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باطنية
د. محمد الشيخ عيسى

عدد الاوراق (4)

22/1/2013

Coma

Coma is a sleeplike state in which the patient makes no purposeful response to the environment and from which cannot be aroused.
■ The eyes are closed and not open spontaneously.
■ The patient dose not speak.
■ There is no purposeful movement of the face or limbs.
■ Verbal stimulation produce no response.
■ Painful stimulation may produce no response or non purposeful reflex movement mediated through spinal cord or brainstem pathways.
Coma results from a disturbance in the function of either the brainstem reticular activating system above the midpons or of both cerebral hemispheres, since these
■ Verbal stimulation produce no response.
■ Painful stimulation may produce no response or non purposeful reflex movement mediated through spinal cord or brainstem pathways.
Coma results from a disturbance in the function of either the brainstem reticular activating system above the midpons or of both cerebral hemispheres, since these are the brain regions that mentain consciousness.




APPROACH TO DIAGNOSIS
1- Emergency measures to stabilize the patient and treat certain life threatening disorders.
2- Establish the etiologic diagnosis.
Emergency management
1- Ensure potency of the airway and adequacy of the ventilation and circulation.
■ If the airway obstructed the obstruction should be cleared and the patient intubated.
■ Adequacy of ventilation can be established by the absence of the cyanosis, respiratory rate >8 per minute, the presence of breath sound on auscultation of the chest and the result of arterial blood gas and pH studies.
2-Assessment of the status of circulation by measuring of the pulse and blood pressure.
3- Insert an intravenous catheter and with draw blood for measurement of :-
- RBS
- S. electrolytes
- Hepatic and renal function tests
- PT, APTT
- CBC, ESR
- Extra tubes for drug screens in certain cases.
4- Begin an IV infusion and administration of 50ml of a 50% dextrose solution to treat possible hypoglycemic coma, with thiamine 100mg IV to avoid precipitation or worsen Wernicke encephalopathy in thiamine deficient patients.
To treat possible opiate over dose, naloxone 0.4-1.2 mg IV should also be administered routinely to comatose patients.
5- Withdraw arterial blood for blood gas and pH determinations.
6- Treatment of seizure if present.
After these measures have been taken, the history (if available) is obtained, general and neurologic examination are performed.


History
The most important point of the history is the time over which coma develop.
1- A sudden onset of coma suggests a vascular origin, especially a brainstem stroke or SAH.
2- Rapid progression from hemispheric signs, such as hemiparesis, hemisensory deficit,
Or aphasia to coma within minutes to hours is characteristic of intracerebral hemorrhage.
3- A more protracted course leading to coma (day to a week or more) is seen with tumor, abscess or chromic subdural hematoma.
4- coma preceded by confusional state or agitation without laterralizing signs or symptoms is probably due to metabolic derangement.

General physical examination

A- Signs of trauma:
1- Inspection of head may reveal signs of basilar skull fracture, including the following:
I- Raccoon eyes (periorbital ecchymoses).
II- Battles sign: swelling and discoloration overlying the mastoid bone behind the ear.
III- Hemotympanum: Blood behind the tympanic membrane.
IV- Cerebrospinal fluid (CSF) rhinorrhea or otorrhea: Leakage of CSF from the nose or ear. CSF rhinorrhea must be distinguished from other causes of rhinorrhea, such as allergic rhinitis. It has been suggested that CSF can be distinguished from nasal mucus by the higher glucose content of CSF, but this is not always the case.
The chloride level may be more useful, since CSF chloride concentrations are 15 to 20 meq/L higher than those in mucus.

2- Palpation of the head may demonstrate a depressed skull fracture or swelling of soft tissues at the site of trauma.

B- Blood pressure:-

Elevation of blood pressure in a comatose patient may reflect long-standing hypertension, which predisposes to intracerebral hemorrhage or stroke. In the rare condition of hypertensive encephalopathy, the blood pressure is above 250/150 mm Hg in chronically hypertensive patients.
Elevation of blood pressure may also be a consequence of the process causing the coma, as in intracerebral or subarachniod hemorrhage or rarely, brainstem stroke.


C- Temperature:-
Hypothermia can occur in coma caused by ethanol or sedative drug intoxication, hypoglycemia, Wernicke encephalopathy, hepatic encephalopathy and myxoedema.
Coma with hyperthermia is seen in heat stroke, status epilepticus, malignant hyperthermia related to inhalational anesthetics, anticholinergic drug intoxication, pontine hemorrhage, and certain hypothalamic lesions.

D- Examination of skin:-

Pallor, Jaundice, Cyanosis, Purpura, Needle marks, Pigmentations etc.

E- Breathing:-

1- Pattern: Ventilatory patterns in coma. Cheyne-stokes respiration and central hyperventilation are seen with metabolic disturbances and with structural lesion at a variety of sites in the brain.
They are therefore not useful for anatomic localization of disorders producing coma. Ataxic and gasping ventilatory patterns are most commonly seen with pontomedullary lesion.

