84 Antenatal obstetric complications

require MSU specimens to be sent to the microbiology Table 6.1 Causes of abdominal pain in
laboratory at each antenatal visit, and low-dose prophy- pregnancy
lactic oral antibiotics may be prescribed. Investigation
Obstetric conditions
should take place after delivery, unless frank haematu-
ria or other symptoms suggest that an urgent diagnosis Early pregnancy (<24 weeks)
is essential. Investigations might include a renal ultra- Ligament stretching
sound scan, renal dimercaptosuccinic acid (DMSA)
Miscarriage
function scan, creatinine clearance, intravenous uro-
gram and cystoscopy. Ectopic pregnancy
Acute urinary retention due to retroverted gravid uterus

Abdominal pain in pregnancy Later pregnancy (>24 weeks)

Labour
Abdominal pain is one of the commonest minor dis-
Placental abruption
orders of pregnancy; the problem is in distinguish-
ing pathological from ‘physiological’ pain. There are HELLP syndrome
many possibilities to exclude and in addition, the Uterine rupture
anatomical and physiological changes of pregnancy
Chorioamnioitis
may alter ‘classical’ presenting symptoms and signs,
making clinical diagnosis challenging. The causes Pregnancy-unrelated conditions
listed in Table 6.1 are not exhaustive, but cover most
possible diagnoses. The crucial point to make is that Uterine/ovarian causes
certain conditions are potentially so dangerous or Torsion or degeneration of fibroid
debilitating (e.g. acute appendicitis), and may be Ovarian cyst accident
masked by the altered anatomy and physiology of
pregnancy, that obstetricians may have to perform Urinary tract disorders
X-rays and arrange invasive assessments to make a Urinary tract infection (acute cystitis and acute
diagnosis. To avoid this, and risk not making an early pyelonephritis)
diagnosis, means that women may not be treated
Renal colic
appropriately for possibly very serious conditions.
Gastrointestinal disorders
Medical gastric/duodenal ulcer
Venous thromboembolism
Acute appendicitis
Venous thromboembolism (VTE) is the most com- Acute pancreatitis
mon cause of direct maternal death in the UK. In the
Acute gastroenteritis
most recent Confidential Enquiries into Maternal
Deaths and Morbidity (2009–2012), there were 26 Intestinal obstruction or perforation
fatalities, giving a maternal mortality rate of 1.08 per
Medical causes
100,000, more than twice that of the next most com-
mon cause (genital tract sepsis). Sickle cell disease (abdominal crisis)
Pregnancy is a hypercoagulable state because of Diabetic ketoacidosis
an alteration in the thrombotic and fibrinolytic sys-
Acute intermittent porphyria
tems. There is an increase in clotting factors VIII, IX,
X and fibrinogen levels, and a reduction in protein S Pneumonia (especially lower lobe)
and antithrombin (AT) III concentrations. The net Pulmonary embolus
result of these changes is thought to be an evolution-
Malaria
ary response to reduce the likelihood of haemor-
rhage following delivery. HELLP, haemolysis, elevated liver enzymes and low platelets.

