Pregnancy is associated with profound anatomical, physiological, biochemical and endocrine changes that affect multiple organs and systems. Red blood cell (RBC) volume falls during the first 8 weeks of pregnancy, increasing back to non-pregnant levels by 16 weeks and then rising to 30 percentage above non-pregnant levels by term. Marked physiological changes of cardiovascular system, respiratory system, renal system, and gastrointestinal system are significantly observed. During pregnancy the skin undergoes a number of changes, mainly thought to be due to hormonal changes. The additional demand for folate during pregnancy leads to a rapid fall in red cell folate and to a high incidence of megaloblastic anaemia in those women taking anticonvulsant drugs for control of epilepsy. For appendicectomy the type of incision depends on the gestation and the location of the appendix. The routine use of urinalysis for monitoring of glycaemic control during pregnancy is unreliable.

Maternal collapse is an acute life-threatening event where the mother becomes unconscious due to cardiorespiratory or neurological compromise at any stage in pregnancy or up to 6 weeks postpartum. During resuscitation, aortocaval compression reduces cardiac output during chest compression. The risk of aspiration during resuscitation is increased due to a more relaxed lower oesophageal sphincter muscle and elevated gastric acid volume production. Amniotic fluid embolism (AFE) can also lead to fetal collapse of unknown origin that precedes maternal collapse. Uncontrolled hypertension can lead to intracranial haemorrhage. Typical clinical signs are severe, never-experienced headache preceding maternal collapse. Hypervolaemia, hypoxia, hyperkalaemia/metabolic disorders, hypothermia, thromboembolism, toxicity, cardiac tamponade, tension pneumothorax are some of reversible causes for maternal cardiac arrest. A cardiac arrest trolley and defibrillator, including wedge for left lateral tilt should be available on all maternity units and checked daily.

The majority of deep vein thrombosis (DVT) in pregnancy is iliofemoral with a greater risk of both embolisation and recurrence. A thrombus may detach from its site of origin in the vein and migrate through the blood stream to reach the lungs (pulmonary embolism (PE)). The rationale for prophylaxis is based on its efficacy, the clinically silent nature of venous thromboembolism (VTE), its prevalence in pregnant or puerperal patients and its potentially disabling or fatal consequences. Compression duplex ultrasound is the preferred initial imaging test in pregnancy as this test has a high sensitivity and specificity when compared with contrast venography. Treatment of acute-phase VTE is done by administering low-molecular-weight heparin (LMWH) either given once daily or in two divided doses subcutaneously with dosage calculated according to the woman's recent weight. The use of thrombolytic therapy during pregnancy should be reserved for women with severe pulmonary thromboembolism with haemodynamic compromise.

This chapter discusses the pathophysiology, key implications, diagnostic signs and management of severe preeclampsia and eclampsia in an obstetric setting. Preeclampsia may affect multiple organ systems. Blood pressure greater than or equal to160/110 mmHg, severe headache with visual disturbance, epigastric pain, clonus and papilloedema are some of the diagnostic signs of severe preeclampsia. Patients should be managed in a high-dependency obstetric care setting with one-to-one experienced midwifery care. Hourly measurement and documentation of maternal observations like (blood pressure, pulse, respiratory rate, oxygen saturation, temperature, urine output, and neurological status) should be done. Magnesium sulphate should be commenced at diagnosis of severe preeclampsia/eclampsia; continuing until 24 hours following delivery/last seizure/commencement of magnesium sulphate therapy, whichever is the later. Antihypersensitives should be administered, and fluid management should be considered. Postpartum haemorrhage should be anticipated and managed efficiently. Regular 'skills drills' should be conducted on management of severe preeclampsia/eclampsia.

This chapter describes the types, key implications and management strategies of massive obstetric haemorrhage. Antepartum haemorrhage due to placental abruption and intrapartum haemorrhage due to uterine rupture are associated with increased perinatal mortality. Visible blood loss greater than 2 litres, ongoing bleeding are some key pointers of massive obstetric haemorrhage. Immediate management involves active resuscitation to ensure a patient airway, breathing and maintaining circulation with intravenous fluids, blood and blood products as well as correction of coagulopathy. In women who are not acutely compromised or bleeding severely, interventional radiology can be considered. If the bleeding is predominantly from the lower segment, a total abdominal hysterectomy is warranted. Women with massive obstetric haemorrhage often need multi-organ support. Hence, transfer to an intensive care unit or high dependency unit should be considered for monitoring. Thromboprophylaxis should be considered once the coagulation parameters return to normal.

This chapter discusses the pathophysiology, implications, diagnostic signs and diagnostic signs of sepsis and septic shock in pregnancy. In severe sepsis the key pathology is endothelial dysfunction (endothelial apoptosis, increased expression of adhesion molecules and increased capillary permeability) and disordered coagulation homeostasis. It is also important to note that the signs and symptoms of sepsis can be non-specific. The principles of treatment revolve around the basic elements of resuscitation (Airways, Breathing, and Circulation), treatment of the underlying infection including surgical drainage or excision, and organ support until recovery. The use of Modified Early Obstetric Warning System (MEOWS) charts has been shown to minimise risk in the unwell obstetric patient. Prophylactic antibiotic administration is recommended in a number of clinical scenarios to prevent infection in women considered to be at risk. Adjuvant interventions includes surgical removal of infections, use of low-dose steroids and administering activated protein C, an exogenous anticoagulant.