2. Blood Volume
Non pregnant BV calculation
– Non-pregnant blood volume ~ 3500 ml
– Pregnant blood vlume~5000ml
3. BV
Pregnant blood volume:
• Increases across GA and plateaus at app.34 weeks
• The increase Varies from 30 - 60 % of calculated
nonpregnant volume
– Usually larger with low normal-range HCT (~30%) and smaller
with high normal-range HCT (~38%)
• Average increase is 40 - 80 % with MF gestation
• Average increase is less in the woman with PE
• severe PE or E blood volume doesnot expand normally
severity is inversely related with volume
– The Mean increase above nonpregnant volume in 29 eclamptic
women at delivery was only 10% Zeeman and colleagues (2009).
• Thus, these women are very sensitive to, or even
intolerant of, what may be considered normal blood loss
4. Blood Volume
• pregnancy-induced hypervolemia usually increases BV by
30 % to 60 %.
1500 to 2000 mL for an average-sized woman (Pritchard, 1965).
Loss of the same volume during delivery is tolerated (no
significant ↓in Hct postpartally)
Thus, if blood loss < the amount added by pregnancy, the
Hct stays the same acutely and during the first several
days.
It eventually increases as normal plasma volume shrinks
postpartum.
If post partum Hct < admission Hct => blood loss
Volume lost= ( 500ml/3%HCt↓ + extra volume of pregnancy)
5. BV
Women who may not have adequate pregnancy
added volume- sensitive for hemorrhage
• Small Woman- even with N BV expansion
which is proportional to their body size /
prepreg BV
• Severe PE/ Eclampatic women ( Eg E ~10%
increase over the prepreg volume)
• Women with Chronic renal insufficiency
6. Little Pregnancy volume expansion ~ 9%
less than that of normotensives
Intolerance of little blood loss
↑ed vasoconstriction
BP maintained with significant blood loss leading to
underestimation of bleeding
↓ UO UO is poor indicator of severity of hemorrhage
/↓ end-organ perfusion secondary to
hemorrhage
it is rather manifestation of severity of PE
7. Classification of Hemorrhage
Clinicians should note that significant drops in
BP are generally not manifested until class III
hemorrhage develops
up to 30% of a patient's blood volume can be lost
before this occurs:
• compensated by vasoconstriction and increased HR that
may attempt to maintain CO and BP
• Clinical Significance of tachypnoea in hemorrhage- not clear-
may indicate impending decompensation
8. Classification of Hemorrhage
• Class I hemorrhage
– involves a blood volume loss of up to 15 %.
– The heart rate is minimally elevated or normal, and
– no change in BP , pulse pressure, or RR .
• Class II hemorrhage – involves 15 – 30% blood volume
loss and is clinicaly manifested as
– tachycardia (HR 100 -120’) ,tachypnea (RR :20 – 24’),
– a decreased pulse pressure, Although SBP changes
minimally if at all.
– The skin may be cool and clammy, and
– capillary refill may be delayed.
9. Classification of Hemorrhage
• Class III hemorrhage- involves a 30 to 40 %
blood volume loss, results in
– a significant drop in BP
– Changes in mental status.
– Markedly elevated HR (≥ 120 and thready) and RR
– Diminished urine output.
– Delayed Capillary refill .
Any hypotension (SBP< 90 mmHg) or drop in BP > 20 -30 % of the
measurement at presentation is cause for concern. While diminished
anxiety or pain may contribute to such a drop, the clinician must
assume it is due to hemorrhage until proven otherwise.
10. Classification of Hemorrhage
Class IV hemorrhage
• involves more than 40 %BV loss leading to
– significant depression in BP and mental status.
– Most patients are hypotensive (SBP < 90 mmHg).
– Pulse pressure is narrowed (≤25 mmHg), and
– tachycardia is marked (>120).
– Urine output is minimal or absent.
– The skin is cold and pale, and
– capillary refill is delayed
11. The classification reflects volume of deficit rather than volume of
loss.
Class 1- 900 ml- 15%
• Asymptomatic
Class 2- 1,200–1,500ml- 20–25 %
• Tachycardia and tachypnea
• Narrowed pulse pressure
• Orthostatic hypotension
• Delayed hypothenar refilling
class 3- 1,800–2,100 ml- 30–35 %
• Worsening tachycardia and tachypnea
• Hypotension
• Cool extremities
Class 4- >2,400 ml 40% Shock Oliguria/Anuria
12. Pulse pressure is a good reflection of
stroke volume and β-1 stimulation.
