Diagnostic Tests for Persistent Vegetative State
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COMA:
DIAGNOSTIC WORKUP
(Algorithmic Diagnosis of Symptoms and Signs)
When one encounters a patient with coma, the first thing to do is to establish an airway. Next, the blood pressure is taken. If there are any signs of shock, an intravenous access is established, and the shock is treated appropriately. A cardiology and surgical consult are obtained. Blood should then be drawn for a CBC, type and cross-match, sedimentation rate, chemistry panel, electrolytes, blood ammonia level, and blood alcohol levels. Before removing the syringe, 50 cc of 50% dextrose is given unless the patient is suspected of having hyperosmolar nonketotic diabetic coma. A urinalysis and urine drug screen must be done also. Arterial blood gas analysis should be done. If the situation is urgent or emergent, a CT scan is done before the results of the laboratory tests are available. If the laboratory tests are inconclusive, a CT scan must be done anyway.
If all of the above studies are negative, a spinal tap is done for cell count, protein, glucose, VDRL test, smear, and culture and sensitivity. This is especially true when there is fever or nuchal rigidity.
If the diagnosis is still in doubt, blood tests for other toxic materials, such as the lead level, and blood cultures and EEG are done. A neurologist or neurosurgeon is usually consulted as soon as one is available.
» READ BOOK EXCERPT ONLINE »
Source: Algorithmic Diagnosis of Symptoms and Signs, 2003
Coma:
Physical examination
(The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter)
A. General examination. A thorough general examination, including vital signs, helps to establish and rule out potential causes of coma. Look for evidence of head trauma or metabolic encephalopathy.
B. Neurologic examination. A detailed neurologic examination, including mental status; motor, sensory, reflex coordination; gait; and cranial nerve testing, will help distinguish the location and degree of dysfunction. Look for the following important features:
1. Level of consciousness. Is the patient responsive at all? To what degree?
2. Brainstem function
a. Pupils: assess cranial nerves (CN) 2 and 3 for anisocoria, miosis, pinpoint, mydriasis, or fixed, midposition pupils.
b. Eye movements: assess conjugate gaze, gaze deviation, nystagmus, and spontaneous movements (CN 3, 4, and 6).
c. Funduscopic examination: assess for papilledema and underlying diseases. Corneal reflexes (CN 5 and 7); gag and cough reflexes (CN 9 and 10).
3. Breathing patterns. Cheyne-Stokes respiration suggests cerebral hemispheric or diencephalic injury or an encephalopathy (hypoxic or metabolic). Central hyperventilation suggests brainstem injury. Ataxic or Biot’s respiration, which can progress to apnea, suggests injury to the reticular formation in the medulla and pons.
4. Sensorimotor activity. Are there spontaneous, volitional movements? Is there other motor activity such as choreoathetosis, decerebrate or decorticate activity, myoclonus, asterixis, or seizure activity? Is the muscle tone flaccid, rigid, spastic, or clonic? Is the response to painful stimuli purposeful, flexion withdraw, abnormal posturing, or no response at all?
5. Tendon reflexes. Are the reflexes asymmetric, increased, or decreased?
6. Glasgow Coma scale. Measures the depth and duration of altered consciousness based on the best response to three actions: eye opening, verbal response, and motor response to commands or painful stimulus.
Testing
A. Clinical laboratory tests. Complete chemistry profile (including electrolytes, glucose, calcium, magnesium, creatinine, blood urea nitrogen), complete blood count, coagulation panel, arterial blood gas, toxicology screen (blood, urine, gastric contents), thyroid function tests, cortisol level, and select cultures (blood, urine, throat, rectal, spinal fluid). Consider performing lumbar puncture after obtaining a computed tomography (CT) scan.
B. Diagnostic imaging. Cerebral CT findings reliably suggest intracranial hemorrhage, cerebral edema, mass lesions, focal infection, or hydrocephalus as diagnoses. Magnetic resonance imaging is preferred for the detection of abscess, tumor, subdural empyema, inflammatory lesions, or demyelinating diseases.
C. Other testing. Electroencephalography rules out seizures, status epilepticus (SE), and nonconvulsive SE. Lumbar puncture, typically after diagnostic imaging, may help determine increased intracranial pressure as well as infectious causes. Evoked potentials, such as brainstem auditory or short-latency somatosensory, provide information about the physiologic state and response to therapy (4).
Diagnostic assessment.
The prognosis in comatose patients is typically poor except for those that are drug-related or result from traumas. In general, the longer the coma lasts, the poorer the prognosis. Coma rarely lasts longer than 4 weeks, after which, transition into a vegetative state or recovery occurs (3).
References
1. Plum F, Posner JB. The diagnosis of stupor and coma, 3rd ed. Philadelphia: FA Davis, 1983.
2. Feske SK. Coma and confusional states: emergency diagnosis and management. Neurol Clin North Am 1998;16:237–256.
3. Giacino JT. Disorders of consciousness: differential diagnosis and neuropathic features. Semin Neurol 1997;17:105–111.
4. Chiappa KH, Hill RA. Evaluation and prognostication in coma. Electroenceph Clin Neurophysiol 1998;106:149–155.
» READ BOOK EXCERPT ONLINE »
Source: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter, 2000
Coma:
Diagnostic Approach
(Field Guide to Bedside Diagnosis)
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.
» READ BOOK EXCERPT ONLINE »
Source: Field Guide to Bedside Diagnosis, 2007
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