SUBJECT SEMINAR SUBJECT SEMINAR ON COMAON COMA

Presenter : Dr.Mohan.T.ShenoyPresenter : Dr.Mohan.T.Shenoy

Chairperson: Dr.ShivasharanappaChairperson: Dr.Shivasharanappa

ReferencesReferences• Nelson Textbook of Pediatrics 18Nelson Textbook of Pediatrics 18thth ed. ed.• Pediatric Neurology – Kenneth.F.Swaiman 3Pediatric Neurology – Kenneth.F.Swaiman 3rdrd ed. ed.• Rogers' Textbook of Pediatric Intensive Care, 4th ed.Rogers' Textbook of Pediatric Intensive Care, 4th ed.• Neurology in clinical practice, 4Neurology in clinical practice, 4thth ed Volume 1 by Walter ed Volume 1 by Walter

George BradleyGeorge Bradley• Roberts - Manual of Clinical Problems in Pediatrics 5Roberts - Manual of Clinical Problems in Pediatrics 5thth ed ed• Meherban Singh Pediatric Emergencies 4Meherban Singh Pediatric Emergencies 4thth ed. ed.• Pediatric & Neonatal emergencies by SachdevaPediatric & Neonatal emergencies by Sachdeva• Fenichel: Clinical Pediatric Neurology, 5Fenichel: Clinical Pediatric Neurology, 5thth ed. ed.• Pediatric Practical neurology by Veena KalraPediatric Practical neurology by Veena Kalra• Management of Pediatric Traumatic Brain Injury

Anaesthesia Tutorial of the week No.127 MARCH 30 2009

Definitions - Plum & Posner,1982

Definitions ConsciousnessConsciousness

State of wakefulness and awareness of self and surroundings.

SleepSleepBiological active state with identifiable behavioral and EEG stages

LethargyLethargy State of reduced wakefulness with attention deficits.

ObtundationObtundationBlunted alertness with decreased interest in environment and

slower than normal reactivity to stimulation.

StuporStupor State of unresponsiveness with little or no spontaneous

movement, resembling deep sleep but differing from coma because vigorous and repeated stimulation induces temporary arousal.

Coma Definition““state of reduced neuronal activity with altered state of reduced neuronal activity with altered

consciousness characterized by loss of both consciousness characterized by loss of both wakefulness (arousal, vigilance) and awareness of the wakefulness (arousal, vigilance) and awareness of the self and environment”self and environment”

Sustained, pathologic stateEyes closedUnarousable unresponsivenessSleep-wake cycles are absent.

Transitory state that can evolve toward

Recovery of consciousnessA minimally conscious state Vegetative state or Brain death.

Consciousstate

Drowsy

Alert and oriented

Sleepy but can be woken up

Stupor

Coma

Unconscious but responds to vigorous stimulation

Unconscious and unresponsive

PVS(PersistentVegetativeState)

All cognitive functions lostMaybe awake But totally unresponsive May last for yearsBreathing, circulation and internal organ functions intact.

Various states of consciousnessVarious states of consciousness

Other TermsOther Terms

Confusional state:

Inability to think without customary speed, clarity and coherence, resulting in inattention and impaired perception or registration of information

misinterpretation of stimulidifficulty following commandsdisorientation (due to decreased cerebral oxygen consumption 20%

below normal)

Delirium

confusional state accompanied by hyperactivity or sympathetic overactivity (diaphoresis, tremor, arterial hypertension, tachycardia)

Conditions Simulating comaConditions Simulating coma

Akinetic MutismLocked in syndrome (pseudocoma)Psychogenic unresponsivenessAbuliaCatatoniaVegetative state (coma vigil)

Akinetic Mutism

Coined by Cairns in 1941.

Characterized by Severe poverty of movement, speech and thought No associated arousal disorder or descending

motor tract impairment. Apathy, and indifference to painful stimuli

Hallmark feature • marked dimunition in drive.

EXAMPLESEXAMPLES

Severe frontal lobe damage -loss of inhibitory control.

Olfactory groove meningioma.

