1. ANTEPARTUM HEMORRHAGE (APH)
PRESENTER:JOY WILLIAMS
19TH/04/2010

2. INTRODUCTION
APH is defined as vaginal bleeding occuring once d fetus has reached viability ie. >24 wks gestation to delivery of d fetus.
It is one of the most ominous complications of pregnancy.
It is one of the three leading causes of maternal death and a major cause of perinatal morbidity and mortality in the U.S.
Differentiation must be made between obstetric and non–obstetrics causes of bleeding.
Placenta praevia n abruption fa=orm over 50% of all causes of APH.

3. AETIOLOGY OBSTETRICS -bloody show -placenta abruption
-placenta praevia
-vasa praevia
-DIC
-uterine rupture
-marginal sinus bleed
NON-OBSTETRICS
-cervical cancer or dysplasia
-cervicitis
-cervical eversion
-cervical polyps
-vaginal laceration
-vaginitis

4. PLACENTA ABRUPTION
Premature separation from the site of uterine implantation before delivery of the fetus.
Two types (a) concealed (b) external
30% antepartum hemorrhage is due to placental separation usually the first hemorrhage is seen after the 26th week
50% occur before the onset of labour and 10-15% are not diagnosed before the second stage of labour.

5. ETIOLOGY
Predisposing factors: previous placental separation, hypertensive states of pregnancy, advanced maternal age, multiparity, uterine distension, vascular disease, thrombophilias, uterine anomalies or tumors, cigarette smoking, alcohol consumption (>14 drinks per week), cocaine use and possibly maternal type O blood.

6. ETIOLOGY
Precipitating factors: circumvallate placenta, trauma, sudden reduction of uterine volume, abnormally short cord, increase venous pressure

7. PATHOPHYSIOLOGY AND PATHOLOGY
Local vascular injury that results in vascular rupture into the decidua basalis, bleeding and hematoma formation, the hematoma shears off adjacent denuded vessels, producing further bleeding and enlargement of the area of separation
Due to an abrupt rise in uterine venous pressure transmitted to the intervillous space leads to engorgement of the venous bed and separation of all or part of the placenta

8. CLINICAL FINDINGS
Larger separations are accompanied by abdominal pain, uterine irritability, hemorrhage may be visible or concealed. If the process is extensive, evidence of fetal distress, uterine tetany, DIC, hypovolemic shock may be seen. Increased uterine tonus and frequency of contractions may provide early clues of abruption, most times patients present with vaginal bleeding

9. LABORATORY FBC Blood group, cross-match
Peripheral blood smear shows reduced platelet counts, presence of schistocytes, fibrinogen depletion with release of fibrin split products
Prothrombin time, PTT, platelet count, fibrinogen and fibrin split products- help determine coagulation status

10. IMAGING
U/S may be helpful in diagnosing placental abruption but it is inconclusive.
Possible findings are hyperechoeic foci posterior to the placenta suggests fresh blood or a hypoechoeic area suggests a formed clot

11. TREATMENT
Expectant management in placental abruption is the exception and not the rule. Appropriate when the mother is stable, fetus immature and fetal heart tracing is reassuring. Continous fetal and uterine monitoring should be done.
Emergency measures, most cases are diagnosed during labour or delivery. Hemorrhage, fetal distress and uterine spasm. Blood should be collected least 4 units of PRBC typed and crossed. Two large bore IV cannulas SHOULD BE PLACED AND CRYSTALLOIDS ADMINISTERED.

12. TREATMENT
Vaginal delivery is indicated if the degree of separation appears to be limited and if continuous FHR is reassuring. When the separation is extensive but the fetus is dead, vaginal delivery is indicated. It is contraindicated when there is massive hemorrhage and operative delivery is necessary to save mother or fetus

13. TREATMENT
Cesarean section is done when vaginal delivery is not imminent for a fetus with a reasonable chance of survival with persistent evidence of distress. It is also indicated when the fetus is in good condition but the situation is not favourable for rapid delivery in d face of progression or severe placental separation
Maternal indications are uncontrollable hemorrhage, rapidly expanding uterus with concealed hemorrhage with or without live fetus

14. COMPLICATIONS Desseminated intravascular coagulation(DIC)
Renal tubular and cortical necrosis
Uterine atony

15. PROGNOSIS
External or concealed hemorrhage, excessive blood loss, shock, nulliparity, closed cervix, absence of labor and delayed diagnosis and treatment are unfavourable
Maternal mortality ranges from 0.5-5%, most die from hemorrhage(immediate or delayed), cardiac or renal failure
Perinatal mortality rate is approx 5%, liveborn infants have a high morbidity rate due to predelivery hypoxia,birth trauma and hazards of prematurity

16. PLACENTA PREVIA
The placenta is implanted in the lower uterine segment within the zone of effacement and dilatation of cervix leads to an obstruction to the descent of the presenting part.
Classified into:
-(a) marginal
-(b) partial
-(c) complete

