In this case I concealed the vital piece of the history (trauma). In real life you would usually know that a patient had experienced major trauma. In quizzes and tests of course the rules are different. This is probably because you should always have your mind open to the possibility of prior trauma as the patient may be unwilling to reveal the history for legal or domestic reasons and there may be elements of lesser trauma that you were not informed of (iatrogenic biopsies etc).
This case demonstrates a kidney with impaired perfusion. There is only preservation of capsular perfusion that originates from smaller vessels, suggesting arterial disruption. Venous infarction usually results in persistent cortico-medullary differentiation. Contrast in the collecting system is always absent in arterial pedicle avulsion but may be present in venous thrombosis. The kidney is a little large, which may occur in arterial or venous infarction, however, in this case this was likely pre-existant as the patient had congenital absence of the right kidney. There is also a large anterior abdominal soft tissue mass. This is heterogeneously dense prompting many to think this was an enhancing mass, possibly pancreatic neoplasm or pancreatitic phlegmon.This mass does not enhance, but was actually hyperdense pre-contrast due to mesenteric haematoma. There is also hyperdense fluid in the left paracolic gutter from haemoperitoneum. In combination the renal findings are best explained by traumatic disruption of the renal artery pedicle which is probably the commonest causes of acute renal infarction of a whole kidney.
Non-traumatic arterial renal infarction may also result from embolism, for example from atrial thrombus or valve vegetations, however, subtotal infarction is commoner and there are usually features of embolic disease in other organs like the spleen. Other explanations include traumatic intimal damage from renal arteriography, or thrombosis of the renal artery related to atherosclerosis, aneurysm or dissection of the aorta and vasculitides. The presence of a capsular rim of enhancement does not imply the kidney is unsalvageable, although clearly the prognosis is poor.
This case demonstrates a kidney with impaired perfusion. There is only preservation of capsular perfusion that originates from smaller vessels, suggesting arterial disruption. Venous infarction usually results in persistent cortico-medullary differentiation. Contrast in the collecting system is always absent in arterial pedicle avulsion but may be present in venous thrombosis. The kidney is a little large, which may occur in arterial or venous infarction, however, in this case this was likely pre-existant as the patient had congenital absence of the right kidney. There is also a large anterior abdominal soft tissue mass. This is heterogeneously dense prompting many to think this was an enhancing mass, possibly pancreatic neoplasm or pancreatitic phlegmon.This mass does not enhance, but was actually hyperdense pre-contrast due to mesenteric haematoma. There is also hyperdense fluid in the left paracolic gutter from haemoperitoneum. In combination the renal findings are best explained by traumatic disruption of the renal artery pedicle which is probably the commonest causes of acute renal infarction of a whole kidney.
Non-traumatic arterial renal infarction may also result from embolism, for example from atrial thrombus or valve vegetations, however, subtotal infarction is commoner and there are usually features of embolic disease in other organs like the spleen. Other explanations include traumatic intimal damage from renal arteriography, or thrombosis of the renal artery related to atherosclerosis, aneurysm or dissection of the aorta and vasculitides. The presence of a capsular rim of enhancement does not imply the kidney is unsalvageable, although clearly the prognosis is poor.
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