STATUS EPILEPTICUS AND RAISED ICP.pptx...

status epilepticus is a imp topic

1. STATUS EPILEPTICUS DR NAVEENA SAJEEVAN FIRST YEAR PAEDIATRICS

2. STATUS EPILEPTICUS 1. Definition of STATUS EPILEPTICUS:OPERATIONAL DEFINITION ILAE Generalized Tonic- Clonic SE: Treatment Initiation (t1 ): 5 minutes of continuous or recurrent generalized convulsive seizures without regaining consciousness. Long-Term Sequelae (t2 ): ≥30 minutes of continuous seizure activity. .

3. Focal Seizures with Impaired Awareness Status epilepticus: t1: 10 minutes. t2: 30 minutes. Absence SE: t1: 10-15 minutes. t2: Unknown. Medical Emergency: SE is a critical condition that requires prompt treatment to prevent long-term neurological damage. Seizures that do not cease in 5 minutes are less likely to terminate without intervention. Hence, a child who is convulsing on arrival into the ED is more likely to continue to convulse and cause respiratory insufficiency unless actively treated

4. Refractory Status Epilepticus : Definition : SE that does not resolve despite treatment with appropriate doses of 2 classes of anticonvulsant medications including benzodiazepines Super-refractory Status Epilepticus : Definition : SE that fails to resolve or recurs after 24 hours or more despite treatment that includes continuous infusion of medications such as: Midazolam Pentobarbital

5. CLASSIFICATION OF STATUS EPILEPTICUS Types of Status epilepticus based on seizure semiology With prominent motor symptoms Convulsive SE generalized tonic, clonic , or tonic- clonic seizures. Focal onset evolving into bilateral convulsive SE Myoclonic SE;with or without coma hyperkinetic Focal motor SE

6. Withoutprominent motor symptoms Nonconvulsive STATUS EPILEPTICUS 1.NCSE WITH COMA 2.NCSE WITHOUT COMA -GENERALISED –ABSENCE -FOCAL -Unknown including autonomic Includes focal seizures with impaired awareness,

7. . INCIDENCE Overall Incidence: Ranges from 10 to 60 per 100,000 population. Children Younger Than 5 Years: Incidence is approximately 100 per 100,000 children 30% of patients presenting with SE are having their first seizure, and approximately 40% of these later develop epilepsy Most Common Type: Febrile status epilepticus Mortality Rate: -Current Rate 4–5%. - Primary Cause: Mortality is primarily due to the underlying etiology Risk of Neurologic Deficits: Overall Risk: Approximately 14%.

8. Loss of GABA AReceptors : GABA A receptors, which mediate the protective effect against seizures, can be destroyed or recycled during ongoing seizure activity. Increased NMDA Receptor Activity : Continued seizure activity leads to the mobilization of excitatory N-methyl-D-aspartate (NMDA) receptors. Outcome : reduced inhibitory control and heightened excitation, contributing to the persistence of status epilepticus. PATHOPHYSIOLOGY OF STATUS EPILEPTICUS

9. ROLE OF Benzodiazepines : Benzodiazepines bind to GABA A receptors and enhance neuronal inhibition, helping to control seizures. Timing of Administration : Given that the number of active GABA Areceptors decreases as SE progresses, it is crucial to administer the first dose of benzodiazepines as early as possible to effectively terminate the seizure activity. Failure of Desensitization of AMPA Glutamate Receptors : Persistent activation of AMPA receptors leads to continued increased excitability and contributes to the maintenance of seizure activity.