Final stages of Creutzfeldt-Jacob disease.

Acute cases of encephalitis lethargica.

Stroke that affects both anterior cerebral territories.

Ablation of cingulate gyrus as in treatment of psychosis.

Locked in syndrome Locked in syndrome (deafferent or ventral pontine (deafferent or ventral pontine

state) (pseudocoma)state) (pseudocoma)

Patient is awake and alert, but unable to move or speak.

Pontine lesions affect lateral eye movement and motor control

Lesions often spare vertical eye movements and blinking.

AbuliaAbulia

not able to use will power or to make decisions, cerebellar vessel infarction

Psychogenic unresponsiveness Psychogenic unresponsiveness The patient, although apparently unconscious, usually shows

some response to external stimuli

An attempt to elicit the corneal reflex may cause a vigorous contraction of the orbicularis oculi

Marked resistance to passive movement of the limbs may be present, and signs of organic disease are absent

CatatoniaCatatonia

Rigid plastic posture of limbs in schizophrenia.

Vegetative state coma vigil, apallic syndrome(

“Persistent unresponsive state with complete unawareness of self and environment accompanied by intact sleep-wake cycles with either partial or complete preservation of hypothalamic and brain stem autonomic functions”

IF COMA PRECEDES

•Re-emergence of eye opening and •Spontaneous control of autonomic functions.

SUMMARYSUMMARY

Vegetative

Locked-in

PATHOPHYSIOLOGY

(Diencephalon)

(Pons, Medulla)

RAS

COMA

COMA

Ascending RAS, from the lower border of the pons to the ventromedial thalamus

• occupy a paramedian area in the brainstem

AROUSAL- the state of consciousnessAROUSAL- the state of consciousness

Depth of coma - Assess using GCSDepth of coma - Assess using GCS

Best eye response (E)

Best verbal response (V)

Best motor response (M)

4 Eyes opening

spontaneously 5 Oriented 6 Obeys commands

3 Eye opening to

speech 4 Confused 5 Localizes to pain

2 Eye opening in response to pain

3 Inappropriate words 4 Withdraws from pain

1 No eye opening 2 Incomprehensible

sounds 3 Flexion in response to

pain

1 None 2 Extension to pain

1 No motor response

Glasgow Coma Scale (GCS)

z

Evaluation Evaluation

of of

Comatose ChildComatose Child

HistoryHistory Sudden onset in an otherwise normal,awake child

Convulsions / Intracranial hemorrhage

Preceded by sleepiness or unsteadinessIngestion of drug/toxin

Precede by fever

Acute Infectious process which lead to complications ADEMReye's syndromeCerebral malaria

Associated headache Raised Intracranial pressure (from hydrocephalus / neoplasm) Migraine syndromes

Use of unkerosenated stove/heaterCarbon Monoxide posioning

Lucid Interval Traumatic brain injury – extradural hematoma

Underlying previous diseases Diabetes – hypoglycemia,ketoacidosisCongenital heart diseases

Intermittent episodes of coma Drug overdosageToxidromes Inborn errors of metabolism Munchausen syndrome by proxy

•RECURRENT ENCEPHALOPATHYRECURRENT ENCEPHALOPATHY

Inborn errors of metabolismInborn errors of metabolism

EpilepsyEpilepsy

Mitochondrial disordersMitochondrial disorders

Mental disordersMental disorders

MigraineMigraine

Substance abuseSubstance abuse

GENERAL PHYSICAL EXAMINATIONGENERAL PHYSICAL EXAMINATION

InspectionInspection

Head,ScalpHead,Scalp

SkinSkin

CyanosisCyanosis IcterusIcterus Extreme pallorExtreme pallor Cherry-red colorCherry-red color RashesRashes HypermelanosisHypermelanosisNeedlemarksNeedlemarks

Odor Odor

FruityFruity

MustyMustyAmmoniacalAmmoniacal

AlcoholicAlcoholic

Signs of trauma

Boggy scalp swellingBattle signRaccoon eyes,Retinal hemorrhages, Hemotympanum, Bruises, hematomas.

