Internal Iliac Aneurysm Repair Outcomes Using a Modification of the Iliac Branch Graft.

OBJECTIVES: Iliac branch grafts (IBGs) are a validated option for the treatment of aorto-iliac aneurysms preserving internal iliac artery (IIA) flow. IIA aneurysm (IIAA) is a relative contraindication to IBG placement. The goal of this study was to review experience in managing aorto-iliac aneurysms with concomitant IIAAs with extension of the IIA branch stent graft into the superior gluteal artery (SGA). METHODS: This retrospective study between May 2009 and November 2014 includes consecutive patients who underwent placement of an IBG (Cook, Bloomington, IN, USA) with extension of the internal iliac component of the branch stent graft into the SGA because of aneurysmal IIA (>15 mm). The stent grafts used were Viabahn (Gore, Karlsruhe, Germany), Fluency (Bard, Flagstaff, AZ, USA), or iCast (Atrium, Hudson, NH, USA) proximally. Imaging follow up was with computed tomography angiography (CTA) within 30 days of device insertion and then annually. RESULTS: The procedure was performed on 15 patients with a mean age of 76.8 years (SD 6.1 years). Twenty IIAAs were treated with a mean IIA and common iliac artery (CIA) diameter of 33 mm (SD 13 mm) and 35 mm (SD 11 mm) respectively. Technical success rate was 100%. One patient who underwent simultaneous IBG and three vessel fenestrated endovascular aneurysm repair died of mesenteric ischemia 2 days after the procedure. Mean imaging follow up with CTA was 18.3 months (SD 15.1 months). Primary patency of the SGA stent grafts was 100%. There was one case of type II endoleak. All patients were free from buttock claudication at follow up (mean: 19.7 months). Two patients who had IIA embolization contralateral to the IBG placement suffered from unilateral lower limb monoparesis. CONCLUSIONS: Extension of the internal iliac component of IBGs into the SGA for distal seal is feasible and safe in the endovascular treatment of aorto-iliac aneurysms with concomitant IIAs. Long-term results are needed to further validate this technique.

Anomalous splenic artery aneurysm.

Aneurysms of the splenic artery are the most common visceral aneurysm. A splenomesenteric trunk, which involves the splenic artery arising from the superior mesenteric artery (SMA), is rare and occurs in less than 1% of patients. Thus splenic artery aneurysms (SAAs) with an anomalous origin from the SMA are quite rare. We report our experience with the surgical management of a 2.6-cm aneurysm involving a splenic artery arising from the SMA in a 40-year-old woman. This was treated with surgical resection with preservation of the spleen. A discussion about SAAs and the management of aneurysms arising from a splenomesenteric trunk follows.

Endovascular ruptured abdominal aortic aneurysm repair--setting up your hospital for an endovascular approach.

In recent years, major improvements have been made, making elective repair of abdominal aortic aneurysm (AAA) a safe procedure. In selected series, mortality rates are less than 5%. Many of the patients with AAA, however, remain asymptomatic until they present with rupture. Once rupture has occurred, the overall mortality approaches 90%. Despite many advances in the management of ruptured AAA, the mortality rate of conventional open surgery has not improved significantly during the last 15 years. Over the last decade, endovascular techniques have been used increasingly to repair AAA, and there is increasing evidence that endovascular aneurysm repair (EVAR) is technically feasible and safe for ruptured AAA. This review studies the evidence and aids the clinician in setting up a practice to manage rAAAs utilizing an endovascular approach.

Effect of complement inhibition with soluble complement receptor 1 on pig allotransplant lung function.

