Management of comatose patient

1. Management of comatose patient DR.H.N.SARKER MBBS,FCPS,MRCP(UK), FRCP(Edin) Associate Professor Medicine

2. Introduction • Consciousness means wakefulness with awareness of self and surroundings. • The state of consciousness is the product of complex interactions between parts of the reticular activating system in brainstem and medial part of thalamus , cortex, and all sensory stimuli.

3. Introduction • For a person, in order to maintain consciousness, the two important neurological components must function perfectly. • 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).

4. Introduction • Injury to either, or both of these components is sufficient to cause a patient to experience altered consciousness.

5. Introduction

6. Introduction • Altered / Disturbed consciousness: definitions of some terms- ■ Clouding of consciousness –means reduced wakefulness and/or self-awareness, sometimes with confusion. ■ Confusion means that the subject is bewildered and misinterprets his/her surroundings. ■ Delirium is a state of confusion, sometimes with visual hallucination, and often high arousal (e.g. delirium tremens, ).

7. Introduction ■ Sleep is normal mental and physical inactivity: the subject can be roused. ■ Stupor is abnormal; a sleepy state from which the subject can be aroused by vigorous or repeated stimuli. The term is also used for psychiatric states, e.g. catatonic and depressive stupor. ■ Coma means unrousable unresponsiveness. Coma is a state of unconsciousness whereby a patient cannot react with the surrounding environment.

8. Mechanisms of coma • Altered consciousness is produced by three mechanisms affecting brainstem, reticular formation and cortex. ■ Diffuse brain dysfunction. Generalized severe metabolic or toxic disorders (e.g. alcohol, sedatives, uraemia, septicaemia) depress overall brain function.

9. Mechanisms of coma ■ Direct effect within the brainstem. A brainstem lesion inhibits the reticular formation. ■ Pressure effect on the brainstem. A mass lesion within the brain compresses the brainstem, inhibiting the reticular formation.

10. Mechanisms of coma • A single focal hemisphere (or cerebellar) lesion does not produce coma unless it compresses or damages the brainstem.

11. Causes of coma • Principal causes of coma Diffuse brain dysfunction • Drug overdose, alcohol abuse • CO poisoning, anaesthetic gases • Hypoglycaemia, hyperglycaemia • Hypoxic/ischaemic brain injury • Hypertensive encephalopathy

12. Causes of coma Diffuse brain dysfunction • Severe uraemia • Hepatocellular failure • Respiratory failure with CO2 retention • Hypercalcaemia, hypocalcaemia • Hypoadrenalism, hypopituitarism and hypothyroidism

13. Causes of coma Diffuse brain dysfunction • Hyponatraemia, hypernatraemia • Metabolic acidosis • Hypothermia, hyperpyrexia • Trauma to brain • Epilepsy

14. Causes of coma Diffuse brain dysfunction • Encephalitis, cerebral malaria, septicaemia • Subarachnoid haemorrhage • Metabolic rarities, e.g. porphyria • Cerebral oedema from chronic hypoxia

15. Causes of coma Direct effect within brainstem • Brainstem haemorrhage or infarction • Brainstem neoplasm, e.g. glioma • Brainstem demyelination • Wernicke–Korsakoff syndrome • Trauma

16. Causes of coma Pressure effect on brainstem • Hemisphere tumour, infarction, haematoma, abscess, • encephalitis or trauma • Cerebellar mass

17. Causes of coma • Common causes of coma (remember by Mnomonic-AEIOU,DAMM ) • A-Alcohol, Abscess • E- Epilepsy, Encephalitis, Endocrine and Electrolyte disturbance • I- Head injury, Brainstem Infarction or haemorrhage

18. Causes of coma • O-Opium,drug Overdose • U- Uraemia • D- Diabetes(Hypoglycaemia, diabetic ketoacidosis, nonketotic hyperosmolar hyperglycemia)

19. Causes of coma • A-Apoplexy, Epidural and subdural hemorrhage, Subarachnoid hemorrhage • M- Meningitis,cerebral Malaria • M-Metabolic(hepatic failure)

20. Causes of coma • A-Apoplexy, Epidural and subdural hemorrhage, Subarachnoid hemorrhage • M- Meningitis, cerebral Malaria • M-Metabolic (hepatic failure)

21. Approach to the Patient: Coma • Immediate assessment Actions that take seconds save lives. • Assess airway, breathing, circulation-resuscitate. • Give 100% O2, monitor pulse oximetry and obtain venous access. • Withdraw blood for glucose, other biochemical parameters and drug screening

22. Immediate assessment • Record the GCS and check the pupil size and reaction. • Check the bedside glucose and the temperature. • Consider the differential diagnosis. • Look for a Medic alert bracelet or necklace.

