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 1",IIN 1) hi 111 , 1, 1111 111 II /
MBBS and Beyond
Emergency obstetric care

© Dr. (Mrs) TRN Fernando

'J I II
 MBBS and Beyond
Emergency obstetric care

Second Edition

Dr (Mrs) TRN Fernando, M BBs, Ms (o&GJ

Consultant o bst et rician and gynaecologist,
~~
~~-
 Table of Contents
page

01. Management of primary post partum

haemorrhage {PPH) 01

02. Management of Secondary PPH 26

03. Management of Antepartum haemorrhage {APH) 31

04. Pre eclampsia, severe pre eclampsia and eclampsia 35

05. Management of umbilical cord prolapse 64

06. Management of shoulder dystocia 71

07. Management of heart disease in pregnancy 79

08. Management of maternal collapse 92

09. Ectopic pregnancy 102

10. Early pregnancy bleeding problems (Miscarriage) 114

01. Primary Post Partum Haemorrhage {PPH)

Intended learning outcomes:

1. Define primary PPH.

2. Recognise PPH as the leading cause of direct maternal deaths in

Sri Lanka.

3. Understand the causes of primary PPH and the underlying patho-

physiology of haemorrhage.

4. Describe the risk factors for PPH.

5. Discuss how to minimise/prevent the primary PPH.

6. Describe the diagnosis and management of primary PPH

7. Understand the principles of task prioritisation, communication,

resuscitation, monitoring, investigations and arresting of
bleeding.

8. A student should be able to arrive at a differential d iagnosis and

outline a management plan for a given case scenario.

Definition

WHO definition of primary PPH is the loss of 500 ml or more of

blood from the genital tract within 24hours of the birth of a ba by.
In anaemic mothers a lower level of blood loss should be the cut off
point for therapeutic interventions.

PPH can be minor (500-1000 ml) or major (more than 1000 ml).
Major could be further divided to moderate (1000-2000 ml), severe
(more than 2000 ml) or massive (mo re than 2500ml).

1
Primary PPH as a cause of maternal deaths in Sri Lanka
Primary PPH is the most common form of major obstetric
haemorrhage. Obstetric haemorrhage remains one of the major
causes of maternal death in both developed and developing
countries. In Sri Lanka, primary PPH was the leading cause of
maternal morbidity and mortality for many decades. 1996 maternal
death review states that there were 61 deaths due to PPH {26% of
maternal deaths were due to direct obstetric causes). PPH accounts
for nearly 25% of maternal deaths during 2000 -2004. However it is
commendable that since 2013 and 2014 number of maternal deaths
due to PPH had markedly reduced in Sri Lanka. PPH is no longer
the leading cause of maternal death but this remains the leading
cause of direct maternal deaths and severe maternal morbidity in
Sri Lanka.
The majority of maternal deaths due to haemorrhage must be
considered preventable. There is substantial evidence of substandard
care in the majority of fatal cases. PPH must be considered as a
priority topic in undergraduate and postgraduate curriculum in Sri
Lanka.
Patho-physiology
• Calculation of blood volume depends on the body weight .
• Approximate blood volume equals weight in kilograms divided
by 12 expressed as liters. [Kg(BW}/12=BV (L)]
• Allowing for the physiological increase in pregnancy, total blood
volume at term is approximately 100 ml/kg (an average 60kg
woman the total blood volume of 6000ml}.
• A blood loss of more than 40% of total blood volume ("'2400 ml)
is generally regarded as 'life threatening'.
2
When estimating the percentage of blood loss, consideration should
be given to body weight and the original haemoglobin level. Low
antenatal haemoglobin (<11 g/dl) should be investigated and treated
appropriately to optimise haemoglobin level before delivery.
Iron is an essential co-factor for enzyme activity at the cellular
level. There is also some evidence that iron deficiency anaemia can
contribute to uterine atony becau se of depleted uterine myoglobin
levels necessary for uterine smooth muscle action.
The "proactive" physiological changes in pregnancy that arrests
bleeding soon after delivery of the placenta are:
1. Structural mechanism of the interlacing myometrial smooth
muscle fiber's contraction and retraction leading to mechanical
occlusion of spiral arterioles. This mechanism is called the 'living
ligatures'.
2. Hyper-coagulable state (fibrinogen doubles, reduction in anti
thrombin Ill activity}.
Clinicians and hea lth care workers must be aware of risk factors for
primary PPH and should take these into account when counseling
women about place of delivery, essential for the safety of both the
mother and the baby. However, most cases of primary PPH have no
identifiable risk factors ante-natally.
Risk factors:
There are abnormalities of underlying patho-physiology of 4 basic
processes in all causes of primary PPH. This can be remembered as
4 Ts.
3
Four T's:- Table 2:
Risk factors that becomes apparent during labour and delivery
1. Tone - uterine atony/inertia.

2. Trauma - to the reproductive organs during delivery. (uterine/

Risk factor Four T's
ce rvical/vaginal tears)
Delivery by emergency Trauma
3. Tissue - retained placental tissue.
caesarean Section
4. Thrombin - coagulation disturbance.
De livery by elective caesa rean section Trauma

The common underlying causes for PPH identified in maternal death Induction of labour Tone/Th rombi n
reviews in Sri Lanka were uterine atony and retained placenta.
Retained placenta Tissue
Table 1:
Media-lateral episiotomy Trauma
Risk factors that are associated with high-moderate risk of PPH
Operative vaginal delivery Tra uma

Prolonged labour (> 12 hours) To ne

Risk factor Four T's
Big baby (> 3.5 kg) Tone/Trauma
Placental abruption Thrombin
Pyrexia in la bou r Throm bin
Pre-eclampsia Thrombin
Age (> 40 years) Tone
Multiple pregnancy Tone

Placenta praevia Ton e Prevention of primary PPH

Previous PPH Tone • Active management of the third stage of labour lowers maternal
blood loss, reduces the risk of primary PPH by about 60% and
Asian ethnicity Tone shortens the third stage.

