Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although patients undergoing acute hemodialysis (HD) constitute a group at risk for heparin-induced thrombocytopenia (HIT), the optimal therapeutic strategy remains undefined. We describe a case of HIT complicated with right subclavian vein thrombosis in a patient with chronic renal insufficiency undergoing acute HD for oligoanuria and pulmonary edema. Circulating anti-heparin-PF4 complex antibodies were detected. Past medical history was relevant for an otherwise unexplained self-limited episode of thrombocytopenia following acute HD one year earlier after an anterior STEMI. All sources of heparin were discontinued and alternative anticoagulation was initiated with argatroban, a direct-thrombin inhibitor with hepatic clearance, followed by transition to warfarin. Prevention of tunneled HD catheter obstruction was accomplished with low-dose alteplase catheter locking solution. No bleeding occurred with argatroban anticoagulation. Platelet count recovered and no further thrombotic complications were observed. The present report illustrates the diagnostic and therapeutic challenges of HIT complicating acute HD.
 ...
PMID:Therapeutic implications of heparin-induced thrombocytopenia complicating acute hemodialysis. 2035 43

Acute lung injury (ALI) and systemic coagulopathy are serious complications of traumatic brain injury (TBI) that frequently lead to poor clinical outcomes. Although the release of tissue factor (TF), a potent initiator of the extrinsic pathway of coagulation, from the injured brain is thought to play a key role in coagulopathy after TBI, its function in ALI following TBI remains unclear. In this study, we investigated whether the systemic appearance of TF correlated with the ensuing coagulopathy that follows TBI in ALI using an anesthetized rat blunt trauma TBI model. Blood and lung samples were obtained after TBI. Compared with controls, pulmonary edema and increased pulmonary permeability were observed as early as 5 min after TBI without evidence of norepinephrine involvement. Systemic TF increased at 5 min and then diminished 60 min after TBI. Lung injury and alveolar hemorrhaging were also observed as early as 5 min after TBI. A biphasic elevation of TF was observed in the lungs after TBI, and TF-positive microparticles (MPs) were detected in the alveolar spaces. Fibrin(ogen) deposition was also observed in the lungs within 60 min after TBI. Additionally, preadministration of a direct thrombin inhibitor, Refludan, attenuated lung injuries, thus implicating thrombin as a direct participant in ALI after TBI. The results from this study demonstrated that enhanced systemic TF may be an initiator of coagulation activation that contributes to ALI after TBI.
 ...
PMID:Early coagulation events induce acute lung injury in a rat model of blunt traumatic brain injury. 2719 65