Life-Threatening Spontaneous Retroperitoneal Hemorrhage Associated with Acenocoumarol Anticoagulation in a Young Patient with a Mechanical Aortic Valve: A Case Report

Abstract

Background

Spontaneous retroperitoneal hemorrhage is an uncommon but potentially fatal complication of anticoagulant therapy. Management is particularly difficult in patients with mechanical heart valves because urgent reversal must be balanced against the risk of valve thrombosis and systemic embolism.

Case Presentation

A 24-year-old man with a mechanical aortic valve receiving acenocoumarol presented with severe abdominal pain, abdominal distension, and syncope. Hemoglobin was 4 g/dL, serum creatinine was 2.5 mg/dL, and the international normalized ratio was 15. Contrast-enhanced computed tomography showed a large left perinephric retroperitoneal hematoma extending into the left iliopsoas muscle and pelvis, without hemoperitoneum or active contrast extravasation. Acenocoumarol was stopped, and he received intravenous vitamin K, fresh frozen plasma because prothrombin complex concentrate was unavailable, packed red blood cells, and intensive monitoring. He improved without invasive intervention, and anticoagulation was cautiously reintroduced after clinical and radiological stabilization.

Conclusion

Spontaneous retroperitoneal hemorrhage should be considered in anticoagulated patients with abdominal or flank pain, syncope, unexplained anemia, hypotension, or acute kidney injury. Prompt diagnosis, urgent reversal, and individualized anticoagulation resumption are essential.

Plain Language Summary

Blood-thinning medicines are essential after mechanical heart-valve replacement, but excessive anticoagulation can occasionally cause severe internal bleeding. We describe a 24-year-old man taking acenocoumarol after mechanical aortic-valve replacement who developed sudden abdominal pain, swelling, fainting, profound anemia, kidney injury, and a very high clotting test result. A CT scan showed a large collection of blood behind the abdominal cavity, around the left kidney and extending into a nearby muscle. The anticoagulant was stopped, and the patient received vitamin K, plasma, blood transfusions, and close monitoring. He recovered without surgery or embolization. This case shows the importance of regular INR monitoring, early CT imaging when internal bleeding is suspected, and careful specialist decisions about when to restart anticoagulation after bleeding has been controlled.

Introduction

Spontaneous retroperitoneal hemorrhage (SRH) is bleeding into the retroperitoneal space without preceding trauma or an invasive procedure. Because this compartment can accommodate a large volume of blood before obvious external signs develop, diagnosis may be delayed and mortality can be substantial.¹ Anticoagulant exposure is a major predisposing factor, and affected patients often present with nonspecific symptoms.²

Vitamin K antagonists, including warfarin and acenocoumarol, remain necessary for thromboembolic prevention in patients with mechanical prosthetic valves. Their narrow therapeutic index creates a clinically important bleeding risk when anticoagulation becomes excessive.³ Retroperitoneal hemorrhage associated with vitamin K antagonist therapy has been described in several anatomical patterns, including renal and perirenal bleeding.⁴

Clinical manifestations may include abdominal or flank pain, progressive anemia, hypotension, syncope, femoral neuropathy, and acute kidney injury caused by hypovolemia or compression of retroperitoneal structures. Early and accurate diagnosis improves the opportunity for effective treatment.⁵ Contrast-enhanced computed tomography (CT) is the principal diagnostic modality because it defines the location and extent of the hematoma and can identify active bleeding. Stable patients without active extravasation may be managed conservatively, whereas persistent instability or ongoing bleeding may require endovascular or surgical intervention.⁶

Patients with mechanical valves present an additional management dilemma: anticoagulation must be reversed during life-threatening bleeding, but prolonged interruption increases the risk of valve thrombosis and systemic embolism.⁷ We report a young patient with a mechanical aortic valve who developed massive SRH, profound anemia, acute kidney injury, and an INR of 15, and who was successfully managed in a resource-limited setting where prothrombin complex concentrate (PCC) and interventional radiology were not readily available.

