Status epilepticus

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Status epilepticus

  1. 1. STATUS EPILEPTICUSDR.SRIRAMA.ANJANEYULU<br />
  2. 2. INTRODUCTION<br />Medical emergency<br />Hunter noted that SE was rare before the advent of powerful antiepileptic drugs, and the consequent risk of drug withdrawal.<br />Incidence of SE have varied from 10 to 60 per 100000 person-years.<br />The annual incidence in the UK is about<br /> 9000–14 000 new cases per year.<br />Accounts for 3.5% of admissions to emergency departments in the developed nations and for 11% in a developing country.(MEENA AK,2000).<br />
  3. 3. INCIDENCE<br />About 5% of all epileptic adult clinic patients will have at least one episode of SE in the course of their epilepsy , and in children the proportion is higher (10-25%).<br />Mortality for SE is about 20%-30% (dying of the underlying condition, rather than the SE itself.)<br /> Mortality is age related, and is much lower in children and higher in the elderly.<br /> The risks of morbidity are greatly increased the longer the duration of the SE episode .<br />
  4. 4. Mortality of status epilepticus<br />Dead of status 1.8% <br />Dead of underlying cause 28.8% <br />Dead other causes 6.5% <br />Alive 63.1% <br />
  5. 5. A comparison of survival by duration in status epilepticus shows a marked increase in mortiality for patients in prolonged status epilepticus.  <br />(Towne et al. 1994)<br />
  6. 6. Five population-based studies of status epilepticus (convulsive and non convulsive)<br />
  7. 7. Seizure type and epilepsy classification in five population-based studies<br />
  8. 8. DEFINITIONS (nanda gopal,pgmj,2006)<br />
  9. 9. ILAE CLASSIFICATION OF SE, Continuous seizure types <br />Generalized status epilepticus<br />Generalized tonic-clonic status epilepticus<br />Clonic status epilepticus<br />Absence status epilepticus<br />Tonic status epilepticus<br />Myoclonic status epilepticus<br />Focal status epilepticus<br />Epilepsiapartialis continua of Kojevnikov<br />Aura continua<br />Limbic status epilepticus (psychomotor status)<br />Hemiconvulsive status with hemiparesis<br />
  10. 10. Revised classification of status epilepticus (shorvon s)<br /> Status epilepticus confined to early childhood<br />Neonatal status epilepticus<br />Status epilepticus in specific neonatal epilepsy syndromes<br />Infantile spasms<br /> Status epilepticus confined to later childhood<br />Febrile status epilepticus<br />Status in childhood partial epilepsy syndromes<br />Status epilepticus in myoclonic-astatic epilepsy<br />Electrical status epilepticus during slow-wave sleep<br />Landau-Kleffner syndrome<br /> Status epilepticus occurring in childhood and adult life<br />Tonic-clonic status epilepticus<br />Absence status epilepticus<br />Epilepsiapartialis continua<br />Status epilepticus in coma (subtle generalized tonic-clonic seizure)<br />Specific forms of status epilepticus in mental retardation<br />Syndromes of myoclonic status epilepticus<br />Non-convulsive simple partial status epilepticus<br />Complex partial status epilepticus<br /> Status epilepticus confined to adult life<br />De novo absence status of late onset<br />
  11. 11. Stepwise approach to classification of status epilepticus<br />
  12. 12. Clinical features and electroencephalographic abnormalities in subtypes of NCSE<br />
  13. 13. SE Vs PSYCHOGENIC SE<br />
  14. 14. Status epilepticus and neuronal damage<br />Cerebral cortex <br />Hippocampus <br />Amygdala<br />Thalamus <br />Cerebellum <br />
  15. 15. Hippocampal atrophy<br />
  16. 16. Drug pharmacokinetics <br />Fast drug absorption is essential in the treatment of status epilepticus<br />Route of administration<br />Volume of distribution<br />Acidosis<br />Hepatic&renal dysfunction due to SE<br />
  17. 17. Diazepam drug levels<br />
  18. 18. Concentration-time profile of acutely administered drugs showing two phases<br />
  19. 19. Stages of status epilepticus<br />Discrete seizures <br />Merging seizures <br />Continuous ictal activity<br />Continuous ictal activity, punctuated by low voltage flat activity <br />Periodic epileptiform discharges on a quiet background <br />(Treiman et al. 1990)<br />
