Category: Resuscitation

Antidotes (2024)

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by Sarah Alzaabi

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Introduction

An antidote is a specific agent designed to counteract the toxic effects caused by drugs or poisons [1]. These substances play a crucial role in toxicology, as they can effectively mitigate or reverse the harmful consequences of various toxic exposures. In clinical practice, the availability of antidotes is somewhat limited, with only a select number approved for use depending on the type of toxin involved [2].

It’s important to note that antidotes are not administered indiscriminately; instead, they are used based on clearly defined clinical guidelines. Each antidote has specific indications that dictate when it should be given, ensuring that patients receive the appropriate treatment in situations of toxicity. Proper identification of the toxin and the clinical scenario is essential to determine the need for an antidote and to maximize its therapeutic efficacy.

Many poisons have no true antidote, and the poison(s) involved may initially be unknown [3, 4]. Furthermore, limiting the differential diagnosis to poisoning can deter the identification of other pathologies that may exist in these patients [3, 4]. Therefore, the initial approach should be to assess and stabilize [4, 5] thoroughly. Similar to any compromised patient, the attention is directed toward securing the airway, breathing, circulation, and decontamination [4, 5]. There are only a few indications where antidotes are prioritized over cardiopulmonary stabilization, i.e., naloxone for opioid toxicity, cyanide antidotes for cyanide toxicity, and atropine for organophosphate poisoning [5]. Otherwise, most patients will have good outcomes with supportive management and a period of observation [1, 3, 4, 5].

Administration of pharmacologic antagonists may worsen the outcome in some situations and is not recommended [2, 3]. Therefore, the physician should know the indications and contraindications of each antidote [2, 3]. When in doubt, consult a poison control center or a medical or clinical toxicologist [2, 4].
In summary, it’s important to understand that antidotes should be utilized as complementary treatments rather than the sole focus in managing poisoning cases [1]. The primary objective should always be to address the patient’s overall condition, taking into account their symptoms and needs, rather than concentrating exclusively on the specific toxin involved [4]. This approach ensures a more comprehensive and effective care strategy for individuals affected by poisoning.

Pregnant Patients and Antidotes

Limited data is available on the use of antidotes in pregnancy [4]. Hence, the teratogenic potential of antidotes is not fully understood [7]. The general initial management principles are the same, and stabilization of the mother is the priority [6].

The risks and benefits of using or withholding antidotes must be assessed. In general, antidotes are not used for uncertain indications, but proven effective treatments should not be withheld from the mother based on theoretical danger to the fetus [4].

There is no known indication for fetal antidote therapy [7]. However, if an antidote is to be given for fetal benefit, it should be done rapidly in the acute setting [7]. This specifically applies to chelators such as dimercaprol, calcium EDTA, and deferoxamine, which will prevent the toxin from passing into fetal circulation [7].

The following section presents information about various antidotes, organized in alphabetical order.

Antidotes

Atropine

General Information

  • Anticholinergic agent, competitive muscarinic antagonist [3, 4, 5, 8].

Indications

  • Organophosphate poisoning, carbamates, nerve agents [3, 4, 5, 8].

Precautions

  • Excessive doses may cause anticholinergic symptoms [5].

Dose/Administration

  • Adults: Start with 1-2 mg IV, double the dose every 2-3 minutes to reach the goal [3, 4, 5, 8].
  • Children: 0.02 mg/kg IV (minimum of 0.1 mg) [3].

Other Notes

  • Large doses may be required.
  • Goal: Drying of respiratory secretions/improved work of breathing [3, 8].
  • Tachycardia is not the endpoint (atropine helps with muscarinic effects; pralidoxime is used for nicotinic effects) [3, 8].

Calcium

General Information

  • Calcium chloride 10% (1 g/10 mL, 27.2 mg/mL elemental Ca).
  • Calcium gluconate 10% (9 mg/mL elemental Ca), one-third strength of calcium chloride [5].

Indications

  • Calcium channel blocker toxicity, hydrofluoric acid exposure, hyperkalemia, hypermagnesemia [4, 5, 9].

Precautions

  • Calcium chloride extravasation can cause soft tissue necrosis; prefer central line administration [9].
  • Continuous monitoring is recommended [9].

Dose/Administration

  • Adults:
    • Calcium chloride: 0.5-1 g IV (5-10 mL) [5, 9].
    • Calcium gluconate: 1-3 g IV (10-30 mL) [5].
  • Children: 0.15 mL/kg calcium chloride IV [5].
  • IV bolus over 5-10 minutes; repeated doses every 10-20 minutes as needed, guided by serum Ca+ or QT interval [9].
  • Infusion available [9].

Other Notes

  • For HF acid skin burns: Topical 2.5% calcium gel or local injection of calcium gluconate [9].
  • Regional block with intra-arterial or IV calcium gluconate for extremity exposure [9].
  • Nebulized calcium gluconate for HF acid inhalation injury [9].

Cyproheptadine

General Information

  • Antihistaminic and antiserotonergic agent; also has anticholinergic activity [10].

Indications

  • Serotonin syndrome [4, 10].

Dose/Administration

  • Adults: 8 mg every 8 hours for 24 hours (if response observed) [10].
  • Children: 4 mg (not well established) [10].

Deferoxamine

General Information

  • Iron-chelating agent that converts iron to a water-soluble complex for renal clearance [3, 11].

Indications

  • Systemic iron toxicity (e.g., severe gastroenteritis, shock, metabolic acidosis, altered mental status) [3, 4, 11].
  • Iron levels >500 µg/dL or multiple pills on radiography [3, 4, 11].
  • Chronic iron overload [3, 4, 11].

Precautions

  • Hypotension may occur at rapid infusion rates; ensure adequate hydration [3].
  • Cardiac monitoring is needed [11].

Dose/Administration

  • Start with IV infusion: 15 mg/kg/h (maximum 1 g/h) over 6 hours; re-evaluate [3, 11].
  • Infusion rate can be increased in critical patients if blood pressure allows [11].

Other Notes

  • Urine may become rusty-red as iron is excreted [3, 11].

Digoxin Immune Fab

General Information

  • Fab fragments of antibodies to digoxin, reversing cardiotoxic effects [1, 3].

Indications

  • Digoxin overdose with potassium >5 mEq/L after acute ingestion, hemodynamic instability, or life-threatening dysrhythmias [3].
  • Poisoning by other cardiac glycosides (e.g., Oleander) [1, 3, 5, 12].

Precautions

  • Close monitoring of digoxin serum levels, vital signs, and ECG. Resuscitation equipment should be ready [12].

Dose/Administration

  • Acute overdose:
    • Stable patients: 5 vials.
    • Unstable patients: 10-20 vials [3, 5].
  • Chronic overdose: Start with 1-2 vials, repeat after 60 minutes if needed [12].
  • Calculate dose if the ingested dose is known (40 mg Fab binds 0.6 mg digoxin) [3, 5].
  • Bolus in life-threatening conditions (e.g., cardiac arrest) or infusion over 30 minutes, monitoring clinical response [3, 12].

Other Notes

  • For other cardiac glycoside poisoning: Start with 5 vials [3, 12].

Dimercaprol (BAL)

General Information

  • Heavy metal chelator [1, 14].

Indications

  • Severe lead, inorganic arsenic, and mercury poisoning [1, 4, 13].

Precautions

  • Severe adverse effects include nephrotoxicity; consider using EDTA or succimer instead if possible [13].

Dose/Administration

  • 3 mg/kg IM every 4 hours for 48 hours, then every 12 hours for 7-10 days based on clinical response [13].

Ethanol

General Information

  • Blocks formation of toxic metabolites of alcohols [14].

Indications

  • Methanol and ethylene glycol poisoning (second-line to fomepizole) [5, 14].

Precautions

  • Maintain blood ethanol concentration between 100-150 mg/dL [14].

Dose/Administration

  • IV:
    • Loading: 10 mL/kg of 10% ethanol.
    • Maintenance: 1-2 mL/kg/h of 10% ethanol [14].
  • Oral:
    • Loading: 1.8 mL/kg of 43% ethanol.
    • Maintenance: 0.2-0.4 mL/kg/hour of 43% ethanol [14].

Flumazenil

General Information

  • Competitive antagonist of GABA-benzodiazepine receptors [1, 2, 3, 15].

Indications

  • Benzodiazepine overdose (limited role), reversal of procedural sedation, accidental pediatric ingestion [1, 3, 5, 15].

Precautions

  • May cause withdrawal or seizures, especially in benzodiazepine dependence or mixed overdoses [2, 3, 15].

Dose/Administration

  • Adults: 0.2 mg IV over 30 seconds, repeat every minute until reversal (maximum 3 mg) [1, 3, 5, 15].
  • Children: 0.01-0.02 mg/kg, repeat every minute [1, 5, 15].

Other Notes

  • Limited role due to risk of seizures [1, 3, 15].

Fomepizole

General Information

  • Alcohol dehydrogenase inhibitor [1, 3, 16].

Indications

  • Methanol and ethylene glycol toxicity (first-line due to better side effect profile) [1, 3, 5, 16].

Dose/Administration

  • Loading dose: 15 mg/kg IV infusion in 100 mL normal saline or 5% dextrose over 30 minutes [1, 3, 16].
  • Maintenance dose: 10 mg/kg every 12 hours for 48 hours, then 15 mg/kg every 12 hours until alcohol concentrations <20 mg/dL [1, 16].
  • In dialyzed patients: Give every 4 hours or continuous infusion of 1 mg/kg/h [16].

Other Notes

  • Continue therapy until alcohol concentrations are <20 mg/dL and the patient is asymptomatic [3].

Glucagon

General Information

  • Increases cyclic AMP (cAMP).
  • Positive inotropic and chronotropic properties, similar to beta-agonists [18].

Indications

  • β-blocker toxicity (adjunct).
  • Calcium channel blocker toxicity [5, 17, 18].

Precautions

  • Induces vomiting; consider anti-emetics and airway management [18, 19].

Dose/Administration

  • Adults: 5-10 mg IV bolus over 1-2 minutes [5, 18, 19].
  • Children: 0.05-0.1 mg/kg IV [19].

Other Notes

  • If there is a clinical response, start an infusion [18].
  • Intravenous fluids, vasopressors, and high-dose insulin with dextrose are first-line treatments for β-blocker toxicity [19].

Hydroxocobalamin

General Information

  • Precursor of Vitamin B12 [20].

Indications

  • Cyanide toxicity (forms cyanocobalamin by displacing hydroxyl group) [3, 5, 20].

Precautions

  • Safe drug with low side effects.

Dose/Administration

  • Adults: 5 g in 100 mL normal saline IV infusion over 15 minutes; repeat if needed [3, 5, 20].
  • Children: 70 mg/kg IV over 15 minutes (maximum 5 g) [3, 5].

Other Notes

  • Causes orange-red discoloration of skin and urine, resolving within 24-48 hours [3].

Insulin (High Dose)

General Information

  • Strong inotropic effects [21].

Indications

  • Calcium channel blocker and β-blocker toxicity [5, 21].

Precautions

  • Monitor for hypoglycemia, hypokalemia, hypomagnesemia, and hypophosphatemia [21].

Dose/Administration

  • Adults:
    • Glucose 25 g (50 mL of dextrose 50%) IV bolus → 1 IU/kg IV bolus of short-acting insulin → 25 g/h glucose and 0.5-1 IU/kg/h short-acting insulin infusion [21].
  • Titrate glucose to maintain levels between 6-8 mmol/L [21].

Intravenous Lipid Emulsion

General Information

  • 20% lipid emulsion as a parenteral nutrient.
  • Expands the lipid compartment within the intravascular space, sequestering lipid-soluble drugs from tissues [1, 5].

Indications

  • Overdose by drugs with high protein binding and large volume of distribution, e.g., local anesthetics (bupivacaine), β-blockers, and calcium channel blockers [1, 5].

Dose/Administration

  • Adults: 100 mL IV bolus over 1 minute (repeat every 5 minutes, maximum 2 doses) → 18 mL/min IV infusion for 20 minutes [5].
  • Children: 1.5 mL/kg IV bolus over 1 minute (repeat every 5 minutes, maximum 2 doses) → 0.25 mL/kg/min IV infusion for 20 minutes [5].

Methylene Blue

General Information

  • Reduces methemoglobin (MetHb) to hemoglobin [5, 22].

Indications

  • Symptomatic methemoglobinemia.
  • MetHb levels >20% in asymptomatic patients.
  • Oxidizing toxins (e.g., nitrites, benzocaine, sulfonamides) [5, 22].

Precautions

  • Pulse oximetry is unreliable in methemoglobinemia.
  • May cause hemolysis in G6PD deficiency [3, 22].

Dose/Administration

  • 1-2 mg/kg slow IV injection over 5 minutes; may repeat after 30-60 minutes [5, 22].

Other Notes

  • Monitor MetHb levels frequently until a consistent decrease is observed [22].

N-acetylcysteine (NAC)

General Information

  • Prevents hepatocellular injury by restoring glutathione stores, which conjugate the toxic metabolite NAPQI [1, 3, 23].

Indications

  • Serum acetaminophen levels above toxic threshold (>4 hours after ingestion).
  • Single ingestion >150 mg/kg.
  • Evidence of liver injury [1, 3, 4, 23].

Dose/Administration

  • Oral: 140 mg/kg loading dose → 70 mg/kg every 4 hours for 17 doses [1, 3, 23].
  • IV: 150 mg/kg in 200 mL of 5% dextrose over 60 minutes → 50 mg/kg diluted in 500 mL of 5% dextrose over 4 hours → 100 mg/kg diluted in 1000 mL of 5% dextrose over 16 hours [1, 3, 23].

Other Notes

  • Oral therapy may not be well tolerated due to taste and odor [23].

Naloxone

General Information

  • Opioid antagonist, diagnostic, and therapeutic agent [1, 2, 3].

Indications

  • Opioid toxicity with respiratory and CNS depression [1, 2, 3, 5].

Precautions

  • Re-sedation may occur due to naloxone’s short half-life; monitor for at least 4 hours.
  • Withdrawal in chronic/opioid-dependent users [1, 2, 3].

Dose/Administration

  • Adults: 0.4-2 mg IV; repeat every 2-3 minutes up to a maximum of 10 mg [1, 2, 3].
  • Children: 0.01 mg/kg IV [1, 3].

Other Notes

  • Goal: Adequate respiratory rate, normal oxygen saturation on room air, improved level of consciousness [3, 5].
  • Miosis is an unreliable indicator [5].

Octreotide

General Information

  • Synthetic analogue of somatostatin [24].

Indications

  • Hypoglycemia secondary to sulfonylurea [24].

Precautions

  • Breakthrough hypoglycemia may occur [24].

Dose/Administration

  • Adults:
    • 50 µg IV bolus → 25 µg/h infusion.
    • Alternatively, 100 µg IM or SC every 6 hours [24].
  • Children: 1 µg/kg IV bolus or SC → 1 µg/kg/h IV infusion [24].

Other Notes

  • Euglycemia needs to be maintained for 12 hours off the infusion before the patient is medically cleared [24].

Physostigmine

General Information

  • Reversible acetylcholinesterase inhibitor [25].

Indications

  • Neurological anticholinergic symptoms, e.g., delirium and seizures (crosses the blood-brain barrier) [5, 25].

Precautions

  • Contraindicated in bradycardia, AV block, and bronchospasm [25].

Dose/Administration

  • Adults: 0.5-1 mg slow IV push over 5 minutes; repeat in 10-30 minutes if needed [25].
  • Children: 0.02 mg/kg IV (maximum dose of 0.5 mg) [25].

Other Notes

  • Confirm absence of conduction defects on a 12-lead ECG before administration.
  • Rapid administration may cause a cholinergic crisis; treat with atropine if this occurs [25].

Pralidoxime

General Information

  • Reactivates acetylcholinesterase inhibition [1, 3, 26].

Indications

  • Early organophosphate poisoning (<2 hours).
  • Nerve agents [1, 3, 5, 26].

Precautions

  • Rapid administration can cause laryngospasm, muscle rigidity, and transient respiratory impairment [3].

Dose/Administration

  • Adults: 1-2 g IV in 100 mL of 0.9% saline over 15-30 minutes → 500 mg/h IV infusion [3, 26].
  • Children: 25-50 mg/kg → 10-20 mg/kg/h infusion [3, 26].

Other Notes

  • Administer in the early phase before irreversible acetylcholinesterase binding occurs.
  • Adequate atropine doses should be given concurrently [1, 3, 26].

Pyridoxine (Vitamin B6)

General Information

  • Vitamin B6, essential for GABA production [3, 27].

Indications

  • Isoniazid, hydrazine, and Gyromitra poisoning.
  • Ethylene glycol poisoning (adjunct therapy) [3, 5, 27].

Dose/Administration

  • Adults:
    • For isoniazid poisoning: 1 g per gram of ingested isoniazid, given as 0.5 g/min infusion until seizures stop. If unknown, give 5 g IV empirically [3, 5, 27].
  • Children: 70 mg/kg IV, maximum 5 g [5, 27].

Other Notes

  • For ethylene glycol toxicity: 50 mg IV every 6 hours [27].

Sodium Bicarbonate

General Information

  • Hyperosmolar sodium bicarbonate injection [28].

Indications

  • Cardiotoxicity due to fast sodium channel blockade presenting as QRS widening and ventricular dysrhythmias (e.g., TCA poisoning).
  • Urine alkalinization [2, 5, 28].

Precautions

  • Monitor for hypokalemia and hypernatremia.
  • Maintain serum pH between 7.50-7.55 [28].

Dose/Administration

  • Start with 1-2 mEq/kg IV over 1-2 minutes → 0.3 mEq/kg per hour IV infusion if needed [5].
  • Repeated doses may require intubation and hyperventilation to maintain pH >7.5-7.55 [28].

Sodium Calcium Edetate (EDTA)

General Information

  • IV heavy metal chelator [29].

Indications

  • Severe lead toxicity with lead levels >70 µg/dL [29].

Precautions

  • Risk of nephrotoxicity, ECG changes, and transaminitis.
  • Hospital admission required [29].

Dose/Administration

  • Dilute 25-50 mg/kg in 500 mL of 0.9% saline or 5% dextrose; infuse over 24 hours, starting 4 hours after the first dose of dimercaprol [29].
  • In encephalopathy, continuous infusion for 5 days until stabilization [29].

Other Notes

  • Once clinically improved, switch to oral succimer if tolerated [29].

Sodium Thiosulfate

General Information

  • Assists the body in detoxifying cyanide [1, 30].

Indications

  • Cyanide poisoning [1, 5, 30].

Precautions

  • In severe cases, use with other antidotes (e.g., hydroxocobalamin) [30].

Dose/Administration

  • Adults: 50 mL of 25% solution (12.5 g; 1 ampoule) IV over 10 minutes [1, 5, 30].
  • Children: 1.65 mL/kg IV; repeat after 30 minutes if clinically indicated [30].

Succimer (DMSA)

General Information

  • Oral heavy metal chelator [31].

Indications

  • Symptomatic lead poisoning.
  • Asymptomatic lead poisoning with lead levels >60 µg/dL in adults or >45 µg/dL in children [5, 31].

Precautions

  • Reversible neutropenia, gastrointestinal upset, and liver function abnormalities [31].

Dose/Administration

  • 10 mg/kg three times a day for 1 week → two times a day for 2 weeks [31].

Other Notes

  • Monitor serum lead levels during treatment [31].

Antidotes play a crucial role in managing toxicological emergencies in the emergency department. While their use is often specific and limited, they provide life-saving interventions in cases of confirmed poisonings such as opioid overdoses, cyanide poisoning, or organophosphate exposure. However, their administration requires careful assessment of indications, contraindications, and potential adverse effects. Emergency clinicians must prioritize stabilizing airway, breathing, and circulation before considering antidote administration, except in scenarios where antidotes are critical to immediate survival. The decision to use an antidote should be guided by clinical judgment, toxicology consultation, and evidence-based guidelines. Ultimately, antidotes should be viewed as adjunctive therapies, emphasizing the principle of treating the patient comprehensively rather than focusing solely on the poison.

Author

Picture of Sarah Alzaabi

Sarah Alzaabi

Sarah Alzaabi, MD is a graduate from the United Arab Emirates University. She is currently a medical intern at Sheikh Shakhbout Medical City, Abu Dhabi, with a longstanding interest in Emergency Medicine. She is a big advocate for the FOAMed movement; and is proud to be a part of the fantastic team at iEM. She is excited to develop innovative ways to provide accessible education for anyone in need. Sarah has a particular interest in lifestyle and nutrition and spends time learning about how to educate others about succeeding in medicine while maintaining a healthy lifestyle.

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References

  1. Chacko B, Peter JV. Antidotes in Poisoning. Indian J Crit Care Med. 2019;23(Suppl 4):S241-S249. doi:10.5005/jp-journals-10071-23310
  2. Erickson TB, Thompson TM, Lu JJ. The Approach to the Patient with an Unknown Overdose. Emerg Med Clin N Am. 2007;25(2):249-81.
  3. Holstege CP, Dobmeier SG, Bechtel LK. Critical care toxicology. Emerg Med Clin North Am. 2008;26(3):715-39.
  4. Nelson LS, Howland M, Lewin NA, Smith SW, Goldfrank LR, Hoffman RS. Principles of Managing the Acutely Poisoned or Overdosed Patient. In: Nelson LS, Howland M, Lewin NA, Smith SW, Goldfrank LR, Hoffman RS. eds. Goldfrank’s Toxicologic Emergencies, 11e. McGraw Hill; 2019. Accessed March 04, 2023. https://accessemergencymedicine-mhmedical-com.uaeu.idm.oclc.org/content.aspx?bookid=2569&sectionid=210267250
  5. Greene S. General Management of Poisoned Patients. Tintinalli’s Emergency Medicine. 8 ed: MC Graw Hill; 2014. p. 1207.
  6. Gei AF, Suarez VR. Poisoning in Pregnancy. In: Foley MR, Strong, Jr TH, Garite TJ. eds. Obstetric Intensive Care Manual, 5e. McGraw Hill; . Accessed March 04, 2023. https://obgyn-mhmedical-com.uaeu.idm.oclc.org/content.aspx?bookid=2379&sectionid=185993887
  7. Bailey, B. (2003), Are there teratogenic risks associated with antidotes used in the acute management of poisoned pregnant women?. Birth Defects Research Part A: Clinical and Molecular Teratology, 67: 133-140. https://doi-org.uaeu.idm.oclc.org/10.1002/bdra.10007
  8. Long N. Atropine. Life in the Fast Lane. https://litfl.com/atropine/. Published November 3, 2020. Accessed March 23, 2023.
  9. Long N. Calcium. Life in the Fast Lane. https://litfl.com/calcium/. Published November 3, 2020. Accessed March 23, 2023.
  10. Long N. Cyproheptadine. Life in the Fast Lane. https://litfl.com/cyproheptadine/. Published November 3, 2020. Accessed March 23, 2023.
  11. Long N. Desferrioxamine. Life in the Fast Lane. https://litfl.com/desferrioxamine/. Published November 3, 2020. Accessed March 23, 2023.
  12. Long N. Digoxine Immune Fab. Life in the Fast Lane. https://litfl.com/digoxin-immune-fab/. Published November 3, 2020. Accessed March 23, 2023.
  13. Long N. Dimercarpol. Life in the Fast Lane. https://litfl.com/dimercaprol/. Published November 3, 2020. Accessed March 23, 2023.
  14. Long N. Ethanol. Life in the Fast Lane. https://litfl.com/ethanol/. Published November 3, 2020. Accessed March 23, 2023.
  15. Long N. Flumazenil. Life in the Fast Lane. https://litfl.com/flumazenil/. Published November 3, 2020. Accessed March 23, 2023.
  16. Long N. Fomepizole. Life in the Fast Lane. https://litfl.com/fomepizole/#:~:text=Fomepizole%20is%20an%20alcohol%20dehydrogenase,methanol%20and%20ethylene%20glycol%20poisoning. Published June 15, 2021. Accessed March 23, 2023.
  17. Long N. Glucagon. Life in the Fast Lane. https://litfl.com/glucagon/. Published November 3, 2020. Accessed March 24, 2023.
  18. Nickson C. Glucagon Therapy. Life in the Fast Lane. https://litfl.com/glucagon-therapy/. Published November 3, 2020. Accessed March 24, 2023.
  19. Atlantic Canada Poison Centre. https://atlanticcanadapoisoncentre.ca/glucagon-pediatric.html. Published March 2017. Accessed March 30, 2023.
  20. Long N. Hydroxocobalamin. Life in the Fast Lane. https://litfl.com/hydroxocobalamin/. Published November 3, 2020. Accessed March 24, 2023.
  21. Long N. Insulin (High dose). Life in the Fast Lane. https://litfl.com/insulin-high-dose/. Published November 3, 2020. Accessed March 24, 2023.
  22. Long N. Methylene Blue. Life in the Fast Lane. https://litfl.com/methylene-blue/. Published November 3, 2020. Accessed March 24, 2023.
  23. Long N. N-acetylcysteine. Life in the Fast Lane. https://litfl.com/n-acetylcysteine/#:~:text=Acetylcysteine%20is%20the%20most%20widely,of%20NAPQI%20(toxic%20paracetamol%20metabolite. Published November 3, 2020. Accessed March 24, 2023.
  24. Long N. Octreotide. Life in the Fast Lane. https://litfl.com/octreotide/. Published November 3, 2020. Accessed March 24, 2023.
  25. Long N. Physostigmine. Life in the Fast Lane. https://litfl.com/physostigmine/. Published November 3, 2020. Accessed March 24, 2023.
  26. Long N. Pralidoxime. Life in the Fast Lane. https://litfl.com/pralidoxime/#:~:text=This%20is%20the%20oxime%20commonly,and%20the%20OP%2FCarbamate%20involved. Published November 3, 2020. Accessed March 24, 2023.
  27. Long N. Pyridoxine. Life in the Fast Lane. https://litfl.com/pyridoxine/. Published November 3, 2020. Accessed March 24, 2023.
  28. Long N. Sodium Bicarbonate. Life in the Fast Lane. https://litfl.com/sodium-bicarbonate/. Published November 27, 2022. Accessed March 24, 2023.
  29. Long N. Sodium Calcium edetate. Life in the Fast Lane. https://litfl.com/sodium-calcium-edetate/#:~:text=Sodium%20Calcium%20Edetate%20(EDTA)%20is,3.38%20micro%20mol%2FL). Published November 3, 2020. Accessed March 24, 2023.
  30. Long N. Sodium thiosulphate. Life in the Fast Lane. https://litfl.com/sodium-thiosul phate/#:~:text=Sodium%20thiosulfate%20enhances%20the%20endogenous,hydroxocobalamin%20in%20severe%20cyanide%20toxicity.Published November 3, 2020. Accessed March 24, 2023.
  31. Long N. Succimer. Life in the Fast Lane. https://litfl.com/succimer/#:~:text=Succimer%20(DMSA)%20is%20an%20orally,2.9%20micro%20mol%2FL). Published November 3, 2020. Accessed March 24, 2023.

Reviewed and Edited By

Picture of Arif Alper Cevik, MD, FEMAT, FIFEM

Arif Alper Cevik, MD, FEMAT, FIFEM

Prof Cevik is an Emergency Medicine academician at United Arab Emirates University, interested in international emergency medicine, emergency medicine education, medical education, point of care ultrasound and trauma. He is the founder and director of the International Emergency Medicine Education Project – iem-student.org, chair of the International Federation for Emergency Medicine (IFEM) core curriculum and education committee and board member of the Asian Society for Emergency Medicine and Emirati Board of Emergency Medicine.

Seizure (2024)

~ iEM Education Project Team ~ Leave a comment

by Ardi Knobel Mendoza, Danielle Charles-Chauvet, Erik J. Blutinger

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Introduction

Seizures are caused by abnormal cortical neuronal activity that manifests as changes in alertness or neurological symptoms. While seizures account for only 1% of all emergency department (ED) visits and 3% of prehospital transports, their potential for significant morbidity undermines the importance of rapid assessment and treatment in emergency settings [1]. The etiology of seizures varies by age group, with the most common causes being fever in infants and metabolic derangements or structural abnormalities in adults over 75. This chapter will explore various seizure presentations, diagnostic assessment tools, and considerations for treatment and disposition decisions in the ED.

You have a new patient!

A 24-year-old female presents to the emergency room after being found on the street. She is minimally responsive, alert, and oriented only to herself. Her heart rate is 87 bpm, blood pressure is 141/94 mmHg, respiratory rate is 14 bpm, and she is afebrile, with oxygen saturation of 99% on room air. She has a gravid uterus with a fundal height of approximately 29 cm (11.4 inches) but is otherwise atraumatic.

a-photo-of-a-24-year-old-female (image was produced by using ideogram 2.0)

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Seizure Presentation and Classification

It is essential to investigate the cause and categorize the type of seizure after an acute episode to inform the diagnostic and treatment plan. Seizures are often classified as provoked, which occur within 7 days of a neurologic, metabolic, or infectious precipitator, or unprovoked, which has no association with an inciting factor. A history of seizures, febrile illness, malignancy, new medications, recreational drug use, or pregnancy can help to elucidate this. A complete neurological examination, which includes an assessment of mental status, should be performed as an altered postictal state follows most primary seizures. In addition to a change in mental status, the postictal state can present as motor deficits or paresis. Postictal paresis suggests a structural lesion as the cause of the seizure and should prompt cranial imaging [2]. Given that seizures are a manifestation of cortical neuronal activity, the extent of cortical involvement can lead to various symptoms at presentation [3].

Partial seizures involve only some of the cortex. They are classified as either simple, in which the patient is alert throughout, or complex, in which the patient has decreased alertness. Seizures can also begin as partial seizures, involving only some of the cortex, and spread to involve the entire cortex. Seizures involving the entire cortex are termed “generalized” seizures, resulting in decreased alertness. Generalized seizures are further classified based on their physical manifestations:

Absence Seizure: no collapse, automatisms (blinking, staring, lip smacking)

Tonic-clonic Seizure: collapse with stiff non-rhythmic convulsive movements.

Atonic Seizure: collapse without convulsions (similar to syncope) [4].

Febrile seizures typically occur in children 6 months-6 years of age with fevers greater than 38℃ and no neurological infection. 80% of febrile seizures are tonic-clonic in presentation, self-limiting, and do not recur after resolution of the inciting fever [5].

Eclamptic seizures are typically tonic-clonic in presentation and are considered unstable, as they carry significant mortality risk to the mother and fetus. Therefore, any pregnant patient with altered mental status and hypertension, identified as systolic >140 or diastolic >90, should be assessed for eclampsia. In cases with high suspicion of preeclampsia or eclamptic seizures, patients should be treated with magnesium for seizure prophylaxis [6].

Psychogenic seizures present similarly to generalized tonic-clonic seizures but are not associated with cortical neuronal derangements. In the ED, it is difficult to differentiate these seizures from neurogenic seizures, as there is limited access to EEG. However, psychogenic seizures present with more rhythmic and symmetric movements, patients are typically completely aware and conversant throughout, and there is no postictal state.

It is important to consider the duration of a seizure episode in all patients. Most seizures last from 30 seconds to 2 minutes. Seizures lasting longer than 5 minutes meet the criteria for status epilepticus. These patients are considered unstable, as prolonged seizure activity is associated with an increased risk of permanent brain damage. Not all patients with status epilepticus have convulsive seizures, so it is important to assess for subtle symptoms of seizure activity in the unresponsive patient, as they may have non-convulsive status epilepticus—a medical emergency.

Medical History

Thorough history taking in patients with seizure disorders is crucial for accurate diagnosis and effective management. This process involves a structured yet flexible approach to gathering relevant information, ensuring that all aspects of the patient’s condition are considered. Key components of this history include the patient’s medical background, seizure characteristics, and psychosocial factors.

Key Components of History Taking

  • Presenting Complaints: Document the chief complaints, including the nature, frequency, and duration of seizures [7].
  • Seizure Onset and Triggers: Investigate the age of onset, potential triggers (e.g., photosensitivity), and environmental factors that may provoke seizures [8].
  • Medical and Family History: Collect information on past medical history, family history of seizures or neurological disorders, and any relevant social history [7,9].
  • Psychosocial Aspects: Assess the impact of seizures on the patient’s daily life, including emotional and social challenges [8].

A comprehensive history-taking process in seizure patients is crucial for accurate diagnosis and effective management of various seizure types. By gathering essential information regarding seizure semiology, triggers, and patient-specific factors, clinicians can develop tailored treatment strategies to improve outcomes. Seizure semiology, for example, provides valuable insights into the nature of seizures, helping to classify them as either focal or generalized [10]. Detailed accounts of auras and observable signs can further indicate the anatomical origins of seizures, guiding appropriate diagnostic testing [10]. Additionally, identifying seizure triggers, such as environmental factors or specific stimuli, plays a vital role in both diagnosis and management. For instance, patients with photosensitivity may require targeted questions to uncover visual triggers that provoke seizures [8]. Together, these aspects of thorough history-taking form the foundation for effective and personalized seizure management.

When conducting history-taking in patients with seizure disorders, clinicians must be mindful of several common pitfalls that can lead to misdiagnosis or ineffective treatment. These issues often arise from inadequate questioning, overemphasizing certain symptoms, and neglecting the broader context of the patient’s experiences.

Inadequate history-taking, such as missing or incomplete accounts from witnesses, can result in misinterpreting seizure types [11]. Failing to gather detailed descriptions of seizure events, including pre-ictal and post-ictal states, may further obscure the diagnosis [12].

Additionally, an overemphasis on specific symptoms, such as those associated with focal seizures, may mislead clinicians, as these symptoms do not always correlate with the seizure type [13].

Another critical factor is the neglect of contextual elements, such as environmental triggers, which may result in missed diagnoses of reflex seizures, especially in photosensitive patients [8]. Furthermore, ignoring psychosocial aspects and the patient’s overall health can complicate the understanding of seizure disorders [14]. While advancements in technology and neuroimaging provide valuable objective data, the art of listening and thorough history-taking remains an irreplaceable cornerstone in the diagnostic process.

While a comprehensive history is essential, it is also important to recognize that some patients may present atypically, necessitating a tailored approach to history taking that considers individual circumstances and variations in symptom presentation.

Physical Examination

A comprehensive physical examination for patients presenting with seizures in the emergency department is essential for accurate diagnosis and effective management. Key components include a thorough neurological assessment, which involves evaluating consciousness, motor function, and sensory responses to identify any neurological deficits [15]. Monitoring vital signs is equally critical, as instability such as hypotension or tachycardia may indicate underlying issues requiring immediate attention [16]. Additionally, a systematic head-to-toe physical examination can help identify signs of trauma or systemic illness that may contribute to seizure activity [15].

In the emergency department, recognizing physical examination findings indicative of a severe or prolonged seizure episode is critical for timely diagnosis and management, particularly in cases of status epilepticus or non-convulsive seizures. Altered mental status, characterized by confusion, disorientation, or a prolonged postictal state, is a key finding that can suggest non-convulsive status epilepticus (NCSE) [17]. Neurological signs, such as subtle twitching, blinking, or fluctuating sensorium, may also indicate ongoing seizure activity [17]. In cases of generalized tonic-clonic seizures (GTCS), convulsive activity manifests with muscle rigidity and jerking movements, making it a more apparent diagnosis [18]. Additionally, focal seizures can result in specific neurological deficits, which may be misinterpreted as other neurological conditions. While these findings are crucial for identifying severe seizure episodes, it is important to acknowledge that some patients may present with atypical symptoms or lack overt signs of seizure activity, complicating the diagnostic process [17].

While the value of a comprehensive examination cannot be overstated, it is also important to recognize that some patients may present with atypical symptoms or underlying conditions that complicate the diagnosis. This highlights the need for a tailored approach to each case, ensuring that individual factors are carefully considered [16].

Alternative Diagnoses

The diagnosis of seizures primarily relies on the patient’s clinical history, with particular emphasis on accounts provided by witnesses. This is especially important because many seizure types involve impaired consciousness, leaving patients unaware of their episodes. Clinical findings can be supported by interictal electroencephalogram (EEG) abnormalities, although it is essential to note that such abnormalities may also occur in healthy individuals and their absence does not rule out epilepsy. It is equally critical to differentiate seizures from other conditions that may present similarly. These include syncope, such as cardiac arrhythmias or vasovagal episodes; metabolic disturbances like hypoglycemia or hyponatremia; and vascular events such as transient ischemic attacks. Additionally, migraine auras, sleep disorders like narcolepsy or night terrors, movement disorders such as paroxysmal dyskinesia, and gastrointestinal conditions like esophageal reflux in neonates and infants can mimic seizures. Psychiatric conditions, including conversion disorders, panic attacks, malingering, or episodes driven by secondary gain, must also be considered [19].

Acing Diagnostic Testing

When considering diagnostic testing such as labs and imaging, there is a lack of consensus on a set of tests required for all seizing patients. Rather, the diagnostic workup for a patient presenting with a seizure depends on a variety of factors, such as the suspected etiology of the seizure and whether the patient has a known seizure disorder or is presenting with a first-time seizure [20]. In patients with known seizure disorders, it is generally accepted test for levels of the anti-epileptic drug (AED) the patient takes, such as levetiracetam, phenytoin, carbamazepine, phenobarbital, or valproic acid. However, levels can often take hours to days to result or may not be available at a certain facility. In patients without a known seizure disorder, or if there is concern for an etiology for a seizure besides breakthrough from AED treatment, a more extensive workup is warranted. Basic testing should include a finger stick glucose, a urine or serum pregnancy test, and serum chemistry, including calcium and magnesium. Urine/serum toxicologies can also be obtained if there is concern for potential toxic ingestion as a cause. A lactic acid can be obtained, which should be markedly elevated immediately after the seizure and normalize after an hour of seizure onset [21].

A Computed Tomography (CT) Head should be obtained in all first-time seizure patients to assess for a structural lesion such as a mass, a bleed either as the etiology or sequelae of the seizure, or signs of an infection. Seizure sequelae such as significant head trauma can also be assessed with CT imaging to look for a large hematoma or skull fracture in patients who fail to return to baseline mental status after a seizure [22]. Magnetic Resonance Imaging (MRI) can be considered to reveal other diagnoses such as a brain abscess or central vascular event such as infarction; however, this imaging modality is often less available in the emergency setting and may require admission vs. outpatient referral to obtain an image [23]. Electroencephalography (EEG)is when diagnostic testing such as labs and imaging is considered, but there is a lack of consensus on a set of tests required for all seizing patients. Rather, the diagnostic workup for a patient presenting with a seizure depends on a variety of factors, such as the suspected etiology of the seizure and whether the patient has a known seizure disorder or is presenting with a first-time seizure [20]. In patients with known seizure disorders, it is generally accepted test for levels of the anti-epileptic drug (AED) the patient takes, such as levetiracetam, phenytoin, carbamazepine, phenobarbital, or valproic acid. However, levels can often take hours to days to result or may not be available at a certain facility. In patients without a known seizure disorder, or if there is concern for an etiology for a seizure besides breakthrough from AED treatment, a more extensive workup is warranted. Basic testing should include a finger stick glucose, a urine or serum pregnancy test, and a serum chemistry, including calcium and magnesium. Urine/serum toxicologies can also be obtained if there is concern for potential toxic ingestion as a cause. A lactic acid can be obtained, which should be markedly elevated immediately after the seizure and normalize after an hour of seizure onset [21].

A Computed Tomography (CT) Head should be obtained in all first-time seizure patients to assess for a structural lesion such as a mass, a bleed either as the etiology or sequelae of the seizure, or signs of an infection. Seizure sequelae such as significant head trauma can also be assessed with CT imaging to look for a large hematoma or skull fracture in patients who fail to return to baseline mental status after a seizure [22]. Magnetic Resonance Imaging (MRI) can be considered to reveal other diagnoses such as a brain abscess or central vascular event such as infarction; however, this imaging modality is often less available in the emergency setting and may require admission vs. outpatient referral to obtain an image [23]. Electroencephalography (EEG)is an important study in patients who are continuing to have seizures without clear signs of convulsions, such as in nonconvulsive status epilepticus (NCSE), patients with persistent altered mental status, or intubated patients. EEGs are often unavailable in the emergency setting but have a role in the inpatient or ICU settings with neurology consultants [24]. ECGs should also be considered in patients with new-onset seizures to exclude cardiac conduction disorders that can cause seizure-like activity, such as syncope, Brugada syndrome, or QTc prolongation or shortening.

Risk Stratification

The presence of comorbidities plays a critical role in the risk stratification, prognosis, and management of epilepsy, highlighting the need for a holistic approach to patient care. In the emergency department, recognizing these comorbidities is crucial for tailoring immediate interventions and ensuring acute and comprehensive follow-up care. Studies reveal that 60-70% of adults and 80% of children with epilepsy experience multimorbidity [25]. Among patients with senile epilepsy, 81% have at least one comorbidity, with neurological (61%) and cardiovascular (45%) conditions being the most prevalent [26]. Emergency clinicians must remain vigilant for these conditions, as they may exacerbate seizure episodes or complicate acute management. These comorbidities significantly impact seizure outcomes, as patients with neurological and psychiatric disorders face a higher risk of recurrent seizures and reduced likelihood of achieving seizure freedom [26]. Conditions like depression and anxiety are particularly associated with a more severe course of epilepsy [27], and their identification in the emergency setting can guide referrals for further psychiatric evaluation. Additionally, multimorbidity is linked to lower health-related quality of life and increased healthcare costs due to frequent hospitalizations [25]. Cognitive and psychiatric comorbidities often impair daily functioning more than the seizures themselves [28], necessitating a multidisciplinary approach starting from the emergency department. Addressing these comorbidities, however, has been shown to improve overall health outcomes and enhance the quality of life for patients, emphasizing the importance of comprehensive, patient-centered care [28].

Management

The most important intervention in a patient actively seizing is ensuring adequate brain oxygenation. The airway should be protected via maneuvers that include rolling the patient on their side, jaw thrusts, applying a nasopharyngeal airway, applying supplemental oxygen, and preventing aspiration with suction as needed. Oxygenation status should be monitored with continuous pulse oximetry and capnography when possible.

Providers should also anticipate the impending decompensation of the clinical course and the need for intubation by preparing airway equipment, medications, and IV access, which will be discussed later in the chapter. Along with oxygenation, patients must be protected from injury, e.g., from falling out of bed and preventing trauma.

Most seizures stop on their own within one to two minutes of onset, but the longer the seizure lasts, the less likely it is to stop on its own and can become self-sustaining.

Seizures that are continuous or intermittent, lasting more than 5 minutes without recovery of consciousness, are known as status epilepticus. Medical therapies to terminate a seizure are divided into three stages based on escalation of need and inability to terminate the seizure.

Benzodiazepines are considered first-line agents in terminating seizures, followed by second-line agents such as Levetiracetam, Valproate, Phenytoin, and Fosphenytoin [29]. The third-line medications are infusions of benzodiazepines, propofol, or barbiturates, prepared for likely intubation with paralytics and continued infusions [30].

The following lists these medications by stage, dose, and considerations [31, 32]:

Midazolam (1st Line Agent – Benzodiazepine)

  • Loading Dose:
    • 10 mg IM or 0.1-0.2 mg/kg IV.
  • Maintenance Dose: 0.001 mg/kg/min.
  • Pediatric Dose:
    • IV or IN: 0.2 mg/kg (max 5 mg).
    • IM:
      • <13 kg: 0.2 mg/kg.
      • 13-39 kg: 5 mg.
      • 39 kg: 10 mg.
  • Considerations:
    • IM dosing can be used if no IV is established.
    • Acts faster than Lorazepam but has a shorter duration.
    • May cause respiratory depression and hypotension.

Diazepam (1st Line Agent – Benzodiazepine)

  • Loading Dose: 10 mg over 2 minutes. Repeat every 5-10 minutes to a max of 30 mg.
  • Maintenance Dose: N/A.
  • Pediatric Dose: 0.15 mg/kg IV.
  • Considerations:
    • May cause respiratory depression and hypotension.

Levetiracetam (2nd Line Agent)

  • Loading Dose: 60 mg/kg (up to a max of 4,500 mg), infused over 10 minutes.
  • Maintenance Dose: Same as the loading dose.
  • Pediatric Dose: Same as loading dose.
  • Considerations:
    • If the patient weighs >75 kg, the dose is 4.5 g.
    • If seizures stop, continue to give Levetiracetam to prevent recurrence.

Phenytoin (2nd Line Agent)

  • Loading Dose: 18-20 mg/kg with a max rate of 50 mg/min.
  • Maintenance Dose: N/A.
  • Pediatric Dose: N/A.
  • Considerations:
    • Cardiac monitoring is necessary for QRS complex widening.

Fosphenytoin (2nd Line Agent)

  • Loading Dose: 15-20 mg/kg with a max rate of 150 mg/min.
  • Maintenance Dose: Same as loading dose.
  • Pediatric Dose: N/A.
  • Considerations:
    • Cardiac monitoring is necessary for QRS complex widening.

Valproate (2nd Line Agent)

  • Loading Dose: 20-40 mg/kg over 10 minutes. Repeat if needed.
  • Maintenance Dose: Same as loading dose.
  • Pediatric Dose: Same as loading dose.
  • Considerations: N/A.

