Biomedical subjects

M J Rohrer

Publications and source records attributed to M J Rohrer.

36 records · Page 2Linked to original sources

PubMed1995

Ultrasound-guided compression of iatrogenic femoral pseudoaneurysm failure, recurrence, and long-term results.

PURPOSE: Iatrogenic femoral pseudoaneurysms (IFP) have traditionally been treated surgically. Recently, this common problem has been successfully treated without operation by use of ultrasound-guided compression (UGC) to induce thrombosis of the false aneurysm cavity, but the risk factors for failure and the long-term outcome have not been defined. METHODS: All patients referred to the vascular laboratory from June 1992 to November 1994 whose femoral pseudoaneurysms were treated by UGC were included in the study. Data were collected prospectively during the last 18 months of the study. Data regarding the location and morphologic characteristics of the pseudoaneurysms and anticoagulation status were documented. Patients who had successful UGC underwent follow-up duplex scanning and ankle-brachial arterial pressure evaluations. RESULTS: Fifty-seven patients with IFP were treated with UGC over a 30-month period; the last 34 were evaluated prospectively. UGC was successful at obliterating the false aneurysm cavity with the initial attempt in 47 (83%). Thrombosis of seven additional pseudoaneurysms was achieved on subsequent UGC attempts for an overall success rate of 95%. Recurrent false aneurysms were noted in two patients 2 and 10 days after initially successful UGC. Both were treated successfully with repeat UGC. Multivariate analysis of 14 variables revealed heparin anticoagulation (chi-square 9.025, p = 0.001) as the only significant risk factor for failure of UGC. There were no episodes of arterial thrombosis, embolization, or femoral nerve injury associated with UGC. Temporary occlusion of femoral artery during UGC and compression intervals of 20 minutes were well tolerated. Long-term follow-up from 30 to 400 days after UGC was available in 36 patients. There was no late recurrence or significant change in ankle-brachial pressures (p > 0.05). CONCLUSION: UGC is a safe and effective treatment for most catheter-induced femoral pseudoaneurysms with a low complication rate and excellent long-term results at a cost substantially lower than operative treatment. Because the natural history of IFP is unpredictable, UGC appears to be the preferred treatment for all IFPs persisting after cessation of heparin anticoagulation.

Adult↗

PubMed1994

Neutrophil cathepsin G modulates the platelet surface expression of the glycoprotein (GP) Ib-IX complex by proteolysis of the von Willebrand factor binding site on GPIb alpha and by a cytoskeletal-mediated redistribution of the remainder of the complex.

The effects of neutrophil cathepsin G on the glycoprotein (GP) Ib-IX complex of washed platelets were examined. Cathepsin G resulted in a concentration- and time-dependent decrease in the platelet surface GPIb-IX complex, as determined by flow cytometry, binding of exogenous von Willebrand factor (vWF) in the presence of ristocetin, and ristocetin-induced platelet agglutination. Cathepsin G resulted in proteolysis of the vWF binding site on GPIb alpha (defined by monoclonal antibody [MoAb] 6D1), as determined by increased supernatant glycocalicin fragment (a proteolytic product of GPIb alpha); decreased total platelet content of GPIb; and lack of effect of either cytochalasin B (an inhibitor of actin polymerization), prostaglandin I2 (an inhibitor of platelet activation), or prior fixation of the platelets. However, cathepsin G resulted in minimal decreases in the binding to fixed platelets of MoAbs TM60 (directed against the thrombin binding site on GPIb alpha) and WM23 (directed against the macroglycopeptide portion of GPIb alpha). In contrast to its proteolytic effect on GPIb alpha, the cathepsin G-induced decrease in platelet surface GPIX and the remnant of the GPIb-IX complex (defined by MoAbs FMC25 and AK1) was via a cytoskeletal-mediated redistribution, as determined by lack of change in the total platelet content of GPIX and the GPIb-IX complex; complete inhibition by cytochalasin B, prostaglandin I2, and prior fixation of platelets. Experiments with Serratia protease-treated and Bernard-Soulier platelets showed that neither platelet surface GPIb nor cathepsin G-induced proteolysis of GPIb were required for the cathepsin G-induced redistribution of the remnant of the GPIb-IX complex or the cathepsin G-induced increase in platelet surface P-selectin. In summary, neutrophil cathepsin G modulates the platelet surface expression of the GPIb-IX complex both by proteolysis of the vWF binding site on GPIb alpha and by a cytoskeletal-mediated redistribution of the remainder of the complex. Prior studies show that, although thrombospondin 1, antiserine proteases, and plasma are all inhibitors of cathepsin G, the effects of cathepsin G on platelets, including an increase in surface GPIIb-IIIa, occur during close contact between neutrophils and platelets in a protective microenvironment (eg, thrombosis and local inflammation).(ABSTRACT TRUNCATED AT 400 WORDS)

Actins↗

PubMed1994

The activation-induced decrease in the platelet surface expression of the glycoprotein Ib-IX complex is reversible.

