A Case Report on Spontaneous Retroperitoneal Hemorrhage

A Case Report on Spontaneous Retroperitoneal Hemorrhage

Spontaneous retroperitoneal hemorrhage (SRH) is a rare but potentially life-threatening condition characterized by the spontaneous rupture of retroperitoneal blood vessels. This condition is often associated with a low diagnostic rate and high mortality, particularly in patients with underlying conditions such as hypertension, diabetes, renal failure, or those undergoing anticoagulation therapy. This case report presents a detailed account of a 49-year-old woman with a complex medical history who developed SRH, ultimately leading to her death despite intensive medical intervention.

The patient, a 49-year-old woman of Han nationality, had a history of hypertension for two years and type 2 diabetes for 19 years. Her diabetes was complicated by diabetic nephropathy, diabetic peripheral neuropathy, diabetic peripheral vascular disease, nephrotic syndrome, renal insufficiency, and coronary heart disease. She was admitted to the hospital due to swelling in both legs, oliguria for one year, and a worsening condition over the preceding half month. On admission, her weight was 75 kg, blood glucose level was 15.47 mmol/L, blood pressure (BP) was 143/102 mmHg, hemoglobin (Hb) was 119 mg/dL, prothrombin time (PT) was 14.70 seconds, activated partial thromboplastin time (APTT) was 37.6 seconds, and international normalized ratio (INR) was 1.11. Imaging studies revealed bilateral pleural effusion and an enlarged heart with a ventricular ejection fraction of 33%.

Upon admission, the patient was treated with diuretics, insulin, anti-creatinine drugs, low molecular weight heparin (3200 U, subcutaneous injection, once daily), aspirin (100 mg, oral, once daily), and supportive treatments. Her hemostasis and coagulation tests remained within normal limits until February 14. However, on February 14, she developed acute left heart failure and was transferred to the Department of Critical Care Medicine. There, she received oxygen inhalation, sedation, antihypertensive therapy, continuous renal replacement therapy (CRRT), CRRT anticoagulation with sodium citrate, dehydration, thoracic drainage, and albumin infusion. Despite these interventions, her condition continued to deteriorate.

On February 19, her Hb dropped to 93 mg/L, prompting the discontinuation of low molecular weight heparin and aspirin. The following morning, she complained of discomfort in the left lower abdomen, and her Hb further decreased to 71 mg/L. Ultrasound revealed an abdominal pelvic effusion in the left lower abdomen measuring 119 x 74 x 89 mm. A diagnostic peritoneal puncture yielded light-yellow transparent fluid. Despite rapid fluid replacement and red blood cell transfusion, her Hb continued to drop to 60 mg/L, and her PT, INR, and APTT increased to 17.3 seconds, 1.44, and 52.5 seconds, respectively. Her heart rate increased to 120 beats per minute, and her BP was 130/90 mmHg with an oxygen saturation of 96%.

Abdominal computed tomography (CT) revealed an area of heterogeneous density under the left kidney, suggestive of retroperitoneal hemorrhage. Lumbar artery rupture and active bleeding were suspected, and emergent lumbar artery embolization was recommended. However, during transit to the catheterization laboratory, the patient lost consciousness, and her BP dropped from 117/84 to 50/30 mmHg. Despite rapid fluid replacement via central venous catheter and vasopressors, her BP could not be maintained, and her heart rate dropped rapidly. Cardiopulmonary resuscitation was initiated, but the patient eventually died. The causes of death were determined to be rupture of retroperitoneal hematoma, hemorrhagic shock, and respiratory and cardiac arrest.

SRH is defined as the spontaneous rupture of retroperitoneal blood vessels, and its etiology remains unclear. Most patients with SRH have underlying vascular diseases such as hypertension and atherosclerosis. Other potential contributing factors include congenital defects or abnormal development of retroperitoneal vessels, pregnancy, and endocrine factors. In this case, the patient’s long-standing diabetes and hypertension likely contributed to structural changes in the arterial wall, including stenosis, hyaline degeneration, deformation, impaired vasodilation, and weakened blood vessel walls. The nephrotic syndrome, characterized by increased vascular permeability and protein leakage into the retroperitoneal cavity, may have also played a role in the development of SRH.

The clinical presentation of SRH is often characterized by the Lenk triad: abdominal pain, shock, and a non-pulsating abdominal mass. The nature of the abdominal pain can vary depending on the location, incidence, and amount of bleeding. Persistent retroperitoneal hemorrhage can lead to increased abdominal pressure due to hematoma enlargement, resulting in severe abdominal distension, anemia, and abdominal compartment syndrome. If the hematoma compresses the femoral nerve, it can cause pain in the lower limbs and buttocks, paresis, and movement disorders. In this case, the patient exhibited an unexplained decrease in Hb, abdominal discomfort, and imaging findings consistent with retroperitoneal hemorrhage.

Diagnostic methods for SRH include ultrasound, diagnostic abdominal puncture, and abdominal CT scans. Ultrasound can be used as a preliminary screening tool, while diagnostic abdominal puncture and CT scans provide more accurate information about the location and extent of the hematoma. Enhanced CT can be performed to assess the need for interventional or surgical treatment. In this case, the patient’s abdominal CT revealed a mass-occupying lesion in the retroperitoneum, and ultrasound showed an abdominal pelvic effusion. However, an enhanced CT scan was not performed due to concerns about further renal damage from the contrast agent.

The treatment of retroperitoneal hematoma requires a multidisciplinary approach and a comprehensive evaluation based on the cause of bleeding. Compression hemostasis can be used if the hematoma is integrated. Conservative treatment is recommended for patients with small hematomas or stable vital signs, while active anti-shock therapy and surgical exploration are necessary for patients with acute bleeding and unstable hemodynamics. Endovascular embolization is preferred for patients with unexplained bleeding and unstable vital signs, followed by selective surgical treatment if necessary. In this case, the patient initially received conservative treatment, but her condition rapidly deteriorated, necessitating emergent interventional therapy. Unfortunately, she died before the procedure could be performed.

In conclusion, SRH is a rare but serious condition that can be challenging to diagnose and treat. Physicians should be aware of the potential for SRH in patients with unexplained decreases in Hb and clinical manifestations such as abdominal pain and shock. Immediate treatment and bleeding risk assessment are crucial in suspected cases. For critically ill patients, interventional therapy should be considered before surgery. Multidisciplinary team (MDT) cooperation and effective communication are essential for achieving satisfactory outcomes. Further research is needed to better understand the etiology, early diagnosis, and treatment of SRH.

doi.org/10.1097/CM9.0000000000001278

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