In the latest Case Record of the Massachusetts General Hospital, a 50-year-old man presented with flank pain and fever. CT of the abdomen and pelvis showed a focal wedge-shaped defect in the left inferolateral kidney.
The differential diagnosis of acute-onset flank pain must begin with a consideration of renal colic due to a renal calculus, which would classically be manifested as flank pain and hematuria, often gross hematuria. Pyelonephritis classically presents with flank pain and fever. Flank pain is most commonly related to renal disease; however, intraabdominal processes such as cholecystitis, pancreatitis, and mesenteric ischemia, which may cause referred pain to the flank, should be ruled out. Renal ischemia is characterized by an acute onset of pain. Patients with renal ischemia are typically able to describe the exact time of onset of the pain and its severity.
• What is the infectious risk in an asplenic patient?
The sinusoids of the spleen filter blood and allow resident mononuclear phagocytes to ingest circulating bacteria. The spleen also contains nearly half of the total B lymphocytes responsible for immunoglobulin production and, therefore, is centrally important for the production of opsonizing antibodies. This function is critical in the clearance of encapsulated organisms. Therefore, an asplenic patient is at risk for postsplenectomy sepsis, a fulminant and often rapidly fatal illness resulting from infections that are normally cleared from the circulation by the spleen. The most common causes of sepsis in asplenic patients relate to bacterial infection with encapsulated organisms, including Streptococcus pneumoniae, H. influenzae, and Neisseria meningitidis; more than 50% of the cases of sepsis and associated deaths are related to S. pneumoniae.
• What is the typical clinical presentation of renal infarction?
Renal infarcts usually present with the abrupt onset of abdominal or flank pain and sometimes they are associated with signs of extrarenal embolization (e.g., neurologic deficits). Renal infarction is often associated with a leukocytosis, an elevated creatinine level, and microscopic hematuria or even proteinuria, although these findings are most consistent with large emboli or bilateral disease.
Morning Report Questions
Q: What is the most common cause of a renal infarct?
A: The most common cause of renal infarction is thromboembolic disease from the heart or aorta due to a left atrial clot in a patient with atrial fibrillation, left ventricular thrombus in a patient with myocardial infarction, or thromboemboli derived from ruptured plaque in the aorta. Other sources of thromboemboli can be valvular vegetations from infective endocarditis. Tumor or fat emboli or a paradoxical embolus from a deep venous thrombosis in a patient with a patent foramen ovale may also result in emboli to the kidney. In situ thrombosis can also occur; it is most often due to renal-artery occlusion from an aortic dissection, but it can be a complication after either an aortic or a renal endovascular intervention. Another consideration is fibromuscular dysplasia, which in a young patient with medial fibroplasia could appear on angiography as a renal infarct.
Q: What is the implication of a diagnosis of S. mutans bacteremia?
A: S. mutans is a member of the viridans group streptococci. Viridans group streptococci are common commensal components of the human oropharyngeal flora, and S. mutans has been identified as a major contributor to tooth decay and dental caries. Streptococcal species (including S. mutans) are the most common cause of native-valve endocarditis in adult patients, accounting for 45 to 65% of cases.