1. Management of comatose patient
DR.H.N.SARKER
MBBS,FCPS,MRCP(UK),
MACP(USA),MRCPS(GLASGOW)
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
In order for a person 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 400mcg of naloxane i.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
Extension 2
No response 1

30. Examination Verbal response (V) Orientated 5 Confused conversation 4
Inappropriate words
Incomprehensible sounds
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.

48. THANK YOU