COMA
Joana Marie E. Gantuangco
Harrison's 20th Edition
Drowsy Stupor Coma
•Light sleep •Can be transiently •Deep sleeplike
•Easy arousal awakened by state
•Persistence of vigorous stimuli •Cannot be aroused
alertness for brief •With motor
periods behavior:
•With confusion withdrawal
•With confusion
Minimally
Vegatative State
Conscious State
•Rudimentary vocal or motor •Awake-appearing; eyelids
behaviors (often may open periodically
spontaneous but some in •Non-responsive
response to touch, visual or •Respiratory and autonomic
command) functions retained
(coughing, swallowing, limb
and head movements)
•With signs of extensive
damage
(decorticate/decerebrate,
absent visual responses)
•Often emerging from coma
Most common causes:
1. Cardiac arrest with cerebral hypoperfusion
2. Head trauma
Syndromes affecting alertness
■ Akinetic mutism
– Partially/fully awake
– Able to form impressions and think
– Remains virtually immobile and mute
– Causes: damage to MTN or frontal lobes (deep or surface)
extreme hydrocephalus
Syndromes affecting alertness
■ Abulia
– Milder form
– Mental and physical slowness
– Diminished ability to initiate activity
– Cause: damage to medial frontal lobes and connections
Syndromes affecting alertness
■ Catatonia
– Hypomobile and mute syndrome
– Part of a major psychosis (schizophrenia or major depression)
– Few voluntary or responsive movements (blink, swallow, may not
appear distressed)
– Responsive signs: eyelid elevation actively resisted, blinking in
response to visual threat, eye movement with head rotation)
– Limbs retain posture in which they have been placed (waxy
flexibility or catalepsy)
– Similar to akinetic mutism but NO evidence of cerebral damage
such as hyperreflexia
Syndromes affecting alertness
■ Locked-in State
– Pseudocoma
– Awake patient has no means of producing speech or
movement
– Retains voluntary vertical eye movement and lid elevation
– Cause: basilar artery thrombosis, hemorrhage to ventral pons
■ Awake, de-efferented states
– Guillain-Barre syndromw
– Critical illness neuropathy
– Pharmacologic neuromuscular blockade
Anatomy and Physiology of Coma
■ Widespread ■ Reduced activity
abnormalities of RAS in the
of cerebral brainstem
hemispheres
Coma due to Cerebral Mass Lesions
and Herniation Syndromes
Coma due to Cerebral Mass Lesions
and Herniation Syndromes
Coma due to Cerebral Mass Lesions
and Herniation Syndromes
3-5mm 6-8mm >9mm
drowsiness stupor coma
Coma due to Metabolic Disorders and
Toxins
■ Interrupting deliver of energy substrates (O2, glucose)
■ Altering neuronal excitability (drugs, alcohol, anesthesia)
Coma due to Metabolic Disorders
■ O2 consumption: 3.5ml/100g/min
75ml/100g/min ■ Glucose utilization: 5mg/100g/min
30ml/100g/min
■ Glucose stores 2mins
■ O2 stores last 8-10s
Hepatic Encephalopathy
Ammonia Ammonia Glutamine
Ammonia Glutamine
Ammonia
Glutamine
Coma ROS RNS
GABA GABA
ROS
RNS
Uremic Encephalopathy
■ Contributors:
– ↑ creatinine, guanidine, brain calcium, inflammation
– ↓ catecholamines
– altered glutamate and GABA, disruption of BBB
– Frequent coexisting vascular disease
■ Urea does NOT cause CNS toxicity
Coma due to Metabolic Disorders
■ Sodium
– <125mmol/L confusion
– <119mmol/L coma and convulsions
■ Osmolarity
– >350mosmol/L coma
■ CO2
– ↑ CO2 ↓ level of consciousness
Coma due to Drugs and Toxins
■ Reversible
■ Leave no residual damage provided there has not been
cardiorespiratory failure
■ Signs of overdose of atropinic medications:
– Dilated puils
