non-traumatic coma and altered mental status
TRANSCRIPT
SYMPOSIUM ON PGIMER PROTOCOLS OF NEUROLOGICAL EMERGENCIES
Non-Traumatic Coma and Altered Mental Status
Atul Jindal & Sunit C. Singhi & Pratibha Singhi
Received: 9 July 2011 /Accepted: 2 August 2011 /Published online: 26 August 2011# Dr. K C Chaudhuri Foundation 2011
Abstract Non traumatic coma in childhood is animportant emergency. It can result from wide range ofetiologies. CNS infections are the most common cause ofnon traumatic coma in children. However, multipleinterrelated factors may be present in one patient.Management of a comatose child goes hand in handwith clinical evaluation. It is an emergency that requiressimultaneous institution of immediate life support,identification of the cause and institution of definitetherapy. The primary goal is to establish airway,breathing and circulation and to identify and treat raisedintracranial pressure and seizures.
Keywords Coma . Encephalopathy . Impairedconsciousness . Intracranial pressure
Introduction
Non traumatic coma in childhood is a common pediatricemergency. The incidence of non traumatic coma is 30/100,000 children per year [1]. The diagnosis and manage-ment of a comatose child in the emergency room is achallenging task. Central nervous system (CNS) infectionsare the most common cause of non traumatic coma inchildren in the authors’ setting [2]. Regardless of the
etiology, initial management of the comatose child inemergency room involves immediate attention to sustainlife and prevent irreversible damage.
Definitions
Consciousness is a state of awareness of self andsurroundings which involves complex interaction of cere-bral cortex and reticular activating system. This state isdetermined by two separate functions:
& Awareness (content of consciousness), depends on anintact cerebral cortex.
& Arousal (level of consciousness), depends on an intactascending reticular activating system (ARAS) and itsconnections with diencephalic structures.
Coma is a state of altered consciousness with loss ofboth wakefulness (arousal) and awareness of self andsurroundings characterized by a state of sustained, patho-logic, unarousable unresponsiveness and absence of sleep-wake cycles, which must last for at least 1 h [3].
Vegetative state describes a condition of completeunawareness of the self and the environment accompaniedby sleep wake cycles with variable preservation ofbrainstem functions [4].
Minimally conscious state is defined as a condition ofseverely altered consciousness in which the patient dem-onstrates minimal but definite behavioral evidence of self-or environmental awareness [5].
Brain death is defined as the permanent absence of allbrain functions including those of the brainstem [6].
Descriptive terms such as somnolence, stupor, obtunda-tion, and lethargy used to denote different levels of
A. Jindal : S. C. Singhi (*) : P. SinghiDepartment of Pediatrics, and Advanced Pediatrics Centre,Postgraduate Institute of Medical Education and Research(PGIMER),Chandigarh 160012, Indiae-mail: [email protected]
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wakefulness are best avoided, given the lack of uniformityin the way these states are defined in the literature [7].
Etiopathogenesis
Common causes of non-traumatic coma seen in children in theauthors’ emergency department are central nervous systeminfections, which includes tubercular meningitis (19%),encephalitis (18%), and bacterial meningitis (16%),toxic-metabolic encephalopathies (19%), status epilepticus (10%),intracranial bleed (7%), and other (4%) [2]. Coma can be dueto a primary/direct insult to the cerebral cortex, diencephalicstructures, midbrain or rostral pons, or a secondary manifes-tation of systemic derangements caused by toxins, metabolicor endocrine disorders (Table 1). However, multiple interre-lated factors may be present in one patient.
Coma can be precipitated by a critical hemispheric lesionif there is bilateral diffuse involvement, or a large unilaterallesion causing midline shift leading to central or tentorialherniation with midbrain compression, compromising prox-
imal elements of ARAS. However, comparatively smallbrainstem and diencephalic lesions that disrupt or impairthe ARAS and its projections can cause coma.
Toxic and metabolic etiologies of coma have been linkedto an interruption in the delivery or utilization of oxygen orsubstrate (hypoxia, hypoglycemia); alterations in neuronalexcitability and signalling (seizures, drug toxicity, acidosis)or changes in brain volume (hyper/hyponatremia).
The degree of neurologic impairment is related to thetime course of the underlying cerebral pathology. An acutelesion is usually associated with depressed consciousnesswhereas a slowly developing lesion at identical location andvolume may be asymptomatic.