BACKGROUND: Lung dysfunction after transplantation continues to be a significant clinical problem. Soluble complement receptor 1 (sCR1) is a potent inhibitor of complement activation. We evaluated the inhibitory effect of sCR1 on complement activation and reperfusion injury in pig lung allografts. METHODS: In a randomized and blinded study, left lung transplantation was performed in 13 pigs. Donor lungs were flushed and then stored for 30 hr at 4 degrees C. Control pigs (n=7) received saline, and the treatment group (n=6) received 15 mg/kg sCR1 1 hr before reperfusion. One hour after reperfusion, the right pulmonary artery was clamped for 10 min to assess the function of the transplanted lung. Pulmonary function was assessed again on day 3. RESULTS: Complement inhibition was 93% in the sCR1 group and returned to baseline (8% inhibition) after 3 days. There was a trend toward a higher partial pressure of oxygen at 1 hr in the sCR1 group compared with the control group (mean +/- SE: 408+/-42 mmHg vs. 288+/-69 mmHg, P = 0.19). Alveolar ventilation was better in the sCR1 group than in the control group (P = 0.01) at 1 hr. Mixed venous saturation was significantly lower in the control group at both 1 hr (P = 0.02) and 3 days (P = 0.001). The wet/dry weight of the lung tissue was lower in the sCR1 group compared with the control group on day 3 (P < 0.05). Chemiluminescence, an index of phagocyte priming, was lower in the sCR1 group when cells were stimulated with complement opsonized zymosan but not when stimulated with zymosan or phorbol myristate acetate. CONCLUSION: sCR1 improves ventilation, reduces pulmonary edema, and may be beneficial in improving posttransplant lung oxygenation.

Mesenteric arterial bypass grafts: early and late results and suggested surgical approach for chronic and acute mesenteric ischemia.

BACKGROUND: The purposes of this study were to determine the early and late results of placement of arterial bypass grafts in the treatment of chronic and acute intestinal ischemia and to ascertain whether multiple grafts provide better late results than a single graft. METHODS: Records of 34 patients who underwent mesenteric vascular graft placement were retrospectively reviewed. RESULTS: All 21 patients with chronic ischemia had a history of intestinal angina and weight loss. Food fear was reported by 33% of patients; also, diarrhea in 57%, constipation in 29%, acalculous cholecystitis in 19%, ischemic gastritis or peptic ulcer in 19%, and elevation of liver enzymes in 22% were reported. Angiogram showed more than 50% stenosis or occlusion of the superior mesenteric artery (SMA) in 100% of patients, celiac artery in 90%, and inferior mesenteric artery in 90%. Although not described previously, a reduction in collateral flow from the internal iliac arteries was caused by severe pelvic disease in 56% of patients. There were no in-hospital deaths. The rate of survival at 1 year was 100%; at 2 years it was 93% +/- 6%, at 3 years 86% +/- 9%, at 5 years 79% +/- 11%, and at 10 years 50% +/- 15%. During follow-up, graft thrombosis occurred in three patients. Of the patients who underwent only a single SMA or celiac bypass, two of five died of bowel infarction; only one of 16 patients who underwent both celiac and SMA bypass had to undergo a repeat surgical procedure because of graft occlusion. Three of 16 retrograde bypasses thrombosed, compared with zero of five prograde bypasses. In nine patients who underwent placement of mesenteric bypass grafts because of acute ischemia caused by acute mesenteric thrombosis, the early mortality rate was 22%; the two deaths were the result of bowel ischemia. The cumulative survival rate was 78% +/- 14% at 1 month, 65% +/- 17% at 1 year, and 52% +/- 16% at 5 years. One of the two late deaths was due to graft thrombosis and bowel infarction. Three of four patients who underwent concomitant mesenteric bypass at the time of aneurysm repair or aortobifemoral bypass survived the surgical procedure. CONCLUSIONS: When chronic and acute mesenteric ischemia are diagnosed and treated with a bypass graft, the early and late results are good. Complete revascularization of the SMA and celiac artery or pelvis or both and prograde bypass may reduce the risk of late bowel ischemia.

Role for tumor necrosis factor as mediator of lung injury following lower torso ischemia.