10. ETHIOLOGY OF STATUS EPILEPTICUS . - New-Onset Epilepsy : Drug Intoxication and Misuse - Drug Withdrawal or Overdose: Issues related to antiepileptic drugs (AEDs). - Metabolic Abnormalities Hypoglycemia Hypocalcemia,Hyponatremia,Hypomagnesemia - Acute Head Trauma - Infections - Encephalitis - Meningitis - Autoimmune Encephalitis: - Anti-NMDA receptor encephalitis - Steroid-responsive encephalopathy associated with autoimmune thyroiditis (SREAT) - Anti-voltage-gated potassium channel complex antibody syndromes - Stroke: Ischemic (arterial or venous) - Intracranial Hemorrhage

11. Metabolic Dependencies: - Folinic acid and pyridoxine/pyridoxal phosphate dependency - Inborn Errors of Metabolism: - Nonketotic hyperglycinemia - MELAS - Ion Channel–Related Epilepsies: Mutations in sodium and potassium channels - Hypoxic-Ischemic Injury Systemic Conditions : - Hypertensive encephalopathy - Posterior reversible encephalopathy - Renal or hepatic encephalopathy -Brain Tumors Other Disorders: Brain malformations, neurodegenerative disorders, progressive myoclonic epilepsy, storage diseases 2.

12. Rare and Specific Conditions - Hemiconvulsion -Hemiplegia-Epilepsy Syndrome: - Febrile Infection-Related Epilepsy Syndrome (FIRES) - Likely parainfectious -autoimmune etiology . - Rasmussen Encephalitis - Infections Leading to SE - Herpes Simplex: - Bartonella: Particularly nonconvulsive status - Epstein-Barr Virus - Mycoplasma: Postinfectious encephalomyelitis - Postinfectious Encephalitis and Acute Disseminated Encephalomyelitis: - HHV-:

13. Physiological status: Unmaintainable airway, respiratory failure, tachycardia, shock with highnormal bloodpressure with convulsive status epilepticus. PRESENTATION OF CONVULSIVE STATUS EPILEPTICUS

14. NONCONVULSIVE STATUS EPILEPTICUS Sudden Unresponsiveness Clinical Signs: Conjugate Deviation of Eyelids , Twitching , Unilateral Clonus: NCSE can develop after convulsive status epilepticus (CSE) during resuscitation, where active convulsions cease but the child remains unresponsive or exhibits abnormal breathing patterns (apneic or tachypneic) and shocky symptoms.

15. 1. New-Onset Refractory Status Epilepticus (NORSE) Definition : SE without a clear etiology after initial investigations (including brain imaging, blood, and CSF analysis) have excluded common causes such as stroke, infection, and toxic/metabolic derangements. flu-like illness before seizures. no prior seizure history. Etiology : . - Possible causes include: - Inflammatory and autoimmune disorders Genetic predispositions (e.g., pathogenic variants in PCDH19) Prognosis - superrefractory status epilepticus .Mortality rate >10%. - Up to two-thirds of patients develop long-term neurological disabilit .

16. COMPLICATIONS OF STATUS EPILEPTICUS Cerebral – Interictal coma , Cumulative anoxia , Altered autoregulation ,Increased cerebral blood flow Autonomic system disturbance – Hyperpyrexia – Excessive sweating, vomiting – Hypersecretion (salivary, tracheobronchial) – Airway obstruction CVS- Cardiac arrest , Hypertension Cardiac failure, hypotension Cardiogenic shock Respiratory system failure – Apnea ,Cheyne-Stokes breathing , Tachypnea ,Neurogenic pulmonary edema ,Aspiration, pneumonia, Respiratory acidosis , RENAL Renal failure – Oliguria, uremia , Acute tubular necrosis ,Rhabdomyolysis , Lower nephron necrosis

17. Metabolic and biochemical abnormalities – Acidosis (metabolic acidosis) ,Anoxemia , Hypernatremia, hyponatremia Hypoglycemia ,Hepatic failure , Dehydration Infection Altered autoregulation – Cerebral metabolic rate for oxygen (CMRO2 ) ,Disseminated intravascular coagulation , Multiple organ dysfunction , Fractures, thrombophlebitis

18. GOALS OF TREATMENT 1. Stabilize patient: Ensure adequate cardio-respiratory function. 2. Correct the correctable: temperature, hypoglycemia , abnormal electrolytes. 3. Prompt control of seizures. 4. Prevent recurrences: Evaluate and treat specific cause. 5. Prevent complications

