| Abstract|| |
Renal artery disease is the most common cause for surgically curable form of hypertension. In a small subset of patients with severe aortic disease where the aorta is not suitable for endovascular technique and to provide an arterial inflow, an extra-anatomic renal bypass surgery (EARBS) is an option. Anesthetic management of such procedures has not been described so far in the literature. We retrospectively analyzed the anesthetic techniques used in all patients who underwent EARBS between February 1998 and June 2008 at this institute. We also further analyzed data concerning blood pressure (BP) control and renal function response following surgery as outcome variable measures. A total of 11 patients underwent EARBS during this period. Five received oral clonidine with premedication. During laryngoscopy, esmolol was used in 4 patients, while lignocaine was used in remaining 7 patients. Of 11 patients, 7 showed significant hemodynamic response to laryngoscopy and intubation; among these, one had oral clonidine with premedicant, and 6 received lignocaine just before laryngoscopy. Intravenous vasodilators were used to maintain target BP within 20% of baseline during perioperative period. All patients received renal protective measures. During follow-up, 10% were considered cured, 70% had improved BP response, while 20% failed to show improvement in BP response. Renal functions improved in 54.5%, remain unchanged in 36.5%, and worsened in 9% of patients. Use of clonidine during premedication and esmolol before laryngoscopy were beneficial in attenuating hemodynamic response to laryngoscopy, while use of vasodilators to maintain target BP within 20% of baseline, and routine use of renal protective measures appear to be promising in patients undergoing EARBS.
Keywords: Anesthetic management, extra-anatomic renal bypass surgery, renovascular hypertension
|How to cite this article:|
Kumar B, Sinha PK, Unnikrishnan M. Anesthetic management of patients undergoing extra-anatomic renal bypass surgery for renovascular hypertension. Ann Card Anaesth 2011;14:97-103
|How to cite this URL:|
Kumar B, Sinha PK, Unnikrishnan M. Anesthetic management of patients undergoing extra-anatomic renal bypass surgery for renovascular hypertension. Ann Card Anaesth [serial online] 2011 [cited 2021 Jan 20];14:97-103. Available from: https://www.annals.in/text.asp?2011/14/2/97/81563
| Introduction|| |
Renal artery disease is the most common cause for surgically curable form of hypertension. In the US, experience incidence of renal arterial hypertension is about 3% of hypertensive population.  The high-grade renal arterial disease discovered incidentally can pose no problem for several years. However, at one point, blood pressure (BP) begins to accelerate and does not respond to the addition of several antihypertensive drugs.  The progressive deterioration of renal function is common, if treated non-operatively, and occurs even in the presence of BP control with drugs. The current indications for considering renal revascularization include resistant hypertension, progressive renal insufficiency, circulatory congestion or recurrent flash pulmonary edema, and refractory congestive heart failure with bilateral renal arterial stenosis.  With increased use of endovascular techniques, patients with more extensive and severe aortic atherosclerosis unsuitable for endovascular revascularization are being referred for surgical reconstruction.
Aortorenal bypass is a preferred surgical revascularization technique. However, in a small subset of patients where the aorta is not suitable to provide an inflow source due to severe aortic atherosclerosis, abdominal aortic aneurysm, aortitis, or previous aortic surgery, transposition of visceral arteries may be performed.  Surgical approaches in such cases include hepatorenal, splenorenal, gastroduodenorenal, mesenteriorenal bypass, and iliorenal artery bypass. These extra-anatomic renal bypass surgeries (EARBSs) avoid the need for cross-clamping of the aorta and is technically more straightforward, allowing for shorter, less traumatic procedure with lower blood loss.