Ischemia and reperfusion of the ischemic lower torso lead to a neutrophil- (PMN) dependent lung injury characterized by PMN sequestration and permeability edema. This mimics the injury seen after infusion of tumor necrosis factor alpha (TNF), a potent activator of PMN and endothelium. This study tests whether TNF is a mediator of the lung injury after lower torso ischemia. Anesthetized rats underwent 4 h of bilateral hindlimb tourniquet ischemia, followed by reperfusion for 10 min, 30 min, 1, 2, 3, and 4 h (n = 6 for each time point). Quantitative lung histology indicated progressive sequestration of PMN in the lungs, 25 +/- 3 (SE) PMN/10 high-power fields (HPF) 10 min after reperfusion vs. 20 +/- 2 PMN/10 HPF in sham animals (NS), increasing to 53 +/- 5 PMN/10 HPF after 4 h vs. 23 +/- 3 PMN/10 HPF in sham animals (P less than 0.01). There was lung permeability, shown by increasing protein accumulation in bronchoalveolar lavage (BAL) fluid, which 4 h after reperfusion was 599 +/- 91 vs. 214 +/- 35 micrograms/ml in sham animals (P less than 0.01). Similarly, there was edema, shown by the lung wet-to-dry weight ratio, which increased by 4 h to 4.70 +/- 0.12 vs. 4.02 +/- 0.17 in sham animals (P less than 0.01). There was generation of leukotriene B4 in BAL fluid (720 +/- 140 vs. 240 +/- 40 pg/ml, P less than 0.01), and in three of six rats tested at this time TNF was detected in plasma, with a mean value of 167 pg/ml. TNF was not detectable in any sham animal.(ABSTRACT TRUNCATED AT 250 WORDS)

Coronary bypass and carotid endarterectomy: does a combined approach increase risk? A metaanalysis.

BACKGROUND: Patients with concomitant carotid and coronary artery disease present a surgical dilemma. We compared the stroke and mortality rates for combined coronary artery bypass grafting and carotid endarterectomy in which both procedures were performed under a single anesthetic, versus a staged approach, in which coronary artery bypass grafting and carotid endarterectomy were performed separately. METHODS: A computerized MEDLINE search supplemented with a manual bibliographic review was performed for all peer-reviewed English language publications that contained both combined and staged coronary artery bypass grafting/carotid endarterectomy patient cohorts. Outcomes of interest were stroke, death, and stroke or death; aggregation of outcome rates was performed with the Mantel-Haenszel method. RESULTS: Sixteen studies were identified with a total of 844 combined patients and 920 staged patients. None of the studies was completely randomized. The combined surgical group had a higher prevalence of unstable angina; the two groups had a similar prevalence of symptomatic carotid disease and severe carotid stenosis. Meta-analysis revealed a significantly increased risk of the composite end point, stroke or death, for patients undergoing combined procedures (relative risk 1.49; 95% confidence interval 1.03-2.15; p = 0.034). There was also a trend toward increased risk during combined procedures for the end points of stroke (relative risk 1.50; 95% confidence interval 0.97-2.32; p = 0.068) and death (relative risk 1.55; 95% confidence interval 0.94-2.53; p = 0.084) considered separately. The crude event rates for stroke were 6.0% versus 3.2% for combined versus staged procedure, 4.7% versus 2.9% for death, and 9.5% versus 5.7% for stroke or death. Two of the 16 individual studies showed a statistically significant increase in the risk of stroke or death for combined procedure (p < 0.05). CONCLUSIONS: Combined coronary artery bypass grafting and carotid endarterectomy may be associated with a higher risk of stroke or death than staged procedures. A randomized trial needs to be performed to determine the optimal management of patients with concomitant carotid and coronary artery disease.

The in vivo gracilis muscle model of skeletal muscle ischemia.

The bilateral canine gracilis muscle has been studied as a model of acute skeletal muscle ischemia. Early investigations demonstrated that preparation of the model did not alter the energy profile of the muscle. Changes in energy metabolism during ischemia and after reperfusion have been extensively investigated using this model. Further investigations are reviewed that have explored the mechanisms of injury during reperfusion, including oxygen free radical production, calcium influx, neutrophil infiltration, and complement activation. These experiments have furthered our understanding of the pathophysiologic changes that occur in skeletal muscle after ischemia and laid the groundwork for future experiments to reduce reperfusion injury and salvage ischemic skeletal muscle.

Two cases of arteriovenous fistula formation between the external iliac vessels following endovenous laser therapy.