19. PREHOSPITAL THERAPY Place the convulsing child in the recovery position to enable drainage of secretions Open airway using the head-tilt chin-lift maneuver (while maintaining the recovery position). Administer midazolam (0.2 mg/kg) via the intramuscular or intrabuccal or intranasal route. Fever a common cause of seizures in children should be controlled rapidly by tepid sponging and placing a rectal suppository of paracetamol

20. AIRWAY At least two members (one doctor and one nurse) must be dedicated for airway management Open the airway using the head-tilt and chin-lift maneuver. C-spine precautions are taken if trauma is suspected. 3. Use a large bore rigid suction catheter to suction oropharyngeal secretions. 4. Rapidly decompress stomach with a nasogastric tube to prevent vomiting and pulmonary aspiration. 5. Introduce an appropriate sized oropharyngeal airway, if feasible. Avoid forcible opening of clenched jaws during a convulsive episode. CALL FOR HELP!!!

21. BREATHING Opening the airway and provision of oxygen without initiating bag-valve-mask ventilation is not enough to correct hypoxia in actively convulsing children in the emergency setting. Almost 50% of children presenting with convulsive SE can be mask ventilated without being intubated. If spontaneously breathing, provide O2 using the flow inflating ventilation device. Oxygen saturations are monitored using pulse oximeter Drugs used in the management of status epilepticus can also lead to respiratory failure.

22. Indications for Intubation in SE ● Failure to maintain optimal saturations despite effective bag-valve-mask technique. ● Features of pulmonary edema or cardiac dysfunction noted at any step in the protocol. ● Hypotensive shock Prior to starting phenobarbitone or midazolam infusion for SE not responding to benzodiazepines and phenytoin. ● Severe traumatic brain injury, where there is a need to provide controlled ventilation. Raised intracranial pressure .

23. CIRCULATION Within the first ½ hour of SE, blood pressure rises. Later blood pressure either becomes normal or hypotensive . ● Secure intravenous access on arrival and provide non-glucose containing isotonic fluids. ● If IV access is unavailable, intraosseous access must be secured. If shock is identified the first bolus of 20 mL/ kg is administered. ● If euvolemic restrict fluids to 2–3 mL/kg/h. ● Shock secondary to idiopathic SE will resolve following administration of 20–30 mL/kg of fluid ● Shock complicated by diarrhea or sepsis will require large volumes to attain therapeutic goals. .

24. . CHALLENGES Drugs and fluid therapy can unmask PULMONARYEDEMA /MYOCARDIAL DYSFUNCTION during management. If signs of PE are not recognized during resuscitation of SE, cardiac arrest can supervene . If signs of pulmonary edema or myocardial dysfunction are identified during fluid administration: – Interrupt fluids. – Initiate an inotrope. – Intubate using ICP precaution

25. Here are the key points related to the initial and ongoing management of status epilepticus (SE), including diagnostic and therapeutic considerations: 1. **Immediate Management**: - **Securing Airway, Breathing, and Circulation**: - Ensure the airway is clear and maintain adequate breathing and circulation. - Continuous monitoring of vital signs, including ECG, is essential. 2. **Determination and Management of Underlying Etiology **: - **Identify and Treat Causes**: - For example, correct hypoglycemia if present. 3. Laboratory Studies Essential Tests: - Blood glucose, sodium, calcium, magnesium. - Complete blood count (CBC). - Basic metabolic panel. - Imaging and Monitoring: after stabilisation - CT Scan: To assess for structural abnormalities. - EEG - Additional Tests: - Blood and spinal fluid cultures. - Toxic drug screens. - Tests for inborn errors of metabolism. - AED levels if the patient is already on antiepileptic drugs.

