Category: Decision Making

Question Of The Day #47

question of the day
~ Joseph Ciano, USA ~ Leave a comment

Which of the following is the most appropriate next step in management for this patient’s condition?

  • A) 1000mL bolus of 0.9% NaCl
  • B) 25g of IV dextrose
  • C) 1mg of IV naloxone
  • D) 100mg of IV thiamine

This patient presents to the Emergency Department with altered mental status.  This presenting symptom can be due to a large variety of etiologies, including hypoglycemia, sepsis, toxic ingestions, electrolyte abnormalities, stroke, and more.  The management and evaluation of a patient with altered mental status depends on the primary assessment of the patient (“ABCs”, or Airway, Breathing, Circulation) to identify any acute life-threatening conditions that need to be managed emergently, the history, and the physical examination.  One mnemonic that may help in remembering the many causes of altered mental status is “AEIOUTIPS”.  The table below outlines this mnemonic.

ALTERED MENTAL STATUS

The initial approach to all Emergency Department patients, especially those with abnormal vital signs, should include a primary survey (“ABCs”, or Airway, Breathing, Circulation).  This patient is breathing independently but at a significantly reduced rate and is hypoxic.  Hypoxia should prompt the administration of supplemental oxygen to the patient and reassessment of the SpO2.  The patient’s reduced respiratory rate, lethargy, and bilateral miosis (constricted pupils) should strongly hint at the possibility of opioid overdose.  Although the patient is lethargic and hypoxic, establishing a definitive airway (endotracheal intubation) should be avoided until after the antidote to opioid overdose is administered.  Naloxone is a mu-opioid receptor antagonist and functions as the antidote to opioid overdose.

 

Administration of 1000mL of 0.9% NaCl (Choice A) is unlikely to fix the patient’s clinical condition.  The patient needs naloxone to improve respiratory status.  25g of IV dextrose (Choice B) would be helpful if this patient’s altered mental status was from hypoglycemia.  A normal glucose level is provided in the question stem.  100mg of IV thiamine (Choice D) may be helpful in the case of Wernicke-Korsakoff Syndrome, a state of thiamine deficiency often associated with malnutrition and alcohol abuse.  Wernicke-Korsakoff Syndrome presents with vision disturbances, ataxia, and confusion.  Typically, this syndrome does not present with severe lethargy or depressed mental status as is seen in this patient.

The best next step in management is 1mg of IV naloxone (Choice C).  If given appropriately, naloxone can prevent the need for intubation.  Naloxone has a very short onset to action (~1min).  If suspicion for opioid overdose is high and there is an inadequate respiratory response after a single naloxone dose, repeat doses of naloxone are appropriate.  Naloxone can be administered in repeat boluses every 3-minutes to a total dose of 10mg IV.  Patients who respond appropriately to naloxone should be observed for recurrent respiratory depression as naloxone is cleared.  Need for repeat doses of naloxone indicates the need for a continuous naloxone infusion and hospital admission.  The typical infusion dose is 2/3 the “wake-up” dose given over 1 hour as a continuous infusion.  For example, if the patient responded to 1mg IV initially, the continuous infusion dose would be 0.6mg/hour of IV naloxone.

Correct Answer: C

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Question Of The Day #46

question of the day
~ Joseph Ciano, USA ~ Leave a comment

Which of the following is the most appropriate next step in management for this patient’s condition?

  • A) 1000mL of IV 0.9% NaCl
  • B) Noncontrast CT scan of head
  • C) 25g of IV dextrose
  • D) 150mL of 3% NaCl

This patient presents to the Emergency Department with altered mental status.  This presenting symptom can be due to a large variety of etiologies, including hypoglycemia, sepsis, toxic ingestions, electrolyte abnormalities, stroke, and more.  The management and evaluation of a patient with altered mental status depends on the primary assessment of the patient (“ABCs”, or Airway, Breathing, Circulation) to identify any acute life-threatening conditions that need to be managed emergently, the history, and the physical examination.  One mnemonic that may help in remembering the many causes of altered mental status is “AEIOUTIPS”.  The table below outlines this mnemonic.

ALTERED MENTAL STATUS

The serum chemistry results provided show elevated BUN and Creatinine with a BUN/Cr ratio of 21.3.  A BUN/Cr ratio greater than 20 indicates decreased perfusion to the kidneys, also known as pre-renal azotemia, which can indicate dehydration, hypovolemia, or shock.  The serum chemistry also shows a severely low sodium level.  Hyponatremia can present with a variety of symptoms, including weakness, fatigue, myalgias, nausea, vomiting, headaches, altered mental status, focal neurologic deficits, seizures, or coma.  Hyponatremia can be acute or chronic, asymptomatic or symptomatic, and mild or severe.  Sodium levels below 120 mEq/L are severely low.  Neurologic symptoms, such as seizures, altered mental status, and focal neurologic deficits, are also considered severe.  Treatment should be based on patient symptoms, rather than the sodium level, as it can be difficult to assess how acute or chronic the hyponatremia state is on initial evaluation.  The presence of any severe neurologic symptoms as is seen in this scenario should prompt administration of hypertonic saline (3% NaCl).  This allows for rapid correction of serum sodium levels, which should in turn relieve the neurologic symptoms.  A 100-150mL IV bolus of 3% NaCl can be given a second time if symptoms continue after 5-10 minutes.  