These patients carry high operative and anesthesia risk due to high incidence of myocardial disease including left ventricular failure and pulmonary edema, and cerebrovascular disease.  Anesthetic challenge in such cases are due to uncontrolled hypertension despite use of multiple antihypertensive drugs, coexistent multiple end organ damage, viz. cardiovascular, cerebrovascular, peripheral vascular disease, diabetes, hyperlipidemia, and chronic obstructive pulmonary disease. Besides this, preservation of residual kidney function before and after EARBS is of paramount importance. To the best of our knowledge, there is no prospective or retrospective study describing anesthetic management of such procedures.
Therefore, the aim of the study was to carry out a retrospective analysis of the anesthetic techniques used for such cases at our center, with outcome in terms of BP and renal function response following surgery.
| Materials and Methods|| |
All patients who underwent EARBS between February 1998 and June 2008 were retrospectively analyzed. After permission from institute review committee, data were collected after reviewing files from medical record departments. A total of 11 such patients were identified. Indication for EARBS included severe or uncontrolled hypertension with and without renal insufficiency, in patients with significant renal artery stenosis and severely diseased aorta. Exclusion criteria included congenital renal artery hypoplasia and emergency surgery after complication of percutaneous transluminal renal artery angioplasty.
All patients were evaluated clinically and with routine laboratory investigations, including hemogram, hepatic and renal function tests, coagulation profile, electrocardiogram, and chest radiography. Further cardiac evaluation included echocardiography (all patients) and coronary angiogram (6 patients). The severity of aortic and renal artery disease and kidney function were assessed using Duplex scan, selective digital subtraction angiography, computerized tomography angiogram of abdomen, and isotopic renogram. Patients dependent on hemodialysis were preoperatively hemodialyzed within 24 hours of surgery.
Anesthesia technique based on our institution protocol was used in all patients. All received general anesthesia with or without thoracic epidural analgesia. Premedication included oral diazepam 0.15 mg/kg night before and in morning of surgery. All antihypertensive medications except angiotensin-converting enzyme inhibitor (ACEI) were continued until morning of surgery. Additional oral clonidine (0.2 mg) was given 90 minute before surgery in patients not receiving this drug.
All patients, except those with preoperative pulmonary edema, received up to 500 ml i.v. lactated ringer before induction of anesthesia. Thoracic epidural catheter was inserted between T8-12 epidural space under local anesthesia while awake in all, except four dialysis-dependent patients. Anesthesia was induced using fentanyl (2 μg/kg) and propofol (1.5-3 mg/kg) or thiopentone (3-5 mg/kg). Atracurium (0.5 mg/kg) was used to facilitate tracheal intubation. Esmolol and lignocaine were used to attenuate hemodynamic response to laryngoscopy in non-b-blocked and b-blocked patients, respectively. Sodium nitroprusside (SNP) or nitroglycerine (NTG) were used during perioperative period to control high BP (target BP = baseline ± 20%) in cases unresponsive to above measures and deepening of anesthesia. Monitoring included American Society of Anesthesiologist routine monitors, direct BP (typically through radial artery), central venous pressure (through a 7.5 F central line catheter in internal jugular vein), pulmonary artery pressure (in two patients with poor left ventricular function), arterial blood gas analysis, and urine output. Anesthesia maintained with fentanyl, isoflurane, nitrous oxide, and oxygen with or without 0.1% sensorcaine and buprenorphine (5 μg/ml) through epidural catheter. The epidural infusion was titrated to achieve postoperative (PO) pain control till 24 hours postextubation. All patients received mannitol (0.5 g/kg) 30 minutes prior to renal artery clamp. Furosemide (0.25-2 mg/kg) was used to maintain adequate urine output during the procedure. Before cross-clamping the renal artery, intravenous heparin (100-150 IU/kg IV bolus followed by incremental doses of 25 IU/kg every hourly) was administered to maintain activated coagulation time between 250 and 300 seconds. After application of renal artery clamp, renal perfusion solution (ringer's lactate,400 ml; mannitol, 10 g; sodium bicarbonate, 25 ml; heparin, 2500 IU; papaverine, 30 mg chilled to 3° C) was administered using Inahara Pruitt catheter (LeMaitre Vascular Inc., Burlington) for renal protection. None of the patients were extubated in OR as per our departmental policy. Following surgery, all patients were shifted to intensive care unit (ICU). Endotracheal extubation was done after achieving usual extubation criteria.
