STATUS EPILEPTICUS.docx - Fiji National UniversityDocument Transcript
STATUS EPILEPTICUS<br />May be defined as seizure activity that lasts longer than 30 minutes or repeated seizures between which the child does not return to the baseline level of consciousness. <br />2 categories<br />
ConvulsiveNon-convulsiveHad prolong, generalized tonic-clonic seizure or repetition of such seizure without a return o full consciousness between episodesProlong twilight or semi-coma stateEpilepsia partialis continuaGeneralized myoclonusComplex partial status epilepticus –involved a small area of the brain, normally the temporal lobeAbsence status epilepticus – generalize seizure affecting whole brain and result in long lasting stupor, staring and unresponse
History<br />In the initial presentation of status epilepticus, a directed history suffices. Obtain a more detailed history after stabilization, including the following details:<br />The course of current seizure activity <br />Time and nature of onset of seizure activity <br />Involvement of extremities or other body parts <br />Nature of movements (eg, eye movements, flexion, extension, stiffening of extremities), including any focal movements and details of postictal neurologic deficit <br />Incontinence <br />Cyanosis (perioral or facial) <br />Duration of seizure activity prior to medical attention <br />Mental status after cessation of seizure activity<br />Fever or intercurrent illnesses <br />Prior history of seizures - If present, specify medications, anticonvulsant use, and compliance. <br />Head injury (recent and remote) <br />Central nervous system (CNS) infection or disease (eg, meningitis, neurocutaneous syndrome) <br />Intoxication or toxic exposure (see Causes for examples) <br />Other CNS abnormality (eg, ventricular-peritoneal shunt, prior CNS trauma) <br />Birth history and developmental delay (eg, anoxic encephalopathy, cerebral palsy) <br />Other medical history (eg, acquired immunodeficiency syndrome, systemic lupus erythematosus, type 1 diabetes mellitus)<br />Physical<br />Perform a rapid, directed physical and neurologic examination during status epilepticus, followed by a detailed examination when the child is stabilized.<br />Signs of sepsis or meningitis <br />Temperature more than 38.5°C; in patients younger than 2-3 months, more than 38.0°C <br />Respiratory distress <br />Cyanosis <br />Poor peripheral perfusion <br />Bulging fontanelles in infant <br />Meningismus (in children >12-18 mo) <br />Presence of petechiae or purpura, herpetic vesicles<br />Evidence of head or other CNS injury <br />Bradycardia, tachypnea, and hypertension (Cushing triad for signs of increased intracranial pressure) <br />Poor pupillary response <br />Asymmetry on neurologic examination <br />Abnormal posturing <br />Gross deformity or soft tissue injury to head<br />Hallmarks of neurocutaneous syndromes (eg, port wine stain)<br />Causes<br />Neonates (first month of life) <br />Birth injury (eg, anoxia, hemorrhage) and congenital abnormalities <br />Metabolic disorders (eg, hypoglycemia, hypocalcemia, hyponatremia) and inborn errors of metabolism (eg, lipidoses, amino acidurias) <br />Infection (eg, meningitis)<br />Early childhood (<6 y) <br />Birth injury <br />Febrile convulsions (3 mo to 6 y) <br />Infection <br />Metabolic disorders <br />Trauma <br />Neurocutaneous syndromes <br />Cerebral degenerative diseases <br />Tumors <br />Idiopathic<br />Children and adolescents (>6 y) <br />Birth injury <br />Trauma <br />Infection <br />Epilepsy with inadequate drug levels <br />Cerebral degenerative disease <br />Tumor <br />Toxins <br />Idiopathic<br />Toxins and medications <br />Topical anesthetics (eg, lidocaine) <br />Anticonvulsant overdose <br />Camphor <br />Hypoglycemic agents (eg, insulin, ethanol) <br />Carbon monoxide <br />Cyanide <br />Heavy metals (eg, lead) <br />Pesticides (eg, organophosphate) <br />Cocaine <br />Phencyclidine <br />Belladonna alkaloids <br />Nicotine <br />Sympathomimetics (eg, amphetamines, phenylpropanolamine [recalled from US market]) <br />Tricyclic antidepressants<br />Pathophysiology<br />
↑ major amino acids excitatory neurotransmitters – glutamate, aspartate and acetylcholine
↓major inhibitory neurotransmitters such as Gamma amino butyric acid (GABA), ↓inhibitor of calcium ion dependent potassium ion current and blockage of N-methyl-d-aspartate (NMDA) by magnesium.
Neurons depolarized<br />Ca enter cells thru NMDA channels<br />3.Neuronal loss-occur in every episodes, especially prolong episodes<br />Hypoxia, ↑various proteins that causes apoptosis<br />Systemic complications<br />
Hypoxemia – due to impaired ventilation; ↑ oxygen consumption, excessive salivation or tracheobronchial secretion; metabolic disturbance (↓brain glucose, lactic acidosis, depletion of brain ATP); impaired myocardial function, and hypotension
Acidemia - ↓pH <7.0 –lactic acidosis and respiratory acidosis
Investigations<br />Initial investigations:<br />Glucose, urea & creatinine, sodium, potassium, calciumAnti-epileptic drug levelsComplete blood countOximetry or arterial blood gasesUrinalysis<br />Further investigations after stabilization:<br />
Liver function tests
not all of the investigations need be performed in every patient;
selection depends on both the patient's history and presentation. Most patients with SE should have a CT scan performed at some stage but patients with established epilepsy who have already had a CT scan do not usually require another scan.
