CAC - Manejo Perioperatorio Del Paciente Con Falla Renal

7/28/2019 CAC - Manejo Perioperatorio Del Paciente Con Falla Renal

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CHAPTER 2

NICHOLAS L. TILNEY, M.D.JULIAN L. SEIFTER, M.D.ROBERT J. RIZZO, M.D.

Renal Dysfunction

Perioperative Management of the Patient with RenalFailure

Renal failure is defined as a general loss of kidney function with(1) alterations in volume regulation and ionic composition of bodyfluids and (2) inadequate excretion of metabolic wastes. Clinical

manifestations vary depending on the extent and rate of functionaldecline: patients with acutely deteriorating kidneys becomesymptomatic earlier than those who have adapted to progressivechronic renal failure (CRF).1 The three stages of renal dysfunctionare diminished renal reserve (creatinine clearance > 30 ml/min), renal failure(creatinine clearance 10 to 30 ml/min), and uremia (creatinine clearance < 10 ml/min).2

Patients with diminished renal reserve are typically asymptomatic. With the onsetand progression of renal failure, the following may occur: hypertension, anemia,carbohydrate intolerance, hyperuricemia, hypertriglyceridemia, acidosis,hyperphosphatemia, hypocalcemia, and hyponatremia. (Hyperkalemia occursinfrequently at this stage unless myonecrosis or hemolysis is present or the patientreceives a depolarizing muscle relaxant during operation.) Care must be taken in

patients with worsening renal failure to prevent or treat acute surgical stressesforexample, hypotension, infection, or use of nephrotoxic agentsthat may furtherdiminish renal function. Finally, as will be described, virtually every major organsystem is adversely affected in patients with uremia, who often present withmalaise, weakness, nausea, vomiting, weight loss, and edema.3

When evaluating a surgical patient with renal compromise or impending orestablished renal failure, the surgeon should first obtain answers to the followingquestions:

1. What are the extent and rate of progression of renal failure?2. Is renal failure acute or chronic? If acute, to what degree is it reversible? What

contributing factors are present, if any, and how can they be corrected?3. What steps must be taken to prevent further renal injury?

4. What steps must be taken to minimize and manage perioperativecomplications?

Extent and Rate of Progression of Renal Failure


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The seriousness of the patients renal dysfunction may not be apparent fromsymptoms or physical examination. Acute renal failure (ARF) rarely produces thephysical findings of severe chronic uremia, so its extent is best ascertained bylaboratory evaluation.

Several methods are used to assess glomerular and tubular function. The

glomerular filtration rate (GFR) is the most practical measure of renal function. GFRmay be estimated clinically by measuring blood urea nitrogen (BUN), the serumcreatinine concentration, or creatinine clearance. BUN depends on severalvariables, including GFR, the rate of urea production, and the rate of tubularreabsorption of urea. Urea production is increased by extrarenal factors, such asblood in the GI tract, a high-protein diet or intravenous nutrition, and administrationof glucocorticoid hormones, which stimulate gluconeogenesis and protein catabolism.4Furthermore, tubular reabsorption of urea is increased by low urine output andvolume depletion. An elevated BUN should not be equated with a low GFR.

The serum creatinine level is affected by GFR as well as by the rate of productionand tubular secretion of creatinine.5 In contrast to BUN levels, the rate of creatinineproduction is relatively constant in an individual because it depends primarily on

products of muscle breakdown and only minimally on increased protein ingestion.Thus, a muscular male with renal dysfunction may have high serum creatininevalues, whereas a small female with severe renal failure may have only minorelevations. Creatinine production also decreases with age (by 1 ml/min every yearafter 35 years of age6) secondary to diminished muscle mass and in proportion todiminished GFR associated with normal aging; therefore, normal creatinineconcentrations in elderly individuals do not reflect the same GFR as they would inyounger patients. Because the rate of tubular secretion in normal kidneys is alsorelatively constant, it does not interfere with the inverse correlation between theGFR and serum creatinine concentrations. GFR has been estimated for males by thefollowing formula (for females, the calculated value is decreased by 15 percent7):