Obesity (BMI >35) Tone • Prophylactic oxytocin should be offered routinely in t he active
management of the third stage of labour in all w ome n (WHO)
Anaemia (<9 g/dl) Tone
• For women wit hout risk factors for primary PPH, delivering
vaginally, oxytocin 5 iu or 10 iu by intramuscular inj ection is the
agent of choice for the third stage of labou r.
4 5
• Fo r women delivering by caesarean section, oxytocin 5 iu by
slow intravenous injection should be used in the 3 rd stage.
• Intramuscular syntometrine (ergometrine SOOµg + Syntocinon
Siu) may be used in th e absence of hypertension in women with
high - moderate risk for PPH as it reduces the risk of minor PPH
(500-1000 ml) but increases vomiting and hypertension.
• Misoprostol is not as effective as oxytocin/ergometrine but it
may be used when oxytocin is unavailable, such as the home-
birth setting (800µg per rectal/vaginal).
• All women who have had a previous caesarean section must have
their placental site determined by ultrasound after 34 weeks of
gestation. Where facilities exist, magnetic resonance imaging
(MRI) may be a useful tool and assist in determining whether an
anterior placenta previa is accreta or percreta.
• Women with placenta accreta/percreta are at very high risk of
major primary PPH. If placenta accreta or percreta is diagnosed
antenatal, there should be consultant-led multidisciplina ry
planning for delivery. As blood flow of the placenta at term is -
500-800ml/minute, a woman with a morbidly adhered placenta
can collapse within 5-10 minutes, in the 3rd stage.
• Consultant obstetrician and anaesthetist should be present ,
prompt availability of blood, fresh frozen pl as ma and platelets
must be confirm ed and the timing and location for delivery
chose n to facilitate consultant prese nce and access to intensive
care .
• Ava il able evidence on prophylactic balloon occlusion or
embolization of pelvic arteries in the management of PPH is
inconcl usive. The outcomes of prophylactic arterial occlusion
require further evaluation.
6 7
Active management of 3rd stage includes:
1. The use of utero-tonics (oxyt ocin)
2. controlled traction of the cord for the delivery of the placenta
• Active management is also associated with an increased
incidence of nausea, vomiting and raised blood pressure,
especially after the use of ergometrine.
Ergometrine + oxytocin (Syntometrine) or oxytocin 5 iu and
•
oxytocin 10 iu alone, have similar efficacy in prevention of
prim ary PPH in excess of 1000ml.
Misoprostol (800µg orally or per vaginally) is not as
•
effective when compared with oxytoci n10iu intravenously
in preventing PPH; it also carries increased adverse effects,
which are dose related.
However, in situation s where oxytocin is unavailable or birth
•
attendants facilities are limited (a home birth) misoprostol
can be used as an alternative to oxytocin. Misoprostol 800µg
per rectally or vaginally can be used as an alternative for oral
route.
• Oxytoci n s iu by slow intravenous injection for prophylaxis in
the context of caesarean delivery. A longer-acting oxytoci n
derivative, carbetocin, a single dose (lOOµg) is as effective
as oxytocin by infusion. Carbetocin is licensed in the UK
specifically for the indication of prevention of PPH in t he
context of caesarean delivery.
 M anagement of primary PPH Tab le 3:
M anage ment involves mainly three components, all of which must Estimation of blood loss (EBL) pi ctora l guide
be undertaken simultaneously and delegate the work among t he
obstetric team appropriately. Pictoral guide EBL

Re member 3 Rs: Fully soaked sanitary t ow el

1. Recognise
100m l
2. Resuscitate

3. Arrest the bleeding

500m l
It is important to be aware that minor PPH can easily progress to
major PPH without being recognized in the immediate post pa rtum
period.

How to recognize primary PPH? 1500m l

• Systolic BP drops $90 mmHg

• Pulse rate rise~ 100/minute 2000m l

• Uterine size rises with intrauterine blood clot formation

• Visual estimation ofthe blood loss (table 3)

Modified Early Warning System (MEWS chart), Shock Index:

The management given in this book is a guide for a woman being 30% blood loss = moderat e shock (Rule of 30)
cared for in a consultant-led maternity unit with access to laboratory
and blood bank facilities and with skilled obstetric and anaesthetic 1. Pulse increase >30 bpm
staff readily available.
2. RR >30/ min
However the basic principles of initial management can be done
3. SBP drop by 30 m m Hg
at any hospital or by any practicing clinician, in view of minimizing
maternal morbidity and mortality. 4. UOP < 30 ml/ hour

5. PCV d rop > 30%

8 9
The new national partogram introduced in 2015 has a component
fo r monitoring the 3rd stage of labour with the above mentioned
fi rst four parameters. These early warning charts help recognize
the PPH early and enable early interventions to prevent maternal
morbidity.

Basic measures for minor PPH (blood loss 500-1000 ml, no clinical
shock):

• Inform the on call house officer/ senior house officer.

• Check with the blood bank for availability of blood .

• Communicate with the emergency theatre and keep the on call
anaesthetists informed.
• Take blood for the basic investigations (*FBC, RFT, LFT, clotting
profile, cross match)
Figurel.1: Probability of survival against time to initiate resuscitation.
Full protocol for major PPH (blood loss more than 1000 ml and
continuing to bleed)
1. Communication:

• Continue monitoring (assess blood loss, pulse, *BP, UOP, O2
saturation)
• The "Golden Hour" is the time in which resuscitation must begin
to achieve maximum survival - with the arrest of bleeding. As
more time elapses between the point of severe shock and the
start of resuscitation, the likelihood of survival of the patient
decreases.
*FBC=full blood count, RFT= renal function tests, LFT=liver function
tests, BP=blood pressure, UOP=urine output, PCV= pack cell
volume, SBP = systolic blood pressure
• Call experienced midwife, nurse in charge
• Call obstetric SHO/ Registra r and alert consultant.
• Call anaesthetic middle grade and alert consultant.
• Alert consultant clinical haematologist on call.
• Alert blood t ransfusion laboratory.
• Ca ll porters for delivery of specimens/blood.
It is vital that junior obstetricians and anaesthetists do not pe rceive
the calling of se nior colleagues as involving 'loss of face'.
Senior staff must be receptive to concerns expressed by juniors.
Communication with the patient and family is important and clear
inform ation of what is happening should be given, as thi s is a very
frightening event.

