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approach to comatose child
The child presented with fever, progressive lethargy, and posturing for 3 days along with vomiting. On examination, the temperature was 40 degrees Celsius. The doctor outlines the approach to managing an altered mental state including coma in children. This involves rapid assessment and stabilization, detailed history and neurological examination, key investigations, identifying the underlying etiology, and specific treatment. The document discusses terminology, common causes, pathophysiology, and goals of therapy for comatose pediatric patients.
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approach to comatose child
- 1. APPROACH TO COMATOSECHILD Dr G.Venkatesh
- 2. • A 5year 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?
- 3. contents Terminology -Statesof altered conciousness. Etiology Approach Rapid assessment & Stabilisation. History. Examination & Neurological assessment. Investigations. Treatment.
- 4. • Consciousness isthe state of awareness of self and environment.
- 5. Impairment of consciousness states •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.
- 6. Impairment of consciousnesswith 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.
- 7. Impairment of consciousnesswith reduced mental state • Drowsiness • Obtundation arousal is present to stimuli • Stupor State Stimulus needed for arousal Drowsiness Verbal and light touch Obtundation Deep touch Stupor Vigorous, painful, or noxious stimulation
- 8. • Coma isa “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.
- 9. • Increased neuronalexcitability Restless/Confusion Delirium Stupor Coma • Decreased neuronal excitability Lethargic Obtunded Stupor Coma
- 10. Etiologies of ImpairedConsciousness and Coma 1.Infectious or Inflammatory A. 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
- 11. Etiology –cont. 2. Structural A.Traumatic Concussion Cerebral contusion Epidural hematoma or effusion Intracerebral hematoma Diffuse axonal injury Abusive head trauma B. Neoplasms C. 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
- 12. Etiology –cont. 3.Metabolic, Nutritional,or Toxic A. 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
- 13. Etiology -cont C. 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
- 14. PATHOPHYSIOLOGY OF COMA •Consciousness has two dimensions – wakefulness and awareness. • Integral Consciousness requires an intact - 1) RAS 2) Cerebral hemispheres, 3) Healthy projections between the two systems.
- 15. ANATOMY AND PHYSIOLOGY- CONSCIOUSNESS Function Site Awake – RAS (Reticular Activating System) •Rostral brainstem (midbrain and upper pontine tegmentum) to the lower thalamus . •The hypothalamus. Awareness (a higher cognitive function) = cognition + affect Cerebral hemispheres.
- 16. Aetio-pathophysiological approach COMA Structural lesionsMetabolic disorders Usually focal Diffuse and symmetric Supratentorial Infratentorial (Hemispheric) (Brainstem).
- 17. • Coma withfocal signs Intracranial hemorrhage Stroke: arterial ischemic or sinovenous thrombosis Tumors Focal infections: brain abscess Post seizure state: Todd’ paralysis Acute disseminated encephalomylelitis
- 18. • Coma withoutfocal 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.
- 19. • 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
- 20. • Post infectiousdisorders: 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
- 21. The goals ofcoma 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.
- 23. Rapid assessment andstabilization • 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.
- 24. • Identify signsof 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).
- 25. • If thereare 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.
- 26. History ,physical examinationand 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 ,
- 27. 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.
- 28. Approach: History • Associatedsymptoms 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
- 29. Approach: History • Recurrentepisodes: 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
- 30. Approach: History • H/oloose 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
- 31. Physical examination • Vitalsigns: – 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)
- 32. – Temp: Feverin 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
- 33. • Any signsof 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
- 34. • CVS: Arrhythmias,Murmurs (Congenital heart disease, Infective endocarditis) • Chest: Signs of lung disease • P/A: Tender hepatomegaly (Hepatitis, Sepsis), Hepatosplenomegaly- malaria
- 35. Clues to etiologyof coma in general examination Look 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
- 36. 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
- 37. 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.
