COMAPresented byDr. 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 waened with outside physical or auditory stimulation. !ome other terms .. Stupor:"efers to a higher degree of arousability in which the patient can be awaened 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 characteri$ed by easy arousal and the persistence of alertness for brief periods. !ome other terms ..%ethargy indicates a patient who is incoherent but arousable and has tendency to sleep and able to communicate &egetative state signifies an awae but unresponsive state %oced in state is a pseudocoma in which an awae patient has no means of producing speech. Pathophysiology 'n order for a patient to maintain consciousness# two important neurological components must function impeccably. The first is the cerebral corte( which is the gray matter covering the outer layer of the brain# and the other is a structure located in the brainstem# called "eticular activating system )"A! or A"A!*. 'n+ury to either or both of these components is sufficient to cause a patient to e(perience a coma. PathophysiologyThe human corte( is a group of tightly dense# ,gray matter, composed of the nucleus of the neurons whose a(ons then form the ,white matter,# and is responsible for the perception of the universe# relay of the sensory input )sensation* via the thalamic pathway# and most importantly directly or indirectly in charge of all the neurological functions# from simple refle(es to comple( thining. Pathophysiology"eticular activating system )"A!* on the other hand is a more primitive structure in the brainstem that is tightly in connection with reticular formation )"-*# a critical anatomical structure needed for maintenance of arousal. "eticular activating system )"A!* taes its name from the effect it has on the reticular formationwhich is via its stimulation. Pathophysiology !o the principal ways to develop coma .Damage to "A! and its pro+ections Damage to both cerebral hemisphere !uppression of reticulo/cerebral function by drugs #to(ins hypoglycemia # hepatic failure or a$otemia etc.. Classification Plum and Posner classify coma either :0* supratentoral)above Tentorium cerebelli# 1* infratentoral )below Tentorium cerebelli*2* metabolic or 3* 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 categori$ed into several levels. Patients may or may not progress through these levels. 'n the first level# the brain responsiveness lessens# normal refle(es are lost# the patient no longer responds to pain and cannot hear. CA4!5! O- COMAMetabolic disturbanceDrug overdose Hyponatraemia 4raemia Hepatic failure "espiratory failure Hypothermia Hypothyroidism Diabetes mellitus. Hypoglycaemia 6etoacidosis Hyperosmolar coma CA4!5!TraumaCerebral contusion 5(tradural haematoma !ubdural haematoma CA4!5!Cerebrovascular disease !ubarachnoid haemorrhage 'ntracerebral haemorrhage 7rain/stem infarction8haemorrhage Cerebral venous sinus thrombosis CA4!5! Infections Meningitis 5ncephalitis Cerebral abscess 9eneral sepsis CA4!5! Others 5pilepsy 7rain tumour Thiamin deficiency Approach to the Patient. ComaAcute respiratory and cardiovascular problems should be attended to prior to neurologic assessment. 'n most instances# a complete medical evaluation# e(cept for vital signs# funduscopy# and e(amination for nuchal rigidity# may be deferred until the neurologic evaluation has established the severity and nature of coma. 9%A!9O: COMA !CA%5Eye-oenin! "E#; !pontaneous3; To speech2; To pain1; ; Confused conversation3; 'nappropriate words2; 'ncomprehensible sounds1; ApproachHistory)0* The circumstances and rapidity with which neurological symptoms developed? )1*The antecedent symptoms )confusion# weaness# headache# fever# sei$ures# di$$iness# double vision# or vomiting*? )2*The use of medications# illicit drugs# or alcohol? and )3*Chronic liver# idney# lung# heart# or other medical disease. Approach 9eneral Physical 5(amination The temperature# pulse# respiratory rate and pattern# and blood pressure should be measured @uicly. -ever suggests a systemic infection# bacterial meningitis# or encephalitis? High body temperature# 31A33BC# associated with dry sin should arouse the suspicion of heat stroe or anticholinergic drug into(ication. Hypothermia is observed with alcoholic# barbiturate# sedative# or phenothia$ine ApproachTachypnea may indicate systemic acidosis or pneumonia. Aberrant respiratory patterns that reflect brainstem disorders. Mared hypertension either indicates hypertensive encephalopathy or is the result of a rapid rise in intracranial pressure )'CP? the Cushing response* most often after cerebral hemorrhage or head in+ury. Hypotension is characteristic of coma from alcohol or barbiturate into(ication# internal hemorrhage# myocardial infarction# sepsis# profound hypothyroidism# or Addisonian crisis. The funduscopic e(amination can detect subarachnoid hemorrhage )subhyaloid hemorrhages*# hypertensive encephalopathy )e(udates# hemorrhages# vessel/crossing changes# papilledema*# and increased 'CP )papilledema*. Cutaneous petechiae suggest thrombotic thrombocytopenic purpura# meningococcemia# or a bleeding diathesis from which an intracerebral hemorrhage has arisen. Approach mm* but not pinpoint pupils are seen in metabolic encephalopathies or in deep bilateral hemispheral lesions such as hydrocephalus or thalamic hemorrhage. &ery small but reactive pupils )E0 mm* characteri$e narcotic or barbiturate overdoses but also occur with e(tensive 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. %id tone# tested by lifting the eyelids and noting their resistance to opening and the speed of closure# is reduced progressively as coma deepens. Hori$ontal divergence of the eyes at rest is normal in drowsiness. As coma deepens# the ocular a(es may become parallel again. Approach "espiratory Patterns !hallow# slow# but regular breathing suggests metabolic or drug depression. Cheyne/!toes respiration in its classic cyclic form# ending with a brief apneic period# signifies bihemispheral damage or metabolic suppression and commonly accompanies light coma. "apid# deep )6ussmaul* 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 nown as the terminal respiratory pattern of severe brain damage. %aboratory !tudies and 'magingchemical/to(icologic analysis of blood and urine# cranial CT or M"'# 559# and C!- e(amination. Arterial blood/gas analysis7lood glucose %aboratory !tudies and 'maging cont FCalcium and phosphate level Coagulation profile7lood count and hemoglobin levelChest G/ray4rea and electrolytes %iver function test %aboratory !tudies and 'maging cont F