Medical disorders during pregnancy
Minor
Symptoms
Gastro-oesophageal reflux due to
relaxation of the sphincter
Difficulty with breathing at night
Oedema and potential carpal tunnel
syndrome, related to increased water
retention, increased blood volume and
prolonged standing
Supine hypotension, due to aortocaval
compression
Postural hypotension due to
obstructed lower limb venous flow
Urinary frequency due to increased
pressure on bladder
Loin pain from ureteric obstruction
Back and pelvic pain from the descent
of fetal head and relaxation of pelvic
ligaments
Symphysis pubis dysfunction where
the joint becomes loose in 3rd trimester
Suggestions
Eat frequent, small meals, avoid
caffeine, spicy food and to take
antacids if severe, stop smoking
Sleep in a supported lateral position
Support hose and regular exercise, and
physiotherapy and wrist splints for
carpal tunnel syndrome
Sleep in lateral position, massage, heat
packs and pelvic rock exercise
Improves after delivery and can Mx
with simple analgesia and a low
stability belt
High-fibre diet and lactulose
Constipation from progesterone
slowing gut motility, weight on the
rectum and iron tablets
Varicose veins and haemorrhoids
Support stockings, avoidance of
caused by relaxation of vascular
standing, simple analgesia
smooth muscle due to progesterone,
local anaesthetics, anti-irritant, highand weight on the IVC
fibre diet
Not so minor
Hyperemesis gravidarum
 Excessive pregnancy-related nausea +/- vomiting that prevents adequate
food and fluid intake and associated with weight loss >5% body weight
 <3% pregnancies, begins at 4-6/52 and peak between 9-13/52.
 In 10-20% of pregnancies, symptoms last for entire pregnancy 
 Complications: Dehydration, nutritional deficiency, metabolic imbalance
 HCG has been thought to be responsible. High levels associated with twin
and molar pregnancies and hyperthyroidism.
 In severe cases the fetus is at risk of growth restriction
 Ddx: Fatty liver of pregnancy and pre-eclampsia (typically in third
trimester), acute appendicitis, UTI, biliary tract disorders, gastroenteritis,
diabetic ketoacidosis, Grave’s disease
Physiology
 Continued vomiting leads to hypokalaemia, hyponatraemia,
hypochloraemic alkalosis and a decrease in ECF volume

Urine output is decreased from the hyperosmolar stiumulation of ADH
and reduced GFR.
Cause
Symptoms
Management
Hypokalaemia
thirst, malaise, dizziness IV normal saline or Hartmann’s
and reduced ECF
when standing and
+ potassium chloride
volume
syncope
supplementation. Do not correct
severe hyponatraemia too
Dehydration
postural hypotension
quickly as this may precipitate
and fever
Hyponatraemia
Listlessness, convulsions, central pontine myelinolysis.
Total parenteral nutrition.
respiratory arrest
Prolonged
vomiting
Mallory Weiss tears
Use anti-emetics with caution in
first 10/52.
1. Metoclopramide,
phenothiazines and 5HT3
antagonists are most
commonly used.
2. Powdered ginger and
vitamin B6 (30mg
pyridoxine daily)
3. Hydrocortisone and
Prednisolone
Nutritional
deficiencies (B1,
B6, B12)
Anaemia, peripheral
neuropathy, Wernicke’s
encephalopathy, pontine
myelinolysis
Vitamin supplements
Ix: Midstream urine, urine dipstick (high specific gravity and ketones), FBE
(haemotocrit increased), U&E, LFT, TFT
Anaemia
Physiological anaemia of pregnancy
 Plasma volume increases more rapidly than the erythrocyte mass
 Lowest Hb at 25-26/52
 Hb < 110 in 1st trimester or <100 in late 2nd and 3rd trimesters
should be investigated further
Iron deficiency anaemia, Thalassemia, Sickle cell syndrome
Isoimmunization
 Fetal cells may cross the placenta during pregnancy and enter maternal
circulation exposing the mother to ‘foreign’ red cell antigens
 Mother develops IgG which are transferred to the fetus and increases
slowly between 12-24/52 and exponentially after that to term
 HDN (haemolytic disease of the newborn) is when the infant’s red cells
are shortened by the action of the mother’s antibodies and its red cells
are removed by the fetal liver and spleen leading to anaemia
 Anti-Rh (D) anti-Rh (c) and anti-Kell cause severe HDN
 Rh E, C, e, Duffy (Fya), Kid (Jka) and Lutheran (Lua) are common but
cause mild to mod HDN.


VTE



PE


Investigate with indirect antiglobulin test (IAT) and monitor antibodies
by titration of quantitation. Other tests: cordocentesis,
spectrophotometric examination of amniotic fluid(to determine presence
of bilirubin), peak systolic middle cerebral artery flow
Give anti-D IgG which will bind to any fetal RhD cells in the mother’s
circulation allowing them to be cleared
1. Give to women with a history of threatened or spontaneous
miscarriage, invasive procedures, trauma, placental abruption
2. routinely at 28 and 34 weeks gestation
3. at delivery if baby is RhD positive.
Pregnancy is pro-thrombotic state with an increase in coagulation
factors, thrombin and plasminogen activation, impairment of venous
return in the lower limbs, immobilisation (hospitalisation) and surgery
(Caesarean section)
Treatment is the same as in non-pregnant state except that warfarin is
not used until post-partum (teratogenic!).
Treat for duration of pregnancy with heparin (unfractionated or more
commonly LMWH), then omitted on the day of delivery and recommenced
until 6/52 postpartum. The woman may change to warfarin post-partum.
PE after caesarean section occurs after 1/52, and 2/52 after vaginal birth.
Treat with therapeutic heparin for 6/12. If the PE is close to the due date,
a venal caval filter may be necessary.