Anesthetic data recorded include preoperative renal and cardiac function, duration of surgery, renal ischemia time, intraoperative urine output, duration of PO ventilation, ICU and hospital stay, intraoperative or PO complication like arrhythmia, myocardial infarction, pulmonary edema, stroke, progressive renal failure, ileus, pancreatitis, hepatic dysfunction, graft thrombosis, and pneumonia. Hemodynamic response to laryngoscopy and intubation and surgery was also noted. Any increase more than 20% in heart rate and/or BP from baseline value was considered as significant. Renal hypertension was assessed using BP measurements at 8 weeks or more following surgery, according to previously published criteria.  Hypertension was considered cured if the BP was ≤140/90 mmHg without antihypertensive medications and improved if diastolic pressure decreased by ≥15 mmHg at the same or lower doses of medication, or patient became normotensive with antihypertensive medications. Treatment failure was designated to patients who did not qualify for the above categories.
Renal function response following surgery was determined from estimated glomerular filtration rate (eGFR) estimated from serum creatinine measured at 3 weeks or more after surgery.  A 20% or more increase in eGFR or removal from dialysis dependence was considered improved renal function, and 20% or more decrease in eGFR leading to serum creatinine ≥1.5 mg/dl was considered worsened function. All other responses were defined as no change.
Follow-up cardiovascular events, morbidity, and mortality including cause of death was obtained from medical records and/or telephone interviews.
All data are presented as the mean ± standard deviation.
| Result|| |
The demographic data of patients and diseases prevalent at the time of presentation are shown in [Table 1]. Severe uncontrolled hypertension was present in all patients (188 ± 34/109 ± 17 mmHg) with duration of 2 to 18 years (5.5 ± 4.69 years). The mean number of preoperative antihypertensive medications needed was 4 ± 1 including 7 patients on b-blocker (3 on metoprolol, 4 on atenolol). The preoperative ejection fraction ranged from 35 to 79% (58.22 ± 12.60). The preoperative serum creatinine level was 3.71 ± 3.81, with eGFR of 41.05 ± 28.34 ml/min/m 2 . Eight patients had a preoperative serum creatinine ≥1.8 mg/dl and were considered to have ischemic nephropathy. Four patients were dependent on hemodialysis prior to intervention. One of these patients presented with left ventricular failure and pulmonary edema besides acute renal failure (ARF) secondary to ACEI administration.
[Table 2] showed type of operative repair done. Total duration of surgery ranged from 5.5 to 9 hours (7.5 ± 1.0 hours). The renal ischemia time varied from 28 to 64 minutes (47.0 ± 15.8 minutes). The duration of PO mechanical ventilation varied from 4.5 to 216 hours (39.95 ± 64.05 hours). The total duration of ICU stay was 48 to 336 hours (115.45 ± 87.43 hours), while hospital stay ranged from 4 to 20 days (12 ± 4.31 days).
The overall mortality rate was 9% (one developed graft thrombosis and underwent thrombectomy and graft revision, subsequently expired on third PO day following progressive renal failure). Of 10 survived, one developed left lung collapse and ventilator-associated pneumonia requiring prolonged ICU stay. Another developed dialysis catheter-induced subclavian vein thrombosis. One patient of hepatorenal bypass developed PO ileus, who was successfully managed conservatively. None of the survived patients developed PO myocardial infarction, pulmonary edema, stroke, pancreatitis, or clinically overt hepatic dysfunction.
