Perioperative management of patients with chronic kidney disease or ESRD PDF

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Best Practice & Research Clinical Anaesthesiology Vol. 18, No. 1, pp. 129 –144, 2004 doi:10.1016/S1521-6896(03)00067-3, available online at http://www.sciencedirect.com 8 Perioperative management of patients with chronic kidney disease or ESRD Paul M. Palevsky* MD Chief Renal Section, VA Pittsbu...

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Best Practice & Research Clinical Anaesthesiology Vol. 18, No. 1, pp. 129 –144, 2004 doi:10.1016/S1521-6896(03)00067-3, available online at http://www.sciencedirect.com

8 Perioperative management of patients with chronic kidney disease or ESRD Paul M. Palevsky*

MD

Chief Renal Section, VA Pittsburgh Healthcare System Professor of Medicine University of Pittsburgh, School of Medicine, Pittsburgh, PA, USA

The perioperative management of patients with chronic kidney disease (CKD) or dialysisdependent end-stage renal disease (ESRD) is complicated by both the underlying renal dysfunction, with associated disturbances of fluid and electrolyte homeostasis and altered drug clearance, and the presence of associated co-morbid conditions, including diabetes mellitus, chronic hypertension and cardiovascular and cerebrovascular disease. The impact of CKD on fluid and electrolyte management, haematological and cardiovascular complications and drug management in the perioperative period are reviewed. Special issues related to the management of haemodialysis and peritoneal dialysis patients in the perioperative period are also reviewed. Key words: chronic kidney disease; end-stage renal disease; dialysis; haemodialysis; peritoneal dialysis; water-electrolyte imbalance; hyperkalaemia; anaesthesia; opioid analgesics; neuromuscular blocking agents; post-operative complications.

The perioperative management of patients with chronic kidney disease (CKD) or dialysis-dependent end-stage renal disease (ESRD) is complicated by both the underlying renal disease, with associated disturbances of fluid and electrolyte homeostasis and altered drug clearance, and the presence of associated co-morbid conditions, including diabetes mellitus, chronic hypertension and cardiovascular and cerebrovascular disease. The perioperative and anaesthesia management of these patients must therefore take into account the specific changes related to renal dysfunction as well as the increased anaesthesia and operative risks associated with these comorbidities.

STRATIFICATION AND EPIDEMIOLOGY OF CHRONIC KIDNEY DISEASE The National Kidney Foundation –Kidney Disease Outcomes Quality Initiative (NKFK/DOQI), has recently proposed a standardized classification scheme for patients with * Tel.: þ 1-412-688-6000; Fax: þ412-688-6908. E-mail address: [email protected] (P. M. Palevsky). 1521-6896/$ - see front matter Published by Elsevier Ltd.

130 P. M. Palevsky

Table 1. Stages of CKD. Stage

Definition

1 2 3 4 5

GFR GFR GFR GFR GFR

$90 ml/minute/1.73 m2 with evidence of kidney damagea 60–89 ml/minute/1.73 m2 with evidence of kidney damagea 30–59 ml/minute/1.73 m2 15–29 ml/minute/1.73 m2 ,15 ml/minute/1.73 m2 or dialysis-dependent

a

Kidney damage defined as pathological abnormalities or markers of damage, including abnormalities of blood or urine tests or imaging studies.

CKD.1 This classification scheme stratifies CKD into five stages based on estimation of glomerular filtration rate (GFR) and documentation of renal injury (Table 1). All individuals with a GFR of less than 60 ml/minute/1.73 m2 for more than 3 months are classified as having CKD, irrespective of other evidence of kidney damage. Because GFR declines with ageing, other evidence of renal disease, such as pathological or anatomical abnormalities, or markers of kidney damage such as proteinuria or haematuria, must be present to define CKD in patients with a GFR $ 60 ml/minute/1.73 m2. Reductions in GFR below this level represent a loss of more than half of the normal adult renal function and are associated with increased risk of progressive disease and associated co-morbidities. Although serum creatinine is the most widely utilized index of renal function in clinical practice, it is a relatively insensitive marker of renal function. Serum creatinine concentration is a function of both creatinine generation, primarily from muscle creatine metabolism, and renal and extra-renal creatinine excretion. Creatinine generation is proportional to muscle mass and is generally higher in men than in women, and in individuals of African descent as compared to other racial groups. In addition, creatinine generation tends to decline with increasing age and will also be decreased in individuals with muscle wasting or malnutrition. Although creatinine excretion occurs primarily through glomerular filtration, a small percentage of creatinine is normally excreted by renal tubular secretion and in the stool. The percentage of creatinine excretion occurring via these non-glomerular routes increases with impaired renal function. As a consequence of these factors, serum creatinine concentration, particularly in elderly or chronically ill patients may be normal or only minimally elevated despite significant reduction in GFR. In order to improve the assessment of renal function from readily available clinical data, multiple prediction equations to estimate creatinine clearance or GFR have been developed. The two most widely utilized equations are the Cockroft– Gault equation for estimation of creatinine clearance2 and the MDRD study equation for calculation of estimated GFR.1,3,4 These equations are Cockroft –Gault equation

