Hypovolaemic shock

This is associated with haemorrhage due to a number of obstetric conditions including:

• Placental abruption
• Placenta praevia and accreta
• Uterine rupture
• Lacerations
• Retained placenta
• Atonic uterus
• Infection

Decreased cardiac output causes catecholamine release with vasoconstriction of skin, kidneys and muscle.

Septic shock

• This is now the most common cause of maternal deaths directly related to pregnancy.^[1] 
• It is commonly caused by postoperative endometritis.
• Escherichia coli O157 is associated with 25-50% of cases but a wide range of Gram-negative and Gram-positive, both aerobic and anaerobic, can be implicated.
• Endotoxin release causes hypotension due to peripheral vasodilation - skin is usually flushed and warm - with lactic acidosis and oliguria.
• Risk of sepsis is increased with:
  • Prolonged rupture of membranes
  • Emergency Caesarean section
  • Retained products after miscarriage, termination of pregnancy or delivery.
  Delivery in water may carry a risk of infection for mother and baby due to faecal contamination of the perineum and genital tract.

Cardiogenic shock

This occurs following pulmonary embolus but also with cardiac disease. Cardiac disease is the most common indirect cause of maternal deaths.^[1]  See separate article Cardiac Disease in Pregnancy.

Anaphylactic shock

This is usually drug-related but may also occur following amniotic fluid embolism (AFE). AFE is a rare and largely unpreventable obstetric complication.

Neurogenic shock

This may occur with uterine inversion.

Epidemiology

Obstetric shock remains a significant cause of maternal and fetal mortality and morbidity in the UK.

Venous thromboembolism

See separate article Venous Thromboembolism in Pregnancy for risk factors.
Thromboembolic events remain the leading cause of direct maternal deaths with a mortality rate of 0.79 per 100,000 deliveries.^[1]  This rate has dropped over the last decade. Pregnancy increases the risk of venous thromboembolism (VTE) by ten, and by greater multiples if there are pre-existing risk factors.
The risk of VTE is increased throughout pregnancy, including the first trimester, but is highest in the puerperium, following vaginal as well as operative delivery.

Postpartum haemorrhage

See separate article Postpartum Haemorrhage for risk factors.
Catastrophic obstetric haemorrhage is the most common cause of maternal mortality worldwide with the burden falling primarily on the developing world. In the UK, the most recent figures suggest a mortality rate for haemorrhage of 0.39 per 100,000 deliveries^[1]  but primary postpartum haemorrhage (PPH) - blood loss of more than 500 ml within the first 24 hours of delivery - is common and occurs in 3-5% of births.

Genital tract sepsis

Maternal morality from infection currently is about 1.13 per 100,000 deliveries. It may occur during pregnancy, following surgical interventions or as puerperal sepsis.
Risk factors include:^[1] 

• Obesity
• Impaired glucose tolerance/diabetes
• Impaired immunity
• Anaemia
• Vaginal discharge
• History of pelvic infection
• History of Group B streptococcal infection
• Amniocentesis, and other invasive intrauterine procedures
• Cervical cerclage
• Prolonged rupture of membranes
• Vaginal trauma
• Caesarean section
• Wound haematoma
• Retained products of conception post-miscarriage or post-delivery

Presentation^[2]

Signs of hypovolaemic shock include:

• Altered mental status
• Dizziness
• Sweating, with cold clammy extremities
• Fast, thready pulse
• Oliguria

The onset of life-threatening sepsis in pregnancy or the puerperium can be insidious with subsequently rapid and sometimes irreversible clinical decline. Signs of septic shock include:

• Systolic blood pressure <60 mm Hg
• Altered mental status
• Unstable temperature (note pyrexia may be absent with severe sepsis)

Pulmonary embolism (PE) presents with:

• Dyspnoea
• Collapse
• Chest pain
• Haemoptysis
• Raised jugular venous pressure
• Faintness
• Focal chest signs
• Possible associated signs of a deep vein thrombosis

Early signs of a PE are often subtle, such as increased breathlessness, and are frequently misdiagnosed, particularly with telephone consultation.^[1] 

Amniotic fluid embolism occurs most commonly during labour, and is often only considered with the onset of severe signs and symptoms such as:

• Respiratory distress
• Chest pain
• Paraesthesia
• Cyanosis
• Restlessness, panic and altered behaviour prior to collapse

Differential diagnosis

The differential diagnosis of acute collapse in pregnancy includes:^[3]

• Acute coronary syndrome
• Acute aortic dissection
• Cerebrovascular incidents
• Anaphylaxis
• Anaesthetic complications

Investigations

In all cases:

• FBC
• Clotting
• Blood for group and crossmatch
• U&Es
• LFTs
• Arterial blood gases

Additional investigations will depend on presentation and may include:

• Chest X-rays
• ECG
• Blood cultures, swabs

Investigations for suspected pulmonary embolism:^[4]

• Bilateral compression duplex ultrasound to examine for deep vein thrombosis
• Ventilation-perfusion lung scan
• CT pulmonary angiography

D-dimer tests are not recommended as their levels are raised normally in pregnancy and are often abnormal by the third trimester and into the postnatal period.
The use of a thrombophilia screen prior to instituting treatment is controversial and is not routinely recommended.

