Coma

Coma: Excerpt from Field Guide to Bedside Diagnosis

Differential Overview

❑ Alcohol intoxication

❑ Drug overdose

❑ Hypoglycemia

❑ Metabolic acidosis

❑ Subdural hematoma

❑ Hypothermia

❑ Heat stroke

❑ Meningitis

❑ Subarachnoid hemorrhage

❑ Head trauma

❑ Ischemic encephalopathy

❑ Epidural hematoma

❑ Pontine hemorrhage

❑ Cerebellar hemorrhage

❑ Psychogenic

Diagnostic Approach

Coma is a state of pathological unconsciousness, where the patient is unaware of their environment and unarousable. It is caused by dysfunction of either the reticular activating system above the level of the mid-pons or both cerebral hemispheres. It should be distinguished from brain death due to cessation of cerebral and cerebellar function, marked by absense of response to stimuli, respiratory drive, and central reflexes (although spinal reflexes may be preserved), and from persistent vegetative state, characterized by diurnal wakefulness but with unawareness and inability to interact with others.

Pupils: Pupillary responses are more sensitive than papilledema in detecting increased intracranial pressure. Normal pupils imply an intact midbrain and CNIII. Preserved pupillary light reflex with other signs of brainstem impairment suggests a toxic/metabolic cause. Asymmetric reactivity is consistent with an acute structural process. A unilaterally dilated pupil suggests ipsilateral uncal herniation. Hypothermia, barbiturates, and midbrain lesions produce midposition unreactive pupils. Pinpoint pupils occur with pontine lesions and opiates. Bilateral dilated unresponsive pupils occur with anoxia, severe midbrain damage caused by transtentorial herni-ation, or anticholinergic drugs. Large pupils that dilate and contract automatically (hippus) but do not react to light suggest a tectal lesion.

Eye deviation: Injection of ice water into the ear (calorics) normally causes deviation of both eyes toward the stimulated ear. Its absence implies dysfunction of the pons or medulla. Cortical mass lesions produce ipsilateral conjugate deviation that can be overcome with calorics. Brainstem and pontine lesions produce contralateral deviation that cannot be overcome with calorics. In metabolic coma or drug overdose coma, eyes move loosely side-to-side opposite the turning of the head. A pontine or cerebellar lesion causes skew deviation (separation of horizontal axes). Ocular bobbing (briskly down, slowly up) is a result of bilateral pontine lesions. Ocular dipping (slow arrhythmic downstroke, followed by a faster upstroke) with normal calorics is consistent with anoxic encephalopathy.

Posturing: Decorticate posturing (arm flexion and leg extension) is found with hemispheric lesions or metabolic derangement. Decerebrate posturing (extension of the legs and arms) implies dysfunction of the midbrain or upper pons on a structural or metabolic basis. In response to noxious stimuli, flexion, extension, and adduction reflexes are found. Shoulder and hip abduction involve cortical activity whereas withdrawal implies voluntary behavior.

Respiratory pattern: If the patient is yawning or swallowing, coma is not very deep and brainstem function is intact. Cheyne-Stokes respiration (crescendo-decrescendo pattern with apneic pauses) is seen with herniation, metabolic encephalopathy, and congestive heart failure. Central neurogenic hyperventilation (rapid deep breathing) indicates damage to the brainstem between the midbrain and pons. Ataxic respiration occurs with midbrain lesions. Apneustic respiration with inspiratory pauses occurs with pontine lesions and precedes respiratory arrest.

Asymmetric resting muscle tone, deep tendon reflexes, or Babinski response suggests a structural lesion. A toxic/metabolic cause is suggested by preceding confusion, disorientation, and somnolence. Myoclonic jerks or clonus provide further support.

The Glasgow Coma Scale is scored as follows: Best Motor Response: 6 obeys commands, 5 localizes pain, 4 withdraws to pain, 3 decorticate (flexion), 2 decerebrate (extension), 1 none. Best Verbal Response: 5 oriented, 4 confused conversational, 3 inappropriate words, 2 incomprehensible sounds, 1 none. Eye Opening: 4 spontaneous, 3 to speech, 2 to pain, 1 none.