Thrombin decreases the platelet surface expression of the glycoprotein (GP) Ib-IX complex. To determine whether this effect is reversible, flow cytometric studies were performed with GPIb-IX-specific monoclonal antibodies. In both whole blood and washed platelet systems, incubation of platelets with thrombin or a combination of adenosine diphosphate and epinephrine resulted in a maximal decrease of the platelet surface expression of GPIb-IX within 5 minutes, after which there was a time-dependent return of the platelet surface GPIb-IX complex, which was maximal by 60 minutes. Exposure of the same platelets to additional exogenous thrombin resulted in a second decrease in platelet surface GPIb-IX, followed by a second reconstitution of platelet surface GPIb-IX. Throughout these experiments there was no measurable release from the platelets of glycocalicin (a proteolytic fragment of GPIb). Experiments in which platelets were preincubated with a biotinylated GPIb-specific MoAb showed that the GPIb molecules that returned to the platelet surface were the same molecules that had been translocated to the intraplatelet pool. The GPIb molecules that returned to the platelet surface were functionally competent to bind von Willebrand factor, as determined by ristocetin-induced platelet agglutination and ristocetin-induced binding of exogenous von Willebrand factor. Inhibitors of protein kinase C and myosin light-chain kinase enhanced the reexpression of platelet surface GPIb. In summary, the activation-induced decrease in the platelet surface expression of the GPIb-IX complex is reversible. Inactivation of protein kinase C and myosin light-chain kinase are important mechanisms in the reexpression of the platelet surface GPIb-IX complex.

Adult↗

PubMed1994

Human neutrophil cathepsin G is a potent platelet activator.

PURPOSE: Neutrophil activation has been implicated in the pathophysiologic condition of ischemia-reperfusion injury, the formation of arterial aneurysms, the progression of myocardial ischemia, and the initiation of deep venous thrombosis. Activated neutrophils release cathepsin G, a serine protease, from their granules, which may cause platelet activation that leads to intravascular thrombosis, tissue infarction, and systemic release of the thrombogenic products of platelet granules. This study used flow cytometry to quantify the extent of cathepsin G-induced platelet activation and degranulation through changes in the expression of platelet surface glycoproteins. METHODS: Increasing concentrations of human neutrophil-derived cathepsin G were incubated with washed platelets or whole blood from healthy human donors. The platelet surface expression of glycoproteins, including P-selectin, a platelet membrane glycoprotein only expressed after platelet alpha granule release, were determined by quantifying the platelet binding of a panel of fluorescently labeled monoclonal antibodies. Results were compared with the effect of a maximal dose of thrombin, the most potent known platelet activator. RESULTS: In a washed platelet system, cathepsin G increased platelet surface expression of P-selectin (an activation-dependent neutrophil binding site), the glycoprotein IIb/IIIa complex (fibrinogen receptor), and glycoprotein IV (thrombospondin receptor), and decreased surface expression of glycoprotein Ib (von Willebrand factor receptor) to an extent comparable to maximal thrombin. However, these effects were not observed in a whole blood system. Further experiments revealed that preexposure to plasma completely inhibited cathepsin G-induced washed platelet activation and degranulation. Prostacyclin treatment of washed platelets markedly inhibited cathepsin G-induced platelet activation. CONCLUSIONS: Cathepsin G is a very potent platelet agonist and degranulator, comparable to maximal thrombin, which alters platelet surface glycoprotein expression for enhanced neutrophil binding and effective platelet aggregation. This study helps to elucidate a possible pathway through which neutrophils may directly activate platelets, leading to intravascular thrombosis, irreversible ischemia, and tissue death in cardiovascular disease states. Patients with diseased endothelium that is deficient in prostacyclin production may be particularly prone to the detrimental effects of neutrophil-derived cathepsin G platelet activation.

Antigens, CD↗

PubMed1994

Reversible inhibition of human platelet activation by hypothermia in vivo and in vitro.