23. Immediate therapy • If hypoglycaemia, give 50 ml 50% glucose i.v. • If hypothermia, start rewarming. • If pupils are small, R rate is low or signs of drug abuse are present, give 400µg of naloxanei.v stat and repeat.

24. Subsequent management • After initial therapy, subsequent assessment is done by taking history and physical examination including General and neurological examination

25. History • All possible information from Relatives Paramedics Ambulance crew Bystanders

26. History • Particularly about the mood of onset and circumstances • Previous medical history- epilepsy, DM, drug history • Clues obtained from pt’s clothing and handbag

27. Examination • A thorough examination of all systems is essential but concentrate on the following. • 1.Trauma requires complete exposure and roll to examine back • 2. Neddle mark

28. Examination • 3. Severity of coma-assessed by Glasgow Coma Scale • Eye opening (E) • Spontaneous 4 • To speech 3 • To pain 2 • No response 1

29. Examination • Motor response (M) • Obeys 6 • Localizes 5 • Withdraws 4 • Flexion 3 • Extension 2 • No response 1

30. Examination • Verbal response (V) • Orientated 5 • Confused conversation 4 • Inappropriate words 3 • Incomprehensible sounds 2 • No response 1

31. Examination • Glasgow Coma Scale = E + M + V (GCS minimum = 3: maximum = 15)

32. Examination

33. Examination

34. Examination 4. Pupil size and reaction-

35. Examination 5.Spontaneous eye movement- Abnormal conjugate deviation suggests intracerebral damage. Dysconjugate deviation implies damage to 3,4 or 6th nerve palsy

36. Examination 6.Respiratory rate and pattern-

37. Examination 7. Signs of Lateralisation suggest focal neurological damage

38. Examination

39. Investigations • Often, the cause is evident (e.g. head injury, cerebral haemorrhage, self-poisoning); • if no cause is evident, further investigations are essential.

40. Investigations • Blood and urine ■ Drugs screen (e.g. salicylates, diazepam, narcotics, amfetamines). ■ Routine biochemistry (urea, electrolytes, glucose, calcium, liver biochemistry). ■ Metabolic and endocrine studies (TSH, cortisol). ■ Blood and urine cultures. ■ Other, e.g. cerebral malaria (request thick blood film).

41. Investigations • Imaging CT or MR brain imaging may indicate an unsuspected mass lesion or intracranial haemorrhage. • CSF examination Lumbar puncture should be performed in coma only after careful risk assessment. It is contraindicated when an intracranial mass lesion is a possibility:

42. Investigations CT is essential to exclude this. CSF examination is likely to alter therapy only if undiagnosed meningoencephalitis or other infection is present. • Electroencephalography EEG is of some value in the diagnosis of metabolic coma and encephalitis.

43. Management • Comatose and stuporose patients – at home or outside, on a trolley, in a ward or ITU – need immediate careful nursing, • meticulous attention to the airway (protected airway) , and • frequent monitoring of vital functions and high flow O2.

44. Management • Longer-term essentials are: ■ skin care – turning (to avoid pressure sores and pressure palsies), removal of jewellery, a suitable pressure-relieving mattress. ■ oral hygiene – mouthwashes, suction ■ eye care – prevention of corneal damage (lid taping, irrigation)

45. Management ■ fluids – intragastric or i.v. ■ calories – liquid diet through a fine intragastric tube, 3000 kcal daily ■ sphincters – catheterization when essential ; rectal evacuation.

46. Management • Broad spectrum antibiotics and/or antivirals should be given empirically if there is any suggestion of bacterial infection or encephalitis . • Half-hourly neuro-observations.

47. Management • Specific treatment- Treatment of specific causes of coma.

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