Evaluation of a Comatose Child
Management of a comatose child goes hand in hand withclinical evaluation. It is an emergency that requiressimultaneous institution of immediate life support, identifi-cation of the cause and definitive therapy.
Table 1 Causes ofnon-traumatic coma inchildren
Infections Metabolic
Tubercular meningitis Hypoglycemia
Viral meningoencephalitis Diabetic ketoacidosis
Bacterial meningitis Uremia
Cerebral malaria Hyperammonemia (hepatic encephalopathy, Reyesyndrome, disorders of fatty acid metabolism)
Rickettsial meningoencephalitis Mitochondrial encephalopathies
Rabies Dyselectrolytemia (hyponatremia, hypernatremia,hypercalcemia, hypermagnesemia, hypophosphatemia)
Brain abscess Acute Porphyria
Subdural/epidural empyema Acidosis/alkalosis
Toxic encephalopathy ( enteric fever, shigellaencephalopathy)
Toxic
Severe systemic infections with shock Opioids
Post infectious Barbiturates
Acute demyelinating encephalomyelitis Organophosphates and carbamates
Acute necrotising encephalopathy Sedatives
Hemorrhagic shock encephalopathy syndrome Tricyclic antidepressants
Post immunisation Lead encephalopathy
Whole cell DPT Snake bite
Semple rabies vaccine Structural
Hypoxia-ischemia Tumor
Shock Hydrocephalus
Cardiac/pulmonary failure Miscellaneous
Near drowning Post ictal state
Vascular Status epilepticus (convulsive, non convulsive)
Arterial ischemic stroke Hypertensive encephalopathy
Sinus venous thrombosis Acute complicated migraine
Intracranial bleed
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Primary Assessment and Emergency Management
& The primary goal is to establish airway, breathing andcirculation and to identify and treat raised intracranialpressure (ICP).
& Establish airway by jaw thrust/ oropharyngeal airwayand give high flow oxygen by mask.
& Perform endotracheal intubation by rapid sequenceinduction and start bag ventilation if the patient hasmodified Glasgow coma score≤8, impaired airwayreflexes, shock or evidence of herniation. Invasiveinterventions can aggravate ICP; avoid trauma as far aspossible and try to keep oxygen saturation above 92%.
& If signs of compensated/ hypotensive shock are present,establish a vascular access and resuscitate with isotonicsaline and inotropes. If there is high BP at contact, it couldbe both cause and effect of coma; reduce it slowly.
& Assess level of consciousness using the modifiedGlasgow coma scale (GCS) (Table 2). If in doubt onscoring, record a lower score initially.
& Examine the fundi for papilledema (rarely seen in acuteencephalopathy; absence does not exclude intracranialhypertension), retinal hemorrhage, and macular starsuggestive of hypertension.
& Look for tonic deviation of the eyes or nystagmus. Ifthere is tonic deviation of the eyes or nystagmus,assume subtle status epilepticus and give benzodiaze-pine (inj. Lorazepam 0.1 mg/kg or inj. diazepam0.3 mg/kg) and load with inj. Phenytoin 20 mg/kg.
& Assess brain stem function (Table 3) and decide whetherthe patient has evidence of herniation or raised ICP
(Table 4). If signs of raised ICP or impending herniationare present, start manual hyperventilation with a bag(PaCO2 30–35 mmHg) and give 20% mannitol (0.5 g/kg)or hypertonic saline (preferred if patient in shock).
& Perform Dextrostix testing and send for simultaneousvenous blood sugar. Give dextrose 2ml/kg of 25% dextroseor 5 ml/kg of 10% dextrose if blood sugar is<60 mg/dl andincrease glucose infusion rate to 6–8 mg/kg/min.
& Take samples for serum electrolytes, arterial bloodgases, lactate, complete blood count, platelet count,blood cultures, liver and kidney function tests, MPsmears, toxicology screen, urine sugar and ketones.
& Maintain normothermia—treat fever and hypothermia.& In a febrile child give empiric first dose of ceftriaxone
(100 mg/kg i.v. in 2 divided doses) and acyclovir/artesunate as indicated, obtain CT scan and decide aboutfurther management.
– In a child with focal neurologic deficit, focal seizures,behavioral changes, aphasia, neuroimaging suggestiveof fronto-temporal involvement or hemorrhagic CSF,give first dose of Acyclovir (30 mg/kg i.v. in 3 divideddoses) and obtain MRI.
– If child is resident of P.falciparum endemic area, andhas hypoglycemia, anemia or absent meningeal signsthen give empiric IV Artesunate/Quinine.