A hypothermia-induced hemorrhagic diathesis is associated with cardiopulmonary bypass, major surgery, and multiple trauma, but its pathophysiological basis is not well understood. We examined the hypothesis that hypothermia reversibly inhibits human platelet activation in vitro and in vivo. Platelet activation was studied in normal volunteers by whole blood flow cytometric analysis of modulation of platelet surface GMP-140 and the glycoprotein (GP) Ib-IX complex in: a) shed blood emerging from a standardized in vivo bleeding time wound; b) peripheral blood activated in vitro with either thrombin (in the presence of gly-pro-arg-pro, an inhibitor of fibrin polymerization) or the stable thromboxane (TX) A2 analogue U46619. Platelets in peripheral whole blood were activated at temperatures between 22 degrees C and 37 degrees C. the forearm skin temperature was maintained at temperatures between 22 degrees C and 37 degrees C prior to and during the bleeding time incision. Platelet aggregation was studied in shed blood by flow cytometry and in peripheral blood by aggregometry. Generation of TXB2 (the stable metabolite of TXA2) was determined by radioimmunoassay. In vitro, hypothermia inhibited both thrombin- and U46619-induced upregulation of GMP-140, downregulation of the GPIb-IX complex, platelet aggregation, and TXB2 generation. These inhibitory effects of hypothermia were all completely reversed by rewarming the blood to 37 degrees C. In vivo, platelet activation was inhibited by hypothermia as shown by 5 independent assays of shed blood: upregulation of GMP-140, downregulation of the GPIb-IX complex, platelet aggregate formation, TXB2 generation, and the bleeding time.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1993

Experimental femoral vein reconstruction with expanded polytetrafluoroethylene grafts seeded with endothelial cells.

The effect of endothelial cell seeding on the patency of small-caliber expanded polytetrafluoroethylene (ePTFE) grafts used for venous replacements in a canine experimental model was evaluated. Grafts were implanted bilaterally in 12 dogs as femoral vein interpositions. In each animal, one graft was seeded with enzymatically derived homologous endothelial cells which had been cultivated for 3 days in vitro before implantation, whereas the contralateral graft was not seeded. In five dogs, venography was performed at 2 weeks, and grafts were then excised. In the remaining seven dogs, venography was performed at both 2 and 4 weeks, with graft excision at 4 weeks. Graft patency at 2 weeks for seeded grafts was 75% (nine of 12) compared with only 33% (four of 12) for unseeded grafts (P < 0.02). There were no new episodes of thrombotic occlusion between 2 and 4 weeks. Five dogs with thrombus in the control graft did not develop thrombus in the contralateral seeded graft. Furthermore, each dog with a patent control graft had no thrombus in the seeded graft. It is concluded that the early patency of seeded ePTFE grafts is superior to that of unseeded ePTFE grafts in the femoral vein.

Animals↗

PubMed1992

Do graduated compression stockings and pneumatic boots have an additive effect on the peak velocity of venous blood flow?

Graduated compression stockings and intermittent pneumatic compression boots reduce the incidence of deep vein thrombosis. Recent studies suggest that the simultaneous use of these devices may have a synergistic prophylactic effect; however, conflicting reports also exist. Using duplex imaging, we analyzed the effect on peak venous velocity in the superficial femoral vein produced by the individual and simultaneous use of graduated compression stockings and intermittent pneumatic compression boots. Normal volunteers and postoperative patients were examined. The use of intermittent pneumatic compression boots significantly increased the peak venous velocity relative to rest, whereas the use of graduated compression stockings did not alter the peak venous velocity. Also, the addition of graduated compression stockings to legs already being treated with intermittent pneumatic compression boots did not produce a further augmentation of peak venous velocity. This study demonstrates that the simultaneous use of graduated compression stockings and intermittent pneumatic compression boots does not produce a synergistic augmentation of peak venous velocity in the superficial femoral vein.

Bandages↗

PubMed1992

Effect of hypothermia on the coagulation cascade.