GFR (ml/min) = (140 - age) weight (kg)/72 serum creatinine

This formula assumes a stable creatinine concentration and thus should not be

used in the setting of ARF, where the creatinine concentration is rising. On the otherhand, estimation of the GFR by measuring creatinine clearance [see II Care in theICU, 6 Acute Renal Failure] does not require a stable creatinine concentration orcorrection for age, but it does require accurate collection of urine. (Normal valuesfor men are from 90 to 130 ml/min; for women, normal values are from 80 to 125ml/min.)8 Because creatinine is secreted preferentially by the renal tubules in renalfailure, estimates of the GFR based on creatinine clearance can be too high by asmuch as 20 percent in normal individuals and by 50 percent when the GFR isreduced to 10 percent of normal.9 In addition, certain conditions increase the serumcreatinine concentration and decrease creatinine clearance without altering GFR.10

For example, ketones11 and some cephalosporins12 produce spuriously elevatedvalues for serum creatinine by interfering with its assay, and cimetidine13 andtrimethoprim-sulfamethoxazole14 inhibit the tubular secretion of creatinine.

Several isotopic methods, including measurement of iodine-125iothalamateclearance, are available for precise measurement of GFR.


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Classification of Renal Failure and Correction of ReversibleFactors

ACUTE RENAL FAILURE

Potentially reversible acute renal failure may be categorized asprerenal, postrenal, or intrarenal in origin [see Table 1].15

Prerenal factors decrease renal perfusion; they include volumedepletion, cardiac failure, systemic vasodilatation, and renovascularobstructive disease. The patient typically presents with oliguria,tachycardia, and hypotension (except for the patient withrenovascular disease, who is typically hypertensive). The urinary sediment isunremarkable, and urine osmolality is high. An isolated urine sample with a sodiumconcentration of less than 10 mEq/L indicates good tubular function and suggests a

prerenal mechanism for the renal dysfunction.The fractional excretion of sodium (FENa) provides a good assessment of prerenal

states; it is often low (less than one percent) because of sodium and waterconservation by the kidneys [see II Care in the ICU, 6 Acute Renal Failure].16 Aspot urine sample rather than a timed collection may be employed to determine FENa.Measurements of pulmonary arterial wedge pressure, cardiac output, and systemicvascular resistance also assist in the diagnosis of ARF17 and indicate the direction ofsubsequent therapy. Correction of prerenal conditions should be aggressive toprevent ischemic renal injury. A special circumstance occurs in the setting ofvolume depletion or renal arterial stenosis when angiotensin-converting enzyme(ACE) inhibitors or angiotensin II antagonists are used. Reversible oliguria andazotemia develop because of a fall in glomerular pressure that follows dilatation of

the efferent arterioles. This development reflects failure of normal autoregulatoryfunction; volume repletion and discontinuance of the drug are required forresolution.

Postrenal factors are typically caused by mechanical complications and are usuallysecondary to urinary tract obstruction or extravasation. Bladder catheterization willrelieve or rule out urethral or bladder outlet obstruction. Ultrasonography is most helpfulin documenting upper urinary tract obstruction, which may be relieved acutely byretrograde cystoscopy or percutaneous means. Urinary extravasation, as in a patientwith a ruptured bladder, is associated with hematuria and may be assessed by meansof intravenous or retrograde pyelography or CT scans. It should be noted that theradiopaque dyes used for contrast studies are not without potential hazards.Intravenous urography contrast agents may cause renal failure in patients with

multiple myeloma or diabetes mellitus as well as in those with other renal diseases.If ARF persists even after prerenal and postrenal factors have been excluded or

corrected, the presence of intrarenal disease must be considered [see Table 1].Differentiation between acute and chronic causes of intrarenal failure may require athorough clinical evaluation [see Table 2].3 The causes of acute intrarenal failuremay be categorized according to the site of the primary parenchymalabnormalitytubules, glomeruli, vessels, interstitium, papillae, or cortex.15

1. The most common cause of ARF in surgical patients is acute tubular necrosis(ATN) from systemic infection, ischemia, or exposure to nephrotoxins18; patients


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with ATN are rarely hypertensive. The urine sediment classically shows pigmented,

granular casts; heme pigment may reflect ATN from hemoglobinuria caused by atransfusion reaction or from myoglobinuria caused by a crush injury or muscleischemia.19 In rhabdomyolysis, serum creatine phosphokinase levels are elevated.20Nonsteroidal anti-inflammatory agents are a common cause of renal failure,particularly in dehydrated patients.

2. Acute glomerulonephritis often follows systemic infection or collagen vasculardisease and is associated with hematuria, proteinuria, hypocomplementemia, andhypertension.