26. Benzodiazepines : Lorazepam : Effective as a first-line treatment. Controls seizures within 3 minutes in about 50% of patients. Longer duration of effect (12-24 hours) compared to diazepam. Less risk of recurrence and respiratory depression. Requires refrigeration, should be diluted, and administered as a bolus over 1 minute. Diazepam : Effective but has a shorter duration of action (about 30 minutes). Higher risk of recurrence if used alone; phenytoin is recommended to prevent further seizures. If used, the full dose should be given to avoid converting convulsive SE to non-convulsive SE. DRUG THERAPY

27. Midazolam : can be administered Im /iv/nasal/buccal Rapid onset of action and effective in 90% of patients. Shorter half-life increases the risk of recurrence; also has a risk of hypotension. Repeat Dosing : A second dose of lorazepam or diazepam can be given 5 minutes after the first dose if seizures are not controlled.

28. Second-Line Drug: - Phenytoin Cardiac Effects: Decreases Automaticity Hypotension Risk Cardiotoxicity: -Severe reactions like atrial and ventricular conduction depression, and ventricular fibrillation, have been reported. Fosphenytoin , a water-soluble phosphoester of phenytoin has been considered less cardiotoxic effects than phenytoin and may be safer

29. Levetiracetam When SE is complicated by pulmonary edema , myocardial dysfunction coagulopathy, liver failure or hypotension Sodium valproate less sedation, good cardiovascular profile and lower risk of respiratory failure compared to other anticonvulsants. ● Sodium valproate should be avoided, if child has evidence of liver disease or metabolic disease or hemostatic abnormalities

30. RAISED INTRACRANIAL PRESSURE

31. INTRODUCTION Intracranial pressure is the total pressure exerted by brain,blood and CSF in intracranial vault NORMAL VALUES OF ICP Term infants-1.5-6mmhg Young children 3-7 mmhg Adults and older children <10-15 mmhg >20 mmhg –raised ICT >40 mmhg –severe life threatening raised ict

32. MONROE-KELLIE DOCTRINE

33. CEREBROSPINAL FLUID The choroid plexus - 70% of CSF production, volumes of CSF are children 4 – 13 years old - 90 mL adults- 150 ml The rate of formation - 0.35 mL/min or 500 mL/day . The rate at which CSF forms remains constant and declines if CSF pressure the rate of absorption increases linearly as CSF pressure exceeds 7 mm Hg. At a pressure of 20 mm Hg, the rate of absorption is three times the rate of formation.

34. CAPACITY OF LATERAL AND THIRD VENTRICLE -20 ML PULSATILE FLOW SYSTOLE –FLOW OUTSIDE VENTRICLE DIASTOLE –TOWARD VENTRICLE

35. CEREBRAL BLOOD FLOW Systemic arterial pressure is the primary determinant of cerebral blood flow. Normal cerebral blood flow is 50 – 60 mL/min/100-g brain weight HYPERCARBIA ------------dilates cerebral blood vessels , CBF Hypocarbia ----------- constricts cerebral blood vessels CBF The Arterial vasodilation or obstruction of cerebral veins and venous sinuses increases intracranial blood volume. intracranial blood volume, increased ICP. PCO2

36. CEREBRAL PERFUSION PRESSURE It defines the pressure gradient driving cerebral blood flow Brain able to maintgain CBF with CPP 50 -150 mmhg by AUTOREGULATION –buffering effect In paediatrics CPP threshold is 40-50 mmhg

37. MEASUREMENT OF CPP

38. ETHIOLOGY OF RAISED ICT Cerebral Edema 1. ; either localized or generalized cerebral edema. VASOGENIC CYTOTOXIC EDEMA INTERSTITIAL EDEMA Increased capillary permeability swelling of neurons, glia, and endothelial cells,constricts the extracellular space. Transependymal movement of fluid brain tumor, abscess, and infection, trauma and hemorrhage. hypoxia and ischemia csf absorption blocked fluid collects chiefly in the periventricular white matter .

