Correspondence
Status Epilepticus
N Engl J Med 1998; 339:409-410August 6, 1998
- Article
To the Editor:
Lowenstein and Alldredge's excellent review of status epilepticus (April 2 issue)1 contains one misunderstanding that we hear often: “Patients should receive 100 percent oxygen by nasal cannula or a nonrebreathing mask.” Airway management and oxygen administration are priorities in the management of status epilepticus. However, there are few methods of ensuring that the patient receives 100 percent oxygen, and all of them involve the placement of a tube (endotracheal or tracheostomy) or an airtight mask (facial or laryngeal), attached to a breathing system with a reservoir (bag or tube) full of oxygen.
1 ReferencesCasiano Barrera Groba, F.R.C.A.
King's College Hospital, London SE5 9RS, United Kingdom1
Lowenstein DH ,Alldredge BK . Status epilepticus. N Engl J Med 1998;338:970-976
Full Text | Web of Science | Medline
To the Editor:
With regard to airway management during status epilepticus, nasal–tracheal intubation has an unnecessarily high rate of complications and a lower success rate than oral rapid-sequence intubation.1,2 In addition, nasal–tracheal intubation is intensely stimulating and will exacerbate elevated intracranial pressure if such a condition is present. Nasal–tracheal intubation is therefore a poor choice for patients with status epilepticus.
Vecuronium in the dose cited in the article (0.1 mg per kilogram of body weight) is inadequate for a protected, rapid-sequence intubation. The appropriate course for most patients with status epilepticus who are thought to require intubation is the combination of succinylcholine at a dose of 1.5 mg per kilogram and a rapid-acting induction agent with anticonvulsant properties, such as sodium thiopental at a dose of 3 mg per kilogram. After intubation, sedation can be maintained with benzodiazepines, and neuromuscular blockade can be maintained, if necessary, with vecuronium at a dose of 0.1 mg per kilogram. If neuromuscular blockade is maintained, continuous electroencephalographic monitoring or frequent clinical reassessment is necessary to ensure that the other anticonvulsant measures have stopped the seizure. If intracranial pressure is thought to be elevated, treatment before intubation with lidocaine at a dose of 1.5 mg per kilogram, fentanyl at a dose of 3 μg per kilogram, and vecuronium at a dose of 0.01 mg per kilogram will help mitigate adverse intracranial-pressure responses to the medications and intubation.3
3 ReferencesRon M. Walls, M.D.
Mark J. Sagarin, M.D.
Brigham and Women's Hospital, Boston, MA 021151
Dronen SC ,Merigian KS ,Hedges JR ,Hoekstra JW ,Borron SW . A comparison of blind nasotracheal and succinylcholine-assisted intubation in the poisoned patient. Ann Emerg Med 1987;16:650-652
CrossRef | Web of Science | Medline2
Walls RM ,Sagarin MJ ,Vissers RJ , et al. Confirmation of endotracheal tube placement -- analysis of 1,288 emergency department intubations. Acad Emerg Med 1998;5:541-541 abstract.3
Walls RM . Rapid-sequence intubation in head trauma. Ann Emerg Med 1993;22:1008-1013
CrossRef | Web of Science | Medline
To the Editor:
Drugs and toxins account for a considerable percentage of cases of status epilepticus, so poisoning must be considered in any patient with seizures who has no history of an underlying seizure disorder or other clear explanation. This is particularly important since patients with drug-induced status epilepticus may require the administration of appropriate antidotal therapy to terminate their seizures, as is the case in patients with status epilepticus brought about by isoniazid.
In New York City, there has been a dramatic increase in the number of patients with isoniazid-induced seizures.1 Seizures following an overdose of isoniazid are common2 and are often refractory to standard management strategies,2 such as those outlined by Lowenstein and Alldredge. Isoniazid interferes with the synthesis of the inhibitory neurotransmitter γ-aminobutyric acid (GABA), and benzodiazepines specifically enhance the neuroinhibitory effects of GABA and require the presence of GABA to be effective.
The intravenous administration of high-dose pyridoxine (vitamin B6) reverses the pharmacologic effects induced by isoniazid and terminates the seizure. Given the high prevalence of isoniazid overdose in New York City and the safety of 5 g of intravenous pyridoxine (70 mg per kilogram in children), we routinely recommend the administration of pyridoxine to all patients with seizures refractory to conventional doses of intravenous benzodiazepines.
2 ReferencesLewis S. Nelson, M.D.
Joseph Rella, M.D.
Robert S. Hoffman, M.D.