CNS infection must be seriously considered in all patients, especially young children with a fever. Lumbar puncture is indicated in patients with fits not controlled with a benzodiazepine and phenytoin, or evidence of craniofacial infection (eg otitis, mastoiditis), or nuchal rigidity. It is contraindicated in those in whom an intracranial space occupying lesion is suspected. Although CT scanning prior to lumbar puncture is not considered, by some, to be mandatory, it should be bourne in mind that in adults CNS tumours are a more common cause of epilepsy than CNS infection and that lumbar puncture is never a life-saving procedure. It has been suggested that, even in suspected meningitis, lumbar puncture be delayed for 30 minutes after a fit because of the transient cerebral oedema that accompanies a fit. Although CSF leucocytosis occurs in 20% of patients with SE, patients with CSF leucocytosis should be treated for suspected meningitis until the diagnosis is excluded by microbiological culture or antibody assays.
Management<br />Prehospital Care<br />Secure the airway. <br />Administer supplemental 100% oxygen. <br />Infuse isotonic intravenous fluids and glucose. <br />Immobilize the cervical spine in patients with possible trauma. <br />Consider rectally administered diazepam (0.5 mg/kg/dose) or intramuscularly administered midazolam (0.1-0.2 mg/kg/dose; not to exceed a cumulative dose of 10 mg).2 <br />Emergency Department Care<br />The principles of treatment are to terminate the seizure while resuscitating the patient, treating complications, and preventing recurrence.<br />Assessment and stabilization of ABCs concurrent with management of the seizure is imperative. <br />Administer 100% oxygen by facemask, assist ventilation, and use artificial airways (eg, endotracheal intubation) as needed. Suction secretions and decompress the stomach with a nasogastric tube. <br />Immobilize the cervical spine if trauma is suspected. <br />Closely monitor vital signs, cardiorespiratory function, and oxygen saturation. <br />Perform rapid blood glucose assay (eg, Dextrostix) at bedside.<br />Establish intravenous access. Use intraosseous (IO) infusion if intravenous access is not immediately available in the child younger than 6 years. Most available anticonvulsants may be administered intravenously or intraosseously. <br />Infuse isotonic intravenous fluids 20 mL/kg with glucose (eg, 200 mL dextrose 5% in normal saline [D5NS] intravenously over 1 h for a 10-kg child). <br />Consider treatment with the following agents: <br />Dextrose - 0.25-0.5 g/kg/dose (1-2 mL of 25% dextrose) intravenously for hypoglycemia; not to exceed 25 g/dose <br />Naloxone - 0.1 mg/kg/dose intravenously preferably (if needed may administer intramuscularly/subcutaneously) for narcotic overdose <br />Thiamine - 100 mg intramuscularly for possible deficiency <br />Pyridoxine - 50-100 mg intravenously/intramuscularly for possible deficiency <br />Antibiotics - If meningitis is strongly suspected, initiate treatment with antibiotics prior to cerebrospinal fluid (CSF) analysis or CNS imaging.<br />Administer anticonvulsant medication. The optimal protocol for management of status epilepticus begins with a benzodiazepine. In the United States, lorazepam is the first drug of choice in patients with intravenous or intraosseous access. For patients without parenteral access, intramuscular midazolam is best. If the seizures cease, no further drugs are immediately necessary, and the etiology of status epilepticus should be investigated. If seizures continue, administer intravenous phenytoin or parenteral fosphenytoin. If these are not effective, administer intravenous phenobarbital titrated to induce barbiturate coma. Finally, consider general anesthesia with pentobarbital or midazolam. <br />The goal is prompt cessation of seizure activity. Patiently allow infused anticonvulsants to act before using additional anticonvulsants. Proceed to the next drug if seizure activity continues. <br />Lorazepam (0.05-0.1 mg/kg intravenously/IO slowly infused over 2-5 min) has rapid onset and long duration of anticonvulsant action. It is preferred over diazepam. <br />Phenytoin (18-20 mg/kg intravenously/IO) or fosphenytoin (15-20 mg/kg intravenously/IO) loading doses: These long-acting anticonvulsants usually are infused if benzodiazepines do not stop the seizures. Phenytoin and fosphenytoin are effective for most idiopathic generalized seizures and for posttraumatic, focal, or psychomotor status epilepticus. Use a slow rate of infusion (<1 mg/kg/min or <50 mg/min) to avoid hypotension or cardiac arrhythmias. A full loading dose should be delivered unless the patient is known to have a current therapeutic level. <br />Midazolam (0.1-0.2 mg/kg intramuscularly) is most effective when intravenous or intraosseous access is not immediately available. Midazolam is the only benzodiazepine that can be administered safely intramuscularly with equivalent rapid onset and moderate duration of action. <br />Phenobarbital (20-25 mg/kg intravenously/IO) is effective for febrile and neonatal status epilepticus and may be infused after lorazepam or other benzodiazepines if the child is likely to have these types of seizures. Phenobarbital's major disadvantages are that it significantly depresses mental status and causes respiratory difficulty. Obtain serum anticonvulsant levels prior to administering additional long-acting anticonvulsants such as phenytoin or fosphenytoin.<br />General anesthesia <br />Pentobarbital (5-10 mg/kg intravenously/IO loading dose followed by 0.5-3 mg/kg/h) or midazolam (0.2 mg/kg intravenously/IO loading dose followed by 0.75-10 mcg/kg/min) <br />All children must be intubated and paralyzed, have continuous cardiorespiratory and EEG monitoring, and be in a pediatric critical care setting.<br />Consultations<br />After initial emergency stabilization, consider consultation with the following specialists:<br />Pediatric emergency or critical care specialist or general pediatrician <br />Pediatric neurologist <br />Pediatric neurosurgeon if needed<br />