10 11
 2. Resuscitation:
• Establish two 14/16-gauge intravenous 2 lines; 20 ml blood
sample should be taken and sent for diagnostic tests, including
full blood count, coagulation screen, urea and electrolytes and
cross match (4 units of blood).
• Commence crystalloid infusion (0.9% NaCl /Hartmann's solution).
• Continue monitoring until bleeding settles.
• Consider oxytocin or ergometrine if suspect uterine atony.
• Empty bladder.
• Fundal massage.
• Bimanual compression of the uterus.
The urgency and measures undertaken to resuscitate and arrest
haemorrhage need to be tailored to the degree of shock. Delegating
work in a team by a team leader is essential. Always remember the
"golden hour".
Immediate measures for major PPH (blood loss > 1000 ml and
continuing to bleed):
• Evaluate circulation (BP, Pulse, UOP, capillary filling)
• Oxygen by mask at 10-15 litres/minute.
• Intravenous access (14/16-gauge 2, cannula, orange/grey
cannulas).
• Position flat.
• Keep the woman warm.
• Transfuse warm blood as soon as possible.
12
• Until blood is available, infuse up to 3.5 liters of crystalloid
I lartmann's solution (2 litres) and/or colloid (1-2 liters) as rapidly
[lS required.
• Find the cause for PPH and arrest the bleeding.
Huid therapy and blood products transfusion:-
• Crystalloid up to 2 liters (Hartmann's solution)
• Colloid up to 1-2 liters until blood arrives.
• If blood is cross matched start blood transfusion immediately
(special blood filters should not be used, as they slow infusions)
• If cross-matched blood is yet unavailable, give uncrossed
matched group-specific blood or give 'O Rh D negative' blood.
• Fresh frozen plasma (FFP)l units for every 2 units of red cells
should be given initially until investigations are available
• If prothrombin time : activated partial thromboplastin time> 1.5,
give FFP 15-20ml/Kg
• Platelets concentrates if PLT count < 50 x 109/1
• Cryoprecipitate (12- 15 ml/kg, total ll) if fibrinogen <2 g/1.
(fibrinogen <2 g/1 in pregnancy and postpartum, non pregnant
<lg/I)
Recombinant factor Vila therapy is not recommended unless as a
pa rt of clinical trial. However this is widely used "offiabel" in PPH.
Recommended dose 90-120 µg/kg, can be repeated after 2 hrs. There
is an increase risk of thromboembolism . Apply clinical judgment on
each situation, before using.
The cornerstones of resuscitation during PPH are restoration of
both blood volume and oxygen-carrying capacity of the red blood
cells.
13
Volum e replacement must be undertaken on the basis that blood
loss is often grossly under estimated. Compatible blood (supplied in
th e form of red cell concentrate) is the best fluid to replace major
blood loss and shou ld be transfused as soon as available.
Main therapeutic goals of management of massive blood loss are
to maintain:
• Haemoglobin> 8g/dl
• platelet count >50 x 109/1
• prothrombin time< 1.5 x mean control
• activated prothrombin times < 1.5 x mean control
• fibrinogen > 2 g/1.
What fluids can be used for volume replacement?
• The nature of fluid infused is of less importance than rapid
administration . Rapid volume replacement until cross-matched
blood is available should be initiated promptly.
• A total volume of 3.5 liters of clear fluids (up to 2L of crystalloids
and 1.5Lof colloid until blood is available) should be the maximu m
that infused while awaiting compatible blood . Maintai ning t he
circulation alone with fluids other than blood for more tha n 30-
45 minutes in a massive PPH may reduce the oxygen carrying
capacity to vital organs.
• Fully cross-matched blood should be available by the tim e that
3.5L of clear fluid have been infused. If full cross-matched blood
is unavailable the best available alternative should be given to
restore oxygen-carrying capacity. Group O RhD-negative blood
may be the safest way to avoid a mismatched transfusion in an
acute emergency.
14
• When the blood loss reaches about 80% of blood volu me, there
will be cl otting factor defects and blood components should
be given. Up to l l of fresh frozen pla sma (FFP) and lOunits of
cryoprecipitate (two packs) may be given empirically in t he f~ ce
of relentless bleeding, wh il e awaiting t he results of coagulation
st udies.
• Documentation of fluid balance, bl oo d, blood products and
procedures is vital in an emergency. Fluid replacement and t he
use of blood and blood produ cts should be st rictly monitored
and the amount given should be dictated by t he lead clin ici an
(consultant anaesthetist, haematologist s or consu ltant
obstetrician).
• The presence of a ce ntral lin e not only provides a means of
accurate central venous pressure (CVP) monitoring but also
a route for rapid fluid replacement. 'Central ve nous and
direct arterial pressure monit oring should be used w hen the
cardiovascular system is compromised by haemorrhage.
• The need to continually re-eva luate the woman's physiological
condition, even when bleeding appears to have stopped, is
essential to recogni se continuing bleeding.
3. Arresting the bleeding:
Identify the underlying cause for PPH
• Tone (abnormalities of uterine co ntraction)
• Tissue (retained products of conception)
• Trauma (of th e genital tract)
• Thrombin (abnormalities of coagulation) .
The most common c~use of primary PPH is ut erine atony.
15
 ~rowded~eti.r, clinl ical examination must be under taken to exclude other • Carboprost (PGF 2} 0.25 mg by intramuscular injection repeated
a ' ona causes such as:-
at intervals of not less than 15minutes to a maximum of 8 doses
1. Retained products (placenta, membranes, clots) (contraindicated in women with asthma).
2. Vaginal/cervical lacerations or haematoma • Direct intra-myometrial injection of carboprost (PGF 2) 0.5 mg (at
3. Ruptured uterus caesarean or laparotomy), with responsibility of the administering
clinician as it is not recommended for intra-myometrial use.
4. Broad ligament haematoma
• Misoprostol 800-1000 µg rectally.
5. Extra genital bleeding (for example, sub-capsular liver rupture)
6. Uterine inversion
Simple mechanical strategies that can be used for primary PPH
7. Clotting disorder
rhe simple mechanical and physiological measures of:
• emptying the bladder,
Management of uterine atony: • 'uterine fundal massage'

:,~en .uterine atony is perceived to be a cause of the bleeding the • bimanual uterine compression
. o. ~w,ng ~echanical and pharmacological measures should The above basic measures would stimulate uterine contractions and
rnrtiated without delay until the bleeding stops: be
represent time-honoured first line management of primary PPH.
• Bi.manual uterine compression (rubbing up the fundus) to
stimulate contractions.
Balloon temponade
• bE~sure bladder is empty (Foley catheter, /eave in place) prior to • Intrauterine balloon temponade is an appropriate first line
,manual compression .
'surgical' intervention for most women where uterine atony is
• Sftyntocino~ 5 units by slow intravenous injection (repeat dose the only or main cause of haemorrhage.
a er 10 minutes).
• A procedure in which a balloon is inflated within the uterine
• Ergometrine o s mg b I . cavity to apply pressure on bleeding blood vessels, compresses
· · · ·. . Y sow intravenous or intramuscular
'~Jection (contrarndrcated in women with hypertension h the vessels, and stops the bleeding. Hydrostatic balloon is
disease). or eart inflated with 300-500ml water/saline.

• Syntocinon infusion (40 units in SOO ml Hart ' I . • Temponade using various types of hydrostatic balloon catheter
125 ml/h ) l mann s so ution at has superseded uterine packing for control of atonic PPH. Case
our un ess fluid restriction is necessary.
series have used a Foley catheter, Bakri balloon, Sengstaken-
• :rane.xemic acid lg slow intravenous bolus Blakemore oesophageal catheter and a condom catheter.
f followed by lg
rn us,on over 8 hours. (BSCH guidelines 2014)
16
17
 • In ~ost cases, 4 - 6hours of temponade should be adequate to
ach 1~ve haemostasis and, ideally, it should be removed during
daytime hours,_ in the presence of appropriate senior staff,
should further intervention be necessary. Before its complete
removal, the balloon could be deflated but left in place to ens
that bleeding does not recur. When no further bleeding rem~::
completely.
• Once the bleeding has been controlled and initial resu scitation
~as b~en completed, continuous close observations in either
~ntens1~e care unit or high -dependency unit on the labour ward
1s required.
• !f ?all_oon temponade fails to stop the bleeding then laparotomy
1s rnd1cated.
• When pharmacological and mechanical measures fail to control
the haemor h · ··
r age, initiate surgical measures sooner rather than
later.
• The following conservative surgical interventions may be
attem~ted, depending on clinical circumstances and available
expertise.
Conservative surgical interventions
• Haemostatic brace suturing· B-Lynch or mod1'fied .
· compression
sutures (pages 20 and 21).
• Bilateral ligation of uterine arteries
• Bilateral ligation of internal iliac arteries
• ~elective arterial embolization (may not be possi ble to arrange
1n an emergency setting).
18
If bleeding occurs at the time of caesarean section, intra -myometrial
injectio n of 0.25mg of carboprost should be used. If laparotomy
is undertaken following failure of pharmacological management,
intra-myometria l carboprost injection should be the fi rst-line
meas ure once the uterus is exposed. (carboprost at present is
unavailable in Sri Lankan government hospit als)
It is recommended that a laminated diagram of the brace technique
be kept in obstetric theatres.
Minor surgical techniques like 'temponade' and 'B-Lynch sutures'
may give immediate arrest of bleeding and faci litate an early
decision, regarding the need for hysterectomy.
Surgical treatment to arrest the bleeding:
Subtotal hysterectomy is the operation of choice in many insta nces
of PPH requiring hysterectomy.
Early recourse to hysterectomy is recommended, especially where
bleeding is associated with placenta accreta or uterine rupture. A
second consultant clinician should be involved in the decision for
hysterectomy (recommendation by RCOG).
The judgment of a senior clinician, taking into account the individual
woman's future reproductive aspirations, is required in deciding the
appropriate sequence of interventions.
ROTEM (Rotational Thrombo-elastrometry)
This is a ve ry useful test now available in many teach ing hospita l
haematology laboratories. This gives a quick result of the blood clot
formation an d fibrinolysis. This has a simple principle of an oscillating
axis inside a cuvette. Resistance to oscillation is measured in mm
plotted against time. Maximum resistance with high est amplitude
the clot is formed and is firm.
19
 100

I
if.
E
ao
60
40
E 20
.!:
0
~ Figure 1.3:
( posterior side of t he
~ uterus w ith 8-Lynch
sutures.
0 10 20 30 40 50 . 60
Time In mln

Figure:1.1- Rotem normal

CT- time for blood to start clotting

CFT/a _an~le . - clot formation time. The a angle will give a

Figure 1.4:
good m_d1cation of platelet function, fibrinogen activity and anterior side of uterus
~oa_gulation factors. A shortening of CFT (or a high a angle) after completion of
indicate hypercoagulability.A prolonged CFT (or a lower a angle) is B-Lynch sutu re.
usually caused by poor platelet function, low platelet count fibrin
polymerization disorders or fibrinogen deficiency. '
Retained placenta
• Placenta can be retained in whole or in parts.