Creatinine clearance ðml=minuteÞ ¼

ð140 2 ageÞ £ weightðkgÞ £ ð0:85 if femaleÞ ð72 £ serum creatinineÞ

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Abbreviated MDRD study equation eGFRðml=minute=1:73 m2 Þ ¼186 £ ðserum creatinineÞ21:154 £ ðageÞ20:203 £ ð0:742 if femaleÞ £ ð1:210 if of African descentÞ Accurate data regarding the prevalence of CKD are not available. Using data from the US Third National Health and Nutrition Examination Survey (NHANES III) it has been estimated that approximately 3% of the adult population in the USA, or 5.3 million patients, have stage 2 CKD as defined by persistent albuminuria and an estimated GFR of 60– 84 ml/minute/1.73 m2.1 An additional 4.7% of the population, or 8.3 million patients, have more advanced renal disease, with a GFR of less than 60 ml/minute.1 In contrast to the paucity of data on the number of patients with early stages of CKD, detailed data are available from the United States Renal Data System (USRDS) on the incidence and prevalence of ESRD.5 In 2000 there were approximately 270 000 ESRD patients receiving chronic dialysis in the USA, with the population of dialysis patients increasing by 3 –5% per year.5 The most common aetiology of renal failure is diabetes mellitus, accounting for over 40% of these patients, with an additional 27% having ESRD as the result of hypertensive renal disease.5 This population is also elderly; 45.6% of chronic dialysis patients are aged 65 or older. The proportion of elderly patients is also increasing, with this age group accounting for 51% of incident patients.5 Based on these epidemiological data it is clear that CKD is a common disease. In addition, given the increased representation of CKD and ESRD in the elderly population, and the high rate of co-morbid conditions, the management of patients with CKD is an important issue for anaesthesiologists.

FLUID AND ELECTROLYTE MANAGEMENT The capacity of the kidneys to maintain the volume and content of the extracellular compartment is normally preserved well into the course of chronic renal insufficiency. In the majority of medically stable patients, extracellular fluid volume and electrolyte composition remain normal until the development of dialysis-dependent end-stage kidney disease.6 This capacity of the failing kidney to maintain volume and electrolyte homeostasis is achieved, however, through adaptive processes which are limited in their capacity to respond to physiological stress. Thus, the patient with chronic renal disease who is well compensated in the pre-morbid state is at high risk for the development of fluid and electrolyte disturbances during the perioperative period. Volume homeostasis The patients with chronic renal insufficiency can usually maintain sodium balance on a fixed sodium intake until end-stage kidney disease is reached.6 – 8 The ability of the chronically injured kidney to respond to extremes of sodium intake or to sudden changes in sodium balance is, however, markedly impaired. Maximal sodium excretion decreases as a function of the decline in GFR.8 – 10 Patients with mild chronic renal insufficiency are generally able to excrete a sodium load and usually do not develop clinical volume overload unless other conditions which independently inhibit renal sodium excretion (e.g. heart failure, cirrhosis or nephrotic

