Surgeons and nephrologists share the management of patients with chronic renal failure, acute renal failure, and structural disease of the urinary tract. The presence of pre-existing chronic renal disease requires modifications to the management of patients undergoing surgery and this is discussed first. Acute renal failure is a dreaded complication of surgery: although dialysis and haemofiltration allow many patients to survive with recovery, the mortality rate remains high. Prevention and management of acute renal failure will be discussed in the second part of this section.

As the safety of surgery increases and the indications for particular procedures widen, surgery is being undertaken in a greater number of older patients and in those with pre-existing illnesses. Surgeons will therefore be operating on patients with pre-existing chronic renal impairment, for conditions unrelated to their renal failure, and performing procedures related to the provision of and complications of renal treatment (e.g. vascular access operations, parathyroid surgery, renal transplantation).

Modification of pre- and postoperative management will depend on the severity of renal failure, which is best assessed by measurement of the glomerular filtration rate. This can easily be measured by the urinary creatinine clearance before elective surgery is undertaken, but in more urgent situations this opportunity may not arise. In this circumstance, the serum creatinine is the best guide to renal function, but reference to age, sex, and body mass (which determine muscle mass and creatinine production rate) is essential in relating serum creatinine level to the adequacy of renal function. An estimate of the glomerular filtration rate (GFR) is provided by the formula: Equation 19

A value of serum creatinine at the upper limit of the ‘normal range’ (150 &mgr;mol/l) would reflect a creatinine clearance of 75 ml/min in a young male weighing 80 kg, but only 18 ml/min in an elderly female weighing 40 kg. Clearly, the implications of a further decline of 5 to 10 ml/min, which might easily arise during apparently uncomplicated surgery, will be quite different in the two patients.

The preoperative examination should include particular attention to the state of hydration: patients with renal disease have a limited capacity to regulate their salt and water excretion and are therefore particularly liable to imbalances in either direction. Clinical signs may, however, be more difficult to interpret. Tachycardia may be obscured by &bgr;-blockade and an acute reduction in systemic blood pressure may have simply brought a previously high blood pressure into the normal range. Useful signs of severe intravascular depletion are cool extremities, peripheral cyanosis, and a postural fall in blood pressure: in very sick patients this may be manifest simply by sitting the patient with their legs over the side of the bed. The jugular venous pressure will be low unless there is coincident myocardial or pericardial disease. Severe overhydration will usually be manifest, as in patients with normal renal function, by a raised jugular venous pressure, and signs of peripheral or pulmonary oedema. Pulmonary oedema is particularly serious, since in those with severe renal failure even large doses of diuretics may not be effective. In such patients, and in any maintenance dialysis patient with pulmonary oedema, emergency dialysis or haemofiltration will be required. In young patients with good cardiovascular function, overhydration is less easily detected and may be manifest as resistant hypertension without significant oedema.

Attention should be directed to the detection and assessment of cardiovascular disease, since severe coronary and hypertensive heart disease is common in patients with renal disease. Coronary disease may be present in young adults, particularly those with renal failure from diabetic glomerulosclerosis in whom myocardial infarction is sometimes painless. Hypertension is associated with all forms of renal disease, although the prevalence varies and increases with the severity of renal failure. About 80 per cent of patients with end-stage renal disease require antihypertensive treatment. The pathogenesis is poorly understood, but in severe renal failure, sodium retention is an important factor. When this is controlled by dialysis, the number of patients requiring antihypertensive treatment can be reduced to about 20 per cent.

Antihypertensive treatment should be maintained during surgery, unless intercurrent illness has produced severe hypotension. This is particularly important with drugs such as clonidine or &bgr;-blockers, the abrupt withdrawal of which may cause rebound phenomena. Hypertension is associated with increased anaesthetic risk and since there is evidence that treatment, particularly with &bgr;-blockers, reduces the incidence of arrhythmias and myocardial ischaemia under anaesthesia, elective surgery is usually deferred when elevated blood pressure is found unexpectedly in the preoperative assessment. It is important, however, to be sure that unexpectedly raised blood pressure in patients with closely monitored renal disease is not simply a manifestation of anxiety. In dialysis patients, unexpected hypertension may be due to fluid overload, which will require removal by dialysis. It is again important to be sure of this diagnosis since removal of excessive fluid by dialysis prior to surgery will increase the risk of dangerous intraoperative hypotension.

When assessing patients on maintenance dialysis much can be learnt from the dialysis records. For instance, in patients with limited cardiac reserve, fluid losses and vasodilation during haemodialysis may provide sudden and severe hypotension, a problem which may also be manifest during anaesthesia. Records of such problems during haemodialysis may forewarn the surgeon and anaesthetist. In addition, dialysis records should indicate pre- and postdialysis weights and blood pressures, which will be of importance in assessing preoperative fluid balance.

Clinical examination and history should usually be supplemented by simple investigations which include a full blood count, measurement of serum creatinine and electrolytes, electrocardiogram, and a chest radiograph. A full blood count will be important in assessing the need for pre- or perioperative transfusions (see below). In acutely ill patients comparison with previous values may indicate serious blood or other fluid loss.

