critical care

Critical Brain Resuscitation

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A patient with an intracranial hemorrhage can look surprisingly stable…until they suddenly don’t. Recognizing the subtle signs of rising intracranial pressure before herniation occurs is one of the most time-critical skills in emergency medicine. In this episode, Drs. James Nardini, Mike Prats, and Kim Bambach discuss a practical, evidence-based approach to critical brain resuscitation, from recognizing early deterioration to implementing tiered ICP management, choosing hyperosmolar therapy, optimizing sedation, and avoiding common pitfalls. Based on the Emergency Neurological Life Support (ENLS) framework, this episode provides a systematic approach you can apply on your next shift.

Guest: James Nardini, MD, MS; Host: Mike Prats, MD and Kim Bambach, MD; Editor: Kim Bambach, MD

🔑 Key Learning Points

1. Recognize deterioration early

  • Elevated ICP often begins with nonspecific symptoms (headache, vomiting, confusion, gait disturbance).
  • Serial neurologic examinations are more valuable than a single assessment.
  • Track:
    • Glasgow Coma Scale (watch for declining scores)
    • Pupillary size and reactivity
    • New focal neurologic deficits
    • Mental status changes
  • A >1 mm change in pupil size may be an early sign of herniation.

2. Understand herniation syndromes

  • Subfalcine: contralateral leg weakness (ACA compression)
  • Uncal (transtentorial):
    • ipsilateral fixed dilated pupil
    • decreased consciousness
    • contralateral hemiparesis
  • Tonsillar:
    • occipital headache
    • neck stiffness
    • progressive brainstem compression
    • eventual Cushing triad

3. Cushing triad is a late finding

  • Hypertension
  • Bradycardia
  • Irregular respirations

Waiting for the full triad means the patient is already critically decompensating.

4. Follow a tiered approach (Emergency Neurological Life Support)

Tier 0: Optimize physiology

  • ABCDE assessment
  • Protect airway, maintain oxygenation and ventilation
  • Normalize glucose
  • Treat fever
  • BP management
  • Elevate head of bed (when appropriate)
  • Provide analgesia and sedation
  • Obtain urgent non-contrast head CT
  • Minimize secondary brain injur

Tier 1: Temporize while arranging for definitive care

  • Hyperosmolar therapy
  • Brief controlled hyperventilation if actively herniating
  • Early neurosurgical consultation and if needed arrange transfer for neurosurgical consultation. You can advocate for your patient.

5. Hypertonic saline vs. mannitol

  • Both improve outcomes and are reasonable first-line agents.
  • Hypertonic saline may provide:
    • more sustained ICP reduction
    • better cerebral perfusion pressure
    • superior ICP control in several studies
  • Don’t delay treatment simply because one agent is unavailable.
  • In selected critically ill patients, both therapies may be used.

6. Monitor sodium carefully

  • Obtain a baseline sodium on patient arrival.
  • Check sodium frequently after hypertonic saline.
  • Typical therapeutic target:
    • 145–155 mEq/L

6. Propofol is the preferred sedative

Benefits:

  • Decreases cerebral metabolic demand
  • Reduces cerebral blood volume
  • Lowers ICP
  • Suppresses seizures

Watch for:

  • Hypotension
  • Reduced cerebral perfusion pressure

Maintain adequate blood pressure while sedating.

7. Common pitfalls

A common pitfall is waiting too long to initiate hyperosmolar therapy. If you’re seriously asking whether the patient needs hypertonic therapy, that may be the moment to act rather than waiting for unmistakable herniation.

8. Emergency physicians are the bridge to definitive care

The goal is to:

  • Recognize deterioration
  • Prevent secondary injury
  • Optimize physiology
  • Initiate temporizing therapies
  • Rapidly connect patients with neurosurgical intervention

9. Ultrasound pearl

Bedside ultrasound may provide additional information:

  • optic nerve sheath diameter measurement
  • optic disc elevation
  • transcranial ultrasound (experienced users)

đź“š Further Resources

  1. Emergency Neurological Life Support Course
  2. Emergency Neurological Life Support Intracranial Hypertension and Herniation Protocol
  3. Guidelines for the Acute Treatment of Cerebral Edema in Neurocritical Care Patients- Neuro Critical Care Society

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Under Pressure: Abdominal Compartment Syndrome

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Abdominal compartment syndrome is an elusive diagnosis that can cause or worsen multi-organ failure in your sickest patients. How can we avoid missing it? It’s a classic case of “if you don’t think of it, you can’t diagnose it.” Dr. Ruben Geeraert, PGY-3 and future critical care fellow, breaks down how we can recognize and treat it.

Guest: Ruben Geeraert, MD
Host: Kim Bambach, MD
Editor: Kim Bambach, MD

Key Take-Aways:

What is it? Abdominal compartment syndrome is sustained pressures > 20 mm Hg in the abdomen with evidence of end-organ damage. End-organ damage can occur with abdominal hypertension > 16 mm Hg.

What’s the pathophysiology? Compressing structures in the abdomen ultimately leads to decreased cardiac output and multi-organ failure due to hypoperfusion.

Why is it so easy to miss? These patients can be easy to miss because they are already critically ill, and multi-organ failure might be attributed to a different cause. Consider it in patients receiving massive fluid resuscitation, massive transfusion protocols (MTP), polytrauma patients, septic patients, patients with an acute abdomen, and any mechanically ventilated patient. It is shockingly common in MICU and SICU patients.

Can’t I just tell based on abdominal exam? Unfortunately, you can’t. It’s important to recognize a tense abdomen, but the abdominal exam is unreliable—only 50% sensitive for this diagnosis!

How do you measure abdominal pressure? Assess for abdominal compartment syndrome by taking a bladder pressure, which you can do with a Foley catheter and arterial line setup.

How is it treated? Initial management is medical (treating the underlying disease process), but the patient may ultimately require decompressive laparotomy. Evidence is limited on the optimal timing of this procedure.

References:

  1. Masneri DA, O’Brien M. Acute Abdominal Pain. In: Tintinalli JE, Ma O, Yealy DM, Meckler GD, Stapczynski J, Cline DM, Thomas SH. eds. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 9e. McGraw-Hill Education; 2020. Accessed February 07, 2024.
  2. EMCrit Project. “Abdominal Compartment Syndrome.” Accessed September 27, 2024. https://emcrit.org/ibcc/abdominal-compartment-syndrome/.
  3. Popowicz, Patrycja, Nalin Dayal, Richard K. Newman, and Elvita Dominique. “Abdominal Compartment Syndrome.” In StatPearls. Treasure Island (FL): StatPearls Publishing, 2024. http://www.ncbi.nlm.nih.gov/books/NBK430932/.
  4. Reintam Blaser, Annika, Adrian Regli, Bart De Keulenaer, Edward J. Kimball, Liis Starkopf, Wendy A. Davis, Patrick Greiffenstein, and Joel Starkopf. “Incidence, Risk Factors, and Outcomes of Intra-Abdominal Hypertension in Critically Ill Patients—A Prospective Multicenter Study (IROI Study).” Critical Care Medicine 47, no. 4 (April 2019): 535. https://doi.org/10.1097/CCM.0000000000003623.
  5. Regli, Adrian, Paolo Pelosi, and Manu L. N. G. Malbrain. “Ventilation in Patients with Intra-Abdominal Hypertension: What Every Critical Care Physician Needs to Know.” Annals of Intensive Care 9, no. 1 (April 25, 2019): 52. https://doi.org/10.1186/s13613-019-0522-y.

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