Changes in platelet count, coagulation and fibrinogen associated with elective repair of asymptomatic abdominal aortic aneurysm and aortic reconstruction for occlusive disease

Abstract

Mortality and morbidity following aortic surgery, particularly repair of ruptured abdominal aortic aneurysm (AAA), is frequently associated with the development of coagulopathy. To examine changes in platelet count (PC), fibrinogen, and coagulation in patients undergoing elective repair of asymptomatic abdominal aortic aneurysm (AAA) and aortic surgery for occlusive disease. Prospective clinical study in a University Department of Vascular Surgery. Thirty-three patients undergoing elective repair of asymptomatic AAA and 19 patients undergoing aortic surgery for occlusive disease. Full blood count (FBC), clotting screen, and fibrinogen measured pre-operatively; 6, 12, 24, 48 h postoperatively; and thereafter as clinically indicated in 23 consecutive patient's undergoing AAA repair (Group 1). Pre- and postoperative PC measured weekly for 4 weeks following operation in a further 10 consecutive patients undergoing AAA repair (Group 2) and perioperative PC measured in 19 consecutive patients undergoing aortic surgery for occlusive disease (Group 3). Group 1: Preoperative haematological parameters were normal. There was no mortality. Postoperatively, 21 (91%) patients developed thrombocytopenia (PC < 150 x 10(9)/l). The postoperative fall in PC (median 90, range 12-160 x 10(9)/l) was significantly related to the duration of aortic cross-clamp (median 46, range 20-127 min, r2 = 0.33, p < 0.01). At 10 days all patients had developed thrombocytosis (PC > 350 x 10(9)/l) Postoperatively, by 48 h, 17 (74%) patients had developed hyperfibrinogenaemia. One patient suffered a myocardial infarction associated with a PC of 105 x 10(9)/l and a fibrinogen of 7.2 g/l. GROUP 2: In a further 10 patients undergoing AAA repair postoperative thrombocytosis was found to persist for several weeks in five of nine survivors. GROUP 3: Patients undergoing aortic surgery for occlusive disease had significantly higher preoperative PC than AAA patients (median 292, range 179-251 x 10(9)/l vs. median 204, range 140-293 x 10(9)/l, p < 0.01). Patients undergoing elective repair of AAA demonstrate similar, albeit less dramatic, changes in platelet count to those we have previously reported in patients undergoing repair of ruptured AAA. Aortic clamping leads to platelet sequestration and thrombocytopenia in the early postoperative period. Later, patients develop hyperfibrinogenaemia and thrombocytosis which may persist for several weeks. Similar changes are seen in patients undergoing aortic surgery for occlusive disease. These changes may represent a hypercoagulable state that predisposes these patients to thrombotic complications.