Pregnancy is often accompanied by complications; although most are benign and seen as more of a nuisance to the mother, some can be severe and life threatening to both mother and baby. This article will look at the minor complications of pregnancy and the more complex, major complications of pregnancy.
The complications experienced by many pregnant women are due to the physiological changes to the body which occur in order to accommodate the developing foetus. The complications listed below are frequent occurences in pregnancy and women may find them distressing. It is important to reassure women that these complications are common. Also listed below are some labour-related complications, details of which can be found in other articles on the site.
Nausea with or without vomiting is experienced by up to 90% of pregnant women. It begins early and usually ceases by the beginning of the second trimester, although a few women may experience symptoms throughout the whole of gestation.
It has been hypothesised that nausea and vomiting may act to protect the growing foetus from toxins and studies have shown that decreased energy intake in the early weeks of gestation increases placental mass and stimulates placental growth. Although the nausea and vomiting in pregnancy has been referred to as "morning sickness", few women will experience symptoms exclusively in the morning.
Anti-emetics may be prescribed, such as metoclopramide, if the vomiting is distressing but not severe. Severe vomiting within the first 12 weeks of pregnancy is uncommon and is known as hyperemesis gravidarum. It is more often associated in women who are suffering from hyperthyroidism or a molar pregnancy. Vomiting may be so severe that the patient is unable to keep down saliva and Mallory-Weiss tears are possible. Intrauterine growth retardation and other serious complications are possible, albeit rare.
Women with hyperemesis gravidarum often require hospital admission as the continual nausea and frequent vomiting causes ketoacidosis and dehydration. It is treated with IV normal saline or Hartmann's solution and the combined use of anti-emetics and anti-reflux medications. Parenteral nutrition and corticosteroids may be considered in refractory cases. The cause of hyperemesis gravidarum is thought to be due to the effects of rising hCG levels, although it is uncertain why it does not occur in all women.
Amniotic fluid fills the amniotic cavity and is secreted by the amniotic cells. It is a clear, watery fluid derived primarily from maternal blood. It acts as a shock-absorber, allows foetal movements and plays a role in foetal lung development. The foetus swallows the amniotic fluid and excretes it via skin and urine. Too much, or, too little amniotic fluid can be pathological.
Polyhydramnios is an excess volume of amniotic fluid (1,500 to 2,000 mL or an amniotic fluid index greater than 25cm) present in the amniotic sac. It may be due to different aetiologies, including gestational diabetes and birth defects. In gestational diabetes the excess amniotic fluid may be due to the larger placenta needed to maintain a macrosomic foetus, and hence greater fluid production, or foetal hyperglycaemia may cause an osmotic diuresis. The foetal anomalies associated with polyhydramnios are ones which prevent adequate foetal swallowing. These include anencephaly and oesophageal atresia. In acute and massive cases of polyhydramnios, the mother suffers from symptoms such as dyspnoea and oedema. Amniocentesis may be required for relief of symptoms, although most women can be managed conservatively with rest. Postpartum haemorrhage is a frequent occurence in women suffering from polyhydramnios, and prophylactic oxytocin should be given.
Oligohydramnios is a paucity of amniotic fluid (less than 400 mL or amniotic fluid index of less than 5cm). It is more common than polyhydramnios and is most often associated with renal agenesis in the fetus. Early oligohydramnios is associated with spontaneous abortion, whereas later, it increases the risk of amniotic band formation, which may lead to limb defects. Distortion of the foetus may also cause club foot and wry neck. The presence of oligohydramnios also increases the risk of pulmonary hypoplasia and umbilical cord compression, which can be lethal to the foetus. An amnioinfusion may be performed, where Ringer's lactate is infused into the amniotic sac under ultrasound guidance.
In multiparous women, due to weakening of the rectus abdominis muscles, the uterus may move forward, causing a "pendulous abdomen". This can be quite uncomfortable for women and can prolong labour as the foetus is unable to engage efficiently. It is managed with an abdominal binder in pregnancy and in labour, the woman is asked to hold her uterus up to help progression.
