OBSTETRIC

EMERGENCIES
LEARNING OBJECTIVE
• obstetric emergencies requiring intensive care management:
• 1.1 pregnancy induced hypertension (pre-eclampsia and eclampsia)
• 1.2 haemorrhage (antepartum and postpartum)
• 1.3 embolism (venous and amniotic fluid)
• 2. correlate the clinical presentation of the above obstetric
emergencies with its pathophysiology
• 3. discuss the critical care management of the following obstetric
• emergencies:
• 3.1 pregnancy induced hypertension (pre-eclampsia and eclampsia)
• 3.2 haemorrhage (antepartum and postpartum)
• 3.3 embolism (venous and amniotic fluid)
• 3.4 obstetric patients with cardiac diseases
• 4. use the nursing process as a framework to formulate
individualized care of patients with the above obstetric
emergencies admitted in the Intensive Care Unit (ICU)
• 5. appreciate the importance of prompt management to the
patient’s clinical prognosis
 PRE ECLAMPSIA
•Pre eclampsia is a syndrome specific
to pregnancy. It has no definitive
biomarkers and is diagnosed
clinically by new onset of
hypertension and proteinuria after
20 weeks gestation with or without
pathologic oedema.
Eclampsia
•Eclampsia, which is considered a
complication of severe preeclampsia, is
commonly defined as new onset of grand
mal seizure activity and/or unexplained
coma during pregnancy or postpartum in a
woman with signs or symptoms of
preeclampsia. It typically occurs during or
after the 20th week of gestation or in the
postpartum period.
• What Is Triploidy?
• Triploidy is a rare chromosomal abnormality. Fetuses with Triploidy,
or Triploid Syndrome, have an extra set of chromosomes in their
cells.

• One set of chromosomes has 23 chromosomes and is called a

haploid set. Two sets, or 46 chromosomes, are called a diploid set.
Three sets, or 69 chromosomes, are called a triploid set.

• Typical cells have 46 chromosomes, 23 inherited from the mother

and 23 inherited from the father. Fetuses with Triploidy inherit an
extra set of chromosomes from one of the parents.

• Triploidy is a lethal condition. Fetuses with the abnormality rarely

survive to birth. Many are spontaneously miscarried during the first
trimester or stillborn before reaching full-term. The few infants that
do survive to term will have severe and multiple birth defects.
These might include growth retardation, heart defects, and neural
tube defects (Spina bifida). Infants born with Triploidy typically will
not live more than a few days after delivery.
•What Causes Triploidy?
•Triploidy is the result of an extra set of
chromosomes. This can be the result of
two sperm fertilizing one normal egg. It
can also occur if a normal sperm fertilizes
an egg that has an extra set of
chromosomes.
Clinical Practice Guideline on
Hypertension (MOH), 2008
• Pre-eclampsia - eclampsia:
• Clinically diagnosed in the presence of de novo hypertension after
gestational
• week 20, and one or more of the following:
• i. Significant proteinuria
• ii. Renal insufficiency: serum creatinine >90μmol/l or oliguria
• iii. Liver disease: raised transaminases and/or severe right upper
quadrant or epigastric pain
• iv. Neurological problems: convulsions (eclampsia), hyperreflexia
with clonus or severe headaches, persistent visual disturbances
(scotoma)
• v. Haematological disturbances: thrombocytopenia, coagulopathy,
haemolysis
• vi. Fetal growth restriction
•Edema is no longer part of the
definition of pre-eclampsia. Either
excessive weight gain or failure to
gain weight in pregnancy may
herald the onset of preeclampsia.
Pathophysiology
•Pre-eclampsia is a systemic disease
characterized by endothelial
dysfunction in pregnant women.

•The mechanisms by which

pre-eclampsia occurs is not certain,
and numerous maternal, paternal,
and fetal factors have been implicated
in its development.
•The factors currently considered to be the
most important include the following:
•Maternal immunologic intolerance
• Abnormal placental implantation
• Genetic, nutritional, and environmental
factors
• Cardiovascular and inflammatory changes
 Clinical Manifestation
• Basic diagnostic criteria for pre-eclampsia:

• Hypertension Systolic arterial pressure >140 mmHg or

• Diastolic arterial pressure* >90 mmHg
• And

• Proteinuria >300 mg protein in a 24-hour collection

Clinical features suggestive of
severe pre-eclampsia:
Management
• The optimal management of a woman with
pre-eclampsia depends on gestational age and disease
severity.

