A 62-year-old woman who underwent an aortic valve replacement for hard aortic valve stenosis developed postoperative thrombocytopenia and adult respiratory distress syndrome simultaneously.

A 62-year-old woman who underwent an aortic valve replacement for hard aortic valve stenosis developed postoperative thrombocytopenia and adult respiratory distress syndrome simultaneously. the pair complications resolved promptly after discontinuing heparin therapy. The demeanor of a heparin-related antiplatelet antibody was lay opened by in vitro testing. The time course of clinical marked occurrences suggests the possibility of a heparin-induced, immune-mediated injury to the pair the pulmonary vascular endothelium and the platelet membrane as an underlying pathophysiologic mechanism.

centurys of thousands of open heart surgery actions performed annually utilize cardiopulmonary bypass (CPB) technique with heparin anticoagulation. Depending onward whether porcine or bovine heparin source is used, clinically important heparin-associated thrombocytopenia (HAT) is a complication in a small clump of patients (1 to 5 percent incidence, respectively).[1]

brace forms of HAT have been described: a mild subclinical form and a more serious immune form. a certain quantity of past studies have described that nearly all patients receiving intravenous heparin may bring out a mild, transient, asymptomatic reduction in platelet think with no clinical sequelae.[2] Other investigators have not been able to propagate this observation.[3] The immune form of HAT usually meet the eyes within 6 to 14 days of initial heparin position and may begin earlier in patients who have had previous heparin position The thrombocytopenia is more rigid in degree. Paradoxically, the immune HAT has also been associated with life-threatening thrombotic complications in as many as 20 percent of those patients.[1] Given the large number of patients undergoing CPB and concomitant heparin therapy, the early diagnosis and management of HAT can be crucial to many patients.

We near herein a case of CPB in a 62-year-old woman with valvular heart disease. Her postoperative course was complicated from the simultaneous occurrence of HAT and adult respiratory distress syndrome (ARDS). the pair HAT and ARDS began resolution upon the discontinuation of heparin administration. We prompt that both HAT and ARDS in this patient may have been promot via a heparin-related immune mechanism.

CASE REPORT

The patient was admitted to the hospital for evaluation of worsening symptoms of dizziness and fatigue. She was lay the foundation of to have the clinical and laboratory features of chaste aortic stenosis without any findings of chronic pulmonary disease. At the time of admission, 8 days prior to surgery unimpaired blood cell count (CBC), platelet cast prothrombin time (PT), activated partial thromboplastin time (APTT), and chest radiograph (CXR) were within normal limits. Four days prior to surgery heparin was first enlist in one's serviceed during a diagnostic cardiac catheterization, which revealed aortic valve stenosis and pulmonary capillary wedge influence (PCWP) of 12 mm Hg the same day prior to surgery, the CBC platelet reckon (191,000/[mm.sup.3]), PT, and APTT were within normal limits. The aortic valve replacement practice using heparin proceeded without complications, and the CPB lasted 60 min. The patient, being hemodynamically stable with PCWP at 12 mm Hg was extubated forward the first postoperative day, the morning following the surgery after dutiful gas exchange was demonstrated on arterial blood gas criteria (prior to extubation in succession a respirator with [FIO.sub.2] 40 percent; [PaO.sub.2]=258 mm Hg; [PCOsub2]=32 mm Hg; pH=748)

by dint of the third postoperative day, however, the patient was observ to be progressively dyspneic and hypoxic (on nonrebreather mask [POsub2]=45 mm Hg; [PCOsub2]=51 mm Hg; pH=743) and she required reintubation. At that time the CXR displayed fresh diffuse bilateral infiltrates and small pleural effusions. Since the measured PCWP was 10 mm Hg a diagnosis of noncardiogenic (nonhydrostatic) pulmonary edema was made. Also, forward the third postoperative day, the CPB-related thrombocytopenia stopped resolving (platelet think 143,000/[mm.sup.3]) and proceeded to become plain thrombocytopenia by the eighth postoperative day (platelet esteem 56,000/[mm.sup.3]) (Fig 1). Postoperative medications included heparin for flushing vascular access lines, quinidine to command premature cardiac contractions, and prophylactic ranitidine (Fig 1) Sputum and relations cultures were negative throughout her hospitalization.

in succession the fifth postoperative day, the patient's serum was plant positive for evidence of a heparin-related antiplatelet antibody via a phase 1 aggregometry way using normal donor platelet controls[4] At this point, all heparin administration was immediately discontinued, and sodium citrate was substituted. Ranitidine therapy was also discontinued upon the same day while quinidine therapy was continued over the patient's hospitalization. by means of the ninth postoperative day the thrombocytopenia and respiratory measurements began to indicate progressive improvement: platelet count, 73000/[mmsup3] and [PaO.sub.2]=148 mm Hg onward respirator with [FIO.sub.2] 40 percent the one and the other PT and APTT remained normal through every part of The patient was extubated in succession the ninth postoperative day accompanied by the agency of continuous return of platelet account CXR findings, and respiratory parameters to normal range (Fig 1)

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