Typically, hyponatremia should be corrected slowly to avoid central pontine myelinolysis.  Increases in sodium greater than 8mEq/L per 24hours should be avoided for this reason.  However, in the case of neurologic symptoms, rapid correction of sodium is opted for to prevent further damage.

Administration of “normal saline”, or 1000mL of IV 0.9% NaCl (Choice A), can increase the sodium level.  However, normal saline is not concentrated enough to rapidly increase the serum sodium to terminate neurologic symptoms.  A noncontrast CT scan of the head (Choice B) is a reasonable investigation for this altered patient, but hypertonic saline should be administered first if hyponatremia is known.  Administration of 25mg IV dextrose (Choice C), also known as “D50”, would be helpful in a patient with hypoglycemia and altered mental status. However, this patient is not hypoglycemic.

Administration of hypertonic saline (Choice D) is the best next step in this patient with severe hyponatremia and neurologic symptoms.

Correct Answer: D

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Question Of The Day #45

question of the day
~ Joseph Ciano, USA ~ Leave a comment

Which of the following is the most appropriate next step in management for this patient’s condition?

  • A) Administer IM haloperidol
  • B) Endotracheal intubation
  • C) Roll patient to lateral decubitus position and suction the airway
  • D) Obtain a 12-lead EKG

This patient presents to the Emergency Department with altered mental status.  This presenting symptom can be due to a large variety of etiologies, including hypoglycemia, sepsis, toxic ingestions, electrolyte abnormalities, stroke, and more.  The management and evaluation of a patient with altered mental status depends on the primary assessment of the patient (“ABCs”, or Airway, Breathing, Circulation) to identify any acute life-threatening conditions that need to be managed emergently, the history, and the physical examination.  One mnemonic that may help in remembering the many causes of altered mental status is “AEIOUTIPS”.  The table below outlines this mnemonic.

ALTERED MENTAL STATUS

This patient’s altered mental status is likely due to a post-ictal state after a first-time seizure.  A seizure occurs when the brain is in a state of neuronal hyperactivity.  First time seizures can be caused by a variety of factors, such as hypoxia, hyperthermia, hypoglycemia, traumatic brain injury, brain tumors, meningitis, encephalitis, hyponatremia, or alcohol withdrawal.  It can sometimes be difficult to differentiate a seizure from a syncopal episode.  Both conditions cause loss of consciousness and both may include body convulsions.  Details that support a diagnosis of seizure over syncope include bowel or bowel incontinence, tongue biting, and confusion after regaining consciousness (post-ictal state).

Management of a patient having a seizure should focus initially on the ABCs (Airway-Breathing-Circulation) and terminating the seizure.  This involves first repositioning the patient to prevent aspiration.  A common maneuver is rolling the patient in the lateral decubitus position, performing a jaw thrust, and suctioning the airway (Choice C).  Administration of IM haloperidol (Choice A) is unlikely to terminate the seizure as it is an antipsychotic, not an antiepileptic medication.  Obtaining a 12-lead EKG (Choice D) is an important aspect of evaluating a patient with a potential seizure, however, the next best step in this seizing patient should focus on the ABCs and terminating the seizure.  Endotracheal intubation (Choice B) may be necessary in this patient to protect the airway, but patient repositioning (Choice C) and antiepileptic (i.e., benzodiazepines) administration are important initial steps prior to considering intubation.  The best next step in this scenario is Choice C.

 Correct Answer: C

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Question Of The Day #44

question of the day
~ Joseph Ciano, USA ~ Leave a comment

Which of the following is the most appropriate next investigation to confirm this patient’s diagnosis?

  • A) Lumbar puncture
  • B) 12-lead EKG
  • C) MRI of brain
  • D) Noncontrast CT scan of head

This patient presents to the Emergency Department with altered mental status.  This presenting symptom can be due to a large variety of etiologies, including hypoglycemia, sepsis, toxic ingestions, electrolyte abnormalities, stroke, and more.  The management and evaluation of a patient with altered mental status depends on the primary assessment of the patient (“ABCs”, or Airway, Breathing, Circulation) to identify any acute life-threatening conditions that need to be managed emergently, the history, and the physical examination.  One mnemonic that may help in remembering the many causes of altered mental status is “AEIOUTIPS”.  The table below outlines this mnemonic.

ALTERED MENTAL STATUS

The information provided indicates that the patient’s headache was maximal at onset, severe, associated with vomiting, and led to a deteriorating mental status ultimately requiring intubation.  This history is very concerning for intracranial bleeding, especially subarachnoid hemorrhage (SAH).  The majority of atraumatic SAHs are caused by the rupture of a saccular aneurysm.  This causes the leakage of blood into the subarachnoid space.  Symptoms of a SAH are sudden onset headache that is maximal intensity at onset (“thunderclap headache”), syncope, vomiting, seizures, and any neurological deficits.  Risk factors for SAH are age over 50years-old, family history of SAH, alcohol abuse, tobacco smoking, Marfan Syndrome, Ehlers-Danlos Syndrome, and Polycystic Kidney Disease.  Diagnosis of SAH takes into account the patient’s history, physical exam, and risk factors. 