Five patients received oral clonidine (0.2 mg) with premedication. Four received esmolol (100 mg), while remaining 7 received lignocaine (1.5 mg/kg) i.v. bolus prior to laryngoscopy. Significant hemodynamic response to laryngoscopy was observed in 6 patients; all had received lignocaine prior to laryngoscopy, while one also had oral clonidine with premedicant. Significant ST elevation (>1 mm) was observed in two coronary artery disease patients who responded with intravenous NTG. None had sustained intraoperative ischemia or arrhythmia that warranted major intervention. During intraoperative period, NTG (1-3 μg/kg/min) and SNP (0.5-2 μg/kg/min) were used in 3 and 1 patients, respectively, to control severe increase in BP unresponsive to deepening of anesthesia. All except 3 patients required vasodilators (NTG/SNP) in dose of 0.5 to 3 μg/kg/min to control BP during 24 to 48 hours postoperatively.
During follow-up of survived 10 surgical patients, 10% were considered cured, 70% had improved BP, and 20% had failed hypertension response. [Table 3] showed data concerning BP control postoperatively. Antihypertensive needed to control BP postoperatively decreased to 2.4 ± 1.3 from 4 ± 1.
Intraoperative urine output was satisfactory in all, except 4 preoperative dialysis-dependant patients (2 of them passed no urine, while remaining 2 peed only150-170 ml). During PO period, urine output was satisfactory in all, except one patient who died on third PO day following progressive renal failure. Overall significant increase in eGFR was noted in all but one patient (preoperative eGFR, 41.05 ± 28.34 ml/min/m 2 vs PO eGFR, 63.95 ± 23.41 ml/min/m 2 ; P = 0.043). Of all, 54.5% of patients had improved renal function, 36.3% were considered unchanged, and 9% were worsened after surgical repair. All four patients who were dialysis dependent preoperatively became dialysis independent following surgery. Two patients with preoperative normal renal function showed more than 20% decreased in eGFR; however, serum creatinine remained ≤1.5 mg/dl, thus was considered as no change renal function response. Greater proportion of patients with high preoperative serum creatinine had improvement in overall PO renal function [Table 4].
|Table 4: Renal function response after surgery in regards to creatinine level postoperatively (n = 10)|
Click here to view
| Discussion|| |
The most common cause of renovascular disease is atherosclerosis.  Aortoarteritis, particularly diffuse form, is prevalent in India. The prevalence of aortoarteritis is about 4 to 5% of cases of hypertension.  Renovascular hypertension seen in significant number of these patients is often refractory to medical therapy and is an independent predictor of poor long-term survival.  Seven of our patients had aortoarteritis, while 4 had atherosclerotic renovascular disease, suggesting common incidence of aortoarteritis in India. 
Anesthetic management for EARBS is quite challenging. The preoperative evaluation should be aimed at the assessment of the target organ damage. The anesthesia technique should take in consideration the cardiac and cerebrovascular status, the renal dysfunction, antihypertensive drug therapy, and control of hemodynamics. The aim should also include avoidance of dysfunction of organ used to provide inflow to renal artery and preservation of residual kidney function.