Clinical Findings

Alcohol intoxication  The odor of alcohol will be apparent on the breath. Be wary when diagnosing the intoxicated patient. There may be another (obscured) cause of coma such as head trauma.

Drug overdose  Narcotic overdose produces pinpoint pupils and hypoventilation. Response to naloxone is rapid and diagnostic. Barbiturate overdose will produce absent doll’s eyes and corneal reflexes, but the pupillary light response will be preserved.

Hypoglycemia  The patient is taking insulin or oral hypoglycemics and responds readily to an injection of 50% dextrose.

Metabolic acidosis  The underlying disease process is usually evident (sepsis, uremia, diabetic ketoacidosis, shock). A clue is hyperventilation with Kussmaul breathing. With diabetic ketoacidosis, there will be a fruity, sweet, acetone odor to the breath.

Subdural hematoma  There will usually be a history of head trauma, headache, and a fluctuating level of consciousness.

Hypothermia  Suspect with environmental exposure and a patient who is cold to the touch. Determination of the core temperature with a special thermometer is essential.

Heat stroke  Consider this in the presence of fever without perspiration.

Meningitis  Subacute onset of prominent headache, fever, and nuchal rigidity with Kernig and Brudzinski signs precede the coma.

Subarachnoid hemorrhage  A severe headache of instantaneous onset followed by meningeal signs, pupillary asymmetry, strabismus (third or sixth nerve palsy), and extensor posturing is the typical evolution.

Head trauma  Suspect with mastoid ecchymoses, subconjunctival hemorrhage, raccoon eyes, or hemotympanum. Clear rhinorrhea suggests basilar skull fracture. The most common cause of coma in the setting of head trauma is subdural hematoma, with gradually evolving cortical signs. Preceding headache in the setting of a head injury (however minor), especially with asymmetric motor or sensory findings suggests supratentorial bleeding. Occipital headache—especially with vertigo, ataxia, diplopia, and vomiting—suggests subtentorial bleeding.

Ischemic encephalopathy  This usually occurs after an episode of profound hypotension (cardiopulmonary arrest) or anoxia (near drowning) and is characterized by repetitive multifocal myoclonic jerks. Hypoxia, as in COPD, is accompanied by central cyanosis. Carbon monoxide poisoning produces a flushed (“cherry red”) face.

Epidural hematoma  Suspect this when there is a history of head trauma, especially a temporal blow/fracture. A gradual middle meningeal bleed produces the classic signs of initial concussion with confusion, followed by a lucid interval, then deepening coma. A unilateral “blown” (fixed and dilated) pupil is an early sign of uncal herniation. Cheyne-Stokes repiration (crescendo-decrescendo pattern with apneic pauses) implies bilateral hemisphere dysfunction with an intact brainstem and may be the first sign of transtentorial herniation.

Pontine hemorrhage  Absent corneal reflexes and doll’s eyes are present, with pinpoint pupils that react to strong light on observation with a magnifying glass. The breathing pattern is apneustic (prolonged inspiratory cramp followed by an expiratory pause).

Cerebellar hemorrhage  Occipital headache, vomiting, gaze paresis, and vertigo with inability to stand is followed by coma.

Psychogenic  There is usually a prior psychiatric history. Pupils are responsive and calorics produce nystagmus. The patient is flaccid or has an avoidance response.

Pictures

Book Source Details

• Book Title: Field Guide to Bedside Diagnosis
• Author(s): David S. Smith
• Year of Publication: 2007
• Copyright Details: Field Guide to Bedside Diagnosis, Copyright © 2007 Lippincott Williams & Wilkins.

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More About This Book: Title: Field Guide to Bedside Diagnosis Authors: David S. Smith Publisher: Lippincott Williams & Wilkins Copyright: 2007 ISBN: 0-78178-165-5

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