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Wakeful and aware------drowsy------confused or delirium-----------stupor----coma Corpus Callosum Medial surface of right hemisphere.

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Presentation on theme: "Wakeful and aware------drowsy------confused or delirium-----------stupor----coma Corpus Callosum Medial surface of right hemisphere."— Presentation transcript:

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2 Wakeful and aware------drowsy------confused or delirium stupor----coma Corpus Callosum Medial surface of right hemisphere

3 Infra tentorial and supra tentorial Corpus Callosum Medial surface of right hemisphere

4 Coma is a state in which the patient makes no purposeful response to environment and from which he or she can not be aroused. Eyes are closed not opened spontaneously Speak------no speak, no verbal response Mechanical stimulation (painful) produce no response or non- purposeful response or elicit non purposeful reflex movement mediated through spinal cord or brainstem. Coma result from a disturbance in the function of either brainstem RAS above mid pons, at thalami? or both C.H. since these brain areas which maintain cons.. Pathophysiologic assess. The most important step in evaluating comatose patient is to decide whether it is result from str. Brain lesion for which an emergent surgical interference is needed or from diffuse encephalopathy, meningitis,or seizure for which surgical treatment is not required. The dilemma we have is how to differentiate between them.

5 1-Structural brain lesion 2-metabolic 1-structural A-supra-tentorial str. Lesion :ex brain tumor the History & examination point to H. disorder early in course of disease like hemi sensory and hemi paresis or aphasia (dominant) and agnosia (nondominant). As the mass expanded-----somnolence supervenes because of compression of other H. or downward pressure on diencephalons. stupor progress to coma step by step as rostro-caudal compression progress where thalamus,MB, pons and medulla become involved. the N. E. revealed dysfunction at lower anatomical level. once pontine level reached fatal outcome is inevitable ipsilateral papillary dilatation and impaired eye adduction (sign of 3rd nerve palsy) indicate uncal H. called uncal syndrome which precede loss of cons.. Corpus Callosum Medial surface of right hemisphere

6 Stages of suprat. lesion: all normal when lesion at brain level but: P. Ref. Reflex e.move* MOTOR R. Early diencephalons 2mm,reactive normal localizing, often asymmetry Late = = = decorticate Midbrain dilated(>7) not r. impair add. Decerebrate Pons ** pin point + impair abd. no resp. or slight flexion * to doll’s or to ear irrigation=caloric test ** pin point pupil(1-1.5), unreactive seen in pontine lesion. Corpus Callosum

7 B-sub-tentorial str. Lesion -- Usually of sudden onset with focal brainstem sign, --with focal MB pupil is mid sized(5 mm) not reacting, --pin point pupil seen in pontine lesion as in hemorrhage. Less often from Infarction and compression due to cerebellar bleed or infarction. --conjugate gaze away from side of lesion or disconjugate E. movement as in INO support sub T. Lesion. motor response is of little value to differentiate between sub and supratentorial.. Ventilation pattern in coma usually is not so helpful in anatomic localization in coma. gasp and ataxic breathing suggest pontmedullary site which can result from trans tentorial

8 2-Diffuse metabolic encephalopathy.— metabolic coma include exogenous toxins as in drug intoxicating or endogenous as in uremia and hepatic failure, hypoglycemia.other process like meningitis,seizure and SAH are of special consideration. C/f : usually no focal sign except in SAH and some times in hypoglycemia. -no sudden onset except in SAH,but there is progressive somnolence to confusion,or delirium and then coma. N E. is often ---symmetrical except in some cases of hyperosmlar state, hypoglycemia and hepatic failure there may be focal sign. ----Asterxis,myoclonus and tremor Decerebrate and decorticate may be seen in uremia, hepatic, anoxic, hypoglycemia and sedative drug induced coma.

9 Metabolic coma The presence reactive pupils of otherwise normal BS function is hallmark of m. coma. the later might be seen in str. coma with transtentorial at early stages but can be distinguished by means of focal n. sign. Exception :Metabolic coma with impaired PLR are Seen in glutithimide overdose, massive barbiturate poisoning( with apnea and hypotension), acute anoxia, marked hypothermia, and anticholinergic poisoning large pupil) ;and pinpoint in opiod overdose even in these condition completely unreactive pupil is unlikely. Reflex eye movement is intact except sedative drug and wernick’s encephalopathy

10 Emergency management 1-Ensure patency of airways, adequacy of ventilation and circulation (ABCDE): E: exposure,D-disability cervical x ray is important in case of trauma when patient need intubations. 2-Insert IV line, draw blood for general laboratory assessment, blood gases, PH, metabolic(LFT,RFT), electrolyte,drug,toxins, and PT,PTT. 3-Give: IV glucose(25-50ml of 50% dextrose), thiamine(100mg) and naloxone (o.4-1.2mg)& atropine. flumazenil? Caution in epilepsy. 4-Draw blood for blood gases and pH. 5-Treatment of seizure if present.

