COMA
DR RABIA RATHORE
ASSISTANT PROFESSOR
WEST MEDICAL WARD
MAYO HOSPITAL/K.E.M.U
COMA
DR RABIA RATHORE
ASSISTANT PROFESSOR
WEST MEDICAL WARD
MAYO HOSPITAL/K.E.M.U
DEFINITION OF COMA
 A state of prolonged unconsciousness
characterized by loss of reaction to
external stimuli or, a state of
unarousable unresponsiveness.
 Consciousness is dependent on the functioning of
two separate anatomical and physiological
systems:
 The ascending reticular activating system (ARAS)
projecting from brainstem to thalamus. This
determines arousal (the level of consciousness)
 The cerebral cortex, which determines the content
of consciousness.
 Impaired functioning of either anatomical system
may cause coma.
FEATURES DISTINGUISHING BETWEEN
COMA AND RELATED STATES
STUPOR
Unconscious but can be aroused with repeated stimuli..
DELIRIUM :
Confused state often with restlessness and hallucinations
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‘LOCKED-IN SYNDROME :
Actually conscious but unable to speak or move may move eyes (massive brainstem
damage). Awarness is present , sleep awake cycles are present, vertical eye
movement /blinking may be seen. Respiration is preserved.
VEGETATIVE STATE :
Apparently awake but unresponsive (brainstem intact but widespread
cortical damage). Awarness is absent ,while sleep awake cycles are
present. There is no purpose movement ,respiration is preserved .
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 COMA:
 The Awarness is absent, sleep awake cycles are
absent.There is no purposeful movement and respiration
is variable..
 BRAIN DEATH :
 There is lack of awarness, sleep awake cycles are
absent.There is no purposeful movement ,respiration is
absent
CAUSES OF COMA
 DIFFUSE BRAIN DYSFUNCTION:
 Drug overdose (accidental or deliberate), including
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alcohol
CO poisoning
Traumatic brain injury
Hypoglycaemia, hyperglycaemia
Severe uraemia
Hepatic encephalopathy
Respiratory failure with CO2 retention
Hypercalcaemia, hypocalcaemia
Hypoadrenalism, hypopituitarism and hypothyroidism
Hyponatraemia, hypernatraemia
 Metabolic acidosis
 Hypothermia, hyperpyrexia
 Seizures – post-ictal state and non-convulsive
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status
Metabolic rarities, e.g. porphyria
Extensive cortical damage
Hypoxic-ischaemic brain injury, e.g. cardiac arrest
Encephalitis, meningitis, cerebral malaria
Subarachnoid haemorrhage
 DIRECT EFFECT WITHIN BRAIN STEM:
 Brainstem haemorrhage, infarction or
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demyelination
Brainstem neoplasm, e.g. glioma
Wernicke–Korsakoff syndrome
PRESSURE EFFECT ON BRAIN STEM:
Tumour, massive hemisphere infarction with
oedema,
haematoma, abscess
Cerebellar mass
IMMEDIATE ASSESMENT OF COMATOSE
PATIENT
 Check the airway, breathing and circulation.
 Check for blood glucose.
 Obtain as much history as possible.
 What were the circumstances?
 Ask paramedics, police, and witnesses. Contact the
patient’s relatives, friends and GP and obtain past
hospital notes.
 Look for drug details/bottles and identification
data.
GENERAL EXAMINATION
 Measure the patient’s temperature.Check for meningism.
 Sniff the patient’s breath for ketones, alcohol and hepatic
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fetor.
Survey the skin for signs of trauma or spinal injury, rash
(meningococcal sepsis), jaundice or stigmata of chronic liver
disease, cyanosis, injection marks.
Respiratory pattern:
Cheyne–Stokes (alternating hyperpnoea and periods of
apnoea indicating bilateral cerebral or upper brainstem
dysfunction)
Acidotic (Kussmaul) respiration (deep, sighing
hyperventilation seen in diabetic ketoacidosis and uraemia).
NEUROLOGICAL EXAMINATION
 Neurological examination aims to determine:
 Depth of coma (GCS)
 Brainstem function
 Lateralization of pathology
BRAIN STEM FUNCTION
 PUPILS:
 Record their size and reaction to light
 Dilatation of one pupil that then becomes fixed to
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light
Compression of the IIIrd nerve.
Bilateral mid-point reactive pupils (i.e. normal
pupils)
Metabolic comas
Sedative drugs except opiates.
 Bilateral light-fixed, dilated pupils:
 Brain death.
 Barbiturate intoxication
 hypothermia.
 Bilateral pinpoint, light-fixed pupils:
 Pontine haemorrhage
 Opiates.
