Case of the Week: Post Arrest to Room 5L

Author: Christian Gerhart, MD

Reviewed by: Jessica Pelletier, DO

You are working in the trauma/critical care (TCC) pod of the ED. You get the following page: “Post-arrest to room 5L…BP 130/70, RR 12, HR 85, O2 sat 97% RA, BG 103.”

Per EMS the patient was at his job, sitting at his computer when someone witnessed him suddenly collapse. They do not think there was any trauma. A bystander reportedly performed CPR briefly, but when EMS arrived the patient had palpable pulses with normal sinus rhythm on the monitor. He had spontaneous respirations and was placed on 2L of NC O2. He did not receive any medications en route to the ED.

The patient arrived and had easily palpable pulses. He exhibited spontaneous respirations but did not open his eyes or grimace to pain. There was no verbal response. He was noted to have extensor posturing in all four extremities with painful stimuli. His pupils were 1 mm bilaterally. 

What would your next steps in management be for this patient?

The patient was intubated with etomidate and succinylcholine on the first attempt. Tube placement was confirmed with end tidal CO2. An EKG was obtained and is shown below: 

Figure 1 -  EKG on arrival to the ED.

What would your next steps be?

The patient was taken emergently to the CT scanner. His non contrast head CT is shown below: 

Figure 2 - CT head without contrast.

What would you do next?

The patient’s non-contrast head CT was interpreted by the ED team in the CT scanner. There did not appear to be any hemorrhage or visible large volume infarct. Given the concern for a large vessel occlusion, rapid CT angiogram (CTA)/CT perfusion (CTP) were performed. A representative image of the CTA is shown below. 

Figure 3 – CTA head and neck.

What do you see on the images?

The images show a basilar artery occlusion. The stroke pager was activated, and the patient was rapidly evaluated by neurology. Given the patient’s symptom onset of less than one hour prior to arrival, he was potentially a candidate for thrombolytic therapy. The patient’s chart was reviewed, and the following history was found:

PMHx: 

Atrial flutter 

L5-S1 discitis 

Ascending aortic aneurysm with Type A aortic dissection 

Chronic Pseudomonas graft infection with aortitis

Aortic regurgitation

Mitral Regurgitation

Hypertension

Dilated cardiomyopathy

PSHx:

Type A dissection graft repair

Prosthetic aortic valve placement

Prosthetic mitral valve placement

Medications:

Amiodarone

Rivaroxaban

Cirpofloxacin

Carvedilol

Hydralazine

Aspirin

Hydrochlorothiazide

In discussion with neurology, the patient was deemed not to be a candidate for thrombolysis as he had a therapeutic anti-Xa level in the context of active rivaroxaban use and an active aortic graft infection placing him at high risk for bleeding. The patient’s CTP showed a favorable quantity of potentially reperfusable tissue. Neuro interventional radiology (IR) was contacted and agreed that the patient would benefit from thrombectomy. He underwent a successful thrombectomy and was transferred to the neuro ICU (NNICU) following the procedure. He had an extended ICU course but ultimately went home from the hospital requiring a walker for ambulation with minimal residual neurological deficits. 

Basilar Artery Occlusion

The basilar artery originates at the intersection of the two vertebral arteries and supplies a large portion of the pons. Presentation of a basilar artery occlusion can be variable depending on where the occlusion is and if it also involves the vertebral arteries or posterior cerebral arteries. Infarction of any location if large enough can cause acute coma. However, smaller lesions may result in subtle, less commonly seen findings on the neurological exam. Lower motor neuron (rather than the usual upper motor neuron) or “crossed” findings, where the patient may have a cranial nerve deficit on one side but weakness or sensory changes on the other side may be present since the fibers may have already crossed midline and a number of cranial nerve nuclei reside in the brainstem. The basilar artery in particular can lead to findings that can be challenging to detect if a thorough exam is not performed. Colloquially, these findings (dysphagia, dysarthria, diplopia, dizziness, dystaxia) are often described as the “deadly D’s”.