The use of serum creatinine in the estimation of renal function has been described. This is a less satisfactory guide to the adequacy of dialysis since the characteristics of dialysis membranes differ from those of the glomerular filter. For instance, in patients maintained by continuous ambulatory peritoneal dialysis a serum creatinine level above 1200 &mgr;mol/l can often be tolerated well, while such levels in a haemodialysis patient would usually indicate inadequate dialysis. Of much greater importance is measurement of the serum potassium: the risk of cardiotoxicity is very high when this rises above 7 mmol/l, and the level which is acceptable preoperatively will depend on whether the patient has renal function or is dialysis dependent, and on the type of surgery planned. For instance, minor surgery in patients with moderate chronic renal failure could proceed if the serum potassium is less than 6 mmol/l whereas in the dialysis patient undergoing major surgery a preoperative serum potassium of less than 4.5 mmol/l should be the aim.

The electrocardiogram may reveal the presence of hypertensive or ischaemic heart disease: the detection of acute ischaemia and arrhythmias is particularly important. The chest radiograph will show the cardiac diameter. A sudden increase in diameter reflects serious overhydration, but may also indicate acute pericardial or myocardial disease. Pulmonary oedema requires prompt treatment.

Analysis of arterial gases will be helpful in selected patients. In the presence of severe anaemia, arterial hypoxaemia is difficult to detect clinically and is also more serious. Patients with acute surgical pathology and severe renal disease will often have an important metabolic acidosis with respiratory compensation. In this situation, sudden and often inadvertent changes in respiration, consequent on sedation, anaesthesia, or analgesia, may cause large changes in arterial pH and consequently the plasma potassium.

Modifications of anaesthetic technique and drug prescription will depend on the severity of renal failure, the presence or absence of disease in other organs, and the type of surgery. In the main these issues are dealt with elsewhere, but certain simple principles should be understood by all involved in the care of the patient.

The use of forearm veins for intravenous infusions may damage potential sites for vascular access, and this is a very serious consideration in any patient who is, or may become dependent on dialysis for life support. It is particularly important to avoid damage to the cephalic venous system. Intravenous infusions should be sited in veins outside the forearm or on the ulnar side of the hand.

Delayed gastric emptying is common in patients with serious renal disease, particularly when renal disease complicates diabetes and severe autonomic neuropathy is present. Premedication with agents such as metoclopramide may be helpful in reducing the risk of gastric aspiration. Most renal patients are all too aware of the increased risk they face during intercurrent illness and anxiolytic drugs such as benzadiazepines will often be helpful. These may be given orally as increased bleeding times in haemodialysis patients are a relative contraindication to intramuscular agents. Opiate analgesia should be used with care (see below).

If substantial fluid loss is expected, particularly in patients with known cardiovascular instability, central venous pressure should be monitored. Blood pressure is best monitored using an automated sphygmomanometer: intra-arterial monitoring is rarely required, but if it is considered essential, the dorsalis pedis artery is the site of first choice in order to avoid damage to vessels which may be required later for creation of vascular access. Where anaemia and cardiorespiratory disease coexist, the use of pulse oximetry to ensure maintenance of optimal blood oxygenation will be helpful.

Anaesthesia may result in sudden hypotension requiring resuscitation with intravenous fluid or even pressor agents. Care must be taken to avoid overhydration, particularly in haemodialysis patients in whom preservation of renal function is not an issue, and excess fluid will require dialysis or haemofiltration for removal. The risk of hypotension is also present during spinal and epidural analgesia, and in these circumstances it may be even more difficult to control. Even in patients without renal disease, renal blood flow is usually reduced and autoregulation is impaired under surgical anaesthesia. A variety of renal vasoconstrictor mechanisms contribute to this, including activation of the sympathetic nervous system and the renin-angiotensin system. An important defence is provided by the vasodilatory action of renal prostaglandins (I&sub2; and E&sub2;). In patients with significant renal disease this mechanism assumes greater importance and prostaglandin synthetase inhibitors should not be used in the perioperative period.

The most serious, and potentially fatal immediate postoperative complication is respiratory depression. With the use of modern muscle relaxants such as atracurium, which are rapidly cleared by mechanisms independent of renal function, the problem of recurarization due to the action of muscle relaxants outlasting their antagonist should not, in theory, occur. Nevertheless, respiratory depression, and even respiratory arrest is a very important, and rather unpredictable risk after major surgery in patients with severe renal failure. Prolonged and excessive action of sedative and analgesic drugs, and impaired gas exchange arising from undiagnosed pulmonary oedema, may contribute.

