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We report on a patient with left upper quadrant pain as a result of splenic infarction; the patient was subsequently found to have a thoracoabdominal aortic thrombus extending through the celiac axis. The patient was successfully treated with an aortic thrombectomy guided by intraoperative transesophageal echocardiography.
A case report of a emphysematous pyelonephritis associated with a splenic infarction is presented. The point of this case is the association of two rare pathologies and their management by the placement of a percutaneous nephrostomy. A review of the literature could not find any similar case.
Techniques for mobilizing the greater curve of the stomach during laparoscopic Nissen fundoplication (LNF) include division of the short gastric vessels (SGV). The splenic artery and vein lie directly posterior to the proper plane of dissection. Uncontrolled bleeding during SGV division places the splenic vessels at risk for inadvertent injury or ligation. We report herein on 2 patients referred to our institution who had left upper quadrant pain and radiographic evidence of segmental splenic infarction (SI) that resulted from a peripheral splenic artery branch injury during LNF. Management strategies included a trial of conservative management and splenectomy for persistent symptoms or complications resulting from SI. Intense inflammation and adhesion formation making laparoscopic splenectomy difficult should be anticipated when operating on the infarcted spleen.
It is well recognized that patients with sickle cell disease are susceptible to splenic infection and infarction. A case of total splenic infarction is presented in which the ultrasound and CT features are atypical.
We report the presence of sickle cell trait in several members of a white Jewish family. The trait was discovered when the propositus developed massive splenic infarction at high altitude. No erythrocyte markers characteristic of African ancestry were detected in any of the family members. This is the first bona fide documentation of sickle trait among white Jews.
Here we describe a 20-year-old pregnant woman with systemic lupus erythematosus who had high anticardiolipin antibodies and presented with splenic infarction.
We describe a case of apparent embolic thrombosis of the superior mesenteric artery that on computed tomography (CT) was noted unexpectedly, making the diagnosis of ischemic bowel disease straightforward. It occurred together with the typical CT findings of renal and splenic infarction. This diagnosis was verified by angiography that provided more information and was confirmed at surgery.
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The authors report a case of symptomatic splenic infarction secondary to cholesterol embolization after coronary artery bypass grafting in a 59-year-old woman. The patient was treated with urgent splenectomy, which was curative. The diagnosis, investigations and management of the condition are discussed.
Thrombotic events are occasionally associated with circulating lupus anticoagulant and may take a variety of clinical forms. The authors report a thrombotic manifestation, spontaneous isolated splenic infarction that occurred in a young man with circulating lupus anticoagulant.
The clinical spectrum of extra-intestinal salmonellosis, comprising enteric fever and invasive infections owing to non-typhoidal Salmonellae, is well known. We report an otherwise healthy patient with isolated splenic infarction caused by group B Salmonella. She was seropositive for the O antigen of Salmonella group B and stool cultures were positive for group B Salmonellae. After appropriate antimicrobial therapy, her complaints disappeared and microbiological tests for Salmonellae became negative.
Incomplete ischemia of the celiac trunk due to arterial thrombosis occurred in a patient infected with the HIV. Ischemia led to infarct of the spleen and pancreatitis. Endoluminal desobstruction of the arterial trunk then medical management after exploratory laparoscopy were successful without splenectomy. The causes, diagnostic methods and treatments for splenic infarction in HIV-infected patients are discussed with a review of the literature.
Many etiologies lead to pleural effusion. The pathogenetic cause is usually located either in the lung parenchyma or in the pleura. Subphrenic causes that lead to pleural effusion are uncommon. Several reports elaborated on the role of splenic hemorrhages in the genesis of left-sided pleural effusion. Splenic infarction is a rare etiology of left-sided pleural effusion, and it has rarely been described in medical literature. We present a case study of an elderly female patient who suffered from polycythemia vera for more than a decade, and was hospitalized for left-sided pleural effusion that appeared following left upper abdominal pain.
We describe a 15-year-old black boy with hemoglobin S-C disease living in Atlanta (altitude 1,034 ft), with no prior history of aircraft or mountain travel, who developed splenic infarction. The clinical picture was characterized by severe left upper quadrant abdominal pain, fever, splenomegaly, and hematologic and scintigraphic evidence of functional asplenia. The diagnosis was suggested by liver/spleen scintigraphy and further confirmed by ultrasonography and computerized tomography (CT) of the spleen. Treatment consisted of analgesics, intravenous fluids, and short-term antibiotic therapy. The child recovered without sequelae.
We describe a case of severe Wegener's granulomatosis associated with asymptomatic splenic infarction. The 4 previous case reports are reviewed and the implication of this finding for preventive strategies is highlighted.
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A 44 year-old man presented to the Emergency Department of American Hospital with severe pain persisting in the left upper quadrant for several hours. A computed tomographic scanning (CT scan) and celiac digital substraction angiography (DSA) of the abdomen demonstrated a splenic infarct. Histopathological examinations showed diffuse acute vasculitis, thrombosis, panvasculitis which led us to diagnose the case as "polyarteritis nodosa". The diagnosis is usually difficult to establish and it is usually delayed due to variable clinical manifestations dependent on the site and the extent of arterial involvement.
There are no generally accepted diagnostic criteria for primary systemic vasculitis, and the application of classification as diagnostic criteria is not feasible and may even be misleading. We report a case of a 13-year-old boy with acute abdomen who was found to have isolated eosinophilic mesenteric vasculitis with extensive thrombosis and splenic infarction. All serological tests were negative, including antineutrophil cytoplasmic antibody. The vasculitis had been successfully controlled with surgical intervention, steroid, and cyclophosphamide therapy. This may be an atypical presentation of Churg-Strauss syndrome.