Cardiovascular system

Cardiac output and plasma volume return to normal within approximately 1 week. There is a fluid loss of 2 L during the first week and a further loss of 1.5 L over the next 5 weeks. This loss is associated with an apparent increase in haematocrit and haemoglobin concentration. There is an increase of serum sodium and plasma bicarbonate as well as plasma osmolality. An increase in clotting factors during the first 10 days after delivery is associated with a higher risk of deep vein thrombosis and pulmonary embolism. There is also a rise in platelet count and greater platelet adhesiveness. Fibrinogen levels decrease during labour but increase in the puerperium.

Endocrine changes

There are rapid changes in the endocrine system in all facets. There is a rapid fall in the serum levels of oestrogens and progesterone and they reach non-pregnant levels by the 7th postnatal day. This is associated with an increase in serum prolactin levels in those women who breastfeed. By the tenth postnatal day, human chorionic gonadotrophin (hCG) is no longer detectable.

Breastfeeding

The breasts and nipples should be washed regularly. The breasts should be comfortably supported and aqueous-based emollient creams may be used to soften the nipple and thus avoid cracking during suckling. Suckling is initially limited to 2–3 minutes on each side, but subsequently this period may be increased. Once the mother is comfortably seated, the whole nipple is placed in the infant’s mouth, taking care to maintain a clear airway (Fig. 13.2). Correct attachment of the baby to the breast is essential to the success of breastfeeding. The common problems such as sore nipples, breast engorgement and mastitis usually occur because the baby is poorly attached to the breast or is not fed often enough. Most breastfeeding is given on demand and the milk flow will meet the demand stimulated by suckling. Once the baby is attached correctly to the nipple, the sucking pattern changes from short sucks to long deep sucks with pauses. It may, on occasions, be necessary to express milk and store it, either because of breast discomfort or cracked nipples or because the baby is sick. Milk can be expressed manually or by using hand or electric pumps. Breast milk can be safely stored in a refrigerator at 2–4°C for 3–5 days or frozen and stored for up to 3 months in the freezer.

In women who choose not to breastfeed, have suffered a stillbirth or intrauterine death or where there is a contraindication to breast feeding, suppression of lactation may be achieved by conservative methods or by drug therapy. Firm support of the breasts, restriction of fluid intake, avoidance of expression of milk and analgesia may be sufficient to suppress lactation. The administration of oestrogens will effectively suppress lactation but carries some risk of thromboembolic disease. The preferred drug therapy is currently the dopamine receptor agonist cabergoline. This can be given as a single dose and will inhibit prolactin release and hence suppress lactation. Bromocriptine is also effective, but the dosage necessary to produce this effect tends to create considerable side effects.

Endometritis

The patient with endometritis usually presents with fever, lower abdominal pain, secondary postpartum haemorrhage and foul smelling vaginal discharge. The organisms involved are group A β-haemolytic streptococci, aerobic Gram negative rods and anaerobes. On examination, the patient often has a fever, is tachycardic and is tender on palpation of the lower abdomen. There may be foul smelling vaginal discharge, bleeding and cervical excitation. The white cell count and C-reactive protein may be raised. Vaginal or blood cultures may identify the organism responsible. Broad spectrum antibiotics are the first-line treatment and resolution should start to occur within the first 48 hours. The complications of endometritis are parametritis, peritonitis, septic pelvic thrombophlebitis, pelvic abscesses and rarer is toxic shock syndrome.

Urinary tract infections (UTIs)

UTIs are the most common cause of puerperal infections. The predisposing factors include a history of previous UTIs, polycystic kidneys, congenital abnormalities of the renal tract, neuropathic bladder, urinary tract calculi but most are idiopathic. Patients present with voiding difficulties (e.g. urgency and frequency), dysuria, fever and pain in the renal angle. Urine analysis may be positive for protein and leucocytes, though nitrites are more sensitive. Urine should be sent for culture before commencing antibiotic treatment. The commonest organisms are Escherichia coli, Enterococcus, Klebsiella, Proteus and Staphylococcus epidermidis.

Mastitis and breast abscess

Presenting symptoms include breast pain, fever and erythema. The commonest organisms are S. aureus, S. epidermidis, or group A, B and F streptococci. Oral antibiotics are usually sufficient for mastitis but intravenous treatment is required for an abscess. In the case of an abscess, fluctuance will be elicited and surgical drainage may be warranted.