Vital signs Vital signs Hypothermia

Sepsis HypothyroidismEnviromental exposure

Hyperthermia

CNS infectionSepsis Heat stroke ThyrotoxicosisStroke Drugs - Salicylates,Anticholinergics,Sympathomimetics)

Hypotension:

•Shock•Sepsis•Drugs•Adrenal insufficiency•Myocardial injury

Hypertension : ICH ThyrotoxicosisExposure to sympathomimmetic agents

Bradycardia

↑ ICPHypothyroidism Calcium channel blockers or ß-blockers

Cheyne-Stokes

Ataxic

Apneustic

Central Neurogenic Hyperventilation

Cluster

NEUROLOGICAL EXAMINATION

Abnormal Posture in Coma

Flexion of the elbows and wrists and arm supination (decorticationdecortication)

It is uncommon in children except after head injury and indicates hemispheric dysfunction with brainstem integrity above the midbrain

Extension of the elbows and wrists with pronation (decerebrationdecerebration)

indicate a more severe disturbance and prognosis. damage to the corticospinal tracts in the midbrain or

caudal diencephalon. Arm extension with minimal leg flexion or flaccid legs

has been associated with lesions in the lower pons.

Metabolic coma, especially after acute hypoxia, also may produce vigorous spontaneous extensor rigidity.

Posturing may coexist with purposeful limb movements, usually reflecting subtotal damage to the motor system

Flaccidity with no response to painful stimuli has gravest prognosis with injury sustained to deep brain structures

Ocular and motor responses

Assess the following to help determine whether etiology is structural or medical. Asymmetry points to a structural lesion.

a. Pupillary size. Normal or asymmetric?

b. Pupillary reflex. Fixed or reactive?

c. Extraocular movements. Normal, asymmetric, or absent?

d. Motor response to pain. Decorticate, decerebrate, or flaccid?

Oculocephalic (doll's head) response

Rotating the head from side to side and observing the position of the eyes.

If the eyes move conjugately in the opposite direction to that of head movement, the response is positive and indicates an intact pons mediating a normal vestibulo-ocular reflex

Reflex movements

•tested by moving the head from side to side or vertically, first slowly then briskly;

•eye movements are evoked in the opposite direction to head movement.

Generated by brainstem mechanisms originating in the labyrinths and cervical proprioceptors.

Normally suppressed by visual fixation mediated by the cerebral hemispheres in awake patients but appear as the hemispheres become suppressed or inactive.

Caloric oculovestibular responses Caloric oculovestibular responses

Requires intact cerebropontine connections.

Installation of ice-cold water into the external auditory meatus, having confirmed that there is no tympanic rupture.

Normal response in a conscious patient

• nystagmus with the quick phase away from the stimulated side.

Ocular movements Ocular movements

The position of the eyes at rest

Presence of spontaneous eye movement

The reflex responses to oculocephalic and oculovestibular maneuvers

Diffuse cerebral involvement but intact brainstem function, slow roving eye movements can be observed

Frontal lobe lesion

• Deviation of the eyes towards the side of thelesion.

Lateral pontine lesion

• Conjugate deviation to the opposite side

Midbrain lesion

• Conjugate deviation downwards

Structural brainstem lesion disconjugate ocular deviation

Signs of lateralization

Unequal pupilsDeviation of the eyes to one sideFacial asymmetryTurning of the head to one sideUnilateral hypo-hypertoniaAsymmetric deep reflexesUnilateral extensor plantar response (Babinski)Unilateral focal or Jacksonian fits

Signs of herniation

Dilated nonreactive pupilPapilledema, Posturing

Increased intracranial pressure

Cushing triad -hypertension, bradycardia, irregular respiration

If present,

provide controlled mild hyperventilation,consider administration of mannitol or normal saline,obtain emergent CT scan of the head and neurosurgical

consultation.