Case Report

A 24-year-old man presented to the emergency department with sudden severe abdominal pain, progressive abdominal distension, dizziness, blurred vision, and a syncopal episode. He had rheumatic heart disease and had undergone mechanical aortic valve replacement six months earlier. He was taking acenocoumarol 3 mg daily, with a documented target INR range of 2.0–3.0.

He denied recent trauma, falls, invasive procedures, alcohol use, liver disease, a known bleeding disorder, herbal medication use, or intentional overdose. He described erratic INR monitoring during the preceding several weeks; however, the exact testing frequency and his most recent pre-presentation INR were not available. The precise cause of the INR elevation could not be established. Possible contributors included inconsistent INR surveillance, dosing variation, dietary vitamin K fluctuation, an unrecognized drug interaction, or intercurrent illness, but none could be confirmed from the available record.

On examination, he was pale and distressed. His heart rate was 120 beats/min, blood pressure was 100/60 mmHg, respiratory rate was 24 breaths/min, and oxygen saturation was 97% on room air. The abdomen was distended and diffusely tender, with ecchymotic discoloration. Mechanical valve clicks were audible, without an additional murmur.

Laboratory testing showed a hemoglobin concentration of 4 g/dL, leukocyte count of 11.2 × 10⁹/L, platelet count of 240 × 10⁹/L, serum creatinine of 2.5 mg/dL, and INR of 15. Liver biochemistry was within normal limits. A retrospective estimate using the 2021 CKD-EPI creatinine equation gave an eGFR of approximately 36 mL/min/1.73 m².

Because life-threatening internal bleeding was suspected, urgent contrast-enhanced CT of the abdomen and pelvis was performed despite the acute kidney injury (Figure 1). The scan demonstrated a large left perinephric retroperitoneal hematoma extending into the left iliopsoas muscle and inferiorly into the pelvis, with mass effect on the left kidney (Figure 2). No hemoperitoneum or active contrast extravasation was identified. The immediate diagnostic value of defining the bleeding source and determining whether active hemorrhage was present was judged to outweigh the potential contrast-associated renal risk.

Figure 1.

Index contrast-enhanced computed tomography (CT) of the abdomen and pelvis. (A) Axial CT image demonstrating a large left perinephric retroperitoneal hematoma causing significant mass effect on the left kidney and adjacent retroperitoneal structures. (B) Inferior axial CT image showing extension of the hematoma into the left iliopsoas muscle and pelvis. No hemoperitoneum is identified. Arrows consistently indicate the hematoma in both panels.

Figure 2.

Coronal (A) and sagittal (B) contrast-enhanced computed tomography (CT) reconstructions confirming the large left perinephric retroperitoneal hematoma, demonstrating marked mass effect on the left kidney and extension into the pelvis.

The patient was admitted to the intensive care unit. Acenocoumarol was stopped immediately. He received intravenous vitamin K 5 mg and four units of fresh frozen plasma because PCC was unavailable, together with four units of packed red blood cells. Serial clinical assessment and laboratory monitoring were undertaken. He remained hemodynamically stable without evidence of continued bleeding. Hemoglobin and INR improved, urine output remained adequate, and renal function recovered with supportive care. Renal replacement therapy was not documented in the available clinical record follow-up CT scan was not performed because the patient improved clinically, and repeat CT was not indicated due to cost considerations. Instead, follow-up ultrasonography confirmed interval reduction of the retroperitoneal hematoma. Therefore, no follow-up CT images are available for inclusion. Following multidisciplinary discussion among cardiology, internal medicine, and cardiovascular surgery teams, anticoagulation was cautiously restarted because of the thromboembolic risk associated with the mechanical valve. The source record documented enoxaparin 0.4 mL twice daily, followed by gradual reintroduction of acenocoumarol. The enoxaparin product strength, patient weight, calculated mg/kg dose, and intended prophylactic or therapeutic intensity were not available for retrospective verification. Enoxaparin was stopped after the INR returned to the therapeutic range.

The patient continued to improve and was discharged in stable condition. At one-month follow-up, renal function and hemoglobin were stable, the INR was therapeutic, and there had been no recurrent bleeding or valve-related complication.

