Obstetrics

Anaemia in pregnancy

Because of the widespread availability of iron supplementation in pregnancy, severe iron deficiency anaemia (microcytosis) is rare. It is managed with iron replacement for six months, and the only twist is if this is not tolerated in an anaemic pregnant woman. Nausea and vomiting associated with iron pills is common, and can be dealt with by taking it after meals, possibly with an anti-emetic. There is some evidence that weekly therapy is nearly as good as daily dosing^[1] once Hb has been restored. There is a role for parenteral iron in severely anaemic patients not responding to a tweaked dose regimen or an alternative oral formulation.

Megaloblastic anaemia in pregnancy is diagnosed and treated in the same way as in non-pregnant individuals. Other causes of anaemia in pregnancy are haemolysis and chronic illnesses – e.g. TB.

Cardiac disease in pregnancy

Cardiac failure developing in the last month of pregnancy or in the first five months thereafter may be due to valvular heart disease, anaemia, thyrotoxicosis or myocardial disease.

Peripartum cardiomyopathy

This is thought to be an immune process. It is defined as heart failure developing in the six month period starting in the last month of pregnancy and continuing for five months after delivery, in the absence of any other cause for cardiac failure. The clinical features are the same as those of any cardiomyopathy (displaced hypodynamic apex in 72%, gallop in 92%^[2]) but the echocardiographic criteria are relatively strict, so a ‘borderline’ LV is probably actually a peripartum cardiomyopathy if the clinical features are compatible. (The ‘stricter’ criteria are^[3]: LVEF < 45% or LVFS < 30% and LVEDD > 2.7cm/m²)

The prognosis is a little variable, but in general the mortality rate is about 15% and about 20-30% recover normal systolic function^[4].

During pregnancy the use of ACE inhibitors is contra-indicated, and overly aggressive diuresis is undesirable so alternative vasodilators should be considered. Possibilities are nitrates and hydralazine. Digoxin can be used, but care should be taken in late pregnancy, as bradyarrhythmias can occur in the newborn. Because pregnancy itself is a prothrombotic state, heparin should be considered (warfarin after the 1^st trimester, then back onto heparin two weeks before delivery.)

After delivery pay careful attention to fluid balance in the first 48-72 hours, as the fluid shifts that occur usually necessitate extra furosemide. Start an ACE inhibitor. It may be possible to reduce anti-failure therapy over the next few months in some patients. An echocardiogram should be done after about six months, during which period it is very important that the patient remain on adequate contraception. If the LV function returns to normal, there is a reasonable but poorly quantified chance (about 80%^[5]) that the problem will not recur during a subsequent pregnancy, but if it does, it may be worse. Another more recent but smaller study^[6] found worsening of cardiac failure in 8 of 15 patients (53%).

Valvular heart disease in pregnancy

Valvular heart disease in pregnancy is common. Regurgitant valvular disease is often relatively innocuous during pregnancy unless very severe. Stenotic diseases (aortic stenosis and mitral stenosis) are more problematic in that vasodilators are not generally an option and so management is basically about diuretics and rate control.

• Investigate and manage anaemia promptly.
• Any infection leading to a fever and tachycardia may result in haemodynamic deterioration. Treat chest infections and urinary tract infections early and well.
• Avoid fluid loads or other causes of tachycardia at delivery – an assisted delivery is often advised, but frequently unnecessary.
• Anticoagulation.
• Digoxin is appropriate if the patient is in rapid atrial fibrillation.
• As with peripartum cardiomyopathies post-delivery fluid shifts should be expected, and should be managed by careful attention to lung bases and pulse before the patient goes into frank pulmonary oedema.

Occasional patients present already pregnant and with quite severe valvular heart disease and there are doubts about the ability to withstand pregnancy. Heart surgery under such circumstances has a high foetal attrition rate, and if the valve lesion is purely mitral stenosis, the option of a balloon valvotomy should be considered.