The action of most opiate analgesics is prolonged in renal failure. This is particularly striking in the case of morphine and probably arises from retention of active metabolites such as morphine 6-glucuronide. Potentially fatal respiratory depression may also unpredictably complicate the use of relatively modest doses of supposedly milder agents such as dihydrocodeine and dextropropoxyphene. Probably the most predictable agent is pethidine, although retention of the pethidine metabolite, norpethidine, has been reported to account for symptoms of neuromuscular excitability. Facilities for the continuous observation of these patients in the first 2 h after surgery are therefore essential.

Patients with chronic renal failure but otherwise good health generally maintain sodium and water balance until the glomerular filtration rate is reduced very severely (below approximately 10 ml/min). This is achieved by a corresponding large increase in the proportion of the filtered sodium and water which is excreted. Similarly, to produce a given change in excretion of sodium and water at low glomerular filtration rate requires a magnification of the tubular response: for instance, a response which is effected by kidneys with a glomerular filtration rate of 120 ml/min from a change in fractional excretion of sodium from 0.5 to 3 per cent, will require a change from 5 to 30 per cent, if the filtration rate is only 12 ml/min. It is therefore not surprising that one of the earliest effects of chronic renal disease is a limitation in the power of the kidney to compensate for changes in sodium and water intake.

In healthy individuals with a normal solute intake, water excretion can be varied from approximately 20 ml to 1500 ml/h; in renal disease this range is reduced in both directions. The reduction in capacity for water excretion will, in most cases, be very much greater than the reduction in glomerular filtration rate, since during surgery other factors such as non-osmotic ADH release impair water excretion. Many patients with severe renal disease will be at risk of water intoxication from commonly prescribed postoperative regimens which include 2 to 3 litres of 5 per cent dextrose/day. Since the precise limitations of renal compensation are difficult to predict, the problem can only be avoided by strict attention to fluid balance, corroborated by daily weighing of the patient.

In some surgical situations, such as the relief of urinary obstruction, and after renal transplantation, massive diuresis and natriuresis may be encountered. In these patients, it may be necessary to adjust the rate of intravenous replacement on an hourly basis, and also to adjust the sodium concentration of the replacement fluid regularly in the light of urinary sodium concentration.

In dialysis patients without residual renal function, great care is required to maintain fluid and electrolyte balance. Patients should be dialysed prior to surgery, but because of increased arrhythmias and haemodynamic instability immediately after dialysis, where possible, an interval of a few hours should be allowed before induction of anaesthesia. Avoidance of hyperkalaemia is of paramount importance, and can sometimes be difficult, even in patients with only mild renal disease. In general, as with sodium and water, although potassium balance is maintained in chronic renal disease, capacity for excretion is severely limited. This may be particularly serious in diabetic patients, who are liable to develop hyporeninaemic hypoaldosteronism which further reduces potassium excretion. In patients with significant renal disease, potassium supplements and potassium-sparing diuretic agents should only be used when serum potassium is low or declining.

In dialysis patients serum potassium should be measured before dialysis is terminated and should be reduced below 4.5 mmol/l. In dialysis patients known to have difficulty in maintaining potassium balance, provision for increased preoperative dialysis should be made and a calcium resonium enema should be given prior to surgery.

Patients with severe renal failure are almost invariably anaemic, but severe anaemia in patients presenting for surgery should be less frequent now that recombinant erythropoietin is available. Anaemia is usually well tolerated, except in patients with coexisting ischaemic heart disease, and major surgery, such as for renal transplantation, is feasible in many patients with haemoglobin levels as low as approximately 6 g/dl. Nevertheless, a higher preoperative haemoglobin level, in the range 8 to 10 g/dl, will provide a greater safety margin in the event of haemorrhage and itself reduces the bleeding time. Blood should be cross-matched for any procedure during which a brisk haemorrhage is possible and, if the surgical indication is not immediate, consideration should be given to preoperative transfusion, particularly in patients with cardiac disease. Patients with renal failure have a bleeding diathesis, which is in part a consequence of abnormal platelet function. Such patients are liable to ooze from incisions and particularly careful attention to surgical haemostasis is required. Medically the problem can be limited by ensuring that the patients are well dialysed, transfused to haemoglobin levels of 8 to 10 g/dl preoperatively, and that heparin used during dialysis has been cleared or reversed. The administration of platelets is not effective but there are measures that can be applied in patients who are at particular risk of bleeding or who continue to ooze after surgery. Cryoprecipitate produces a temporary improvement in bleeding time. The synthetic vasopression analogue l-deamino 8- d-arginine vasopression (0.3 &mgr;g/kg IV) is effective for about 48 h. Conjugated oestrogens provide an improvement in bleeding time which lasts up to 14 days.

Special care must be taken with the use of all drugs, not only because their elimination may be slowed and their bioavailability altered in patients with renal failure, but also because they may directly or indirectly reduce residual renal function. Before prescribing it is prudent to ask whether these considerations apply and, if they do, whether prescription is essential, whether there is an alternative drug, and whether the dose needs to be modified. A list of commonly used drugs that may adversely affect renal function is given in Table 1 94.

