Engidaw Ambelu

1. Maru M/MD/
For Anesthesia 2nd
09/09/2010Ec

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)

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

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%

28. Thank You
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