BACKGROUND AND METHODS: The development of a multifactorial coagulopathy after massive transfusion is a well-recognized clinical problem that is almost always accompanied by hypothermia. The purpose of this study was to investigate the isolated effect of alterations of temperature on the integrity of the coagulation cascade. Prothrombin times and partial thromboplastin times were each performed 15 times on samples of pooled normal plasma at the temperatures of 37 degrees C, 34 degrees C, 31 degrees C, and 28 degrees C, as well as 39 degrees C and 41 degrees C. RESULTS: Mean prothrombin time results increased from 11.8 +/- 0.3 (SD) secs at 37 degrees C to 12.9 +/- 0.5, 14.2 +/- 0.5, and 16.6 +/- 0.2 secs at 34 degrees C, 31 degrees C, and 28 degrees C, respectively (p < or = .001 for each). Partial thromboplastin time determinations increased from 36.0 +/- 0.7 (SD) secs at 37 degrees C to 39.4 +/- 1.0, 46.1 +/- 1.1, and 57.2 +/- 0.6 secs at 34 degrees C, 31 degrees C, and 28 degrees C, respectively (p < or = .001 for each). Both prothrombin time and partial thromboplastin time determinations were only minimally shortened at hyperthermic temperatures. CONCLUSIONS: The series of enzymatic reactions of the coagulation cascade are strongly inhibited by hypothermia, as demonstrated by the dramatic prolongation of prothrombin time and partial thromboplastin time tests at hypothermic deviations from normal temperature in a situation where factor levels were all known to be normal. Clinicians who deal with critically ill massively transfused hypothermic patients all recognize the inevitable appearance of a coagulopathy that has a multifactorial origin. Unless specifically considered, the contribution of hypothermia to the hemorrhagic diathesis may be overlooked since coagulation testing is performed at 37 degrees C, rather than at the patient's actual in vivo temperature.

Blood Coagulation Disorders↗

PubMed1992

High-dose heparin suppresses platelet alpha granule secretion.

Platelet degranulation has been implicated in the pathophysiology of acute arterial thrombosis, intimal hyperplasia, and atherogenesis. Most previous studies that examined the effect of heparin on platelet function have used platelet aggregometry. These studies have resulted in contradictory data and, by the nature of the assay, reveal no information with regard to platelet degranulation. In contrast, flow cytometry allows accurate quantification of the extent of platelet degranulation by measurement of the platelet surface binding of a GMP-140 specific monoclonal antibody (S12). GMP-140 is only expressed on the platelet surface after platelet alpha granule release. In the present study increasing concentrations of heparin were added to whole blood anticoagulated with sodium citrate. Platelets were activated with a panel of agonists, and the extent of platelet degranulation was quantified by whole blood flow cytometry. Heparin concentrations as high as 100 units/ml were found to suppress platelet alpha granule release induced by either a thromboxane A2 analog (U46619) or a combination of adenosine diphosphate and epinephrine. Heparin suppressed alpha granule release induced by thrombin both in whole blood and in washed platelets. The addition of heparin after platelet activation had no effect on S12 binding. In summary, heparin in high concentrations is a potent inhibitor of platelet degranulation, an action that is unrelated to its effect on the coagulation cascade. Although the heparin concentrations used in this study exceed those used clinically by a factor of 10 or more, future studies of heparin fractions may allow the separation of the anticoagulant and antiplatelet properties of the molecule and allow the administration of an agent that selectively suppresses platelet degranulation without the humoral anticoagulant effect.

Adenosine Diphosphate↗

PubMed1992

A prospective randomized study comparing surgical and percutaneous removal of intraaortic balloon pump.

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.

Aged↗

PubMed1992

Precoating expanded polytetrafluoroethylene grafts alters production of endothelial cell-derived thrombomodulators.

Although the use of extracellular matrix proteins to precoat small-caliber vascular grafts before endothelial cell seeding has been shown to improve cell attachment, proliferation, and adherence, the effect of precoating on the thrombomodulatory properties of the seeded cells is unknown. The use of vascular prostheses lined with confluent endothelial cell monolayers expressing optimal thromboresistant properties may enhance patency rates. In this study human saphenous vein endothelial cells were seeded onto expanded polytetrafluoroethylene (ePTFE) graft material, both unmodified and precoated with fibronectin, type I collagen, or fibronectin and type I collagen (fibronectin/type I collagen). After 3 days of in vitro cultivation, endothelial cell production of prostacyclin, tissue plasminogen activator, and plasminogen activator inhibitor was evaluated under basal conditions and after stimulation with arachidonate or thrombin. Production of tissue plasminogen activator by endothelial cells cultured on fibronectin-ePTFE was significantly greater compared with production by endothelial cells grown on noncoated or fibronectin/type I collagen-ePTFE under basal conditions (p values less than 0.01 and less than 0.05, respectively) and in response to thrombin (p values less than 0.002 and less than 0.003, respectively). Plasminogen activator inhibitor-1 production was not detected in any of the four experimental groups. Endothelial cells cultured on fibronectin-ePTFE also synthesized significantly more prostacyclin than endothelial cells grown on type I collagen- or fibronectin/type I collagen-ePTFE, under basal conditions (p values less than 0.02 and less than 0.01, respectively) and in response to arachidonate (p values less than 0.03 and less than 0.002, respectively) and thrombin (p values less than 0.003 and less than 0.002, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Vessel Prosthesis↗

PubMed1990

Axillary artery compression and thrombosis in throwing athletes.