Patients that arrive in the Emergency Department under 6hours since symptom onset should initially get a noncontrast CT scan of the head (Choice D).  When a noncontrast head CT is performed in this time window, its sensitivity reaches 98-100%.  Noncontrast head CTs performed within the first 24hrs since headache onset have a sensitivity of about 90%.  Patients with signs and symptoms concerning for SAH who have a negative CT head should get a lumbar puncture (Choice A) to evaluate for xanthochromia.  This is especially important if the patient’s symptoms have been for over 6 hours.  A 12-lead EKG (Choice B) can show ST and T wave changes, but an EKG alone cannot be used to make a diagnosis of SAH.  A brain MRI (Choice C) can make the diagnosis of SAH, but a CT scan would be preferred due to greater CT scan accessibility, cost, and the shorter time of this imaging test.  The best next investigation would be a noncontrast CT of the head (Choice D).

Correct Answer: D

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Question Of The Day #43

question of the day
~ Joseph Ciano, USA ~ Leave a comment

Which of the following is the most likely cause for this patient’s altered mental status?

  • A) Diabetic ketoacidosis
  • B) Sepsis
  • C) Intracerebral hemorrhage
  • D) Hypothyroidism

This patient presents to the Emergency Department with altered mental status and fever.  Altered mental status can be due to a large variety of etiologies, including hypoglycemia, sepsis, toxic ingestions, electrolyte abnormalities, stroke, and more.  The management and evaluation of a patient with altered mental status depends on the primary assessment of the patient (“ABCs”, or Airway, Breathing, Circulation) to identify any acute life-threatening conditions that need to be managed emergently, the history, and the physical examination.  One mnemonic that may help in remembering the many causes of altered mental status is “AEIOUTIPS”.  The table below outlines this mnemonic.

ALTERED MENTAL STATUS

This patient has confusion, fever, lower abdominal pain, dysuria, and no focal neurological deficits on exam.  Diabetic ketoacidosis (Choice A) is unlikely as the patient does not have marked hyperglycemia (>250mg/dL (13.8mmol/L)), polyuria, or polydipsia.  Intracranial hemorrhage (Choice C) is unlikely as the patient has no headache, history of trauma, focal neurologic deficits, or coma.  Severe hypothyroidism (Choice D), known as myxedema coma, can cause altered mental status.  This condition is marked by somnolence or coma, hypothermia, nonpitting edema on the hands and feet, dry skin, macroglossia (enlarged tongue), and hair loss.  This patient does not have symptoms consistent with severe hypothyroidism. 

Sepsis (Choice B), especially in elderly individuals, can cause altered mental status.  The patient’s fever, confusion, lower abdominal pain, and dysuria all point to a likely diagnosis of urosepsis.  Sepsis is the most likely cause of this patient’s disoriented state.  Treatment with early IV hydration and antibiotics will help remedy the patient’s altered mental status.  Correct Answer: B

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Question Of The Day #42

question of the day
~ Joseph Ciano, USA ~ Leave a comment

Which of the following is the most appropriate next step in management for this patient’s condition?

  • A) IV insulin continuous infusion
  • B) IV hypertonic 3% NaCl
  • C) IV 0.9% NaCl bolus
  • D) IV insulin bolus

This patient presents to the Emergency Department with altered mental status.  This presenting symptom can be due to a large variety of etiologies, including hypoglycemia, sepsis, toxic ingestions, electrolyte abnormalities, stroke, and more.  The management and evaluation of a patient with altered mental status depends on the primary assessment of the patient (“ABCs”, or Airway, Breathing, Circulation) to identify any acute life-threatening conditions that need to be managed emergently, the history, and the physical examination.  One mnemonic that may help in remembering the many causes of altered mental status is “AEIOUTIPS”.  The table below outlines this mnemonic.

ALTERED MENTAL STATUS

This patient has a markedly elevated glucose level.  All patients with altered mental status should have a point of care glucose test as both hypoglycemia and severe hyperglycemia can cause altered mental status.  Some diagnoses to consider in this patient are diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS).  Both of these diagnoses can present with hyperglycemia and altered mental status, but HHS more often presents with higher glucose levels (greater than 600mg/dL (33mmol/L)) and more pronounced Central Nervous System depression.  Patients with HHS may have severe somnolence to the point of coma and may require intubation for airway protection.  In both DKA and HHS, patients are severely dehydrated by osmotic diuresis.  High glucose levels in the serum create an osmotic gradient that causes increased urination and fluid loss.  The first step in treatment for DKA and HHS is volume resuscitation. 

IV fluids (Choice C) should be given prior to the initiation of insulin therapy (Choices A and D).  After adequate IV hydration and correction of electrolyte derangements, insulin can be started to normalize glucose levels.  Bolus doses of IV insulin (Choice D) are harmful in both DKA and HHS and increase the risk of cerebral edema development.  For this reason, an IV insulin continuous infusion (Choice A) is always preferred over an insulin bolus (Choice D).  IV hypertonic 3% NaCl (Choice B) is the treatment for severe hyponatremia causing altered mental status or seizure.  Severe hyperglycemia can cause pseudohyponatremia, but this can be corrected for using the standard sodium correction formula (see references below).  The question stem provides an explanation for this patient’s altered mental status (hyperglycemia), so hypertonic saline should not be given with the information provided.  IV fluid administration (Choice C) is the next best step. Correct Answer: C

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References

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The Case of the Perplexing Crepitations

perplexing crepitations
~ Gayatri Lekshmi Madhavan, India ~ 1 Comment

Occam’s Razor – the simplest explanation is most likely to be correct.