3. Vasculitides involving glomeruli present in much the same way as acuteglomerulonephritis, but serum complement levels are normal. Other signs ofsystemic diseases may be present. A test for antineutrophil cytoplasmic antibodiesshould be performed.

4. The urine sediment in interstitial nephritis from medication allergy orpyelonephritis may contain eosinophils and mononuclear leukocytes.

5. Acute papillary necrosis may be precipitated by analgesic abuse, diabetes, orurinary tract infection or obstruction; sloughed papillae may lodge in the ureter,creating painful obstruction.21

6. Acute cortical necrosis is particularly likely to occur in an obstetric patient as aconsequence of profound shock and disseminated intravascular coagulation after acomplicated labor and delivery.22

7. Atheroembolic disease is an important cause of subacute renal failure in patientswho have undergone vascular procedures or have received anticoagulants.

Most patients with ARF are oliguric, producing urine volumes of less than 400ml/day, although nonoliguric (high-output) renal failure is not uncommon and is

characteristic of aminoglycoside-related ATN.23 Complete anuria suggests bilateralrenal artery occlusion, obstructive uropathy, cortical necrosis, or rapidly progressiveglomerulonephritis. Severe disease or obstruction of a single kidney and inadvertentureteral ligation during a difficult retroperitoneal surgical dissection should be ruledout as causes of acute anuria.CHRONIC RENAL FAILURE

Irreversible, progressive CRF has many possible causes, includingglomerulonephritis, hypertensive nephrosclerosis, diabetic nephropathy,tubulointerstitial disease, obstructive uropathy, chronic pyelonephritis, polycystickidney disease, and congenital hypoplasia.24 Consequently, the differential diagnosis

requires a complete clinical evaluation [see Table 2].3 The history should recordsymptoms of urinary tract dysfunction, systemic diseases that could affect thekidneys, exposure to nephrotoxins or infectious agents, and family history of renaldisease. The physical exam should evaluate blood pressure, the retinas, thecardiovascular system, and the kidneysincluding the presence or absence of renalartery bruits. Urine volume is not usually helpful in evaluating CRF. Many patientscontinue to excrete urine, at least until dialysis is begun. Broad casts that aregranular and waxy are often seen in the urine sediment, reflecting compensatoryhypertrophy of surviving nephrons.


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1. Maintenance of an alkaline urine to diminish free heme pigment, which can bedirectly toxic to tubular cells (a urine pH > 6 usually discourages dissociation of hemefrom hemoglobin or myoglobin32).2. Avoidance of nephrotoxins, with levels of potentially nephrotoxic agents(e.g., aminoglycoside antibiotics) carefully maintained in the nontoxic range.

3. Adequate hydration before33 and during surgical exposure to protect against thenephrotoxicity of contrast agents, aminoglycosides, antineoplastic agents, hemepigment, and hypercalcemia.344. Smaller doses of medications for elderly patients, whose GFR is lower given the

same serum creatinine level.355. Aggressive treatment of urinary tract infections and other factors that may causedeterioration of kidney function.34

6. Dietary protein restriction, which may slow the progression of renal failure bydecreasing glomerular hyperfiltration.36,37

Perioperative Complications of Renal Failure

Both elective and emergency operations can be performed inpatients with renal failure, provided that physiologic homeostasis isreestablished by judicious and aggressive perioperative dialysis.38,39Dialysis particularly improves abnormalities of hemostasis that arecaused largely by platelet dysfunction40; however, anticoagulants

and antiplatelet medications that are used to maintain patency ofarteriovenous fistulae may also contribute to excessive bleeding[see Discussion, Hematologic System, below]. In addition, heparinmay still be active in patients undergoing operation soon after hemodialysis, andheparin rebound may occur because of the shorter action of protamine in relation toheparin.41 Abnormal prothrombin times are correctable by means of fresh frozenplasma or vitamin K, although such measures are usually unnecessary; in fact,angioaccess devices commonly thrombose after operation. Attention tointraoperative hemostasis and technique is also important for a successful outcome.

