Cryptic Shock – Identifying the Unseen (PART 1)

Case Presentation

A 68-year-old man presented to the Emergency Department with complaints of breathing difficulty and fever for three days. The patient is a known diabetic and hypertensive.

After detailed history taking, clinical examination, and radiological workup, the patient was diagnosed with right-sided lobar pneumonia (Community-acquired) and immediately started on intravenous antibiotics. In addition, necessary cultures and blood samples were taken for evaluation.

At the time of presentation, his vitals were HR – 92/min, BP – 130/70mmHg, RR – 30/min, SpO2 – 90% with RA à 96% with 2L O2. He underwent bladder catheterization.

During the 1st hour in the ER, the patient had a very low urine output, which continued for the next few hours. Lactate levels were more than 4mmol/L.

Based on the symptoms, oliguria, and hyperlactatemia, the patient was diagnosed to have sepsis and was initiated on fluid resuscitation. After 2 hours, the patient remained oliguric still, and his BP declined to 120/70mmHg.

After 6 hours, the patient’s BP became 110/60mmHg (MAP – 77). He became anuric and developed altered sensorium. Since he did not meet the criteria of septic shock, he was continued on IV fluids and antibiotics.

After 12 hours, the BP became 80/40mmHg (MAP – 63mmHg) à developed Multiorgan Dysfunction Syndrome. He was then started on vasopressors and mechanical ventilation.

By day 3, the patient further deteriorated and went into cardiac arrest. ROSC was not achieved.

Case Analysis

The treatment initiated was based on protocols like Surviving Sepsis Guidelines and Septic Shock management. So how did the process fail in order to adequately resuscitate this patient? Could something have been done more differently?

The case you read above is a very common scenario. Approximately 30% of the people coming to the ER are hypertensive, and around 10% have diabetes mellitus. They form a huge population, among whom the incidence of any other disease increases their morbidity and early mortality.

Before we delve into the pathology in these patients, let us look at the basic definitions of shock/hypotension.

  • SBP < 90mmHg
  • MAP < 65 mmHg
  • Decrease in SBP > 40mmHg
  • Organ Dysfunction
  • Hyperlactatemia
  • Shock: A state of circulatory insufficiency that creates an imbalance between tissue oxygen supply (delivery) and demand (consumption), resulting in end-organ dysfunction.
  • Septic Shock: Adult patients can be identified using the clinical criteria of hypotension requiring the use of vasopressors to maintain MAP of 65mmHg or greater and having a serum lactate level greater than 2 mmol/L persisting after adequate fluids resuscitation.
  • Cryptic Shock: Presence of hyperlactatemia (or systemic hypoperfusion) in a case of sepsis with normotension.

Based on all the information given above;

  1. what do you think was wrong with our patient?
  2. What kind of shock did he have?
  3. Could we have managed him any other way?
  4. When should we have started inotropes?
  5. Did the fact that he was hypertensive and diabetic have to do with his early deterioration? If so, how?
  6. When did the patient-first develop signs of shock?
  7. What are the different signs and symptoms of shock, and how are they recognized in the ER?

Keep your answers ready… 

Part 2 of Cryptic Shock Series – Vascular Pathology and What is considered ‘Shock’ in Hypertensive patients

Part 3 of Cryptic Shock Series – Individualised BP management

Part 4 of Cryptic Shock Series – Latest Trends

References and Further Reading

  1. Ranzani OT, Monteiro MB, Ferreira EM, Santos SR, Machado FR, Noritomi DT; Grupo de Cuidados Críticos Amil. Reclassifying the spectrum of septic patients using lactate: severe sepsis, cryptic shock, vasoplegic shock and dysoxic shock. Rev Bras Ter Intensiva. 2013 Oct-Dec;25(4):270-8. doi: 10.5935/0103-507X.20130047.
  2. Singer M, Deutschman CS, Seymour CW, Shankar-Hari M, Annane D, Bauer M, Bellomo R, Bernard GR, Chiche JD, Coopersmith CM, Hotchkiss RS, Levy MM, Marshall JC, Martin GS, Opal SM, Rubenfeld GD, van der Poll T, Vincent JL, Angus DC. The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3). JAMA. 2016 Feb 23;315(8):801-10. doi: 10.1001/jama.2016.0287.
  3. Shankar-Hari M, Phillips GS, Levy ML, Seymour CW, Liu VX, Deutschman CS, Angus DC, Rubenfeld GD, Singer M; Sepsis Definitions Task Force. Developing a New Definition and Assessing New Clinical Criteria for Septic Shock: For the Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3). JAMA. 2016 Feb 23;315(8):775-87. doi: 10.1001/jama.2016.0289.
  4. Education Resources – Sepsis Trust
  5. The Research of Predicting Septic Shock – International Emergency Medicine Education Project (iem-student.org)
  6. Sepsis – International Emergency Medicine Education Project (iem-student.org)
  7. Empiric Antibiotics for Sepsis in the ED Infographics – International Emergency Medicine Education Project (iem-student.org)
  8. Sepsis – An Overview and Update – International Emergency Medicine Education Project (iem-student.org)
Cite this article as: Gayatri Lekshmi Madhavan, India, "Cryptic Shock – Identifying the Unseen (PART 1)," in International Emergency Medicine Education Project, October 4, 2021, https://iem-student.org/2021/10/04/cryptic-shock/, date accessed: December 4, 2021

