COMATOSE CHILD

Coma is a clinical state of varied etiology, characterized by altered consciousness, from which the child cannot be aroused by ordinary verbal or physical stimuli.

Pathophysiology: Maintenance of consciousness, i.e.

TABLE 18.7: Modified Glasgow coma scale

*Combined score of lt; 7 suggests definite coma. (also see text)

While many terms are used for altered states of con­sciousness, it may be broadly classified as:

• States of depressed consciousness, e.g. obtundation, stupor or coma of variable severity.

• States of hyp er excitability, e.g. agitation, confusion, delusions, hallucinations or delirium.

• Vegetative state, i.e. a wakeful state with preserved sleep-wake cycle but without any awareness about surroundings.

Clinically, presence and severity of coma is usually best assessed on Modified Glasgow coma scale or GCS (Table 18.7), using three variables, i.e. Eye opening (E_1-4), motor response to painful stimuli (M_1-6) and response to verbal commands (V_1-5). A GCS score of lt;7 indicates definite coma, though most cases with score of 7 or 8 are also comatose. GCS score may also be described in terms of individual variables, e.g. as E₄M₅V₃.

In routine clinical practice, depth of coma may also be simply graded as:

• Grade I (stupor): Momentarily arousable on verbal/ physical stimuli,

• Grade II (light coma): Not arousable, but moans on painful stimuli with limb withdrawal,

• Grade III (deep coma): No response to painful stimuli with decorticate/decerebrate posture,

• Grade IV (brain death): No pupillary reaction and spontaneous breathing, though spinal reflexes may be present.

Persistence of grade IV coma for more than 4 hours, may be considered as an indicator of irreversible brain damage.

Etiology of coma may be broadly divided into four groups: (a) Infections, (b) Hypoxia/Ischemia, (c) Metabolic/Toxic disorders, and (d) Traumatic head injury (Table 18.8). It is also a terminal event in vascular or degenerative neurological disorders as well as a sign of severely raised intracranial pressure (ICP).

Diagnostic evaluation in comatose patients may be delayed till initial resuscitation restoring patent airways, adequate breathing and circulation, and includes:

A. Detailed history, specially related to:

• Onset and progress of coma

TABLE 18.8: Causes of coma in childhood

• Infective

Local—meningitis, encephalitis, brain abscess Systemic—cerebral malaria, septicemia, typhoid

• Metabolic

Hypoglycemia, diabetic ketoacidosis

Hepatic encephalopathy, Reye syndrome

Uremia — acute or end-stage renal failure

Severe dehydration or water intoxication Dyselectrolytemia — hyper/hyponatremia, acidosis

• Toxic

Poisonings - barbiturates, narcotics, and others Snake bite, scorpion sting

• Traumatic: Head injury

• Hypoxic

Acute respiratory failure

Accidents: CO poisoning, near-drowning

• Vascular

Shock/syncope

Hypertensive encephalopathy

Cerbrovascular strokes

Cerebral edema (raised ICP)

• Others

Status epilepticus (post-ictal)

Heat stroke, severe hypothermia

Hysteria (conversion reaction)

± Sudden: Vascular, toxic or traumatic etiology

± Gradual: ICSOL or degenerative lesions

• Preceding illness, e.g.

• Head injury, accidents and poisoning

• Fever (infective, heat stroke)

• Family history of epilepsy or psychiatric problems.

B. General examination:

• Temperature

± Hypothermia: Poisonings, shock, etc.

± Fever: Infection, subarachnoid hemorrhage, etc.

± Hyperthermia: Heat stroke, pontine lesions.

• Heart rate

± Bradycardia: Raised ICP, narcotic poisonings.

± Tachycardia: Shock, atropine poisoning.

• Blood pressure

± Hypertension: Raised ICP, encephalopathy.

± Hypotension: Shock, poisonings.

• Respiration

- Cheyne-Stokes breathing: Bilateral cortical damage.

- Irregular and deep: Brainstem lesions.

- Irregular and shallow: Narcotic poisoning.

- Acidotic: Diabetic ketoacidosis, salicylism, etc.

- Breath odor: Fruity in diabetic ketoacidosis, Fetor hepaticus in liver disease, foul in uremia.

• Pupils

- Bilateral fix and dilated: Atropine poisoning, terminal.

- Unilateral fix and dilated: Tentorial herniation.

- Fixed in mid-position: Mid-brain lesions.

- Pin-point: Morphine poisoning, pontine lesion.

• Eye movements

- Spontaneous movements: Conjugate deviation in cortical lesion, contralateral in irritation of gaze centers, ipsilateral in complete injury.

- Oculocephalic (Doll's eye) response: Absent in brainstem lesion, preserved in cortical lesions.

- Oculovestibular response, i.e. ipsilateral deviation of eyes on cold-water irrigation of auditory canal is absent in brainstem lesion.

- Absent oculocephalic and oculovestibular response but preserved light reflex is a hallmark of metabolic encephalopathy.

- Nystagmus: Cerebellar or posterior fossa lesion.

• Skin/mucosal findings:

- #936; sweating/salivation in atropine poisoning

- #8593; sweating/salivation in organophosphorus poisoning

- Icterus in hepatic failure

- Purpuric spots signs of intracranial hemorrhage

- Abnormal smells in poisonings

- External injury marks in traumatic coma

C.

