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At least 19 recordsLinked to original sources
PubMed1989

[Splenic infarction].

Splenic infarction is a recognized sequel of a number of diseases but, until recently, it has been difficult to verify. Employing the new imaging techniques, the spleen has become diagnostically more accessible and increase in the number of splenic infarctions diagnosed must be anticipated. The commonest basic cause is cardiovascular disease but the etiology may be manifold. Whereas the infarct as such is of lesser significance, splenic abscess, eg after bacterial endocarditis, is a life-threatening condition. The treatment consists of surgical drainage and, frequently, splenectomy. The lethality is reduced from nearly 100% to approximately 10% when the correct treatment is employed.

Humans↗
PubMed1977

Unusual cause of acute abdomen. Sickle cell trait and nonhypoxic splenic infarction.

Splenic infarction under hypoxic conditions is a well-known complication of sickle cell trait (Hgb AS). However, this case illustrates that it may occur without any clinical conditions of circumstances associated with decreased Pao2. In addition, sickle cell trait should be included in the differential diagnoses of splenic infarction even if the patient is not of African ancestry.

Abdomen, Acute↗
PubMed1991

Case report: splenic infarction and acute splenic sequestration in adults with hemoglobin SC disease.

While acute splenic sequestration and splenic infarction are commonly observed in infants and young children with sickle cell anemia, they are rarely experienced by adult hemoglobin S homozygotes because the recurrent splenic infarction that takes place during childhood is typically followed by scarring, atrophy, and splenic fibrosis. Both acute splenic sequestration and splenic infarction do remain relatively common in adults with the other sickle hemoglobinopathies. These episodes are almost certainly a consequence of the persistently enlarged and distensible spleens that often remain present in these conditions. In this report, the authors describe two adult patients with hemoglobin SC disease: one who developed acute splenic sequestration and one with splenic infarction. In neither case was there a history of recent air travel or exposure to altitude. The clinical course of these two syndromes is presented, and the hematologic, radiologic, and pathologic manifestations are discussed. Because they can sometimes be difficult to distinguish from one another, and because a failure to identify acute splenic sequestration can be catastrophic, these two entities must be included in the differential diagnosis for any hemoglobin SC patient who present with an unexplained fall in hemoglobin, left upper quadrant pain, unexplained fever, or symptomatic splenomegaly.

Acute Disease↗
PubMed1990

Splenic infarction: sonographic patterns, diagnosis, follow-up, and complications.

Forty splenic infarcts in 23 patients were examined with ultrasound (US). At clinical presentation, splenic infarction was associated with severe left upper quadrant pain (n = 10) or diffuse abdominal pain (n = 4) or was asymptomatic (n = 9). In this retrospective study, predominantly wedge-shaped (n = 17) or round (n = 23), irregularly delineated (n = 33) or smooth (n = 7), hypoechoic (n = 40) and anechoic (n = 5) lesions were found at first examination. During follow-up observation, four patients died because of complications unrelated to infarct, and five patients underwent splenectomy as a consequence of US findings. Expanding intralienal liquefaction, increasing subcapsular hemorrhage, free peritoneal blood (even in spleens shown to have an intact surface at sonography), and flow phenomena in the area of infarction demonstrated at B-mode pulsed Doppler US were identified as infarct-related complications associated with the risk of splenic rupture. Despite the high self-healing tendency in splenic infarction, short-term follow-up with US is recommended for early recognition of these possible complications.

Abdominal Pain↗
PubMedDate not supplied

Splenic infarction complicating pediatric liver transplantation: incidence and CT appearance.

In children it is often necessary to ligate the splenic artery and the main collateral supply to the spleen during liver transplantation. The complication of splenic infarction has been observed on postoperative CT in such patients. The purpose of our study was to determine the incidence and CT appearance of splenic infarction and to correlate its occurrence with a vascular cause related to the operative procedure. During a 2 year period, 26 of 94 (28%) children receiving liver transplants developed splenic infarction as shown by CT. Infarction generally occurred within 2 weeks of transplantation. Computed tomography demonstrated variable portions of splenic involvement with hypodense lesions. Twenty-two of 39 (56%) patients whose splenic artery was ligated developed splenic infarctions. Only 4 of 55 (7%) patients whose splenic artery was left intact had splenic infarctions on postoperative CT. We conclude that there is an increased incidence of splenic infarction in pediatric liver transplant recipients. The incidence of infarction is related to ligation of the splenic artery and collateral pathways.

Adolescent↗
PubMedDate not supplied

[Splenic infarction in Plasmodium falciparum malarial attack].

Splenic infarct during P. falciparum malaria is rare but well known. We report one case where ultrasonography and computed tomography suggested the diagnostic, showing respectively in splenic parenchyma a peripheral hypoechoic lesion and a low attenuation lesion. Diagnostic was confirmed by spontaneous regression during following days. We shall encounter more frequently than nowadays this rare entity due to expanding tourism and P. falciparum resistance.

Adult↗
PubMed1976

Massive splenic infarction in cirrhosis: report of a case with spontaneous disappearance of hypersplenism.

A cirrhotic patient with massive splenic infarction is described. Celiac angiography showed normally opacified splenic artery and vein and a markedly enlarged spleen with large avascular zones. Splenic infarction was associated with the spontaneous disappearance of a syndrome of hypersplenism. The spleen was surgically removed. Histological examination showed multiple thromboses of the small arterial and venous vessels. The cause of this infarct remained unclear.

