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Approach to

Approach to. Contents. Clinical Evaluation History Examination Lab Evaluation Management. Basics. Wakefulness depends on the integrity of both cerebral hemi- spheres and the ascending reticular activating formation of the brain stem . Cont.

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Approach to

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  1. Approach to

  2. Contents • Clinical Evaluation History Examination • Lab Evaluation • Management

  3. Basics Wakefulness depends on the integrity of both cerebral hemi- spheres and the ascending reticular activating formation of the brain stem.

  4. Cont.. • The management of an unconscious patient is never an easy task in clinical practice The duty of physician is • Arrive at diagnosis • Predict the eventual outcome

  5. History

  6. Onset of coma (abrupt, gradual) ii) Recent complaints ( headache, depression, focal weakness, vertigo ) iii) Recent injury iv) Previous medical illness ( diabetes,uraemia, heart disease ) v) Access to drugs ( sedatives,psychotropic drugs )

  7. Examination

  8. General physical Examination i) Vital signs ii) Evidence of trauma iii) Evidence of acute or chronic system illness iv) Evidence of drug ingestion ( needle marks alcohol breath ) v) Nuchal rigidity (examine with care)

  9. Neurological Examination

  10. State of consciousness Obtundation; responds-to verbal stimuli although slow and inappropriate. Stupor; the subject can be aroused only by vigorous and repeated noxious stimuli. Coma; unarousable and unresponsive. Stupor; the subject can be roused only by vigorous and repeated noxious stimuli.

  11. Respiratory pattern a ) Hyperventilation - midbrain and upper pons lesion metabolic diseases e.g. hepatic coma, diabetes and generalised raised intracranial pressure in its early stages. ( b ) Hypoventilation - medullary, upper cervical spinal lesion Drug overdose and later stages of cerebral herniation. ( e ) Cheyne-Stoke respiration – usually diencephalic lesion central transtentorial herniation and obstructive hydrocephalus. ( d ) Ataxic respiration (completely irregular breathing) brain-stem dysfunction of a diffuse nature

  12. Pupillary size and reaction Medium to dilated symmetrical pupils fixed to light structural disease of the brain stem. Small symmetrical pupils reactive to light metabolic diseases and drug overdose. Unequal pupil fixed to light intracranial mass lesion producing 3rd nerve palsy e.g in unilateral uncal herniation.

  13. Eye movements Vestibulo-ocular reflexes – douching of one ear with cold water produces ipsi-lateral deviation of both eyes with a contralateral quick phase nystagmus lasting for 1—2 minutes. Use of hot water produces the opposite effect i.e. contralateral deviation with ipsilateral quick phase nystagmus. Bilateral douching with cold water gives rise to downward deviation with upward nystagmus and with hot water the opposite response. Absence or abnormal response indicates brain-stem dysfunction. Oculo-cephalic reflexes (Doll's eye movement ) - Normal response consist of deviation of both eyes to the opposite direction of head rotation. Again absence or abnormal response indicates brain-stem dysfunction.

  14. Motor Responses This is elicited by applying peripheral noxious stimuli e.g. pinching of limbs rubbing the sternum to elicit pain. ( a ) Appropriate response – brushing away the source of stimulus. { b ) Inappropriate response - decerebrate or decorticate rigidity. Motor response is also of localising value. Paralysed limb will show no response and presence of hemiplegia can therefore be evident. Decerebrate rigidity indicates brain-stem damage and if bilateral is usually associated with a very poor prognosis. Complete flaccidity with no response to noxious stimuli is often indicative of severe central nervous system depression due to drug overdose.

  15. Laboratory Evaluation

  16. Supratentorial lesions • Skull radiograph • Computerised tomographic scan CTscan) • Carotid angiography • EEG ( electroencephalogram )

  17. Infratentorial lesions • Skull radiograph • CT scan • Vertebral angiography • EEG • Ventriculography

  18. Diffuse neuronal lesions • Examination of CSF ( cerebro spinal fluid ) • Serum glucose, calcium, Na, K, magnesium • Blood gases and PH • Liver and renal functions • Drug levels

  19. Management

  20. Initial Management • Airway • Breathing • Circulation • Deformity • Exposure

  21. Definitive Management In general, management of the comatose patient depends on the cause. However, while the patient is undergoing evaluation, it is essential to : • pressure area care • care of the mouth, eyes and skin • physiotherapy to protect muscles and joints • risks of deep vein thrombosis • risks of stress ulceration of the stomach • nutrition and fluid balance • urinary catheterization • monitoring of the CVS • infection control • maintenance of adequate oxygenation, with the assistance of artificial ventilation

  22. You are in emergency department when an unconscious patient land in emergency with B.P 90/50 pulse 92/min and attendants tell u that the patient suddenly fell unconscious, how will you approach ?

  23. APPROACH • ABC • Immediate management • Examination • History • Investigations

  24. ABC

  25. Immediate management • Maintain i.v line, oxygen inhalation • Blood sample for RBS • Control seizures • Consider i.v glucose, thiamine, naloxone, flumazenil

  26. Examination

  27. CONTD. Vitals 1.Pulse tachycardia • Hypovolemia/haemorrhage • hyperthermia • Intoxication bradycardia • Raised intracranial pressure • Heart blocks

  28. CONTD. 2.Temperatureincreased • Sepsis • Meningitis ,encephalitis • Malaria ,Pontine haemorrhage Decreased • Hypoglycemia • Hypothermia (less than 31 C) • Myxedema • Alcohol, barbiturate ,sedative or phenothiazine intoxication.

  29. CONTD. 3.Blood pressure increased • Hypertensive encephalopathy • Cerebral haemorrhage • Raised intracranial pressure Decreased • Hypovolemia /hgr • Myocardial infarction • Intoxication/poisoning • Profound hypothyroidism, Addisonian crisis

  30. CONTD. 4.Respiratoryrate Increased(tachypnae) • Pneumonia • Acidosis (DKA, renal failure) • Pulmonary embolism • Respiratory failure Decreased • Intoxication/poisoning

  31. CONTD. Skin petechial rash • Meningococcal meningitis • Endocarditis • Sepsis,thrombotic thrombocytopenic purpura • Rickettsial infection RMS (rocky mountain spotted fever)

  32. CONTD. Multiple injection marks • Drug addiction • Acute endocarditis • Hepatitis B /C with encephalopathy • HIV

  33. CONTD. Neurological assessment; • General posture • Level of conciousness

  34. CONTD. Posture; • Lack of movements on one side • Intermittent twitching • Multifocal myoclonus • DECORTICATION • DECEREBRATION

  35. CONTD. Level of conciousness • Glasgow coma scale (GCS) Best motor response Best verbal response Eye opening GCS score 3 –severe injury less than or equal to 8 – moderate injury 9 to 12 – minor injury

  36. CONTD. • An abbreviated coma scale is used in the assessment of critically ill patient (primary servey) AVPU A –alert V – respond to voice stimulus P – respond to pain U - unresponsive

  37. Brainstem reflexes • Pupillary responses to light • Spontaneous and elicited eye movements • Corneal responses • Respiratory movements

  38. CONTD.Ocular movements • Conjugate deviation of eyes to a side – ipsilateral hemisphere frontal leison or contralateral pontine leison. Rarely eyes may turn paradoxically away from the side of deep hemisphere leison (WRONG-WAY EYES) • Downward conjugate deviation of eyes – mesencephalic leison.

  39. CONTD. • Eyes turn down and inward in – thalamic hgr and upper midbrain leison. • Ocular bobbing – is diagnostic of pontine hgr. • Ocular dipping - indicates diffuse cortical anoxic damage. • Dysconjugate ocular deviation – brainstem leison.

  40. CONTD. • Oculocephalic reflex (Doll’s eyes response) – brisk in cortical depression ,lost in brainstem leison. • Oculovestibulo responses –two components 1.Conjugate ocular movement – loss in brainstem damage. 2.Nystagmus – loss in damage to cerebral hemisphere

  41. CONTD.Pupillary changes;

  42. CONTD.

  43. CONTD.Respiratory movements • Has less localizing value then other brainstem reflexes. • Cheyen-stokes respiration(classic cyclic form ending with a brief apneic period – B/L hemisphere damage or metabolic depression. • Rapid ,deep breathing (Kussmaul) –in metabolic acidosis and in pontomesencephalic leison.

  44. Neck rigidity; • Meningitis • Subarachnoid haemorrhage

  45. Fundoscopy • Raised intracranial pressure • Hypertensive changes • Subarachnoid haemorrhage • Diabetic retinopathy

  46. History • Onset of the symptoms • Antecedent symptoms • Use of medications • Chronic liver ,kidney ,lung or heart disease

  47. CAUSES OF UNCONCIOUSNESS

  48. Causes of unconciousness • Metabolic Drugs, poisoning e.g CO ,alcohol Hypoglcemia, hyperglycemia (keto acidoti or HONK) Hypoxia, carbondiaoxide narcosis (COPD) Septicemia Hypothermia Myxedema ,addisonian crisis Hepatic / uremic encephalopathy

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