• Because delivery of the placenta and fetus is the only

cure for pre-eclampsia, clinicians must try to minimize
maternal risk while maximizing fetal maturity.

• Before delivery and during immediate postpartum

period management is supportive and focused on
• control of blood pressure
• prevention of seizures
• maintenance of placental perfusion
• prevention of complications.
1) General measures
•Mother: lateral or semi-lateral position,
•H2 antagonists
• routine monitoring (frequent clinical
assessment
•blood pressure
• ECG
• pulse oxymeter
• fluid balance).
Advantages of Left-Sided
Sleep Position
• There are advantages to the left-sided sleep position during
pregnancy besides improved wellness for mother and the
baby. The bulk of the stomach is on the left side of the
abdomen. When lay on the left side, the food in the stomach
is below the esophagus and this leads to less heartburn in the
middle of the night. Also the heart is in the left side of your
chest. When lay on the left side the blood returns from the
head and neck more easily than when lay on the right side.
This means less nasal congestion and snoring which can be big
problems as the pregnancy progresses.
• This will:
• Improve blood flow to you and the baby
• Reduce heartburn
• Reduce snoring and nasal congestion
•Fetus: fetal heart rate,
prophylactic dexamethasone for
lung maturity.
•Serial blood investigation to
monitor disease progression: FBC,
Coagulation profile,electrolytes,
uric acid, renal profile, liver
function test, urinalysis.
2) Anti Hypertensive therapy
• The aim of anti HPT therapy is to prevent maternal
complications
• intracerebral hemorrhage
• cardiac failure
• abruption placenta) while
• maintaining placental blood flow (maintain BP around 140/90
mmHg).

• severe hypertension (SBP >160 mmHg; DBP >110 mmHg) Anti

HPT treatment is recommended.
Recommended anti HPT
drugs for acute treatment:
3) Anti convulsant therapy
• The basic principles of airway, breathing, and circulation (ABC)
should always be followed as a general principle of seizure
management.

• Magnesium sulfate is the first-line treatment for the

prevention of primary and recurrent eclamptic seizures.

• For eclamptic seizures that are refractory to magnesium

• sulfate, diazepam and phenytoin may be used as second-line
agents.

• If seizures are refractory, thiopental and suxamethonium

should be given and airway secured.
•Active seizures should be treated with IV
magnesium sulfate as a first-line agent.

•A loading dose of 4-6 g should be given by

an infusion pump over 20 minutes,
followed by an infusion of 1-2 g/h
maintained for 24 hours after the last
seizure.
•Recurrent seizures should be treated with
an additional bolus of 2 g or an increase in
the infusion rate to 1.5 g or 2 g per hour.
•Prophylactic treatment with
magnesium sulfate is
indicated for all patients
with severe preeclampsia.
Guidelines for administration
of magnesium sulphate:
•Renal function and tendon reflexes
should be monitored. Reduce dose
and monitor serum concentrations in
oliguria or renal impairment. (1 g
magnesium sulphate = 98 mg = 4.06
mmol = 8.12 mEq elemental
magnesium)
•Suggested target serum concentration is
2-3.5 mmol/l (4-7 mEq/l or 4.8-8.4 mg/l).
Magnesium toxicity is associated with
muscle weakness and may lead to:

• respiratory paralysis (>7.5 mmol/l)

• increased conduction time with increase
PR, QT intervals and QRS
•duration and can lead to sinoatrial and
atrioventricular block (>7.5 mmol/l)
• cardiac arrest in diastole (>12.5 mmol/l).
•Toxicity is unlikely when deep tendon
reflexes are present. Magnesium
toxicity can be treated with small
intravenous doses of calcium.
Magnesium crosses placental blood
barrier and can cause neonatal
flaccidity and respiratory depression.
4) Fluid management
•Despite the presence of
peripheral edema, patients
with pre-eclampsia are
intravascularly volume
depleted, with high peripheral
vascular resistance.
•Diuretics should be avoided.
•Aggressive volume resuscitation may lead
to pulmonary edema, which is a common
cause of maternal morbidity and mortality.

