Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Splenic Infarction”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 973 records · Page 54Linked to original sources
PubMed2002

Colonic infarction following endovascular AAA repair: a multifactorial complication.

PURPOSE: To report a case of colonic infarction following endovascular abdominal aortic aneurysm (AAA) repair in a patient with both internal iliac arteries (IIA) unobstructed by the endograft. CASE REPORT: A 73-year-old man presented with blue toes as a result of emboli from a 6.4-cm AAA. As he was medically at high risk for open repair and his aneurysm morphology was suitable for a modular bifurcated endovascular graft, a Zenith endograft was used to exclude the aneurysm. Twenty hours after the successful procedure, in which both IIAs were preserved, the patient regurgitated coffee-ground vomit; an upper gastrointestinal endoscopy found a small Mallory-Weiss tear and antral gastritis. A proton-pump inhibitor was begun, but his symptoms progressed. Laparotomy revealed transmural ischemia and infarction of the upper rectum, sigmoid, descending colon, and the splenic flexure; a colonic resection with formation of Hartmann's pouch and colostomy was performed. He made a slow but uncomplicated recovery. CONCLUSIONS: Colonic necrosis can complicate endovascular AAA repair even when both IIAs are preserved. Advantageously, the clinical signs of severe colonic ischemia in endograft patients are not obscured by aftereffects of a laparotomy.

Aged↗
PubMed1992

The splenic snood: an improved approach for the management of the wandering spleen.

A wandering spleen is in constant danger of torsion and infarction. Splenectomy, the traditional treatment, leaves children in danger of postsplenectomy sepsis. Three children with wandering spleens were treated by a new splenopexy technique, the splenic snood. After detorsion, the spleens were wrapped in polyglycolic mesh and anchored by the mesh subdiaphragmatically in the left upper quadrant. All have retained their spleens which have remained where anchored up to a 4-year follow-up. The simplicity and technical ease of the splenic snood operation recommend it as an improved method to avoid splenectomy and safely normalize intraabdominal anatomy in the management of the wandering spleen.

Child↗
PubMed1999

[Thoracic splenosis with symptoms of coronary heart disease].

HISTORY AND REASON FOR ADMISSION: A 53-year-old man, who had undergone a splenectomy for a traumatic splenic tear 20 years previously, was admitted because an acute myocardial infarction was suspected. 20 years ago, a splenectomy had been performed because of traumatic rupture. INVESTIGATIONS: Laboratory values were normal except for a microcytic anaemia, thrombocytopenia (109,000/microliter) and a raised ferritin level (547 ng/ml). Coronary heart disease as well as other cardiac and upper gastrointestinal abnormalities were excluded. Computed tomography revealed a space-occupying mass in the left lower lobe of the lung near the heart. This filled with contrast medium on coelangiography at the same time as the liver and a subphrenic mass thought to be an accessory spleen. TREATMENT AND COURSE: At thoracotomy numerous splenic masses, maximally 7 cm in diameter, were removed from near the heart, the costal pleura and the lung margin. There were haematological changes similar to those after splenectomy: leucocytosis (32,400/microliter) and thrombocytosis (637,000/microliter) on the 11th postoperative day and Howell-Jolly bodies noted on the 16th day. CONCLUSION: In splenosis the disseminated pieces of splenic tissue can partly substitute for the normal spleen's functions. Splenosis tissue should, therefore, not be removed in every case, especially, if it does not cause symptoms.

Diagnosis, Differential↗
PubMed1992

[Splenic complications in inflammatory pancreatic diseases].

Pancreatitis in combination with splenic and vascular complications is dangerous and potentially lethal. The most common complications are intestinal or intraperitoneal hemorrhage resulting directly from either vascular changes, such as erosion of the splenic artery, formation of a pseudoaneurysm, hemorrhage into a pseudocyst, or rupture of a pseudocyst with perforation into the colon, or complications in the spleen, such as anemic or hemorrhagic infarction, abscess or rupture. CT is the method of choice for the diagnosis of splenic complications of pancreatitis. Angiography is indicated in every severe hemorrhage in the presence of pancreatitis, to demonstrate vascular changes and to localize the source of hemorrhage. In addition, acute arterial bleeding can be successfully treated with catheter embolization.