Caesarean wound infections and perineal infections

Puerperal infection is more common in caesarean sections than vaginal deliveries. Intraoperative antibiotics have helped reduce the incidence. The commonest organisms involved are S. aureus, methicillin-resistant S. aureus (MRSA), skin flora and those involved with endometritis. Complications include wound dehiscence and necrotizing fasciitis. Infection may also occur in episiotomy wounds or perineal tears, although these infections are relatively uncommon because the vascularity of the perineum provides a higher resistance to infection. The perineum becomes tender and reddened and may be seen to exude purulent discharge. Where wound breakdown occurs, the wound should be kept clean and allowed to heal by secondary intention. Resuturing should not be performed unless the wound is clean and there is no residual inflammation around the wound margins.

Other infections

Once more common sites of infection have been excluded, one must consider other sites of infection or sepsis. These include pneumonia, meningitis, bacterial endocarditis or even influenza, malaria and H1N1. The incidence of chest infection is greater in caesarean sections than vaginal births due to reduced mobility and reduced air entry secondary to pain or if the patient has had a general anaesthetic.

This is the commonest form of thromboembolic disease and tends to arise within the first 3–4 days after delivery. Localized inflammation, tenderness and thickening occur in the superficial leg veins. Although the condition is painful and may spread along the leg veins, it rarely leads to serious embolic disease and does not require anticoagulant treatment. Anti-inflammatory drugs and local applications of glycerine and ichthyol should be used.

Primary and secondary postpartum haemorrhage (PPH)

Please see Chapter 12.

Anaemia

If the haemoglobin (Hb) is less than 7–8 g/dL in the postnatal period, where there is no continuing or threat of bleeding, the decision to transfuse should be made on an informed individual basis. In fit, healthy, asymptomatic patients there is little evidence of the benefit of blood transfusion. If severe bleeding was encountered and if bleeding disorders were suspected, appropriate investigations should be made. These investigations should be repeated on a non-urgent basis at least 3–6 months after delivery when pregnancy-related coagulation changes have settled.

Oral iron should be the preferred first-line treatment for iron deficiency. Parenteral iron is indicated when oral iron is not tolerated, absorbed or patient compliance is in doubt. Parenteral therapy offers a shorter duration of treatment and a quicker response than oral therapy. It is, however, more invasive and expensive to administer. Iron sucrose is given in multiple doses whereas iron dextran may be given as a single total-dose infusion. Recombinant human erythropoietin (rHuEPO) is mostly used in the anaemia of end-stage renal disease.

Maternal collapse

Maternal collapse is defined as an acute event involving the cardiorespiratory systems and/or brain, resulting in a reduced or absent conscious level (and potentially death), at any stage in pregnancy and up to 6 weeks after delivery. An obstetric early warning score chart should be used routinely for all women, to allow early recognition of the woman who is becoming critically ill. In some cases maternal collapse occurs with no prior warning, although there may be existing risk factors that make this more likely. Antenatal care for women with significant medical conditions at risk of maternal collapse should include multidisciplinary team input with a pregnancy and delivery management plan in place.

There are many causes of collapse, and these may be pregnancy-related or result from conditions not related to pregnancy and possibly existing before pregnancy. The common reversible causes of collapse in any woman can be remembered using the 4 Ts and the 4 Hs employed by the Resuscitation Council (UK) (Table 13.1). In the pregnant woman, eclampsia and intracranial haemorrhage should be added to this list.

Haemorrhage is the most common cause of maternal collapse. In most cases of massive haemorrhage leading to collapse, the cause is obvious, but concealed haemorrhage should not be forgotten, including following caesarean section. Other rare causes of concealed haemorrhage include splenic artery rupture and hepatic rupture.

In the UK, thromboembolism is the most common cause of direct maternal death. Appropriate use of thromboprophylaxis has improved maternal morbidity and mortality, but improvements in clinical risk assessment and prophylaxis are still required.

Amniotic fluid embolism (AFE) presents as collapse during labour or delivery or within 30 minutes of delivery in the form of acute hypotension, respiratory distress and acute hypoxia. Seizures and cardiac arrest may occur. There are different phases to disease progression; initially, pulmonary hypertension may develop secondary to vascular occlusion either by debris or by vasoconstriction. This often resolves and left ventricular dysfunction or failure develops. Coagulopathy often occurs resulting in a massive postpartum haemorrhage. The underlying pathophysiological process has been compared to anaphylaxis or severe sepsis. Clinically, an AFE can be suspected, but a definitive diagnosis can only be made on post-mortem.