•Pulmonary edema occurs most frequently

48-72 hours postpartum, probably due to
mobilization of extravascular fluid.

•Careful measurement of fluid input and

output is advisable, particularly in the
immediate postpartum period.
5) Post partum care
• Pre-eclampsia resolves after delivery. However, patients
may still have an elevated BP postpartum.

• Liver function tests and platelet counts must be

performed to document decreasing values.

• In addition, one third of seizures occur in the

postpartum period, most within 24 hours of delivery, and
almost all within 48 hours.

• Therefore, magnesium sulfate seizure prophylaxis is

continued for 24 hours postpartum.
•Anti HPT drugs may be reduced
according to the blood pressure.
Some patients may require a
change to oral medication. Full
recovery from the organ
dysfunction of pre-eclampsia is
normally expected within 6
weeks.
SEVERE OBSTETRIC
HAEMORRHAGE
•Obstetric bleeding may be vaginal and
external, or, internal, into the
abdominal cavity. Typically bleeding is
related to the pregnancy itself, but
some forms of bleeding are caused by
other events. Can be categorized as:
•a) Antepartum hemorrhage
•Bleeding mostly from placenta
previa or abruption placenta and
both are ultimately managed by
delivery.
b) Postpartum hemorrhage
(PPH)
• Bleeding usually from uterine atony or placenta
accreta. Blood loss of more than 500mls
following vaginal delivery, or 1000mls of blood
following cesarean section. A loss of these
amounts within 24 hours of delivery is termed
early or primary PPH, whereas such losses are
termed late or secondary PPH if they occur 24
hours after delivery.
Pathophysiology
•Uterine atony is a failure of the
uterine myometrial fibers to
contract and retract.
•This is the most important cause
of PPH and usually occurs
immediately following delivery of
the baby, up to 4 hours after the
delivery.
• Trauma to the genital tract (ie, uterus, uterine
cervix, vagina, labia, clitoris) in pregnancy results
in significantly more bleeding than would occur
in the nonpregnant tate because of increased
blood supply to these tissues.

• The trauma specifically related to the delivery of

the baby, either vaginally in a spontaneous or
assisted manner or by cesarean delivery, can also
be substantial and can lead to significant
disruption of soft tissue and tearing of blood
vessels.
Clinical Presentation
•The usual presentation of PPH is
one of heavy vaginal bleeding that
can quickly lead to signs and
symptoms of hypovolemic shock.
Clinical Findings in Obstetric
Hemorrhage:
 Management
• Rapid recognition and diagnosis of PPH is essential
to successful management.

• Resuscitative measures, the diagnosis and

treatment of the underlying cause must occur
quickly before sequelae of severe hypovolemia
develop.

• The major factor in the adverse outcomes

associated with severe hemorrhage is a delay in
initiating appropriate management.
Outline of management:
• 1) Organization
• 2) Resuscitation (fluid, blood and blood
component)
• 3) Correct defective blood coagulation
• 4) Evaluate response towards management
• 5) Find the underlying cause of bleeding
•The two therapies used in
management of a patient with PPH are:

•a) Medical therapy: Resuscitation and

management of obstetric hemorrhage
and hypovolemic shock
Fluid resuscitation
• Perform the initial resuscitation with crystalloid solution,
either normal saline (NS) or Lactated Ringer’s solution
(LRS), through peripheral intravenous sites.

• Central venous access is not required for the vast

majority of patients with PPH, but do not delay
establishing such access if necessary.

• NS is a reasonable solution in the labor ward setting

because of its compatibility with most drugs and blood
transfusions. The risk of hyperchloremic acidosis is very
low in the setting of PPH.
•PPH of up to 1500 mL in a healthy
pregnant woman can usually be
managed by crystalloid infusion
alone if the cause of bleeding is
arrested. Blood loss in excess of
this usually requires the addition
of a PRBC transfusion.
Blood transfusion
• The goal is to rapidly transfuse 2-4 packed of
PRBCs to replace lost oxygen-carrying capacity
and to restore circulating volume.