Propofol (3rd Line Agent)

  • Loading Dose: 1-2 mg/kg IV over 5 minutes (max load 10 mg/kg).
  • Maintenance Dose: 50-80 mcg/kg/min (3-5 mg/kg/hr) as an infusion.
  • Pediatric Dose: N/A.
  • Considerations:
    • May cause respiratory depression and hypotension.

Phenobarbital (3rd Line Agent)

  • Loading Dose: 10-15 mg/kg bolus up to 60 mg/min.
  • Maintenance Dose: 120-240 mg every 20 minutes.
  • Pediatric Dose: N/A.
  • Considerations: N/A.

Midazolam (for 3rd Line use) (3rd Line Agent)

  • Loading Dose: 0.2 mg/kg IV.
  • Maintenance Dose: 0.1-2 mg/kg/hr.
  • Pediatric Dose: N/A.
  • Considerations:
    • Can be used in patients with hypotension.

Once the provider considers 3rd line medications and starting infusions, they should prepare for intubation as the patient is likely in status epilepticus, requiring continued medication and airway protection. Induction medications for intubation are often the same medications listed above in the 3rd stage of treatment, such as propofol or midazolam, and can be on board before paralytics. Paralytics are used to stop the seizure-like activity and aid in intubation, but it is important to remember that they are not meant to terminate the seizure. Patients can still have seizures despite the lack of tonic-clonic seizure activity such as NCSE. Rocuronium is the preferred paralytic agent as it is not associated with the hyperkalemia seen in succinylcholine, which is a risk for patients seizing for an extended period who could develop rhabdomyolysis. Rocuronium paralysis lasts much longer, which should be a consideration when monitoring for further seizures with EEG.

Finally, other conditions can cause seizures or seizure-like activity that require their own treatment strategies, which are discussed below:

Eclampsia, a life-threatening condition often associated with pregnancy, is treated with magnesium to control seizures, benzodiazepines for acute management, and blood pressure control to address underlying hypertension. For seizures due to isoniazid toxicity, the recommended treatment is pyridoxine (vitamin B6), which counteracts the drug’s neurotoxic effects. In cases of hypoglycemia, seizures can be managed by administering Dextrose 50% in Water (D50W) to restore blood glucose levels rapidly. Hypocalcemia, another potential seizure trigger, requires the administration of calcium gluconate or calcium chloride to normalize calcium levels. For seizures induced by hyponatremia, 3% hypertonic saline is used to increase serum sodium levels safely.

In cases of toxicity from aspirin, tricyclic antidepressants (TCAs), or lithium, hemodialysis is indicated to effectively remove the offending agents from the bloodstream. For seizures caused by meningitis, prompt initiation of appropriate antibiotics is critical to address the underlying infection and prevent further complications.

Special Patient Groups

Pediatrics

Seizures in pediatric patients can present with diverse etiologies ranging from febrile seizures to more serious underlying conditions such as intracranial infections, metabolic disturbances, or congenital disorders. In children under 5, febrile seizures are the most common cause of convulsions and are generally self-limited, though they require careful differentiation from more serious causes like meningitis or encephalitis. Clinical reasoning should prioritize a detailed history, including the onset of the seizure, vaccination status, and any family history of epilepsy or neurodevelopmental disorders. Laboratory tests and imaging may be indicated if there is a high suspicion of an underlying structural or metabolic issue, such as in children with a prolonged postictal state or a first-time seizure without a clear precipitant. In the emergency department (ED), rapid assessment of the child’s airway, breathing, and circulation (ABCs) is paramount, along with ensuring the seizure is appropriately controlled, often with medications like lorazepam or diazepam. Close follow-up is necessary to assess for recurrent seizures or potential neurological sequelae.

Geriatrics

Seizures in elderly patients often present a diagnostic challenge due to the overlap with other common age-related conditions, such as syncope, transient ischemic attacks (TIA), or dementia-related behavioral changes. In this population, new-onset seizures should prompt an urgent evaluation for reversible causes, including cerebrovascular events, metabolic disturbances (such as hyponatremia or hypoglycemia), brain tumors, or infections like meningitis or encephalitis. Seizures in older adults may also be a manifestation of progressive neurodegenerative diseases, including Alzheimer’s or Parkinson’s disease. Emergency management in the ED should focus on stabilizing the patient while considering potential drug interactions, as elderly patients are more likely to be on multiple medications that may lower the seizure threshold (e.g., antipsychotics, antidepressants, or antihypertensives). Antiepileptic drug (AED) therapy initiation, while necessary in recurrent or long-duration seizures, must be approached cautiously due to age-related pharmacokinetic changes and the increased risk of side effects. A thorough evaluation for underlying causes, including neuroimaging and laboratory tests, is critical.

Pregnant Patients

Seizures during pregnancy present unique challenges in both diagnosis and treatment. The differential diagnosis includes pregnancy-specific conditions like eclampsia, in addition to the possibility of preexisting epilepsy or new-onset seizures due to metabolic derangements or intracranial pathology. In a pregnant patient with a seizure, the clinical priority is to ensure both maternal and fetal well-being. Eclampsia, a severe complication of preeclampsia, must be ruled out, as it presents with generalized tonic-clonic seizures and may lead to maternal and fetal morbidity if not promptly treated. Once eclampsia is excluded, consideration should be given to other causes such as hypoglycemia, cerebrovascular accidents, or drug toxicity (e.g., withdrawal from anticonvulsant medications). Emergency management in the ED should prioritize seizure control, typically with benzodiazepines, while avoiding teratogenic medications. Magnesium sulfate is the treatment of choice for eclampsia. Fetal monitoring should be initiated, and careful planning for delivery may be required depending on the severity of the condition and gestational age. The clinical approach should balance the need for immediate seizure control while minimizing risks to both the mother and fetus.

When To Admit This Patient

Few definitive practice guidelines are available to emergency physicians making disposition decisions for seizure episodes. However, all critically ill patients must be admitted to the inpatient setting since overall risk assessment is important for deciding whether to safely discharge patients home. For alternative clinical presentations, the physician should reliably assess whether the patient’s overall presentation warrants further medical interventions in a clinical setting.

For emergency physicians, seizure recurrence, morbidity, and mortality are useful measures to consider for safe discharge. Studies suggest that seizure recurrence most often depends upon EEG findings and the underlying cause—normal EEG and undetectable cause are associated with lower recurrence rates [33]. With positive neuroimaging findings (e.g., structural findings), initiating AED therapy for first-time seizures is recommended given a high 1-year recurrence risk of up to 65% [34].

Any patients with abnormal neurologic signs or symptoms who have not fully recovered from their seizure should not be discharged. Other important clinical benchmarks are the presence of normal vital signs, CT head imaging, EKG, basic lab results (especially renal function and blood counts), and follow-up. As part of the physician’s risk assessment of the patient’s overall condition, social factors must also be taken into account: lack of follow-up care, history of being lost to follow-up, and insufficient assistance available at home should all weigh towards admitting the patient for further monitoring (and possible seizure workup).

Generally, stable patients are those who return to their baseline mental status, do not exhibit any new neurological deficits, have no significant lab result abnormalities, and remain at low risk for recurrent seizure activity in the short term. Coordinating reliable follow-up is important, and all patients should be educated about the “red flag” signs and symptoms that warrant urgent evaluation and treatment.

Revisiting Your Patient

Altered mental status in the gravid, hypertensive patient is concerning for eclampsia. This patient should be started on 2mg of Mg as seizure prophylaxis. Obstetrics should be consulted as urgent delivery via cesarean section is the definitive treatment for this patient’s seizures. After delivery, the patient should be monitored closely for postpartum eclamptic seizures, which can occur up to 6 weeks postpartum.

Authors

Picture of Ardi Knobel Mendoza

Ardi Knobel Mendoza

Ardi Mendoza, MD is a resident at the Mount Sinai Hospital Emergency Medicine Program. He is interested in Health System and Emergency System Strengthening and local partner/local government-led collaborations. He has prior experiences in the field of Global Surgery while at Rutgers Robert Wood Johnson Medical School, assessing financial risk protection from impoverishing and catastrophic expenditure due to surgical care in the Colombian Healthcare System. He lived in Lima, Peru for a year working with Peruvian researchers at the University Cayetano Heredia as a research coordinator helping to develop a point-of-care diagnostic screening tool for Autism using eye-tracking technology.

Picture of Danielle Charles-Chauvet

Danielle Charles-Chauvet

Danielle Charles-Chauvet, MD is an Emergency Medicine resident at the Mount Sinai Hospital in New York. She is deeply invested in medical education and health disparities and, in affiliation with Harlem Children's Zone, has led several community-based educational initiatives to address these disparities. She designed and taught a course entitled Health and Structures of Oppression at Brown University's medical school. Her dedication to education earned her the 2022 National Outstanding Medical Student Award from the Academic College of Emergency Physicians and the 2021 Medical Education Award from the Society of Academic Emergency Medicine. She is currently working to expand her impact internationally by building Haiti's medical education infrastructure.

Picture of Erik J. Blutinger

Erik J. Blutinger

Erik J. Blutinger, MD, MSc, FACEP is a full-time emergency physician at Mount Sinai Queens Hospital in New York City and Medical Director to the Community Paramedicine program at Mount Sinai Health Partners. He completed his residency training at the University of Pennsylvania, Master's at the London School of Hygiene & Tropical Medicine, and has worked on a variety of health initiatives in quality and patient experience with formal leadership training in Quality Improvement (QI). Erik has worked in multiple national healthcare systems and underserved communities, including townships in South Africa and Guatemala, Bhutan, India, and Austria.

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References

  1. Jagoda, (2010). Seizures: An issue of Emergency Medicine Clinics. Elsevier Saunders.
  2. Werhahn, J. (2010). Weakness and focal sensory deficits in the postictal state. Epilepsy & Behavior, 19(2), 138–139. https://doi.org/10.1016/j.yebeh.2010.06.029
  3. Kim, , Cho, J.-W., Lee, J., Joo, E. Y., Hong, S. C., Hong, S. B., & Seo, D.-W. (2011). Seizure duration determined by subdural electrode recordings in adult patients with intractable focal epilepsy. Journal of Epilepsy Research, 1(2), 57–64. https://doi.org/10.14581/jer.11011
  4. Kumar, , Sharma Maini, K., & Arya, K. (n.d.). Simple partial seizure. National Center for Biotechnology Information. Retrieved April 10, 2023, from https://pubmed.ncbi.nlm.nih.gov/29763181/
  5. Heon, (n.d.). Febrile seizures. Core EM. Retrieved April 10, 2023, from https://coreem.net/core/febrile-seizures/
  6. Wagner, K. (2004, December 15). Diagnosis and management of preeclampsia. American Family Physician. Retrieved April 10, 2023, from https://www.aafp.org/pubs/afp/issues/2004/1215/p2317.html
  7. Hiroshi, S., Hallett, M., ‘History taking’, The Neurologic Examination: Scientific Basis for Clinical Diagnosis, 2 edn (2022; online edn, Oxford Academic, 1 Aug. 2022), https://doi.org/10.1093/med/9780197556306.003.0002, accessed 1 Dec. 2024.
  8. Brinciotti, M., Bouilleret, V, Masnou, P. (2021). Optimizing the Patient’s History: A Modern Approach. 10.1007/978-3-319-05080-5_26.
  9. Dulak SB. A practical guide to a thorough history. RN. 2004;Suppl:14-21.
  10. Wolf P, Benbadis S, Dimova PS, et al. The importance of semiological information based on epileptic seizure history. Epileptic Disord. 2020;22(1):15-31. doi:10.1684/epd.2020.1137
  11. Smith PE. If it’s not epilepsy… J Neurol Neurosurg Psychiatry. 2001;70 Suppl 2(Suppl 2):II9-II14. doi:10.1136/jnnp.70.suppl_2.ii9
  12. Trevathan E. Patient page. The diagnosis of epilepsy and the art of listening. Neurology. 2003;61(12):E13-E14. doi:10.1212/wnl.61.12.e13
  13. Henry JC. Comment: Be careful what you ask when interviewing patients with epilepsy. Neurology. 2015;85(7):594. doi:10.1212/WNL.0000000000001843
  14. Kanner, A. (2008). Common Errors Made in the Diagnosis and Treatment of Epilepsy. Seminars in neurology. 28. 364-78. 10.1055/s-2008-1079341.
  15. Wan, XH & Zeng, R. (2020). Handbook of Clinical Diagnostics. 10.1007/978-981-13-7677-1.
  16. Bank, A & Bazil, C. (2019). Emergency Management of Epilepsy and Seizures. Seminars in Neurology. 39. 073-081. 10.1055/s-0038-1677008.
  17. Hasan, Ahmed. (2016). Non-Convulsive Status Epilepticus in Emergency Department: A Diagnostic Challenge. Journal of Medical Science And clinical Research. 10.18535/jmscr/v4i8.103.
  18. Virani, D., Sangani, S., Patel, C, Patel, V., Saha, J., Kalsariya, R. (2024). 5. Study of Clinical Profile, Management and Outcome of Patients Presented with Seizures in Emergency Medicine Department. BJ Kines: National Journal of Basic & Applied Sciences, doi: 10.56018/bjkines2024065
  19. Ko DY. Epilepsy and Seizures Differential Diagnoses (updated Jul 26, 2002). From https://emedicine.medscape.com/article/1184846-differential?&icd=login_success_email_match_fpf Accessed: Nov 1,
  20. Burgess M, Mitchell R, Mitra B. Diagnostic testing in nontrauma patients presenting to the emergency department with recurrent seizures: A systematic review. Acad Emerg Med. 2022 May;29(5):649-657. doi: 10.1111/acem.14391. Epub 2021 Oct 1. PMID: 34534387.
  21. Teran F, Harper-Kirksey K, Jagoda A. Clinical decision making in seizures and status epilepticus. Emerg Med Pract. 2015 Jan;17(1):1-24.
  22. Harden CL, Huff JS, Schwartz TH, Dubinsky RM, Zimmerman RD, Weinstein S, Foltin JC, Theodore WH; Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology. Reassessment: neuroimaging in the emergency patient presenting with seizure (an evidence-based review): report of the Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology. Neurology. 2007 Oct 30;69(18):1772-80. doi: 10.1212/01.wnl.0000285083.25882.0e. PMID: 17967993.
  23. Gelisse P, Crespel A, Genton P, Jallon P, Kaplan PW. Lateralized Periodic Discharges: Which patterns are interictal, ictal, or peri-ictal? Clin Neurophysiol. 2021 Jul;132(7):1593-1603. doi: 10.1016/j.clinph.2021.04.003. Epub 2021 Apr 27. PMID: 34034086.
  24. Rosenthal Seizures, Status Epilepticus, and Continuous EEG in the Intensive Care Unit. Continuum (Minneap Minn). 2021 Oct 1;27(5):1321-1343. doi: 10.1212/CON.0000000000001012. PMID: 34618762.
  25. Gaitatzis A, Majeed A. Multimorbidity in people with epilepsy. Seizure. 2023;107:136-145. doi:10.1016/j.seizure.2023.03.021
  26. Cao, Z., Li, Y., Liu, S. et al.Clinical characteristics and impact of comorbidities on the prognosis of senile epilepsy in Southwest China: a retrospective cohort study. Acta Epileptologica 6, 11 (2024). https://doi.org/10.1186/s42494-024-00153-8
  27. Kanner, A.M., Ribot, R. and Mazarati, A. (2018), Bidirectional relations among common psychiatric and neurologic comorbidities and epilepsy: Do they have an impact on the course of the seizure disorder?. Epilepsia Open, 3: 210-219. https://doi.org/10.1002/epi4.12278
  28. Mula M, Coleman H, Wilson SJ. Neuropsychiatric and Cognitive Comorbidities in Epilepsy. Continuum (Minneap Minn). 2022;28(2):457-482. doi:10.1212/CON.0000000000001123
  29. Silbergleit R, Durkalski V, Lowenstein D, Conwit R, Pancioli A, Palesch Y, Barsan W; NETT Intramuscular versus intravenous therapy for prehospital status epilepticus. N Engl J Med. 2012 Feb 16;366(7):591-600. doi: 10.1056/NEJMoa1107494. PMID: 22335736; PMCID: PMC3307101.
  30. Falco-Walter JJ, Bleck Treatment of Established Status Epilepticus. J Clin Med. 2016 Apr 25;5(5):49. doi: 10.3390/jcm5050049. PMID: 27120626; PMCID: PMC4882478.
  31. Brophy GM, et : Guidelines for the evaluation and management of status epilepticus. Neurocrit Care 17:3-23, 2012.
  32. Seizure: Emergency Medicine, Second Editor; Adams, James G., MD, 2013, 2008 by Saunders, an imprint of Elsevier Inc. Book Chapter 99
  33. Berg AT, Shinnar The risk of seizure recurrence following a first unprovoked seizure: a quantitative review. Neurology 1991;41:965–72.
  34. Jagoda A; Gupta, K. “The Emergency Department Evaluation of the Adult Patient Who Presents with a First-Time ” Emergency Medicine Clinics of North America, U.S. National Library of Medicine, https://pubmed.ncbi.nlm.nih.gov/21109101/.

Reviewed and Edited By

Picture of Arif Alper Cevik, MD, FEMAT, FIFEM

Arif Alper Cevik, MD, FEMAT, FIFEM

Prof Cevik is an Emergency Medicine academician at United Arab Emirates University, interested in international emergency medicine, emergency medicine education, medical education, point of care ultrasound and trauma. He is the founder and director of the International Emergency Medicine Education Project – iem-student.org, chair of the International Federation for Emergency Medicine (IFEM) core curriculum and education committee and board member of the Asian Society for Emergency Medicine and Emirati Board of Emergency Medicine.

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Peripheral Intravenous Line Access and Blood Sampling (2024)

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by Omar F. Al- Nahhas, Mansoor M. Husain

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Introduction

Peripheral IV Cannulation is a critical skill for healthcare providers in the Emergency Department, clinics, and the field. Knowing that it is one of the most essential procedures in the United States, where it is estimated that more than 25 million patients have peripheral intravenous (IV) catheters placed each year for vascular access for the administration of medications and fluids and the sampling of blood for analysis [1], makes it essential to master the technique, understand the subtleties of anatomy, and perform the procedure frequently to maintain this skill.

IV access plays a critical role in the emergency department as it permits the administration of medicines and fluids directly into the patient’s bloodstream, allowing prompt treatment of severe conditions such as dehydration, shock, and severe infections. The speed of treatment delivery is crucial in emergency scenarios, and peripheral IV access provides an efficient and effective way to deliver life-saving therapies. Additionally, it enables the frequent and easy sampling of blood, which is crucial for diagnosing and monitoring the patient’s condition. Therefore, healthcare providers in the emergency department must develop quick and reliable peripheral IV access skills to guarantee the best possible patient outcomes.

Indications

  • Administration of fluids: Patients who are dehydrated or unable to tolerate oral fluids may require IV fluids to maintain hydration and electrolyte balance [2].
  • Medication administration: Certain medications, such as antibiotics, chemotherapy drugs, and pain relievers, may need to be administered intravenously to achieve the desired effect.
  • Blood transfusions: Patients who have lost a significant amount of blood due to trauma or surgery may require a blood transfusion via an IV cannula.
  • Monitoring: IV access may be necessary for frequent blood draws or to monitor certain parameters, such as blood glucose levels.
  • Contrast material administration: Some imaging studies, such as CT scans, require the administration of contrast material via IV cannulas to help visualize certain structures.

Contraindications

There are no absolute contraindications. Relative contraindications include

  • Coagulopathy
  • The presence of local infection
  • Burns, or compromised skin at the intended site of insertion
  • Previous lymphatic nodal clearance, arteriovenous fistula formation, or deep venous thrombosis on the affected limb.

In such cases, clinical judgment must be used to balance the benefits and risks of proceeding with line placement at that site [2].

Equipment and Patient Preparation

Equipment

  • Gloves
  • Skin disinfectant (Povidine and Alcohol Swabs),
  • 16-18 gauge IV catheter (smaller catheters are better used in the pediatric population)
  • Tape
  • Syringe
  • 3-way stopcock
  • Tourniquet

Optional

  • Topical anesthetic, e.g., EMLA ( 2.5% lidocaine and prilocaine),
  • Transilluminator light
  • Ultrasound with a vascular probe.

Patient Preperation

To perform the procedure, obtaining consent from the patient after discussing the procedure and its associated risks and benefits is important. The preferred site for cannulation is the Cephalic vein in the forearm, followed by the Medial Brachial Vein in the Antecubital Sulcus.  The dorsum of the hand is also a common site, but this can be more painful for the patient, and often, smaller gauge cannulas are used. Always use universal precautions, such as wearing gloves, during the procedure. The selected vein should be visualized and palpated, as it will have a slight “give” compared to surrounding tissue.

The overlying skin should be disinfected, and a topical anesthetic may be applied as desired. While transillumination or ultrasound may provide additional guidance, care should be taken to avoid contamination of the clean, prepped site to be accessed.

Procedure Steps

The procedure for peripheral IV cannulation involves several steps [3]:

  1. Apply a tourniquet or blood pressure cuff inflated above the diastolic reading proximal to the intravenous site.
  2. Prepare the site with an antiseptic solution.
  3. Insert the IV catheter using a no-touch technique distal to and along the line of the vein at a 10 to 15-degree angle to the skin.
  4. Slowly advance the needle and catheter into the vein, waiting for a flash of blood to enter the catheter, which may not always occur.
  5. Slowly advance the needle an additional 1 to 2 millimeters and slide the cannula into the vein while securing the needle in place.
  6. Remove the needle while pressing on the overlying skin over the cannula proximal to the insertion site to stem the blood flow.
  7. Attach a 3-way stopcock and flush the stopcock and cannula with 5 ml of saline to prevent clotting. Assess the fluid flow through the catheter and watch for skin bulge, which may suggest fluid extravasation.
  8. Secure the catheter with tape or dressing and release the tourniquet or blood pressure cuff.
  9. Attach intravenous tubing to the 3-way stopcock, attach it to the fluid of choice, and initiate flow. Watch again for fluid extravasation. Medications may be administered through another port of the stopcock or added to the IV solution as desired.
  10. Ensure that the tourniquet is removed before administering drug or fluid infusion.
  11. If fluid extravasation occurs, remove the catheter and repeat the procedure at a more proximal site, avoiding distal attempts.
  12. These steps should be performed carefully and with appropriate attention to detail to ensure successful IV cannulation.

Blood Sampling

Blood sampling is a fundamental procedure in clinical practice for diagnostic and monitoring purposes. Various tubes are available for collecting blood samples, each designed for specific laboratory tests. For instance, the Vacutainer system offers a range of tubes with different additives to facilitate accurate test results. The choice of the tube depends on the required analyses, such as complete blood count (CBC), basic chemistry panels, coagulation studies, blood cultures, or specialized tests. Adhering to the appropriate tube selection based on the intended tests is crucial for obtaining reliable laboratory results. The amount of blood required for each tube varies depending on the specific test being conducted.

Generally, a CBC requires 2-4 mL of blood to obtain sufficient quantities of plasma or serum for cell counting and differential analysis [4]. Basic chemistry panels often necessitate larger volumes, ranging from 5-10 mL, to provide enough serum or plasma for multiple analytes, such as electrolytes, liver function tests, and renal function tests [4].On the other hand, blood culture bottles usually require 10 mL of blood to optimize the sensitivity of microbial detection [5]. Understanding the recommended blood volumes for each tube is crucial for ensuring adequate sample collection and accurate test results.

In summary, proper tube selection is essential for blood sampling to ensure accurate laboratory results. Various tubes with specific additives are available and tailored for different tests. The amount of blood needed for each tube varies depending on the type of analysis being conducted. Familiarity with the recommended blood volumes for each tube is crucial to obtaining sufficient sample quantities and optimizing diagnostic accuracy.

Complications

Despite the widespread use, IV cannulation is not without complications.

Phlebitis: This refers to vein inflammation, which can cause redness, warmth, and pain at the catheter site. The incidence of phlebitis ranges from 2% to 50% in adult patients and is related to various factors, including catheter gauge, insertion site, and duration of catheterization. [6]

Catheter-related bloodstream infections (CRBSIs): These are serious infections that can result from the colonization of the catheter by microorganisms. The incidence of CRBSIs is estimated to be 1-10% and is associated with prolonged catheterization, immunocompromised patients, and inadequate catheter site care.[7]

Infiltration and extravasation: Infiltration occurs when the fluid administered leaks into the surrounding tissue, while extravasation occurs when the medication or solution irritates the surrounding tissue, leading to tissue damage. The incidence of infiltration ranges from 4% to 38%, while extravasation occurs in less than 6% of patients. [8]

Hematoma: This is a collection of blood at the site of the catheter, which can occur due to trauma during catheter insertion or catheter displacement. Hematoma is reported in 0.5-8% of cases. [9]

Nerve injury: Nerve injury can occur due to direct trauma during catheter insertion, leading to motor and sensory deficits. The incidence of nerve injury is low, reported in less than 1% of cases. [10]

In conclusion, peripheral IV catheterization is a commonly performed procedure but not without complications. Careful attention to technique and site care can help minimize the risks of complications.

Hints and Pitfalls

To successfully perform peripheral IV cannulation, it’s important to use the correct technique and select an appropriate site with a visible vein.

  • Start by applying heat and a tourniquet to enhance blood flow, making the vein more prominent.
  • Once you have identified the vein, stabilize it and insert the cannula at an angle of 10 to 30 degrees, advancing it slowly while monitoring for proper placement.
  • Finally, secure the cannula using a transparent dressing or tape, ensuring it is not too tight.

Proper care and maintenance of peripheral intravenous (IV) lines are crucial to prevent complications and ensure patient safety. According to evidence-based guidelines, dressing care plays a vital role in IV line maintenance. Transparent semipermeable dressings are recommended by the Infusion Nurses Society (INS) as they provide a barrier against contamination and allow easy visualization of the insertion site [11]. Regular inspection of the dressing is important to identify any issues such as loosening, soiling, or moisture accumulation, and compromised dressings should be promptly replaced using sterile technique to reduce the risk of infection.

Flushing and locking peripheral IV lines are essential for maintaining patency. The INS recommends flushing with 0.9% sodium chloride (normal saline) solution before and after medication administration and at least every 8-12 hours for continuous infusions [11]. This practice helps prevent blood clot formation and ensures proper line functioning. When intermittent infusion is not expected for an extended period, the INS suggests using a saline or heparin lock to maintain line patency [11].

Vigilant monitoring and assessment of the peripheral IV site are critical to detect any signs of infection or complications. According to the Centers for Disease Control and Prevention (CDC), routine site inspection should be performed at least daily, paying close attention to redness, swelling, warmth, tenderness, or drainage [12]. Timely reporting and appropriate intervention in case of any abnormalities are crucial to prevent complications like phlebitis or infiltration.

Patient education is an essential aspect of peripheral IV line care. Educating patients and their caregivers about proper hand hygiene, signs of infection or complications, and when to seek medical assistance is vital. Patients should receive clear instructions to promptly report any pain, tenderness, or changes at the IV site.

It is important to note that specific institutional protocols may vary, and adherence to local guidelines is essential. These recommendations are based on current evidence and best practices in peripheral IV line care, aiming to promote patient safety and achieve optimal outcomes.

There are some pitfalls to avoid. Failure to use proper technique or choosing an inappropriate site can increase the risk of infection and complications such as infiltration, extravasation, or phlebitis. Applying too much heat or pressure with the tourniquet can cause burns or damage to the veins. Failure to stabilize the vein or inserting the cannula at the wrong angle can make cannulation more difficult or cause complications. Advancing the cannula too quickly or over-tightening the dressing can cause pain or discomfort, restrict blood flow, or damage the vein.

In time-critical cases with known difficult peripheral access or where multiple attempts at peripheral line placement have already failed, an ultrasound-guided technique may be necessary, or the clinician may consider using alternative routes of drug administration (such as oral, intramuscular, intraosseous, or central venous access).

Special Patient Groups

Certain populations, including pediatric, geriatric, and pregnant patients, require special considerations during peripheral IV catheterization.

Pediatrics

Pediatric patients have unique anatomical and physiological differences that affect the success of IV catheterization. The smaller size of their veins and thinner skin can make it challenging to locate and access suitable sites for catheter insertion [13]. 

Additionally, children have a higher risk of experiencing pain, discomfort, and anxiety during the procedure, which can lead to complications such as vasovagal syncope and catheter dislodgement. Therefore, healthcare providers need to use appropriate-sized catheters and consider non-pharmacological interventions, such as distraction techniques and topical anesthetics, to minimize the pain and discomfort associated with the procedure [13].

Geriatrics

Geriatric patients also require special consideration during peripheral IV catheterization. As individuals age, their veins become less elastic and more fragile, making it challenging to cannulate veins and increasing the risk of complications such as hematoma, infiltration, and extravasation. Furthermore, geriatric patients often have multiple comorbidities and take multiple medications, which can increase the risk of adverse reactions and interactions with IV medications. Therefore, healthcare providers must assess the patient’s venous status and consider alternative routes of medication administration when appropriate [14].

Pregnant Patients

Pregnant patients pose unique challenges during peripheral IV catheterization due to the physiological changes that occur during pregnancy. Increased blood volume, decreased venous compliance, and increased peripheral resistance make locating and accessing suitable veins for catheter insertion difficult. Additionally, certain medications and fluids can affect the mother and fetus, requiring careful consideration of the medication’s safety and potential risks. Therefore, healthcare providers can use ultrasound guidance and consider the patient’s gestational age, medical history, and current medications when selecting the site and medication for IV catheterization [15].

In summary, peripheral IV catheterization requires special considerations in pediatric, geriatric, and pregnant patients. Healthcare providers should assess the patient’s anatomical and physiological status and select appropriate-sized catheters. They should also consider non-pharmacological interventions to reduce pain and discomfort and carefully select the site and medication for IV catheterization to minimize the risk of complications.

Authors

Picture of Omar F. Al- Nahhas

Omar F. Al- Nahhas

Dr. Omar Al-Nahhas is a Senior Emergency Medicine Resident at STMC, Al-Ain, UAE, and an MSc Candidate in Medical Education at the University of Warwick. He is an Adjunct Clinical and Simulation Tutor at Ajman University and a certified BLS and ACLS Instructor. With publications in emergency medicine, his interests include Trauma, Sports Medicine, Critical care and Advanced Emergency Medicine, emphasizing education, research, and resuscitation practices.

Picture of Mansoor M. Husain

Mansoor M. Husain

Consultant Emergency Medicine, Tawam Hospital – Alain

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References

  1. Chopra V, Anand S, Hickner A, Buist M, Rogers MA, Saint S, Flanders SA. “Risk of venous thromboembolism associated with peripherally inserted central catheters: a systematic review and meta-analysis.” Lancet. 2013 Jul 27;382(9889):311-25. doi: 10.1016/S0140-6736(13)60592-9. Epub 2013 May 30. PMID: 23726390.
  2. Beecham GB, Tackling G. Peripheral Line Placement. [Updated 2022 Jul 25]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK539795/
  3. Keith A. “Intravenous (IV) Line Access” (n.d.). International Emergency Medicine Education Project, Available athttps://iem-student.org/intravenous-iv-line-access/.
  4. Clinical and Laboratory Standards Institute (CLSI). (2017). Procedures for the Collection of Diagnostic Blood Specimens by Venipuncture; Approved Standard—Eighth Edition. CLSI Document GP41-A8. CLSI.
  5. Clinical and Laboratory Standards Institute (CLSI). (2020). Principles and Procedures for Blood Cultures; Approved Guideline—Third Edition. CLSI Document M47-A3. CLSI.
  6. Helm RE, Klausner JD, Klemperer JD, et al. Accepted but unacceptable: peripheral IV catheter failure. J Infus Nurs. 2015;38(3):189-203.
  7. Blot SI, Depuydt P, Annemans L, et al. Clinical and economic outcomes in critically ill patients with nosocomial catheter-related bloodstream infections. Clin Infect Dis. 2005;41(11):1591-1598.
  8. Dougherty L, Lister S. Infusion Nursing: An Evidence-Based Approach. Elsevier Health Sciences; 2014.
  9. Feleke Y, Mekonnen N, Assefa A. Magnitude and associated factors of intravenous catheter-related hematoma in the adult emergency department of Tikur Anbessa Specialized Hospital, Addis Ababa, Ethiopia. BMC Emerg Med. 2018;18(1):10.
  10. Wallis MC, McGrail M, Webster J, et al. Risk factors for peripheral intravenous catheter failure: a multivariate analysis of data from a randomized controlled trial. Infect Control Hosp Epidemiol. 2014;35(1):63-68.
  11. Infusion Nurses Society. (2021). Infusion therapy standards of practice. Journal of Infusion Nursing, 44(1S), S1-S224.
  12. Centers for Disease Control and Prevention. (2021). Guidelines for the Prevention of Intravascular Catheter-Related Infections. Retrieved from https://www.cdc.gov/infectioncontrol/guidelines/bsi/index.html
  13. Naik VM, Mantha SSP, Rayani BK. Vascular access in children. Indian J Anaesth. 2019 Sep;63(9):737-745. doi: 10.4103/ija.IJA_489_19. PMID: 31571687; PMCID: PMC6761776.
  14. Gabriel, J. (2017). Understanding the challenges to vascular access in an ageing population. British Journal of Nursing, 26(14), S15–S23. doi:10.12968/bjon.2017.26.14.s
  15. Tan PC, Mackeen A, Khong SY, Omar SZ, Noor Azmi MA. Peripheral Intravenous Catheterisation in Obstetric Patients in the Hand or Forearm Vein: A Randomised Trial. Sci Rep. 2016 Mar 18;6:23223. doi: 10.1038/srep23223. PMID: 26987593; PMCID: PMC4796788.

Reviewed and Edited By

Picture of Arif Alper Cevik, MD, FEMAT, FIFEM

Arif Alper Cevik, MD, FEMAT, FIFEM

Prof Cevik is an Emergency Medicine academician at United Arab Emirates University, interested in international emergency medicine, emergency medicine education, medical education, point of care ultrasound and trauma. He is the founder and director of the International Emergency Medicine Education Project – iem-student.org, chair of the International Federation for Emergency Medicine (IFEM) core curriculum and education committee and board member of the Asian Society for Emergency Medicine and Emirati Board of Emergency Medicine.

Toxidromes (2024)

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by Phalguni Sai Preethi Asapu & Thiagarajan Jaiganesh 

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You have a new patient!

A 24-year-old male university student was brought into the Resuscitation area of the Emergency department via ambulance after his friends found him collapsed and confused on the floor at a party. His friends tell you that this is not the first time and has happened to him in the past. He has had a history of recreational drug usage in the past. No further history is known. On arrival, you notice that the patient is confused, moves to localized pain, and opens their eyes to speech with GCS 12/15. His vitals T = 36.8. C, BP = 82/74 mmHg, HR = 52 bpm, RR = 8 bpm, O2% saturation = 90% on room air. On a quick examination, you notice that the patient has needle marks like train track appearances. His pupils are pinpoint.

a-photo-of-a-24-year-old-male-(image was produced by using ideogram2.0)

What do you need to know?

Importance

Toxidrome, a term coined by Mofenson and Greensher in 1970, refers to a clinical fingerprint that comprises a specific set of characteristic signs and symptoms. These symptoms arise from neurochemical and autonomic processes triggered by exposure to a particular class of toxins [1]. For physicians, recognizing these toxidromes is crucial for saving lives, as they serve as a valuable tool for the prompt detection and management of toxic exposures. Additionally, this recognition aids in differentiating between toxins that may present similarly.

In this chapter, we will discuss the five major toxidromes: Cholinergic, Anticholinergic, Sympathomimetic, Sedative-Hypnotics, and Opioids. However, a detailed examination of each toxidrome is beyond the scope of this chapter.

Epidemiology

A major cause of morbidity and mortality worldwide is both accidental and intentional poisoning from illicit substances. The second most common presentation involves pediatric patients under 6 years of age with accidental poisoning [2]. 

The American Association of Poison Control Centers reported over two million human exposure calls in 2018. The rates of poisoning cases presented to the emergency department appear to be increasing annually worldwide, with the majority being adults with intentional overdoses [2].

Studies have shown that the most common classes of drugs involved are analgesics, antidepressants, and opioids [3]. Additionally, accidental poisoning from pharmaceuticals, envenomation, and environmental and occupational exposure from either agricultural or industrial agents are also sources of potential toxicity. 

Pathophysiology

Cholinergic Toxicity

This particular toxidrome includes nicotinic toxicity, carbachol methacholine bethanechol or pilocarpine overdose, pyridostigmine toxicity, etc., results from inhibition or binding of acetylcholinesterase causes increased levels of acetylcholine in the synaptic clefts leading to an overstimulation of the parasympathetic portion of the autonomic nervous system which maintains the rest and digest functions. The typical presentation of these types of patients includes fluids coming out of every orifice [4,5].

Anticholinergic Toxicity

Anticholinergic toxidrome is frequently encountered because many pharmaceuticals have antimuscarinic properties with drugs such as diphenhydramine, tricyclic antidepressants, doxylamine, and scopolamine. It inhibits the muscarinic cholinergic neurotransmission, therefore blocking the acetylcholine from binding to the receptors, causing an alteration in the normal homeostatic balance between the sympathetic and parasympathetic arms of the autonomic nervous system. This allows the sympathetic side to function unopposed and generates a state of relative sympathomimetics. Therefore, this toxidrome is very similar to sympathomimetic toxicity [4,5].

Sympathomimetic Toxicity

This Toxidrome is defined by increased catecholamines such as epinephrine, norepinephrine, and dopamine, reducing the catecholamine reuptake in the preganglionic synapse. Simply a sympathomimetic excess leading to a fight or flight reaction. This class includes cocaine, amphetamines, phencyclidine hydrochloride (PCP), and lysergic acid diethylamide (LSD) [4,5].

Sedative Hypnotic Toxicity

This toxidrome is frequently encountered in the ED as it includes ethanol intoxication, hence presenting with sedation, and occurs on a spectrum depending on the particular substance, route, and potency. The pathophysiology typically involves an increase in GABA (gamma-aminobutyric acid) neurotransmission in the case of CNS Depressants and enhanced effects of GABA at GABA-A receptor in the case of benzodiazepines [4,5].

Opioid Toxicity

This toxidrome is similar to sedative/hypnotic toxidrome as it also involves sedation and depressed respiratory drive. Opioids stimulate three receptors Mu, Kappa, and Sigma. Receptors are found all over the central and peripheral nervous system producing effects analgesia by inhibiting the nociceptive information to the brain. Increasing the dopamine from the mesolimbic pathway causes euphoria and causing noradrenergic effects in the locus coeruleus producing anxiolysis [4,5].

Medical History

Although intuitive, history is always the key for identifying the etiologies of poisoning; therefore, focused history is paramount. Often, patients are unable and unreliable to provide history due to their clinical state of being obtunded, confused, uncooperative, or even following intentional ingestion. Hence, history must be procured from paramedics, family members, friends, primary care physicians, medical records, and pharmacists as they can offer an in-site that must be correlated with signs and symptoms, physical examination, and laboratory values [6].

The elements that should be focused on during history taking include the type of substance consumed, timing and quantity of ingestion as the management can vary depending on the timing of presentation to the emergency department, intent, whether it was suicidal or homicidal, to be able to obtain all the medications found at the site since multiple drugs can be ingested at once and if there are any forms of chemical exposure or obtaining a product safety protocol.

Physical Examination

Physical examination of poisoned patients provides invaluable clues regarding the agent involved; namely, vital signs, mental status examination, and pupillary size are useful elements. It is also important to examine the skin and mucus membrane with attention to discoloration, moisture levels, track marks, and ulcerations. 

A full neurological examination focusing on motor examination should be performed. The Image below highlights the features each patient presents with toxidromes [6,7]:

Alternative Diagnoses

There is a frequent encounter in which the patient presents with some level of delirium. Excluding pathological causes of altered mental status is important, such as acidosis, encephalopathy, electrolyte abnormalities, infection, uremia, trauma, insulin-related seizures/stroke, and psychosis. Identifying reversible causes, such as hypoglycemia and nutritional deficiencies, is vital. Having broad differentials, including toxicological and non-toxicological causes, is crucial for the management of the patient and helps avoid premature conclusions. 

Acing Diagnostic Testing

Diagnostic testing in toxicology is guided by clinical findings and suspected toxins in a patient. The following basic tests can be performed in the ED, depending on the presentation.

Electrocardiogram (ECG)

  • Provides diagnostic and prognostic information; hence, it should be performed on all patients on arrival.
  • Keeping an eye out for QT prolongation and widening of QRS interval aids in diagnosis as sodium channel blockers (tricyclic antidepressants, cocaine, carbamazepine) and potassium efflux (most antipsychotics and sotalol), respectively [8].
  •  

Toxicology Screens [9-11]

  • It helps to aid diagnosis, although its use can be limited since drugs such as LSD, mushroom, and mescaline are not part of the panel.
  • Urine toxicology screens are superior to blood toxicology screens as they are more reliable and have a longer period for positive detection, 24-72 hrs. We need to understand that urine toxicology panel is a qualitative measure, not a quantitative test, and false negatives can occur. Hence, it should not delay therapy.
  • General toxicology panel coverage:
    • Amphetamines
    • Cocaine
    • Ecstasy
    • Methamphetamines
    • Opiates
    • Phencyclidine
    • Marijuana
    • Benzodiazepines
    • Barbiturates
    • Methadone
    • Tricyclic antidepressants
    • Oxycodone
  •  

Serum Acetaminophen and Salicylate levels

Serum acetaminophen and salicylate levels should be measured routinely in all patients with suspected drug overdose or substance abuse, as these are among the most commonly implicated substances in acute poisoning cases [12].

Basic Laboratory Testing

  • Symptomatic patients and those with an unknown/unreliable history should undergo a complete blood count, urinalysis, serum electrolytes, blood urea nitrogen, creatinine, and glucose as a minimum to rule out any pathological cause before a toxic cause.
  • In severely ill patients, serum ketones, renal function tests, liver function tests, creatinine kinase, ionized magnesium, and calcium should be measured.
  • If there is suspicion of toxic alcohol ingestion, then additional tests, such as serum osmolality, can be performed [10].
  •  

Arterial and Venous Blood Gas Analysis

Blood gas analysis, both arterial and venous, plays a vital role in the evaluation and management of patients presenting with toxidromes. These analyses provide critical insights into acid-base balance, oxygenation, ventilation, and the metabolic status of the patient, all of which can be profoundly affected by various toxic agents.

Routine Pregnancy Tests

Routine pregnancy testing is recommended for all women of childbearing age presenting with suspected poisoning [10], as pregnancy can significantly influence both the clinical presentation and management of toxic exposures. 

Radiological Imaging

This is not of much value except in cases of radiopaque toxins, ingested drug packets, non-cardiogenic pulmonary edema, and acute respiratory syndrome due to exposure to certain toxins [10].

Risk Stratification

Risk stratification is essential in managing patients with toxidromes to prioritize care, allocate resources, and guide treatment decisions. It involves assessing the severity of the toxic exposure, identifying life-threatening symptoms, and evaluating patient-specific factors that may influence outcomes. Key considerations include the type and amount of toxin ingested, the time since exposure, and clinical manifestations such as altered mental status, hemodynamic instability, respiratory compromise, or significant acid-base disturbances. Laboratory findings, such as elevated lactate, anion gap metabolic acidosis, or co-oximetry results, provide additional insights into systemic effects of the toxin. Patient factors such as age, comorbidities, and pregnancy status further impact risk categorization. Stratifying patients into low, moderate, or high-risk categories ensures that those with critical conditions receive immediate interventions, such as airway support or antidotal therapy, while lower-risk patients can be managed with observation or symptomatic care. This systematic approach optimizes outcomes by tailoring interventions to the urgency and severity of each case.

Any patient with significant toxicity along with any of the following should be admitted to the ICU [13,14].  

  1. CNS depression, lethargy, coma.
  2. Patients with agitation who require either chemical or physical restraints.
  3. If PCO2 >45 mmHg, hypoxia or respiratory failure, endotracheal intubation.
  4. If the patient’s systolic blood pressure is  ≤80 mmHg.
  5. Prolonged or recurring seizures.
  6. On an ECG, if a second or third-degree AV block is present.
  7. On an ECG, presence of non sinus cardiac rhythm.
  8. Any significant acid-base disturbances, such as metabolic acidosis with pH ≤7.2.
  9. Any significant metabolic abnormalities requiring either close monitoring or aggressive correction, such as symptomatic hypoglycemia following sulfonylurea or insulin overdose.
  10. Patients with temperatures are at extremes, such as hyperthermia with T >104°F.
  11. Patients who ingest “toxic time bombs” like Ingested drug packets, sustained-release preparations, and ingestion of quantitative level of the drug have unfavorable outcomes.
  12. If the patient needs invasive hemodynamic monitoring such as pulmonary artery catheter, arterial line, or cardiac pacing.
  13. If the patient requires whole bowel irrigation to enhance GI elimination of the toxin.
  14. If the patient is in need of emergency hemodialysis, hemoperfusion, or hemofiltration.
  15. If the patient requires an emergency antidote that requires close monitoring, such as crotalid antivenin, Digi bind, physostigmine, or naloxone drip.
  16. If the patient experiences ischemic chest pain from toxins, namely cocaine and carbon monoxide.
  17. If the patient is exposed to TCA or other drugs with QRS >120 msec or QTc >500 msec.

