Peripartum convulsions

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Peripartum convulsions

  1. 1. PERIPARTUMCONVULSIONSDR. RAJEEV SOODDept of OBGIGMC, SHIMLA
  2. 2. CONVULSIVE DISORDERS Are episodic neurological dysfunction & leading to sensory or motor manifestations in the form of sensory, cognitive, emotional or abnormal motor movements Always originate from central nervous system May be confined to one area of brain or involve whole brain So can be focal, partial or generalized
  3. 3. In obstetrics & gynecology4.Obstetric causes- 98%7.Non obstetric causes- 2%
  4. 4. Obstetric cause Eclampsia
  5. 5. ECLAMPSIAIs a disease complex confined to pregnancy where patient has2.High blood pressure3.Convulsions4.Proteinuria
  6. 6. Non obstetric causes In pregnant constitute 2% of the patientst Epilepsy 0.5-1% (idiopathic)h Focal lesions in the brain Tumours  primary or metastatics Tuberculomas Other infective lesions e.g cystecercosisl Tetanusl Cerebral malaria
  7. 7. NON OBSTETRIC CAUSES CONT..Vascular causeso Cerebral venous thrombosiso Thrombosis of cavernous sinuses or other venous sinuses in braino Thromboembolismo Vascular malformations
  8. 8. NON OBSTETRIC CAUSES CONT…Metabolic causeso Uremiao Hepatic failureo Hypo or hyperglycemia
  9. 9. NON OBSTETRIC CAUSES CONT…o Electrolyte abnormalityHyponatremiaHypernatremiaHypocalcemiaHypercalcemiaPyridoxine deficiencyHypomagnesemia
  10. 10. NON OBSTETRIC CAUSES CONT…OthersoFebrile convulsionsoTraumaoPoisoningoAlcohol
  11. 11. OBSTETRIC CAUSES 98%ECLAMPSIA:o Obstetric patient with seizure should be treated as eclampsia until proven otherwiseo Eclampsia is occurrence of seizures or coma not attributable to any cause other than pregnancy
  12. 12. ECLAMPSIAo Incidence varies from 1 in 30 to 500 pregnancyo Eclampsia can start without any prior symptoms or can have warning symptoms like High blood pressure Excessive weight gain >1 kg/week in last trimester Significant proteinuria >2+ on dipstick
  13. 13. ECLAMPSIAMostly a disease ofPrimigravidae- 75%Multiple pregnancyIn low socio economic group
  14. 14. TYPES OF ECLAMPSIA Antepartum 50% Intrapartum 30% Postpartum 20% usually within 48 hrs & fits beyond 7 days reasonably rule out eclampsia, but has been reported as long as 23 days after delivery
  15. 15. ATYPICAL ECLAMPSIA Before 20 weeks of gestation or 48 hrs after delivery Any patient presents with hypertension & proteinuria & additional feature of blindness without convulsions should be treated as eclampsia About 10% of the eclamptic patients can be normotensive
  16. 16. Presentation can be Antepartum 50% Peripartum 30% Postpartum 20% Majority have hypertension but 10% of patients never have high BP Headache 80% Visual disturbances 40-50% Pain epigastrium before seizure 30% Hyperactive deep tendon reflexes 30%
  17. 17. ECLAMPTIC CONVULSION OR FITS Premonitary stage(30 sec): twitching of face, tongue, limbs, eye balls turn to one sidey Tonic stage opisthotonus (30 sec): limbs flexed & hands clenched, respiration caeses, tongue protrude in between teeth, cyanosis appeare Clonic stage (1-4 min): alternate contraction & relaxation of voluntary musclesl Stage of coma: for brief period in some or continue to next convulsionStatus eclampticus: in quick succession
  18. 18. ECLAMPSIA20-35% of patients have signs & symptoms of pre eclampsia.40% patients have no symptoms & present first time with convulsions