Immediate Management of Paediatric Traumatic Brain Injury

Traumatic brain injury (TBI) has been noted as a leading cause of death and disability in infants, children, and adolescence (Araki, Yokota and Morita, 2017). In the UK alone, it’s approximated 1.4 million individuals attend the emergency department (ED) with head injury, and of those, 33%-50% are children under the age of 15; on top of this, a fifth of those patients admitted have features suggesting skull fracture or brain damage – that’s no small figure (NICE, 2014)! The particular importance of TBI in the paediatric population is that the treatment and management approach differs to adults; this is largely due to the anatomical and physiological differences in children. Furthermore, neurological evaluation in children proves more complex. All in all, children are complicated, and it is of great importance that we are aware of these differences when a paediatric patient arrives at the ED with TBI presentations.

Why is the paediatric population at risk for TBIs?

To delve slightly deeper into physiology and anatomy, there are several reasons children are at high risk of acquiring serious injury from TBIs. The paediatric brain has higher plasticity and deformity. As such, their less rigid skulls and open sutures allow for greater shock absorbance and response to mechanical stresses (Ghajar and Hariri, 1992). This ‘shaking’ of the brain inside the skull can stretch and tear at blood vessels in the brain parenchyma, resulting in cerebral haemorrhage.

Children also have a larger head-to-body size ratio, making the probability of head involvement in injury consequently higher (in comparison to adults); the head is also relatively heavier in a child, making it more vulnerable (especially in injury caused by sudden acceleration).

Young children have weaker neck muscles on top of having relatively heavier heads. Ligaments in the neck are relied on for craniocervical stability more so than the vertebrae. Hence, not only are TBIs more likely, but craniocervical junction lesions can also result from traumatic injury.

How does TBI in children come about?

The common causes of TBI in the paediatric population varies with age (Araki, Yokota and Morita, 2017). Some of these causes can be seen in the table below, which has been adopted from Araki, Yokota, and Morita (2017).

Table 1 Injury characteristics according to age and development

How can TBI in children present?

  • History: dangerous mechanism of injury (e.g. road traffic accidents or fall from a height greater than 1 meter)
  • Glasgow Coma Scale (GCS) less than 15 (at 2 hours after injury)
  • Visible bleeding, bruise, swelling, laceration
  • Signs of base-of-skull fracture:
    •  ‘Panda’ eyes – haemotympanum
    • Battle’s sign – cerebrospinal fluid leakage from ear or nose
  • Seizure (ask about history of epilepsy)
  • Focal neurological deficit
  • Vomiting
  • Loss of consciousness
  • Amnesia lasting more than 5 minutes
  • Abnormal drowsiness 

Note some children won’t have any of these signs, but if there is any suspicion of possible TBI, it should be investigated further.

Immediate management

There are various causes to paediatric TBI – also subdivided into primary and secondary TBI. Primary TBI includes skull fractures and intracranial injury. Secondary TBI can be caused by diffuse cerebral swelling. Primary and secondary TBI will be managed similarly in initial treatment (i.e. in the ED). The goal of baseline treatment is to:

  1. maintain blood flow to the brain
  2. prevent ischaemia (and possible secondary injury)
  3. maintain homeostasis 

Analgesia, Sedation, Seizure Prophylaxis

A level of anaesthesia needs to be achieved to allow for invasive procedures, such as airway management and intracranial pressure (ICP) control. Normally opioids and benzodiazepines are using in combination for analgesia and sedation in children. Instances where a child presents with a severe TBI (defined as a ‘brain injury resulting in a loss of consciousness of greater than 6 hours and a Glasgow Coma Scale of 3 to 8’), a neuromuscular block is used to improve mechanical ventilation, stop shivering, and reduce metabolic demand.

Anticonvulsants have been used in children, in particular infants, as they have a lower seizure threshold. Risk factors for early onset of seizures in infants under the age of 2 include hypotension, child abuse, and a GCS of ≤ 8; note, all of which may occur as a result of, or preceding, a TBI! For severe paediatric TBI cases, immediate prophylactic administration of anticonvulsants has been recommended.