Management

Optimal management of a poisoned patient depends on various parameters, including the type of poisoning involved, presenting symptoms, severity, and the time elapsed between exposure and presentation.  Resuscitation is a crucial initial step for any poisoned patient coming through the ED. Subsequently, a structured risk assessment should identify patients who would benefit from supportive care, decontamination, antidotes, and enhanced elimination techniques. Further assistance can be obtained from a medical toxicologist. The generalized initial evaluation for all poisoned patients in an ED setting includes the following approach. 

Primary Survey [15,16]

A: Airway

  • Assess whether the airway is patent or obstructed.
  • If not patent: Perform immediate intubation using rapid sequence intubation with pre-oxygenation and neuromuscular blockade.
    • Exception: In cases of suspected opioid overdose, administer naloxone to reverse respiratory depression while ensuring adequate oxygenation and ventilation.
  • Always rule out hypoglycemia as a potential cause before proceeding with intubation.

B: Breathing

  • Evaluate respiratory rate (RR), effort, chest expansion, presence of abnormal sounds, and oxygen saturation (SpO₂).
  • Administer high-flow oxygen to all critically ill patients with suspected overdoses, regardless of SpO₂ levels.

C: Circulation

  • Assess heart rate (HR), blood pressure (BP), central and peripheral pulses, capillary refill time (CRT), and temperature to evaluate circulatory status.

D: Disability (Neurological Status)

  • Examine Glasgow Coma Scale (GCS), pupil size, and blood glucose levels.
  • Once Airway, Breathing, and Circulation (ABC) are secured, focus on neurological stabilization.
  • The traditional “Coma Cocktail” (dextrose, oxygen, naloxone, thiamine) is no longer recommended as a blanket approach. Instead, each component should be administered selectively based on clinical indications [15].

E: Exposure and Environmental Control

  • Conduct a thorough external examination, assessing for temperature abnormalities, skin findings, injuries, trauma, or signs of transdermal medication patches and external contaminants.
  • Remove clothing, external contaminants, and concealed items such as drugs or weapons that might provide clues to the history of poisoning.
  • Manage temperature extremes:
    • Severe Hyperthermia (> 40°C): Requires aggressive treatment with sedation, paralysis, and ice bath cooling [17].
    • Severe Hypothermia (< 30°C): Requires rapid rewarming. For unconscious patients who achieve return of spontaneous circulation after cardiac arrest, consider therapeutic hypothermia [17].

Secondary Survey

  • SAMPLE history should be taken, including site, allergies, medications, past medical conditions, last meal, and event history, which have been discussed in this chapter’s history and physical examination section. 
  • A complete neurological examination should be performed. 

Management of Patients Depending on The Toxidrome

The general management of a patient after stabilization involves supportive care, which remains the cornerstone of management, decontamination, and specific antidotal therapy when indicated since they do not exist for every potential poisoning.

Anticholinergic Toxidrome Management [18]

Initial management should focus on evaluating and stabilizing cardiovascular and neurological toxicity. If a patient is agitated or having seizures, administer benzodiazepines (lorazepam or diazepam). On an ECG, if the QRS interval is prolonged >120 msec, depicting sodium channel blockade, then Sodium bicarbonate boluses of 50 mEq can be given in adults.

If a patient with anticholinergic toxicity comes to the Emergency department within 2 hours of ingestion and the patient is cooperative, then consider gastrointestinal tract decontamination with activated charcoal. The most common reason for emergency intervention is when the patient presents with delirium, then an antidote, Physostigmine, should be administered since it reversibly inhibits cholinesterase in both central and peripheral nervous systems, allowing acetylcholine accumulation and competition with the antimuscarinic blocking agent occupying the receptor. Its dosage is 0.5 mg – 1 mg IV over 15 minutes, with a maximum of up to  2 mg in the first hours. If more than 3 doses are required in a span of 6 hours, start IV infusion; 1-2 mg followed by 1mg/hr. Reassess after a 12-hour period. Caution: if  QRS >100, Na blockade signs and narrow-angle glaucoma, then Physostigmine are contraindicated.

Disposition [19]

  • Discharge if the patient has minimal symptoms after 6 hours of observation in the ED.
  • If the patient has had large ingestions, then observe for up to 24-48 hours, even if asymptomatic.
  • Admission is required if physostigmine is administered since the half-life of physostigmine is often shorter than the ingested drug).
  • The patient can be discharged if he remains asymptomatic within 6 hours of the last antidote dose.

Cholinergic Toxidrome Management

The management of patients presenting with cholinergic toxicity is directed towards Decontamination, supportive care, and reversal of acetylcholine excess and toxin binding at receptor sites on cholinesterase molecules. 

Decontamination includes using universal PPE (full-face air purifying cartilage mask, eye shield, chemical-resistant suites, boots, nitrile/ butyl rubber gloves) to protect the providers due to the contaminant’s dermal absorption. All clothing is removed by thoroughly flushing the skin with water. Activated charcoal or gastric lavage is of no use.

Stabilization and supportive care, Airway management remain crucial due to the high probability of respiratory failure followed by death. Intubation should be considered with either Rocuronium 1mg/kg or Vecuronium, non-depolarizing paralytic agents, since cholinesterases do not metabolize them. Succinylcholine, which is long used in an emergency setting, should be avoided at all times since it is metabolized by cholinesterase and prolongs the duration of effect around 4-6 hours in this particular setting [20].

Antidote therapy is a definitive treatment aimed at reducing the effects and levels of acetylcholine at various receptor sites. Atropine is one of them, and it acts as a competitive inhibitor of acetylcholine at the muscarinic sites. The dosage includes 0.6 – 1 mg atropine can be given. If severely poisoned, then administer 3mg. If there is no response with the first dose, double the dose after 5 minutes until clinical improvement is observed. Sometimes, it may require prolonged administration, which can be done via infusion. The initial loading doses should be followed by an infusion using 20% per hour of the total bolus dose. Note that the endpoint of atropinization includes drying of respiratory secretions, respiratory effort, and normalizing respiratory rate. The second part includes regenerating the acetylcholinesterase function by using an oxime that binds to the organophosphate-cholinesterase complex, leading to a conformational change that allows cholinesterase to function normally. This can be used if there is respiratory depression or failure, seizures, fasciculations, hemodynamic instability, dysthymias, or large amounts of repeated doses of atropine to completely control the signs and symptoms of this type of poisoning. Commonly used agents are Pralidoxime chloride 1-2 g over 30 minutes followed by a continuous infusion at 0.5 to 1 g/hour for several days. Alternatively, Obidoxime can be given in a loading dose of 4 mg/kg over 20 minutes, followed by an infusion of 0.5 mg/kg/hour. It is usually given as 250 mg loading dose in adults followed by 750 mg every 24 hours [20].

Disposition

  • If the patient is asymptomatic and has had minimal exposure for at least 12 hours after the ingestion, then the patient can safely be discharged.
  • If there is any evidence of self-harm, consult psychiatry.

Sympathomimetic Toxidrome Management

Patients with this type of toxicity should first undergo stabilization and supportive care, which includes loading the patient with IV fluids to avoid renal failure secondary to rhabdomyolysis. For decontamination, 50 g of activated charcoal can be used if the patient has ingested the toxin within an hour and their airway is protected. Moreover, Benzodiazepines are the key to managing sympathomimetic toxicities as they provide the cleanest pharmacological approach in treating agitated patients because they act by facilitating the binding of the inhibitory neurotransmitter GABA at various GABA receptors throughout central nervous system, such as 10-20 mg oral or IV diazepam or 1-2 mg lorazepam. If the patient remains agitated and has no respiratory depression, then proceed with further boluses via IV. If Oral or IV are unavailable, consider giving via IM 1-2 mg lorazepam or 5-10 mg Midazolam and repeat as necessary.

Another medication is haloperidol (5-10 mg intramuscular), which blocks the postsynaptic dopamine 2 receptors in the mesolimbic system of the brain. It can be used in agitated patients who are unresponsive to two or more doses of benzodiazepines. Ketamine, an N-methyl-D-aspartate receptor antagonist that induces a dissociative state, is used in the setting of uncontrollable agitation in sympathomimetic toxicity [21, 22]. 

Disposition

  • Discharge is no symptoms once symptoms resolve after 6 hours of observation.

Opioid Toxidrome Management

Physicians should prioritize stabilizing the airway, oxygenation, and ventilation. Most opioids are extended-release preparation that decreases gastric motility. Activated charcoal can be used, although discouraged due to lack of sufficient evidence to support its use in opioid poisoning. The key management is the use of Naloxone, a competitive opioid antagonist, therefore reversing opioid intoxication effects. Its use is indicated when a patient experiences significant respiratory or central nervous system effects. In general, starting with lower doses and subsequently increasing the doses as needed to alleviate symptoms is an optimal choice. Doses range from 0.04 – 15mg intravenously; starting dose of 0.04 mg is recommended, followed by titration of the subsequent dosages. It can be given via IV, IM, or SC but is ineffective when given orally due to first-pass metabolism [23].

Disposition

  • If the patient is on long-acting opioids, then admit to an observation unit.
  • Consider discharge after 6 hours of observation if the patients are asymptomatic.
  • Asymptomatic body packers should be admitted until the packets are passed or retrieved.

Sedative/Hypnotic Toxidrome Management

Benzodiazepine Toxicity

Initially, patients need to be stabilized, which includes endotracheal intubation with close respiratory and end-tidal carbon dioxide monitoring when obligated, and should not be delayed by the administration of an antidote. Administer activated charcoal (50 g) only if the patient arrives at the emergency department within one hour of ingestion and the patient’s airway is protected. An antidote that can be administered in these cases is Flumazenil, a nonspecific competitive antagonist at the benzodiazepine receptor site, which reverses benzodiazepine sedation after overdose, procedural sedation, and general anesthesia. It is to be noted that Flumazenil reverses the central nervous system depressant effects more than respiratory depression. Flumazenil is not recommended for routine use in the emergency department [23, 24]. It can precipitate acute withdrawal who are chronically dependent on benzodiazepine, leading to status epilepticus. The decision should be based on balancing risk and benefits and the reliability of the user. The dosage includes 0.2 mg IV over 30 seconds. A second dose of 0.2 mg followed by 0.2 mg at a minute interval to a total of 1 mg [25].

Disposition

  • Asymptomatic patients, after 4 hours of ED observation, can be discharged.
  • If there is a deliberate overdose, consult psychiatry.
Barbiturates Overdose

Patients with barbiturate toxicity should initially be stabilized by maintaining the airway (Eg. mechanical ventilation), administering IV fluids and vasopressor to eliminate hypotension (Systolic blood pressure >90 mmHg), and adequate urine output, rewarming measures to annihilate hypothermia. There is no specific antidote for barbiturates overdose. Decontamination with 50 g of activated charcoal can be applied if the patient presents within one hour of ingestion and the airway is secured. Dialysis plays a role as enhanced elimination only in patients ingesting phenobarbital, and who are deteriorating despite aggressive supportive care because routine use of it has limited evidence since phenobarbital is a weak acid, alkalization of the urine increases the amount of drug present in ionized form, therefore, minimizing tubular reabsorption and increases drug clearance [25].

Disposition

  • Consider discharge if the patient shows improvement in the neurological status and vital signs over 6-8 hours.
  • If symptoms continue after 6 hours, admit the patient.

Special Patient Groups

There aren’t any significant differences in identifying and managing toxidromes in children, pregnant women, or the geriatric population except for the drug dosages. The clinical features remain the same, and the management involves following primary and secondary surveys followed by supportive care, decontamination, antidotes, and enhanced elimination techniques depending on the toxic syndrome involved.

Revisiting Your Patient

Let’s revisit the case discussed at the beginning of the chapter. A patient presents to the ED

collapse and confused on the floor at a party with a history of drug usage of GCS 12/15.

Vitals shows T = 36.8. C, BP = 82/74, HR = 52, RR = 8, O2 sat = 90 on room air. You notice needle track marks on the skin and pinpoint pupils during quick examination. Discussed below is how one should approach this case.

  • Connect the patient to the monitors and establish two IV access points, along with a 12-lead ECG, to look for abnormal rhythm patterns.
  • Maintain a clear airway with adequate ventilation since opioids cause respiratory depression.  
  • Administer Naloxone immediately (Begin with small doses of 0.05 mg IV or 0.1 mg IM when the dependence is possible and ventilation can be maintained, then double the dose until respiratory depression is reversed) since the patient’s consciousness level is impaired. Consider referring the patient to the intensive care unit.
  • Expose the patient and look for transdermal medication patches or concealed drug packets.
  • Simultaneously with the resuscitative efforts, Obtain the necessary laboratory investigations, such as CBC, U&Es, glucose, LFTs, and CK, a toxic screen, APAP and salicylate levels, and ABG (metabolic acidosis).
  • Ensure adequate hydration to maintain a good urine output (0.5 mL/kg/hour) and perfusion.
  • Check for infection at injection sites and for clinical signs of endocarditis, pneumonia, and pulmonary edema.
  • Discuss testing for HIV and hepatitis in all patients using intravenous drugs.
  • The secondary survey obtains a thorough history with a neurological examination of the patient.

Authors

Picture of Phalguni Sai Preethi Asapu

Phalguni Sai Preethi Asapu

Dr. Preethi Asapu, is currently a first-year emergency medicine resident at Tawam Hospital, Al Ain, UAE. She graduated with an MBBS from Ras Al Khaimah Medical and Health Sciences University in 2021 and completed her internship at NMC Royal Hospital, Abu Dhabi, UAE. Dr. Asapu is competent researcher with publications to her name. She has Keen interest in Emergency Medicine and Toxicology.

Picture of Thiagarajan Jaiganesh

Thiagarajan Jaiganesh

Dr. Jaiganesh is a Chairman and Consultant in Adult and Pediatric Emergency Medicine and serves as an Adjunct Assistant Professor at UAE University. As the former Director of the Emergency Medicine Residency Program at Tawam Hospital in Al Ain, UAE, Dr. Jaiganesh is dedicated to training the next generation of emergency medicine professionals. With a strong academic and professional background, Dr. Jaiganesh has published numerous peer-reviewed articles on emergency medicine and contributes as a Section Editor and Chapter Author for notable medical texts, including the Oxford Handbook for Medical School. A sought-after speaker, Dr. Jaiganesh has been invited to present at numerous national and international conferences and serves as an instructor in various life support courses. Additionally, Dr. Jaiganesh is an expert in medico-legal and clinical negligence matters, providing valuable insights into complex legal and ethical cases in healthcare.

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References

  1. Mofenson HC, Greensher J (1970). “The nontoxic ingestion”. Pediatric Clinics of North America. 7 (3): 583-90. doi.1016/s0031-3955(16)32453-1.
  2. Gummin DD, Mowry JB, Beuhler MC, et al. 2019 Annual Report of the American Association of Poison Control Centers’ National Poison Data System (NPDS): 37th Annual Report. Clin Toxicol (Phila) 2020; 58:1360.
  3. Spyres MB, Farrugia LA, Kang AM, et al. The Toxicology Investigators Consortium Case Registry-the 2018 Annual Report. J Med Toxicol 2019; 15:228.
  4. Timothy JM. Care of a poisoned patient. In Ron MW ed. Rosen’s Emergency Medicine concepts and clinical practice. 10th Elsevier; 2022:1828-1830.
  5. Kloss B, Bruce T. Toxicology in a box. McGraw Hill Professional;2013.
  6. Erickson TB, Thompson TM, Lu JJ. The approach to the patient with an unknown overdose. Emerg Med Clin North Am 2007; 25:249.
  7. Olson KR, Pentel PR, Kelley MT. Physical assessment and differential diagnosis of the poisoned patient. Med Toxicol 1987; 2:52.
  8. Yates C, Manini AF. Utility of the electrocardiogram in drug overdose and poisoning: theoretical considerations and clinical implications. Curr Cardiol Rev 2012; 8:137.
  9. Hammett-Stabler CA, Pesce AJ, Cannon DJ. Urine drug screening in the medical setting. Clin Chim Acta 2002; 315:125.
  10. Timothy JM. Care of a poisoned patient. In Ron MW ed. Rosen’s Emergency Medicine concepts and clinical practice. 10th Elsevier; 2022:1832.
  11. DAST – Drug Abuse Screening Test | Dr. Lal PathLabs. Dr Lal PathLabs Blog. Published January 7, 2015. Accessed April 10, 2023. https://www.lalpathlabs.com/blog/screening-tests-for-drug-abuse-dr-lal-pathlabs/
  12. Sporer KA, Khayam-Bashi H. Acetaminophen and salicylate serum levels in patients with suicidal ingestion or altered mental status. Am J Emerg Med 1996; 14:443.
  13. Brett AS, Rothschild N, Gray R, Perry M. Predicting the clinical course in intentional drug overdose. Implications for use of the intensive care unit. Arch Intern Med 1987; 147:133.
  14. Lee HL, Lin HJ, Yeh ST, et al. Presentations of patients of poisoning and predictors of poisoning-related fatality: findings from a hospital-based prospective study. BMC Public Health 2008; 8:7.
  15. Sivilotti ML. Flumazenil, naloxone and the ‘coma cocktail’. Br J Clin Pharmacol 2016; 81:428.
  16. Adnet F, Borron SW, Finot MA, et al. Intubation difficulty in poisoned patients: association with initial Glasgow Coma Scale score. Acad Emerg Med 1998; 5:123.
  17. Ebi KL, Capon A, Berry P, et al. Hot weather and heat extremes: health risks. Lancet 2021; 398:698.
  18. Rosenbaum C and Bird SB. Timing and frequency for physostigmine redosing for antimuscarininc toxicity. J Med Toxicol. 2010;6:386-92.
  19. Hoppe JA, Monte AA, Anticholinergics, In Walls RM, ed. Rosen’s Emergency Medicine Concepts and Clinical Practice. Elsevie, 2022:1872-1875.
  20. Eyer P. The role of oximes in the management of organophosphorus pesticide poisoning. Toxicol Rev 2003; 22:165.
  21. McCarron MM, Wood JD. The cocaine ‘body packer’ syndrome. Diagnosis and treatment. JAMA 1983; 250:1417.
  22. Timothy JM. Care of a poisoned patient. In Ron MW ed. Rosen’s Emergency Medicine concepts and clinical practice. 10th Elsevier; 2022:1832.
  23. Nikolaides JK, Thompson TM. Opioids. In: Walls RM, ed. Rosen’s Emergency Medicine concepts and clinical practice. 10th Elsevier; 2022:1958-1961
  24. Penninga EI, Gradual N, Ladekarl MB, Jurrgens G. Adverse events associated with flumazenil treatment for the management of suspected benzodiazepine intoxication – a systemic review with meta-analyses of randomized control trials, Basic Clin Pharmacol Toxicol 2016. http://doi.org/10.1111/bcpt.12434.
  25. Overbeek DL, Erickson TB. Sedative-Hypnotics. In Wall RM, ed. Rosen’s Emergency Medicine Concepts and Clinical Practice. Elsevier;2022:1986-1993.

Reviewed and Edited By

Picture of Arif Alper Cevik, MD, FEMAT, FIFEM

Arif Alper Cevik, MD, FEMAT, FIFEM

Prof Cevik is an Emergency Medicine academician at United Arab Emirates University, interested in international emergency medicine, emergency medicine education, medical education, point of care ultrasound and trauma. He is the founder and director of the International Emergency Medicine Education Project – iem-student.org, chair of the International Federation for Emergency Medicine (IFEM) core curriculum and education committee and board member of the Asian Society for Emergency Medicine and Emirati Board of Emergency Medicine.

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Cardiac Monitoring (2024)

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by Stacey Chamberlain

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Definitions and Overview

Cardiac monitoring in the emergency setting is continuous monitoring of a patient’s cardiac activity in order to identify conditions that may require emergent intervention. These conditions include certain arrhythmias, ischemia and infarction, and abnormal findings that could signal impending decompensation. This chapter focuses specifically on cardiac monitoring or electrocardiography; additional methods of continuous hemodynamic monitoring in the emergency department (ED) include pulse oximetry, end-tidal CO2 monitoring, central venous pressure monitoring, and continuous arterial blood pressure monitoring. Of note, telemetry is the ability to do cardiac monitoring from a remote location; in practice, this is often a centralized system that might be located at a nursing station where multiple patients can be monitored remotely.

Cardiac monitoring differs from a 12-lead electrocardiogram in that it is done continuously over a period of time rather than capturing one moment in time in a static image. The benefit of this is that it captures transient arrhythmias and ectopic beats or monitors for changes over time. A disadvantage of cardiac monitoring is that typically, only 2 leads are displayed instead of a full 12 leads, giving a less comprehensive view of the heart and limiting its utility for looking for anatomic patterns. For example, on the 12-lead EKG, ED practitioners usually group the inferior, anterior, and lateral leads when looking for ischemic or infarct patterns. These may be less evident on a monitor with only two leads. Additionally, the static EKG allows the ED physician to carefully study it for subtle findings, for example, to make measurements of intervals, whereas in real-time monitoring, this is very difficult. In practice, both modalities are commonly used in conjunction for many ED patients.

The American Heart Association (AHA) published a consensus document in 2004 establishing practice standards for electrocardiographic monitoring in hospital settings, which was updated in 2017 [1,2]. These comprehensive documents outline the indications for cardiac monitoring, the specific skills required of the practitioner for cardiac monitoring, and specific ECG abnormalities that the practitioner should recognize. The 2017 update addressed the overuse of arrhythmia monitoring among certain populations, appropriate use of ischemia and QT-internal monitoring among select populations, alarm management, and documentation in electronic health records [2].

Cardiac monitoring is essential for those patients who are at risk for an acute, life-threatening arrhythmia and can also be used to evaluate for developing ischemia, response to therapy, and as a diagnostic tool. The AHA guidelines divide indications for cardiac monitoring in the inpatient setting into four classes based on varying degrees (level A, B, C) of evidence. Cardiac monitoring is considered indicated in patients in Class I. In Class IIa, it “is reasonable to perform” cardiac monitoring, whereas in Class IIb, it “may be considered.” For Class III, cardiac monitoring is not indicated as there is no benefit or there may actually be harm. Newer guidelines tailor the recommendations based on specific patient populations and whether the cardiac monitoring is for arrhythmia or continuous ST-segment ischemic monitoring [2]. Specific patient populations that are considered include patients with:

  1. Chest pain or coronary artery disease.
  2. Major cardiac interventions such as open heart surgery.
  3. Arrhythmias.
  4. Syncope of suspected cardiac origin.
  5. After electrophysiology procedures/ablations.
  6. After pacemaker or ICD implantation procedures.
  7. Pre-existing rhythm devices.
  8. Other cardiac conditions (acute decompensated heart failure or infective endocarditis).
  9. Non-cardiac conditions (e.g., post-conscious sedation or post-non-cardiac surgery).
  10. Specific medical conditions (e.g., stroke, imbalance of potassium or magnesium, drug overdose, or hemodialysis).
  11. DNR/DNI status.

Table 1 lists Class I-III recommendations. The AHA Scientific Statement provides a more comprehensive and detailed list.

Table 1 – Select Indications for Cardiac Monitoring

Class I Indications

Early phase ACS or after MI

 

After open-heart surgery or mechanical circulatory support

 

Atrial tachyarrhythmias

 

Symptomatic sinus bradycardia

 

2nd or 3rd degree AV block (exception as noted below for asymptomatic Wenckebach)

 

Congenital or genetic arrhythmic syndrome (e.g. WPW, Brugada, LQTS)

 

After stroke

 

With moderate to severe imbalance of potassium or magnesium

 

After drug overdose

Class IIa and IIb Indications

Non-sustained VT

 

Asymptomatic, significant bradycardia with negative chronotropic medications initiated

 

After non-cardiac major thoracic surgery

 

Chronic hemodialysis patients without other indications (e.g. hyperkalemia, arrhythmia)

Class III Indications

After non-urgent PCI without complications or after routine diagnostic coronary angiography

 

Patients with chronic atrial fibrillation, sinus bradycardia, or asymptomatic Wenckebach who are hemodynamically stable and admitted for other indications

 

Asymptomatic post-operative patients after non-cardiac surgery

 

DNR/DNI patients when the data will not be acted on and comfort-focused care is the goal

Ischemia Monitoring

Continuous ST-Segment Ischemia Monitoring was highlighted in the 2017 AHA guidelines as a specific indication for cardiac monitoring for patients most at risk for ischemia. Older monitors may not have this capability, but more modern monitors are programmed with automated ischemia monitoring that identifies abnormal ST-segment elevation or depression; manufacturers do not automatically enable this capability, and it may be turned on or off. To reduce unnecessary alarms, it is recommended (IIa level) to enable this function only in high-risk patients in the early phase of ACS and to individualize which lead should be prioritized based on the coronary artery suspected to be affected by an ischemic process. High-risk patients would include those being evaluated for vasospastic angina, those presenting with MI, post-MI patients without revascularization or with residual ischemic lesions, and newly diagnosed patients with a high-risk lesion such as a left main blockage.

QTc Monitoring

QTc monitoring aims to assess the safety of QT-prolonging medications and avoid Torsade de Pointes (TdP). Most hospitals do not have fully automated continuous QTc monitoring, so QTc monitoring and measurements may need to be performed manually or semi-automated with digital calipers. Regardless of the method, in general, recommendations for QTc monitoring are for patients with specific risk factors for TdP who are started on anti-arrhythmic drugs with a known risk for TdP (e.g., dofetilide, sotalol, procainamide, quinidine, and others), patients with a history of prolonged QTc started on non-anti-arrhythmic drugs with risk for TdP, those undergoing targeted temperature management, specific electrolyte derangements, and select drug overdoses. As with ischemic monitoring, QTc monitoring is not universally recommended for all patients, so consulting the 2017 guidelines for select patient scenarios is best.

Rhythm Interpretation

One of the most critical skills of an ED physician is in interpreting both static EKGs and interpreting arrhythmias on a cardiac monitor. A skilled practitioner must be able to diagnose common arrhythmias and be well-versed in the management of acute arrhythmias, recognizing which arrhythmias necessitate immediate action and which are less worrisome. Table 2 from the 2004 AHA guidelines lists the specific arrhythmias that the ED physician must be able to recognize. How and whether to treat an arrhythmia depends on many factors. The AHA has established algorithms for specific rhythms, including ventricular fibrillation (v-fib)/pulseless ventricular tachycardia (v-tach) and pulseless electrical activity (PEA)/asystole, as well as for non-specific rhythm categories such as bradycardia and tachycardia [3]. Additionally, they have published algorithms for clinical scenarios, including cardiac arrest, acute coronary syndrome, and suspected stroke.

The first step in the assessment of any rhythm is a clinical assessment of the patient. The premier issue of concern is if the patient is perfusing vital organs. A quick survey of the patient assessing mental status and pulses is essential to determining management. The management of a patient with v-tach will be substantially different if the patient is unresponsive and pulseless versus if the patient is awake with good pulses. As another example, the physician can quickly distinguish artifact from v-fib on the cardiac monitor by assessing the patient, as v-fib is not a perfusing rhythm.

The initial assessment of tachyarrhythmias (heart rate > 100) is to determine if the rhythm is “narrow-complex” (i.e., a QRS duration < 0.12s) or “wide-complex” (i.e., a QRS duration of 0.12s or greater). A narrow complex rhythm is considered a supraventricular rhythm (originating above the ventricles). Supraventricular tachycardia is a generic term encompassing any narrow-complex tachycardias originating above the AV node. Colloquially, when many practitioners refer to “SVT,” however, they are referring to a specific subcategory of supraventricular tachycardia called AV nodal re-entrant tachycardia (AVNRT). Wide complex tachycardias either originate in the ventricles or could originate in the atria and have an associated bundle branch block. Different criteria have been developed to help the practitioner distinguish between ventricular tachycardia and an SVT “with aberrancy” (i.e., aberrant conduction either due to an accessory path such as in Wolff-Parkinson-White or with a bundle branch block), the most well known of which are the Brugada criteria [4,5]. Practically speaking, many ED practitioners will assume the more dangerous and potentially unstable rhythm (v-tach) until proven otherwise; of course, the clinical picture and the patient’s vital signs are of utmost importance in determining the management of these patients. An excellent summary of this issue with rhythm strip examples is provided on the FOAM site “Life in the Fast Lane” [6].

Table 2 – Specific Arrythmias (adapted from AHA Scientific Statement [1])

Normal rhythms

 

 

Normal sinus rhythm

 

Sinus bradycardia

 

Sinus arrhythmia

 

Sinus tachycardia

Intraventricular conduction defects

 

 

Right and left bundle-branch block

 

Aberrant ventricular conduction

Bradyarrhythmias

 

 

Inappropriate sinus bradycardia

 

Sinus node pause or arrest

 

Non-conducted atrial premature beats

 

Junctional rhythm

AV blocks

 

 

1st degree

 

2nd degree Mobitz I (Wenckebach) or Mobitz II

 

3rd degree (complete heart block)

Asystole

 

Pulseless electrical activity (PEA)

 

Tachyarrhythmias

 

 

Supraventricular

Paroxysmal supraventricular tachycardia (AV nodal reentrant, AV reentrant)

Atrial fibrillation

Atrial flutter

Multifocal atrial tachycardia

Junctional ectopic tachycardia

Accelerated ventricular rhythm

Ventricular

Monomorphic and polymorphic ventricular tachycardia

Torsades de pointes

Ventricular fibrillation

Premature complexes

 

 

Supraventricular (atrial, junctional)

 

Ventricular

Pacemaker electrocardiography

 

 

Failure to sense

 

Failure to capture

 

Failure to pace

ECG abnormalities of acute myocardial ischemia

 

 

ST-segment elevation, depression

 

T-wave inversion

Muscle or other artifacts simulating arrhythmias

 

While each rhythm has distinctive management, it is worth noting for the novice learner that only v-fib and pulseless v-tach warrant asynchronized mechanical defibrillation (i.e. “shocking” the patient). Many students are stunned upon observing an asystolic cardiac arrest code to learn that shocking a “flatline” (i.e., asystolic) patient is an inappropriate treatment perpetuated by fictitious TV shows and movies. For unstable patients with arrhythmias but still have palpable pulses, synchronized cardioversion may be used.

Regarding medications, for certain rhythms and clinical scenarios, only vasopressor types of medications are used (e.g., epinephrine for asystole). For other rhythms and scenarios, antiarrhythmic medications are used (e.g., amiodarone for v-tach). Atrioventricular (AV) nodal blocking agents are often necessary for supraventricular tachyarrhythmias. One author suggests using a five “As” approach to treating emergency arrhythmias, keeping in mind the medications adenosine, amiodarone, adrenaline (epinephrine), atropine, and ajmaline [7]. Ajmaline is an antiarrhythmic that is not commonly used in English-speaking countries where procainamide is more common as an alternative to amiodarone for unstable v-tach.

Additional interventions may include pacemaker placement for symptomatic heart blocks. In many cases, the ED practitioner must also determine the underlying precipitant of the arrhythmia and tailor treatment to that cause. The emergency physician must familiarize himself with each rhythm and its unique management in any given clinical scenario.

At the end of this chapter, some good internet resources for the ED practitioner to practice interpreting EKGs and cardiac rhythms are provided.

Case Example

A 44-year-old male patient with a history of hypertension and end-stage renal disease on hemodialysis presents with shortness of breath after missing dialysis for 6 days. He reports gradual onset shortness of breath associated with orthopnea and increased lower extremity edema. He denies chest pain or palpitations. He does not have any cough or fever. On physical exam, he is in no distress, afebrile with a heart rate of 60, respiratory rate of 20, blood pressure of 140/78 mmHg, and oxygen saturation of 98% on room air. He has a regular rate and rhythm without murmurs and has crackles bilaterally to the inferior 1/3 of the lung bases and 1+ pitting edema of the bilateral lower extremities.

You decide to get an EKG, which shows the following:

Figure 1 (EKG from http://www.lifeinthefastlane.com)

You send a blood chemistry test, place the patient on a cardiac monitor, and one hour later note the following on the monitor:

Figure 2 - (EKG from liftl.com)

What are the indications for cardiac monitoring in this patient? What EKG abnormalities do you see? What does the rhythm strip show? What is the treatment?

Case Discussion

The ED practitioner should recognize potentially life-threatening conditions that a patient who has missed hemodialysis is at risk for are fluid overload (leading to pulmonary edema) and hyperkalemia. This patient could be considered to meet the Class I monitoring criteria for “needing intensive care” and possibly with “pulmonary edema”; however, even if the patient had no symptoms, the patient is indeed at risk for an acute life-threatening arrhythmia that would necessitate cardiac monitoring.

The EKG demonstrates peaked T waves indicative of acute hyperkalemia. Given the clinical picture of missed dialysis and the peaked Ts on the EKG, the ED physician should immediately initiate treatment for acute hyperkalemia without waiting for a confirmatory blood test (unless immediate point-of-care tests are available). If the patient’s hyperkalemia progressed, the patient could develop QRS widening with the morphology as shown on the rhythm strip called a “sine wave.” This dangerous finding could precipitously deteriorate into a life-threatening arrhythmia such as pulseless v-tach with cardiac arrest and should prompt immediate action. It is important to note that hyperkalemia can manifest in a variety of different EKG findings and does not always follow a consistent pattern from peaked Ts to QRS widening to sine waves; therefore, the patient should be treated at the first indication of any hyperkalemia-related EKG changes.

Conclusions

Cardiac monitoring is an important tool to monitor patients at risk for acute arrhythmias (including those at risk specifically for TdP) and acute or worsening cardiac ischemia. It can be helpful to immediately identify patients with life-threatening arrhythmias who need immediate intervention, to assess the response to medications for arrhythmias, and to help exclude arrhythmias as a likely etiology of a patient’s symptoms (e.g., a patient with syncope) [9]. Given the limited resources and the lack of benefits for many patients, the purpose and duration of cardiac monitoring should be carefully considered. Overuse can not only waste resources but can also contribute to alarm hazards, including “alarm fatigue,” where clinicians are barraged by so many false or nonactionable alarm signals that they become desensitized and do not respond to real events. Therefore, appropriate use and staff education are critical to maximizing the benefits of cardiac monitoring.

Author

Picture of Stacey Chamberlain

Stacey Chamberlain

Dr. Stacey Chamberlain is a board certified emergency physician who is a Professor in the Department of Emergency Medicine at the University of Illinois at Chicago (UIC). She also serves as the Director of the Global Emergency Medicine Fellowship Program and the Co-Director of the Social Emergency Medicine Fellowship Program. In addition to her work in Emergency Medicine, she is the Director of Academic Programs at the UIC Center for Global Health. In this role, she oversees the Global Medicine (GMED) Program for UIC medical students and the graduate global health certificate programs. Dr. Chamberlain has done clinical, educational, public-health, disaster-response, and emergency medicine development work, including working with several globally-focused NGOs, spanning five continents. Her global health work focuses on capacity building in emergency care in Uganda.

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2018 version of this topic – https://iem-student.org/cardiac-monitoring/

References

  1. Drew BJ, Califf RM, Funk M, Kaufman ES, Krucoff MW, et al. AHA Scientific Statement:  Practice Standards for Electrocardiographic Monitoring in Hospital Settings. Circulation. 2004; 110: 2721-2746. doi: 10.1161/01.CIR.0000145144.56673.59
  2. Sandau KE, Funk M, Auerbach A, Barsness GW, Blum K, Cvach M, Lampert R, May JL, McDaniel GM, Perez MV, Sendelbach S, Sommargren CE, Wang PJ; American Heart Association Council on Cardiovascular and Stroke Nursing; Council on Clinical Cardiology; and Council on Cardiovascular Disease in the Young. Update to Practice Standards for Electrocardiographic Monitoring in Hospital Settings: A Scientific Statement From the American Heart Association. Circulation. 2017 Nov 7;136(19):e273-e344. doi: 10.1161/CIR.0000000000000527. Epub 2017 Oct 3. PMID: 28974521.
  3. ACLS Training Center. Algorithms for Advanced Cardiac Life Support 2015. Dec 2, 2015.  Accessed at: https://www.acls.net/aclsalg.htm, Dec 10, 2015.
  4. Wellens HJJ. Ventricular tachycardia: diagnosis of broad QRS complex tachycardia. Heart2001;86:579-585 doi:10.1136/heart.86.5.579.
  5. Brugada P, Brugada J, Mont L, Smeets J, Andries EW. A new approach to the differential diagnosis of a regular tachycardia with a wide QRS complex. Circulation. 1991; 83: 1649-1659. doi: 10.1161/01.CIR.83.5.1649
  6. Burns E. VT versus SVT with aberrancy. Life in the Fast Lane. Accessed at: http://lifeinthefastlane.com/ecg-library/basics/vt_vs_svt/, Dec 10, 2015.
  7. Trappe H-J. Concept of the five ‘A’s for treating emergency arrhythmias. J Emerg Trauma Shock. 2010 Apr-Jun; 3(2): 129–136. doi:  10.4103/0974-2700.62111
  8. Ramzy M. Duration of Electrocardiographic Monitoring of Emergency Department Patients with Syncope. REBEL EM blog; June 13, 2019; Available at: https://rebelem.com/duration-of-electrocardiographic-monitoring-of-emergency-department-patients-with-syncope/.

Additional Online Resources

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Picture of Arif Alper Cevik, MD, FEMAT, FIFEM

Arif Alper Cevik, MD, FEMAT, FIFEM

Prof Cevik is an Emergency Medicine academician at United Arab Emirates University, interested in international emergency medicine, emergency medicine education, medical education, point of care ultrasound and trauma. He is the founder and director of the International Emergency Medicine Education Project – iem-student.org, vice-chair of the International Federation for Emergency Medicine (IFEM) core curriculum and education committee and board member of the Asian Society for Emergency Medicine and Emirati Board of Emergency Medicine.

Heat Illnesses (2024)

~ iEM Education Project Team ~ Leave a comment

by Patrick Joseph G. Tiglao, Rhodney P. Canada, & Emmanuel Luis S. Mangahas

Authors
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You have a new patient!

A 24-year-old man was brought to your Emergency Department by his football coach. His coach informed you that he started “behaving strangely” and responding inappropriately to questions a few hours ago during a practice session on the football field. His initial vital signs are BP 80/50 mmHg, HR 115 bpm, RR 24 bpm, T 41.5oC, and SpO2 98%. His GCS is 13 (E3V4M6).

What do you need to know?

Climate change is widely considered the greatest threat to human health globally in the coming decades [1]. According to the assessment of the Intergovernmental Panel on Climate Change (IPCC), the next decades might witness global warming above 1.5 °C, exceeding the goals of the Paris Agreement [2]. Concomitantly, heat-related mortality has developed as a growing public health concern. Populations with pre-existing chronic diseases are more sensitive to climate change, warranting closer attention and more effective interventions to manage heat-related health risks [3]. Therefore, a comprehensive medical understanding of heat-related illnesses is required as the world faces climate change [1].

Heat-related illnesses include a spectrum of diseases, ranging from mild and self-limiting conditions such as heat edema, heat cramps, and heat stress to the life-threatening condition known as heat stroke. These conditions occur when the body’s thermoregulatory mechanisms fail to keep body temperature within normal limits in a hot and humid environment [4].

The emergency physician needs to have a high index of suspicion for heat stroke because these patients can mistakenly be diagnosed with other conditions that may present similar to heat stroke.  Some examples are sepsis, intracranial bleeding, stroke, thyroid storm, anticholinergic toxicity, or other conditions where patients may have high fevers or altered mental status, similar to heat stroke. The most critical initial intervention in heat stroke is rapid cooling to <39°C. A misdiagnosis can result in a delay in rapid cooling.  Failing to implement this intervention results in higher mortality [5].

According to the World Health Organization, more than 166,000 people died due to extreme temperatures between 1997 and 2017.  This includes 70,000 deaths in the 3-month European heatwave of 2003 and 53,000 deaths in the 44-day Russian heatwave of 2010 [5]. A 2003 prospective study from France reported a 28-day and 2-year mortality rate of 58% and 71%, respectively, for patients diagnosed with heat stroke [6].

Body temperature is controlled by the hypothalamus. The body gains heat from metabolism and the environment, and this heat must be dissipated to maintain core body temperature between 36°C and 38°C (96.8°F and 100.4°F). Thermoregulation relies on four primary mechanisms: dilatation of blood vessels, particularly in the skin, increased sweat production and subsequent evaporation, decreased heat production, and behavioral heat control. Vasodilation contributes to the orthostatic pooling of interstitial fluid in the lower extremities, as seen in heat edema. When these processes are overwhelmed, core temperature will rise and may result in heat stress [4].

Cellular injury can begin when the core body temperature exceeds 39oC, especially if the elevation in temperature is sustained [7]. As the body temperature rises to 40°C, an acute phase response is elicited from heat-stressed cells.  This involves the release of cytokines and heat shock proteins, materials that can cause damage to organ systems and result in heat stroke [4,8]. The incremental damage to cells and organ systems as body temperature rises above 39oC exemplifies the importance of rapid cooling in a patient with hyperthermia.

Heat stroke due to high external temperature and humidity without much contribution from physical exertion is termed classical heat stroke (CHS).  Heat stroke is due to increased heat generation from strenuous physical activity, usually under extreme heat conditions and in a poorly acclimatized and conditioned body, and is termed exertional heat stroke (EHS). For example, classical heat stroke may be seen in elderly individuals sitting in poorly cooled and ventilated homes during the summer; exertional heat stroke may be seen in athletes exercising hours in the sun during a prolonged sporting event or race. Another heat-related illness that may be encountered in the athlete patient is heat cramps. These cramps occur from relative deficiencies in electrolytes such as sodium, potassium, and magnesium brought about by replenishing lost fluids with hypotonic drinking solutions after vigorous physical activity. This leads to painful involuntary contractions of skeletal muscles, most commonly the calves [4].

The exercising body has thermoregulatory mechanisms it utilizes when exposed to prolonged heat. During exercise, blood vessels dilate to release heat, the heart rate increases, and stroke volume decreases. Sweat production and evaporation from the skin surface also assist in cooling the body during exercise. These mechanisms may be diminished in patients with underlying cardiovascular disease (e.g., congestive heart failure) or those taking certain medications (e.g., beta-blockers or anticholinergic medications). These patient groups are at increased risk of heat-related illnesses during exercise [9].

Medical History

Ask patients with heat edema about exposure to hot and humid environments. The presence of other symptoms, such as dyspnea, easy fatigability, orthopnea, paroxysmal nocturnal dyspnea, and oliguria, are red flags that may point to alternative causes of the edema, such as congestive heart failure or kidney failure [4].

For patients with heat cramps, verify recent participation in strenuous activities, such as sports events and practices, military exercise, or procession-like activities. Ask if the patient took fluid during exertional activities and, if so, what type of fluid was consumed. Drinking hypotonic solutions, such as plain water, puts patients at risk for relative deficiencies in electrolytes and subsequent heat cramps. Ask about vomiting, diarrhea, and medications, like diuretics or antihypertensives, which can also put the patient at risk for electrolyte disturbances [4].

Heat stress is a diagnosis of exclusion because patients usually come in febrile with non-specific symptoms such as nausea, headache, weakness, and dizziness [4]. Again, patients with a recent history of exposure to hot and humid environments are at increased risk of heat stress. Still, the emergency physician should be aware of other more dangerous conditions, such as sepsis, CNS infection, endocrine dysfunction, myocardial infarction, and drug overdose. Ask for recent history of dyspnea, cough, dysuria, and headache, which may point to infectious diseases such as pneumonia, urinary tract infection, and CNS infection.

To diagnose heat stroke, the patient must have both Central Nervous System (CNS) impairment and a core temperature greater than 40°C. The spectrum of neurological abnormalities ranges from mild confusion to coma with a GCS of 3. Situational awareness is a vital skill for emergency physicians, as one should be aware of days with high ambient temperatures and high humidity that can increase the risk of CHS. Usage of medications that impair sweating, like anticholinergic medications, is another risk factor for developing heat illnesses. Generally speaking, CHS is uncommon in geographical areas where the average temperature throughout the year is high, as communities living there will develop behavioral tactics to avoid the heat. Intense exercise, military training, sports competitions, or prolonged labor, on the other hand, puts patients at risk for EHS. Patients not trained in hot environments may not be physiologically acclimatized, increasing their risk for EHS [4].

Physical Examination

Whenever heat illnesses are considered in the differential diagnosis of a given patient, measuring a core body temperature (e.g., rectal temperature) is the most important physical assessment. Using the physical exam to evaluate for other causes of elevated body temperature is important.  Physical signs of infection (e.g., cellulitis, abscess, drainage from wounds, asymmetric breath sounds), intoxication (e.g., dilated pupils), and endocrine dysfunction (e.g. goiter) should be assessed.

