Left testicular venous infarction secondary to large spontaneous retroperitoneal haematoma compressing left testicular vein: a case report
- 1 Department of General Surgery, Alfred Health, Melbourne, Victoria, Australia
- 2 Department of Medicine at Alfred Medical Research and Education Precinct, Monash University, Melbourne, Victoria, Australia
- Correspondence to Dr Thomas Vu; tomvu90@gmail.com
Abstract
A man in his early 50s presented with a spontaneous large left-sided retroperitoneal haematoma (RPH), on a background of therapeutic anticoagulation with warfarin for homozygous factor V Leiden. His international normalised ratio was found to be supra-therapeutic at 9.0 on presentation. He was treated non-operatively with prompt reversal of the coagulopathy and close monitoring. On day 4 of the admission, the patient reported scrotal pain and swelling. An urgent scrotal ultrasound revealed infarction of the left testis and the patient was taken to an emergency scrotal exploration. Intraoperatively, the left testis was found to be no longer viable with the left spermatic vein and venules completely thrombosed with extensive clots, while the left testicular artery remained intact. Consequently, a left orchidectomy was performed. Therapeutic anticoagulation was recommenced on day 3 postoperatively. It is thought that the large RPH caused extrinsic compression of the left testicular vein, in addition to the patient’s pre-existing factor V Leiden, which resulted in thrombosis of the blood vessel.
Background
Spontaneous retroperitoneal haematoma (RPH) is a rare but recognised condition seen in patients with bleeding disorders, on anticoagulation therapies or haemodialysis.1 Documented complications of RPH include local mass effects such as femoral neuropathy, abdominal compartment syndrome, obstructive uropathy and persistent pain, as well as systemic effects secondary to hypovolaemia.2 While compression of the testicular vein causing thrombosis, venous ischaemia and infarction of the testis is also a potential complication due to the anatomical course of this vessel within the retroperitoneal space, it is yet to be reported.
We present a case of a large spontaneous left-sided RPH in a patient with therapeutic anticoagulation for underlying homozygous factor V Leiden, causing compression on the left testicular vein. This resulted in extensive venous thrombus and subsequent left testicular venous infarct, causing severe pain requiring emergent surgery for scrotal exploration and left orchidectomy. To our knowledge, this is the first case report documenting testicular venous infarct as a complication of RPH in the literature.
Case presentation
A man in his early 50s presented to our emergency department with a 4-day history of severe abdominal pain and constipation. He had no nausea or vomiting and there were no urinary symptoms. There was no history of trauma. His medical history included homozygous factor V Leiden, diagnosed after an unprovoked episode of deep vein thrombosis and pulmonary embolism 6 years prior to this admission. The patient’s usual warfarin dose was 10 mg daily, with a therapeutic target international normalised ratio (INR) between 2 and 3; however, he had been non-compliant with regular INR monitoring. Clinical examination revealed a soft and distended abdomen, with tenderness in the left upper and lower quadrants, as well as positive Grey-Turner’s and Cullen’s signs. The patient was haemodynamically stable.
His admission blood results revealed abnormal blood parameters with a low haemoglobin count of 79 g/L, mildly elevated white cell count of 12.23×1o9/L, elevated platelets of 300×1o9/L, significantly raised INR and lactate of 9.0 and 3.8 mmol/L, respectively. An urgent CT with intravenous contrast of the abdomen–pelvis was performed, which revealed a large 24 cm left retroperitoneal haematoma with multiple foci of contrast extravasation indicating active bleeding (figure 1). A haematological opinion was sought to promptly reverse the effect of warfarin by administration of 1 unit of fresh frozen plasma, intravenous vitamin K and prothrombin factor complex (Prothrombinex). The patient was also transfused 1 unit of packed red cells with an appropriate resultant haemoglobin increment. A CT angiogram of the abdomen–pelvis was performed after resuscitation and correction of coagulopathy which showed a stable haematoma without further evidence of active bleeding. The decision was subsequently made by the surgical and interventional radiology team to hold off an initially planned angioembolisation at this point of time. After 24 hours of close monitoring in the intensive care unit, the patient was discharged to the ward for ongoing expectant management of the RPH, with haematology input for recommendation of anticoagulation restart.
CT of the abdomen–pelvis on presentation (left–coronal, right–axial) showing a large left-sided retroperitoneal haematoma with multifocal contrast extravasations (red arrows).
