Coagulopathy and hyperfibrinolysis in ruptured abdominal aortic aneurysm repair.

Perioperative hemorrhage is one of the principal causes of death in patients with ruptured abdominal aortic aneurysm (AAA). This study examines perioperative coagulation and fibrinolysis in patients undergoing ruptured AAA repair complicated by coagulopathy. Eight patients (8 men of median age 74, range 69-87, years) who developed clinical and laboratory evidence of coagulopathy during attempted repair of ruptured infrarenal AAA were prospectively studied. Platelet count, fibrinogen, clotting times, prothrombin fragment (PF) 1+2, and tissue plasminogen activator (t-PA) and plasminogen activator inhibitor (PAI) activities were measured preoperatively, immediately before, and 5 min and 24 hr after aortic declamping. Six patients died, three intraoperatively, one within 24 hr, and two in the late postoperative period. All patients had thrombocytopenia and prolonged clotting times intraoperatively with evidence of increased thrombin generation (as demonstrated by elevated PF 1+2). Five patients had increased systemic fibrinolysis (as demonstrated by elevated t-PA activity) preoperatively and/or before aortic declamping and all of these patients died. Three patients had perioperative inhibition of systemic fibrinolysis (as demonstrated by elevated PAI activity) and two survived. These data demonstrate that coagulopathy in ruptured AAA repair may be associated with a hyperfibrinolytic state. Further research is required to determine if (a) a causal relationship exists between hyperfibrinolysis and coagulopathy and (b) whether antifibrinolytic agents can improve outcome if targeted at this group of patients.

von Willebrand factor and platelet count in ruptured abdominal aortic aneurysm repair.

OBJECTIVE: von Willebrand factor (vWF) is essential for the formation of platelet aggregates at sites of vascular endothelial cell (EC) injury. Peri-operative thrombocytopenia is associated with poor outcome in ruptured abdominal aortic aneurysm (AAA) repair. This prospective study examines the relationship between vWF and platelet count (PC) in ruptured AAA repair. METHODS: plasma vWF antigen, PC and C-reactive protein (CRP) were measured pre-operatively, and immediately before and 5 min after aortic clamp release, and on post-operative days 1 and 2 in 20 patients (18 men and 2 women of median age 74, range 63-86, years) with ruptured AAA. RESULTS: elevated vWF was present in 13 (65%) patients pre-operatively, and 14 of 16 (88%) survivors at 24 h post-operatively. All patients demonstrated an intra-operative fall in vWF. There was no significant difference in vWF levels between survivors and non-survivors. PC was below the normal range in 8 (40%) patients pre-operatively and all patients at 24 h. Eighteen (90%) patients demonstrated an intro-operative fall in PC. PC was significantly lower in non-survivors pre-operatively (p=0.007), immediately before (p=0.009) and 5 min (p=0.009) and 24 h (p=0.02) after clamp release. There was a significant positive correlation between vWF and PC pre-operatively (r= +0.48, p=0.033), and immediately before (r= +0.47, p=0.044) and 5 min after clamp release (r= +0.5, p=0.043). There was a significant positive correlation between peak vWF level and the greatest fall in PC (r= +0.65, p=0.006). There was a significant negative correlation between vWF and CRP and operative blood loss; and between PC and CRP, operative blood loss and aortic clamp time. CONCLUSIONS: these data demonstrate that EC activation, the acute phase protein response, operative blood loss and aortic clamp time all contribute to the peri-operative fall in PC in patients with ruptured AAA. The peri-operative fall in circulating levels of vWF and PC may represent consumption secondary to macro- and microvascular thrombus formation. The resultant procoagulant state may partly explain the association between low PC and poor outcome in ruptured AAA.

Comparison of cardiac troponin I and creatine kinase ratios in the detection of myocardial injury after aortic surgery.

BACKGROUND: Perioperative myocardial infarction may not be diagnosed correctly because World Health Organization criteria are often not met and creatinine kinase myocardial fraction (creatinine kinase/creatinine kinase MB isoenzyme; CK/CK-MB) ratios can be difficult to interpret. Cardiac troponin (cTn) I and cTnT are the most sensitive and specific markers of myocardial cell necrosis currently available but are not widely used in surgical practice. The aim was to compare cTnI and CK/CK-MB ratios in the detection of myocardial injury following aortic surgery. METHODS: This was a prospective study of 59 patients undergoing elective (n = 28) or ruptured (n = 24) abdominal aortic aneurysm repair or elective aortofemoral bypass (n = 7). cTnI level was measured before operation and at 6, 24 and 48 h after surgery. The CK/CK-MB ratio was measured where cTnI was detectable. RESULTS: Some 14 of 24 emergency and ten of 35 elective patients had detectable cTnI (greater than 0.5 ng/ml) at one or more time-points. The CK/CK-MB ratio was greater than 5 per cent in only four of 24 patients having an emergency operation and in none of the elective patients with detectable cTnI. CONCLUSION: Over half of patients undergoing emergency operation and more than a quarter of those having elective aortic surgery suffered myocardial necrosis as determined by detectable cTnI levels. This was accompanied by a raised CK/CK-MB ratio in less than one-fifth of patients.

Myocardial injury and systemic fibrinolysis in patients undergoing repair of ruptured abdominal aortic aneurysm: a preliminary report.

BACKGROUND: ruptured abdominal aortic aneurysm (AAA) is associated with inhibition of systemic fibrinolysis. Hypofibrinolysis is a risk factor for ischaemic myocardial injury, one of the commonest complications of ruptured AAA repair. Cardiac troponin I (cTnI) is one of the most sensitive and specific marker of myocardial injury currently available. OBJECTIVE: To examine, for the first time, the relationship between fibrinolytic activity and myocardial injury in patients operated for ruptured AAA. METHODS: Twenty patients (18 men and 2 women of median age 74, range 65-86 years) undergoing repair of ruptured AAA were prospectively studied. Plasma tissue plasminogen activator (t-PA) and plasminogen activator inhibitor (PAI-1) activity were measured pre-operatively, immediately before and five minutes following aortic clamp release. Serum cTnI was measured pre-operatively, 6 and 24 h following clamp release. Results cTnI was detectable at one or more sample points in 13 (65%) patients, and in 7 out of 8 patients who suffered major cardiac complications. There was a significant negative correlation between pre-operative t-PA activity and cTnI before operation (r =-0.55, p = 0.01) and 6 h ( r =-0.51, p =0.02) after clamp release. There was a significant positive correlation between pre-operative PAI activity and cTnI before operation (r =+0.50, p =0.03), 6 h ( r =+0.47, p =0.04) and 24 h ( r =+0.50, p =0.03) after clamp release. There was no correlation between pre- and intra-operative hypotension or blood transfusion requirement and cTnI release. CONCLUSIONS: Hypofibrinolysis during ruptured AAA repair is associated with the development of peri-operative myocardial injury. The causal mechanisms underlying this state are not clear but treatment of this prothrombotic/hypofibrinolytic diathesis may help to limit myocardial cell necrosis.