Obtaining an accurate and continuous core body temperature is a crucial part of the physical examination. Core temperature should be assessed and monitored using rectal, bladder, or esophageal probes. Peripheral temperature measurements, like oral, axillary, or temporal temperatures, are unreliable and may not reflect actual core temperatures. A common pitfall in measuring rectal temperature is not inserting the probe to a sufficient depth, rendering readings inaccurate, mainly if ice packs have been applied to the groin area for cooling. Rectal probes, in general, have to be inserted 15 cm inside the rectum to mitigate the effects mentioned above, but manufacturers may recommend different depths.  Note that unlike heat stroke and heat stress, heat edema, and heat cramps will not have an increased core temperature [4]. Tachycardia and hypotension may be seen on examination as a response to thermoregulatory peripheral vasodilation. This phenomenon contributes to other heat illnesses, such as heat edema and heat syncope.

After vital signs, a head-to-toe physical exam should be conducted with special care in conducting a thorough neurological examination. A hallmark finding of heat stroke, other than a core temperature above 40°C, is an abnormal neurological exam. CNS effects might range from mild confusion to deep coma. Ataxia and slurred speech may also be seen. CNS effects help distinguish heat stress from heat stroke, as only heat stroke will have CNS changes [4].

Assess for neurologic signs such as nuchal rigidity, lateralizing spasticity, and pathologic reflexes (e.g. extensor toe reflex) to determine the possibility of a central neurologic etiology. Seizures, in general, are common in heat stroke and might be confused with shivering during cooling.  Both seizures and shivering should be treated for neural protection and prevention of heat generation, respectively.  Benzodiazepines are appropriate for treating both conditions.

Alternative Diagnoses

Minor heat illnesses, like heat cramps and heat edema, can be diagnosed clinically based on the history. Alternative diagnoses for heat edema include congestive heart failure, renal failure, and chronic hepatic disease. The presence of exertional dyspnea, orthopnea, or paroxysmal nocturnal dyspnea would suggest congestive heart failure. Progressively decreasing urine output and generalized edema would suggest renal failure. A jaundiced patient with progressively enlarging abdomen would indicate a chronic hepatic disease. Alternative diagnoses for heat cramps are infectious conditions and electrolyte derangements. Many viral syndromes, like influenza, COVID-19, or Dengue, can be associated with myalgias.  Other conditions, like Leptospirosis, can also present with lower extremity myalgia and calf tenderness. However, the absence of decreasing urine output, fever, and jaundice would make this diagnosis unlikely.

Heat stroke, with its cardinal features of hyperpyrexia and altered sensorium, has numerous alternative diagnoses.  Some important diagnoses to consider are sepsis, CNS infections, thyroid storm, sympathomimetic or anticholinergic toxidromes, serotonin syndrome, alcohol withdrawal, stroke, or status epilepticus. Investigate accordingly for a focus of infection for these patients. Thyroid storm patients may also present with atrial fibrillation, diarrhea, and a trigger (e.g., missed thyroid medications, infection, or surgery). The presence of signs and symptoms such as sudden-onset lateralizing weakness, slurring of speech, headache, nuchal rigidity, and recurrent seizures despite adequate cooling may suggest central neurologic etiology for the patient’s condition. It may require a more tailored neurologic work-up.  Reported illicit substance or alcohol use, or lack thereof, would support intoxication or withdrawal. Epilepsy history, missed doses of antiepileptic medications, or active seizure activity during the exam would support status epilepticus as a diagnosis.

Acing Diagnostic Testing

Heat stroke and other heat illnesses are diagnoses made clinically.  However, diagnostic testing can help rule out alternative diagnoses and evaluate for concurrent organ dysfunction and metabolic derangements.

Immediately test point-of-care glucose because hypoglycemia is a common and easily reversible cause of altered sensorium. Hypoglycemia also sometimes accompanies exertional heat stroke since glucose reserves may become depleted from physical activity. Blood work-ups can include a complete blood count to evaluate for infection, creatinine to rule out acute kidney injury, and metabolic profile to assess for electrolyte imbalance. Hypernatremia may be present in severe dehydration. Hyponatremia and hypercalcemia may be present in patients who are dehydrated with hypotonic solutions after extreme physical activity. Hyperkalemia may be associated with acute kidney injury.

Blood gas analysis may help differentiate classical and exertional heat stroke. Classical heat stroke usually presents with respiratory alkalosis from hyperventilation as a compensatory mechanism to extreme heat. In contrast, exertional heat stroke may present with lactic acidosis from repeated muscular contractions from physical exertion [4]. Moreover, elevation of liver enzymes is very common in both EHS and CHS, mainly due to direct thermal injury and hypoxia from splanchnic vascular redistribution. Hepatic damage is almost always mild and reversible despite rare reports of fulminant hepatic failure from heat stroke [4,10].

Concerns for a central neurologic etiology for the patient’s encephalopathy can be assessed with CT brain imaging and CSF analysis.  These studies should be especially considered if focal neurologic deficits, slurring of speech, nuchal rigidity, or meningeal signs persist despite lowering the core temperature.

Risk Stratification

Minor heat illnesses are generally self-limited and have good outcomes. Heat stroke, on the other hand, is a life-threatening emergency. Mortality rate is correlated with the maximum core temperature and time to initiate cooling methods [4]. A study in 2018 also showed that the presence of disseminated intravascular coagulation is an independent prognostic factor for hospital mortality in patients with heat stroke [11]. Patients suffering from multiple organ injuries due to thermal injury also have poorer prognosis, so it is imperative to closely monitor renal, hepatic, and cardiovascular status of heat stroke patients [10,12].

Management

A core temperature above 40°C should prompt the clinician to consider heat stroke and initiate rapid cooling. 

Heat stroke is a time-sensitive condition where cooling takes precedence over everything else, including confirmation of the diagnosis. Every patient should be approached with the ABCDE assessment to ensure that all critical decisions are made promptly. Heat stroke is not an exception to this role, as the disturbance in consciousness could result in significant airway complications. A complete airway assessment should be immediately performed when the patient arrives in the emergency department while cooling measures are being set up. Many heat stroke patients may have a depressed level of consciousness, but the decision to intubate is ultimately clinical and based on local resources. Airway protection is paramount and should take priority over any other diagnostic or therapeutic procedures. Peripheral blood pooling is a component of heat stroke pathology, so hypotension is common in these patients. Intravenous fluid administration should be judicious, as blood pressure usually picks up as the core temperature drops. Aliquots of 250cc of crystalloids should be used when fluids are needed, and repeated dosing should take place after volume status assessments.

In heat stroke, external cooling methods are the main pillar of therapy. Antipyretics, such as Paracetamol, have no proven benefit in such cases. The fastest way to cool patients is through conduction, the direct transfer of heat between molecules. Full body water immersion can do this, and although this is theoretically the best cooling method, it is clinically challenging. Immersion of the patient in water poses a risk of aspiration and renders the patient’s accessibility quite difficult. Alternatively, ice packs can be placed on the patient’s neck, axilla, and groin areas. Convection, heat loss due to gas movement around the body, combined with evaporation, can achieve a cooling speed similar to full-body immersion. This combination can be achieved by spraying the patient with lukewarm water followed by fanning with warm air. Mist fans are very convenient and have the added benefit of their ability to fan multiple patients at once.

Figure 1- monitor showing the current vitals while the patient is cooled.
Figure 2. The row of beds with mist fans in a sunstroke unit. A cooling unit can be seen at the far right.
Figure 3. Fiberglass grooved beds with waterproof mattresses in a sunstroke unit.

One complication of these cooling maneuvers is shivering. Shivering needs to be controlled as it increases internal heat generation. This can be overcome by administering benzodiazepines. It should be noted that high ambient temperature and high humidity make convection and evaporation less effective. For this reason, if these patients are encountered in the prehospital setting, the first priority is to remove them from the hot and humid environment [4,7].

Internal cooling procedures, such as cold IV fluids and internal cold fluid lavages, do not have high quality to support their safety and efficacy in heat stroke patients [4]. Internal cooling with cardiopulmonary bypass can be considered in severe cases that do not respond to typical cooling methods. However, it is costly, resource-intensive, and unavailable in many contexts [4]. Rapid and aggressive external cooling with evaporative cooling, cold water immersion, and ice packs should be prioritized as the initial preferred cooling methods. Invasive measures, like thoracic, bladder, rectal, or peritoneal lavage, should only be used when other measures fail.

Special Patient Groups

Patients at extremes of age are at increased risk for heat-related illnesses and should be carefully considered for these conditions when presenting with fever [4].

Pediatrics

Classical heat stroke can occur in pediatric patients, but these patients are also at risk of another type of heat stroke known as confinement hyperpyrexia. This happens when a child is left inside a vehicle with poor ventilation during extreme heat. Pediatric patients are especially susceptible to heat stroke because they still lack adequate thermoregulatory mechanisms and the instinctive capacity to replace their fluid losses [4]. Child abuse should be considered, and necessary actions should be taken to protect the child from abuse or maltreatment.

Pregnant Patients

Pregnant individuals are particularly vulnerable to heat-related illnesses due to physiological changes that increase metabolic and cardiovascular demands. Conditions such as heat cramps, heat exhaustion, and heat stroke can arise from prolonged heat exposure, posing risks to both maternal and fetal health, including preterm birth and low birth weight. Management involves moving the patient to a cooler environment, ensuring hydration with non-caffeinated drinks or intravenous fluids if needed, applying cooling measures like wet cloths and fans, and monitoring vital signs closely. Preventive measures are crucial and include staying hydrated, wearing lightweight clothing, avoiding outdoor activities during peak heat, and utilizing air-conditioned spaces. Recognizing early symptoms, such as excessive sweating, dizziness, or confusion, and seeking immediate medical care when necessary are critical to preventing complications.

Geriatrics

Geriatric patients may have comorbidities or take daily medications that impair thermoregulation or mobility, making them prone to heat-related illnesses. This population has a higher heat stroke mortality rate and is more likely to experience complications of heat stroke [4]. Advocating for closer community ties, monitoring by family or peers, and improved socioeconomic support may help elderly patients evade health-related illnesses.

Mass Gatherings

Preparing for a mass gathering event should involve mitigation measures for a possible mass casualty incident of heat stroke and heat exhaustion patients, especially during hot or humid summer months. Public education should be employed to seek shade, drink enough fluids, and use umbrellas. Preparations should also include installing mist pipes, vent fans, and nearby cooling stops.

When to admit this patient

Patients with minor heat illness (e.g., heat edema, cramps, and stress) can generally be discharged home. They should be advised to refrain from strenuous activities during extreme heat conditions, drink plenty of fluids, and wear light and loose-fitting clothing. Those who suffer from heat cramps should be advised to avoid hypotonic solutions for fluid replacement to prevent relative electrolyte deficiencies [4].

Consider admission for patients with minor heat illness but have comorbidities, such as congestive heart failure and renal failure, and those with severe electrolyte abnormalities. Patients suffering from heat stroke must be admitted after resuscitation and rapid cooling in the emergency department.  Heat stroke patients need admission to adequately monitor core temperature and possible occurrence of late complications, such as renal failure, hepatic injury, and electrolyte abnormalities. Patients who are intubated or unstable hemodynamically require ICU admission for closer monitoring [4].

Revisiting Your Patient

You immediately assess the patient’s ABCDEs as part of the primary survey. You assess the patient’s airway for the presence of stridor and pooling of oral secretions. The airway is normal. The patient is able to speak in sentences, albeit confused. He is tachypneic but has normal work of breathing and clear breath sounds. Again, you note that the patient is hypotensive at BP 80/50, tachycardic at HR 115, and hyperthermia at 41.5oC. You start infusing 500 mL of normal saline intravenously as a bolus. The patient was confused but did not exhibit lateralizing weakness, slurring of speech, or nuchal rigidity. Point-of-care glucose was done to rule out hypoglycemia, which revealed 146 mg/dL. You did not elicit any history of trauma, and you did not note any obvious abrasions, lacerations, or bleeding. After the IV bolus, reassessment was as follows: BP 90/60, HR 110, RR 24, T 41.5oC, SpO2 98%, and GCS 13 (E3V4M6)

On further history taking, you elicit that the patient has no allergies, no daily medications, no known comorbidities, and last ate 3 hours ago. You learn the patient was at football team practice for 2 hours at noon today when they noted that the patient had decreased verbal responses, responded inappropriately, and was extremely warm to touch. There was no vomiting, headache, lateralizing weakness, or trauma noted during the incident. There was no history of cough, dyspnea, and fever in the preceding days. The coach said the patient had only joined the football team 4 days prior. You insert a rectal thermometer and note a temperature of 42.0oC. With this information, you suspected that the patient may be suffering from an exertional heat stroke and decided that the goal was to decrease the core temperature to less than 39oC as soon as possible. You immediately remove the patient’s clothing while still maintaining modesty. You direct a vent fan to the patient by incorporating water sprays and placing ice packs on the patient’s neck, axillary, and groin areas.

After 30 minutes of cooling, you observe shivering. To decrease the internal heat production that shivering may cause, you administer diazepam 2.5 mg IV, and the shivering subsides. A cardiac monitor with pulse oximetry is connected, and blood samples are drawn to evaluate for organ dysfunction and possible sepsis. After reaching a rectal temperature of 39°C, you direct your team to dry cover the patient with a light bed sheet. Upon subsequent examination, the patient was conscious, alert, and oriented. Vitals are BP 110/60, HR 105, RR 22, T 38.5oC O2Sat 96% on room air. Laboratories are remarkable for metabolic acidosis and elevated liver enzymes. Complete blood count is unremarkable. You admit the patient to a general medical ward for further monitoring and management.

Authors

Picture of Patrick Joseph G. Tiglao

Patrick Joseph G. Tiglao

Dr. Patrick Joseph G. Tiglao, FPCEM is a practicing Emergency Medicine Physician at the University of the Philippines - Philippine General Hospital. He is also affiliated with DOH regional hospitals in the other parts of the Philippines namely, Corazon Locsin Montelibano Memorial Regional Hospital in Bacolod City, Negros Occidental and Eastern Visayas Medical Center in Tacloban City, Leyte Province.

Picture of Rhodney P. Canada

Rhodney P. Canada

Dr. Rhodney P. Canada graduated, being the top of his class, Doctor of Medicine from the University of St. La Salle – Bacolod in 2018. He spent a year of post-graduate internship at the University of the Philippines Manila – Philippine General Hospital from 2018-2019. Currently, he is a senior 4th year and Chief Resident of the Department of Emergency Medicine in Corazon Locsin Montelibano Memorial Regional Hospital, Bacolod City, Negros Occidental, Philippines.

Picture of Emmanuel Luis S. Mangahas

Emmanuel Luis S. Mangahas

Philippine General Hospital

Acknowledgement

The authors would like to express their utmost gratitude to Dr. Abdulaziz Al Mulaik, the author of this chapter in the previous edition.

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References

  1. Zhou L, He C, Kim H, et al. The burden of heat-related stroke mortality under climate change scenarios in 22 East Asian cities. Environ Int. 2022; 170
  2. Tollefson J. Top climate scientists are sceptical that nations will rein in global warming. Nature. 2021; 599(7883):22-24.
  3. Yang J, Zhou M, Ren Z, et al. Projecting heat-related excess mortality under climate change scenarios in China. Nat Commun. 2021; 12 (1039)
  4. LoVecchio F. Heat Emergencies. In Tintinalli J, ed. Emergency Medicine A Comprehensive Study. 9th ed. USA: McGraw Hill; 2020: 1345-1350
  5. Heat and Health. World Health Organization. https://www.who.int/news-room/fact-sheets/detail/climate-change-heat-and-health. Published June 2018. Accessed April 2023.
  6. Argaud L, Ferry T, Le QH, et al. Short- and long-term outcomes of heatstroke following the 2003 heat wave in Lyon, France. Arch Intern Med. 2007;167(20):2177-2183
  7. Beltran G. Heat-related Illneses. In Cone D, ed. Emergency Medical Services Clinical Practice and Systems Oversight. 3rd ed. New Jersey, USA: John Wiley & Sons; 2021: 403-409
  8. Benedetto W. Heat Stroke. In Parsons P, Wiener-Kronish J, ed.Critical Care Secrets. 5th ed. Mosby; 2013: 541-544
  9. Hifumi T, Kondo Y, Shimizu K, Yasufumi M: Heat stroke. J Intens Care. 2018: 6(30)
  10. Grogan H, Hopkins PM. Heat stroke: implications for critical care and anaesthesia. BJA. 2002: 88(5):700–707
  11. Hifumi T, Kondo Y, Shimazaki J, et al. Prognostic significance of disseminated intravascular coagulation in patients with heat stroke in a nationwide registry. J Crit Care. 2018;44:306-311
  12. Liu S, Xing L, Wang J, et al. The Relationship Between 24-Hour Indicators and Mortality in Patients with Exertional Heat Stroke. Endocr Metab Immune Disord Drug Targets. 2022;22(2):241-246

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Reviewed and Edited By

Picture of Joseph Ciano, DO, MPH, MS

Joseph Ciano, DO, MPH, MS

Dr. Ciano is a board-certified attending emergency medicine physician from New York, USA. He works in the Department of Emergency Medicine and Global Health at the Hospital of the University of Pennsylvania. Dr. Ciano’s global work focuses on capacity building and medical education and training in low-middle income countries. He is thrilled to collaborate with the iEM Education Project in creating free educational content for medical trainees and physicians.

Picture of Arif Alper Cevik, MD, FEMAT, FIFEM

Arif Alper Cevik, MD, FEMAT, FIFEM

Prof Cevik is an Emergency Medicine academician at United Arab Emirates University, interested in international emergency medicine, emergency medicine education, medical education, point of care ultrasound and trauma. He is the founder and director of the International Emergency Medicine Education Project – iem-student.org, chair of the International Federation for Emergency Medicine (IFEM) core curriculum and education committee and board member of the Asian Society for Emergency Medicine and Emirati Board of Emergency Medicine.

Mechanical Ventilation (2024)

~ iEM Education Project Team ~ Leave a comment

by Elham Pishbin, Hamidreza Reihani

Authors
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You have a new patient!

A 70-year-old male with a history of severe chronic obstructive pulmonary disease (COPD) presents to the emergency department (ED) with complaint of progressive dyspnea and productive cough. Vital signs are as follows: PR=108/min, RR=46/min, BP=130/90 mm Hg, T=37.8°C (axillary), SpO2=76% (with 5 L/min O2with nasal cannula). He is awake but confused. You request a blood gas test and initiate standard medical treatment for COPD exacerbation (Nebulized short-acting beta-agonists, antibiotics, and systemic glucocorticoids). You are concerned about the patient’s respiratory status and prepare for the possibility that he may need additional respiratory support in the emergency department.

Introduction

Mechanical ventilation (MV) is often essential to successfully managing critically ill patients. Patients may require MV because of respiratory failure, airway protection, or as part of the management of their illness to support their respiratory function and to reduce the work of breathing. Emergency physicians should have a solid understanding of mechanical ventilation and its indications, modes, and troubleshooting. Here, we provide a simplified guide to managing MV in the emergency department (ED) setting.

Physics of MV

MV involves pumping air with a positive pressure into the patient’s lungs and allowing the patient to exhale the air spontaneously.  The aim is to deliver oxygen to the lungs, keep the distal airways open for oxygen exchange, and allow carbon dioxide release upon exhalation. The ventilator uses pressurized air to overcome the resistance of ventilator tubing, the endotracheal tube (ETT), and airways. When the resistance to airflow increases or lung compliance decreases (lung compliance is inversely related to the elastic recoil of the lungs), higher pressure is required to inflate the lung [1, 2]. Common causes of high resistance are obstruction of the ETT by tube biting or a mucus plug, airway secretions, and bronchospasm. Common causes of poor compliance are pneumothorax, alveolar oedema, right main stem intubation, and air trapping [2].

Exhalation occurs passively due to pressure differences between the alveoli (higher pressure) and the ventilator (lower pressure). Notably, ventilators can administer a positive end-expiratory pressure (PEEP) to decrease this pressure gradient, thereby preventing the lungs from excessive collapse [2].

Control Variables and Ventilator Modes

The control variables on a ventilator determine how to pump the air (the air volume, the time over which the air is delivered, the frequency of delivering the air over a minute, and the speed at which the air travels). The alarms and monitors show whether the controls we set are appropriate and how the lungs respond [3]. 
After a patient is intubated and connected to a ventilator, the ventilator mode and settings should be established.  First, specify volume-controlled ventilation (VC) or pressure-controlled ventilation (PC) [1].

VC ventilation

VC ventilation is the most familiar and the most commonly used of MV modes in the ED [4].

The key parameters which should be set on the ventilator include [2]:

  1. Tidal volume (Vt): the amount of air pumped into the patient in each breath (measured in milliliters)
  2. Respiratory rate (RR)
  3. Fraction of inspired oxygen (FiO2)
  4. Positive end-expiratory pressure (PEEP): the baseline airway pressure at the end of expiratory. PEEP stents open the distal airways for gas exchange.
  5. Flow rate*: the speed at which Vt is pumped through the circuit (measured in liters per minute)
  6. Inspiratory time (Ti) *: the time (in seconds) over which the ventilator pumps the Vt

(*These parameters are often automatically set, but this depends on the ventilator)

In VC ventilation, pressure cannot be set as it depends on airway resistance and lung compliance. Increased airway resistance or worsened lung compliance will increase pressures in the airways, increasing the risk of barotrauma. Barotrauma due to elevated pressures is one disadvantage to VC. The advantage of VC ventilation is that the VT is guaranteed, and minute ventilation is stable.

PC ventilation

PC ventilation applies constant inspiratory pressure throughout inspiration, whether the ventilator or the patient triggers the breath [2]. In PC ventilation, the Vt cannot be set directly, so the operator sets the inspiratory pressure instead of Vt. Flow rate and Vt are dependent variables in PC ventilation. This is a disadvantage of PC ventilation since increased resistance or decreased compliance will lead to smaller Vt delivery, diminished ventilation, and carbon dioxide retention. Other key parameters, like Vt, PEEP, RR, and FiO2, are the same as VC ventilation. The advantage of PC ventilation is that airway and pulmonary pressures are set at the inspiratory pressures, preventing barotrauma. In addition, the patients can regulate their inspiratory flow rate and increase it according to their inspiratory efforts. This improves patient-ventilator synchrony [2].

A ventilator mode is a specific setting on the ventilator that determines how the ventilator assists the patient by giving a breath. It also defines the amount of respiratory support that the ventilator provides for the patient [5].

It is important to note that each ventilator mode has advantages and disadvantages.  There is no perfect ventilation mode that fits all patients. The best mode is the mode with which you and your team are most familiar [2].

Two primary ventilator modes that are most commonly used in the ED are Assist/Control Ventilation (ACV) Mode and Synchronous Intermittent Mandatory Ventilation (SIMV) Mode [4].

Assist/Control ventilation (ACV)

This mode is designed to offer full respiratory support for patients with minimal or no spontaneous breathing by delivering a preset number of mandatory breaths. However, if the patient tries to breathe, the ventilator will also assist that breath [5]. The patient will always receive at least the preset number of breaths (regardless of his/her respiratory effort). In this regard, ACV is the most appropriate initial mode in ED patients who are initially paralyzed and sedated [1].

ACV can be set as either volume-control or pressure-control. In VC/ACV, we set these parameters: Vt, flow rate, basal respiratory rate, and sensitivity to the patient’s respiratory effort (trigger). We can adjust the sensitivity control to make it easier or harder for the patient to trigger an assisted breath from the ventilator.
In PC/ACV, instead of Vt, we set the Ti.  In this mode, Vt is dependent on the patient’s lung compliance and airway pressure. The advantage is avoiding barotrauma, but the disadvantage is that a specific preset Vt cannot be guaranteed [4].

To ensure ventilator synchronization, a breath initiated by the patient takes precedence over a preset breath. If the ventilator is programmed to deliver 12 breaths per minute, it will provide a breath every five seconds in the absence of spontaneous breathing. However, if the patient makes a spontaneous effort, the ventilator will provide an extra breath and reset the timer for another five seconds. The main challenge is that patient-initiated breaths are not proportional to his effort. When the patient makes an inspiratory effort, the ventilator provides a full Vt, which can lead to hyperventilation and poor patient-ventilator synchronization. Adequate sedation is necessary to prevent spontaneous breathing efforts when a patient is ventilated in the ACV mode. [1].

Synchronous Intermittent Mandatory Ventilation (SIMV)

This mode offers intermittent ventilatory support to patients by delivering mandatory breaths and supporting spontaneous breaths. Mandatory breaths are delivered at a preset rate. The ventilator delivers at least a preset number of mandatory breaths to the patient, similar to ACV. Patients with no respiratory effort, will receive the preset number of breaths. Patients with spontaneous breathing at a lower rate than the ventilator preset rate will receive the preset number of breaths with full Vt. In these two scenarios, SIMV is very similar to ACV. However, if a patient has spontaneous breathing at a rate higher than the preset respiratory rate, additional respiratory effort beyond the preset rate will only be partially supported proportional to the patient’s respiratory effort. This makes SIMV an appropriate mode for less sedated patients with some degree of spontaneous breathing [1].

Pressure Support Ventilation (PSV)

In this mode, the ventilator assists the patient’s spontaneous breaths during the inspiratory phase of breathing. It is often used to help the patient overcome the airway resistance caused by the endotracheal tube and the ventilator circuit. The patient should be alert or on light sedation and able to follow commands. When the patient triggers a breath, the ventilator supports it by adding pressure to facilitate breathing. The operator sets the FiO2, PEEP, and inspiratory pressure on the ventilator based on how much support the patient needs to receive. In PSV, RR, Ti, and flow rate are determined by the patient. The higher the pressure support, the easier it will be for the patient to take a breath. The ventilator supports inspiration until the inspiratory flow falls below a preset measure [2,6].

When choosing PSV, it is also necessary to set an appropriate backup mode (for example, SIMV) and ventilator alarms [6].

Typical initial ventilator settings: Although required settings depend on whether PC or VC ventilation is selected, the principles are similar in both modes [1]. Typical initial ventilator settings include the following: [1,2,4]

  1. Tidal volume (Vt): a Vt of 6 to 8 mL/kg of estimated ideal body weight (IBW) is appropriate for most patients. The inspiratory pressure should be set in PC ventilation to achieve these Vt targets. Ongoing patient assessment is necessary to avoid excessive Vt. Regardless of VC or PC, initial pressure targets should not exceed 30 cm H2O.
  2. Respiratory rate: a rate of 12 to 18 breaths per minute would be reasonable for most patients and provide adequate ventilation. In special situations, such as patients with severe metabolic acidosis, the respiratory rate should be increased to match pre-intubation minute ventilation.
  3. FiO2: initially should be set at 100%, then lowered to target a SpO2 of 92% – 96% (PaO2 of 60 to 100 mmHg)
  4. PEEP: is routinely set initially at 5 cm H2O, but it can be set at 4 to 20 cm H2O
  5. I/E time ratio: The ratio of inspiratory time to expiratory time. It is commonly set as a ratio of 1:2. In some modes, it is automatically set based on other parameters. In some other modes, it needs to be set by the operator.
  6. Flow rate: is typically set at 60 L/min. (Vt will be delivered at the speed of 60 L/min). Increasing the flow rate will deliver the set Vt faster, reducing the inspiratory time. (It is found in VC modes)
  7. The trigger is a preset change in pressure or flow detected by the ventilator as the patient tries to initiate a breath, and the ventilator supports that breath. It should be set at a level that enables the patient to trigger the ventilator without great effort. For most patients, pressure sensitivity trigger from -0.5 to -2 cm H2O is effective and safe. The 1–3 L/min threshold is appropriate for the flow trigger setting.

When choosing a ventilator mode and parameters, it is essential to ensure adequate ventilation, but it is also important to ensure that the pressure in the ventilator circuit (including the lung) is appropriate [1]. Some important pressures are:

  • Peak inspiratory pressure (PIP) is the maximum pressure during inspiration. It is a dynamic pressure measured during the inspiration, so it incorporates airflow and reflects the resistance to airflow. It is also reflective of dynamic compliance of the entire respiratory system. Decreasing compliance or increasing resistance to airflow will increase PIP. It can never be lower than P. plat [4].
  • Plateau pressure (P. plat) is a static pressure that can be measured at the end of inspiration with a short breath-hold (Figure 1). The goal is to be less than 30 cm H2O. Decreasing the compliance will increase P. plat. Decreasing the Vt will decrease P. plat [4]
Figure.1: Airway pressure-time curve demonstrating PEEP, PIP, Pplat (Provided by the authors)
  • Positive End-Expiratory Pressure (PEEP) is the airway pressure at the end of expiration. It helps to keep the smaller airways and the alveoli open, prevents atelectasis, and improves oxygenation. Increased levels of PEEP may lead to lung injury. Additionally, high PEEP can depress cardiac output and lead to hemodynamic compromise [1,4]. When talking about PEEP, most authors mean extrinsic PEEP (PEEPe). In this chapter, when we use PEEP, we refer to PEEPe.
  • Intrinsic PEEP or auto-PEEP (PEEPi) results from air trapping in the airways. It occurs due to increased expiratory resistance (e.g., bronchospasm, kinked ETT), impaired elastic recoil (e.g., emphysema), and increased minute ventilation (inadequate expiratory time). PEEPi can lead to hemodynamic instability similar to high levels of PEEP [2,4].

Noninvasive ventilation (NIV)

NIV provides continuous positive pressure throughout the breathing cycle via a tight-fitting mask (nasal, oro-nasal, or full-face mask, as shown in Figure 2) rather than an endotracheal tube [7].

Figure.2: NIV masks: A, B: Oro-nasal mask, C: Nasal mask, D: Full face mask (provided by authors)

No mandatory breath is given by the ventilator so the patient must have spontaneous breathing. The ventilator provides a preset level of pressure when the patient initiates a breath, but inspiratory flow and Ti are completely patient-dependent [4,7]NIPPV can be delivered as continuous positive airway pressure (CPAP) or bi-level positive airway pressure (BiPAP).

CPAP provides constant positive pressure throughout the entire respiratory cycle. Its main effect is applying positive pressure at the end of expiration and exerts a minimal effect on inspiration [4,7].

BiPAP supplies a positive airway pressure during inspiration (IPAP) and a lower positive airway pressure during expiration (EPAP) [4].

IPAP provides pressure support and decreases the patient’s work of breathing. Increasing the IPAP will improve tidal volume and minute ventilation, thereby helping to eliminate CO2 from the alveoli.

EPAP acts similar to PEEP and improves alveolar recruitment and oxygenation by maintaining positive pressure at the end of expiration. EPAP prevents the lung from being fully deflated at the end of expiration, aiding in oxygen exchange across the alveolar-capillary membrane. Therefore, when you need to improve oxygenation, you should increase the EPAP.

The difference between the IPAP and EPAP is called delta pressure. The delta pressure is the same as pressure support in invasive ventilation. When the difference between the IPAP and EPAP is larger, the patient is able to have a larger tidal volume. Therefore, when you need to increase the clearance of CO2, you need to increase the delta pressure. [1,7].

Contraindications to NIV are patients who are uncooperative, hemodynamically unstable, lack protective airway reflexes, lack good respiratory effort, or have maxillofacial trauma. [7,8]

Initial NIV Settings

Initial settings depend on the amount of support that the patient requires, patient comfort, and patient cooperation.

BiPAP usually is initiated at 10 cm H2O for IPAP and 5 cm H2O for EPAP. Based on the patient’s clinical response, these parameters can be titrated later by 1 to 2 cm H2O at a time. However, the maximum pressure for IPAP should not exceed 20 cm H2O because this may lead to barotrauma [8,9].

Typical initiated settings for CPAP are 5 to 15 cm H2O [4,7].

Ventilator Troubleshooting

Patient-ventilator dys-synchrony refers to patients who develop respiratory distress after undergoing mechanical ventilation [10]. Emergency physicians must be familiar with patient-ventilator interactions so that life-threatening complications of mechanical ventilation can be promptly identified and managed [11]. In Figure 3, we present a systematic approach to detect life-threatening conditions in patients who suddenly deteriorate and become hemodynamically unstable (profound hypotension or cardiac arrest) under mechanical ventilation [1, 10].

Figure-3: Evaluation of respiratory distress in hemodynamically unstable mechanically ventilated patients (Provided by authors)

Revisiting Your Patient

After 30 minutes, you reevaluate your patient. The patient remains in respiratory distress with SpO2 of 79%, despite nebulized beta-agonists, steroids, antibiotics, and the use of 7 L/min O2 via face mask. The patient’s blood gas reveals a pH of 7.22, PCO2 of 80 mm Hg, and PaO2 of 55 mmHg. You decide to put him on NIV using an oro-nasal mask. You choose BiPAP mode and set IPAP=12 cm H2O, EPAP=7 cm H20, and FIO2= 90%.  After 5 minutes, the patient becomes agitated on the NIV mask, even with verbal direction and support. The pulse oximeter remains low at a SpO2 of 85%.

What would be the next appropriate step in the management of this patient?

You recognize your patient has not sufficiently improved despite maximal medical therapies. You decide to prepare for intubation and mechanical ventilation. The patient is fully sedated, paralyzed, and intubated using RSI (rapid sequence intubation). You prepare to choose a ventilation mode and set the parameters on your ventilator.

Which mode of ventilation and control parameters are most ideal for your patient?

The patient is sedated and paralyzed during RSI, so the VC/ACV mode is the best choice. Your senior says, “The best mode is the mode most familiar to you.”  No data suggest the advantage of PC over VC (or vice versa) in patients with COPD. You review your goals in MV of your COPD patient: improve oxygenation and ventilation, minimize PEEPi, and prevent barotrauma. 

You set the ventilator as:

  • Mode: ACV (VC/ACV)
  • FiO2= 100%
  • Vt= 500 cc
  • Respiratory rate= 14
  • PEEP= 5cm H2O
  • I/E: 1/4

You base your tidal volume on the patient’s 170 cm height and weight of 90 kg. You set the I/E ratio at 1:4 to optimize a longer expiratory time and titrate the FiO2 until the SpO2 falls between 88% to 92% [12]. A chest X-ray confirms the tip of the endotracheal tube is located above the carina.  The patient is admitted to the medical ICU for further management and treatment.

Authors

Picture of Elham Pishbin

Elham Pishbin

Elham Pishbin is a full-time associate professor of emergency medicine (EM) with 16 years of experience as a faculty member of the department of EM at Imam Reza Hospital, affiliated with Mashhad University of Medical Sciences, Mashhad, Iran. She is a member of the Iranian national board of EM and contributed to establishing the first EM residency program at Mashhad University of Medical Sciences in 2008, the fifth EM residency program in Iran, and a significant milestone in the development of EM in the country.

Picture of Hamidreza Reihani

Hamidreza Reihani

Dr. Hamidreza Reihani, a professor of emergency medicine at Mashhad University of Medical Sciences in Iran, is also a member of the national board of emergency medicine. He holds fellowships in medical education, research, and clinical informatics. With 15 years of experience in emergency medicine, he has made significant contributions, including founding an academic Emergency Department (ED) at his university and educating over 100 specialists in the field. Dr. Reihani has also been actively involved in interdisciplinary and undergraduate education, research (with more than 60 published articles), peer review, and editorial roles for two academic journals. His expertise and dedication are reflected in his contributions to both the previous and current editions of this book.

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References

  1. Seigel T.A, Johnson N.J. Mechanical ventilation and noninvasive ventilatory support. In: Walls R.M, ed. Rosen’s emergency medicine: concepts and clinical practice. 10th ed. Philadelphia PA: Elsevier; 2023:24-33
  2. Ward J, Noel C. Basic Modes of Mechanical Ventilation. Emerg. Med. Clin. N. Am. 2022;40(3):473-88
  3. Gomersall C, Joynt G, Cheng C, et al. Basic Assessment and Support in Intensive Care. Hong Kong: Chinese University of Hong Kong; 2013:37-54.
  4. Santanilla J.I. Mechanical Ventilation. In Roberts J.R, Hedges J.R, eds. Roberts and Hedges’ clinical procedures in emergency medicine and Acute Care. 7th ed. Philadelphia PA: Elsevier; 2018:152-172.
  5. Hickey S, Giwa A. Mechanical ventilation. StatPearls. 2023 Jan 26.
  6. Abramovitz A, Sung S. Pressure Support Ventilation. StatPearls. 2022. Sep 18.
  7. Gill HS, Marcolini EG. Noninvasive mechanical ventilation. Emerg. Med. Clin. N. Am. 2022;40(3):603-13.
  8. Carlson J.N, Wang H.E. Noninvasive Airway Management. In: Tintinalli J.E, ed. Tintinalli’s emergency medicine: a comprehensive study guide, 9th ed. McGraw Hill Education; 2020: 178-183.
  9. Baker DJ, Baker DJ. Basic Principles of Mechanical Ventilation. Artificial Ventilation: A Basic Clinical Guide. 2020:113-37.
  10. Keith RL, Pierson DJ. Complications of mechanical ventilation: a bedside approach. Clinics in chest medicine. 1996 Sep 1;17(3):439-51.
  11. Gilstrap D, MacIntyre N. Patient–ventilator interactions. Implications for clinical management. American journal of respiratory and critical care medicine. 2013 Nov 1;188(9):1058-68.
  12. Atchinson P.R, Roginski M.A. Chronic obstructive pulmonary disease. In: Walls R.M, ed. Rosen’s emergency medicine: concepts and clinical practice. 10th ed. Philadelphia PA: Elsevier; 2023:806-815

Free open access resources for study

Reviewed and Edited By

Picture of Joseph Ciano, DO, MPH, MS

Joseph Ciano, DO, MPH, MS

Dr. Ciano is a board-certified attending emergency medicine physician from New York, USA. He works in the Department of Emergency Medicine and Global Health at the Hospital of the University of Pennsylvania. Dr. Ciano’s global work focuses on capacity building and medical education and training in low-middle income countries. He is thrilled to collaborate with the iEM Education Project in creating free educational content for medical trainees and physicians.

Picture of Arif Alper Cevik, MD, FEMAT, FIFEM

Arif Alper Cevik, MD, FEMAT, FIFEM

Prof Cevik is an Emergency Medicine academician at United Arab Emirates University, interested in international emergency medicine, emergency medicine education, medical education, point of care ultrasound and trauma. He is the founder and director of the International Emergency Medicine Education Project – iem-student.org, chair of the International Federation for Emergency Medicine (IFEM) core curriculum and education committee and board member of the Asian Society for Emergency Medicine and Emirati Board of Emergency Medicine.

Tachyarrhythmias (2024)

~ iEM Education Project Team ~ Leave a comment

by Keith Sai Kit Leung, Rafaqat Hussain & Abraham Ka Cheung Wai 

Authors
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You have a new patient!

A 28-year-old female patient presented with 3 weeks history of palpitations. She started with a new-onset shortness of breath and dizziness this morning, which prompted her to attend ED. The patient also complains of recent unintentional weight loss, restlessness, insomnia, passing loose stool more frequently, menstrual disturbances, and some degree of chest pain. No other significant medical history was noted. On physical examination, she looks well-perfused, with bilateral equal air entry and normal vesicular breath sounds throughout, heart sound I+II with no added sound. Vital signs monitoring showed a temperature of 38.1°C, heart rate of 142 bpm, respiratory rate of 21, blood pressure of 155/98, peripheral CRT of 3s, and SpO2 96% on air. ECG is shown below:

(Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8496558/)

What do you need to know?

Tachyarrhythmia is an abnormal heart rate over 100 bpm. It can be classified by site of origin (sinus, supraventricular, ventricular), in relation to QRS complexes (narrow or board-complex), or regularity.

Importance

Tachycardia is an extremely common finding in patients presenting to the emergency department; it involves a wide range of differential diagnoses, from normal variants to physiological responses to life-threatening conditions like shock and cardiac arrest. Studies have shown that patients with tachycardia have an increased risk of post-discharge mortality [1, 2], with higher rates of future re-visit to ED [3].

Epidemiology and Pathophysiology

Sinus tachycardias usually occur as part of a normal physiological response (e.g., exercise, pregnancy) or a compensatory pathological response to secondary underlying conditions (e.g., pulmonary embolism, hyperthyroidism, anemia, infection). It is important to note that sinus tachycardia can be abnormal, secondary to cardiac dysautonomia. These conditions are postural orthostatic tachycardia syndrome or inappropriate sinus tachycardia.

(Reused from Jones, S. A. (2009). ECG Notes: Interpretation and Management Guide. F.A. Davis Company.)

Supraventricular tachycardias is an umbrella term that includes a number of arrhythmias that arise above the bundle of His, i.e., the sinoatrial (SA) node, atria, and atrioventricular (AV) node; these are typically narrow complex tachycardia except WPW syndrome. The most prevalent types of SVTs, in descending order, are atrial fibrillation, atrial flutter, atrioventricular nodal re-entrant tachycardia (AVNRT), atrioventricular re-entrant tachycardia (AVRT), with atrial tachycardia (AT) and junctional tachycardia being the least common types [4, 5]. Three arrhythmogenic mechanisms have been proposed: Re-entry, enhanced automaticity, or triggered activity [6].

Starting with atrial fibrillation (AF) and atrial flutter (AFL), the latest data from the Global Burden of Disease Study 2019 showed that there are 59.7 million affected individuals worldwide [7], with a male predominance in the older population. Common causes of AF include PIRATES [Mnemonic for Pulmonary embolism, Ischaemic heart disease/Idiopathic, Rheumatic valvular disorder, Anaemia/Alcohol, Thyroid (hyperthyroidism), Electrolytes imbalance/Elevated BP (hypertension), Sepsis/Sick sinus syndrome]. The arrhythmogenic mechanism of AF is by increased automaticity, leading to ectopic focal activities and the creation of micro re-entrant circuits in the atrial muscles. Without organized contractility, blood pools in the atria, predisposing to thrombus formation and increasing stroke risk.

(Reused from Jones, S. A. (2009). ECG Notes: Interpretation and Management Guide. F.A. Davis Company.)

Atrial flutter is less common than AF, but they both share similar aetiologies and may coexist. The difference between both is that AF presents with an irregularly irregular heartbeat, while AFL presents with a regularly irregular heartbeat, as a macro re-entrant circuit exists in the atrium, producing a rapid regular atrial rate at 300 bpm. Depending on the conduction ratio, affected patients have a fixed ventricular rate at 150 bpm (2:1), 100 bpm (3:1), or 75 bpm (4:1).

(Reused from Jones, S. A. (2009). ECG Notes: Interpretation and Management Guide. F.A. Davis Company.)

Atrioventricular nodal re-entrant tachycardia (AVNRT) has a prevalence of 2.25 cases per 1000 people in the general population, with a female/male ratio of 2:1 among all age groups [8]. It is the most common cause of paroxysmal SVT and occurs in about 50% of cases. Hence, it is often used synonymously with the term SVT. AVNRT is usually idiopathic, i.e., patients have structurally normal hearts. In AVNRT, re-entry is the main arrhythmogenic mechanism. Naturally, the AVN has dual pathways with different conduction velocities (a fast and slow pathway). Usually, conduction passes via the fast pathway, which blocks incoming current from the slow pathway, while in SVT, the slow pathway becomes the dominant anterograde conduction pathway, uses the fast pathway for retrograde conduction, and creates a re-entrant loop. 90% of AVNRT is slow-fast type [9].

(Reused from Jones, S. A. (2009). ECG Notes: Interpretation and Management Guide. F.A. Davis Company.)

Atrioventricular re-entrant (or reciprocating) tachycardia (AVRT) is another form of paroxysmal SVT, accounting for 30% of cases. It is caused by an anatomical re-entrant circuit with the normal AV conduction system and an AV accessory tract. The most commonly known accessory pathway is called Bundle of Kent, causing Wolff-Parkinson-White (WPW) pre-excitation syndrome; hence, WPW and AVRT are often used interchangeably. It has been estimated to affect 1-3 persons per thousand people. [10]

(Reused from Jones, S. A. (2009). ECG Notes: Interpretation and Management Guide. F.A. Davis Company.)

Atrial tachycardia (AT) accounts for the remaining 10-20% of cases, as opposed to other subtypes; it is usually caused by increased atrial automaticity independent from the AV conduction system or accessory pathways. Other causes include sinoatrial scarring, digoxin toxicity, or conditions that cause atrial dilation (COPD, CHF). Note that there are 2 types of AT, focal and multifocal AT; the former is caused by one ectopic arrhythmogenic focus and later with multiple arrhythmogenic foci within the atria. The firing rate of the ectopic focus is faster than that of the SA node, which overrides its activity. [11]

(Reused from Jones, S. A. (2009). ECG Notes: Interpretation and Management Guide. F.A. Davis Company.)
(Reused from Jones, S. A. (2009). ECG Notes: Interpretation and Management Guide. F.A. Davis Company.)
(Reused from Srinivasan C, Balaji S. Neonatal supraventricular tachycardia. Indian Pacing Electrophysiol J. 2019;19(6):222-231. DOI:10.1016/j.ipej.2019.09.004) – Open Access (https://www.sciencedirect.com/science/article/pii/S0972629219301159)

Junctional tachycardia occurs when there is increased automaticity in the AV node and decreased automaticity in the SA node. This causes ECG changes, which commonly present as retrograde p waves around the QRS complex. [12]

(Reused from Jones, S. A. (2009). ECG Notes: Interpretation and Management Guide. F.A. Davis Company.)