• Placenta is considered retained if undelivered after 30 minutesrd

of actively managed 3rd stage or 60 minutes of physiological 3
stage.
• Retained placenta may not always follow haemorrhage but
MEWS chart should be maintained with monitoring Pulse and
BP every 10 minutes.
• When placenta is partially separated physiological mechanisms
fail to prevent haemorrhage from the placental site.
Figurel.2:
• A retained placenta in a previous uterine scar m ust be treated
Anterior aspect of
with caution as placenta could be morbidly adhe red to the
the uterus of B- lynch
sutures (brace suture). previous scar.
21
20
 However NICE guideline on intra-partum care (2014), 1.14.22
Causes for retained placenta: recommends: Do not use umbilical vein agents if the placenta is

1. Full bladder retained.

• Start resuscitation with crystalloids, colloids and th en with blood
2. Poor management of the 3rd stage (active or physiological)
and blood products as management of primary post partum
3. Snapped cord haemorrhage. Then attempt MROP.
4. Morbidly/ abnormally adhered placenta (placenta accrete)
Manual removal of placenta(MROP) principals of management:
5. Uterine abnormality
1. Strictly steri le conditions
6. Constriction ring formation of the cervix
2. Adequate anaesthesia
Management: 3. Informed consent
• If no significant bleeding and . 4. Done by an trained birth attendant
stable following active m woman is haemodynamically
anagement of 3rd stag .
45- 60 minutes with cIose monitoring
. . e wait 5. Best performed in an operating theater (OT)
The pi t up to
spontaneously separate given few more e~tra minu:ectn a may
6. Antibiotic prophylaxis
• Start breast feeding to stimulate the release of oxytocin.

• Empty the bladder Procedure of manual removal

SHO/senior doctor.' mas sage t he f undus and alert the on call (best understood by observing a video presentation)
• After getting the informed consent observe strict st erility. Scrub
• Intravenous access .
and sterile gowns and glows should be used.
• If bleeding and vital parameters wo . . .
withtwo 14/16 . rsenmg imm ediate IV access • Preferably performed under anaesthesia, in an operating t heater.
-gauge intravenous 2 lines· 20 ml blo d I
should be taken and s t f d. , o samp e
above (page 10). en or ,agnostic tests as mentioned • Empty the bladder.
• Keep one hand over the abdomen and continue to stabilize the
• Intravenous oxytocin 10 iu stat d . uterine fundus.
intravenous infusion of ox t . . o~e continued with an
125ml/hr. y ocm 401u m 500ml normal saline • Then gently introduce the other hand into the vagina following
the umbilical cord in to the uterine cavity via the open cervical
• Intra umbilical vein injectio .
20ml as closer to the vulva n ~an ~e used with oxytocin 20 iu in os.
w en intravenous access is delayed.
23
22
 • Follow the umbilical cord and find its insertion to the placenta.
From there approach the edge of the placenta and the placental
uterine interphase.
• Keep your fingers Curved together and the cleavage movement
towards the uterine cavity. This movement will minimize uterine
perforation and retained placental parts.
• When the whole surface of the placenta is separated withdraw
the hand with the placenta in hand. Check the placental surfaces
to reassure that the whole placenta is removed.
• At low resource setting when anaesthesia and operating theater
is unavailable MROP has to be performed in the delivery room
place. Using IV Pethidine, Morphine or Ketamine as analgesics,
under sterile condition.
• Prophylactic antibiotics can be given in above settings to prevent
sepsis.
Figurel.5:
MROP; note
the fundal
stabilization and
scoop movement
of hand in
uterus.
24
omplications of retained placenta and MROP:
1.. PPH
2. Haemorrhagic shock
3. Infection
4. Uterine perforation and its consequences
5. Uteri ne inversion
6. Retained placenta or membrane parts
It is very important to detect any complication follo~i.ng. MROP
immediately and take appropriate measures to mm1m1ze t he
morbidity and mortality.
Uterine perforation can lead to internal haemorrhage and i~ter~~I
organ damage. W hen bowel is perforated it can lead to perit onitis
and septicaemia .
It is in the best interest that an ultrasound scan be pe rformed before
the woma n is send home to exclude any retained placental parts
after MROP.
References:
01. UNICEF. Guidelines for monitoring the availa bil ity and use of
obstetric services. UNICEF; 199 7 ,
02. Prevention and management of postpartum haemorrhage.
RCOG Green-top Guideline No.52. May 2oo 9
03. S Paterson-Brown. Obstetric emergencies. Dewhurt's text
book of obstetrics and gynaecology. 7th edition. Chapte r 18.
Pages 149-152.
25
02. Secondary PPH ~ After evacuation if the bleeding continues apply balloon
temponade.
Definition
• Last resort to settle the bleeding is open laparotomy ligation of
Secondary PPH is defined as vaginal bleeding between 48 hours and internal iliac arteries, B-Lynch sutures or hysterectomy.
6 weeks after delivery. In developed countries the incidence is about • There are no randomized control trials to compare the most
2%, this may be higher for low resourced settings.
effective management option in secondary PPH. Therefor~ a
senio r consult ant should make the decision on the best option
Causes of treatment according to the severity of the haemorrh age.

1. Retained parts of placenta • If genital tract tear identifi ed it shou ld be repaired under
anesthesia and good light.
2. Endometritis

3. Necrosis of cervix or vaginal wall due to obstructed prolonged What measures can be taken to ensure optimal management of
labour
PPH?
4. Caesarean wound breakdown(dehiscence) o Trainingfor all birth attendants in the management of postpartum
5. Genital tract tear haemorrhage is recommended.

6. Coagulopathy • A forma l follow-up meeting w hich analyses the case and

addresses what could be done better in the future should be
triggered for every significant PPH.
Management of Secondary PPH
• Accurate documentation of a delivery with postpartum
• The most commonly encountered cause for secondary PPH is haemorrhage is essential.
infection following retained placental parts.
--~--- ·---·-·--
• Secondary PPH could be mild or severe. In mild cases observation,
investigation and broad-spectrum antibiotics may be all what
the patient needs.

• When the secondary PPH is severe resuscitation, antibiotics and

evacuation of retained placental parts should be done. Figure 2.1:
BT-Cath®
• Always use suction curettage when evacuating infected retained Balloon
parts, as risk of uterine perforation is very high as uterine walls Tampo nade
are thinned due to infection. Catheter Set.