  20. 20. Aetiologies of status epilepticus<br />
  21. 21. Drugs and Other Substances that Can Cause Seizures<br />
  22. 22. Aetiologies of status epilepticus<br />
  23. 23. PATHOPHYSIOLOGY<br />SE requires a pool of neurones capable of initiating and sustaining abnormal firing.<br />Abnormal discharge is facilitated by loss of inhibitory synaptic transmission mediated by gamma-amino butyric acid (GABA) and sustained by excitatory transmission mediated by glutamate.<br />Postsynaptic GABA(A) and N-methyl-D-aspartate receptors have a vital role in the inhibitory and excitatory transmissions, respectively.<br />Increased neuronal activity can also lead to loss of inhibition by accelerated internalisation of the GABA(A) receptor.<br />Neuropeptide Y and galanin serve as endogenous anticonvulsants that terminate status epilepticus.<br />Brain injury from trauma, epilepsy, infections and other causes leads to increased cortical excitability and impaired seizure termination.<br />
  24. 24. PATHO PHYSIOLOGY OF SE<br />
  25. 25. Medical management <br />Oxygen and cardiorespiratory resuscitation<br />Monitoring<br />Emergency anticonvulsant therapy<br />Intravenous lines<br />Emergency investigations<br />Intravenous glucose and thiamine<br />Acidosis<br />Establish aetiology<br />Seizure and EEG monitoring<br />Long-term anticonvulsant therapy<br />
  26. 26. Diagnosis and early management ofseizures<br />
  27. 27. Protocol for drug treatment, general measures, and emergency investigations of convulsivestatus epilepticus as function of time from the onset of the seizure<br />
  28. 28. Protocol for drug treatment, general measures, and emergency investigations of convulsivestatus epilepticus as function of time from the onset of the seizure<br />
  29. 29. Diazepam vslorazepam<br />Four randomised trials of anticonvulsants in patients with status epilepticus showed that both lorazepam and diazepam are effective as initial treatment.<br />Intravenous lorazepam given by trained paramedics in prehospital settings was also found to be therapeutically beneficial.<br /> Ease of administration, longer effective duration of action and better side effect profile,most prefer lorazepam to diazepam for the initial treatment.<br />
  30. 30. Diazepam was effective in controlling brief (10 min) seizuresbut lost potency after prolonged (45 min) seizures in a lithium pilocarpine ,rat model of status epilepticus. <br />
  31. 31. Protocol for drug treatment, general measures, and emergency investigations of convulsivestatus epilepticus as function of time from the onset of the seizure<br />
  32. 32. phenytoin or fosphenytoin?<br />Fosphenytoin advantages.<br />It can be infused using standard intravenous solutions, whereas phenytoin should not be given in dextrose containing fluids (because of drug precipitation).<br /> It can be given intramuscularly.<br />Rate of infusion is three times as fast with fosphenytoin.<br />
  33. 33. Phenytoinvsphosphenytoin<br />
  34. 34. treatment protocol for RSE<br />
  35. 35. Protocol for drug treatment, general measures, and emergency investigations of convulsivestatus epilepticus as function of time from the onset of the seizure<br />
  36. 36. rse<br />
  37. 37. Se protocol<br />
  38. 38. Mayo Clin Protocol<br />
  39. 39. Pharmacotherapy of generalised convulsive status epilepticus<br />
  40. 40. Pharmacotherapy of generalised refractory status epilepticus<br />
  41. 41. Non-convulsive status epilepticus<br />1/3rd of all cases of SE.<br />14-24 per 100000 population per year.<br />The diagnosis of non-convulsive status epilepticus is critically dependent on EEG.<br />In patients of epilepsy,any prolonged change in personality, prolonged postictal confusion (greater than 30 min) or recent onset psychosis should be investigated.<br />Subtle manifestations such as twitching of the limbs, or facial muscles or nystagmoid eye jerking.<br />
