articol statusul epileptic

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    Summary

    Status epilepticus (SE) is a major neurological emergency [1,2,3], potentially

    life-threatening that requires immediate and vigorous treatment [1,2,3] to stop

    the ongoing seizures, in order to prevent severe neuronal injuries, associated

    complications or even death [3,4].

    This study was designed to evaluate the incidence of SE in the neurological

    intensive care unit, the basic etiology favored the development of SE, the

    management in stopping the seizures and recurrence prevention.

    In the study was performed a retrospective analysis of the medical records ofthe Emergency Hospital over a period of 3 years (01.01.2008-01.10.2011) that

    included evaluation of 220 patients hospitalized with SE. The mean age of

    patients was 53.52.6 years with the highest percentage among males (54.1%).

    The most common cause of SE was appreciated to be of toxico-dysmetabolic

    genesis (47.27%).According to the morphology of seizures the highest incidence

    returns to SE generalized convulsive (SECG) type (85%). In the study group

    was found that every patient has more than one probable cause of SE

    development of which alcohol abuse was in 41.1%, on the second being placed

    history of stroke (16.81%). To elderly patients acute and chronic

    cerebrovascular pathology together form more than 50% of cases.

    Clinical outcome during the period immediately after finalization was

    characterized by a polymorphism of neurological and systemic symptoms thatappreciate entirely the clinical picture and severity of the process.

    The management was performed according to international and institutional

    protocols, which was primary directed on early seizure termination and

    prevention of recurrence, in parallel with treatment of underlying etiology and

    secundary complications. The mortality due to consequences of SE in this group

    was 16.81%.

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    Introduction

    SE constitute a potentially fatal medical emergency, that occurs as a result of

    primary neurologic disease or secondary to critical illness [2,3,4,6] and is

    manifested by continuous seizure activity >30min. or 2 sequential seizures

    during this period without full recovery of consciousness [3,6], being associated

    with a high rate of morbidity and mortality [3,4,5]. SE accounts for 3.5% of

    admissions to emergency departments in the developed nations and for 11% in

    developing country [4,6]. The average incidence of SE is 20/100.000 for

    industrialized countries [1,5]. SE affects males and females equally, the major

    causes in adults are: cerebrovascular diseases (23-25%), trauma (4.6%),

    ethanol/drug-related (12.2%) tumors (4.3%), CNS infections (1.8%) [2,4,6].

    Approximately 25% of SE occurs in patients with epilepsy and more than 15%

    of patients with epilepsy experience at least one episode of SE [1,3].

    Complications of SE include: epilepsy (20-40%), encephalopathy (6-15%) and

    focal neurological deficits (9-11%) [1,4,5]. SE mortality rates are 15-20% [4,6].

    Death usually occurs as a consequence of brain injury underlying the

    development of SE and no more than 2% of patients die directly from it [1,5].

    Fortunately, SE responds to relatively simple treatment, but when simple

    interventions fail, refractory SE requires more aggressive measures to prevent

    complications [3,5,6].

    Purpose of the study: Analysis of SE incidence, etiology, the management

    features and mortality rates.

    Materials and Methods: This study was based on retrospective analysis of

    medical records from the Stroke/Intensive Care Unit and Neurology departments

    over a period of 3 years (01.01.2008-01.01.2011). All medical records were

    standardized according to: general data, medical history/pathological history,

    etiology, type of SE, methods of diagnosis, management of SE.

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    Results: During the period 01.01.2008-01.01.2011 in Neurological Clinic of

    Emergency Hospital, 220 patients were admitted with the diagnosis of SE,

    patient age ranged from 15-88 years, mean age 53.5years 2.6. Structure of the

    patients according to age is presented in Table 1.

    Table 1. Structure of the patients according to age (%)

    Age (years)

    80 Total

    Total 8 50 101 57 4 220

    % 3,63 22,72 45,90 25,90 1,81 100

    The distribution by sex was: females -101p (45.9% 3.2) respectively males -

    119p (54.1% 3.3).

    Structure of the SE etiology is represented in Table 2.

    Tabel 2. Structure of the SE etiology (%)

    The polymorphism of SE according to seizures morphology is represented inFigure1.