Although elective surgery may be acceptable in presence of chronic moderate hypertension, a severe or labile hypertension, especially if symptomatic, must be controlled in preoperative period. The target BP level should be less than 130/80 mmHg for individual with measurable loss of kidney functions.  Most of the patients require complex antihypertensive regimens including ACEI. The survival of patients with renovascular hypertension is better when ACEI are part of therapy than when they are not. , However, major concern in its use for renovascular hypertension is their potential to cause functional ARF.  The risk factors for developing ARF includes global renal ischemia (either bilateral renal artery stenosis or stenosis to a solitary kidney), congestive heart failure, treatment with vasodilators or diuretics, and volume contraction. Adequate volume management with judicious use of diuretics and close monitoring is crucial during chronic treatment with ACEI in these patients. In our study, one patient presented with ACEI-induced ARF and pulmonary edema and required hemodialysis before surgery. With exception of ACEI, we continued all other antihypertensive medication till morning of surgery, since continuing ACEI has shown to be associated with hypotension during induction of anesthesia.  The clonidine use in dose of 0.1 to 0.3 mg preoperatively has been shown to produce dose-related sedation, reduced hemodynamic response to intubation, and marked intraoperative hemodynamic stability.  We used oral clonidine (0.2 mg) with premedicant in 5 patients, none except one showed significant hemodynamic response to intubation and surgery. A single 100 mg intravenous bolus esmolol given before laryngoscopy has been shown to control heart rate and BP without excessive hypotension in hypertensive patients treated with non-b-blocker drug.  Intravenous lignocaine has also been used commonly for this purpose.  We used esmolol and lignocaine for attenuating hemodynamic response to laryngoscopy and intubation and found that lignocaine was not as effective as esmolol. This correlates with previous finding of Miller and Warren.  NTG/SNP was needed during intraoperative and immediate PO period to control BP in some cases. In our knowledge, there is no clear-cut guideline regarding what should be the ideal BP in patients with severe uncontrolled hypertension. However, we feel that over jealous reduction in BP can compromise vital organ perfusion because these organs are used to have this for their perfusion, so we kept target less than 20 to 30% of baseline value. This was also important to maintain adequate perfusion to the organ which provided inflow to the kidney.
Preexisting chronic kidney disease is a strong risk factor for development of ARF. Preservation of residual renal function could be achieved by preventing volume depletion, optimization of hemodynamic status, correction of acid-base disturbance, and avoidance of sepsis and nephrotoxic drugs. The volume depletion and hypotension if persistent can induce renal ischemia and tubular cell apoptosis. Patients with renovascular hypertension have reduced plasma volume, so we administered up to 500 ml of intravenous crystalloid before induction of anesthesia in all, except 4 patients who presented with pulmonary edema, and further fluid therapy was guided by CVP. Among the nephrotoxic agents, nonsteroidal anti-inflammatory drugs (NSAID) cause ARF by inhibiting the synthesis of prostaglandins which act to preserve renal blood flow and GFR in subjects with volume depletion, preexisting renal insufficiency, and congestive heart failure.  We avoided the use of NSAID in perioperative period. Intraoperative as well as PO epidural analgesia was achieved using continuous infusion of sensorcaine fentanyl mixture in all, except 4 dialysis-dependant patients in whom intraoperative fentanyl and PO tramadol were used for analgesia. To date, several pharmacologic maneuvers have been used to prevent or improve ARF, but none has proven their efficacy in human beings. Traditionally, dopamine has been used at low renal dose to improve renal blood flow, but multiple studies have failed to show its renoprotective effect. In contrast, it may exacerbate the severity of renal tubular injury during the early PO period.  Fenoldopam, a selective dopamine receptor (DA1) agonist, has been used in prevention of ARF. However, it did not reduce contrast-induced renal dysfunction in patients with chronic kidney disease.  It causes systemic hypotension which may offset its benefit obtained from improved renal perfusion. Atrial natriuretic peptide (ANP) has shown to reverse ARF and improve renal histopathology in laboratory animals.  However, Anaritide, a 25-aminoacid synthetic form of ANP, did not improve the overall rate of dialysis-free survival in patients with acute tubular necrosis as a result of ischemic and nephrotoxic insults.  We avoided the use of dopamine as a renal protective agent. Fenoldopam and ANP were also not used in many of our patients.
Mannitol confers renal protection by expanding intravascular volume, increasing tubular flow rate by preventing water absorption in the proximal tubule, acting as a free radical scavenger, and by release of intrarenal prostaglandins. Loop diuretics facilitate diuresis by counteracting the increased response of antidiuretic hormone to surgical stress. Also, by inhibition of the Na-K ATPase pump that decreases active tubular sodium chloride transport and tubular oxygen consumption, resulting in resistance against ischemic injury. We used both mannitol and furosemide during perioperative period. In addition, we used chilled renal preservative solution to protect renal parenchyma during period of renal ischemia. The maintenance of renal parenchymal hypothermia during ischemia is most important in renal preservation technique. The warm ischemia time in excess of 30 minutes are associated with increasing degree of loss of excretory function.  Furthermore, more than one hour of warm ischemia is associated with increasing amount of permanent loss of renal function. Although the mean ischemia time in our cases was 47 ± 15 (range, 28-64) minutes, the use of such a chilled perfusates might have extended the period of tolerable ischemia to one hour or so. We strongly believe that this might have contributed to the preservation of renal parenchyma. The renal preservative solution have been used previously for renal parenchymal protection during splenorenal anastomosis with beneficial effect. 