 Mydriatic drugs
 previous pupillary surgery
LATERALIZING SIGNS
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Coma makes it difficult to recognize lateralizing signs. These
are helpful:
Asymmetry of response to visual threat in a
stuporose patient: suggests hemianopia
Asymmetry of face. Drooping or dribbling on one side,
blowing in and out of mouth when the paralysed cheek
does not move
Asymmetry of tone. Unilateral flaccidity or spasticity
may be the only sign of hemiparesis
Asymmetry of decerebrate and decorticate posturing
Asymmetrical response to painful stimuli
Asymmetry of tendon reflexes and plantar responses.
Both plantars are often extensor in deep coma.
CLINICAL PRESENTATION
CASE SCENARIO NO:1
 A young college boy had high grade fever for 3 days.
Fever was associated with photophobia.Now for the
last 5 hours he developed sudden severe headache
all around the head, 2 episodes of vomiting which
were projectile in nature followed by altered state
of consciousness.His examination revealed a young
male who was unconscious with pulse of 55 beats
per minute ,blood pressure 160/90, signs of
meningeal irritation were present.
 What is the differential diagnosis?
 Acute Bacterial Meningitis
 Subarachnoid haemorrhage
 Migraine
CAUSES OF MENINGITIS
 Bacteria
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Neisseria meningitidis
Streptococcus pneumoniaea
Staphylococcus aureus
Streptococcus Group B
Listeria monocytogenes
Gram-negative bacilli, e.g. E. coli
Mycobacterium tuberculosis
Treponema pallidum
• Viruses
• Epstein–Barr virus
• Enteroviruses
• Coxsackie virus
• Poliomyelitis
• Mumps
• Herpes simplex
• HIV
 Fungi
 Cryptococcus neoformans
 Candida albicans
 Coccidioides immitis, Histoplasma capsulatum,
 Blastomyces dermatitidis (USA)
CLINICAL CLUES IN MENINGITIS
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Clinical feature
Petechial rash
Skull fracture
Ear disease
Congenital CNS lesion
Immunocompromised
patients
Rash or pleuritic pain
International travel
Occupational
(work in drains, canals,
polluted water, recreational
swimming)
 Possible cause :
 Meningococcal infection
 Pneumococcal infection
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HIV opportunistic infection
Enterovirus infection
Malaria
Leptospirosis
CLINICAL FEATURES
MENINGOCOCCAL RASH
 How will you investigate him?
INVESTIGATIONS
 Blood complete examination & ESR
 Blood cultures
 CT scan
 Lumbar puncture
CSF PICTURE
COMPLICATIONS OF MENINGITIS
 ACUTE COMPLICATIONS:
 Seizures
 cranial nerve lesions
 venous sinus thrombosis
 severe cerebral oedema
 hydrocephalus
 CHRONIC COPMLICATIONS:
 Focal neurological
 Behaviour disorder
 Language deficit
 Deafness
 Seizure disorder
CASE SCENARIO NO 2
An old retired army officer who is diabetic and
hypertensive with poor compliance of medicine
developed severe headache and two episodes of vomiting,
just after the last episode of vomiting he fell down to the
ground ,developed altered state of consciousness and was
brought to emergency by his son . On examination GCS
was 3/15 there were pin point pupil ,horizontal eye
movements of eyes were absent while vertical eye
movements were present . His BP was 230/140mm of
Hg and temperature was 104*F. Respiratory rate was
32/min and was having qudreplegia.
 What is the diagnosis?
 PONTINE HEMORRHAGE
 How will you investigate him?
 The purpose of investigations in stroke is:
 To confirm the clinical diagnosis and distinguish
between haemorrhage and thromboembolic
infarction;
 To look for underlying causes and to direct therapy;
 To exclude other causes, e.g. tumour.
 Sources of embolus should be sought.
 Routine bloods (for ESR, polycythaemia, infection,
 vasculitis, thrombophilia, syphilitic serology, clotting
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studies, autoantibodies)
Fasting Lipid profile
Chest X-ray
ECG
E chocardiography
Carotid Doppler studies
MR angiography
PT/APTT
Bleeding time/Clotting time
 Imaging in Acute Stroke.
 Non-contrast CT:
 will demonstrate haemorrhage immediately but
cerebral infarction is often not detected or only subtle
changes are seen initially.
CT SCAN BRAIN
MR angiography showing
internal carotid artery occlusion.
DEFINITION
 Stroke
 Stroke is defined as a syndrome of rapid onset of cerebral
deficit (usually focal) lasting >24 h or leading to death,
with no cause apparent other than a vascular one.
Transient ischaemic attack (TIA)
means a brief episode of neurological dysfunction due to
temporary focal cerebral or retinal ischaemia without
infarction.
