Obstetric Shock

Shock occurs when there is inadequate perfusion of tissues with oxygenated blood. In obstetrics this is usually due to haemorrhage (hypovolaemic shock) or sepsis.

• Hypovolaemic shock This is associated with haemorrhage due to a number of obstetric conditions including abruptio placentae, placenta praevia and accreta; rupture of the uterus; lacerations; retained placenta, atonic uterus, infection. Decreased cardiac output causes catecholamine release with vasoconstriction of skin, kidneys and muscle.
• Septic shock The commonest cause in obstetrics is postoperative endometritis. E. coli 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), lactic acidosis and oliguria.
  Risk of sepsis is increased after prolonged rupture of membranes, emergency caesarian section or if products are retained 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.¹
• Cardiogenic shock e.g. Pulmonary embolus
• Anaphylactic shock Usually drug related, also amniotic fluid embolism
• Neurogenic shock Uterine inversion

Obstetric shock remains a significant cause of maternal and fetal mortality and morbidity in the UK with thromboembolic events the leading cause of direct maternal deaths. Pregnancy increases the risk of venous thromboembolism (VTE) by ten, and by greater multiples if there are pre-existing risk factors.
Risk factors for VTE in pregnancy:²

• >35 years
• Immobility
• Obesity
• Operative delivery
• Surgical procedure during pregnancy or puerperium
• Pre-eclampsia
• Parity>4
• Congenital or acquired thrombophilia
• Excess blood loss
• Sickle cell disease
• Inflammatory disorders or infection
• Dehydration

It is important to note that the risk of VTE is present from the first trimester and also following vaginal delivery and that many of the maternal deaths fall into these categories.³
Catastrophic obstetric haemorrhage is the commonest cause of maternal mortality world-wide with the burden falling primarily on the developing world. In the UK, there were 17 maternal deaths due to haemorrhage between 2000 and 2002.¹

Primary PPH (blood loss of more than 500 ml within the first 24 hours of delivery) occurs in 3-5% of births.

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 BP <60 mmHg, altered mental status, unstable temperature and sometimes sinusoidal fluctuations in BP. Pyrexia may be absent in some cases of severe sepsis.

Pulmonary embolism (PE) presents with dyspnoea, collapse, chest pain, haemoptysis, raised JVP, faintness, focal chest signs and possible associated signs of a DVT.

Amniotic Fluid embolism is very rare, occurring most commonly during labour and is often only considered with the onset of severe signs and symptoms such as respiratory distress, cyanosis, restlessness and altered behaviour prior to collapse.

In all cases: FBC, clotting, blood for crossmatch, U & Es, arterial blood gases, chest X-rays
Where septicaemia is a possibility, take blood cultures.
Investigations for suspected PE: D-dimers, Ventilation-perfusion lung scan, MRI, angiography or spiral CT(post delivery), bilateral leg doppler

• All cases of obstetric shock require rapid and coordinated response. Units should have well rehearsed protocols for dealing with these emergencies.
• Institute immediate resuscitation - give high flow oxygen, wide bore peripheral IV and central access to replace blood volume (if bleeding) and reverse hypotension with crystalloids/colloids/blood guided by urine output and central pressures.
• Assemble the most senior team available - obstetrician, anaesthetist/intensivist, haematologist, radiologist etc.
• Ascertain cause of shock and institute appropriate treatment.

Haemorrhagic shock⁶

Need to replace blood volume and find and control source of bleeding. 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.⁷

The development of 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 and seek haematological advice. Serial monitoring is essential.

Oxytocin infusion and prostaglandin (carboprost 250 mcg given by deep intramuscular injection and repeated as necessary) can correct uterine atony. Rubbing up contractions and bimanual compression may also help.

Surgical intervention is required for traumatic bleeding - ligation of the uterine, ovarian and internal iliac arteries will usually control uterine bleeding. Arterial embolisation is another option where interventional radiology expertise is available.⁸ Uterine packing is a conservative option that can be applied.⁹ Where bleeding is not controlled, hysterectomy can be life-saving and should not be delayed.

Treatment where shock is non-haemorrhagic in origin.⁵

Septic shock

Early aggressive treatment of suspected sepsis with adequate doses of appropriate parenteral broad-spectrum antibiotics (for example, ampicillin, gentamicin & clindamycin) is critical. Microbiology should be involved early to ensure appropriate antibiotic treatment. Look carefully for infected or necrotic foci that may require surgical removal. If chorioamnioitis is the cause of sepsis, delivery should be expedited.

Clinically suspected PE

Treated with heparin whilst objective testing is performed. If confirmed, heparin is usually continued until after delivery and into the puerperium.²

Amniotic fluid embolism

Managed supportively, optimising maternal oxygenation, maintaining cardiac output and blood pressure and correcting any associated coagulopathy.

Acute uterine inversion

Requires replacement of the uterus either manually, surgically or with hydrostatic pressure.

Haemorrhagic shock

Fetal - changes in uteroplacental blood flow can cause fetal hypoxia, acidosis, placental abruption, intracranial haemorrhage and death.
Maternal - acute renal failure, Sheehan's syndrome, DIC, death.

Septic shock

Acute respiratory distress syndrome, arrhythmias, hepatic failure, renal insufficiency, fetal and maternal death.

• Risk of PPH is much reduced with an actively managed 3rd stage of labour.¹⁰
• 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 instituted and the significance of developing symptoms recognised. This is particularly important with rapid postpartum discharge.
• Identification of women with risk factors for VTE in early pregnancy and implementation of appropriate thromboprophylaxis.³