39. 2.Mass Lesions Mass lesions (e.g., tumor , abscess, hematoma, and arteriovenous malformation) increase ICP by occupying space at the expense of other intracranial compartments MECHANISM cerebral edema, blocking the circulation and absorption of CSF, increasing blood flow, and obstructing venous return

40. CLINICAL FEATURES OF RAISED ICP In Infants Symptoms Poor feeding Irritability Shrill cry vomiting Lethargy Seizures SIGNS Bulging fontanelle 6 th nerve palsy macrocephaly Dilated scalp veins sutural diasthesis Papilledema is not common hypertonia • Transillumination + (hydrocephalus) ,Impaired upward gaze (setting sun sign)

41. Children Symptoms Headache Projectile Vomiting Visual disturbances Drowsiness,seizures Altered mental status/COMA SIGNS Depressed level of consciousness Diplopia/strabismus 6 th nerve palsy Sunset sign(hydrocephalus) Papilledema(RARE) Raised intracranial pressure’ must be presumed in all comatose children

42. Late signs of Intracranial hypertension CUSHINGS TRIAD hypertension

43. HERNIATION SYNDROMES Due to raised ict there is displacement of brain tissue from one compartment to another

44. TYPES MECHANISM PRESENTATION Subfalcine /cingulate Displacement of the brain beneath the free edge of falx cerebri Impaired consciousness Contralateral leg weakness due to compression of ACA Central transtentorial Downward displacement of both cerebral hemispheres and diencephalon through tentorial notch Lateral transtentorial / uncal Displacement of uncus of temporal lobe over the free edge of tentorium Impaired consciousness, abnormal respirations, ipsilateral third nerve palsy , ipsilateral hemiparesis Tonsillar downward displacement of cerebellar tonsils and medulla Impaired consciousness, neck rigidity, opisthotonus, irregular respirations, apnea and bradycardia

45. STAGES OF CENTRAL TRANSTENTORIAL PUPILLARY CHANGES OCULAR REFLEX/MOVT POSTURE RESPIRATION Diencephalic Symmetrical small reactive pupils preserved oculocephalic oculovestibular reflexes decorticate posturing Cheyne-Stokes breathing Midbrain-upper pons Midposition unreactive pupils absent decerebrate posturing hyperventilation Lower pons-medullary midposition fixed pupils Absent ocular movements/reflexes lower extremities may withdraw to plantar stimulation ataxic respiration Medullary midposition fixed pupils Absent ocular movements/reflexes Flaccid Irregular/gasping

46. SUBFALCINE UNCAL TONSILLAR

47. UNILATERAL DIALATED PUPIL-UNCAL HERNIATION STRABISMUS IPSILATERAL THIRD NERVE PALSY

48. OPISTHOTONOS

49. NEUROIMAGING CT SCAN FEATURES OF RAISED ICT Obliterated sulci an gyri Poor gray white differentiation Compressed lateral ventricles Loss of basal cisterns MRI For posterior fossa and white matter pathology

50. INTRACRANIAL PRESSURE MONITORING Indications a patient with GCS score of 3–8 (after resuscitation) with either an abnormal admission head CT motor posturing hypotension. It is been found beneficial for the outcome and in determining a treatment threshold in TBI CONTRAINDICATION COAGULOPATHIES

51. Intracranial Pressure Monitoring Devices The most common methods used for ICP monitoring are intraventricular and intraparenchymal catheters. The gold standard for ICP monitoring is intraventricular catheter or ventriculostomy drain. The ventricular catheter is connected to standard pressure transducer. The reference point for ICP monitor is foramen of Monro, although practically, the external auditory meatus is used as a landmark.

52. VENTRICULOSTOMY CATHETERS INTRAPARENCHYMAL CATHETERS ADVANTAGE ability to perform external calibration and therapeutic CSF drainage. easy to insert and have lower risk of infections DISADVANTAGE difficulty in placement when ventricles are effaced higher rate of infection it cannot be calibrated in vivo and may show zero drift over time

53. Intracranial Pressure Waveforms Normal ICP waveform consist of three arterial components— percussion wave (reflects the ejection of blood from heart and transmitted to choroid plexus), tidal wave (reflects brain compliance) dicrotic wave (which reflects aortic valve closure).

