Approach to the Patient with Coma Protocol

Emergency Neurological Life Support

Approach to the Patient with Coma Protocol
Version 5.0

Authors
Sara Stern-Nezer, MD, MPH
Katrina Peariso, MD, PhD
Prem A. Kandiah, MD

Last updated: May 2022

Protocol developed by:

Aarti Sarwal, MD, FNCS, FAAN
Sara Stern-Nezer, MD
Approach to the Patient with Coma Protocol
Approach to the Patient with Coma Algorithm
Approach to the Patient with Coma Protocol
Checklist
☐ Evaluate/treat circulation, airway, breathing, and ventilation issues
☐ Ensure adequate immobilization of cervical spine if warranted
☐ Exclude/treat hypoglycemia or opioid/benzodiazepine overdose
☐ Serum chemistries, arterial blood gas, urine toxicology screen
☐ Emergent cranial CT (CT angio brain if appropriate) to determine if coma etiology is
structural or vascular

Communication
☐ Physician and advanced provider communication
☐ Clinical presentation and time last seen well if known including history from
bystanders, witnesses, contextual or environmental observations (e.g., pill bottles,
seizures, trauma, etc.)
☐ Findings on neurological examination including details on GCS components and any
abnormality with brainstem reflexes, if found
☐ Relevant past medical history/surgical history
☐ Relevant laboratory tests including glucose, blood gas, renal and hepatic function
☐ Brain imaging, LP, or EEG results (if available)
☐ Treatments administered so far
☐ Nursing, physician/advance practice provider communication

Sample Sign-off Narrative:

“54-year-old male patient was found unresponsive at home with agonal respirations. Unknown
last well time. Bottle of narcotics found at bedside. He was intubated on scene without
sedatives, paralytics. Given naloxone at scene without significant improvement in exam.
Hypertensive with SBP in 190s; given labetalol, now in the 140s. No spontaneous respirations
on ventilator on controlled mechanical ventilation at 100% FiO2 with tidal volume of 350 ml and
PEEP 8 saturating 95%, PaCO2 on blood gas was 38 mmHg; 5.06 kPa (goal PCO2 35–40
mmHg; 4.6–5.3 kPa). On exam, GCS is 4T, X time after intubation. He is not responsive, does
not attend. He has absent brainstem reflexes with extension to motor response to pain but
pinpoint pupils. Toxicology screen positive for opioids and cocaine. Neurological consults or
neuroimaging CT angio are not available here; hence being transferred.”
Approach to the Patient with Coma Protocol

Unconscious Patient
Eyes closed, unresponsive

A patient who has eyes closed and is unresponsive is considered comatose.

Determine unresponsiveness:
• Observation: eyes closed, immobility, lack of facial expression, obliviousness to
environmental stimuli.

Examiner evaluates response to graded stimulus:

• Verbal stimulus - Ask "Are you OK?" or "What is your name?" Other auditory
stimulus may be a loud handclap.
• Tactile stimulus to body parts with large cortical representation - face and hands.
• Noxious stimulus - should be intense but not cause tissue injury. Recommended
maneuvers include sternal rub, nail-bed pressure, pressure on supraorbital ridge or
on posterior aspect of mandibular ramus.
 Approach to the Patient with Coma Protocol
Assess ABCs and C-Spine
The unconscious patient’s ABCs should be quickly assessed and concurrently treated (see
ENLS protocol Airway, Ventilation, and Sedation). Verifying patency of the airway is an
overriding initial priority to ensure adequate oxygenation and ventilation. The patient’s cervical
spine should be immobilized if the possibility of injury cannot be ruled out.

• Airway, breathing and circulation are assessed and concurrently treated as detailed
in ENLS protocol Airway, Ventilation and Sedation.
• Rapid survey of head and neck, chest, abdomen, and extremities. Cervical spine is
immobilized if there is any likelihood of traumatic instability.
• Bedside glucose testing is performed on all unconscious patients. If blood glucose is
< 70 mg/dl administer 20-50 ml of 50% dextrose. Thiamine 100 mg IV should be
given prior to dextrose in patients at risk for nutritional deficiency (e.g., chronic
alcohol users, bariatric surgery patients, patients with malabsorptive states) (see
Table 3, Prehospital pharmacological therapy for coma).
• If there is suspicion of opioid toxidrome (e.g., history of drug use, coma, apnea or
bradypnea, small pupils), administer naloxone 0.04-0.4 mg IV/IM and repeat as
needed in total dosing up to 4 mg. 1–2 mg per nare into both nares can be given
initially but switch to IV/IM when possible (see Table 3, Prehospital pharmacological
therapy for coma).
 Approach to the Patient with Coma Protocol

Neurological Assessment
Focused neuro exam

The emergency neurological assessment of the unconscious patient has four parts: level of
consciousness, brainstem assessment, evaluation of motor responses, and appraisal of
breathing patterns. Many scales are available to aide in emergent neurological assessment of
a comatose patient.

See Table 4 for Adult Glasgow Coma Scale

See Table 5 for Pediatric Glasgow Coma Scale
See Tables 6 for pupillary changes
See Chart 1 for respiratory changes reflecting underlying etiology
See Figure 2 for FOUR Score

• Level of consciousness: Refer to Glasgow Coma Scale (see Tables 4 and 5) or

FOUR Score (see Figure 2). Assess additional potential signs of arousal including
visual fixation, visual pursuit (tracking), and forced eye closure resisting the
examiner.
• Brainstem (cranial nerve) examination:
o Pupillary size, reactivity, and symmetry (see Table 6 for pupillary changes
reflecting underlying etiology)
o Corneal reflex
o Visual threat response
o Oculocephalic reflex (doll’s eyes - only if no suspicion of cervical instability)
o Gag reflex
o Cough reflex
• Motor function: Spontaneous muscle position/posture, spontaneous movements,
response to verbal command, response to noxious stimulus. Examiner should
distinguish purposeful from reflexive activity. Examples of purposeful activity include
following commands, pushing examiner away, reaching for endotracheal tube,
localizing to noxious stimulus. Examples of reflexive activity include withdrawal,
flexion, or extension to noxious stimulus.
• Breathing pattern: The breathing pattern may have localizing value in comatose
patients with brainstem lesions (see Chart 1 for respiratory pattern reflecting
underlying etiology)
o Cheynes stokes-global metabolic encephalopathy, impaired forebrain or
diencephalon
o Central neurogenic hyperventilation: metabolic encephalopathy, high brainstem
tumors (rare)
o Apneusis bilateral pons lesion
o Cluster breathing or ataxic breathing - pontomedullary junction lesion
o Apnea – lesions affecting ventrolateral medulla bilaterally
 Approach to the Patient with Coma Protocol
Assess for Readily Reversible Conditions
Prehospital and initial hospital evaluation should focus on assessing and treating readily
reversible conditions like airway compromise, hypotension, hypoglycemia, opioid overdose
(see table 3, Prehospital pharmacological therapy for Coma).

STAT CTH
Consider CTA

Head CT will help assess for possibility of acute intracranial process. Primary neurological
etiologies of coma are described in Table 7, many of which may be apparent on noncontrast
CT head. Use caution in ruling out ischemic stroke and brainstem pathology as head CT may
be negative early on. See Table 9 for metabolic, toxic and environmental etiologies of coma,
for which relevant laboratory testing should be performed routinely in the initial management of
coma.

Non-contrast cranial CT should be obtained emergently in unconscious patients with a

presumed structural cause of coma and in patients with an unclear cause of coma after initial
assessment of ABCs and cervical spine stabilization.

If an acute ischemic stroke is suspected, cranial CT angiography and CT perfusion can provide
valuable information on vascular patency and regional perfusion (see ENLS protocol Acute
Ischemic Stroke). Basilar artery thrombosis is a consideration in sudden onset coma and CT
angiography will be diagnostic. If CT alone is done, look at the basilar artery and see if it is
abnormally hyperdense - this may suggest basilar artery thrombosis. A rapid sequence MRI
may be obtained if there is a presumption of hyperacute ischemic stroke or when the cause of
coma is not explained by other tests.

When a CNS infection is being considered, cranial CT with and without contrast should be
obtained to evaluate for abscess, extra-axial fluid collections, hydrocephalus, hemorrhagic
transformation, and vasculitic infarcts.
 Approach to the Patient with Coma Protocol
Focused History/PMH
Patient history is obtained concurrently with resuscitative measures. Historical information
elicited from witnesses, friends, family, co-workers, or EMS personnel may suggest the cause
of coma. EMS personnel may have valuable details about the circumstances in which the
patient was found. Medical and surgical history, medications, alcohol and illicit drug use, and
environmental exposures or evidence of trauma should be systematically queried.

The time course of the alteration in consciousness may be helpful in suggesting etiology. An
abrupt onset suggests a stroke, seizure, or a cardiac event with impaired cerebral perfusion. A
more gradual onset of coma suggests a metabolic or possibly infectious process.
Approach to the Patient with Coma Protocol
STAT Labs
Unless a readily reversible cause of unresponsiveness has been discovered and corrected,
additional laboratory work (serum chemistries, CBC, coags, EtOH level, blood gas, urine
toxicology, cultures) is obtained emergently. Point of care (POC) testing should be utilized
where available.
• Serum chemistries including Na, K, creatinine, BUN, and transaminases
• Hematological panel including hemoglobin/hematocrit, platelets, and white blood cell
count; coagulation studies
• Arterial blood gas
• Toxicology: Blood alcohol level; urine toxicology screen for opioids,
benzodiazepines, illicit drugs. (Note: Some toxins that cause unconsciousness are
not detectable in common toxicology screens); acetaminophen & salicylate levels if
warranted
• Microbiology: Urinalysis; urine culture; blood cultures
 Approach to the Patient with Coma Protocol
Causes of Coma
Three possibilities

Information accrued so far is used to establish a preliminary impression of either a structural

cause, a nonstructural cause, or an unclear cause. Structural and nonstructural causes of
coma may coexist. Caution must be exercised in patients with non-focal exam and
noncontributory CT head as brainstem stroke or nonconvulsive seizures can present without
focal or structural abnormalities apparent initially. Orofacial dyskinesias and posturing may be
seen in brainstem stroke and may be mistaken for seizures. Please see Tables 7 and 8 for
neurological and non-neurological causes of coma.
Approach to the Patient with Coma Protocol
Unclear Etiology
In many patients, the etiology of coma cannot be easily identified after initial assessment or
emergent non-contrast cranial CT. Advanced imaging like CT angiogram, perfusion imaging or
rapid sequence MRI or contrast imaging should be considered if suspicion of ischemic stroke
or occult pathology exists based on risk factors. If diagnostic uncertainty persists, a lumbar
puncture (LP) and EEG. A LP may be indicated for suspicion of CNS infection,
neuroinflammatory and autoimmune disorders, and suspected central nervous system
involvement of hematological or solid organ cancers. Additionally, when there is clinical
suspicion of an aneurysmal subarachnoid hemorrhage presenting more than 24 hours after
onset of headache, an LP should be obtained even if the non-contrast CT is negative.
 Approach to the Patient with Coma Protocol
Structural
(Focal Exam)

Structural causes of coma include Traumatic Brain Injury, Acute Ischemic Stroke, Intracerebral
Hemorrhage, Meningitis and Encephalitis, and brain tumor and other mass lesions.

Management should be initiated in consultation with Neurology and/or Neurosurgery.

Asymmetric or focal findings on physical examination suggest a localized brain lesion or

disturbance. A structural etiology is suggested by:
• History: trauma, acute onset of symptoms, immunodeficiency, malignancy
• Physical examination: asymmetric cranial nerve findings, asymmetric motor
responses (e.g., hemiparesis)
• Absence of an obvious toxic-metabolic etiology

Unless proven otherwise, coma is presumed to be structural in origin and should be

immediately assessed with a non-contrast cranial CT since emergent neurosurgical
management may be needed. Emergent CT angiography should be considered in any patient
with an exam concerning for focal brainstem findings or suspected vertebrobasilar ischemia.

Patients with a new onset of seizures, a change in seizure pattern, or status epilepticus should
be evaluated for a possible structural focus. See ENLS protocol Status Epilepticus.
Approach to the Patient with Coma Protocol
Nonstructural
Caution must be exercised in patients with non-focal exam and noncontributory CT head as
brainstem stroke or nonconvulsive seizures can present this way.

A nonstructural cause of coma is suggested by:

• Progressive, gradual onset of symptoms
• History of medication, alcohol, or illicit drug use, or environmental toxic exposure
• Non-focal neurological exam with symmetric cranial nerve and motor findings (Table
8 highlights some important, non-neurological causes of coma).
 Approach to the Patient with Coma Protocol
Metabolic Coma
Global or metabolic causes

Common nonstructural causes of coma include anoxic-ischemic encephalopathy, seizures,

metabolic alterations, endocrinopathies, systemic infections, CNS infections, medication
overdose, alcohol and illicit drug use, and exposure to nonpharmacologic neurotoxic
compounds (Tables 7 & 8).

Treatment is guided by the underlying etiology. Where appropriate, specific

antagonists/antidotes should be administered. For example:
• Opioid overdose: naloxone (Table 3)
• Acetaminophen overdose: N-acetylcysteine (Table 3)
• In some cases, a primary metabolic encephalopathy may evolve toward a structural
process, such as acute liver failure leading to cerebral edema and herniation. Table
9 lists causes of hyperammonemia
• Severe hyponatremia can contribute to coma and should be managed according to
the algorithm outlined in Table 10
• Wernicke’s encephalopathy may not present with the full classic triad of
encephalopathy, ataxic gait and ophthalmoplegia. High dose thiamine should be
initiated in patients with coma and risk factors for Wernicke’s Encephalopathy (see
Table 11)
• Seizures and status epilepticus commonly are not associated with any detectable
lesion on cranial CT. However, in patients with new onset seizures or a change in
seizure pattern, a structural cause must be excluded with cranial CT or MRI. CNS
infections may have no structural correlate on non-contrast CT or MRI; however, this
study should be obtained with and without contrast to exclude brain abscess.
• Remember to initiate antimicrobials and dexamethasone (if indicated) prior to the
head CT if you suspect infectious meningoencephalitis and specifically do not delay
therapy for a diagnostic lumbar puncture. Do not forget to treat empirically for
Listeria in at risk populations (immunocompromised, neonates, elderly, etc) or for
HSV meningitis with acyclovir if the clinical situation is suggestive, such as a patient
with fever and seizures.
Approach to the Patient with Coma Protocol
Persisting Uncertainty
Next steps

Depending on the history and presentation, advanced imaging like CT angiogram, perfusion
imaging, rapid sequence MRI must be considered if initial CT head is non-contributory. Stat
EEG may be considered to assess for non-convulsive seizures.

When diagnostic uncertainty persists despite initial assessment, additional test measures
include:
• Non-contrast head CT is obtained in all comatose patients with an undiagnosed
etiology if not done already.
• Consider basilar artery thrombosis (look for a hyperdense basilar artery sign on non-
contrast head CT); CT-Angiography (CTA) or MR-Angiography (MRA) is definitive.
• EEG to evaluate for non-convulsive seizures or status epilepticus, burst
suppression, or patterns consistent with metabolic encephalopathy. Be aware of
dyskinesias seen in brainstem stroke that may mimic seizures.
• Lumbar puncture (LP) is obtained if there is suspicion of CNS infection,
inflammation, infiltration with lymphoma or malignant cells, or to substantiate a
suspicion of aneurysmal subarachnoid hemorrhage in patients with negative CT
findings. A space occupying lesions should be ruled out with non-contrast head CT
prior to performing the LP.
• MRI is obtained when the cause of coma is not explained by other tests or if there is
a presumption of hyperacute ischemic stroke.
• Consultation with a specialist.