Maintaining Cerebral Perfusion

The gold standard to measure ICP is an external ventricular drain (EVD); which can be used not only to measure ICP but can also be opened to drain additional CSF to reduce ICP. An intraparenchymal intracranial pressure sensor is an immediate invasive method used to detect early increased ICP in children with TBI. Monitoring of both ICP and cerebral perfusion pressure (CPP) is considered standard practice in TBI management in both paediatric and adult populations, as it is associated with better outcomes.

CPP is the pressure gradient which allows for cerebral blood flow. If this pressure is not maintained, the brain will lose adequate blood flow (Ness-Cochinwala and Dwarakanathan, 2019). Elevated CPP can accelerate oedema and increase chances of secondary intracranial hypertension.

Cerebral Perfusion Pressure (CPP) = Mean Arterial Pressure (MAP) – Intracranial Pressure (ICP)

A CPP of around 40-60 mmHg (40-50mmHg in 0-5 year-olds and 50-60mmHg in 6-17 year-olds) is considered ideal. Achieving an adequate CPP can be done by increasing MAP or reducing ICP (using the above equation). Hence it is necessary to have a good understanding of what good target values for MAP and ICP are.

A good target value for MAP is the upper end of ‘normal’ for the child’s age. Reaching this can be done by using fluids (if fluid deficient) or by use of inotropes. The recommended ICP target is < 20mmHg (normal is between 5-15 mmHg and raised ICP is regarded as values over 20mmHg).

When thinking about ICP, it’s useful to remember a mass in the brain; a mass being possible haemorrhage or any other space-occupying lesion. In TBI, oedema is most prominent at around 24-72 hours post-injury. As a result of increased mass, the initial consequence is a displacement of cerebrospinal fluid (CSF) into the spinal cord. Following this, venous blood in the cranium will also be displaced.

If ICP is further elevated, herniation can result – which is serious and often fatal! Signs of uncal herniation can present as unilateral fixed and dilated pupil. Signs of raised ICP can include pupillary dilatation and series of responses known as the ‘Cushing’s Triad’: irregular, decreased respiration (due to impaired brainstem function), bradycardia, and systolic hypertension (widened pulse pressure). Cushing’s triad results from the response of the body to overcome increased ICP by increasing arterial pressure.

Using the Monroe-Kellie Doctrine as a guide, we can predict how to reduce ICP. One management is head positioning. Head-of-bed should be elevated to 30˚, with the head in mid-line position, to encourage cerebral venous drainage. The EVD can also be used to drain CSF.

Commonly, intravenous mannitol and hypertonic saline are used to manage intracranial hypertension in TBI. Mannitol is traditionally used at a dosage of 20% at 0.25-1.0 g/kg – this is repeatedly administered. The plasma osmolality of the patient needs to be kept a close eye on; it should be ≤ 310 mOsm/L. 3% NaCl can be used to raise sodium levels to 140-150 mEg/L – this is slightly higher than normal sodium levels as a higher blood osmolarity will pull water out of neurons and brain cells osmotically and reduce cerebral oedema (Kochanek et al., 2019). Mannitol works in the same manner, however, use with caution as mannitol, being an osmotic diuretic, can cause blood pressure drops and compromise CPP! In last-resort emergency cases, where ICP need to be immediately reduced, a decompressive craniotomy can be performed.

Intravascular Volume Status

Measuring the patient’s central venous pressure (CVP) is a good indicator of the child’s volume status; 4-10 mmHg have been used as target thresholds. Alternatively, you can also monitor urine output (>1mL/kg/hr), blood urea nitrogen, and serum creatinine. Low volume status should be corrected with a fluid bolus. If the patient’s volume status is normal or high, but they remain hypotensive, vasopressors may improve blood pressure. At all costs, hypotension must be avoided, as if can lead to reduced cerebral perfusion and lead to brain ischaemia; on the other end, hypertension can cause severe cerebral oedema and should also be kept an eye on.

Other considerations​ - There have been reports of pituitary dysfunction in 25% of paediatric TBIs (during the acute phase). Do consider this if the patient had refractory hypotension – keep ACTH deficiency in mind!

Ischaemia

Prevent hypoxia at all costs! Hypoxia goes hand-in-hand with cerebral vasodilation – and as we already know, this increases the pressure in the cranium. Additionally, with hypoxia, there will be ischaemia. A minimum haemoglobin target of 7.0 g/dl is advised in a severe paediatric TBI case.

Other considerations​ - Whilst we are on the blood topic, also take care to correct and control any coagulopathies.

Ventilation

At a Paediatric Glasgow Coma Scale (PGCS) of less than 8, airways must be secured with a tracheal tube and mechanical ventilation commenced. SpO2 should be maintained at greater than 92%.

Of course, hypercapnia (CO2 > 6 kPa) and hypocapnia (CO2 < 4 kPa) are both not ideal, and we should maintain paCO2 at 4.5 – 5.3 kPa. However, some sources have suggested a quick fix to reduce ICP is to acutely hyperventilate the patient (as low CO2 results in cerebral vasoconstriction) – it’s suggested that paCO2 can safely go as low as 2.67 kPa before ischaemia kicks in! Mild hyperventilation is recommended (3.9 – 4.6 kPa)(Araki, Yokota and Morita, 2017).