Management

Haemorrhagic shock^[1] [5]

See additional article Antepartum Haemorrhage and the separate Postpartum Haemorrhage article.
There is an urgent need to replace blood volume and find and control source of bleeding (eg damaged blood vessel, ruptured uterus, placenta percreta):

• Hypovolaemia should be rapidly corrected with crystalloids and red cells as first priority.
• The degree of hypotension is the main indicator of blood loss (except with an abruption).
• Inotropes may be required.
• The use of anti-shock garments has also been trialled in obstetric haemorrhagic shock.^[6]

The development of disseminated intravascular coagulation (DIC) is a risk and may require corrective fresh frozen plasma (FFP), platelets and clotting factors, as indicated by haematocrit, coagulation tests, platelet count and clinical features. Seek haematological advice. Serial monitoring is essential.

For uterine atony:

• Syntocinon and ergometrine are the first-line agents for the treatment of uterine atony in the UK. IM Syntometrine® should be given immediately after delivery where there is a high risk of postpartum haemorrhage (PPH), eg prolonged labour, 2nd stage hysterectomy.
• Syntocinon infusion and prostaglandin (carboprost 250 micrograms, given by deep IM injection and repeated as necessary) may also be required.
• Rubbing up contractions and bimanual compression are widely used.
• The use of sublingual misoprostol may be as effective as the use of IV oxytocin and easier to use, particularly in resource-poor countries, but this remains controversial.^[7]

Surgical intervention is required for traumatic bleeding:

• Ligation of the uterine, ovarian and internal iliac arteries will usually control uterine bleeding.
• Intrauterine balloon tamponade has also been explored.^[8]
• Arterial embolisation is another option where interventional radiology expertise is available.^[9] Uterine packing is a conservative option that can be applied.^[10]
• Where bleeding is not controlled, hysterectomy can be life-saving and should not be delayed. Peripartum hysterectomy occurs at a rate of 41/100,000 deliveries in the UK.

Septic shock^[1] 

See separate article Puerperal Pyrexia.

• Sepsis is often insidious in onset with a fulminating course. DIC and rapid multisystem failure may occur with little warning.
• With increasing early discharge following delivery in hospital, the impetus is on community midwives and GPs to be vigilant. Monitoring pulse, blood pressure, respiratory rate, temperature and lochia regularly in the early postnatal period may mean sepsis is detected and treatment instigated.
• Where sepsis is suspected, early aggressive treatment with adequate doses of appropriate parenteral broad-spectrum antibiotics (eg cefuroxime and metronidazole) is critical. Do not wait for microbiology results. Ensure serum levels are within therapeutic range. Microbiology should be involved early to ensure appropriate antibiotic treatment. Where there is no response within 24-48 hours, or if clinically a woman is worsening, antibiotics should be changed, with the addition of gentamicin or alternative antibiotics with advice from a microbiologist.
• The source of sepsis should be removed where possible, eg delivery or evacuation of retained products.

Venous thromboembolism^[4]

See separate Venous Thromboembolism in Pregnancy article.

• In clinically suspected deep vein thrombosis (DVT) or pulmonary embolism (PE), treatment with low molecular weight heparin (LMWH) should be started whilst objective testing is performed to exclude the diagnosis, unless there are strong contra-indications.
• Where venous thromboembolism (VTE) is confirmed, heparin is usually continued until after delivery (stop 24 hours prior to planned delivery or until the spontaneous start of labour) Following delivery, heparin or oral anticoagulation is usually continued for at least 6 weeks.
• Collapsed, shocked women with suspected VTE should be managed by a multidisciplinary resuscitation team. Treatment options include IV unfractionated heparin, thrombolytic therapy or thoracotomy and surgical embolectomy.

Amniotic fluid embolism

See separate Amniotic Fluid Embolism article.
This is managed supportively, optimising maternal oxygenation, maintaining cardiac output and blood pressure and correcting any associated coagulopathy. The use of recombinant factor VIIa, ventricular assist devices, inhaled nitric oxide, cardiopulmonary bypass and intra-aortic balloon pump with extracorporeal membrane oxygenation have all been reported in the management of this devastating condition but, despite aggressive resuscitation efforts, maternal and fetal outcome is usually poor.^[11]

Complications

Haemorrhagic shock

• Fetal - changes to the uteroplacental blood flow can cause fetal hypoxia, acidosis, placental abruption, intracranial haemorrhage and death
• Maternal - acute renal failure, Sheehan's syndrome, disseminated intravascular coagulation (DIC), death

Septic shock

• Acute respiratory distress syndrome
• Arrhythmias
• DIC
• Hepatic and renal failure
• Fetal and maternal death

Prevention^[1] 

• Risk of postpartum haemorrhage (PPH) is much reduced with an actively managed 3rd stage of labour.^[12]
• Women at high risk of haemorrhage should not be delivered in isolated units or facilities without immediate access to specialist consultant care, blood products or intensive care.
• A woman who declines blood products should have a management plan, in case of haemorrhage, agreed with them before delivery is anticipated.
• Any problems that may lead to sepsis should be communicated to the community carers at the time of discharge so that appropriate follow-up can be instituted and the significance of developing symptoms recognised. This is particularly important with rapid postpartum discharge.
• Identification of women with risk factors for venous thromboembolism (VTE) should occur prior to pregnancy or in early pregnancy, with implementation of appropriate thromboprophylaxis. Reassessment of risk should take place prior to delivery. Women with BMIs >35 should be referred for specialist assessment.