For the uremic patient, whose host defense mechanisms are often altered ordepressed,42 broad-spectrum antibiotics should be administered perioperatively toprevent infection.43 In patients receiving long-term steroid therapy, coverage with

stress steroids may be required [see 9 Adrenal Insufficiency].PREOPERATIVE CONSIDERATIONS IN ELECTIVE SURGERY

Preoperative preparation of the stable renal failure patient for elective surgery isroutine. For the unstable patient, however, preoperative dialysis should be performedto correct volume overload; requirements depend on the severity of renal failure andthe potential extent of the operative procedure.1 Patients on long-term maintenancedialysis are usually dialyzed the day before and the day after operation, most often


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against a low-potassium bath in anticipation of the increased intraoperative releaseof potassium that occurs secondary to muscle relaxant administration,44 tissuemanipulation and breakdown, and blood transfusions.1 Patients in whom acute renalfailure develops require earlier and more aggressive dialysis, particularly if they arehypercatabolic.3

Indications for dialysis before elective surgery are less clear in patients with

compromised renal function who do not yet require maintenance dialysis.1Conservative correction of fluid, electrolyte, and metabolic abnormalities usuallysuffices unless the condition necessitating operation could possibly increasecatabolism and the potential for uremic complications. Asymptomatic patients whohave a normal physical examination and reasonable blood chemistries usually do notrequire preoperative dialysis, but this prophylactic treatment should be employed atthe first sign of need.

PREOPERATIVE CONSIDERATIONS IN EMERGENCY SURGERY

If dialysis cannot be performed preoperatively, evidence of hyperkalemia shouldprompt aggressive treatment by other methods.1 Aggressive measures are especiallynecessary in hypercatabolic patients who have suffered trauma or severe burns,because these patients may experience a rapid elevation of serum potassium levels.In these patients, prompt initiation of aggressive dialysis may be lifesaving. Inaddition, administration of calcium may be necessary. Calcium (5 to 10 ml of 10percent calcium chloride solution I.V. over a two-minute period) directly antagonizesthe cardioplegic effects of hyperkalemia and allows time for instituting less dramaticmeasures:

1. Sodium bicarbonate (44 mEq I.V. over a five-minute period), glucose (250 ml of20 percent dextrose), and insulin (10 to 25 U I.V. over a 30-minute period) all driveextracellular potassium into cells.2. Sodium polystyrene sulfonate (Kayexalate), a potassium-binding ion exchangeresin, can be given orally every three to four hours in doses of 25 to 50 gadministered with 100 ml of 20 percent sorbitol to decrease constipation.(Given alone, Kayexalate can cause extensive colonic concretions that may bedifficult to remove. For this reason, Kayexalate and aluminum-containing phosphatebinders should not be given simultaneously.) Alternatively, 50 g of Kayexalate with50 g of sorbitol in 200 ml of water can be given every one to two hours as aretention enema; however, this treatment should be avoided in the immediate

postoperative period because of the potential hazard of colonic necrosis.45

Preoperative correction of other renal failure abnormalities can be done moreleisurely. Excess intravascular fluid can be removed by plasmapheresis, packed redblood cells can be used to correct anemia and to establish some hematologicreserve, and sodium bicarbonate can be given to correct acidosis as well as toreduce hyperkalemia1provided that volume status will allow the sodium load.

ANESTHETIC CONSIDERATIONS


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drains, and skin or retention sutures but aggressive in treating suspected surgicalcomplications.1

Protein malnutrition impairs both wound healing and immunity. Nutritional supportwith a diet high in carbohydrates and essential amino acids (or their alphaketoanalogues) has been shown to limit protein catabolism without eliciting uremicsymptoms.37 Endogenous urea may be used as a source of nonessential amino acids

for protein synthesis.52 In undernourished patients, protein-containing nutrition shouldnot be withheld to maintain a low BUN. It is better to provide nitrogen via aminoacids and then to dialyze if necessary. Techniques for continuous renal replacementtherapy are now available. These procedures (e.g., continuous arteriovenous andvenovenous hemodialysis) are particularly useful in hypercatabolic patients in theICU, who require large volumes of replacement fluid and intravenous nutrients.

Drug dosages should be modified in renal failure patients. Consideration should begiven to the absence of renal excretion and the possible dialytic removal ofmedications.53 Consideration should also be given to the potential systemic toxicity ofmedications. For example, meperidine should not be given to patients with renalfailure because of the possibility of serious neurologic sequelae.