– Tachycardia
– Dry skin
■ Signs of overdose of opiates:
– Pinpoint pupils <1mm
Epileptic Coma
Exhaustion of
reserves, Coma (self-
Seizure limited; post-
Locally toxic ictal state)
molecules
Come due to Widespread Damage to
Cerebral Hemispheres
■ Extensive bilateral structural damage
■ E.g. Hypoxic-ischemic
■ May also be from disorders that occlude widespread small blood
vessels
– Cerebral malaria
– TTP
– Hyperviscosity
■ May be from diffuse white matter damage from trauma or
inflammatory demyelinating disease
Approach to the Patient
■ ABC
■ Vitals, nuchal rigidity, funduscopy
■ Neurologic exam assess severity and nature of coma
■ Complete medical exam
Approach: History
■ Circumstances and rapidity with which neuro symptoms
developed
■ Antecedent symptoms (confusion, weakness, headache,
fever, seizures, dizziness, double vision, vomiting)
■ Use of medication drugs, or alcohol
■ Chronic liver, kidney, lung, heart, or other disease
Approach: General PE
■ Fever: infection, bacterial meningitis, encephalitis, heat stroke, malignant
hyperthermia, anticholinergic drug intoxication; “central fever” last to consider
■ Hypothermia: alcohol, barbiturate, sedative, phenothiazine intoxication,
hypoglycemia, peripheral circulatory failure, extreme hypothyroidism; itself causes
coma if <31C
■ Tachypnea: acidosis, pneumonia
■ Hypertension: hypertensive enceph, stroke, head injury
■ Hypotension: alcohol, barbiturate, internal hemorrhage, MI, sepsis
■ Funduscopy: papilledema, SAH, hypertensive enceph
■ Cutaneous petechiae: TTP, meningococcemia, bleeding diathesis
■ Cyanosis/Anemia: carbon monoxide, or others
Approach: Neuro PE
■ Multifocal myoclonus metabolic disorder, particularly uremia,
anoxia, drugs
■ Bilateral asterixis metabolic enceph, or drugs
Bilateral Bilateral
damage damage CAUDAL
ROSTRAL to to midbrain
midbrain
Approach: Neuro PE
■ Brainstem reflexes
– Pupillary size and reaction to light
• Reactive and small (1-2.5mm): metabolic enceph, hydroceph, thalamic hemorrhage
• Pinpoint (<1mm): narcotic/barbiturate overdose, extensive pontine hemorrhage
– Spontaneous and elicited eye movements
• Horizontal divergence at rest is normal in drowsiness
• ”Eyes look toward a hemispheral lesion and away from a brainstem lesion”
• Ocular bobbing; ocular dipping
• Doll’s eyes: reduced cortical influence on brainstem, intact brainstem pathways
• COWS
– Corneal responses
– Respiratory pattern
• Cheyne-Stokes: bilateral damage or metabolic suppression
• Kussmaul: metabolic acidosis
• Agonal gasps: medullary damage; terminal respiratory pattern
Laboratories and Imaging
■ Ethanol levels in non-habituated patients
– 0.2 g/dl impair mental activity
– 0.3 g/dl stupor
■ Herpesvirus enceph or prion disease EEG
– Delta/triphasic waves: metabolic coma (hepatic failure)
– Widespread fast B activity: sedative drugs
– Alpha coma: pontine or diffuse cortical damage; poor prognosis
Brain Death
■ Irreversible cessation of all cerebral and brainstem function
■ With preservation of cardiac activity and respiratory and somatic function by
artificial means
■ Criteria:
– No confounding factors are present
– Widespread cortical destruction reflected by deep coma and unresponsiveness
– Global brainstem damage
■ Delay clinical testing for at least 24h if cardiac arrest caused brain death (or
unknown)
Treatment
■ Immediate goal: prevent further CNS damage
■ Ischemic stroke: IV TPA
■ Anticholinergic overdose: physostigmine
■ Ethylene glycol ingestion: fomepizole