  19. 19. CAUSES OF CONVULSIONS• Hypoxia or anoxia  spasm of cerebral vasculature• Cerebral oedema• Cerebral dysrhythmia  due to hypoxia & oedema• Disseminated intravascular coagulation in cerebral microcirculation
  20. 20. ECLAMPSIA The convulsions are not related with level of hypertension as they are not as a result of hypertensive encephalopathy, as they are not associated with retinal hemorrhage, exudates & may not be associated with even papillodema
  21. 21. INVESTIGATIONSLAB FINDINGS:2. Complete hemogram which include platelet count3. Coagulation profile Bedside BT, CT, CRT Lab findings prothrombin time partial thromboplastin time
  22. 22. LAB FINDINGS (CONTD) Haemoconcentration leads to Increased Hb Increased urea Increased serum creatinine level once raised reflects deranged glomerular functiono Serum uric acid level  increased & reflects deranged tubular functiono Tubular functions are knocked out about 4-6 weeks prior to the glomerular functiono Liver function are affected more in patients who have pain epigastrium & is reflected by Increased serum transaminases (increased SGOT, SGPT) more so in HELLP SYNDROME
  23. 23. LAB FINDINGS (CONTD) Lactatedehydrogenase are reflection of endothelial damage HELLP syndrome One form of eclampsia showing Hemolysis Elevated liver enzymes 10% of eclamptic Low platelet count patients Urinary protein estimation in clean catch sample and 24 hr urinary protein estimation
  24. 24. CT SCAN (OPTIONAL) Cerebral oedema Diffuse white matter low density area Patchy areas of low density Occipital white matter oedema Loss of normal cortical sulci Reduced ventricular size Acute hydrocephaluso Cerebral haemorrhage Intraventricular haemorrhage Parenchymal haemorrhage (high density)o Cerebral infarction Low attenuation areas Basal ganglia infarctionSimilar findings are observed in MRI
  25. 25. FUNDUS EXAMINATIONTo differentiate between the chronichypertensive patient and eclampticpatient
  26. 26.  Doppler studies shows vasoconstriction Angiography EEG: findings are non specific apart form eclampsia seen in Polycythemia Hypoxia Renal disease Hypocalcemia Hypercalcemia Water intoxication
  27. 27. MANAGEMENT
  28. 28. MANAGEMENT• PRINCIPLES are• To keep the patient in quiet environment• Keep the airway clear & put patient in left lateral position with head end slightly low on the bed with the rails• Secure the I/V line• Maintain vitals• Avoid injury  bed side rails, mouth gag if patient is unconscious• Control convulsions by anti convulsives (Magsulph)• Treat hypertension (anti- hypertensives)
  29. 29. MANAGEMENT
  30. 30. MANAGEMENT (CONTD.)• Monitor hypoxia & fluid balance(SpO2 & CVP monitor)• Organize investigation• Prevent recurrence of convulsion• Delivery of the woman safely as soon as possible• Postpartum care• Catheterize the bladder for monitoring hourly urine output
  31. 31. MANAGEMENT DURING FITIn premonitary stage:2.Place mouth gag between teeth3.Air passage cleaned4.Patient head turned to one side to prevent aspiration
  32. 32.  DON’T DO VIGOROUS TREATMENT DURING THE FIT AS USUALLY TENDENCY IS TO RUSH THE DRUGS IN THE FIT TO CONTROL IMMEDIATELY IT MAY PROVE COUNTERPRODUCTIVE DUE TO RAPID INFUSION OF DRUG (diazepam & magsulf) WHICH MAY DANGEROUSLY INCREASE THE BLOOD LEVEL OF DRUG LEADING TO CARDIAC ARREST