Discussion

This case demonstrates that severe vitamin K antagonist-associated bleeding can occur in young patients, although much of the anticoagulation safety literature has focused on older populations.⁸ The patient presented with abdominal pain, syncope, borderline hypotension, profound anemia, and acute kidney injury, a combination that should trigger immediate investigation for occult internal hemorrhage.

Severe spontaneous bleeding during anticoagulant therapy is not confined to vitamin K antagonists or the retroperitoneum. A previously published case of apixaban-associated subdural hematoma in an elderly patient with heart failure similarly illustrates the need to consider major occult hemorrhage when anticoagulated patients deteriorate unexpectedly.⁹ The relevance of that report to the present case is supportive rather than directly comparative because both the anticoagulant and bleeding site were different.

CT was central to diagnosis and management. The hematoma was predominantly left perinephric, extended into the iliopsoas muscle and pelvis, compressed the left kidney, and showed no active extravasation. Warfarin-associated retroperitoneal hematoma has also been reported in patients with renal impairment, emphasizing the interaction between bleeding, renal dysfunction, and anticoagulant exposure.¹⁰ In the present case, contrast imaging was undertaken because determining the bleeding extent and excluding active hemorrhage was immediately relevant to survival. The patient maintained urine output and recovered renal function without documented dialysis.

For life-threatening vitamin K antagonist-associated bleeding, contemporary guidance supports immediate interruption of the anticoagulant, intravenous vitamin K, and rapid factor replacement; four-factor PCC is generally preferred to plasma because it reverses anticoagulation more rapidly and with a lower infused volume.¹¹ Fresh frozen plasma is an alternative when PCC is unavailable. In this resource-limited setting, vitamin K, plasma, transfusion support, and intensive monitoring achieved hemostatic and clinical stabilization. FFP should not be interpreted as equivalent to PCC, and the treatment used here reflected local availability rather than preferred first-line reversal.

Restarting anticoagulation required balancing the risk of recurrent bleeding against the risk of mechanical valve thrombosis and systemic embolism. Current valvular-heart-disease guidance emphasizes lifelong vitamin K antagonist therapy for mechanical valves and individualized decisions about interruption, bridging, and resumption after major bleeding.¹² In this patient, anticoagulation was resumed only after hemodynamic stability, improvement in hemoglobin and renal function, and radiological reduction of the hematoma. The exact enoxaparin dose intensity could not be verified retrospectively, which limits detailed evaluation of the bridging strategy.

Published evidence on the optimal timing and intensity of anticoagulation resumption after life-threatening extracranial bleeding in patients with mechanical valves remains limited, and decisions must account for valve position, thromboembolic risk, bleeding control, renal function, and available monitoring.¹³ This report is further limited by its single-patient design, the absence of PCC and advanced interventional radiology, incomplete documentation of the cause of INR elevation and the enoxaparin dose, and the inability to draw general conclusions about the best restart strategy.

Conclusion

Spontaneous retroperitoneal hemorrhage should be considered in anticoagulated patients presenting with abdominal or flank pain, syncope, hypotension, severe anemia, or acute kidney injury. Conservative treatment can be successful in selected hemodynamically stable patients without active bleeding on CT. PCC is preferred for urgent vitamin K antagonist reversal when available, while FFP may be used when PCC cannot be obtained. In patients with mechanical prosthetic valves, the timing and intensity of anticoagulation reintroduction require individualized multidisciplinary assessment.

Ethical Approval

Ethics committee approval was not required for this case report according to institutional policy for single-patient case reports. The study was conducted in accordance with the Declaration of Helsinki.

Informed Consent

Written informed consent was obtained from the patient for publication of this case report and accompanying images.

Author Contributions

All authors made a significant contribution to the work reported, whether that is in the conception, study design, execution, acquisition of data, analysis and interpretation, or in all these areas; took part in drafting, revising or critically reviewing the article; gave final approval of the version to be published; have agreed on the journal to which the article has been submitted; and agree to be accountable for all aspects of the work.

Disclosure

The authors declare no conflicts of interest.