Dr. Raj Gopal. V: Tuesday, March 10, 2015
Dr. Raj Gopal. V: Tuesday, March 10, 2015
Dr. Raj Gopal. V: Tuesday, March 10, 2015
2015
Definition of COMA
Coma is defined as a sleeplike state with total absence
of awareness of self and the environment, even after
vigorous external stimulation. Coma is the most severe
form of unresponsiveness, and by definition, comatose
patients lie with their eyes closed.
In general a
comatose person is:
Apparently asleep.
Closing the eyes.
Not talking.
Unresponsive to instructions.
Without any voluntary movements.
Tuesday, March 10,
2015
Conscious
state
Drowsy
Stupor
Coma
PVS
(Persistent
Vegetative
State)
Pathophysiology of coma
Primarily 2 mechanisms:
A diffuse insult to both cerebral hemispheres.
A focal lesion in the Reticular Activating
System (RAS) in the upper Pons, midbrain or
the Diencephalon.
The Big-3 causes: Stroke, Trauma, Drug
overdose (STD!).
Tuesday, March 10,
2015
COMA
RAS
(Diencephalon)
COMA
(Pons,
Medulla)
Dr. Raj
Gopal.
V
Causes of COMA
Two broad categories: Structural or surgical
and Metabolic or Medical.
Structural/Surgical: Diffuse damage to both cerebral
hemispheres due to vascular damage or raised
intracranial pressure.
Medical/Metabolic: Diffuse insult to both cerebral
hemispheres by toxins, either from within or from
outside.
Causes of COMA
Remember AEIOU-TIPS
A: Alcohol.
E: Epilepsy or Exposure to heat and cold
I: Insulin (Diabetic emergencies)
O: Overdose or Oxygen deficiency
U: Uremia (kidney failure)
T: Trauma (Shock or head injury)
I: Infection or Iatrogenic.
P: Psychosis or poisoning.
S: Strokes.
There are 424 causes of COMA!
Tuesday, March 10,
2015
Differences
Differences between Structural or surgical and
Metabolic or Medical.
Structural/Surgical: Focal neurological signs, dilated
and unreactive pupils and increased intracranial
pressure.
Medical/Metabolic: Reactive pupils, no focal
neurological signs and normal intracranial pressures.
Diagnosis of COMA
History from third parties like family, friends and
emergency medical personnel. Ask relevant
questions.
Clinical Examination: Quick and precise.
Rapid and appropriate investigations: To find cause
and institute appropriate treatment.
Assessment of COMA
The level of coma is assessed by the Glasgow
Coma Scale. A quick assessment is the AVPU
scale, used by emergency medical personnel:
A:
V:
P:
U:
Alert.
Responds to verbal commands.
Responds to pain.
Unresponsive - - - - - Proceed to GCS.
Assessment of COMA
The level of coma is assessed by the Glasgow
Coma Scale. GCS assesses:
Best verbal response.
Best motor response.
Level of stimulus needed to make the patient
open the eyes.
MOTOR RESPONSE
4
3
2
1
Obeys
Localizes
Withdraws
Abnormal flexion
Extension Posturing
No response
VERBAL RESPONSE
Oriented
Confused conversation
Inappropriate words
Incomprehensible sounds
No response
Tuesday, March 10,
2015
5
4
3
2
1
6
5
4
3
2
1
Total score: E + M + V
Range: 3 15.
Mild coma: 13 15
Moderate coma: 9 12
Severe coma: < 8
Dr. Raj Gopal. V
Neurological examination
The neurological examination focuses on 4
components.
Respiratory patterns.
Pupillary responses.
Eye movements.
Motor responses.
The most important examination in coma (to identify the
cause) is the examination of the pupillary response
and eye movements.
Tuesday, March 10,
2015
Respiratory patterns
Pattern
Lesion
Description
Cheyne-Stokes
Forebrain to
pons
Hyperventilation and
hypoventilation with pauses.
Apneustic
breathing
Pons
Cluster breathing
High
medullary
lesions
Ataxic breathing
Medulla
Pupillary responses
Most important part of examination.
Pupils that react to light and are equal in size: Metabolic or
medical coma.
Unreactive, unequal and dilated pupil: Neurosurgical
emergency.
Pinpoint pupils: Pontine lesions or opiate toxicity.
Bilateral dilated, unresponsive pupils: Anoxia, severe
midbrain damage or anticholinergic drugs.
No pupillary abnormality: Excludes lesions below pons and
above thalamus.
