Status Epilepticus in Children. Azhar Daoud Professor of Child Neurology Jordan Univ of science and Tech

Transcription

1 Status Epilepticus in Children Azhar Daoud Professor of Child Neurology Jordan Univ of science and Tech

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3 Status epilepticus (SE) presents in a multitude of forms, dependent on etiology and patient age (myoclonic, tonic, subtle, tonic-clonic, absence, complex partial etc.) Generalized, tonic-clonic SE is the most common form of SE The following presentation refers to generalized, tonic-clonic SE

4 Definition Conventional definition: Single seizure > 30 minutes Series of seizures > 30 minutes without full recovery

5 Definition If appropriate therapy is delayed, SE can cause permanent neurologic sequelae or death thus any child who presents actively convulsing should be assumed to have SE. Haafiz A. Pediatr Emerg Care 1999;15(2):119-29

6 Types of Status Convulsive Generalized convulsive status epilepticus (GCSE) is the most common and the most dangerous form of SE If untreated, may progress to subtle status Get an electromechanical dissociation (nonconvulsive) Nonconvulsive Absence considered benign Complex-partial not benign; get cycling between levels of responsiveness and unresponsiveness

7 The longer SE persists, the lower is the likelihood of spontaneous cessation the harder is it to control the higher is the risk of morbidity and mortality Treatment for most seizures needs to be instituted after > 5 minutes of seizure activity Bleck TP. Epilepsia 1999;40(1):S64-6

8 Climate and Geography Jordan has a combination of Mediterranean and arid desert climates, with Mediterranean prevailing in the North and West of the country. while the majority of the country is desert. Generally, the country has warm, dry summers and mild, wet winters The annual average temperatures ranges from 12 to 25 C Petra

9 Causes Fever Medication change Unknown Metabolic Congenital Anoxic Other (trauma, vascular, infection, tumor, drugs) 36% 20% 9% 8% 7% 5% 15% DeLorenzo RJ. Epilepsia 1992;33 Suppl 4:S15-25

10 Drugs which can cause seizures Antibiotics Penicillins Isoniazid Metronidazole Anesthetics, narcotics Halothane, enflurane Cocaine, fentanyl Ketamine Psychopharmaceuticals Antihistamines Antidepressants Antipsychotics Phencyclidine Tricyclic antidepressants

11 Mortality Adults Children 15 to 22% 3 to 15% Reviewed in: Fountain NB. Epilepsia 2000;41 Suppl 2:S23-30

12 Prolonged seizures Temporary systemic changes Life threatening systemic changes Death

13 Respiratory Hypoxia and hypercarbia - ventilation (chest rigidity from muscle spasm) - Hypermetabolism ( O 2 consumption, CO 2 production) - Poor handling of secretions - Neurogenic pulmonary edema?

14 Hypoxia Hypoxia/anoxia markedly increase (triple?) the risk of mortality in SE Seizures (without hypoxia) are much less dangerous than seizures and hypoxia Towne AR. Epilepsia 1994;35(1): ):27-34

15 Neurogenic pulmonary edema Rare complication of SE in children Likely occurs as consequence of marked increase of pulmonary vascular pressure during SE Johnston SC. Postictal pulmonary edema requires pulmonary vascular pressure increases. Epilepsia 1996;37(5):428-32

16 Acidosis Respiratory Lactic Impaired tissue oxygenation Increased energy expenditure

17 Hemodynamics Sympathetic overdrive Massive catecholamine / autonomic discharge Hypertension Tachycardia High CVP Exhaustion Hypotension Hypoperfusion 0 min 60 min

18 Cerebral blood flow - Cerebral O2 requirement O2 requirement Blood flow Blood pressure Seizure duration Hyperdynami c phase CBF Exhaustion phase CBF drops as hypotension sets in Autoregulation exhausted Neuronal damage ensues

19 Glucose 30 min Glucose SE SE + hypoxia Seizure duration Hyperdynamic phase Hyperglycemia Exhaustion phase Hypoglycemia develops Hypoglycemia appears earlier in presence of hypoxia Neuronal damage ensues

20 Hyperpyrexia Hyperpyrexia may develop during protracted SE, and aggravate possible mismatch of cerebral metabolic requirement and substrate delivery Treat hyperpyrexia aggressively Antipyretics, external cooling Consider intubation, relaxation, ventilation

21 Other alterations Blood leukocytosis (50% of children) Spinal fluid leukocytosis (15% of children) K + creatine kinase Myoglobinuria

22 A First line Oxygen, oral airway. Avoid hypoxia! B Consider bag-valve mask ventilation. Consider intubation C IV/IO access. Treat hypotension, but NOT hypertension

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24 Treatment Arterial blood gas? All children in SE have acidosis. It often resolves rapidly with termination of SE Intubate? It may be difficult to intubate the actively seizing child Stop or slow seizures first, give O2, consider BVM ventilation If using paralytic agent to intubate, assume that SE continues

25 Initial investigations Labs Na, Ca, Mg, PO4, glucose CBC Liver function tests, ammonia Anticonvulsant level Toxicology