Similarly DBP is a reflection of systemic
vasoconstriction.
Therefore, the SBP represents the
interrelationship between these entities
13. When a large hemorrhage occurs, RBF is
reduced and redirected from the outer
renal cortex to the juxtamedullary region.
In this region, increased water and
sodium absorption occur, resulting in
• less urine volume,
• lower urinary sodium concentration, and
• increased urine osmolarity.
A urine sodium concentration <10 to 20
mEq/L or a urine/serum osmolar ratio > 2
indicates significantly reduced renal
perfusion in the face of hemorrhage.
14. Class 2 volume deficit, the sympathoadrenal system is
activated, resulting in a diversion of blood away from
nonvital organs (skin, muscle, kidney) and a
redistribution of the circulation to vital body organs,
the brain, and heart.
The end result is
• increased vasoconstriction,
• increased DBP, maintenance of SBP, and
• a narrowing of the pulse pressure.
With greater narrowing of the pulse pressure, more
compensatory vasoconstriction is occurring to
accommodate for a loss in stroke volume
16. Obstetrical Hemorrhage
• Obstetrics is "Bloody Business.“
• Hemorrhage is the single most important cause of
maternal death worldwide.
• Obstetrical hemorrhage (OH) accounts for almost
half of all postpartum deaths in developing
countries
• Fatal hemorrhage is most likely in circumstances in
which blood or components are not available
immediately
17. Obstetrical Hemorrhage
• Generally speaking,OH
– may be antepartum (28 wk to delivery of last fetus)—
such as with placenta previa or placental abruption
– or more commonly it is postpartum—from uterine
atony or genital tract lacerations.
18. Special considerations
The following may be sensitive for a blood loss
considered normal
• Small women-
– proportionally small BV despite normal
pregnancy induced expansion
• Preeclamptic/ Eclamptic
• Chronic renal insufficiency
• Inadequate pregnancy induced hypervolemia
20. Causes and Predisposing Factors of OH
Small Maternal Blood Volume
• Small women
• Pregnancy hypervolemia
not yet maximal
• Pregnancy hypervolemia
constricted
• Severe preeclampsia
• Eclampsia
• Sepsis syndrome
• Chronic renal insufficiency
Other Factors
• Obesity
• Previous PPH
Uterine Atony
• Overdistended uterus
– Large fetus
– Multiple fetuses
– Hydramnios
– Distension with clots
– Labor induction
• Anesthesia or analgesia
• Halogenated agents
• Conduc anatlgesia with
hypotension
• Exhausted myometrium
• Rapid labor
• Oxytocin or PG stimulation
• Chorioamnionitis
• Previous uterine atony
21. Causes and Predisposing Factors of OH
• Coagulation Defects—Intensify Other Causes
– Massive transfusions
– Placental abruption
– Sepsis syndrome
– Severe preeclampsia and eclampsia
– Anticoagulant treatment
– Congenital coagulopathies
– Amnionic fluid embolism
– Prolonged retention of dead fetus
– Saline-induced abortion
22. Causes and Predisposing Factors of OH
• One factor not generally considered as "predisposing" to
exsanguination is the lack of adequate obstetrical and
anesthetic services.
• According to the 2002 Confidential Enquiry into Maternal
and Child Health (CEMACH), however, most maternal
deaths from hemorrhage in the UK were associated with
substandard care.
• Moreover, from Japan, Nagaya and associates (2000)
concluded that many hemorrhage-related maternal deaths
were preventable and were associated with inadequate
facilities.
• Zwart and co-workers (2008) provided similar observation
from the Netherlands
23. Percentages are approxima-tions because of different classification schemata
used. DIC = disseminated intravascular coagulation. (Data from Al-Zirqi,
2008;Berg, 2010; Chichakli, 1999; Zwart, 2008.) Will 24th
Contributions to maternal death from
various causes of obstetrical hemorrhage
24. Antepartum Hemorrhage
“Bloody Show"
• common, Slight vaginal bleeding in active
labor
• The consequence of effacement and dilatation
of the cervix, with tearing of small vessels
• insignificant blood loss.
Uterine bleeding, however, coming from above the cervix, is
cause for concern
25. Antepartum Hemorrhage
APH may follow
• some separation of a placenta in
– placenta previa- implanted in the immediate vicinity of the
cervical canal.
– placental abruption- located elsewhere in the uterine
cavity.
• Vasaprevia-
– velamentous insertion of the umbilical cord, rare~ 1%
BVesselss overlie the cervix extending from the cord insertion
(within the membranes)
– hemorrhage may follow laceration of these vessels at the
time of membrane rupture (digital manipulation, fetal
descent).
