33 CONFUSION, STUPOR, AND COMA
Harrison’s Manual of Medicine
CONFUSION, STUPOR, AND COMA
Disorders of consciousness are common in medical practice. Assessment should determine whether there is a change in level of consciousness (drowsy, stuporous, comatose) and/or content of consciousness (confusion, perseveration, hallucinations). Confusion is a lack of clarity in thinking with inattentiveness; stupor, a state in which vigorous stimuli are needed to elicit a response; coma, a condition of unresponsiveness. Patients in such states are usually seriously ill, and etiologic factors must be assessed (Table 33-1).
Table 33-1 Approach to the Differential Diagnosis of Coma
Approach to the Patient
Support vital functions.
Administer glucose, thiamine, and naloxone if etiology is not clear.
Utilize history, examination, and laboratory and radiologic information to rapidly establish the cause of the disorder.
Provide the appropriate medical and surgical treatment.
The pt should be aroused, if possible, and questioned regarding use of insulin, narcotics, anticoagulants, other prescription drugs, suicidal intent, recent trauma, headache, epilepsy, significant medical problems, and preceding symptoms. Witnesses and family members should be interviewed, often by phone. History of sudden headache followed by loss of consciousness suggests intracranial hemorrhage; preceding vertigo, nausea, diplopia, ataxia, hemisensory disorder suggest basilar insufficiency; chest pain, palpitations, and faintness suggest cardiovascular cause.
Vital signs should be evaluated, and appropriate support initiated. Blood should be drawn for glucose, Na, K, Ca, BUN, ammonia, alcohol, liver transaminase levels; also screen for presence of toxins. Fever, especially with petechial rash, should suggest meningitis. Fever with dry skin suggests heat shock or intoxication with anticholinergics. Hypothermia suggests myxedema, intoxication, sepsis, exposure, or hypoglycemia. Marked hypertension occurs with increased intracranial pressure (ICP) and hypertensive encephalopathy.
Focus on establishing pt’s best level of function and uncovering signs that enable a specific diagnosis. Although confused states may occur with unilateral cerebral lesions, stupor and coma are signs of bihemispheral dysfunction or damage to midbrain-tegmentum (reticular activating system).
RESPONSIVENESS Stimuli of increasing intensity are applied to body parts to gauge the degree of unresponsiveness and any asymmetry in sensory or motor function. Motor responses may be purposeful or reflexive. Spontaneous flexion of elbows with leg extension, termed decortication, accompanies severe damage to contralateral hemisphere above midbrain. Internal rotation of the arms with extension of elbows, wrists, and legs, termed decerebration, suggests damage to diencephalon or midbrain. These postural reflexes can occur in profound encephalopathic states.
PUPILS In comatose pts, equal, round, reactive pupils exclude midbrain damage as cause and suggest a metabolic abnormality. Pinpoint pupils occur in narcotic overdose (except meperidine, which causes midsize pupils). Small pupils also occur with hydrocephalus and thalamic or pontine damage. A unilateral, enlarged, often oval, poorly reactive pupil is caused by midbrain lesions or compression of third cranial nerve, as occurs in transtentorial herniation. Bilaterally dilated, unreactive pupils indicate severe bilateral midbrain damage, anticholinergic overdose, or ocular trauma.
EYE MOVEMENTS Spontaneous and reflex eye movements should be examined for limitations of movement, involuntary movements, and misalignment of ocular axes. Intermittent horizontal divergence is common in drowsiness. Slow, to-and-fro horizontal movements suggest bihemispheric dysfunction. An adducted eye at rest with impaired ability to turn eye laterally indicates an abducens (VI) nerve palsy, common in raised ICP or pontine damage. The eye with a dilated, unreactive pupil is often abducted at rest and cannot adduct fully due to third nerve dysfunction, as occurs with transtentorial herniation. Vertical separation of ocular axes (skew deviation) occurs in pontine or cerebellar lesions. Doll’s head maneuver (oculocephalic reflex) and cold caloric– induced eye movements allow accurate diagnosis of gaze or cranial nerve palsies in pts who do not move their eyes purposefully. Doll’s head maneuver is tested by observing eye movements in response to lateral rotation of head (significant neck injury is a contraindication); loose movement of eyes with the doll’s head maneuver occurs in bihemispheric dysfunction. In comatose pts with intact brainstem function, raising head to 60° above the horizontal and irrigating external auditory canal with ice water causes tonic deviation of gaze to side of irrigated ear. In conscious pts, it causes nystagmus, vertigo, and emesis.
RESPIRATIONS Respiratory pattern may suggest site of neurologic damage. Cheyne-Stokes (periodic) breathing occurs in bihemispheric dysfunction and is common in metabolic encephalopathies. Respiratory patterns composed of gasps or other irregular breathing patterns are indicative of lower brainstem damage; such pts usually require intubation and ventilatory assistance.
OTHER Comatose pt’s best motor and sensory function should be assessed by testing reflex responses to noxious stimuli; carefully note any asymmetric responses, which suggest a focal lesion. If possible, pts with disordered consciousness should have gait examined. Ataxia may be the prominent neurologic finding in a stuporous pt with a cerebellar mass.
Lesions causing raised ICP commonly cause impaired consciousness. CT or MRI scan of the brain is often abnormal in coma but is not usually diagnostic in metabolic encephalopathy, meningitis, early infarction, early encephalitis, diffuse anoxic injury, or drug overdose. Postponing appropriate therapy in these pts while awaiting a CT or MRI scan may be deleterious. Pts with disordered consciousness due to high ICP can deteriorate rapidly; emergent CT study is necessary to confirm presence of mass effect and to guide surgical decompression. CT scan is normal in some pts with subarachnoid hemorrhage; the diagnosis then rests on clinical history combined with RBC in spinal fluid. Cerebral angiography or magnetic resonance angiography is frequently necessary to establish basilar artery insufficiency as cause of coma in pts with brainstem signs.
This results from total cessation of cerebral function and blood flow at a time when cardiopulmonary function continues but is dependent on ventilatory assistance. The pt is unresponsive to all forms of stimulation, brainstem reflexes are absent, and there is complete apnea. Demonstration of apnea requires that the PCO2 be high enough to stimulate respiration, while PO2 and bp are maintained. EEG is isoelectric at high gain. The absence of deep tendon reflexes is not required because the spinal cord may remain functional. Special care must be taken to exclude drug toxicity and hypothermia prior to making a diagnosis of brain death. Diagnosis should be made only if the state persists for some agreed upon period, usually 6–24 h.
For a more detailed discussion, see Ropper AH: Acute Confusional States and Coma, Chap. 24, p. 132, HPIM-15.