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syndrome) are present.8,9 Volume overload may develop, however, if large volumes of saline solutions are rapidly administered. In advanced chronic renal insufficiency, the ability to excrete even a modest sodium load is impaired and volume overload can rapidly develop following the administration of only modest quantities of enteral or intravenous fluids. The administration of large volumes of intravenous fluids to patients with CKD should be avoided. If volume overload develops, intravenous fluids should be discontinued and diuretic therapy initiated. Diuretics inhibiting sodium transport in the thick ascending limb of the loop of Henle, such as furosemide and bumetanide, are the most effective agents. Sequential nephron blockade using a combination of a loopacting diuretic and oral metolazone or an intravenous thiazide diuretic may significantly increase the diuresis in patients resistant to a loop-acting diuretic alone.11 In patients with ESRD, volume overload may precipitate the need for urgent dialysis. Paradoxically, patients with mild to moderate chronic renal insufficiency are also at increased risk for the development of extracellular fluid volume depletion. The chronically injured kidney maintains sodium balance at the expense of an increased fractional excretion of sodium; when challenged with sudden sodium restriction, maximal sodium conservation cannot be rapidly achieved.8 A sudden decrease in sodium intake or increased extrarenal losses due to diarrhoea, nasogastric suction, vomiting, enterocutaneous fistulas, burns or fever may therefore be associated with relative renal ‘salt-wasting’ and clinically significant volume depletion. This volume depletion may be further exacerbated by the injudicious use of diuretics. Volume depletion in the patient with chronic renal insufficiency is frequently not recognized until significant complications, including pre-renal azotaemia and systemic hypotension, develop. The prescription of intra- and perioperative fluids must therefore take this increased risk for volume depletion into consideration. Sufficient fluids need to be provided to replace obligate renal and extrarenal losses while avoiding volume overload. Central haemodynamic monitoring is frequently necessary to guide fluid management, especially in patients with concomitant cardiac or hepatic dysfunction. Tonicity homeostasis The ability to conserve or excrete free water in CKD is limited and patients are predisposed to the development of disturbances of body fluid tonicity. Although patients with advanced renal insufficiency usually retain the ability to dilute their urine, maximal free water clearance is reduced in proportion to the decrease in GFR.8 – 10 Thus, while a normal individual may have a maximal free water excretion in excess of 20 l per day, a patient with a GFR of 15 ml/minute is limited to a free water excretion of approximately 2 –3 l per day. While this is sufficient to prevent water intoxication and hypotonicity in the medically stable patient, excessive free-water administration to patients with chronic renal insufficiency may result in significant hypotonicity. In contrast, renal concentrating ability is lost relatively early in the course of renal disease, primarily due to impairment of the generation and maintenance of the medullary solute gradient.8 – 10 The inability to elaborate a concentrated urine is not, however, generally associated with the development of hypertonicity as water intake is independently modulated by thirst in response to changes in plasma tonicity. During the perioperative period, when access to water is restricted, the risk of developing hypertonicity is increased.12 Adequate free water must therefore be prescribed to replace insensible, gastrointestinal and renal water losses.

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Intraoperative and perioperative fluid management in the patient with renal insufficiency must therefore take into account the reduced capacity for both water excretion and conservation. Excessive free water administration must be avoided to prevent iatrogenic hypotonicity, while providing sufficient free-water to prevent hypertonicity. Electrolyte status should be monitored frequently and water administration adjusted if hypo- or hypernatraemia ensue. Potassium homeostasis Maintenance of the extracellular potassium concentration is dependent upon both total body potassium balance and on the distribution of potassium between the extracellular and intracellular compartments.13,14 Renal potassium excretion is primarily dependent upon potassium secretion in the collecting duct and is not directly impaired by reductions in GFR. In the absence of disease directly involving the distal nephron or associated with mineralocorticoid deficiency, renal potassium excretion is maintained until late in the course of CKD and hyperkalaemia usually does not ensue until the onset of ESRD.6 The ability to tolerate an acute potassium load is, however, markedly impaired in patients with CKD. During the perioperative period, patients with CKD are therefore susceptible to the development of hyperkalaemia from either exogenous administration of potassium or from sudden shifts of potassium from the intracellular into the extracellular space. Excessive administration of potassium must therefore be avoided, with particular attention paid to the potassium content of intravenous fluids. Routine prescription of potassium-containing fluids, such as lactated Ringer’s solution, should be avoided. Other sources of exogenous potassium administration include blood transfusions and medications administered as potassium salts (e.g. antibiotics). Preservative solutions for kidney transplants and cardioplegia solutions may also provide substantial potassium loads. A variety of renal and systemic diseases are associated with tubular defects in potassium secretion, and predispose to the development of hyperkalaemia at lesser degrees of renal insufficiency. These include systemic lupus erythematosus15, sickle-cell disease16, obstructive uropathy17, chronic interstitial nephritis18 and renal transplantation.19 Mineralocorticoid deficiency may also impair renal potassium excretion in association with a wide variety of diseases, including diabetes mellitus20, chronic interstitial nephritis20, systemic lupus erythematosus21, acquired immune deficiency syndrome22, and sickle-cell disease.20 Inhibitors of aldosterone secretion, such as angiotensin-converting enzyme inhibitors, angiotensin receptor antagonists, betaadrenergic receptor blockers, non-steroidal anti-inflammatory drugs (both nonselective COX-1/COX-2 inhibitors and selective COX-2 inhibitors) and heparin, impair potassium tolerance and may also contribute to the development of hyperkalaemia.13,23,24 The potassium-sparing diuretics amiloride, triamterene and spironolactone inhibit tubular potassium secretion – amiloride and trimethoprim through inhibition of the epithelial sodium channel (ENaC) and spironolactone through antagonism of the intracellular mineralocorticoid receptor.13,24 Trimethoprim also contributes to hyperkalaemia through inhibition of the epithelial sodium channel.25 A combination of mechanisms underlies the hyperkalaemia associated with cyclosporin A and tacrolimus.26,27 Patients with chronic renal insufficiency are also more susceptible to the development of hyperkalaemia from transcellular potassium shifts. Factors that may produce transcellular potassium shifts and precipitate hyperkalaemia include