The choice of anesthetic drugs is governed by presence of renal dysfunction. Drugs associated with nephrotoxicity should be avoided, whereas drugs which are largely excreted by kidney might have accumulative effect. Among anesthetic induction agents, etomidate is useful with minimal cardiodepressant effect and pharmacokinetics that is not affected significantly by renal impairment.  Thiopentone is still popular; however, a reduced dose is indicated to prevent undesired cardiodepressant effect because of relative hypovolemia and reduced protein binding. Propofol can be used safely in uremia; however, with the usual induction dose, it may cause marked peripheral vasodilatation. We used either thiopentone or propofol in titrated doses for induction of anesthesia. Among inhalational anesthetics, isoflurane is preferred because it preserves renal blood flow, produces low renal toxicity and only mild cardiodepressive effect.  Isoflurane, desflurane, and halothane produce negligible levels of nephrotoxic inorganic fluoride, and thus are safe. Although sevoflurane metabolism may result in higher fluoride production, it has been found to be safe in uremia.  Enflurane metabolism can result in nephrotoxic level of inorganic fluoride, so its use should be avoided. Morphine and meperidine both produce metabolites which are renally eliminated and potentially neurotoxic, so these agents should be better avoided. Fentanyl is most suitable alternative in these cases. Alfentanil and sufentanil are also suitable agent and dose modification is unnecessary.  Remifentanil undergo rapid inactivation by blood nonspecific esterases; however, the excretion of its principal metabolite is delayed in chronic renal failure, but it does not produce significant opioid effect.  Among muscle relaxants, rocuronium are unlikely to accumulate after intubating and maintenance doses for general anesthesia, but vecuronium infusion in ICU may cause accumulation of active metabolite, 3-decetylevecuronium. Atracurium and cisatracurium undergo spontaneous Hoffman elimination in the blood and are totally independent of renal function for their clearance, thus can be used safely. We used fentanyl, isoflurane, and atracurium in our series.
The overall outcomes following surgery were comparable with previously described series. The efficacy in improving or curing hypertension in this series is 80% which is comparable with the results of Reilly et al.  who reported improvement or cure in 85% of their patients. The reduction in average number of antihypertensive needed during PO period from 4 ± 1 to 2.4 ± 1 in our series were also comparable with decrease from 2.4 to 1.7 in their series.  Geroulakos et al. also showed the decrease in the average number of antihypertensive medications needed from preoperative average of 2.63 to 1.9 (P = 0.001) following EARBS. 
Renal function remained constant or improved in 90% of patients. These results are similar to others that report stable or improved renal function in 69 to 100% patients. , The overall mortality rate was 9% and complication included ventilator-associated pneumonia, subclavian vein thrombosis, and transient ileus in one patient each, all were treated successfully without any sequel. Previous series have reported a transient rise in liver enzyme, without any permanent or major problem with hepatic function following hepatorenal shunt. , None of our patients showed hepatic dysfunction during PO period. This may be attributed to the maintenance of adequate perfusion pressure and avoidance of toxic drug in perioperative period in our series.
