Postpartum collapse

Abstract

Abrupt deterioration in the mother’s condition may occur postpartum as a result of a broad array of conditions, many of them rare. Maternal survival depends on aggressive resuscitation, rapid precise diagnosis and the institution of disease-targeted therapy. Additionally there may be implications for any future pregnancy. A case of sudden maternal collapse postpartum is presented, the differential diagnosis is discussed, and the management plan and outcome for a subsequent pregnancy reviewed.

Case

A 24-year-old woman became acutely unwell minutes following an otherwise uneventful 9 h labour and vaginal delivery of a healthy 4030 g male infant with epidural anaesthesia. This was her third child and her two previous vaginal deliveries had been uncomplicated. The woman complained of shortness of breath and rapidly became centrally cyanosed and unresponsive. Her past history was significant for exercise-induced anaphylaxis (EIA).

The woman’s airway appeared obstructed with audible stridor. Oxygen saturation was 83% while breathing 6 l/min via a Hudson mask. No bronchospasm was audible on auscultation. Pulse was 140 beats/min and regular, blood pressure was 60 mmHg systolic and the woman was afebrile. A generalized fine erythematous rash was present without features of urticaria.

The woman was intubated. At laryngoscopy significant laryngeal mucus was present with minimal laryngeal oedema. Adrenaline and hydrocortisone were administered intravenously, and the epidural infusion ceased. The woman was transferred to the intensive care ward with a provisional diagnosis of amniotic fluid embolism. It was noted that intramuscular oxytocin was given minutes before the woman’s deterioration. Latex precautions were not taken at this stage.

Electrolytes, coagulation profile, and renal and liver function tests were normal. White blood cell count (WBC) was 20.7 × 10⁹/l, neutrophil count was 16 × 10⁹/l, with normal haemoglobin and platelet count. Serum tryptase was 34.2 µg/l (<13.5). Computerized axial tomography pulmonary angiography and echocardiography were normal.

The woman remained stable with blood pressure supported by a noradrenaline infusion. An oxytocin infusion was administered briefly for postpartum blood loss without further haemodynamic instability. Sixteen hours post-delivery the woman was extubated with normal gas exchange on room air. Mother and baby were discharged on the fourth day postpartum. Further allergy testing was not performed.

Six years later the woman presented at 13 weeks of gestation in her fourth pregnancy. Review of medical records disclosed an oxytocin infusion for induction in her first pregnancy without adverse effect. The woman wanted a vaginal delivery with epidural anaesthesia. Multidisciplinary team meetings were held regularly involving midwives, obstetricians, anaesthetists and obstetric physicians, with advice from immunologists, as the most likely cause was felt to be anaphylaxis to latex. Induction at 38 weeks of gestation was planned, in a latex-free environment, and the room kept cool. The use of a single dose of omalizumab a fortnight prior to induction was discussed; however, the woman declined. Prednisone, diphenhydramine and ranitidine were commenced three days prior to delivery, and intravenous hydrocortisone given peripartum.^1–3 Extracorporeal membrane oxygenation was available and the intensive care unit notified. It was planned to avoid oxytocin and use ergometrine in the third stage of labour.

The mother proceeded to an uneventful vaginal delivery of a healthy male infant birthweight 3540 g. The postpartum course was uncomplicated. Skin testing for latex allergy is planned once the mother has completed breastfeeding.

Discussion

Many conditions may result in haemodynamic collapse postpartum (Table 1). The abrupt deterioration in this previously well woman is most suggestive of anaphylaxis, amniotic fluid embolism, undiagnosed pulmonary hypertension or pulmonary embolism.

Table 1.

Causes of sudden postpartum cardiorespiratory collapse.

