Table 3. Details of patients for which the early suspected etiology using the SEEIT was incorrect.
Pt | Age | Gender | Previous seizures |
Etiology generated using the SEEIT |
Final etiology | Case description | Explanation |
---|---|---|---|---|---|---|---|
1 | 54 | F | No | Cryptogenic | Brain glioma | Small temporal glioma was missed in the CT performed in ED, but seen on MRI later. Of note, because seizures were focal, the tool advised an MRI |
Etiology missed on CT |
2 | 76 | M | No | Cryptogenic/ encephalitis? |
Brain glioma | Because of new-onset refractory epilepsy with normal CT and normal CSF analysis, SEEIT evoked a cryptogenic SE or encephalitis in early phase/autoimmune process. The later MRI revealed a glioma |
Etiology missed on CT |
3 | 40 | F | Yes | Drug related (ciprofloxacin) |
Known epilepsy without provocative factors |
Patient with known epilepsy experienced SE in the context of ciprofloxacin prescribed for UTI without systemic involvement. The discharge summary did not retain ciprofloxacin as provocative factor |
Disagreement on causality judgment of minor precipitants |
4 | 57 | F | No | Meningoencephalitis (infectious) |
Carcinomatous leptomeningitis |
SE after lumbar surgery for vertebral metastasis (breast cancer). CSF showed a pleocytosis (115 whitecells/ mm3). Infectious meningitis was proposed by the SEEIT. Further CSF analysis revealed metastatic cells |
CSF data misinterpreted |
5 | 21 | F | No | Meningoencephalitis (infectious) |
NMDA encephalitis |
Presented with refractory SE and mild CSF pleocytosis. Possible CNS infectious was retained using the SEEIT. Further analysis didnot find any infectious agent and revealed NMDA antibodies |
Failure to identify a complex disease in the emergency setting |
6 | 72 | M | No | Remote ischemic stroke |
Lymphomatous meningitis |
Known for Waldenstrom disease. Initial imaging showed an old previously asymptomatic stroke retained as responsible using the SEEIT. LP done because of unexpected evolution revealed lymphomatous meningitis |
Remote brain pathology incorrectly retained |
7 | 19 | F | Yes | Known epilepsy without provocative factors |
Cryptogenic | History revealed a couple febrile seizures during childhood and no other explanation. Because of the long time before recurrence of seizure, she was not considered as having epilepsy before the SE episode and thus considered as cryptogenic |
Disagreement on causality judgment of minor precipitants |
8 | 71 | F | No | Drug related (clozapine) |
Posterior reversible encephalopathy syndrome (PRES) |
In the context of severe anxiety for 3 days, clozapine was prescribed and increased. Then the patient presented with altered mental status and visual hallucinations. Focal SE was diagnosed after EEG. Initial imaging was nonconclusive. The etiology retained using the SEEIT was related to the clozapine. Later MRI revealed a PRES |
Etiology missed on CT |
9 | 67 | F | No | Meningoencephalitis (infectious) |
Cryptogenic | Refractory SE and fever at the presentation. Despite a mild pleocytosis, the CSF remained sterile. The pleocytosis was attributed to seizures |
CSF data misinterpreted |
10 | 75 | M | No | Cryptogenic | HSV-1 encephalitis |
Because of fever and new onset SE, the SEEIT suggested a CSF analysis, which was normal (four white cells). Later, PCR came back positive for HSV-1. LP was performed early (ca. 36 h after onset), so the SEEIT warned against “false” normal CSF in early phase of an encephalitis |
CSF data misinterpreted |
11 | 46 | F | Yes | Sepsis | Possible posterior reversible encephalopathy syndrome (PRES) |
SE in the context of sepsis (pulmonary origin) and known epilepsy. So, using the SEEIT, sepsis was considered as a provocative factor. Later MRI was consistent with a PRES. However, it was not excluded for certain that the MRI changes were due to seizures |
Etiology missed on CT |
12 | 40 | F | Yes | Sepsis | Known epilepsy without provocative factors |
SE in the context of fever, systemic inflammatory response syndrome (SIRS) and known epilepsy. So, using the SEEIT, sepsis was considered as a provocative factor. The complete evaluation did not find any infectious source. The SIRS was attributed to the SE itself |