26 27
References:

01.
UNICEF. Guidelines for monitoring the availability and use of
obstetric services. UNICEF; 1997.
02.
Prevention and management of postpartum haemorrhage.
RCOG Green-top Guideline No.52. May 2009
03.
S Paterson-Brown. Obstetric emergencies. Dewhurt's text
book of obstetrics and gynaecology. 7th edition. Chapter 18.
Pages 149-152.
Summary
Major PPH (blood loss> 1000ml and continuing to bleed
or clinical shock}
Communication, resuscitation, investigation, monitoring
and arrest the bleeding should be done simultaneously
by delegating tasks working as a team.
1. Call for help
Alert senior obstetrician, anaesthetist, senior nurse,
midwives, blood bank, operating theatre.

PRIMARY PPH 2. Resuscitation (airway, breathing, circulation)

• 0 2 by mask
Loss of ~SOO ml of blood from the genital tract within 24hours
of the birth of a baby. • Two 14/ 16 G cannula
• Blood for investigations
1. Minor PPH: ~500-1000 ml of blood loss.
• Fluid replacement (Crystalloids 2L, collo ids 1.SL)
2. Major PPH: >1000 ml of blood loss.
• Blood transfusion
Moderate: ~1000-2000 ml
• FFP, cryo
Severe: ~2000 ml
Massive: ~2500ml 3. Investigations:

Causes for PPH : (4Ts) • Group & cross match (4 units)

1. Tissue • FBC,LFT, RFT, Coagulation profile, Fibrinogen
2. Tone
• ROTEM
3. Thrombin
4. Trauma 4. Monitoring
• Pulse oximeter (0 2 Saturation)
Principles of management:
• UOP
1. Prevention - active management of the 3rd stage • Pulse
2. Management/ treatment • BP
• Recognise • Central line or arterial line
• Resuscitation • Estimate blood loss
• Arrest the bleeding

28
29
 11, Antepartum haemorrhage (APH)

Arrest bleeding (uterine atony) ,,, t nition

1. Empty bladder 1111 is defined as bleeding from the genital tract ~ 24 weeks of
1111 ·gnancy to the birth of the baby. APH complicates about 3-5% of
2· Bimanual uterine compression
111 1•gnancies and 20% of very pre-term babies are born due to APH.
3. 10 units IV oxytocin stat dose I II ,re is an association of high maternal and perinat al morbidity and

4. 40 units IV infusion of oxytocin in 500 ml saline 111ortality.

5 . 500 µg of ergometrine IV (exclude HD/PIH)
6. lg Tranexemic acid slow IV bolus ·auses:

7. 250 µg of carboprost IM every 15 minutes x 3 I . Placenta previa ("' 30%)

) . Placental abruption ("'25%)
8. 1000 µg of misoprostol per rectal or vaginal 1. Local causes - cervix, vagina or vulva (Cervicitis, cervical
9. Look for retained placental tissue ectropian, polyp or cancer) ("'45%)
10. Look for trauma to genital tract 4. Preterm labour
5. Vasa previa (rare)
11. Consider intrauterine balloon tamponade 6. Bleeding disorders (rare)
12. Correct coagulation dysfunctions 7. Trauma (accidents, domestic violence)
APH can occur spontaneously or provoked by intercourse or clinical
Operating theatre (laparotomy/ following LSCS) examination depending on the underlying cause.

• Brace sutures/ B- Lynch sutures

• Bilateral uterine artery ligation Management

• Bilateral internal iliac artery ligation 1. Assessment (clinical and biochemical)

• Haemodynamic stability (pulse, BP, 0 2saturation)
• Hysterectomy

• MROP if retained products • Estimation of blood loss

• Repair of cervical/vaginal tears if identified • Symptoms: abdominal pain and its nature
• Abdominal tenderness, uterine contractions, Fetal heart
sounds

