1. Define Coma
2. What anatomical structures must be malfunctioning to produce coma?
3. What are the initial steps in managing a patient with coma?
4. How do you go about diagnosing the cause of coma?
5. Give pathological reasons for the following signs
purpuric rash
'Battle' sign
bilateral large fixed pupils
unilateral large fixed pupil
nuchal rigidity
gynaecomastia and spider naevi
bilateral pinpoint pupils
unilateral chemosis and proptosis
myoclonus
quadriplegia, loss of lower cranial nerve function but retained vertical eye movements
6. How dos the finding of a new focal abnormality on neurological examination affect the management of the comatose patient?
7. Does a nonfocal neurological examination in a comatose patient exclude a mass as the cause of coma?
8. What initial laboratory investigations should be performed in coma of uncertain aetiology?
9. What is the approach to the comatose trauma patient?
10. What are the common causes of coma in the ICU?
Integrates disease process, pathophysiology, and clinical presentation
A normal level of consciousness
(wakefulness) depends upon activation of the cerebral hemispheres by neurons
located in the brainstem RAS. Both of these components and the connections
between them must be preserved for normal consciousness to be maintained. The
principal causes of coma are therefore: (1) widespread damage in both
hemispheres from ischemia, trauma, or other less common brain diseases; (2)
suppression of cerebral function by extrinsic drugs, toxins, or hypoxia or by
internal metabolic derangements such as hypoglycemia, azotemia, hepatic
failure, or hypercalcemia; and (3) brainstem lesions that cause proximate
damage to the RAS.
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Differential Diagnosis of Coma |
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Pathological Site |
Primary Cause |
Secondary Cause |
Location |
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INTRACRANIAL |
Vascular |
Haemorrhage |
intracerebral |
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subarachnoid |
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subdural |
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extradural |
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Infarction |
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Infection |
Meningitis |
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Encephalitis |
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Abscess |
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Tumour |
Mass effect |
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Cerebral oedema |
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Post epileptic |
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Head injury |
Vascular effects |
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Hypoxic encephalopathy |
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Cerebral oedema |
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Psychiatric |
Conversion disorder |
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Depression |
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Catatonia |
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EXTRACRANIAL |
Cardiovascular |
Shock (any cause) |
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Severe hypertension |
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Infection |
Septicaemia |
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Metabolic |
Hyper/hypo-osmolar states |
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Hyper/hypoglycaemia |
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Hormonal insufficiency |
Pituitary |
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Adrenal |
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Thyroid |
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Electrolyte disorders |
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Hypoxia |
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Carbon monoxide poisoning |
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Hypercarbia |
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Hepatic encephalopathy |
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Uraemic encephalopathy |
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Drugs |
Sedatives |
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Analgesics |
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Alcohol |
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Major tranquillizers |
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Physical injury |
Hyper/hypothermia |
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Electrocution |
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Begin simply and accurately - then get specific
A Alert
V responds to Verbal stimuli
P responds to Painful stimuli
U Unresponsive
Eye Opening Spontaneous 4
To speech 3
To pain 2
Nil 1
Best Motor Response Obeys commands 6
Localises to pain 5
Withdraws to pain 4
Abnormal flexion 3
Extensor response 2
Nil 1
Verbal Response Orientated 5
Confused conversation 4
Inappropriate words 3
Incomprehensible words 2
nil 1
Maximum possible 15 Minimum possible 3 Intubate if
GCS < 10generally
The individual components are more important than the total number!
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Approaches
to Diagnosis - Clues |
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purpuric rash |
meningococcemia |
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battle sign |
base of skull fracture |
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bilateral large fixed pupils |
atropine poisoning |
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unilateral large sluggish pupils |
III nerve lesion temporal cone |
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mid position pupils no light response |
midbrain lesion |
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nuchal rigidity |
meningitis |
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gynaecomastia/spider naevi |
hepatic encephalopathy |
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bilateral pinpoint reactive pupils |
narcotic overdose |
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Horner's syndrome |
medullary lesion |
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myoclonus |
hypoxic encephalopathy |
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hyperventilation |
brainstem (usually pulmonary) |
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Cheynes Stokes breathing |
deep bilateral subcortical lesion |
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Apneustic breathing |
pontine lesion |
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