These physiological changes predispose a woman
to thromboembolism and this is further exacerbated
by venous stasis in the lower limbs due to the weight
of the gravid uterus placing pressure on the IVC in
late pregnancy and immobility, particularly in the
puerperium.
Pregnancy is associated with a 6–10-fold increase
in the risk of VTE compared to the non-pregnant
situation. Without thromboprophylaxis, the inci-
dence of non-fatal pulmonary embolism (PE) and
deep vein thrombosis (DVT) in pregnancy is about
0.1% in developed countries; this increases following
delivery to around 1–2% and is further increased fol-
lowing emergency caesarean section.
Risk factors for
thromboembolic disease
• Pre-existing:
• maternal age (>35 years);
• thrombophilia;
• obesity (>80 kg);
• previous thromboembolism;
• severe varicose veins;
• smoking;
• malignancy.
• Specific to pregnancy:
• multiple gestation;
• pre-eclampsia;
• grand multiparity;
• caesarean section, especially
if emergency;
• damage to the pelvic veins;
• sepsis;
• prolonged bed rest.
Thrombophilia
Some women are predisposed to thrombosis through
changes in the coagulation/fibrinolytic system that
may be inherited or acquired. There is growing
evidence that both heritable and acquired throm-
bophilias are associated with a range of adverse
pregnancy outcomes, particularly recurrent fetal
loss. The major hereditary forms of thrombophilia
currently recognized include: deficiencies of the
endogenous anticoagulants protein C, protein S and
Venous thromboembolism 85
AT III; abnormalities of procoagulant factors, factor
V Leiden (caused by a mutation in the factor V gene)
and the prothrombin mutation G20210A. It seems
probable that there are still some thrombophilias not
yet discovered or described. Heritable thrombophil-
ias are present in at least 15% of Western populations.
Acquired thrombophilia is most commonly
associated with antiphospholipid syndrome (APS).
APS is the combination of lupus anticoagulant with
or without anticardiolipin antibodies, with a history
of recurrent miscarriage and/or thrombosis. It may
(or, more commonly, may not) be associated with
other autoantibody disorders such as systemic lupus
erythematosus (SLE).
If thrombophilic disorders are taken together,
more than 50% of women with pregnancy-related
VTE will have a thrombophilia. It is therefore vital
that women with a history of thrombotic events are
screened for thrombophilia. The presence of throm-
bophilia, with a history of thrombotic episode(s),
means that prophylaxis should be considered for
pregnancy.
Diagnosis of acute venous
thromboembolism
Clinical diagnosis of VTE is unreliable. Therefore,
women who are suspected of having a DVT or PE
should be investigated promptly.
Deep vein thrombosis
The commonest symptoms are pain in the calf with
varying degrees of redness or swelling. Women’s legs
are often swollen during pregnancy, therefore unilat-
eral symptoms should ring alarm bells. The signs are
few, except that often the calf is tender to gentle touch.
It is mandatory to ask about symptoms of PE (see later),
as a woman with PE might present initially with a DVT.
Compression ultrasound has a high sensitivity
and specificity in diagnosing proximal thrombosis
in the non-pregnant woman and should be the first
investigation used in a suspected DVT. Calf veins are
often poorly visualized; however, it is known that a
thrombus confined purely to the calf veins with no
extension is very unlikely to give rise to a PE.
Venography is invasive, requiring the injection
of contrast medium and the use of X-rays. It does,
however, allow excellent visualization of veins both
below and above the knee.
86 Antenatal obstetric complications
Pulmonary embolus
It is crucial to recognize PE, as missing the diagno-
sis could have fatal implications. The most common
presentation is of mild breathlessness or inspira-
tory chest pain in a woman who is not cyanosed
but may be slightly tachycardic (>90 bpm) with a
mild pyrexia (37.5°C). Rarely, massive PE may pres-
ent with sudden cardiorespiratory collapse (see
Chapter 14, Obstetric emergencies).
If PE is suspected, initial electrocardiogram
(ECG), chest X-ray and arterial blood gases should
be performed to exclude other respiratory diagno-
ses. However, these investigations are insufficient on
their own to exclude or diagnose PE and it may be
sensible to investigate the lower limbs for evidence of
DVT by ultrasound, and if positive treat with a pre-
sumptive diagnosis of PE. If all the tests are normal
but a high clinical suspicion of PE remains, a ven-
tilation perfusion (V/Q) scan or computed tomog-
raphy pulmonary angiogram (CTPA) should be
performed. In both cases the radiation to the fetus is
below the threshold considered potentially danger-
ous to the fetus.
D-dimer is now commonly used as a screening
test for thromboembolic disease in non-pregnant
women, in whom it has a high negative predictive
value. Outwith pregnancy, a low level of D-dimer
suggests the absence of a DVT or PE, and no
further objective tests are necessary, while an
increased level of D-dimer suggests that throm-
bosis may be present and an objective diagnostic
test for DVT and/or PE should be performed. In
pregnancy, however, D-dimer can be elevated due
to the physiological changes in the coagulation
system, limiting its clinical usefulness as a screen-
ing test in this situation.
Treatment of VTE
Warfarin is given orally and prolongs the prothrom-
bin time (PT). Warfarin is rarely recommended for
use in pregnancy (exceptions include women with
mechanical heart valves) as it crosses the placenta
and can cause limb and facial defects in the first tri-
mester and fetal intracerebral haemorrhage in the
second and third trimesters.
Low molecular weight heparins (LMWHs)
are now the treatment of choice. They do not cross
the placenta and have been shown to be at least as
safe and effective as unfractionated heparin (UFH)
in the treatment of VTE, with lower and fewer haem-
orrhagic complications in the initial treatment of
non-pregnant subjects. In addition, LMWH is safe
and easy to administer. Women are taught to inject
themselves and can continue on this treatment for
the duration of their pregnancy.
Following delivery, women can choose to convert
to warfarin (with the need for stabilization of the
doses initially and frequent checks of the interna-
tional normalized ratio (INR) or remain on LMWH.
Both warfarin and LMWH are safe in women who
are breast feeding. Newer anticoagulants such as
fondaparinux (a direct factor Xa inhibitor) and lepi-
rudin (a direct thrombin inhibitor) are not licensed
for use in pregnancy and experience with them is
limited.
Graduated elastic stockings should be used for
the initial treatment of DVT and should be worn for
2 years following a DVT to prevent post-thrombotic
syndrome.
Prevention of VTE in
pregnancy and postpartum
The Royal College of Obstetricians and
Gynaecologists has recently released updated guide-
lines on the prevention of thrombosis and embo-
lism in pregnancy and the puerperium (Green-top
Guideline No. 37a, April 2015) and these are sum-
marized in Figure 6.2.
KEY LEARNING POINTS
• Screening for thrombophilias should be carried out in
those with a strong family or personal history of VTE.
• Rapid treatment of suspected VTE in pregnancy
should be commenced while awaiting diagnosis.
• LMWHs are the treatment of choice.
• Graduated compression stockings should be fitted
and worn for 2 years to reduce the incidence of post
thrombotic syndrome.
Substance abuse in pregnancy
Approximately one-third of adults who access drug ser-
vices are women of reproductive age. There are approx-
imately 6,000 births to problem drug users in the UK
 Antenatal assessment and management (to be assessed at Postnatal assessment and management (to be assessed
booking and repeated if admitted) on delivery suite)

