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Query: UMLS:C0243026 (sepsis)
 52,417 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sixteen dogs with splenic infarction due to causes other than splenic torsion were identified. Dogs with splenic infarction often had multiple concurrent diseases, and surgical management of splenic infarction was associated with high mortality. Splenic infarction occurred in dogs with hypercoagulable conditions associated with liver disease, renal disease, and hyperadrenocorticism, or as a consequence of uniform splenomegaly, neoplasia, or thrombosis associated with cardiovascular disease. Clinical signs and common laboratory findings generally reflected the underlying disease process. A variety of splenic abnormalities were detected by abdominal ultrasound in 15 dogs, with the ventral extremity of the spleen being most often abnormal. Four dogs were euthanized or died because of the presence of severe systemic disease, whereas 12 dogs underwent laparotomy. Complete splenectomy was performed in 9 dogs and partial splenectomy was performed in 2 dogs. Seven dogs died in the immediate postoperative period, 3 required chronic veterinary care, and 2 had uncomplicated long-term recoveries. Splenic infaraction should be regarded as a sign of altered blood flow and coagulation, rather than as a primary disease, and surgical management should be reserved for patients with life-threatening complications such as hemoabdomen or sepsis.
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PMID:Splenic infarction in 16 dogs: a retrospective study. 767 15

A recent Ethiopian immigrant to Israel presented with pneumococcal sepsis, massive splenomegaly and lymph-adenopathy. Investigations revealed many features of both hairy cell leukaemia (HCL) and hyperreactive malarious splenomegaly (HMS). Proguanil therapy for HMS was followed by rapid, marked decrease in spleen size, disappearance of the tartrate-resistant acid phosphatase-positive cells characteristic of HCL, and increasing eosinophilia, but unchanged lymphadenopathy.
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PMID:Massive splenomegaly responsive to proguanil and with features of hairy cell leukaemia. 777 47

The traditional method of splenectomy involves a 7- to 10-cm abdominal incision, with its attendant morbidity that includes sepsis. Recently, the laparoscopic technique has been adopted for splenectomy. Many surgeons still believe that laparoscopic splenectomy should be carried out only for idiopathic thrombocytopenia purpura and Hodgkin's disease with a normal-sized spleen. A 16-year-old girl with marked splenomegaly (spleen size for times normal and weighing 600 g) due to congenital spherocytosis underwent laparoscopic splenectomy and retrieval of the spleen through the umbilical trocar site. Preoperative arterial embolization was not used, and the operative blood loss was estimated to be only 250 mL. Her postoperative course was uncomplicated, and she was discharged on the 4th postoperative day. The operative technique is described and the advantages of laparoscopic splenectomy are discussed.
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PMID:Laparoscopic splenectomy for congenital spherocytosis with splenomegaly: a case report. 788 14

We review the clinical manifestations and long-term outlook of patients with chronic natural killer (NK) cell lymphocytosis. After reviewing more than 1,500 peripheral blood lymphoid flow cytometry reports and molecular genetics data from patients with suspected large granular lymphocyte (LGL) proliferation, we identified 10 patients (median age at diagnosis, 60 years; range, 35 to 76 years; male:female ratio, 3:2) with persistent (greater than 6 months) increase in phenotypically determined NK cells (CD3-CD16+). Southern blot analysis performed on 9 patients showed no clonal T-cell receptor gene rearrangements. Disease duration was measured from time of initial recognition of LGL or NK cell excess (greater than 40% of the lymphocyte fraction). Clinical data from these 10 patients were compared with those from 68 patients with T-cell LGL (T-LGL) leukemia. Currently, all patients are alive (median disease duration, 5 years; range, 0.8 to 8 years). Associated disease manifestations included pure red blood cell aplasia, recurrent neutropenia, recurrent neutropenic sepsis, and vasculitic syndromes, all of which were responsive to immunosuppressive therapy. No patient had palpable lymphadenopathy or splenomegaly. Compared with the patients with T-LGL leukemia, patients with chronic NK cell leukemia has similar lymphocyte counts, associated conditions, treatment responses, and survival but had less neutropenia and anemia.
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PMID:Chronic natural killer cell lymphocytosis: a descriptive clinical study. 791 84

Life-threatening portal hypertension (PHN) in patients with chronic myeloproliferative disorders may result from increased portal flow caused by marked splenomegaly or an increased resistance to portal flow from either a large vein thrombosis or an intrahepatic obstruction usually associated with agnogenic myeloid metaplasia (AMM). The former cause is correctable by splenectomy alone, whereas the latter requires portal-systemic shunt surgery. Few data exist regarding the outcome of portal-systemic shunt surgery in patients with AMM and intrahepatic obstruction. During the past 25 years, 13 patients with chronic myeloproliferative disorders underwent portal-systemic shunt surgery at our institution. The cause of PHN was intrahepatic obstruction in ten patients and hepatic vein thrombosis in three. Ten of the thirteen patients had AMM as initial diagnosis. Only one patient had intraoperative complications, and four patients had either sepsis or thrombosis during the postoperative period. Twelve patients survived the postoperative period and had a median postsurgical survival of 3 years (range, 0.25 to 19 years). The long-term complications of the operation were very few and included hepatic encephalopathy (one patient), portal vein thrombosis (one patient), and shunt occlusion (one patient). The procedure was successful in alleviating complications of PHN in all but one patient. Deterioration of hepatic function and subsequent hepatomegaly were unusual. Portal-systemic shunt surgery seems to be a useful option in patients with AMM and life-threatening PHN from intrahepatic obstruction.
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PMID:Outcome of portal-systemic shunt surgery for portal hypertension associated with intrahepatic obstruction in patients with agnogenic myeloid metaplasia. 803 84

Hypersplenism is defined as the association of anemia, leukopenia, or thrombocytopenia with bone marrow hyperplasia and splenomegaly. Hypersplenism is common in liver cirrhosis and frequent in patients with portal hypertension. The effects of portacaval shunt are variable; hypersplenism hardly ever improves but rarely develops after surgery. Since the spleen is a major component of the mononuclear phagocyte system, splenectomy reduces antibody synthesis. Although splenectomy abolishes hypersplenism, it may lead to sepsis. Recently, partial splenic embolization, using gelform injected directly into the splenic artery, has been performed in patients with cirrhosis. Partial splenic embolization induces an increase in the number of circulating blood cells. In addition, the levels of albumin, hepaplastintest, cholesterol and cholinesterase are increased significantly after treatment. Partial splenic embolization rarely causes problems and may actually be beneficial.
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PMID:[Hypersplenism in liver cirrhosis]. 811 16

Eighty-two consecutive cases of acute leukaemias in adult Ethiopians were admitted to the Tikur Anbessa (Black Lion) Hospital, a teaching and referral hospital in Addis Abeba, Ethiopia, from January 1982 to December 1992. These cases were studied to describe the clinical and haematological findings, response to therapy and prognosis. The age range was 13-78 (mean 29.6) years. The male to female ratio was 1.6:1. Acute myeloblastic (AML) and acute lymphoblastic (ALL) leukaemias occurred in 53.7% and 46.3%, respectively. The commonest symptoms were anaemia, fever and bleeding tendencies. The commonest signs were pallor, fever, sternal tenderness and purpura. Splenomegaly was more commonly seen in ALL patients. The haematological findings were anaemia (mean Hgb 6.35 g%), leucocytosis (mean WBC count 88,507/mm3) and thrombocytopenia (mean platelet count 31,700/mm3). Of the patients eligible for evaluation treated with chemotherapeutic agents, only 38.4% of ALL and 6.2% of AML achieved complete remission. Twenty-seven patients with ALL died from one day to 84 (median 1.0) months after diagnosis. Ten are lost to follow-up from two weeks to 36 (median 2.5) months, one is still alive 40 months after diagnosis. Thirty-nine of the AML patients died from one day to nine (median 0.3) months after diagnosis. Five are lost to follow-up from two weeks to two and a half (median 2.0) months. The causes of death were sepsis and bleeding, separately or in combination. Increasing numbers of acute leukaemia patients are being referred to this centre. Therefore, attempts should be made to equip it for the treatment of such cases.
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PMID:Acute leukaemias in adult Ethiopians in a teaching hospital. 818 78

Atraumatic splenic ruptures in the course of infectious diseases are rare but have been reported. Various germs of viruses can be at the origin of such rupture. The more often quoted viral disease is infectious mononucleosis. The more frequently involved bacteria are Streptococcus non pneumoniae, Pseudomonas, staphylococci and Clostridium. Rupture mechanism is not clearly elucidated; it can be connected with sepsis diffusion at spleen level via haematogenic way and consequently splenomegaly. Splenic rupture following septicaemia does not always entail major splenomegaly nor abscess formation but the attack of the splenic tissue itself is sometimes sufficient to bring about the rupture. The present case of atraumatic splenic rupture on spleen sepsis, no abscess, starting from a pulmonar infection with Streptococcus pneumoniae is, to our knowledge, the first case reported in literature.
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PMID:Atraumatic splenic rupture in the course of a pneumonia with Streptococcus pneumoniae. Case report and literature review. 847 Apr 45

To halt bleeding in patients with severe thrombocytopenia due to bone marrow failure, it is desirable to achieve a post-transfusion blood platelet count of 40 x 10(9)/L by platelet transfusions. Based on calculations of corrected count increments, each 1 x 10(11) platelets transfused will increase the blood platelet count approximately 10 x 10(9)/L per each square meter of patient body surface area. Thus, the post-transfusion blood platelet count will be approximately 20 x 10(9)/L following transfusion of 3 x 10(11) platelets to a 5 foot, 8 inch patient weighing 170 pounds (2.0 m2), who is bleeding because of a pre-transfusion platelet count of 5 x 10(9)/L. The post-transfusion platelet count likely will be even lower in sick patients (sepsis, amphotericin B plus antibiotic therapy, splenomegaly, graft-vs.-host disease, etc.) or if platelets are lost from the unit by leukofiltration before transfusion. Although a dose of 3 x 10(11) platelets is acceptable, in a regulatory sense for product quality, it is inadequate to control bleeding in most thrombocytopenic adult patients. Adjusting dose for body size, bleeding patients with pre-transfusion blood platelet of < 10 x 10(9)/L and weighing > 120 pounds should receive approximately 6 x 10(11) platelets, those weighing 30 to 120 pounds should receive 3 x 10(11) platelets, and infants weighing < 30 pounds (15 kg) should receive 5-10 ml/kg of platelet concentrate.
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PMID:Clinical perspectives of platelet transfusions: defining the optimal dose. 858 93

The authors present rare case of splenic necrosis during meningococcal sepsis in an eight-month-old infant. The diagnosis was based on ultrasonographic examination and confirmed by CT. These investigations were conducted because of splenomegaly and gastrointestinal tract disturbances. Splenectomy gave good results.
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PMID:[Splenic necrosis during meningococcal sepsis treated with splenectomy]. 864 62


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