CAUSES

MNEMONIC for causes of COMAMNEMONIC for causes of COMA

Tips from vowels

T - Trauma, Head injuryI - Intussuception,Insulin,Hypoglycemia,Inborn errors of

metabolismP – PsychogenicS – Seizures,Shock, StrokeA - Alcohol ingestion, AbuseE – Electrolytes,EncephalopathyI – InfectionsO - Overdose, IngestionU - Uremic encephalopathy

ADEMADEM Monophasic autoimmune demyelinating disease of the CNS

following a vaccinationnonspecific upper respiratory tract infections

CENTRAL NERVOUS SYSTEM INFECTION

MeningitisMeningoencephalitisEncephalitisSubdural or epidural empyema, and Brain abscess

Important treatable causes

Bacterial meningitis, Herpes simplex encephalitis, Bacterial abscess, Cerebral toxoplasmosis, and Tuberculosis meningitis

Complications

Cerebrovascular infarctionCerebritisCranial nerve compressionDevelopment of hydrocephalussubdural effusionscerebral edemacerebral herniation.

MANAGEMENTMANAGEMENT

RAISED

Intracranial

Pressure

Reference RangesReference Ranges

2 mm Hg (27 mm H2O) in neonates

5 mm Hg (68 mm H2O) in young infants

6–13 mm Hg (82–177 mm H2O) in 1–7 years of age

5–15 mm Hg (65–204 mm H2O) in adults.

Threshold of 20 mm Hg usually accepted for starting active treatment

Cerebral perfusion pressure = systemic arterial pressure – ICP

Normal cerebral perfusion pressure is between 50 to 55 mm of Hg.

A drop below 50 mm is generally associated with ischemic brain injury

Increased ICP reduces cerebral blood flow

CT scan may be normal if ICP elevation occurs acutely.

Infants develop less ICP due to sutural seperation

Most patients with non-traumatic encephalopathies have raised ICP,although papilledema may be absent

Systolic Blood Pressure

Monro-Kellie doctrineMonro-Kellie doctrine

“Skull is a rigid cavity and that its contents are relatively non-compressible and consist of the brain parenchyma, intravascular blood and CSF and Expansion in the volume of any one compartment is likely to occur at the expense of the other two”

Intracranial volume

brain tissue (70%),cerebrospinal fluid (10%), cerebral blood volume (10%)interstitial water (10%).

Although the Monro-Kellie doctrine is a useful concept, it is not as consistently applicable to infants as it is to adults.

Monroe- Kellie Principle

Rogers (1996) Textbook of Pediatric Intensive Care p. 646

Treatment of raised intracranial Treatment of raised intracranial pressurepressure

1. Maintain adequate cerebral perfusion pressure and cerebral perfusion

Treatment of shockLimitation of excessive hyperventilation

2. Prevent hypoxia and hypercarbia

Tracheal intubation/controlled ventilationSeizure treatment and prophylaxis

3. Decrease cerebral blood volume

Acute hyperventilation

Treatment (contd.)Treatment (contd.)4. Decrease brain tissue volume

MannitolDexamethasone for vasogenic edema

5. Decrease cerebrospinal fluid (CSF) volume

CSF drainageAcetazolamide

6. Removal of mass lesion

Surgical removal/decompression

ComplicationsThe clinical course of a child in coma largely depends

on the underlying illness and timing of treatment.

Because the child's neurologic function will evolve over time, frequent serial examinations may be essential for diagnosis, identification of complications, and prognostication.

Neurologic complications of coma include

autonomic dysfunction, increased ICP,cerebral herniation, seizures, and metabolic derangements that may prolong the comatose state.

Signs of Herniation / Increased ICP

Headache, nausea, vomitingDecreasing LOCSixth nerve paresis (one or both eyes adducted)Decreased respiratory rateCushing reflex

(hypertension/bradycardia/bradynpea)PapilledemaDevelopment of signs of herniation

Fixed and dilated pupilContralateral hemiparesisPosturing

Clinical Factors Associated with Cerebral Edema

Prolonged IllnessSevere acidosis - low PA CO2Severe dehydrationBicarbonate therapyPersistent hyponatremiaExcessive fluid admistration

Core investigationsCore investigationsA Dextrostix reading should be taking on all children

at the initial evaluation.