Hypertension in pregnancy

Gestational proteinuric hypertension (pre-eclampsia-eclampsia) is a multisystem disorder characterised by a diastolic blood pressure >90 mmHg on more than one occasion or any single reading >110 mmHg, with proteinuria of >0.3g/day, with or without oedema. A spot protein/creatinine ratio of more than 0.03g/mmol is a reasonable predictor of concerning proteinuria (>0.3g/d) with a LR+ of 11.6. (sens 0.93, spec 0.92)^[7]. The findings of elevated liver enzymes and a coagulopathy (elevated D-dimer, although PTT and INR often normal) suggest that delivery should be expedited. A falling platelet count, even if still in the normal range, may be another clue^[8]. A frequent question is whether the hypertension could have antedated the pregnancy. In the absence of evidence of end-organ damage from long-standing hypertension, this assessment can be difficult, although clues might be older age, multiparity and perhaps most helpfully, a note documenting elevated blood pressure before 20 weeks. Obstetric management of GPH now centres on the use of magnesium; the internal medicine question is usually about which antihypertensives are appropriate in individuals with chronic (pre-pregnancy) hypertension.

The best studied, although not necessarily the most effective agent is methyldopa in a dose of 250 mg 3x/d, increasing to 500 mg 3x/day if tolerated.

Nfedipine (5 mg 3x/d), increasing to 10mg 3x/d) appears safe. The safety of amlodipine is less clear (Category C).

Hydralazine can be added if control is inadequate, in a dose of 25 mg 3x/d, increasing to 50 mg 3x/d, then 75 mg 3x/d.

Do NOT use ACE inhibitors which are associated with growth retardation, oligohydramnios and anuric renal failure in the foetus. Thiazide diuretics are also associated with growth retardation and with gestational diabetes.

The information about beta-blockers is somewhat shaky – atenolol has been associated with growth retardation and so is probably not a good idea in the third trimester. It may be considered if other agents are not working. The alpha-blocker doxazosin is another option (0.5 mg test dose, then 1 mg nocte, increasing gradually to 4 mg nocte – up to 16 mg/d has been used).

Stroke in pregnancy.

Subarachnoid bleeds – usually due to aneurysms or arteriovenous malformations, and occasionally due to bleeding problems such as DIC or over-enthusiastic anticoagulation. Management should be the same as in the non-pregnant patient – i.e. CT, angiography, and consideration for surgery. It is unclear whether there is a higher risk of bleeding associated with straining at delivery, but elective caesarean section at 38 weeks is commonly recommended in individuals with documented aneurysms.

Cerebral infarction. Management and investigation is broadly similar to that of a stroke in a young person who is not pregnant. CT scanning with adequate abdominal screening is probably justifiable as the radiation risk to the foetus is relatively small.

Epilepsy in pregnancy

Probably the commonest causes for worsening seizure frequency during pregnancy are lack of pills and lack of sleep.

It is safer to keep the patient on a working antiepileptic regimen than to fiddle and risk breakthrough seizures during drug weaning and overlap. The evidence for major differences between various agents in terms of their teratogenic risk is not particularly impressive, although valproate in high doses is concerning.

Swopping during pregnancy, especially after the first trimester, and generating a vicious cycle of poorly controlled seizures is not ideal for either the mother or the baby. Getting onto stable lamotrigine monotherapy before pregnancy is helpful.

Perspective – risk of various anti-epileptics

A systematic review and network meta-analysis which looked at this this showed that some agents are more of an issue than others¹. The risk of a any congenital malformation in the control groups (no anti-epileptics) was 2.6%, and this was not increased by use of lamotrigine or levetiracetam, but was increased for most other agents or combinations of agents (odd ratios for valproate and ethosuximide 3, phenytoin 1.7, and carbamazepine 1.3.)

Jaundice in pregnancy

A number of causes of hepatic disease are pregnancy-related; however all liver diseases that can occur outside of pregnancy should also be considered.

Associated with GPH – hypertension, renal impairment. If high aminotransferases the consider HELLP, but usually only a modest rise in other cases.

Acute fatty liver of pregnancy – high alkaline phosphatase, moderate aminotransferase rise, late pregnancy (after 34^th week) and sometimes renal failure. Leukocytosis can be quite impressive. Treatment is supportive – FFP for coagulopathy, glucose for hypoglycaemia.

Benign cholestasis of pregnancy – marked itching, deep ‘chronic’ jaundice with moderate alkaline phosphatase rise, and INR usually fine until very late. Cholestyramine may help the itch.

Viral hepatitis – always check serology for Hepatitis A and B before making any of the other diagnoses

Drug induced hepatitis – same as in the non-pregnant patient

Budd-Chiari syndrome – sudden onset of hepatic pain and ascites due to hepatic vein thrombosis.