In the Emergency Room, we are faced with a multitude of cases, and Occam’s Razor serves best when we need to narrow down on the differential diagnoses.

Sometimes, a few cases may evade this category and continue to baffle us even after a thorough history is obtained or a detailed clinical examination is performed. If we are lucky enough to get the point-of-care (POC) lab tests in time (or the mere availability of POC), they aid in the diagnosis and decision-making. At times, these POC lab tests also may not provide much help.

I have described one such case – a 21-year-old male with fever, dyspnea, desaturation, and multiple petechiae of 3 days duration.

Case Presentation

A 21-year-old male came at 9.30 pm to the ER with fever and breathlessness for three days. Being a healthcare worker himself, he had suspected pneumonia and started oral Amoxiclav, oral Clarithromycin, and Paracetamol. Despite this, there was no improvement in clinical status. He had progressively worsening breathlessness and continuous low-grade fever. On day 3, he developed a few petechial spots over his arms and minimal subconjunctival hemorrhage.

He recalls having myalgia in the lead up to these symptoms, for which he had received several injections of intramuscular Diclofenac. The injection sites now had developed small hematomas. There were no other visible bleeding manifestations. He clearly said that he had had no contact with any infectious patients and had self-isolated after developing these symptoms. His workplace had sent blood and sputum cultures – which came back negative. Their only concern was a continuous rise in the WBC count and sent to our hospital for further management.

Assessment

The patient was very ill-looking and extremely dyspneic with obvious usage of accessory respiratory muscles. He was profusely diaphoretic, had bilateral subconjunctival hemorrhage, multiple petechiae, anasarca, dyspnea, and 99.6⁰F. His Vitals were heart rate – 134/min, blood pressure – 110/70mmHg, respiratory rate – 34/min, SpO2 – 72% in room air; 98% with NIV. There were bilateral crepitations in all lung fields + no obvious abnormalities on CVS, CNS, and abdominal examination. POC ultrasound revealed multiple B-lines in all lung areas. Dilated IVC. The remaining cardiac, abdomen, and limb USGs were normal. ABG revealed Type 1 respiratory failure with elevated lactates. Bedside CXR and chest CT revealed diffuse bilateral lung infiltrates – not typical of pulmonary edema or pneumonia. Probable ARDS was mentioned. Blood samples had been sent for necessary investigations, including cultures and peripheral blood smear.

Management

Meanwhile, opinions were obtained from critical care consultants and pulmonologists regarding further management. Based on the clinical findings, it was decided to start the patient on broad-spectrum antibiotics (BSA), albumin transfusion, diuretics for the fluid overload status, and NIV for respiratory failure [all in suspicion of sepsis with MODS]. The patient was started on BSA before shifting to the ICU. Meanwhile, the blood reports arrived, suggestive of possible Myelodysplastic Syndrome (WBC – 95,000 cu.mm), Hb – 7g/dl. Peripheral Blood Smear report was Acute Myeloid Leukemia – possible M2 or M3.

The patient was immediately started on IV fluids, and oncology consultation was immediately obtained for chemotherapy initiation. Albumin and diuretics were withheld in suspicion of blast crisis and leukostasis / leukemic infiltration of the lungs. The patient was started on Cisplatin and other chemotherapeutic agents; bicarbonate infusion for urine alkalinization; allopurinol to treat hyperuricemia due to cytolysis; aggressive IV fluids for prevention of AKI due to chemotherapy and hyperuricemia [Tumour Lysis Syndrome]. Bone marrow biopsy was done during his hospital stay, which confirmed blast crisis AML-M3. His clinical condition improved considerably, and he was discharged from the hospital on Day 7.

Lessons Learnt

  1. Recognising leukostasis and hyperviscosity in the ED in an undiagnosed AML patient is extremely difficult. https://link.springer.com/chapter/10.1007/978-3-030-22445-5_3
  2. While considering different diagnoses based on clinical findings, always keep an open eye. Rare diseases present to the ED just like all others. https://www.medscape.com/viewarticle/860747_3
  3. Aggressive fluid management is needed in hyperviscosity syndrome. If we had started this patient on diuretics as planned, the blood would have become more viscous and lead to multisystem thrombosis. https://pubmed.ncbi.nlm.nih.gov/22915493/
  4. Increased metabolism in AML can present as pyrexia. With the other features of anemia, leucocytosis, petechiae, and anasarca, we are likely to diagnose this as sepsis. When in doubt, look through other causes of pyrexia (PUO). https://onlinelibrary.wiley.com/doi/full/10.1111/imj.13180
  5. Anasarca in leukemia does not warrant albumin transfusion as this may worsen fluid status. They may actually be in need of steroid therapy. https://www.hindawi.com/journals/crihem/2012/582950/
  6. Point of Care Lab testing is essential to reduce the number of diagnostic errors in the ED. https://acutecaretesting.org/en/articles/
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Recent Blog Posts By Gayatri L. Madhavan

STEMI Limitations

STEMI Limitations
~ Israa M Salih, UAE ~ Leave a comment

In 2000, the ST-Elevation Myocardial Infarction (STEMI) paradigm revolutionized the management of Acute Coronary Syndrome (ACS), substituting the previous dichotomy between Q-wave versus non-Q wave myocardial infarcts (MI). Subcategorizing aimed to predict completely occluded arteries and the need for immediate intervention, namely, emergent cardiac catheterization to open an occluded coronary artery in STEMI. However, literature has shown that STEMI and occlusion myocardial infarction (OMI) are not interchangeable, with clear evidence of benefit from early reperfusion in both entities. Moreover, definitions STEMI and Non-ST-elevation myocardial (NSTEMI) can miss a large proportion of acute coronary occlusions; STEMI as a category can miss 30% of occlusion MI up to 50% in left circumflex, and NSTEMI was only associated with total MI in a quarter of cases.