    Etiologic factor Number of

    cases

    % eP

    Idiopathic epilepsy 11 5,9 1,58

    Secondary

    epilepsy

    vascular 41 18,63 2,62

    posttraumatic 24 10,90 2,1

    Secondary epilepsy withunspecified etiology

    8 3,63 1,26

    Encephalopathy toxico-

    dysmetabolic

    93 42,27 3,52

    Anoxic encephalopathy (CO

    intoxication)

    1 0,45 0,44

    Stroke ischemic 22 10 2

    hemorrhagic 9 4,09 1,31

    Secondary purulent

    meningoencephalitis

    2 0.9 0,63

    Cerebral arterio-venous

    malformation

    2 0,9 0,63

    Expansive process 2 0,9 0,63

    Brain metastases 1 0,45 0,44

    Fluid and electrolyte disorders 2 0,9 0,63

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    Figure 1. Polymorphism of SE according to seizures morphology.

    In study group have been determined the antecedents and comorbidities present

    in patients, which would be favored the installation of SE, shown in Table 3.

    Tabel 3. The structure based on antecedents and present comorbidities.

    Of all patients diagnosed with idiopathic epilepsy (11p) reduced compliance

    to treatment was recorded at 5p (45.45% 3.35), canceling treatment because of

    side-effects without medical advice -3p (27.27%3.0), change of the preparation

    -2p (18.18% 2.6) causes that induced SE development.

    85%

    4.09% 8.18% 1.36% 1.36%0%

    10%

    20%30%

    40%

    50%

    60%

    70%

    80%

    90%

    SEGC SE simple

    partial

    Partial SE with

    secundary

    generalization

    SENC SE polimorph

    SE- Status Epilepticus

    SEGC- SE generalized convulsiveSENC- SE non-convulsive

    Antecedents/Comorbidities Absolute number % eP

    Idiopathic epilepsy 11 5 1,46Trauma 31 14,09 2,31

    Antecedents of stroke 39 17,72 2,57

    Neurosurgical intervention 5 2,27 1,0

    Meningoencephalitis 1 0,45 0,44

    Chronic alcoholism 92 41,81 3,32

    Drug addiction 2 0,9 0,63

    Hepatic cirrhosis 10 4,54 1,4

    Diabetes mellitus 6 2,72 1,09

    Tuberculosis 5 2,27 1,0

    Cerebral arterio-venous

    malformation

    3 1,36 0,77

    Pulmonary adenocarcinoma 1 0,45 0,44

    Expansive intracerebral process 2 0,9 0,63

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    Clinical evolution of SE in the period immediately after completion was

    characterized by an polymorphism of clinical symptoms which appreciated

    integral and defined the gravity of the process, so vegetative disorders with

    systemic involvement were appreciated to the forefront such as deviations in

    blood pressure -hypertension/hypotension 89.54% (2.06) cases, these

    symptoms being associated with cardiac rhythm disturbances -arrhythmias/

    tachycardias -57, 26% (3.33). Have been present and clinical manifestations

    generated by the inflammatory process -pneumonia (22.72% 2.82), fever

    (51.3% 3.36) with the association of pulmonary edema in 16.8% (2.51) cases.

    The severity of the process was determined by metabolic disturbances especially

    -metabolic acidosis (3.63% 1.26), hyperglycemia (15.9% 2.46), renal failure

    (8.63% 1.8). Signs of cerebral involvement with different degrees of

    expressions of the consciousness disturbances were in 100% of cases, the most

    severe cases being associated with cerebral edema (33.18% 3.17), coma and

    death.

    Methods used for establishing the etiology of SE have included: general

    laboratory analysis and instrumental investigations such as: computerized EEG-

    104p (47.27% 3.36), cerebral CT -139p (63.18% 3.25 ) Angio-CT cerebral -

    3p (1.36% 0.78), chest radiography -86p (39.1% 3.18), lumbar puncture -18p

    (8.18% 1.84), ultrasonography -62p (28.18% 3.03), transcranial Doppler -19p

    (8.63% 1.83), EKG -170p (77.27 2.82%).