New York City Poison Control Center, New York, NY 100161
Shah BR ,Santucci K ,Sinert R ,Steiner P . Acute isoniazid neurotoxicity in an urban hospital. Pediatrics 1995;95:700-704
Web of Science | Medline2
Sullivan EA ,Geoffroy P ,Weisman R ,Hoffman R ,Frieden TR . Isoniazid poisonings in New York City. J Emerg Med 1998;16:57-59
CrossRef | Medline
To the Editor:
Psychogenic seizures are common1 and can sometimes look like status epilepticus.2 Given that more than 80 percent of physiologic seizures cease after the administration of intravenous benzodiazepines, phenytoin, or both,3 the physician should consider the diagnosis of psychogenic seizures if a patient continues to have seizures after administration of these two anticonvulsant medications.
The distinction between psychogenic seizures and physiologic seizures is not easy to make; clinical features are unreliable,2 and electroencephalographic monitoring may not be readily available. In our experience, patients with pseudo–status epilepticus often have a history of similar events. Consequently, while waiting for the completion of the phenytoin infusion (which takes approximately 20 minutes), we routinely review the chart of each patient who presents with prolonged seizure activity. This facilitates the early diagnosis of psychogenic seizures and allows the institution of appropriate treatment, including counseling and supportive care.4
4 ReferencesBryan J. Traynor, M.D., M.R.C.P.I.
Orla Hardiman, M.D., M.R.C.P.I.
Beaumont Hospital, Dublin 9, Ireland1
Chabolla DR ,Krahn LE ,So EL ,Rummans TA . Psychogenic nonepileptic seizures. Mayo Clin Proc 1996;71:493-500
CrossRef | Web of Science | Medline2
Leis AA ,Ross MA ,Summers AK . Psychogenic seizures: ictal characteristics and diagnostic pitfalls. Neurology 1992;42:95-99
Web of Science | Medline3
Lowenstein DH ,Alldredge BK . Status epilepticus at an urban public hospital in the 1980s. Neurology 1993;43:483-488
Web of Science | Medline4
Pakalnis A ,Drake ME Jr ,Phillips B . Neuropsychiatric aspects of psychogenic status epilepticus. Neurology 1991;41:1104-1106
Web of Science | Medline
Author/Editor Response
The authors reply:
To the Editor: For the management of patients in status epilepticus, we agree that oral rapid-sequence intubation is almost always preferable to nasal–tracheal intubation in the hospital setting. However, there continues to be a role for nasal–tracheal intubation in the prehospital setting, since most emergency medical systems have not incorporated rapid-sequence intubation into their protocols for airway management.1 Some patients, especially those with a pronounced postictal depression of consciousness, can be intubated orally without the use of a rapid-sequence–intubation medication protocol. Nonetheless, nasal–tracheal intubation may be the only option in the prehospital setting for patients who have ongoing convulsions or those who have clinical respiratory failure and have regained consciousness.
Dr. Groba raises a semantic issue. He reminds us that introducing a source of 100 percent oxygen in the vicinity of the nasopharynx does not necessarily result in the delivery of 100 percent oxygen into the respiratory system.
Psychogenic or other nonepileptic seizures must always be considered in the differential diagnosis of status epilepticus, and we fully agree with Traynor and Hardiman's practice of including a very prompt chart review during the immediate management of status epilepticus. We also appreciate Nelson et al. for bringing attention to the importance of isoniazid toxicity as a cause of status epilepticus. Their suggestion for the routine use of pyridoxine in geographic regions of high risk is a good one. As stated in our review, status epilepticus due to drug toxicity is associated with relatively high morbidity and mortality, and it is often resistant to anticonvulsant therapy.2-4 A toxicologic evaluation should therefore be performed routinely in patients with status epilepticus of unknown cause, and poisonings should be identified rapidly and treated aggressively.
4 ReferencesDaniel H. Lowenstein, M.D.
Brian K. Alldredge, Pharm.D.
University of California, San Francisco, San Francisco, CA 94143-06221
McDonald CC ,Bailey B . Out-of-hospital use of neuromuscular-blocking agents in the United States. Prehosp Emerg Care 1998;2:29-32
CrossRef | Medline2
Lowenstein DH ,Alldredge BK . Status epilepticus. N Engl J Med 1998;338:970-976
Full Text | Web of Science | Medline3
Lowenstein DH ,Alldredge BK . Status epilepticus at an urban public hospital in the 1980s. Neurology 1993;43:483-488
Web of Science | Medline4
Towne AR ,Pellock JM ,Ko D ,DeLorenzo RJ . Determinants of mortality in status epilepticus. Epilepsia 1994;35:27-34
CrossRef | Web of Science | Medline
- Citing Articles (2)
Citing Articles
1
Cecil D. Hahn, Sam D. Shemie, Elizabeth J. Donner. 2011. Status Epilepticus. , 837-848.
CrossRef2
Fabio Minicucci, Giancarlo Muscas, Emilio Perucca, Giuseppe Capovilla, Federico Vigevano, Paolo Tinuper. (2006) Treatment of Status Epilepticus in Adults: Guidelines of the Italian League Against Epilepsy. Epilepsia 47:s5, 9-15
CrossRef