As any Emergentologist at any level can relate, it was only recently when my ED held a morbidity and mortality meeting for a presumably delayed cath lab activation. The patient had all the risk factors, a typical chest pain which resolved in the ED, normal vitals and an ECG that didn’t meet the STEMI criteria; however, when he went for urgent angiography, the LAD was totally occluded.

A new paradigm: OMI vs. NOMI

The OMI manifesto, introduced by Dr Stephen Smith, Dr Pendell Myers, and Dr Scott Weingart might provide a better solution in the management of ACS. The fundamental question is: Does the patient have an acute coronary occlusion that would benefit from immediate intervention? Based on this question, the following diagram was suggested to substitute STEMI versus NSTEMI paradigm. The manifesto also contains rules to diagnose acute MI in certain categories of patients, such as patients with left bundle branch block (LBBB), left ventricular paced rhythm, terminal QRS distortion, normal ST-elevation vs. left anterior descending artery (LAD) occlusion, anterior ventricular aneurysm vs. acute MI, ST depression in aVL.

https://emcrit.org/emcrit/omi-manifesto/

Basic concepts

ACS is a spectrum of clinical presentations divided into STEMI, NSTEMI and unstable angina, based on ECG findings and cardiac markers. The American Heart Association/American College of Cardiology (AHA/ACC) and European Society of Cardiology (ESC) define STEMI as new ST elevation at the J point in the absence of LV hypertrophy or LBBB in at least 2 contiguous leads. The elevation must be at least 2 mm (0.2 mV) in men or 1.5 mm (0.15 mV) in women in leads V2–V3 and/or 1 mm (0.1 mV) in other contiguous chest leads or the limb leads.

AHA/ACC recommends primary percutaneous coronary intervention (PCI) for patients with STEMI and ischemic symptoms of less than 12 hours’ duration. In NSTEMI, the recommendation is to perform urgent/immediate angiography with revascularization if appropriate in patients who have refractory angina or hemodynamic or electrical instability.

A meta-analysis of 46 trials with a total of 37 757 patients, including data from the International Study of Comparative Health Effectiveness with Medical and Invasive Approaches (ISCHEMIA) and Complete versus Culprit-Only Revascularization Strategies to Treat Multi-vessel Disease after Early PCI for STEMI (COMPLETE) trials demonstrated that PCI prevents death, cardiac death, and MI in patients with unstable coronary artery disease (CAD). The study defined unstable CAD as post-MI patients who haven’t received reperfusion therapy, multi-vessel disease following STEMI, non–ST-segment–elevation acute coronary syndrome.

STEMI Equivalents

For patients with persistent chest pain, hemodynamic instability and certain patterns of EKGs, it’s advisable to consider immediate/urgent PCI. The following patterns were found consistent with total occlusion or critical ischemia of the coronaries so every Emergentologist should familiarize her/himself with those: (All displayed ECGs are from Life in the Fast Lane ECG library)

De Winter T-wave: LAD occlusion.

Prominent T wave with upsloping ST depression in precordial leads
Prominent T wave with upsloping ST depression in precordial leads. https://litfl.com/de-winter-t-wave-ecg-library/

Wellen's Syndrome: Severe proximal LAD stenosis.

Biphasic or deep inverted T waves in V2 V3
Biphasic or deep inverted T waves in V2 V3 https://litfl.com/wellens-syndrome-ecg-library/

LBBB with positive Sgarbossa criteria

Concordant ST elevation in aVL
Concordant ST elevation in aVL https://litfl.com/sgarbossa-criteria-ecg-library/#:~:text=The%20original%20three%20criteria%20used,ve%20QRS%20complex%20(score%20)

New LBBB without meeting Sgarbossa criteria is not considered an indication for cath lab activation any longer. Smith modified Sgarbossa criteria are:

  • Concordant ST elevation ≥ 1 mm in ≥ 1 lead
  • Concordant ST depression ≥ 1 mm in ≥ 1 lead of V1-V3
  • Proportionally excessive discordant STE in ≥ 1 lead anywhere with ≥ 1 mm STE, as defined by ≥ 25% of the depth of the preceding S-wave

Positive Sgarbossa criteria in ventricular paced rhythm

Ventricular paced rhythm with Concordant ST depression in V2 to V6
Ventricular paced rhythm with Concordant ST depression in V2 to V6 https://litfl.com/sgarbossa-criteria-ecg-library/#:~:text=The%20original%20three%20criteria%20used,ve%20QRS%20complex%20(score%202)

Posterior MI: Left Circumflex (LCx) Artery or right coronary artery (RCA) occlusion

Infero-lateral STEMI with ST depression in V1 to V4 suggesting posterior MI
Infero-lateral STEMI with ST depression in V1 to V4 suggesting posterior MI https://litfl.com/posterior-myocardial-infarction-ecg-library/
Same patient with posterior EKG showing ST elevation in posterior leads
Same patient with posterior EKG showing ST elevation in posterior leads https://litfl.com/posterior-myocardial-infarction-ecg-library/

