Diagnosis of Persistent Vegetative State
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COMA:
Ask the following questions:
(Algorithmic Diagnosis of Symptoms and Signs)
- Is there a history of drug or alcohol ingestion? This is a very important question to ask, as many cases of coma are due to acute alcohol intoxication, delirium tremens, opium poisoning, barbiturate poisoning, and other toxic cerebral depressants.
- Is there a history of trauma? Most of the time it will be obvious that the patient has suffered a blow to the head. However, there are many times when one must contact the family or other people who witnessed the onset of the coma to determine if there was trauma.
- Are there focal neurologic signs? Focal neurologic signs would make one think of a stroke, brain abscess, brain tumor, or epidural or subdural hematoma.
- Is there papilledema? Papilledema certainly would indicate a possible space-occupying lesion such as a brain tumor, brain abscess, or subdural hematoma.
- Is there a sweet odor to the breath? A sweet odor to the breath should make one think of a diabetic coma or alcoholism.
- Is there fever? If there is fever, one should be thinking of meningitis, subarachnoid hemorrhage, or acute encephalitis. However, aspiration pneumonia, urinary tract infection (UTI), or septicemia may explain the fever.
- Is there nuchal rigidity? The presence of nuchal rigidity suggests a meningitis or subarachnoid hemorrhage.
- Are there sibilant or crepitant rales on examination of the lung? Sibilant rales would suggest the possibility that pulmonary emphysema is responsible for the coma, whereas crepitant rales would suggest that there is congestive heart failure or possibly pneumonia.
DIAGNOSTIC WORKUP
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:
Differential Diagnosis
(In A Page: Pediatric Signs and Symptoms)
-
Infection
–Meningitis/encephalitis
–Bacteria, virus, fungi, spirochete
-
Increased intracranial pressure
–Tumor, abscess, hydrocephalus
-
Vascular
–Intracranial hemorrhage, stroke
–Hypoxic ischemic injury (hypotension,
cardiac arrest, arrhythmia, near-drowning)
–Vasculitis
-
Toxins
–Uremia, ethanol, atropine, opiates, lead, substance abuse
-
Trauma: Concussion, contusion
-
Seizure
–Nonconvulsive status epilepticus
–Postconvulsive state (postictal state)
-
Electrolyte imbalance
–Hyponatremia, hypernatremia
–Hypomagnesimia
–Hypoglycemia, hyperglycemia
–Hypercalcemia, hypocalcemia
-
Postinfectious
–Acute disseminated encephalomyelitis (ADEM)
-
Endocrine disorders
–Adrenal insufficiency
–Thyroid disorders
-
Degenerative and metabolic diseases
–Urea cycle disorders
–Reye syndrome
–Mitochondrial disease
-
Systemic infection and sepsis
-
Hepatic encephalopathy
-
Psychogenic
The mnemonic AEIOU-TIPS has been used to recall portions of the differential diagnosis:
Alcohol ingestion and acidosis
Epilepsy and encephalopathy
Infection
Opiates
Uremia
Trauma
Insulin overdose or inflammatory disorders
Poisoning and psychogenic causes
Shock
Workup and Diagnosis
-
History
–Trauma, seizures, diabetes; cardiac, liver, renal disease
–Presence of delirium before the onset of coma
–Fever, neck stiffness, headache
–Possible toxins at home
-
Physical exam
–Vital signs, temperature
–Pattern of breathing (Cheyne-Stokes, apneustic, ataxic)
–Retinal hemorrhages, otorrhea, spinal fluid rhinorrhea
–Thyroid, cardiac rhythm, murmur
–Skin (cyanosis, petechiae, splinter hemorrhages)
–Hepatosplenomegaly, meningismus
-
Neuro exam: Response to voice and noxious stimulation
–Papilledema, pupillary size, and light reflex
–Eye movements (spontaneous, doll's, calorics), corneals
–Gag, motor response to pain, DTRs, Babinski
–Decerebrate or decorticate posturing, muscle tone
-
Labs
–Toxicology screen, glucose, electrolyes
–CBC, ABG, LFT, ammonia
–BUN, creatinine, TSH, blood culture
-
Studies
–Neuroimaging: CT or MRI
–Lumbar puncture (after herniation has been ruled out)
–If subarachnoid hemorrhage or infection is suspected
–EEG to rule out nonconvulsive status epilepticus, gives clues to a metabolic process (triphasic waves)
» READ BOOK EXCERPT ONLINE »
Source: In A Page: Pediatric Signs and Symptoms, 2007
COMA AND SOMNOLENCE:
Approach to the Diagnosis
(Differential Diagnosis in Primary Care)
Obviously, the neurologic examination and a good history from a member of the family or friend are invaluable in the diagnosis of coma. However, one should not delay ordering laboratory work until the examination and history are accomplished. A CBC, BUN, fasting blood sugar (FBS), serum osmolality, electrolytes, blood gases, urinalysis, and drug screen are ordered immediately. If there is little or no history available and insulin shock is suspected, glucose or glucagon is administered before the laboratory reports are back, although this is done with more caution today for fear of aggravating a case of nonketotic, hyperosmolar diabetic coma.
