Approach to child with coma
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Approach to child with coma
- 1. UTHSCSA PediatricResidentCurriculumforthePICU MANAGEMENT AND EVALUATION OF THE COMATOSE CHILD REF : 1. INDIAN JOURNAL OF PEDIATRICS , SEPT 2010 2. SWAIMAN’S PEDIATRIC NEUROLOGY 3. swartz clinical handbook of pediatrics 5th ed. 2013 4. Roger’s text book of critical care pediatrics
- 2. UTHSCSA PediatricResidentCurriculumforthePICU OBJECTIVES • Primary Objective: The pediatrician should be able to stabilize, evaluate, and treat the comatose patient in the emergent setting. • The pediatrician should understand this involves an organized, sequential, prioritized approach.
- 3. UTHSCSA PediatricResidentCurriculumforthePICU The Comatose Patient Primary Objectives • Airway • Breathing • Circulation • Treatment of rapidly progressive, dangerous metabolic causes of coma (hypoglycemia) • Evaluation as to whether there is significant increased ICP or mass lesions. • Treatment of ICP to temporize until surgical intervention is possible.
- 4. UTHSCSA PediatricResidentCurriculumforthePICU The Comatose Patient Secondary Objectives • The pediatrician should understand and recognize: • Coma • Herniation syndromes • Signs of supratentorial mass lesions • Signs of subtentorial mass lesions • The pediatrician should be able to develop the differential diagnosis of metabolic coma.
- 5. UTHSCSA PediatricResidentCurriculumforthePICU consciousness • Spontaneous occuring state of awareness of self and environment. • Two componant 1. Wakefulness 2. Awareness Awareness require wakefulness, wakefulness can be present without awareness (eg. Vegetative state)
- 6. UTHSCSA PediatricResidentCurriculumforthePICU The Comatose Patient Neurophysiology • Consciousness requires: • An intact pontine reticular activating system • An intact cerebral hemisphere, or at least part of a hemisphere • Coma requires dysfunction of either the: • Pontine reticular activating system, or • Bihemispheric cerebral dysfunction
- 7. UTHSCSA PediatricResidentCurriculumforthePICU Stage of consciousness • Clouding of consciousness • Confusion • Delirium • Somnolence • Obtundation • Stupor • Coma
- 8. UTHSCSA PediatricResidentCurriculumforthePICU Consciousness • Spontaneous occurring state of awareness of self and environment. • Two component 1. Wakefulness 2. Awareness Awareness require wakefulness, wakefulness can be present without awareness (eg. Vegetative state)
- 9. UTHSCSA PediatricResidentCurriculumforthePICU Terminology • Clouding of consciousness : – Minimal reduction of wakefulness or awareness main difficulty is attention or vigilance • Confusion : – State of impaired ability to think and reason clearly at developmentally and intellectually appropriate level
- 10. UTHSCSA PediatricResidentCurriculumforthePICU • Somnolence : • Excessive drowsiness, little response to external stimuli • Obtundation : • Mild to moderate reduction in alertness , clower than normal reactivity to stimulus. • Appear abnormally drowsy, and often sleeps when left alone
- 11. UTHSCSA PediatricResidentCurriculumforthePICU • Stupor : “ state of unresponsiveness with little or no spontaneous movement resembling deep sleep from which patient can only be aroused by repetitive and vigorous stimuli. Without stimuli, pt returns to prestimulation state.
