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Febrile syndrome and febrile convulsions

Febrile syndrome and febrile convulsions. Department of pediatrics. F ebril e syndrome. Generalities.

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Febrile syndrome and febrile convulsions

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  1. Febrile syndrome and febrile convulsions Department of pediatrics

  2. Febrile syndrome

  3. Generalities • The central temperature ofhuman beingsis, asin another animalswith warm blood, a constant, which is naming homeothermia, in contrast with that ofanimalswithcold blood (fish, reptiles, etc.) which is variable.

  4. Homeothermia resultsfromequilibriumbetweenwarmth production, orthermogenesis (alimentation, physical exercise…), and the means to combat it, or thermolysis (more or less abundant sweating, waterintake). • There are, however, variationsof central temperatureduring one day by 0,6ºC, the most decreased temperaturebeing registeredin morningand the most increased evening.

  5. It’s important to memorize that, normally, the children seems to havea temperatureslightly more that the normal temperatureof adults, and can sometimes achieve until 38ºC, and even 38,5ºC in evening.

  6. The thermic metabolism in newborns • Insufficient thermoproduction. • Incapacityto increase the thermic losses in the case of hyperthermiaand the thermoproductionin the case of overcooling. • Incapacity topresenta typical febrile reaction (causedby insufficient sensibility of hypothalamic neurons to the pyrogenic leucocytary substancesandincreased concentration of arginin-vasopressin which decreases the body temperature). • Only at the age of 2-3 yearsthe circadian rhythm of body temperatureis installing in children.

  7. The forms and basic mechanisms of body t0increasing • We speak about feverwhen the body temperatureis mai more than 38°C. A febrile sensation canappearwhenthe temperatureexceeds the mediumnormal value of 37°C. • The febrile state appears whenthe function of de thermoregulationcenters from hypothalamus is not disturbed, but under the action of pyrogenic substances (exogenous – lipopolysacharides, or endogenous – macrophages, granulocytes, neutrophils, eosinophils,inconsequence of phagocytosisthe genetically determined “point of body t” (set point) is changing. The febrile states have a positive biologic character of organism defense.

  8. The forms and basic mechanisms of body t0increasing (cont.) hyperthermic reaction (tºhigher than 38,0 – 38,50 C), which appears on the background of disturbance and decompensationof thermoregulation mechanismsfunction (intensifyingwith metabolism decompensation, pathological disorders of thermoregulartion centers. The hyperthermic reactions are often met in pediatric practice, especially in neuroinfections, different viroses etc. and have not biologic sense for organism. They have only pathologic character.

  9. The forms and basic mechanisms of body t0increasing (cont.) Hyperthermiacorrespondsto central body temperatureincreasing provoked by thermogenesis increasing, in the time of some intense muscular exercise, for example, and/ordiminishing thermolysis, having a connection with very high exterior temperature, diminishing of sweating and/orinsufficiencyof hydric intakes (overheating, dehydration, etc).

  10. Due to hyperthermia all forms of metabolism aredecompensating, the endogenous intoxication of organism increases(cascadeof intermediary metabolits), the disorders of vital centers – respiratoryand cardiovascular are observed, the convulsions appear, the cerebral edema increases. The hyperthermic reactionsare not stopping with antipyretics, but the physical methods are useful: frictionsof body with wet gauze and ensuring of local hypothermiain the region ofheadand magistral vessels (towels, wet swaddling clothes etc).

  11. Infectious causes Bacterial infections Mycoplasma Chlamidias Parasitoses Mycosesetc. Etiology of fever

  12. Etiology of fever (cont.) Noninfectious • Immunopathological (collagenoses, systemic vasculites, allergies) • Tumors (lymphogranulomatosis, lymphomas, neuroblastomas) • Intracranial traumas • Hemorrhages • Endocrine diseases • Vaccination • Malignanthyperthermia etc.

  13. Levels of fever • Subfebrile (until 380C) • Moderated fever (38,10C – 39,00C) • High fever (39,00C - >) • Hyperpyrexia (more than 410C)

  14. Thermic curves • Continuous fever– oscillation in 24 hrsno more than 10C (abdominal typhus) • Remittent fever- oscillation in 24 hrs more than 10C (virotic and bacterial infections) • Irregular or atypical fever– oscillations are irregular– the most frequent form offeverindifferent pathologies • Hectic fever– correlation between remittent and irregular fever with oscillations more than 2-3 0C • Intermittent fever– short periods of high temperaturewhichcorrelateswith the periodsof physiological temperature (tuberculosis, purulent diseases) • Recurrent fever– the alternation of febrile crisis in the time of 2-7 dayswith the periodsof apyrexiaby 1-2 daysis characteristic (malaria).

