Babak Tamizi Far MD. Assistant professor of internal medicine Al-zahra hospital, Isfahan university of medical sciences

Babak Tamizi Far MD. Assistant professor of internal medicine Al-zahra hospital, Isfahan university of medical sciences

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Level of consciousness is depressed Stuporous patients respond only to repeated vigorous stimuli Comatose patients are unarousable and unresponsive

Coma is a major complication of serious CNS disorders Coma can result from seizures, hypothermia, metabolic disturbances, or structural lesions causing bilateral cerebral hemispheric dysfunction or a disturbance of the brainstem reticular activating system A mass lesion involving one cerebral hemisphere may cause coma by compressing the brainstem ۵

Abrupt onset of coma suggests Subarachnoid hemorrhage Brainstem stroke Intracerebral hemorrhage A slower onset and progression of coma occur with other structural or mass lesions A metabolic cause is likely with a preceding intoxicated state or agitated delirium ۶

In stupor, response to painful stimuli Purposive limb withdrawal from painful stimuli implies that sensory pathways from and motor pathways to the stimulated limb are functionally intact Unilateral absence of responses to stimuli to both sides of the body implies A corticospinal lesion Bilateral absence of responses suggests brainstem involvement Bilateral pyramidal tract lesions Psychogenic unresponsiveness ٧

Decorticate posturing occurs With lesions of the internal capsule and rostral cerebral peduncle With dysfunction or destruction of the midbrain and rostral pons In the arms accompanied by flaccidity or slight flexor responses in the legs in patients with extensive brainstem damage extending down to the pons at the trigeminal level ٨

Hypothalamic disease processes may lead to unilateral Horner syndrome Bilateral diencephalic involvement or destructive pontine lesions leads to small but reactive pupils Ipsilateral pupillary dilation with no response to light occurs with compression of the third cranial nerve, eg, with uncal herniation Pupils are slightly smaller than normal but responsive to light in many metabolic encephalopathies Pupils may be fixed and dilated following overdosage with atropine, scopolamine, or glutethimide Pupils may be pinpoint (but responsive) with opioids Pupillary dilation for several hours after cardiopulmonary arrest implies a poor prognosis ٩

Conjugate deviation to the side suggests the presence of an ipsilateral hemispheric lesion or a contralateral pontine lesion A mesencephalic lesion leads to downward conjugate deviation Dysconjugate ocular deviation in coma implies a structural brainstem lesion (or preexisting strabismus) ١٠

In response to brisk rotation, flexion, and extension of the head, conscious patients with open eyes do not exhibit contraversive conjugate eye deviation (doll's-head eye response) unless there is voluntary visual fixation or bilateral frontal pathology With cortical depression in lightly comatose patients, a brisk doll's-head eye response is seen With brainstem lesions, this oculocephalic reflex becomes impaired or lost, depending on the lesion site ١١

Tested by caloric stimulation using irrigation with ice water In normal persons, jerk nystagmus is elicited for about 2 or 3 minutes, with the slow component toward the irrigated ear In unconscious patients with an intact brainstem, the fast component of the nystagmus disappears, so that the eyes tonically deviate toward the irrigated side for 2 3 minutes before returning to their original position With impairment of brainstem function, the response is perverted and disappears In metabolic coma, oculocephalic and oculovestibular reflex responses are preserved, at least initially ١٢

Cheyne-Stokes respiration may occur with bihemispheric or diencephalic disease or in metabolic disorders Hyperventilation occurs with lesions of the brainstem tegmentum Apneustic breathing (prominent end-inspiratory pauses) suggests damage at the pontine level Atactic breathing (completely irregular pattern, with deep and shallow breaths occurring randomly): associated with lesions of the lower pons (pontine tegmentum) and medulla ١٣

Brain death Persistent vegetative state Locked-in syndrome ١۴

Serum glucose, electrolyte, and calcium levels Arterial blood gases Liver and kidney function tests Toxicologic studies ١۵

CT scan to identify a structural lesion ١۶

The diagnostic workup of the comatose patient must proceed concomitantly with management Lumbar puncture (if CT scan reveals no structural lesion) to exclude subarachnoid hemorrhage or meningitis ١٧

Dextrose 50% (25 g), naloxone (0.4 1.2 mg), thiamine (50 mg) are given intravenously ١٨

Treatment of coma depends on underlying cause Emergency measures Supportive therapy for respiration or blood pressure is initiated In hypothermia, all vital signs may be absent; all such patients should be rewarmed before the prognosis is assessed The patient is positioned on one side with the neck partly extended, dentures removed, and secretions cleared by suction If necessary, the patency of the airways is maintained with an oropharyngeal airway ١٩

WHEN TO REFER All patients WHEN TO ADMIT All patients to an ICU ٢٠

In coma because of cerebral ischemia and hypoxia, the absence of pupillary light reflexes at the time of initial examination implies little chance of regaining independence By contrast, preserved pupillary light responses, the development of spontaneous eye movements (roving, conjugate, or better), and extensor, flexor, or withdrawal responses to pain at this early stage imply a relatively good prognosis ٢١

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MENINGEAL CAUSES Subarachnoid hemorrhage (uncommon) Bacterial meningitis Encephalitis Subdural empyema ٢۴

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