Because the elimination of many drugs is dependent on renal function, the dose and frequency of administration must be changed in patients with renal failure (Table 2) 95. In a patient receiving maintenance dialysis the mode of dialysis also has an important effect: for example, haemodialysis removes gentamicin from the circulation very rapidly so that it should be administered at the end of dialysis, following which high levels will persist in the plasma until the next treatment. In contrast peritoneal dialysis will remove gentamicin continuously at a low rate.

Acute renal failure following surgery may be defined operationally as ‘a reduction in renal function sufficient to cause clinical problems’ to distinguish it from the very much more common occurrence of acute renal functional impairment, often recognized simply by a rise in the plasma creatinine concentration. A reduction in excretory capacity may occur on a background of pre-existing chronic renal functional impairment, when it is referred to as ‘acute on chronic renal failure’. In this situation a relatively minor reduction in renal function can cause clinically important problems.

The annual incidence of severe acute renal failure requiring dialysis is 30 to 60/million population/year, but less than half of these cases have a surgical cause. In addition, five to ten times as many patients develop transient renal impairment, which can be managed without recourse to dialysis, but which requires careful attention to water and electrolyte balance.

In Oxford, between 1988 and 1990, 190 patients with acute renal failure were referred for renal support and of these 39 per cent had a surgical cause (Table 3) 96. This compares with the 32-year experience of the General Infirmary at Leeds where 1347 patients were treated between 1956 and 1988. In 638 (47.4 per cent) of these the acute renal failure arose from surgical conditions (Table 4) 97. These figures are typical of Western civilian practice, except that in the United States of America trauma is a more common cause of surgical acute renal failure than in the United Kingdom.

Prospective audit of surgical practice has defined circumstances associated with a particularly high risk of acute renal failure. There is, for example, a 20 per cent incidence of acute renal failure following abdominal aortic aneurysm rupture compared to only 3 per cent following elective repair. About 10 per cent of patients undergoing hepatobiliary surgery develop renal impairment but only 3 per cent require renal support. Two other high risk situations are acute pancreatitis and extensive burns: about 20 per cent of patients with greater than 15 per cent burns and 4 per cent of those with acute pancreatitis develop acute renal failure, and in both circumstances the mortality rate is high.

The causes of acute renal failure are generally classified according to whether they act at prerenal, renal or postrenal sites (Table 5) 98.

Prerenal failure arises in an otherwise healthy kidney as a simple consequence of hypoperfusion. The low perfusion pressure may be confined to the kidney, as with bilateral renal artery stenoses (Fig. 1) 72 or stenosis of the artery to a single functioning kidney, but hypoperfusion is more often systemic and in surgical practice most commonly arises from hypovolaemia or sepsis.

Postrenal causes are those of obstruction to urine flow. For obstruction to cause acute renal failure it must either be bilateral or affect a single functioning kidney. Bilateral ureteric obstruction is most often caused by retroperitoneal fibrosis, retroperitoneal lymphoma (Fig. 2) 73, or malignant disease invading the base of the bladder. Bladder outflow obstruction is usually a result of prostatic disease or urethral stricture. Renal stones and sloughed papillae cause acute on chronic renal failure when they obstruct the only or better functioning of two kidneys.

Acute renal failure arising from intrinsic damage to the kidney is commonly due to ‘acute tubular necrosis’. Definition is difficult since the pathogenesis in man is poorly understood, but this form of renal disease is generally associated with a severe haemodynamic disturbance or nephrotoxic exposure; acute renal failure is presumed to arise from tubular damage. The term ‘necrosis’ is widely used but inaccurate, since frank necrosis of tubular cells is not usually striking when tissue is examined histologically.

In most clinical settings, the risk of acute tubular necrosis is rather unpredictable: a particular reduction of systemic blood pressure, or loss of intravascular volume cannot be precisely related to the risk of acute renal failure. Following exposure to potential nephrotoxins such as aminoglycoside antibiotics, haem proteins and radiographic contrast media, the risk of acute renal failure is usually low, not clearly dose dependent, and more obviously related to the coincidence of other potentially damaging influences. Many of the agents commonly listed as causing acute tubular necrosis might therefore more accurately be termed risk factors. Risk will also depend on the patient's underlying condition (Table 6) 99: those with conditions such as heart failure, chronic liver disease, obstructive jaundice, chronic hypertension, or diabetes, in which there are pre-existing abnormalities of renal haemodynamics will be at greater risk from a particular insult. The type of surgery is also important: operations or conditions associated with sepsis or severe tissue injury (for instance after trauma, burns, or major vascular occlusion) are associated with an increased risk of acute tubular necrosis.

Patients with acute renal failure caused by glomerular or interstitial disease usually present to physicians but may be referred to urologists when the striking symptoms are of haematuria or renal pain.