- 38. Glasgow coma scale ACTIVITY BESTRESPONSE Adults/Older Children Infants ( modified GCS ) Score Eye Opening ( E ) 1. Spontaneous 2. To speech 3. To pain 4. None 1. Spontaneous 2. To speech 3. To pain 4. None 4 3 2 1 Verbal ( V ) 1. Appropriate speech 2. Confused speech 3. Inappropriate words 4. Incomprehensible or none specific sounds 5. None 1. Coos, babbles 2. Irritable, cries but consolable 3. Cries, inconsolable 4. Moans to pain 5. None 5 4 3 2 1 Motor ( M ) 1.Obeys commands 2.Localizes pain 3.Withdraws to pain 4.Decorticate to pain 5.Decerebrate to pain 1. Normal spontaneous movement 2. Withdraws to touch 3. Withdraws to pain 4. Decorticate to pain 5. Decerebrate to pain 6 5 4 3 2
- 39. Significance of Glasgowcoma 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
- 40. B. Size andreactivity of pupils Pupils 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
- 42. 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.
- 43. D. Motor response •Single best indicator of the depth and severity of coma 1. Spontaneous movements. 2. Tone and reflexes 3. Induced movements.
- 44. Motor responses tonoxious stimuli. A, Localization of pain as patient attempts to remove stimulus. B, Decorticate posturing. C, Decerebrate posturing. D, Flaccid patient with no response.
- 45. • Decorticate posturingwith 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.
- 46. 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.
- 47. A.Cheyne-Stokes respiration-bilateral cerebral/diencephalon dysfunction ,preceding to transtentorial herniation B.Central neurogenic hyperventilation.- midbrain C, Apneusis-pons D, Cluster breathing.-lower pons,cerebellum E, Ataxic breathing-medullary lesion
- 48. Herniation syndromes • Braintissue deforms intracranially and moves from higher to low pressure when there is asymmetric, unilateral or generalised increase in intracranial pressure. • Signs of cerebral herniation 1. Glasgow coma score <8 2. Abnormal pupil size and reaction (unilateral or bilateral) 3. Absent doll’s eye movements 4. Abnormal tone (decerebrate/decorticate posturing, flaccidity) 5. Hypertension with bradycardia 6. Respiratory abnormalities (hyperventilation, Cheyne- Stokes breathing, apnea, respiratory arrest) 7. Papilledema
- 50. • In transtentorialor 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.
- 51. Central vs uncalherniation Central uncal •Arousal •Breathing •Pupils •Oculocephalic responses •Motor signs •Impaired early, before other signs •Sighs , yawns, sometimes Cheyne-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 motor paresis 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
- 52. Metabolic vs structuralcoma 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 signs Rostral to caudal progression • Infratentorial destructive or mass lesions: Preceding brainstem dysfunction Sudden onset of coma Cranial nerve palsies Early respiratory disturbances
- 53. Investigations 1. neuroimaging: • CTscan: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.
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- 55. Acute epidural hematomaand midline shift
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- 60. electroencephalography EEG findings Interpretation •Highvoltage 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
- 61. TREATMENT • Emergency measures(immediate life support) • Specific therapy
- 62. SPECIFIC THERAPY • Acutefebrile encephalopathy: In sick children with Acute febrile encephalopathy, empirical therapy with antibiotics, acyclovir, antimalarials should be considered while awaiting for reports.
- 63. Specific therapy-Acute febrileencephalopathy: • 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.
- 64. Specific therapy • Treatdyselectrolytemia 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
- 65. prognosis • The prognosisfor 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
- 66. 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.
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- 71. Alert: Fullyconscious 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:
- 72. • Minimally ConsciousState “a condition of severely altered consciousness in which the person demonstrates minimal but definite behavioral evidence of self or environmental awareness”
- 73. • Vegetative State “conditionof 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”
- 74. Severe Disorders ofConsciousness Condition Self- Awareness Pain and Suffering Sleep– Wake Cycles Motor Function Respiratory Function Coma Absent No Absent No purposeful movement Variably depressed Vegetative state Absent No Intact No purposeful movement Normal Minimally conscious State Very limited Yes Intact Severe limitation of movement Variably depressed
- 75. 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, Hypoglycemia Inborn 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
- 76. • A Alcoholingestion, 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
- 78. 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
- 79. Kussumaul’s breathing: • Diabeticketoacidosis Uremia • Characterized by rapid, deep respiration Biot’s breathing: • Fast & deep respirations with apnoea in between Ataxic breathing: • Lesion: Medulla • Inco-ordination in breathing