An easily misdiagnosed and rare cause of traumatic back pain: bilateral renal infarction caused by traumatic bilateral renal artery dissection

Dear editor,

The incidence of renal infarction in patients admitted to the emergency department (ED) is approximately 0.004%.[1] Among patients with renal infarction, bilateral renal involvement has been reported in 28.6% of patients.[2] However, there are very few cases of bilateral renal infarction after a traumatic injury.

Renal artery thrombosis is the main cause of renovascular injury including renal infarction after trauma.[3] However, traumatic renal artery dissection is a rare cause. Most cases of traumatic renal artery dissection have unilateral involvement, and cases of bilateral involvement are extremely rare. The injury mechanism in patients with bilateral renal infarction caused by traumatic bilateral renal artery dissection is unclear.

Herein, we describe an easily misdiagnosed and rare case of bilateral renal infarction caused by traumatic bilateral renal artery dissection. We also review the injury mechanisms and clinical courses of similar cases reported in the literature.

CASE

A 44-year-old man who complained of back pain after an automobile accident was admitted to the ED. The vital signs were as follows: blood pressure 135/90 mmHg (1 mmHg=0.133 kPa); heart rate 71 beats/min; respiratory rate 20 breaths/min; and body temperature 36.5 °C. The emergency medical technician reported that the patient’s car stopped in front of the pedestrian crossing and was struck by a bus that was behind it. The patient claimed that he was fastening his seat belt while driving and could not clearly remember the accident because he had lost consciousness. The emergency physician initially presumed that the patient had sustained minor injuries, such as a lumbar sprain and a cerebral concussion. One hour after admission, while waiting for radiography in an observation unit, the patient complained of abdominal pain and hematuria, and the blood pressure significantly decreased to 88/50 mmHg.

Emergent computed tomography (CT) was performed to identify the cause of hemodynamic instability. The results showed bilateral renal infarction caused by traumatic bilateral renal artery dissection (Figure 1). Initially, the patient’s hemoglobin level was 15.8 g/dL, and the coagulation test and electrocardiography results were normal. Many red blood cells were detected on urinalysis. He was successfully treated with percutaneous endovascular stenting with a balloon expandable stent (Express SD, Boston Scientific, USA) 16 h after the accident (supplementary Figure 1) and transferred to an intensive care unit. He received low-molecular-weight heparin for 6 d. After the patient was transferred to a general ward, his brother (witness) claimed that the patient’s car was thrown 15 m away from the collision site and the driver’s seat had flipped backward; the seat and the patient’s back may have directly collided with an electric guitar amplifier placed in an empty space in front of the rear seat (Figure 2).

Figure 1.

Enhanced computed tomography scan. A: occlusion of the right renal artery (white arrow); renal parenchymal ischemia (red arrow) in the upper and middle segments of the right kidney; B: occlusion of the accessory left renal artery; hematoma surrounding the artery (white arrow); C: ischemia of the right and left kidneys (white and red arrows) on a coronal reformatted image.

Figure 2.

Schematic diagram of the injury mechanism. A: an electric guitar amplifier.

The patient denied the current use of any medications except antihypertensive drugs and claimed that his blood pressure was well controlled before the accident. There was no other significant family history except hypertension. In the outpatient department 6 weeks after the accident, the patient’s blood pressure was 116/77 mmHg, and the blood urea nitrogen and creatinine levels were 17.2 mg/dL and 1.05 mg/dL, respectively. A ^99mTc dimercaptosuccinic acid (DMSA) renal scan, performed 4 months later, showed reduced perfusion of the bilateral kidneys and the relative function of the right and left kidneys was 32 vs. 68 (supplementary Figure 2). Bilateral renal blood flows via the stents were well-maintained on CT performed 5 months later (supplementary Figure 2). No clinical complications occurred at the end of a five -month follow-up.

DISCUSSION

Although the emergency physician could not determine the injury mechanism, the patient was initially misdiagnosed with minor injuries. However, after the patient’s condition deteriorated, an urgent CT was performed, which revealed bilateral renal infarction caused by traumatic bilateral renal artery dissection. Many emergency physicians, including residents in training, often encounter patients injured in traffic accidents similar to this case. Caution is needed in such cases because the clinical course could worsen.

The following mechanisms may have caused traumatic renal artery dissection.[4,5] During sudden deceleration, there may have been a direct vessel wall contusion against the vertebral bodies. Alternatively, the relatively mobile kidneys may have been displaced anteriorly after deceleration, opposite to the renal pedicles. Hence, subintimal dissection may have occurred. Most traumatic renal artery dissection cases that correlated with these mechanisms had unilateral involvement. Including our case, only seven cases with bilateral involvement have been reported.[4,6-10] Of these, four involved bilateral renal infarction caused by traumatic bilateral renal artery dissection (supplementary Table 1).

In these cases, the injury mechanism correlated with traumatic bilateral renal artery dissection was multiple direct blunt trauma or deceleration injury. The patients complained of hematuria, back pain, and flank pain. Traumatic shock and hypotension might have occurred, which could have resulted in death. Transient hypotension in our case could be due to bleeding; this can be inferred from bilateral perivascular hematomas indicating the occurrence of extravasation of arterial blood. Although our patient recovered from hypotension after the rapid infusion of crystalloid, caution is needed in cases with perivascular hematoma due to the possibility of developing traumatic shock. Therapeutic options, including interventional treatments, are controversial in cases of renal artery dissection. Some researchers have suggested the following indications for interventional treatments: (1) hemodynamically stable or stabilized blunt renal injuries; (2) dissection of segmental renal arteries (similar to our case), preocclusive main renal artery dissection, renal artery stenosis without flow limitation, and thrombogenic renal artery intimal tears in imaging patterns on CT; and (3) within 12–24 h after injuries (as early as possible).[7,11] The main known complications of renal artery injury that include renal artery dissection are deterioration of renal function and renovascular hypertension.[7] Among seven reviewed cases with traumatic bilateral renal artery dissection, hypertension occurred in one and renal dysfunction occurred in four cases.

CONCLUSIONS

In patients with blunt injury due to deceleration, bilateral renal infarction caused by traumatic bilateral renal artery dissection could develop. If emergency physicians do not accurately determine the injury mechanism, the diagnosis of this critical condition could be missed. Hence, emergency physicians must strive to identify the injury mechanism appropriately.