Since the kidney has a high resting blood flow, a low arterial–venous oxygen difference, and good autoregulatory capability it is not immediately clear why it should be susceptible to hypoperfusion injury. Regional disparities in oxygenation are well recognized and may leave certain regions at risk despite high overall blood flow, or renal perfusion may suffer an unusually severe reduction in certain forms of haemodynamic shock. The risk of renal injury is strongly dependent on the type of shock, being high in septicaemic shock and low in simple haemorrhagic shock (e.g. following gastrointestinal haemorrhage). The most severe threat to renal perfusion probably arises from multiple interactions such as activation of vasoconstrictor mechanisms, including the sympathetic nervous system and renin angiotensin system, loss of compensatory vasodilation such as by inhibition of prostaglandin production, and vascular injury itself, which may complicate septicaemia and endotoxaemia.

For some risk factors, a direct nephrotoxic action is clear. These include exposure to heavy metals such as cis-platinum, organic solvents, polyene antibiotics, amphotericin B, and prolonged administration of aminoglycoside antibiotics. Other precipitating factors such as myoglobin, haemoglobin,and radiographic contrast media have a clear association with acute renal failure, but renal injury is by no means invariable, and the mechanism of damage is not yet adequately explained.

Several mechanisms have been proposed to explain the near complete loss of renal function associated with acute tubular necrosis (Table 7) 100. Tubular injury may prevent function directly, either by luminal blockage or by permitting back leakage of filtrate; or filtration itself may be reduced, either primarily, or secondary to feedback signals arising from impaired tubular transport or raised luminal pressures. Since these mechanisms may all operate at different times or may coincide and interact, it has been impossible to obtain a simple unifying explanation, even for the relatively simple animal models of acute renal failure.

The most immediate consequence of an abrupt loss of renal function is, of course, retention of the waste products of metabolism. The rate of accumulation is dependent not only on the severity of renal failure but on the rate of production. Increased catabolism is observed postoperatively and is particularly severe in patients with sepsis, burns, or trauma. Acute renal failure in this setting is marked by particularly rapid rises in urea, creatinine, urate, phosphate, acidaemia, and most importantly potassium. Massive muscle injury, which is not always traumatic, and may for instance complicate sepsis, ischaemia, prolonged coma, unusually strenuous exercise, or alcoholic intoxication, will lead to the particularly rapid onset of dangerous hyperkalaemia, hypocalcaemia, and hyperphosphataemia.

Acute renal failure is usually detected by a rise in the plasma creatinine or urea concentrations, or as a fall in urine output. Normal urine output alone can be falsely reassuring since many patients with acute renal failure are not oliguric; it is essential to monitor urea and creatinine in any patient at risk of developing postoperative renal failure.

Essential early diagnostic steps are the exclusion of urinary obstruction, the exclusion or treatment of prerenal failure, and the detection of pre-existing chronic renal disease. In each case assessment of the clinical history is vital. Urethral obstruction should be excluded immediately by palpation of the bladder.

The risk of ureteral obstruction depends on the underlying pathology, being increased following pelvic or retroperitonal surgery for malignant pathologies, or in the presence of a single kidney. It may lead to renal pain or to the classical pattern of alternating polyuria and oliguria. Ultrasound examination is the key investigation and will detect almost all cases, with occasional failures when the investigation is performed early after acute obstruction or when the urinary system is encased with malignant tissue.

The possibility of prerenal failure should be apparent from clinical examination. Although systemic blood pressure will not always be low in a supine patient there will generally be evidence of impaired circulation, such as cool extremities and postural hypotension. If external fluid losses are not apparent, the possibility of fluid sequestration, sepsis, or cardiac dysfunction must be considered. The diagnosis of prerenal failure is made by restoration of renal function when the haemodynamic problem is corrected.

The type of replacement fluid (blood, colloid, or crystalloid) should ideally reflect what has been lost. In circumstances where this is not clinically apparent or where blood is not available immediately, circulatory resuscitation should be commenced with isotonic crystalloid or colloid solutions. Controversy still surrounds the arguments for and against crystalloid or colloid solutions and in most circumstances either is acceptable. Colloid solutions are more expensive and have the potential to cause anaphylactoid reactions, but they are confined, at least partially, to the vascular compartment for a short period of time and can increase plasma oncotic pressure. Although the action on Starling forces may be slight and short-lived it may be significant in patients with coincident lung or cardiac disease who are on the verge of developing pulmonary oedema. Our practice is to use isotonic crystalloid solution in most circumstances and reserve the use of colloid solutions for resuscitation of shocked patients and those in whom intravascular depletion is combined with interstitial oedema. Colloid solutions are either albumin-containing preparations such as plasma protein fraction or carbohydrate polymer solutions such as Haemacel. Because of rapid availability and freedom from vasodilatory effects sometimes seen with plasma protein fraction, Haemacel is very suitable while blood becomes available, and up to 1500 ml may be infused. Some concern has been raised by the reporting of acute renal failure apparently occurring as a consequence of dextran infusions. The risk is small and may not be present with all carbohydrate polymers, but it is wise to use plasma protein fraction if large volumes of colloid replacement are to be given.

