Warfarin induced spontaneous gastric intramural haematoma presenting with palpitations

Abstract

Spontaneous gastric intramural haematoma is an uncommon complication associated with anticoagulant therapy. A patient receiving chronic warfarin for paroxysmal atrial fibrillation was admitted due to atrial fibrillation with rapid ventricular response (RVR). An incidental intra-abdominal mass was detected on a CT scan. Following the initiation of the amiodarone infusion, the patient experienced bleeding attributed to warfarin-amiodarone-induced coagulopathy, with no identifiable bleeding source. Subsequent CT scans revealed an enlargement of the intra-abdominal mass, suggesting gastric intramural haematoma. After coagulopathy reversal, the haematoma is managed conservatively. Our case underscores the potential for incidental bleeding even when the international normalised ratio is within the normal range in patients on chronic warfarin therapy. When managing such patients with atrial fibrillation with RVR, physicians should maintain a high index of suspicion for bleeding, emphasising the importance of prompt coagulopathy reversal.

Background

Spontaneous gastric intramural haematoma is a rare complication of anticoagulant therapy. Here we present a case of incidental gastric intramural hematoma with an atypical presentation in a patient with chronic use of warfarin.

Case presentation

A man in his 70s with a history of hypertension, diabetes mellitus type 2, congestive heart failure, paroxysmal atrial fibrillation on home warfarin 5 mg daily, chronic obstructive pulmonary disease, obstructive sleep apnoea, chronic kidney disease (CKD) and morbid obesity presented to the emergency department (ED) with a sudden onset of palpitation. He denied having abdominal pain, diarrhoea, nausea, vomiting or melena. He denied any recent trauma or procedures.

Investigations

At the ED, his temperature was 97.5°F, blood pressure was 92/66 mm Hg, heart rate was 153 beats per minute, respiratory rate was 20 breaths per minute and oxygen saturation was 95% on room air. A physical examination was significant for a distended abdomen and reducible umbilical hernia with mild tenderness on palpation of the hernia. Initial laboratory workup showed haemoglobin of 13.3 g/dL (normal range: 14–18 g/dL), creatinine of 2.4 mg/dL (normal range: 0.7–1.3 mg/dL), lactate of 7.7 mmol/L (normal range: 0.5–2 mmol/L), prothrombin time of 28.5 s (normal range: 12.2–14.9 s), partial prothrombin time of 35.9 s (normal range: 23.2–37.4 s) and international normalised ratio (INR) of 2.67. The ECG revealed atrial fibrillation with rapid ventricular response (RVR). A CT of the abdomen and pelvis without contrast showed a 16.43×15×13.44 cm mass in the upper abdomen, inseparable from the left hepatic lobe and stomach (figure 1A and B). Carcinoembryonic antigen, carbohydrate antigen 19–9 and alpha-fetoprotein tests were negative. The patient was admitted to the intensive care unit (ICU) for management of atrial fibrillation with RVR.

Figure 1.

CT of the abdomen and pelvis without contrast findings in the patient. CT images demonstrate the gastric intramural haematoma (asterisks). (A) Axial and (B) coronal images were taken on the day of admission to the ICU. (C) Axial and (D) coronal images were taken on ICU day 3. Subtle cleavage between the haematoma and the adjacent liver was found in (C) and (D) (outlined by yellow arrows). ICU, intensive care unit.

On admission to the ICU, the patient was initiated on a diltiazem, digoxin and amiodarone infusion. Warfarin was continued at the home dose, as no coagulopathy or active bleeding was suspected. On ICU day 2, cardioversion was performed, converting atrial fibrillation to a normal sinus rhythm. The laboratory workup showed dropped haemoglobin of 8.3 g/dL, elevated INR of 4.09 and normal lactate of 1.5 mmol/L. Therefore, warfarin was suspended. On day 3, his haemoglobin further dropped to 6.2 g/dL, and his INR increased to 5.8, suggesting severe bleeding due to coagulopathy. He then received four units of packed red blood cells, 10 mg of phytonadione and three units of fresh frozen plasma. Subsequently, his haemoglobin increased to 7.1 g/dL, and the INR decreased to 1.1. Repeat CT showed further enlargement of the mass arising from the anterior wall of the stomach, measuring 22.3×13.6×17.3 cm, accompanied by subtle cleavage from the adjacent liver (figure 1C and D). The patient underwent an ultrasound-guided biopsy of the intra-abdominal mass, revealing a haematoma. Then, he underwent oesophagogastroduodenoscopy (OGD), which revealed large extrinsic compression on the gastric body with normal gastric mucosal tissue (figure 2). Then, the patient remained haemodynamically stable and was then discharged home on day 14 of hospitalisation.

Figure 2.

Endoscopic examination showed marked narrowing of the gastric lumen. Large extrinsic compression was seen in the anterior wall of the body (black arrows). No gastric mass was found.