17. ETIOLOGY
Multiparity, advancing age, previous C/S, scarred or poorly vascularized endometrium in the corpus, large placenta, succenturiate lobe, multiple gestation.
Bleeding in placenta praevia is due to (a)mechanical separation from its implantation site during formation of the lower uterine segment or during effacement and cervical dilatation (b)placentitis (c) rupture of poorly supported venous lakes in d decidua basalis that have been engorged with venous blood

18. DIAGNOSIS
Every patient suspected to have placenta previa should be hospitalized and cross match hand.
Vaginal and rectal examination should not be performed to avoid hemorrhage
95% are diagnosed via U/S

19. SYMPTOMS AND SIGNS
Painless, sudden and profuse bleeding , bright red clotted blood. Bleeding rarely produces shock.
Uterus is soft, relaxed and non-tender
High presenting cannot be pressed into the pelvic inlet
Infant will pressent in a transverse or oblique in approx 15%

20. DIFFERENTIAL DIAGNOSIS
Placenta abruption
Circumvallate placenta

21. TREATMENT
Depends on the amount of uterine bleeding, duration of pregnancy and viability of fetus, degree of placenta previa, presentation, position and station of fetus, gravidity and parity of the patient, status of the cervix and whether or not labour has begun
Patient should be admitted and blood should be readily available for transfusion

22. TREATMENT
Expectant therapy because hemorrhage may occur early in pregnancy before pulmonary maturity, transfusions to replace blood loss, use of tocolytic agents to prevent premature labour and prolong pregnancy to about weeks
C/S is the delivery of choice. Vaginal delivery is usually indicated for marginal placenta previa and when the presentation is cephalic plus there should be constant FHR monitoring any signs of distress do C/S

23. COMPLICATIONS
Maternal: hemorrhage, shock, death, operative trauma, infection and embolism, placenta previa accreta
Fetal: prematurity, fetal hemorrhage due to tearing of the placenta occurs with vaginal manipulation and upon entry into the uterine cavity as C/S is done

24. PROGNOSIS
Maternal: due to rapid recourse to C/S, use of banked blood and expertly administered anaesthesia the mortality has fallen to less than 1 in 1000
fetal: perinatal mortality has reduced to approx 1%. Premature labour, placenta abruption, cord accidents and uncontrollable hemorrhage cannot be avoided, can be reduced with ideal obsteric and newborn care

25. COMPARISON OF HAEMORRAGE FROM P PRAEVIA & ABRUPTION
PLACENTA PRAEVIA(PP)
PLACENTA ABRUPTION(PA)
Painless(80%)
Patient is less distressed
Soft abdomen
Abnormal lie & presentation
CTG usually normal
No particular association with pre-eclampsia
No coagulation defect initially
Painful
Patient is distressed
Tender, tense abdomen
Normal lie & presentation
Abnormal CTG likely
May be associated with pre-eclampsia
Coagulation defect may occur early

26. UTERINE RUPTURE
Tearing of d uterus occurs most commonly in association with a previous scar on d uterus.
Major cause of maternal death
Two types:
-(a) complete: traumatic and spontaneous
-(b) incomplete

27. RISK FACTORS Hysterotomy Trauma Uterine over-distension
Uterine anomalies
Placenta percreta
Invasive mole
Choriocarcinoma
Neglected obstructed labour
Improper use of oxytocin

28. CLINICAL FINDINGS Fetal heart rate abnormalities
Increased suprapubic pain and tenderness with labour
Sudden cessation of uterine contractions with a tearing sensation
Vaginal bleeding or bloody urine
Recession of the fetal presenting part

29. TREATMENT Prepare the patient for URGENT C/S
Control of maternal haemorrage

30. COMPLICATIONS Haemorrage Shock Postoperative infection
Bladder or ureteral damage
Thrombophlebitis
Amniotic fluid embolus
DIC
Pituitary failure
Death

31. PREVENTION Identify patients @ risk of uterine rupture
Early diagnosis of abnormal presentation
Correct administering of oxytocin during labour
Good obstetric assessment and technique
Correct use of partograph

32. PROGNOSIS Maternal mortality rate is 4.2%
Perinatal mortality rate is 46%

33. VASA PRAEVIA
Is d term used where umbilical cord vessels abnormally transverse d membranes n overlie d internal cervical os.
Occurs in 1 in 3000 pregnancies.
Is associated with either a velamentous insertion of d cord into d placenta(from d side) or with a succenturiate(satellite or accessory) lobe of d placenta.
D vessels are at risk of tearing wen dey are stretched during cervical dilatation in labor or amniotomy.

34. Fetal mortality from vasa praevia is 35-95%, there is no significant risk to d mother.
Diagnosis must, therefore, be suspected clinically by a combination of relatively small volume bld loss(<500ml), no maternal pain n an abnormal CTG, oft following ARM.
May also be diagnosed antenatally on ultrasound with demonstration of doppler flow in d vessels beneath d fetus.

35. TREATMENT
Immediate CS performed
Transfusion of d neonate.

36. THANK YOU