• Abnormal posture

- Decorticate (cortical)

- Decerebrate (brain-stem lesion)

• Neck rigidity in meningitis, subarachnoid bleed.

• Localizing motor signs in ICSOL, strokes.

• Signs of raised ICP in infections, metabolic, ICSOL, etc.

• Abnormal movements, e.g. Athetosis/myoclonus in hypoxic/metabolic coma. Seizures are of little diagnostic value.

• Fundus examination is essential in all cases to detect papilledema, and retinal hemorrhages.

D. Laboratory investigations, depend on suspected cause and include:

• CSF examination

• Biochemical studies, e.g.

- Blood sugar

- Serum electrolytes sp. Na⁺, Ca⁺⁺ and HCO₃

- Liver function tests including serum ammonia

- Renal function tests, e.g. BUN, serum creatinine

- Arterial blood gases

- Metabolic screening for inborn errors

• Hematological studies

- Peripheral smear for malaria

- Platelet count and clotting profile for IC bleeding

• Urinalysis

- Benedict test for diabetic ketoacidosis

- Ferric chloride test in selected cases

- Purple color in ketosis or salicylate poisoning

- Green color in phenothiazine or INH poisoning

• Gastric aspirate for toxic screen in poisoning

• Neuroimaging with CT/MRI

• EEG for HSV encephalitis, seizure disorder

• Microbial cultures from CSF/blood/other sites

• Serology, e.g. antibody titers for viral or autoimmune encephalitis

Management: Coma is a medical emergency and all cases need intensive care. Important components of care include—(a) Restoration of vital functions, (b) General nursing care, (c) Continuous monitoring, (d) Treatment of complications, e.g. seizures and raised ICT, and (e) Treatment of primary cause.

a. Immediate resuscitation (ABC):

• Airway patency needs to be ensured with repeated suction and oral airway.

• Breathing support with oxygen and ventilator assis­tance, if needed.

• Circulatory support with fluids and inotropic agents, e.g.

b. General nursing care:

• Nursing position, preferably in lateral head-down (recovery) position to facilitate draining of secretions and prevent aspiration.

• Nutrition via IV route in initial stages. Nasogastric feeds may be given in stable, prolonged coma.

• Care of back with frequent change of posture, keeping the under-bed dry and application of fine dusting powder on back, to prevent bed-sores.

• Care of bladder with regular emptying of bladder by manual compression/hot fomentation to prevent urinary stasis and infection. As indwelling catheters carry higher risk of UTI, condom catheterization is preferred to prevent soiling.

• Care of bowel with regular bowel enema in cases with constipation or fecoliths.

• Care of skin (frequent sponging), eyes (moistening/ antibiotic eye drops to prevent exposure keratitis) and oral cavity (frequent rinsing), etc.

• Prevention of contractures by physiotherapy and splints, etc.

• Prevention of respiratory complications with regular chest physiotherapy

c. Monitoring for progression and early detection of complications includes:

• Continuous clinical monitoring for depth of coma, vital signs, intake-output chart and complications, e.g. aspiration, infection, bedsores, etc.

• Periodic electrolyte and arterial blood gas estimations, specially till stabilization.

d. Treatment of complications:

• Fluid and electrolyte imbalance: Regular intake output monitoring, clinical suspicion and periodic electrolyte estimations should guide fluid/electrolyte therapy in comatose child. As SIADH is common, fluid intake must be restricted to 2/3^rd of calculated requirements.

• Control of seizures: Prompt anticonvulsant therapy is essential to prevent seizure-induced brain damage and cerebral edema. Prophylactic anticonvulsants are generally not indicated.

• Control of raised ICP by—(a) IV 3% Nacl 0.5-1 ml/ kg/hr (with serum sodium monitoring) or IV mannitol 10/20% (0.5-1.0 gm/kg/dose q4-6hr) or

(b) steroids, e.g.

• Control of infections with rational antimicrobials, though prophylactic antibiotics are not necessary.

e. Treatment of primary cause, e.g. infections (antibiotics), poisoning (antidotes, dialysis etc), metabolic problems and liver or renal disease, is discussed in related chapters.

Delirium

Delirium denotes acute behavioral changes due to neuronal hyperexcitability, which may be a precursor of coma, though psychiatric problems need to be excluded.

Clinically, these cases present with bizarre behavioral patterns, as follows:

• Agitation, i.e. a state of behavioral hyperexcitability with irrational vocalization or motor activity, which is difficult to control.

• Confusion, i.e. a state of rapid changes between hyper and hypoexcitability with unpredictable behavior.

• Delusion, i.e. fixed beliefs, which cannot be altered with reasoning.

• Hallucination, i.e. perception of a sensory stimuli that is not present. Visual hallucinations are mostly organic, while auditory hallucinations usually indicate psychiatric illness or temporal lobe disorders.

Diagnostic evaluation of delirium largely depends on history, as clinical and neurological signs may not be established till the child progress to comatose state.

Some common indicators of probable etiology include:

• Preceding events, e.g. trauma, seizures

• History of exposure to drugs/toxins

• Family history of epilepsy, migraine or psychic illness

• Recent adverse event/conflict at home or school

• Preceding viral illness or systemic disease

Examination of these children should be as elaborate as in comatose child, supported by relevant investigations, before considering the possibility of a psychiatric illness.

18.4