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Biomedical subjects

R Y Rhee

Publications and source records attributed to R Y Rhee.

24 records · Page 2Linked to original sources

Heparin-induced thrombocytopenia: pathophysiology.

HIT is a procoagulant disorder that is associated with significant morbidity and mortality if undetected and untreated. It occurs in approximately 5% of all patients receiving heparin therapy. HIT can be separated into two different types based on the clinical presentation and the pathophysiological mechanism. Type I HIT is an early, mild form of thrombocytopenia that is thought to be non-immune-mediated. No therapy is necessary for this type of HIT. Type II HIT has a delayed onset and is immunologically mediated. It is the more severe form and is associated with the development of HITT. Once suspected or diagnosed, all heparin therapy must be withdrawn. The thrombocytopenia will generally resolve within several days to a week. Minimizing the risk to the patient for developing HIT is the best form of prevention currently available.

Anticoagulants↗

Iliocaval complications of retroperitoneal fibrosis.

BACKGROUND: Retroperitoneal fibrosis can compress ureters, nerves, and blood vessels in the abdomen. However, clinically significant large-vein obstruction secondary to this process is rare. METHODS: Three hundred forty patients with retroperitoneal fibrosis were treated at our institution between 1976 and 1993. The clinical data from seven of these patients, who were treated for iliocaval complications of retroperitoneal fibrosis, were reviewed. RESULTS: Six patients had signs and symptoms of chronic obstruction, and one patient presented with acute iliocaval thrombosis and underwent attempt at venous thrombectomy in the referring hospital. All patients exhibited extremity edema and three had venous claudication. Iliocaval occlusion was confirmed in all patients by venography, computed tomography, or magnetic resonance imaging. The obstructive process involved the iliocaval tree (four patients), the inferior vena cava alone (two patients), and the iliac vein alone (one patient). Five patients were managed conservatively with leg elevation, compression stockings, and anticoagulation. Two patients received prednisone. One patient underwent an iliocaval bypass from the external iliac vein to the juxtarenal cava using a ringed polytetrafluoroethylene graft with a femoral arteriovenous fistula. A second patient with an isolated left common iliac vein obstruction underwent a left-to-right femorofemoral saphenous vein bypass. Four patients treated conservatively continued to have extremity edema. The two patients managed surgically remain asymptomatic from venous insufficiency, with patent grafts at 25 and 12 months after surgery, respectively. CONCLUSION: Iliocaval obstruction is an unusual complication of retroperitoneal fibrosis. Although most cases can be managed conservatively, reconstruction is an option for patients who have failed medical treatment and are symptomatic secondary to chronic venous obstruction. Lifelong anticoagulation should be considered for all patients with progressive iliocaval obstruction secondary to retroperitoneal fibrosis.

Acute Disease↗

Mesenteric venous thrombosis: still a lethal disease in the 1990s.

PURPOSE: This study was designed to evaluate progress in diagnosis, management, and clinical outcome of mesenteric venous thrombosis (MVT). METHODS: We retrospectively reviewed the clinical course of 72 patients treated for mesenteric venous thrombosis between 1972 and 1993. RESULTS: Fifty-three patients had acute and 19 had chronic mesenteric venous thrombosis. Fifty-seven patients had secondary mesenteric venous thrombosis; previous abdominal surgical procedure and hypercoagulable states were the most prevalent associated conditions. Computed tomography was abnormal in all patients who underwent this test for acute mesenteric venous thrombosis and in 93% of those who had chronic disease. Angiography diagnosed acute mesenteric venous thrombosis in five (72%) of seven patients. Acute mesenteric venous thrombosis presented most frequently as abdominal pain (83%), anorexia (53%), and diarrhea (43%). Thirty-three (75%) had symptoms longer than 48 hours. Thirty-four (64%) patients with acute mesenteric venous thrombosis underwent a surgical procedure. Bowel resection was necessary in 31 patients. One patient had unsuccessful mesenteric venous thrombectomy. Seven patients with acute mesenteric venous thrombosis underwent anticoagulation without a surgical procedure, and 12 were observed. All patients with chronic mesenteric venous thrombosis were observed; nine of the 19 underwent anticoagulation. The median delay in diagnosis for patients with acute mesenteric venous thrombosis was 48 hours and did not decrease during the last decade. Mesenteric venous thrombosis recurred in 19 (36%) patients. The 30-day mortality was 27%. Long-term survival of patients with acute mesenteric venous thrombosis was significantly worse than that of those with chronic disease (36% vs 83% survival at 3 years). The patients with acute mesenteric venous thrombosis who underwent anticoagulation with and without surgical procedure had improved survival when compared with the observed group. CONCLUSION: Acute mesenteric venous thrombosis remains a lethal disease. Mortality has not improved in the last 22 years. Computed tomography is the most sensitive diagnostic test. Anticoagulation and surgical procedure enhanced survival in the acute subgroup. The underlying disease determined survival in chronic disease.