• Administer the blood transfusion through a set

with an integrated filter, and use a blood warmer
if the infusion rate (>100 mL/min) or the total
volume infused is high.

• A rapid infusion set with an integrated warmer

or a pressure cuff may be used to increase the
infusion rate.
Coagulopathy
•Thrombocytopenia is likely after
1.5-2.0 times the blood volume
has been replaced.

•If surgical intervention is

necessary, maintain the platelet
count at more than 80-100 x
109/L.
• Cryoprecipitate may be useful along with FFP
because of the markedly depressed fibrinogen
levels.

• Cryoprecipitate provides a more concentrated

form of fibrinogen and other clotting factors
(VIII, XIII, von Willebrand factor) and is faster to
prepare in the blood bank.

• It is commonly given in 6- to 12-U doses and

may also be helpful immediately before any
surgical intervention in patients with abnormal
coagulation test results.
•b) Surgical therapy:
Identification and
management of the underlying
cause(s) of the haemorrhage
•Various techniques including
laparotomy, hysterectomy, arterial
embolization, balloon tamponade,
uterine compression sutures, and
iliac artery ligation or uterine
devascularization.
uterine artery embolization
(UAE).
•
EMBOLISM
•1. Venous thromboembolism
•Venous thromboembolism (VTE) refers
to the formation of a thrombus within
•veins. This can occur anywhere in the
venous system but the clinically
•predominant sites are in the vessels of
the leg (giving rise to deep vein
•thrombosis (DVT)) and in the lungs
(resulting in a pulmonary embolus (PE)
•Pregnancy is associated with five
fold increase in thromboembolism
because of:
•a) venous stasis
•b) hypercoagulable state
•c) vascular injury associated with
delivery
Risk factors specific to pregnancy:
•Venous stasis
• Maternal age of ≥35 years
• Multiparity
• Gestation <36 weeks
• Instrument-assisted or Caesarean
delivery
• Haemorrhage
• Pre-eclampsia
• Prolonged labour
Pathophysiology
•Venous thrombus formation and
propagation most usually depend on
the presence of one or more of the
following:
•venous stasis
• blood vessel wall trauma or
abnormality
• increased risk of blood coagulation
•These elements are known collectively as
Virchow’s triad.
•a) Venous Stasis
•Venous stasis occurs when there’s a
decrease in movement of blood,causing
venous congestion in the lower
extremities; this may occur after
prolonged immobility or confinement to
bed.
b) Vein injury
• The endothelium (lining) of a healthy vein is smooth
and provides a physical barrier between the
circulating blood and the thrombogenic tissues
beneath.

• When the vein becomes injured the lining loses its

normal negative charge,becoming rough and
provoking platelet aggregation and adhesion.

• Endothelial injury may be caused by a previous

DVT, venous distension,trauma and surgery.
 c) Hypercoagulability
•Changes in blood chemistry causing
hypercoagulability (increased blood
stickiness) can occur as a result of
many factors including
dehydration,malignancy, surgery or
trauma, oestrogen therapy and
systemic inflammatory diseases.
Clinical Presentation
• Presentation is similar to non-pregnant patients with
DVT or Pulmonary embolism (PE):

• DVT: leg pain and discomfort, swelling, tenderness,

oedema, increased temperature and a raised white
cell count. The difficulty is that some of these
• symptoms may be found in normal pregnancies. The
patient may also be asymptomatic with a
retrospective diagnosis being made following a PE.
• PE: dyspnoea, pleuritic chest pain, haemoptysis,
faintness, collapse. The patient may have focal
signs in the chest, tachypnoea, a raised jugular
• venous pressure (JVP) and there may be ECG
changes (S1Q3T3). Arterial blood gases taken with
the patient sitting down may show respiratory
• alkalosis and hypoxaemia. There may also be
symptoms or signs of a DVT.
•Accurate diagnosis of VTE is
crucial. Test for diagnosing include
Doppler ultrasonography, D dimer
testing, venography, pulmonary
angiography, lung perfusion scan
and helical CT scan.
Management
• Medical anticoagulation is the treatment of choice
for acute VTE.
• Subsequently, surgical interventions may be
considered: patients suffering from recurrent PEs
despite adequate anticoagulation (or where there is
an absolute contra-indication to anticoagulation)
may benefit from placement of a temporary caval
filter and, in those cases where there is limb or
lifethreatening embolus, a surgical embolectomy or
thrombus fragmentation may be attempted.
Anticoagulation is the most
common treatment option.
• Heparin is the most frequently used drug, being
non-toxic to the fetus (it does not cross the placental
barrier).

