Postpartum haemorrhage.ppt

Obstetrics

1. POSTPARTUM
HAEMORRHAGE
W. STANEY ALEMI-RHU

2. Postpartum Haemorrhage
Traditional Definition
Blood loss of > 500ml. following vaginal delivery
Blood loss of >1000ml. following cesareandelivery
Functional Defination: Excessive bleeding that makes a
patient symptomatic ( e.glightheadedness, vertigo,
syncope) and/or results in signs of hypovolemia( e.g
hypotension, tachycardia oliguria)
A 10% decrease in postpartum HB concfrom prepartum
levels
Incidence
About 5% of all deliveries

3. Classification of Postpartum
haemorrhage
Primary( Early PPH) –Occurs in first 24
hours after delivery
Secondary (Late PPH)–Occurs after first 24
hours and within six weeks post partum

4. Etiology of Postpartum haemorrhage
Tone –Uterine atony
Tissue –Retained tissue/clots
Trauma –laceration, incisions, rupture,
inversion
Thrombopathy-coagulopathy

5. Uterine Atony
Defn: Lack of effective contraction of the uterus
after delivery
Commonest cause of PPH( 80 –90%) cases
Atony related to;
1: Overdistension( xple
gestation,polyhydramnios,macrosomia)
2: Uterine
fatigue/exhaustion(prolonged,rapid,induced,aug
umented labour)

6. Uterine Atony-Cont’d
3: High parity –Uterine fatigue/exhaustion
4: Uterine infxn–
chorioamnionitisis,prolongedPROM
5: Uterine inversion
6: Some general anaesthetics-
halogenated hydrocarbons
7: Poorly perfused myometrium –
hypotension –APH
8: Uterine atonyin previous pregnancy

7. Predisposing Factors for PPH -Antepartum
Previous PPH or manual removal of placenta
Placental abruption especially if concealed
Intrauterine fetal demise
Placenta previa
Gestational hypertension
Over distended uterus (e.g twins,
polyhydramnios)
Prexisting maternal bleeding disorder.

8. Predisposing Factors for PPH -Intrapartum
Operative delivery –cesarean or assissted
vaginal delivery
Prolonged labour
Rapid labour
Induction or augmentation
Chorioamnionitis
Shoulder dystocia
Internal podalic version
Acquired coagulopathy

9. PPH –Postpartum causes
Lacerations or episiotomy
Retained placenta /placental abnormalities
Retained blood clots
Uterine rupture
Uterine inversion
Uterine anormalies/uterine fibroids
Acquired coagulopathy

10. Prevention
Be prepared
Active management of the third stage
-Prophylactic oxytocin with delivery of anterior shoulder
or immeidately after delivery
10 U IM or 5 U IV bolus
10-20 U/L N/S IV run rapidly at 100-150 ml/hr
-Early cord clamping and cutting
-Palpate the uterine fundus and confirm the uterus is
contracted
-Controlled cord traction (gentle) with suprapubic
countertraction
-Uterine massage after delivery of the placenta, as
approriate
-If placenta has not delivered after 15 minutes, infuse
oxytocin at 20 units/L of cristalloid at 100-150ml/hr
-Consider oxytocin infusion after placental delivery

11. Diagnosis –Is this a PPH?
Consider predisposing factors
Observe vaginal loss
Express blood from vagina following C/S
REMEMBER
-Blood loss is consistently underestimated
-Ongoing trickling can lead to significant blood
loss
-Blood loss is generally well tolerated to a point

12. Diagnosis –What is the cause?
Assess the fundus
Inspect the lower genital tract
Explore the uterus
-retained placental fragments
-uterine rupture
-uterine inversion
Assess coagulation

13. Postpartum haemorrhage-
Management
A=Airway
B=Breathing
C=Circulation
D = DRUGS

14. Management –ABC’s
Talk to and assess woman
Get HELP
Monitor vital signs
Remember that compensatory responses to blood loss in
these patients are excellent & may give you a false
sense of security
Large bore 2 IV access: active fluid resuscitation
Crystalloid –lots!
CBC, cross match and consider coagulation studuies
Elevate the legs to increase return of blood to the heart
Foley catheter

15. Management –Assess the fundus
Simultaneous with ABC’s
Atony is the leading cause of PPH
Uterine massage
If boggy –bimanual massage
Rules out uterine inversion
May feel lower tract injury
Evacuate clot from vagina and/or cervix
May consider manual exploration at this time

16. Management –Oxytocin
5 units IV bolus
20 units per L N/S IV wide open
10 units intramyometrial given
transabdominally

17. Manual Exploration: Is there a need?
No need for routine manual exploration
Risks:
-Infections
-Hemorrhages
-Pain

18. If no response to:
Uterine massage
Bimanual massage
Oxytocin

19. Proceed to Manual Exploration
Manual exploration is need to :
Rule out uterine inversion
Palpate cervical injury
Remove retained placenta or clot from
uterus
Rule out uterine rupture or dehiscence

20. Management –Additional Uterotonics
Ergometrine –caution in hypertension
-o.25 mg IM or 0.125mg IV
-Intervals of 5 mins maximum dose 1.25mg
Hemabate (carboprost tromethamine) –asthma
is relative contraindication
-15 methyl –prostaglandin F2alpha
-O.25mg IM or intramyometrial
-Intervals of 15 –90 mins maximum of 8 doses
(2mg)

21. Management –Additional Uterotonics
Cytotec (misoprostol) caution in asthma
-800/1000 micrograms pr; 200 mcg po +
400mcg sublingual; & 200mcg po +
400mcg sL + 400mcg pr
Duratocin (carbetocin-long acting oxytocin
agonist)
-100 micrograms IM or 100 micrograms IV
over 1 min.