The aim of correcting the deficit as precisely and rapidly as possible is best achieved by administering fluid rapidly, but in relatively small aliquots: about 250 to 500 ml should be administered over approximately 30 min, and central venous pressure should be measured accurately after each aliquot of fluid. As vascular capacitance is filled this will remain low, but it will rise rapidly once repletion is achieved, and 250 ml aliquots of fluid are appropriate once any shift has been discerned. In some situations, such as severe haemorrhage, venoconstriction will be important. This will relax as volume replacement proceeds and may lead to a further fall in central venous pressure, which requires differentiation from continued fluid loss. If renal function does not immediately improve great care must be taken to avoid overhydration. Once volume replacement is achieved it is common to give an intravenous dose of either mannitol (10–20 g) or frusemide (40–80 mg) to promote a diuresis. This manoeuvre is justified on several grounds. First it provides reassuring evidence that renal perfusion has been re-established somewhat sooner than might otherwise be the case. Secondly, these agents might actually reduce the risk of acute tubular necrosis (see below). If in a volume-replete patient these manoeuvres do not induce a diuresis of at least 40 ml in the following hour then ‘acute tubular necrosis’ has probably become established.

Much is made of the importance of urinary electrolyte measurements in the assessment of the oliguric patient. Classically, in prerenal failure, tubular function should be intact and is reflected by a urine specific gravity of above 1.030 and an osmolality greater than 400 mosmol/kg H&sub2;O, a urine to plasma urea ratio above 7, and a fractional excretion of sodium of less than 1 per cent. The distinction is often blurred by diuretic therapy and pre-existing renal disease, and is not a great help in management. The over-riding concern is to achieve prompt and precise correction of the haemodynamic problem, something which will often require a period of continuous bedside medical attendance.

The possibility or pre-existing renal failure should have been excluded in the preoperative assessment but if not may be suspected from a history of renal disease or hypertension, unexplained anaemia, or if reduced kidney size is demonstrated by ultrasonography. If these exclusions are made, renal failure develops postoperatively in a situation of recognized risk, and the urine deposit is not very cellular, a presumptive diagnosis of acute tubular necrosis can be made. In other situations, for instance if renal failure is found on admission, diagnostic assessment of the full range of renal diseases will be required. History should involve careful enquiry about drug or toxin exposure. Examination should include a search for cutaneous signs of vasculitis and microscopic examination of fresh urine looking for red cells, red cell casts, white cells, and bacteria.

Renal failure is often recognized rather late, presenting the clinician with the need to treat dangerous hyperkalaemia immediately and assess the need for urgent dialysis. The risk from hyperkalaemia is of sudden arrhythmic death; early electrocardiographic abnormalities are increased ‘T’ wave amplitude, while later, ominous changes are broadening of the QRS complex, and flattening and eventual disappearance of the P wave. Eventually, the electrocardiogram comes to resemble a sine wave and cardiac standstill follows. Treatment is required urgently if the serum potassium is above 8 mmol or there are electrocardiographic changes (Fig. 3) 74.

The immediate management is intravenous administration of calcium. Calcium gluconate (10 ml of 10 per cent) should be given over 1 to 2 min and repeated until the electrocardiogram improves. Additional measures should be undertaken to reduce the serum potassium. In patients without serious fluid overload, hypertonic sodium bicarbonate (4.2 per cent) may be given intravenously in a dose of 50 mmol (100 ml). Entry of potassium into cells is promoted by correction of acidosis and also by the hypertonic sodium. Serum potassium may also be reduced acutely by insulin, which promotes cellular entry by stimulation of Na, K-ATPase. To prevent hypoglycaemia, glucose is given concurrently, a typical regimen being 50 g glucose intravenously with 15 units soluble insulin. Monitoring is required to detect hypoglycaemia in unconscious patients and if this cannot be provided (e.g. during a transfer) it is safer, in non-diabetic patients, to omit insulin and rely on the endogenous insulin response to glucose infusion. Following control of hyperkalaemia by these measures, provision for urgent dialysis should be made unless renal function has been restored.

Fluid overload manifesting as pulmonary oedema is also an immediate indication for ultrafiltration using a dialysis machine, haemofiltration, or peritoneal dialysis (see below). A marked metabolic acidosis should be treated with sodium bicarbonate only if there is hyperkalaemia or cardiogenic shock. This will have only temporary benefit and is not a substitute for dialysis or measures to improve tissue perfusion.

Since many treatments when applied before the insult are effective in ameliorating or preventing acute renal failure in experimental models, it might be expected that prophylactic measures would be important in surgery. However, since many of the measures, such as use of vasodilators, may exacerbate hypotension they are difficult or dangerous to apply in clinical practice. Prophylactic administration of dopamine, mannitol, or frusemide, coupled with intravenous fluid sufficient to maintain or even expand the plasma volume, will almost certainly reduce the incidence of acute renal failure after high-risk procedures such as aortic surgery and surgery in jaundiced patients. Of these measures, the most important is maintenance of blood volume. The use of prophylactic mannitol is also established practice in aortic surgery, a suitable regimen consisting of infusion of 10 g as a hypertonic 20 per cent solution after induction of anaesthesia followed by infusion at a rate of 10 g/h during the procedure.

