APPROACH TO COMATOSE CHILD

Dr G.Venkatesh

• A 5 year old child was brought with history of fever, progressive lethargy and posturing for 3 days . He had been vomiting several times since morning. His temperature was 40 degree celsius.

• how will you manage this patient?

contents

Terminology -States of altered conciousness.EtiologyApproach

Rapid assessment & Stabilisation. History. Examination & Neurological assessment. Investigations. Treatment.

• Consciousness is the state of awareness of self and environment.

Impairment of consciousnessstates

• Impairment of consciousness with activated mental state

• Impairment of consciousness with reduced mental state

• Impairment of consciousness along the continuum of coma–vegetative state–minimally conscious state.

Impairment of consciousness with activated mental state

• Confusion: state of impaired ability to think and reason clearly, resulting in difficulty with orientation, simple cognitive processing, and acquisition of new memory.

• Delirium is an activated mental state that may include disorientation, irritability, fearful-responses, and sensory misperception. Patients may be hyperactive and have signs of increased sympathetic tone.

Impairment of consciousness with reduced mental state

• Drowsiness• Obtundation arousal is present to stimuli

• StuporState Stimulus needed for arousalDrowsiness Verbal and light touchObtundation Deep touchStupor Vigorous, painful, or noxious

stimulation

• Coma is a “state of deep, unarousable, sustained pathologic unconsciousness with the eyes closed that results from dysfunction of the ascending reticular-activating system in the brainstem or in both cerebral hemispheres”

• Patients in coma lack both wakefulness and awareness.

• Increased neuronal excitability Restless/Confusion Delirium Stupor Coma

• Decreased neuronal excitability Lethargic Obtunded Stupor Coma

Etiologies of Impaired Consciousness and Coma

1.Infectious or InflammatoryA. Infectious

• Bacterial meningitis• Viral encephalitis• Rickettsial infection• Protozoan infection• Helminth infestation

B. Inflammatory• Sepsis-associated encephalopathy• Vasculitis, collagen vascular disorders• Demyelination• Acute disseminated encephalomyelitis• Multiple sclerosis

Etiology –cont.2. StructuralA. Traumatic

Concussion Cerebral contusion Epidural hematoma or

effusion Intracerebral hematoma Diffuse axonal injury Abusive head trauma

B. NeoplasmsC. Focal Infection

• Abscess• Cerebritis

D. Hydrocephalus

E.Vascular Disease• Cerebral infarction

Thrombosis Embolism Venous sinus thrombosis

• Cerebral hemorrhage Subarachnoid hemorrhage Arteriovenous malformation Aneurysm

• Congenital abnormality or dysplasia of vascular supply

• Trauma to carotid or vertebral arteries in the neck

Etiology –cont.3.Metabolic, Nutritional, or

ToxicA. Hypoxic-Ischemic

Encephalopathy Shock Cardiac or pulmonary failure Near-drowning Carbon monoxide poisoning Cyanide poisoning Strangulation

B. Metabolic Disorders Sarcoidosis Hypoglycemia Fluid and electrolyte

imbalance Endocrine disorders

With acidosis Diabetic ketoacidosis Aminoacidemias Organic acidemias

With hyperammonemia Hepatic encephalopathy Urea cycle disorders Disorders of fatty acid

metabolism Reye’s syndrome Valproic acid encephalopathy

Uremia Porphyria Mitochondrial disorders Leigh’s syndrome

Etiology -contC. Nutritional

Thiamine deficiency Niacin or nicotinic acid

deficiency Pyridoxine dependency Folate and B12 deficiency

D. Exogenous Toxins and Poisons Alcohol intoxication Over-the-counter

medications Prescription medications

(oral and ophthalmic)

Herbal treatments Heavy-metal poisoning Mushroom and plant

intoxication Illegal drugs Industrial agents

E. Hypertensive Encephalopathy

F. Burn Encephalopathy

PATHOPHYSIOLOGY OF COMA

• Consciousness has two dimensions – wakefulness and awareness.

• Integral Consciousness requires an intact - 1) RAS2) Cerebral hemispheres, 3) Healthy projections between the two

systems.

ANATOMY AND PHYSIOLOGY - CONSCIOUSNESS

Function SiteAwake – RAS (Reticular Activating System)

•Rostral brainstem (midbrain and upper pontine tegmentum) to the lower thalamus .•The hypothalamus.

Awareness(a higher cognitive function) = cognition + affect

Cerebralhemispheres.

Aetio-pathophysiological approachCOMA

Structural lesions Metabolic disorders

Usually focal Diffuse and symmetric

Supratentorial Infratentorial(Hemispheric) (Brainstem).

