ENLS Version 4.

0
Approach to the Patient with Coma
Content: Aarti Sarwal, MD; Sara Stern-Nezer, MD, MPH; Deborah S. Tran
DNP, RN, CNRN, SCRN, NE-BC
Slides: George A. Lopez, MD PhD
 Presenter:
Your name
Your institution

Conflicts:
No conflicts
 Editors’ Note: Global Considerations
The intent of the editors, authors, and reviewers of this ENLS topic was not to
address all the variations in international practice for the different diseases. We
have discussed major practice variances (e.g., the availability of diagnostic
testing, or the type of medications used) and encourage learners to use the
ENLS algorithms as a framework on which any relevant local practice
guidelines can be incorporated.
 The Comatose Patient
Learning Objectives
• Perform a neurological exam in a comatose
patient
• Assess airway and need for assisted
ventilation
• Establish a diagnosis for the cause of coma
• Treat presumptively for the most likely
cause of coma if indicated
 What is coma?

Arousal: wakefulness, eye opening

Awareness: able to follow commands, content

processing
Checklist for the 1st hour
☐ Evaluate/treat circulation, airway, breathing and cervical-spine

☐ Exclude/treat hypoglycemia or opioid/benzodiazepine overdose

☐ Serum chemistries, ABG, urine toxicology screen

☐ Emergent cranial CT (and CT-angio brain if appropriate) to

determine if coma etiology is structural or vascular in etiology
Approach to the Patient with Coma
• Assess level of consciousness
• Airway
• Breathing
• Circulation
• Cervical-spine immobilization
• IV/IO access
Prehospital Checklist and Handoff
• Airway, breathing, ventilation issues
• GCS, pupils, and vital signs on presentation
• IV or IO access, site and patency (IV)
• Ruled out hypoglycemia
• History from bystanders, witnesses, contextual or
environmental observations (pill bottles, signs of trauma or
seizure activity)
• Medications administered, dose and response (naloxone,
dextrose etc.)
• Time when patient was last seen normal
• Prodromal symptoms when last seen
Approach to the Patient with Coma

• Level of responsiveness
• Assess for brainstem reflexes
• Evaluation of motor responses,
tone and reflexes
• Note any asymmetry in the exam
• Appraisal of breathing patterns
 Level of Responsiveness
• Glasgow Coma Scale (GCS)
▪ Eye response (4 points)
▪ Verbal response (5 points)
▪ Motor response (6 points)
• Full Outline of UnResponsiveness Scale (FOUR)
▪ Eye opening
▪ Motor response
▪ Brainstem response
▪ Respiratory response
 Brainstem Assessment
• Pupillary response
▪ Pinpoint: raises concern of pontine damage
▪ Large, unreactive: midbrain damage, 3rd nerve compression
• Corneal reflex
• Visual threat response
• Eye movements
▪ Spontaneous
▪ Oculocephalic Reflex (Doll’s Eyes)
▪ Vestibulo-ocular Reflex (cold caloric testing)
• Cough reflex, gag reflex
 Pupillary Responses
Pupillary change Possible etiologies/localization
Pinpoint pupil Opioids
Cholinergic intoxication
Pontine damage (interrupts descending sympathetic pathways)
Dilated, non-reactive pupils Cerebral anoxia, global
Barbiturates
Atropine
Hypothermia
Brain death
Dilated, reactive pupils Pretectal lesions
Stimulants (cocaine, methamphetamine), hallucinogens including
PCP/LSD
Anisocoria (pupillary 3rd nerve compression from uncal herniation
asymmetry) Localized drug effect (e.g. ipratropium, tropicamide)
Mid-position, fixed or irregular Midbrain lesion
 Motor Function
• Spontaneous movement or to noxious stimuli
• Posturing in structural & metabolic coma
▪ Flexor (decorticate)
▪ Extensor (decerebrate)
• Muscle tone
• Reflexes
• Distinguish between purposeful and reflex
activity
 Breathing Pattern
• Breathing patterns may help localize
• Neurogenic hyperventilation
▪ Midbrain and pons
• Cluster breathing
▪ Pons
• Ataxic breathing
▪ Medulla
Respiratory pattern Pattern
Cheyne-Stokes
Central neurogenic
hyperventilation
Localization
Global/metabolic encephalopathy
Impaired forebrain or diencephalon
Metabolic encephalopathy
High brainstem tumors (rare)

Apneusis Bilateral pontine lesions

Cluster
breathing/ataxic Pontomedullary junction lesions
breathing
Lesions affecting ventrolateral medulla bilaterally
Apnea
(ventral respiratory group)
Approach to the Patient with Coma
• D50 (Dextrose 50%) IV if
glucose < 70 mg/dL
• Thiamine 100 mg IV before
dextrose, in at risk patients
• Administer naloxone if opiate
overdose is concern
▪ IV, IM, IO, Sub-Q, ETT, Nasal
Approach to the Patient with Coma