Acute Disease↗

A biomechanical study of the collateral ligaments of the proximal interphalangeal joint.

Collateral ligament injuries of the proximal interphalangeal joint are common. A significant number of these injuries result in complete rupture of the ligament. The forces that damage the ligaments are abduction and adduction stresses. Previous studies have investigated laxity, angulation, and patterns of failure, but detailed biomechanical rupture studies are scant. Sixty-eight proximal interphalangeal joints from fresh human cadaver fingers (average age, 67 years) were stressed at velocities of 1 mm/sec, 4 mm/sec, and 10 mm/sec. Sectioning studies were also done. Four distinct rupture patterns were noted: midsubstance tear, proximal detachment, distal detachment, and distal avulsion fracture. The prevalence of these patterns differed with the rate at which the ligaments were stressed. Lower speeds tended to produce midsubstance tears, while higher speeds yielded distal damage. The study confirmed that the lateral collateral ligament is the primary restraint against medial-lateral stress and that other supporting structures (the extensor hood and the palmar plate) did not contribute significantly to side-to-side stability.

Analysis of Variance↗

Future alternatives to heparin: low-molecular-weight heparin and hirudin.

The antithrombotic effects of standard heparin were compared with those of low-molecular-weight heparin (LMWH) and hirudin by use of an in vitro perfusion system. Fresh blood collected from human volunteers was treated with varying doses of these three agents and perfused in a recirculating system over everted porcine vein segments. A low shear rate (100/sec) was selected to simulate conditions in large arteries and veins. Platelet and fibrinogen deposition were evaluated with indium 111 and iodine 125 radiolabels, respectively. Anticoagulant activity was assessed by measuring the activated clotting time (ACT). Anti-Xa activity was assayed to determine the degree to which these agents used antithrombin III pathways. Low-molecular-weight heparin was the weakest anticoagulant, requiring 32 micrograms/ml blood to double the ACT. By contrast, the ACT doubled with only 0.75 and 1.10 micrograms/ml blood of heparin and hirudin, respectively. Heparin and hirudin inhibited platelet and fibrin deposition at equivalent doses. Low-molecular-weight heparin was a less potent inhibitor of fibrin than heparin or hirudin. Hirudin, a direct thrombin inhibitor, exhibited minimal anti-Xa activity, contrasted with 0.14 anti-Xa units/micrograms for LMWH and 0.13 anti-Xa units/mg for heparin. These data suggest that heparin and hirudin are more potent anticoagulants and antiplatelet agents than LMWH.

Analysis of Variance↗

Low dose heparin therapy: in vitro verification of antithrombotic effect.

Low dose heparin therapy has been used routinely for prophylaxis of deep venous thrombosis, yet in vitro data regarding its antithrombotic effects are sparse. The effects of heparin on venous thrombus formation were studied in an in vitro perfusion system. Fresh blood collected from human volunteers was treated with varying heparin doses and perfused at a shear rate of 100 sec-1 over everted, injured porcine vein segments, simulating conditions in the venous circulation. Platelet and fibrin deposition were measured by use of indium 111 and iodine 125 radiolabels, respectively. The effects of heparin on the intrinsic coagulation cascade were monitored by the activated clotting time. Increasing doses of heparin resulted in significant reductions in fibrin and platelet deposition (ANOVA F = 2.67 and 3.17, respectively, p less than 0.05). At a dose of only 0.19 USP units/ml blood, equivalent to a 1000 unit bolus of heparin in a 70 kg man, a noticeable reduction in both fibrin and platelet deposition was observed without an increase in the activated clotting time. These data confirm the antithrombotic effects of heparin at low dose ranges and may explain the clinically observed phenomenon of deep venous prophylaxis without an appreciable alteration in the conventional coagulation assays.

Animals↗