Any previous VTE

HIGH RISK HIGH RISK
Anyone requiring antenatal LMWH
Requires antenatal prophylaxis High-risk thrombophilia At least 6 weeks’
Any previous VTE except a single event
with LMWH postnatal prophylactic LMWH
related to major surgery Low-risk thrombophilia + FHx
Refer to trust-nominated thrombosis
in pregnancy expert/team
Caesarean section in labour
Hospital admission
BMI ≥40 kg/m2
Single previous VTE related to major surgery
Readmission or prolonged admission INTERMEDIATE RISK
High-risk thrombophilia + no VTE (≥3 days) in the puerperium
Medical comorbidities (e.g. cancer, heart failure, At least 10 days’
active SLE, IBD or inflammatory polyarthro- Any surgical procedure in the puerperium except postnatal prophylactic LMWH
INTERMEDIATE RISK
pathy, nephrotic syndrome, type I DM with immediate repair of the perineum
Consider antenatal prophylaxis NB If persisting or >3 risk factors
nephropathy, sickle cell disease, current IVDU)
with LMWH consider extending
Any surgical procedure (e.g. appendicectomy) Medical comorbidities (e.g. cancer, heart failure,
thromboprophylaxis with LMWH
active SLE, IBD or inflammatory polyarthropathy;
OHSS (first trimester only) nephrotic syndrome, type I DM with nephropathy,
sickle cell disease, current IVDU)

Obesity (BMI >30 kg/m2)

Age >35 years
Age >35 years
Obesity (BMI >30 kg/m2)
Parity ≥3 Four or more risk factors: Two or
Parity ≥3 more risk
Smoker prophylaxis from first trimester
Smoker factors
Gross varicose veins
Three risk factors: Elective caesarean section
Current pre-eclampsia
prophylaxis from 28 weeks Family history of VTE
Immobility (e.g. paraplegia, PGP)
Low-risk thrombophilia
Family history of unprovoked or oestrogen
Fewer than Gross varicose veins
provoked VTE in first-degree relative
three risk
Low-risk thrombophilia Current systemic infection
factors
Multiple pregnancy Immobility (e.g. paraplegia, PGP, Fewer than
long-distance travel) two risk
IVF/ART factors
Current pre-eclampsia
LOWER RISK
Transient risk factors:

Substance abuse in pregnancy

Multiple pregnancy
Dehydration/hyperemesis; current systemic Mobilization and
avoidance of dehydration Preterm delivery in this pregnancy (<37 +° weeks)
infection; long-distance travel
Stillbirth in this pregnancy LOWER RISK
Midcavity rotational or operative delivery Early mobilization and
APL, antiphospholipid antibodies (lupus anticoagulant, anticardiolipin antibodies,
avoidance of dehydration
β2-glycoprotein 1 antibodies); ART, assisted reproductive technology; BMI based on booking weight; Prolonged labour (>24 hours)
DM, diabetes mellitus; FHx, family history; gross varicose veins, symptomatic, above knee or associated
PPH >1 litre or blood transfusion
with phlebitis/oedema/skin changes; high-risk thrombophilia, antithrombin deficiency, protein
C or S deficiency, compound or homozygous for low-risk thrombophilias; IBD, inflammatory bowel
disease; immobility, ≥ 3 days; IVDU, intravenous drug user; IVF, in vitro fertilisation; LMWH, low-molecular- Antenatal and postnatal prophylactic dose of LMWH
weight heparin; long-distance travel, >4 hours; low-risk thrombophilia, heterozygous for factor V Leiden Weight <50 kg = 20 mg enoxaparin/2,500 units dalteparin/3,500 units tinzaparin daily
or prothrombin G20210A mutations; OHSS, ovarian hyperstimulation syndrome; PGP, pelvic girdle pain Weight 50–90 kg = 40 mg enoxaparin/5,000 units dalteparin/4,500 units tinzaparin daily
with reduced mobility; PPH, postpartum haemorrhage; thrombophilia, inherited or acquired; Weight 91–130 kg = 60 mg enoxaparin/7,500 units dalteparin/7,000 units tinzaparin daily
VTE, venous thromboembolism. Weight 131–170 kg = 80 mg enoxaparin/10,000 units dalteparin/9,000 units tinzaparin daily
Weight >170 kg = 0.6 mg/kg/day enoxaparin/ 75 u/kg/day dalteparin/ 75 u/kg/day tinzaparin