Right Ventricular MI: Complicates inferior STEMI, RCA occlusion

ST elevation in V1, ST elevation in III more than II
ST elevation in V1, ST elevation in III more than II https://litfl.com/right-ventricular-infarction-ecg-library/
ST elevation in V4R
ST elevation in V4R https://litfl.com/right-ventricular-infarction-ecg-library/

ST elevation in aVR with diffuse ST depression: Left Main Coronary Artery (LMCA), proximal LAD, or triple vessel occlusion

ST elevation in aVR with diffusion ST depression
ST elevation in aVR with diffusion ST depression https://litfl.com/st-elevation-in-avr/

ST depression and T-wave inversion in aVL: RCA, LCx, or LAD occlusion

Reciprocal ST depression in avL
Reciprocal ST depression in avL https://litfl.com/inferior-stemi-ecg-library/

Hyperacute T-waves: LCx occlusion

Broad asymmetrical T wave
Broad asymmetrical T wave https://litfl.com/t-wave-ecg-library/

References and Further Reading

  • Amsterdam, E. A., Wenger, N. K., Brindis, R. G., Casey, D. E., Ganiats, T. G., Holmes, D. R., … & Zieman, S. J. (2014). 2014 AHA/ACC guideline for the management of patients with non–ST-elevation acute coronary syndromes. Journal of the American College of Cardiology, 64(24), e139-e228.
  • Chacko, L., P. Howard, J., Rajkumar, C., Nowbar, A. N., Kane, C., Mahdi, D., … & Ahmad, Y. (2020). Effects of percutaneous coronary intervention on death and myocardial infarction stratified by stable and unstable coronary artery disease: a meta-analysis of randomized controlled trials. Circulation: Cardiovascular Quality and Outcomes, 13(2), e006363.
  • Coven, D. L. (2020). Acute Coronary Syndrome. Retrieved April 9, 2021, from https://emedicine.medscape.com/article/1910735-overview
  • Khan, A. R., Golwala, H., Tripathi, A., Bin Abdulhak, A. A., Bavishi, C., Riaz, H., … & Bhatt, D. L. (2017). Impact of total occlusion of culprit artery in acute non-ST elevation myocardial infarction: a systematic review and meta-analysis. European heart journal, 38(41), 3082-3089.
  • Kreider, D., Berberian, J. (2019). STEMI Equivalents: Can’t-Miss Patterns. EMResident. Retrieved April 9, 2021, from https://www.emra.org/emresident/article/stemi-equivalents/
  • Life in the Fast Lane. (n.d.). ECG Library. Retrieved April 9, 2021, from https://litfl.com/ecg-library/
  • Meyers, P. (2018). Guest Post – Down with STEMI – The OMI Manifesto by Pendell Meyers. EM Crit RACC. Retrieved April 9, 2021, from https://emcrit.org/emcrit/omi-manifesto/
  • O’gara, P. T., Kushner, F. G., Ascheim, D. D., Casey Jr, D. E., Chung, M. K., De Lemos, J. A., … & Zhao, D. X. (2013). 2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction. Circulation, 127(4), 529-555.
  • Wang, T. Y., Zhang, M., Fu, Y., Armstrong, P. W., Newby, L. K., Gibson, C. M., … & Roe, M. T. (2009). Incidence, distribution, and prognostic impact of occluded culprit arteries among patients with non–ST-elevation acute coronary syndromes undergoing diagnostic angiography. American heart journal, 157(4), 716-723.
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Recent Blog Posts By Israa Salih

Question Of The Day #41

question of the day
~ Joseph Ciano, USA ~ Leave a comment

Which of the following is the most appropriate next step in management for this patient?

  • A) CT scan of head without contrast
  • B) IV hypertonic 3% NaCl
  • C) IV dextrose
  • D) IV potassium chloride

This patient presents to the Emergency Department with altered mental status. This presenting symptom can be due to a large variety of etiologies, including hypoglycemia, sepsis, toxic ingestions, electrolyte abnormalities, stroke, and more. The management and evaluation of a patient with altered mental status depend on the primary assessment of the patient (“ABCs,” or Airway, Breathing, Circulation) to identify any acute life-threatening conditions that need to be managed emergently, the history, and the physical examination. One mnemonic that may help in remembering the many causes of altered mental status is “AEIOUTIPS.” The infographic below outlines this mnemonic.

ALTERED MENTAL STATUS

This patient is awake and moving all extremities, but with obvious confusion and dysarthria. Ordering a CT scan of the head without contrast (Choice A) may be helpful in this patient to evaluate for intracerebral hemorrhage, stroke, or a brain mass. However, the question stem indicates that this patient has a low glucose level. Glucose is considered low at levels below 70mg/dL (3.9 mmol/L); however, the absence of any symptoms can be reassuring. Glucose levels that are more severely low (less than 40mg/dL (2.2 mmol/L)) are more concerning than levels that are only moderately low (less than 70mg/dL (3.9mmol/L)). All patients with altered mental status should have a point of care glucose test. Both hypoglycemia and severe hyperglycemia can cause altered mental status. Hypoglycemia, if left untreated, can cause permanent brain damage. For this reason, the prompt identification of low blood glucose is critical so it can be treated rapidly.

