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Maru M/MD/
For Anesthesia 2nd
09/09/2010Ec
 Spontaneous preterm labor -50%
 Spontaneous PROM -30%
 Medically necessary delivery- 20%
)
 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/
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.
 Fetal: Multiple pregnancy, Congenital
malformations, IUFD
 Placental: Infarction, thrombosis, Abruption
3. Iatrogenic: wrong GA estimation
4. Idiopathic: Half of cases
 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
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.
Mechanisms:
-increase release of CRH-
“Placental Clock”
-increased release of foetal pituitary
ACTH (fig)
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
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
Pathological uterine distension
-formation of gap junctions,
-up regulation of oxytocin receptors
-production of PGE2 &F2 & MLCK
 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
 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
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
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
 Bed rest
 Adequate hydration
 Prophylactic antibiotics**
 Tocolytic agents: delay labor for adminstration of
corticosteroids and in utero referral
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
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
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
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
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
-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!
 RDS
 Birth injury
 IVH
 Metabolic complications: Hypocalcemia,
hypoglycemia, hypomagnesmia
 Hypothermia
 NEC
 Hyperbilirubinemia
 Infection
 Malnutrition
 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%
Thank You
???

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preterm labor

  • 1. Maru M/MD/ For Anesthesia 2nd 09/09/2010Ec
  • 2.
  • 3.  Spontaneous preterm labor -50%  Spontaneous PROM -30%  Medically necessary delivery- 20% )
  • 4.  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/
  • 5. 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.
  • 6.  Fetal: Multiple pregnancy, Congenital malformations, IUFD  Placental: Infarction, thrombosis, Abruption 3. Iatrogenic: wrong GA estimation 4. Idiopathic: Half of cases
  • 7.  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
  • 8. 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.
  • 9. Mechanisms: -increase release of CRH- “Placental Clock” -increased release of foetal pituitary ACTH (fig)
  • 10.
  • 11. 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
  • 12.
  • 13. 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
  • 14. Pathological uterine distension -formation of gap junctions, -up regulation of oxytocin receptors -production of PGE2 &F2 & MLCK
  • 15.  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
  • 16.  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
  • 17. 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
  • 18. 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
  • 19.  Bed rest  Adequate hydration  Prophylactic antibiotics**  Tocolytic agents: delay labor for adminstration of corticosteroids and in utero referral
  • 20. 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
  • 21. 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
  • 22. 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
  • 23. 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
  • 24. 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
  • 25. -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!
  • 26.  RDS  Birth injury  IVH  Metabolic complications: Hypocalcemia, hypoglycemia, hypomagnesmia  Hypothermia  NEC  Hyperbilirubinemia  Infection  Malnutrition
  • 27.  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%