Comatose child

Consciousness Confusion State of wakefulness with awareness of self and surrounding . Confusion Altered consciousness (the subject misinterprets his surrounding) .

Delirium state of high arousal ( acute confusion ) There is confusion and visual hallucination . Stupor Is abnormal sleepy stat from which the subject can be aroused by repeated stimuli .

What is a coma ?

Coma ( or unconsciousness ) Is a state in which a patient is totally unaware of both self and external surroundings. Coma is not a disease. It is a symptom of disease or a response to an event.

Pathophysiology: A reduction in neuronal function resulting from disruption of cerebral cortical or brain stem integrity.

Causes

* Encephalopathy: * Infection: * Pressure effects: hypoxia ischemia seizures and post ictal states * Infection: encephalitis meningitis septicemia * Pressure effects: cerebral edema hydrocephalus space occupying lesions

* Diseases of other systems: * Vascular: - hemorrhage : extradural, subdural, subarachnoid, intraventricullar - hypertensive encephalopathy * Diseases of other systems: - hepatic coma - uremic encephalopathy - respiratory failure with C02 narcosis * Endocrine: - adrenal insufficiency - DKA / hypoglycemia - hypothyroidism - hypopituitarism

- H20, Na, K, Mg and Ca imbalance * Trauma. * Exogenous intoxication: - sedatives - salicylates - heavy metals - carbon monoxide * Fluid and acid-base balance: - H20, Na, K, Mg and Ca imbalance * Trauma.

How to approach to comatose patient ?

History Infection: Metabolic: Fever, irritability, lethargy, poor feeding, rash, seizure. Metabolic: Hx of DM, hx of previous loss of consciousness, hepatomegaly, jaundice, oligurea, hypertension.

Poisoning: Ask about drugs in the family, tablets, and alcohol. Seizure: Past hx of seizure, neurocutaneous lesions, developmental delay, abnormal eye movement, focal neurological signs.

Raised intracranial pressure: Trauma: Hx of road traffic accident, fall, bruising, hemorrhage, fractures. Raised intracranial pressure: Headache, vomiting, focal neurological signs: ataxia, squint. Papilloedema, retinal hemorrhage.

Physical Examination General Examination Neurological Examination

PULSE BLOOD PRESSURE In General Examination: Vital Signs:- IRREGULAR – Cardiac diseases ABSENT – Peripheral emboli FEEBLE – Circulatory collapse PULSE BLOOD PRESSURE - CVA - hypertensive encephalopathy - Cardiogenic shock - Septicemia - Addison’s disease

TEMPERATURE HYPOTHERMIA FEVER - Systemic infection : malaria - Meningitis / encephalitis - Heat stroke - Drugs : Barbiturate - Circulatory failure - Myxoedema

Skin and mucous membranes:- JAUNDICE CYANOSIS PURPURA SKIN RASH 18

Head - scalp :- ENT :- Fundoscopy Neck - Cx. Spine:- fractures, hematomas ,ant fontanels. ENT :- discharge, blood Fundoscopy Neck - Cx. Spine:- fracture, neck stiffness, carotid pulses

Neurological examination Determine level of consciousness by GCS

* The Glasgow Coma Scale is used to determine the severity of a brain injury. It is often used at the emergency scene or emergency room. * The scale is used as part of the initial evaluation of a patient, but does not assist in making the diagnosis the cause of coma * Motor, verbal, and eye responses are rated.

4 3 2 1 Spontaneous To loud voice To pain None   Eye Opening

Verbal Response 5 4 3 2 1 smile, follows objects. spontaneous irritable cry Cries only to pain Moans to pain None Oriented disoriented and converses inappropriate words Incomprehensible sounds Verbal Response

Motor Response 6 5 4 3 2 1 Obeys commands Localizes pain Withdraws from pain Abnormal flexion (decorticate posture) AbnormalExtension (decerebrate posture) None Abnormal Extension (decerebrate posture) Motor Response

GCS Mild=13-15 Moderate=9-12 Severe=3-8 Minimum=3 - Maximum=15

Core Neurological Exam (for coma); 1)Respiratory rate 2)Pupil 3)Extra ocular muscle, function muscle 4)Motor exam 5)Ciliospinal reflexes