  15. Clinical signs • Circulator system: pulse increasingwith 8-10 beatsat fever increasingwith 1 degree. In thecases oflong – term febrile states and manifested with high values the collapse, cardiac failure, DIC syndrome are determining. • Nervous system: fatigue, headache, delirium, insomniaor somnolence.

  16. Clinical signs (cont.) • Respiration – in the first phase of fever thefrequence of respiration decreases, thenincreaseswith 4 respiratory movementsateach degree of fever. In the same time, the volume ofrespirationnot increases, but even decreases beingthe cause ofhypoxia appearance aspathogenetic mechanism of affection in fever. • The digestive system is characterizing by motoryand fermentative activity decreasing, gastric juice acidity decreasing.

  17. Management • The diagnosisis performing on the base of thermometria, clinical manifestations ofbasic diseaseand routineparaclinical examinations. • The treatment includes thefollowing measures: • Diet • Physical methods of cooling • Using of antipyretics

  18. Febrile convulsions

  19. The peculiarities of nervous systemin early age children • The immaturityof cellular elementsand nervous fibers, which determine adiffuse affection of brain. • Increased sensibilityto noxious factors and decreased excitability threshold, which can provoke the convulsive status. • Increased hydrophylia of nervous tissue which contributesto rapid development of cerebral edema. • Intolerance ofCNSto the immune system, whichconditions theappearance of anticerebral autoantibodies in the case of hematoencephalic barrier affection. • Plasticityand high compensatorypossibilities of thebrain.

  20. Definitions The convulsionsare paroxystic or rhythmic or saccadated muscular contractions, enclosedin tonic, clonic or tonico-clonic crises. The convulsionscan have epilepticandnonepileptic (occasional) origin. The seconds arereleasedby intercurrent events (fever, metabolic disorders, neuroinfectionsetc.).

  21. Febrile convulsions They representa critical disorderswhich appear in children between 6 months and 5 years, inassociation with fever, but without the signs of intracranian infection and without afebrile crises in antecedents. The majority of crises, until 90%, appear before 3 years age, with the incidence peakat 15 months.

  22. The causes of febrile convulsions • Infections of nervous system. • The fever can act as a trigger factor of convulsions. • Febrile convulsions, as expression of some genetic predisposition connected with the age.

  23. Most frequently, the crises of febrile convulsions follow the virotic infectionsofrespiratory tract, severe gastroenteritiscaused by Shigellaoranotherinfectionswhichprovokeminimal fever by 37,80 – 38,5 0C. • The crises appear usually with the first episode of feverorare the first symptom of fevermanifestation in 25 – 42% of cases.

  24. International classification ofepilepsies, epileptic syndromesand critical disorders Localized crises (focal, partial): I.1. Idiopathic (primary) I.2. Symptomatic (secondary) I.3. Criptogenic Generalized crises: II.1. Idiopathic II.2. Symptomatic II.3. Criptogenic or symptomatic • Undetermined syndromes(with focal character or generalizedundetermined): neonatal crises, myoclonic severe epilepsyofthe child, acquired epilepticaphasia , epilepsywithpeak – wave complexes continuesin the time of sleeping. • Special syndromes (situational, occasional crises).

  25. Clinical manifestations • Tonic crises– sudden disturbance of consciousness, hypertonia of axialmusculaturewith the membersin extension, apnea, perioronasal cyanosis, contracture of masseters, revulsioned eyes; • Tonico-clonic crisesarecharacterizingby tonic phase withduration of10-12 seconds, followedby clonic phasewith muscular symmetricaland bilateral clonus, withshortrelaxationsduring until 2 minutes, the tongue wounding can appear, sanguinolent foam, elimination of urineandstools; the resolutive phaseischaracterizingby postcritical coma with ample, noisy respirations, bilateral midriasis; • Atonic crises – sudden loss of muscular tonus during one or a few seconds, sudden falling of the head on the chest.

  26. Clinical manifestations (cont.) • Loss of consciousness authenticatedby ocularrevulsion . • Neuro-vegetative disorders – respiratory,vasomotory (accessesof pallor),rhythm irregularities, cyanosis.

