Management of comatose patient

DR.H.N.SARKER

MBBS,FCPS,MRCP(UK), FRCP(Edin) Associate Professor Medicine

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.

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).

Introduction

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

Introduction

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, ).

Introduction

■ inactivity: the subject can be roused.

■ ■ Sleep is normal mental and physical 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.

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.

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.

Mechanisms of coma

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

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

Causes of coma

Diffuse brain dysfunction

    

Severe uraemia Hepatocellular failure Respiratory failure with CO2 retention Hypercalcaemia, hypocalcaemia Hypoadrenalism, hypopituitarism and hypothyroidism

Causes of coma

Diffuse brain dysfunction

 Hyponatraemia, hypernatraemia    Metabolic acidosis Hypothermia, hyperpyrexia Trauma to brain  Epilepsy

Causes of coma

Diffuse brain dysfunction

 Encephalitis, cerebral malaria, septicaemia    Subarachnoid haemorrhage Metabolic rarities, e.g. porphyria Cerebral oedema from chronic hypoxia

Causes of coma

Direct effect within brainstem

• Brainstem haemorrhage or infarction • Brainstem neoplasm, e.g. glioma • Brainstem demyelination • Wernicke–Korsakoff syndrome • Trauma

Causes of coma

Pressure effect on brainstem

• Hemisphere tumour, infarction, haematoma, abscess, • encephalitis or trauma • Cerebellar mass

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

Causes of coma

   O-Opium,drug Overdose U- Uraemia D- Diabetes(Hypoglycaemia, diabetic ketoacidosis, nonketotic hyperosmolar hyperglycemia)

Causes of coma

   A-Apoplexy, Epidural and subdural hemorrhage, Subarachnoid hemorrhage M- Meningitis,cerebral Malaria M-Metabolic(hepatic failure)

Causes of coma

   A-Apoplexy, Epidural and subdural hemorrhage, Subarachnoid hemorrhage M- Meningitis, cerebral Malaria M-Metabolic (hepatic failure)

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

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.

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 naloxane i.v stat and repeat.

Subsequent management

 After initial therapy, subsequent assessment is done by taking history and physical examination including General and neurological examination

History

 All possible information from Relatives Paramedics Ambulance crew Bystanders

History

   Particularly about the mood of onset and circumstances Previous medical history epilepsy, DM, drug history Clues obtained from pt’s clothing and handbag

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

Examination

  3. Severity of coma-assessed by

Glasgow Coma Scale Eye opening (E)

• Spontaneous • To speech • To pain • No response 4 3 2 1

Examination



Motor response (M)

• Obeys • Localizes • Withdraws • Flexion • Extension • No response 6 5 4 3 2 1

Examination



Verbal response (V)

• Orientated • Confused conversation • Inappropriate words 3 • Incomprehensible sounds 2 • No response 5 4 1

Examination

 Glasgow Coma Scale = E + M + V (GCS minimum = 3: maximum = 15)

Examination

Examination

Examination

4. Pupil size and reaction-

Examination

5.Spontaneous eye movement Abnormal conjugate deviation suggests intracerebral damage.

Dysconjugate deviation implies damage to 3,4 or 6th nerve palsy

Examination

6.Respiratory rate and pattern-

Examination

7.

Signs of Lateralisation suggest focal neurological damage

Examination

Investigations

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

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).

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:

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.

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.

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)

Management

■ fluids – intragastric or i.v.

■ calories – liquid diet through a fine intragastric tube, 3000 kcal daily ■ sphincters – catheterization when essential ; rectal evacuation.

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.

Management

 Specific treatment Treatment of specific causes of coma.