- 12. UTHSCSA PediatricResidentCurriculumforthePICU coma • State of deep, unarousable, sustained pathological unconsciousness with the eyes closed. • Result from dysfunction of ARAS or Both Cerebral Hemisphere • Require period of unconsciousness that persist > 1 hr
- 13. UTHSCSA PediatricResidentCurriculumforthePICU Etiology • 1) Coma with focal signs • 2) Coma without focal signs and without meningeal irritation • 3) Coma without focal signs and with meningeal irritation
- 14. UTHSCSA PediatricResidentCurriculumforthePICU Coma with focal sign • Intracranial hemorrhage • Stroke: arterial ischemic or sinovenous thrombosis • Tumors • Focal infections-brain abscess • Post seizure state: Todd’s paralysis • Acute disseminated encephalomyelitis
- 15. UTHSCSA PediatricResidentCurriculumforthePICU Coma without focal sign without meningeal irritation • Hypoxia-Ischemia: – Cardiac or pulmonary failure, Cardiac – arrest, – Shock, – Near drowning – Carbon monoxide poisoning – Cyanide poisoning
- 16. UTHSCSA PediatricResidentCurriculumforthePICU • Metabolic disorders: – Hypoglycemia ; Acidosis • Organic acidemias, • diabetic keto-acidosis – Hyperammonemia • Hepatic encephalopathy • urea cycle disorders • valproic acid encephalopathy, • disorders of fatty acid metabolism, • Reye syndrome – Uremia, – Fluid and Electrolyte disturbances (dehydration, hyponatremia, hypernatremia) – Endocrine : Myxedema coma, Addison’s disease – Thiamine, pyridoxin, niacin deficiency
- 17. UTHSCSA PediatricResidentCurriculumforthePICU Systemic infections gram-negative sepsis, meningitis, toxic shock syndrome, cat-scratch disease, Shigella encephalopathy, Enteric encephalopathy • Post infectious disorders: Acute necrotizing encephalopathy, ADEM, Hemorrhagic shock and encephalopathy syndrome
- 18. UTHSCSA PediatricResidentCurriculumforthePICU • Post immunization encephalopathy: – Whole cell pertussis vaccine, – Semple Rabies vaccine • Drugs and toxins • Cerebral malaria • Rickettsial: Lyme disease, Rocky mountain spotted fever • Hypertensive encephalopathy (PRES) • Post seizure states • Non-convulsive status epilepticus • Post migraine
- 19. UTHSCSA PediatricResidentCurriculumforthePICU Coma without focal sign with meningeal irritation • Meningitis, • Encephalitis • Subarachnoid hemorrhage
- 20. UTHSCSA PediatricResidentCurriculumforthePICU Coma • Medical and neurological emergency – Rapid stabilization – Identification of cause – Specific treatment
- 21. UTHSCSA PediatricResidentCurriculumforthePICU Hitory and neurological assessment • Fever, headache, vomiting, irritability, seizure, rash • Trauma, • drug, toxin exposure, • dog bite, seizure • Fever (infectious vs noninfectious) – ADEM – Reye’s syndrome – Mitochondrial disorder – Some IEM
- 22. UTHSCSA PediatricResidentCurriculumforthePICU • Past history – Similar episode ( intermittant metabolic disease) (recurrent toxic ingestion) – Convulsion / head injury • Devlopment history : • family history – AR disorder (metabolic disorders) – Neuro cutaneous syndromes – Unexplained coma/ death
- 23. UTHSCSA PediatricResidentCurriculumforthePICU Examination : • Vitals : • Fever : • infective ( sepsis, pneumonia, meningitis, encephalitis, brain abscess) • Non infective : impaired hypothalamic temp regulatory mechanism, heat stroke • Hypothermia: • cold exposure, • sepsis, • hypoglycemia, • hypothyroidism, • Addison disease, • ingestion (alcohol, barbiturates, opioids, and sedatives)
- 24. UTHSCSA PediatricResidentCurriculumforthePICU • Tachycardia • Fever, septic or hypovolemic shock, arrhythmia, heart failure • Toxin ingestion / ingestion of sympathomimetic drugs • Eg. Amphetamines, cocaine, hallucinogens • Bradycardia : raised ICT, myocarditis • (sepsis, hypoxia, toxin induced)
- 25. UTHSCSA PediatricResidentCurriculumforthePICU • Tachpnoea with incr. WOB • Pneumonia, pneumothorax, empyema, asthma • Quite tachypnoea : acidosis • DKA, Uremia, Ethylene glycol poisoning • Hypertention : • hypertensive encephalopathy, • raised ICT (with bradycardia as cushing’s tried) • Stroke
- 27. UTHSCSA PediatricResidentCurriculumforthePICU • Hypotention : • sepsis, • cardiac dysfunction, • toxin, • adrenal insufficiency Decreased cerebral perfusion Infarct in watershed area or diffuse HIE
- 28. UTHSCSA PediatricResidentCurriculumforthePICU General Physical examination Look for Think of Pallor Cerebral malaria, ICH, HUS Icterus Hepatic encephalopathy, leptospirosis, comp. malaria Rashes Meningococcemia, dengue, measels, rikettsial fever, Arbovirus disease Petechiae Dengue, meningococcemia, Hemorrhagic fever Fat emboli due to long bone # Head and scalp hematoma Trauma/ non accidental injury Dysmorphism, neurocutaneous markers Possibility of seizure Abnormal odour DKA, Hepatic coma Lymphadenopathy Cat scratch disease
- 29. UTHSCSA PediatricResidentCurriculumforthePICU G/E cont… • Posture • Flaccid • Decorticate : (flexion of UL , extention of LL) • Suggest bihemispheric lesion with intact brainstem • Decerebrate: extention and internal rotation of all limbs • global metabolic derangements or brain stem involvement
- 30. UTHSCSA PediatricResidentCurriculumforthePICU Systemic examination • R/S : pneumonia, empyema • CVS : congenital or rheumatic heart disease – Prone to IE disseminated ic abscess • P/A : HS Megaly
- 31. UTHSCSA PediatricResidentCurriculumforthePICU Neurological examination 1. level of consciousness 2. Pupillary abnormality 3. Brainstem function 4. Motor response 5. Herniation syndrome
- 32. UTHSCSA PediatricResidentCurriculumforthePICU Evaluation of the Comatose Patient Disability - Neurologic • Glasgow coma scale – Provides easily reproducible and somewhat predictive basic neurologic exam – This allows rapid assessment and record of baseline neurologic status – Allows physician to track neurologic changes over time and multiple examiners
- 35. UTHSCSA PediatricResidentCurriculumforthePICU 2.Pupillary abnormality • Clue to brainstem and 3rd nerve dysfunction • If dilated with mydriatics, order sheet should specifically mention about it • Light reflex – resistant to metabolic dysfn • U/L dilatation + coma = oculomotor nerve compression due to UNCAL HERNIATION until prove otherwise.
