Profound Hypokalaemia Resulting in Maternal Cardiac Arrest: A Catastrophic Complication of Hyperemesis Gravidarum?

Author:

Walch Anna123ORCID,Duke Madeline456,Auty Travis278,Wong Audris9101112

Affiliation:

1. Doctor of Medicine (MD), Griffith University, Australia

2. Lecturer, School of Medicine, Griffith University, Australia

3. Obstetrics and Gynaecology Principal House Officer, Gold Coast University Hospital, Australia

4. Bachelor of Medicine and Bachelor of Surgery (MBBS), Bond University, Australia

5. Obstetric Medicine Fellow, Royal Brisbane and Women’s Hospital, Australia

6. Endocrine Advanced Trainee, Royal Brisbane and Women’s Hospital, Australia

7. Bachelor of Medicine and Bachelor of Surgery (MBBS), Griffith University, Australia

8. Intensive Care Unit Registrar, Gold Coast University Hospital, Australia

9. Obstetrics and Gynaecology Staff Specialist, Gold Coast University Hospital, Australia

10. FRANZCOG (Fellowship of the Royal Australian and New Zealand College of Obstetricians and Gynaecologists), Australia

11. MRCOG (Membership of the Royal college of Obstetricians and Gynaecologist), UK

12. MRCPI (Membership of the Royal College of Physicians in Ireland (Obstetrics and Gynaecology and General Medicine)), Ireland

Abstract

We present a case of a 39-year-old G8P6 Pacific Islander woman who at 15+5 weeks’ gestation had an out-of-hospital cardiac arrest secondary to profound hypokalaemia which was associated with severe hyperemesis gravidarum (HG). Her clinical course after arrest was complicated by a second 5-minute cardiac arrest in the Intensive Care Unit (ICU) (pre-arrest potassium 1.8), anuric renal failure requiring dialysis, ischaemic hepatitis, and encephalopathy and unfortunately fetal demise and a spontaneous miscarriage on day 2 of admission. Despite these complications, she was discharged home 4 weeks later with a full recovery. Following a plethora of inpatient and outpatient investigations, the cause of her cardiac arrest was determined to be profound hypokalaemia. The hypokalaemia was presumed second to a perfect storm of HG with subsequent nutritional deficiencies causing electrolyte wasting, extracellular fluid (ECF) volume reduction, and activation of the renin-angiotensin-aldosterone axis (RAAS). This combined with the physiological changes that promote potassium wasting in pregnancy including volume expansion, increased renal blood flow, increased glomerular filtration rate, and increase in cortisol contributed to the patient having a profoundly low total body potassium level. This diagnosis is further strengthened by the fact that her pre- and post-pregnancy potassium levels were within normal limits in the absence of supplementary potassium. This case highlights the potentially life-threatening electrolyte imbalances that can occur with HG and the importance of recognising the disease, comprehensive electrolyte monitoring, and aggressive management in pregnancy.

Publisher

Hindawi Limited

Subject

Obstetrics and Gynecology

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