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Introduction

Hyperemesis gravidarum, characterized by intractable vomiting with fluid and electrolyte disturbances, affects 0.3 to 2% of pregnant women [1]. Excessive vomiting may lead to a variety of metabolic disturbances and mechanical trauma, both of which occurred in the present case.

Case report

A 29-year-old woman was admitted with a three-week history of nausea and vomiting. Her symptoms had begun when she was six weeks pregnant, but had increased in severity during the ten days before admission to the extent that she was vomiting continuously throughout the day and night. She complained of thirst, had noticed that her urine had been dark and had been constipated for five days. She had no other symptoms.

Apart from undergoing an appendicectomy at the age of 24 years, she had no previous medical history and was receiving no medication. She was single, lived with her partner, and had three children. She was a housewife who did not smoke or drink alcohol.

On examination, she was dehydrated and jaundiced. There were no stigmata of chronic liver disease and she was apyrexial. The abdomen was normal, and, in particular, there was no hepatosplenomegaly. Auscultation of the heart revealed a soft ejection systolic murmur in the pulmonary area and widespread crackles were heard over the entire praecordium, which varied both with respiration and with the cardiac cycle. Subcutaneous emphysema was not detected.

Investigations

Haemoglobin 16.3 g/dl, white blood cells 15.1 x 10⁹ /l, platelets 357 x 10⁹/l; sodium 138 mmol/l, potassium 3.0 mmol/l, urea 21.4 mmol/l, creatinine 146μmol/l; albumin 46g/l, globulin 33g/l, alanine transaminase 92U/l, alkaline phosphatase 161U/l, bilirubin 192μmol/l; corrected calcium 3.03 mmol/l. The chest X-ray showed the typical appearances of mediastinal emphysema and surgical emphysema (Fig. 1).

Fig. 1 Chest radiograph showing subcutaneous (white arrow) and mediastinal (black arrow) emphysema.

Barium swallow - to exclude rupture of the oesophagus - was normal, as was the ultrasound examination of the liver and biliary tract.

The patient was diagnosed as suffering from hyperemesis gravidarum. The severity of this condition had resulted in marked metabolic disturbances including dehydration, uraemia, jaundice, and hypercalcaemia. Moreover, the mechanical effects of profuse vomiting had led to a leak of air - either from the oesophagus or the respiratory tract - resulting in mediastinal emphysema.

Management comprised intravenous fluids. Over the ensuing week, the laboratory evidence of dehydration resolved, the disturbance in renal and liver function returned to normal, and the hypercalcaemia was fully corrected (Fig. 2).

Fig. 2 Graphs showing initially abnormal laboratory results returning to normal with IV hydration (blue dotted line indicates normal values for pregnancy)

Clinical recovery was complete within one week and she underwent a previously planned termination of pregnancy before discharge from hospital.

Discussion

While hyperemesis gravidarum often results in dehydration and mild impairment of renal function, the other complications present in this patient are very unusual.

Jaundice in pregnancy [2] may, of course, be due to liver or biliary tract disease not associated with the pregnancy - acute viral hepatitis, gallstones, adverse drug reactions, congenital hyperbilirubinaemia, chronic auto-immune hepatitis, and, uncommonly, established cirrhosis.

However, jaundice may also result from diseases of the liver which are specific to pregnancy. Intrahepatic cholestasis of pregnancy is related to hormonal changes, there may be a family history of the condition or a previous history of cholestasis while receiving oral contraceptive drugs; patients complain predominantly of intense pruritis, some may have obstructive jaundice and the symptoms resolve after delivery. Acute fatty liver of pregnancy is a rare condition presenting initially with non-specific symptoms followed by the development of jaundice and subsequent fulminant hepatic failure; the high mortality in this condition is greatly reduced by rapid termination of the pregnancy. Severe pre-eclampsia may be complicated by the HELLP syndrome (haemolysis, elevated liver enzymes and low platelets); this condition, which should be treated by delivery of the foetus, is associated with significant maternal and foetal mortality. All of these potentially life-threatening liver diseases characteristically present in the third trimester and, hence, were easily excluded in the current case.

Disturbance of liver function is unusual in hyperemesis gravidarum, occurring only in those patients whose symptoms are severe enough to warrant admission to hospital. Typically liver enzymes are increased and mild hyperbilirubinaemia (<70 μmol/l) is present in up to 50% [3] [4]. In the present case, the bilirubin level was exceptionally high although it returned to normal rapidly as expected. Liver histology has been reported to be normal or to show fatty change [3] [5]. Although the mechanism of liver damage is unclear, it appears to be related to the metabolic disturbance associated with profuse vomiting. Correction of fluid and electrolyte depletion results in prompt resolution of the jaundice and a return to normal liver function.

Pneumomediastinum results from an escape of air either from the respiratory tract (alveolar rupture with tracking of air or direct leak from damage to trachea or bronchi) or from the oesophagus. Spontaneous rupture of the oesophagus (Boerhaave's syndrome) is a rare complication of severe vomiting [6]. Both of the above have been reported in hyperemesis gravidarum [1]. In this patient, the origin of the pneumomediastinum is uncertain although a small oesophageal tear, which had sealed before the barium examination, remains likely.

This case demonstrates the spectrum of problems that may arise in patients with severe hyperemesis gravidarum. The metabolic consequences in this patient included uraemia, hypercalcaemia and disturbed liver function tests associated with an unusually high level of bilirubin. In addition, the mechanical trauma resulted in pneumomediastinum, most probably from a small full-thickness tear of the oesophagus. The patient made a complete recovery.

This article was first published on GastroHep.com in 2007.

References

1. Eliakim R, Abulafia O, Sherer DM. Hyperemesis gravidarum: A current review. Am J Perinatology 2000;17(4); 207-18.

2. Knox TA & Olans LB. Liver disease in pregnancy. New Eng J Med 1996; 335; 569-76.

3. Adams RH, Gordon J, Combes B. Hyperemesis gravidarum: Evidence of hepatic dysfunction. Obstet Gynaecol 1968; 31; 659-64.

4. Wallstedt A, Riely CA, Shaver D, et al. Prevalence and characteristics of liver dysfunction in hyperemesis gravidarum. Clin Res 1990; 38; 970A.

5. Larrey D, Rueff B, Feldmann G et al. Recurrent jaundice caused by recurrent hyperemesis gravidarum. Gut 1984; 25; 1414-5.

6. Walker WS, Cameron EWJ, Walbaum PR. Diagnosis and management of spontaneous transmural rupture of the oesophagus (Boerhaave's syndrome). Br J Surg 1985; 72; 204-7.

This article was first published on GastroHep in May 2007.

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