Jaundice during pregnancy
Try out this gastrointestinal case and test your clinical knowledge. The answers are at the bottom.
Questions
You are a FY2 doctor on your obstetrics placement. A 32-year-old G2P1 lady who is 36-weeks pregnant attends the antenatal clinic. She reports a one-day history of severe vomiting and yellowing of the eyes. She has vomited over five times, bringing up bilious liquid and no blood. She denies any abdominal pain, diarrhoea or fever. She denies any recent travel, although reports dining at a Chinese restaurant 3 days ago.
She has no past medical history or family history of note. She has one 3-year-old child who was delivered via normal vaginal delivery, with no complications during pregnancy or labour. She denies any medication use other than some multi-vitamins prescribed by her midwife.
On examination, she is alert and oriented. There is no asterixis. There are no peripheral stigmata of chronic liver disease, but there is obvious scleral icterus. Her abdomen is distended in keeping with pregnancy, and there is mild RUQ tenderness on palpation. It is difficult to assess for organomegaly on abdominal examination due to pregnancy.
Observations
BP 106/60
HR 110
Sats 100% OA
RR 16
Temp 36.9
Bloods
Hb 145, WCC 8.6, Plt 600
Na 139, K 5.2, Ur 4.2, Cr 72, eGFR > 90
ALT 1320, ALP 160, Bil 130, Alb 40
PT 12, INR 1.0
CRP 97.2
Urine dip – Negative for protein, leukocytes and nitrites
Q1: What additional blood tests would you request urgently?
Q2: What imaging test would you request?
Q3: What are your differential diagnoses?
The further blood tests you conduct show a positive HEV IgM. Imaging shows hepatomegaly, normal renal tract and a single live foetus with no complications.
Q4: What is the most appropriate initial management of this patient?
Answers
Reveal the Answers
Answer to Question 1
You would request an urgent non-invasive liver screen. This includes, but is not limited to, the following tests:
- Immunoglobulins
- Liver autoimmune profile (Anti-LKM, ANA, ANCA, AMA, anti-smooth muscle antibodies)
- Viral hepatitis screen
- Hepatitis A IgM and IgG
- Hepatitis B core AB, sAg, eAg, eAB, sAB and if indicated, viral load
- Anti HCV antibody
- Hepatitis E IgM and IgG
- Hepatitis D testing is only indicated if there is evidence of active Hepatitis B infection
- Iron and transferrin saturations
- Copper and caeruloplasmin
- Alpha-feto protein
Answer to Question 2
This patient requires urgent imaging of her liver and of the foetus. An ultrasound scan is the safest and most readily available initial imaging modality which will allow visualisation of the patient’s liver, spleen and the foetus. It carries no radiation risk to the foetus.
Answer to Question 3
The following are potential differential diagnoses:
- Acute fatty liver disease of pregnancy
- HELLP syndrome
- Acute viral hepatitis
- Drug-induced liver injury
- Ischaemic hepatitis
Acute fatty liver disease of pregnancy is a rare and potentially fatal complication that occurs due to abnormalities in foetal fatty acid metabolism. It presents in the third trimester of pregnancy or early post-partum period and has a high risk of morbidity and mortality associated with fulminant liver failure. Patients typically present with fever and jaundice, or signs of fulminant liver failure such as encephalopathy, deranged clotting and occasionally multi-organ failure. Laboratory investigations typically reveal a raised WCC, deranged clotting with elevated PT and INR, significantly raised ALP (although note a mild ALP increase is normal in pregnancy) and ALT (although typically < 500), with jaundice. Ultrasound typically shows fatty infiltration of the liver.
HELLP (haemolysis, elevated liver enzymes, low platelets) syndrome is a potential life-threatening complication of pre-eclampsia. Patients typically present in the third trimester with abdominal pain, headache, visual disturbance, nausea, vomiting and elevated BP. Serious cases can progress to seizures. Laboratory investigations typically reveal jaundice with deranged ALT (although typically < 500) and coagulopathy with low platelets. A urine dip typically shows proteinuria.
Acute viral hepatitis presents similarly in pregnant patients as it does in the general population. Patients typically present with acutely deranged liver function, most often with a hepatitic pattern (ALT rise more significant than ALP) and jaundice. Ultrasound often shows hepatomegaly. Most patients are tested for Hepatitis B and C at the early stages of pregnancy. Hepatitis A and E are transmitted via the faecal-oral route and are typically caused by the consumption of contaminated food or water.
Many drugs can cause an acute liver injury, so it is imperative that a full and thorough medication history is obtained from patients, including the use of any over the counter, herbal and recreational drugs. Drugs can cause a hepatitic, cholestatic (ALP rise more significant than ALT) or mixed picture of liver injury.
Ischaemic hepatitis is a result of ischaemic insult to the liver, typically caused by hypotension or embolic disease to the hepatic vasculature. Patients typically have a history of concurrent illness, recurrent hypotension or risk of embolism (e.g atrial fibrillation). Laboratory investigations typically show a predominantly hepatitic pattern of liver injury.
An ALT of > 1000 is typically caused by drugs, ischaemia or viral hepatitis.
Answer to Question 4
This patient has acute hepatitis E (likely from consuming contaminated pork at the Chinese restaurant) and should be managed conservatively with intravenous fluids and anti-emetics. Early delivery of the foetus should be considered. Given that she is 36-weeks pregnant, the foetus is likely to be viable if delivered. The baby will also require testing for Hepatitis E after delivery.
Drugs such as Ribavarin or Interferon-alpha are contraindicated in pregnancy due to risk of teratogenicity and should be avoided. The patient should be monitored closely for any signs of fulminant hepatic failure, as there is a significant risk of this in pregnant patients with Hepatitis E. This involves close monitoring of her laboratory markers (liver function, renal function and coagulation), as well as clinical monitoring for signs of encephalopathy
St Mark’s hospital, London
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