Decreasing Metabolic Demand of the Brain

Body Temperature

What we want is to prevent hyperthermia, as it increases cerebral metabolic demands. Normothermia (36.5˚C – 37.5˚C) can be maintained by use of cooling blankets or antipyretics. There has been debate on whether therapeutic hypothermia has shown any benefit. Some studies have shown that moderate hypothermia for up to 48 hours, followed by slow rewarming, has prevented rebound intracranial hypertension as well as decreased ICP, however, there have not been any confirmed functional outcomes or decreased mortality rates benefits of this method (Adelson et al., 2013; Hutchinson et al., 2008).

Glycaemic control

Persistent hyperglycaemia (glucose > 10 mmol/L) should be treated. Hypoglycaemia (< 4 mmol/L) is much more dangerous. Persistent hyperglycaemia can be managed by reducing the dextrose concentration in IVF (which is usually administered in the first 48 hours of ICU care), or by starting an insulin drip.

A comment on imaging methods

In the UK, the initial investigation choice for detecting acute brain injuries is a CT head scan. A CT scan should be done within an hour of suspected head injury.
If there are no indications for a CT head scan (i.e. the signs/symptoms listed previously), a CT head scan should be performed within 8 hours of injury (NICE, 2014).

MRI scans are not usually done as the initial investigation, however, they have shown to provide information on the patient’s prognosis.

A final and most important note:

Don’t ever forget Safeguarding in children. Unfortunately, child maltreatment is common and can present anywhere. Have a look at the NICE guidelines below for more on how to identify child maltreatment.

Further reading

References

  • Adelson PD, Wisniewski SR, Beca J, Brown SD, Bell M, Muizelaar JP, Okada P, Beers SR, Balasubramani GK, Hirtz D; Paediatric Traumatic Brain Injury Consortium. Comparison of hypothermia and normothermia after severe traumatic brain injury in children (Cool Kids): a phase 3, randomised controlled trial. Lancet Neurol. 2013 Jun;12(6):546-53. doi: 10.1016/S1474-4422(13)70077-2.
  • Araki T, Yokota H, Morita A. Pediatric Traumatic Brain Injury: Characteristic Features, Diagnosis, and Management. Neurol Med Chir (Tokyo). 2017;57(2):82-93. doi:10.2176/nmc.ra.2016-0191
  • Finnegan R, Kehoe J, McMahon O, Donoghue V, Crimmins D, Caird J, Murphy J. Primary External Ventricular Drains in the Management of Open Myelomeningocele Repairs in the Neonatal Setting in Ireland. Ir Med J. 2019 May 9;112(5):930.
  • Ghajar J, Hariri RJ. Management of pediatric head injury. Pediatr Clin North Am. 1992;39(5):1093-1125. doi:10.1016/s0031-3955(16)38409-7
  • Hutchison JS, Ward RE, Lacroix J, Hébert PC, Barnes MA, Bohn DJ, Dirks PB, Doucette S, Fergusson D, Gottesman R, Joffe AR, Kirpalani HM, Meyer PG, Morris KP, Moher D, Singh RN, Skippen PW; Hypothermia Pediatric Head Injury Trial Investigators and the Canadian Critical Care Trials Group. Hypothermia therapy after traumatic brain injury in children. N Engl J Med. 2008 Jun 5;358(23):2447-56. doi: 10.1056/NEJMoa0706930.
  • Kochanek PM, Tasker RC, Bell MJ, Adelson PD, Carney N, Vavilala MS, Selden NR, Bratton SL, Grant GA, Kissoon N, Reuter-Rice KE, Wainwright MS. Management of Pediatric Severe Traumatic Brain Injury: 2019 Consensus and Guidelines-Based Algorithm for First and Second Tier Therapies. Pediatr Crit Care Med. 2019 Mar;20(3):269-279. doi: 10.1097/PCC.0000000000001737.
  • National Institute for Health and Care Excellence. Head injury: assessment and early management. 2014. Available at: https://www.nice.org.uk/guidance/cg176
  • Ness-Cochinwala M., Dwarakanathan D. Protecting #1 – Neuroprotective Strategies For Traumatic Brain Injury. Paediatric FOAMed. 2019. 
Cite this article as: Nadine Schottler, Great Britain, "Immediate Management of Paediatric Traumatic Brain Injury," in International Emergency Medicine Education Project, November 16, 2020, https://iem-student.org/2020/11/16/paediatric-traumatic-brain-injury/, date accessed: December 4, 2021

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Triads in Medicine – Rapid Review for Medical Students

triads in medicine

One of the most convenient ways of learning and remembering the main components of disease and identifying a medical condition on an exam are Triads, and medical students/interns/residents swear by them.

