The hyperemesis gravidarum and pulmonary embolism: A case report and review of literature.

Abstract

Background: Nausea and vomiting occur in more than 70% of pregnant women,¹ and only 2% of these females progress into hyperemesis gravidarum (HG).² HG is the persistent and excessive vomiting before the 22nd week of gestation. HG patients can develop life-threatening electrolyte disturbances or thromboembolism. Pulmonary embolism (PE) is a thromboembolism that blocks and stops blood flow to an artery in the lung. Both HG and PE increase morbidity and mortality in pregnant patients. HG patients developing PE are reported only in two patients with fatal outcomes in the literature. We report a case of PE in a hospitalized HG patient with a better outcome.

Case presentation: A 26-year-old previously healthy gravida 3 and para 2 patient was admitted to the Women Wellness and Research Center with HG at 10 weeks of gestation. She developed nausea and vomiting at 6 weeks of gestation and was treated in the emergency department, where she was started on intravenous (IV) fluids for hydration, an antiemetic, and deltaparin for prevention of deep venous thrombosis (DVT), as she was pregnant and dehydrated. She was on potassium replacement therapy for hypokalemia. The patient was improving; still had vomiting, but less frequent. On day 3, following admission, the patient suddenly developed hemoptysis, chest pain, and palpitation. She was tachycardic (120 bpm) and tachypneic (30 breaths per minute). She was feeling dizzy, and her oxygen saturation (Spo₂) was around 95%. Her chest was clear on examination. Computerized tomographic pulmonary angiography showed bilateral PE. She was admitted to the highdependency unit. The patient was tachypneic and tachycardic and required non-invasive ventilation. A therapeutic dose of enoxaparin (1 mg/kg) was started and supplemented with fentanyl plus paracetamol for analgesia, continued IV fluids, and promethazine.Her respiratory symptoms and tachycardia improved by day 6, she was transferred to the ward from there and discharged home by day 10, on enoxaparin therapeutic dose (1 mg/kg), and follow up in outpatient clinics showed no issues, and she is doing fine.

Discussion: HG is a severe clinical disease in pregnancy where patients have intractable nausea and vomiting with increased morbidity and even mortality. These patients frequently present with ketonuria, dehydration, electrolyte abnormalities, and a weight loss of 7%. Rarely, these patients' present with severe vitamin deficiency, causing a neurological emergency called Wernicke's encephalopathy. The occurrence of DVT is one of the main risk factors due to prothrombotic conditions in pregnancy in combination with dehydration in these patients. The occurrence of PE is reported in two cases of HG in the post-mortem. Our patient developed bilateral PE, a medical emergency due to immobility, dehydration, and prothrombotic predominance during pregnancy. PE was detected early and managed, leading to a better outcome.

Conclusion: HG should be diagnosed early, followed by admission of the patient to the hospital. Our patient with HG was complicated by a rare bilateral PE due to a combination of pregnancy, dehydration, and immobility, despite DVT prophylaxis with a favorable outcome. Clinicians should have an index of suspicion for DVT and PE in these dehydrated pregnant patients. A high index of suspicion, early diagnosis, and management by a multidisciplinary team are key for better outcomes of PE in our HG patient.