• However, its main disadvantages are

• that it has to be parentally administered and, in the
long-term, may give rise to heparin-induced
osteoporosis and thrombocytopenia.

• In some patients, it can also provoke a painful,

localised allergic reaction on administration.
•o Warfarin is the other treatment
option in the postnatal patient but it
must be avoided antenatally as it
is teratogenic and can also cause
placental abruption and
fetal/neonatal haemorrhage.
•In clinically suspected DVT or PE,
treatment with unfractionated
heparin (UFH) or low molecular
weight heparin (LMWH) should be
given until the
•diagnosis is excluded by objective
testing, unless treatment is
strongly contraindicated.
•LMWH is preferred over UFH for the
prevention and treatment of VTE because of
ease of use and better efficacy and safety
profile. Anticoagulants should be
administered for at least 6 weeks
postpartum (for a minimum total duration of
therapy of 6 month).
2. Amniotic Fluid Embolism
•Amniotic fluid embolism (AFE) is a rare
obstetric emergency in which it is
postulated that amniotic fluid, fetal
cells, hair, or other debris enter the
maternal circulation, causing
cardiorespiratory collapse. Incidence
varies between 1in
•8000 and 1 in 80000 deliveries.
Pathophysiology
• The pathophysiology of AFE is speculative; various
theories have been published. Three distinct
responses or a combination of clinical responses to
• circulating fetal debris are suggested:

• 1) transient pulmonary vasospasm - caused by

amniotic microemboli that trigger the release of
arachidonic acid metabolites and lead to pulmonary
• hypertension, intrapulmonary shunting,
bronchoconstriction, and severe hypoxia.
•2) negative inotropism and left
ventricular failure resulting in
increasing pulmonary edema and
hypotension quickly leading to
shock.

•3) neurological response to the

respiratory and hemodynamic
injury, which may include seizures,
confusion, or coma
Clinical Presentation
• Currently no definitive diagnostic test exists. The
United States and United Kingdom, AFE registries
recommend the following four criteria, all of which
must be present to make the diagnosis of AFE.

• 1. Acute hypotension or cardiac arrest

• 2. Acute hypoxia
• 3. Coagulopathy or severe hemorrhage in the
absence of other explanations
• 4. All of these occurring during labor, cesarean
delivery, dilation and evacuation, or within 30
minutes postpartum with no other explanation of
findings
• In case reports, patients are described as
developing acute shortness of breath,
• sometimes with a cough, followed by severe
hypotension. The following signs
• and symptoms are indicative of possible
AFE:
• Hypotension: Blood pressure may drop significantly
with loss of diastolic measurement.
• Dyspnea: Labored breathing and tachypnea may
occur.
• Seizure: Tonic clonic seizures are seen in 50% of
patients.
• Cough: This is usually a manifestation of dyspnea.
• Cyanosis: As hypoxia/hypoxemia progresses,
circumoral and peripheral cyanosis and changes in
mucous membranes may manifest.
• Fetal bradycardia: In response to the hypoxic
insult, fetal heart rate may drop to less than
110 beats per minute (bpm).
• Pulmonary edema: This is usually identified
on chest radiograph.
• Cardiac arrest
• Uterine atony: Usually results in excessive
bleeding after delivery.
• Failure of the uterus to become firm with
bimanual massage is diagnostic.
•Coagulopathy or severe hemorrhage in
absence of other explanation (DIC
occurs in 83% of patients.)
• Altered mental
status/confusion/agitation
•The diagnosis of AFE has traditionally
been made at autopsy when fetal
squamous cells are found in the
maternal pulmonary circulation;
however, fetal
•squamous cells are commonly found in
the circulation of laboring patients who
do not develop the syndrome.
Management
• Treatment is supportive.
• ∙ Administer oxygen to maintain normal
saturation. Intubate if necessary.
• ∙ Initiate cardiopulmonary resuscitation
(CPR) if the patient arrests. If she does not
respond to resuscitation, perform emergent
cesarean delivery.
• ∙ Treat hypotension with crystalloid and blood
products. Use vasopressors as necessary.
•Consider pulmonary artery
catheterization in patients who are
hemodynamically unstable.
•Continuously monitor the fetus.
• Treat coagulopathy with FFP for a
prolonged aPTT, cryoprecipitate for a
fibrinogen level less than 100 mg/dL,
and transfuse platelets for platelet
•counts less than 20,000/μL.
OBSTETRIC PATIENTS WITH CARDIAC
DISEASES