A 28-year-old major league baseball pitcher sustained an axillary artery thrombosis which was successfully treated with intraarterial urokinase. Subsequent angiography and duplex scanning with the arm elevated in the pitching position demonstrated inducible compression of the axillary artery by the humeral head as well as compression at the thoracic outlet. To determine the incidence of axillary and subclavian artery compression and to investigate the mechanism of injury, brachial artery blood pressures and duplex scans of the subclavian and axillary arteries were performed in both the neutral position and the throwing position in the 92 extremities of 19 major league baseball pitchers, 16 non-pitching major league players, and 11 nonathlete controls. A drop in blood pressure of greater than 20 mm Hg was noted in the position in 56% of extremities tested, with a loss of a detectable blood pressure in 13%. Compression of the axillary artery by the humeral head was documented in 83% of extremities, but in only 7.6% was a greater than 50% stenosis inducible. No statistical difference was found in the incidence of arterial compression between the three groups tested or between their dominant and nondominant extremities. Dissection of the axillary artery in two cadavers documented that abduction and external rotation of the arm causes compression of the axillary artery by the humeral head, which acts as a fulcrum. We conclude that the repetitive mechanical trauma of the throwing motion can cause intermittent compression and contusion of the axillary artery by the humeral head and predisposes the athlete who throws to thrombosis of the axillary artery.

Adult↗

PubMed1990

Clinical management of the symptomatic but unruptured abdominal aortic aneurysm.

Pain or tenderness of an abdominal aortic aneurysm is widely believed to signify acute expansion and imminent rupture. To assess the potential benefit of emergency operation for the group of patients with an acutely expanding aneurysm, the clinical course of 19 patients with a symptomatic but unruptured expanding abdominal aortic aneurysm was compared with 117 patients undergoing elective abdominal aortic aneurysm resection, and 69 patients having operation for a ruptured abdominal aortic aneurysm. Postoperative morbidity was high in the patients with an expanding abdominal aortic aneurysm, and included a 21% incidence of myocardial infarction, a 10% incidence of stroke, a 37% risk of ventilatory failure, and a 31% incidence of acute renal failure, which was not statistically different from the results in patients having ruptured abdominal aortic aneurysm resection. Patients undergoing elective abdominal aortic aneurysm resection had only an 8% risk of myocardial infarction, and only a 2% risk of stroke, ventilatory failure, or renal failure. The mortality rate for expanding abdominal aortic aneurysm resection was 26% compared to 35% for ruptured abdominal aortic aneurysm (p = 0.31). Both emergency operations had a mortality rate more than five times greater than the 5.1% after elective procedures (p = 0.008). Our findings emphasize the need for early and aggressive treatment of abdominal aortic aneurysm in the elective setting, even in the patient at high risk, and suggest that the preoperative assessment and modification of risk factors is important to prevent the cardiac, cerebrovascular, pulmonary, and renal complications seen accompanying an emergency operation of this magnitude.

Acute Kidney Injury↗

PubMed1989

Extended indications for placement of an inferior vena cava filter.

To study the morbidity and mortality rates after placement of an inferior vena cava filter and to define the appropriate indications for interruption of the inferior vena cava, the records of all patients who underwent insertion of a Greenfield filter during the decade January 1978 to December 1987 were reviewed. Patients were designated as having either a traditional or extended indication for placement of an inferior vena cava filter. Two hundred sixty inferior vena cava filters were placed in 264 attempts, with no deaths related to insertion of the filter. An extended indication was the primary reason for placement of the Greenfield filter in 66 (25%) of the patients. In patients with extended indications there were no cases of air embolism or filter misplacement and only three wound complications (4.5%). Pulmonary embolism after insertion of the inferior vena cava filter occurred in three patients (4.5%), with one fatality (1.5%). Inferior vena cava occlusion was documented in three cases (4.5%), and manifestations of the postphlebitic syndrome in early follow-up were present in two patients (3.0%). As the procedures to prevent fatal pulmonary embolism have become safer, more efficacious, and less morbid, the number of patients in whom the potential benefits of insertion of an inferior vena cava filter outweigh the risks has become larger. Our results support the liberalized use of Greenfield filters in those patients who do not necessarily have one of the traditional indications for placement of an inferior vena cava filter but are at a high risk of having a fatal pulmonary embolus.