Differential diagnosis

Concerned about the patient’s elevated lactate levels and mild abdominal tenderness, our initial suspicion was bowel ischaemia related to the umbilical hernia. Given the patient’s haemodynamic instability and pre-existing CKD, we opted for further investigation using a CT of the abdomen and pelvis without contrast. The imaging revealed an incidental intra-abdominal mass, prompting a shift in our working diagnosis towards a potential gastric or liver tumour, despite negative tumour marker tests. A visceral aneurysm was also considered a differential diagnosis; however, it is worth noting that visceral aneurysms typically do not present with such a large mass.¹ Subsequent CT scans, displaying an enlarging mass, led us to consider the possibility of a bleeding neoplasm or haematoma secondary to warfarin-induced coagulopathy. To confirm the diagnosis, we conducted an ultrasound-guided biopsy, which demonstrated the presence of blood without malignant cells, suggesting gastric intramural haematoma.

Treatment

The gastric intramural haematoma was managed conservatively, and anticoagulant therapy was discontinued throughout the entire hospitalisation.

Outcome and follow-up

Following discharge, the patient received ongoing care at the cardiology clinic. Approximately 1.5 months postdischarge, the cardiologist commenced the patient on apixaban 5 mg two times per day, to prevent embolus formation. Considering the patient’s elevated risk of bleeding, the cardiologist recommended the implantation of a WATCHMAN device. Unfortunately, the patient declined this procedure, citing financial constraints stemming from the prior hospitalisation. At 3-month follow-up, the patient was doing well and had no complaints. The patient became lost to follow-up thereafter, with no subsequent re-evaluation of the gastric intramural haematoma through repeated CT scans.

Discussion

Gastric intramural haematoma is a rare complication of anticoagulant therapy, with only a few cases documented in the literature.^2–7 Clinical manifestations of gastric intramural haematoma are non-specific and can range from mild abdominal pain to severe shock resulting from internal bleeding.⁶ Our case was atypical as our patient only presented with localised mild tenderness on palpation of umbilical hernia, despite the substantial haematoma growth during hospitalisation. Given the non-specific symptoms of gastrointestinal haematomas, CT stands as the primary diagnostic tool for gastrointestinal haematomas.² However, without contrast-enhanced CT or angiography, it was initially unclear to us if the mass was a haematoma. In addition, the initial CT failed to reveal a distinct margin between the haematoma and the liver, further complicating the diagnostic process by hindering the identification of the source of the mass. To overcome these challenges, we used combined information from serial CT scans, OGD and ultrasound-guided biopsy, which is a diagnostic method not previously described in the literature.

Bleeding is the major adverse event in anticoagulant treatment, including vitamin K antagonist (VKA) use.⁸ The major determinants of VKA-induced bleeding are the intensity of the anticoagulant effect, inherent patient characteristics and the duration of therapy.⁸ 39.6% and 4.5% of the patients experienced haematoma and gastrointestinal bleeding, respectively, within 1 year after the initiation of VKA therapy.⁹ Overcoagulation, characterised by supratherapeutic INR, is associated with an increased risk of both major and minor bleeding.⁸ Interestingly, our patient presented with an incidental gastric intramural haematoma on admission, despite INR within the therapeutic range of INR 2.0–3.0. We speculated that chronic bleeding might trigger atrial fibrillation with RVR in our patient. This emphasises the necessity of a high index of suspicion for bleeding events, regardless of the INR value, when managing patients on long-term VKA therapy.

Amiodarone, classified as a class III antiarrhythmic agent, has been shown to be effective in converting atrial fibrillation to sinus rhythm and controlling ventricular rate in patients who are critically ill.¹⁰ Given the frequent use of warfarin for stroke prevention in atrial fibrillation, the concomitant administration of these medications is common.¹¹ Of note, amiodarone acts as a cytochrome P450 2C9 inhibitor, impeding warfarin hydroxylation and consequently intensifying anticoagulation effects.¹² During hospitalisation, the haematoma exhibited a significant increase in size attributed to the coagulopathy induced by the warfarin–amiodarone interaction. As a result, the cost of hospitalisation increased due to the need for blood product transfusions and long ICU stays. Current guidelines recommend discontinuing warfarin and considering optional vitamin K administration for hospitalised patients with no active bleeding and an INR between 4.5 and 10.¹³ In the specific context of atrial fibrillation with RVR, aggressive treatment to reverse coagulopathy may be warranted in patients on chronic use of warfarin who initiate an amiodarone infusion. In conclusion, our case serves as a reminder that variations in clinical expression attributed to anticoagulant-associated bleeding should be anticipated.

Learning points.

• Warfarin-induced gastric intramural haematomas can develop silently, despite an International normalised ratio (INR) within the therapeutic range and the absence of abdominal tenderness.

• Warfarin–amiodarone interaction can potentiate coagulopathy when treating atrial fibrillation with rapid ventricular response.

• A decrease in the warfarin dosage might be warranted, even if the INR is within the therapeutic range when it is administered concurrently with intravenous amiodarone.

• There may be a need for aggressive interventions to reverse coagulopathy in patients with a history of chronic warfarin use who initiate amiodarone infusion.

Ethics statements

Patient consent for publication

Consent obtained directly from patient(s).