- 37. UTHSCSA PediatricResidentCurriculumforthePICU 3.Brainstem abnormality • Oculocephalic, oculovestibular, corneal, cough, gag reflex +ce = intact observe Think of Conjugate lateral deviation of eye I/L hemispheric lesion c/l hemispheric seizure focus Damage to c/l pontine horizontal gaze center (pprf) Lateral Gaze palsy Central herniation Compression of b/l 6th nerve Tonic upward gaze B/L hemispheric damage
- 39. UTHSCSA PediatricResidentCurriculumforthePICU 4.Motor response • Focal deficit : (trunk, limb position, spontaneous movement, response to stimuli) – postictal todd’s palsy, – structural anomaly • Posturing : sign of brain stem herniation • Seizure : myoclonic jerks : – anoxic or hepatic encephalopathy • Dystonia : extrapyramidal involvement » JE/TBME/IEM/metoclopromide toxicity
- 40. UTHSCSA PediatricResidentCurriculumforthePICU • Fundus : retinal hemorrhage • Cherry red spot in some IEM • papilledema : very rare in acute encephalopathy Neck rigidity meningitis, tonsillar herniation, craniocervical trauma Meningeal irritation Meningitis, encephalitis, SAH Kernings and brudzinski are more reliable signs
- 41. UTHSCSA PediatricResidentCurriculumforthePICU Herniation syndrome 1. Subfalcine herniation. The cingulate gyrus shifts across midline under the falx cerebri 2. Uncal herniation. The uncus (medial temporal lobe gyrus) shifts medially and compresses the midbrain and cerebral peduncle. 3. Central transtentorial herniation. The diencephalon and midbrain shift caudally through the tentorial incisura. 4. Tonsillar herniation. The cerebellar tonsil shifts caudally through the foramen magnum. 1. Monoparesis of c/l lower extrimities 2. IL 3rd nerve palsy/CL hemiparesis Prominent brainstem sign, downward gaze deviation (upgaze palsy) decerebrate posturing 3. Decortictae evolving to decerebrate posturing, symmetrical, small reactive or midposition fixed reactive pupil, abn respiration 4. Neck rigidity, opisthotonus, decerebrate rigidity, vomiting, irregular respiration, apnoea , bradycardia
- 42. UTHSCSA PediatricResidentCurriculumforthePICU Herniation syndrome Search for Think for Subfalcine herniation (medially to cingulate gyrus Monoparesis of c/l lower extrimities Central transtentorial (downward of diencephalic structure Decortictae evolving to decerebrate posturing, symmetrical, small reactive or midposition fixed reactive pupil, abn respiration Lateral trans tentorial (downward and medially of uncus and paraheppocampal gyrus 3rd nerve palsy/ hemiparesis Upward transtentorial(upward of cerebellar vermis and midbrain Prominent brainstem sign, downward gaze deviation (upgaze palsy) decerebrate posturing Transforaminal (downward of cerebellar tonsil and medulla) Neck rigidity, opisthotonus, decerebrate rigidity, vomiting, irregular respiration, apnoea , bradycardia
- 43. UTHSCSA PediatricResidentCurriculumforthePICU Investigations • BSR • CBC and Blood C&S • MP PROFILE, DENGUE SEROLOGY, widal • PS for cell morphology • S. BIOCHEMISTRY including RFT & LFT • ABG • S. lactate • Urine R&M, C&S, reducing substances and ketone • Serology for leptospira, mycoplasma, rikettsia
- 44. UTHSCSA PediatricResidentCurriculumforthePICU Neuro imaging and CSF • Unless pt is a c/o known metabolic encephalopathy, CT Brain must be ordered. • “Normal CT does not rule out raised ICT” • In CT scan …… with contrast….. • MRI : stroke pt ct change may take up to 24 hours Fronto temporal pathology Herpes simplex type 1 Thalamic involvement Japanese encephalitis Demyelination ADEM Necrotizing lesion Acute necrotizing encephalopathy
- 47. UTHSCSA PediatricResidentCurriculumforthePICU Supratentorial Mass Lesions Acute epidural hematoma and midline shift