Administration of IV hypertonic 3% NaCl (Choice B) would be helpful in a patient with severe hyponatremia with altered mental status or seizure. However, the question stem provides a cause for the patient’s symptoms (low glucose). IV potassium chloride (Choice D) would be helpful in the case of hyperkalemia to stabilize the cardiac membrane. Severe hyperkalemia can cause weakness and arrythmias, but does not cause dysarthria. This patient is at higher risk for hyperkalemia as he is a hemodialysis patient, but no evidence is given that he has hyperkalemia (i.e., peaked T waves on EKG or widened QRS interval). Again, a low glucose level is given in the question stem, which should be treated first.

IV dextrose (Choice C) is the best next step in management for this patient’s hypoglycemia. This patient has had poor oral intake and has end-stage renal disease. Insulin is excreted by the kidneys, so patients with end-stage renal disease are more prone to insulin “buildup” and hypoglycemia. In addition to administering IV dextrose (i.e., D50 bolus), providing food with complex carbohydrates is important to prevent recurring hypoglycemic episodes. If the patient continues to have persistent hypoglycemia despite an IV dextrose bolus and food, a continuous IV dextrose infusion (i.e., D10W at 100cc/hour) and admission for further evaluation should be considered. Correct Answer: C

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References

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VIP-EM POP QUIZ: What do you do?

~ Anthony Rodigin, USA ~ Leave a comment

During your emergency care career, you will not be able to avoid seeing the so-called VIP (very important…) patients from time to time. Whether it’s a VIP according to someone else higher up, general society or even your own perceptions actually does not matter – the end game is one and the same.

The best time to ponder and prepare regarding your future approach to VIP patients is now – before you are in the midst of the actual situation.

Now, if you are an idealist, things may seem blatantly easy. You shall and you of course will evaluate each one of your patients the same, regardless of anything about them! It may in fact feel insulting if someone were to insinuate that this case deserves or requires that “special” or “above and beyond” care. Doesn’t that imply that all of your other patients so far have been getting just average or so-so treatment?

A VIP patient is like a parcel box that arrives with a “handle with care” stamp. And the question is – are we not caring that way already?

Unfortunately, that is now how things may appear to others – exactly why patients and family members put on institutional badges or start mentioning names as you walk in the room. In a short while, random suits whom you have never met or knew existed descend from upstairs to “check on things”, as they seek you out to shake hands and make eye contact. And the general atmosphere affecting not only yourself, but also your nurses and everyone around slowly starts to resemble the buzz felt near a transformer booth.

The ethics and the philosophy of VIP-EM (I’m patenting the podcast name if you’re not) would take up a heavy volume.  For our purposes, we will make it simple:

VIP-EM situations will potentially push you toward one of two things:  either withholding what you normally would have done, or doing what you otherwise wouldn’t have done. 

Let’s take an example of either situation to illustrate.

  • A secretary of a hospital network CEO arrives with her 3-week old having a fever at home. Someone had called the charge nurse ahead of time, and they are given a priority room, ahead of others. The baby looks fine and is, oh, so cute! You, unfortunately, know what needs to happen, and so does the useless WBC count.  But…lumbar punctures hurt, and the mother is seeking out in your eyes the permission to defer it. So you send the happy baby home to its life-saving next day pediatrician follow up appointment and its Listeria meningitis demise…or do you?
  • A local TV station news anchor, and a friend of the Chief of the surgery department, pulls a shoulder while attempting a muscle up as part of the new IM-50X weight loss program. Physical exam findings are minimal, the XRay is normal and there is no concern for any neurological or vascular injury. You are requested to order a STAT MRI and to perform a shoulder steroid injection. Instead of the orthopedist on call, a special sports specialist catering to the town football team will be arriving in 3 hours to evaluate the patient, who will continue to hold up the ED bed. You will of course be prescribing narcotics for home…or will you?

Thinking about such hypothetical scenarios now to understand who you are and how you would behave will serve you well when the time comes. Regrettably, such education is often omitted from official medical school “handling difficult patients” curricula and cultural sensitivity training.

While I’m not an ethics professor, I do think there are three special circumstances within the entire VIP conundrum to consider.

The first is about returning someone injured in the line of public service to active duty. Whether it’s a colleague with a needle stick, a fireman needing clearance from minor inhalation or a police officer inadvertently embedded with a taser dart by one of his own – if you can return them to work rapidly and ahead of others, you should probably do it. First heal the healer goes a long way not only in major disasters, but in everyday life as well. It’s the basic utilitarian argument.

The second has to do with taking extra steps to ensure someone’s privacy.  If the patient is the kind of a persona who has paparazzi following them day and night, going the extra mile to create conditions of confidentiality that are no more than usual is probably okay.

Third, I do want to mention that while the sense of entitlement to extra or special care among the VIPs may be prevalent, the latter trend does not encompass everyone. Just like you will never plant the seed of suicidality by asking a patient if he or she is suicidal, you are unlikely to offend a potential VIP by asking directly if it is okay for you to treat them as everyone else. You will be amazed, but quite a few people who have to carry out their lives in full view of the public or are subjected to immense professional responsibilities never want to be treated differently in the first place.  Getting what I call a brief “fame holiday” may in fact be therapeutic and exactly what they need.

There are very few things in EM that are both deadlier and more unfair than VIP-medicine. Anticipating and mitigating potential fallout before it happens is a tough skill to learn. Knowing that such situations are unavoidable is the first step.

