Management of the Azotemic Patient

Saturday, March 2, 1996

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5. Eisenberg JM, Clarke JR, Sussman SA. Prothrombin and partial thromboplastin times as preoperative screening tests. Arch Surg 1982; 117:48-51. 6. Kaplan EB, Sheiner LB, Boeckmann AJ, et al. The usefulness of preoperative laboratory screening. JAMA 1985; 253:35763581. 7. Suchman AL, Mushlin AI. How well does the activated partial thromboplastin time predict postoperative hemorrhage? JAMA 1986; 256:750-753. 8. Turnbull JM, Buck C. Value of preoperative screening investigations in otherwise healthy individuals. Arch Intern Med 1987; 147:1101-1105. 9. Rohrer MJ, Michelotti MC, Nahrwold DL. Prospective evaluation of the efficacy of preoperative coagulation testing. Ann Surg 1988; 208:554-557. 10. Suchman AL, Griner PF. Diagnostic uses of the activated partial thromboplastin time and prothrombin time. Ann Intern Med 1986; 104:810-816. 11. Ritter DM, Rettke SR, Lunn RJ, et al. Preoperative coagulation screen does not predict intraoperative blood product requirements in orthotopic liver transplantation. Transplant Proc 1989; 21: 3533-3534. 12. Wagner JD, Moore DL. Preoperative laboratory testing for the oral and maxillofacial surgery patient. J Oral Maxillofac Surg 1991; 49:177-182. 13. Vincent GM, Brown W. Prothrombin time and partial thromboplastin time tests are unnecessary before routine cardiac catheterization. J Intervent Cardiol 1990; 3:

1-4. 14. Wilson NY, Corne JM, Given-wilson RM. Critical appraisal of coagulation studies prior to transfemoral angiography. Br J Radiol 1990; 63:147-148. 15. Fellin FM, Murphy S. Perioperative evaluation of patients with hematologic disorders. In: Merli GJ, Weitz HH, eds. Medical Management of the Surgical Patient. Philadelphia: WE Saunders, 1992; 84-115. 16. Macpherson DS, Snow R, Lofgren RP. Preoperative screening: value of previous tests. Ann Intern Med 1990; 113:969-973. 17. Development Task Force of the College of American Pathologists. Practice parameters for the use of fresh frozen plasma,

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cryoprecipitate, and platelets. JAMA 1994; 271:777-781. 18. Jensen R, Ens GE. Platelet component therapy. Clin Hemost Rev 1994; 8:1-9. 19. Walker RH. Special report: transfusion risks. Am J Clin Pathol 1987; 88:374-378. 12:50 pm

Management of the Azotemic Patient Louis G. Martin, MD

Learning objectives: (1) To identify basic anatomic, pathologic, and physiologic principles as they apply to acute and chronic renal insufficiency. (2) To use these principles to assess and manage azotemic patients more effectively before, during, and after interventional treatment. Management of the azotemic patient presents special problems for the interventional radiologist. Azotemic patients are more susceptible to infection and hemorrhage and are more sensitive to contrast material. Perhaps less understood are the actions that interventional radiologists can take to lessen procedural risks. At issue are the effects of contrast material, hydration, salt load, medications, and diet on azotemic patients. The patient's primary care physician, nephrologist, cardiologist, and anesthesiologist are members of a team whose talents are necessary and should be used for the safe treatment of these patients. The role of the interventional radiologist, however, should not be minimized in this setting. Frequently, they are the most qualified to judge the risk-benefit ratio of a treatment or diagnostic test that is being proposed. The following information is generalized, may not have been proved by randomized prospective studies, and tends to oversimplify the problem. Proposed solutions may require modifications during use. Definitions The word "azotemia" is derived from two Greek words: "azote," meaning absence of life (used by Lavoisier to name nitrogen because of its inability to sustain life), and "haima," meaning blood. An excess of urea or other nitrogenous bodies in the blood is characteristic of the azotemic state, which is caused by the body's inability to clear or eliminate these products of metabolism.

Acute renal failure is a clinical syndrome characterized by a sudden reduction in the glomerular

Saturday, March 2, 1996 filtration rate (GFR), diagnosed by an increase in the serum creatinine level of at least 0.5 mgldL if the baseline is <3.0 mgldL or an increase of 1.0 mgldL if the baseline is >3.0 mgldL. It has many causes that most often afflict patients with no underlying renal disease. However, commonly, it may be "superimposed" over chronic renal failure. A knowledge of the patient's baseline renal function and medical history may be essential in distinguishing one from the other. If the patient survives, renal function may return to normal or may be permanently impaired. Impairment is steady and nonprogressive. The cardinal feature of chronic renal failure is a progressive decrease in the GFR due to the relentless destruction of nephrons, resulting ultimately in renal function so poor that life cannot be sustained. The slowly progressive nature of chronic renal failure selves to distinguish it from acute renal failure. Acute tubular necrosis occurs if oxygen delivery to renal tissue is Significantly impaired. Prerenal acute renal failure and ischemic acute tubular necrosis account for more than twothirds of the cases of acute renal failure that are seen or develop in the hospital. Classification and Etiology Acute renal failure is classified according to the anatomic location of its cause into prerenal, intrinsic renal, and postrenal categories. Prerenal failure is caused by decreased effective intravascular volume most commonly associated with trauma and hemorrhage but also associated with volume redistribution, which might occur with sepsis or anaphylaxis, cardiac dysfunction, and renal artery stenosis or occlusion. Imrinsic failure is due to conditions caused by infections, toxins, pigments, and vasculopathies, for example, that primarily affect the glomeruli, renal tubules, or microvasculature. Postrenal failure is caused by processes that occlude urinary outflow from both kidneys (or all of the functional renal tissue). In males, bladder outflow obstruction due to prostatic hypertrophy is the most common reason, whereas a pelvic neoplasm is most likely in females. Other causes include retroperitoneal fibrosis, calculi, blood clots, and functional neuropathy.