Be it a question during rounds, a multiple-choice exam question to be solved, or even in medical practice, the famous triads help physicians recall important characteristics and clinical features of a disease or treatment in an instant.

Since exam season is here, this could serve as a rapid review to recall the most common medical conditions.

While there are a vast number of triads/pentads available online, I have listed the most important (high-yy) ones that every student would be asked about at least once in the duration of their course.

1) Lethal Triad also known as The Trauma Triad of Death
Hypothermia + Coagulopathy + Metabolic Acidosis

2) Beck’s Triad of Cardiac Tamponade
Muffled heart sounds + Distended neck veins + Hypotension

3) Virchow’s Triad – Venous Thrombosis
Hypercoagulability + stasis + endothelial damage

4) Charcot’s Triad – Ascending Cholangitis
Fever with rigors + Right upper quadrant pain + Jaundice

5) Cushing’s Triad – Raised Intracranial Pressure
Bradycardia + Irregular respiration + Hypertension

6) Triad of Ruptured Abdominal Aortic Aneurysm
Severe Abdominal/Back Pain + Hypotension + Pulsatile Abdominal mass

7) Reactive Arthritis
Can’t See (Conjunctivitis) + Can’t Pee (Urethritis) + Can’t Climb a Tree (Arthritis)

8) Triad of Opioid Overdose
Pinpoint pupils + Respiratory Depression + CNS Depression

9) Hakims Triad – Normal Pressure Hydrocephalus
Gait Disturbance + Dementia + Urinary Incontinence

10) Horner’s Syndrome Triad
Ptosis + Miosis + Anydrosis

11) Mackler’s Triad – Oesophageal Perforation (Boerhaave Syndrome)
Vomiting + Lower Thoracic Pain + Subcutaneous Emphysema

12) Pheochromocytoma
Palpitations + Headache + Perspiration (Diaphoresis)

13) Leriche Syndrome
Buttock claudication + Impotence + Symmetrical Atrophy of bilateral lower extremities

14) Rigler’s Triad – Gallstone ileus
Gallstones + Pneumobilia + Small bowel obstruction

15) Whipple’s Triad – Insulinoma
Hypoglycemic attack + Low glucose + Resolving of the attack on glucose administration

16) Meniere’s Disease
Tinnitus + Vertigo + Hearing loss

17) Wernicke’s Encephalopathy- Thiamine Deficiency
Confusion + Ophthalmoplegia + Ataxia

18) Unhappy Triad – Knee Injury
Injury to Anterior Cruciate Ligament + Medial collateral ligament + Medial or Lateral Meniscus

19) Henoch Schonlein Purpura
Purpura + Abdominal pain + Joint pain

20) Meigs Syndrome
Benign ovarian tumor + pleural effusion + ascites

21) Felty’s Syndrome
Rheumatoid Arthritis + Splenomegaly + Neutropenia

22) Cauda Equina Syndrome
Low back pain + Bowel/Bladder Dysfunction + Saddle Anesthesia

23) Meningitis
Fever + Headache + Neck Stiffness

24) Wolf Parkinson White Syndrome
Delta Waves + Short PR Interval + Wide QRS Complex

25) Neurogenic Shock
Bradycardia + Hypotension + Hypothermia

Further Reading

Cite this article as: Sumaiya Hafiz, UAE, "Triads in Medicine – Rapid Review for Medical Students," in International Emergency Medicine Education Project, June 12, 2020, https://iem-student.org/2020/06/12/triads-in-medicine/, date accessed: December 4, 2021

The list of useful scores and rules for ED

useful rules for ed

SAFE-BBOP! – A mnemonic for anaphylaxis management in the emergency department

anaphylaxis

While recently experiencing eight incredible weeks of Emergency Medicine rotations, I was reviewing my approach to anaphylaxis. Coincidentally, there was a real case a few days later, and I found the following mnemonic useful. If you’re having trouble remembering the different components of management for adult cases of anaphylaxis in the emergency department, think of SAFE-BBOP

This is not the exact order in which anaphylaxis should be approached, but it may facilitate memorizing commonly-used treatment modalities while learning and reviewing the general approach. The ABC algorithm should be applied first (see: https://iem-student.org/abc-approach-critically-ill/). Following the diagnosis of anaphylaxis, epinephrine should be administered promptly, as delayed administration has been associated with increased mortality (1-4).

SAFE BBOP

S - Steroids

Prednisone 50mg PO or methylprednisolone 125mg IV. Glucocorticoids are theoretically used to prevent a possible biphasic reaction; however, there is limited evidence for this.

A - Antihistamines (H1 and H2)

Ranitidine 150mg PO/50mg IV, Diphenhydramine 25-50mg PO/IV. Their use is based on studies of urticaria and should only be used as an adjunct therapy.