Even if results are normal, laboratory glucose testing should be requested for confirmation, as hypoglycemia alone may cause coma, and hypoglycemia in association with other etiologies may worsen outcome.

Hypoglycemia (capillary glucose <2.6 mmol/L) must be treated urgently with an IV dextrose infusion.

Hyperglycemia may occur in diabetic ketoacidosis (capillary glucose >11 mmol/L, pH <7.3, and urine ketones).

Electrolytes should be measured on all patients, as abnormalities may cause coma or may occur secondary to intracranial abnormalities.

A complete blood count with differential is indicated in all patients to detect infection, anemia, disseminated intravascular coagulopathy, lead encephalopathy, or sickle cell disease.

A blood gas should be performed on every patient.

Liver function tests should be performed, as hepatic encephalopathy may cause coma, and liver injury can occur in the setting of systemic hypoxic ischemic injury.

Blood, urine, and stool cultures should be obtained in most patients to investigate infectious etiologies.

Toxin screens should be performed in all children and include acetaminophen, salicylate, and ethanol.

Specific tests for medications found in the home should be conducted as necessary.

Ammonia, lactate, and pyruvate tests may be performed in all patients to screen for metabolic disorders.

If history is suggestive of metabolic disease, measurement of organic acids, amino acids, and acylcarnitine profile may be indicated.

CT HEAD After resuscitation, a head CT should be performed

in all children to detect

Intracranial hemorrhage,

Space-occupying lesions (such as tumor or abscess),

Edema,

Focal hypodensities (such as acute disseminated encephalitis, herpes simplex encephalitis, infarct) Hydrocephalus.

If a patient is febrile, infection is suspected, or no other etiology can be determined, then a lumbar puncture should be performed. If clinical or radiologic evidence is present for intracranial hypertension, lumbar puncture should be deferred and treatment should be initiated for possible infections (bacterial and viral). A normal CT does not rule out elevated ICP.

Cell count (both the first and last tubes should be tested to help differentiate true findings in the case of a traumatic tap), glucose, protein, Gram stain, bacterial culture, viral polymerase chain reaction, and additional cultures when suspected clinically (fungal or tubercular).

Cerebrospinal fluid

EEGEEG

Diagnostic as well as a prognostic role in coma

History of seizures Eyelid blinking Unexplained nystagmus Nonconvulsive status epilepticus

An EEG may detect useful background changes (such as triphasic waves suggestive of metabolic encephalopathy or sharp waves associated with herpes simplex encephalitis) and may identify subclinical seizures.

EEG may be required to detect subclinical seizures.

If the cause of coma remains unknown, additional studies may be directed at uncommon causes of coma in children, such as Hashimoto encephalitis (thyroid function tests and thyroid autoantibodies), cerebral vasculitis (erythrocyte sedimentation rate, ESR; antinuclear antibody, ANA, panel; and possibly angiography), or paraneoplastic disorders.

Once the patient has been stabilized and the etiology of coma remains unclear, a brain MRI may be performed for diagnostic and prognostic purposes.

EEG findings in some conditions EEG findings in some conditions causing comacausing coma

Two Classes of Brain Injury

PRIMARY

SKULL FRACTURE

CONTUSION/ BRUISING OF THE BRAIN

HEMATOMA/BLOOD CLOT ON THE BRAIN

DIFFUSE AXONAL INJURY

SECONDARY

BRAIN SWELLING/EDEMA INCREASED INTRACRANIAL

PRESSURE INTRACRANIAL INFECTION EPILEPSY HYPOXEMIA (LOW BLOOD

OXYGEN) HIGH OR LOW BLOOD

PRESSURE ANOXIA/HYPOXIA (LACK OF

OXYGEN TO THE BRAIN)

Primary Brain Injury

Occurs at the time of in initial injury

May result in

brain contusion, laceration,haematoma formation diffuse axonal injury.