54. MANAGEMENT OF RAISED ICT Therapy must be rapid and systematic and focus on the following aspects: A. Immediate stabilization (airway, breathing, circulation) B. Control of ICP and CPP management C. Monitoring in the PICU D. Supportive management E. Evaluation and treatment of underlying disorder

55. ABC Patients with raised ICP will not be able to maintain or protect their airway because of altered mentation and loss of airway tone. Early control of the airway is paramount to prevent airway obstruction and aspiration. Indications for intubation: - GCS < 8 or fall in GCS > 3 points - Evidence of herniation - Airway compromise - Irregular respiratory efforts - Hypoxemia and/or hypercarbia

56. DRUG REGIMEN FOR INTUBATION Lignocaine (1 mg/kg): Used for cough suppression and to prevent ICP surges. Deep Sedation: Thiopentone (2-5 mg/kg): Use lower doses if hypotensive; ensure fluid resuscitation and vasopressor support. Propofol (2-3 mg/kg): Monitor for hypotension. Ketamine: Historically thought to worsen ICP, but recent evidence shows it may be neuroprotective and hemodynamically stable. Vecuronium (0.1-0.2 mg/kg): Provides muscle relaxation; monitor neuromuscular function.

57. CIRCULATION Ensure normovolemia Rapid correction of shock with isotonic saline 2/3 maintainence fluids should be started and titrated to maintain urine output >1ml/kg/hour Fluid of choice –NS Vasopressers can be used to maintain MAP to attain targeted cpp Noradrenaline can be used (through central line). If associated myocardial dysfunction s uspected, an inotrope such as dobutamine should be added.

58. POSITIONING Head end elevation head end of bed 30° with head in neutral position, avoid jugular compression (pro mo tes venous drainage from brain).

59. SEDATION AND ANALGESIA Maintain Deep Sedation: Use continuous infusions of midazolam with opioids (morphine or fentanyl) to keep sedation stable. Manage Pain and Agitation: Administer boluses of fentanyl (1-2 mcg/kg) before suctioning or other stimuli. Neuromuscular Blockade: Only use vecuronium (0.1-0.2 mg/kg) for critical hypoxemia. Note: Always monitor for pain, discomfort, and agitation to avoid ICP spikes.

60. Maintaining of temperature Monitor core temperature. Maintain body temperature normal to mildly hypothermic. Fever is harmful!! Control fever with paracetamol, tepid sponging and cooling blankets. Monitor for and aggressively treat fever and sepsis . Maintain euglycemia. Add glucose to the maintenance fluid at sufficient concentrations to maintain serum glucose between 100-150 mg%.

61. Investigations and monitorin g during therapy of raised I CP ■ Heart rate, invasive arterial blood pressure CVP monitoring . ■ Intracranial pressure monitoring □ Precise hourly fluid balance monitoring. An in dwelling urinary catheter usually necessary. . ABG Q4H, continuous capnography and pulse oximetry. ■ Blood glucose Q2 -4lh hourly, electrolytes every 6-12 hours. ■ Serum osmolality Q12H, BUN daily. ■ Hemogram, LFT,infection screen , coagulation profile eeg . Cranial imaging as necessary Do not postpone stabilization while waiting for etiology to be identified Lumbar Puncture LP may be performed when the child becomes hemodynamically stable with no clinical or radiological evidence of raised ICP.

62. OSMOTHERAPY -1.HYPERTONIC SALINE children who are hypovolemic or hypotensive . It will restore cellular membrane potential and improve cardiac output preferred IN renal failure or serum osmolality greater than 320 mOsmol /kg. For Impending Herniation: Administer 1-3 mL/kg, up to 250 mL over 20 minutes. Fluid Management: Limit fluid intake to 2/3 of maintenance Severe TBI: Use 6.5–10 mL/kg . Acute CNS Infections Continuous Infusion: Give 0.1–1.0 mL/kg/hour to achieve a serum sodium level of 145–155 mEq /L.

63. OSMOTHERAPY 2.20% Mannitol It is an osmotic diuretic and also decreases blood viscosity and hematocrit and increases CBF and cerebral oxygen delivery. Urinary fluid losses should be replaced with normal saline to avoid volume depletion. Serum osmolality must be maintained < 320 mO sm /L to prevent renal toxicity.