  42. 42. definitions of nonconvulsivestatus epilepticus<br /> (a) Unequivocal electrographic seizure activity.<br /> (b) Periodic epileptiform discharges or rhythmic discharge with clinical seizure activity.<br /> (c) Rhythmic discharge with either clinical or electrographic response to treatment.<br />
  43. 43. Typical absence status epilepticus<br />Prolonged absence attacks with continuous or discontinuous 3 Hz spike and wave occurring in patients with primary generalized epilepsy.<br /> Absence status epilepticus can be divided into<br />Childhood absence status epilepticus (those usually already receiving treatment).<br /> Late onset absence status epilepticus with a history of primary generalized history (often a history of absences in childhood) .<br /> Late onset absence status epilepticus developing de novo (usually following drug or alcohol withdrawal).<br /> No evidence that absence status induces neuronal damage,and thus aggressive treatment is not warranted.<br /> Responds rapidly to intravenous benzodiazepines.<br />Sodium valproate is one of the alternative.<br />
  44. 44. Complex partial status epilepticus<br />‘A prolonged epileptic episode in which focal fluctuating or frequently recurring electrographic epileptic discharges, arising in temporal or extratemporal regions, result in a confusional state with variable clinical symptoms‘.<br />Oral clobazam over a period of 2-3 days given early at home.<br />Persistent or resistant complex partial status epilepticus intravenous therapy should be used , and lorazepam followed by phenytoin (or fosphenytoin) are the drugs of choice.<br />
  45. 45. Non-convulsive status epilepticus in coma<br />Electrographic status epilepticus in coma is not uncommon and is seen in up to 8% of patients in coma with no clinical evidence of seizure activity.<br />Non-convulsive status epilepticus in coma consists of three groups: <br />Those who had convulsive status epilepticus.<br /> Those who have subtle clinical signs of seizure activity .<br />Those with no clinical signs.<br />Should be treated aggressively with deep anaesthesia and concomitant antiepileptic drugs.<br />
  46. 46. Atypical absence status epilepticus<br />Associated with the epileptic encephalopathies such as Lennox-Gastaut syndrome.<br />Should be considered if there is change in behaviour, personality, cognition or increased confusion in a patient with one of these epilepsies.<br />The EEG characteristics are usually that of continuous or frequent slow (<2.5Hz) spike and wave.<br />Oral rather than intravenous treatment is usually more appropriate, and the drugs of choice are valproate, lamotrigine,clonazepam, clobazam and topiramate.<br />
  47. 47. Tonic status epilepticus<br />Tonic status epilepticus is not uncommon in patients with syndromes such as Lennox-Gastaut.<br />Tonic status epilepticus can also rarely occur in the setting of normal premorbid intelligence.<br />The tonic seizures may not necessarily be clinically apparent; the EEG, however, demonstrates bursts of paroxysmal, generalized fast discharges.<br />Worsened with benzodiazepines.<br />Stimulants such as methylphenidate can be effective.<br />Oral lamotrigine, ACTH and corticosteroids can be helpful.<br />
  48. 48. Epilepsiapartialis continua<br />Status equivalent of simple partial motor seizures.<br />Defined as regular or irregular clonic muscular twitching affecting a limited part of the body, occurring for a minimum of 1 h, and recurring at intervals of no more than 10 s.<br />Can result from structural abnormalities such as stroke, trauma, cerebral infarction, cerebral abscess, neuronal migration disorders and vascular malformation.<br />50% of cases, the MRI is normal.<br />Associated with a variety of encephalitides, commonly Rasmussen's encephalitis, but also SSPE,CJD.<br />Treatment is best targeted at the underlying cause.<br />Oral corticosteroid, nimodipine.<br />Neurosurgical resection.<br />
  49. 49. TREATMENT OF NCSE<br />
  50. 50. The use of valproate and new antiepileptic drugs in status epilepticus<br />VALPROATE<br />LEVETIRACETAM<br />TOPIRAMATE<br />

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