To conclude, use of clonidine with premedicant and esmolol before laryngoscopy were beneficial in attenuating hemodynamic response to laryngoscopy, while vasodilators to maintain target BP within 20% of baseline and routine use of renal protective measures appear promising in preserving residual kidney function among patients undergoing EARBS.
| References|| |
|1.||Brest AN, Bower R. Renal arterial hypertension: Incidence, diagnosis and treatment. Amer J Card 1966;17:612-6. |
|2.||Textor SC. Progressive hypertension in a patient with incidental renal artery stenosis. Hypertension 2002;40:595-600. |
|3.||Vesna DG, Stephen CT. Renovascular hypertension and Ischemic nephropathy. Circulation 2005;112:1362-74. |
|4.||Moncure AC, Brewster DC, Darling RC, Atnip RG, Newton WD, Abbott WM. Use of splenic and hepatic arteries for renal revascularization. J Vasc Surg 1986;3:196-203. |
|5.||Pickering TG, Herman L, Devereux RB, Sotelo JE, James GD, Sos TA, et al. Recurrent pulmonary oedema in hypertension due to bilateral renal artery stenosis: Treatment by angioplasty or surgical revascularization. Lancet 1988;2:551-2. |
|6.||Khauli RB, Novick AC, Ziegelbaum M. Splenorenal bypass in the treatment of renal artery stenosis: Experience with sixty-nine cases. J Vasc Surg 1985;2:547-51. |
|7.||Rolin HA, Hall PM, Wei R. Inaccuracy of estimated creatinine clearance for predictors of iothalamate glomerular filtration rate. Am J Kidney Dis 1984;4:48-54. |
|8.||Krijnen P, Van Jaarsveld BC, Steyerberg EW, Man in't Veld AJ, Schalekamp MA, Habbema JD. A clinical prediction rule for renal artery stenosis. Ann Intern Med 1998;129:705-11. |
|9.||Padmavati S, Arora AP, Kasliwal RR. Aortoarteritis in India. J Assoc Phys India 1987;35:442-4. |
|10.||Subramanyan R, Joy J, Balakrishnan KG. Natural history of aortoarteritis (Takayasu's disease). Circulation 1989;80:429-37. |
|11.||Novick AC, Stewart R, Hodge EE, Golfarb D. Use of the thoracic aorta for renal arterial reconstruction. J Vasc Surg1994;19:605-9. |
|12.||Chobanian AV, Bakris GL, Black HR, Cushman WC, Green LA, Izzo JL jr, et al. The seventh report of the Joint Nation Committee on prevention, Detection, Evaluation and Treatment of High Blood Pressure: The JNC Report. JAMA 2003;289:2560-72. |
|13.||Khauli RB, Novick AC, Coseriu CV, Beven EG, Hertzer NR: Superior mesenterorenal bypass for renal revascularization with infrarenal aortic occlusion. J Urol 1985;133:188-90. |
|14.||Losito A, Gaburri M, Errico R, Parente B, Cao PG. Survival of patients with renovascular disease and ACE inhibitor. Clin Nephrol 1999;52:339-43. |
|15.||Hricik DE, Browning PJ, Kopelman R, Madias NE, Dzau VJ. Captopril induced functional renal insufficiency in patients with bilateral renal artery stenosis or renal artery stenosis in a solitary kidney. N Eng J Med 1983;308:373-6. |
|16.||Coriat P, Richer C, Douraki T, Gomez C, Hendric KS, Giudicelli JF, et al. Influence of chronic angiotensin converting enzyme inhibition in anesthetic induction. Anesthesiology 1994;81:299-307. |
|17.||Carabine UA, Wright PMC and Moore J. Preanesthetic medication with clonidine: A dose response study. Br J Anaesth 1991;67:79-83. |
|18.||Sharma S, Mitra S, Grover VK, Kalra R. Esmolol blunts the hemodynamic response to tracheal intubation in treated hypertensive patients. Can J Anesth 1996;43:778-82. |