64. Use an initial bolus of 0.25–1 g/kg (the higher dose for more urgent reduction of ICP) followed by 0.25–0.5 g/kg bolus repeated 2–6 hours as per requirement. Its duration of effect is 3–5 hours. Emergency therapy for herniation syndromes : 1.0-1.5 g/kg of 20% mannitol; subsequent dose 0.25-0.5 g/kg q4-6h , measure serum osmolality CONTRAINDICATIONS Hypotension, renal failure ,Serum osmolality > 320 mOsm /kg - Intracranial bleed - HYPERTONIC SALINE . ANY CHILD WITH RAISED ICP TRAUMATIC BRAIN INJURY ALSO SHOULD BE SUSOECTED

65. 1.Excess diuresis--Hypovolemia, fall in CPP- Lower doses CONCERNS WHILE USING MANNITOL 2.Use in focal pathology with midline shift Mannitol may cause ' selective debulking" of normal brain parenchyma with increase in midline shift Mannitol should be reserved for features of severely ICP or impending herniation 3.Worsening edema after discontinuation Limit use to less than 48-72 hours. Use smaller doses. Avoid concurrent hypotonic IV fluid

66. SECOND TIER THERAPIES NEUROWORSENING/ICP STILL HIGH AFTER TIER 1 TREATMENT Worsening of GCS >2 Loss of pupillary reactivity Pupillary asymmetry > 2mm New focal motor deficit Herniation syndromes

67. Hyperventilation Hyperventilation: Lowers CBF by constricting cerebral blood vessels. Adjust the ventilator rate to keep PCO2 between 30–35 mm Hg. Caution in Children with traumatic brain injury: Aggressive hyperventilation can reduce CBF too much, worsening cerebral ischemia. Best Use: Hyperventilation is most effective for sudden increases in ICP or signs of impending herniation.

68. Barbiturate Coma Thiopentone/ Pentobarbital can be used to induce burst suppression and control ICP by reducing metabolic activity. A commonly used protocol is to use loading dose of 10 mg/kg over 30 min followed by 1 mg/ kg/hour. The complication rate of barbiturate therapy is high and includes hypotension, hypokalemia, respiratory complications, infections, hepatic dysfunction and renal dysfunction. Bp should be monitored Ionotropic support needed when given in large doses

69. Hypothermia studies do suggest a lowered ICP during the hypothermia therapy in children.32-34 c So in children with refractory raised ICP controlled hypothermia may be tried.

70. SURGICAL OPTIONS Early decompression of hydrocephalus Even when ventricles are not dilated, early insertion of a ventricular drain is useful as ICP monitor and therapeutic m odality (permits CSF drainage). ICSOL- early resection

71. DECOMPRESSIVE CRANIECTOMY This may be considered if above measures fail to control ICP in salvageable patients. Bilateral removal of skull flaps and lifting dura allows decompression of the underlying brain and can prevent herniation and cerebral ischemia . Best for: Children with potentially recoverable brain injurieswho show secondary worsening within 48 hours. Medically refractory intracranial hypertdension Less Effective: Children with severe secondary injuries at the time of presentation may not benefit as much.

72. Seizures that do not cease in 5 minutes are less likely to terminate without intervention. Hence, a child who is convulsing on arrival into the ED is more likely to continue to convulse and cause respiratory insufficiency unless actively treated PHENYTOIN shldnt be given in pulmonary edema A second dose of lorazepam or diazepam can be given 5 minutes after the first dose if seizures are not controlled. Raised intracranial pressure’ must be presumed in all comatose children RAISED ICT is not a contraindication for shock correction 2/3 maintainence fluids Do not postpone stabilization while waiting for etiology to be identified Lp should be done only once icp normalises and hemodynamically stable TAKE HOME MESSAGE SE /RAISED ICP ARE MEDICAL EMERGENCIES

73. CASE SCENARIO