Cardiac disease was the most common overall cause of maternal death in the UK from 2006 to 2008. The majority of deaths secondary to cardiac causes occur in women with no previous history. The main cardiac causes of death are myocardial infarction, aortic dissection and cardiomyopathy. Primary cardiac arrest in pregnancy is rare and most cardiac events have preceding signs and symptoms. Aortic root dissection can present with central chest or interscapular pain and a wide pulse pressure, mainly secondary to systolic hypertension. A new cardiac murmur must prompt referral to a cardiologist and appropriate imaging. The incidence of congenital and rheumatic heart disease in pregnancy is increasing secondary to improved management of congenital heart disease and increased immigration. Other cardiac causes include dissection of the coronary artery, acute left ventricular failure, infective endocarditis and pulmonary oedema.

Bacteraemia, which can be present in the absence of pyrexia or a raised white cell count, can progress rapidly to severe sepsis and septic shock leading to collapse. The most common organisms implicated in obstetrics are the streptococcal groups A, B and D, Pneumococcus and E. coli.

Drug toxicity/overdose should be considered in all cases of collapse, and illicit drug overdose should be remembered as a potential cause of collapse outside of hospital. In terms of therapeutic drug toxicity, the common sources in obstetric practice are magnesium sulphate in the presence of renal impairment and local anaesthetic agents injected intravenously by accident. Effects initially include a feeling of inebriation and lightheadedness followed by sedation, circumoral paraesthesia and twitching; convulsions can occur in severe toxicity. On intravenous injection, convulsions and cardiovascular collapse may occur very rapidly. Local anaesthetic toxicity resulting from systemic absorption of the local anaesthetic may occur sometime after the initial injection. Signs of severe toxicity include sudden loss of consciousness, with or without tonic–clonic convulsions, and cardiovascular collapse.

Eclampsia as the cause of maternal collapse is usually obvious in the inpatient setting, as often the diagnosis of pre-eclampsia has already been made and the seizure witnessed. Intracranial haemorrhage is a significant complication of uncontrolled, particularly systolic, hypertension, but can also result from ruptured aneurysms and arteriovenous malformations. The initial presentation may be maternal collapse, but often severe headache precedes this.

Anaphylaxis causes a significant intravascular volume redistribution, which can lead to decreased cardiac output. Acute ventricular failure and myocardial ischaemia may occur. Upper airway occlusion secondary to angioedema, bronchospasm and mucous plugging of smaller airways all contribute to significant hypoxia and difficulties with ventilation. Common triggers are a variety of drugs, latex, animal allergens and foods.

Other causes of maternal collapse include hypoglycaemia and other metabolic/electrolyte disturbances, other causes of hypoxia such as airway obstruction secondary to aspiration/foreign body, air embolism, tension pneumothorax and cardiac tamponade secondary to trauma and, rarely, hypothermia.

The management of maternal collapse in the UK follows the Resuscitation Council (UK) guidelines using the standard A, B, C approach: airways, breathing and circulation. The airway should be protected as soon as possible by intubation with a cuffed endotracheal tube and supplemental oxygen should be administered. Bag and mask ventilation should be undertaken until intubation can be achieved. In the absence of breathing despite a clear airway, chest compressions should be commenced immediately. Two wide-bore cannulae should be inserted as soon as possible, to enable an aggressive approach to volume replacement. Abdominal ultrasound by a skilled operator can assist in the diagnosis of concealed haemorrhage. The same defibrillation energy levels should be used as in the non-pregnant patient. There should normally be no alteration in algorithm drugs or doses. Common, reversible causes of maternal cardiopulmonary arrest should be considered throughout the resuscitation process. If cardiac output is not restored after 3 minutes of CPR in a woman who is still pregnant the fetus should be delivered by caesarean section as this will improve the effectiveness in maternal resuscitation efforts and may save the baby. Resuscitation efforts should be continued until a decision is taken by the consultant obstetrician, and consultant anaesthetist in consensus with the cardiac arrest team. Senior staff with appropriate experience should be involved at an early stage. Accurate documentation in all cases of maternal collapse, whether or not resuscitation is successful, is essential. Debriefing is recommended for the woman, her family and the staff involved in the event. All cases of maternal collapse should generate a clinical incident form and the care should be reviewed through the clinical governance process. All cases of maternal death should be reported to CMACE.