Acute Disease↗
PubMed1986

Clinical and pathologic findings in dogs with atherosclerosis: 21 cases (1970-1983).

Atherosclerosis was diagnosed on necropsy in 21 dogs in a 14-year period. Nine dogs died and 12 were euthanatized because of complications associated with the disease. The mean age was 8.5 +/- 0.5 years; 18 dogs were male. Three breeds (Miniature Schnauzer, Doberman Pinscher, and Labrador Retriever) had a higher prevalence of the disease than other breeds in the canine necropsy population of The Animal Medical Center. Most common clinical signs were lethargy, anorexia, weakness, dyspnea, collapse, and vomiting. Hypercholesterolemia, lipidemia, and hypothyroidism were common in affected dogs tested, and protein electrophoresis revealed high values for alpha 2 and beta fractions in all dogs tested. Electrocardiography indicated conduction abnormalities and myocardial infarction in 3 of 7 dogs. Necropsy revealed that affected arteries (including coronary, myocardial, renal, carotid, thyroidal, intestinal, pancreatic, splenic, gastric, prostatic, cerebral, and mesenteric) were yellow-white, thick and nodular, and had narrow lumens. Myocardial fibrosis and infarction also were observed in the myocardium. Histologically, affected arterial walls contained foamy cells or vacuoles, cystic spaces, mineralized material, debris with or without eroded intima, and degenerated muscle cells.

Animals↗
PubMed1996

First report of reversal of organ dysfunction in sickle cell anemia by the use of hydroxyurea: splenic regeneration.

Much of the morbidity associated with sickle cell anemia (SCA) is due to ongoing infarction resulting in organ dysfunction. Because the spleen is often the first organ damaged in this illness, there is a significant impairment of the immune system in these patients. Hydroxyurea (HU) has been shown to increase fetal hemoglobin (HbF) and decrease painful episodes in patients with this disease. It is unclear whether HU can prevent organ damage. We treated two SCA patients with HU for several years and found evidence of reversal of previously documented splenic dysfunction. Patient no. 1 was treated for 30 months with an increase in HbF to 30%. HU was stopped because of cytopenia. She developed left upper quadrant pain. A splenectomy was performed due to the possibility of splenic abscesses. A pathologic review found no evidence of infection and an enlarged spleen that showed active germinal centers. Patient no. 2 was treated for 24 months with HU before developing splenomegaly. His HbF levels were 25% to 30%, his pit counts averaged 2%, and his liver spleen scans showed uptake. These two cases show that chronic HU therapy may reverse splenic dysfunction in certain patients and suggest that this drug may have efficacy beyond the elimination of pain in SCA.

Adult↗
PubMed1986

[CT morphology of the splenic vessels in splenoportal fistula].

CT examination of a 53-year-old patient with endocarditis and clinical signs of hepatosplenomegaly revealed an atypical vascular morphology in the hilum of the spleen, for which no diagnosis could be established. Angiography indicated the presence of a symptom-free splenoportal fistula, the histological study of which suggested its congenital genesis. The paper describes the morphology, as ascertained by CT, of the splenic vessels characterised by changed haemodynamics due to a hilar splenoportal fistula.

Angiography↗
PubMed1976

Spontaneous rupture of the spleen. An unusual complication of anticoagulant therapy.

A 44-year-old man, who had been taking warfarin sodium because of a previous myocardial infarct, suddenly developed abdominal pain and signs of peritoneal irritation, requiring exploratory laparotomy. The spleen was ruptured. There were not any systemic diseases nor antecedents of trauma that could be considered predisposing factors for the apparently spontaneous rupture of the spleen. The only abnormality recorded was an elevated prothrombin time. Thus, a coagulopathy produced by the anticoagulants appeared to be the only possible predisposing factor for his splenic rupture.

Adult↗
PubMed2001

[Torsion of the accessory spleen: an atypical etiology for acute abdomen].

