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 PRE -ECLAMPSIA
PRE -ECLAMPSIA
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preterm labor

  1. 1. Maru M/MD/ For Anesthesia 2nd 09/09/2010Ec
  2. 2.  Spontaneous preterm labor -50%  Spontaneous PROM -30%  Medically necessary delivery- 20% )
  3. 3.  Cause is unknown in 50% of cases  Cause is of multifactorial and associated with different factors 1. High risk factors:  Previous history of preterm labor, induced or spontaneous abortion  Asymptomatic Bactriuria/UTI  Smoking  Low socioeconomic status/ Nutritional status/vt c def/
  4. 4. 2. Complications in current pregnancy: Maternal, fetal or placental  Maternal: - Pregnancy complications: APH, PROM, Preeclampsia, polyhydraminos - Uterine anomalies: Cervical incompetence, malformations of the uterus - Medical & surgical illness: acute fever, appendicitis, etc. - Genital tract infections: BV, T vaginalis chlamydial, etc.
  5. 5.  Fetal: Multiple pregnancy, Congenital malformations, IUFD  Placental: Infarction, thrombosis, Abruption 3. Iatrogenic: wrong GA estimation 4. Idiopathic: Half of cases
  6. 6.  Labor initiation mechanism is not known as is in normal labor. But probable mechanisms include: 1. Activation of fetal hypothalamic-pituitary- adrenal axis 2. Bacterial colonization(infection) 3. Decidual hemorrhage 4. Pathologic uterine enlargement
  7. 7. Activation of HPA axis -Premature activation can initiate PTB -Physical or psychological stress of the mother -Uteroplacental vasculopathy –major -evidence of placental ischemia -severe preeclampsia is associated with three fold increase # 25-50% of PTD display evidence of uteroplacental vasculopathy.
  8. 8. Mechanisms: -increase release of CRH- “Placental Clock” -increased release of foetal pituitary ACTH (fig)
  9. 9. Infection - link between spontaneous PTB & both systemic & ascending genital infection -may account for 50% PTB before 30 weeks -inflammatory response is the final common pathway
  10. 10. Decidual haemorrhage -thrombin binds to decidual membrane receptors that regulate the expression of proteases & metalloproteinases -degradation of foetal membrane extracellular matrix , which can result PPROM
  11. 11. Pathological uterine distension -formation of gap junctions, -up regulation of oxytocin receptors -production of PGE2 &F2 & MLCK
  12. 12.  symptoms/ signs  general physical examination  sterile speculum examination -pH , fern, pooled fluid cervical examination - cervix >=3cm/80% effaced –PTL confirmed, evaluate for tocolysis -cervix 2-3cm & <80% effaced –PTL likely but not established -cervix<2cm & 80% effaced- PTL diagnosis is uncertain  transabdominal ultrasound
  13. 13.  use of cervical ultrasound -cervical length <20mm & contraction criteria met(4 in 20min,8 in 60min) PTL -cervical length 20-30mm & contraction criteria met – probable PTL -cervical length >30mm – PTL very unlikely regardless of contraction frequency
  14. 14. Goals & Efficacy of Treatment Ultimate goal- delivery of an infant who suffers none of the sequelea of prematurity! The goals of treating acute episode of idiopathic PTL are:  Administration of corticosteroids  Safe transport of the mother  Prolong pregnancy  Antibiotic prophylaxis Initial evaluation of the patient: -risks & benefits of continuing the pregnancy -potential causes of PTL should be sought
  15. 15. Prerequisites for treatment :  presence of PTL  gestational age < 34 weeks -lowest gestational age –controversial 15 weeks , 20 weeks,24wks -upper gestational age- 34weeks Contraindications to labor inhibition:  IUFD  Lethal foetal anomaly  NRFHR pattern  Severe IUGR  Chorioamnionitis  Maternal haemorrhage with hemodynamic instability  Severe preeclampsia
  16. 16.  Bed rest  Adequate hydration  Prophylactic antibiotics**  Tocolytic agents: delay labor for adminstration of corticosteroids and in utero referral
  17. 17. 1. Prostaglandin synthase inhibitors. Eg. Indomethacin, Sulindac 2. Calcium Channel Blockers. Eg. Nifedipine 3. β- Adrenergic agonists. e.g. Ritodrine , terbutaline , salbutamole 4. Magnesium Sulfate
  18. 18. Mechanism of action: prevention of PGs production by inhibiting cyclo-oxygenase enzymes  PGs are important for - Increase gap junction - facilitate cervical ripening - increase free intracellular ca+2 , etc
  19. 19. Mechanism of action:  Decrease intracellular calcium  Inhibits release of ca+2 from intracellular storage sites ↓↓ Ca+2 ↓↓M L C K ↓↓M – C interaction  ↑↑myometrial muscle relaxation
  20. 20. Mechanism of action:  inhibiting myosin light chain phosphorylation  reducing intracellular ca+2 ion concentration - ↓↓ ca+2 release from storage sites - ↑↑ ca+2 efflux - ↓↓ ca+2 influx
  21. 21. Mechanism of action:  It is a calcium antagonist*  Inhibits uterine contractility by competition with ca+2 for entry in the calcium channel of the myocytes  Has neuroprotection effect for the fetus  Not FDA approved
  22. 22. -Foetal monitoring -tolerate labor poorly -course of labor is significantly shorter -delivery –principal goals of intrapartum management are : -avoidance of perinatal acidosis -avoidance of birth trauma -generous episiotomy -prophylactic forceps- no benefit ! -C/S delivery: not routine!
  23. 23.  RDS  Birth injury  IVH  Metabolic complications: Hypocalcemia, hypoglycemia, hypomagnesmia  Hypothermia  NEC  Hyperbilirubinemia  Infection  Malnutrition
  24. 24.  High perinatal mortality & morbidity  With good NICU: survival for 1000-1500gm is 90%  With help of surfactant, neonates born at 28 weeks have survival of 75%
  25. 25. Thank You ???

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