 TIAs may herald a stroke
 Risk factor for Ischemic stroke :
 Hypertension
 Diabetes
 Smoking
 Lifestyle
 High cholesterol
 Atrial fibrillation
 Obesity
 Severe carotid stenosis
 RARE CAUSES:
 Hyperviscosity states.
Thrombocythaemia,
Polycythaemia
Thrombophilia
Anti-cardiolipin and lupus anticoagulant antibodies
 oral contraceptive.
 Migraine
 Vasculitis
 Systemic lupus erythematosus (SLE),
 Polyarteritis
 Giant cell arteritis
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granulomatous CNS angiitis
Amyloidosis.
Hyperhomocysteinaemia
Neurosyphilis
mitochondrial disease
Drugs :
Sympathomimetic drugs
cocaine
Vasoconstrictors
neuroleptics
CADASIL (cerebral dominant arteriopathy with
subcortical infarcts and leucoencephalopathy)
 WHAT IS THE LESION ?
 WHERE IS THE LESION ?
CASE SCENARIO
 An 18 years old girl is brought to emergency in
unconscious state .Her mother gave a history that she
was havimg polyuria and polydipsia for the last few
months.2 days back she complained of abdominal
pain which worsened gradually,7-8 episodes of
vomiting and now has developed altered state of
consciousness which was gradual in onset.On
examinationshe was in a stuporous state with
evidence of dehydration, rapid deep breathing with
“fruity” breath odor of acetone .Her pulse was 110
bpm and BP.60/40 mm of Hg.
 What is the diagnosis?
 DIABETIC KETO ACIDOSIS
 HOW ARE U GOING TO INVESTIGATE HER?
INVESTIGATIONS
 BLOOD COMPLETE EXAMINATION
 BLOOD SUGAR LEVEL
 URINE FOR KETONES/COMPLETE EXAMINATION
 SERUM KETONES
 SERUM ELECTROLYTES
 SERUM OSMOLALITY
 mosm/kg =Measured[Na ]+Glucose (mg/dL)
18
 Blood urea nitrogen
 Serum creatinine
 Arterial blood gases
TERMS USED IN UNCONTROLLED
DIABETES
 Ketonuria
 Detectable ketone
levels in the urine; it
should be appreciated
that ketonuria occurs
in fasted non-diabetics.
 Ketosis
 Elevated plasma
ketone levels in the
absence of acidosis
 Diabetic ketoacidosis
 Hyperosmolar
Hyperglycaemic state
 A metabolic emergency
in which hyperglycaemia
is associated with a
metabolic acidosis due to
greatly raised (>5
mmol/L) ketone levels.
 A metabolic emergency
in which uncontrolled
hyperglycaemia induces
a hyperosmolar state
in the absence of
significant ketosis
 Lactic acidosis
 A metabolic
emergency in which
elevated lactic acid
levels induce a
metabolic acidosis and
associated with
biguanide therapy
CASE SCENARIO NO:3
 A middle aged female had a history of slowness in her
activities, dry brittle hairs and thick-skin.She also
complains of deep-voice with weight gain, cold
intolerance and constipation.There is also history of
oligomenorrhoea.Now has presented in emergency in
semi conscious state.On examination she had puffy
eyes ,loss of lateral 1/3of eye brows,peripheral non
pitting edema .Her pulse was 55 bpm.Heart sounds
were muffled.Her temperature was below normal.
 What is the diagnosis?
 Myxoedema coma
CASE SCENARIO NO:3
A young female was brought in emergency when
she was found unconscious in room by his
husband.Past history revealed that she has been on
treatment for depression since 4-5 months after the
death of her son.On further inquiring her husband
it was found that she had a fight with her husband
on some minor issue one day back .Examination
revealed that she had dilated pupils, dry mouth,
flushed skin and muscle twitching.Her pulse was
120/minute and she was in deep coma.
 What is the diagnosis?
 TRICYCLIC ANTIDEPRESSANT POISONING
MANAGEMENT
 Cardio toxic sodium channel-depressant effects of
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tricyclic antidepressants may respond to boluses of
sodium bicarbonate (50–100 mEq intravenously).
Prolongation of the QT interval or torsades de pointes is
usually treated with intravenous magnesium.
Severe cardio toxicity in patients with overdoses
has responded to intravenous lipid emulsion.
Plasma exchange using albumin has been reported to
b successful in few cases.
Mild serotonin syndrome may be treated with
benzodiazepines.
 Moderate cases may respond to cyproheptadine (4
mg) orally or via gastric tube hourly for three or
four doses) or chlorpromazine (25 mg
intravenously).
 Severe hyperthermia should be treated with
neuromuscular paralysis and endotracheal
intubation in addition to external cooling
measures.