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COMA

Presented by Dr. Mahmudul Hasan

What is a "coma"?

Coma is a state of unconsciousness whereby a patient cannot react with the surrounding environment. The patient cannot be wakened with outside physical or auditory stimulation.

Some other terms ..


Stupor: Refers to a higher degree of arousability in which the patient can be awakened only by vigorous stimuli, accompanied by motor behavior that leads to avoidance of uncomfortable or aggravating stimuli. Drowsiness: which is familiar to all persons, simulates light sleep and is characterized by easy arousal and the persistence of alertness for brief periods.

Some other terms ..


Lethargy indicates a patient who is incoherent but arousable and has tendency to sleep and able to communicate Vegetative state signifies an awake but unresponsive state Locked in state is a pseudocoma in which an awake patient has no means of producing speech.

Pathophysiology
In order for a patient to maintain consciousness, two important neurological components must function impeccably. The first is the cerebral cortex which is the gray matter covering the outer layer of the brain, and the other is a structure located in the brainstem, called Reticular activating system (RAS or ARAS). Injury to either or both of these components is sufficient to cause a patient to experience a coma.

Pathophysiology
The human cortex is a group of tightly dense, "gray matter" composed of the nucleus of the neurons whose axons then form the "white matter", and is responsible for the perception of the universe, relay of the sensory input (sensation) via the thalamic pathway, and most importantly directly or indirectly in charge of all the neurological functions, from simple reflexes to complex thinking.

Pathophysiology
Reticular activating system (RAS) on the other hand is a more primitive structure in the brainstem that is tightly in connection with reticular formation (RF), a critical anatomical structure needed for maintenance of arousal. Reticular activating system (RAS) takes its name from the effect it has on the reticular formation which is via its stimulation.

Pathophysiology
So the principal ways to develop coma : Damage to RAS and its projections Damage to both cerebral hemisphere Suppression of reticulo-cerebral function by drugs ,toxins hypoglycemia , hepatic failure or azotemia etc..

Classification
Plum and Posner classify coma either : 1) supratentoral (above Tentorium cerebelli, 2) infratentoral (below Tentorium cerebelli) 3) metabolic or 4) diffuse. This classification is merely dependent on the position of the original damage that caused the coma, and does not correlate with severity or the prognosis. The severity of coma impairment however is categorized into several levels. Patients may or may not progress through these levels. In the first level, the brain responsiveness lessens, normal reflexes are lost, the patient no longer responds to pain and cannot hear.

CAUSES OF COMA
Metabolic disturbance
Drug overdose Hyponatraemia Uraemia Hepatic failure Respiratory failure Hypothermia Hypothyroidism Diabetes mellitus:
Hypoglycaemia Ketoacidosis Hyperosmolar coma

CAUSES
Trauma Cerebral contusion Extradural haematoma Subdural haematoma

CAUSES
Cerebrovascular disease Subarachnoid haemorrhage Intracerebral haemorrhage Brain-stem infarction/haemorrhage Cerebral venous sinus thrombosis

CAUSES
Infections Meningitis Encephalitis Cerebral abscess General sepsis

CAUSES
Others Epilepsy Brain tumour Thiamin deficiency

Approach to the Patient: Coma


Acute respiratory and cardiovascular problems should be attended to prior to neurologic assessment. In most instances, a complete medical evaluation, except for vital signs, funduscopy, and examination for nuchal rigidity, may be deferred until the neurologic evaluation has established the severity and nature of coma.

GLASGOW COMA SCALE


Eye-opening (E) Spontaneous4 To speech3 To pain2 Nil1 Best motor response (M) Obeys6 Localises5 Withdraws4 Abnormal flexion3 Extensor response2 Nil1 Verbal response (V) Orientated5 Confused conversation4 Inappropriate words3 Incomprehensible sounds2 Nil1 Coma score = E + M + V Minimum3 Maximum15

Approach
History (1)The circumstances and rapidity with which neurological symptoms developed; (2)The antecedent symptoms (confusion, weakness, headache, fever, seizures, dizziness, double vision, or vomiting); (3)The use of medications, illicit drugs, or alcohol; and (4)Chronic liver, kidney, lung, heart, or other medical disease.