26 Initial investigations Lumbar puncture Always defer LP in unstable patient, but never delay antibiotic/antiviral rx if indicated CT scan Indicated for focal seizures or deficit, history of trauma or bleeding d/o

27 Treatment Give glucose (2-4 ml/kg D25%, infants 5 ml/kg D10%), unless normo- or hyperglycemic Hyperglycemia has no negative effect in SE (as long as significant hyperosmolality is being avoided)

28 Treatment The longer you wait with anticonvulsant, the more anticonvulsant you will need to stop SE Most common mistake is ineffective dose

29 Anticonvulsants Rapid acting Plus Long acting

30 Anticonvulsants - Rapid acting Benzodiazepines Lorazepam 0.1 mg/kg i.v. over 1-2 minutes Diazepam 0.2 mg/kg i.v. over 1-2 minutes If SE persists, repeat every 5-10 minutes

31 Benzodiazepines Lorazepam Low lipid solubility Action delayed 2 minutes Anticonvulsant effect 6-12 hrs Less respiratory depression than diazepam Midazolam May be given i.m. Diazepam High lipid solubility Thus very rapid onset Redistributes rapidly Thus rapid loss of anticonvulsant effect Adverse effects are persistent: Hypotension Respir depression

32 Lorazepam Superiority IV Treatment in Out-of-hospital SE SE at Time of Arrival at the ER Lorazepam Diazepam Placebo SE terminated 39 (59.1%) 29 (42.6%) 15 (21.1%) Ongoing SE 27 (40.9%) 39 (57.4%) 56 (78.9%) Alldredge BK, et al. N Eng J Med

33 Anticonvulsants - Long acting Phenytoin 20 mg/kg i.v. over 20 min ph 12 Extravasation causes severe tissue injury Onset min May cause hypotension, dysrhythmia Cheap Fosphenytoin 20 mg PE/kg i.v. over 5-7 min PE = phenytoin equivalent ph 8.6 Extravasation well tolerated Onset 5-10 min May cause hypotension Expensive

34 Cutaneous Reactions in Patients Receiving IV Phenytoin: Purple Glove Syndrome (PGS) PGS = delayed, soft-tissue injury of the hand and forearm following IV administration of phenytoin PGS is frequently, but not exclusively, associated with phenytoin extravasation PGS is characterized by pain, edema, and purplish discoloration Skin may blister or slough prior to resolution Retrospective study of 152 patients who received IV phenytoin over 3 months at the Mayo Clinic 9 patients (5.9%) developed PGS O'Brien TJ et al. Neurology. 1998;51:

35 Purple Glove Syndrome Hanna DR. J Neurosci Nur. 1992;24:

36 Anticonvulsants - Long acting Phenobarbital 20 mg/k g i.v. over min Onset min May cause hypotension, respiratory depression

37 Third-Line Agents Valoproat load 20mg/kg at 3mg/kg/min +no associations with hypotension or arrhythmias +don t need to place patient on monitor +very few side effects even at high doses -minimal data (80% effective in 2 trials) Phenobarbital load 15mg/kg at 100mg/min +a lot of clinical experience with this -prolonged sedation, hypotension, respiratory depression Pentobarbital like phenobarb. but faster acting, shorter t1/2 Propofol don t use in kids (metabolic acidosis and rhabdomyolysis) -load 2mg/kg, then 5-10 mg/kg/hr

38 Start EEG; do not delay treatment unless EEG necessary to verify diagnosis Lorazepam 0.1 mg/kg by IV push (<2 mg/min) Seizures continue Fosphenytoin 20 mg PE/kg (up to 150 mg PE/min). If only phenytoin is available: 20 mg/kg (<50 mg/min) Seizures continue Additional fosphenytoin 5-10 mg PE/kg Seizures continue Call for help Phenobarbital (PB) 20 mg/kg (<100 mg/min) OR Induce barbiturate coma: Pentobarbital (5-15 mg/kg) slowly as loading dose, then mg/kg/hr Valproate 20 mg/kg (3 mg/kg/min) is an alternative to PB Seizures continue Continuous infusion propofol 1 mg/kg over 5 min, then 2-4 mg/kg/hr OR Time (Minutes) Midazolam 0.2 mg/kg bolus, then mg/kg/hr

39 If SE persists Propofol infusion 5-10 mg/kg/hr after bolus 2 mg/kg Midazolam infusion 1-10 mcg/kg/min after bolus 0.15 mg/kg Pentobarbital infusion 1-3 mg/kg/hr after bolus 10 mg/kg Paraldehyde Isoflurane Leviteracetam? Lacosamide?

40 Non - convulsive status epilepticus How do you tell that patient s seizures have stopped?

41 Non - convulsive SE? Neurologic signs after termination of SE are common: Pupillary changes Abnormal tone Babinski Posturing Clonus May be asymmetrical

42 Non - convulsive SE? Up to 20% of children with SE have non - convulsive SE after tonic - clonic SE

43 Non - convulsive SE? If child does not begin to respond to painful stimuli within minutes after tonic - clonic SE, suspect non - convulsive SE Urgent EEG

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