Minimally invasive treatment of varicose veins is becoming increasingly popular with both patients and physicians. Endovenous laser therapy has been shown to be safe and effective but the rare complication of iatrogenic creation of arteriovenous fistulas has been described. One case of fistulation between the external iliac artery and vein has been published. We report two further cases and describe their management.

Anomalous splenic artery aneurysm.

Aneurysms of the splenic artery are the most common visceral aneurysm. A splenomesenteric trunk, which involves the splenic artery arising from the superior mesenteric artery (SMA), is rare and occurs in less than 1% of patients. Thus splenic artery aneurysms (SAAs) with an anomalous origin from the SMA are quite rare. We report our experience with the surgical management of a 2.6-cm aneurysm involving a splenic artery arising from the SMA in a 40-year-old woman. This was treated with surgical resection with preservation of the spleen. A discussion about SAAs and the management of aneurysms arising from a splenomesenteric trunk follows.

C5 complement inhibition attenuates shock and acute lung injury in an experimental model of ruptured abdominal aortic aneurysm.

BACKGROUND: Ruptured abdominal aortic aneurysm (RAAA) is associated with a systemic inflammatory response syndrome and multiple organ dysfunction. The potential role of a novel C5 complement inhibitor in attenuation of pathological complement activation and tissue injury was explored in a model of RAAA. METHODS: Anaesthetized rats were randomized to sham (control) or shock and clamp (SC) groups. Animals in the SC group underwent 1 h of haemorrhagic shock (mean arterial pressure 50 mmHg or less), 45 min of supramesenteric aortic clamping and 2 h of reperfusion. They were randomized to receive an intravenous bolus of a functionally blocking anti-C5 monoclonal antibody (C5 inhibitor), at a dose of 20 mg/kg, or saline. Lung injury was assessed by permeability to 125I-labelled albumin, tissue myeloperoxidase (MPO) activity, and semiquantitative reverse transcriptase-polymerase chain reaction (RT-PCR) for mRNAs encoding tumour necrosis factor (TNF) alpha and interleukin (IL) 6. RESULTS: The lung permeability index was significantly increased in the SC compared with the sham group (P = 0.032); this was prevented by the C5 inhibitor (P = 0.015). Lung MPO activity was significantly increased in the SC compared with the sham group (P < 0.001), and this increase was attenuated by treatment with the C5 inhibitor (P < 0.001). Semiquantitative RT-PCR in SC group demonstrated downregulation of TNF-alpha mRNA (P = 0.050) and upregulation of IL-6 mRNA (P < 0.001), which were both prevented by the C5 inhibitor (P = 0.014 and P < 0.001 respectively). CONCLUSION: These results indicated that C5 complement inhibition can reduce shock and acute lung injury in an experimental model of RAAA.

Acute pulmonary injury in a model of ruptured abdominal aortic aneurysm.

PURPOSE: The purpose of this study was to determine whether the combined insults of hemorrhagic shock and aortic clamping simulating ruptured abdominal aortic aneurysm repair had a synergistic effect on the production of pulmonary injury, indicating remote organ injury. METHODS: Animals were randomized to one of three groups, infrarenal clamp plus 1 hour of shock, infrarenal clamp plus 2 hours of shock, and supramesenteric clamp plus 1 hour of shock. Each of these groups had four subgroups; sham, shock (mean arterial pressure of 50 mm Hg), clamp, or combined [shock plus clamp]). All animals had a laparotomy with aortic clamping in only the clamp and combined groups. Five hours after clamp removal lung permeability index and neutrophil sequestration were quantified. RESULTS: Lung permeability index (6.60 +/- 0.63, p < 0.05 vs all other groups) and neutrophil sequestration (3.72 +/- 0.45 vs sham and clamp, p < 0.05) were significantly increased when shock and supramesenteric clamp were combined. After 1 or 2 hours of shock and infrarenal clamping, no increase in lung permeability index was noted, although neutrophil sequestration was increased in the 2-hour shock group. CONCLUSIONS: These results demonstrate the additive effect of shock and supramesenteric clamping, which initiated a cascade of injurious events that resulted in a rapid pulmonary injury. The high mortality rate related to remote organ failure in ruptured abdominal aortic aneurysm may be related to the synergy of these two injurious processes.