Discussion

Pathophysiological Mechanisms in Renal Failure

The pathophysiological mechanisms in renal failure include the progression ofkidney disease and the effects of the uremic syndrome on metabolism and the majorbody systems. The general pathophysiology of renal failure has been thoroughly

reviewed elsewhere [see II Care in the ICU, 6 Acute Renal Failure].PROGRESSION OF KIDNEY DISEASE

The progression of kidney disease is related to underlying aggravating factors,which may include dehydration, infection, obstruction, poorly controlled hypertension,and intrarenal deposition of crystals.54 In addition, the processes of adaptation mayactually induce further damage. Progressive glomerulosclerosis may develop in thenormal nephrons that remain after surgical removal of large amounts of kidneytissue.55 Both the rate of progression of injury and the magnitude of the glomerularhemodynamic changes in the remaining nephrons correlate directly with theproportion of tissue removed. Moderate dietary protein restriction may blunt

adaptive hyperperfusion and hyperfiltration of the kidney remnants, thus limitingfurther glomerular injury.56

Treatment with ACE inhibitors, which decrease arteriolar and glomerular capillarypressures, also limits glomerular injury in patients with diabetic and nondiabetic renaldisease.57THE UREMIC SYNDROME

The uremic syndrome is a clinical state resulting from loss of renal function;


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regulation of body fluid volume and ionic composition, excretion of endogenous andexogenous metabolic wastes, and participation in endocrine metabolic processes aresubsequently impaired. The resulting adverse effects hamper a range of intracellularand systemic body processes.

The Effects of Uremia on Major Organ Systems

Although severe uremia can impair the function of most major body systems, the

most obvious and profound effects seldom occur today because of prompt andaggressive treatment. These effects must be considered, however, when patientswith CRF are evaluated for surgery.

Cardiovascular system Cardiovascular complications are responsible for morethan half of the deaths in patients with chronic renal disease,58 primarily because ofthe frequency of severe atherosclerosis in this population.59,60 Cardiac hypertrophy iscommon, often occurring secondary to hypertension. Deposition of calcium andoxalate crystals may cause decreased myocardial function, leading to congestive

heart failure, arrhythmias, and, sometimes, sudden death.61Potential myocardial toxins include phenol,62 parathyroid hormone, and cobalt.63

Large arteriovenous fistulas used for dialysis access may also contribute tohigh-output myocardial failure.64 Improvement of myocardial function with dialysishas been correlated specifically with increased plasma levels of calcium.65

Pericarditis may present as chest pain, fever, pericardial friction rub, or acutecardiovascular collapse; hypotension, jugular venous distention, and pulsus paradoxusmay appear during dialysis secondary to hemopericardium and pericardialtamponade. Constrictive pericarditis also may result in circulatory instability.66 The

etiology of uremic pericarditis is unknown, but it may be a response to uremic toxins,fluid overload, or infection.67

Pericardial effusion can be diagnosed by ultrasonography, tamponade byequalization of atrial pressures, and constrictive pericarditis by angiography andcatheterization.68 Aggressive dialysis is indicated for uremic patients withpericarditis, and fluid balance must be carefully managed. Acute tamponade orenlarging effusions call for drainage, and constrictive pericarditis may necessitatepericardiectomy.69

Pulmonary system Abnormal pulmonary function in renal failure patients isassociated with anemia, fluid overload, and the direct effects of toxins on pulmonarytissue.70 In the uremic lung, increased densities in the perihilar and inner lung zonesform a butterfly appearance on x-ray.71 As pulmonary vascular permeability

increases,72 pulmonary edema may occur with relatively low pulmonary arterialpressures.73,74

In uremic pneumonitis, membranes formed within alveoli and fibrin deposited inthe interstitium eventually give rise to interstitial fibrosis.75 Restrictive pulmonaryinsufficiency may occur secondary to diffuse pulmonary calcification.76 Fibrinouspleuritis, which may also cause a restrictive defect, responds to dialysis andthoracentesis; only rarely is surgical decortication required.77

Gastrointestinal system Severe uremia may alter the entire GI tract fromnasopharynx to rectum because urea diffuses into the lumen and is converted to


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individuals; in anemic patients with normal renal function, however, serumerythropoietin levels may be markedly increased and therefore are not useful forpredicting the response to exogenous erythropoietin.

