Examination of the Comatose Patient
GOAL
The goal of the history and examination of the comatose patient is to look for clues to the localization and etiology of the process causing coma.
PATHOPHYSIOLOGY OF COMA
Normal consciousness depends on the cerebral hemispheres to provide cognition and the reticular formation of the upper brainstem (from the midpons and above) to provide alertness. Coma, the absence of consciousness, can occur only due to dysfunction of both cerebral hemispheres, dysfunction of the upper brainstem, or a combination of bilateral hemisphere and upper brainstem dysfunction.
Much of the examination of the comatose patient focuses on assessing brainstem function. This is because most structural brainstem processes causing coma produce easily identified abnormalities on examination, but structural disorders of the hemispheres or diffuse metabolic disorders generally show preservation of brainstem function on examination. Therefore, if the brainstem is functioning normally, a structural brainstem process (such as a brainstem stroke or brainstem compression) is unlikely to be the cause of coma; the process causing coma would then most likely be due to structural lesions affecting both of the hemispheres or a diffuse metabolic process.
TAKING THE HISTORY OF A COMATOSE PATIENT
The history needs to be obtained from witnesses, family, or friends for any clues they may provide to the cause of the patient’s problem. If possible, try to obtain information regarding the temporal course of development of impaired consciousness, any recent systemic or neurologic symptoms, head trauma, the patient’s past medical and social history, medications, and any other potentially relevant available historical information.
HOW TO EXAMINE THE COMATOSE PATIENT
General Examination
As part of a detailed general and neurologic examination, look in the fundi for evidence of papilledema (see Fig. 11-2), which would suggest increased intracranial pressure, or retinal hemorrhages (see Fig. 11-3), which would suggest subarachnoid hemorrhage. Look for evidence for a basilar skull fracture by looking in the ear canals for blood, inspecting the mastoid areas for ecchymosis (Battle’s sign), or finding ecchymosis around the eyes (raccoon eyes). Fever suggests the possibility of meningitis, encephalitis, or sepsis. Meningismus (see Chapter 45, Examination of the Patient with Headache) is a clue to meningitis or subarachnoid hemorrhage but may be an insensitive sign in deep unconsciousness.
Assess the Level of Consciousness
Assess the patient’s level of consciousness within the continuum from drowsiness to coma by looking at the response to external stimuli, as follows:
Assess response to verbal stimuli by calling the patient’s name loudly or asking the patient to follow a simple command, such as “open your eyes,” “blink your eyes,” or “stick out your tongue.”
Assess response to visual stimuli first by opening the patient’s eyes and seeing if the patient attends to you. Test the patient’s response to visual threat by holding the patient’s eyes open and assess whether the patient blinks when you make a quick motion with your hands in front of each eye. To avoid inadvertently producing a corneal reflex from air pushed into the cornea, bring your hands in from the sides when testing visual threat.
In any potentially comatose patient, ensure that the patient does not actually have the locked-in syndrome by holding the patient’s eyes open and asking the patient to look down. Patients with the locked-in syndrome are not comatose. They are awake but quadriplegic and have paralysis of horizontal eye movements; they can communicate only by looking down or blinking on command. This syndrome occurs due to large lesions of the base of the pons, usually infarction.
Assess Resting Eye Position
Open the patient’s eyes and look at the resting position of the eyes for any tonic (persistent) deviation of the eyes to one side (called a gaze preference), as follows:
A gaze preference away from the side of a hemiparesis is consistent with a large acute cerebral hemispheric lesion. This is because the frontal eye fields (see Chapter 14, Examination of Eye Movements) of each hemisphere move the eyes to the contralateral side; therefore, a large lesion of one of the hemispheres causes the eyes to deviate toward the damaged hemisphere because of the unopposed action of the intact frontal eye field from the opposite healthy hemisphere. In other words, the eyes look to the side of an acute hemispheric lesion and away from the hemiparesis.Related posts:
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