31
30
 • Feta! maturity and viability
• Speculum examination to exclude any local cause for bleeding
•
•
Blood group and cross match
Placental localization
2. Communication
• Call for senior help. Multi-disciplinary team with obstetrician,
anaesthesiologists, neonatologists and haematologists to plan
management and time delivery.
• Communicate with the woman and her family clearly about the
maternal and fetal condition .
3. Resuscitation
• Resuscitation will depend on the degree of shock. Degree
of shock will not correlate to the blood loss when there is a
concealed haemorrhage in placental abruption.
• Placental abruption is characterized by sudden onset, continuous,
localized abdominal pain with a tender tense abdomen to touch.
• Follow the basic resuscitation steps as given in PPH for major
APH(page 12, 13)
• If the fetus is viable and less than 34 weeks antenatal
corticosteroids should be administered as soon as possible.
• Those women with an APH where immediate resuscitative
measures are not required monitoring of vital parameters
should be continued until maternal and fetal safety is ensured .
Fet al heart monitoring should be done until plan to deliver.
32
1. Delivery of the baby
Tme to deliver and the mode of delivery depends on the materna~
• I dition and the fetal maturity and viability. If. matern~
c~:mod namic state can only be improved by delivery,. t_h1s
:hould :econsidered, irrespective of gest ational age. Dec1s1on
to deliver should be taken by a consultant.
. tances even a dead fetus has to be delivered b~ a
• Some ins secu·on to save a mother's life when there is a m ass ive
caesarean
placental abruption.
• Extremely premature babies will need to be delivered ~ it~Pu~
antenatal corticosteroid to be effe_ctive when a ma ssive
occur with a placenta previa abruption.
Dela to deliver the baby and placenta with a placental abrupti~n
• can ~ad to disseminated intravascular coagulation (DIC)_and ,t~
Therefore diagnosis of placental abruption a_n
~~~~~~~ e;c~~livery are two important factors that will decide
the prognosis of both mother and the baby.
complications of APH
Maternal:
1. Anaemia
2. Infection
3. PPH
4 . coagulopathy and DIC
5. Complications of blood transfusion
6. Prolonged hospital stay
7. Psychological sequale
33
 Fctal:

1. Prematurity
04. PRE ECLAMPSIA (PE}, SEVERE PRE-ECLAMPSIA AND
ECLAMPSIA
2. Fetal hypoxia
Intended learning outcomes:
3. Fetal death
I. Define pre-eclampsia, severe pre-eclampsia and eclampsia.
4 . Growth restriction
2. Describe the clinical features of severe pre-eclampsia.
3. Describe the initial assessment and diagnosis of sever pre-
eclampsia.
4. Recognise the warning indices of worsening condition.
5. Describe the management of severe pre-eclampsia.
6. Understand 4 main components of management.
7. Recall the basic pharmacology of anti-hypertensive and anti-
convulsants used for severe pre-eclampsia and eclampsia.
8. Student should be able to arrive at a differential diagnosis and
outline a management plan for a given clinical case scenario.
Figure : Couvelaire uterus.
Severe pre eclampsia and eclampsia as a cause of maternal deaths
Hemorrhagic process in uterine m I Severe pre-eclampsia and eclampsia are relatively rare condition s
severe abruptio placentae E t uscu ature that may accompany
muscle fibrils and under th x ~av~sated blood effuses between the but can give rise to serious complications of pregnancy. Worldwide,
on a purplish color and doesenu terme peritoneum. The uterus takes each year, more than four million women will develop pre-eclampsia
o contract well. and approximately 100 OOO women will have eclamptic convulsions,
with over 90% occurring in developing countries.
References
Pre-eclampsia complicates 2%-3% of all pregnancies {5%-7% in
1. Green top guideline no·63 by RCOG N b nulliparous women) and 2% of women with pre-eclampsia will
· ovem er 2011 develop eclampsia. WHO estimates that worldwide approximately
60,000 women die each year from pre-eclampsia. This remains a
common cause of death in pregnancy, in developing countries.

Hypertension in pregnancy is common occurring in about 1:5 wom en

after 20weeks of gestation. Incidence of pre-eclampsia is less than
34
35
 be affected with pre eclampsia
1:20 pregnant women. PIH and pre-eclampsia had remained the • Virtually any organ s~st~mn~~~e cerebral oedema, pulmonary
second leading cause of maternal deaths in Sri Lanka from 1996 - then lead to comphca.tio t liver failure HELLP syndrome,
ute renal failure, acu e '
2005. oe d ema, ac t ill lead to severe materna 1
haemolytic ureamic syndro~e, e c, :th restriction, intrauterine
In 2007 it had declined to 41h, then declined further to 10th cause morbidity. Placental a~rup~on, gro erinatal morbidity and
death and prematurity, increase p
in 2014. However in some districts in Sri Lanka (Nuwereliya, Badulla,
Monaragala, Rathnapura) hypertensive disorders remain a leading mortality.
cause for maternal morbidity and mortality.
Clinical features of severe pre-eclampsia

Definition of severe pre eclampsia and eclampsia

• Symptoms:
• Pre-eclampsia (PE) is pregnancy-induced hypertension (PIH) in severe headache
association with proteinuria(>300mg in 24 hours) ± oedema visual disturbance (blurring or flashing before the eyes)
appearing in the second half (~20weeks) of pregnancy up to 6
weeks post partum . epigastric pain
vomiting
• There is consensus that severe hypertension is confirmed with
a diastolic blood pressure (DBP) ~llOmmHg on two occasions right hypochondria! pain
or systolic blood pressure (SBP) ~170 mmHg on two occasions sudden swelling of the face, hands or feet
(6 hours apart) and that, together with significant proteinuria
(>3g/litre).
• Signs:
• Severe pre eclampsia is also called imminent eclampsia or clonus
impending eclampsia. DBP ~100 mmHg on two occasions and
liver t enderness
significant proteinuria with at least two signs or symptoms of
imminent eclampsia will also include many women with severe papil\oedema
pre-eclampsia.

• Eclampsia is defin ed as the occurren ce of one or more • HELLP syndrome :

convulsions superimposed on pre-eclampsia. Some women who platelet count falling to below 100 x 109/L .
prese nt with eclampsia may not have prodromal signs. Clinicians . (ALT or AST rising to above 70 ,u/L)
abnormal liver enzymes
should be aware that pre-eclampsia may occasionally occur
with hypertension in the absence of proteinuria and proteinuria
without hypertension
37
36

-
 Assessment and diagnosis:
1. Initial assessment at the time of presentation
• Initial assessment should be clinical and biochemical.
• C!inical symptoms are important components of
disease, particularly headache and abdominal pain. worsening
• Increasing oedema · t . .
is no rn itself a sign that should dete .
management. rm1ne
• ~=i:~;nal tendon reflexes, ~lthough useful to assess magnesium
Y, are not of value in assessing the . k f .
although the presence of clonus may be. rrs o convulsion,
• Continuous oxygen saturatio · · . testing, usually by 24hour urine collection, is reco mmended
is valuable, as it will ofte . n moln1t?rrng with a pulse oximeter
• n give ear y signs of pulmonary oedema.
Some women wHI present with convulsions abdominal p .
general malaise In th ' arn or
considered and ~he bi es~ cases, pre-eclampsia should always be
• . oo pressure taken and the urine analysed.
::n1or obstetric and anaesthetic staff should be involved in
e assessment and manag f
eclampsia and eclampsia. ement o women with severe pre-
2. How should the blood pressure be taken?
• It is important to standardise methods of blood
assessment with the woman appropriately positioned. pressure
• :;~ng :~~i~~~aloodl press ure, the woman should be rested and
ng e.
• The blood pressure cuff should b f
should be placed at the level of th: ~ea\~~ appropriate size and
• Multiple readings should be used to confirm the diagnosis.
• Korotkoff phase v is th . at least daily when the results are normal but more often if the
bi oo d pressure. e approprrate measurement of diastor1c
38
3. How should proteinuria be measured?
• The usual screening test is visual dipstick assessment. A two plus
dipstick measurement can be taken as evidence of proteinuria.
• Ideally a more accurate test to quantify (either a spot urinary
protein creatinine ratio or id ea lly a 24-hour urine collection) is
required.
• Significant proteinuria is diagnosed if the urinary
protein:creatinine ratio (PCR) is >30 mg/mmol or a valid ated
24-hour urine collection result shows ~300 mg protein.
• In view of the high false positive rates with dipsticks, laboratory
to confirm significant proteinuria, unless the clinical urgency
dictates immediate delivery.
• Urine dipstick testing, approximate equivalent is: 1+ = 0.3 g/1,
2+ = 1 g/1 and 3+ = 3 g/1.
