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Decreased level of consciousness Ali Shoeibi MD, assistant professor of neurology, Mashhad University of Medical Sciences
Consciousness State of awareness
of self
and surroundings
Types Level of arousal
Cognitive and affective function
dementia
delusions
Confusion
inattention
APPROACH TO THE PATIENT IN COMA Stabilize vital functions such as blood pressure and oxygenation (A,B,C)
Brief history & examination
I.V. line & sampling
Treat reversible causes of coma
supplemental oxygen
intravenous thiamine (at least 100 mg)
intravenous 50% dextrose in water (25 g)
Naloxone hydrochloride may be given parenterally, preferably intravenously, in doses of 0.4 to 2.0 mg
APPROACH TO THE PATIENT IN COMA Comprehensive history & examination
The neck should be stabilized in all instances of trauma
until cervical spine fracture or subluxation can be ruled out
in unconscious patients with a history of trauma, peritoneal lavage by an experienced surgeon may be warranted
Causes of Coma
Causes of Coma More than half of all cases of coma are due to metabolic brain dysfunction (Almost half of these are drug poisonings)
Differentiating Toxic-Metabolic Coma from Structural Coma When the history is available, the patient's underlying illnesses and medications, or the setting in which they are found, often help guide the physician to the appropriate cause
The time course of the illness resulting in coma can be helpful. Generally, structural lesions have a more abrupt onset, whereas metabolic or toxic causes are more slowly progressive
The response to initial emergency therapy may help differentiate metabolic or toxic causes of coma
In general, structural lesions have focal features or at least notable asymmetry on neurological examination. Toxic, metabolic, and psychiatric diseases are characterized by their symmetry
State of consciousness Patients with metabolic problems often have milder alterations in arousal, typically with waxing and waning of the behavioral state
Patients with acute structural lesions tend to stay at the same level of arousal or progressively deteriorate
Toxins may also cause progressive decline in level of arousal
Respiration Deep, frequent respiration most commonly is due to metabolic abnormalities, though rarely it is caused by pontine lesions or by neurogenic pulmonary edema secondary to acute structural lesions
Funduscopic examination Subhyaloid hemorrhage or papilledema are almost pathognomonic of structural lesions
Papilledema due to increased ICP may be indicative of an intracranial mass lesion or hypertensive encephalopathy
Papilledema does not occur in metabolic diseases except hypoparathyroidism, lead intoxication, and malignant hypertension
Pupil size The pupils usually are symmetrical in coma from toxic-metabolic causes.
Patients with metabolic or toxic encephalopathies often have small pupils with preserved reactivity.
Exceptions
methyl alcohol poisoning, which may produce dilated and unreactive pupils
late in the course of toxic or metabolic coma if hypoxia or other permanent brain damage has occurred. In terminal asphyxia the pupils dilate initially and then become fixed at midposition within 30 minutes
Pupil reactivity Pupillary reactivity is relatively resistant to metabolic insult and usually is spared in coma from drug intoxication or metabolic causes, even when other brainstem reflexes are absent.
Exceptions
Hypothermia may fix pupils
severe barbiturate intoxication may fix pupils
neuromuscular blocking agents produce midposition or small pupils
glutethimide and atropine dilate pupils
common mistakes the use of insufficient illumination
preexisting ocular or neurological injury may fix the pupils or result in pupillary asymmetry
Seizures may cause transient anisocoria
Local and systemic medications may affect pupillary function
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