In patients with established acute tubular necrosis such measures can usually increase the urine output moderately, but there is no evidence that they lessen the severity or duration of renal failure or that they improve survival. However, when renal failure is first detected it is difficult to know whether any reversible element exists. In this situation it is usual to attempt to improve renal perfusion and urine flow by the intravenous administration of dopamine (1–2 &mgr;g/kg.min) and frusemide (5–10 mg/min) for 1 to 2 h. Whilst there is no certain evidence of efficacy, there is little short-term risk associated with these procedures.

Apart from the control of fluid and electrolyte balance a number of measures have become part of the routine management of patients with acute renal failure and are based on common sense, and knowledge of the causes of death and morbidity, rather than on the results of rigorous clinical trials.

The first is the prevention and prompt treatment of infection. To avoid nosocomial infection the number of intravascular catheters should be kept to a minimum and there should be a low threshold for changing these. Bladder catheters should either be removed or connected to a closed drainage system. Samples should be examined frequently for bacteria and Candida. Fever should be promptly investigated. Antibiotic treatment will often be required before microbiological identification of the pathogen is available. The usual sites of sepsis are surgical wounds, the abdominal cavity, the lungs, central venous catheters, and the urinary tract. Surgeons should have a low threshold for re-exploring the abdomen in patients who have developed renal failure following abdominal surgery or penetrating injury since in these seriously ill patients clinical signs and imaging are too insensitive to detect residual sepsis.

The second general measure is the maintenance of adequate nutrition. This is more difficult in patients with renal failure, but with attention to fluid balance it is usually possible to provide both sufficient calories and sufficient nitrogen. The nutritional requirements will depend on the degree of catabolism. Depending on the method of renal replacement being used, adjustments in the potassium, phosphate, and sodium concentrations of parental nutrition solutions will be required. Gastro-intestinal haemorrhage was a common cause of death but is seldom fatal today, perhaps because anticoagulation is minimized and the prescription of H&sub2;-receptor antagonists or cytoprotective agents is routine. Most patients with surgical acute renal failure have received broad-spectrum antibiotics and therefore are at risk of developing Clostridium difficile toxin-related colitis. Stools should be tested regularly for the toxin, and prompt treatment with oral metronidazole or vancomycin should be instituted.

Finally it should again be emphasized that the metabolism and excretion of many drugs is altered in renal failure. Each prescription should be checked to determine whether dose modifications are required (see Table 2 95).

Peritoneal dialysis via a rigid catheter inserted percutaneously or by surgical implantation of a soft catheter is still widely used for the treatment of acute renal failure as it is inexpensive and can be instituted without recourse to specialized equipment. Continuous peritoneal dialysis has three possible advantages over haemodialysis: a lower risk of exacerbating bleeding because heparinization is not required, less cardiovascular instability, and a lower risk of disequilibration. In practice these problems can be minimized or overcome with modern haemodialysis techniques. Peritoneal dialysis requires an intact peritoneum, a watertight abdomen, and a safely inserted dialysis catheter. It also needs a significant amount of nursing supervision. Other potential problems include difficulties in maintaining dialysate flow, peritoneal infection, protein losses, limited efficacy in hypercatabolic patients and, when a rigid catheter is used, immobilization of the patient. The choice of peritoneal dialysis is often made for practical reasons such as lack of haemodialysis equipment, but it is the treatment of choice in infants. It should not be used in hypercatabolic patients or those with any past or recent intra-abdominal pathology, because adhesions make catheter placement hazardous.

Intermittent haemodialysis is the orthodox treatment for acute renal failure and it is the most practical way to treat mobile patients. Access to the vascular system is either via catheters placed in central veins or by the use of an arteriovenous shunt. Treatment should be started before complications make it urgent. The first dialysis treatment is generally short, lasting 2 to 3 h. Depending on whether the patient is severely catabolic, subsequent treatments will need to be undertaken daily or on alternate days, aiming to keep the pretreatment blood urea below 33 mmol/l and to avoid fluid overload. In patients with an unstable cardiovascular system bicarbonate-buffered dialysate is used in preference to acetate. The dialysis treatment is used as an opportunity to administer blood transfusions, allowing the extra fluid to be removed by ultrafiltration.

The risk of bleeding can be minimized if low doses of heparin are used, and if necessary this can be reversed at the end of dialysis by the administration of protamine sulphate. There is some evidence to suggest that the use of low molecular weight heparin reduces the risk of bleeding, and this is used in some units for patients requiring dialysis in the early postoperative period. Heparin requirements can be further reduced by the use of prostacyclin to inhibit platelet function. The drug is short-lived and is given as an infusion immediately before, and during, the dialysis treatment. In most regimens prostacyclin does not replace heparin, but is used in combination with a reduced dose. The disadvantages are expense and hypotension. If a patient is actively bleeding when dialysis is required, dialysis can even be performed without heparin, provided the lines have been primed with heparin-containing saline and the blood flow is maintained over 200 ml/min.