11 Then history and examination should obtained from relative or witness and perform G. and N. exam. To reach diagnosis. 1-history: time and course is important. a-sudden onset-----in vascular cause ex; brainstem and SAH. b-rapid progression from H. sign like aphasia or hemiparesis consistent with ICH. C-More long progression days-a week). think about SOL as a cause. d-a state of confusional state or agitation with out localizing sign goes with metabolic cause. 2-general exam. a-look for signs of trauma. n/ p: in rhinorrhea, CSF chloride and glucose is higher than in mucous b-BP checking. c-temp. hypothermia raise possibility of ethanol toxicity. hypoglycemia,sedative drug intoxication,myxedema,hepatic and wernick’s encephalopathy. coma with hyperthermia seen in heat stroke, status E.,pontine hemorrhage, antichol. drug and malignant hyperthermia from inhalation anesthesia and hypotha. Lesion. d-signs of m. irritation. May be lost in deep coma in presence of SAH and m. e-optic fundi

12 3-neurological exam. This is crucial for diagnosis. it include 3 main elements A-pupillary reflex; either normal 3-4mm reacting bilaterally and briskly in supratent str. and metabolic coma thalamic pupil: slightly small reactive seen in early stages of thalamic compression with early herniation (interruption of sympathetic ocular supply) fixed dilated (>7mm)not reacting. Seen in 3rd nerve compression less likely anticholinergic or sympathetic drug intoxication. pinpoint (<1,5mm): seems to be not reacting but really reacting with magnification seen in opioid overdose, pontine lesion,also in neurosyphilis, miotic eye drop and organophosphorus. In 20% of population have asymmetry in pupil size called aniscoria where both reacting to same extent. the one less reacting in comparism to the other indicate MB or 3rd nerve lesion in that side.

13 B-Extraocular movement; Tested by stimulation of vestibular system either by doll’s head movement (oculo-cephalic reflex: normally eye deviated to side away from direction of rotation) or irrigation against the tympanic membrane (calorie test: normally there is tonic deviation of both eyes to side of irrigation of ice water). If it is fixed or abnormal= brainstem lesion If one or both eyes down ward deviated after cold cal. Test=sedative drug poisoning. Both are normal in comatose in cases of metabolic ( with exception*) and H. lesion with out BS affection (from pons –MB level) involvement. *Sedative drug intoxication with predilection to brainstem and some time there is tonic deviation of eyes (one or both) downward in caloric test stimulation.

14 c-Motor response to pain: already discussed assessed by deep pressure at supraorbital, sternal or nail bed. it is of help in localizing the level of cerebral dysfunction and assess the depth of coma. In C. lesion of mod. Severity the patient may localize or do semi purpseful movement which difficult to differentiate it from reflexic movement (never an abduction). In thalamic lesion direct or sec. to downward pressure from large H. lesion causing decorticate response. More sever brain dysfunction lead to Decerebrate posture (MB function is compromised). Bilateral symmetric posturing seen in both str. and metabolic coma Unilateral and asymmetrical posture seen in controlateral str. cerebral or brainstem lesion. In pontine or medullary,there is no response or slight flexion in legs Useful in Glasgow coma scale? EVM =15 GRADE

15 Stages of suprat. lesion: all normal when lesion at brain level but: P. Ref. Reflex e.move* MOTOR R. Early diencephalons 2mm,reactive normal localizing, often asymmetry Late = = = decorticate Midbrain dilated(>7) not r. impair add. Decerebrate Pons ** pin point + impair abd. no resp. or slight flexion * to doll’s or to ear irrigation=caloric test ** pin point pupil(1-1.5), unreactive seen in pontine lesion.

16 etiology Metabolic: Drug overdose diabetes including-hypoglycemia, hyperglycemia &hyperosmlar coma uremia hepatic failure hyponitremia respiratory F. Hypothyroidism Hypothermia Trauma: Cerebral contusion,subdural hematoma,extradural H. Cerebrovascular Disease SAH Intracerbral Hematoma Cerebral V. thrombosis. Brainstem infarction and bleeding. Infection Meningitis Encephalitis Cerebral abscess General abscess Others: Epilepsy, thiamin deficiency, brain tumor.

17 Glasgow Coma scale

18 BRAIN DEATH Irreversible and persistent cessation of all brain function In comatose patient (unresponsive) on ventilator not due to hypothermia (<32 c),sedative, neuro-muscular agent or shock.* *Child should be diagnosed with caution

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