Septicaemia – check WCC and think about source – e.g. urinary tract infection.

Biliary tract disease – do an ultrasound to exclude obstructive lesions.

HIV cholangiopathy. This is a difficult diagnosis to make during pregnancy, but would be strengthened by non-resolution of the condition after delivery.

Renal disease in pregnancy

Acute kidney injury in late pregnancy

All the causes that can affect non-pregnant persons can occur in pregnancy. Most obstetric-related septic and hypotensive aetiologies are obvious. Others are:

Cortical necrosis. Aetiology similar to ATN, but tends to be commoner in older multiparous women, perhaps reflecting a degree of pre-existing renal damage. Recovery is slower and may be incomplete.

Acute fatty liver of pregnancy – associated with relatively mild renal impairment.

Postpartum renal failure should be considered if there is no clear hypotensive or septic episode, the renal failure presents within a few weeks of delivery, and the BP is quite high.

Treating urinary tract infections in pregnancy.

The diagnosis of UTI is the same as in a non-pregnant patient – lower abdominal symptoms and suprapubic tenderness with leukocytes and nitrites on dip sticks suggests cystitis; back pain and renal angle tenderness suggests that this has progressed to pyelonephritis. Many women have back pain in pregnancy, so differentiate the new pain from previous ones. It is important to take urinary tract infections seriously, as deterioration in pregnancy can be quite rapid.

Mild cystitis – amoxyclav 500/125 mg 8 hourly for 7 days. Pyelonephritis – ceftriaxone 1g daily IV for 7 days, or an alternative second or third generation cephalosporin. Fosfomycin 3 g stat PO is another option. Gentamicin crosses the placenta and may in theory cause ototoxicity or nephrotoxicity, and is probably best avoided unless the patient is very ill and allergic to cephalosporins. The duration of therapy in pyelonephritis in pregnancy is unclear but because the incidence of recurrence can be quite high (e.g. 23%^[9]), a 14 day course is sometimes recommended^[10].

1. Ekstrom E, Ziauddin Hyder S, Mushtaque A, et al. Efficacy and trial effectiveness of weekly and daily iron supplementation among pregnant women in rural Bangladesh: disentangling the issues. Am J Clin Nutrition. 2002;76:1392-1400. ↑

2. Desai D, Moodley J, Naidoo D. Peripartum cardiomyopathy experiences at King Edward VII Hospital, Durban South African and a review of the literature. Trop Doct. 1995;25:118-23. ↑

3. Hibbard JU, Lindheimer M, Lang RM. A modified definition for peripartum cardiomyopathy and prognosis based on echocardiography. Obstet Gynecol 1999;94:311-16. ↑

4. Silwa K, Fett J, Elkayam U. Peripartum cardiomyopathy. Lancet 2006; 368:687-93. ↑

5. Elkayam U, Tummala PP, Rao K et al. Maternal and fetal outcomes of subsequent pregnancies in women with peripartum cardiomyopathy. N Engl J Med. 2001;344:1567-71. ↑

6. Fett JD, Christie LG, Murphy JC. Brief communication: outcome of a subsequent pregnancy after peripartum cardiomyopathy: a case series from Haiti. Ann Intern Med. 2006;145:30-34. ↑

7. Saudan PJ, Brown MA, Farrell T, et al. Improved methods for assessing proteinuria in hypertensive pregnancy. Br J Obstet Gynaecol. 1997;104:1159-64. ↑

8. Redman CW, Bonnar J, Beilen L. Early platelet consumption in pre-eclampsia. BMJ. 1978;1:467-9. ↑

9. Gilstrap LC, Cunningham FG, Whalley PJ. Acute pyelonephritis in pregnancy: an anterospective study. Obstet Gynecol. 1980;57:409-13. ↑

10. Barron WM, Linheimer MD. Medical disorders during pregnancy. Mosby 2000, p420. ↑

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1. Veroniki, A.A., Cogo, E., Rios, P. et al. Comparative safety of anti-epileptic drugs during pregnancy: a systematic review and network meta-analysis of congenital malformations and prenatal outcomes. BMC Med 15, 95 (2017). https://doi.org/10.1186/s12916-017-0845-1 ↩

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