Preoperative factors that predict hospital length of stay after distal arterial bypass.

PURPOSE: The purpose of this study was to identify the preoperative factors that are predictive of prolonged hospital length of stay (LOS) and to discuss strategies that might assist in minimizing LOS for this select group of patients. METHODS: Two hundred seventy-five arterial bypass procedures with the in situ technique were performed between 1986 and 1993. The relationship between 14 preoperative variables and hospital LOS was analyzed with both univariate (Kaplan-Meier) and multivariate (Cox regression) statistical techniques. A model was developed to determine the significant preoperative variables that were associated with prolonged LOS. RESULTS: The primary and secondary patency rates and limb salvage rates at 4 years were 73.3% +/- 3.2%, 78.9% +/- 2.9%, and 81.9% +/- 3.2%, respectively. The median postoperative LOS was 15 days, with a mean +/- SD of 17.8 +/- 12.3 days (range 4 to 93 days). With Cox regression analysis, the variables that were significant predictors of LOS (with a model p value < 0.002) were age (greater than 74 years vs less than 75), history of cerebrovascular disease (transient ischemic attack, stroke, past carotid endarterectomy vs nil), and operative indication (limb salvage vs disabling claudication). CONCLUSIONS: This study illustrates that certain preoperative variables are predictive of prolonged postoperative LOS after in situ bypass. The significant preoperative factors identified should be used to direct specific care and discharge planning for these individuals.

Plasma activation of neutrophil CD18 after skeletal muscle ischemia: a potential mechanism for late systemic injury.

Reperfusion of acutely ischemic skeletal muscle is associated with neutrophil activation, which may augment local injury or cause damage to distant organs. Polymorphonuclear neutrophil glycoprotein CD18 plays a role in this injury, since its blockade substantially reduces damage; however, its mechanisms of control during reperfusion are poorly understood. The purpose of this study was to investigate the importance of circulating plasma factors to CD18-dependent neutrophil function during reperfusion and to relate these to quantitative expression of CD18. Eight rabbits were subjected to hindlimb ischemia for 5 h, followed by 48 h of reperfusion. Plasma collected at seven intervals was incubated with unstimulated neutrophils from uninjured rabbits. CD18-specific neutrophil activation was evaluated by quantifying adherence to protein-coated polystyrene and by measuring oxidant production, detected by chemiluminescence after exposure to complement-opsonized zymosan. CD18 was quantified cytofluorometrically. Plasma collected at end ischemia and during early reperfusion affected no significant alterations of adhesion, oxidant production, or CD18. Late reperfusion plasma (between 8 and 48 h) significantly increased adherence and oxidant production (to 4.11 +/- 0.61 and 2.60 +/- 0.32 times the values of preischemic plasma, P < 0.006). Peak adherence, oxidant production, and CD18 expression were evoked synchronously by 24 h plasma. CD18 expression increased only at 24 h and did not increase proportional to increases in adherence and oxidant production. Control plasma (nonischemic, n = 5) elicited no significant differences of any inflammatory measure during sham ischemia or reperfusion. These results indicate that endogenous mediators may evoke a progressive systemic inflammatory response after ischemia by stimulating CD18-dependent neutrophil function in a delayed but prolonged manner.

Rupture of an abdominal aortic aneurysm causes priming of phagocytic oxidative burst.

