Michael M. Farooq
Medical College of Wisconsin
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Surgery | 1996
Michael M. Farooq; Julie A. Freischlag; Gary R. Seabrook; Marc R. Moon; Charles Aprahamian; Jonathan B. Towne
BACKGROUNDnDespite improvements in emergency medical services, surgical technology, and postoperative critical care, ruptured abdominal aortic aneurysm (AAA) is associated with constantly high morbidity and mortality. To determine the effect of the duration of symptoms, transport time to hospital, and length of emergency department assessment on outcome, we evaluated 124 consecutive patients with ruptured AAA treated during the past decade.nnnMETHODSnThe medical records for 122 patients were abstracted for preoperative hypotension, cardiopulmonary resuscitation (CPR), blood loss, and three time intervals: symptom onset to operation, transport time to hospital, and emergency department assessment.nnnRESULTSnIntraoperative mortality was 26% (n = 32), 30-day mortality was 51% (n = 63), and cumulative hospital mortality was 56% (n = 69). Death occurred in 52 (64%) of 81 patients with hypotension compared with 14 (35%) of 40 patients without hypotension (p < or = 0.01). Hypotension was present in 37 (82%) of 45 patients who arrived in the operating room in 2 hours or less compared with 26 (60%) of the 43 patients who arrived later than 2 hours (p < or = 0.05). Death followed in 21 (91%) of 23 patients who received CPR compared with 46 (46%) of 99 patients who did not receive CPR (p < or = 0.01). Bowel ischemia was observed in 18 (30%) of 60 patients who received more than 10 units of blood compared with 3 (5%) of 61 patients who received 10 units or less (p < or = 0.01).nnnCONCLUSIONSnFor patients with ruptured AAA, prolonged presurgical time was associated with a more hemodynamically stable patient and a lower mortality. Progressive bleeding in those hemodynamically stable patients was reflected by a larger blood transfusion requirement. Such patients exhibited an increased incidence of ischemic bowel complications, perhaps caused by splanchnic arterial ischemia augmented by preexisting atherosclerosis, as well as extrinsic compression by mesenteric hematomas.
Vascular Surgery | 1997
Michael M. Farooq; Julie A. Freischlag; Brian T. Carlsen; Robert A. Cambria; Gary R. Seabrook; Jonathan B. Towne
Consumption of adenosine triphosphate (ATP) during ischemia leads to the failure of cell membrane ATP-dependent ion pumps, cell lysis, and activation of the inflammatory cascade, which contributes to endothelial injury during reperfusion. Adenosine is a lipidsoluble precursor in ATP metabolism that may be depleted during reperfusion, exacerbating this injury. The purpose of this study was to examine the effect of adenosine administration with reperfusion on endothelium-dependent relaxation in the rabbit superficial femoral artery. New Zealand white rabbits underwent 3 hours of complete unilateral hindlimb ischemia followed by 2 hours of reperfusion. Animals received an intraarterial infusion of adenosine (0.35 mg/kg/min) or an equivalent volume of normal saline (1 cc/min) during the first 20 minutes of reperfusion. A sham group underwent aortoiliac collateral ligation and 5 hours of anesthesia without ischemia. A control group underwent immediate superficial femoral artery explantation with no collateral ligation or prolonged anesthesia. The superficial femoral arteries were explanted and suspended as 3 mm segments upon isometric force transducers within organ bath chambers. Contraction was evaluated with potassium chloride (KCl) and maximal norepinephrine (NE). Acetylcholine (Ach) relaxation was determined after NE submaximal contraction. No difference in contractile response to KCl was observed among the four groups. A significant increase in contraction to maximum NE was observed for vessels in the adenosine group (P<0.05). A significant increase in relaxation was noted over four consecutive doses of Ach administered to vessels from the adenosine, sham, and control groups when compared with the saline group (P<0.05). Adenosine administered during reperfusion preserved endothelium-dependent relaxation after ischemia and reperfusion in the rabbit superficial femoral artery. Adenosine may act as a substrate for ATP resynthesis and maintain cellular integrity during reperfusion. This form of pharmacologic therapy may prove clinically useful in the treatment of extremity ischemia/reperfusion injury.
Annals of Vascular Surgery | 2006
Sidney Glazer; Jean Diesto; Peter A. Crooks; Hock Yeoh; Noel Pascual; David Selevan; Stephen F. Derose; Michael M. Farooq
Annals of Vascular Surgery | 1999
Robert A. Cambria; Michael M. Farooq; Mark W. Mewissen; Julie A. Freischlag; Gary R. Seabrook; Martin R. Crain; Matthew I. Goldblatt; Ricardo Paz-Fumagalli; Jonathan B. Towne
Journal of Surgical Research | 1999
Julie A. Freischlag; Dawn Johnson; Michael M. Farooq; Jonathan Doty; Robert A. Cambria; Gary R. Seabrook; Jonathan B. Towne
Journal of Surgical Research | 1996
Curtis A. Erickson; Richard E. Carballo; Julie A. Freischlag; Gary R. Seabrook; Michael M. Farooq; Robert A. Cambria; Jonathan B. Towne
Journal of Surgical Research | 1996
Philip C. Chiang; David K. Traul; Michael M. Farooq; Robert J. Lesniak; Gary R. Seabrook; Jonathan B. Towne; Julie A. Freischlag
Journal of Vascular Surgery | 2001
Michael M. Farooq; Alexandre Serra; Peter J. Newman; Robert A. Cambria; Gary R. Seabrook; Jonathan B. Towne; Julie A. Freischlag
Journal of Surgical Research | 1999
Michael M. Farooq; Julie A. Freischlag; Holly Kelly; Gary R. Seabrook; Robert A. Cambria; Jonathan B. Towne
Journal of Surgical Research | 1996
Curtis A. Erickson; Richard E. Carballo; Julie A. Freischlag; Gary R. Seabrook; Michael M. Farooq; Robert A. Cambria; Jonathan B. Towne