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Biomedical subjects

Craig S Kitchens

Publications and source records attributed to Craig S Kitchens.

9 recordsLinked to original sources
PubMed2007

Chronic oral anticoagulant therapy for extrahepatic visceral thrombosis is safe.

BACKGROUND: Patients with hypercoagulability may thrombose visceral veins with resultant portal hypertension, esophagogastric varices, and hemorrhage. The role of chronic oral anticoagulant therapy in such patients is unclear. On the one hand, such patients are prone to significant hemorrhage and thus anticoagulant therapy may seem contraindicated. On the other hand, because the causal pathophysiology is typically hypercoagulability, it would seem rational to treat these patients with chronic anticoagulant therapy in order to both prevent other visceral and systemic thromboses and perhaps, over time, reduce the degree of portal hypertension. Experience and poor prognosis associated with the more common portal hypertension due to hepatic cirrhosis may bias judgment. METHODS: We retrospectively reviewed the course of chronic oral anticoagulant therapy regarding both the safety and effectiveness using our long-term follow-up of a cohort of seven patients with visceral thrombosis resulting in extrahepatic non-cirrhotic portal hypertension. RESULTS: Seven consecutive patients encountered over the past 19 years were observed for 78 patient-years, the first 14 patient-years prior to anticoagulant therapy and the latter 64 patient-years on oral anticoagulant therapy. No patients rethrombosed either visceral or systemic vessels while on oral anticoagulant therapy. There were no fatal or serious hemorrhagic events on oral anticoagulant therapy; in fact, upper gastrointestinal bleeding decreased from 1.2 to 0.2 bleeds/year. The endoscopic grade of esophageal varices decreased in four of five patients who underwent serial endoscopy, and platelet counts increased in all seven patients. CONCLUSIONS: Chronic oral anticoagulant therapy is safe and not associated with an increase in upper gastrointestinal bleeding in such patients. Additionally, and by inference, perhaps in conjunction with the natural history of portal hypertension, such therapy is possibly effective in reducing portal hypertension in patients with hypercoagulability-induced extrahepatic portal hypertension.

Administration, Oral↗
PubMed2005

A feasibility study of continuing dose-reduced warfarin for invasive procedures in patients with high thromboembolic risk.

BACKGROUND: The management of perioperative anticoagulation therapy for patients having a high risk of thromboembolism who are receiving long-term oral anticoagulant therapy is uncertain. The prevalent approach is to discontinue oral anticoagulation therapy and initiate heparin therapy. Another potential strategy is to continue oral anticoagulation therapy with a temporary adjustment of warfarin intensity to a preoperative international normalized ratio (INR) of 1.5 to 2.0. Such moderate-dose anticoagulation therapy with warfarin has been shown to be hemostatically safe yet effective in the prevention of thromboembolism after hip or knee replacement. METHODS: Over an 11-year period (ie, 1993 to 2003), our hemostatic consultative service prospectively identified 100 consecutive patients for whom we continued warfarin therapy at adjusted doses during the perioperative period, targeting a goal for the INR of 1.5 to 2.0. Patients were assigned a score for venous thromboembolic risk as well as overall surgical risk using published instruments. Score assignment was based on what was deemed to be extremely high risk for thromboembolism in patients who were receiving long-term warfarin therapy. Although the patients were accrued prospectively, the final retrospective analysis was made after all patients were treated. RESULTS: The most common indication (62%) for high-risk assignment was a thromboembolic event within the past 6 months. The second most prevalent reason was prior postoperative venous thromboembolism (VTE) [11%]. Indications for long-term anticoagulation therapy were recent VTE (62%), inherited thrombophilia (7%), antiphospholipid syndrome (13%), mechanical heart valves (18%), and prior cerebrovascular accident (4%). The prevalence of inherited thrombophilia probably has been grossly underestimated, as neither factor V Leiden mutation nor prothrombin 20210 mutation had been described during the bulk of the accrual time. Most surgical procedures (58%) were significantly invasive (Johns Hopkins category 3 to 5). The mean INR values were 2.1 on the day prior to surgery (SD, 0.9594; range, 1.2 to 6.5; n = 65), 1.8 on the day of surgery (SD, 0.4899; range, 1.2 to 4.9; n = 75), and 1.8 on the first postoperative day (SD, 0.4436; range, 1.1 to 3.3; n = 70). Two patients had major bleeding, and four patients had minor bleeding. One patient developed deep venous thrombosis. Several weeks after surgery, one patient with a prosthetic heart valve died from an embolic stroke, which was associated with a failure to increase his anticoagulation to therapeutic levels. CONCLUSIONS: Moderate-intensity anticoagulant therapy with warfarin, targeting a goal INR of 1.5 to 2.0, appears to be a safe and feasible method for preventing thromboembolic complications in high-risk surgical patients who are receiving long-term oral anticoagulant therapy. This may be considered a reasonable method to afford thromboprophylaxis in highly selected patients who are occasionally seen in clinical practice. This observational study does not prove equality, let alone superiority, to other proposed methods of anticoagulation therapy.