Focussed History
A detailed history may not be available during initialresuscitation phase of the comatose child but it should be
Table 2 Modified Glasgowcoma scale [8] >5 y <5 y
Eye opening
4 Spontaneous
3 To voice
2 To pain
1 None
Verbal
5 Orientated 5Alert, babbles, coos, words or sentences—normal
4 Confused 4 Less than usual ability, irritable cry
3 Inappropriate words 3 Cries to pain
2 Incomprehensible sounds 2 Moans to pain
1 No response to pain 1 No response to pain
Motor
6 Obeys commands 6 Normal spontaneous movements
5 Localises to supraocular pain (>9 mo) 5 Localises to supraocular pain
4 Withdraws from nailbed pressure 4 Withdraws from nailbed pressure
3 Flexion to supraocular pain 3 Flexion to supraocular pain
2 Extension to supraocular pain 2 Extension to supraocular pain
1 No response to supraocular pain 1 No response to supraocular pain
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Table 3 Focussed ClinicalExamination and Localisationin Coma
Italics refers to clinical signs ofpotentially reversible cerebralherniation
Respiratory pattern Normal Brainstem intact
Cheyne-Stokes Diencephalic
Hyperventilation Midbrain/upper pontine
Ataxic, shallow Lower pontine
Gasping, slow, irregular Medullary
Posture Normal Brainstem intact
Hemiparesis Uncal herniation
Decorticate Diencephalic
Decerebrate Midbrain/upper pontine
Flaccid Lower pontine
Response to pain Flexion to supraocular pain Diencephalic
Extension to supraocular pain Midbrain/upper pontine
None Lower pontine
Tone/reflexes/plantars Normal Brainstem intact
Unilateral pyramidal Uncal herniation
Bilateral pyramidal Diencephalic
Flaccid/extensor plantars Lower pontine
Oculocephalic (doll’s eye) Saccadic eye movements Normal forebrain control
Exclude cord injury Full deviation eyes away Diencephalic
Turn head from side to side, watch eyes Minimal deviation eyes Midbrain/upper pontine
No movement eyes Lower pontine
Pupil size Normal midpoint Midbrain/upper pontine
Small Diencephalic
Unilaterally large Uncal herniation
Bilaterally large Lower pontine
Pupil response to light Brisk Brainstem intact
Bright torch Unresponsive Midbrain/upper pontine
Table 4 Clinical signssuggestive of various herniationsyndromes
Italics refers to clinical signs ofpotentially reversible cerebralherniation
Uncal Unilateral fixed dilated pupil
Unilateral ptosis
Minimal deviation of eyes on oculocephalic/oculovestibular testing
Hemiparesis
Diencephalic Small or midpoint pupils reactive to light
Full deviation of eyes on oculocephalic/oculovestibular testing
Flexor response to pain and/or decorticate posturing
Hypertonia and/or hypereflexia with extensor plantars
Cheyne–Stokes respiration
Midbrain/upper pontine Midpoint pupils, fixed to light
Minimal deviation of eyes on oculocephalic/oculovestibular testing
Extensor response to pain and/or decerebrate posturing
Hyperventilation
Lower pontine Midpoint pupils, fixed to light
No response on oculocephalic/oculovestibular testing
No response to pain or flexion of legs only
Flaccidity with extensor plantars
Shallow or ataxic respiration
Medullary Pupils dilated and fixed to light
Slow, irregular, or gasping respiration
Respiratory arrest with adequate cardiac output
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obtained as quickly as possible, as it may be crucial foridentification of the cause of coma. The history shouldinclude details of events prior to coma, with specialattention to timing, exposures, and accompanying symp-toms. Sudden onset of coma suggests spontaneous intra-cranial hemorrhage or seizure. Slowly worsening state ofconsciousness suggests hydrocephalus, an expanding masslesion, or indolent infection. Recent history of feversuggests an infectious etiology but other disorders such asAcute Demyelinating Encephalomyelitis (ADEM), Reyesyndrome or mitochondrial disorders must also be consid-ered. Ask for history of seizures, rash, diabetes, trauma,toxin exposure, snake bite, heat exposure, diarrhea, pastmedical illness and family history. Suspect child abuse if aninfant/toddler develops sudden unexplained coma.