Blood losses from the GI tract, menstruation, multiple laboratory determinations, oreven dialysis itself can also contribute to anemia. It has been estimated that theaverage dialysis patient loses about 2.5 L of blood a year, and this figure does not

includeoccasional large losses caused by rupture of the dialysis coil, bleeding from accessdevices, or surgical procedures.90Patients with uremia also have increased bleeding tendencies, even though theirprothrombin times, partial thromboplastin times, and platelet counts are usuallynormal.91 Heparin anticoagulation during dialysis, combined with abnormal plateletfunction, may predispose the patient to epistaxis, hemopericardium, intracranialhemorrhage, retroperitoneal bleeding, and other complications.92-94 Subduralhematoma may mimic dialysis dysequilibrium syndrome.

The most important clotting defect in uremiaone that correlates directly with theseverity of renal failureinvolves platelet dysfunction, which is measured asdecreased release of platelet factor 3 and diminished platelet aggregation and

adhesiveness and which is believed to be related to the presence ofguanidinosuccinic acid, a dialyzable toxin in uremic plasma.95 Phenolic acid, cyclicadenosine triphosphate (cATP), hypermagnesemia, and elevated prostacyclin levelsmay be toxic to platelets; peritoneal dialysis markedly inhibits these adverseeffects.

On the other hand, the nephrotic syndrome (usually associated with membranousglomerulonephritis in patients who are not yet in end-stage renal failure) has been

associated with a hypercoagulable state that may produce renal vein thrombosis;antithrombin III deficiency may become significant when the serum albumin levelhas fallen to less than 2 mg/dl.96,97 Anticoagulation may be necessary to preventthrombosis, but the condition may be resistant to heparin. Hemodialysis may inducea transient thrombocytopenia through contact activation on dialyzer membranes, butantiplatelet agents such as short-acting prostacyclins can block this effect.

Operative blood loss secondary to platelet dysfunction is rare if the patient is welldialyzed.98 However, the use of heparin during dialysis and the extended use ofcoumadin or antiplatelet drugs to maintain the patency of dialysis accesses maypotentiate intraoperative blood loss. In addition, even if heparinization is regionalduring the preoperative dialysis, heparin rebound may occur during operation.99Therefore, the surgeon must be aware of the type and the degree of preoperative

anticoagulation. The effects of heparin can generally be reversed intraoperatively bythe intravenous infusion of protamine; the prothrombin times of patients on long-termcoumadin regimens can be normalized by the administration of vitamin K. Moreurgent reversal can be accomplished with fresh frozen plasma. Occasionally, bloodloss is excessive even when such coagulation defects have been reversed,particularly with retroperitoneal dissection for procedures on the abdominal aorta orthe iliac arteries. The surgeon must also be aware of the increased likelihood ofclotting of the arteriovenous fistula postoperatively.

Treatment of anemia in patients with end-stage renal disease should include iron


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replacement if iron stores are depleted, as determined by measuring transferrin ironsaturation (a value of < 20 percent signals depletion). Until the 1990s, blood transfusionswere the mainstay of therapy. Since then, however, recombinant erythropoietin hascome to play a prominent role. The availability of recombinant human erythropoietinconstitutes a tremendous advance in the care of patients with end-stage renal disease.The drug largely eliminates the need for transfusions, thereby not only improving the

anemia but also avoiding the acute and chronic hazards of transfusion (viral infectionand iron overload).100,101 Recombinant human erythropoietin also corrects clottingchanges.100,101 Indeed, most patients who are now receiving erythropoietin havenormal bleeding times. The drug has other benefits as well, including increasedenergy level, greater exercise tolerance, and improved overall well-being.

The most effective approach to uremic bleeding is prevention by means ofadequate dialysis. Regional heparinization may be used with good results; patientscome to surgery after dialysis with their clotting ability reasonably intact.Cryoprecipitate, conjugated estrogens, and 1-desamino-8-D-arginine vasopressin(DDAVP) may be administered postoperatively as needed to correct bleedingdisorders; conjugated estrogens may take several days to influence bleeding times.102In most cases, however, none of these measures are necessary if dialysis is

adequate.Immune system Alteration of leukocyte and immunologic function in renal failure

patients is thought to contribute to their increased susceptibility to infection.43Neutrophil counts are usually normal but may decrease transiently afterhemodialysis because of leukocyte sequestration in pulmonary capillaries, possibly

related to complement activation.103 Chemotaxis of granulocytes and phagocytes isalso depressed, both by inhibitors in uremic serum104 and by an intrinsic cell defect,105

and it is worsened by hemodialysis (although less so by peritoneal dialysis).Transplantation restores depressed chemotaxis.105,106