Acute Coma

This case, which initially presented as a “post-arrest”, was actually a devastating stroke. We are experts at making decisions with limited information, but sometimes we need to reframe the information we are given. The initial report of a patient who was “post-arrest” can serve as a distractor and create anchoring bias. One thing that should lead the clinician away from the diagnosis of cardiac arrest is the fact that the patient had normal vital signs without any intervention. This would be very unlikely for a patient who suffered a cardiac arrest. Though the neurological exam can vary tremendously in post-arrest patients, extensor posturing with pinpoint pupils should raise concern for a primary neurological etiology. This patient’s presentation would be better characterized as acute coma, rather than post-arrest. This significantly changes our differential diagnosis. In a patient with acute coma, especially with the reported abrupt decompensation in this case, primary neurological causes become much more likely. Although a toxicologic ingestion, electrolyte abnormality, cardiac dysrhythmia, myocardial infarction, or seizure could present similarly, an acute, hemorrhagic or large vessel occlusion ischemic stroke is of highest concern with this clinical history. As always, stabilization of the airway, breathing, and circulation, as well as obtaining a rapid point of care glucose, should occur before proceeding further down a diagnostic pathway as these patients are often unstable. Hypo- or hyperthermia should also be ruled out as potential etiologies of acute coma. Unless the diagnosis is obvious, a broad toxic/metabolic workup including a CBC, CMP, TSH, magnesium, phosphorus, and acetaminophen/ethanol/salicylate should be sent. Further toxicologic workup with a urine drug screen or specific toxicologic testing can be considered depending on the clinical scenario. 

The history of acute coma in a patient later found to be on anticoagulation with chronic aortitis placing them at high risk for mycotic aneurysms should raise initial concern for spontaneous intracranial hemorrhage. However, after a negative head CT in a patient with acute coma, the differential must be broadened to include large vessel occlusion strokes, particularly a basilar artery occlusion. The National Institute of Health Stroke Scale (NIHSS) focuses on the anterior circulation and lateralizing findings. However, strokes of the posterior circulation, of which the basilar is often the deadliest, can have vague, poorly localizing symptoms. Though this patient’s NIHSS would be very high if formally calculated, stroke can be missed in the absence of lateralizing findings. Consider a rapid CTA of the head and neck in a patient where the history and exam are suspicious for an intracranial hemorrhage but the non-contrast CT is negative. A negative CTA should prompt further consideration of the need for an LP to assess for meningitis or encephalitis, or an EEG to evaluate for non-convulsive status epilepticus. A CT venogram can be considered for patients in whom cerebral venous sinus thrombosis is suspected. Posterior reversible encephalopathy syndrome (PRES) is a diagnosis that should be considered in hypertensive patients with negative CT imaging, as this can result in a significantly depressed level of consciousness if severe. MRI is the test of choice for suspected PRES. 

Take Home Points:

• Avoid anchoring bias; acute coma can mimic the post cardiac arrest state

• Acute coma requires a broad differential

• In a patient who has a high pretest probability of an acute intracranial hemorrhage but a normal non-contrast head CT, consider a CTA of the head and neck to assess for a large vessel occlusion

• In a patient with acute coma and negative CT imaging consider an LP/EEG/MRI (if available) to further evaluate the etiology

References:

Farkas J. Approach to Stupor & Coma - EMCRIT Project. EMCrit Project. https://emcrit.org/ibcc/coma/. Published February 12, 2023. Accessed September 30, 2023.

Salerno A, Strambo D, Nannoni S, Dunet V, Michel P. Patterns of ischemic posterior circulation strokes: A clinical, anatomical, and radiological review. Int J Stroke. 2022;17(7):714-722. doi:10.1177/1747493021104675

Booth CM, Boone RH, Tomlinson G, Detsky AS. Is this patient dead, vegetative, or severely neurologically impaired? Assessing outcome for comatose survivors of cardiac arrest. JAMA. 2004;291(7):870-879. doi:10.1001/jama.291.7.870

Traub SJ, Wijdicks EF. Initial Diagnosis and Management of Coma. Emerg Med Clin North Am. 2016;34(4):777-793. doi:10.1016/j.emc.2016.06.017

Sciacca S, Lynch J, Davagnanam I, Barker R. Midbrain, Pons, and Medulla: Anatomy and Syndromes. Radiographics. 2019;39(4):1110-1125. doi:10.1148/rg.2019180126