Focussed Examination
Look and record vitals. Fever is often a pointer to meningitis,encephalitis, sepsis, pneumonia or brain abscess and some-times of ADEM, Reye syndrome or heat stroke. Hypothermiais seen in shock. Bradycardia is seen with raised ICP,hypothermia, or hypoxia; tachycardia may be caused byfever, raised ICP, shock states, myocarditis. Tachypnea maybe seen in sepsis, shock, pneumonia, and acidosis. Hypoten-sion is seen in shock and may result in hypoxic ischemicinjury. Hypertension may be a feature of raised ICP or it maybe because of hypertensive encephalopathy. In hypertensiveencephalopathy there will be diastolic hypertension, withassociated findings of left ventricular hypertrophy (on ECGand ECHO) and there may be changes in retina suggestive ofhypertensive retinopathy.
General Physical Examination
Presence of cyanosis, jaundice (hepatic encephalopathy,complicated malaria, leptospirosis, enteric fever), pallor(intracranial bleed, dengue, malaria), hyperpyrexia >40°C(neuroleptic malignant syndrome, heat stroke), rash (den-gue, measles, rickettsia, meningococcemia, mycoplasma,viral exanthem), petechiae (dengue, DIC secondary tosevere sepsis, meningococcemia), edema (dengue, sepsis,liver failure), dysmorphism, abnormal odour(sweet inDKA, musty in hepatic and urine like in uremia), neuro-cutaneous markers or any evidence of trauma could provideimportant clue to the etiology.
Systemic Examination
Hepato-splenomegaly (malaria, enteric fever, viral hepatitis,sepsis), murmurs (congenital heart disease, rheumatic fever,infective endocarditis), signs of infective endocarditis, andevidence of pneumonia may be helpful clues to the cause.
Neurological Examination
The neurologic examination is directed toward localisingbrain dysfunction, identifying etiology, and determiningearly indicators of prognosis. In a comatose child, exami-nation requiring patient cooperation (mental status, sensorytesting) cannot be performed and hence examination isdirected towards assessing response to stimuli and brain-stem and motor functions.
Level of consciousness Record level of consciousnessobjectively by GCS score in children >5 y and modifiedGCS score in children <5 y. GCS has several importantlimitations. Subtle alterations in wakefulness and brainstemfindings may not be picked by GCS. It is difficult tocomment on the GCS of patients who are sedated orintubated. It is always better to record detailed descriptionof clinical findings and detects changes over time in such asituation.
Cranial nerves Cranial nerve evaluation helps in identifyingbrainstem and cortical control of cranial nerve pathways.
Fundus examination gives information about retina andoptic nerve. Papilledema is seen in raised ICP, however itsabsence does not rule out raised ICP as it takes hours todays to develop papilledema. Retinal haemorrhages areseen in inflicted child trauma and disorders of coagulation.Soft and hard exudates with flame shaped hemorrhages areseen in hypertensive encephalopathy.
Pupils should be examined for size, shape, symmetry,and response to light. Pupillary size and reactivity arecontrolled by centres in the brainstem which are adjacentto those that maintain consciousness, and hence, brainstem lesions commonly lead to abnormality of pupillaryreactivity and size. These pupillary changes are a valuableguide to the presence and location of brain lesions andalso help in differentiating between metabolic encephalo-pathies and structural lesions; these signs appear late inmetabolic encephalopathies. Unilateral pupillary dilatationin a comatose patient is a sign of oculomotor nervecompression from ipsilateral uncal herniation until provedotherwise. (Table 5 for pupillary abnormalities in differentconditions.)
Brainstem function The details are given in Table 3.
Meningeal signs Seen in meningitis, subarachnoidhemorrhage.
Herniation syndromes The details are given in Table 4.Also look for focal deficits which may suggest presence
of intracranial space occupying lesion (abscess, tuber-culoma, infarcts).
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Investigations
First Line Investigations
The first line investigations that should be performed in allchildren with non-traumatic coma are already listed undersection ‘Primary assessment and Emergency management’.In febrile coma: Perform malaria card test, send smear formalarial parasite, and blood for serological tests—JE virus,dengue, widal, herpes simplex virus, leptospira, rickettsia,and mycoplasma.
Perform a lumbar puncture in every febrile patient withcoma unless contraindicated. The contraindications includeclinical features of raised ICP, focal signs, thrombocytope-nia, local infection, shock. CSF should be tested for cellcount, glucose, protein, gram stain, culture, latex aggluti-nation, Ziehl-Neelsen stain and AFB culture(if symptom-atology for more than 1 wk), Herpes PCR and serology, JEPCR and serology, and additional tests as guided by clinicalsuspicion.