Up to 10% of women may have a retroverted uterus (in contrast to the usual anteverted position) and in some, this may remain retroverted during pregnancy. The growing foetus compresses the bladder and if left for long enough, overflow incontinence will result. Rarely, spontaneous abortion or rupture of the uterus may occur. If a retroverted uterus has not corrected itself by around 14 weeks gestation, manual correction is indicated. If left towards the end of gestation, delivery by Caesarean section may be indicated.
The cervix and occasionally the uterine body may prolapse through the vagina in early pregnancy. This will usually correct itself in later pregnancy. Uterovaginal prolapse is more common in multiparous women and those who have had previous traumatic vaginal deliveries.
Skin changes are very common in pregnancy; increased pigmentation, spider naevi and striae are seen in many pregnant women. However, there are some specific dermatoses of pregnancy.
Polymorphic eruption or pregnancy (PEP) and prurigo of pregnancy are benign skin conditions which although uncomfortable, do not cause any harm to mother or foetus. Pemphigoid gestationis (also known as herpes gestationis), however, is a serious autoimmune skin disease. It presents with an extremely itchy eruption around the umbilicus in mid to late pregnancy. It then spreads to the extremities before developing into tense bullae. Symptoms may gradually resolve as pregnancy continues, but there is usually a flare at or after delivery.
Diagnosis is by biopsy, which will demonstrate IgG antibodies against a protein found in the basement membrane; it therefore has a similar aetiology to bullous pemphigoid. This finding helps to differentiate pemphigoid gestationis and PEP.
Pemphigoid gestationis is treated with topical or oral corticosteroids, depending on severity. Antihistamines may help to relieve pruritis.
Complications of pemphigoid gestationis may include a low birth weight baby, premature labour and intrauterine death. Foetal monitoring is therefore important. In rare cases, the baby may develop blisters, which although alarming, will clear promptly.
Gestational diabetes mellitus (GDM) is defined as glucose intolerance occuring in pregnancy. Women who are at risk for developing GDM (for example, obesity or GDM in a previous pregnancy) should be screened using the oral glucose tolerance test. If blood glucose is found to be more than 7.8 mmol/L two hours after an oral glucose load, GDM can be diagnosed. Women who develop GDM are usually obese and have insufficient pancreatic beta cell capacity to maintain normal blood glucose. Many of these women will develop type II diabetes in later life, so should be followed up closely after delivery.
Diabetes diagnosed before pregnancy should be well controlled before the woman attempts to conceive. An HbA1c of less than 6.1% is recommended and 500mg of folic acid should be taken daily up until 12 weeks gestation. Metformin can be continued in pregnant women, but many may need additional insulin treatment. Maternal complications of diabetes in pregnancy include a greater risk of hypertension and pre-eclampsia and progression of co-morbidities associated with diabetes such as retinopathy and renal disease.
Diabetes in pregnancy is a major cause of foetal malformation. The most common malformations seen are sacral agenesis and congenital heart defects. The infant of a mother who has diabetes in pregnancy will also be large (known as macrosomic). This increases the risk of emergency Caesarean section, birth trauma such as shoulder dystocia, and foetal hypoxia. Babies born to diabetic mothers must be monitored carefully; they have an increased risk of neonatal hypoglycaemia which may require treatment with IV glucose. Babies may also be more prone to developing complications such as jaundice and infant respiratory distress syndrome.
Obstetric cholestasis is a rare disorder which usually manifests itself in the third trimester with severe pruritis, which worsens as pregnancy continues. Other symptoms include anorexia, pale stools, dark urine and jaundice. Malabsorption may result in vitamin K deficiency, which can cause a coagulopathy. Obstetric cholestasis is important as it can precipitate foetal distress and intrauterine death, the cause of which is unknown.
Liver function tests will show an increased serum bile concentration and raised transaminases. Pruritis is relieved with ursodeoxycholic acid, although this is unlicensed in pregnancy. Labour is often induced before 34 weeks to prevent a stillbirth and vitamin K should be given to reduce the risk of postpartum haemorrhage. Obstetric cholestasis will resolve following delivery, although they are at an increased risk of recurrence in further pregnancies and also of gallstones.