  33. 33.  First aid treatment outside hospital Patient should be transferred to tertiary hospital as soon as possible Control of convulsion: zero hour treatment Magnesium sulphate Phenytoin DiazepamMagnesium sulphate should be given zero hour dose at peripheral institution
  34. 34. PRITCHARD REGIMEN• (50% magsulph ) 2ml  1 gram• 4 gram 20% I/V slowly in 3-4 minutes• 4 ampoules (8ml) to be diluted to make it 20 ml• 5 gram (5%) in each buttock• Total dose 14 grams• Monitored by7. Tendon reflexes8. Urine output >100ml in 4 hrs9. Respiratory rate > 16/ minute
  35. 35. ZUSPAN REGIMEN:Loading dose 4 gm I/V (20%)Followed by 1 gm/ hr I/V infusionSEBAI REGIMEN:Loading dose 6 gm I/VFollowed by 2gm/ hr infusion
  36. 36. DHAKA REGIMEN:(Begam R etal) Loading dose 4 gm I/V & 3 gm IM in each buttock(10 gm total) Followed by 2.5 gm I/M every 4 hrly Magnesium sulphate prophylaxis has to be continued 24 hours after delivery A combination of magsulf with nifedipine should be avoided  it decreases the blood pressure dangerously low as both act on calcium channels
  37. 37. MAGNESIUM SULPHATE LEVELSCLINICAL FINDINGS SERUM LEVELLoss of patellar reflex 8-10 µg/dlFeeling of warmth, flushing 9-12 µg/dlDouble vision & slurred speech & 10-12 µg/dloliguriaMuscular paralysis 15-17 µg/dlRespiratory difficulty 15-17 µg/dlCardiac arrest 30-35 µg/dl
  38. 38. MANAGEMENT OF MAGNESIUMSULPHATE TOXICITY• Discontinue magsulf administration• Begin oxygen administration• Administer 1gm calcium gluconate (10cc of 10% calcium gluconate)• If respiratory arrest occurs then cardio pulmonary resuscitation
  39. 39. ANTI HYPERTENSIVES STARTING DOSE MAXIMUM DOSEHYDRALAZINE 5-10 MG I/V every 20 30 mg minLABETALOL 20-40 mg I/V every 220 mg 10-15 minNIFEDIPINE 10-20 mg per orally 120 mg/d every 30 minDILTIAZEM 120-180 mg QID 540 mg/dATENELOL 50 mg QID 100 mg/dAIM is to lower the B P between 95-100 mm Hg diastolic &mean arterial pressure between 105-115 mm Hg
  40. 40. PHENYTOIN: Loading dose 15-25 mg/kg I/V in 2 hrs Under ECG tracing 100 mg 6 hrlySIDE EFFECTS:5. Cardiac toxicity6. Nystagmus7. Hypotension8. Ataxia9. Lethargy
  41. 41. DIAZEPAM:Lean regimen :10mg I/V every 2 minutes to maximum 40 mgfollowed by 40 mg in 500 ml normal saline in 24 hrs
  42. 42. Definitive treatment is termination of PregnancyAfter stabilisation of the patient P/V examination done Ripening agent put & delivery conducted in next 8-12 hrs Labour managed partographically
  43. 43. OMINOUS FEATURES OFECLAMPSIA1. Long interval between the onset of fits and commencement of treatment2. Antepartum eclampsia early in pregnancy3. Number of seizures more than ten4. Systolic BP > 200 mm Hg5. Temperature > 102º F6. Oliguria7. Non response to treatment8. Jaundice
  44. 44. INDICATION OFLSCS1. Uncontrolled fits inspite vigorous therapy2. General condition of the patient deteriorating very fast3. Patient not responding to ripening agent & induced labour4. Other obstetric indications
  45. 45. CARRY HOMEMESSAGE Identification of high risk patient in the antinatal period Early referral of high risk patients to experts Administration of anti hypertensives to the subjects & regular anti natal care in the indoors Procurement & Administration of magsulph to the severely pre-eclamptic and emplamptic patiets in zero hour before referral Management of the severely pre-eplamptic and eplamptic patients in the tertiary institutes under team of experts

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