- 48. UTHSCSA PediatricResidentCurriculumforthePICU Severe head trauma with basilar skull fracture, right temporal hematoma, cerebral edema, hydrocephalus, and pneumocephalus
- 50. UTHSCSA PediatricResidentCurriculumforthePICU MRI Brain Cranial MRI revealed either mixed intensity or hypointense lesion on T(1) and hyperintense or mixed intensity lesion on T(2) in thalami in all except two patients. The MRI lesions were also noted in basal ganglia in 11, midbrain in 18, pons in 8, cerebellum and cerebral cortex in 6 patients each and subcortical white matter in 2 patients. MRI was more sensitive than CT scan in revealing thalamic and extrathalamic abnormalities. Thalamic changes may be helpful in the diagnosis of JE especially in endemic area.
- 51. UTHSCSA PediatricResidentCurriculumforthePICU • a T1-weighted image showing bilateral high signal lesions in the thalamus and extensively in the left hemisphere. • b T2-weighted image showing a low-signal rim surrounding high- signal lesions in the thalamus. The left frontal region gives low signal, while the temporoparietal region gives increased signal. Periventricular high signal is also seen
- 52. UTHSCSA PediatricResidentCurriculumforthePICU Second line investigations • Metabolic Testing • (before stopping feed and starting treatment) – Blood ammonia and lactate – S. amino acid – Urine for organic acid – Plasma free fatty acid and carnitine levels • Cause of hyperammonemia – IEM - liver failure – Reye’s syndrome - valproate toxicity • Urine for toxicological screen • Thyroid function test • Workup for CNS vasculitis
- 53. UTHSCSA PediatricResidentCurriculumforthePICU Ix cont… • Drug levels ( suspected anti epileptic toxicity) • ESR and autoimmune screen for cerebral vasculitis
- 54. UTHSCSA PediatricResidentCurriculumforthePICU EEG IN COMATOSE CHILD • Diffuse theta and delta activity, absence of faster frequency, intermittent rhythmic delta activity characteristic of severe encephalopathy • Specific epileptiform activity of absence seizure or complex partial seizure • Triphasic wave of hepatic or uremic encephalopathy • PLED of herpes encephalitis
- 55. UTHSCSA PediatricResidentCurriculumforthePICU Approach to the Comatose Patient Initial Treatment • Airway • Breathing • Circulation • ABC - identify and address life threatening inadequacies • Treat rapidly progressive metabolic disorders -- hypoglycemia • Evaluate for intracranial hypertension and imminent herniation and treat
- 56. UTHSCSA PediatricResidentCurriculumforthePICU Management of the Comatose Patient Airway • Evaluate -- is airway patent. Can patient move air without obstruction. Is there trauma or foreign body obstructing airway • Try chin lift to help open airway -- protect cervical spine • Place airway if indicated - nasal or oral airway, intubation, or surgical airway
- 57. UTHSCSA PediatricResidentCurriculumforthePICU Management of the Comatose Patient Airway • Intubate (protecting neck) “anyone who will let you” – Any of the following are adequate criteria • GCS < 9 • Airway not secure or open • Respiration not adequate • Any significant respiratory failure • Uncertainty regarding direction or rate of mental status changes, particularly if constant observation not available (during CT scans, etc..) • Fluid refractory shock
- 58. UTHSCSA PediatricResidentCurriculumforthePICU Management of the Comatose Patient Breathing • Evaluate - is patient moving adequate air, is respiratory rate appropriate, is gas exchange adequate, are breath sounds adequate and symmetrical • Must assure oxygenation and ventilation • If intubated don’t forget to ventilate • Identify and immediately treat problems - pneumothorax, airway obstruction, etc..