Ventricular arrhythmias are life-threatening conditions that cause sudden cardiac death (SCD); subtypes include monomorphic and polymorphic ventricular tachycardia (VT), Torsades de Pointes (TdP, variant of PVT), ventricular fibrillation (VF). It has been estimated that over 356,000 people suffer from out-of-hospital cardiac arrest in the USA annually, nearly 1000 cases each day [13], and SCD remains the world’s leading cause of death, costing 17 million lives each year [14]. Over the years, VT/VF has decreased incidence; they account for 23% of initial cardiac arrest rhythm, with the most commonly encountered ones being asystole (39%) and PEA (37%). This trend is likely due to the advancement of devices like implantable cardiac defibrillators and improvement in preventative cardiology practice [15]. The most common causes of VT/VF include acute coronary syndrome, cardiomyopathies, congenital channelopathies (BrS, LQTS, CPVT), QT-prolonging drugs (macrolides, TCA), electrolytes imbalance, etc. (Consider 4H 4T causes in cardiac arrest).

(Reused from Jones, S. A. (2009). ECG Notes: Interpretation and Management Guide. F.A. Davis Company.)
(Reused from Jones, S. A. (2009). ECG Notes: Interpretation and Management Guide. F.A. Davis Company.)
(Reused from Jones, S. A. (2009). ECG Notes: Interpretation and Management Guide. F.A. Davis Company.)
(Reused from Jones, S. A. (2009). ECG Notes: Interpretation and Management Guide. F.A. Davis Company.)

The diagram below shows a decision-making algorithm.

(Reused from Srinivasan C, Balaji S. Neonatal supraventricular tachycardia. Indian Pacing Electrophysiol J. 2019;19(6):222-231. DOI:10.1016/j.ipej.2019.09.004) – Open Access (https://www.sciencedirect.com/science/article/pii/S0972629219301159)

Medical History

As tachyarrhythmias present with an extensive list of differential diagnoses, a detailed history taking is essential to direct clinicians to the next-step management. The most common clinical presentations in patients suffering from tachycardias include palpitations (84%), chest pain (47%), dyspnoea (38%), syncope (26%), light-headedness (19%) and sweating (18%) [16]. Symptoms can be explored with a simple mnemonic SOCRATES (site/specify, onset, character/change, rhythm/radiation, associated features, timing, exacerbating and relieving factors, severity). As patients often confuse medical terms with other meanings, it is important to ask and clarify what the term means to them (palpitations vs heart attack). Understanding the onset and progression of symptoms would allow us to determine the acuity and chronicity of the presentation. For timing, we need to ask if the presentation constantly existed since the onset, if it is intermittent, and if it comes on at a particular time of the day. In terms of exacerbating and relieving factors, when it comes to cardiac problems, it is particularly important to ask about the difference between exertion and rest and whether the patient tried anything over the counter. As non-cardiac problems cause tachycardia too, it is necessary to perform a systems review from head to toe to rule out other causes (for example, diarrhea, weight loss, heat intolerance, menstrual disturbance in hyperthyroidism). Past medical and family history should never be missed; these help us to identify risk factors, e.g., hypertension, diabetes, familial hypercholesteremia (predispose to MI), and HOCM (predispose to SCD). In the end, remember to ask for medication history (both prescribed and illicit) and social history (especially smoking and alcohol intake).

If the patient is unconscious, collateral histories from friends and family members are ideal candidates to gain some basic understanding of the patient’s background. It is also worthwhile to communicate with EMTs and paramedics and see if any other valuable information can be obtained.

Adverse features (red flags) for tachyarrhythmias are mainly myocardial infarction, syncope, new-onset heart failure, and deteriorating vital signs, i.e., increased capillary refill time, hypotension (indicative of shock), altered consciousness/reduced GCS.

Physical Examination

If the patient is unconscious or has no palpable pulse, manage the patient with basic life support and advanced life support protocols.

Evaluation of all other patients with the A-E approach is critical as they are still undifferentiated. If the patient is conscious, start inspecting the patient. Key features to observe include cyanosis (poor perfusion peri-arrest), pallor (anemia), dyspnea (heart failure, myocardial infarction/injury), diaphoresis (myocardial infarction/injury), and peripheral edema (heart failure). Start peripherally at hands, observe for clubbing (indicative of infective endocarditis, congenital heart diseases, hyperthyroidism), and assess radial and carotid pulse for its rate, rhythm, and volume. Look for visible jugular venous pulse (elevated – heart failure), presence of corneal arcus (familial hypercholesterolemia) in eyes, and scars on the chest (sternotomy, pacemaker). To assess murmurs, auscultate in all 4 valvular areas (2ndICS left sternal border – pulmonary area, 2nd ICS, right sternal border – aortic area, 4th ICS left sternal border – tricuspid area, 5th ICS mid-clavicular line – mitral area). Be sure to examine other systems, including respiratory, neurological, and ENT.

Alternative Diagnoses

As mentioned above, most tachyarrhythmias are idiopathic or secondary to cardiac and non-cardiac causes. It is extremely important to keep an open mind and an extensive list of differentials so we won’t miss the actual diagnosis. The table below lists differentials for palpitations, the chief complaint of tachyarrhythmias.

Causes of Palpitations

Cardiac Causes

Noncardiac Causes

Atrial fibrillation/flutter

Atrial myxoma

Atrial premature contractions

Atrioventricular reentry

Atrioventricular tachycardia

Autonomic dysfunction

Cardiomyopathy

Long QT syndrome

Multifocal atrial tachycardia

Sick sinus syndrome

Supraventricular tachycardia

Valvular heart disease

Ventricular premature contractions

Ventricular tachycardia

Alcohol

Anemia

Anxiety/stress

Beta-blocker withdrawal

Caffeine

Cocaine

Exercise

Fever

Medications

Nicotine

Paget disease of bone

Pheochromocytoma

Pregnancy

Thyroid dysfunction

(Reuse from Wexler RK, Pleister A, Raman SV. Palpitations: Evaluation in the Primary Care Setting. Am Fam Physician. 2017;96(12):784-789.) – Open Access (https://www.aafp.org/pubs/afp/issues/2017/1215/p784.html)

Acing Diagnostic Testing

Any patients with adverse features and life-threatening presentations should be placed in a resuscitation bay with a multi-parameter vitals monitor/defibrillator connected and a point-of-care portable ultrasound ready. For stable patients, stepwise management should be initiated. Proceed with bedside tests: perform a 12-lead ECG, measure heart rate, assess SpO2 with an oximeter, and record blood pressure. Collect blood samples, including a Full Blood Count, Urea and Electrolytes, serum Magnesium, Calcium, Thyroid Function Tests, Liver Function Tests, and a coagulation panel. Additional tests can be considered based on the clinician’s clinical decision and the patient’s presentation, for example, Troponin for suspected MI, D-dimer for suspected PE, etc. Chest X-rays should be performed in any patients presenting with chest pain. Advanced imaging again depends on clinical presentation, coronary angiogram for Myocardial Infarction, Computed Tomography Pulmonary Angiography for Pulmonary Embolism, etc. The risk stratification tool (more details in the section below) can be used to facilitate decisions for advanced interventions involving intensive care input. Cardiology input will be required for further investigations involving Holter monitoring, implantable loop recorder, electrophysiological study, echocardiogram, cardiac Magnetic Resonance Imaging, etc.

Management

Sinus Tachycardia

Sinus tachycardia is often a physiological response to an underlying cause such as sepsis, hypovolemia, or anemia. Management should focus on identifying and addressing these causes rather than targeting the heart rate itself. For example, in a septic patient, early fluid resuscitation and antibiotics are critical, while in a patient with anemia, blood transfusion or treatment of iron deficiency may resolve the tachycardia. Clinicians should avoid unnecessary use of beta-blockers or calcium channel blockers unless sinus tachycardia persists after the underlying cause has been addressed.

Atrial Fibrillation

Management of atrial fibrillation requires a careful evaluation of the patient’s hemodynamic stability, symptom duration, and underlying comorbidities.

  1. Hemodynamically Stable Patients with Symptoms >48 Hours or Uncertain Timeline:

    • Rate control is the priority to prevent further decompensation. Start with beta-blockers (e.g., bisoprolol) or calcium channel blockers (e.g., diltiazem).
    • Consider digoxin for patients with congestive heart failure who may not tolerate beta-blockers.
    • Avoid cardioversion without anticoagulation if the symptom duration is >48 hours or unclear, as this increases the risk of thromboembolic events.

  2. Hemodynamically Stable Patients with Symptoms <48 Hours or a Reversible Cause:

    • Focus on rhythm control with cardioversion, which can be electrical or pharmacological (e.g., flecainide or amiodarone).
    • Ensure anticoagulation with heparin before cardioversion unless contraindicated.
    • Use an echocardiogram to rule out structural abnormalities, as this guides drug selection (e.g., flecainide for structurally normal hearts; amiodarone for structural heart disease).

  3. Patients with Adverse Features (Shock, Syncope, Acute Heart Failure, or Myocardial Ischemia):

    • Immediate electrical cardioversion is required, typically using synchronized shocks. Time is critical—any delay could worsen outcomes.

  4. Paroxysmal AF:

    • Counsel patients on the use of “pill-in-the-pocket” therapies such as flecainide or sotalol for intermittent symptoms. Ensure they understand the signs of structural heart disease, which would contraindicate these medications.

Always consider underlying conditions such as hyperthyroidism, electrolyte disturbances, or alcohol-related atrial fibrillation (Holiday Heart Syndrome). Addressing these causes can prevent recurrence. In elderly patients or those with heart failure, weigh the benefits of rhythm versus rate control.

Atrial Flutter

Management of atrial flutter parallels that of atrial fibrillation. Rate control is often sufficient in stable patients, but rhythm control may be prioritized for symptomatic relief. In acute settings, electrical cardioversion may be more effective than pharmacological approaches.

Atrial flutter is frequently associated with underlying structural heart disease or atrial enlargement. Evaluate for these conditions with echocardiography and address them to improve long-term outcomes.

AVNRT (Atrioventricular Nodal Reentrant Tachycardia)

AVNRT is often well-managed with non-pharmacological measures in stable patients.

Conservative Management:

  • Initiate vagal maneuvers (e.g., Valsalva maneuver or carotid massage). These can terminate the tachycardia in many cases. Ensure the patient is monitored for safety, especially in older adults where carotid massage could induce complications.

Pharmacological Management:

  • Administer IV adenosine, starting at 6 mg and escalating to 12 mg or 18 mg if needed. Warn the patient about the transient sensation of chest discomfort or flushing.
  • If adenosine is contraindicated (e.g., in asthmatic patients), use a calcium channel blocker such as verapamil.

Persistent Cases:

  • Consider beta-blockers, digoxin, or amiodarone if initial treatments fail.

Hemodynamically Unstable Patients:

  • Proceed with immediate cardioversion to stabilize the patient.

In recurrent AVNRT, evaluate for underlying triggers such as excessive caffeine or stimulant use. Discuss long-term options such as catheter ablation for definitive treatment.

AVRT/WPW (Atrioventricular Reentrant Tachycardia/Wolff-Parkinson-White Syndrome)

In patients with WPW, rapid and accurate diagnosis is critical to avoid inappropriate treatment.

Stable Patients:

  • Treat with amiodarone, flecainide, or procainamide. Avoid digoxin and calcium channel blockers, as these can worsen pre-excitation and lead to ventricular fibrillation.

Unstable Patients:

  • Immediate cardioversion is indicated.

In young patients presenting with sudden palpitations and syncope, always consider WPW and obtain a 12-lead ECG for diagnosis. Educate patients on avoiding stimulants that may precipitate episodes.

Atrial Tachycardia

For atrial tachycardia, management depends on the patient’s stability. Rate control is often effective for stable patients, while cardioversion may be required in unstable cases.

Investigate underlying causes such as digoxin toxicity or structural heart disease, as addressing these may resolve the tachycardia.

Ventricular Tachycardia (VT)

Management of VT hinges on the patient’s hemodynamic stability.

Stable VT:

    • Administer amiodarone (300 mg IV STAT followed by a 900 mg infusion over 24 hours). Monitor for potential side effects such as hypotension or bradycardia.

Unstable VT, pulse positive:

    • Follow the ALS (Advanced Life Support) algorithm, prioritizing cardioversion.

VT, no pulse:

  • Follow the ALS (Advanced Life Support) algorithm, prioritizing defibrillation and CPR.

In patients with recurrent VT, assess for underlying ischemic heart disease or electrolyte abnormalities. Long-term management may require ICD placement or catheter ablation.

Ventricular Fibrillation (VF)

VF is a life-threatening emergency requiring immediate intervention. Follow the ALS algorithm, which includes high-quality CPR and defibrillation.

Always assess for reversible causes of VF, such as acute myocardial infarction or electrolyte imbalances (e.g., hypokalemia or hypomagnesemia), and treat these aggressively to prevent recurrence.

Tachycardia and advanced life support algorithms are provided below.

(Reuse from Soar J, Böttiger BW, Carli P, et al. European Resuscitation Council Guidelines 2021: Adult advanced life support [published correction appears in Resuscitation. 2021 Oct;167:105-106]. Resuscitation. 2021;161:115-151. DOI:10.1016/j.resuscitation.2021.02.010) – Open Access (https://www.cprguidelines.eu/)
(Reuse from Soar J, Böttiger BW, Carli P, et al. European Resuscitation Council Guidelines 2021: Adult advanced life support [published correction appears in Resuscitation. 2021 Oct;167:105-106]. Resuscitation. 2021;161:115-151. DOI:10.1016/j.resuscitation.2021.02.010) – Open Access (https://www.cprguidelines.eu/)

Special Patient Groups

The management of most tachyarrhythmias is similar among pregnant women and pediatric populations, with the exception of ventricular cardiac arrest rhythms.

Pregnant Patients (Obstetric Cardiac Arrest ) [17]

  • A normal supine position will result in aortocaval compression from the gravid uterus; this reduces cardiac output. Hence, placing the patient in a left lateral position is crucial, especially at> 20 weeks gestation.
  • The position of the rescuer’s hands for chest compression ideally should be slightly higher than usual, taking the elevation of the diaphragm and abdominal contents caused by the gravid uterus into account.
  • The defibrillator pad position should be adjusted to maintain the left lateral position.
  • Magnesium sulfate (4 g IV) should be given in patients with eclampsia.
  • Patients should be intubated early due to the higher risk of pulmonary aspiration and Mendelson syndrome from gastric contents.
  • Emergency delivery of the fetus (>20 weeks) with resuscitative hysterotomy should happen within 5 minutes in the event of cardiac arrest, given that the initial resuscitation attempt has failed. This is a definitive procedure to decompress IVC to facilitate venous return and increase cardiac output.
  • As this is an obstetric emergency, get help from the OB/GYN and neonatal team early; resuscitative hysterotomy should not wait even if not all surgical equipment is immediately available; one scalpel is enough to start the procedure.

Pediatrics (Cardiac Arrest) [17]

  • Most pediatric cardiac arrests are secondary to respiratory failure; hence, giving 5 rescue breaths is essential prior to chest compressions.
  • Pulse checks use brachial or femoral pulses as opposed to carotid pulses in adults.
  • It is a similar compression site but with a compression: breath ratio of 15:2, as opposed to 30:2 in adults.
  • In infants, compress the chest using two fingers or an encircling technique (two thumbs). For children over one year old, use one or two hands.
  • Intraosseous (IO) access is preferred for circulation access, as obtaining venous access can be difficult in children.
  • Adrenaline is given in 10 mcg/kg, and Amiodarone is given in 5 mg/kg.
  • Note that PALS is different from newborn life support (NLS), which is not mentioned here.

* Please refer to European Resuscitation Council (ERC) Paediatric Life Support and Special Circumstances Guidelines (https://www.cprguidelines.eu/)

Risk Stratification

There is no single risk stratification tool for tachyarrhythmias, developed scoring systems are usually condition-specific or presentation-specific. We listed some of the important ones related to tachyarrhythmias below:

  • Cardiac Arrest Hospital Prognosis (CAHP) score – predicts prognosis in patients suffering from out-of-hospital cardiac arrest. [18]
  • Cardiac Arrest Risk Triage (CART) Score – predicts the risk of in-hospital cardiac arrest in hospitalized patients. [19]
  • CHA₂DS₂-VASc Score – calculate stroke risk in patients with atrial fibrillation and guide initiation of anticoagulation therapy. [20]
  • HEART score – predicts patients presenting with chest pain for a 6-week risk of major adverse cardiac events (MACE). It can also classify patients into low, moderate, and high-risk groups to facilitate decisions for discharge from ED, admission for observation, or urgent intervention required. [21]
  • Thrombolysis In Myocardial Infarction (TIMI) score and Global Registry of Acute Coronary Events (GRACE) score – estimate mortality for patients with acute coronary syndrome, guide decision for coronary revascularisation needs. [22]
  • Well’s Score – calculate the clinical probability of DVT/PE and guide the decision to consider alternative diagnosis or perform immediate CTPA/anticoagulation. [23]
  • Pulmonary Embolism Rule Out Criteria (PERC) – effectively rules out PE if scored 0. [24]
  • Pulmonary Embolism Severity Index (PESI) – predicts 30-day mortality in patients with PE. [25]
  • Emergency Heart Failure Mortality Risk Grade (EHMRG) estimates 7-day mortality in patients with congestive heart failure and guides the decision to admit them [26].
  • San Francisco syncope rule (SFSR), Canadian syncope risk score (CSRS), and Evaluation of Guidelines in SYncope Study (EGSYS) Score – both SFSR and CSRS predict adverse outcomes in patients presenting with syncope (7-day and 30-day, respectively), EGSYS helps determine whether syncope is cardiac or non-cardiac cause (these includes vasovagal, situational, postural hypotension). [27-29]
  • Multi-parametric models – predict the prognosis of patients with Brugada syndrome for future major arrhythmic events (VT/VF) and guide decisions for implantable cardioverter defibrillator placement. [30]

* Please browse these calculators on MDCalc website (https://www.mdcalc.com/)

When To Admit This Patient

Patients with adverse features and hemodynamic instability require immediate intervention and admission. The aforementioned risk stratification tools can be used based on clinical signs and symptoms. If initial investigations yielded no clinical significance, patients could be discharged with education, reassurance, and safety netting advice. Explain that palpitations are usually transient and harmless; if they are recurring, ask patients to note down the onset, timing, and duration and measure BP and HR if monitoring is available at home. Advise them to reattend ED if symptoms persist or worsen or new-onset red flag symptoms emerge; lifestyle advice, for example, avoid certain known stimulants like caffeine, alcohol, and nicotine. If the patient is known to have SVT, educate about self-performing Valsalva maneuver to try terminating it before medical assistance arrives. Arrange follow-up with a family physician and review the need for further investigations and specialist input. Patients should be referred urgently for detailed investigations, including Holter monitoring if non-specific new clinical findings are yielded. Other options may be explored, such as an echocardiogram, implantable loop recorder, and electrophysiology study. [31, 32]

Revisiting Your Patient

The case reminds us that tachyarrhythmias can be secondary to non-cardiac causes. This is a classical presentation of hyperthyroidism, with ECG showing fast-rate atrial fibrillation. Atrial fibrillation occurs in 15% of patients with hyperthyroidism. A detailed history taking with appropriate systems review (as symptoms suggest) would point us towards hyperthyroidism. Clinical examination may reveal clubbing (thyroid acropachy), exomphalos (thyroid eye disease), pretibial myxoedema, goiter, and an irregular heartbeat with mid-systolic scratchy murmur (Means–Lerman scratch) might be heard on auscultation. The investigation here, starting from bedside, would be to obtain a complete set of vital signs (blood pressure, heart rate, respiratory rate, temperature, SpO2), 3-lead continuous monitoring, and 12-lead ECG; blood including complete blood count, urea and electrolytes, thyroid function tests, troponin (serial), venous blood gas, other electrolytes (Ca2+). The management approach of this patient is to treat the underlying hyperthyroidism primarily. Hence, endocrinologist referral will be required, with cardiologists’ input on managing the fast Atrial Fibrillation. Propranolol (reduces peripheral conversion of T4 to T3) and anti-thyroid drugs like carbimazole (inhibits thyroid peroxidase action) are the mainstay management (details see thyroid disorder chapter). However, as the patient also complains of anginal pain, rate control with cardio-selective beta-blockers should be initiated as well. It also helps with alleviating symptoms of hyperthyroidism, including palpitations, tremors, anxiety, heat intolerance, etc., due to the increased sympathetic tone caused by excess thyroid hormone production. The need for anticoagulation is assessed on an individual basis. In most cases, Atrial Fibrillation reverses to sinus rhythm spontaneously after the euthyroid state has been achieved. However, if Atrial Fibrillation persists, cardioversion may be considered. This, nevertheless, would be a cardiologist’s decision. [33]

Authors

Picture of Keith Sai Kit Leung

Keith Sai Kit Leung

Keith is an academic foundation doctor (emergency medicine themed) in the UK. He graduated both BSc and MBChB with distinction, and has published over 30 peer-reviewed articles till date. He is interested in Pre-Hospital Emergency & Retrieval Medicine, Intensive Care, Cardiology and Medical Education. He main research interests are arrhythmias and cardiac electrophysiology, cardiac arrest and resuscitation, ACS, POCUS, ECMO, airway and trauma management. He aims to work as an academic PHEM/HEMS physician and pursue a MD (Res)/PhD in the near future.

Picture of Rafaqat Hussain

Rafaqat Hussain

Dr Rafaqat Hussain is working as Specialty Doctor in Emergency Department at SWBH NHS trust. He had done MBBS.MRCEM. FRCEM.EBCEM. He has involved in training and teaching for junior doctors and medical students at University of Birmingham. He is enthusiastic in pursuing his career in being an Emergency Medicine Consultant.

Picture of Abraham Ka Cheung Wai

Abraham Ka Cheung Wai

Dr Abraham Wai, Clinical Associate Professor at the University of Hong Kong (HKU), is a dynamic force in the field of emergency medicine. His journey from specialist training to impactful research and innovative teaching has left an indelible mark on the healthcare landscape.

Listen to the chapter

References

  1. Pinto DS, Ho KK, Zimetbaum PJ, Pedan A, Goldberger AL. Sinus versus nonsinus tachycardia in the emergency department: importance of age and heart rate. BMC Cardiovasc Disord. 2003;3:7. doi:10.1186/1471-2261-3-7
  2. Gabayan GZ, Sun BC, Asch SM, et al. Qualitative factors in patients who die shortly after emergency department discharge. Acad Emerg Med. 2013;20(8):778-785. doi:10.1111/acem.12181
  3. Wilson PM, Florin TA, Huang G, Fenchel M, Mittiga MR. Is Tachycardia at Discharge From the Pediatric Emergency Department a Cause for Concern? A Nonconcurrent Cohort Study. Ann Emerg Med. 2017;70(3):268-276.e2. doi:10.1016/j.annemergmed.2016.12.010
  4. Sohinki D, Obel OA. Current trends in supraventricular tachycardia management. Ochsner J. 2014;14(4):586-595.
  5. Kotadia ID, Williams SE, O’Neill M. Supraventricular tachycardia: An overview of diagnosis and management. Clin Med (Lond). 2020;20(1):43-47. doi:10.7861/clinmed.cme.20.1.3
  6. Tse G. Mechanisms of cardiac arrhythmias. J Arrhythm. 2016;32(2):75-81. doi:10.1016/j.joa.2015.11.003
  7. Li H, Song X, Liang Y, et al. Global, regional, and national burden of disease study of atrial fibrillation/flutter, 1990-2019: results from a global burden of disease study, 2019. BMC Public Health. 2022;22(1):2015. doi:10.1186/s12889-022-14403-2
  8. Orejarena LA, Vidaillet H Jr, DeStefano F, et al. Paroxysmal supraventricular tachycardia in the general population. J Am Coll Cardiol. 1998;31(1):150-157. doi:10.1016/s0735-1097(97)00422-1
  9. George SA, Faye NR, Murillo-Berlioz A, Lee KB, Trachiotis GD, Efimov IR. At the Atrioventricular Crossroads: Dual Pathway Electrophysiology in the Atrioventricular Node and its Underlying Heterogeneities. Arrhythm Electrophysiol Rev. 2017;6(4):179-185. doi:10.15420/aer.2017.30.1
  10. Chhabra L, Goyal A, Benham MD. Wolff Parkinson White Syndrome. [Updated 2023 Jan 28]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK554437/
  11. Liwanag M, Willoughby C. Atrial Tachycardia. [Updated 2022 Jun 27]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK542235/
  12. Hafeez Y, Grossman SA. Junctional Rhythm. [Updated 2023 Feb 5]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK507715/
  13. Srinivasan NT, Schilling RJ. Sudden Cardiac Death and Arrhythmias. Arrhythm Electrophysiol Rev. 2018;7(2):111-117. doi:10.15420/aer.2018:15:2
  14. Tsao CW, Aday AW, Almarzooq ZI, et al. Heart Disease and Stroke Statistics-2022 Update: A Report From the American Heart Association [published correction appears in Circulation. 2022 Sep 6;146(10):e141]. Circulation. 2022;145(8):e153-e639. doi:10.1161/CIR.0000000000001052
  15. Keller SP, Halperin HR. Cardiac arrest: the changing incidence of ventricular fibrillation. Curr Treat Options Cardiovasc Med. 2015;17(7):392. doi:10.1007/s11936-015-0392-z
  16. Yetkin E, Ozturk S, Cuglan B, Turhan H. Clinical presentation of paroxysmal supraventricular tachycardia: evaluation of usual and unusual symptoms. Cardiovasc Endocrinol Metab. 2020;9(4):153-158. doi:10.1097/XCE.0000000000000208
  17. Maupain C, Bougouin W, Lamhaut L, et al. The CAHP (Cardiac Arrest Hospital Prognosis) score: a tool for risk stratification after out-of-hospital cardiac arrest. Eur Heart J. 2016;37(42):3222-3228. doi:10.1093/eurheartj/ehv556
  18. Banerjee, A., & Oliver, C. (2017). Revision notes for the FRCEM intermediate SAQ paper (2nd). Oxford University Press.
  19. Churpek MM, Yuen TC, Park SY, Meltzer DO, Hall JB, Edelson DP. Derivation of a cardiac arrest prediction model using ward vital signs. Crit Care Med. 2012;40(7):2102-2108. doi:10.1097/CCM.0b013e318250aa5a
  20. Lip GY, Nieuwlaat R, Pisters R, Lane DA, Crijns HJ. Refining clinical risk stratification for predicting stroke and thromboembolism in atrial fibrillation using a novel risk factor-based approach: the euro heart survey on atrial fibrillation. Chest. 2010;137(2):263-272. doi:10.1378/chest.09-1584
  21. Brady W, de Souza K. The HEART score: A guide to its application in the emergency department. Turk J Emerg Med. 2018;18(2):47-51. doi:10.1016/j.tjem.2018.04.004
  22. de Araújo Gonçalves P, Ferreira J, Aguiar C, Seabra-Gomes R. TIMI, PURSUIT, and GRACE risk scores: sustained prognostic value and interaction with revascularization in NSTE-ACS. Eur Heart J. 2005;26(9):865-872. doi:10.1093/eurheartj/ehi187
  23. Wells PS, Anderson DR, Rodger M, et al. Excluding pulmonary embolism at the bedside without diagnostic imaging: management of patients with suspected pulmonary embolism presenting to the emergency department by using a simple clinical model and d-dimer. Ann Intern Med. 2001;135(2):98-107. doi:10.7326/0003-4819-135-2-200107170-00010
  24. Freund Y, Cachanado M, Aubry A, et al. Effect of the Pulmonary Embolism Rule-Out Criteria on Subsequent Thromboembolic Events Among Low-Risk Emergency Department Patients: The PROPER Randomized Clinical Trial. JAMA. 2018;319(6):559-566. doi:10.1001/jama.2017.21904
  25. Aujesky D, Obrosky DS, Stone RA, et al. Derivation and validation of a prognostic model for pulmonary embolism. Am J Respir Crit Care Med. 2005;172(8):1041-1046. doi:10.1164/rccm.200506-862OC
  26. Lee DS, Lee JS, Schull MJ, et al. Prospective Validation of the Emergency Heart Failure Mortality Risk Grade for Acute Heart Failure. Circulation. 2019;139(9):1146-1156. doi:10.1161/CIRCULATIONAHA.118.035509
  27. Quinn J, McDermott D, Stiell I, Kohn M, Wells G. Prospective validation of the San Francisco Syncope Rule to predict patients with serious outcomes. Ann Emerg Med. 2006;47(5):448-454. doi:10.1016/j.annemergmed.2005.11.019
  28. Thiruganasambandamoorthy V, Kwong K, Wells GA, et al. Development of the Canadian Syncope Risk Score to predict serious adverse events after emergency department assessment of syncope. CMAJ. 2016;188(12):E289-E298. doi:10.1503/cmaj.151469
  29. Kariman H, Harati S, Safari S, Baratloo A, Pishgahi M. Validation of EGSYS Score in Prediction of Cardiogenic Syncope. Emerg Med Int. 2015;2015:515370. doi:10.1155/2015/515370
  30. Chung CT, Bazoukis G, Radford D, et al. Predictive risk models for forecasting arrhythmic outcomes in Brugada syndrome: A focused review. J Electrocardiol. 2022;72:28-34. doi:10.1016/j.jelectrocard.2022.02.009
  31. Moulton KP, Bhutta BS, Mullin JC. Evaluation Of Suspected Cardiac Arrhythmia. [Updated 2023 Feb 9]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK585054/
  32. RCEMLearning. https://www.rcemlearning.co.uk/reference/palpitations/. Published July 27, 2021. Accessed April 13, 2023.
  33. Parmar MS. Thyrotoxic atrial fibrillation. MedGenMed. 2005;7(1):74.

Reviewed and Edited By

Picture of Arif Alper Cevik, MD, FEMAT, FIFEM

Arif Alper Cevik, MD, FEMAT, FIFEM

Prof Cevik is an Emergency Medicine academician at United Arab Emirates University, interested in international emergency medicine, emergency medicine education, medical education, point of care ultrasound and trauma. He is the founder and director of the International Emergency Medicine Education Project – iem-student.org, chair of the International Federation for Emergency Medicine (IFEM) core curriculum and education committee and board member of the Asian Society for Emergency Medicine and Emirati Board of Emergency Medicine.

Blood Transfusion And Its Complications (2024)

~ iEM Education Project Team ~ Leave a comment

by Yaman Hukan, Thiagarajan Jaiganesh

Authors
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You have a new patient!

A 68-year-old male with a history of controlled HTN, DM, and Ischemic heart disease presents to the Emergency Department with complaints of easy fatiguability that started 2 months ago. He reports a gradual onset of symptoms and inability to tolerate his usual morning walk. He denies chest pain or palpitations. Upon further questioning, he mentioned that he noticed his clothes getting loose, and his family noticed he had lost weight. On review of systems, he states he has bouts of diarrhea with dark stools. Upon arrival, his vitals are Temp 36.9 C, HR 105 BPM, BP 122/68 mmHg, RR 17 BPM, and SpO2 of 98% on RA.  Blood investigations reveal an Hgb level of 5.0 g/dL. Therefore, you decide to initiate a Packed RBC transfusion in the ER. One hour after starting the transfusion, you are called by the nurse as the patient is becoming distressed. You attend to the patient and notice him to be in severe respiratory distress.

What do you need to know?

Often, patients presenting to Emergency Departments require a blood transfusion. According to the National Blood Collection and Utilization survey administered by the US Department of Health and Human Services, 2019 around 1 million RBC transfusions took place in EDs across the United States [1]. The clinical conditions necessitating a blood transfusion include upper and lower gastrointestinal bleeding, traumatic shock, symptomatic anemia, etc., to name a few. Therefore, medical trainees and emergency physicians must be aware of complications that may arise from blood transfusions and manage them appropriately.

Commonly administered blood products in the emergency department (ED) include packed red blood cells (PRBCs), fresh frozen plasma (FFP), platelet concentrates, and cryoprecipitate. PRBCs are frequently used to increase oxygen-carrying capacity in patients with significant anemia or hemorrhage. FFP provides essential clotting factors, making it valuable in cases of coagulopathy or massive transfusion protocols. Platelet concentrates are utilized to manage thrombocytopenia or platelet dysfunction, while cryoprecipitate supplies fibrinogen, von Willebrand factor, and other clotting factors, supporting hemostasis in patients with severe bleeding or fibrinogen deficiency.

The choice of components should be directed by the patient’s clinical condition, rate of bleeding, cardiopulmonary status, and operative intervention, with the goal of restoring volume and oxygen-carrying capacity [2].

Administering blood and blood products to patients has resulted in numerous adverse reactions. These reactions are broadly classified as either Acute (onset within 24 hrs), such as febrile nonhemolytic reactions, or Delayed (onset beyond 24 hrs), such as delayed hemolytic reactions [3].

Data from the National Healthcare Safety Network Hemovigilance Module in the United States demonstrate that 1 in 455 blood components transfused was associated with an adverse reaction. However, the incidence of serious reactions was much lower, at 1 in 6224. Despite the relatively lower rates of serious reactions, 23 fatalities were recorded between 2013 and 2018 [4].

Severe adverse reactions result from transfusing incompatible (ABO or Rh) blood. The ABO blood group system remains of extreme importance in blood transfusions, as it is the most immunogenic of all blood group antigens [5]. The four blood groups are A, B, O, and AB.

The table shows the summary of ABO Antigens and Antibodies contained within each blood type.

 

A

B

O

AB

Antigens

A

B

None

A and B

Antibodies

Anti-B

Anti-A

Anti-A & Anti-B

None

There are several ABO blood group antigens expressed on every RBC cell. Each blood group early on during life forms antibodies against ABO antigens not found on the surface of RBCs. When an individual is transfused ABO-incompatible blood, preformed antibodies in its own serum react against the donor’s red blood cells, causing rapid acute intravascular hemolysis, a life-threatening transfusion reaction.

The second significant blood grouping system is the Rh system. The presence of Rh Antigen implies that the patient is Rh(+) (e.g., Blood group O+). Patients who are Rh(-) lack the RhD antigen. Therefore, their blood develops antibodies against Rh(+) blood groups if they are ever exposed to it. This incompatibility can lead to a hemolytic reaction, but it is much less likely than a hemolytic reaction due to ABO incompatibility. The clinical significance of the Rh system lies in the pregnancy setting when a Rh(-) mother is pregnant with an Rh(+) fetus. Upon first exposure to the positive blood from the fetus, the mother’s blood would form antibodies against Rh-blood. In case of a repeated pregnancy with Rh+ fetus, the mother’s antibodies cross the placenta and attack the RBCs of the fetus, which can lead to a condition called hemolytic disease of the newborn [6]. This is the reason why women of childbearing age should always receive O(-) blood in the setting of acute hemorrhage needing a blood transfusion, as opposed to men who may receive O(+) blood safely.

Medical History

Should a patient receiving or recently received a blood or a blood product transfusion develop new signs and symptoms, consider a transfusion reaction. Commonly encountered signs and symptoms of mild transfusion reactions include:

  • Increase in body temperature/fever,
  • Chills/Rigors,
  • Pruritis, New rash, or swelling of the mucous membranes.

Severe reactions include:

  • Difficulty in breathing,
  • Respiratory distress,
  • Altered level of consciousness,
  • Decreased urinary output.

Reaction Types

Acute Transfusion Reactions

Febrile nonhemolytic transfusion reaction

This is one of the most common transfusion reactions, occurring at a rate of around 1:900 [7]. It has been attributed to cytokines released from white blood cells and their accumulation in blood products [8].

Diagnostic criteria

  • A reaction which occurs during or within 4 hours of cessation of transfusion,

AND

  • Either Fever (> 38 C° and a change of at least 1 C° from pretransfusion value) OR Chills/Rigors is present [9].

Caution must be exercised when distinguishing between febrile nonhemolytic transfusion reactions and hemolytic reactions, which could also present with fever. Febrile nonhemolytic transfusion reaction is considered a diagnosis of exclusion [8]. In the case of first onset of a febrile reaction, a hemolytic reaction must be suspected until proven otherwise.

Allergic and anaphylactic transfusion reactions

Another very common non-infectious transfusion reaction is allergy. Allergic reactions vary in severity from mild to severe. Mild reactions are primarily characterized by itching and hives. They occur at a rate of 1:1200 transfusions. However, rates may be much higher due to underreporting [7].

On the other hand, anaphylactic reactions are typically more severe and occur at a rate of around 1:30000 blood transfusions [7]. Anaphylactic reactions are acute systemic allergic reactions characterized most significantly by hypotension and/or respiratory compromise. They typically arise abruptly within 0-4 hours of initiating the transfusion.

Allergic reactions are thought to be multifactorial in etiology, mainly caused by an antibody-mediated response to donor proteins. These reactions fall under Type 1 hypersensitivity reactions and involve pre-existing IgE antibodies [10].

The criteria for a definitive diagnosis of an allergic reaction encompasses two or more of the following during or within 4 hours of cessation of transfusion: conjunctival edema, edema of lips, tongue, and uvula; Erythema and edema of the periorbital area, generalized flushing, hypotension, localized angioedema, maculopapular rash, pruritis (itching), respiratory distress/bronchospasm, and urticaria (hives) [9].

Acute hemolytic transfusion reaction

The hemolytic transfusion reaction is perhaps the most severe and life-threatening transfusion reaction. They account for 5% of all severe adverse reactions of blood transfusions.  Reactions due to ABO incompatibility occur at a rate of 1:200000 [7]. The rate significantly increases in the setting of uncross-matched blood transfusions in bleeding patients (e.g., major trauma), where the rate reaches as high as 1:2000 [11].

Despite their relative rarity, mainly due to growing hemovigilance procedures and schemes, acute hemolytic transfusion reactions can lead to significant morbidity and mortality. Mortality rates increase with the increase in the volume of the incompatible transfused blood. However, even a volume of as low as 30 mL could lead to a severe fatal reaction [12].

Reactions due to ABO system incompatibility most often occur due to a clerical or laboratory error, including misidentification of patient or mislabelling blood samples collected from the recipient for crossmatching. The recipient’s blood contains pre-existing antibodies against ABO antigens that are not present in their blood. When incompatible blood is administered, those pre-existing antibodies attack the donor’s RBCs. Through complement activation and membrane attack complex, the donor’s RBCs are destroyed, leading to intravascular hemolysis, which subsequently gives rise to the clinical features of hemolysis, including acute tubular necrosis, renal failure, hypotension, disseminated intravascular coagulopathy (DIC), and shock [13].

The criteria for the definitive diagnosis of acute hemolytic transfusion reactions is complex and includes components that can be obtained from clinical presentation combined with laboratory studies, detailed below [9]:

Decision-Making Algorithm for Suspected Hemolytic Transfusion Reaction
1. Identify New-Onset Symptoms

Check if the patient has developed any new symptoms during the transfusion or within 24 hours of transfusion cessation. The presence of any of the following symptoms warrants further investigation:

  • Back or flank pain
  • Chills or rigors
  • Disseminated intravascular coagulation (DIC)
  • Epistaxis (nosebleed)
  • Fever
  • Hematuria (indicative of gross hemolysis)
  • Hypotension
  • Oliguria or anuria (reduced or absent urine output)
  • Pain and/or oozing at the IV site
  • Renal failure

AND

Check for Laboratory Evidence of Hemolysis
Confirm the presence of at least two of the following laboratory findings:

  • Decreased fibrinogen
  • Decreased haptoglobin
  • Elevated bilirubin
  • Elevated lactate dehydrogenase (LDH)
  • Hemoglobinemia
  • Hemoglobinuria
  • Plasma discoloration consistent with hemolysis
  • Spherocytes visible on blood film

AND EITHER

Determine the Mechanism of Hemolysis. Differentiate between immune-mediated and non-immune-mediated hemolysis.

IMMUNE-MEDIATED HEMOLYSIS

  • Perform a Direct Antiglobulin Test (DAT) to detect anti-IgG or anti-C3.
  • Conduct an elution test to detect any alloantibodies on the transfused red blood cells. If the DAT or elution test is positive, this suggests an immune-mediated HTR.

NON-IMMUNE-MEDIATED HEMOLYSIS

  • If serologic testing is negative and there is evidence of a physical cause (e.g., thermal, osmotic, mechanical, or chemical), consider a non-immune etiology. A confirmed physical cause indicates a non-immune-mediated HTR.
Transfusion related acute lung injury (TRALI)

Transfusion-related acute lung injury (TRALI) is an infrequent but incredibly serious blood transfusion reaction. Despite only occurring at the rate of 1:60000 [7], TRALI is reported to be one of the most life-threatening complications according to data from the US Food and Drug Administration, coming in 2nd place among the most fatal blood transfusion reactions in the United States between 2016 and 2020, causing 21% of reported fatalities [14].

TRALI results in a constellation of symptoms that manifest as acute respiratory distress along with hemodynamic instability and can occur with virtually all blood components. The proposed mechanism is complex and involves activation of pulmonary endothelium and polymorphonuclear leucocytes and transfusion of plasma-containing antibodies directed against antigens on the surface of those leucocytes, leading to their activation [15].

The TRALI diagnosis remains clinical and significantly overlaps with other respiratory conditions (e.g., ARDS and Transfusion-associated circulatory overload). A set of clinical features have been adopted to define TRALI, including [9]:

  • No evidence of acute lung injury prior to transfusion, AND,
  • Acute lung injury onset during or within 6 hours of cessation of transfusion, AND,
  • Hypoxemia defined by any of the following methods:
      • PaO2/FiO2 less than or equal to 300 mmHg
      • Oxygen saturation less than 90% on room air
      • Other clinical evidence

AND,

  • Radiographic evidence of bilateral infiltrates
  • No evidence of left atrial hypertension (i.e., circulatory overload)
Transfusion associated circulatory overload (TACO)

The last of the acute transfusion reactions is transfusion-associated circulatory overload (TACO), which carries the highest mortality risk among all reactions. Between 2016 and 2020, 34% of recorded fatalities due to reactions to blood transfusions were caused by TACO [14]. It is relatively more common than TRALI, occurring at an estimated rate of 1:9000 transfusions [7]. TACO can present on a spectrum of mild symptoms to life-threatening ones. Significant overlap exists between TRALI and TACO as both may cause respiratory distress and potentially lead to hemodynamic instability.

TACO is a form of volume overload leading to pulmonary edema. Patients who are older than 70 years of age, suffer from pre-existing cardiac disease, or have a history of renal dysfunction are at increased risk of developing this complication [16].

The criteria for diagnosing TACO have evolved several times over the years. Currently, establishing a definitive diagnosis would require the following [9]:

New onset or exacerbation of 3 or more of the following within 12 hours of cessation of transfusion:

At least 1 of the following two items:-

  1. Evidence of acute or worsening respiratory distress (dyspnea, tachypnoea, cyanosis, and decreased oxygen saturation values in the absence of other specific causes) and/or 
  2. Radiographic or clinical evidence of acute or worsening pulmonary edema (crackles on lung auscultation, orthopnea, cough, a third heart sound, and pinkish frothy sputum in severe cases) or both

             AND;

  • Elevated brain natriuretic peptide (BNP) or NT-pro BNP relevant biomarker
  • Evidence of cardiovascular system changes not explained by underlying medical condition (Elevated central venous pressure, evidence of left heart failure including development of tachycardia, hypertension, widened pulse pressure, jugular venous distension, enlarged cardiac silhouette, and/or peripheral edema)
  • Evidence of fluid overload

Delayed Transfusion Reactions

In addition to acute blood transfusion reactions, there are certain reactions which could appear days or weeks following blood transfusions.

Delayed hemolytic transfusion reaction

Delayed hemolytic transfusion reactions are less severe forms of hemolytic reactions in patients receiving blood transfusions. They appear to be caused by secondary (anamnestic) responses in patients who have already received transfusions. They rarely cause life-threatening or serious manifestations [17]. Those reactions may occur up to 4 weeks following the completion of the transfusion. They are less common than acute hemolytic transfusions, occurring at a rate of 1:22000 transfusions [7].

The criteria for definitive diagnosis of delayed hemolytic transfusion reactions include [9]:

Positive direct antiglobulin test (DAT) for antibodies developed between 24 hours and 28 days after cessation of transfusion

AND EITHER

  • Positive elution test with alloantibody present on the transfused red blood cells OR
  • Newly identified red blood cell alloantibody in recipient serum

AND EITHER

  • Inadequate rise of post-transfusion hemoglobin level or rapid fall in hemoglobin back to pre-transfusion levels OR
  • Otherwise, unexplained appearance of spherocytes
Transfusion associated graft vs. host disease

Transfusion-associated graft vs. host disease is an extremely rare and exceptionally dangerous complication of transfusions, occurring at a rate of 1 in every 13 million [7]. It can present any time up to 6 weeks following the transfusion. It is thought to be caused by viable lymphocytes in the donor’s blood recognizing their new host’s cells as foreign and attacking them, often leading to fatal outcomes [17].