|19.||Tam S, Chung F, Cambell M. Intravenous lidocaine: Optimum time of injection before tracheal intubation. Anesth Analg 1987;66:1036-8. |
|20.||Miller CD, Warren SJ. IV lignocaine fails to attenuate cardiovascular response to laryngoscopy and tracheal intubation. Br J Anaesth 1990;65:216-9. |
|21.||Feldman, Kinman JL, Berlin JA, Hennessy S, Kimmel SE, Farrar J, et al. Parenteral Ketorolac: The risk of acute renal failure. Ann Intern Med 1997;126:193-9. |
|22.||Woo EB, Tang AT, El-Gamel A, Keevil B, Greenhalgh D, Patric M, et al. Dopamine therapy for patients at risk of renal dysfunction following cardiac surgery: Science or fiction! Eur J Cardiothorac Surg 2002;22:106-11. |
|23.||Stone GW, McCollough PA, Tumlin JA, Lepor NE, Madyoon H, Murray P, et al. CONTRAST Investigators: Fenoldopam mesylate for the prevention of contrast induced nephropathy: A randomized controlled trial. JAMA 2003;290:2284-91. |
|24.||Nakamoto M, Shapiro Jl, Shanley PF, Chan L, Schrier RW. In vitro and in vivo protective effect of atriopeptin III on ischemic acute renal failure. J Clin Invest 1987;80:698-705. |
|25.||Allgren RL, Marbury TC, Rahman SN, Weisberg LS, Fenves AZ, Lafayette RA, et al. Anaritide in acute tubular necrosis: Auriculin Anaritide Acute Renal Failure Study Group. N Eng J Med 1997;336:828-34. |
|26.||Ward JP. Determination of the optimum temperature for regional renal hypothermia during temporary renal ischemia. Br J Urol 1975;479:17-24. |
|27.||Brewster DC, Darling RC. Splenorenal arterial anastomosis for renovascular hypertension. Ann Surg 1979;189:353-8. |
|28.||Giese JL, Stanley TH. Etomidate: A new intravenous anesthetic induction agent. Pharmacotherapy1983;3:251-8. |
|29.||Mazze RI, Cousins MJ, Barr GA. Renal effects and metabolism of isoflurane in man. Anesthesiology 40;1974:536-42. |
|30.||Arthu AA. Renal effects of sevoflurane during condition of possible increased risk. J Clin Anesth 1998;10:531-8. |
|31.||Fyman PN, Reynolds JR, Moser F, Avitable M, Casthely PA, Butt K. Pharmacokinetics of sufentanil in patients undergoing renal transplantation. Can J Anesth 1988;35:312-5. |
|32.||Hoke JF, Shulman D, Dershwitz M, Michalowski P, Malthouse-Difore S, Connors PM, et al. pharmacokinetics and pharmacodynamics of remifentanil in persons with renal failure compare with healthy volunteers. Anesthesiology 1997;87:533-41. |
|33.||Reilly JM, Rubin BG, Thompson RW, Allen BT, Anderson CB, Sicard GA. Long-term effectiveness of extra-anatomic renal artery revascularization. Surgery 1994;116:784-90. |
|34.||Geroulakos G, Wright JG, Tober JC, Anderson L, Smead WL. Use of the splenic and hepatic artery for renal revascularization in patients with atherosclerotic renal artery disease. Ann Vasc Surg 1997;11:85-9. |
|35.||Fichelle JM, Colacchio G, Farkas JC, Tugaye A, Priollet P, Laurian C, et al. Renal revascularization in high risk patients: The role of iliac renal bypass. Ann Vasc Surg 1992;6:403-7. |
|36.||Sicard GA, Valentin LI, Freeman MB, Allen BT, Anderson CB. Renal autotransplantation: An alternative to standard renal revascularization procedures. Surgery 1988;104:624-30. |
|37.||Chibaro EA, Libertino JA, Novick AC. Use of hepatic circulation for revascularization. Ann Surg 1984;199:406-11. |
Prabhat Kumar Sinha
Campbellton Regional Hospital, Campbellton, NB, E3N1R1
Source of Support: None, Conflict of Interest: None
[Table 1], [Table 2], [Table 3], [Table 4]