•Principle Management
•Patients with preexisting
cardiac lesions should be
counseled in advance about
•the risk of pregnancy.
General Principles of
Management
• All women of reproductive age with congenital or
acquired heart disease should have access to
specialized multidisciplinary preconception
counseling.

• All women with heart disease should be assessed

clinically as soon as possible by a multidisciplinary
team and appropriate investigations undertaken.

• A clear plan for the management of labour and the

puerperium in women with heart disease should be
established in advance and well documented.
•The main aims of management are: to
optimize the mother's condition during
the pregnancy (e.g. considering
ß-blockers, thromboprophylaxis, or
•pulmonary arterial vasodilators in
appropriate cases); to monitor for
deterioration; and minimize any
additional load on the cardiovascular
system
•from delivery and the post-partum
period.
• In the post-partum period, high-level maternal
surveillance is required until the main
haemodynamic changes after delivery have
resolved. A recent review of parturients with heart
disease found that the worst cardiac compromise
did not always occur at the time of delivery.

• The occurrence of chest infection or development of

peripartum cardiomyopathy (which may occur
anytime from 1 month pre-delivery up to 5 months
post-delivery) in some cases lead to worse
compromise post-delivery.
Nursing Care of Patients
with Acute Obstetric
Emergency
• Problem 1: Inadequate tissue perfusion related to
massive blood loss secondary to placenta previa
abruption.
• Clinical Assessment Findings
• ∙ Pallor
• ∙ Tachycardia
• ∙ MAP <70 mmHg
• ∙ Capillary refill >2 seconds
• ∙ Urine output <0.5 ml/kg/hour
• ∙ Fetal heart rate <140 beat/min
• ∙ Anxiety
Intervention
• Monitor hemodynamic status and oxygenation
(blood pressure, heart rate,
• ECG)
• - Keep MAP >70 mmHg
• - Observe ECG for myocardial ischemia
• - SpO2 >92%
• - Respiration >12/min
• - Observe CTG and keep fetal heart rate between
140-160 beat/min
• 2. Estimate ongoing fluid losses
• - Measure blood loss
• 3. Replace volume with prescribed fluids
(crystalloids/colloids)/ transfused blood
• - Keep MAP >70 mmHg
• - Capillary refill <2 seconds
• 4. Measure urine output continuously
• - Keep Urine output >0.5 ml/kg/hr
• 5. Psychological support
• - Complete rest in bed
• - Assist patient with activity daily living (ADL)
Problem 2: ‘Fluid volume deficit’ related to
massive blood loss secondary
to uterine atony
• Clinical Assessment Findings
• ∙ Pallor
• ∙ Tachycardia
• ∙ MAP <70 mmHg
• ∙ CVP <7 mmHg
• ∙ Capillary refill >2 seconds
• ∙ Urine output <0.5 ml/kg/hour
• ∙ Anxiety
Intervention
• 1. Monitor hemodynamic status and oxygenation
(blood pressure, heart rate,
• ECG)
• ∙ Keep MAP >70 mmHg
• ∙ Observe ECG for tachycardia
• ∙ SPO2 >95%
• 2. Estimate ongoing fluid losses
• ∙ Measure blood loss
• 3. Replace volume with prescribed fluids
(crystalloids/colloids)/ transfused blood
• ∙ Keep MAP >70 mmHg
• ∙ CVP >7 mmHg
• ∙ Capillary refill <2 seconds
• 4. Measure urine output continuously
• ∙ Keep Urine output >0.5 ml/kg/hr
• ∙ Psychological support
• 5. Complete rest in bed
• ∙ Assist patient with activity daily living (ADL)