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hypertonicity (most commonly due to hyperglycaemia), insulin deficiency, betaadrenergic receptor blockade and acidaemia. Of particular concern in perioperative management, the use of intravenous beta-adrenergic receptor blockers for the acute management of hypertension has been associated with the development of severe hyperkalaemia in patients with advanced CKD.28,29 For this reason, these agents, and in particular intravenous labetalol, should be used with great caution in the management of intraoperative and post-operative hypertension in patients with advanced renal failure. The depolarizing muscle relaxant succinylcholine has also been associated with acute hyperkalaemia.30,31 Use of this agent in normal individuals is associated with a transient increase in serum potassium concentration of between 0.5 and 1.0 mmol/l within 3 – 5 minutes and lasting 10 –15 minutes.32 The mechanism for the hyperkalaemia is believed to be related directly to muscle depolarization at the neuromuscular junction. In patients with trauma, burns or neuromuscular disorders, this hyperkalaemic response may be exaggerated. Case reports of severe hyperkalaemia associated with succinylcholine use in patients with CKD has lead to the recommendation that it not be used in this population.30,31 In an extensive review of the literature, however, Thapa and Brull conclude that succinylcholine is not associated with an excess risk of hyperkalaemia in CKD and that its use in patients with advanced renal disease is safe, so long as there is no pre-operative hyperkalaemia, repeated doses are not administered and other conditions that predispose to hyperkalaemia (e.g. trauma, burns, neuromuscular disorders) are not present.31 Acute hyperkalaemia must be promptly treated.33 If cardiac toxicity is present, intravenous calcium should be administered to antagonize the membrane effects of hyperkalaemia, normalizing the associated EKG changes. The use of intravenous calcium has no effect on the serum potassium concentration and must be followed immediately by interventions to shift potassium from the extracellular fluids into the intracellular compartment. Intravenous insulin (accompanied by glucose infusion to prevent hypoglycaemia in non-hyperglycaemic patients), and intravenous or inhaled beta-adrenergic agonists are the most effective agents, with an onset of action within 10 –20 minutes and durations of action of 1 – 2 hours.33 Sodium bicarbonate, which previously had been recommended for the treatment of hyperkalaemia, has now been shown to be a relatively ineffective agent, with little utility in the acute treatment of hyperkalaemia, particularly in ESRD patients.33 – 35 Its use should be reserved for patients with concomitant metabolic acidosis. Decreasing total body potassium is the final step in the treatment of hyperkalaemia. In non-oliguric patients, renal potassium excretion may be enhanced with loop-acting diuretics. Sodium polystyrene sulphonate (Kayexalatew) may be used as an exchange resin in the gastrointestinal tract; when given orally in sufficient sorbitol to promote elimination, each gram binds approximately one millimole of potassium. Although less effective, sodium polystyrene sulphonate may also be administered as a rectal retention enema. If treatment with sodium polystyrene sulphonate is ineffective or cannot be employed due to gastrointestinal disease, acute haemodialysis should be performed. Although continuous renal replacement therapy is highly effective for the control of hyperkalaemia over a course of hours, potassium removal is not sufficiently rapid for this modality to be used for acute treatment. Many patients with advanced CKD or ESRD are chronically hyperkalaemic. The need for pre-operative normalization of serum potassium in these patients has not been rigorously evaluated. Anecdotal experience suggests that these patients are not at significantly increased risk for hyperkalaemic arrhythmias if the serum potassium is

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