Administration, Oral↗
PubMed2004

Thrombocytopenia due to acute venous thromboembolism and its role in expanding the differential diagnosis of heparin-induced thrombocytopenia.

Thrombocytopenia is an uncommon but serious consequence of heparin administration. Occasionally patients with massive acute venous thromboembolism (VTE) will develop thrombocytopenia. As heparin or some thrombin inhibitor is strongly indicated in acute VTE, it is important to distinguish this event from heparin-induced thrombocytopenia (HIT). Four patients are presented who developed thrombocytopenia so early in their course of VTE and/or therapy with heparin that HIT was considered unlikely. The mean nadir platelet count for these four patients was 60,000/microl occurring at a mean time of 18 hr after the initiation of heparin therapy. Because of strong indications to continue heparin for their acute VTE in the face of a very low likelihood that they did have HIT, heparin was continued with excellent results and resolution of the thrombocytopenia. The literature of this subject is reviewed. Thrombocytopenia following VTE is actually rather common, but it is usually milder than in these four cases. In some cases such as these four, the thrombocytopenia can be sudden and rather severe causing diagnostic confusion with HIT.

Acute Disease↗
PubMed2002

The contact system.

OBJECTIVES: To review the literature for conditions, diseases, and disorders that affect activity of the contact factors, and further to review the literature for evidence that less than normal activity of any of the contact factors may be associated with thrombophilia. DATA SOURCES: MEDLINE search for English-language articles published from 1988 to 2001 and pertinent references contained therein, as well as search of references in recent relevant articles and reviews. STUDY SELECTION: Relevant clinical and laboratory information was extracted from selected articles. Meta-analysis was not feasible because of heterogeneity of reports. DATA EXTRACTION AND SYNTHESIS: Evidence for association of altered levels of the contact factors and thrombophilia was sought. A wide variety of disorders is associated with decreased activity of the contact factors; chief among these disorders are liver disease, hepatic immaturity of newborns, the antiphospholipid syndrome, and, for factor XII, being of Asian descent. These disorders are more common than homozygous deficiency. The few series and case reports of thrombophilic events in patients homozygous for deficiency of contact factors are not persuasive enough to support causality. The apparent association between levels consistent with heterozygosity (40%-60% of normal) of any of the contact factors (but especially factor XII) in persons with antiphospholipid antibodies appears to be due to falsely decreased in vitro activity levels of these factors, which are normal on antigenic testing. The apparent association with thrombosis is better explained by the antiphospholipid syndrome than by the modest reduction of the levels of contact factors. CONCLUSIONS: Presently, it is not recommended to measure activity of contact factors during routine evaluation of patients who have suffered venous or arterial thromboembolism or acute coronary syndromes.

Blood Coagulation↗