Search

This study was undertaken to determine if warfarin anticoagulation could be safely continued during surgery and in the perioperative period. An animal model was followed by a prospective human study of all patients on heparin or warfarin at the time of surgery. Twenty-four rabbits underwent laparotomy, during which a controlled liver injury was created and repaired. Group 1 (Warf) was anticoagulated with warfarin to raise the mean international normalization ratio (INR) to 2.5-3.0. Group 2 (Hep) was anticoagulated with heparin to raise the activated partial thromboplastin time to 1.5-2.0 times control. The heparin was then stopped 6 hr prior to surgery and resumed 6 hr postoperatively without a bolus. Group 3 (control) was not anticoagulated and received saline infusion. For the human study, data were collected on 40 patients undergoing 50 operations from October 1996 to January 1998. The results of this study reveal that (1) bleeding was less in the group anticoagulated with warfarin throughout surgery in the animal model, (2) bleeding complications were less in the patients continued on warfarin through surgery than those on heparin (3) older patients may have an increased risk of bleeding, and (4) an INR of >3 at the time of surgery may increase the risk of bleeding.

Protamine sulfate (PS) neutralization of heparin (HEP) given during carotid endarterectomy (CEA) has been previously associated with an increased postoperative stroke rate. Dosing regimens of PS have varied in previous studies. The accuracy of PS dosing and its effect on postoperative complications was analyzed. The medical records of all patients undergoing elective CEAs from January 1993 to June 1996 in our institution were reviewed. A hematoma was defined as either an event requiring return to the operating room or when repeatedly identified in the medical record. The accuracy of dosing PS was determined utilizing a formula calculating the logarithmic exponential decay of HEP, which determined the residual HEP at the time of PS dosing. An ideal PS dose was then calculated and compared to the dose given. Statistical analyses was performed using a Fisher's exact test as well as the Student's t-test. Four hundred-seven CEAs were performed in 365 patients. There were 10/407 (2.5%) postoperative strokes (STROKE) and 11/407 (2.7%) hematomas, 3 of which required reoperation. Results indicate that (1) the administration of PS significantly reduced the incidence of postoperative hematoma; (2) there appears to be an association between the administration of PS and STROKE; (3) the inaccuracy in dosing PS appears to be based on a decision to dose PS to the total HEP given rather than the residual HEP on board at the time of neutralization. The effect of PS overdosing is unclear, but it may play a role in STROKE.

Elevated elastase activity in patients with chronic obstructive pulmonary disease (COPD) is attributable to the direct effect of nicotine. COPD is also known to be an independent predictor of abdominal aortic aneurysm (AAA) growth and rupture. The purpose of this study is to determine the effect of nicotine on elastase activity release from neutrophils of AAA patients. Human neutrophils were extracted from the blood of subjects in the following six groups, n = 10 in each group: smoking AAA (SAAA), nonsmoking AAA (NSAAA), smoking aortic occlusive disease (SAOD), nonsmoking aortic occlusive disease (NSAOD), smoking controls (SC), and nonsmoking controls (NSC). After incubation with varying nicotine concentrations (0-1000 microg/ml), the released elastase activity was determined. There is generally an elevation in elastase activity release by neutrophils of smokers compared to nonsmokers. Nicotine exposure stimulated increased elastase activity release in AOD and AAA, and the increase was especially pronounced in the SAAA and SAOD groups. The elevation was greatest in the SAAA group while the release was lowest in the NSAOD group. There is a direct correlation between elastase activity release and nicotine concentration. The data suggest that COPD and AAA development, which may occur by similar initial mechanisms may also be aggravated by nicotine-induced neutrophil elastase activity release. In addition, the results indicate that nicotine is playing an active role in the development of vascular disease by inducing neutrophils to release elastase activity.

Patients undergoing abdominal aortic aneurysm repair routinely have a depressed core body temperature during surgery, and hypothermia is known to cause abnormalities in coagulation. This study was designed to determine whether platelet function is altered as a result of hypothermia or heparin during abdominal aortic aneurysm repair. Ten patients scheduled for abdominal aortic aneurysm surgery were prospectively studied. Bleeding times and temperature were measured every hour beginning preoperatively. Each patient was heparinized intraoperatively, and the effects reversed with protamine sulfate prior to closure. Despite efforts to keep the patients warm, all of them developed hypothermia (mean lowest core temperature 34.8 +/- 0.7 degrees C). A significant linear relationship between the change in core temperature and the change in bleeding time was demonstrated. In 7 of 10 cases the greatest change in bleeding time occurred when patients experienced the lowest mean core temperature and not when they were heparinized. These data suggest that hypothermia has a marked effect on platelet function during abdominal aortic aneurysm repair. Although heparin can cause abnormalities in platelet function, hypothermia may be a more important role in inhibiting normal platelet function. By preventing severe hypothermia (< 35 degree C), excessive bleeding associated with abdominal aortic aneurysm repair may be minimized without the concomitant risk of blood product transfusion.