Anticoagulants↗

PubMed1988

Long-term survival and quality of life following ruptured abdominal aortic aneurysm.

To document both the long-term survival and the quality of life of patients following surgery for ruptured abdominal aortic aneurysm (AAA), the records of 65 patients with ruptured AAA resection were compared with those of 100 who underwent elective AAA resection. The actuarial survival following ruptured aneurysm surgery was 92%, 51%, and 51% at 1, 5, and 10 years, respectively, and did not differ statistically for patients after elective AAA surgery or for an age- and sex-matched sample from the general population. Based on responses to a quality of life survey, there were no discernible differences in life-style, degree of independence, or productivity following either ruptured or elective AAA surgery. Survivors of ruptured AAA have an excellent long-term prognosis and expectation for a good quality of life.

Age Factors↗

PubMed1988

Improved long-term patency of infragenicular polytetrafluoroethylene grafts.

This article reviews late graft patency and the incidence of postoperative complications in 75 infragenicular polytetrafluoroethylene bypass grafts (20 posterior tibial, 26 anterior tibial, and 29 peroneal). All patients received a heparin infusion after operation and were switched to warfarin before discharge to maintain coagulation parameters (prothrombin time and partial thromboplastin time) approximately twice that of control subjects. Primary procedures were done in 14 patients (19%), and the remaining patients had one or more previous procedures. Ninety-seven percent of patients had limb-threatening ischemia. Graft patency was confirmed by interval examinations and Doppler ankle pressure measurements. The mean follow-up was 36 months, and long-term graft patency (4 years) was determined by life-table analysis. The 2-year cumulative patency rate for this group was 45% and the 4-year patency rate was 37%. The latter is significantly better than the patency rates of 12% reported for similar untreated randomized grafts. Anticoagulation was subtherapeutic in 15 patients at the time of graft thrombosis, and if these were excluded, the 2- and 4-year patency rates were 58% and 50%, respectively. Hematomas requiring drainage occurred in 10 patients (13.3%) and six patients (8%) developed wound infections, but graft infection occurred in only two patients. Two patients (2.6%) developed late bleeding complications necessitating cessation of the warfarin. There was one fatal perioperative myocardial infarction (1.3%) and four late deaths, none of which were related to the warfarin therapy. Although the incidence of postoperative hematoma and wound infection was increased, late complications occurred infrequently.(ABSTRACT TRUNCATED AT 250 WORDS)

Amputation, Surgical↗

PubMed1988

A prospective evaluation of the efficacy of preoperative coagulation testing.

The efficacy of routine screening coagulation tests was studied to identify occult coagulopathies in patients prior to elective general and vascular surgery procedures. The efficacy of screening tests was compared to that of indicated tests performed for predefined clinical indications, which were elicited by history and physical examination and a detailed coagulation history questionnaire. Tests were prothrombin time (PT), partial thromboplastin time (PTT), platelet count (PC), and bleeding time (BT). Of 514 screening tests done in the 282 patients, 4.1% were abnormal, but none of them identified a clinically significant coagulopathy. Of the 605 indicated tests, 7.4% were abnormal, and all significant coagulopathies were found in this group. The study shows that preoperative screening tests for coagulopathies not suspected on the basis of detailed clinical information are unnecessary and should not be done. In the authors' institution 46% of screening coagulation tests could be eliminated.

Adult↗

PubMed1988

Placement of two Greenfield filters in a duplicated vena cava.

Congenital anomalies of the inferior vena cava (IVC) are not unusual and may complicate the placement of caval interruption devices. A duplicated IVC was demonstrated by venography in a patient with left iliofemoral venous thrombosis. A Greenfield filter was placed in each cavum from a right internal jugular vein approach. Because anomalies of the IVC are common, ascending venograms should be obtained in all patients who undergo caval interruption to document the number and position of the IVC, the location of the caval bifurcation, and the diameter of the IVC, as well as to identify the presence of thrombus within the lumen of the IVC. Unrecognized anomalies of the IVC may contribute to the incidence of recurrent pulmonary embolus after Greenfield filter placement.

Aged↗