PURPOSE: The purpose of this investigation was to determine whether rupture and repair of an abdominal aortic aneurysm induced activation of phagocyte oxidant burst, reflecting a systemic inflammatory state, when compared with elective abdominal aortic aneurysm (AAA) repair. METHODS: Blood samples were harvested from 22 patients with elective AAA and 15 patients with ruptured AAA. Phagocyte oxidant activity was measured in response to a panel of activators with luminol and lucigenin as chemiluminescent substrates. Activity of the complement pathways was measured with plasma levels of C3a des arg. RESULTS: Elective AAA repair resulted in significant elevation in phagocyte count and oxidative activity after surgery in response to maximal dose phorbol myristate acetate (PMA) when compared with the baseline sample. In patients with ruptured AAA the oxidative activity of phagocytes was significantly increased in response to both unopsonized zymosan (899.8 +/- 192 ruptured vs 300 +/- 40 elective, p < 0.01) and maximal dose PMA (8769 +/- 2011 vs 3508 +/- 382, p < 0.01) compared with elective cases at the initial sampling. Phagocyte priming has occurred by way of two distinct pathways: receptor-mediated (unopsonized zymosan, CR3 receptor) and receptor-independent (PMA, protein kinase c). CONCLUSIONS: Rupture of an AAA resulted in priming of the phagocyte oxidant capacity before operative repair compared with elective AAA. Phagocyte activation is a critical component of the systemic inflammatory response that may contribute to the high incidence of systemic organ dysfunction and death in this patient group.

The effect of ischemia/reperfusion on adenine nucleotide metabolism and xanthine oxidase production in skeletal muscle.

Prolonged ischemia to skeletal muscle as occurs after an acute arterial occlusion results in alterations in adenine nucleotide metabolism. Adenosine triphosphate continues to be used for cellular functions, and an ischemia-induced degradation of phosphorylated adenine nucleotides is initiated. In this experiment we demonstrated the time-dependent aspect of adenine nucleotide depletion during ischemia and the production of large quantities of soluble precursors. In addition, we studied the rate of conversion of xanthine dehydrogenase to xanthine oxidase, a potential source of oxygen-free radicals, after controlled periods of total normothermic ischemia (4 hours and 5 hours) and during the reperfusion phase. During ischemia complete depletion of creatine phosphate occurred in both groups, and adenosine triphosphate fell from 22.1 +/- 1.3 to 10.3 +/- 1.4 mumol/gm dry weight after 4 hours and from 21.6 +/- 0.7 to 3.9 +/- 0.8 mumol/gm dry weight after 5 hours (p less than 0.05). During reperfusion, creatine phosphokinase resynthesis occurred in both groups, but adenosine triphosphate levels were not significantly increased (p greater than 0.05). A washout of lipid soluble products of adenine nucleotide metabolism occurred equally in both groups. The relationship between phosphorylated adenine nucleotides as measured by the energy charge potential fell significantly in both groups (p less than 0.05), but after the shorter period of ischemia (4 hours it returned to normal during early reperfusion but did not after 5 hours of ischemia. There was 21% +/- 4% necrosis after 4 hours and 51% +/- 8% after 5 hours of ischemic stress when assessed at 48 hours. In conclusion, the degree of adenine nucleotide degeneration as determined primarily by the length of the ischemic period, may be the most important determinant of the ultimate extent of skeletal muscle ischemic necrosis that results from an acute interruption of circulation.

Management of upper extremity central venous obstruction using interventional radiology.

Upper extremity central vein stenosis/occlusion is responsible for significant morbidity. The objective of this report is to review our management using interventional radiological techniques and to determine the long-term clinical results. All radiological interventions for central vein stenosis/occlusion (n = 59) between July 1991 and July 1996 at our institution were reviewed. The interventions consisted of thrombolytic therapy alone in 10 cases, PTA in 40 cases (combined with initial thrombolytic therapy in 6 cases), and deployment of a venous stent in 9 cases. At follow-up, the cumulative success (patency and relief of symptoms) was determined (Kaplan-Meier method). The involved vein was the subclavian, axillary, or innominate (SUB-AX-INN) in 45 cases and the superior vena cava (SVC) in 14 cases. The etiology was secondary to an indwelling foreign body (catheter, pacemaker lead) in 53 cases (90%), and spontaneous in only 6 cases (10%). The average follow-up after intervention was 17.2 months, with a cumulative success of 70 +/- 7.5% at 2 years, with rapid decline thereafter. Analysis of the failure quantiles revealed that 25% failed by 17 months, 50% failed by 26.6 months, and 75% failed by 33.8 months. There were no subgroup differences (log-rank test) for stenosis versus occlusion (p = 0.526), SUB-AX-INN versus SVC (p = 0.744), or if the intervention was begun < 5 days versus > or =5 days after symptom onset (p = 0.240), or whether or not a stent was deployed (p = 0.893). Interventional radiological techniques should be considered when symptoms from upper extremity central vein stenosis/occlusion are severe and disabling, or when veno-access or maintenance of patency of an ipsilateral arteriovenous (A-V) access is necessary. These results suggest an acceptable short-to medium-term solution.