• Coma with focal signs Intracranial hemorrhage Stroke: arterial ischemic or sinovenous thrombosis Tumors Focal infections: brain abscess Post seizure state: Todd’ paralysis Acute disseminated encephalomylelitis

• Coma without focal signs and with meningeal irritation: Meningitis Encephalitis Subarachnoid hemorrhage

• Coma without focal signs and without meningial irritation: Hypoxic-ischemia: cardiac or pulmonary failure,

shock, near drowning.

• Metabolic disorders: Hypoglycemia Acidosis: Diabetic ketoacidsis, organic acidemis Hyperammonemia: hepatic encephalopathy, urea

cycle disorders, valproic acid encephlopathy, Reyes syndrome.

Uremia Fluid and electrolyte disturbance (dehydration,

hyponatremia, hypernatremia)• Systemic infections :

Gram negative sepsis, toxic shock syndrome, enteric encephalopathy, shigella encephlopathy

• Post infectious disorders: ADEM Hemorrhagic shock and encephalopathy syndrome

• Post immunisation encephalopathy Whole cell pertusis vaccine

• Drugs and toxins • Cerebral malaria• Rickettsial : lyme disease, rocky mountain spotted

fever• Hypertensive encephalopathy• Post seizure states• Non-convulsive status epilepticus

The goals of coma therapy(a) Adhere to the principles of neuroresuscitation, the A, B,

and Cs

(b) Immediately identify signs of intracranial pathology: herniation, increased intracranial pressure (ICP), or a focal neurologic signs, head trauma.

(c) Identify and specifically treat the underlying cause.

(d) Determine prognosis.

(e) Plan appropriate long-term therapy.

Rapid assessment and stabilization• Establish and maintain airway: intubate if

GCS<= 8 ,impaired airway reflexes, abnormal breathing pattern, signs of raised ICT, oxygen saturation<92% despite high flow oxygen, fluid refractory shock.

• Circulation: establish IV access, take samples (serum electrolytes), fluid bolus if in circulatory failure (20ml/kg NS), inotropes if required

• Blood glucose : regent strip testing , if <50mg/dl give 10% D 2ml/kg.

• Identify signs of cerebral herniation or raised ICT: ( if GCS<8,abnormal pupil size and reaction, absent dolls eye movements,abnormal tone or posturing, hypertension with brdycardia, abnormal respiratory pattern) Must act immediately (Elevate the Head end of bed 30 degrees, short term Hyperventilation, 20% Mannitol (0.5-1g/kg) or 3% NaCl(if in shock).

• If there are seizures: give IV lorazepam 0.1-0.2mg/kg , then phenytoin 20mg/kg loading.

• Immobilisation of cervical spine in suspected cases of traumatic coma.

• Manage hypo/hyperthermia accordingly.

History ,physical examination and neurological assesment

• History: age Infant Child Adolescent

CNS infection (meningitis,encephalitis)

Ingestion Drug/Alcohol overdose

Systemic infection with shock CNS infection Intentional poisoning

Metabolic disorders Seizure Trauma, seizures

Abuse / Trauma, Abuse / Trauma CNS infection,

Inborn errors of metabolism,seizures

DKA, Rey’s syndrome

DKA, , Rey’s syndrome

Post immunisation encephalopathy, hemorrhagic shock and encephalopathy syndrome ,

Approach: History

• Onset : – Sudden onset: vascular catastrophy or a

convulsion– Acute onset in normal child: ingestion of drug,

toxin, poison.– Gradual onset : infectious process, metabolic

derangement.

Approach: History• Associated symptoms of CNS causes:– Fever – Infections– Headache, Vomiting, Diplopia – Increased ICP– Neck stiffness – Meningitis, SAH– Rash - Meningococcemia– H/o excess cry, irritability, enlarging head in infants

– Meningitis, Hydrocephalus– H/o Trauma (Severity, Bleeding from ear/nose)– Seizures – ICH, ICSOL, Epilepsy, Post-ictal

Approach: History• Recurrent episodes: Epilepsy, Inborn errors of

metabolism

• H/o recent infectious diseases – eg. Mumps (Parotid swelling), measles (rash)

• Failure to thrive, vomiting, peculiar skin odour – Metabolic cause

• Jaundice, abdominal distension, hematemesis, melena, bleeding - Hepatic encephalopathy

• ↓ Urine output, swelling, periorbital puffiness, Nausea, vomiting, loss of appetite – Uremic encephalopathy

Approach: History

• H/o loose stools- HUS, Hypovolemia ,Ingestion of toxins/poisons, medications

• H/o Immunocompromised state (Cryptococcal meningitis, TBM), malignancy

• Family h/o TB, migraine, epilepsy

• Birth H/o: Birth asphyxia, h/o recurrent hypoglycemia

• Developmental delay or regression

• h/o envenomation

Physical examination• Vital signs:

– HR: Bradycardia (↑ ICT, myocardial injury due to hypoxia, sepsis), Tachycardia (Shock, Infections, Atropine); Irregular (Arrhythmia).