• However in many hospitals in Sri Lanka still perform heat t est
for urine protein a practice we should change and adapt urin e
dipstick test.
4. How should the woman be monitored?
• The blood pressure should be checked each 15 minutes until
the woman is stabilised and then every 30minutes in the initial
phase of assessment.
• The blood pressure should be checked 4hourly if a conservative
management plan is in place and the woman is stable and
asymptomatic.
• Biochemical assessment of the woman requires a full blood count,
liver function and renal function tests. These should be repeated
clinical condition changes or if there are abnormalities.
39
 • Serial assessment will allow timing of delivery to be op~mis;:,
• Clotting studies are not required if the platelet count is over 100
X 10 /l.
9
• Fluid balance with charting of input and output is essential.
• Growth restriction is usually asymmetrical so measurement ~f
• A catheter with an hourly urometer is advisable in the acute
situation, especially in the immediate postpartum period.
5. What are the warning indices of worsening condition?
• In pre-eclampsia, there can be a rise in uric acid that correlates
with poorer outcome for both mother and baby.
• This rise confirms the diagnosis of pre-eclampsia and confers
an increased risk to the mother and baby but the levels, in
themselves, should not be used for clinical decision-making
• Renal function is generally maintained in pre-eclampsia until the
late stage unless HELLP syndrome develops.
• A falling platelet count is associated with worsening disease and
is itself a risk to the mother. However, it is not until the count is
less than 100 x 109/L that there may be an associated coagulation
abnormality.
• A platelet count of less than 100 x 109/L should be a consideration
for delivery.
• An AST level of above 75 iu/L is seen as significant and a level
above 150 iu/L is associated with increased morbidity to the
mother.
6. How should the fetus be assessed?
• In the acute setting, an initial assessment with cardiotocography
(CTG) should be undertaken if the fetus is viable . If feta I maturity
is <34 weeks fetal heart detection with Doppler is preferable.
• If conservative management is planned then further assessment
of the fetus with ultrasound measurements of feta I size, umbilical
artery Doppler and liquor volume should be undertaken.
40
The value of Doppler in other fetal vessels other t an e
umbilical artery has yet to be clarified.
the abdominal circumference is the best method o: asse~sme~ i
Reduced liquor volume is also associated with p acen a
insufficiency and fetal growth restriction.
01 f eclamptic pregnanci es.
• IUGR occurs in aroun d 30 10 o pre-
. . labour then continuous electronic fetal
• If the woman ts in . ffectin the
monitoring is appropriate. The main pat~olog~ ~ g .
fetus, apart from prematurity,. is placental insufficiency leading
to intrauterine growth restriction (IUGR).
Management of severe pre-eclampsia/impending eclampsia
·1n·1cal and biochemical (as decribed in page 38-40)
• Assessment - Cl
• Stabilisation - control BP, prevention/treatment of convulsions,
fluid balance
• Monitoring - mother and the fetus
• Delivery - at the optimal time for the mother and her baby
Stabilisation:
l. Control the blood pressure
Severe PIH : . omen
• Antihypertensive treatment should be started in w ·th
with a SBP 2:160 mmHg or a DBP ~110 mmHg. In women w 1
other markers of potentially severe disease,. treatment can
be considered at lower degrees of hypertension. .
• Labetalol given orally or intravenously, nifedipine given
orally and intravenous hydralazine can be used for the ~~u~e
management of severe hypertension. Labetalol shou e
avoided in women with known asthma.
41
 H (150/lOOmmHg) should be maintained for
Moderate PIH: MAP of 125mm g . . mild hypertension may
• Treatment may assist prolongation of the pregnancy. i ,tero-placental cihrc~lati~;~e::.~~:;efore mild hypertension is
lead to fetal growt 1mpa , '
Clinicians should use agents with which they are familiar. l) etter monitored than treated.
With treatment a prolongation of pregnancy of an average ·11 not reduce the risk of pre-
of 15 days is possible as long as there is no other reason to • f reatment of hypertension w1
deliver. cclampsia.
• There is also a consensus that, if the BP <160/100 mmHg,
there is no immediate need for antihypertensive therapy. An .babetalol
exception may be if there are markers of potentially more Labetalol (a and 13-adrenergic blocking agent) has fewer ~ide
severe disease, such as heavy proteinuria or abnormal liver d h Id be considered as first-line therapy. It is a
or haematological test results . :~:~:filn se~e~:ve a1 blocker and a r:r'ixed no~-selective 13
• Atenolol, angiotensin converting enzyme (ACE) inhibitors, blocker. The !3:a antagonism of labetalol 1s about 3.1.
angiotensin receptor-blocking drugs (ARB) and diuretics
should be avoided. ACE inhibitors and ARBs are
contraindicated because of unacceptable feta I adverse effects.
• ~~bd~;;~~::~s ~~,~~~~::i\::;~!",!:~: ~~: ';~::~~;i~e~~~;,,~
Diuretics are relatively contraindicated for hypertension and alteration of heart rate or cardiac output.
should be reserved for pulmonary oedema only. d erve utero-placental
• Labetalol is not teratogenic an may pres.
• Nifedipine should be given orally not sublingually. blood flow better than other antihypertens1ve drugs.
a ra id absorption and peak serum
Anti-hypertensives used in PIH and preeclampsia • Oral labe~alol ha~ 20-30~inutes following labeta\ol ingestion.
concentration occu · to 60
• Anti-hypertensive should be started in patients with severe Food can delay the time to peak serum concentrations up
hypertension in order to prevent maternal end-organ damage minutes.
and stroke. BP control does not, however, alter the progression
of pre-eclampsia.
Dosing:
• One retrospective study found SBP was 159 - 198 mmHg
. I d se of labetalol is 100 mg twice
immediately pre-stroke in 24 of 24 patients. The recommended starti~g ora do b 100 mg twice daily every 2-3
. d th dose can be increase Y
• The best practice is to initiate antihypertensive therapy in pre- da1 1y an e f the BP Usual maintenance doses are
days based on the response o .
eclamptic women when the SBP is ::::150 mm Hg and the DBP is
200-400 mg twice daily.
::::100 mm Hg, or less if symptoms may be attributable to elevated
pre eclampsia: Initial first-line
blood pressure. Severe Hypertension/severe
• Mean arterial pressure (MAP} of >150mmHg will cause loss of management is with Labetalol.
cerebral circulation and risk of cerebral haemorrhage.
43
42
 SBP measurement is ~160 mmHg or if DBP measurement i!
~llOmmHg or BP~160/110mmHg:
• Initial dose of labetalol can be given 200mg stat.
• If no response second oral dose can be repeated in 30 minutes.
• If no response to oral treatment or if oral drugs cannot be
tolerated IV labetalol is indicated.
• Initiate feta I surveillance if fetus is viable.
• Pre load ~ith normal saline or Hartman solution 500ml,
60 drops/ mrnute before administering IV labetalol.
• A vial of Labetalol contains 100mg in 20ml; 5mg in 1 ml. Draw
the labetalol in to a 20ml syringe and label it.
• Administer 4 ml labetalol (20 mg) IV over 2 minutes. Be cautious
not to spill the labetalol over the skin.
• Repeat BP measurement in 10 minutes and record results.
• Aim should be to reduce the DBP by 10mmHg.
• If BP still exceeded 160/110 mmHg, administer 8ml labetalol
(40 mg) IV over 2 minutes.
• If B~ is below threshold: SBP 150 mmHg and DBP lOOmmHg,
continue to monitor BP.
• Repeat BP measurement in 10 minutes and record results.
• If ei~h:r BP still exceeded160/110 mmHg, administer the
remarnmg 8 ml labetalol (40mg) IV over 2 minutes.
• If BP is below threshold, continue to monitor BP closely.
• Repeat BP measurement in 10 minutes and record results.
• !f BP. threshold is still 160/110 mmHg, administer IV labetalol
rnfus,on.
44
•,yringe pump infusion:
• Draw 2 vials of labetalol 40 ml undiluted to a syringe (200mg in
40 ml), add sticker "labetalol 5mg in lml". Start the infusion with
an initial rate of 4ml/hour (20mg/hour) .
• Repeat BP measurement in 20 minutes and record results.
• If either BP threshold is still exceeded double the infusion rate
every 30 minutes.
• If BP is within expected range continue the sa me rate. Titrate to
stabilise the BP by halving or doubling the infusion rate every 30
minutes. If BP decreases precipitously stop the infusion.
• Once the BP thresholds are achieved, repeat BP measurement
every 10 minutes for 1 hour, then every 15 minutes for 1 hour,
then every 30 minutes for 1 hour, and then every hour for 4
hours.
• Discontinue the IV labetalol infusion weaning over 1-2 hours
when BP is constantly below 155/95 mmHg.