Cause	Incidence	Predisposing	Symptoms/signs
Massive postpartum haemorrhage	1 : 1000	Abnormal placentation, placental abruption, severe preeclampsia, personal/family history, intrauterine fetal demise, high parity, bleeding diathesis
Pulmonary embolism	1 : 1600	Multiple	Pleuritic chest pain, haemoptysis, dyspnoea, signs deep vein thrombosis, signs pulmonary hypertension
Mitral stenosis	Variable	Rheumatic fever	Abrupt onset pulmonary oedema, atrial fibrillation
Peripartum cardiomyopathy	1 : 3000	African ethnicity, preeclampsia, multiple gestation, cocaine use	Dyspnoea, cough, orthopnoea, haemoptysis, oedema, signs heart failure
Aortic dissection	1 : 5000	Marfan, Ehlers–Danlos, Loeys–Dietz and Turner's syndromes; bicuspid aortic valve, vascilitis	Chest/back pain, cardiac murmur, neurologic deficits
Uterine rupture	1 : 8000	Loeys-Dietz and Ehlers-Danlos syndromes, abnormal placentation, older age, multiple gestation	Fetal bradycardia, uterine pain and tenderness, vaginal bleeding
Uterine inversion	1 : 10,000	Macrosomia, rapid delivery, retained placenta, severe preeclampsia	Vaginal bleeding, inability to palpate fundus, mass protruding from cervix
Septic shock	1 : 10,000	Premature rupture of membranes, chorioamniotitis, pyelonephritis, pneumonia, puerperal sepsis	Peripherally shutdown, fever or hypothermia, altered mental status, abdominal pain
Myocardial infarction	1 : 16,000		Chest pain, dyspnoea, presyncope
Coronary artery dissection		Connective tissue disease, vasculitis
Atheromatous		Diabetes, smoking, hypertension, lipids
Coronary artery spasm		Asian, migraine, Raynauds
Illicit drug use		Cocaine
Amniotic fluid embolism	1 : 30,000	Preeclampsia, placental abnormalities	Sudden collapse in labour/within 30 min delivery, DIC, seizures
Anaphylaxis	1 : 40,000	Oxytocin, latex, misoprostol, antibiotics, anaesthetic agents, NSAIDs, breastfeeding	Angioedema, rash
Splenic aneurysm rupture	Rare	Portal hypertension	Left upper quadrant pain
Hepatic rupture	Rare	Preeclampsia, tumours, acute fatty liver pregnancy	Right upper quadrant pain, abdominal distension
Pulmonary hypertension	Rare	Connective tissue disorders	Sudden collapse/death peripartum, signs right heart failure
Magnesium toxicity	Rare	Neuromuscular disorders	Respiratory failure
Cortisol deficiency	Rare	Prior glucocorticoid therapy, Sheehan’s syndrome, hypophysitis, antiphospholipid syndrome	Hyponatraemia, hypoglycaemia
Pheochromocytoma	Rare	Neurofibromatosis, MEN2, Von Hippel–Lindau syndromes	Cardiomyopathy, pulmonary oedema
Tension pneumothorax	Rare	Marfan syndrome, lymphangioleiomyomatosis	Hypoxia, tracheal deviation, absent breath sounds
Local anaesthetic induced sympathetic block/toxicity	Rare	Renal/liver/cardiac disease	Slurred speech, tinnitus, agitation, confusion, respiratory depression, seizures, hypotension, arrhythmias

All may be associated with tachycardia, hypotension or hypoxia. DIC: disseminated intravascular coagulation; MEN2: Multiple Endocrine Neoplasia type 2; NSAID: Non-steroidal anti-inflammatory drug.

Anaphylaxis has been estimated to complicate approximately 1 in 40,000 deliveries, 74% of episodes occurring with caesarean section. The most common aetiologic agents associated with peripartum anaphylaxis are β lactam antibiotics, natural rubber latex, oxytocin, neuromuscular blockers, epidural medications, chlorhexidine and blood products.⁴ Symptoms usually occur within minutes of receiving the precipitating substance. One case report of anaphylaxis suspected to be due to EIA with labour and delivery has been reported.⁵ Laryngopathia gravidarum is a rare condition of progressive hoarseness in pregnancy due to oedema of the superficial layer of the lamina propria. Severe cases of laryngopathia gravidarum with preeclampsia may mimic laryngeal obstruction with anaphylaxis.

Amniotic fluid embolism usually presents during labour or within 30 min of delivery with sudden rapidly progressive cardiovascular collapse, hypoxia and subsequent disseminated intravascular coagulation (DIC). Cardiac arrest is usually due to sustained pulseless ventricular tachycardia or ventricular fibrillation.⁶ If the woman survives the initial event, haemorrhage due to DIC occurs in more than 80% of cases. Serum tryptase may be elevated, and decreased C3 and C4 complement are seen in 90–100% of cases.