- Smell for:

□ Drugs
□ Alcohol
□ Acetone smell
□ Fetor hepaticus: bad odor due to some chronic liver diseases.

Neurologic Examination

The neurologic examination is the key to etiologic diagnosis is the comatose patient pupillary size and reactivity and oculocephalic and oculovestibular reflexes and the motor response to pain should be evaluated in detail
A- Pupils:-
1- Normal pupil normal pupils 3-4mm in diameter and equal, constrict briskly and symnetrically in response to light and acommidation .
2- Fixed dilated pupils greater than 7mm in diameter and fixed result from compression of the III CN and anticholinergic or sympathomimetic drug intoxication.
And in comatose patient is due to transtentorial herniation of medial temporal lobe from supratentorial mass.
3- Pinpoint puplis (1-1.5mm in diammer) caused by opioid over dose, pontine hemorrhage and organophosphate poisoning, miotic eye drops and neurosyphilis.
B- Optic fundi:-
Examination of the optic fundi may reveal papilledema or retinal hemorrhages compatible with chronic or acute hypertension or an elevation in the intracranial pressure.
Subhyaloid (superficial retinal) hemorrhages in an adult strongly suggest subarachnoid hemorrhage.


C- Signs of meningeal irritation:-
For example: neck stiffness or the Brudzinski,s sign and kernig,s sign are of great importance in leading to the prompt diagnosis of meningitis or subarachnoid hemorrhage, but they are lost in deep coma.

D- Motor response to pain:-

The motor response to pain is tested by applying strong pressure on the supra orbital ridge, sternum or nail beds. The response to such stimuli may be helpful in localizing the level of cerebral dysfunction and providing a guide to the depth of coma.
1- With cerebral dysfunction of only moderate severity, patient may localize the offending stimulus.
2- A decorticate response to the pain (flexion of the arm at the elbow , adduction at the shoulder and extension of the leg and ankle) occur due to lesion involve the thalamus directly or large hemispheric mass compress it from above.
3- A decerebrate response ((extension of the elbow, internal rotation at the shoulder and forearm and leg extension)) occur when midbrain function is compromised and indicate more sever brain dysfunction.
4- Unilateral or asymmetric
Posturing suggests structural disease in the contralateral cerebral hemispher.
5- In patient with pontine and medullary lesion show no response to pain but occasionally some flexion at the knee is noted (spinal reflex).

Glasgow Coma Scale

In order to asses the state of coma and to scale the progression or regression of the comatos patients state, there have been put many scales, but the most agreeable one the Glasgow Coma Scale which is as follows:-


This scaling is performed successively by the medical staff to asses the current status of the patient and to determine whether its going good or going down.

Etiology

Supratentorial structural lesions
1- Subdural hematoma diagnosis made by CT scan or MRI.
2- Ebidural hematoma.
3- Cerebral contusion.
4- Intracerebral hemorrhage.
5- Brain abscess.
6- Cerebral infarction (stroke).
7- Brain tumor.


Subtentorial structural lesion

1- Basilar artery occlusion.
2- Pontine hemorrhage.
3- Cerebillar hemorrhage or infarction.
4- Posterior fossa sabdural or epidural hematomas.

Diffuse encephalopathy

1- Meningitis and encephalitis.
2- Subarachnoid hemorrhage.
3- Hypoglycemia.
4- Global cerebral ischemia.
5- Drug intoxication.
■ Sedative-Hypnotic drugs.
■ Ethanol.
■ Opioids.
6- Hepatic encephalopathy.
7- Hyperosmalar coma.
8- Hyponatremia.
9- Hypothermia.
10- Hyperthermia.
11- Seizure or Prolonged postictal state.




BRIAN DEATH
Irreversible cessation of all brain function is required for a diagnosis of brain death .
The diagnosis o f brain death in children younger than 5 years must be made with caution .

Cessation of Brain Function
A . Unresponsiveness :
The patient must be unresponsive to sensory input, including pain and speech .
B . Absent Brainstem Reflexes :
Pupillary , corneal , and oropharyngeal responses are absent , and attempts to elicit eye movements with the oculocephalic and vestibuloocular maneuvers are unsuccessul .

Respiratory responses are also absent without ventilatory effort after the patient PCO2 is permitted to rise to 60 mm Hg for maximal ventilatory stimulation, while oxygenation is maintained by giving 100% oxygen by a cannula inserted into the endotracheal tube (apnea test ) .
IrreversibirIrlity Brain Dysfunction
The cause of coma must be known ; it must be adequate to explain the clinical picture ; and it must be Irreversible.
Sedative drug intoxication , hypothermia (32.2C), neuromuscular blockade , and shock must be ruled out . ۫

Persistence of Brain Dysfunciton

The criteria for brain death described above must
Persist for an appropriate length of time as follows
1. Six hours with a confirmatory isoelectric (flat) EEG, performed according to the technical standards of the American electroencephalographic society
2. Twelve hours without a confirmatory isoelectric EEG
3. Twenty-four hours for anoxic brain injury without a confirmatory isoelectric EEG.










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