F - Fluids

Normal saline or Ringer’s lactate 1-2 L IV.

B - Beta-blocked

If a patient is on a beta-blocker and is refractory to the administered epinephrine, consider glucagon 1-5mg slow IV bolus over 5mins, followed by an infusion at 5-15mcg/min, titrated to effect.

B - Bronchodilators

For persistent bronchospasm despite epinephrine, an inhaled bronchodilator can be considered, such as salbutamol 2.5-5mg nebulized or 4-8 puffs by MDI with spacer q20 mins x 3. This is based on studies of acute asthma exacerbation and should only be used as an adjunct therapy.

O - Oxygen

Every patient, who is critically ill, requires supportive oxygen treatment.

P - Positioning

Recumbent position with lower extremity elevation (consider left lateral decubitus position for pregnant patients to prevent inferior vena cava compression).

As for disposition considerations, the SAFE system below was introduced by Lieberman et al. (2007) to recognize the four basic actions to address with patients prior to discharge from the emergency department (5).

  • Seek support
  • Allergen identification and avoidance
  • Follow-up for specialty care
  • Epinephrine for emergencies

For a detailed review of anaphylaxis definitions, signs and symptoms, refer to this great Life in the Fast Lane article: https://litfl.com/anaphylaxis/

References

  1. Prince, B.T., Mikhail, I., & Stukus, D.R. (2018). Underuse of epinephrine for the treatment of anaphylaxis: missed opportunities. J Asthma Allergy, 11, 143-151.
  2. Sheikh, A., Shehata, Y., Brown, S.G., & Simons, F.E. (2009). Adrenaline for the treatment of anaphylaxis: Cochrane systematic review. Allergy, 64(2), 204.
  3. Simons, F.E. (2008). Emergency treatment of anaphylaxis. BMJ, 336(7654), 1141.
  4. McLean-Tooke, A.P., Bethune, C.A., Fay, A.C., & Spickett, G.P. (2003). Adrenaline in the treatment of anaphylaxis: what is the evidence? BMJ, 327, 1332.
  5. Lieberman, P.,Decker, W., Camargo, C.A. Jr., Oconnor, R., Oppenheimer, J., & Simons, F.E. (2007). SAFE: a multidisciplinary approach to anaphylaxis education in the emergency department. Ann Allergy Asthma Immunol 98(6), 519-23. 
 

Further Reading

Cite this article as: Nada Radulovic, Canada, "SAFE-BBOP! – A mnemonic for anaphylaxis management in the emergency department," in International Emergency Medicine Education Project, December 11, 2019, https://iem-student.org/2019/12/11/a-mnemonic-for-anaphylaxis-management/, date accessed: December 4, 2021

A 19-year-old female presents with sharp right flank pain and shortness of breath

by Stacey Chamberlain

A 19-year-old female presents with sharp right flank pain and shortness of breath that started suddenly the day prior to arrival. The pain is worse with deep inspiration but not related to exertion and not relieved with ibuprofen. She denies anterior chest pain, cough, and fever. She denies leg pain or swelling and recent travel, immobilization, trauma, or surgery. She has no anterior abdominal pain, no dysuria or hematuria and no personal or family history of gallstones, kidney stones, or blood clots. She’s never had this pain before, has no significant past medical history and her only medication is birth control pills. On exam, her vital signs are within normal range, she has normal cardiac and pulmonary exams, no costovertebral angle tenderness, no chest wall or abdominal tenderness and no leg swelling.

Do you need to do any studies to evaluate this patient for a pulmonary embolism?

Pulmonary Embolism Rule-Out Criteria (PERC)

  • Age ≥ 50
  • Heart rate ≥ 100
  • O2 sat on room air < 95%
  • Prior history of venous thromboembolism
  • Trauma or surgery within 4 weeks
  • Hemoptysis
  • Exogenous estrogen
  • Unilateral leg swelling

The PERC CDR was originally derived and validated in 2004 and with a subsequent multi-study center validation in 2008. In the larger validation study, the rule was only to be applied in those patients with a pre-test probability of < 15%, therefore incorporating clinical gestalt prior to using the rule. PERC is a one-way rule, as mentioned above, which tried to identify patients who are so low-risk for pulmonary embolism (PE) as to not require any testing. It does not imply that testing should be done for patients who do not meet criteria, and it is not meant for risk stratification, as opposed to the Wells’ and Geneva scores.

Case Discussion

In order to apply the PERC CDR to the case study patient, the ED physician pre-supposes a pre-test probability of < 15%. If the ED physician has a higher pre-test probability than that, he/she should not use the PERC CDR. If the ED physician, in this case, did indeed have a pre-test probability of < 15%, the case study patient would fail the rule-out due to her use of oral contraceptives. In that case, the ED physician would need to determine if he/she would do further testing which could include a D-dimer, CT chest with contrast, ventilation/perfusion scan, or lower extremity Doppler studies to evaluate for deep vein thromboses (DVTs). The PERC CDR gives no guidance in this case.