Last, while dignitary emergency medicine (DEM?) is not (yet) a legitimate EM fellowship, you can certainly read more about what’s being thought on this topic within the general medical field:

Al Mulhim MA, Darling RG, Kamal H, Voskanyan A, Ciottone G. Dignitary Medicine: A Novel Area of Medical Training. Cureus. 2019 Oct 22;11(10):e5962. doi: 10.7759/cureus.5962. PMID: 31799098; PMCID: PMC6863586.

 

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Recent Blog Posts By Anthony Rodigin

Immediate Management of Paediatric Traumatic Brain Injury

~ Nadine Schottler, Great Britain ~ Leave a comment

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. 
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Hypoglycemia – A Rural Perspective

hypoglycemia - a rural perspective
~ Carmina Shrestha, Nepal ~ Leave a comment

Waiting for patients is among some of the weird perks of working in a rural ER. “Too little isn’t fun as well”, said an enthusiastic new paramedic at Beltar PHC. Later that night, I’d find a funny connection between what he said and what followed.

A 56Y/M patient is brought to the ER on a particularly silent evening. Following the usual ER premise; I reach the department from upstairs. The patient was unconscious when I arrived. A paramedic was trying to open a peripheral line, and a nurse was taking a pulse oximeter reading while keeping the patient at 2L via nasal cannula. The bystanders who brought him had no clue of what had happened or if the patient had any comorbidity. As I grabbed the glucometer from the drawer, I could not help but remember how in med school exams all the hypoglycemic patients were medics who injected themselves with insulin. As I poked the patient with a lancet and measured his blood glucose, I realized the paramedic had already given up trying to get IV access. “I couldn’t get in”, he said. The glucometer beeped exactly then as if to confirm “this is trouble” – 37! “That is hypoglycemia”, I exclaimed!

Although there is no universally accepted definition of hypoglycemia (low blood glucose), a level below 60 rings the bell. As I tried to establish the line, I requested my nurse to prepare a thick paste of glucose powder. Of all the medicine I was taught, one thing I’ve found the most useful is the “available” medicine. Sure, start with a bolus of the glucose-containing solution: D50 or D10, if you cannot get IV access go for IM glucagon and so forth. But when you’re working in a setting where you second guess yourself for wasting a lancet while checking a patient’s blood glucose, IM glucagon becomes nothing more than a very good test question.

I could not get the line started either. Minutes after we applied the glucose paste on the buccal mucosa, the patient woke up. The sigh of relief was audible in the small ER of our PHC. Eventually, we were able to feed the patient per oral. The patient turned out to be diabetic who thought, “insulin is a medicine, hence should not be ignored, but the food is optional.”

Clinical hypoglycemia is sometimes defined as blood glucose low enough to cause symptoms. For most people, this occurs at 50-60 mg/dL. Clinically significant hypoglycemia is confirmed by the presence of the ‘Whipple triad’. Yap, that’s the same Allen Whipple, the American surgeon who also coined the Whipple procedure! The presence of symptoms consistent with hypoglycemia, a low serum glucose level, and resolution of the symptoms and signs of hypoglycemia with the administration of glucose is what confirms hypoglycemia.

Because diabetics are most prone to get hypoglycemic, in a diabetic patient, hypoglycemia is defined as a self-monitored blood glucose level ≤ 70mg/dL. Everyone else must have a documented experience of Whipple’s triad for the diagnosis. There is also something called relative hypoglycemia, it occurs when a patient with diabetes reports hypoglycemic symptoms, but the blood glucose remains above 70 mg/dL. This still requires treatment. Remember, we treat patients, not numbers.

The causes of hypoglycemia can be diverse, but the horses include missed meals or overnight fasting but still using hypoglycemic agents (sulphonylureas, insulin) in a person with diabetes. Be vigilant about recent exercise enthusiasts, alcohol ingestion, weight loss, and renal failure (which can reduce insulin clearance).

Signs and symptoms of hypoglycemia in non-diabetic patients are generally fairly obvious. Sympathetic autonomic nervous system activation symptoms like nervousness, anxiety, tremulousness, sweating, palpitations, shaking, dizziness, hunger, and symptoms due to decreased availability of glucose to the brain; confusion, weakness, drowsiness, speech difficulty, incoordination, odd behavior are seen below the commonly quoted glycemic values of 50-60. In severe cases, hypoglycemia may result in seizures, coma, or death.

A logical treatment flowchart should start with a glucose-containing solution: D50 or D10. In regards to D50, be aware that the bolus may cause rebound hypoglycemia, may overshoot glycemic targets and is hypertonic hence should be given slowly over 2-5 minutes. There has been extensive debate over D50 vs D10, here is what I try to keep in mind; If using D50, give 1 amp at a time over 2-5 mins. If D10, a 100ml bolus over 2 mins. Check the patients’ glucose levels often.

Remember both of those approaches require you to have IV access. Intramuscular glucagon (5mg) may be given to raise serum glucose levels. Keep in mind two things: the efficacy of glucagon is dependent upon hepatic glycogen stores. Patients with prolonged hypoglycemia may have a minimal response and repeating glucagon does not make much sense.

If the blood glucose goes back to > 60mg/dL in a non-diabetic patient, and >70mg/dL in a diabetic patient and/or there is an improvement in symptoms, patients who can eat should do so otherwise IV dextrose drip (D5W at 75-100 mL/hr) is the way to go.

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