Coagulopathy and massive bleeding plays a major role in the mortality of thoraco-abdominal aneurysm repair. Increasing supraceliac aortic cross-clamp time from 0 to 90 minutes increases the degree of disseminated intravascular coagulation, which occurs as a result of occlusion and reperfusion of the superior mesenteric artery. The purpose of this study was to investigate the mechanism of the superior mesenteric artery reperfusion disseminated intravascular coagulation. Twenty dogs were divided into four groups: cross-clamp time of 30 minutes; cross-clamp time of 60 minutes; cross-clamp time of 90 minutes; and control. Permeability was determined by lactulose/mannitol absorption. The venous effluent was sampled for endotoxin, potassium, bacteria, and pH every hour and urine was collected for six hours. Lactulose absorption was significantly higher in all of the experimental groups. There was increased permeability in the 60 and 90 minute groups which correlated significantly with time. Venous endotoxin, potassium, and blood cultures for bacteria did not change significantly. The pH was significantly lower every hour for six hours in the 90 minute group. These data suggest that intestinal permeability is increased with supraceliac aortic clamping and can be kept to a minimum for clamp times of under one hour.

Aortic elastase and neutrophil elastase is higher in patients with abdominal aortic aneurysms. The purpose of this study was to determine if these proteolytic elevations occur after abdominal aortic aneurysms have been repaired. Specifically, we studied the stimulation and inhibition of elastase degranulation from neutrophils in postoperative abdominal aortic aneurysm patients compared to aortic occlusive disease patients. Neutrophil elastase was determined in postoperative abdominal aortic aneurysm and aortic occlusive disease patients in response to calcium and the ionophore A23187. Inhibition of elastase release was determined with the calcium channel blocking agent Verapamil. Neutrophil elastase secretion was significantly higher in the abdominal aortic aneurysm patients (47%) versus aortic occlusive disease (20%) (p less than .05), while the effect of Verapamil in blocking this response was significantly lower in the abdominal aortic aneurysm patients (14%) compared to aortic occlusive disease patients (27%) (p less than .02). The time for degranulation to occur was longer in the abdominal aortic aneurysm patients (14.7 minutes) versus aortic occlusive disease patients (3.5 minutes), but the rate of secretion was not different between the two groups. These data indicate that, (1) neutrophils secrete more elastase in response to a calcium stimulus in abdominal aortic aneurysm patients; (2) it takes longer to secrete the increased amount of elastase in abdominal aortic aneurysm patients since the rate of secretion is similar between the two groups; and (3) Verapamil blocks elastase secretion ineffectively in abdominal aortic aneurysm patients. We conclude that the proteolytic alterations in abdominal aortic aneurysm patients are more likely a primary event and not a response to the abdominal aortic aneurysm and that Verapamil is a poor drug to use to medically manipulate the protease system in abdominal aortic aneurysm patients.

Purpura fulminans is an uncommon catastrophic syndrome that occurs in children, typically one to four weeks after a seemingly benign infectious process. The child usually presents with a high fever, purpuric ecchymosis, hypotension, disseminated intravascular coagulation, and gangrene of the extremities. We have recently treated six children, whose mean age was 22 months; three were male and three were female. Five of the six had a change of mental status upon initial examination. Their mean temperature was 104 degrees F. All six children had purpuric involvement of their extremities; three had involvement of their hands, two had involvement of their faces, and two had involvement of their trunks. All had absent palpable pulses and sluggish capillary refill in the involved hands and feet. Two patients died shortly after admission as a result of severe end-stage sepsis. The platelet counts in these two patients, and the white blood cell counts were markedly depressed. The mean platelet count of the survivors was 370,000 and the mean white blood cell count was 25,000. Lumbar punctures were positive for bacterial meningitis in five patients and viral meningitis in one patient. All patients were treated with intravenous heparin. Of the four survivors, two lost significant tissue and required multiple plastic reconstructive procedures, and two improved on heparin alone with no tissue loss. In addition to systemic support and intravenous antibiotics, the mainstay of treatment is one of immediate heparinization and a continuous heparin drip. Heparin prevents subsequent small vessel thrombosis and limits tissue loss due to ongoing purpura. Conservative management of the purpuric lesions is the treatment of choice until final demarcation occurs.