Acute fatty liver of pregnancy (AFLP) is rare, but can be fatal for both the mother and foetus. It is associated with first pregnancies, pre-eclampsia, male foetuses, multiple pregnancy and maternal obesity. Women most often present in the third trimester with nausea, vomiting, malaise, anorexia and abdominal pain. Jaundice soon appears and pruritis may be marked. Liver failure may lead to disseminated intravasular coagulation or encephalopathy. Liver function tests are abnormal with a marked increase in transaminases and also increased neutrophils. It may be differentiated from other liver disorders by hypoglycaemia and hyperuricaemia.
Management is with immediate delivery. The mother must be supported with blood transfusion, fresh frozen plasma, albumin, platelets and 50% dextrose. Following delivery liver function usually returns to normal within a few weeks, but some may require a liver transplant.
Hypertensive disorders of pregnancy are very important as they may lead to eclampsia in the mother.
Essential hypertension prior to conception may require different management during pregnancy. Diuretics and ACE inhibitors are contraindicated and labetolol is the drug of choice. The patient should be monitored carefully and any signs of deterioration in mother or baby should be investigated promptly.
Gestational hypertension is hypertension which develops in a woman at or after 20 weeks gestation who did not have hypertension before pregnancy. It can be divided into mild, moderate and severe forms.
Mild and moderate hypertension is managed with observation and foetal monitoring. Patients with severe hypertension, however, need to be admitted to hospital until their blood pressure is lowered below 150/100mmHg. First line treatment is with oral labetalol and blood pressure and testing urine for protein is carried out frequently.
Pre-eclampsia is hypertension in association with proteinuria; the threshold is 0.3g of protein excreted in 24 hours. It usually requires hospital admission for close observation to prevent progression to eclampsia. The aetiology of pre-eclampsia is not fully understood, but it is thought that aberrant trophoblastic invasion of the spiral arteries leads to endothelial dysfunction of maternal blood vessels. Early pre-eclampsia is often asymptomatic, but in its severe form, it can present with headache, visual distubrances and epigastric and right upper abdominal pain. Signs severe pre-eclampsia include fluid retention, brief reflexes, more than three beats of ankle clonus and intrauterine growth retardation.
The definitive treatment for pre-eclampsia is delivery, but this can be a difficult decision to make if the patient presents before 34 weeks. The woman with mild to moderate pre-eclampsia may be managed expectantly before 34 weeks but severe pre-eclampsia and eclampsia are indications for immediate delivery.
Eclampsia occurs when the patient experiences a seizure in the context of pre-eclampsia. To prevent this occuring, severe pre-eclampsia should be managed by lowering blood pressure, providing anticonvulsants (magnesium sulphate), careful fluid maintenance and preparation for delivery. Before 34 weeks gestation betamethasone needs to be given to promote foetal lung maturation. If a seizure occurs, the patient should be nursed in the left lateral position, the airway secured, and magnesium sulphate given. The patient is then stabilised as for severe pre-eclampsia described above.
Throughout management blood results should be monitored carefully, since haemolysis, abnormal liver function and thrombocytopaenia are complications of pre-eclampsia, known as the HELLP syndrome (Haemolysis, Elevated Liver enzymes and Low Platelet count). HELLP syndrome is managed similarly to eclampsia with stabilisation and urgent delivery.
Pre-eclampsia and eclampsia can be lethal; multiple organ faillure, disseminated intravascular coagulation, cerebral oedema and pulmonary oedema can all contribute to death of the mother. Foetal death is most often due to complications arising from intrauterine growth retardation and premature delivery.
A detailed description of antepartum haemorrhage can be found here.
1. Oats J, Abraham S. Llewellyn-Jones Fundamentals of Obstetrics and Gynaecology. 9th ed. St-Louis: Mosby Elsevier; 2010.
2. Chamberlain G, Steer P. Turnbull's Obstetrics. 3rd ed. London: Churchill Livingstone; 2001.
3. Baker PN. Obstetrics by Ten Teachers 18th ed. London: Hodder Education; 2006.
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