DR RABIA RATHORE ASSISTANT PROFESSOR - PowerPoint Presentation

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DR RABIA RATHOREASSISTANT PROFESSORWEST MEDICAL WARDMAYO HOSPITAL/K.E.M.U

COMA

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DR RABIA RATHOREASSISTANT PROFESSORWEST MEDICAL WARDMAYO HOSPITAL/K.E.M.U

COMA

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DEFINITION OF COMA

A state of prolonged unconsciousness characterized by loss of reaction to external stimuli or, a state of

unarousable

unresponsiveness.

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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.

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FEATURES DISTINGUISHING BETWEEN COMA AND RELATED STATES

STUPOR

Unconscious but can be aroused with repeated stimuli..

DELIRIUM :

Confused state often with restlessness and hallucinations

.

‘

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

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CAUSES OF COMA

DIFFUSE BRAIN DYSFUNCTION: Drug overdose (accidental or deliberate), including 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

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Metabolic acidosisHypothermia, hyperpyrexia Seizures – post-ictal

state and non-convulsive status Metabolic rarities, e.g. porphyria

Extensive cortical damage

Hypoxic-

ischaemic

brain injury, e.g. cardiac arrest

Encephalitis, meningitis, cerebral malaria

Subarachnoid

haemorrhage

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DIRECT EFFECT WITHIN BRAIN STEM: Brainstem haemorrhage

, infarction or demyelination Brainstem neoplasm, e.g.

glioma

Wernicke–Korsakoff

syndrome

PRESSURE EFFECT ON BRAIN STEM:

Tumour

, massive hemisphere infarction with

oedema

,

haematoma

, abscess

Cerebellar

mass

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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.

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GENERAL EXAMINATIONMeasure the patient’s

temperature.Check for meningism

.

Sniff the patient’s breath for

ketones

, alcohol and hepatic 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

).

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NEUROLOGICAL EXAMINATIONNeurological examination aims to determine:

Depth of coma (GCS) Brainstem function Lateralization of pathology

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BRAIN STEM FUNCTION

PUPILS:Record their size and reaction to lightDilatation of one pupil that then becomes fixed to light

Compression of the

IIIrd

nerve.

Bilateral mid-point reactive pupils (i.e. normal pupils)

Metabolic comas

Sedative drugs except opiates.

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Bilateral light-fixed, dilated pupils: Brain death. Barbiturate intoxication

hypothermia.Bilateral pinpoint, light-fixed pupils:

Pontine

haemorrhage

Opiates.

Mydriatic

drugs

previous

pupillary

surgery

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LATERALIZING SIGNSComa 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.

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CLINICAL PRESENTATION

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CASE SCENARIO NO:1A 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.

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What is the differential diagnosis?

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Acute Bacterial MeningitisSubarachnoid haemorrhage

Migraine

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CAUSES OF MENINGITIS

Bacteria Neisseria

meningitidis

Streptococcus

pneumoniaea

Staphylococcus

aureus

Streptococcus Group B

Listeria

monocytogenes

Gram-negative bacilli, e.g.

E. coli

Mycobacterium tuberculosis

Treponema

pallidum

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Viruses

Epstein–Barr virus

Enteroviruses

Coxsackie virus

Poliomyelitis

Mumps

Herpes simplex

HIV

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FungiCryptococcus

neoformans

Candida

albicans

Coccidioides

immitis

,

Histoplasma

capsulatum

,

Blastomyces

dermatitidis

(USA)

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CLINICAL CLUES IN MENINGITIS

Clinical featurePetechial 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

HIV opportunistic infection

Enterovirus

infection

Malaria

Leptospirosis

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CLINICAL FEATURES

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MENINGOCOCCAL RASH

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How will you investigate him?

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INVESTIGATIONSBlood complete examination & ESR

Blood cultures CT scanLumbar puncture

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CSF PICTURE

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COMPLICATIONS OF MENINGITIS

ACUTE

COMPLICATIONS

:

Seizures

cranial nerve lesions

venous sinus thrombosis

severe cerebral

oedema

hydrocephalus

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CHRONIC COPMLICATIONS:Focal neurological

Behaviour disorderLanguage deficit

Deafness

Seizure disorder

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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

.

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What is the diagnosis?

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PONTINE HEMORRHAGE

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How will you investigate him?

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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.

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Routine bloods (for ESR, polycythaemia, infection,

vasculitis, thrombophilia, syphilitic serology, clotting studies,

autoantibodies

)

Fasting Lipid profile

Chest X-ray

ECG

E

chocardiography

Carotid Doppler studies

MR angiography

PT/APTT

Bleeding time/Clotting time

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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

.

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CT SCAN BRAIN

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MR angiography showinginternal carotid artery occlusion.

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DEFINITION

StrokeStroke 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

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Risk factor for Ischemic stroke :HypertensionDiabetes

Smoking Lifestyle High cholesterol

Atrial

fibrillation

Obesity

Severe carotid

stenosis

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RARE CAUSES:

Hyperviscosity states. Thrombocythaemia,

Polycythaemia

Thrombophilia

Anti-

cardiolipin

and lupus

anticoagulant antibodies

oral contraceptive.

Migraine

Vasculitis

Systemic

lupus

erythematosus

(SLE),

Polyarteritis

G

iant 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

)

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WHAT IS THE LESION ?WHERE IS THE LESION ?

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CASE SCENARIOAn 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.

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What is the diagnosis?

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DIABETIC KETO ACIDOSIS

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HOW ARE U GOING TO INVESTIGATE HER?

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INVESTIGATIONSBLOOD COMPLETE EXAMINATION

BLOOD SUGAR LEVELURINE FOR KETONES/COMPLETE EXAMINATION

SERUM KETONES

SERUM ELECTROLYTES

SERUM OSMOLALITY

mosm

/kg

=Measured[Na ]+Glucose (mg/

dL

)

18

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Blood urea nitrogen Serum creatinine

Arterial blood gases

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TERMS USED IN UNCONTROLLED DIABETES

Ketonuria

Ketosis

Detectable

ketone

levels in the urine; it should be appreciated that

ketonuria

occurs in fasted non-diabetics.

Elevated plasma

ketone

levels in the absence of acidosis

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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

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Lactic acidosis

A metabolic emergency in which

elevated lactic acid levels induce a metabolic acidosis and associated with

biguanide

therapy

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CASE SCENARIO NO:3A 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.

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What is the diagnosis?

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Myxoedema coma

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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.

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What is the diagnosis?

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TRICYCLIC ANTIDEPRESSANT POISONING

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MANAGEMENT

Cardio toxic sodium channel-depressant effects of 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.

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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.

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