It has been my experience that the neurologic examination is best performed simultaneously with the taking of a history from a relative or friend. In this way, various telltale neurologic signs can be found with alacrity. A unilateral dilated pupil (suggesting a subdural hematoma or aneurysm), acetone breath (suggesting diabetic acidosis), contusion of the skull (suggesting cerebral concussion or hematoma), and nuchal rigidity (suggesting a subarachnoid hemorrhage in meningitis) are just a few of the signs that can help identify the cause of the coma rapidly.
Coma without focal neurologic findings should suggest a metabolic or toxic cause. In that case, an intensive laboratory workup as listed below would be indicated. A spinal tap maybe indicated if there is fever as well. On the other hand, coma with focal neurologic signs suggests tumor, abscess, hematoma or cerebral embolism, thrombosis, or hemorrhage. The clinician should proceed with a skull x-ray film and CT scan immediately. When these are not available, immediate referral to a large medical center is necessary. Electroencephalography (EEG) and a spinal tap may identify the cause. A spinal tap should be considered with extreme caution even if there is no papilledema. Of course, a spinal tap is never done in the presence of papilledema unless a neurologist is consulted and CT findings are negative. One indication for a spinal tap under these circumstances might be meningitis. Another might be “benign intracranial hypertension.”
» READ BOOK EXCERPT ONLINE »
Source: Differential Diagnosis in Primary Care, 2007
Coma:
History
(The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter)
A. Characteristics. Coma patients essentially behave in a reflex manner without spontaneous or purposeful movements, language cognizance or expression, or specific localizing responses (3).
B. Confounding conditions include some medications, mechanical ventilation, immobilized extremities, facial edema, and diurnal variations.
C. Differential diagnosis. Less severe conditions of altered consciousness include vegetative state, the minimally conscious state, akinetic autism, and locked-in syndrome (3).
Physical examination
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.
» READ BOOK EXCERPT ONLINE »
Source: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter, 2000
Coma:
Differential Overview
(Field Guide to Bedside Diagnosis)
❑ Alcohol intoxication
❑ Drug overdose
❑ Hypoglycemia
❑ Metabolic acidosis
❑ Subdural hematoma
❑ Hypothermia
❑ Heat stroke
❑ Meningitis
❑ Subarachnoid hemorrhage
❑ Head trauma
❑ Ischemic encephalopathy
❑ Epidural hematoma
❑ Pontine hemorrhage
❑ Cerebellar hemorrhage
❑ Psychogenic
Diagnostic Approach
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
COMA AND SOMNOLENCE:
Approach to the Diagnosis
(Differential Diagnosis in Primary Care)
Obviously, the neurologic examination and a good history from a member
of the family or friend are invaluable in the diagnosis of coma. However,
one should not delay ordering laboratory work until the examination and
history are accomplished. A CBC, blood urea nitrogen (BUN), fasting blood
sugar (FBS), serum osmolality, electrolytes, blood gases, urinalysis, and
drug screen are ordered immediately. If there is little or no history
available and insulin shock is suspected, glucose or glucagon is
administered before the laboratory reports are back, although this is done
with more caution today for fear of aggravating a case of nonketotic,
hyperosmolar diabetic coma.
It has been my experience that the neurologic examination is best performed
simultaneously with the taking of a history from a relative or friend. In
this way, various telltale neurologic signs can be found with alacrity. A
unilateral dilated pupil (suggesting a subdural hematoma or aneurysm),
acetone breath (suggesting diabetic acidosis), contusion of the skull
(suggesting cerebral concussion or hematoma), and nuchal rigidity
(suggesting a subarachnoid hemorrhage in meningitis) are just a few of the
signs that can help to rapidly identify the cause of the coma.
Coma without focal neurologic findings should suggest a metabolic or toxic
cause. In that case, an intensive laboratory workup as listed below would be
indicated. A spinal tap may be indicated if there is fever as well. In
contrast, coma with focal neurologic signs suggests tumor, abscess, hematoma
or cerebral embolism, thrombosis, or hemorrhage. The clinician should
proceed with a skull x-ray film and CT scan immediately. When these are not
available, immediate referral to a large medical center is necessary.
Electroencephalography (EEG) and a spinal tap may identify the cause. A
spinal tap should be considered with extreme caution even if there is no
papilledema. Of course, a spinal tap is never done in the presence of
papilledema unless a neurologist is consulted and CT findings are negative.
One indication for a spinal tap under these circumstances might be
meningitis. Another might be “benign intracranial hypertension.”
» READ BOOK EXCERPT ONLINE »
Source: Differential Diagnosis in Primary Care, 2007
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