Cite this article as: iEM Education Project Team, "A 19-year-old female presents with sharp right flank pain and shortness of breath," in International Emergency Medicine Education Project, June 17, 2019, https://iem-student.org/2019/06/17/a-19-year-old-female-presents-with-sharp-right-flank-pain-and-shortness-of-breath/, date accessed: December 4, 2021

A 28-year-old man presents to the ED with left ankle pain

by Stacey Chamberlain

A 28-year-old man presents to the ED with left ankle pain after twisting his ankle playing basketball. He is able to bear weight and notes pain and swelling to the lateral aspect of the ankle (he points to just below the lateral malleolus). He denies weakness, numbness, or tingling and has no other injuries. On exam, he is neurovascularly intact. Edema and tenderness are noted slightly anterior and inferior to the lateral malleolus. There is no point tenderness to the distal posterior malleoli bilaterally.

Should you get an X-ray to rule out fracture?

Ottawa Ankle Rule

Pain in the malleolar zone and any one of the following:

  • Bone tenderness along the distal 6 cm of the posterior edge or tip of the tibia (medial malleolus), OR
  • Bone tenderness along the distal 6 cm of the posterior edge or tip of the fibula (lateral malleolus), OR
  • An inability to bear weight both immediately after the trauma and in the ED for four steps.

Ottawa Foot Rule

Pain in the midfoot zone and any one of the following:

  • Bone tenderness at the base of the fifth metatarsal, OR
  • Bone tenderness at the navicular bone, OR
  • An inability to bear weight both immediately after the trauma and in the ED for four steps.

Case Discussion

In the above case, using either CDR, an X-ray is unnecessary.

Cite this article as: iEM Education Project Team, "A 28-year-old man presents to the ED with left ankle pain," in International Emergency Medicine Education Project, June 10, 2019, https://iem-student.org/2019/06/10/a-28-year-old-man-presents-to-the-ed-with-left-ankle-pain/, date accessed: December 4, 2021

A 36-year-old woman slipped on ice. CT or Not CT?

by Stacey Chamberlain

A 36-year-old woman slipped on ice and fell and hit her head. She reports loss of consciousness for a minute after the event, witnessed by a bystander. She denies headache. She denies weakness, numbness or tingling in her extremities and no changes in vision or speech. She has not vomited. She remembers the event except for the transient loss of consciousness. She doesn’t use any blood thinners. On physical exam, she has a GCS of 15, no palpable skull fracture and no signs of a basilar skull fracture.

Should you get a CT head for this patient to rule out a clinically significant brain injury?

Canadian CT Head Rule

High-Risk Criteria (rules out the need for neurosurgical intervention)

Medium Risk Criteria (rules out clinically important brain injury)

  • GCS < 15 at two hours post-injury
  • Suspected open or depressed skull fracture
  • Any sign of basilar skull fracture (hemotympanum, Raccoon eyes, Battle’s sign, CSF oto or rhinorrhea)
  • Retrograde amnesia to event  ≥ 30 minutes
  • Dangerous mechanism (pedestrian struck by motor vehicle, ejection from the motor vehicle, fall from > 3 feet or > 5 stairs)

The Canadian CT Head Rule (CCHR) only applies to patients with an initial GCS of 13-15, witnessed loss of consciousness (LOC), amnesia to the head injury event, or confusion. The study was only for patients > 16 years of age. Patients were excluded from the study if they had “minor head injuries” that didn’t even meet these criteria. Patients were also excluded if they had signs or symptoms of moderate or severe head injury including GCS < 13, post-traumatic seizure, focal neurologic deficits, or coagulopathy. Other studies have looked at different CDRs for traumatic brain injury including the New Orleans Criteria (NOC). However, CCHR has been found to have superior sensitivity and specificity.

Case Discussion

By applying this rule to the above case, the patient should be considered for imaging due to the mechanism. A fall from standing for an adult patient would constitute a fall from > 3 feet; therefore, although the patient would not likely be high risk and need neurosurgical intervention, the patient might have a positive finding on CT that in many practice settings would warrant an observation admission.

Cite this article as: iEM Education Project Team, "A 36-year-old woman slipped on ice. CT or Not CT?," in International Emergency Medicine Education Project, June 7, 2019, https://iem-student.org/2019/06/07/a-36-year-old-woman-slipped-on-ice/, date accessed: December 4, 2021

A 24-year-old woman presents with headache

by Stacey Chamberlain

A 24-year-old woman presents with headache that began three hours prior to arrival to the ED. The patient was at rest when the headache began. The headache was not described as “thunderclap,” but it did reach maximum severity within the first 30 minutes. The headache is generalized and rated 10/10. She denies head trauma, weakness, numbness, and tingling in her extremities. She denies visual changes, changes in speech and neck pain. She has not taken anything for the headache. She does not have a family history of cerebral aneurysms or polycystic kidney disease. On physical exam, she has a normal neurologic exam and normal neck flexion.