The purpose of this study was to determine whether aortic elastase could be activated by distant operative trauma unrelated to direct aortic injury. One hundred rabbits were divided into five groups: group I - anesthesia only; group II - laparotomy only; group III - cecal resection; group IV - aortic mobilization; and group V - aortotomy with repair. Animals were sacrificed at one hour, three hours, six hours, one day, two days, and five days after surgery, and the aorta was analyzed for elastase activity. Operative trauma such as laparotomy, bowel resection, and mobilization of the aorta without direct aortic injury resulted in a significant increase in rabbit aortic elastase. The pattern of activation of rabbit aortic elastase within the laparotomy, aortic mobilization, and aortotomy groups was one of a slow rise to peak activation at 6-24 hours with a subsequent fall towards baseline at five days after surgery. This pattern differed in the cecal resection group in which activation occurred immediately with a slow fall towards baseline at five days. In none of the four surgical groups did the elastase activity return to baseline by five days after surgery. These data suggest that aortic elastase in rabbits can be activated by intraabdominal surgery unrelated to direct aortic injury.

The current study was undertaken to determine if cold crystalloid perfusion of the mesenteric circulation or continuous arterial shunting into the superior mesenteric artery would prevent the subsequent development of disseminated intravascular coagulation in a dog model. Twenty-two dogs were divided into four groups: those with distal aortic occlusion; those with isolated washout of the mesenteric circulation via the superior mesenteric artery with cold crystalloid; those with continuous isolated arterial perfusion of the superior mesenteric artery via an open proximal aorta; and those with shunting of blood into the superior mesenteric artery from the proximal aorta with an Inahara-Pruitt shunt. Coagulation parameters were measured for 24 hours and compared to the results with 32 dogs in the following groups: sham operation; supraceliac aortic occlusion for 30 minutes, 60 minutes, 90 minutes; superior mesenteric occlusion for 90 minutes; and celiac axis occlusion for 90 minutes. Shunting or direct arterial perfusion of the superior mesenteric artery prevented disseminated intravascular coagulation from occurring. Infrarenal aortic occlusion resulted in no change in any of the coagulation factors, whereas crystalloid perfusion of the superior mesenteric artery resulted in death in all animals. These results indicate that the disseminated intravascular coagulation that occurs with supraceliac aortic occlusion or superior mesenteric occlusion of greater then one hour can be prevented by continuous arterial perfusion of the superior mesenteric artery during proximal aortic clamping.

The purpose of this study was to analyze hospital resource consumption in any of the nine non-complicating conditions covered under stratified, peripheral vascular surgical Diagnosis-Related Groups (DRGs) using the new DRG prospective All Payer System in effect in New York. There is significant health policy debate at the level of the United States Congress regarding the improvement of the equity of DRG hospital payment. Although there have been a number of recommendations by federal advisory bodies to further stratify DRGs by complications and comorbidities, no major revision of DRGs along these lines has been implemented. The all payer system uses the DRG format to pay for all patients. We analyzed 788 peripheral vascular surgical patients by payer (Medicare, Medicaid, Blue Cross and commercial insurance) in these stratified, peripheral vascular surgical DRGs with no complications or comorbidities for a three year period. Our study demonstrated that patients within each DRG with more complications and comorbidities generated higher total hospital costs, a longer hospital length of stay, a greater percentage of procedures per patient, financial risk under DRG payment, more outliers, and a higher mortality, compared to patients in these same DRGs with fewer complications and comorbidities. These findings suggest that new, prospective DRG all payer systems may be inequitable to certain groups of patients or types of hospitals in these stratified peripheral vascular surgical DRGs with no complication or comorbidities. This analysis suggests that these peripheral vascular surgical DRGs should be stratified by the numbers and types of complications and comorbidities to more equitably reimburse hospitals under DRGs.(ABSTRACT TRUNCATED AT 250 WORDS)

Massive coagulopathy and bleeding continues to play a major role in the operative mortality and perioperative multi-system failure of patients requiring elective thoracoabdominal aneurysm repair. It was the purpose of this study to determine the coagulation defect that occurs with supraceliac aortic clamping and the effects of increasing aortic cross-clamp time (AXCT) on the coagulation system and its recovery. Through a standard thoracoabdominal incision, 16 mongrel dogs had their aortas cross-clamped simultaneously just above the diaphragm and at the aortic bifurcation. Animals were divided into four groups of four animals each; sham operation, 30 minute AXCT, 60 minute AXCT, and 90 minute AXCT. Central venous blood was sampled prior to aortic cross clamping (AXC), during AXC and 1 hour, 2 hours, 5 hours, 7 hours, 12 hours, and 24 hours after the clamp was removed. All samples were assayed for platelets, fibrinogen, fibrin split products, prothrombin time (PT) and partial thromboplastin time (PTT). Platelets and fibrinogen decreased as PT and PTT increased with increasing AXCT consistent with disseminated intravascular coagulation (DIC) (P less than .001). Fibrin split products were positive in the 90 minute AXCT group only. The drop in platelets was greater for increasing AXCT and continued to fall in the 30, 60 and 90 minute AXCT groups at 24 hours (p less than .001). Fibrinogen dropped to the lowest levels between two and twelve hours after AXC and returned to normal at twenty-four hours in the 60 and 90 minute AXCT groups (p less than .05).(ABSTRACT TRUNCATED AT 250 WORDS)