Infusion pump:
• Draw 200mg (40ml/2 vials) add to 60 ml of normal saline to the
infusion. A sticker "labetalol 2mg/lml".
• Start infusion 20mg/hour (10 ml/hour).
• Titrate to stabilise the BP by doubling, halving or maintaining the
infusion rate every 30 minutes.
• Discontinue the IV labetalol infusion weaning over 1-2 hours
when BP is constantly below 155/95 mmHg.
45
2, Nifedipine (Ca++ channel blocker)
• The calcium antagonist used for acute severe PIH and severe PE
• A rapid and a significant fall in blood pressure by an average of
20 mmHg are seen within 20minutes after administration.
• The principal side effects were headache and cutaneous flushing,
No adverse fetal effects were detected.
• Hypotensive effect is not significant unless combined with
Magnesium sulfate (MgS04 ).
• Sublingual nifedipine has previously been used in hypertensive
emergencies. This was found to be dangerous, and has been
abandoned. Sublingual nifedipine causes blood-pressure
lowering through peripheral vasodilation. It can cause an
uncontrollable decrease in blood pressure, reflex tachycardia,
and a "steal phenomenon" in certain vascular beds (A symptom
complex that occurs whenever there are extensive anastomoses
between two vascular beds, and the arterial supply to one of
the beds is occluded). There have been multiple reports in the
medical literature of serious adverse effects with sublingual
nifedipine, including cerebral ischemia/infarction, myocardial
infarction, complete heart block, and death.
Recommended dosage for severe PIH or severe PE:
• Nifedipine 20-30mg oral, repeat every 30 minutes up to 80mg
•
maximum per 24 hours.
When BP is controlled, maintain SBP 140-159mmHg and DBP
90-109 mmHg with 20-30mg slow release preparation 12 hourly
until delivery and postpartum.
• The efficacy of oral nifedipine and intravenous hydralazine is
similar when used in acute severe PIH/PE but the side effects are
more with iv hydralazine than to oral nifedipine.
46
lnnavenous Hvdralazine
• 1lydralazine is a second line drug for severe PIH/PE.
/\ single vial contains 20mg(ml. Best used ~ir::~ d~l~~:z~n:'.th
distilled water in a 20ml synnge. Then 1ml - g Y
• Then administer slow intravenous injection of Smg-10mg
(5-10 ml) and continue monitoring pulse and BP.
If no response the above dose can be repeated in 30 minutes.
• If no further response in 30 minutes IV infu sion. One vial 20mg
dilute in 20ml. administer with an infusion pump 3ml/hr, double
every 30 minutes up to 18ml/hr.
• Tachycardia precedes the fall of BP. T~e usual time taken for the
antihypertensive response is 20- 30mmutes.
• Severe hypotension is a known adverse effect.
. n 500ml normal saline drip 80ml/hour can be
• As a precau ti o
started with the hydralazine injection.
Methyl dopa
I BP by stimulating central inhibitory alpha-
~d~::~1;~:e::~to~;ef:lse neurotransmission, and/or reduction of
plasma renin activity. .
on~et of actitonkepe
action may a 2
~o~:~:~~n;: ~~~; i~~~:~~~::~~~ ~~~~::~:~:
excreted in urine (70%).
Start dose 250-SOOmg 8 hourly per oral.
the side effects and late onset of action Methyldopa is no
~un~~~ used as a first line drug in severe hypertension in pregnancy.
47
 ~an~ ~linical trials have shown greater efficacy of labetalol and
nifed1prne compared with traditional methyldopa.
Side effects include; postural hypotension, altered sleep pattern
polstpartum depression, constipation, haemolytic anaemia and
ga actorrheoa .
2, Prevention of seizures:
• MgS04 ~hould be considered for women with severe pre-
eclamps1a for whom there is concern about the risk of eclampsia.
• This is usually in the context of severe pre-eclampsia once
a delivery decision has been made and in the immediate
postpartum period.
• ln·tdomen with less severe disease the decision is less clear and
WI epend on individual case assessment.
• If MgSO
. 4 is given, ·t
, shou Id be continued for 24 hours followin
de:1very or 24 hours after the last seizure, whichever is the late~
un ess there is a clinical reason to discontinue.
• When MgSO · ·
4 is given, regular monitoring of the urine output
~aternal reflexes, respiratory rate and oxygen saturation i;
important.
• When co~servative management of a woman with severe
hypertension and a premature fetus is made, it would be
reasonable not to start MgS04 until the decision to deliver has
been made.
48
,,,., venous MgS04
MgS04 reduces the risk for eclampsia by >50%, and probably
, educes the risk of maternal death.
I he Magpie trial indicated that the use of prophylactic MgS04
reduced the risk of eclampsia and caused no harmful effects to
the mother or baby in the short term .
• I\ follow-up study also found that its use caused no associated
mortality or morbidity to the woman after 2 years. Exposure
of the fetus to MgS04 in utero is not associated with a clear
difference in the risk of morbidity or disability for chi ldren at 18
months of age.
• The mode of action of MgS04 is unclear, but it is believed to have
a neuro-muscular blocking action, which relaxes smooth muscles
including the vasculature, thereby reducing cerebral ischaem ia.
The blocking of aspartate receptors in the brain reduces ca lcium
influx that is responsible for causing cell injury in the neurons.
• MgS04 is mostly excreted in urine.
,
Key points
o MgS04 should be considered for women with severe pre-
eclampsia/imminent eclampsia. This is usually in the context of
severe pre-eclampsia once a delivery decision has been made or
in the immediate postpartum period.
o MgS04 should not be prescribed for the prevention of eclam psia
without discussion with the Consultant Obstetrician on ca ll,
unless in an urgent situation of imminent eclampsia.
o Before commencement of IV Mg504 check and document
that: the deep tendon reflex is present, the respiratory rate is
> 12/minute and urine output is >30ml/hour.
o Remember the therapeutic and toxic range of the IV MgS0 4 is
very narrow. Therefore follow all the precautions given below
when administering MgS04.
49
 Loading dose:
Monitoring during administration of IV MgS04in ahigh depend ency
• Infuse 4g of MgS04 slow IV over 20 mi . 1init (HDU)
infusion rate of lSOmL P h f nutes. This equates to an
saline in an infusion pu;;). our or 20 minutes (4g/50ml normal I. Deep Tendon Reflexes
/.. Respiratory rate
• The loading dose is given for· r h I . 3. Oxygen saturation
treatment of an initial . . p op Y ax,s to prevent seizures or
administered. seizure where no prior MgS04 has been /J.. Blood pressu re
5. Fetal heart rate (before delivery)
• If an infusion pum · .
4g MgS04 in 2oomto:\~~~~~1la~!e use a biuret pump with Monitoring should be done every 15 minutes during the first 2 hours
used. same over 20 minutes can be of therapy, then hourly thereafter. Th ese should be documented
clearly.
• The slow administration of the I d. . .
avoid toxicity (cardiac and re . toa tg dose ,s important to
can cause cardiac and respi s~1ra ory of Mg. Rapid IV injection Fluid Balance Management
acted promptly. ra ory arrest and even death if not • Maintain a strict fluid balance chart and document.
• Total intake of fluids should be limited to 80 ml/hour or 1 ml/kg/
MgSO4 maintenance regimen:
hour.
• The dose for maintenance infusion is 1 • The regime of fluid restriction should be maintained until t here
equates to an infusion rate of 12 5 L g of MgS04 per hour. This is a postpartum diuresis, as oliguria is common w ith severe pre-
of 8g of MgSO in 100ml b . . m. per hour where a solution
4 ag ,s used in an infusion pump. eclampsia.
• The recommendation is all M S . . • Increased pe ripheral resistance leads to generalised vasospasm
infusion pump. g 04 infusions must be given via an and hypertension. The intravascular compartment is reduced.
Endothelial damage leads to increased vascular permeability
• Women on MgSO ther h
d d . 4 apy s ould be cared for in the h' h and oedema.
epen ency Un,t (HOU) until th ,g
normally 24 hours followin th I erapy. has ceased, which is • Women with pre eclampsia have leaky capilla ry membranes
(whichever is the latter). g e ast seizure or after the birth and a predisposition to low albumin levels: the refore if fluid
administration is excessive or unmonitored, they are prone to
developing pulmonary oedema.
MgS04 regime for recurrent seizures:
• The MgS04 therapy may need to be reduced or stopped if there
• IV MgSO4 2g ·is given
· over 5 minutes Th· is <20ml/hour of urine output. MgSO 4 is eliminated via the renal
rate of 300m/s per hour for 5 . . ,_s equates to an infusion
system. Toxicity can occur in the presence of oligu ria. The infusion
25 ml) where a solution of 8 ~1~utes (1_,e. the woman receives
gO gS04 in 100ml bag is used. should be discontinued if signs of toxicity become evident.
so
51
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