CT scan should be performed in all children with comaexcept those with a known cause of coma such ashypoglycemia and post-ictal state. CT will readily identifyintracranial bleed, hydrocephalus, cerebral edema, compart-mental shifts, stroke, abscess or ICSOL. Initial normal CTdoes not rule out an evolving lesion of an infection ormetabolic disorder as well as raised intracranial pressure. Inherpes simplex encephalitis CT head is abnormal inapproximately 50% of cases but may be normal in the first4–5 d [9]. CT should be done only after stabilization of thechild and one should weigh the information generated fromCT against risk of transporting a critically ill child.
Second Line Investigations
Electroencephalography (EEG) Serial EEG’s are moreuseful than single isolated EEG. EEG helps in detectionof non convulsive status epilepticus as a cause of coma. It isrelatively specific in herpes simplex encephalitis (periodic
lateralised epileptiform discharges). Triphasic waves maybe seen in hepatic or uremic or other metabolic encepha-lopathies. Diffuse theta and delta activity, absence of fasterfrequencies are seen in severe encephalopathies. It alsoassists in prognosis of later neurologic outcome (poor withlow amplitude EEG, generalised burst suppression or lossof reactivity to external stimuli).
Magnetic Resonance Imaging (MRI) MRI should be donein patients with unexplained coma and normal or equivocalCT findings. MRI is useful in diagnosing many conditionsincluding stroke and encephalitis. It is abnormal in around70–80% of herpes simplex encephalitis. In herpes simplexencephalitis, asymmetrical hyperintensities in T2 weightedimages are seen in fronto-temporal lobe, insular cortex andcingulated gyrus. Basal ganglia and thalamic involvementmay be seen in Japanese B encephalitis. Patchy demyelin-ation in the brain and spinal cord is seen in ADEM.Meningeal and gyral enhancement may be seen inmeningitis. Certain inborn errors of metabolism alsohave specific MRI features. Severity of the MR changesalso helps in prognostication. MRI should be done onlyafter stabilization of the child. The procedure may takean hour to do and one should weigh the informationgenerated from it against the risk of transporting acritical child.
Metabolic testing Blood ammonia, TMS, GCMS, thyroidfunction tests, ANA, ANCA.
Treatment
Once the child is stabilised with emergency management asdescribed above, next comes:
1. Specific management according to etiology2. Prevention and treatment of secondary complications
(Fig. 1).
Table 5 Pupil abnormalities incoma Etiology/localization Pupil appearance
Pontine Pinpoint
Opiate/ Organophosphate poisonings Pinpoint
Hypothalamic Small reactive
Metabolic Small reactive
Midbrain Mid position, fixed
Oculomotor nerve, uncal herniation Ipsilateral pupil fixed and dilated
Hypoxic ischemic encephalopathy Bilateral fixed dilated
Tectal Large, nonreactive, hippus
Anticholinergic, sympathomimetic, antidepressant poisoning Dilated and fixed
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Specific Management
1. Treatment of neuroinfections—Start with inj. Ceftriax-one 100 mg/kg/d in 2 divided doses and inj Acyclovir30 mg/kg/d in 3 divided doses.
2. Start antimalarials (quinine/artesunate) if there isclinical suspicion of malaria.
3. Try antidotes: Naloxone (0.1 mg/kg) in suspectedopioid poisoning, Flumazenil in benzodiazepine over-
dose. Atropine and pralidoxime in organophosphoruspoisoning.
4. Try Antisnake venom in snake bite.5. Corticoteroids (Methyl prednisolone, hydrocortisone)
are useful in ADEM, enteric encephalopathy, andTBM.
6. Treatment of metabolic coma- DKA, Hepatic, uremicand other metabolic encephalopathies according tospecific protocols.
Coma
Assess and optimise the airway (A), breathing (B) and circulation (C) to ensure that brain is being adequately perfused and maintain cerebral oxygenation.