The impact of multiple organ dysfunction on mortality following ruptured abdominal aortic aneurysm repair.

The in-hospital mortality for a patient with a ruptured abdominal aortic aneurysm (RAAA) ranges from 30% to 70% and remains unchanged despite aggressive surgical, anesthetic, and intensive-care management. The purpose of this investigation is to determine the relationship between the development of organ dysfunction and mortality in ruptured AAA patients. Eighty-eight consecutive patients admitted to the Toronto Hospital for repair of RAAAs were studied. APACHE II and multiple organ dysfunction (MOD) scores were calculated for all patients. The MOD scoring system measures daily alterations in the function of six key organs, with increased dysfunction indicated by an increasing score. The overall 30-day mortality rate was 40%; 10% of patient deaths occurred intraoperatively. ICU mortality was bimodal; 11.5% deaths occurred within the first 48 hours compared to 18.2% after 48 hours (late deaths). The APACHE II score was significantly higher in those who died within 48 hours of ICU admission (28.5 +/- 6.36) compared to both those who died late (17.2 +/- 5.7, p < 0.0001) and survivors (11.2 +/- 4.2, p < 0.0001). The survivors' daily mean MOD scores did not increase significantly, while the MOD scores for late deaths increased progressively (p < 0.01). The renal and hepatic dysfunction components of the MOD score were significantly lower in the survivors compared to late deaths (p < 0.001), however the respiratory MOD score did not differ between the groups (p > 0.05). The change in MOD (delta MOD) score over the intensive care stay was significantly greater in late deaths compared to survivors (p < 0.01). The rates of infection were similar in both groups and were not responsible for mortality. We conclude that mortality is better predicted following RAAA by the development of renal and hepatic dysfunction rather than by initial physiologic derangement measured by the APACHE II score.

Salvage of skeletal muscle with free radical scavengers.

Extensive skeletal muscle necrosis may occur after prolonged ischemia to the lower extremity, with serious consequences both locally and systemically. The extent of necrosis is a combination of cellular damage that occurs during both the period of ischemia and the period of reperfusion. The purpose of this study was to reduce the extent of reperfusion-induced muscle necrosis by therapeutic interventions administered only during the initial period of reperfusion. Indeed, the pretreatment of patients who have an acute arterial occlusion is rarely possible and only interventions applicable to the reperfusion phase would be clinically relevant. By perfusing the isolated gracilis muscle in a controlled manner with reduced oxygen concentrations alone and in combination with free radical scavengers, we were able to reduce the extent of muscle necrosis. By means of controlled oxygen delivery alone, muscle necrosis was reduced from 87% +/- 8% in the control muscle to 67% +/- 9% (p less than 0.05) in the treated muscle. The combination of reduced oxygen delivery and free radical scavengers reduced necrosis from 78% +/- 8% in the control muscle to 53% +/- 7% (p less than 0.01) on the experimental side. We conclude that controlled oxygen delivery and free radical scavengers can reduce skeletal muscle necrosis occurring after prolonged normothermic ischemia.

Can Hypertensive Patients Tell When Their Blood Pressure is Elevated? A Cross-Sectional Study of 104 Patients.

A study was undertaken to see if a group of patients could estimate their blood pressure (BP). One hundred and thirteen hypertensive patients were asked whether they could tell when their BP was high, and if so, how. Patients were also asked to give a categorical and a numerical estimate of their current BP. We found that patients did not appear to be able to predict their BP any more accurately than they could be expected to by chance. Patients who predicted correctly, and those who were incorrect, used the same symptoms to predict elevated BP. These were headache, a feeling of warmth, nervousness, dizziness, and pounding heart.