In some patients, lymphocytopenia with impaired cellular immunity develops.107 Tcell function is depressed by uremic serum but improved by dialysis.108 Bcellmediated antibody response to some stimuli may also be attenuated,109 althoughserum immunoglobulin levels are not always decreased110 and response to vaccinesis usually normal.111

Musculoskeletal system Myopathy in renal failure may be secondary tomalnutrition,112 hyperparathyroidism,113 abnormal vitamin D metabolism,114 oraluminum accumulation115; correction requires 1,25-dihydroxyvitamin D3administration,116 aluminum chelation,115 or renal transplantation. Uremic bursitismay be a result of generalized serositis.117 The olecranon bursa of the access arm

has an increased predilection for bursitis from prolonged pressure on the bed orchair during hemodialysis.118 The incidence of tendon ruptures increases inassociation with hyperparathyroidism,119 in which crystal deposition120 and septicarthritis are common.121 Dialysis amyloidosis is a debilitating condition that includesarthropathy and is attributable to retention of b2-macroglobulin in tissues.

Bone demineralization may result from altered vitamin D metabolism andsecondary hyperparathyroidism,122,123 aluminum intoxication from dialysate oraluminum-containing phosphate binders,124 or metabolic acidosis requiring bufferingof hydrogen ion with bone salts.125 Renal osteodystrophy may result, with osteitis


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fibrosis, osteomalacia, osteosclerosis, osteoporosis, and growth retardation. Physicalmanifestations of renal osteodystrophy include bone pain, proximal muscleweakness, pruritus, calciphylaxis (ischemic lesions of soft tissues and skin, withvascular calcifications), and skeletal deformities.123 Treatment consists ofadministration of aluminum and calcium carbonate phosphate binders126 and calciumsupplements,127 an increased dialysate calcium level,128 1,25-dihydroxyvitamin D3

administration,129 and aluminum chelation with deferoxamine.130 A few patientsrequire parathyroidectomy,131 although bone biopsies should be performed first torule out aluminum-related osteomalacia that is unresponsive to parathyroidectomy.132Nervous system The neurologic effects of uremia include encephalopathy andneuropathy.133 Manifestations of uremic encephalopathy include confusion, tremorand asterixis, myoclonic seizures, delirium, and coma. Severity varies directly withthe degree and rate of development of renal failure and its response to dialysis.

Uremic neuropathy is typically a mixed motor and sensory distal polyneuropathythat affects the lower extremities preferentially and symmetrically; the etiology ofaxonal degeneration with demyelination is unclear. An early manifestation is restlesslegs syndrome: pulling sensations and pruritus relieved by movement. Autonomic andcranial nerve dysfunction, particularly affecting the eighth cranial nerve, is also

associated with uremia. Uremic polyneuropathy may mimic diabetic neuropathy.Dialysis itself is associated with several central nervous system disorders. Dialysis

dysequilibrium syndrome, associated with rapid hemodialysis (particularly when it isinitiated in a patient with an extremely elevated BUN), causes headache, nausea,vomiting,cramps, restlessness, tremors, blurred vision, hypertension, confusion, syncope,seizures, and arrhythmias. Short, frequent dialyses or continuous ambulatoryperitoneal dialysis134 can prevent dialysis dysequilibrium syndrome. Dialysisdementia is a chronic, progressive, and often fatal disorder associated with long-termhemodialysis135; dialysis dementia may be part of a syndrome that includes

osteomalacia, proximal myopathy, and anemia. Because of this disorders frequentassociation with aluminum intoxication from dialysate contamination, administrationof aluminum chelators such as deferoxamine may be beneficial. The incidence ofaluminum toxicity has in fact decreased as a result of improved management ofdialysis. Intracranial hemorrhage is associated with anticoagulation during dialysis,93hypertension, and abnormal hemostasis. Nonketotic hyperosmolar coma may occurbecause of high glucose concentrations in the dialysate.136

Dermal system Pruritus commonly complicates uremia137 and may be related toskin gland atrophy or to altered calcium and phosphate metabolism and

hyperparathyroidism.138 Cutaneous calcification also causes pruritus.139Hyperpigmentation is common and is the result of retained urochromes140 andincreased melanin deposition.141


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CAC - Manejo Perioperatorio Del Paciente Con Falla Renal

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