  27. Simple febrile convulsions They appear in a child with negative neurologic anamnesis, in the age from 6 months until 5 yrs, on the background of fever, are primarly generalized, have duration until 15 minutes, arenot repeated during the same febrile episode or in afebrility. The relatingsabout the febrile convulsions inheredo-collateralantecedents are possible.

  28. Complicated febrile convulsions Duration over 15 minutes, age over 10 months, they can generate convulsive status, are repeating in seriesin the same day, often are focal, with lateralization, the motory postcritical deficits–Todd paralysis can remain. They can develop epilepsyin 2-3% of cases.

  29. Diagnosis It is necessary to exclude some infectious diseases withlocalizationat the level of CNS. Thisimposesa decisionabout the performance of some paraclinical investigations, lombar puncture, neuroimagistics, EEG.

  30. Differential diagnosis The epileptic originof crises will be sustainedin thebase ofsome crises recurrencywith stereotip character, without evidence of some trigger factors, with typical changeson E.E.G. It is made with the following diseases: • Primary infectionsof CNS; • acute encephalopathy; • syncope; • febrile delirium;

  31. The treatmentOF FEBRILE CONVULSIONS IN CHILDREN General principles: • Selection ofoptimal preparation in dependence of theconvulsions type. • Selection of optimal dose– usually minimal, which permits thecomplete control of crises. • Respecting of anticonvulsivant monotherapy (asexception 2-3 preparationsin convulsionsresistantto treatment after exhausting of monotherapy), because the polytherapycan lead to chronic intoxication, undesirable interaction of preparationswith efectului therapeutic effect diminishing.

  32. The medicamentous treatment is administering dailyat thesame hour for to obtain acontinuous therapeutic concentration. • The optimal duration of treatment (from1 until 3 months). • Annulation of treatment ismaking gradually with clinicaland electroencephalographic monitoring. • Avoidance of factors, whichrelease convulsive crises andrespecting of optimal regime of life (infections, traumas, intoxications, alcohol, coffee, concentrated tea, ciocolite, regime ofsleeping-wakefulness).

  33. The treatmentof febrile convulsions will be performed with usual anticonvulsivantsand in specific dosage, as these recommendedin the treatment of epileptic status. The means of body temperaturedecreasingand the treatment ofinfection responsable forfever will be associated.

  34. The recommended medicationis phenobarbital or valproat, the single anticonvulsivants efficient in febrile convulsions. • The prophylactic intermittent therapyhashowevera general acceptation. There are a lot of recommended protocols. But the most often the medication is effectuated with Diazepam per os 0,3 mg/kg, Diazepam rectal 0,5 mg/kg.

  35. The treatment of convulsive status [afterPaul Moe, Alan Seay, 1991] • The primordial measures ABC [A –air; B - breath; C - circulation]: • Liberation of respiratory pathways • oxygen supply of respiration • Maintaining of pulse, APby optimal perfusionofliquids 20-30 ml/kg. • Initial solution- glucose 20% i/v, 1 ml/kg. • Monitoring of sanguine gases level, of electrolytes, ureaand anticonvulsivants levelin blood and of intracranian.

  36. The treatment of convulsive status (cont.) • Intravenousanticonvulsivant treatment: • diazepam 0,1-0,3-0,5 mg/kg (20mg) can be repeated after 5-20 min, its maximal actionis after 20 min: canprovoke respiratoriy depression; • lorazepam 0,05-0,2 mg/kg (has more prolonged that diazepam action); • fenitoin (difenin) 10-20 mg/kg; • phenobarbital 10-20 mg/kg. • Correction of metabolic disorders (acidosis, etc.).

  37. The treatment of convulsive status (cont.) • If the convulsionsare repeating again we introduce: • fenitoin 5 mg/kg and phenobarbital 5 mg/kg; monitoring of their concentrationin blood, the respiration and arterial pressure are maintaining in optimal limits; • i/v paraldehid 4% or per rectrum 0,1-0,3 ml/kg (1:1 witholives oil) • valproic acid in suspension 30-60 mg/kg per os or per rectum. • After exit from convulsive status fenitoin and phenobarbital (5-10 mg/kg) and calcium preparations will be administered.

  38. Prognosis In febrile convulsions it is este favourable. In 70% of cases one self convulsivant episode will exist and only in 9 % of cases more than 3 episodes will exist. Increased risk of FC recurrenceis more inchildren until1 year. After 4 years the riskofrecurrenceis10 %. The risk of epilepsydevelopment is 4 times more in a child with febrile convulsions.

  39. Thank you for attention!

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