The particular limitation of intermittent haemodialysis is the need to establish fluid balance for a 24- to 48-h period during a 3- to 4-h treatment. Thus to control fluid balance ultrafiltration has to be rapid, risking hypotension, cardiac ischaemia, and arrhythmias. Haemodialysis treatment also needs to be frequent to avoid rapid and large changes in the concentrations of plasma urea and other molecules which may generate transcellular osmotic gradients leading to ‘disequilibration’; a syndrome which probably arises from the rapid entry of water into the brain cells and which leads to coma and fits. Another disadvantage of haemodialysis is the sequestration of white cells which occurs in the lungs as a result of complement activation at the dialysis membrane. Although this sequestration is short-lived it can aggravate hypoxia.

These limitations of intermittent haemodialysis stimulated the development of the continuous treatments, which are particularly applicable to the immobilized patient with multiple system failure being managed in the intensive care or high dependency unit. The advantages of these forms of treatment are that they can be used in patients with low systolic blood pressures and provide continuous metabolic control and fluid balance with very little perturbation to the cardiovascular system. This means that there are no constraints on the administration of parenteral nutrition, blood products, and drugs. A disadvantage is the need for continuous heparinization, but with low doses and removal by the filter this should not lead to dangerous systemic anticoagulation. The treatments can only be safely used if the patient has continuous bedside nursing supervision, is immobile, and is unlikely to dislodge the catheters. The use of these catheters is not without its problems. Arterial catheters can cause limb ischaemia in patients with pre-existing peripheral vascular disease, and damage to the vessel wall can lead to thrombosis, aneurysm formation, and leakage of blood into the retroperitoneal space.

There are a number of forms of continuous renal replacement treatment. The simplest is continuous arteriovenous or venovenous haemofiltration, with continuous replacement of the filtrate with fluid which has the electrolyte composition of plasma but which is buffered with lactate rather than bicarbonate (Fig. 3) 74. Using either a Quinton-Scribner shunt, or femoral vascular catheters, a circuit containing a low pressure filter is established. This allows production of ultrafiltration that can be varied from 2 to 3 l/day to 24 l/day by altering the pressure across the filter and the blood flow. Venovenous circuits require a blood pump: since this introduces the risk of potentially fatal air embolism a venous air trap detector and automatic safety switch is mandatory. Low volume haemofiltration (6 l/day) controls fluid balance and substitutes partially for dialysis but needs to be supplemented by haemodialysis treatments, which can be shorter and less frequent. High volume haemofiltration (in excess of 15 ml/min) makes haemodialysis unnecessary but fluid imbalance can occur very rapidly and scrupulous monitoring is needed. This can be achieved by computerized pumped haemofiltration fluid replacement or by using a simple gravity feed device controlled by a balance system (see Fig. 4 75) which returns fluid in direct proportion to that removed.

Another variation is continuous arteriovenous haemodialysis. The circuit is the same as that for continuous arteriovenous haemofiltration, but a low resistance dialysis filter is used. The blood flow is kept low (less than 100 ml/min) and the negative pressure across the membrane is adjusted to control ultrafiltration. The additional component is the slow pumping of dialysis fluid, countercurrent through the dialysate compartment of the filter. Full equilibration in the dialyser is necessary to provide optimal clearance of nitrogenous waste products (15–20 ml/min). The effluent from the filter consists of dialysate and ultrafiltrate. Since most of the membranes used have a high ultrafiltration capacity, scrupulous attendance to fluid balance on an hourly basis, or by a continuous replacement system is again required.

The survival of patients with acute renal failure following surgery depends largely on the underlying disease. The majority of deaths occur in the first week of acute renal failure, and are due to cardiorespiratory or multisystem failure. Sepsis, gastrointestinal haemorrhage, pancreatitis, liver failure, and cerebral damage also contribute to mortality. Overall survival has almost certainly improved over the three decades since dialysis was introduced, although this has not always been easy to demonstrate. In the Leeds series survival improved from 38.4 per cent in patients treated between 1956 and 1959 to 47.4 per cent in the 1980 to 1988 cohort. This improvement was confined to the older patient group (over 45 years), probably because improvements in postoperative care, antibiotics, parental nutrition, and renal support systems have been balanced by the risks of performing more complex surgery in older and less healthy patients.

Treatment for acute renal failure is usually undertaken in the hope that if the patient survives the kidneys will recover. This is not always the case. Persistent renal failure is sometimes seen after severe shock, where the pathology is usually cortical necrosis. Chronicity is also more likely in the elderly and in those with pre-existing renal impairment. When acute renal failure occurs in certain settings or is associated with particular complications the prognosis is particularly poor (Table 9) 102. There is, however, no proven method of establishing that the prognosis of a patient with acute renal failure is hopeless, so that decisions to discontinue renal support in severely ill patients must be made individually.

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