– BP: (HTN in ↑ICP, HTN encephalopathy), Hypotension (shock, barbiturates, adrenal insufficiency)

– Temp: Fever in Infections, Hyperpyrexia, Hypothalamic lesion or pontine hemorrhage, atropine poisoning, Hypothermia in Sepsis, shock, alcohol, barbiturate poisoning, hypoglycemia

– RR: Bradypnea/ Apnea (Drug intoxication, septicemia), Tachypnea (Metabolic Acidosis, Brainstem lesions, Pneumonia), Cheyne-Stoke breathing (B/L cortical damage with intact brainstem), Irregular (medulla involved

• Any signs of trauma (Scalp laceration/swelling/fracture, ENT Bleeding)

• Pallor - hypoxia, bleeding disorders

• Icterus – Hepatic encephalopathy, Sepsis

• Cyanosis – Cyanotic congenital heart disease, Hypoxia

• Oedema – CHF, Renal failure

• Dehydration – Hypovolemic shock, HUS

• Skin- Meningococcal rash, Petechiae

• Signs of meningeal irritation

• CVS: Arrhythmias, Murmurs (Congenital heart disease, Infective endocarditis)

• Chest: Signs of lung disease• P/A: Tender hepatomegaly (Hepatitis, Sepsis),

Hepatosplenomegaly- malaria

Clues to etiology of coma in general examinationLook for if present ,think of

Pallor Cerebral malaria, intracranial bleed, hemolytic uremic syndrome

Icterus Hepatic encephalopathy, leptospirosis, complicated malaria

Rashes Meningococcemia, dengue , measles, rickettsial diseases, arboviral diseases

Petechiae Dengue, meningococcemia , hemorrhagic fevers

Head and scalp hematomas

Traumatic/ non accidental injury

Dysmorphism,neurocutaneusmarkers

Possibility of seizures

Abnormal odour DKA, hepatic coma

Rapid neurogical assesment

• The goal of neurologic examination are:To determine depth of coma.To localise the process leading to coma.

• Includes Level of consciousness Pupillary responses Eye movements(spontaneous or induced) Motor response Respiratory pattern

A.Level of conciousness

• The level of conciousness must be recorded in the form of an objective scale. • The Glasgow coma scale is a useful tool for the

grading of the degree of altered consciousness and the severity of CNS insult.

• Glasgow coma scale is used for adults and older children and its modification is used in infants and young children.

Glasgow coma scaleACTIVITY

BEST RESPONSE

Adults/Older Children Infants ( modified GCS ) Score

Eye Opening( E )

1. Spontaneous2. To speech3. To pain4. None

1. Spontaneous2. To speech3. To pain4. None

4321

Verbal( V )

1. Appropriate speech2. Confused speech3. Inappropriate words4. Incomprehensible or

none specific sounds5. None

1. Coos, babbles2. Irritable, cries but

consolable3. Cries, inconsolable4. Moans to pain

5. None

54

32

1

Motor( M )

1.Obeys commands

2.Localizes pain3.Withdraws to pain4.Decorticate to pain5.Decerebrate to pain6.None

1. Normal spontaneous movement

2. Withdraws to touch3. Withdraws to pain4. Decorticate to pain5. Decerebrate to pain6. None

6

54321

Significance of Glasgow coma scores:

• Diagnosis of different grades of altered consciousness.

• Coma is defined as: No eye opening (1), No recognizable words uttered (2 ), Not obeying commands (5), ie, score = 8 or less.

• Fall of GCS of 2 or more – Indicates deterioration and need of active intervention

• Prediction of prognosis of comatose child:– GCS >8: Good chances of recovery– GCS 3-5: Fatal brain damage

B. Size and reactivity of pupilsPupils Lesion/Dysfunction

Pinpoint Pons, opiates, cholinergic intoxication

Mid position –fixed or irregular

Midbrain lesion

Unilateral , dilated and fixed

Uncal herniation

Bilateral , dilated and fixed

Diffuse damage, central herniation, global hypoxia ischemia, barbiturates, atropine

C. Eye movements

• Oculocephalic or Doll’s eye response: Shows Intact Brainstem.• Oculovestibular response: Lost in pontine lesions,

labyrinthitis, Sedatives, Phenytoin induced coma• Both lost but intact pupillary reflexes present in metabolic

encephalopathy• Stimulation of cortical centre for gaze e.g. seizure focus →

conjugate deviation of eye to contralateral side• Destructive lesion at gaze centre → conjugate deviation of

eye to same side .• Neuropthalmolgic examination is incomplete without fundus

examination.