Approach
General Physical Examination The temperature, pulse, respiratory rate and pattern, and blood pressure should be measured quickly. Fever suggests a systemic infection, bacterial meningitis, or encephalitis; High body temperature, 4244C, associated with dry skin should arouse the suspicion of heat stroke or anticholinergic drug intoxication. Hypothermia is observed with alcoholic, barbiturate, sedative, or phenothiazine

Approach
Tachypnea may indicate systemic acidosis or pneumonia. Aberrant respiratory patterns that reflect brainstem disorders. Marked hypertension either indicates hypertensive encephalopathy or is the result of a rapid rise in intracranial pressure (ICP; the Cushing response) most often after cerebral hemorrhage or head injury. Hypotension is characteristic of coma from alcohol or barbiturate intoxication, internal hemorrhage, myocardial infarction, sepsis, profound hypothyroidism, or Addisonian crisis.

The funduscopic examination can detect subarachnoid hemorrhage (subhyaloid hemorrhages), hypertensive encephalopathy (exudates, hemorrhages, vessel-crossing changes, papilledema), and increased ICP (papilledema). Cutaneous petechiae suggest thrombotic thrombocytopenic purpura, meningococcemia, or a bleeding diathesis from which an intracerebral hemorrhage has arisen.

Approach
Neurologic Examination First, the patient should be observed without intervention by the examiner. Tossing about in the bed, reaching up toward the face, crossing legs, yawning, swallowing, coughing, or moaning denote a state close to normal awakeness. Lack of restless movements on one side or an outturned leg suggests a hemiplegia. Intermittent twitching movements of a foot, finger, or facial muscle may be the only sign of seizures.

Multifocal myoclonus almost always indicates a metabolic disorder, particularly uremia, anoxia, or drug intoxication. In a drowsy and confused patient bilateral asterixis is a certain sign of metabolic encephalopathy or drug intoxication.

Approach
Level of Arousal A sequence of increasingly intense stimuli is used to determine the threshold for arousal and the optimal motor response of each side of the body. The results of testing may vary from minute to minute and serial examinations are most useful. Tickling the nostrils with a cotton wisp is a moderate stimulus to arousalall but deeply stuporous and comatose patients will move the head away and rouse to some degree.

Approach
Using the hand to remove the offending stimulus represents an even greater degree of responsiveness. Stereotyped posturing in response to noxious stimuli indicates severe dysfunction of the corticospinal system. Abduction-avoidance movement of a limb is usually purposeful and denotes an intact corticospinal system. Pressure on the knuckles or bony prominences and pinprick stimulation are humane forms of noxious stimuli;

Approach
Brainstem Reflexes Assessment of brainstem function is essential to localization of the lesion in coma The brainstem reflexes that are conveniently examined are: pupillary responses to light, spontaneous and elicited eye movements, corneal responses, and the respiratory pattern.

1. 2. 3. 4.

Approach
Pupillary Signs:
Pupillary reactions are examined with a bright, diffuse light (not an ophthalmoscope); if the response is absent, this should be confirmed by observation through a magnifying lens. Normally reactive and round pupils of midsize (2.55 mm) essentially exclude midbrain damage, either primary or secondary to compression. One unreactive and enlarged pupil (>6 mm) or one that is poorly reactive signifies compression of the third nerve from the effects of a mass above.

Approach
An oval and slightly eccentric pupil is a transitional sign that accompanies early midbrainthird nerve compression. The most extreme pupillary sign, bilaterally dilated and unreactive pupils, indicates severe midbrain damage, usually from compression by a supratentorial mass. Ingestion of drugs with anticholinergic activity, the use of mydriatic eye drops, and direct ocular trauma are among the causes of misleading pupillary enlargement.