Figure 6.2 Obstetric thromboprophylaxis risk assessment and management. (Adapted from RCOG Green-top Guideline No. 37a, April 2015.)

87

Thrombosis and
thromboembolism
Thrombosis and thromboembolism is once again
the leading cause of direct maternal death in
the 2009–2012 triennium, resulting in 26 direct
maternal deaths (rate of 1.08 per 100,000 preg-
nancies). Venous thromboembolism (VTE) is 10
times more common in pregnancy compared with
non-pregnant women. Women with VTE may be
asymptomatic or present with a range of symp-
toms (specific and non-specific) including calf or
groin pain and/or swelling that is often unilat-
eral, low-grade pyrexia to more extreme presenta-
tions including haemoptysis, shortness of breath,
collapse and death.
Thrombosis and thromboembolism:
prevention/risk factors/
warning signs
• Prevention: thrombosis assessment should
be performed on all patients early in preg-
nancy as per RCOG guideline, to assess
need for antenatal thromboprophylaxis and
on each admission to hospital to assess for
additional risk factors; managing patients
where possible as outpatients and limiting
bed rest; thromboembolic stockings; pro-
phylactic low-molecular-weight heparin for
at-risk patients.
• Risk factors: immobility, obesity, increased
maternal age (≥35), underlying medical
conditions, pre-eclampsia, dehydration,
multiple pregnancy, raised body mass index
(BMI) (≥30 kg/m2), smoker, grand multiparity,
thrombophilia.
• Warning signs: immobility, dehydration, calf
pain, shortness of breath.
When deep vein thrombosis (DVT) is sus-
pected clinically, compression duplex ultrasound
should be undertaken. If this is negative and there
is a low level of clinical suspicion, anticoagulant
treatment can be discontinued. If clinical sus-
picion remains high or symptoms fail to resolve,
ultrasound may be repeated or magnetic resonance
venography may be performed. When pulmonary
embolus is suspected, investigative options include
Uterine inversion 267
chest X-ray (to rule out other respiratory causes
of chest symptoms such as pneumonia), low limb
Doppler to rule out lower limb VTE and finally
a ventilation perfusion (V/Q scan) or computed
tomography pulmonary angiography. The mea-
surement of D-dimers is not helpful and should not
be performed as they are often elevated secondary
to physiological changes in the coagulation system
in pregnancy. Treatment of confirmed or suspected
VTE is with therapeutic low-molecular-weight
heparin given daily in two divided doses according
to the patient’s weight. In the case of a collapsed
patient with pulmonary embolus, management
options include intravenous unfractionated hepa-
rin, thrombolytic therapy or thoracotomy and
surgical embolectomy. This complex management
decision is taken by the multidisciplinary resusci-
tation team including senior physicians, obstetri-
cians and radiologists.
Uterine inversion
Uterine inversion occurs when the uterus is partially
or wholly inverted (Figure 14.10). Four degrees of
inversion have been described: first degree when the
inverted fundus extends to but not through the cer-
vix; second degree when the inverted fundus extends
through cervix but remains within the vagina; third
degree when the inverted fundus extends outside
the vagina; finally, total inversion occurs when the
vagina and uterus are inverted. Prompt recognition
is essential as the longer it is inverted the more dif-
ficult it becomes to replace as a retraction ring form
forms, preventing eversion.
Uterine inversion: prevention/
risk factors/warning signs
• Prevention: senior inhouse supervision and
help to deal with this emergency.
• Risk factors: full dilatation sections, mal-
presentations, prolonged second stage,
intravenous Syntocinon™ prior to a decision
to deliver by caesarean section, unsuccess-
ful instrumental delivery, prolonged second
stage, hyperstimulated uterus.
• Warning signs: see risk factors.