D. Motor response

• Single best indicator of the depth and severity of coma

1. Spontaneous movements.2. Tone and reflexes3. Induced movements.

Motor responses to noxious stimuli. A, Localization of painas patient attempts to remove stimulus. B, Decorticate posturing. C,Decerebrate posturing. D, Flaccid patient with no response.

• Decorticate posturing with flexion of the upper extremities and extension of the lower extremities suggests involvement of the cerebral cortex and preservation of brainstem function.

• Decerebrate posturing with rigid extension of the arms and legs is indicative of cortical and brainstem damage.

• The flaccid patient with no response to painful stimuli has the gravest prognosis with injury sustained to deep brainstem lesions.

E. Respiratory pattern

• Patient breathing pattern is also helpful in localising area of CNS dysfunction. They are :

• Cheyne-Stokes respiration.• Central neurogenic hyperventilation.• Apneustic breathing.• Cluster breathing.• Ataxic breathing.

A.Cheyne-Stokes respiration-bilateral cerebral /diencephalon dysfunction ,preceding to transtentorial herniation

B.Centralneurogenic hyperventilation.- midbrain

C, Apneusis-pons

D, Cluster breathing.-lower pons,cerebellum

E, Ataxic breathing-medullary lesion

Herniation syndromes• Brain tissue deforms intracranially and moves from

higher to low pressure when there is asymmetric, unilateral or generalised increase in intracranial pressure.

• Signs of cerebral herniation1. Glasgow coma score <82. Abnormal pupil size and reaction (unilateral or bilateral)3. Absent doll’s eye movements4. Abnormal tone (decerebrate/decorticate posturing, flaccidity)5. Hypertension with bradycardia6. Respiratory abnormalities (hyperventilation, Cheyne- Stokes breathing, apnea, respiratory arrest)7. Papilledema

• In transtentorial or central herniation, the diencephalon is displaced through the notch of the tentorium cerebelli into the posterior fossa, with progressive rostral - caudal compression and ischemia of the brainstem.

• In Uncal herniation, medial displacement of the uncus compresses upon the oculomotor nerve leading to unilateral dilated fixed pupil with ptosis.

Central vs uncal herniationCentral uncal

•Arousal

•Breathing

•Pupils

•Oculocephalic responses

•Motor signs

•Impaired early, before other signs

•Sighs , yawns, sometimesCheyne-Stokes respirations

•First , small reactive (hypothalamus), then one or both approach midposition

•Initially sluggish, later tonic conjugate

Early hemiparesis opposite to hemispheric lesion followed late by ipsilateral motorparesis and extensor plantar response

•Impaired late, usually with other signs•No early change

•Ipsilateral pupil dilates, followed by somatic third nerve paralysis•Unilateral third nerve paralysis

•Motor signs late, sometimes ipsilateral to lesion

Metabolic vs structural coma METABOLIC, TOXIC, INFECTIOUS CAUSES

• Confusion or stupor precede motor signs

• Pupillary reactions preserved

• Symmetrical motor responses

• Asterixis, myoclonus• Hyper or hypoventilation

STRUCTURAL• Supratentorial destructive

or mass lesions:Initial focal signsRostral to caudal progression

• Infratentorial destructive or mass lesions:Preceding brainstem dysfunctionSudden onset of comaCranial nerve palsiesEarly respiratory disturbances

Investigations

1. neuroimaging:• CT scan:Any comatose child or infant in whom

the neurological findings suggest a structural lesion or in whom the clinical diagnosis is evasive, done after stabilistion of a patient.

• Magnetic Resonance Imaging (MRI) of brain is valuable in identifying evidence of herpes simplex encephalitis or an acute demyelinating process, such as acute disseminated encephalomyelitis.

Subdural Hematoma

Acute epidural hematoma and midline shift

Cerebral Abscess

Cerebral edema

Biochemical investigations

investigations

electroencephalography

EEG findings Interpretation

•High voltage slow waves

•Slowing of background activity•Triphasic waves•PLEDS Periodic Lateralised Epileptiform Discharges

•Underlying supratentorial lesion•Metabolic coma

•Hepatic coma

•Herpes encephalitis

EEG findings in coma

TREATMENT

• Emergency measures (immediate life support)

• Specific therapy

SPECIFIC THERAPY

• Acute febrile encephalopathy: In sick children with Acute febrile

encephalopathy, empirical therapy with antibiotics, acyclovir, antimalarials should be considered while awaiting for reports.