    The management constituted: primary assessment of ABC, the airways was

    secured with Guedel tube or nasopharyngeal, continuous O2 flow and cardio-

    respiratory function monitoring, blood pressure. The next step was the

    establishment of the i/v approach and administration of anticonvulsant

    preparations. As preparations of first line in resolving SE were used the

    benzodiazepines (Diazepam 10mg) i/v or rectal tube, followed by intravenous

    infusion of Phenytoin (Phenydan) 15-20 mg/kg with speed 50mg/min in order to

    prevent recurrence, in parallel with treatment of the underlying etiology that

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    favored the installation of SE. From all patients, about -55p (25% 2.91) have

    been registered repeated recurrent seizures in a period from several hours to

    several days after solving SE that were resolved by the administration of sol.

    Luminal (phenobarbital 15-18 mg/kg i/v infusion rate of 25-60 ml/min).

    The mortality rate was 37 cases (16.81% 2.5) from which 16p (43.24% 3.3)

    men and respectively 21p (56.76% 3.33) women. Age of the deceased ranged

    from 18-82 years, average age 54.05 3.7 years.

    Discussion: Analyzing the obtained data was appreciated that the highest

    incidence of SE was in the age group 41-60 years (45.9%), with predominant

    involvement of male patients (54.1%). Therefore, results that the incident is

    higher in the elderly population and in males in comparison with females in

    adult population. Considering the aging of the population in the future SE will

    become a major problem, increasingly, in the public health and practice.

    According to the etiology, SE has developed mainly on the background of

    toxico-dysmetabolic disorders (42.27%), on second place being the secondary

    epilepsy (31.81%) and only 5.09% of cases assigned to idiopathic epilepsy.

    Thus, in the study group, SE was present predominantly in patients with

    secondary generalized epilepsy than in those with idiopathic generalized

    epilepsy. Pursuant to the type of SE, predominant type was SECG in 85% of

    cases and just 1.36% is assigned to type SE non-convulsive (SENC). Evaluating

    patient's history and comorbidities was determined that in the study lot has

    prevailed on the forefront the alcohol abuse (41.81%) and 16.81% belonging to

    history of stroke that have been aggravated with SE. As we notice in the Table 2

    and 3 for each patient is present more than a cause responsible to the

    development of SE, which includes both an acute and chronic determinant (to a

    patient returning to four cases).

    The management was performed according to international and institutional

    treatment protocols approved. Therefore treatment is continued simultaneously

    in several directions and focused on early seizure termination, prevention of

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    recurrent seizures, identification of underlying etiology, and treatment of

    secondary complications. The mortality rate constituted 16.81% of cases; the

    patient's age at diagnosis, etiology of SE, severity of the underlying disease, and

    duration of SE are the main predictors of increased short-term mortality.

    Conclusions:

    1. SE is a major emergency, potentially fatal which requires prompt

    recognition according to diagnostic schemes and the use of treatment protocols

    adopted in neurological intensive care unit to prevent serious neurological

    complications.

    2. The toxico-dysmetabolic etiology constituted primary cause (42.27%) of

    development of the SE in this study group.

    References:

    1. DeLorenzo RJ, Pellock JM, Towne AR, Boggs JG. Epidemiology of statusepilepticus. J Clin Neurophysiol 1995; 12:31625.

    2. Edward M. Manno, MD. New Management Strategies in the Treatment ofStatus Epilepticus. Mayo Clin Proc. 2003;78:508-518

    3. Groppa St. Antiepilepticele i tratamentul Epilepsiei. Chiinu, 2006. 176 p.4. Hussam Seif-Eddeine, David M Treiman. Problems and controversies in

    status epilepticus: a review and recommendations. Expert Review of

    Neurotherapeutics 12/2011; 11(12):1747-58.

    5. Nathan B. Fountain Status Epilepticus: Risk Factors and Complications.Epilepsia, 41(Suppl. 2):S23-S30, 2000

    6. Shorvon S D. The management of status epilepticus. J Neurol NeurosurgPsychiatry 2001. 70II22II27.II27.

    7. Susanne Knake, Felix Rosenow, Mathias Vescovi. Incidence of StatusEpilepticus in Adults in Germany: A Prospective, Population-Based Study.

    Epilepsia Volume 42, Issue 6, pages 714718, June 2001

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