Pulmonary hypertension is associated with maternal mortality of approximately 30%.⁷ Sudden cardiac death may occur immediately postpartum, or up to three weeks after delivery. Previous symptoms of presyncope, shortness of breath and peripheral oedema may be attributed to physiological changes of pregnancy. Pulmonary hypertension should be particularly considered in women with congenital heart disease, connective tissue disease (scleroderma, mixed connective tissue disease, SLE, primary antiphospholipid syndrome), portal hypertension and sickle cell disease.

Pulmonary embolism in the immediate peripartum period is rare. Lee et al.⁸ reported just six cases of diagnosed pulmonary embolism occurring within 24 h of 57,092 deliveries (0.01%). In almost all cases reported in the literature, pulmonary embolism peripartum occurred with caesarean rather than with vaginal delivery.

We believe the most likely cause for the woman’s collapse was anaphylaxis due to latex allergy triggered by oxytocin administration. Latex use is ubiquitous in medicine, being found in gloves, masks, tubing, ventilator hoses, adhesive tapes, catheters, drains, and stoppers and bungs in medication vials. Severe contact urticaria has been reported with latex in the tape of cardiotocographs, and airborne exposure to latex may lead to anaphylaxis in sensitized individuals.^9,10 Groups at high risk of latex allergy include health care workers, women with a history of multiple surgical procedures, individuals with allergies to fruit and with conditions requiring chronic bladder care. The incidence of latex allergy amongst operating theatre staff had been shown to be 3–6.4% compared with 1% in the general population. Obstetric and gynaecological procedures account for approximately 50% of reactions to latex. Latex allergy intraoperatively is associated with 3.4–6% mortality. Oxytocin has been implicated as a trigger for anaphylactic responses to latex and may potentiate cardiovascular and respiratory effects of anaphylaxis due to its negative inotropic, chronotropic, vasodilatory, hypotensive and bronchoconstrictive properties.¹¹ Numerous cases have been described where individuals with allergy to latex had anaphylaxis triggered by the administration of oxytocin, though were able to tolerate oxytocin only hours later without adverse effect, and without evidence of a reaction to oxytocin on allergy testing. Patatin latex antigens have a high structural homology with oxytocin (six contiguous amino acids) suggesting the possibility of cross-reaction.¹² Oxytocin administration may facilitate antigen recognition in the setting of previous sensitization to latex.

Anaphylaxis to topical chlorhexidine is most commonly reported with mucous membrane contact.

Anaphylaxis during breastfeeding is also rare, and attributed to rapidly falling progesterone levels, the risk potentially increased by concurrent use of nonsteroidal anti-inflammatory drugs.

The benefits of skin tests, challenge/provocation tests, desensitization and immunotherapy during pregnancy need to be considered against the risk of inducing anaphylaxis. Maintenance dose allergy immunotherapy may be continued during pregnancy. Skin testing with latex should be deferred until postpartum.

Omalizumab is a recombinant, humanized, monoclonal antibody against human immunoglobulin E approved for use in severe allergic asthma and chronic urticaria. Omalizumab has been used off-label in many allergic conditions including prevention of anaphylaxis with exercise, food allergy, drug allergy, mastocytosis and during immunotherapy. The Xolair pregnancy registry found no increased risk of major congenital anomalies, prematurity, low birth weight or small for gestational age in 169 pregnancies with first trimester exposure to omalizumab.¹³ Omalizumab has been shown to have clinically relevant ocular and skin anti-allergic activity in health care workers with occupational latex allergy, and to improve latex-induced contact urticaria.^14,15 Care must be taken in the administration of omalizumab to individuals with latex allergy as the needle cap on the prefilled syringe may contain latex.

Serum tryptase is elevated in 4–6% of the general population.¹⁶ Causes of elevated tryptase include anaphylaxis, amniotic fluid embolism, assay interference by heterophile antibodies (especially with previous infliximab exposure), myocardial infarction, mast cell disorders, myeloid leukaemias, hypereosinophilic disorders, following the administration of stem cell factors, and severe renal failure.

The maternal WBC rises significantly following vaginal delivery, with mean levels of 15.3 × 10⁹/l, and levels as high as 37.3 × 10⁹/l reported in healthy pregnancy.¹⁷ In this case the administration of adrenaline may have contributed to neutrophil leucocytosis, as WBC rises within 5 min of adrenaline therapy. The rise in WBC following hydrocortisone is usually delayed by at least 1 h.

Conclusion

A number of conditions may cause abrupt postpartum collapse. Latex allergy needs to be considered where anaphylaxis occurs peripartum, particularly where acute deterioration follows oxytocin administration.