Younger children are more likely to develop subdural haematomas and diffuse cerebral oedema without a skull fracture

Adolescents more likely to develop skull fractures, contusions and extradural haematomas are more common.

Secondary Brain Injury

Occurs in the minutes to days after the initial injury

May be due to hypotension, raised intracranial pressure or cerebral ischaemia.

Worsened by hypoxia, hypercarbia, anaemia, pyrexia, hypoglycaemia or hyperglycaemia.

May be modified by simple clinical interventions, avoidance of hypotension and hypoxia.

Traumatic Head Injury

ALL-NET Pediatric Critical Care Textbook Source: LifeART EM Pro (1998) Lippincott Williams & Wilkins.

Cerebral ContusionCerebral Contusion

•Frontal lobe•Temporal lobes

oFocal haemorrhage

edema under impact

oSusceptible areas

Gyri in close contact with the skull

Cerebral haemorrhage

History of significant head injury

Extradural haemorrhage may be present even if lucid afterwards

Subdural haematoma & retinal haemorrhages

consider non-accidental injury caused by shaking or direct trauma.

Extradural haemorrhageExtradural haemorrhage

Usually associated with a skull fracture.

Usually following direct head trauma.

Arterial/venous bleeding into the extradural space

Subarachnoid Hemorrhage

Much more common in adults.

Presentation is usually with acute onset headache, neck stiffness and occasionally fever, seizures and coma may develop.

Retinal haemorrhage is usually present.

Haemodynamic stress in the susceptible intracranial arteries

Saccular or berry aneurysms

Polycystic Kidney diseaseEhlers–Danlos syndrome Marfan syndrome

Onset is unpredictable

Overall appears to occur at a surprisingly low rate.

Likelihood of having multiple intracranial aneurysms estimated to be around 20%.

Incidentally discovered unruptured aneurysms bleed at a rate depending on size.

Size<1 cm bleed @ 0.05% to 0.5% per year

Size >1 cm bleed @ 1% to 2%.

About 40% die following the initial hemorrhagebut at a later stage.

Rebleeding

• Rebleeding is the principal cause of death, usually by raised ICP

• Occurs with a peak incidence in 1st 24 hours after the initial event.

If the aneurysm is left unsecured,

• 20% in the first 2 weeks, • 50% in the first 6 months,

• Thereafter 3% to 4% per year.

Subdural haematoma

Acute subdural

In neonates by rupture of the vein of Galen.

Chronic subdural

Tearing of veins as they cross the subdural space between the arachnoid and pia mater

Subdural haematoma

Characteristic lesion in non-accidental injury caused by shaking or direct trauma in infants or toddlers.

Retinal haemorrhages are usually present.

Occasionally seen following a fall from a considerable height.

Intracerebral HemorrhageIntracerebral Hemorrhage

MOST common cause: Hypertensive

•Other causes:

•Traumatic•Contusion, •Coup/Contracoup

Rupture of small blood vessels with bleeding inside parenchyma

PutamenCerebellarThalamicPontine ( 3 P’s)

In young children

Initial presentation may be with anaemia and shock. Often a lucid interval until the conscious level deterioratesSeizures occur due to the enlarging haematoma acting as a

space-occupying lesion.

Focal neurological signs

dilatation of the ipsilateral pupil, paresis of the contralateral limbs and a false localising uni- or bilateral VIth nerve paresis.

Diagnosis confirmed with a CT scan.

Management : Correct hypovolaemia.

Surgical evacuation of the haematoma and arrest of the bleeding may be required and can be urgent in some situations.

INVESTIGATIONSINVESTIGATIONS

A CT scan of the head usually identifies blood in the CSF.

A lumbar puncture in the acute situation is best avoided as haemorrhage may extend following the release of intracranial pressure.

The cause is often an aneurysm or arterio-venous malformation (AVM). It can be identified on MR angiography (MRA) or CT or conventional angiography.

Treatment can be neurosurgical or with interventional radiography.

CHILD ABUSE

Nonaccidental trauma (NAT), or Child abuse

Hypoxia and IschemiaHypoxia and Ischemia

• Hypoxia = reduced blood oxygen content• Ischemia = reduced tissue perfusion.

