Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0034065 (pulmonary embolism)
 14,979 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Extremity tourniquets are widely used to achieve bloodless dissection in the surgical field. Excision of venous stasis ulcers (VSU) is aided by tourniquet use because of large dilated veins associated with venous stasis disease. We present 3 patients with hypotensive shock occurring 10 to 15 minutes after tourniquet release after excision of venous stasis ulcers. All patients had long histories of venous stasis changes and two-thirds had prior histories of deep vein thromboses and pulmonary embolism. Mean tourniquet inflation time was 34 minutes and there were electrocardiographic changes in two-third of the patients. All patients responded rapidly to standard resuscitation measures and in all 3 postoperative testing for pulmonary embolus and myocardial infarction was negative. Wound cultures revealed no organisms in 1 patient, mixed Gram-positive cocci in another, and greater than 10(5) Serratia marcescens in the third patient. Although small decreases in blood pressure and blood pH, and increases in blood lactate, PcO2, and creatinine phosphokinase, are normally associated with the use of extremity tourniquets, hypotensive shock has not been reported. The combined effect of tourniquet ischemia and venous stasis changes may cause hypotensive shock by (1) an endotoxic bolus upon tourniquet release, (2) pulmonary microembolization of platelet, fibrin, and leukocyte aggregates causing vasoactive substance release, and (3) synergistic effects of platelet-activating factor, a known mediator of endotoxic shock. The untoward events noted in these patients may be prevented by (1) proximal to distal dissection of the ulcer with initial ligation of large veins, (2) pretreatment with steroids and/or platelet-activating factor antagonists, and/or (3) slow release of the tourniquet.
 ...
PMID:Tourniquet-related hypotension in venous stasis ulcer excision. 836 87

Acute deep vein thrombosis (DVT) is associated with significant morbidity in the form of acute limb-threatening compromise from phlegmasia cerulea dolens, development of the postthrombotic syndrome (PTS), and even death secondary to pulmonary embolism. Initial therapy for DVT is anticoagulation, which inhibits thrombus propagation but lacks the thrombolytic properties to facilitate active thrombus removal. The existing thrombus burden can cause increased venous hypertension from occlusion as well as damage to venous valves by initiating an inflammatory response, which can ultimately result in PTS in up to half of patients on anticoagulation. The manifestations of PTS include leg pain, swelling, lifestyle-limiting venous claudication, skin hyperpigmentation, venous varicosities, and, in rare cases, venous stasis ulcers. Furthermore, patients with iliocaval DVT and large, free-floating thrombus are at an increased risk for pulmonary embolism despite adequate anticoagulation. Early attempts at thrombus removal with surgical thrombectomy or systemic thrombolysis or both demonstrated reductions in the incidence of PTS but were of limited utility owing to their invasiveness and increased risk of bleeding complications. New minimally invasive endovascular therapies, such as pharmacomechanical catheter-directed thrombolysis, have been proposed, which focus on rapid thrombus removal while decreasing the rate of bleeding complications associated with systemic therapy. This article provides an overview of the current pharmacomechanical catheter-directed thrombolysis protocol utilized at the Mount Sinai Hospital for acute iliocaval DVT.
...
PMID:Catheter-directed interventions for acute iliocaval deep vein thrombosis. 2484 Sep 64