1. Obtain immediate blood glucose and correct if it is low. 2. Identify and treat seizures.
Features of raised ICP
Identify signs of impending herniation
Measures to reduce ICP e.g. Head end elevation, adequate sedation and analgesia, hyperventilation, mannitol/hypertonic saline
Focussed history and neurological examination*
* Assess the level of consciousness (table 2) *Focussed neurological examination (table 3,4,5)
Yes
First line investigations in all patients
FeverYes No
Features of CNS infections
YesNo
Refer to protocol for Febrile encephalopathy
Sepsis – broad spectrum antibiotics DKA – Insulin, fluid and other supportive therapy. Hepatic encephalopathy – refer to protocol for acute liver failure. Uremia – refer to protocol for acute renal failure. Heat stroke- specific treatment
Afebrile encephalopathy
Focal signs with or without raised ICP
Raised ICP without focal signs
Normal ICP and No Focal Signs
Urgent neurosurgery evaluation and MRI if possible
Todd’s paresis Stroke
Dyselectrolytemia Toxins – naloxone, flumazenil Metabolic Snake Bite - ASV Hypoxic DKA Postictal
Diabetic ketoacidosis Acute hydrocephalus
Reye’s syndrome
If no improvement or no cause is ascertained, do second line investigations
ADEM – Steroids Stroke
MRI
NCSE – Antiepileptics
EEG TMS, GCMS, Ammonia
Metabolic causes – treat as per protocol
Drug levels Thyroid function test
ESR & autoimmune screen
Urgent CT Scan
Normal Abnormal
Stroke – refer to protocol for stroke. ICSOL Intracranial bleed Brain abscess
Fig. 1 Flow chart showingStepwise approach to child withnon-traumatic coma ADEM;Acute demyelinating encephalo-myelitis, EEG; Electroencepha-lography, ICP; IntracranialPressure, GCMS; Gas Chroma-tography Mass Spectrometry,NCSE ; Non convulsive Statusepilepticus, TMS; Tandem MassSpectrometry
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Prevention and Treatment of Secondary Complications
All comatose children should be transferred to PICU. Tillthen following measures should continue:
1. Maintain ABC, correction of hypoglycemia.2. Treatment of seizures.3. Maintain normothermia and euglycemia.4. Correct electrolyte and acid base abnormalities.5. Ensure adequate intravascular volume by use of N/2 or
normal saline with added glucose in full maintenancedoses. Restriction of fluids does not improve theoutcome.
6. Measures to control raised ICP: Keep head in midlinewith 30° elevation to promote cerebral venous drainage(but may be kept flat if the child is in shock or if themean arterial blood pressure falls with change inposition).
7. Gentle suctioning and avoid vigorous physiotherapy,catheterise the bladder to prevent urinary bladderdistension and surge in ICP, ensure deloading of colonwith use of laxatives, and early institution of nasogas-tric feeds.
8. General care: Minimal handling, care of eyes to preventexposure keratitis, frequent change of position toprevent pressure sores, adequate analgesia (morphine)and sedation (benzodiazepines).
9. Look for and treat nosocomial infections.
Monitoring
Monitor continuously for vital signs (at least hourly),changing level of consciousness (GCS hourly), neurologi-cal status, brainstem signs, ICP, Cerebral perfusion pressure,SpO2 and EtCO2 or ABG, assess adequate sedation andanalgesia, input and output daily, weigh daily if possibleand if not contraindicated (raised ICP, ventilated), urineoutput, bowel sounds, blood counts, serum electrolytes,blood sugar, serum and urine osmolality, EEG.
Follow Up
These children should be followed up to ensure earlydetection and development for long duration. They shouldbe looked for early development of -
& Neurologic sequelae like motor, visual and hearingdeficits.
& Developmental and intellectual disabilities.& Learning and behaviour problems.& Seizures
Prognosis
Prognosis largely depends on the underlying etiology andseverity of brain injury. A patient with delayed initiation oftreatment also will have poor prognosis. In a study of 100consecutive patients in the authors’ Unit , survival rate was65%. Among those who died, deep coma (GCS<6),abnormal respiration patterns, abnormalities of vitals likehypothermia, hypotensive shock, abnormal tone (flaccidity)were suggestive of poor prognosis. Among acute CNSinfections, rabies, herpes encephalitis, severe stages ofTBM had poor prognosis. Among metabolic encephalopa-thies, children with hepatic coma had high mortality [2].
Key Messages
& Urgent management is required in any child with coma.& Stabilization of ABC in emergency room is most
important to sustain life and prevent secondary braininjury.
& Secure airway, oxygenate, bag ventilate to keep CO2
within low normal range.& Identify the signs of impending brain herniation and
treat immediately.& Identify and treat seizures.& Identify and treat reversible and acute causes (e.g.,
hypoglycemia) immediately.& Diagnosis and specific treatment depends on the
etiology of coma.& Prognosis largely depends on the etiology and extent of
brain damage.
Conflict of Interest None.
Role of Funding Source None.
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