COMA Dr. BASHAR SHAKER

Definition Is a sleeplike state in which the patient makes no purposeful response to the environment and from which he or she cannot be aroused. The eyes are closed and do not open spontaneously. The patient does not speak, and there is no purposeful movement of the face or limbs. Verbal stimulation produces no response. Mechanical (e.g. painful) stimulation may produce no response or may elicit nonpurposeful reflex movements mediated through spinal cord or brainstem pathways.

Anatomic basis of coma Consciousness is maintained by the normal functioning of the brainstem reticular activating system above the mid pons and its bilateral projections to the thalamus and cerebral hemispheres. Coma results from lesions that affect either the reticular activating system or both hemispheres.

Pathophysiology Coma results from a disturbance in the function of either the brainstem reticular activating system above the midpons or both cerebral hemispheres since these are the brain regions that maintain consciousness.

APPROACH TO MANAGEMENT The approach to management of the comatose patient consists first of emergency measures to stabilize the patient and treat certain life-threatening disorders, followed by efforts to establish an etiologic diagnosis.

Ensure patency of the airway and adequacy of ventilation and circulation If the airway is obstructed, the obstruction should be cleared and the patient intubated. If there is evidence of trauma that may have affected the cervical spine, however, the neck should not be moved until this possibility has been excluded by x-rays of the cervical spine. In this case, if intubation is required, it should be performed by tracheostomy. Adequacy of ventilation can be established by the absence of cyanosis, a respiratory rate greater than 8/min, the presence of breath sounds on auscultation of the chest, and the results of arterial blood gas and pH studies. If any of these suggest inadequate ventilation, the patient should be ventilated mechanically. Measurement of the pulse and blood pressure provides a rapid assessment of the status of the circulation. Circulatory embarrassment should be treated with intravenous fluid replacement, pressors, and antiarrhythmic drugs, as indicated.

Insert an intravenous catheter and withdraw blood for laboratory studies These studies should include measurement of serum glucose and electrolytes, hepatic and renal function tests, prothrombin time, partial thromboplastin time, and a complete blood count. Extra tubes of blood should also be obtained for additional studies that may be useful in certain cases, such as drug screens, and for tests that become necessary as diagnostic evaluation proceeds.

Begin an intravenous infusion and administer dextrose, thiamine, and naloxone 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. Since 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. To treat possible opiate overdose, the opiate antagonist naloxone, 0.4–1.2 mg intravenously, should also be administered routinely to comatose patients.

Withdraw arterial blood for blood gas and pH determinations In addition to assisting in the assessment of ventilatory status, these studies can provide clues to metabolic causes of coma

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 The most crucial aspect of the history is the time over which coma develops 1- A sudden onset of coma suggests a vascular origin, especially a brainstem stroke or subarachnoid hemorrhage. 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 (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: alcohol, barbiturates and other sedative drugs, opiates, etc. B. Metabolic disturbances: anoxia, diabetic acidosis, uremia, hepatic failure, nonketotic hyperosmolar hyperglycemia, hypo- and hypernatremia, hypoglycemia, addisonian crisis, profound nutritional deficiency, carbon monoxide, thyroid states including Hashimoto encephalopathy C. Severe systemic infections: pneumonia, peritonitis, typhoid fever, malaria, septicemia, WaterhouseFriderichsen syndrome. D. Circulatory collapse (shock) from any cause. E. Postseizure states and convulsive and nonconvulsive status epilepticus F. Hypertensive encephalopathy and eclampsia 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 due to basilar artery thrombosis or embolism C. Brain abscess, subdural empyema, Herpes encephalitis D. Epidural and subdural hemorrhage and brain contusion E. Brain tumor F. Cerebellar and pontine hemorrhage. G. Miscellaneous: cortical vein thrombosis, viral encephalitis (herpes), focal embolic infarction due bacterial endocarditis,

A. Subarachnoid hemorrhage from ruptured aneurysm. B. Acute bacterial meningitis C. Some forms of viral encephalitis

General Physical Examination A. SIGNS OF TRAUMA 1- Inspection of the head may reveal signs of basilar skull fracture, including the following: a. Raccoon eyes—Periorbital ecchymoses. b. Battle's sign—Swelling and discoloration overlying the mastoid bone behind the ear. c. Hemotympanum—Blood behind the tympanic membrane. d. 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 15–20 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 subarachnoid hemorrhage or, rarely, brainstem stroke.

C. TEMPERATURE Hypothermia can occur in coma caused by ethanol or sedative drug intoxication, hypoglycemia, Wernicke's encephalopathy, hepatic encephalopathy, and myxedema. 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 : Air hunger Cheyne- stokes 2- Smell : Drugs Alcohol Acetone smell Fetor hepaticus

F. SIGNS OF MENINGEAL IRRITATION Signs of meningeal irritation [eg, nuchal rigidity or the Brudzinski sign are of great importance in leading to the prompt diagnosis of meningitis or subarachnoid hemorrhage, but they are lost in deep coma.

G.PUPIL SIZE : constricted;Pontine hemorrhage Organophosphorous poisioning dilated;Anticholinergic drugs H. OPTIC FUNDI Examination of the optic fundi may reveal papilledema or retinal hemorrhages compatible with chronic or acute hypertension or an elevation in intracranial pressure. Subhyaloid (superficial retinal) hemorrhages in an adult strongly suggest subarachnoid hemorrhage

DROWSINESS STUPOR CONFUSION SEMICOSCIOUSNESS

Glasgow Coma Scale