METHODS OF ELICITING MOTOR RESPONSE Supra-orbital nail-bed sternum 27

PUPILS – SIZE AND REACTION TO LIGHT METABOLIC Normal, reactive DIENCEPHALIC Small, reactive MIDBRAIN Large, fixed PONS pinpoint III NERVE (UNCAL) dilated, fixed 28

OCULAR-VESTIBULAR REFLEXES OCULO-CEHPHALIC REFLEX (Doll’s eye movement) When the head is turned to one side the eyes move to the opposite direction. yes (brain stem intact) no (brain stem damage) 29

PATTERN OF BREATHING - Chyne-Stoke breathing (cerebral hemisphere lesion) - Central Neurogenic Hyperventilation (midbrain) - Apneustic breathing (pons) - Ataxic breathing – gasping (medulla)

INVESTIGATION Drugs screen(eg_salicylates- -diazepam-narcotics-amphetamines) -Routine biochemistry (urea-electrolytes-glucose-calcium-liver biochemistry) -Metabolic and endocrine studies (TSH-serum cortisol) - Blood cultures such as cerebral malaria(thick blood film) -If the explanation remains unclear ,further investigation are needed .

IMAGING CT or MRI brain imaging may indicate an otherwise unsuspected mass lesion or intracranial hemorrhage.

CSF examination Lumber puncture should be performed in coma only after careful risk assessment .it is usually contraindicated when an intracranial mass lesion is a possibility .CT is necessary to exclude this. CSF examination is likely to alter therapy only if undiagnosed meningoencephalitis or other identifiable infection is present .

lumbar puncture….

Electroencephalography EEG is of some value in the diagnosis of metabolic coma and encephalitis .

Management of comatose patient Immediate Therapy Specific Therapy

IMMEDIATE MANAGEMENT C IRCULATION A IRWAY B REATHING 37

GIVE 50% GLUCOSE 50ML INTRAVENOUSLY IMMEDIATE MANAGEMENT GIVE 50% GLUCOSE 50ML INTRAVENOUSLY * THE RISK OF PERMANENT BRAIN DAMAGE IN THE HYPOGLYCEMIC PATIENT OUTWEIGHS THE TEMPORARY WORSENING DUE TO INDUCED HYPERGLYCAEMIC STATE. * ABSENCE OF HYPOGLYCAEMIA SYMPTOMS DOES NOT EXCLUDE HYPOGLYCAEMIA. * HYPOGLYCAEMIA AT ‘NORMOGLYCAEMIC LEVEL’ IN DIABETIC PATIENTS. 38

Restore the hydration by IV fluids. IMMEDIATE MANAGEMENT Restore the hydration by IV fluids. Treat the hyperthermia/ hypothermia hyperthermia is more danger than hypothermia 39

TREAT RAISED INTRACRANIAL PRESSURE SPECIFIC THERAPY LOOK FOR ANY SEIZURE ACTIVITY (signs can be subtle like just twitching of mouth and eyes) GIVE DIAZEPAM 10mg IV SLOWLY FOLLOWED BY PHENYTOIN 15mg/Kg IV @ 50mg/min TREAT RAISED INTRACRANIAL PRESSURE HYPERVENTILATION (PaCO2 25-29mm. Hg) 25%MANNITOL (1.5 to 2.0G/Kg) FRUSEMIDE 40 to 120mg IV DEXAMETHASONE 12 to 18mg IV 40

IF SUSPECT MENINGITIS/ ENCEPHALITIS SPECIFIC THERAPY IF SUSPECT MENINGITIS/ ENCEPHALITIS START ANTIBIOTICS (3rd generation cephalosporin) IV ACYCLOVIR IV 10mg/Kg. 8 hourly for HSE QUINIDINE IV for strong suspicion of cerebral malaria RESTORE THE ACID-BASE BALANCE METABOLIC ACIDOSIS – cardiac abnormality METABOLIC ALKALOSIS – respiratory depression RESPIRATORY ACIDOSIS - presages respiratory failure RESPIRATORY ALKALOSIS – cardiac arrhythmias 41

SEMI-PRONE TRENDELERG – ONE MOMENT PLEASE… POSITION OF THE PATIENT SEMI-PRONE TRENDELERG – post-ictal state, drowning, metabolic causes ELEVATION OF HEAD END TO 300 IN SUPINE raised intracranial pressure due to any cause ELEVATION OF THE LEG END circulatory failure CATHETER THE URINARY BLADDER 42