• Often go hand in hand because sustained changes in tissue oxygenation have secondary circulatory effects.

• Asphyxia = impaired gas exchange, as carbon dioxide accumulates as oxygen falls.

• Longer periods of hypoxia produce cellular injury.

• Neurons are more vulnerable than glial cells to hypoxia and hypoglycemia.

• Oligodendrocytes are generally more vulnerable than astrocytes

• Factors determining selective vulnerabilityof certain neuronal populations still incompletely understood.

• Neurons in certain areas of the brain such as the basal ganglia and the hippocampal CA1 pyramidal neurons are particularly vulnerable to asphyxial injury.

• By contrast, spinal cord neurons tolerate longer periods of occlusion than do cerebral neurons.

Encephalopathy

Encephalopathy from poor or absent cerebral perfusion (both hypoxia and ischemia) often heralds a poorer outcome than that from trauma; the physician has little to offer to improve the outcome.

Often there is diffuse, global brain injury.

These children may have experienced a period of asystole and may have required CPR, such as after near-drowning episodes, acute life-threatening events, smoke inhalation, upper or lower airway obstruction, shock, or electrical injury.

Severe anaemia

Apnoea

AsphyxiationCarbon monoxideDrowning

Respiratory failure

Shock (adrenal crisis, cardiogenic, septic, hypovolaemic)

Cerebrovascular event.

PROGNOSIS

A poor prognosis is associated with

Low GCS score (<5) Hypotension Cerebral edema Persistent apnea CPR for >25 min Persistent loss of cranial nerve reflexes

(gag,corneal) Coma for >24 hr

MANAGEMENT OF TRAUMATIC BRAIN INJURY

Children with head injury must be assessed and appropriate management started immediately.

Delays worsen outcome

particularly hypoxia, hypotension

The following signs are worrying and merit admission of the child to hospital for close monitoring, including regular neurological assessments:

Patients who are not fully alert Persistent vomiting Severe headache

Minor head injuryMinor head injury

Moderate to severe head injuryModerate to severe head injury All children SHOULD be admitted for rapid assessment.

The following features in the history and clinical condition indicate the possibility of a severe head injury:

History of a fall from a height, High-speed road traffic accident, Road traffic accident where the child is a pedestrian or a cyclist Loss or reduced level of consciousness External sign of skull fracture, including base of skull fracture

(‘panda eyes’, blood or CSF in the ear, bruising of the mastoid process behind the ear)

A Glasgow coma score of </= 8 or loss of ability to localise pain on the motor category

Subacute onset with late development of coma. Marked ketoacidosis, usually above 40 mmol/l,

together with ketonuria. Secondary lactic acidosis (DD severe anoxia or

methyl alcohol or paraldehyde poisoning) Patients are dehydrated, rapid, shallow breathing,

occasionally acetone on the breath. The plantar responses are usually flexor until coma

supervenes.

Disturbance of glucose metabolism

Diabetic Ketoacidosis

PATHOGENESISPATHOGENESIS

Osmotic

Diuresis

Renal Hypoperfusion

Impaired Excretion of

Ketones & Hydrogen ions

Fluid & Electrolyte Depletion

Vomiting

AcidosisHyperglycaemia

Glycosuria

Glucose Ketones

Ketoacidosis is a state of

uncontrolled catabolism associated with

insulin deficiency.

More commonly seen in the elderly. Coma is more common than with ketoacidosis. Profound cellular dehydration, risk of

developing cerebral venous thrombosis, which may contribute to the disturbance of consciousness.

It may be induced by drugs, acute pancreatitis, burns, and heat stroke

Hyperglycaemic non-ketotic diabetic coma

Much more rapid onset. Symptoms appear with blood sugars of less

than 2.5 mmol/lInitially autonomic: sweating and pallor, and

then inattention and irritability progressing to stupor, coma, and frequent seizures.

May present with a focal onset (hemiparesis) Plantar responses are frequently extensor. Patients may be hypothermic.