– Common in placenta previa and multiple gestation
26. APH
Unexplained APH
• The source of uterine bleeding is not always identified. In
that circumstance, antepartum bleeding typically begins
with few, if any, symptoms and then stops.
• At delivery no anatomical cause is identified. In many of
these cases, bleeding likely is the consequence of slight
marginal placental separation.
• A pregnancy with such bleeding remains at increased risk
for a poor outcome even though the bleeding soon stops
and placenta previa appears to have been excluded by
sonography
• delivery should be considered in any woman at term with
unexplained vaginal bleeding.
27. Placenta Previa
• PP- implantation of the placenta over or very
near to the internal cervical OS
• Current classification
– True placenta previa
– low lying
• Incidence-~ 1/300 deliveries
28. Risk Factors
Incidence of PP increases with
• Advancing age
• Multiparity
• Multifetal gestation
• Prior Cesarean delivery
• Smoking
• Elevated MSAFP at early screening
29. PPH
• The most common definition of PPH is EBL
– ≥500 mL after vaginal birth or
– ≥1000 mL after cesarean delivery..
– > 1500 after cesarean bhysterectomy
• This is problematic because half of all women delivered
vaginally shed that amount of blood or more when
losses are measured quantitatively
• The inadequacy of this definition was illustrated in
studies that assessed blood loss using various objective
methods:
– the mean blood loss reported after vaginal and CD was
approximately 400 to 600 mL and 1000 mL, respectively,
and clinicians were more likely to underestimate than
overestimate the volume of blood lost
30. PPH DEFINITION AND DIAGNOSIS
• PPH is best defined and diagnosed clinically as
excessive bleeding that makes the patient symptomatic
(eg, pallor, lightheadedness, weakness, palpitations,
diaphoresis, restlessness, confusion, air hunger,
syncope) and/or results in signs of hypovolemia (eg,
hypotension, tachycardia, oliguria, low oxygen
saturation [<95%]) .
• Vaginal bleeding is usually noted, but may not be
present in cases where hemorrhage is related to
abdominal bleeding from a cesarean delivery or a
broad ligament hematoma after a sulcus laceration.
• A timely, accurate diagnosis of PPH is important in
order to initiate intervention (eg, drugs, surgery,
referral) and improve outcome
31. PPH DEFINITION AND DIAGNOSIS
• Another classic definition of PPH is a 10 % decline
in postpartum hemoglobin concentration from
antepartum levels.
• not useful clinically for several reasons:
rapid blood loss may trigger a medical emergency
prior to observation of a fall in hemoglobin
concentration;
laboratory changes that are not correlated with
events that endanger the patient should not be used
to define a medical emergency;
and antepartum hemoconcentration (eg, from
preeclampsia or dehydration) may cause a large fall in
serlum hemoglobin concentration following delivery
in the absence of excessive intrapartum blood loss.
32. PPH- Incidence Markers
Direct measurement of blood loss
– a two center investigation in Argentina and Uruguay (Sosa, 2009) using
specialized collecting drapes during vaginal delivery
– > 500ml loss in10.8%
– > 1000 ml loss in 1.9%
These estimates likely are too low
Predetermined value of Hct decline
clinically significant blood loss in vaginally delivered women was defined as 6% decline
in hct postpartally by Tia and collegues (2012) ~ 1000ml loss in average sized woman
– 4th ( 25%) of pts had PPH ( agrees with Pritchards findings in the graph)
Transfusion Rates
• Tita and co (2012)- > 6% of vaginally delivered women had intervention
including transfusion
• Of 66,000 women delivered at Parkland H in 2002-06, 2.3% Transfused for
hypovolemia ( 50% CD) , with calculated average blood loss -3500ml
(Hernandez 2012)
• In Australia, 1.6 % of women delivered in 2010 were transfused (Patterson,
2014).
CONC- it is apparent that signifcant blood loss accompanies about a fourth of
vaginal deliveries. The amounts and proportions for CD are much greater.
33. PPH
• Pritchard and associates (1962) used precise methods
and found that app 5 % of women delivering
vaginally lost more than 1000 mL of blood.
– > 500ml loss ~ 30%??? From the graph
• They also reported that estimated blood loss is
commonly only approximately half the actual
loss.
• Because of this, EBL in excess of 500 mL should
call attention to mothers who are bleeding
excessively.
34. Blood loss associated with vaginal delivery, repeat CD , and
repeat CD plus hysterectomy. (Data from Pritchard, 1962.)
35. PPH
• Primary- in the 1st 24 hrs
• secondary (late) PPH- after 24 hrs PP
– in 1% of women
36. PPH
• Postpartum blood volume with serious
hemorrhage
• Assume acute return to nonpregnant total volume—
with fluid resuscitation—because pregnancy
hypervolemia will not be attained again
37. PPH-Etiology (IJGO,117,2012)
• It may be helpful to think of the causes of PPH
in terms of the 4 “T”s:
– Tone: uterine atony, distended bladder.
– Trauma: uterine, cervical, or vaginal injury.
– Tissue: retained placenta or clots.
– Thrombin: pre-existing or acquired coagulopathy
38. Postpartum Hemorrhage
• PPH describes an event rather than a diagnosis, and when
encountered, its etiology must be determined.
• Common causes include
– bleeding from the placental implantation site,
– trauma to the genital tract and adjacent
structures, or both
39. Predisposing Factors and Causes of Immediate Postpartum
Hemorrhage
Bleeding from Placental Implantation
Site
Hypotonic myometrium—
uterine atony:
• Some GAs- halogenated HCs
• Poorly perfused
myometrium—hypotension
• Hemorrhage
• Conduction analgesia
• Overdistended uterus: large
fetus, twins, hydramnios
• Prolonged labor
• Very rapid labor
• Induced or augmented labor
• High parity
• Uterine atony in previous pregnancy
• Chorioamnionitis
• Retained placental tissue
• Avulsed lobule, succenturiate lobe
• Abnormally adhered: accreta,
increta, percreta
Trauma to the Genital Tract
• Large episiotomy, including
extensions
• Lacerations of perineum, vagina, or
cervix
• Ruptured uterus
Coagulation Defects
• Intensify all of the above
40. Hemostasis at the Placental Site
• Near term, it is estimated that at least 600 mL/min of
blood flows through the intervillous space .
• This flow is carried by the spiral arteries—which
average 120 in number—and their accompanying
veins.
• With separation of the placenta, these vessels are
avulsed .
• Hemostasis at the placental implantation site is
achieved by
– contraction of the myometrium that compresses this
formidable number of relatively large vessels .
– This is followed by subsequent clotting and obliteration
of their lumens
• Thus, adhered pieces of placenta or large blood clots
that prevent effective myometrial contraction can
impair hemostasis at the implantation site
41.
42. PPH-Clinical Characteristics
• Postpartum bleeding may begin before or after
placental separation.
• Instead of sudden massive hemorrhage, there usually
is steady bleeding.
• At any given instant, it appears to be only moderate,
but may persist until serious hypovolemia develops.
• Especially with hemorrhage after placental delivery,
constant seepage can lead to enormous blood loss.
• The effects of hemorrhage depend to a considerable
degree on
– the nonpregnant blood volume and
– the corresponding magnitude of pregnancy-induced
hypervolemia.
43. PPH-Clinical Characteristics
• In some women after delivery, blood may not
escape vaginally but instead may collect
within the uterine cavity, which can become
distended by 1000 mL or more of blood
44. PPH-Clinical Characteristics
Bp and PR-poor markers of magnitude of blood
loss (treacherous)
– change moderately until large volume is lost=>
hypovolemia is identified late
– Bp may initially↑ in response to hemorrhage in
the normotensive pt.
– Hypertensive pt. ,with significant bleeding, may
appear normotensive
45. PPH-Diagnosis
• The diagnosis of PPH should be obvious Except
possibly when
– IU and intravaginal accumulation of blood is not
recognized, or
– in some instances of ux rupture with intraperitoneal
bleeding,.
• The differentiation between bleeding from
uterine atony and that from genital tract
lacerations is tentatively determined by
predisposing risk factors and the condition of the
uterus .
– If bleeding persists despite a firm, well-contracted
uterus, the cause most likely is from lacerations.
– Bright red blood also suggests arterial blood from
lacerations.
46. Symptoms related to blood loss with PPH Uptodate
Blood loss, % (mL) BP, mm Hg Signs and symptoms
10 -15 (500 to 1000) Normal
Palpitations,
lightheadedness,
tachycardia
15 to 25 (1000 to 1500) Slightly low
Weakness, sweating,
tachycardia
25 to 35 (1500 to 2000) 70 to 80
Restlessness,
confusion, pallor,
oliguria
35 to 45 (2000 to 3000) 50 to 70
Lethargy, air hunger,
anuria, collapse
47. PPH Management
• Inspect the genital trrepairact for laceration
and
• If Placental defect is noticed- manual
exploration of the uterine cavity and removal
of RPCs
• Atony- uterotonics and massage
• Surgical intervention If refractory
48. 3rd Stage Management
Active Vs Expectant (physiological)
• The Bristol [8] and Hinchingbrooke [9] studies
clearly demonstrated lower PPH incidence
with AMTSL
– Bristol-5.9% with AMTSL vs 17.9% with expectant
management; and
– Hinchingbrooke-6.8% with AMTSL vs 16.5%
without
49. PPH Prevention-AMTSL
• AMTSL reduces the incidence of PPH, the quantity
of blood loss, and the need for blood transfusion,
• should be included in any program of intervention
aimed at reducing death from PPH .
• The usual components of AMTSL include:
– Administration of oxytocin (the preferred storage of oxytocin is
refrigeration but it may be stored at temperatures up to 30 °C for up to 3
months without significant loss of potency) or another uterotonic
drug within 1 minute after birth of the infant.
– Controlled cord traction.
– Uterine massage after delivery of the placenta
50. AMTSL
1.Uteroonic adminstration
• Oxytocin 10 IU IM Within 1 minute of delivery of the
infant,( palpate the abdomen to rule out the presence
of an additional infan/(s)
• Oxytocin is preferred over other uterotonic drugs
because it is effective 2–3 minutes after injection, has
minimal adverse effects, and can be used in all women.
• If oxytocin is not available, other uterotonics can be
used, such as:
– ergometrine or methylergometrine 0.2 mg IM;
– syntometrine (a combination of oxytocin 5 IU and
ergometrine 0.5 mg per ampoule IM or
– misoprostol 600 μg orally.
51. Uterotonics- storage
Uterotonics require proper storage:
◆Ergometrine or methylergometrine:
– 2–8 °C and protect from light and from freezing.
◆ Misoprostol:
– in aluminum blister pack, room temperature, in a
closed container.
◆ Oxytocin:
– 15–30 °C, protect from freezing.
• Counseling on the adverse effects and
contraindications of these drugs should be given
52. Fig. 1. Muscle fibers of the uterus. Image reproduced, with permission,
from Ref. [6]
53. Ergot alkaloids- Caution
• contraindicated in patients with hypertension, cardiac disease
or occlusive vascular disorders, severe hepatic or renal
disease, and sepsis
• not routinely given intravenously to avoid inducing sudden
hypertensive and cerebrovascular accidents.
– If considered a lifesaving measure, however, intravenous
methylergonovine should be given slowly during no less than 60
seconds with careful monitoring of blood pressure
• FDA has added a warning to the package insert
recommending a 12-hour delay between the last
methylergonovine dose and breast feeding. Despite this, no
adverse effects attributable to this drug in breast milkhave
been reported (Briggs, 2011). (will 24th )
54. Misoprostol
• This PGE1 analogue has proved inferior to oxytocin
for PPH prevention (Tunçalp, 2012).
• Although oxytocin is preferred, in resource-poor
settings that lack oxytocin, misoprostol is suitable
for hemorrhage prophylaxis and is given as a single
oral 600-μg dose (Mobeen, 2011; World Health Organization, 2012).
• SEs include shivering in 30 % and fever in 5 %.
• Unlike some other prostaglandins, nausea or
diarrhea is infrequent (Derman,2006; Lumbiganon, 1999; Walraven,
2005). Will 24°
55. Step 2: How to do controlled cord traction
• If the newborn is healthy, you can clamp the cord
close to the perineum
• Once cord pulsations stop or after approximately 2
minutes and
• hold the cord in one hand (immediate cord
clamping may be necessary if the newborn requires
resuscitation)
56. CCT
• Place the other hand just above the woman's pubic
bone and stabilize the uterus by applying counter-
pressure during controlled cord traction.
• Keep slight tension on the cord and await a strong
uterine contraction (2–3 minutes).
• With the strong uterine contraction, encourage the
mother to push and very gently pull downward on the
cord to deliver the placenta.
• Continue to apply counter-pressure to the uterus.
• If the placenta does not descend during 30–40 seconds
of controlled cord traction, do not continue to pull on
the cord:
57. • Gently hold the cord and wait until the uterus
is well contracted again.
• With the next contraction, repeat controlled
cord traction with counter-pressure.
• Never apply cord traction (gentle pull) without
applying countertraction (push) above the
pubic bone on a well-contracted uterus
