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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In adult normothermic cats cerebral blood flow was interrupted for 1 hour by clamping the innominate and subclavian arteries. Following ischemia the brains were recirculated with blood, and the coagulation system was investigated by measuring coagulation times and blood content of fibrinogen and platelets. Ischemia induced progressive consumption coagulopathy with an increase in coagulation times and a decrease of platelets and fibrinogen by more than 40%. Coagulopathy was accompanied by a respiratory distress syndrome with a significant increase in the alveolar-arterial carbon dioxide gradient from --3.3 to --13.5 mm Hg. A correlation was found between plasma fibrinogen concentration, cerebral blood flow and electrophysiological function, indicating that a relationship exists between the severity of postischemic coagulopathy and functional recovery following prolonged cerebral ischemia.
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PMID:Coagulopathy following experimental cerebral ischemia. 84 91

Coagulation mechanisms were examined in the dog after a 70 per cent hepatectomy and the additional effect of varying periods of ischemia on the liver remnant. Dogs were submitted to a 70 per cent partial hepatectomy, and the liver remnant was rendered ischemic by occluding the vascular inflow. Portal decompression during ischemia was accomplished by allowing portal venous flow through the lobes subsequently resected. Dogs in the control group, those undergoing hepatectomy alone and those undergoing hepatectomy together with 60 minutes of ischemia time exhibited a fall in hemoglobin and hematocrit values, a transient leukocytosis, a small increase in kaolincephalin clotting time and a decline in platelet count but no significant thrombocytopenia. Prothrombin time was changed in dogs undergoing hepatectomy, but this was not affected by ischemia. The characteristic rise in plasma fibrinogen postoperatively was abolished, and fibrinogen levels were lower in dogs undergoing hepatectomy alone and fell significantly in dogs subjected to 30 to 60 minutes of ischemia of the liver remnant. Factors V and VII were decreased after hepatectomy, and Factor V was more severely reduced after 30 to 60 minutes of ischemia. There was no overt bleeding tendency. In ten dogs, the liver remnant was subjected to ischemia for 75 minutes. Four of these died within three days of operation, two with severe hypoglycemia and two with postoperative bleeding. All six surviving dogs exhibited gross coagulation defects. Prothrombin time rose, kaolin-cephalin clotting time increased and platelets fell to a greater degree than in any of the other dogs. Plasma fibrinogen level showed a profound fall, as did Factor V, the magnitude of these changes being greater than after a shorter period of ischemia. Factor VII was also decreased, but this did not appear to be related to the ischemic interval. In the clinical situation in which intrinsic coagulation mechanisms are shown to be impaired, treatment with Factor V and VII concentrates may be the best way of correcting the coagulation defect.
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PMID:The mechanism of impaired coagulation after partial hepatectomy in the dog. 93 55

The reports of 8 patients with acute or subacute abdominal pain related to venous mesenteric ischemia were reviewed. None of the patients presented local or regional predisposing factors for venous thrombosis. In 4 patients, a localized segment of ischemic small bowel (median length 125 cm; range: 30-350) was resected without immediate anastomosis and postoperative anticoagulation therapy was given. Two of these patients developed recurrent ischemia involving the bowel adjacent to the stoma, treated successfully in 1 case by a repeat resection. The 4 other patients hospitalized with intestinal obstructive symptoms (1 case) or abdominal angina (3 cases) were treated by long term anticoagulation in 3 cases and artificial nutrition in 2 cases. None of them developed mesenteric infarction with a median follow up of 34 months. In 7 of the 8 patients, a coagulopathy was found: primary myeloproliferative disorder (1 case), hypercoagulation state (5 cases), autoimmune hemolytic anemia (1 case). These observations suggest that venous mesenteric ischemia included two different entities on the basis of clinical and morphological criteria: mesenteric infarction and subacute transient ischemia without bowel infarction. Most of apparently idiopathic cases of acute or subacute venous mesenteric ischemia are related to hypercoagulation states requiring a long term anticoagulation.
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PMID:[Syndromes of venous mesenteric ischemia: infarction and transient ischemia]. 133 Jul 93

This prospective randomized study of 50 patients compares the prevalence of complications between surgical and percutaneous methods of removal of intraaortic balloons. All patients who had percutaneous placement of a 9.5F intraaortic balloon during a 6-month period were eligible for the study. Patients were excluded if the intraaortic balloon was placed surgically, if a coagulopathy was present, or if acute leg ischemia developed at any time after insertion. After informed consent, 25 patients were randomized to each method of removal. Two complications occurred in the surgical group, including a wound infection and a lymph fistula. In one patient in the percutaneous group, a false aneurysm of the femoral artery developed. There was no significant difference between the mean of 59 minutes for percutaneous removal and 47 minutes for operative removal of the balloon (p = 0.74). The percutaneous method is therefore more cost-effective, because it does not require the use of operating room personnel or equipment necessary for surgical removal. The results of this study indicate that the majority of percutaneously placed intraaortic balloons may be safely removed percutaneously. Surgical removal of 9.5F intraaortic balloons is recommended for patients with bleeding diatheses, hemorrhagic or ischemic complications, or for those in whom the intraaortic balloon was inserted with a surgical procedure.
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PMID:A prospective randomized study comparing surgical and percutaneous removal of intraaortic balloon pump. 154 57

Several significant advances in the treatment of hepatic injuries have evolved over the past decade. These trends have been incorporated into the overall treatment strategy of hepatic injuries and are reflected in experiences with 411 consecutive patients. Two hundred fifty-eight patients (63%) with minor injuries (grades I to II) were treated by simple suture or hemostatic agents with a mortality rate of 6%. One hundred twenty-eight patients (31%) sustained complex hepatic injuries (grades III to V). One hundred seven patients (83.5%) with grades III or IV injury underwent portal triad occlusion and finger fracture of hepatic parenchyma alone. Seventy-three surviving patients (73%) required portal triad occlusion, with ischemia times varying from 10 to 75 minutes (mean, 30 minutes). The mortality rate in this group was 6.5% (seven patients) and was accompanied by a morbidity rate of 15%. Fourteen patients (11%) with grade V injury (retrohepatic cava or hepatic veins) were managed by prolonged protal triad occlusion (mean cross-clamp time, 46 minutes) and extensive finger fracture to the site of injury. In four of these patients an atrial caval shunt was additionally used. Two of these patients survived, whereas six of the 10 patients managed without a shunt survived, for an overall mortality rate of 43%. Over the past 4 years, six patients (4.7%) with ongoing coagulopathies were managed by packing and planned re-exploration, with four patients (67%) surviving and one (25%) developing an intra-abdominal abscess. One additional patient (0.8%) was managed by resectional debridement alone and survived. During the past 5 years, 25 hemodynamically stable and alert adult patients (6%) sustaining blunt trauma were evaluated by computed tomography scan and found to have grade I to III injuries. All were managed nonoperatively with uniform success. The combination of portal triad occlusion (up to 75 minutes), finger fracture technique, and the use of a viable omental pack is a safe, reliable, and effective method of managing complex hepatic injuries (grade III to IV). Juxtahepatic venous injuries continue to carry a prohibitive mortality rate, but nonshunting approaches seem to result in the lowest cumulative mortality rate. Packing and planned reexploration has a definitive life-saving role when used adjunctively in the presence of a coagulopathy. Nonoperative management of select hemodynamically stable adult patients, identified by serial computed tomography scans after sustaining blunt trauma is highly successful (95-97%).
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PMID:Significant trends in the treatment of hepatic trauma. Experience with 411 injuries. 161 86

Endotoxemia remains the leading cause of death in horses, being intimately involved in the pathogenesis of gastrointestinal disorders that cause colic and neonatal foal septicemia. Endotoxins, normally present within the bowel, gain access to the blood across damaged intestinal mucosa, or endotoxemia occurs when gram negative organisms proliferate in tissues. Endotoxins are removed from the circulation by the mononuclear phagocyte system, and the response of mononuclear phagocytes to these lipopolysaccharides (LPS) play an important role in determining the severity of clinical disease. Macrophages become highly activated for enhanced secretory, phagocytic and cidal functions by LPS. Macrophage-derived cytokines are responsible for many of the pathophysiologic consequences of endotoxemia. The arachidonic acid metabolites, prostacyclin and thromboxane A2 likely mediate early hemodynamic dysfunction and the leukotrienes may potentiate tissue ischemia during endotoxemia. Interleukin 1 (IL-1) induces fever and is responsible for the inflammatory cascade, which constitutes the acute phase response. Tumor necrosis factor (TNF), an important proximal mediator of the effects of LPS, acts to initiate events and formation of other molecules that affect shock and tissue injury. Systemic administration of TNF produces most of the physiologic derangements that are associated with endotoxemia and antibodies that are directed against TNF significantly reduce LPS-induced mortality in experimental animals. In response to endotoxins, mononuclear phagocytes express thromboplastin-like procoagulant activity (PCA), which initiates microvascular thrombosis. Both IL-1 and TNF induce PCA expression, creating a positive feedback loop for LPS-induced coagulopathy. A macrophage-derived platelet activating factor contributes to coagulation dysfunction and further stimulates arachidonic acid metabolism. The ultimate consequences of endotoxemia are multiple system organ failure and death. The numerous feedback loops and intertwining cascades of mediators during endotoxemia defy simplistic methods of treatment. The optimal therapy likely involves methods to alter the generation of inflammatory mediators by mononuclear phagocytes.
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PMID:Endotoxemia in horses. A review of cellular and humoral mediators involved in its pathogenesis. 192 Feb 54

The potential for hypothermia to prevent or ameliorate ischemic injury to the central nervous system is well known. To determine if a more prolonged period of metabolic suppression with blood substitution is possible, a method was developed to lower body temperature to near the freezing point. Eight adult mongrel dogs underwent closed-chest extracorporeal circulation with both external and internal body cooling. As they were cooled, progressive hemodilution was employed until complete exsanguination and blood substitution with an aqueous solution was accomplished. Continuous circulation and a core temperature at a mean of 1.7 degrees C were maintained from 2 1/2 to 3 hours. After rewarming to 20 degrees C, the animals were autotransfused and allowed to recover. Of the eight animals, two died due to technical factors related to cardiac defibrillation. Of the six surviving animals, five survived over a long period and one died on the 10th postoperative day with hepatorenal failure resulting from a presumed blood transfusion incompatability reaction. All six showed normal neurological function and kennel behavior, except one dog with mild weakness of a hindlimb. When the dogs were sacrificed 1 to 2 months postoperatively, all organs were histologically normal. Specifically, there was no gross or microscopic evidence of ischemic or hypoxic injury to any central nervous system structures. This pilot study demonstrates that it is possible to successfully achieve complete exsanguination, blood substitution, and ultraprofound body temperature, while continuous circulation of the blood substitute is maintained. With the capability of controlling and repeatedly performing washout of the extracellular environment and by reaching lower temperatures, it may be possible to attain greater cellular metabolic suppression. This perhaps will extend the allowable times for circulatory arrest procedures. In addition, "bloodless ischemia" may be beneficial in removing both blood substances and formed elements which may mediate organ ischemia. With replacement of blood at warm temperatures, coagulopathy is avoided. This preliminary evidence demonstrates potential in the combination of ultraprofound hypothermia and complete blood component substitution. However, further study is required to confirm the potential of achieving circulatory arrest of longer duration.
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PMID:Ultraprofound hypothermia with complete blood substitution in a canine model. 201 79

We have reviewed the literature and supplemented it with our own experience to provide a current viewpoint on emergency coronary bypass in three settings in which cardiogenic shock did not exist preoperatively. Acute failure of coronary angioplasty led to emergency operation in 701 patients with 25 (3.6%) deaths. There was a 37.6% incidence of perioperative infarction. Thrombolytic therapy for acute myocardial infarction, sometimes followed by angioplasty, led to emergency operation within 8 hours in 145 instances with four (2.1%) deaths. Emergency coronary bypass was primary therapy for 1,051 patients with acute myocardial infarction with 51 (4.9%) hospital deaths. Emergency operation for failed angioplasty is frequently mandated in the setting of surgical standby and iatrogenic ischemia although some operations could be postponed to an elective status. Emergency operation after thrombolytic therapy has been used for unsuccessful angioplasty of the infarct vessel, left main stenosis of greater than 50%, left main equivalent, multivessel disease with complex lesions not amenable to angioplasty, or failure to restore patency of the infarct vessel with thrombolysis. Operation within 12 hours of thrombolytic therapy is associated with a coagulopathy causing increased bleeding, the need for transfusion, and a greater incidence of reoperation for perioperative bleeding.
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PMID:Emergency coronary bypass not associated with preoperative cardiogenic shock in failed angioplasty, after thrombolysis, and for acute myocardial infarction. 272 Sep 40

A previous article (Part I) described the patient population and operative management of 666 patients who had surgery for nonruptured abdominal aortic aneurysms. This article details the perioperative complications and, by chi-square and logistic regression analysis, identifies the variables that are associated with each complication. In summarizing the results (below) the incidence of each complication is listed, along with the predictive risk factors in parentheses that have significance levels less than 0.05. Vascular morbidity data are as follows: intraoperative bleeding, 4.8%; postoperative bleeding requiring transfusion, 2.3% or repeat operation, 1.4% (large volume of blood transfusion and/or use of an autotransfusion device); intraoperative limb ischemia, 3.5%; graft thrombosis, 0.9% (femoropopliteal disease and/or distal anastomosis at the femoral level); distal thromboembolism, 3.3% (male sex, femoral popliteal disease, and/or intraoperative graft thrombosis); amputation, 1.2%; graft infection, 1 case. General morbidity data are as follows: cerebrovascular event, 0.6%; paraplegia, 1 case; cardiac event, 15.1% (age, previous episode of congestive heart failure, and/or electrocardiogram [ECG] evidence of a previous myocardial infarction); myocardial infarction, 5.2% (advancing age, angina, and/or prolonged aortic cross-clamp time); congestive heart failure, 8.9% (previous history of congestive heart failure, ECG evidence of ischemia, and/or chronic obstructive lung disease); arrhythmia requiring treatment, 10.5% (preoperative ventricular premature beats and/or respiratory failure requiring ventilation for more than 48 hours); new arrhythmia, 8.4% (angina and/or chronic obstructive lung disease); respiratory failure, 8.4% (chronic obstructive lung disease, large volume of blood transfused, and/or occurrence of postoperative bleeding, cerebrovascular accident, congestive heart failure, or myocardial infarction); renal damage with rise in creatinine or blood urea nitrogen, 5.4% and/or renal failure requiring dialysis, 0.6% (elevated preoperative creatinine, suprarenal aortic cross-clamping, and/or renal vein ligation); diarrhea without evidence of ischemia colitis, 7.1% and ischemic colitis, 0.6% (pelvic flow interrupted); prolonged ileus, 11.0% (aortoiliac occlusive disease, deterioration of renal function, prolonged ventilation, and/or preoperative history of angina); superficial wound infection, 1.5% and deep infection, 0.5% (femoral anastomosis and/or female sex); coagulopathy, 1.1% (large volume of blood transfused).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Multicenter prospective study of nonruptured abdominal aortic aneurysm. Part II. Variables predicting morbidity and mortality. 264 60

Periarteritis Nodosa (P.A.N.) is a systemic connective tissue disease with a variety of manifestations that includes ocular involvement in 20% of cases. The diagnosis of this condition is difficult due to the absence of any specific clinical signs or laboratory findings. However, histologic studies have demonstrated a segmental vasculitis that is often necrotic. Ocular findings frequently include choroidal involvement that is characteristic. Nevertheless, angiographic studies of this disease are extremely rare. The findings in three patients suspected of having P.A.N. are presented. Fluorescein angiography established the diagnosis of P.A.N. in two cases and ruled-out its presence in the third case. In the first case angiography demonstrated a retinal vasculitis with multiple arteriolar and capillary occlusions. There was also ischemic involvement of the choriocapillaris and a mild anterior optic nerve vasculitis. All findings resolved, leaving numerous Elschnig spots. In the second case the angiogram showed acute multifocal ischemia of the choriocapillaris. The ocular examination and fluorescein angiogram in the third case were entirely normal, thereby ruling-out P.A.N. on the basis of insufficient criteria. Acute multifocal choroidal ischemia is present in a variety of rare conditions: Toxemia of pregnancy, Disseminated Intravascular coagulopathy, Moskowitz Disease (T.T.P.), Leukemia and Malignant Hypertension. However, the presence of multifocal choroidal ischemia in the presence of a systemic connective tissue disorder strongly favors the diagnosis of P.A.N. The relative contributions of co-existent Malignant Hypertension and P.A.N. in producing choroidal ischemia are discussed. The spectrum of clinical manifestations and laboratory findings in P.A.N. as well as hypotheses concerning pathogenesis (immune-complex deposition) are described. Among all systemic vasculitis , only P.A.N., and rarely Scleroderma, feature choroidal involvement. This is possibly due to the fact that the degree of vasculitis in P.A.N. is sufficiently severe to cause clinically significant choroidal involvement.
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PMID:[Fluorescein angiography in the diagnosis of periarteritis nodosa]. 614 75


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