Eye movements
Roving, slow, conjugate, lateral to and fro movements: Metabolic
encephalopathies or bilateral lesions above brainstem.
Ocular bobbing: Rapid downward jerk and slow return to
midposition of both eyes: Bilateral pontine lesions.
Ocular dipping: Slow downward dipping followed by brisk return:
Diffuse cerebral damage.
Skew deviation in horizontal plane; Cerebellar or pontine lesion.
Dolls eye reflex: Normally when the head is turned in a lateral
plane the eyes move in the opposite direction. Absence of this
response indicates brainstem lesion.
Caloric testing: 40-60 mL of ice cold water in the ears will cause
the eyes to move towards the irrigated ear. Absence indicates
brainstem damage.
Tuesday, March 10,
2015
Motor responses
Spontaneous movements always good sign.
One side paralyzed: Suspect lesion in brain on the side
not moving.
Decorticate posturing: Arms flexed and legs extended
indicates lesions above brainstem or a metabolic cause.
Decerebrate posturing; Arms extended and legs extended
indicates bilateral midbrain or pontine lesion. Worse
prognosis. Also seen in metabolic conditions sometimes.
Myoclonus: Non-rhythmic jerking in single or multiple
muscle groups suggests metabolic encephalopathies
(hepatic chiefly).
Investigations
Full blood counts: Infections.
Biochemistry: Electrolytes, sugar, LFTs, KFTs.
Arterial blood gases: Oxygen, CO2, pH, HCO3.
Blood cultures.
Alcohol levels.
Drug screen (urine and blood)
Lumbar puncture: Infections.
CT Scans in case of trauma, bleeds, hemorrhage.
MRIs where possible.
Thyroid function tests (rarely)
Electroencephalogram (EEG) & ECG.
CXR.
Blood slides for Malaria!!
Tuesday, March 10,
2015
Management
Immediate management in hospital:
Never forget ABC: Airway, Breathing, Circulation.
COMA COCKTAIL: 50 mL of 50% Dextrose + Thiamine
100 mg + Naloxone 0.4 mg (adults).
Stop seizures with anti-epileptics.
Treat metabolic disturbances.
Lower intracranial pressure.
Treat infections.
Mechanical ventilation, IV lines and Ryles tubes.
Specific Management
Further management depends on the cause always.
Diabetes, hepatic coma, electrolyte imbalances, endocrine
causes etc: Correction of metabolic derangements.
Trauma: Neurosurgery.
Strokes, heart attacks, respiratory failure, hypoxia,
hypothermia: Correct underlying causes.
Medication/drug overdose: Specific antidotes.
Meningitis and infections: Antibiotics.
Raised ICP: Mannitol and Dexamethasone.
Long-term Management
Intensive nursing care.
Recovery position.
Mechanical ventilation.
Pressure sores prevention.
Care of the eyes.
Airway clearance by bronchial toilet.
Fluid and nutrition.
Catheterization of bladder.
Bowel care Disposable diapers.
Physio to protect muscles and joints.
DVT prophylaxis?
Vital signs monitoring.
Neurological monitoring.
Tuesday, March 10,
2015
WORST PROGNOSIS:
Structural damage
Subarachnoid Hemorrhage
Cerebrovascular causes
On Day I:
No corneal reflex
No pupillary reflex
Decerebrate posture
GOOD PROGNOSIS:
Metabolic causes.
If no recovery in 4 weeks
progresses to PVS.
INDICATORS OF PROGNOSIS:
Depth of coma as by GCS
Pupillary reflexes.
Eye movements.
Motor responses.
Age.
Complications
Pressure sores.
Bladder infections.
Pneumonia: Hospital acquired or ventilator
associated.
Persistent Vegetative State.
Brain death
Brain death is different from coma and PVS
Complete lack of activity anywhere in the brain.
Kept alive through artificial means.
Clinically and legally dead.
Confirmatory EEG for legal purposes: Isoelectric flat line.
Tests: Shine a light into eyes, corneal reflex, pain
sensation, caloric tests, gag or cough reflex tested and
removal from ventilator for short period to see if it stimulates
respiration.
Organs for transplantation if there is consent.
SUMMARY
Quick history from relatives and friends.
Quick medical examination.
Immediate transfer to specialized centers.
Assessment of Coma depth.
Detailed neurological evaluation.
Basic Laboratory investigations.
Specialized investigations.
Correct underlying cause where possible.
Refer for specialist care if required.
Ongoing care of the patient.
Recovery --------- Congratulations!
Progression to PVS or brain death.
Tuesday, March 10,
2015