Should you do a head CT and/or a lumbar puncture to evaluate for a sub-arachnoid hemorrhage in this patient?

Ottawa SAH Rule

Investigate if ≥1 high-risk variables present

  • Age ≥ 40
  • Neck pain or stiffness
  • Witnessed loss of consciousness
  • Onset during exertion
  • Thunderclap headache (instantly peaking pain)
  • Limited neck flexion on exam

A CDR to determine risk for sub-arachnoid hemorrhage (SAH) was derived and has been externally validated in a single study. The CDR’s purpose was to identify those at high risk for SAH and included those with acute non-traumatic headaches that reached maximal intensity within one hour and who had normal neurologic exams. Of note, the rule has many inclusion and exclusion criteria that the ED physician must be familiar with and was only derived for patients 16 years or older. The study authors note that the CDR is to identify patients with SAH; it is not an acute headache rule. In the validation study, of over 5,000 ED visits with acute headache, only 9% of those met inclusion criteria. Also, clinical gestalt again plays a role as the authors suggest not to apply the CDR to those who are ultra-high risk with a pre-test probability for SAH of > 50%.

The Ottawa SAH Rule was 100% sensitive but did not lead to reduction of testing vs. current practice. The authors state that the value of the Ottawa SAH Rule would be to standardize physician practice in order to avoid the relatively high rate of missed sub-arachnoid hemorrhages.

Case Discussion

By applying the Ottawa SAH Rule, this patient is low risk and does not require further investigation for a SAH.

Cite this article as: iEM Education Project Team, "A 24-year-old woman presents with headache," in International Emergency Medicine Education Project, May 29, 2019, https://iem-student.org/2019/05/29/a-24-year-old-woman-presents-with-headache/, date accessed: December 4, 2021

Mnemonic for Right Lower Quadrant Pain

Open fracture! Antibiotic choice.

ERic Motorcycle accident

A 20-year-old male presents to your ED with a 5 cm wound after he fell off his motorbike. On physical exam, the wound overlays a fractured left tibia but does not show extensive soft tissue damage nor any signs of periosteal stripping or vascular injury. 

Which antibiotic should you give to this patient?

To learn more about it, read chapters below.

Read "Scores" Chapter
Read "Lower Extremity Injuries" Chapter

Quick Read

Gustilo-Anderson Classification

Gustilo-Anderson classification is used for fractures with open wounds and antibiotic coverage.

Gustilo-Anderson Classification

TypeDefinition
Type IOpen fracture, clean wound, wound <1cm in length
Type IIOpen fracture, wound >1cm in length without extensive soft tissue damage, flaps, avulsions
Type IIIOpen fracture with extensive soft tissue laceration, damage, or loss or an open segmental fracture. This type also includes open fractures caused by farm injuries, fractures requiring vascular repair, or fractures that have been open for 8 hours prior to treatment.
Type III AType III fracture with adequate periosteal coverage of the fractured bone despite extensive soft tissue laceration or damage
Type III BType III fracture with extensive soft tissue loss and periosteal stripping and bone damage. Usually associated with massive contamination. It will often need further soft tissue coverage procedure (i.e. free or rotational flap).
Type III CType III fracture associated with arterial injury requiring repair, irrespective of degree of soft tissue injury

According to the above classification, each class should receive the following antibiotics:

  • Type I: 1st generation cephalosporin
  • Type II: 1st generation Cephalosporin +/- Gentamycin
  • Type III: 1st generation Cephalosporin + Gentamycin +/- Penicillin

To learn more about it, read chapters below.

Read "Scores" Chapter
Read "Lower Extremity Injuries" Chapter

Shock Index

A 57-year-old male presented to the ED with severe abdominal pain for 1 day. No allergies or significant past medical history. His vitals are: Temp 37.6 Celsius, BP 100/55, HR 110/min, RR 20/min and O2 Saturation is 99% on room air. 

What level of care does this patient require?

To learn more about it, read chapters below.

Read "Shock" Chapter

Read "Scores" Chapter

Quick Read

Shock Index

SHOCK INDEX (SI) = Heart Rate / Systolic Blood Pressure

Application

SI can be used to identify patients needing a higher level of care despite vital signs that may not appear strikingly abnormal. This index is a sensitive indicator of left ventricular dysfunction and can become elevated following a reduction in left ventricular stroke work.

Interpretation

The answer to the above clinical scenario: By applying the above equation, (110/100 = 1.1), this patient has a high shock index and requires a high level of care.

To learn more about it, read chapters below.

Read "Shock" Chapter

Read "Scores" Chapter