22. If bogginess or haemorrhage continues
Consider abdominal aortic compression that is a
life saving intervention when there is a heavy
bleeding (whatever the cause)
-Circulating blood volume is restricted to the
upper part of the body and thereby to the vital
organs
-BP is kept up
-Blood is prevented from reaching the
bleeding are in the pelvis
-Volume is conserved

23. If bogginess or haemorrhage continues
Other emergency therapies:
tamponade with esophageal catheter,
emergency embolization, emergency
laparotomy with pelvic vessel ligation or
hysterectomy

24. Tamponade
Uterine packs-pack entire uterine cavity
with gauze. Thought to be dangerous &
ineffective by most obstetrians.
Should give i.v antibiotics
Regardless of form of tamponade used Hb
& urine output shd be closely monitored
Important esp. with the gauze pack bse a
large amt of blood can collect behind the
pack.

25. Arterial embolisation
Done by an interventional radiologist
Patient haemodynamically stable
Selective procedure done with single
bleeding vessel & it can be occluded
With diffuse bleeding area/single bleeding
vessel cant b identified-large artery
feeding multiple smaller vessels in
bleeding area is occluded

26. Laparatomy
Incision –midline vertical
Retractor –self retaining for adequate
lateral exposure
If descrete vessel bleeding –clamp it-ligate
with appropriate suture material
Atony or bleeding adjacent to the uterus &
difficult to control –do uterine atery
ligation

27. Uterine vessel ligation
Bilateral ligation(o’ leary stitch) becoming first line
procedure to control bleeding
Advs.
(1)uterine arteries easily accessible vs internal illiac artery
(2) procedure > successful
(3)field of dissection generally not near the ureters & illiac veins
Procedure:
identify the ureter
No. 0 chromic catgut/polyglycolic acid suture on a large curved
needle
Needle passed thru lateral aspect of lower uterine seg. As close to
the cervix as possible, then back thru the broad ligament just
lateral to the uterine vessels tied to compress the vessels
If above not successful vessels of the utero-ovarian arcade are
ligated just distal to the cornua by passing a suture thru the
myometrium just medial to the vessels

28. Compression sutures
B-lynch suture; a pair of vertical brace no.
2 chromic sutures are secured around the
uterus, appearing as suspenders,to
compress together the ant & post uterine
walls.

29. Internal iliac artery ligation
Techinically difficult
Usually successful in < half of patients in which
its attempted
Need adequate exposure
Peritoneum over common iliac artery opened &
dissected down to bifurcation of external &
internal iliacs
Then areolar sheath covering internal iliac is
incised longtudinally & a right-angle clamp is
carefully passed beneath the artery.

30. Internal iliac ligation cont’d
Careful not to perforate contiguous large
veins esp internal iliac vein.
Non-absorbable suture is inserted into
open clamp, jaws closed,suture carried
around vessel & vessel ligated.
NB: Pulsations in external iliac if present
before tying the ligature shd be present
after as well.

31. Internal iliac atery ligation cont’d
Mechanism of action here is an 85% reduction
in pulse pressure in the arteries distal to the
ligation.
This converts an arterial pressure system into
one with pressures close to those in the venous
circulation which are more amenable to
hemostasis via simple clot formation.
Bilateral ligation doesn’t seem to interfere with
subsequent reproduction
NB: HYSTERECTOMY-Last option

32. Management –Bleeding with firm uterus
Explore the lower genital tract
Requirements -appropriate analgesia
-good exposure and lighting
Surgical repair of vaginal and cervical
lacerations
May temporize with packing

33. Management –Continued uterine bleeding
Consider currettage
Correct possible coagulopathy –PTT, fibrinogen
If coagulation is abnormal
-Correct with clotting factors, platelets and
PRBC’s, cryoprecipitate
If coagulation is normal
-Rule out uterine rupture or inadequate
incision repair
-Consider uterine ligation, hysterectomy.

34. Management
ABC –ENSURE that you are always ahead
with your resuscitation
All obstetrical providers should have
access to medications to treat PPH
Consider need for more expert help

35. conclusion
Be prepared
Practise prevention
Assess the loss
Assess maternal loss
Resuscitate vigorously and appropriately
Diagnose the cause
Treat the cause

36. Secondary PPH
Occurs in approx 1% cases
Aetiology:
Retained placental fragments
Intrauterine infection(often coexists with the above)
Submucous fibroid
Lacerations and haematomas
Trophoblastic disease(a very rare but important
cause)
Chronic uterine inversion

37. management
Intravenous crystalloid
X-match blood
Intravenous antibiotics if any signs of sepsis
Under anaesthesia try to remove any placental
tissue
Follow this with cautious curettage
NB: Any tissue shd always be sent for
histopathological diagnosis-keeping in mind the
very rare case of trophoblastic disease