Coma Flashcards

1
Q

Quais os dados mais importantes da história de um doente em coma?

A

In many cases, the cause of coma is immediately evident (e.g., trauma, cardiac arrest, or reported drug ingestion). In the remainder, certain points are especially useful: (1) the circumstances and rapidity with which neurologic symptoms developed; (2) the antecedent symptoms (confusion, weakness, headache, fever, seizures, dizziness, double vision, or vomiting); (3) the use of medications, illicit drugs, or alcohol; and (4) chronic liver, kidney, lung, heart, or other medical disease. Direct interrogation of family, observers, and ambulance technicians on the scene, in person or by telephone, is an important part of the evaluation.

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2
Q

Como fazer o exame neurológico do tronco no doente em coma? (Diferenciar metabólico de estrutural)

A

(1) Reactive and round pupils of midsize (2.5–5 mm) essentially exclude midbrain damage, either primary or secondary to compression
(2) The eyes are first observed by elevating the lids and noting the resting position and spontaneous movements of the globes
(3) The oculocephalic reflexes, elicited by moving the head from side to side or vertically and observing eye movements in the direction opposite to the head movement, depend on the integrity of the ocular motor nuclei and their interconnecting tracts that extend from the midbrain to the pons and medulla (Fig. 17-3). The movements, called somewhat inappropriately “doll’s eyes” (which refers more accurately to the reflex elevation of the eyelids with flexion of the neck), are normally suppressed in the awake patient. The ability to elicit them therefore indicates both reduced cortical influence on the brainstem and intact brainstem pathways, indicating that coma is caused by a lesion or dysfunction in the cerebral hemispheres. The opposite, an absence of reflex eye movements, usually signifies damage within the brainstem but can result infrequently from overdoses of certain drugs. Normal pupillary size and light reaction distinguishes most drug-induced comas from structural brainstem damage.
(4) Thermal, or “caloric,” stimulation of the vestibular apparatus (oculovestibular response) provides a more intense stimulus for the oculocephalic reflex but provides essentially the same information. The test is performed by irrigating the external auditory canal with cool water in order to induce convection currents in the labyrinths. After a brief latency, the result is tonic deviation of both eyes to the side of cool-water irrigation and nystagmus in the opposite direction. The presence of corrective nystagmus indicates that the frontal lobes are functioning and connected to the brainstem; thus functional or hysterical coma is likely
(5) By touching the cornea with a wisp of cotton, a response consisting of brief bilateral lid closure is normally observed. The corneal reflex depends on the integrity of pontine pathways between the fifth (afferent) and both seventh (efferent) cranial nerves; in conjunction with reflex eye movements, it is a useful test of pontine function. he corneal (and pharyngeal) response may be lost for a time on the side of an acute hemiplegia.

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3
Q

Como são as síndromes das doenças cerebrovasculares que causam coma?

A

When cerebrovascular disease is the cause of coma, diagnosis can be difficult (Chap. 27). The most common diseases are (1) basal ganglia and thalamic hemorrhage (acute but not instantaneous onset, vomiting, headache, hemiplegia, and characteristic eye signs); (2) pontine hemorrhage (sudden onset, pinpoint pupils, loss of reflex eye movements and corneal responses, ocular bobbing, posturing, hyperventilation, and excessive sweating); (3) cerebellar hemorrhage (occipital headache, vomiting, gaze paresis, and inability to stand); (4) basilar artery thrombosis (neurologic prodrome or warning spells, diplopia, dysarthria, vomiting, eye movement and corneal response abnormalities, and asymmetric limb paresis); and (5) subarachnoid hemorrhage (precipitous coma after headache and vomiting). The most common stroke, infarction in the territory of the middle cerebral artery, does not generally cause coma, but edema surrounding large infarctions may expand during the first few days and act as a mass.

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4
Q

Quais as etapas fundamentais da morte encefálica?

A

They contain three essential elements: (1) widespread cortical destruction that is reflected by deep coma and unresponsiveness to all forms of stimulation; (2) global brainstem damage demonstrated by absent pupillary light reaction and by the loss of oculovestibular and corneal reflexes; and (3) destruction of the medulla, manifested by complete apnea.

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5
Q

Como posso prever o prognóstico de um coma?

A

(1) Metabolic comas have a far better prognosis than traumatic ones.
(2) In an attempt to collect prognostic information from large numbers of patients with head injury, the Glasgow Coma Scale was devised; empirically, it has predictive value in cases of brain trauma.
(3) For anoxic and metabolic coma, clinical signs such as the pupillary and motor responses after 1 day, 3 days, and 1 week have been shown to have predictive value .

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6
Q

Quais os mecanismos do coma?

A

(1) lesions that damage the RAS in the upper midbrain or its projections; (2) destruction of large portions of both cerebral hemispheres; and (3) suppression of reticulocerebral function by drugs, toxins, or metabolic derangements such as hypoglycemia, anoxia, uremia, and hepatic failure.

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