Alcoholism↗
PubMed1990

[Contribution of sectional imaging, echography and MRI, for the diagnosis of splenic infarction in Osler endocarditis. Apropos of a case].

A case of symptomatic splenic infarct in an 11 year-old girl suffering from bacterial endocarditis is reported; this occurrence is a rare and serious condition in this disease. The diagnosis of haemorrhagic splenic infarct was suggested by ultrasonography and confirmed by MRI. No splenic abscess developed and this was correlated to a rapid improvement of the clinical state following an antibiotic treatment only. The authors discuss the role of sonography and MR in the etiologic diagnosis of splenic involvement in patients suffering from bacterial endocarditis.

Child↗
PubMed1977

[Splenic infarcts in Goodpasture's syndrome: its significance for diagnosis, prognosis, and treatment (author's transl)].

Necrotising splenic arteritis with numerous extensive anaemic splenic infarcts was found in four cases of Goodpasture's syndrome with the necrotising variant of rapidly progressive glomerulonephritis. The disease was rapidly fatal. Early scanning of splenic infarcts for diagnostic, prognostic and therapeutic purposes of the fulminating form of Goodpasture's syndrome is recommended.

Adult↗
PubMed1990

Pulmonary embolism and splenic infarction in a patient with sickle cell trait.

A 43 year-old black man with sickle cell trait documented by hemoglobin electrophoresis presented with severe pleuritic chest pain and hypoxemia three weeks after discharge following abdominal surgery. A pulmonary embolus was diagnosed by angiography and he was treated with heparin; the minimum arterial pO2 was 55 torr while O2 was being administered at a rate of 3 L/min. During this therapy, he developed abdominal pain. Computerized tomography suggested splenic infarction, which was documented by radionuclide liver-spleen scan and magnetic resonance imaging (MRI); the patient's spleen had been normal at exploratory laparotomy three weeks previously. No source for emboli was identified in the deep venous system by MRI. Although splenic infarction has been reported in patients with sickle cell trait at high altitude, this is the first reported case of splenic infarction secondary to the hypoxemia of pulmonary embolism in a patient with sickle cell trait. The spleen is subject to infarction in sickle cell trait because blood flow is slow through a hypoxemic and acidemic environment. The additional hypoxemia due to pulmonary embolism is presumed, in our patient, to have created a local splenic environment which permitted infarction to occur.

Adult↗
PubMed1978

Echography of splenic infarct in a case of systemic lupus erythematosus.

A 29 year old female with systemic lupus erythematosus had a splenic infarct. The echogram showed a 4 x 4 x 5 cm cluster of echoes. After splenectomy the preoperative echograms were matched to the gross pathological findings and a post mortem water bath scan. In this single patient, the echosplenograms were of considerable aid in confirming the accuracy of the diagnosis of splenic infarct.

Adult↗
PubMedDate not supplied

Gastric and splenic infarction: a complication of intraarterial vasopressin infusion.

Gastric and splenic infarction following intraarterial infusion of vasopressin in a patient's left gastric artery is reported. None of the previously described factors predisposing to infarction were present and the cause appears to have been hyperconstriction of vessels in response to vasopressin. Computed tomography (CT) scanning was used to confirm the extent of involvement.

Adult↗
PubMed1975

Howell-Jolly bodies. A clue to splenic infarction.

A 74-year-old woman with secondary erythrocytosis was found to have Howell-Jolly bodies in peripheral blood erythrocytes following acute splenic infarction. The Howell-Jolly bodies were a transitory finding and disappeared six days after the infarction, although the spleen remained abnormal by isotope scanning for several weeks. Careful inspection of the peripheral blood film may be an aid in the diagnosis of acute splenic infarction.

Aged↗
PubMed1989

[The trial use of alpha-IFN in treating a case of chronic myelomonocytic leukemia with splenic infarction].

A 75-year-old man, previously diagnosed as having chronic myelomonocytic leukemia, suffered an attack of severe left hypochondralgia in July 1986. A splenic infarction was diagnosed by both ultrasound tomography and computerized tomography. The patient was treated with alpha-Interferon (600 M.U./day i.m.) for cytoreduction in order to prevent a recurrence of the splenic infarction. Twenty-one days later, the peripheral white blood cell count decreased from 44,110 microliters to 9800/microliters and the monocytoid immature cells disappeared. However, severe dementia appeared and so alpha-Interferon therapy was abandoned. In this report the beneficial effects and side effects of alpha-interferon in the treatment of chronic myelomonocytic leukemia are discussed.

Aged↗
PubMed1992

Splenic infarction: a complication of cardiac catheterization.

Patients with extensive atherosclerosis are at increased risk of developing embolic complications during cardiac catheterization. We describe a 51-year-old man with unstable angina and bilateral leg claudication who developed fever and right upper abdominal pain shortly after cardiac catheterization. Liver-spleen scintigraphy demonstrated a wedge-shaped filling defect compatible with splenic infarction, and serial scans performed over a period of five months showed resolution of this finding. Splenic infarction tends to be under-diagnosed, and physicians should be aware of this potentially serious complication of cardiac catheterization.

Cardiac Catheterization↗
PubMed1979

Splenic infarction in a white man with sickle cell trait.

We report the third case of splenic infarction from sickle cell trait in a young white man traveling through mountains. Apparently the hypoxemia at 10,800 feet, along with a relatively high hemoglobin S concentration of 40%, interacted with the known conditions of splenic blood flow to cause sickling and infarction, even though our patient was not exercising. The optimal management for this rare complication of sickle cell trait remains unknown, but surgery may not be required for either diagnosis or therapy.

Adult↗