- 59. UTHSCSA PediatricResidentCurriculumforthePICU Management of the Comatose Patient Circulation • Is patient in shock? • Check pulses, heart rate, blood pressure, perfusion • Remember hypotension is late sign of shock • Start treatment for shock • Do not restrict fluids in comatose patient with inadequate intravascular volume. • Cardiac output and cerebral perfusion are much more important than fluid restriction
- 60. UTHSCSA PediatricResidentCurriculumforthePICU Management of the Comatose Patient Circulation • Use isotonic solutions and blood, as indicated. • Do not use hypotonic solutions to treat shock, particularly patients with coma or possible cerebral edema • Identify life threatening hemorrhage and control it.
- 61. UTHSCSA PediatricResidentCurriculumforthePICU Management and Evaluation of the Comatose Patient Practicalities • During ABC’s and secondary survey: – Have someone start IV and obtain labs • ABG’s • Chem 7, LFT’s, ammonia, coagulation studies • Toxin screens • Dextrostick – As soon as IV in and labs drawn, give • Glucose (D25, 2 - 4 cc per kilogram) • Consider thiamin
- 62. UTHSCSA PediatricResidentCurriculumforthePICU Management of the Comatose Patient Secondary Survey • Do a quick general exam of the entire body to identify acute life threatening conditions • In general, major thoracic or abdominal trauma takes precedence after ABC’s • Only very rarely is acute neurosurgical intervention appropriate before other acute life threatening injuries are stabilized (except protection of c spine by immobilization)
- 63. UTHSCSA PediatricResidentCurriculumforthePICU Neurologic Examination Secondary Survey • General motor exam – look for focal deficits, posturing (decerebrate or decorticate) • Reflexes, tone • Cranial nerve and brainstem function – Pupillary response - diencephalon, midbrain, brainstem, CN’s II and III – Corneal Reflex - CN’s V, VII, brainstem – Oculocephalic Reflex - not if neck injury possible. Tests CN’s III, IV, VI, VIII, and brainstem. – Oculovestibular (calorics) can be done if neck questionable.
- 64. UTHSCSA PediatricResidentCurriculumforthePICU Neurologic Exam Oculovestibular Testing • Check for tympanic perforation • Instill 120 cc cold water over 2 minutes • Conscious patient - COWS • Coma with intact pathways - tonic eye deviation to side of cold
- 65. UTHSCSA PediatricResidentCurriculumforthePICU Management and Evaluation of the Comatose Patient • Does the patient have a rapidly progressive intracranial lesion? • Assume yes, if: – 1. Any evidence of brainstem abnormality – 2. Any evidence of rostral caudal progression – 3. Any focal deficits – 4. Progression of motor exam from withdrawal to posturing
- 66. UTHSCSA PediatricResidentCurriculumforthePICU Does the patient have a rapidly progressive intracranial lesion? 1. Identification of herniation syndrome and raised ICP • Positioning (elevated head end of bed) • Neutral position of head • Hyperventilation • Mannitol ( 0.25-1 gm / kg bolus followed by 0.25-0.5 g/kg bolus repeated every 2-6 hrly • 3%NS as continuous infusion 0.1-1.0 ml/kg/hr to target sodium level 145-155 meq/L
- 67. UTHSCSA PediatricResidentCurriculumforthePICU 2. Identify and treat hypoglycemia BSR< 50 (2ml/kg D-10%, then GIR 6-8 mg/kg/min) 3. Identify seizure and start treatment – Lorazepam 0.1mg/kg – Phenytoin 20 mg/kg loading “Non convulsive status epilepticus should be looked for in all children with unexplained encephalopathy” 4. Treat electrolyte and acid base disorder
- 68. UTHSCSA PediatricResidentCurriculumforthePICU Acute febrile encephalopathy • Hyperthermia : manage aggresively with antipyretics or cooling devices • If csf is contra indicated or if delay in csf is expected, • Empirical therapy • Ceftriaxone +/- vancomycin • Acyclovir : in sporadic meningo encephalitis with or without focal neurological findings, behaviour changes, aphasia, CT s/o fronto temporal changes, hemorrhagic csf • Steroids : Meningococcemia with shock, enteric encephalopathy, ADEM, or prior to antibiotic dose in pyogenic meningitis • Antimalarial : smear/ RDT +ve case • In resident of resistant p. falci malaria endemic area, • Short history <48 hours, anemia, hypoglycemia, retinal hemorrhage
- 69. UTHSCSA PediatricResidentCurriculumforthePICU • DKA: fluids, insulin, other Mx • Hypertensive encephalopathy : antihypertensive • Toxidrome : – Opiate overdose : naloxone – Benzodiazepine overdose : flumazenil – OP poisoning : atropine, pralidoxime – Envenomation : antivenom • “ Be alert to possibality of child abuse in an infant or toddler with sudden unexplained altered consciousness.”