The accessory spleen is often a incidental discovery. The accessory post-accidental spleen are unusual. The torsion of a movable spleen is possible and represent about 0.2 to 0.3% of splenectomy. But the torsion of an accessory spleen is exceptional. A case of acute torsion of an accessory spleen is reported. In a 26-year-old women was admitted with acute abdominal pain. The abdominal ultrasound and the abdominal X-Ray are no specific. In the face of the acute pain, a laparoscopy was necessary. At laparoscopy, the patient was found to have torsion and infarction of an accessory spleen in the pelvis. The treatment was a splenectomy and the evolution was favorable.

Abdominal Pain↗
PubMed1983

Mesenteric vein thrombosis and vascular plasminogen activator.

A 60-year-old woman with livedo reticularis was examined for defective release of vascular plasminogen activator by a newly described chromogenic assay. Her activator level was only 0.007 Committee on Thrombolytic Agents (CTA) units/mL, compared with a mean of 0.19 CTA units/mL for 84 female controls. Subsequently, the patient died as a result of thrombosis of the portal, splenic, hepatic and superior mesenteric veins with small-bowel infarction. The patient's family had a history of deep and superficial vein thrombosis. Her family's medical history was similar to a recently described pedigree, with low levels of releasable plasminogen activator associated with venous thrombosis. We believe that mesenteric vein thrombosis is a serious potential consequence of defective release of vascular plasminogen activator.

Female↗
PubMed1987

[Partial splenectomy in non-traumatic benign lesions of the spleen].

Partial splenectomy was performed in a patient with cystic lymphangioma and two patients with splenic pseudo-cysts, one of traumatic origin and the other necrotic following infarct. Anatomical features on which this operation is based, together with the technique employed, are exposed and the criteria of efficacy examined. Partial splenectomy was performed to reduce splenomegaly complicated with hypersplenism, and is also applicable for exeresis of cystic and pseudo-cystic splenic lesions. These indications are worthy of more extensive application in young adults.

Adult↗
PubMed2001

Hemolytic anemia, thrombosis, and infarction in male and female F344 rats following gavage exposure to 2-butoxyethanol.

2-butoxyethanol (BE; ethylene glycol monobutyl ether) is used extensively in the manufacture of a wide range of domestic and industrial products which may result in human exposure and toxicity. BE causes severe hemolytic anemia in male and female rats and mice. In a recent report, female F344 rats exposed to 500 ppm BE by inhalation and sacrificed moribund on day 4 of treatment exhibited disseminated thrombosis associated with infarction in several organs. In contrast, no such lesions were observed in male rats similarly exposed to BE. Additional studies were therefore undertaken to compare the effects of BE in rats of both sexes. Rats received 250 mg BE/kg/day by gavage for 1, 2 or 3 days and were sacrificed 24 or 48 hr after the last dose. Control rats received 5 ml/kg water. Progressive time-dependent hemolytic anemia--macrocytic, hypochromic, and regenerative--was observed in both sexes of rats exposed to BE. Additionally, BE caused significant morphological changes in erythrocytes, first observed 24 hr after a single dose, including stomatocytosis, macrocytosis with moderate rouleaux formation, and spherocytosis. These morphological changes became progressively more severe as BE dosing continued and included the occasional occurrence of schistocytes and ghost cells, rouleaux formation in rats of both sexes, and an increased number of red blood cells with micronuclei in female rats. Overall, the progression of hemolytic anemia and morphological changes as a function of the number of days of exposure varied with gender and suggested a faster onset of hemolysis in female rats. The range of BE-related histopathological changes noted in both sexes was comparable; however, while these lesions were observed in female rats following a single dose, similar effects were first observed in males after 3 consecutive days of exposure to BE. Pathological changes involved disseminated thrombosis in the lungs, nasal submucosa, eyes, liver, heart, bones and teeth, with evidence of infarction in the heart, eyes, teeth and bones. Hemoglobinuric nephrosis and splenic extramedullary hematopoiesis were also noted. An apparent correlation between the severity of hemolytic anemia and subsequent disseminated thrombosis in BE-treated rats is proposed. Thrombosis may be related to intravascular hemolysis, which could be triggered by procoagulant release and/or alterations in erythrocyte morphology, as well as increased rigidity.

Administration, Oral↗