SIRS incorrectly suspected |
13 | 54 | F | No | Acute ischemic stroke |
Brain abscess due to Bacillus cereus endocarditis |
Patient known for acute myeloid leukemia. Initial CT showed a probable new ischemic stroke. Subsequent MRI revealed an abscess. Endocarditis was subsequently found |
Etiology missed on CT |
14 | 60 | M | No | Cryptogenic | Alcohol withdrawal |
Alcohol withdrawal was denied during initial assessment |
Incomplete history information |
15 | 79 | M | No | Dementia | Chronic lymphocytic leukemia with CNS infiltration |
Known for advanced dementia and chronic lymphocytic leukemia. Initial imaging was nonconclusive. MRI was performed 4 days later and showed focal lesions likely due to infiltrative lymphoma |
Remote brain pathology incorrectly retained |
16 | 69 | F | No | Toxic-metabolic (in the context of a known CNS B lymphoma) |
Microangiopathic hemolytic anemia |
Initial laboratory testing showed renal and liver impairments of unknown origin. The extensive evaluation revealed a microangiopathic hemolytic anemia |
Failure to identify a complex disease in the emergency setting |
17 | 71 | M | No | Meningoencephalitis (infectious) |
Diffuse large B-cell lymphoma with CNS infiltration |
Presented with SE preceded by rapid cognitive decline. CSF showed pleocytosis (728 white cells/mm3). CNS infection was suspected. Extensive evaluation did not find any etiology. A malignant edema leaded to herniation. Autopsy showed a diffuse CNS infiltration by large B-cell lymphoma |
CSF data misinterpreted |
18 | 36 | M | No | Brain lesion of unclear origin |
Cerebral toxoplasmosis |
Known for HIV. The evaluation in the emergency department identified a newly diagnosed mass without clear precision. The complete evaluation revealed a cerebral toxoplasmosis |
Failure to identify a complex disease in the emergency setting |
19 | 76 | M | No | Cryptogenic | Remote subarachnoid hemorrhage |
The previous history of subarachnoid hemorrhage was unknown at initial presentation |
Incomplete history information |
20 | 68 | F | No | Toxic-metabolic | Acute ischemic stroke |
Presented with several mild metabolic disturbances and the initial CT was considered as normal. Subsequent MRI advised by the SEEIT because of focality in the clinical manifestation, revealed an acute stroke |
Etiology missed on CT |
21 | 83 | F | No | Cryptogenic | Acute ischemic stroke |
Initial imaging was considered as normal. Subsequent MRI advised by the SEEIT because of focality in the clinical manifestation, revealed an acute ischemic stroke |
Etiology missed on CT |
22 | 79 | F | No | Drugs intoxication | Dementia | Patient had mild increase in antipsychotic treatment in setting of dementia and very mild hypernatremia. However, the features identified by the SEEIT were not considered as sufficient to provoke SE |
Disagreement on causality judgment of minor precipitants |
23 | 49 | F | Yes | Known epilepsy without provocative factors |
ASD related | Patient known for epilepsy treated with LEV, VPA, and LCM. There was no evidence of nonadherence in initial evaluation. Later, low level of VPA level became available and pointed out nonadherence |
Incomplete history information |
24 | 27 | F | No | CNS infection | Cryptogenic (NORSE) |
Presented with flu-like symptoms a week before entering a prolonged refractory nonconvulsive SE in coma. The CSF in early phase showed a mild lymphocytosis (15 white bloodcells/mm3). Despite a very broad evaluation including wide infectious and autoimmune panels, no etiology was found. She left the hospital 74 days later with significant cognitive problems |
CSF data misinterpreted |
CNS, central nervous system; CSF, cerebrospinal fluid; CT, computed tomography; ED, emergency department; F, female; HIV, human immunodeficiency virus; HSV, herpes simplex virus; LCM, lacosamide; LEV, levetiracetam; LP, lumbar puncture; M, male; MRI, magnetic resonance imaging; NMDA, N-methyl-d-aspartate; NORSE, new onset refractory status epilepticus; PCR, polymerase chain reaction; SE, status epilepticus; SEEIT, Status Epilepticus Etiology Identification Tool; UTI, urinary tract infection; VPA, valproic acid; WC, white cells.