On day 4 of the admission, the patient reported a 3-day history of scrotal pain and swelling to the medical team for the first time during his inpatient stay. Clinical examination revealed a diffusely enlarged and tender scrotum with widespread ecchymoses, worse on the left side compared with the right. An urgent testicular ultrasound was performed, which showed infarction of the left testis but was unable to clearly rule out testicular torsion (figure 2). The INR was 1.6 at this stage, compared with 9.0 on admission. Despite the elevated INR, the decision was made to proceed for emergency scrotal exploration with the urology team with the hope, although unlikely, for testicular salvage. Intraoperatively though, the scrotal skin was grossly oedematous, and the left testis was found to be diffusely congested and no longer viable. The left spermatic vein and venules were completely thrombosed with extensive clots (figure 3); however, the left testicular artery remained intact. Consequently, a left orchidectomy was performed. The right hemiscrotum was also explored with normal findings.
Ultrasound images of the normal right testis (left) and the infarcted left testis (right) with minimal blood flow.
Infarcted left testis with extensive venous thrombosis.
The patient recovered well from the surgical perspective; however, his inpatient stay was complicated by hospital-acquired pneumonia and postoperative pulmonary embolism requiring intravenous antibiotics and high-flow nasal prongs. A prophylactic dose of enoxaparin was administered immediately following surgery, and therapeutic anticoagulation was recommenced on day 3 postoperatively with enoxaparin 1 mg/kg two times per day, followed by transition to oral anticoagulant (rivaroxaban) on discharge.
Outcome and follow-up
The patient was followed up in the general surgical and urology outpatient clinic 3 weeks after his initial acute presentation with an ultrasound of the abdomen showing a small reduction in size of the left RPH. The scrotal surgical wound had healed well and the patient reported that he had returned to his normal daily activities without any further issues.
Discussion
RPH is commonly associated with blunt or penetrating trauma.3 In non-traumatic RPH, the majority of patients are on either anticoagulation or antiplatelet therapy, reported to be as high as 84.7% of all spontaneous bleeds, with 41.6% on warfarin therapy.4 The management of RPH includes ongoing resuscitation, correction of coagulopathy, close monitoring, and angioembolisation or surgery for ongoing bleeding and haemodynamically unstable patients. Complications of RPH can be classified as systemic due to hypovolaemia or hypotension, and local due to mass effects. These include pelvic or femoral neuropathy, bowel obstruction, obstructive uropathy, abdominal compartment syndrome and persistent pain.3 Large RPH can also cause compression on various retroperitoneal venous structures including the renal veins and the inferior vena cava.5 6 The testicular vein is a structure that could be potentially obstructed due to its anatomical course within the retroperitoneum; however, there have been no reported cases of this complication in the literature.
In this particular case, the large RPH caused extrinsic compression of the left testicular vein resulting in venous stasis with consequent thrombosis. This was further exacerbated by his underlying factor V Leiden with warfarin being withheld, which led to extensive thrombus within the left testicular vein as well as in the venous channels within the left testis. This resulted in venous ischaemia and ultimately infarction of the testis, requiring an orchidectomy.
Testicular venous thrombosis is an uncommon condition that is often associated with regional malignancy in proximity with the testicular vein.7 There are also case reports of the condition in patients with hypercoagulopathy such as antiphospholipid syndrome.8 9 The combination of external compression caused by the large RPH and the hypercoagulable state in this case put the patient at significantly higher risk of developing a thrombotic event.
In conclusion, a large RPH can cause a variety of local complications from its mass effect. Spontaneous RPH tends to occur more frequently in patients on anticoagulation therapy, which often indicates that they have an underlying hypercoagulable condition. Treatments then would include withholding their anticoagulation agents, hence putting patients at higher risks of developing thrombosis in retroperitoneal venous structures, including the testicular veins. Therefore, scrotal examination should form part of a routine physical examination when monitoring patients with large RPH.
Learning points
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Spontaneous retroperitoneal haematoma can occur in patients on anticoagulation/antiplatelet therapies.
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Although rare, large retroperitoneal haematoma could cause compression in testicular veins leading to testicular venous infarct.
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Scrotal assessment is an important part of a complete abdominal clinical examination.
Ethics statements
Patient consent for publication
Footnotes
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Contributors TV is a general surgery registrar responsible for the patient’s care, the primary and corresponding author, and contributed to the writing, editing and submission of the manuscript. SL is a urology fellow responsible for the reviewing and editing of the manuscript. SB is a general surgery consultant and the lead clinician of the patient’s care, and contributed to the reviewing and editing of the manuscript. JG is a urology consultant who contributed to the reviewing and editing of the manuscript.
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Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.
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Case reports provide a valuable learning resource for the scientific community and can indicate areas of interest for future research. They should not be used in isolation to guide treatment choices or public health policy.
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Competing interests None declared.
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Provenance and peer review Not commissioned; externally peer reviewed.
- © BMJ Publishing Group Limited 2022. No commercial re-use. See rights and permissions. Published by BMJ.
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