Approach
Unilateral miosis in coma has been attributed to dysfunction of sympathetic efferents originating in the posterior hypothalamus and descending in the tegmentum of the brainstem to the cervical cord. Reactive and bilaterally small (12.5 mm) but not pinpoint pupils are seen in metabolic encephalopathies or in deep bilateral hemispheral lesions such as hydrocephalus or thalamic hemorrhage. Very small but reactive pupils (<1 mm) characterize narcotic or barbiturate overdoses but also occur with extensive pontine hemorrhage.

Approach
Ocular Movements The eyes are first observed by elevating the lids and noting the resting position and spontaneous movements of the globes. Lid tone, tested by lifting the eyelids and noting their resistance to opening and the speed of closure, is reduced progressively as coma deepens. Horizontal divergence of the eyes at rest is normal in drowsiness. As coma deepens, the ocular axes may become parallel again.

Approach
Respiratory Patterns
Shallow, slow, but regular breathing suggests metabolic or drug depression. Cheyne-Stokes respiration in its classic cyclic form, ending with a brief apneic period, signifies bihemispheral damage or metabolic suppression and commonly accompanies light coma. Rapid, deep (Kussmaul) breathing usually implies metabolic acidosis but may also occur with pontomesencephalic lesions. Agonal gasps are the result of lower brainstem (medullary) damage and are well known as the terminal respiratory pattern of severe brain damage.

Laboratory Studies and Imaging


chemical-toxicologic analysis of blood and urine, cranial CT or MRI, EEG, and CSF examination. Arterial blood-gas analysis Blood glucose

Laboratory Studies and Imaging cont


Calcium and phosphate level Coagulation profile Blood count and hemoglobin level Chest X-ray Urea and electrolytes Liver function test

Laboratory Studies and Imaging cont


Normal CT scan excludes anatomic lesions as the cause of coma is also erroneous. Bilateral hemisphere infarction, acute brainstem infarction, encephalitis, meningitis, Nevertheless, if the source of coma remains unknown, a scan should be obtained. EEG is useful in metabolic or drug-induced states but is rarely diagnostic.

Treatment
Coma is a medical emergency, and attention must first be directed to: maintaining the patient's respiration and circulation, using intubation and ventilation, administration of intravenous fluids blood and other supportive care as needed. Once a patient is stable and no longer in immediate danger, the medical staff may concentrate on maintaining the health of patients physical state.

Treatment
The concentration will be directed on preventing infections such as pneumonias, bedsores (decubitus ulcers) and providing a balanced nutrition. These infections may appear from the patient not being able to move around, and being confined to the bed. The nursing staff will move the patient every 23 hours from side to side and depending on the state of consciousness sometimes to a chair. The goal is to move the patient as much as possible to try to avoid bedsores, atelectasis and pneumonia.

Treatment
Pneumonia can occur from the persons inability to swallow leading to aspiration, lack of gag reflex or from feeding tube, (aspiration pneumonia. Physical therapy may also be used to prevent contractures and orthopedic deformities that would limit recovery for those patients who emerge from coma. A person in a coma may become restless, or seize and need special care to prevent them from hurting themselves. Medicine may be given to calm such individuals. Patients who are restless may also try to pull on tubes or dressings so soft cloth wrist restraints may be put on. Side rails on the bed should be kept up to prevent patient from falling.

Follow up
BP 2 hourly Temperature 2 hourly Strict intake output chart 4 hourly blood gases Continuous monitoring of oxygen saturation with pulse oxymetry Blood glucose 4 hourly Ca and ph 12 hourly Urea and electrolytes twice daily

Prognosis
Children and young adults may have ominous early clinical findings such as abnormal brainstem reflexes and yet recover, so that temporization in offering a prognosis in this group of patients is wise. Metabolic comas have a far better prognosis than traumatic ones. The absence of the cortical waves of the somatosensory evoked potentials has also proved a strong indicator of poor outcome in coma from any cause.