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Transcript
COMA
Is a sleeplike state in which the patient makes no purposeful response to the environment
and from which he or she cannot be aroused.
Coma results from lesions that affect either the reticular activating system or both
hemispheres since these are the brain regions that maintain consciousness
APPROACH TO MANAGEMENT
Ensure patency of the airway and adequacy of ventilation and circulation
Insert an intravenous catheter and withdraw blood for laboratory studies
Begin an intravenous infusion and administer dextrose, thiamine, and naloxone
1-Every comatose patient should be given 25 g of dextrose intravenously, typically as 50 mL
of a 50% dextrose solution, to treat possible hypoglycemic coma.
2-administration of dextrose alone may precipitate or worsen Wernicke's encephalopathy in
thiamine-deficient patients, all comatose patients should also receive 100 mg of thiamine by
the intravenous route.
3-To treat possible opiate overdose, the opiate antagonist naloxone, intravenously, should
also be administered .
Institute treatment for seizures, if present
Persistent or recurrent seizures in a comatose patient should be considered to represent
status epilepticus and treated accordingly
History
1- A sudden onset of coma suggests a vascular origin
2- Rapid progression from hemispheric signs, is characteristic of
intracerebral hemorrhage
3- A more protracted course leading to coma (days to a week or more) is seen with tumor,
abscess, or chronic subdural hematoma
4- Coma preceded by a confusional state or agitated delirium, without lateralizing signs or
symptoms, is probably due to a metabolic derangement
Lateralizing (Focal ) Signs
1- Assymmetry of pupils.
2- Squint
3- Assymmetry of the face
4- Gaze palsy
5- Assymmetry of motor response, reflexes
& plantar response
Diseases that cause no focal or lateralizing
neurologic signs
A. Intoxications:
B. Metabolic disturbances: anoxia, diabetic
acidosis, uremia, hepatic failure,
C. Severe systemic infections
D. Circulatory collapse (shock)
E. Postseizure states and convulsive
F. Hypertensive encephalopathy
G. Hyperthermia and hypothermia. state,
H. Concussion
I. Acute hydrocephalus
Diseases that cause focal brainstem or
lateralizing cerebral signs
A. Hemispheral hemorrhage or massive
infarction
B. Brainstem infarction
C. Brain abscess
D. Epidural and subdural hemorrhage
E. Brain tumor
F. Cerebellar and pontine hemorrhage.
G. Miscellaneous: cortical vein thrombosis,
viral encephalitis
In these cases no focal sing present as at involve all of brain
A. Subarachnoid hemorrhage from ruptured aneurysm. B. Acute bacterial meningitis
C. Some forms of viral encephalitis
General Physical Examination
A. SIGNS OF TRAUMA
B. BLOOD PRESSURE
Elevation of blood pressure may also be a consequence of the process causing the coma, as
in intracerebral or subarachnoid hemorrhage
C. TEMPERATURE
Hypothermia can occur in coma caused by ethanol or sedative drug intoxication, and
hypoglycemia.
Coma with hyperthermia is seen in heat stroke, status epilepticus, malignant hyperthermia .
E- Breathing
1- Pattern : Air hunger  indicate metabolic cause as aspirin over dose or renal failure or
metabolic ketoacidosis
Cheyne- stokes  indicate intracranial or cardiac cause
2- Smell : Drugs
Alcohol
Acetone smell  metabolic ketoacidosis
Fetor hepaticus  hepatitis
Abnormal gait
skeletal abnormalities, usually characterised by pain producing
Gaits that do not fit either pattern may be due to psychiatric disorders and are usually
incompatible with any anatomical or physiological deficit .
Pyramidal gait  Upper motor neuron (pyramidal) lesions
Foot drop  lower motor neuron lesion
Myopathic gait  proximal muscle weakness, usually caused by muscle disease
Ataxic gait  lesions in the cerebellum , vestibular apparatus or peripheral nerves
Sensory ataxia  Impairment of joint position sense
Apraxic gait  higher cerebral dysfunction
Extrapyramidal gait  in Parkinson disease and other extrapyramidal diseases
INVOLUNTARY MOVEMENTS
Rest tremor  pathognomonic of Parkinson disease . It is characteristically pill rolling
Physiological tremor  most common type of action tremor It is common in normal subjects
and exaggeration occurs in anxiety and in Fatigue, Toxins , Alcohol withdrawal
Essential tremor  The condition is often inherited , Alcohol often suppresses it, distinct from
a physiological tremor, although resembling it superficially
Intention tremor  occurs in cerebellar disease , characterised by oscillation at the end of a
movement
Asterixis (flapping tremor)  seen in metabolic disturbances, result of intermittent failure of
the parietal mechanisms required to maintain a posture. Causes of asterixis : Renal failure
Liver failure, Hypercapnia, Acute focal parietal or thalamic lesion
Chorea, athetosis, ballism
These are due to disturbance of balance of activity in the basal ganglia
Chorea : Jerky, smallamplitude, purposeless
involuntary movements
causes : Hereditary , Cerebral
birth injury , Cerebral trauma
, Drugs
, Endocrine disease, Infective
inflammatory
Hemiballismus: More
dramatic ballistic flying
violent movements of the
limbs usually occur
unilaterally in vascular
lesions of the subthalamic
structures.
Athetosis : Slower writhing
movements of the limbs .
These are often combined
with chorea (and have a
similar list of causes) and are
then termed 'choreoathetoid' movements
Dystonia  sustained involuntary contraction that causes abnormal posture or movement.
It may be generalised in various diseases of the basal ganglia or may be focal or segmental,
segmental dystonias can be treated by the administration of botulinum toxin to a few of the
responsible muscles
Tics  Tics are repetitive semi-purposeful movements such as blinking , distinguished from
other involuntary movements by the ability of the patient to suppress their occurrence, at
least for a short time.