Hypoglycaemic comaHypoglycaemic coma

Diagnosis of Hypoglycemic ComaDiagnosis of Hypoglycemic Coma

Patient known to be taking insulin. Spontaneous hypoglycaemia with insulinomas

are usually diagnosed late. May be a long history of intermittent symptoms

and in relation to fasting or exercise. May also be precipitated by

hepatic diseasealcohol intakeHypopituitarismAddison's disease

Treatment

Glucose, together with thiamine

Unless treated promptly, hypoglycaemia results in irreversible brain damage.

Cerebellar purkinje cells, cerebral cortex, and particularly the hippocampus and basal ganglia are affected

Dementia and a cerebellar ataxia are the clinical sequelae of inadequately treated hypoglycaemia.

Hepatic encephalopathyHepatic encephalopathy

1. Raise head end2. IV cefotaxim and cloxacillin3. IV fluid N/5 in 10% Dextrose4. KCl added as per serum potassium5. Lactulose through NG tube6. Hepatic Coma feed7. IV Rantidine 12 hrly8. Mannitol 20% bolus then in maintenence doses8. IV Vitamin K

Brain Death Brain Death

Guidelines suggested by American Academy of Neurology (1995) are generally accepted.

The Academy urged caution in applying the criteria to children younger than 5 years old, but subsequent experience supports the validity of the standards in newborns and through childhood.

Absence of cerebral blood flow is the earliest and most definitive proof of brain death.

BRAIN DEATHBRAIN DEATH

Prognosis in coma Prognosis in coma In general, coma carries a serious prognosis

Main determinants => Etiology,Duration,Depth

Poor prognosis: Length of coma and increasing age.

Brainstem reflexes early in the coma are an important predictor.

In general, cardiorespiratory arrest ,absence of pupillary light and corneal reflexes 6 hours after the onset of coma is very unlikely to be associated with survival

RECOVERY PROSPECTS

Recovery BEST in children due to primary epilepsy

CNS infections have good survival rates.

EXCELLENT for Coma due to depressant drugs carries an provided that resuscitative and supportive measures are available and anoxia not sustained.

Metabolic causes, apart from anoxia, carry a better prognosis than structural lesions and head injury

POOR OUTCOMEPOOR OUTCOME

o Shock

o Hypothermia

o GCS < 6

o Flaccidity

o Non-reactive pupils

o Areflexia

o Absent corneal reflexes

o Decerebrate / Decorticate posturing

o Fixed dilated pupils > 2hrs

CONCLUSIONCONCLUSION

Coma describes a state of altered wakefulness and awareness caused by multiple conditions that affect the brainstem or cortex diffusely.

Coma is a medical emergency that requires rapid and accurate evaluation.

Management in a PICU with adequate monitoring till child improves.

Appropriate investigations required to find out cause which in turn determines treatment.

Complications, such as elevated ICP and seizures, must be recognized and managed to prevent secondary neurologic injury.

Herniation Syndromes

CPP = MAP – ICP: Must keep CPP >60 mm HgUncal Herniation:

Occurs when unilateral mass pushes the uncus (temporal lobe) through the tentorial incisa, prersenting as:

Ipsilateral pupil dilatationContralateral hemiparesisDeepening comaDecorticate posturingApnea and death

Herniation Syndromes

Cerebellar HerniationDownward displacement of cerebellar tonsils

through the foramen magnum.Presents as :

Medullary compressionPinpoint pupilsFlaccid quadriplegiaApnea and circulatory collapse

BRAIN INJURY

Congenital brain injury

Pre-birth During birth

Acquired Brain Injury

After birth process

Traumatic Brain Injury(external physical force)

Closed Head Injury

Open Head

Injury

Non-traumatic Brain Injury

Savage, 1991

Stroke

Brain Infection

Tumor

Anoxia

Exposure to Toxic Substances

Neither definition includes “acquired” Neither definition includes “acquired” brain injuries caused by internal brain injuries caused by internal conditions, such as:conditions, such as: