MANAGEMENT OF POST PARTUM HAEMORRHAGE(1).doc

8/17/2019 MANAGEMENT OF POST PARTUM HAEMORRHAGE(1).doc

1/20

CHAPTER I

INTRODUCTION

Postpartum Haemorrhage (PPH) is commonly defined as a blood loss of 500 ml or more within 24 hours after birth.1 PPH is the leading cause of maternal mortality in lowincome countries and the primary cause of nearly one !uarter of all maternal deaths globally."ost deaths resulting from PPH occur during the first 24 hours after birth. #he ma$ority of these could be a%oided through the use of prophylactic uterotonics during the third stage of labour and by timely and appropriate management. &mpro%ing health care for women duringchildbirth in order to pre%ent and treat PPH is an essential step towards the achie%ement of the "illennium 'e%elopment oals.12*

Hypertensi%e disorders in pregnancy contribute to significant mortality and morbidityworldwide and affect 5+ of pregnancies.4 ,apid onset interstitial fluid accumulation in thelungs acute pulmonary oedema (-P) is a potential complication of maternal hypertensionseen particularly in women with preeclampsia and eclampsia. -P has also been lin/ed toincreased maternal age deli%ery %ia aesarean section body mass inde parity undiagnosedcardiomyopathy multiple gestation corticosteroid use colloid therapy and magnesiumsulphate ("g4) use.5 3ndothelial damage and resulting fluid lea/age into the al%eolar space contributes to the de%elopment of acute pulmonary oedema in these women thus may

be in part eplained by the endothelial dysfunction seen in women with preeclampsia beingan endothelial disease. &atrogenic causes lin/ed to nonrestricti%e intra%enous crystalloid fluidadministration policies ha%e also been noted. #he negati%e inotropic effect attributed to

commonly used antihypertensi%e medications in the obstetric setting such as nifedipine andlabetalol has also been !uestioned as a contributing factor in the de%elopment of acute

pulmonary oedema.5 &ncreasing use of nonsteroidal antiinflammatory drugs (-&')which can cause fluid retention may also be a contributing factor. "aternal morbidity iscurrently underreported in the obstetric literature. #his confounds the ability to bothdetermine rates of acute pulmonary oedema among hypertensi%e pregnant women andidentify potential causati%e factors. 6est estimates of rates are deduced from randomisedcontrolled trials and obser%ational data.7 #his method has inherent problems of accuracy dueto issues such as small sample si8e and sample and publication biases. ,eported rates of acute pulmonary oedema in the obstetric setting %ary widely with rates as high as 0.5+ of alldeli%eries being cited. &n women with se%ere disease9H3::P syndrome (haemolysis ele%ated

li%er en8ymes lowplatelets) acute pulmonary oedema was seen in between 4.*+ and 15+of cases (1415). &n women with eclampsia the reported rates are between 5+ and **+.-cute pulmonary oedema was a contributing cause of death in 17.2+ of women affected byhypertension during pregnancy in a recent outh -frican study.;

1


2/20

CHAPTER II

LITERATUR REVIEW

I. Post Partum Haemorrhage

Postpartum hemorrhage defined as the loss of more than 500 m: of blood after

deli%ery occurs in up to 1; percent of births. 6lood loss eceeding 1000 m: is considered

physiologically significant and can result in hemodynamic instability.1 3%en with appropriate

management approimately * percent of %aginal deli%eries will result in se%ere postpartum

hemorrhage. &t is the most common maternal morbidity in de%eloped countries and a ma$or cause of death worldwide.2 omplications from postpartum hemorrhage include orthostatic

hypotension anemia and fatigue which may ma/e maternal care of the newborn more

difficult. Postpartum anemia increases the ris/ of postpartum depression. 6lood transfusion

may be necessary and carries associated ris/s. &n the most se%ere cases hemorrhagic shoc/

may lead to anterior pituitary ischemia with delay or failure of lactation (i.e. postpartum

pituitary necrosis). ccult myocardial ischemia dilutional coagulopathy and death also may

occur. 'elayed postpartum hemorrhage bleeding after 24 hours as a result of sloughing of the

placental eschar or retained placental fragments also can occur.2*

,is/ factors for postpartum hemorrhage include a prolonged third stage of labor

multiple deli%ery episiotomy fetal macrosomia and history of postpartum hemorrhage. *

Howe%er postpartum hemorrhage also occurs in women with no ris/ factors so physicians

must be prepared to manage this condition at e%ery deli%ery. trategies for minimi8ing the

effects of postpartum hemorrhage include identifying and correcting anemia before deli%ery

being aware of the mother


3/20

seconds has the benefit of increasing iron stores and decreasing anemia which is especially

important in preterm infants and in lowresource settings.1* #he delay has not been shown to

increase neonatal morbidity or maternal blood loss. Prophylactic administration of oytocin

(Pitocin) reduces rates of postpartum hemorrhage by 40 percentA this reduction also occurs if

oytocin is gi%en after placental deli%ery.

151

ytocin is the drug of choice for pre%enting postpartum hemorrhage because it is at least as effecti%e as ergot al/aloids or prostaglandins

and has fewer side effects. "isoprostol (ytotec) has a role in the pre%ention of postpartum

hemorrhage (# B 1;)A this agent has more side effects but is inepensi%e heatand light

stable and re!uires no syringes.1*14

I.I Diagnosis and Management

#he diagnosis of postpartum hemorrhage begins with recognition of ecessi%e

bleeding and methodic eamination to determine its cause. #he C@our #sD mnemonic (#one#rauma #issue and #hrombin) can be used to detect specific causes.15

3


4/20

4


5/20

Tone

Eterine atony is the most common cause of postpartum hemorrhage. 6ecause

hemostasis associated with placental separation depends on myometrial contraction atony is

treated initially by bimanual uterine compression and massage followed by drugs that

promote uterine contraction. Eterine "assage. 6ris/ blood flow after deli%ery of the placenta

should alert the physician to perform a bimanual eamination of the uterus. &f the uterus is

soft massage is performed by placing one hand in the %agina and pushing against the body of

the uterus while the other hand compresses the fundus from abo%e through the abdominal

wall.1

#he posterior aspect of the uterus is massaged with the abdominal hand and the

anterior aspect with the %aginal hand. Eterotonic agents include oytocin ergot al/aloids

and prostaglandins. ytocin stimulates the upper segment of the myometrium to contract

rhythmically which constricts spiral arteries and decreases blood flow through the uterus.

ytocin is an effecti%e firstline treatment for postpartum hemorrhageA 10 international units

(&E) should be in$ected intramuscularly or 20 &E in 1 : of saline may be infused at a rate of

250 m: per hour. -s much as 500 m: can be infused o%er 10 minutes without complications.

"ethylergono%ine ("ethergine) and ergometrine (not a%ailable in the Enited tates) are ergot

al/aloids that cause generali8ed smooth muscle contraction in which the upper and lower

segments of the uterus contract tetanically.171; - typical dose of methylergono%ine 0.2 mg

administered intramuscularly may be repeated as re!uired at inter%als of two to four hours.

6ecause ergot al/aloid agents raise blood pressure they are contraindicated in women with

preclampsia or hypertension.1= ther ad%erse effects include nausea and %omiting.

Prostaglandins enhance uterine contractility and cause %asoconstriction. #he prostaglandinmost commonly used is 15methyl prostaglandin @2a or carboprost (Hemabate). arboprost

can be administered intramyometrially or intramuscularly in a dose of 0.25 mgA this dose can

be repeated e%ery 15 minutes for a total dose of 2 mg. arboprost has been pro%en to control

hemorrhage in up to ;7 percent of patients. &n cases where it is not effecti%e chorioamnionitis

or other ris/ factors for hemorrhage often are present. Hypersensiti%ity is the only absolute

contraindication but carboprost should be used with caution in patients with asthma or

hypertension. ide effects include nausea %omiting diarrhea hypertension headache

flushing and pyreia. "isoprostol is another prostaglandin that increases uterine tone and

decreases postpartum bleeding. "isoprostol is effecti%e in the treatment of postpartumhemorrhage but side effects may limit its use. &t can be administered sublingually orally

%aginally and rectally. 'oses range from 200 to 1000 mcgA the dose recommended by @&

is 1000 mcg administered rectally. Higher pea/ le%els and larger doses are associated with

more side effects including shi%ering pyreia and diarrhea. -lthough misoprostol is widely

used in the treatment of postpartum hemorrhage it is not appro%ed by the E.. @ood and

'rug -dministration for this indication.20

5


6/20

Trauma

:acerations and hematomas resulting from birth trauma can cause significant blood

loss that can be lessened by hemostasis and timely repair. utures should be placed if direct

pressure does not stop the bleeding.21 3pisiotomy increases blood loss and the ris/ of anal

sphincter tears and this procedure should be a%oided unless urgent deli%ery is necessary and

the perineum is thought to be a limiting factor. Hematomas can present as pain or as a change

in %ital signs disproportionate to the amount of blood loss. mall hematomas can be managed

with close obser%ation. Patients with persistent signs of %olume loss despite fluid

replacement as well as those with large or enlarging hematomas re!uire incision and

e%acuation of the clot. #he in%ol%ed area should be irrigated and the bleeding %essels ligated.

&n patients with diffuse oo8ing a layered closure will help to secure hemostasis and eliminatedead space.22

Uterine Inersion

#echni!ue of bimanual massage for uterine atony. 6imanual uterine compression

massage is performed by placing one hand in the %agina and pushing against the body of the

uterus while the other hand compresses the fundus from abo%e through the abdominal wall.

#he posterior aspect of the uterus is massaged with the abdominal hand and the anterior

aspect with the %aginal hand. -cti%e management of the third stage of labor may reduce the

incidence of uterine in%ersion .2* @undal implantation of the placenta may lead to in%ersionA

the roles of fundal pressure and undue cord traction are uncertain. #he in%erted uterus usually

appears as a bluishgray mass protruding from the %agina. Faso%agal effects producing %ital

sign changes disproportionate to the amount of bleeding may be an additional clue. #he

placenta often is still attached and it should be left in place until after reduction. 3%ery

attempt should be made to replace the uterus !uic/ly .24 #he Gohnson method of reduction

begins with grasping the protruding fundus with the palm of the hand and fingers directed

toward the posterior forni. #he uterus is returned to position by lifting it up through the

pel%is and into the abdomen. nce the uterus is re%erted uterotonic agents should be gi%ento promote uterine tone and to pre%ent recurrence. &f initial attempts to replace the uterus fail

6


7/20

or a cer%ical contraction ring de%elops administration of magnesium sulfate terbutaline

(6rethine) nitroglycerin or general anesthesia may allow sufficient uterine relaation for

manipulation. &f these methods fail the uterus will need to be replaced surgically.25

Uterine Ru!ture.

-lthough rare in an unscarred uterus clinically significant uterine rupture occurs in

0. to 0.7 percent of %aginal births after cesarean deli%ery in women with a low trans%erse or

un/nown uterine scar.20 #he ris/ increases significantly with pre%ious classical incisions or

uterine surgeries and to a lesser etent with shorter inter%als between pregnancies or a

history of multiple cesarean deli%eries particularly in women with no pre%ious %aginal

deli%eries. ompared with spontaneous labor induction or augmentation increases the rate of

uterine rupture more so if prostaglandins and oytocin are used se!uentially. Howe%er the

incidence of rupture is still low (i.e. 1 to 2.4 percent). "isoprostol should not be used for

cer%ical ripening or induction when attempting %aginal birth after pre%ious cesarean deli%ery.

6efore deli%ery the primary sign of uterine rupture is fetal bradycardia. 24 #achycardia or late

decelerations can also herald a uterine rupture as can %aginal bleeding abdominal

tenderness maternal tachycardia circulatory collapse or increasing abdominal girth.

ymptomatic uterine rupture re!uires surgical repair of the defect or hysterectomy. hen

detected in the postpartum period a small asymptomatic lower uterine segment defect or

bloodless dehiscence can be followed epectantly.22

Tissue

lassic signs of placental separation include a small gush of blood with lengthening

of the umbilical cord and a slight rise of the uterus in the pel%is. Placental deli%ery can be

achie%ed by use of the 6randt-ndrews maneu%er which in%ol%es applying firm traction on

the umbilical cord with one hand while the other applies suprapubic counterpressure.2 #he

mean time from deli%ery until placental epulsion is eight to nine minutes. :onger inter%alsare associated with an increased ris/ of postpartum hemorrhage with rates doubling after 10

7


8/20

minutes. ,etained placenta (i.e. failure of the placenta to deli%er within *0 minutes after

birth) occurs in less than * percent of %aginal deli%eries. ne management option is to in$ect

the umbilical %ein with 20 m: of a solution of 0.= percent saline and 20 units of oytocin. 27

#his significantly reduces the need for manual remo%al of the placenta compared with

in$ecting saline alone. -lternati%ely physicians may proceed directly to manual remo%al of the placenta using appropriate analgesia. &f the tissue plane between the uterine wall and

placenta cannot be de%eloped through blunt dissection with the edge of the glo%ed hand

in%asi%e placenta should be considered. &n%asi%e placenta can be life threatening. #he

incidence has increased from 0.00* percent to 0.04 percent of deli%eries since 1=50sA this

increase is li/ely a result of the increase in cesarean section rates. lassification is based on

the depth of in%asion and can be easily remembered through alliterationI placenta accreta

adheres to the myometrium placenta increta in%ades the myometrium and placenta percreta

penetrates the myometrium to or beyond the serosa. ,is/ factors include ad%anced maternal

age high parity pre%ious in%asi%e placenta or cesarean deli%ery and placenta pre%ia

(especially in combination with pre%ious cesarean deli%ery increasing to 7 percent with four

or more).2; #he most common treatment for in%asi%e placenta is hysterectomy. Howe%er

conser%ati%e management (i.e. lea%ing the placenta in place or gi%ing wee/ly oral

methotreate until b human chorionic gonadotropin le%els are ) is sometimes successful.

omen treated for a retained placenta must be obser%ed for late se!uelae including infection

and late postpartum bleeding.

Thrombin

oagulation disorders a rare cause of postpartum hemorrhage are unli/ely to respond

to the measures described abo%e.25 "ost coagulopathies are identified before deli%ery

allowing for ad%ance planning to pre%ent postpartum hemorrhage. #hese disorders include

idiopathic thrombocytopenic purpura thrombotic thrombocytopenic purpura %on

illebrand


9/20

preeclampsia amniotic fluid embolism sepsis placental abruption and prolonged retention

of fetal demise. -bruption is associated @igure. 6randt-ndrews maneu%er for cord traction.

@irm traction is applied to the umbilical cord with one hand while the other applies

suprapubic counterpressure. 3cessi%e bleeding can deplete coagulation factors and lead to

consumpti%e coagulation which promotes further bleeding.

27

oagulation defects should besuspected in patients who ha%e not responded to the usual measures to treat postpartum

hemorrhage and in those who are not forming blood clots or are oo8ing from puncture sites.

3%aluation should include a platelet count and measurement of prothrombin time partial

thromboplastin time fibrinogen le%el and fibrin split products (i.e. ddimer).2; "anagement

consists of treating the underlying disease process supporting intra%ascular %olume serially

e%aluating coagulation status and replacing appropriate blood components. -dministration of

recombinant factor F&&a or clotpromoting medications (e.g. traneamic acid >y/lo/apron?)

may be considered.2;

II. Pree"#am!sia Indu"e Post !artum Haemorrhage

Postpartum haemorrhage is a leading cause of maternal morbidity and mortality

worldwide.*1 &dentifying ris/ indicators for postpartum haemorrhage is crucial to predict this

life threatening condition. -nother ma$or contributor to maternal morbidity and mortality is

preeclampsia. Pre%ious studies show conflicting results in the association between

preeclampsia and postpartum haemorrhage.*2

- nationwide cohort was used containing prospecti%ely collected data of women

gi%ing birth after 1= completed wee/s of gestation from Ganuary 2000 until Ganuary 200; (n B1 457 57). 'ata were etracted from the etherlands Perinatal ,egistry co%ering =+ of all

deli%eries in the etherlands. #he main outcome measure postpartum haemorrhage was

defined as blood loss of J1000 ml in the 24 hours following deli%ery. #he association

between preeclampsia and postpartum haemorrhage was in%estigated with uni and

multi%ariable logistic regression analyse.**

omen with P3 were more often older nulliparous had multiple pregnancies a

lower gestational age and a lower socioeconomic status. #hese indicators are also associated

with increased ris/ for PPH which could eplain a slight decrease in ris/ for PPH after

ad$ustment for confounders. >;11K1522*K*=? ,emar/ably noninduced women with P3

who deli%ered %aginally re%ealed an e%en stronger ad$usted association with PPH (ad$usted

, 2.2= =5+ & 2.0 to 2.55). 3cept for women undergoing electi%e caesarean section all

other subgroups showed women with P3 had an increased ris/ for PPH suggesting the

association is independent for onset of labour or mode of deli%ery. #he obser%ed shift in ris/

when assessing the se%erity of P3 could indicate a positi%e sideeffect in the management of

P3A induction possibly reduces the ris/ for PPH in women with se%ere P3. *5

omen with preeclampsia ha%e a 1.5* fold increased ris/ for postpartum

haemorrhage.* linicians should be aware of this and use this /nowledge in the management

of preeclampsia and the third stage of labour in order to reach the fifth "illenium

'e%elopmental oal of reducing maternal mortality ratios with 75+ by 2015.*7

9


10/20

III. A"ute Pu#monar$ Oedema in Pregnant Women

-cute pulmonary oedema in pregnant women is a lifethreatening e%ent. 'espite

impro%ements in the management of congesti%e heart failure in nonpregnant adults itcontinues to cause significant morbidity and mortality in pregnancy.*;

-cute pulmonary oedema is a significant cause of morbidity and mortality in pregnantand recently pregnant women . &t is characterised by suddenonset breathlessness may beaccompanied by agitation and is often the serious clinical manifestation of a %ariety of

pathophysiological processes.*= #he cottish onfidential -udit of e%ere "aternal"orbidity one of the largest maternal morbidity audits reported that acute pulmonaryoedema was the fourth most common form of maternal morbidity.40 &t is also fre!uently thereason for intensi%e care admission and may occur during the antenatal intrapartum or

postpartum periods. 3stimated rates of acute pulmonary oedema in pregnancy %ary from aslow as 0.0;+ to as high as 0.5+ . #he wide ranges reported are due the poor reporting of maternal morbidity and lac/ of minimal reporting datasets of /ey outcomes in pregnancy andthe postpartum period.41

-cute pulmonary oedema may be caused by a %ariety of perturbations of any one of the /ey determinates of cardio%ascular function and fluid flow into the pulmonaryinterstitium. Hydrostatic pressures colloid osmotic pressures and capillary permeabilitydetermine the amount of fluid within the pulmonary interstitium and are described bytarling


11/20

pulmonary circulation can occur both of which can be fatal. - system in balance isrepresented by cardiac output achie%ed at the lowest left %entricular enddiastolic pressurethat meets the metabolic needs of the tissues and that e!uals %enous return. -cute pulmonaryoedema or acute congesti%e cardiac failure represents a system out of balance and unabletomeet the metabolic needs to the tissues which if left untreated leads to death. &t follows

that factors that increase hydrostatic pressure (leading to ele%ated left %entricular enddiastolic pressure) factors that decrease colloid osmotic pressure or factors that increase capillary permeabilitywill predispose a woman to the de%elopment of acute pulmonary oedema. &t isnow recognised that not only is fluid accumulation and retention a mechanism for acute

pulmonary oedema but so too is fluid redistribution from the systemic circulation to the pulmonary circulation due to %enoconstriction or %asoconstriction in a person who iseu%olaemic.44#herapies for the treatment of acute pulmonary oedema re%erse one or more of these factors with reabsorption of pulmonary oedema both a passi%e and an acti%e process.@re!uently more than one ris/ factor is present with iatrogenic fluid administration a ma$or

pre%entable factor. pecific aetiologies causing acute pulmonary oedema ha%e an increasedli/elihood of occurring during specific time periodsA for eample tocolytic therapy in the

antenatal period and fluid o%erload in combination with preeclampsia in thepostpartum period.

ther contributory factors include baroreceptormediated arginine %asopressinrelease leading to fluid accumulation and hyponatremia a situation that occurs in somewomen with preeclampsia. -cute pulmonary oedemaA represents a form of decompensatedacute cardiac failure and is a system out of balance.45 lassifications of acute cardiac failureha%e used the terms diastolic and systolic failure to describe whether the cardiac failureoccurs in the presence of normal or impaired %entricular function respecti%ely. ystoliccardiac failure refers to a failure of ade!uate myocardial contractilit. 'iastolic failure refers toa failure of ade!uate myocardial relaation (lusitropy) usually due to structural changeswithin the myocardium secondary to hypertension (left %entricular hypertrophy). #his leadsto reduced compliance ele%ated enddiastolic pressure and impaired left %entricular filling .#he associated ele%ated pulmonary %enous pressure at rest reduces lung complianceincreases the wor/ of breathing and results in the sub$ecti%e feeling of breathlessness. #hesesymptoms are made worse by eercise.4* ith respect to understanding diastolic cardiacfailure the presence of a preser%ed or normal e$ection fraction does not imply anade!uatecardiac output and the terms e$ection fraction and cardiac output should not be usedsynonymously. ardiac failure with preser%ed e$ection fraction may be associated with acute

pulmonary oedema with hypertension. #he cardiac output in this situation despite an e$ectionfraction within the normal reference range represents a le%el that is inade!uate to meet there!uirements of the metabolising tissues. #here is reduced oygen deli%ery as the presence of

pulmonary oedema limits respiratory gas echange and leads to hypoaemia. @ollowing thisin the more chronic heart failure setting mechanisms are acti%ated to correct this imbalance. 42

#he main response is through the reninangiotensinaldosterone system and thesympathetic ner%ous system which attempt to increase cardiac output through increasingheart rate cardiac contractility fluid redistribution and fluid retention to increase stro/e%olume.4* @urther deterioration may occur leading to cardiac arrest and staff should be

prepared to institute ad%anced life support and consider perimortem caesarean section.#ransthoracic echocardiography can assist in differentiating a low cardiac output from a highcardiac output state as well as eclude other important causes of acute pulmonary oedema.44

3lectrocardiography chest Lray blood pressure oygen saturation heart rate respiratoryrate temperature and fluid balance monitoring should be considered mandatory. Pulmonary

artery catheters for haemodynamic monitoring are rarely re!uired and ha%e significantsideeffects. 'espite the ris/s of aspiration nonin%asi%e %entilation should be tried as the initial

11


12/20

techni!ue before tracheal intubation as it pro%ides increased inspired oygen concentrationdisplaces fluid from the al%eoli into the pulmonary and subse!uently systemic circulationdecreases the wor/ of breathing and decreases the need for tracheal intubation. 45 #he use of nonin%asi%e %entilation also a%oids the complications associated with tracheal intubation in

pregnant or recently pregnant women who are hypertensi%e such as intracerebral

haemorrhage.4*

IV. %LUID MANA&EMENT

12


13/20

@luid management for the patient with pregnancyinduced hypertension (P&H) presents a challenge for the obstetrician. #his is especially true for the subset of patients with preeclampsia.4 #he etiology and pathophysiology of P&H are incompletely understood. -s a

result considerable contro%ersy eists regarding optimal therapy for most aspects of P&H.@luid therapy is no eception. &n general P&H is characteri8ed by a failure to achie%e thenormal pregnancyassociated plasma %olume epansion. :ater in gestation this is combinedwith manifestations of ecess interstitial fluid.47 #he parado of intra%ascular %olumedepletion combined with increased etracellular %olume leads to di%ergent opinions regardingoptimal fluid management. Folume replacement has been ad%ocated by some because of theintra%ascular hypo%olemia whereas others ha%e recommended %olume restriction and e%endiuretics because of the etracellular fluid ecess.4;

e suggest that management plans be tailored to the clinical situation. &nuncomplicated P&H a crystalloid infusion limited to between 75 and 125 m:9hour throughout

the intrapartum and early postpartum period (12 to 24 hours) is appropriate.4=

linicalresolution of the disease will begin in most patients during this time with a bris/ spontaneousdiuresis.50 &n more complicated cases or when other therapeutic inter%entions are plannedthe patientMs intra%ascular %olume status becomes an important management consideration.liguria pulmonary edema antihypertensi%e therapy and regional analgesia or anesthesiaare clinical settings where meticulous fluid management is important. 51

&n the presence of oliguria defined as urine output of less than *0 m:9hour o%er a 2

hour period an initial fluid challenge of 500 to 1000 m: of crystalloid is indicated. &f

ade!uate urine output does not result further therapy should be guided by careful assessment

of oygenation status and if compromised by in%asi%e hemodynamic monitoring.52

omplications such as pulmonary cerebral or laryngeal edema can result from o%er8ealous

%olume infusion. Esing the pulmonary artery catheter in oliguric patients who failed to

respond to an initial fluid challenge lar/ and associates defined three hemodynamic subsets

based on left %entricular function PP and F,.5* #he first group ehibited a relati%e

intra%ascular %olume depletion and responded to further crystalloid infusion. #he

hemodynamic profile of the second group was not one of intra%ascular %olume depletion and

the postulated mechanism for oliguria was selecti%e renal arteriospasm. &mpro%ement in this

group was seen with %asodilator therapy.51 &n this clinical scenario consideration could be

gi%en to lowdose dopamine which causes selecti%e renal artery %asodilation. - single patient

constituted the final group and this case was characteri8ed by intra%ascular fluid o%erloaddecreased left %entricular function and %asospasm. #reatment consisted of fluid restriction

and %asodilator therapy. #his group may alternati%ely benefit from diuretic therapy.52

&n the future the pulse oimeter may ser%e as an alternati%e to in%asi%e hemodynamicmonitoring in some oliguric patients. e are currently comparing changes in oygensaturation measured by pulse oimetry to central hemodynamic parameters obtained with the

pulmonary artery catheter after fluid bolus.54

&n patients re!uiring %olume epansion colloids would seem to be an ideal choiceconsidering the /nown early postpartum decrease in colloid osmotic pressure and the further decrease noted with the use of intrapartum intra%enous fluids. Howe%er Nirshon and

colleagues found no benefit in fetal outcome by using colloids to raise P unless there was

13


14/20

a %ery prolonged negati%e PPP gradient. #hey did note an increased re!uirement for diuretic therapy in the group recei%ing colloids due to an ele%ated PP.50

Pulmonary edema associated with P&H occurs after deli%ery in 70+ to ;0+ of cases.Postpartum mobili8ation of interstitial fluids contributes to the occurrence of pulmonaryedema by increasing PP.51 #he associated increase in hydrostatic pressures decrease in

P and increase in %ascular permeability resulting from endothelial damage all combine toincrease the ris/ of pulmonary edema. "anagement consists of supplemental oygen fluidrestriction diuretics and possibly %asodilators to facilitate afterload reduction. Ese of the

pulmonary artery catheter in etremely complicated cases to aid therapy should beencouraged.52

-ntihypertensi%e agents are often necessary during the peripartum course of P&H.&ntra%ascular hypo%olemia can complicate the use of these medications. &ntrapartum %olumeepansion alone has been reported to decrease peripheral resistance and increase cardiacoutput whereas "-P remains unchanged or e%en decreases. - bolus in$ection of hydrala8ineis commonly used for acute blood pressure control during the intrapartum period. &teffecti%ely lowers "-P and F, while increasing cardiac output but indi%idual patient

responses are !uite %ariable. Folume loading before hydrala8ine therapy may pre%ent anabrupt and precipitous drop in blood pressure.4 #his is particularly important antepartumwhen a significant decrease in blood pressure can lead to decreased uterine perfusion andfetal hypoia. imilar beneficial effects were seen when %olume epansion was performed

before administration of intra%enous nitroglycerin in patients with se%ere P&H. ith pretherapy hydration decreases in PP cardiac inde and oygen deli%ery were pre%ented and the degree of decrease in "-P was reduced.47

#he use of regional analgesia or anesthesia in P&H patients re!uires similar considerations concerning %olume status as those re!uired by antihypertensi%e medications.&n uncomplicated pregnancy the sympathetic bloc/ade causes %asodilation. ithout ade!uaterehydration significant hypotension can occur. #he intra%ascular hypo%olemia present in P&Hcan compound the sympathetic bloc/ resulting in a profound drop in blood pressure. -nassociated decrease in uteroplacental perfusion occurs and fetal wellbeing may be ad%erselyaffected.4; -ttempts to resol%e the hypotension with fluid boluses may lead to o%erhydration

placing the mother at ris/ of de%eloping pulmonary or cerebral edema particularly in the postpartum period. &n the past the potential for these complications had led some to ad%isethe a%oidance of epidural anesthesia in se%ere preeclampsia. #hese same sources ha%e morerecently softened their positions and ha%e suggested that cautious use of epidural anesthesiain se%ere preeclampsia by eperienced operators is appropriate as increasing e%idence of itssafety has been reported. thers emphatically state that when properly used regionalanalgesia or anesthesia is safe and should be considered the method of choice ecept when a

coagulopathy eists.4=

e%eral beneficial fetal and maternal effects of epidural anesthesia ha%e beendemonstrated. &ntra%illous blood flow is impro%ed. "-P can be appropriately reducedwithout a significant change in cardiac inde pulmonary or systemic %ascular resistancecentral %enous pressure or PP. #his may be due in part to a reduction in maternalcatecholamine le%els. &n %aginal deli%eries "oore and colleagues found no difference inmaternal hypotensi%e episodes or neonatal outcome between those recei%ing labor epidural or local anesthesia. &n the same report comparing epidural to general anesthesia for cesareansection patients again there was no significant difference in hypotensi%e episodes but therewas a significantly higher systolic pressure associated with intubation. #here was also greater

blood pressure %ariation.51 eonatal outcome was better in the epidural groupA howe%er

much of this could be attributed to the fetal condition before anesthesia. -ll of these patientswere placed in a leftlateraltilt position to pre%ent aortoca%al compression and 500 to 1000

14


15/20

m: of lactated ,ingerMs solution was administered before epidural placement to reduce theris/ of hypotension.52

@luid management in the pregnant patient with P&H is comple and should be tailored

to the specific clinical situation. areful fluid therapy in which inta/e and output are balanced

is ade!uate for most uncomplicated cases. hen complications arise or therapeutic

inter%entions that lower blood pressure are contemplated %olume epansion may be

desirable. &n particularly difficult cases pulmonary artery catheteri8ation may help guide

fluid therapy.5*

H-P#3, &&&

15


16/20

:E&

1. Postpartum hemorrhage defined as the loss of more than 500 m: of blood after deli%ery

occurs in up to 1; percent of births. 6lood loss eceeding 1000 m: is considered

physiologically significant and can result in hemodynamic instability.1 3%en with

appropriate management approimately * percent of %aginal deli%eries will result in

se%ere postpartum hemorrhage. &t is the most common maternal morbidity in

de%eloped countries and a ma$or cause of death worldwide.2

2. #he diagnosis of postpartum hemorrhage begins with recognition of ecessi%e bleeding and

methodic eamination to determine its cause. #he C@our #sD mnemonic (#one

#rauma #issue and #hrombin) can be used to detect specific causes.15

*. omen with P3 were more often older nulliparous had multiple pregnancies a lower gestational age and a lower socioeconomic status. #hese indicators are also associated

with increased ris/ for PPH.4. -cute pulmonary oedema is a significant cause of morbidity and mortality in pregnant and

recently pregnant women . &t is characterised by suddenonset breathlessness may be

accompanied by agitation and is often the serious clinical manifestation of a %ariety

of pathophysiological processes.5. @luid management in the pregnant patient with P&H is comple and should be tailored to the

specific clinical situation. areful fluid therapy in which inta/e and output are

balanced is ade!uate for most uncomplicated cases. hen complications arise or

therapeutic inter%entions that lower blood pressure are contemplated %olume

epansion may be desirable. &n particularly difficult cases pulmonary artery

catheteri8ation may help guide fluid therapy. Pulmonary edema associated with P&H occurs after deli%ery in 70+ to ;0+ of cases.

Postpartum mobili8ation of interstitial fluids contributes to the occurrence of

pulmonary edema by increasing PP.51 #he associated increase in hydrostatic

pressures decrease in P and increase in %ascular permeability resulting from

endothelial damage all combine to increase the ris/ of pulmonary edema.

"anagement consists of supplemental oygen fluid restriction diuretics and

possibly %asodilators to facilitate afterload reduction. Ese of the pulmonary arterycatheter in etremely complicated cases to aid therapy should be encouraged.5

,3@3,33

16


17/20

1. #he Pre%ention and "anagement of Postpartum HaemorrhageI ,eport of #echnicalor/ing roup ene%a * Guly 1=;=. ene%aI orld Health rgani8ation 1==0.

2. 3lbourne ', Prendi%ille G arroli ood G "c'onald . Prophylactic use of

oytocin in the third stage of labour. ochrane 'atabase yst ,e% 2001A(4)I'001;0;.

*. 6ais G" 3s/es " Pel " 6onsel G 6le/er P. Postpartum haemorrhage innulliparous womenI incidence and ris/ factors in low and highris/ women. - 'utch

populationbased cohort study on standard (O or B 500 m:) and se%ere (O or B 1000m:) postpartum haemorrhage. 3ur G bstet ynecol ,eprod 6iol 2004A115I172.

4. ciscione - &%ester # :argo8a "G" hlossman P olmorgen H. -cute pulmonary oedema in pregnancy. -m G bstet ynecol 200*A101I511K515.

5. east G' Halberstadt "eyer 6- ohen , #horp G-. #he ris/ of pulmonaryoedema and colloid osmotic pressure changes during magnesium sulfate infusion.-m G bstet ynecol 1==*A1=I15K1571.

. otton '6 oni/ 6 pillman # 'orman N@. &ntrapartum to postpartum changes incolloid osmotic pressure. -m G bstet ynecol 1=;4A14=I174K7.

7. 6enedetti # Nates , illiams F. Hemodynamic obser%ations in se%ere preeclampsia complicated by pulmonary oedema. -m G bstet ynecol1=;5A152I**0K4.

;. "athai ". ,e%iewing maternal deaths and complications to ma/e pregnancy andchildbirth safer. ,egion Heath @orum 2005A=I27K=.

=. "agann 3@ 3%ans hauhan P :anneau @is/ -' "orrison G. #he length of the third stage of labor and the ris/ of postpartum hemorrhage. bstet ynecol005A105I2=0.

10. orwin 3G "urrayNolb :3 6eard G:. :ow hemoglobin le%el is a ris/ factor for Postpartum depression. G utr 200*A1**I41*=42.

11. 3/eroma -G -nsari - tirrat ". 6lood transfusion in obstetrics and gynaecology.6r G bstet ynaecol 1==7A104I27;;4.

12. "aternal and perinatal outcome in %arying degrees of anemia. &nt G ynaecol bstet2002A7=I=*100.

1*. ingla -N :apins/i ,H 6er/owit8 ,: aphier G. -re women who are Geho%ah


18/20

1=. haparro " eufeld :" #ena -la%e8 3guia:i8 edillo , 'ewey N. 3ffectof timing of umbilical cord clamping on iron status in "eicaninfantsI a randomisedcontrolled trial. :ancet 200A*7I1==72004.

20. ,abe H ,eynolds 'ia8,ossello G. 3arly %ersus delayed umbilical cord clampingin preterm infants. ochrane 'atabase yst ,e% 2004(4)I '00*24;.

21. Fan ,heenen P 6rabin 6G. :ate umbilical cordclamping as an inter%ention for reducing iron deficiency anaemia in term infants in de%eloping and industrialisedcountriesI a systematic re%iew. -nn #rop Paediatri 2004A24I*1.

22. ordstrom : @ogelstam N @ridman :arsson - ,ydhstroem H.,outine oytocinin the third stage of labourI a placebo controlled randomised trial. 6r G bstetynaecol 1==7A104I7;1.

2*. "c'onald -bbott G" Higgins P. Prophylactic ergometrineoytocin %ersusoytocin for the third stage of labour. ochrane 'atabase yst ,e% 2004A(1)I'000201.

24. ulme8oglu -" @orna @ Fillar G Hofmeyr G. Prostaglandins for pre%ention of postpartum haemorrhage. ochrane 'atabase yst ,e% 2004A(1)I'0004=4.

25. 'erman ,G Nod/any 6 oudar eller 3 ai/ F 6ellad "6 et al. ralmisoprostol in pre%enting postpartum haemorrhage in resourcepoor communitiesI arandomised controlled trial. :ancet 200A*;I124;5*.

2. -nderson G 3tches ' mith '. Postpartum hemorrhage. &nI 6aley 3. -d%anced:ife upport in bstetrics course syllabus. 4th ed. :eawoodNan.I -merican-cademy of @amily Physicians 2001.

27. 6lan/s -" #hornton . #he role of oytocin in parturition. 6G 200*A110(suppl20)I451.

2;. oriano ' 'ulit8/i " chiff 3 6ar/ai "ashiach eidman '. - prospecti%ecohort study of oytocin plus ergometrine compared withoytocin alone for

pre%ention of postpartum haemorrhage. 6r G bstet ynaecol 1==A10*I10;7*.2=. 'e osta . t -nthonydoi?.

*2. Nhan N o$dyla ' ay : ulme8oglu -" Fan :oo/ P@ (200) H analysis

of causes of maternal deathI a systematic re%iew. :ancet *7I 10K 1074. 01407*(0);*=7= >pii?A10.101901407*(0);*=7= >doi?.**. orld Health rgani8ation (200=) H guidelines for the management of

postpartum haemorrhage and retained placenta. ene%aI H Press. -%ailableIhttpI99apps.who.int9rhl9guidelines9postpartumShaemorrhage9en9 . -ccessed 'ecember 12th 2012.

*4. , (2011) Pre%ention and management of postpartum haemorrhage (reentop52). :ondonI ,. -%ailableI httpI99www.rcog.org.u/9files9rcogcorp9#52PostpartumHaemorrhage0411.pdf. -ccessed 'ecember 12th 2012.

*5. tafford & 'ildy - lar/ : 6elfort "- (200;) Fisually estimated andcalculated blood loss in %aginal and cesarean deli%ery. -m G bstet ynecol 1==I

51=K7. 0002=*7;(0;)005012 >pii?A10.1019$.a$og.200;.04.04= >doi?.

18

http://apps.who.int/rhl/guidelines/postpartum_haemorrhage/en/http://www.rcog.org.uk/files/rcog-corp/GT52PostpartumHaemorrhage0411.pdf.%20Accessed%20December%2012th%202012http://www.rcog.org.uk/files/rcog-corp/GT52PostpartumHaemorrhage0411.pdf.%20Accessed%20December%2012th%202012http://www.rcog.org.uk/files/rcog-corp/GT52PostpartumHaemorrhage0411.pdf.%20Accessed%20December%2012th%202012http://www.rcog.org.uk/files/rcog-corp/GT52PostpartumHaemorrhage0411.pdf.%20Accessed%20December%2012th%202012http://apps.who.int/rhl/guidelines/postpartum_haemorrhage/en/


19/20

*. Nnight " allaghan " 6erg -leander 6ou%ierolle "H et al.(200=)#rends in postpartum hemorrhage in high resource countriesI a re%iew andrecommendations from the &nternational Postpartum Hemorrhage ollaborati%eroup. 6" Pregnancy hildbirth =I 55. 14712*=*=55>pii?A10.11;914712*=*=55 >doi?.

*7. 'oran G,


20/20

4;. ,oberts G" #aylor , "usci #G et alI PreeclampsiaI -n endothelial cell disorder.-m G bstet ynecol 11I 1200 1=;=

4=. asserstrum I &ssues in fluid management during laborI "aternal plasma %olumestatus and %olume loading. lin bstet ynecol *5I 514 1==2

50. Pearson G@I @luid balance in se%ere preeclampsia. 6r G Hosp "ed 4;I 47 1==251. attinoni : 6ra88i : Pelosi P et alI - trial of goaloriented hemodynamic therapy

in critically ill patients. 3ngl G "ed ***I 1025 1==552. :undbert 'I Practice parameter for the use of freshfro8en plasma cryoprecipitate

and platelets. G-"- 271I 777 1==453.Hebert P ells "arshall G et alI #ransfusion re!uirements in critical care.

G-"- 27*I 14*= 1==5

20

MANAGEMENT OF POST PARTUM HAEMORRHAGE(1).doc

Documents

Transcript of MANAGEMENT OF POST PARTUM HAEMORRHAGE(1).doc