Specific therapy-Acute febrile encephalopathy:• Empiric antibiotic therapy: IV ceftriaxone+

amikacin• Acyclovir - in sporadic meningo-encephalitis

with or without: focal neurological findings,behaviour changes, aphasia, suggestive CT(frontotemporal changes), hemorrhagic CSF.

• Antimalarials: (quinine/artesunate)- smear positive, rapid tests positive , empiric treatment if short history(<48 hours),P.falciparum endemic area, absent meningial signs,anemia, hypoglycemia,retinal hemorrhages.

Specific therapy

• Treat dyselectrolytemia and acid-base imbalance• Space occupying lesions require prompt

neurosurgical management.• Antihypertensives for hypertensive

encephalopathy.• Hepatic encephalopathy – Lactulose, systemic

antibiotics, vitamins, protein restriction• Medical management and Dialysis for ARF, CRF• Poisoning – Gastric lavage, Antidotes

prognosis• The prognosis for recovery from coma depends primarily

on the cause, rather than on the depth of coma.• Coma from drug intoxication and metabolic causes carry

the best prognosis.• Prolonged coma after a global hypoxic ischemic insult

carries a poor prognosis.• Infectious encephalopathies have a good outcome with

mild or moderate difficulties only.• Children who survive traumatic injury have a better

prognosis than children who suffer a global hypoxic-ischemic injury

appropriate long-term therapy

• Early rehabilitation, by a team comprising doctors, teachers, physiotherapist, occupational and speech therapist and a psychologist is often very much rewarding.

• It is essential to test hearing early, particularly after meningitis.

• Many children, who had seizures acutely, do not develop epilepsy at follow up and may be weaned off from their anticonvulsants after three to six months.

Management approach-outline

Thank you

Alert: Fully conscious

Lethargic: appear somnolent, but may be able to maintain arousal

Obtunded: requires touch or voice to maintain arousal

Stuporous: unresponsiveness from which the individual can be aroused only by painful stimulus

Comatose: State in which the patient is unable to arouse or respond to noxious stimuli and is completely unaware of self and surroundings

Levels of Consciousness:

• Minimally Conscious State “a condition of severely altered consciousness

in which the person demonstrates minimal but definite behavioral evidence of self or environmental awareness”

• Vegetative State “condition of complete unawareness of the

self and the environment, accompanied by sleep–wake cycles with either complete or partial preservation of hypothalamic and brainstem autonomic functions”

Severe Disorders of Consciousness

Condition Self-Awareness

Pain andSuffering

Sleep–WakeCycles

Motor Function RespiratoryFunction

Coma Absent No Absent No purposeful movement

Variablydepressed

Vegetativestate

Absent No Intact No purposeful movement

Normal

MinimallyconsciousState

Very limited

Yes Intact Severe limitation of movement

Variablydepressed

Causes of Coma• T Trauma, head injury Shaken baby syndrome: non-specific

history, retinal hemorrhages.

• I Intussusception Mental status changes may precede abdominal finding

Insulin, HypoglycemiaInborn errors of metabolism

• P Psychogenic Common in adolescents

• S Seizures Postictal states, non-convulsive status may masquerade as undifferentiated coma.

Shock, stroke Coma secondary to poor brain perfusion, arterial and venous infarcts

Shunt Blocked or infected ventriculo-peritoneal shunts

• A Alcohol ingestion, abuse• E Electrolytes Disturbances of sodium, calcium,

magnesium Encephalopathy Hypertensive, Reye syndrome, hepatic

failure, urea cycle defects, lead encephalopathy

• I Infections Encephalitis, meningitis, malaria• O Overdose, ingestion Consider with unexplained loss of

consciousness

• U Uremic encephalopathy

Apneustic breathing:• Lesion: Lower pons• Characterized by inspiratory pause, lasting for 2-3

sec, often alternating with end expiratory pauses.• Pontine infarctions Anoxic encephalopathy

Central neurogenic hyperventliation:• Lesion: Mid brain

Kussumaul’s breathing:• Diabetic ketoacidosis Uremia• Characterized by rapid, deep respirationBiot’s breathing:• Fast & deep respirations with apnoea in betweenAtaxic breathing:• Lesion: Medulla• Inco-ordination in breathing