• Head CT to assess for

structural etiologies
• Consider CTA for possible
vascular cause
▪ Basilar thrombosis
Approach to the Patient with Coma

• Historical account
• Comorbidities
• Medications
• Exposures
Focused Presenting History and Past
Medical History
Valuable clues to the etiology of coma:
• Time course of unconsciousness
▪ Abrupt
▪ Gradual
• PMH, PSH
• Social history
Case: Unresponsive Patient

 60-year-old male
 Unresponsive to voice
 Found in hotel room by
housekeeper
 Last known well night before
 Brought to the ED by EMS
Case: Unresponsive Patient
• Vitals:
▪ Hypothermic, T 34ºC
▪ HR 60 bpm
▪ BP 185/95 mmHg
▪ RR 10 /min
▪ SpO2 92%
• GCS 3 (E1, V1, M1)
 Case : Unresponsive Patient
What is the next step?

A. Treat the elevated BP with nicardipine drip

B. Assess ABCs
C. STAT head CT
D. Apply warming blankets to treat hypothermia
 Case : Unresponsive Patient
What is the next step?

A. Treat the elevated BP with nicardipine drip

B. Assess ABCs
C. STAT head CT
D. Apply warming blankets to treat hypothermia
Case: Neurological Assessment

• Eyes closed, gaze disconjugate, OCR

present
• Pupils are symmetric, reactive and
enlarged
• No response to pain, motor tone
diminished, no DTRs
• Wife is contacted over the phone
 Case
• ABCs assessed
• Patient was intubated with concern for
unknown cervical spine stability and
possible elevated ICP
• Labs sent
 Case
PMH MEDS
Coronary Artery Dz Aspirin
DVT Apixaban
DM Type 2 Metformin
Amitriptyline at night
Depression
Desvenlafaxine daily

Pharmacy contacted for possible emergent need of

PCC as patient on apixaban
Recommended STAT Labs
LABS
☐ Bedside blood glucose, if not done
☐ Serum chemistries
☐ Arterial blood gas
☐ CBC
☐ Toxicology studies:
☐ETOH
☐Urine toxicology screen
☐ Microbiology studies
☐ Consider co-oximetry
Initial Formulation
 Causes of Coma
Neurologic Causes Toxic Metabolic Causes
Trauma (severe) Drug overdose
Neurovascular (stroke) Metabolic
endocrine
electrolyte
hepatic, renal
hypercapnia, hypoxia
CNS infection (encephalitis) Environmental toxins
Neoplasm (primary, metastasis)
Seizure/status epilepticus
Neuroinflammatory
Autoimmune encephalitis, ADEM
Other: PRES, HIE
 Back to the Case

Structural insult? (Stroke/hemorrhage)

Metabolic
• Hx CAD • Hx DM
• Rapid onset • Hx depression
• Abnormal pupils Medication overdose?
• Motor exam & reflexes versus • Opioids
 Case

What is the next step?

A. Brain MRI
B. Naloxone 0.4 mg IV, then head CT
C. Hyperventilate patient
D. Head CT
 Case

What is the next step?

A. Brain MRI
B. Naloxone 0.4 mg IV, then head CT
C. Hyperventilate patient
D. Head CT
Brain Imaging

Unclear cause or focal exam

• Non-contrast head CT STAT
• CT angiography (CTA) and CT
perfusion (CTP)
▪ Concern for ischemic stroke
• CT with contrast
▪ Concern for CNS infection
 Case Conclusion

• CT head with diffuse intraventricular hemorrhage and

hydrocephalus
• Pharmacy notified for urgent need and dosing of PCC
• Neurosurgery consulted for emergent EVD
• Patient hyperventilated until EVD placed
• Mannitol infused
Persistent Uncertainty?

Additional testing
• MRI
• Lumbar Puncture
• Continuous EEG
 Pediatric Considerations
• ABCs as in adults
• Children < 5 yrs modified GCS
• TBI and infection leading causes of coma
• Septic shock is common presentation of meningitis in
children
• Other causes: hypoglycemia, diabetes, hypothermia,
acid-base and electrolyte imbalances, seizures,
intoxications
• STAT neuroimaging if exam focal or unclear etiology
 Clinical Pearls
• Key findings on the neurological examination of comatose patients can
identify changes to suggest toxic syndromes that can lead to the rapid
treatment of coma.
• Suspect basilar thrombosis in comatose patients with the degree of
coma out of proportion to imaging findings or metabolic
derangements/intoxication; early identification and revascularization is
key to improve outcome.
• Elevated ICP can be seen in a variety of processes and cannot be
excluded by imaging alone.
Communication
☐ Clinical presentation
☐ Relevant past medical/surgical history
☐ Findings on neurological examination
☐ Relevant labs
☐ Brain imaging, LP, or EEG results if available
☐ Treatments administered so far
Questions?