Diagnosis is made when the following characteristics appear between 2 days to 6 weeks from cessation of transfusion [9]:

  • Characteristic rash: erythematous, maculopapular eruption centrally that spreads to extremities and may, in severe cases, progress to generalized erythroderma and hemorrhagic bullous formation.
  • Diarrhea
  • Fever
  • Hepatomegaly
  • Liver dysfunction (i.e., elevated ALT, AST, Alkaline phosphatase, and bilirubin)
  • Marrow aplasia
  • Pancytopenia

AND

  • Characteristic histological appearance of skin or liver biopsy
Post transfusion purpura

This reaction may appear up to 2 weeks post-transfusion and involves platelets [17]. Its prevalence is thought to be around 1 in 57,000 transfusions [7]. A definitive diagnosis may be reached by the following two findings [9]:

  • Alloantibodies in the patient directed against human platelet antigens (HPAs) or other platelet-specific antigens detected at or after the development of thrombocytopenia AND
  • Thrombocytopenia (i.e., decrease in platelets to less than 20% of pre-transfusion count)

Physical Examination

Transfusion reactions could manifest in several organ systems. It is important to exercise vigilance when approaching a patient with a suspected transfusion reaction, as clinical features significantly overlap between several reactions.

One unified step in the physical examination of patients with suspected transfusion reactions is to obtain a complete set of vital signs. This can provide important clues to the diagnosis. For instance, a rise in baseline temperature could indicate a Febrile nonhemolytic reaction, Acute hemolytic reaction, or even TRALI.

Hypotension is a feature of anaphylaxis or acute hemolysis. In addition, while keeping in mind that TRALI can present with either Hypotension or Hypertension, hypotension is more common in TRALI [18] and can help distinguish it from TACO, which can present with respiratory distress coupled with hypertension. Tachypnea and desaturation can be signs of respiratory distress, which would point to either TRALI or TACO as possible diagnoses. Following vitals, emphasis should be on signs relating to the suspected reactions.

Chills and rigors might be observed in acute hemolytic transfusion reaction, along with fever and hypotension. Respiratory status examination is essential and could yield signs of acute distress, including tachypnea, oxygen desaturation, use of accessory muscles, and wheezing. Patients would be anxious, with some reporting a sense of impending doom. Additionally, urine frequency and color should be observed for oliguria or dark-colored urine, pointing to acute hemolysis.

Observe any signs of maculopapular urticarial rash in suspected allergic reactions. Also, look for any signs of dyspnea, wheezing, anxiety, and angioedema. Anaphylaxis could further present with hypotension which could pose a diagnostic dilemma.

There are significant similarities between TRALI and TACO. Examination should look for dyspnea, tachypnoea, cyanosis, and decreased oxygen saturation. Furthermore, auscultation for crackles might be evidence of pulmonary edema. Orthopnea, cough, a third heart sound, and pinkish frothy sputum could all be clues leading to the diagnosis of these reactions.

Alternative Diagnoses

When new symptoms arise after blood transfusions, the diagnosis of transfusion reactions should be established. However, an extensive differential diagnosis list must be carefully formulated depending on the presentation.

In the context of transfusions, certain signs and symptoms may indicate potential complications or adverse reactions. A new rash or swelling of mucous membranes could suggest an allergic reaction, anaphylaxis, urticaria, food allergies, or angioedema. Dyspnea, or respiratory distress, may be indicative of transfusion-related acute lung injury (TRALI), transfusion-associated circulatory overload (TACO), anaphylaxis, cardiogenic pulmonary edema, acute respiratory distress syndrome, or acute chest syndrome. Hypotension could point to anaphylaxis, TRALI, septic shock, hemorrhagic shock, or neurogenic shock. Lastly, the presence of fever may indicate a febrile non-hemolytic reaction, an acute hemolytic reaction, an infection from any source, or sepsis. Identifying these symptoms promptly is essential to manage and mitigate potential adverse events during transfusions.

The table summarizes signs&symptoms and potential differential diagnoses. 

Signs and Symptoms

Differential Diagnoses

New rash, or swelling of mucous membranes

Allergic reaction, Anaphylaxis, Acute, Urticaria, Food Allergies, Angioedema

Dyspnea (Respiratory distress)

TRALI, TACO, Anaphylaxis, Cardiogenic pulmonary edema, Acute respiratory distress syndrome, Acute chest syndrome

Hypotension

Anaphylaxis, TRALI, Septic shock, Hemorrhagic shock, Neurogenic shock

Fever

Febrile nonhemolytic reaction, Acute hemolytic reaction, infection of any source, sepsis

Acing Diagnostic Testing

While most transfusion reaction diagnoses are primarily clinical, few diagnostic tests may assist clinicians in establishing a diagnosis.

  1. Visual inspection of the pre-transfusion sample for its color and any unusual clumps [19].
  2. Allergic reactions: IgA levels could also be obtained in patients with suspected IgA deficiency, although the diagnosis for moderate or severe allergic reactions is usually clinical. Eosinophilia could indicate allergic reactions but may not always be present [10].
  3. Hemolytic reactions: Elevated Lactate dehydrogenase levels (LDH) as well as indirect bilirubin levels with decreased haptoglobin levels would suggest a hemolytic reaction arising out of an ABO incompatibility. Elevated PTT and PT/INR, as well as D-Dimer coupled with decreased fibrinogen, would suggest the presence of DIC. Blood film can be examined for schistocytes or spherocytes [12]. Dark urine could suggest hemoglobinuria. Direct antiglobulin test (DAT) for anti-IgG or anti-C3 and elution test with alloantibody present on the transfused red blood cells would help.
  4. TRALI & TACO: arterial blood gas (ABG) is used to calculate the PaO2/FiO2 ratio, and Chest XR is used to evaluate the presence of bilateral infiltrates or features of pulmonary edema. Bedside ultrasound can confirm the absence of circulatory overload in TRALI, which is a distinguishing feature from TACO. Additionally, a BNP level should be obtained when evaluating for TACO.

Risk Stratification

Unfortunately, no objective risk stratification tool exists that would lead to recognizing patients with worse outcomes due to transfusion reactions.

Characteristics which place patients at increased risk of developing transfusion reactions are:

  • Previous transfusion history,
  • Abortions or termination of pregnancy history,
  • Longer blood storage time,
  • Receiving three or more units of blood [3].
  • Critically ill and surgical patients (Risk of mortality due to TRALI appears to be higher) [20].

Management

In case of transfusion reactions, the ABCDE algorithm for managing conditions in the emergency department should be followed. The airway must be assessed for patency and secured if needed, followed by addressing breathing and circulation.

The cornerstone of managing most transfusion reactions is stopping the transfusion and maintaining Intravenous access. In all reactions, the next step is to confirm the details of the transfused unit, make sure no clerical error occurred, and then report the reaction to the concerned blood bank [17].

Febrile nonhemolytic reaction:  Management of this reaction encompasses frequent monitoring of vital signs and administering antipyretics. Transfusion can be continued in stable patients with no other symptoms [12]. However, this remains a diagnosis of exclusion, and other reactions must be considered.

Mild allergic reaction: An H1 antihistamine (e.g., Diphenhydramine 25-50 mg IV) should be administered for symptom management in case of a mild allergic reaction. Restart the transfusion under direct supervision at a slower rate upon resolution of symptoms. In case of recurrence, transfusion must be suspended [17].

Anaphylaxis reaction: Manage as per standard institutional protocol or as delineated in an earlier chapter within this textbook (e.g., IM 1:1000 Epinephrine, H1 antihistamine, e.g., IV Diphenhydramine, Beta-adrenergic drugs, e.g., Salbutamol nebs in case of wheezing and/or bronchospasm, Steroids, e.g., Hydrocortisone and IV Fluids as required) [17].

Acute hemolytic transfusion reaction: The onset of hemodynamic instability will indicate an acute hemolytic transfusion reaction, and it is imperative to immediately halt the transfusions. Treatment is largely supportive. Focus on supporting the respiratory, cardiovascular, and renal systems and treating possible complications such as DIC to halt the patient’s condition [21].

Transfusion-related acute lung injury (TRALI): Similar to acute hemolytic reaction, treatment of TRALI is supportive. Most importantly, support of ventilatory status should be established with noninvasive or invasive means. Most patients who develop TRALI require ventilatory support [22]. As most patients with TRALI develop hypotension, supporting hemodynamics with IV fluids and possible vasopressors may be needed to ensure adequate organ perfusion.

Transfusion-associated circulatory overload (TACO): Since TACO reflects a volume overload status, this condition can be treated similarly to other conditions that result in volume overload. In deteriorating patients, ventilatory support may be needed through noninvasive or mechanical ventilation. Furosemide 0.5/1 mg/kg may be used. In addition, IV Nitroglycerin 50 – 100 mcg as an initial dose may theoretically have a role in clinical status improvement [16,17].

Special Patient Groups

Pregnant Patients

This patient population should always receive O(-) blood when prompt uncross-matched blood is needed for transfusion to minimize the risk of Rh(-) mothers developing antibodies against the Rh(+) fetus, leading to subsequent hemolytic disease of the newborn [5].

Geriatrics

About half of RBC units are administered to patients aged 70 and above [23]. They are frail, have various comorbid conditions, and age-related altered physiology. Clinicians must base their transfusion decisions on the risk-benefit ratio for elderly patients [24]. TACO is the most common transfusion reaction in elderly patients. It occurs at a substantially higher rate in this population compared to younger patients, and those with more comorbidities are at higher risk. Slower transfusion rates are recommended to mitigate the risk [25]. In addition, several studies have mentioned that blood transfusions in the elderly are linked to the risk of developing delirium, although the causation is unknown [26].

Pediatrics

According to a recent meta-analysis, the incidence of transfusion reactions is higher in children than in adults, including rare transfusion reactions [27], due to their size difference (volume-related) and immature liver [28].

When To Admit This Patient

It is advisable to observe patients with hemodynamic instability or severe reactions following a blood transfusion (e.g., ICU for Acute hemolytic reaction). No clear guidelines exist on the criteria for admission for patients with transfusion reactions, and the decision might need to be made on a case-by-case basis, depending on the clinician’s experience and clinical evaluation.

Revisiting Your Patient

Recall that your patient was started on a blood transfusion for a Hgb of 5.0 g/dl and then developed respiratory distress. You arrive at the room and connect to the patient on a monitor. His vitals now show a temperature of 38 C, HR of 132 BPM, RR of 35, BP of 205/120, and SpO2 of 75% on Room Air. You immediately assess the airway and note that the patient is talking clearly but cannot complete full sentences. No secretions in the oral cavity. You judge the airway to be patent and move to assess breathing. He is tachypneic and desaturating, and you immediately place him on 15L O2 via a nonrebreather mask. The patient’s SpO2 picks up to 90%. Upon chest inspection, you hear diffuse crackles. The patient is also unable to lie supine. Hypertension and tachycardia are noted, as well as elevated Jugular venous pressure.

By now, you judge the patient has developed a transfusion reaction, and you immediately order the nurse to suspend the transfusion and notify the blood bank.

An X-ray was ordered, and it showed features of pulmonary edema as well as blunting of the costophrenic angles. Arterial blood gas shows a PaO2/FiO2 ratio 190 and a lactate 4. A BNP is sent and returns at 25,000 pg/mL

Upon review of the patient, he is in significant distress despite the nonrebreather mask, so the respiratory therapist is contacted to initiate BiPAP treatment. You diagnose TACO and, in addition, start the patient on 100 mcg/min of IV Nitroglycerin and a 40 mg dose of IV Furosemide.

The patient started improving shortly after and stated that his breathing was improving. The patient was admitted to the ICU for further stabilization and management of his condition.

Author

Picture of Yaman Hukan

Yaman Hukan

Yaman Hukan is an Emergency Medicine resident at Tawam Hospital in the United Arab Emirates. He completed his bachelor's of medicine (MBBS) degree in 2018 from the University of Sharjah. He is interested in humanitarian medicine. As a medical student, he joined the Syrian American medical society (SAMS) on several of their missions to provide healthcare for Syrian refugees in Jordan. His interests also include resuscitation and toxicology, a field in which he hopes to pursue further training.

Picture of Thiagarajan Jaiganesh

Thiagarajan Jaiganesh

Dr. Jaiganesh is a Chairman and Consultant in Adult and Pediatric Emergency Medicine and serves as an Adjunct Assistant Professor at UAE University. As the former Director of the Emergency Medicine Residency Program at Tawam Hospital in Al Ain, UAE, Dr. Jaiganesh is dedicated to training the next generation of emergency medicine professionals. With a strong academic and professional background, Dr. Jaiganesh has published numerous peer-reviewed articles on emergency medicine and contributes as a Section Editor and Chapter Author for notable medical texts, including the Oxford Handbook for Medical School. A sought-after speaker, Dr. Jaiganesh has been invited to present at numerous national and international conferences and serves as an instructor in various life support courses. Additionally, Dr. Jaiganesh is an expert in medico-legal and clinical negligence matters, providing valuable insights into complex legal and ethical cases in healthcare.

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References

  1. Mowla SJ, Sapiano MRP, Jones JM, Berger JJ, Basavaraju SV. Supplemental findings of the 2019 National Blood Collection and Utilization Survey. Transfusion. 2021;61 Suppl 2(Suppl 2):S11-S35. doi:10.1111/trf.16606
  2. Kumar TA, Geet A. Blood transfusion therapy and related complication. In: Richhariya D, ed. Textbook of Emergency Medicine including intensive care and trauma. New Delhi: Jaypee brothers medical publishers; 2022: 990
  3. Gelaw Y, Woldu B, Melku M. Proportion of Acute Transfusion Reaction and Associated Factors Among Adult Transfused Patients at Felege Hiwot Compressive Referral Hospital, Bahir Dar, Northwest Ethiopia: A Cross-Sectional Study. J Blood Med. 2020;11:227-236. Published 2020 Jun 30. doi:10.2147/JBM.S250653
  4. Kracalik I, Mowla S, Basavaraju SV, Sapiano MRP. Transfusion-related adverse reactions: Data from the National Healthcare Safety Network Hemovigilance Module – United States, 2013-2018. Transfusion. 2021;61(5):1424-1434. doi:10.1111/trf.16362
  5. Dean L. The ABO Blood Group. In: internet, ed. Blood Groups and Cell Antigens. Bethesda MD: National Center for Biotechnology Information (US); 2005: 25-31
  6. Dean L. The ABO Blood Group. In: internet, ed. Blood Groups and Cell Antigens. Bethesda MD: National Center for Biotechnology Information (US); 2005: 39-44
  7. Goel R, Tobian AAR, Shaz BH. Noninfectious transfusion-associated adverse events and their mitigation strategies. Blood. 2019;133(17):1831-1839. doi:10.1182/blood-2018-10-833988
  8. Shmookler AD, Flanagan MB. Educational Case: Febrile Nonhemolytic Transfusion Reaction. Acad Pathol. 2020;7:2374289520934097. Published 2020 Jul 14. doi:10.1177/2374289520934097
  9. Division of healthcare quality promotion. National healthcare safety network biovigilance component hemovigilance module surveillance protocol. Atlanta, GA: Center of disease control and prevention; February 2023: 9-22
  10. Tobian A. Immunologic transfusion reactions. UpToDate. https://www-uptodate-com.eu1.proxy.openathens.net/contents/immunologic-transfusion-reactions?search=anaphylaxis%20transfusion&source=search_result&selectedTitle=1~150&usage_type=default&display_rank=1 . Updated on Sep 06, 2022. Accessed on March 15, 2023.
  11. Fiorellino J, Elahie AL, Warkentin TE. Acute haemolysis, DIC and renal failure after transfusion of uncross-matched blood during trauma resuscitation: illustrative case and literature review. Transfus Med. 2018;28(4):319-325. doi:10.1111/tme.12513
  12. San Miguel C. & Kaide C. Blood and Blood Components. In: Walls R., ed. Rosen’s Emergency Medicine: Concepts and Clinical Practice. Philadelphia, PA: Elsevier; 2023: 1452-1561
  13. Panch SR, Montemayor-Garcia C, Klein HG. Hemolytic Transfusion Reactions. N Engl J Med. 2019;381(2):150-162. doi:10.1056/NEJMra1802338
  14. Center for Biologics Evaluation and Research. Fatalities reported to FDA following blood collection and transfusion. United States: Food and drug administration; 2020: 4-5
  15. Otrock ZK, Liu C, Grossman BJ. Transfusion-related acute lung injury risk mitigation: an update. Vox Sang. 2017;112(8):694-703. doi:10.1111/vox.12573
  16. van den Akker TA, Grimes ZM, Friedman MT. Transfusion-Associated Circulatory Overload and Transfusion-Related Acute Lung Injury [published correction appears in Am J Clin Pathol. 2022 Nov 3;158(5):665]. Am J Clin Pathol. 2021;156(4):529-539. doi:10.1093/ajcp/aqaa279
  17. Delaney M, Wendel S, Bercovitz RS, et al. Transfusion reactions: prevention, diagnosis, and treatment. Lancet. 2016;388(10061):2825-2836. doi:10.1016/S0140-6736(15)01313-6
  18. Vlaar AP, Juffermans NP. Transfusion-related acute lung injury: a clinical review. Lancet. 2013;382(9896):984-994. doi:10.1016/S0140-6736(12)62197-7
  19. Al-Riyami AZ, Al-Hashmi S, Al-Arimi Z, et al. Recognition, Investigation and Management of Acute Transfusion Reactions: Consensus guidelines for Oman. Sultan Qaboos Univ Med J. 2014;14(3):e306-e318.
  20. Gajic O, Rana R, Winters JL, et al. Transfusion-related acute lung injury in the critically ill: prospective nested case-control study. Am J Respir Crit Care Med. 2007;176(9):886-891. doi:10.1164/rccm.200702-271OC
  21. Tobian A. Hemolytic transfusion reactions. UpToDate. https://www-uptodate-com.eu1.proxy.openathens.net/contents/hemolytic-transfusion-reactions?sectionName=DELAYED%20HEMOLYTIC%20TRANSFUSION%20REACTIONS%20AND%20DELAYED%20SEROLOGIC%20TRANSFUSION%20REACTIONS&search=blood%20transfusion%20reaction&topicRef=95132&anchor=H354791&source=see_link#H354791. Updated on Jan 05, 2022. Accessed on March 15, 2023
  22. Vlaar AP, Binnekade JM, Prins D, et al. Risk factors and outcome of transfusion-related acute lung injury in the critically ill: a nested case-control study. Crit Care Med. 2010;38(3):771-778. doi:10.1097/CCM.0b013e3181cc4d4b
  23. Bosch MA, Contreras E, Madoz P, et al. The epidemiology of blood component transfusion in Catalonia, Northeastern Spain. Transfusion. 2011;51(1):105-116. doi:10.1111/j.1537-2995.2010.02785.x
  24. Boureau AS, de Decker L. Blood transfusion in older patients. Transfus Clin Biol. 2019;26(3):160-163. doi:10.1016/j.tracli.2019.06.190
  25. Menis M, Anderson SA, Forshee RA, et al. Transfusion-associated circulatory overload (TACO) and potential risk factors among the inpatient US elderly as recorded in Medicare administrative databases during 2011. Vox Sang. 2014;106(2):144-152. doi:10.1111/vox.12070
  26. van der Zanden V, Beishuizen SJ, Swart LM, de Rooij SE, van Munster BC. The Effect of Treatment of Anemia with Blood Transfusion on Delirium: A Systematic Review. J Am Geriatr Soc. 2017;65(4):728-737. doi:10.1111/jgs.14564
  27. Wang Y, Sun W, Wang X, et al. Comparison of transfusion reactions in children and adults: A systematic review and meta-analysis. Pediatr Blood Cancer. 2022;69(9):e29842. doi:10.1002/pbc.29842
  28. Sostin N, Hendrickson JE. Pediatric Hemovigilance and Adverse Transfusion Reactions. Clin Lab Med. 2021;41(1):51-67. doi:10.1016/j.cll.2020.10.004

Reviewed and Edited By

Picture of Arif Alper Cevik, MD, FEMAT, FIFEM

Arif Alper Cevik, MD, FEMAT, FIFEM

Prof Cevik is an Emergency Medicine academician at United Arab Emirates University, interested in international emergency medicine, emergency medicine education, medical education, point of care ultrasound and trauma. He is the founder and director of the International Emergency Medicine Education Project – iem-student.org, chair of the International Federation for Emergency Medicine (IFEM) core curriculum and education committee and board member of the Asian Society for Emergency Medicine and Emirati Board of Emergency Medicine.

The ABCDE Approach to Undifferentiated Critically Ill and Injured Patient (2024)

~ iEM Education Project Team ~ Leave a comment

by Roxanne R. Maria, Hamid A. Chatha

Authors
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You have a new patient!

A 40-year-old male, a truck driver, is involved in a head-on collision with another vehicle. He has been brought in by ambulance. According to the paramedics, the vehicles were traveling at approximately 85 km/hr, and the patient was restrained by a seatbelt. On arrival at the Emergency Department (ED), the patient is agitated and mildly disoriented. He is tachypneic with a respiratory rate of 30/min, maintaining an O2 saturation of 95% on 12 L/min oxygen via a non-rebreather mask, heart rate of 128 beats/min, blood pressure of 90/52 mmHg, and temperature of 36.1°C. The patient also received 1 L of 0.9% normal saline and 1 unit of O-negative packed red cells in the ambulance. Despite this, his respiratory rate, heart rate, and level of disorientation have worsened.

Emergency Department

In the ED, patients present with a variety of clinical presentations, including both life-threatening and non-life-threatening. Some may have been seen and referred by a clinician before arrival or brought to the department after pre-hospital assessment and care by the emergency medical services (EMS) [1]. Health emergencies affect all age groups and include conditions like acute coronary syndrome, strokes, acute complications of pregnancy, or any chronic illness. Emergency health care providers should respond to these clinically ‘undifferentiated’ patients with symptoms for which the diagnosis may not be known [2].  The root cause of most life-threatening conditions in the ED may be medical or surgical, infection or trauma [2].

In the Emergency Department (ED), there are several potentially life-threatening presentations that demand immediate stabilization. These include trauma, which can result from various forms of accidents or injuries, and shortness of breath, which might indicate critical respiratory distress. An altered mental state also requires prompt attention, as it may signal underlying neurological or systemic issues. Shock, often evidenced by dangerously low blood pressure. Chest pain or discomfort, which could be indicative of a cardiac event, are other urgent concerns. Additionally, cases of poisoning, ingestion of harmful substances, or exposure to toxic materials also necessitate rapid intervention to prevent further harm. Each of these presentations is a medical priority, highlighting the importance of timely and effective response in the ED to ensure patient safety and stability.

These symptoms maybe the only picture that the patients present with, and may constitute the early stage of a critical illness requiring rapid, appropriate intervention and resuscitation, even when the patient seems to appear relatively well [2].

Emergency conditions often require immediate intervention long before a definitive diagnosis is made to stabilize the critically ill patient [3]. Thus, this chapter intends to briefly introduce a basic systematic approach to identifying and managing acute, potentially life-threatening conditions in these patients. This approach will enable all frontline providers, including students, nurses, pre-hospital technicians, and physicians, to manage these patients even in the setting of limited resources [2].

A complete assessment and management of each of the presentations mentioned above is beyond the scope of this chapter. However, the initial approach remains the same, regardless of the patient population or setting [4].

History of the ABCDE approach

The ABC mnemonic’s origins may be traced back to the 1950s. The first two letters of the mnemonic, A and B, resulted from Dr Safar’s description of airway protection techniques and administration of rescue breaths. Kouwenhoven and colleagues later added the letter C to their description of closed-chest cardiac massage [3].

Styner is credited with further developing the Airway, Breathing, Circulation, Disability, and Exposure (ABCDE) approach. After a local aircraft disaster in 1976, Styner and his family were taken to a local healthcare facility, where he saw an insufficiency in the emergency treatment offered. He then founded the Advanced Trauma Life Support course, emphasizing a methodical approach to treating severely injured patients.

The ABCDE approach is universally accepted and utilized by emergency medicine clinicians, technicians, critical care specialists, and traumatologists [3]. Thus, this approach is recommended by international guidelines for suspected serious illness or underlying injury, irrespective of the diagnosis [5]. It is also the first step in post-resuscitation care after the patient achieves return of spontaneous circulation (ROSC) from a cardiac arrest [3]. This systematic approach also aims to improve coordination among the team members and saves time to make critical decisions [3].

The ABCDE approach

Since time is of the essence, the ABCDE method is a systematic approach that can be easily and quickly practiced in the ED. This is incorporated into what is known as ‘Initial patient assessment,’ one of the most crucial steps in evaluation [6]. At each step of this approach, life-threatening problems must be addressed before proceeding to the next assessment step. After the initial assessment, patients must be reassessed regularly to evaluate the treatment response. Anticipate and call for extra help early [7]. Appropriate role allocation and good communication are important for effective team working [7]. Once the patient is stabilized, a secondary survey should be conducted, which includes a thorough history, physical examination, and diagnostic testing [8]. Finally, the tertiary survey is done within 24 hours of presentation to identify any other missed injuries in trauma. Once it is recognized that the patient’s needs exceed the facility’s capabilities, the transfer process must be initiated to an appropriately specialized care center accordingly [8].

Ensure Safe Environment

Before initiating the ABCDE approach, it is essential to ensure both personal safety and a secure environment. This preparation includes addressing any potential risks, such as unexpected or violent behavior, environmental hazards, and the risk of exposure to communicable diseases. Health professionals should consider using appropriate personal protective equipment (PPE) suited to the situation, which may include gloves, gowns, masks, goggles, and thorough hand washing. These precautions are vital to protect both the healthcare provider and the patient, ensuring a safe environment for medical intervention [4].

Initiate First Response

The Resuscitation Council UK (RCUK) (2015) recommends performing a range of initial activities before proceeding with the ABCDE approach [4].

Examine the patient in general (skin color, posture, sensorium, etc.) to determine whether they seem critically ill [4].

After introducing yourself, an initial assessment can be completed in the first 10-15 seconds by asking patients their names and about their active complaints. If they respond normally, it means the airway is patent and brain perfusion is expected [9]. Check for breathing and pulse if the patient appears unconscious or has collapsed. If there is no pulse, call for help and immediately start cardiopulmonary resuscitation (CPR), adhering to local guidelines [9].

Detailed ABCDE Evaluation

Primary Survey

Patients are assessed and prioritized according to their presentations and vital signs. In primary survey, critically ill patients are managed efficiently along with resuscitation. The approach represents the sequence of steps as described below [10]:

A – Airway (with C spine control in Trauma patients)

B – Breathing and Ventilation

C – Circulation (With Hemorrhage control in active bleeding)

D – Disability

E – Exposure / Environment control

A – Airway

Airway obstruction is critical! Gain expert help immediately. If not treated, it can lead to hypoxia, causing damage to the brain, kidneys, and heart, resulting in cardiac arrest and death [4].

Airway management remains the cornerstone of resuscitation and is a specialized skill for the emergency clinician [9].

Assessment of airway patency is the first step. Can the patient talk? If yes, then the airway is patent and not in immediate danger. If not, look for the signs of airway compromise: Noisy breathing, inability to speak, presence of added sounds, stridor or wheezing, choking or gagging, cyanosis, and use of accessory muscles.

The next step is to open the mouth and look for anything obstructing the airway, such as secretions, blood, a foreign body, or mandibular/tracheal/laryngeal fractures [10].

While examining and managing the airway, great care must be taken to restrict excessive movement of the cervical spine and assume the existence of a spinal injury in cases of trauma [11].

Several critical factors can compromise a patient’s airway and must be addressed promptly in emergency settings. A depressed level of consciousness, which may result from conditions such as opioid overdose, head injury, or stroke, can impair airway protection and lead to significant risk [10]. Additionally, an inhaled foreign body, or the presence of blood, vomit, or other secretions, can obstruct the airway and necessitate immediate intervention. Fractures of the facial bones or mandible further complicate airway management due to potential structural damage. Soft tissue swelling, whether caused by anaphylaxis (angioedema) or severe infections like quinsy or necrotizing fasciitis, also seriously threatens the airway. These conditions highlight the importance of vigilant monitoring and rapid response to maintain airway patency and prevent complications.

angioedema - DermNet New Zeeland, CC BY NC ND 3.0
uvula edema - WikiMedia Commons - CC-BY-SA-3.0

Intervention: Several basic maneuvers can help maintain a clear airway. Suctioning should be performed if there are any secretions or blood present. Additionally, using the head-tilt, chin-lift, and jaw-thrust maneuvers can aid in keeping the airway open. For patients with a low Glasgow Coma Scale (GCS) score, placing an oropharyngeal or nasopharyngeal airway can be beneficial in maintaining airway patency. It’s also important to inspect the airway for any obvious obstructions; if a visible object is within reach, it may be removed carefully using a finger sweep or suction. It is crucial to remember that assistance from an anesthetist may be required in some cases. 

Head-Tilt, Chin-Lift maneuver

In trauma patients, to protect the C-spine, perform a jaw-thrust rather than a head-tilt chin-lift maneuver and immobilize the C-spine with a cervical collar [9].

A definitive airway, such as endotracheal intubation, may be necessary in patients with airway obstruction, GCS ≤ 8, severe shock or cardiac arrest, and at risk of inhalation injuries [8].

If intubation has failed or is contraindicated, a definitive airway must be established surgically [11].

B – Breathing and Ventilation

Effective ventilation relies on the proper functioning of the lungs, chest wall, and diaphragm, along with a patent airway and sufficient gas exchange to optimize oxygenation [10]. To assess breathing and ventilation, clinicians should evaluate oxygen saturation, monitor the respiratory rate for any signs of abnormality—such as rapid breathing (tachypnea), slow breathing (bradypnea), or shallow breathing (Kussmaul breathing)—and observe for increased work of breathing, such as accessory muscle use, chest retractions, or nasal flaring. Other critical assessments include checking for neck vein distention, examining the position of the trachea, chest expansion, and any injuries or tenderness, as well as auscultating for bilateral air entry and any additional sounds. Chest percussion should be performed to identify dullness, which may indicate hemothorax or effusion, or hyperresonance, suggestive of pneumothorax. Certain pathologies, like tension pneumothorax, massive hemothorax, open pneumothorax, and tracheal or bronchial injuries, can rapidly disrupt ventilation. Other conditions, including simple pneumothorax, pleural effusion, simple hemothorax, rib fractures, flail chest, and pulmonary contusion, may compromise ventilation to a lesser degree [10].

Interventions:

  • Oxygen – Ensure all patients are adequately oxygenated, with supplemental oxygen delivered to all severely injured trauma patients [11]. Place them on well-fitted oxygen reservoir masks with a flow rate > 10 L/min, which can then be titrated as needed to maintain adequate saturations. Other means of oxygen delivery (nasal catheter, nasal cannula, non-rebreather) can also be used.
  • Bag mask valve ventilation with oxygen – should be given to unconscious patients with abnormal breathing patterns (slow or shallow respiration).
  • Other interventions include salbutamol nebulizers, epinephrine, steroids, needle decompression, chest tube insertion, and the use of noninvasive ventilation and pressure support in different clinical scenarios.

C – Circulation (With Hemorrhage control in active bleeding)

Major circulatory compromise in critically ill patients can result from either blood volume loss or reduced cardiac output. In trauma cases, hypotension is assumed to be due to blood loss until proven otherwise. To assess the hemodynamic status, several key evaluations should be performed. These include checking the level of consciousness, as an altered state may indicate impaired cerebral perfusion, and assessing skin perfusion for signs like pallor, cyanosis, mottling, or flushing. Vital signs such as heart rate and blood pressure should be monitored for abnormalities like tachycardia, bradycardia, hypotension, or hypertension. Auscultation can reveal muffled heart sounds, which may suggest cardiac tamponade or pneumothorax, as well as murmurs or a pericardial friction rub that could indicate pericarditis. Checking the extremities for capillary refill and skin temperature is also essential. Additionally, palpation of the abdomen for tenderness or a pulsatile mass may reveal an abdominal aortic aneurysm, while peripheral edema, such as pedal edema, might indicate heart failure.

Interventions:

  • Two large-bore IV cannulations must be placed. If this attempt fails, intraosseous access is necessary. Hemorrhagic shock—A definitive control of bleeding along with replacement of intravascular volume is essential. Initial resuscitation should start with warm crystalloids, and blood products should be used. Massive Transfusion Protocol (MTP) should be activated according to local guidelines. In hemorrhagic shock, vasopressors and reversal of anticoagulation (if required) can be considered.
  • Hemorrhage control: External hemorrhage can be controlled by direct manual pressure over the site of the wound or tourniquet application.
  • In the case of pelvic or femur fractures, placement of pelvic binders or extremity splints may help to stabilize, although definitive management may be surgical or interventional radiological procedures.
  • Obstructive shock – Immediate pericardiocentesis for cardiac tamponade, chest tube insertion for tension pneumothorax, and thrombolysis for massive pulmonary embolism.
  • Distributive shock – intramuscular epinephrine for anaphylactic shock, empiric antibiotics for sepsis, and hydrocortisone for adrenal crisis.
  • Appropriate antihypertensives in hypertensive emergency.

D – Disability

Evaluate neurological status either with AVPU (Alert, Verbal, Pain and Unresponsive) [5] or GCS (Glasgow Coma Scale).

Evaluate for agitation, head and neck trauma, focal neurological signs (seizure, hemiplegia, etc), lateralizing signs, meningeal signs, signs of raised intracranial pressure, and pupillary examination (size and symmetry). Identify any classic toxidromes (sympathomimetic, cholinergic, anticholinergic, opioid, serotonergic, and sedative-hypnotic toxidromes). 

Choose the best response of patient
EYE OPENING
4: Spontaneously
3: To verbal command
2: To pain
1: No response
BEST VERBAL RESPONSE
5: Oriented and converses
4: Disoriented and converses
3: Inappropriate words; cries
2: Incomprehensible sounds
1: No response
BEST MOTOR RESPONSE
6: Obeys command
5: Localizes pain
4: Flexion withdrawal
3: Flexion abnormal (decorticate)
2: Extension (decerebrate)
1: No response
Glasgow Coma Score (GCS) (Modified from Teasdale, G., & Jennett, B. (1974). Assessment of coma and impaired consciousness: a practical scale. The Lancet, 304(7872), 81-84.) - Please read this article to get more insight regarding GCS.

The Glasgow Coma Scale (GCS) is a critical tool for assessing the level of consciousness in critically ill patients, providing a score based on eye, verbal, and motor responses. A GCS score ranges from 3 to 15, with lower scores indicating more severe impairment. Scores of 13-15 generally indicate mild impairment, 9-12 suggest moderate impairment, and scores of 8 or below (comatose patient) represent severe impairment and a high risk of poor outcomes. In critically ill patients, a declining GCS score can signal worsening neurological status, potentially due to factors like traumatic brain injury, hypoxia, or systemic deterioration, and often warrants immediate intervention to address underlying causes.

E – Exposure and Environmental control

It is necessary to expose the patient appropriately whilst maintaining dignity and body temperature.

Look at the skin for any signs of trauma (burns, stab wounds, gunshot wounds, etc.), rashes, infected wounds, ulcers, needle track marks, medication patches, implantable devices, tubes, catheters, and stomas; measure core body temperature, and perform logroll (trauma).

Do not forget to check frequently concealed and overlooked areas such as the genital, inguinal, perineal, axilla, back and under dressings [8].

Interventions:

  • Use specialized personal protective equipment (PPE), remove all possible triggers such as wet or contaminated clothing, and maintain core body temperature.
  • Minimize hypothermia (external rewarming, warm IV fluids) and hyperthermia (surface cooling, cold IV fluids, antipyretics for fever).

Adjuncts to primary survey

1. Electrocardiography (ECG)
2. Pulse oximetry
3. Carbon dioxide (CO2) monitoring
4. Arterial blood gas (ABG) analysis
5. Urinary catheterization (to assess for hematuria and urine output)
6. Gastric catheterization (for decompression)
7. Blood lactate level measurement
8. Chest and pelvis X-rays
9. Extended focused assessment with sonography for trauma (eFAST)

These adjuncts help provide a comprehensive evaluation of the patient’s condition [10].

Secondary Survey

After the initial primary survey and stabilization, proceed to the secondary survey. This includes a detailed history (SAMPLE)and a head-to-toe examination, including reassessment of vital signs, as there is a potential for missing an injury or other findings in an unresponsive patient [10].

The SAMPLE mnemonic is a structured approach for gathering essential patient history in emergency settings. It stands for Signs and Symptoms, Allergies, Medications, Past Medical History, Last Oral Intake, and Events leading to the illness or injury [5].

  • “Signs and Symptoms” involves asking the patient, family, or other witnesses about any observable signs or reported symptoms.
    “Allergies” are crucial to identify to prevent harm and may help recognize conditions like anaphylaxis.
  • “Medications” requires a comprehensive list of all current and recent medications, including any changes in dosage.
  • “Past Medical History” provides insights into underlying health conditions that may influence the current illness.
  • “Last Oral Intake” is important for assessing risks of aspiration or complications if the patient requires sedation or surgery.
  • Finally, understanding the “Events” surrounding the illness or injury aids in determining its cause and severity.

Together, these components guide healthcare providers in developing a more accurate and effective treatment plan.

In the secondary survey, a thorough approach is taken to ensure comprehensive care for the patient. This includes performing relevant and appropriate diagnostic tests based on the clinical assessment to confirm diagnoses and guide further treatment. Critical, targeted treatments should be initiated promptly, along with adequate supportive care to stabilize the patient’s condition. If necessary, specialized consults are obtained to address specific medical needs. Additionally, the healthcare team must assess the need for escalation of care or consider an interfacility transfer if the patient requires more specialized resources or advanced care options [8]. This structured approach ensures that all aspects of the patient’s condition are managed effectively. 

Adjuncts to secondary survey

Additional x-rays for the spine and extremities, CT scans of the head, chest, abdomen, and spine, urography and angiography with contrast, transesophageal ultrasound, bronchoscopy, and other diagnostics [10].

If the patient starts to deteriorate, immediately go back to the ABCDE approach and reassess!

Special Patient Groups

In recent ATLS updates, the ABCDE approach has been modified to the xABCDEF approach, where “x” stands for eXsanguinating eXternal hemorrhage control and “F” stands for further factors such as special groups (pediatric, Geriatric, and Pregnancy).  While the xABCDEF approach is universal and applies to all patient groups, specific anatomic and physiological differences in different populations should be considered while evaluating and treating life-threatening conditions. Some special population groups are discussed here:

Pediatrics [10]

Children have smaller body mass but higher body surface area than their body mass and proportionately larger heads than adults. These characteristics cause children to have increased energy transfer, hypothermia, and blunt brain trauma.

A useful adjunct is the Broselow® Pediatric Emergency Tape, which helps to rapidly identify weight-based medication doses, fluid volumes, and equipment sizes.

The ABCDE approach in children should proceed in the same manner as in adults, bearing in mind the anatomical differences.

Airway – Various anatomical features in children, such as large tissues of the oropharynx (tongue, tonsils), funnel-shaped larynx, more cephalad and anteriorly placed larynx and vocal cords, and shorter length of the trachea, make assessment and management of the airway difficult. Additionally, in smaller children, there is disproportionality in size between the cranium and the midface, making the large occiput in passive flexion of the cervical spine, resulting in the posterior pharynx being displaced anteriorly. The neutral alignment of the spine can be achieved by placing a 1-inch pad below the entire torso of the infant or toddler.

The most preferred technique for orotracheal intubation is under direct vision, along with restriction of the cervical spine, to achieve a definitive airway.

Infants are more prone to bradycardia due to laryngeal stimulation during intubation than older children and adults. Hence, when drug-assisted intubation is required, the administration of atropine sulfate pretreatment must be considered. Atropine also helps to dry out oral secretions, further enhancing the view of landmarks for intubation.

When the airway cannot be maintained by bag-mask ventilation or orotracheal intubation, a rescue airway with either a laryngeal mask airway (LMA), an intubating LMA, or a needle cricothyroidotomy is required.

Red flag signs in children include stridor, excessive drooling, airway swelling, and the child’s unwillingness to move the neck. Examine the airway carefully for any foreign bodies, burns, or obstruction.

Breathing and ventilation – Children’s respiratory rates decrease with age. The normal tidal volumes in infants and children vary from 4-6 ml/kg to 6-8 ml/kg while assisting in ventilation. Care must be taken to limit pressure-related barotrauma during ventilation. It is recommended that children weighing less than 30 kg use a pediatric bag valve mask.

Injuries such as pneumothorax, hemothorax, and hemopneumothorax should be treated by pleural decompression, for tension pneumothorax, and needle decompression in the 2nd intercostal space (over the top of the third rib) at the midclavicular line. The site for chest tube insertion remains the same as in adults.

The most common cause of pediatric cardiac arrest is hypoxia, and the most common acid-base abnormality encountered is respiratory acidosis due to hypoventilation.

Circulation – Important factors in assessing and managing circulation and shock are looking for signs of circulatory compromise, ascertaining the patient’s weight and circulatory volume, gaining timely peripheral venous access, delivering an appropriate volume of fluids with or without blood replacement, evaluating the adequacy of resuscitation, and aiming for thermoregulation.

Children have increased physiological reserves. A 30% decrease in the circulating blood volume may be required for a fall in the systolic blood pressure. Hence, it is important to look for other subtle signs of blood loss, such as progressive weakening of peripheral pulses, narrow pulse pressure to less than 20 mm Hg, skin mottling (in infants and young children), cool extremities, and decreased level of consciousness.

The preferred route is peripheral venous access, but if this is unsuccessful after two attempts, intraosseous access should be obtained.

Fluid resuscitation must be commenced at 20 ml/kg boluses of isotonic crystalloids. If the patient has ongoing bleeding, packed red blood cells may be initiated at 10 ml/kg as soon as possible. Given that children have increased metabolic rates, thinner skin, and lack of substantial subcutaneous tissue, they are prone to develop hypothermia quickly, which may impede a child’s response to treatment, increase coagulation times, and affect the central nervous system (CNS) function. Therefore, overhead lamps, thermal blankets, as well as administration of warm IV fluids, blood products, and inhaled gases may be required during the initial phase of evaluation and resuscitation.

Disability – Hypoglycemia is a very common cause of altered mental state in children, and children can present with altered mental state or seizures. Check for blood glucose in children; if low, administer glucose (IV D10 or D25).

Geriatric [10]

In cases of trauma in geriatric patients, physiological events that may have led to it (e.g., cardiac dysrhythmias) must be considered. A detailed review of long-term medical conditions and medications, along with their effect on vital signs, is necessary. Risk factors for falls include physical impairments, long-term medication use, dementia, and visual, cognitive, or neurological impairments.

Elderly patients are more prone to sustaining burn injuries due to decreased reaction times, hearing and visual impairment, and inability to escape the burning structure. Burn injury remains the cause of significant mortality.

Airway – Due to loss of protective airway reflexes, airway management in the elderly can be challenging and requires a timely decision to establish a life-saving definitive airway. Opening of the mouth and cervical spine maneuvering may be challenging with arthritic changes. Loose dentures should be removed, while well-fitted dentures should be better left inside. Some patients may be edentulous, making intubation easier, but bag-mask ventilation is difficult.

While performing rapid sequence intubation, it is recommended to lower the doses of barbiturates, benzodiazepine, and other sedatives to 20% to 40% to avoid the risk of cardiovascular depression.

Breathing – Elderly patients have decreased compliance of the lungs and the chest wall, which leads to increased breathing work, placing them at a higher risk for respiratory failure. Aging also results in suppressed heart rate during hypoxia, and respiratory failure may present alongside.

Circulation – These patients may have increasing systemic vascular resistance in response to hypovolemia, given that they may have a fixed heart rate and cardiac output. Also, an acceptable blood pressure reading may truly indicate a hypotensive state, as most elderly patients have preexisting hypertension.

A systolic blood pressure of 110 mm Hg is used as a threshold for identifying hypotension in adults over 65.

Several variables, namely base deficit, serum lactate, shock index, and tissue-specific lab markers, can be used to assess for hypoperfusion. Consider early use of advanced monitoring of fluid status, such as central venous pressure (CVP), echocardiography, and bedside ultrasonography, to guide resuscitation.

Disability – Traumatic brain injury is one of the significant complications among the elderly. The dura becomes more adherent to the skull with age, which increases the risk of epidural hematoma. Moreover, these patients are commonly prescribed anticoagulant and antiplatelet medications, which puts these individuals at a higher risk of developing intracranial hemorrhage. Therefore, a very low threshold is indicated for further CT scan imaging in ruling out acute intracranial and spinal pathologies.

Exposure – Increased risk of hypothermia due to loss of subcutaneous fat, nutritional deficiencies, chronic medical illnesses, and therapies. Complications of immobility, such as pressure injuries and delirium, may develop.

Rapid evaluation and relieving from spine boards and cervical collars will help to reduce these injuries.

Pregnant [10]

Evaluation and management of pregnant individuals can be challenging due to the physiological and anatomical changes that affect nearly every organ system in the body. Therefore, knowledge of the physiological and anatomical changes during pregnancy regarding the mother and the fetus is important to provide the best and most appropriate resuscitation and care for both.  

The best initial treatment for the fetus is by providing optimal resuscitation of the mother.

Female patients in the reproductive age who present to the ED must be considered pregnant until proven by a definitive pregnancy test or ultrasound exam.

A specialized obstetrician and surgeon should be consulted early in the assessment of pregnant trauma patients; if not available, early transfer to an appropriate facility should be sought.

The uterus is an intrapelvic organ until the 12th week of gestation, around 34 to 36 weeks when it rises to the level of the costal margin. This makes the uterus and its contents more susceptible to blunt abdominal trauma, whereas the bowel remains somewhat preserved. Nevertheless, penetrating upper abdominal trauma in the late gestational period can cause complex intestinal injury due to displacement.

Amniotic fluid embolism and disseminated intravascular coagulation are significant complications of trauma in pregnancy. In the vertex presentation, the fetal head lies in the pelvis, and any fracture of the pelvis can result in fetal skull fracture or intracranial injury.

A sudden decrease in maternal intravascular volume can lead to a profound increase in uterine vascular resistance, thus reducing fetal oxygenation regardless of normal maternal vital signs.

The volume of plasma increases throughout pregnancy and peaks by 34 weeks of gestation. Physiological anemia of pregnancy occurs when there is an increase in red blood cell (RBC) volume, leading to decreased hematocrit levels. In normal, healthy pregnant individuals, blood loss of 1200 to 1500 ml can occur without showing any signs or symptoms of hypovolemia. Nonetheless, this compromise may be seen as fetal distress, indicated by an abnormal fetal heart rate on monitoring.

Leukocytosis is expected during pregnancy, peaking up to 25,000/mm3 during labor. Serum fibrinogen and other clotting factors may be mildly increased, with shorter prothrombin and partial thromboplastin times. However, bleeding and clotting times remain the same.

During late pregnancy, in a supine position, vena cava compression can cause a decrease in cardiac output by 30 % due to lesser venous return from the lower extremities.

In the third trimester of pregnancy, heart rate increases up to 10-15 beats/min than the baseline while assessing for tachycardia in response to hypovolemia. Hypertension, along with proteinuria, indicates the need to manage preeclampsia. Be mindful of eclampsia as a complication during late pregnancy, as its presentation can be similar to a head injury (seizures with hypertension, hyperreflexia, proteinuria, and peripheral edema)

An increase in the tidal volume causes increases in the minute ventilation and hypocapnia (PaCO2 of 30 mm Hg), which is common in the later gestational period. Therefore,

Maintaining adequate arterial oxygenation during resuscitation as oxygen consumption increases during pregnancy is also important.

By the seventh month of gestation, the symphysis pubis widens to about 4 to 8 mm, and sacroiliac joint spaces increase. These alterations must be kept in mind while evaluating pelvic X-ray films during trauma. Additionally, the pelvic vessels that surround the gravid uterus can become engorged, leading to large retroperitoneal hemorrhage after blunt trauma with pelvic fractures.

Every pregnant patient who has sustained major trauma must be admitted with appropriate obstetric and trauma facilities.

Pregnant individuals may present to the ED with non-obstetric causes such as intentional (intimate partner violence, suicide attempt) and unintentional trauma (MVC, fall), and obstetric causes such as ectopic pregnancy, vaginal bleed, contractions, abdominal pain, decreased fetal movement, etc.

“To optimize outcomes for the mother and fetus, assessment and resuscitation of the mother is performed first and then the fetus, before proceeding for secondary survey of the mother.”

Primary Survey - Mother

Airway – Ensure the patient has a patent and maintainable airway with adequate ventilation. In cases where intubation is necessary, maintain appropriate PaCO2 levels according to the patient’s gestational age.  Due to the superior displacement of abdominal organs and delayed gastric emptying, there is an increased risk of aspiration during intubation.

Breathing – These patients may have an increased rate of respiration due to pressure effects or hormonal changes. Pulse oximetry and arterial gas must be monitored as adjuncts. It must be remembered that normal maternal bicarbonate levels will be low to compensate for the respiratory alkalosis.

Circulation – Attempt to manually reposition the uterus towards the left side to relieve the pressure on the inferior vena cava and improve the venous return.

Since pregnant individuals have increased intravascular volumes, they can lose a large amount of blood before the onset of tachycardia, hypotension, or other signs of hypovolemia. Therefore, it is essential to remember that the fetus and the placenta are deprived of perfusion, leading to fetal distress while the maternal conditions appear stable.

Administer crystalloid IV fluids and type-specific blood. Vasopressors must be used only as a last resort to raise maternal blood pressure, as these agents can further cause a reduction of the uterine blood flow, leading to fetal hypoxia.

Primary Survey - Fetus

Leading causes of fetal demise include maternal shock and death, followed by placental abruption.

Assess for signs of abruptio placentae (vaginal bleeding, uterine tenderness, frequent uterine contractions, uterine tetany, and irritability). Another rare injury is the uterine rupture (abdominal tenderness, rigidity, guarding or rebound tenderness, abnormal fetal lie, etc.) accompanying hypovolemia and shock.

By 10 weeks of gestation, fetal heart tones can be assessed by Doppler ultrasound, and beyond 20-24 weeks of gestation, continuous fetal monitoring with a tocodynamometer must be performed. At least 6 hours of continuous monitoring in patients with no risk factors for fetal death is recommended, and 24 hours of monitoring in patients with a high risk of fetal death.

Secondary Survey

Perform the secondary survey for non-pregnant individuals, as mentioned.

An obstetrician should ideally examine the perineum, including the pelvis. The presence of amniotic fluid in the vagina, PH greater than 4.5, indicates chorioamniotic membrane rupture.

All pregnant patients with vaginal bleeding, uterine irritability, abdominal tenderness and pain, signs and symptoms of shock, fetal distress, and leakage of amniotic fluid should be admitted for further care.

All pregnant trauma patients with Rh-negative blood group must receive Rh immunoglobulin therapy unless the injury is remote from the uterus within 72 hours of injury.

Obese Patients [10]

In the setting of trauma, procedures such as intubation can be challenging and dangerous due to their anatomy. Diagnostic investigations such as E-FAST, DPL, and CT scans may also be challenging. Moreover, most of these patients have underlying cardiopulmonary diseases, which hinders their ability to compensate for the stress and injury.

Athletes [10]

Owing to their prime conditioning, they may not exhibit early signs such as tachycardia or tachypnea in shock cases. Additionally, they usually have low systolic and diastolic blood pressure.

Revisiting Your Patient

Let’s get back to the patient we discussed earlier and start assessing him:

Airway – The patient maintains his airway but finds breathing hard. Intervention: Apply 15L Oxygen via a nonrebreather mask.

Breathing—A strap mark contusion is seen with multiple bruises. His chest expansion is asymmetrical, with reduced breath sounds on the right side of his chest. There is a dull percussion note on the right lower half of his chest. He maintains oxygen saturation. Intervention: Prepare for chest tube insertion on the right side.

Circulation – Heart sounds are muffled with marked engorgement of the external jugular veins in the neck, a good pulse still palpable in his left radial, but cold clammy extremities. His pulse is 128/min, and his blood pressure is 92/50 mm Hg. Bedside ultrasound FAST (Focused Assessment Sonography in Trauma) shows a pericardial tamponade. Intervention: IV access was gained with two large-bore IV cannulas, blood was drawn for labs, the massive transfusion protocol for blood products was activated, a Foley catheter was inserted to monitor urinary output, and the surgery team was on board to plan for emergent pericardiocentesis.

Disability – Patient’s GCS remains 15, unremarkable pupillary examination and POC glucose is 7 mmol/dl.

Exposure – you notice the strap mark on his chest secondary to his seatbelt restraint, and the multiple bruises. The remaining evaluation is unremarkable, with no head, spine, abdomen, or limb injury.

Adjunct investigations – A portable chest x-ray shows increased cardiac shadow and multiple bilateral rib fractures. There is opacification in the right lung [12]. 

Discussion

This patient sustained a blunt trauma leading to pericardial tamponade and right-sided hemothorax, leading to hypovolemic shock. The most common cause of shock in a trauma patient is hypovolemic shock due to hemorrhage. However, other types of shock like cardiogenic shock (due to myocardial dysfunction), neurogenic shock (due to sympathetic dysfunction), or obstructive shock (due to tension pneumothorax, obstruction of great vessels) can occur.

Early signs of shock include tachycardia, which is the body’s attempt to preserve cardiac output and cool peripheries, and reduced capillary refill time caused by peripheral vasoconstriction. This is caused by the release of catecholamine and vasoactive hormone, which leads to increased diastolic blood pressure and reduced pulse pressure. For this reason, measuring pulse pressure rather than systolic blood pressure allows earlier detection of hypovolaemic shock, as the body can lose up to 30% of its blood volume before a drop in systolic blood pressure is appreciated.

Initiate fluid resuscitation in these patients and do not wait for them to develop hypotension.
The main aim is to maintain organ perfusion and tissue oxygenation. In children, start with crystalloid fluid boluses of 20 ml/kg, and in adults, an initial 1 L can be given. In patients who have sustained a major blood loss, consider initiating the Massive Transfusion Protocol (MTP) for blood products as soon as possible.

A few current trauma guidelines have recommended ‘permissive hypotension’ or ‘balanced resuscitation,’ where the principle is to stabilize any blood clots that may have been formed, and aggressive blood pressure resuscitation may disrupt this ‘first formed clot’ and may contribute to further hemorrhage.

To evaluate response to fluid resuscitation, assess the level of consciousness, improvement in tachycardia, skin temperature, capillary refill, and urine output (>0.5 ml/kg/hour in adults).
Besides administering packed red blood cells, do not forget to transfuse platelets, fresh frozen plasma, or cryoprecipitate, as large blood loss can develop coagulopathy in 30% of these injured patients. Tranexamic acid (TXA), an antifibrinolytic, can be utilized in addition as a 1 g bolus over 10 minutes followed by 1 g over 8 hours within 3 hours of trauma without an increased risk of thromboembolic events [11].

This systematic approach focuses on identifying and treating this hemorrhagic shock case. Bedside adjuncts such as FAST examination and portable chest X-ray can provide valuable clues to the cause of shock. A trauma CT scan is only performed once the patient is stable enough to go to the scan room.

This patient’s vital signs improve slightly but remain unstable, and blood is kept draining into the chest drain. The patient is taken to the operation theatre for an emergency thoracotomy [12].

Authors

Picture of Roxanne R. Maria

Roxanne R. Maria

Picture of Hamid A. Chatha

Hamid A. Chatha

Listen to the chapter

References

  1. Initial Assessment of Emergency Department patients, The Royal College of Emergency Medicine, Feb 2017
  2. World Health Organization. BASIC EMERGENCY CARE : Approach to the Acutely Ill and Injured.World Health Organization; 2018.
  3. Thim T. Initial assessment and treatment with the airway, breathing, circulation, disability, exposure (ABCDE) approach. International Journal of General Medicine. 2012;5(5):117-121. doi:https://doi.org/10.2147/IJGM.S28478
  4. Peate I, Brent D. Using the ABCDE Approach for All Critically Unwell Patients. British Journal of Healthcare Assistants. 2021;15(2):84-89. doi:https://doi.org/10.12968/bjha.2021.15.2.84
  5. Schoeber NHC, Linders M, Binkhorst M, et al. Healthcare professionals’ knowledge of the systematic ABCDE approach: a cross-sectional study. BMC Emergency Medicine. 2022;22(1). doi:https://doi.org/10.1186/s12873-022-00753-y
  6. Learning Objectives. https://www.moh.gov.bt/wp-content/uploads/moh-files/2017/10/Chapter-2-Emergency-Patient-Assessment.pdf
  7. Resuscitation Council UK. The ABCDE Approach. Resuscitation Council UK. Published 2021. https://www.resus.org.uk/library/abcde-approach#:~:text=Use%20the%20Airway%2C%20Breathing%2C%20Circulation
  8. Management of trauma patients – Knowledge @ AMBOSS. http://www.amboss.com. https://www.amboss.com/us/knowledge/Management_of_trauma_patients/
  9. Oxford Medical Education. ABCDE assessment. Oxford Medical Education. Published 2016. https://oxfordmedicaleducation.com/emergency-medicine/abcde-assessment/
  10. HENRY SM. ATLS Advanced Trauma Life Support 10th Edition Student Course Manual, 10e. 10th ed. AMERICAN COLLEGE OFSURGEO; 2018.
  11. Walls RM, Hockberger RS, Gausche-Hill M, Erickson TB, Wilcox SR. Rosen’s Emergency Medicine : Concepts and Clinical Practice. Elsevier; 2.
  12. Eamon Shamil, Ravi P, Mistry D. 100 Cases in Emergency Medicine and Critical Care. CRC Press; 2018.

Reviewed By

Picture of Arif Alper Cevik, MD, FEMAT, FIFEM

Arif Alper Cevik, MD, FEMAT, FIFEM

Prof Cevik is an Emergency Medicine academician at United Arab Emirates University, interested in international emergency medicine, emergency medicine education, medical education, point of care ultrasound and trauma. He is the founder and director of the International Emergency Medicine Education Project – iem-student.org, chair of the International Federation for Emergency Medicine (IFEM) core curriculum and education committee and board member of the Asian Society for Emergency Medicine and Emirati Board of Emergency Medicine.

Maxillofacial Trauma (2024)

~ iEM Education Project Team ~ Leave a comment

by Maitha Ahmad Kazim & David O. Alao

Authors
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You have a new patient!

A 48-year-old man was brought to the ED by ambulance shortly after sustaining blunt trauma to the face. The patient was off-loading his quad bike from a truck when it accidentally flipped over and fell directly on his face. He could not recall the incident.

Upon arrival, his vitals were BP: 144/85 mmHg, HR: 104 bpm, T: 36.8°C, RR: 23 bpm, and SPO2: 99% on room air. He was awake on the AVPU score. On examination, the patient was bleeding profusely from his nostrils, breathing from his mouth, and having diffuse facial swelling. You are concerned about the extent of the injuries sustained, and you assemble a team to manage the patient.

Importance

The significance of proficiently managing maxillofacial trauma in the fast-paced emergency medicine setting cannot be overstated. Not only do these traumas cause direct physical harm, but they also impact the patient’s appearance and their ability to perform vital functions like breathing, speaking, and chewing. Given the complex and sensitive nature of the maxillofacial region, emergency physicians must comprehensively understand how to manage such injuries effectively. Proficiency in diagnosing and managing maxillofacial trauma ensures timely and appropriate treatment and prevents potential complications and long-term sequelae. 

Epidemiology

Maxillofacial injuries are a prevalent global health concern. There were an estimated 7.5 million new facial fractures globally in 2017, with 1.8 million individuals living with a disability from a facial fracture [1]. Undoubtedly, the incidence and prevalence vary significantly from one country to another. Singaram et al. reported that the prevalence varied between countries from 17% to 69% [2]. In many regions, inadequate infrastructure, limited access to healthcare, and poor safety regulations contribute to a higher incidence of maxillofacial injuries.

Pathophysiology

Road traffic accidents, interpersonal violence, industrial accidents, and sports-related incidents are the most common etiologies of maxillofacial injuries globally. However, the predominant causes differ in developed and developing countries. Assault is the most common mechanism of injury in developed countries, while motor vehicle accident (MVA) is the most common mechanism in developing countries [3].

Low or high-impact forces can cause maxillofacial injuries. The force needed to cause damage differs from one bone to another. For instance, the zygoma and nasal bones can be damaged by low-impact forces. In contrast, the frontal bone, supraorbital rim, maxilla, and mandible are damaged by high-impact forces [4].

Furthermore, the etiology of maxillofacial trauma can predict the type of facial injuries and fractures sustained. For example, MVAs have been associated with higher instances of mandibular fractures. That is mainly due to its position compared to the rest of the facial bones and its relatively thin structure [5].

Medical History

Maxillofacial injuries often occur in association with other injuries and, thus, can be missed initially. Obtaining a systemic and thorough history can aid the diagnosis. At the initial presentation, the mnemonic “AMPLE” (Allergies, Medications currently used, Past illness/Pregnancy, Last meal, Events/Environment related to the injury) can be used to assess the patient’s pre-injury health status. Then, the following should be probed:

  • What was the mechanism of injury?
    Understanding the cause of the injury (e.g., fall, vehicle collision, assault) provides insights into potential injuries and the extent of trauma. Different mechanisms (blunt vs. penetrating, low vs. high-impact) influence the pattern and severity of injuries and aid in anticipating associated injuries.

    • Environment related to the injury
      Environmental context (e.g., construction site, sports field) can highlight additional risk factors or clues about the nature and potential complications of the injury. It may also help assess the likelihood of secondary injuries or infections.

    • Blunt vs. penetrative
      The type of trauma affects the damage pattern. Blunt trauma may result in fractures or soft tissue injuries, while penetrating trauma may involve more focal injury with a higher risk of infection and internal damage.

    • Low vs. high-impact force
      High-impact injuries are more likely to cause fractures and significant soft tissue damage. Knowing the force helps anticipate the severity and depth of injuries.

    • Direction of force
      The direction can indicate which structures might be compromised (e.g., anterior force could affect the nose, mandible, and dental structures, while lateral force may impact the zygomatic arch or TMJ).

  • Was there a loss of consciousness or an altered level of consciousness?
    Altered consciousness or loss of consciousness may indicate a head injury or neurological involvement, which necessitates further investigation and monitoring for brain injury.

  • Are there any visual disturbances?
    Vision changes can signal orbital fractures or injuries to the optic nerve, potentially affecting ocular function or indicating damage to the orbit and nearby structures.

  • Is there any change in hearing? Is the patient experiencing tinnitus or vertigo? Did they notice any discharge from the ears (clear or bloody)?
    Hearing changes, tinnitus, vertigo, or ear discharge suggest possible basilar skull fractures or damage to the auditory system, which are essential to identify to avoid long-term complications.

  • Any trouble breathing through the nose? Did they notice any discharge (clear or bloody)?
    Difficulty breathing through the nose or nasal discharge may indicate nasal fractures, airway obstruction, or cerebrospinal fluid (CSF) leakage if clear, which is critical to address in traumatic injuries.

  • Any pain while talking? Do the teeth come together normally?
    Pain when speaking or abnormal occlusion may signal fractures in the mandible, maxilla, or TMJ dislocation, impacting facial symmetry, function, and long-term outcomes.

  • Is there difficulty opening or closing the mouth? Is there any pain when biting down the teeth?
    Difficulty or pain in mouth movement often suggests mandibular fractures or TMJ injury. Restricted movement can help identify specific injury locations and aid in planning management.

  • Numbness or tingling sensation in any area of the face?
    Sensory changes suggest possible nerve damage, often related to fractures affecting the infraorbital, mental, or other facial nerves. This information helps predict potential complications and guides treatment planning.

Consider the following symptoms when obtaining a history from maxillofacial trauma patients:

  • Orbital floor fractures commonly present with symptoms such as tingling or numbness around the nose, upper lip, and maxillary gums due to infraorbital nerve damage, along with difficulty looking upward or laterally, double vision (diplopia), and pain during eye movement.
  • Nasal fractures are characterized by swelling, pain, and nosebleeds (epistaxis).
  • Nasoethmoidal fractures can cause cerebrospinal fluid (CSF) rhinorrhea, epistaxis, and tearing (epiphora) due to nasolacrimal duct obstruction.
  • Zygomaticomaxillary complex (ZMC) fractures may lead to numbness around the nose and upper lip, issues with eye movement, double vision, and difficulty opening the mouth (trismus).
  • Maxillary fractures often result in CSF rhinorrhea or epistaxis and may cause mobility in the upper teeth and gingiva.
  • Alveolar fractures are typically associated with gingival bleeding.
  • Mandibular fractures can present as painful jaw movements and tingling or numbness affecting half of the lower lip, chin, teeth, and gingiva.

Red Flags in History

Due to the complex nature of the maxillofacial region, one should be vigilant for red flags when taking history from the patients. Its proximity to the brain and central nervous system makes injuries to these very likely. Thus, identifying them early on can prevent irreversible sequelae and medicolegal implications. Red flags include memory loss, fluctuations in the level of consciousness, nausea/vomiting, and headache that does not improve with analgesia [6].

Neurological involvement can further be assessed by asking about the presence of diplopia or a change in visual acuity. Vision loss usually occurs immediately, but in 10%, symptoms are delayed [7]. Another red flag that is associated with high morbidity and mortality is cervical cord syndrome. Maxillofacial injuries associated with falls are often associated with cervical spinal injury. The patient may complain initially about neck pain or a loss of motor/sensory function in the arms [8].

Physical Examination

Maxillofacial trauma is commonly associated with polytrauma [9]. Thus, it often gets missed in examinations. Physical examination should be done systematically to ensure that all injuries are noted. Like all trauma cases, life-threatening injuries should be addressed first, and the ATLS protocol should be applied accordingly. After that, a physical examination of maxillofacial trauma would involve several key steps. Hard and soft tissue injuries (hematoma, laceration, foreign body, swelling, missing tissue, bleeding, or clear discharge) should be noted upon general inspection of the head and face. Symmetry and alignment of the face should also be noted, bearing in mind that asymmetry may be hidden by edema [10]. Facial elongation and flattening can be seen in midface fractures. Increased intercanthal distance, also known as telecanthus, indicates a nasoethmoidal injury.

Palpation of the whole face should follow, going from top to bottom to avoid missing any injury. Identify step-offs, crepitus, instability or excessive mobility, and malocclusion. Le Fort fractures, complex midface fractures, can be identified during physical examination. 

Next, a complete ocular examination should be done. Assess visual acuity, visual field, pupillary reflex, anterior chamber, and extraocular movements. An ophthalmologic consultation is recommended if any abnormalities are present [10]. The nose and septum should be inspected for any hematoma, bulging mass, or CSF leakage and palpated for any signs of fracture. The oral cavity should be inspected for palatal ecchymoses, lacerations, malocclusion, or missing teeth. Manipulate each tooth individually for movement or pain. Palpate the entire mandible for step-offs or injury. Motor and sensory functions of the face should be evaluated. A thorough cranial nerve examination will help identify sensorimotor injuries. 

Le Fort Classification

Le Fort I Fracture: A Le Fort I fracture, often referred to as a “floating palate,” is a horizontal maxillary fracture that separates the teeth from the upper face. The fracture line passes through the alveolar ridge, lateral nose, and the inferior wall of the maxillary sinus. Patients with this fracture often present with a swollen upper lip, open bite malocclusion, and ecchymosis of the hard palate. When the forehead is stabilized, the maxilla may also have noticeable mobility (including the hard palate and teeth).

Le Fort II Fracture: Known as a “floating maxilla,” the Le Fort II fracture builds upon the characteristics of Le Fort I but extends to involve the bony nasal skeleton, giving it a pyramidal shape. This fracture often leads to a widening of the intercanthal space, bilateral raccoon eyes, epistaxis, and open bite malocclusion. Physical examination may reveal mobility of the maxilla and nose, ecchymosis of the hard palate, and cerebrospinal fluid (CSF) rhinorrhea. Patients may also experience sensory deficits in the infraorbital region extending to the upper lip.

Le Fort III Fracture: Referred to as a “floating face” or “craniofacial disjunction,” the Le Fort III fracture involves a separation of the midfacial skeleton from the base of the skull. The fracture line extends from the frontozygomatic suture across the orbit and through the base of the nose and ethmoid region, running parallel with the skull base. Physical signs include bilateral raccoon eyes, ecchymosis of the hard palate, and a dish-face deformity characterized by elongation and flattening of the face. Additional signs may include enophthalmos (sunken eyes), Battle’s sign (ecchymosis over the mastoid bone), CSF rhinorrhea or otorrhea, and hemotympanum.

Red Flags in Examination

Look for “red flags” during physical examination. These red flags include cervical spine injuries, loss of teeth, Battle’s sign/Raccoon eyes with CSF rhinorrhea, and Le Fort fractures. Facial bones should not be manipulated until cervical spine injuries, which are present in 2.2% of cases, have been ruled out [11]. The oral cavity should be carefully examined for loss of teeth, as it may be aspirated during the injury. For missing teeth, a chest X-ray should be done to rule out or confirm aspiration.

Moreover, facial fractures can extend to the cranium [4]. Depending on the mechanism of injury, the patient may suffer from a concomitant base of the skull fracture, which may present with Battle’s sign and Raccoon eyes as well as CSF rhinorrhea in some cases [11]. LeFort fractures are complex fractures of the midface and are further classified into LeFort I, II, and III. These fractures are considered a red flag as they may cause airway obstruction and life-threatening bleeding [12].

Alternative Diagnoses

Given that the cause is usually known, doctors must identify the injuries sustained and the extent of injuries sustained. While blunt trauma to the face is an apparent cause of maxillofacial injuries, concomitant and alternative diagnoses should not be missed. Patients with maxillofacial trauma can present with a wide range of symptoms that are similar to those from intracranial and cervical spinal injuries.

Acing Diagnostic Testing

The diagnosis of maxillofacial injuries is not based on a single diagnostic test. It is a correlation between history, physical examination, and imaging studies. Given that the etiologies of the injury vary, the differentials are vast, and the clinical presentation differs from one patient to another. Thus, bedside testing and laboratory studies should be tailored to each patient’s clinical presentation and existing symptoms.

Bedside Testing

ECG monitoring is essential for all trauma patients. Dysrhythmias, atrial fibrillation, and ST segment changes can be seen in blunt cardiac injury. Point-of-care (POCT) glucose testing quickly assesses the patient’s glucose level. Hypoglycemia can cause confusion and an altered mental status, which are common findings in patients with maxillofacial trauma. Point-of-care blood gas testing may be beneficial in case of excessive bleeding or airway compromise. In case of tissue hypoperfusion and shock, metabolic acidosis and elevated lactate levels may be noted. Oxygen saturation and carbon dioxide should be monitored in case of midface fractures and suspected airway compromise. A POCT pregnancy test should be done in women of childbearing age, as almost all maxillofacial trauma patients require imaging for diagnosis.

Laboratory Testing

A complete blood count (CBC), particularly hemoglobin and hematocrit, is indicated when the patient is bleeding profusely. LeFort II and III have been associated with an increased risk of life-threatening hemorrhage compared to other facial fractures [12]. Therefore, blood typing and crossmatching are crucial if the patient needs a blood transfusion. A coagulation panel is done to rule out trauma-induced coagulopathy, a preventable factor for progressive brain injury and massive bleeding [13].

A CSF analysis is warranted when there are secretions from the nose or ear. Beta-2 transferrin testing is the current preferred test to confirm the presence of a CSF leak [14]. Other less used methods include beta-trace protein, double-ring sign, and glucose oxidase test. A blood ethanol test and urine toxicology screen can be considered in agitated patients or those with altered levels of consciousness.

Imaging Studies

CT scans are the “gold standard” diagnostic modality for evaluating maxillofacial trauma [15]. Using narrow-cut CT scans without contrast provides detailed cross-sectional images of the facial structures, thus allowing for a comprehensive evaluation of complex fractures. In addition to identifying facial fractures, it can detect head and cervical spinal injuries, air and fluid in the intracranial space and sinuses, periorbital injury, soft tissue injury, and embedded foreign bodies. A non-contrast head CT helps identify intracranial bleeding and distinguish between the types of bleeds if present. This is recommended, especially when the patient experiences loss of consciousness for several minutes. Because maxillofacial trauma is highly associated with cervical spine injury, the physician must have a high index of suspicion for cervical spine fractures. The NEXUS criteria is used to guide imaging in these situations. 

Plain radiographs of the head are used when CT scans are not available. They may be used to screen for fractures and provide some insight into displaced fragments, but they have low sensitivity for detecting and establishing the extent of the injuries. A chest x-ray should be done when a missing tooth is noted on physical examination, as the patient may have aspirated it.

Ultrasound is a helpful bedside diagnostic tool in any trauma patient, and it has been shown to be an accurate diagnostic method when evaluating orbital trauma [16]. It is used when an isolated orbital injury is suspected or a CT scan is not readily available. It can pick up muscle entrapment, soft-tissue herniation, and orbital emphysema.

Risk Stratification

Several risk stratification tools have been developed for maxillofacial trauma. However, these are commonly used in clinical research to assess injury severity and determine the appropriate course of action. Although no specific tool was developed for use in an emergency department, other nonspecific tools like the Glasgow Coma Scale (GCS) and NEXUS criteria come in handy. The GCS score is used to rapidly assess the patient’s level of consciousness, guiding immediate interventions. The NEXUS criteria is used to clear patients from cervical injury clinically without imaging. 

The diagnosis of maxillofacial trauma is based on a combination of clinical assessment and diagnostic imaging. A thorough evaluation of both helps predict the risk. Some common clinical factors that may contribute to poorer outcomes include severe and complex fractures, extensive soft tissue injury, high-energy trauma, open fractures, ocular injuries, and pediatric and geriatric age groups [17,18].

Management

Initial Stabilization

Treating patients with maxillofacial trauma aims to restore function and optimize appearance. However, the primary focus upon presentation is to stabilize the patient. Initial management begins with a primary survey, which constitutes the “ABCDE” approach to identify life-threatening conditions and treat them promptly. 

Airway

Airway patency is a serious concern in maxillofacial trauma, and the nature of the injury often complicates airway management. Airway compromise may be complete, partial, or progressive [9]. Early signs of airway compromise include tachypnea, inability to speak in complete sentences, and abnormal noisy breathing. Agitation and abnormal behavior may indicate hypercapnia.

If the patient has obstruction from soft tissue, perform a jaw thrust maneuver. Cervical spine injury should be presumed in all maxillofacial injury patients until proven otherwise. Therefore, avoid mobilizing the neck until it is cleared. Inspect the oral cavity for any bleeding or secretions and suction accordingly. Consider manual removal with a finger sweep or forceps if a foreign body or debris is identified. Control patients with nasopharynx or oropharynx bleeding with nasal packing or compression with gauze [19].

The need for airway protection increases with severe maxillofacial fractures, expanding neck hematoma, stridor, profuse bleeding or continuous vomiting, and unconsciousness [9]. A nasopharyngeal airway is indicated in a conscious patient without a midface trauma. If the patient was unconscious or had a midface injury, an oropharyngeal airway may help temporarily. However, a definitive airway must be secured in patients who cannot maintain airway integrity. Definitive airway control is done by an endotracheal intubation (nasal or oral). Nasal endotracheal intubation is contraindicated in a base of skull fracture. Given the area’s delicacy and complexity of the injuries sustained, fiberoptic intubation by a skilled physician may provide immediate confirmation of tracheal placement and avoid further complications [10]. If the previous methods cannot be accomplished, a surgical airway (cricothyroidotomy or tracheostomy) should be considered. 

Breathing

The patient’s breathing, ventilation, and oxygenation should be assessed. Check the alignment of the trachea and listen to the patient’s chest bilateral for air entry and added sounds. Deviated trachea and decreased air entry upon auscultation increase the likelihood of tension pneumothorax, and a needle decompression should be performed. Look for soft tissue abnormalities and subcutaneous emphysema.

The patient should be connected to a pulse oximeter to monitor adequate hemoglobin oxygen saturation. If the patient is hypoxic, they should receive oxygen supplementation. Non-invasive ventilation should precede invasive ventilation methods. However, in severe injuries, mask ventilation may be difficult due to the disrupted anatomy of the face [20].

Like all trauma patients, a “full stomach” should be presumed in patients with maxillofacial trauma as digestion stops during trauma. In addition, blood is often swallowed and accumulates in the stomach. Regurgitation and aspiration are a big risk in such patients, and evacuation of stomach content is recommended [20]. A nasogastric tube is contraindicated in a skull base fracture. An orogastric tube is recommended instead to prevent intracranial passage [21].

Circulation

Maxillofacial trauma can cause profuse bleeding that can lead to shock. Monitor blood pressure and heart rate, auscultate, and check capillary refill and hand warmth. Tachycardia precedes low blood pressure in shock. Establish bilateral IV access with two large bore cannulas and draw blood for type and crossmatch. Fluid therapy with crystalloids should be initiated. Identify the source of hemorrhage. If external or intraoral bleeding occurs, apply direct pressure, pack, and suture. Carefully examine the tongue, as persistent bleeding can obscure the airway. In the case of epistaxis, anteroposterior packing will control the bleeding in most cases [10]. Additionally, topical tranexamic acid can be used in anterior epistaxis. In cases of LeFort fractures, intermaxillary fixation might be required when packing fails to stop the bleeding [10]. If the previously mentioned measures fail, consult IR, ENT, or surgery for more advanced interventions like arterial embolization and fracture reduction [22].

Disability

The patient’s mental status and neurologic function should be assessed initially. Glucose is measured at this point if not done upon arrival. The Glasgow Coma Scale helps assess the patient’s level of consciousness. Note any change in the mental status. A brief neurological exam is recommended. 

Exposure

Expose the patient fully while keeping them warm. Look for bruises, bite marks, lacerations, and other injuries, as the etiology of maxillofacial trauma is broad and often presents as polytrauma. Decontamination might be required depending on the nature of the trauma.

Medications

Isotonic crystalloid fluids and blood products are common treatments in trauma patients. Adequate pain management should be provided with NSAIDs, opioids, or local anesthesia. There are no guidelines on the use of prophylactic antibiotics in maxillofacial trauma. Nonetheless, there are specific scenarios where prophylactic antibiotics administration is recommended. Depending on the type of injury sustained, additional medications might be required. Refer to Table to explore the additional medications used in the setting of maxillofacial trauma:

Drug name (Generic)

Potential Use

Dose

Frequency

Cautions / Comments

Acetaminophen

mild-moderate pain (can be given with NSAIDs, with or without Opioids)

325-1,000 mg PO

 

Max Dose: 4 g daily

q4-6h

  • Ask for allergies
  • Ask for if/when they took Acetaminophen at home

Ibuprofen

mild-moderate pain (can be given with Acetaminophen)

600 mg PO

 

Max Dose: 3,200 mg daily

q6h

  • Can cause GI upset and increase risk of GI bleed
  • Renal insufficiency

Hydromorphone

Moderate – severe pain

0.5-4 mg IV/IM/SC

 

Max Dose: n/a

q4-6h

  • Risk of respiratory depression
  • Risk of addiction and abuse

Morphine sulfate

Moderate – severe pain

2.5-10 mg IV/IM/SC

 

Max Dose: n/a

q2-6h

  • Risk of respiratory depression
  • Risk of addiction and abuse
  • Hypotension

Metoclopramide

Nausea and vomiting (to prevent risk of aspiration)

1 to 2 mg/kg/dose IV

 

Max Dose: n/a

Every 2 hours for the first two doses, then every 3 hours for the subsequent doses.

  • Extrapyramidal side effects
  • If acute dystonic reactions occur, 50 mg of diphenhydramine may be injected IM.

Ondansetron

Nausea and vomiting (to prevent risk of aspiration)

0.15 mg/kg IV (not to exceed 16 mg)

 

Max Dose: n/a

q8hr PRN

  • Increased risk of QT prolongation, which increases the risk of cardiac arrhythmia and cardiac arrest.

Amoxicillin-clavulanic acid

Nasal packing (ppx for epistaxis – TSS)

 

Facial fractures communicating with open wounds of the skin

 

Mandibular fractures that extend into the oral cavity

2g PO (extended-release tablets)

 

Max Dose: n/a

q12h (7 days)

  • Ask for allergies
  • Ask if they have taken any antibiotic recently.
  • Hives and skin rash

Procedures

Epistaxis: Epistaxis is a common issue in maxillofacial trauma due to damage to the nasal structures and blood vessels. Managing epistaxis is crucial to prevent blood loss and ensure the airway remains clear. For anterior epistaxis, anterior nasal packing can effectively apply pressure to stop the bleeding. If the bleeding source is posterior, posterior nasal packing using a balloon catheter or Foley’s catheter may be necessary. These techniques help control bleeding and stabilize the patient, especially in cases where blood loss might obstruct the airway or lead to hemodynamic instability.

Inability to Protect Airway: In cases of severe maxillofacial trauma, there may be a risk of airway compromise due to swelling, bleeding, or physical obstruction from broken facial structures. If a patient cannot protect their airway, endotracheal intubation is required to secure it and maintain ventilation. Intubation provides a definitive airway, bypassing obstructions and ensuring adequate oxygenation, which is critical in trauma patients to prevent hypoxia and support life-sustaining measures.

Failed Intubation: Occasionally, intubation may be unsuccessful, particularly in patients with extensive facial injuries or anatomical challenges. In such cases, a cricothyroidotomy is performed. This emergency surgical procedure creates an opening in the cricothyroid membrane, providing an alternative airway route directly into the trachea. Cricothyroidotomy is a life-saving measure when intubation fails, ensuring oxygen can still be delivered to the lungs when other methods are ineffective.

Tension Pneumothorax: Maxillofacial trauma can sometimes be associated with thoracic injuries, leading to complications like tension pneumothorax, where air is trapped in the pleural cavity and compresses the lungs and heart, causing a life-threatening situation. Needle decompression is the first step in relieving the pressure by inserting a needle into the pleural space to allow trapped air to escape. This is followed by a tube thoracostomy (chest tube placement) to maintain the release of air and prevent the recurrence of tension pneumothorax. This procedure is essential to restore normal lung function and stabilize the patient’s respiratory status.

Special Patient Groups

Pediatrics

Pediatric patients’ anatomical and developmental differences should be considered when evaluating them for maxillofacial trauma. An infant’s frontal bone dents, while a child’s frontal bone experiences a depressed fracture under a force that causes facial fractures in adults [4]. Smaller force loads are needed to damage the facial bones than adults [4]. Given pediatric patients’ underdeveloped facial skeletons and sinuses, growth dysplasia is a common outcome of suboptimal treatment. Standard facial radiographs often miss fractures; a CT scan is more reliable in this age group [23]. Assess for orbital fracture thoroughly, as children’s orbital floor is pliable, increasing the risk of entrapment and rectus muscle ischemia [6].

Geriatrics

The impaired physiologic response and frailty of geriatric patients make their treatment more challenging. Although they are subject to the same mechanism of maxillofacial trauma as the other age groups, their response to the injuries differ. They are at a high risk of intracranial hemorrhage, but their basal vital signs often do not reflect signs of hemorrhage or hypoperfusion, making diagnosing shock difficult. Comorbidities and polypharmacy in this age group further mask the normal shock response. In addition, the likelihood of associated injuries in this group is high [24]. Elderly patients were reported to have more frequent cerebral concussions and internal organ injuries [25]. Nonetheless, a GCS of <15 has also been associated with higher mortality rates, especially in those older than 70 years [25]. Putting all of this into perspective when assessing elderly patients, a lower threshold for extensive investigations and referral is necessary.

When to admit this patient

Definitive repair of facial fractures is not a surgical emergency, and patients can be discharged home with a close follow-up in the clinic in most cases. An awake patient with good home care and isolated stable injuries (i.e., mandibular or nasal fracture) may be discharged home. However, admission should be considered in a number of situations. These include severe complex facial fractures, open fractures, the presence of comorbidities, and cases of associated injuries that need close monitoring. Admission is made to the intensive care unit or a surgical ward with a high level of monitoring.

Revisiting Your Patient

A 48-year-old male was brought to the ED by ambulance shortly after sustaining blunt trauma to the face. The patient was loading his quad bike off a truck when it accidentally flipped over and fell directly on his face and upper body. He could not recall what happened thereafter.
Upon arrival, his vitals were BP: 144/85 mmHg, HR: 104 bpm, T: 36.8°C, RR: 23 bpm, and SPO2: 99% on room air. He was awake on the AVPU score. On examination, the patient was bleeding profusely from his nose, breathing from his mouth, and having diffuse facial swelling. You are concerned about the extent of injuries sustained and have assembled your team to manage the patient adequately.

History was taken from his brother, who witnessed the incident. The brother confirmed that the patient had no LOC, dizziness, or vomiting but reported that the patient kept complaining of neck pain. He is known to have L5-S1 disc prolapse, does not take any medication, and has no known allergies.

You worry that the patient might suffer from airway compromise and quickly begin your primary survey. You hear gurgling noises and check the patient’s mouth to find it filled with blood. You suction and look for sources of bleeding in the mouth but find none. The airway becomes patent. You notice that EMS has placed a C-spine collar on the patient already. His lungs are clear bilaterally, and you insert an orogastric tube to suction his stomach contents. He is bleeding profusely from his nostrils, so you pack his nose anteriorly. This does not stop the bleeding, and the patient is spitting out blood. You then apply topical tranexamic acid and more packs, and the bleeding stops. His pulses are present, extremities are warm, and capillary refill time is less than 2 seconds. His GCS is 15/15, and his pupils are reactive to light. Upon exposing him, you notice lacerations on his lips and ears but no other injuries on the rest of his body.

Two large bore IV lines are inserted peripherally, blood is drawn for laboratory investigations, and intravenous normal saline is administered immediately. A 12-lead ECG demonstrated sinus tachycardia. You perform a bedside E-FAST to rule out pneumothorax/hemothorax, pericardial fluid, and peritoneal fluid. You ask for urgent CT scans, including a CT Head and Neck without contrast and a Maxillofacial CT. The CT scan report confirms no C-spine fractures, skull fractures, or brain injury. However, it identifies a Le Fort 1 fracture and fracture involving the right orbital wall. You safely remove the c-spine collar. You consult the Oral and Maxillofacial surgeon and the Ophthalmologist, and both agree to see the patient. You give the patient morphine to alleviate his pain.

You performed a secondary survey to ensure the patient was not deteriorating and to identify any additional injuries. The patient remained stable, and he was admitted to the surgical floor.

Figure: Fracture of the lateral wall left maxilla (long arrow) and a tripod fracture of the right zygoma (short arrows).

Author

Picture of Maitha Ahmad Kazim

Maitha Ahmad Kazim

Dr. Maitha Ahmad Kazim is an Emergency Medicine Resident at Dubai Health, recognized for her dedication in patient care and medical research. She earned her Doctor of Medicine degree from the United Arab Emirates University, where she graduated with distinction. Dr. Kazim is known for her commitment to advancing emergency care, demonstrated by her active engagement in research, mentorship, and medical education.

Picture of David O. Alao

David O. Alao

David is a senior consultant in emergency medicine and associate professor of medicine College of Medicine and Health Sciences, United Arab Emirates University, Al Ain, UAE
He graduated from the University of Ibadan, Nigeria. After initial training in general surgery in Leeds and Newcastle Upon-Tyne, United Kingdom, he had higher specialist training in emergency medicine in the South West of England.
He was a consultant in emergency medicine for 15 years at the University Hospitals Plymouth, United Kingdom where he was a Clinical Tutor, Academic Tutor and, Assistant professor at Plymouth University Peninsular School of Medicine and Dentistry (PUPSMD) UK.
David is a fellow of the Royal College of Surgeons of Edinburgh and the Royal College of Emergency Medicine UK.
His interests are undergraduate and postgraduate medical education, skills training and transfer, trauma systems development and resuscitation science. He has published over 30 papers in peer-reviewed journal.

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References

  1. Lalloo R, Lucchesi LR, Bisignano C, et al. Epidemiology of facial fractures: incidence, prevalence and years lived with disability estimates from the Global Burden of Disease 2017 study. Inj Prev. 2020;26(Supp 1):i27-i35. doi:10.1136/injuryprev-2019-043297
  2. Singaram M, G SV, Udhayakumar RK. Prevalence, pattern, etiology, and management of maxillofacial trauma in a developing country: a retrospective study. J Korean Assoc Oral Maxillofac Surg. 2016;42(4):174. doi:10.5125/jkaoms.2016.42.4.174
  3. Nalliah RP, Allareddy V, Kim MK, Venugopalan SR, Gajendrareddy P, Allareddy V. Economics of facial fracture reductions in the United States over 12 months. Dent Traumatol Off Publ Int Assoc Dent Traumatol. 2013;29(2):115-120. doi:10.1111/j.1600-9657.2012.01137.x
  4. Pappachan B, Alexander M. Biomechanics of Cranio-Maxillofacial Trauma. J Maxillofac Oral Surg. 2012;11(2):224-230. doi:10.1007/s12663-011-0289-7
  5. Sharifi F, Department of Oral & Maxillofacial Surgery, Mashhad University of Medical Sciences, Mashhad, Iran., Samieirad S, et al. The Causes and Prevalence of Maxillofacial Fractures in Iran: A Systematic Review. WORLD J Plast Surg. 2023;12(1):3-11. doi:10.52547/wjps.12.1.3
  6. Van Gijn D. Tips for GP trainees working in oral and maxillofacial surgery. Br J Gen Pract. 2012;62(594):50-51. doi:10.3399/bjgp12X616490
  7. Lynham A, Tuckett J, Warnke P. Maxillofacial trauma. Aust Fam Physician. 2012;41(4):172-180.
  8. Philip MR, Soumithran CS. Prevalence of Neurologic Deficits in Combined Facial and Cervical Spine Injuries: A Retrospective Analysis. Craniomaxillofacial Trauma Reconstr. 2021;14(1):49-55. doi:10.1177/1943387520940182
  9. Saigal S, Khan MM. Primary Assessment and Care in Maxillofacial Trauma. Oral and Maxillofacial Surgery for the Clinician. 2021:983-995. doi:10.1007/978-981-15-1346-6_48
  10. Truong T. Initial Assessment and Evaluation of Traumatic Facial Injuries. Semin Plast Surg. 2017;31(02):069-072. doi:10.1055/s-0037-1601370
  11. Mukherjee S, Abhinav K, Revington P. A review of cervical spine injury associated with maxillofacial trauma at a UK tertiary referral centre. Ann R Coll Surg Engl. 2015;97(1):66-72. doi:10.1308/003588414X14055925059633
  12. Patel BC, Wright T, Waseem M. Le Fort Fractures. In: StatPearls. StatPearls Publishing; 2023. Accessed August 12, 2023. http://www.ncbi.nlm.nih.gov/books/NBK526060/
  13. Peng N, Su L. Progresses in understanding trauma-induced coagulopathy and the underlying mechanism. Chin J Traumatol. 2017;20(3):133-136. doi:10.1016/j.cjtee.2017.03.002
  14. Das D, Salazar L. Maxillofacial Trauma: Managing Potentially Dangerous And Disfiguring Complex Injuries. Emerg Med Pract. 2017;19(4):1-24.
  15. Meara DJ. Diagnostic Imaging of the Maxillofacial Trauma Patient. Atlas Oral Maxillofac Surg Clin North Am. 2019;27(2):119-126. doi:10.1016/j.cxom.2019.05.004
  16. Forrest CR, Lata AC, Marcuzzi DW, Bailey MH. The role of orbital ultrasound in the diagnosis of orbital fractures. Plast Reconstr Surg. 1993;92(1):28-34. doi:10.1097/00006534-199307000-00004
  17. Sharma R, Parashar A. Unfavourable outcomes in maxillofacial injuries: How to avoid and manage. Indian J Plast Surg. 2013;46(2):221. doi:10.4103/0970-0358.118597
  18. Krausz AA, Krausz MM, Picetti E. Maxillofacial and neck trauma: a damage control approach. World J Emerg Surg. 2015;10(1):31. doi:10.1186/s13017-015-0022-9
  19. Hutchison I, Lawlor M, Skinner D. ABC of major trauma. Major maxillofacial injuries. BMJ. 1990;301(6752):595-599. doi:10.1136/bmj.301.6752.595
  20. Barak M, Bahouth H, Leiser Y, Abu El-Naaj I. Airway Management of the Patient with Maxillofacial Trauma: Review of the Literature and Suggested Clinical Approach. BioMed Res Int. 2015;2015:724032. doi:10.1155/2015/724032
  21. Spurrier E, Johnston A. Use of Nasogastric Tubes in Trauma Patients – A Review. J R Army Med Corps. 2008;154(1):10-13. doi:10.1136/jramc-154-01-04
  22. Jose A, Nagori S, Agarwal B, Bhutia O, Roychoudhury A. Management of maxillofacial trauma in emergency: An update of challenges and controversies. J Emerg Trauma Shock. 2016;9(2):73. doi:10.4103/0974-2700.179456
  23. Stewart C, Fiechtl JF, Wolf SJ. Maxillofacial trauma: Challenges in ED diagnosis and management. Emerg Med Pract. 2008;10(2):1-18.
  24. Shumate R, Portnof J, Amundson M, Dierks E, Batdorf R, Hardigan P. Recommendations for Care of Geriatric Maxillofacial Trauma Patients Following a Retrospective 10-Year Multicenter Review. J Oral Maxillofac Surg. 2018;76(9):1931-1936. doi:10.1016/j.joms.2017.10.019
  25. Kokko LL, Puolakkainen T, Suominen A, Snäll J, Thorén H. Are the Elderly With Maxillofacial Injuries at Increased Risk of Associated Injuries?. J Oral Maxillofac Surg. 2022;80(8):1354-1360. doi:10.1016/j.joms.2022.04.018

Reviewed By

Picture of Arif Alper Cevik, MD, FEMAT, FIFEM

Arif Alper Cevik, MD, FEMAT, FIFEM

Prof Cevik is an Emergency Medicine academician at United Arab Emirates University, interested in international emergency medicine, emergency medicine education, medical education, point of care ultrasound and trauma. He is the founder and director of the International Emergency Medicine Education Project – iem-student.org, chair of the International Federation for Emergency Medicine (IFEM) core curriculum and education committee and board member of the Asian Society for Emergency Medicine and Emirati Board of Emergency Medicine.

Fundamentals of ACLS (2024)

~ iEM Education Project Team ~ Leave a comment

by Mohammad Anzal Rehman

Authors
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You have a new patient!

A 56-year-old man presents to the Emergency Department with complaints of chest pain and dizziness that began an hour ago. Upon assessment by the triage nurse, his vital signs are as follows: his heart rate is 107 beats per minute, and his respiratory rate is 22 breaths per minute. His blood pressure is  96/70 mmHg, and his oxygen saturation is at 90% on room air. His temperature is 36.8°C.

You are the student on shift when this patient arrives, and immediately, your mind begins to jump across differential diagnoses for this patient. As you rush toward the patient’s room to join your senior, you prepare to list out all the potential causes of chest pain proudly. This must be a Myocardial Infarction, or maybe even an Aortic Dissection. Perhaps it is that rare Boerhaave syndrome you read about last night!

You finally catch up to the Emergency Physician, but before you can open your mouth to wax lyrical about esophageal ruptures, the Doctor states “Let’s begin by evaluating the ABCs.”

Initial Assessment

Emergency Medicine is one of the few specialties in medicine where patient evaluation begins in the same way for every patient, regardless of the probable diagnosis. Most clinicians are wired to jump straight to the ‘mystery-solving’ component of clinical presentation, with many undergraduate curriculums based around disease recognition. Emergency Medicine, however, places an emphasis on systematic assessment of the patient, starting with ‘The Primary Survey’.

The Primary Survey – ABCDE Approach

The Primary Survey aims to identify life-threatening conditions rapidly and systematically in critically ill patients, with appropriate stabilizing interventions performed when an abnormality is recognized. Besides streamlining the process in a high-stakes and often chaotic environment, the alphabetical order is designed first to address the most severe causes of mortality [1].

The Primary Survey aims to identify life-threatening conditions rapidly and systematically in critically ill patients, with appropriate stabilizing interventions performed when an abnormality is recognized. Besides streamlining the process in a high-stakes and often chaotic environment, the alphabetical order is designed first to address the most severe causes of mortality [1].

Airway

A patient’s airway connects air, and therefore oxygen, from outside the body to the lungs. Airway management is a term used to evaluate and optimize the passage of oxygen in the upper airway, which may be impaired when there is a blockage or narrowing of this pathway. The most common cause of upper airway obstruction is the tongue, which may ‘close’ the oropharynx posteriorly in patients who are comatose or in cardiopulmonary arrest, for example.

Assessment of the airway typically starts by evaluating any external features that may impact the passage of air through the naso- and oro-pharynx, such as facial or neck trauma, fractures, deformities, and any masses or swelling that may disrupt the airway tract. Allergies, especially anaphylaxis, and significant burns may cause edema of the laryngeal airway and produce obstruction. Excessive secretions may also congest the oropharynx and produce airway obstruction.

A patent or ‘normal’ airway allows a responsive patient to speak in full sentences without difficulty, implying a non-obstructed air passage down the oropharynx and through the vocal cords.

Clinical signs of obstruction may include stridor, gurgling, drooling, choking, gagging, or apnea. A physician may also identify an impending airway obstruction where loss of gag reflex, intractable vomiting, or worsening laryngeal edema may inevitably compromise the passage of air to the lungs and produce a failure to oxygenate or ventilate, prompting a decision to secure the tract through intubation.

Management

In the responsive patient, allow for the patient to be seated or lying in their most comfortable position as you assess the patency of the airway.

‘Opening’ the airway involves positioning the patient’s head in the ‘sniffing position’. In this position, a slight extension of the head with flexion of the neck, keeping the external auditory meatus in line with or above the sternal notch, is used to optimally align the pharyngeal and laryngeal airway segments, preventing obstruction posteriorly by the tongue (Figure 1). This is useful in patients who are unresponsive and cannot consciously protect their airway.

Figure 1 – Use of ‘sniffing position’ to open the airway

Two maneuvers are helpful in opening an unresponsive or sedated patient’s airway, optimizing air entry to the lungs:

1. Head tilt chin lift (Figure 2A) – Using fingertips under the chin, lift the mandible anteriorly while simultaneously tilting the head back using the other hand. Do not use this if cervical spine injury is suspected!

Figure 2A – Head-tilt chin lift

2. Jaw thrust (Figure 2B) – With thenar eminences of both hands anchored over both maxillary regions of the patient’s face, use your fingers at both angles of the mandible to lift it anteriorly. This maneuver is preferable in cases of suspected cervical spine injury as it does not cause hyperextension of the neck.

In unresponsive patients with excessive secretions, use of a rigid suction device can clear fluid and particulate matter such as vomitus.

Intubation may be performed if airway assessment deems it necessary to protect or secure the airway tract in a definitive way. If intubation is required, it should be performed as early as possible to prevent the evolution of a difficult airway, which would lower the chances of a successful intubation. It may also be useful to establish the risk of an inherently difficult airway using the L-E-M-O-N airway assessment method as below:

Look externally – facial trauma, large incisors and/or tongue, hairy beard, or moustache

Evaluate the 3-3-2 rule – where optimal distance between incisors on mouth opening should be 3 finger breadths. Similarly, 3 finger breadths (patient’s fingers) should span the distance from chin to hyoid bone, while the distance from hyoid to thyroid should measure 2 finger breadths.

Mallampati score – grades the view of an open mouth, with class 3 or more predicting a difficult intubation

Obesity/obstruction – Epiglottitis or a tonsillar abscess can inhibit easy passage of an endotracheal tube.

Neck mobility – if limited, positioning is difficult and causes suboptimal views during intubation.

iEM-infographic-pearls-airway - Assessing Airway Difficulty
assessing airway difficulty

Cervical spine immobilization

When the patient arrives in the Emergency Department (ED) following a significant physical trauma, such as head injury or motor vehicle collision, it is crucial to consider the integrity of the cervical spine. If injury is present in this region, further manipulation or movement of the neck may lead to spinal cord damage. Therefore, evaluation and management of airway for these patients should go hand in hand with cervical spine immobilization.

If no specialized equipment is available, or until one is prepared for use, attempts to limit neck movement can be done using manual in-line stabilization, where the provider’s forearms or hands may be positioned at the sides of the patient’s head to prevent indirect movements that could exacerbate underlying injury (see Figure 3).

Cervical spine immobilization is then performed using a rigid cervical collar. It may be augmented with head blocks on lateral sides to limit movement further as the patient is evaluated for injury (see Figure 4). The thoracolumbar region of the spine is immobilized using a spinal backboard, which keeps the patient in a supine position with minimal external force on the spine. Frequently utilized in Emergency Medical Services (EMS) during extrication and transport, all efforts should be made to transition the patient off the spinal board in the ED as it is quite uncomfortable, with prolonged use associated with pressure ulcers and pain.

Breathing

The lungs perform the vital function of delivering oxygen from the airway to the alveoli through ventilation. Perfusion at the alveoli allows for gas exchange; therefore, effective ventilation and perfusion both play a key role in the availability and utilization of oxygen by the human body. Evaluation of the Breathing component assesses factors that would indicate a compromise in ventilation.

The chest inspection should look for respiratory rate, use of accessory muscles, position of trachea (midline versus deviated), symmetry of chest rise, and/or any visible trauma to the thorax. Auscultation evaluates breath sounds for any bilateral inequal air entry or presence of crackles, crepitus, or wheeze. Percussion, though sometimes useful, is often difficult to perform adequately in a resuscitation environment.

Let’s compare the findings in normal lungs, pleural effusion, and pneumothorax based on chest rise, trachea position, percussion, and auscultation.

Normal Lungs: Chest rise is symmetrical with the trachea in the midline position. Percussion reveals a resonant sound. Auscultation presents vesicular breath sounds peripherally and bronchovesicular sounds over the sternum, with no added sounds.

Pleural Effusion: Chest rise remains symmetrical, and the trachea is midline. Percussion is dull over the area of effusion, and auscultation shows decreased breath sounds in the region of the effusion.

Pneumothorax: Chest rise is unequal, and the trachea may be deviated in cases of tension pneumothorax. Percussion reveals a hyper-resonant sound in the area of the pneumothorax, and auscultation shows decreased breath sounds over the pneumothorax region.

Measuring oxygen saturation using pulse oximetry (spO2) provides a percentage of oxygen in circulating blood, with normal levels typically at 95% or above. However, in patients with chronic lung disease, baseline oxygen saturation levels may decrease and can be as low as 88% in many cases. For patients experiencing shortness of breath and showing signs of hypoxia, pulse oximetry readings below 94% suggest that supplemental oxygen may be necessary. This can be administered through various oxygen delivery systems, as outlined in Figure 5 and described below.

Figure 5 – Common equipment used in airway management 1- Nasal cannula, 2- Simple face mask, 3- Nebulizer,* 4- Non-rebreather mask, 5- Venturi mask valves, 6- Rigid suction tip, 7- Bag-valve mask device, 8- Oropharyngeal airway (OPA), 9- Nasopharyngeal airway (NPA), 10- Direct Laryngoscope, 11- Endotracheal tube with stylet, 12- Colorimetric end-tidal CO2 detector, 13- Bougie, 14- Laryngeal Mask Airway (LMA) *NOT an oxygen delivery device, used to administer inhaled medication such as bronchodilators and steroids CO2: Carbon dioxide

General concepts—We typically breathe in room air, which contains 21% oxygen. Each Liter per minute of supplemental oxygen provides an additional 4% inspired oxygen (FiO2) to the patient.

Nasal cannula – Administered through patient nostrils, can provide a maximum flow rate of 4-6 Liters per minute of oxygen, which equals roughly 37 – 45% FiO2

Simple face mask – Applied over the patient’s nose and mouth, can provide a maximum flow rate of 6-10 Liters per minute of oxygen, which equals roughly 40 – 60% FiO2

Venturi mask – Typically used in COPD, where over-oxygenation is avoided. Different colors deliver various flow rates to limit oxygen delivery to the required amount only; Blue (2-4L/min, FiO224%), White (4-6L/min, FiO2 28%), Yellow (8-10L/min, FiO235%), Red (10-12 L/min, FiO2 40%), Green (12-15 L/min, FiO260%)

Non-rebreather mask – Utilizes an attached bag with a reservoir of oxygenated air along with one-way valves on the mask to prevent rebreathing of expired air, optimizing oxygenation. It can provide a maximum flow rate of 15 Liters per minute of oxygen, which equals roughly 85 – 90% FiO2.

Non-invasive ventilation (CPAP/BiPAP) is a tight-fitting mask device that uses high positive pressure to keep the airway open and enhance oxygenation. It is particularly useful in conditions such as COPD exacerbation, acute pulmonary edema/heart failure, and sleep apnea.

Bag-valve mask device: A self–inflating bag attached to a reservoir delivers maximal, high-flow 100% oxygen. This method of manual ventilation is used in rescue breathing and oxygen delivery in nonresponsive or cardiopulmonary arrest patients.

Circulation

The circulation component of the Primary Survey evaluates the adequacy of perfusion by the cardiovascular system. The patient’s general appearance is assessed for signs of pallor, mottling, diaphoresis, or cyanosis, which indicate inadequate or deteriorating perfusion status. Pulses are checked centrally (e.g. carotid pulse, especially if patient with impaired breathing) and peripherally (e.g. radial) alongside hemodynamic assessment, including blood pressure and heart rate checks. Information from this segment also provides valuable insight into potential signs of shock. Extremities are palpated in order to determine any delays in capillary refill time (more than 2 seconds signifies inadequate perfusion, e.g. hypovolemia), peripheral edema in lower extremities (signs of heart failure), and skin temperature (cool or warm to touch).

In cases of trauma, systematic evaluation of circulation also seeks to ascertain areas of potential blood loss or collection, with interventions for any long-bone deformities and/or bleeding from open wounds performed as they are discovered.
Intravenous (IV) line insertion is also performed as part of the management of circulation, as any required fluid or blood products can then be administered through a large-bore IV line (16 gauge or higher). If IV insertion is difficult on multiple attempts, when volume resuscitation is urgently required, Intraosseous (IO) access should be sought to prevent delay in any needed treatment. Insertion of a peripheral venous line often occurs concomitant to blood extraction for any urgent laboratory investigations and/or point-of-care testing. Some common examples of tests performed on critically ill patients include venous blood gas, complete blood count, type and crossmatch, troponin, urea, electrolytes, and creatinine.

Finally, circulation assessment requires an evaluation of cardiac rhythm. Basic auscultation may reveal the rate and regularity of rhythm along with murmurs. However, a critically ill patient will also benefit from the immediate attachment of cardiac pads to the bare chest and connection to a cardiac monitoring device, which provides the physician with the patient’s current cardiac rhythm.

A normal sinus rhythm (Figure 6) consists of a P wave (atrial depolarization), followed by a QRS wave (ventricular depolarization – normally less than 120 ms), with a subsequent T wave (ventricular repolarization). P-R intervals typically have a duration of 120 – 200 ms. A regular rhythm, with a consistent P wave preceding QRS complexes, with a normal heart rate (between 60 – 100 beats per minute (bpm)) is required to consider a rhythm to be normal sinus on the cardiac monitor.

Figure 6 – Normal sinus rhythm

The American Heart Association’s (AHA) Advanced Cardiac Life Support (ACLS) course and guidelines outline a series of internationally recognized cardiac rhythms and their general management when encountered [2]. Some of the most important rhythms, along with the AHA bradycardia and tachycardia algorithms, are summarized below:

Figure 7.1 - Sinus bradycardia (HR < 50 bpm)

Several different conditions, including abnormal heart conduction, damage to the myocardium, metabolic disturbances, or hypoxia, can cause bradycardia. A lower heart rate can result in decreased perfusion to end-organs, such as the brain, with resultant signs and symptoms such as dizziness, confusion, shortness of breath or chest pains. Management (Figure 7.2) aims to treat the underlying cause and increase the heart rate (atropine, dopamine/epinephrine and/or cardiac pacing) if needed to restore the heart’s ability to perfuse organs adequately.

Figure 7.2 – American Heart Association’s Bradycardia Algorithm

Tachycardia (Figure 8.1) is a heart rate of more than 100 bpm that may present as several types of waveforms on the cardiac monitor. Supraventricular tachycardia (SVT) originates in the upper chambers of the heart. The rapid heart rate prevents adequate filling of the heart between contractions, causing signs and symptoms such as dizziness, palpitations, or chest pain.

Figure 8.1 - Supraventricular Tachycardia (SVT)

Management (Figure 8.2) typically involves Valsalva maneuvers, medication (e.g. adenosine), and/or synchronized cardioversion as needed to revert the rhythm back to baseline.

Figure 8.2 – American Heart Association’s Tachycardia Algorithm

SVT produces a narrow-complex tachycardia (QRS segments < 120 ms). In comparison, monomorphic Ventricular Tachycardia (Figure 8.3) originates in the lower chambers of the heart and produces a wide-complex (QRS segments > 120 ms) tachycardia on the cardiac monitor. Similarly, this rhythm may cause dizziness, shortness of breath, or chest pain and is managed with medication or synchronized cardioversion.

Figure 8.3 - Ventricular Tachycardia

ACLS algorithms often divide patients based on “stable” and “unstable” categories. This grouping aims to ascertain which individuals have a pathology severe enough to impair cardiac output to the point of causing serious inadequacies in end-organ perfusion. This ‘instability’ is manifested by altered mental status, ischemic chest pain, drastically low hemodynamic parameters (e.g. systolic BP < 90 mmHg), signs of shock, and signs of acute decompensated heart failure.

Disability

This segment evaluates the level of consciousness and responsiveness of the patient. Level of consciousness may be assessed generally using the AVPU scale (below);

Alert: fully alert patient
Verbal: some form of verbal response is present, though not necessarily coherent.
Pain: response to painful stimulus
Unresponsive: no evidence of motor, verbal or eye-opening response to pain

or more explicitly, using the Glasgow Coma Scale (GCS)

Choose the best response of patient
EYE OPENING
4: Spontaneously
3: To verbal command
2: To pain
1: No response
BEST VERBAL RESPONSE
5: Oriented and converses
4: Disoriented and converses
3: Inappropriate words; cries
2: Incomprehensible sounds
1: No response
BEST MOTOR RESPONSE
6: Obeys command
5: Localizes pain
4: Flexion withdrawal
3: Flexion abnormal (decorticate)
2: Extension (decerebrate)
1: No response
Glasgow Coma Score (GCS) (Modified from Teasdale, G., & Jennett, B. (1974). Assessment of coma and impaired consciousness: a practical scale. The Lancet, 304(7872), 81-84.) - Please read this article to get more insight regarding GCS.

Exposure

Complete exposure of the patient may be necessary to completely evaluate for any external signs of infection, injury, and rash. This is especially useful in trauma, where log-rolling of the patient is included to ensure the back and spine are also included in a complete assessment for any traumatic injuries. As you expose the patient, obtain consent, be mindful of their dignity, and uncover each segment of the body sequentially, covering it back to prevent any hypothermia for the patient. A core temperature reading also completes vital sign measurements for the patient.

Practical implementation of the Primary Survey

The “cursory” primary survey

It may seem surprising to consider that virtually every patient who enters the Emergency Department, despite the severity of the illness, undergoes some form of a Primary Survey by the treating physician. However, the practicality of this becomes quite obvious when you consider a simple question frequently asked at the beginning of a patient encounter:

“How are you?”

An adequate response of “I am all right” or “Well, I have had this pain in my stomach…” seems fairly standard, but it addresses most of the components detailed in the previous section. A patient who can form words without difficulty or added sounds generally has an intact or patent Airway. Their ability to form words depends on air that has been sufficiently ventilated and moving through the vocal cords, hence the Breathing is adequate. An appropriate response to the question allows us to assume that Circulation adequately perfuses the brain to allow comprehension and formulation of new words oriented to the circumstances of the encounter, hence providing insight into Circulation and, to a degree, Disability.

Synchrony in the Emergency Department

Although systematic assessment during the Primary Survey is laid out in order, it is also important to note that an Emergency Department consists of teams of healthcare professionals who often have the personnel and resources to simultaneously perform tasks to efficiently address all components of the Primary assessment, without delay between segments.
In practice, an example of how synchrony works would involve a patient who, on initial, immediate assessment, is deemed to be in significant distress and/or critically ill. The patient is immediately moved into the ED to a resuscitation area, where team members expose the chest, attach cardiac pads to connect the patient to a cardiac monitor, obtain a fresh set of vital signs, including spO2monitoring, with IV cannula insertion, blood extraction for testing as needed. At the same time, a primary survey is conducted simultaneously by another physician who moves through Airway, Breathing, Circulation, Disability and Exposure. In more advanced systems, a member may be dedicated to each component of the Primary Survey.

Adjuncts

A number of resources are accessible to the Emergency Physician that may aid in diagnosing and investigating the critically ill patient. Utilizing these alongside the initial Primary Survey provides valuable, relevant information that can further guide clinical decision-making and diagnosis during evaluation.

  1. Electrocardiogram – A 12-lead electrocardiogram provides a complete picture of the heart’s electrical activity in various vectors and segments, allowing for a more accurate evaluation for rhythm disturbances, such as in acute myocardial infarction, hyperkalemia, bundle branch blocks, and torsade de pointes. This often ties into the Circulation assessment and allows for a more comprehensive look into the heart’s electrophysiology.
  2. Portable X-rays – Particularly in trauma, urgent chest and pelvic X-ray films can often be obtained without having to transfer the patient to Radiology, hence providing more information on suspected lung pathologies (e.g. pneumothorax, effusion/hemothorax) and pelvic abnormalities (e.g. fracture, displacement).
  3. Urinary/ gastric catheters – Urinary catheters are useful to evaluate fluid status and monitor output for the patient undergoing volume resuscitation. When relevant, gastric tube insertion can assist in gastrointestinal decompression, if needed, as well as minimize the risk of aspiration in certain patients.
  4. Point-of-Care Ultrasonography (PoCUS) – A rapidly evolving and increasingly prevalent modality in the ED is the ultrasound.[3] Various probes, at different frequencies, utilize ultrasound waves to provide the physician with real-time visualization of the body’s internal structures. These images are fast and often very reliable in determining major findings that can guide decision-making in critically ill patients (e.g. presence of post-traumatic intra-abdominal free fluid, pneumothorax, cardiac tamponade). Figure outlines some examples of information that can be extracted using PoCUS.

 

HI-MAP in Shock

Reassessment

Each intervention performed in the Primary Survey should ideally be accompanied by a reassessment of vital signs and patient clinical status and a restarted Primary Survey beginning from Airway. Identifying any improvements, deteriorations, or non-responses that will be pivotal in guiding the initiation or discontinuation of further intervention as per the clinical case is crucial.

Focused History and Secondary Survey

If the patient is appropriately evaluated and stabilized following the Primary Survey, the treating physician may proceed with a focused history and secondary survey appropriate to the clinical circumstances. One example of a focused history incorporates the mnemonic SAMPLE to organize pertinent information as follows:

S – Signs/symptoms of presenting complaint

A – Allergies to any food or drugs

M – Medications (current, recent changes)

P – Pertinent past medical history

L – Last oral intake

E – Events leading to the illness or injury

A secondary survey in the Emergency Department is a more comprehensive physical examination performed systematically in a head-to-toe fashion to investigate any clinically relevant findings. In case of trauma, this also involves careful inspection for any missed injuries, deformities, or signs of underlying blood collection.

As the secondary survey is performed, relevant investigations and/or imaging may be ordered to augment the evaluation of the present clinical condition (e.g. Computerized Tomography (CT) of the brain after signs of basal skull fracture noted on inspection of the face and head). Information gathered from the survey and results of any ordered investigations, coupled with the clinical condition and/or response to therapy in the ED, if any, is used to determine patient disposition at the end of the ED encounter.

Revisiting Your Patient

You assist the Emergency Physician in performing a Primary Survey. The airway is patent, with the patient phonating in full sentences and breathing with mild tachypnea but no added sounds on auscultation. You initiate supplemental oxygen through a non-rebreather mask, with an increase in spO2 to 99%. You reassess and proceed through Airway, Breathing, and Circulation. As you discuss initiating IV fluids with your senior, the patient complains of worsening chest pain, palpitations, and dizziness.You attach the patient to the cardiac monitor and notice the rhythm below:

Cardiac pads have already been attached to the patient. Noting the presence of ischemic chest pain, you correctly identify the patient as having an unstable, narrow-complex tachycardia, most likely an SVT and prepare for synchronized cardioversion. Conscious sedation is conducted after explaining the procedure and obtaining consent from the patient. 50 joules of biphasic energy is then administered for synchronized electrical cardioversion. The rhythm changes on the monitor to the reading below:

You observe an organized rhythm but note that the patient is now unresponsive, with eyes closed and no palpable carotid pulse.

Basic Life Support

Cardiopulmonary arrest occurs when the heart suddenly stops functioning, resulting in lack of blood flow to vital organs in the body, such as the lungs and brain. Therefore, signs of arrest are manifested as a lack of breathing (apnea), lack of pulse and unresponsiveness. The most common cause of cardiac arrest is coronary artery disease.[4] Respiratory arrest refers to a cessation of lung activity, but with a present, palpable pulse and functioning heart.
The International Liaison Committee on Resuscitation (ILCOR) and the American Heart Association (AHA) are some of the key figures who have developed international guidelines on the recognition and management of cardiac arrest patients.[5] Basic Life Support (BLS) and Advanced Cardiac Life Support (ACLS) courses were established to optimize the workflow and, therefore, patient outcomes in Cardiopulmonary Resuscitation (CPR).

CPR forms the cornerstone of BLS to effectively maintain the victim’s circulatory and ventilatory function until circulation either spontaneously returns or is hopefully restored through intervention. The general concepts within BLS are outlined below:

1. A person who has a witnessed collapse, lack of response or who is suspected of being unresponsive due to cardiac arrest should be approached for further assessment and management. However, it is important for the rescuer to first determine whether the scene is safe around the patient before attempting any intervention. An example of this would be a victim drowned in water, who should be removed from the body of water onto a dry surface prior to attempting life-saving chest compressions or defibrillation.

Figure 9 - Witness
Figure 10 - Check for responsiveness

2. Check for responsiveness. Firmly tapping both shoulders with the palms of your hands and a clear, verbal prompt, such as “Hey, are you okay?” should be incorporated to ensure that the victim is, indeed, unresponsive to an otherwise arousable stimulus.

3. You have determined that the patient is unresponsive. If you are alone, shout loudly and clearly for help and assistance. If no help is nearby, call Emergency Medical Services using your mobile phone.

Figure 11 - Call for help
Figure 12 - Open airway, palpate carotid artery, observe the chest

4. Open the patient’s airway (tilt chin upward into sniffing position). Palpate the carotid pulse by placing two fingers (index and middle finger) just lateral to the trachea on the side closest to you while simultaneously observing the chest for any spontaneous chest rise (breathing). The pulse check should take a minimum of five (5) seconds but no more than 10 seconds to avoid delay in life-saving intervention.

5. When help is available, the chain of survival begins by activating the Emergency Response System. In addition to activating the Emergency Response, ask the person who has responded to your call for help getting an Automated External Defibrillator (AED) device. An example of instruction to a bystander (out of hospital) would be to ‘call an ambulance and get an AED!’. Inside a hospital, if another healthcare provider has come to aid, you may ask them to ‘activate the Emergency Response System/’Code Blue’ and get the crash cart/AED.’

6. Begin high-quality chest compressions. Hands are placed with fingers interlaced to exert pressure using the heel of one hand at the center of the chest, over the lower half of the breastbone (sternum), in line with the nipples (in men), with shoulders directly over your hands and arms straight at a perpendicular angle to the victim’s chest. High-quality chest compression is one of the few variables which have been evidenced to improve patient survival in cardiac arrest.

Figure 13 - Chest compression

Keep the following features in mind to maintain high-quality chest compressions:

  • More than 80% of the time in resuscitation or more should be spent on compressions (Chest compression fraction of > 80%)
  • The frequency of compressions should follow a rate of 100–120 compressions per minute.
  • Compression depth in adults is at least 2 inches. In infants and children, depth should be at least one-third of the anterior-posterior diameter of the chest.
  • After each compression, the hands should be withdrawn to allow adequate chest recoil and fill the heart between compressions.
  • Minimize interruptions in chest compression
  • Avoid hyperventilation (see next point).
Figure 14 - Bag-Valve-Mask Ventilation. Two-Hand technique

7. Compressions should follow the ratio 30:2, that is, 30 compressions followed by 2 rescue breaths delivered by a mouth barrier device (pocket mask) in the sniffing position or a Bag-valve mask (BVM) device if another rescuer is present to manage the airway in hospital. The BVM’s mask should be held with a tight seal using the E-C technique over the bridge of the nose and covering the mouth. 

Breaths should be over 1 second, with enough air pushed in to observe a chest rise and no hyperventilation or excessive bagging of the BVM to avoid gastric insufflation. Two attempts at rescue breaths are performed, minimizing time to under 10 seconds and resuming chest compressions immediately after. If a definitive airway (e.g. endotracheal tube) is in place, resume compressions without pause at a rate of 100-120 compressions per minute while breaths are delivered once every 6 seconds.

8. Once an AED or cardiac monitor/defibrillator is available, place the pads on the victim’s bare chest (dry the skin if wet) in either an anterior-lateral or anterior-posterior position.When in doubt, follow the machine’s prompts and the instructions on the pads themselves to guide placement.

Figure 15 - Correct placement of transcutaneous pacing pads.jpg

9. Follow the prompts on the AED. Stop compressions when the device analyzes rhythm and stay clear of the patient (not touching any part of the patient’s body). During an in-hospital resuscitation, as per ACLS workflow, stay clear, as the team leader should analyze the initial rhythm to ascertain the presence of a shockable or non-shockable rhythm. Either way, the device or team leader should prompt whether a shock is advised. Continue compressions as the device charges, but ensure that all rescuers are clear of the patient when the shock is delivered using the AED/defibrillator device.

Figure 16 - Shock delivery.

A victim who is unresponsive but has a palpable pulse has respiratory arrest, which is managed using rescue breathing only. Breaths are delivered once every 6 seconds without chest compressions while transport to a higher level of care and/or management of any underlying cause for the condition is initiated.

Advanced Cardiac Life Support

The Advanced Cardiac Life Support algorithms were designed to deliver a higher level of resuscitative care where providers with increased training and improved resources are available. This type of augmented management is customary to the Emergency Department, where a Rapid Response Team or Code Blue team would respond when activated and initiate a more team-based approach to cardiopulmonary resuscitation.

Instead of an AED, in-hospital settings have a cardiac monitor/defibrillator, usually mounted atop a crash cart consisting of a CPR back-board (to support chest compressions by providing a firm surface to use under the patient’s chest), drawers with medication used during cardiac arrest, and various equipment for airway management and IV/IO access. Once brought to the bedside, the cardiac pads are similarly placed on the patient’s chest while BLS maneuvers (chest compressions and rescue breaths) continue. Once placed, however, compressions should be paused to assess the cardiac monitor’s cardiac rhythm. The type of rhythm should be identified as ‘shockable’ or ‘non-shockable’ (Figure 17s).

Figure 17.1 - NON-SHOCKABLE - Asystol
Figure 17.2 - NON-SHOCKABLE - Pulseless electrical activity – organized rhythm in the absence of palpable pulse
Figure 17.3 - SHOCKABLE - Pulseless Ventricular Tachycardia
Figure 17.4 - SHOCKABLE - Ventricular fibrillation

“Shockable” rhythms (pulseless Ventricular Tachycardia and Ventricular Fibrillation) are a product of aberrant electrical conduction of the heart. Rapid, early correction of this rhythm is the most important step in returning the body to its normal circulatory function. Early defibrillation is one of the few variables that has been evidenced to improve patient survival in cardiac arrest, the other notable one being high-quality chest compressions.[6]

Defibrillation involves using an asynchronous 200J of biphasic (360J if monophasic) energy, delivering an electric current through the cardiac pads attached to the patient’s chest to revert the heart to a rhythm that can sustain spontaneous circulation. Chest compressions should be ongoing while charging, but all persons should stay clear of the patient when shock is being delivered, and this is frequently verified with verbal feedback (‘Clear!’) before pressing the defibrillator button to deliver the shock. Immediately after the shock, chest compressions should resume to minimize interruptions between compressions.

Two minutes of chest compressions and rescue breaths make up each cycle of CPR, at the end of which a rhythm check should be performed for any changes and/or presence of pulse. Figure 18 outlines the ACLS algorithm used to manage shockable and non-shockable rhythms in cardiac arrest. Early shock in shockable rhythms is followed by a cycle of CPR, a second shock if still with a shockable rhythm, after which 1mg of IV epinephrine is given, with subsequent doses every 3 to 5 minutes. During the third cycle of CPR, after 3 shocks have been delivered for a persistent shockable rhythm, a bolus of IV Amiodarone 300mg is typically administered, with a dose of 150mg in a subsequent CPR cycle if still with a shockable rhythm.

“Non-shockable” rhythms (pulseless electrical activity (PEA) and asystole) are not typically a product of disorganized electrical activity in the heart. Instead, an underlying cause has resulted in cardiac arrest for these patients. While the majority of cardiac arrest is caused by coronary artery disease, the consideration of reversible causes by use of the H’s (hypovolemia, hypoxia, hyper-/hypokalemia, hydrogen ions (acidosis), and hypothermia) and T’s (thrombosis/embolism, toxins, tension pneumothorax, and cardiac tamponade) may help recognize and manage other possible etiologies in patients.

The management of non-shockable rhythms focuses on consistent, high-quality CPR, with regular pulse checks every 2 minutes, addressing reversible causes, and administering IV epinephrine 1mg every 3 to 5 minutes.
A palpable pulse with measurable blood pressure signals the Return of Spontaneous Circulation (ROSC).

Figure 18 - ACLS Adult Cardiac Arrest Algorithm

Resuscitation Team Dynamics

The Emergency Department is equipped with the resources and personnel to provide care beyond basic life support. Resuscitation is optimized when multiple providers work together to effectively perform tasks toward management of the patient, thereby multiplying the chances of a successful outcome for the patient. A high-performance team typically consists of members allocated to the following roles and responsibilities:

  • Airway – Opens and maintains the airway. Manages suctioning, oxygenation, and ventilation (Bag-valve mask) and assesses the need for a definitive airway if needed.
  • Medication – Inserts and maintains IV/IO access. Manages medication administration and fluids.
  • Monitor/defibrillator – Ensures attached cardiac pads and AED/cardiac monitor/defibrillator device are working appropriately to display the patient’s cardiac rhythm in clear view of the team leader. Administers shocks using the devices as needed. May alternate with the compressor every 5 cycles or 2 minutes to prevent compression fatigue
  • Compressor – Performance of high-quality chest compressions as part of CPR for the cardiac arrest patient. Focuses on quality and consistency of compressions. You may switch to another standby compressor or monitor/defibrillator every 5 cycles or 2 minutes if compressions are affected by fatigue.
  • Recorder – Documents the timing of medication, intervention (shocks, compression), and communicates these to the Team Leader, with prompts to enable timely dosing of frequent medication (e.g., ensuring epinephrine every 3 to 5 minutes is administered as per the verbalized order)
  • Team leader – A defined leader who coordinates the team’s efforts and organizes them into roles and responsibilities that are clear, well-understood, and within their individual limitations. Provides explicit instructions and direction to the resuscitation effort, focused on patient care and optimized performance from all team members. Promotes understanding and motivates members, identifying any potential deficit or depreciation of quality during resuscitation and facilitating improvement in performance as needed.

All team members are encouraged to conduct themselves with mutual respect and practice closed-loop communication, where each message or order is received with verbal confirmation of understanding, then execution of the order, centralizing all information back to the team leader. Figure 19 provides an example of the possible placement of each member during resuscitation that may optimize their workflow through the resuscitation attempt. Ideally, the team leader remains at the foot of the bed, in clear view of all members, with involvement limited to coordination of the team’s efforts and minimal direct execution of tasks.

Figure 19 - An example of optimized team placement during resuscitation

Post Arrest Care

If the patient is found to have Return of Spontaneous Circulation (ROSC), post-cardiac arrest care should be initiated to enhance the preservation of brain tissue and heart function. This involves a sequential assessment and optimization of Airway, Breathing, and Circulation in the initial stabilization phase. A definitive airway may be placed so ventilation is more appropriately controlled, with parameters set to optimize oxygen administered with ventilatory function. Figure 20 outlines the ACLS algorithm and parameters often used to help guide post-cardiac arrest care. Circulation incorporates fluids, vasopressors, and/or blood products to achieve an adequate systolic blood pressure above 90 mmHg, with Mean Arterial Pressure of at least 65 mmHg typically indicating perfusion within stable parameters.

It is imperative to obtain a 12-lead ECG early to ascertain the presence of an ST-elevation myocardial infarction (STEMI), which will require expedited transfer of the patient to a Cath Lab for definitive reperfusion therapy. The patient’s responsiveness should be reassessed, and the determination for additional investigation should be performed in conjunction with other critical care management as needed.

Of note, unresponsive patients may benefit from Targeted Temperature Management (TTM), which involves the maintenance of core body temperature at a target of 32 – 36 ℃ for 24 hours, or preferably normothermia at 36 °C to 37.5 °C with an emphasis on prevention of hyperthermia, in order to protect and optimize brain recovery post-arrest.[7]

Almost all cardiac arrest survivors will require a period of intensive care observation and management. If no immediate intervention is needed (e.g., reperfusion therapy), patients inside a hospital will need to be transitioned to an Intensive Care Unit (ICU) for further care.

Figure 20 – Post-Cardiac Arrest Care

What do you need to know?

  • Emergency Medicine, especially in critical care, emphasizes a systematic approach to the unwell patient.
  • The Primary Survey is designed to recognize and address life-threatening conditions effectively and timely.
  • The Primary Survey components are Airway (& and C-spine in trauma), Breathing, Circulation, Disability, and Exposure.
  • If an intervention is performed at any level of the survey, you must reassess the patient by commencing the Primary Survey again, starting with Airway.
  • Reassess and review your patient for changes frequently.
  • Many of the actions performed in the initial assessment of the critically ill patient may occur simultaneously when more team members are present in an Emergency Department. Do not let the chaos of the scene distract you from completing each step of the assessment.
  • The AHA has well-established guidelines for assessing and managing patients through the Primary Survey. Use the algorithms and the patient’s status as ‘stable’ or ‘unstable’ to guide the management of recognized pathologies, especially in Circulation.
  • The ED is home to a variety of adjuncts, including portable X-rays, ECG, and point-of-care ultrasound, which can provide the physician with rapid, readily accessible information to guide management.
  • Remember the SAMPLE mnemonic for a focused history in the critically ill patient.
  • An unresponsive patient should be immediately recognized, and Emergency Response Systems should be activated.
  • Performance of Basic and Advanced cardiac life support focuses on preserving blood circulation transiently to maintain the perfusion of organs, such as the brain, until the cause of the condition is reversed or managed.
  • The majority of cardiac arrest is caused due to coronary artery disease.
  • The two most important predictors of patient survival in cardiac arrest are high-quality CPR and early defibrillation (for a shockable rhythm)
  • An effective resuscitation in the ED often relies on the concerted efforts of multiple team members, led by a team leader who coordinates tasks in an organized, effective way to improve patient survival and outcomes.

Author

Picture of Mohammad Anzal Rehman

Mohammad Anzal Rehman

EM Residency Graduate from Zayed Military Hospital in Abu Dhabi, UAE. Founder/President of the Emirates Collaboration of Residents in Emergency Medicine (ECREM). Editor-in-Chief for the Emirates Society of Emergency Medicine (ESEM) Monthly Newsletter. I have a vested interest in sharing updated knowledge and developing teaching tools. As a healthcare professional, I continually strive to incorporate the newest clinical research into practice and am an active advocate for the use of Point of Care Ultrasonography (POCUS) in the ED.

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References

  1. Reynolds T. Basic Emergency Care: Approach to the Acutely Ill and Injured. World Health Organization; 2018.
  2. 2020 Advanced Cardiac Life Support (ACLS) Provider Manual. American Heart Association; 2021.
  3. Hashim A, Tahir MJ, Ullah I, Asghar MS, Siddiqi H, Yousaf Z. The utility of point of care ultrasonography (POCUS). Ann Med Surg (Lond). 2021;71:102982. Published 2021 Nov 2. doi:10.1016/j.amsu.2021.102982
  4. Cardiac Arrest Registry to Enhance Survival (CARES) 2022 Annual Report; 2022, https://mycares.net/
  5. Wyckoff MH, Singletary EM, Soar J, et al. 2021 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science With Treatment Recommendations: Summary From the Basic Life Support; Advanced Life Support; Neonatal Life Support; Education, Implementation, and Teams; First Aid Task Forces; and the COVID-19 Working Group. Resuscitation. 2021;169:229-311. doi:10.1016/j.resuscitation.2021.10.040
  6. Soar J, Böttiger BW, Carli P, et al. European Resuscitation Council Guidelines 2021: Adult advanced life support [published correction appears in Resuscitation. 2021 Oct;167:105-106]. Resuscitation. 2021;161:115-151. doi:10.1016/j.resuscitation.2021.02.010
  7. Lüsebrink E, Binzenhöfer L, Kellnar A, et al. Targeted Temperature Management in Postresuscitation Care After Incorporating Results of the TTM2 Trial. J Am Heart Assoc. 2022;11(21):e026539. doi:10.1161/JAHA.122.026539

Acknowledgements

  • Marina Margiotta – Illustrator
  • Paddy Kilian – Emergency Physician – Mediclinic City Hospital, Dubai, Director of Academic Affairs – Mohammed Bin Rashid University Of Medicine and Health Sciences
  • Rasha Buhumaid – Consultant Emergency Physician – Mediclinic Parkview Hospital, Dubai, Assistant Professor of Emergency Medicine – Mohammed Bin Rashid University Of Medicine and Health Sciences, President of the Emirates Society of Emergency Medicine (ESEM)
  • Amog Prakash – Medical Student – Mohammed Bin Rashid University Of Medicine and Health Sciences
  • Fatima Al Hammadi- Medical Student – Mohammed Bin Rashid University Of Medicine and Health Sciences

Reviewed By

Picture of Arif Alper Cevik, MD, FEMAT, FIFEM

Arif Alper Cevik, MD, FEMAT, FIFEM

Prof Cevik is an Emergency Medicine academician at United Arab Emirates University, interested in international emergency medicine, emergency medicine education, medical education, point of care ultrasound and trauma. He is the founder and director of the International Emergency Medicine Education Project – iem-student.org, chair of the International Federation for Emergency Medicine (IFEM) core curriculum and education committee and board member of the Asian Society for Emergency Medicine and Emirati Board of Emergency Medicine.