Chronic renal failure, unlike acute renal failure, is diagnosed by documenting a reduction in nephron mass. In >50% of cases, chronic renal failure is secondary to diabetic nephropathy or hypertensive arteriolar nephrosclerosis. Less

common causes include chronic glomerulonephritis, polycystic renal disease, and chronic interstitial nephritis.

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Acute renal failure may also be subdivided into oliguric «20 mL of urine production per hr), nonoliguric (20-100 mL per hr), and polyuric (>100 mL of urine production per hr) categories. Disease Course As previously mentioned, the pathologic proc-

ess is usually limited in acute renal failure, resulting in complete recovery, fixed functional defiCit, or death. In chronic renal failure, the disease course that results in progressive renal destruction occurs in a well-defined manner. Although the rate of progression may differ among patients, its progression is linear or curvilinear, and follows a predictable course. Therefore, a deViation, such as sudden worsening of renal function, must be explained by a superimposed etiologic process, such as an adverse reaction to medication or a critical vascular stenosis. Laboratory Diagnosis Urinary pH is a measure of the kidneys' ability to acidify urine. The inability to excrete acidic urine in the presence of systemic acidosis suggests renal insufficiency.

Plasma has a specific gravity of 1.010 and an osmolarity of 290 mOsm/kg. Urinary specific gravity and osmolarity are indexes of renal tubular function. Excretion of concentrated urine (1.030 specific gravity and 1.050 mOsm/kg) indicates excellent tubular function, whereas urinary osmolarity approaching plasma levels indicates renal disease. Urinary concentration is normal in prerenal azotemia and abnormally low in intrinsic and postrenal causes of azotemia. Massive proteinUria (>750 mg/d) is always abnormal and usually suggests severe glomerular damage. Creatinine is freely filtered at the glomerulus and, apart from an almost negligible increase in content due to secretion in the distal nephron, is neither reabsorbed nor secreted. Therefore, serum creatinine measurements reflect glomerular function. A specific measurement of glomerular function and creatinine clearance is the GFR. Serum creatinine concentration and clearance are better indicators of kidney function and GFR than similar measurements of urea nitrogen. The latter are subject to wide individual

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Saturday, March 2, 1996 variations secondary to changes in hydration, rate of urine flow, and dietary protein intake. Sodium, potassium, cWoride, and bicarbonate concentrations usually remain normal until frank renal failure is present, at which point metabolic acidosis, hyponatremia, and hyperkalemia develop. Interventional Therapy of the Azotemic Patient Percutaneous transluminal angioplasty or thrombolysis is usually done for relief of renovascular obstruction or postrenal obstruction in the urinary collecting system; this may require percutaneous nephrostomy, stone extraction, ureteral stenting, abscess drainage, or tumor treatment.

Ideally, the fluid and electrolyte balance should be as close to normal as possible before the operation. The patient with azotemia will, characteristically, have an increase in both intracellular and extracellular fluid and will be hyponatremic and hyperkalemic. Preoperative fluid and electrolyte administration or restriction will depend on whether the patient's treatment has included diuretics, fluid, and salt restriction and whether renal failure is acute or chronic. Major procedural risks to the patient are most commonly due to the contrast material used and the cardiotoxic effect of hyperkalemia. The patient should not be dehydrated before administration of contrast material. This will frequently be a problem because many patients will have been treated with diuretics. Volume depletion and electrolyte imbalance must also be treated before interventional therapy. The risk of acute renal failure can be reduced for patients with chronic renal insufficiency who are at high risk for contrast-material toxicity. After proper hydration with normal saline, these patients should be given mannitol (25 g) and furosemide (200 mg, intravenously) over 20 minutes. This infusion should be started 3060 minutes before the interventional study. The combination of volume expansion and interruption of afferent arteriolar vasoconstriction increases renal blood flow and sodium and water excretion. Hyperkalemia is a serious risk factor for patients undergoing an interventional procedure. These patients are especially prone to cardiac arrhythmias. If fluid and electrolyte balance cannot be attained, dialysis should be done before the procedure.

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Most drugs are weak electrolytes and lipid soluble in the un-ionized state. Therefore, they are extensively reabsorbed by renal tubular cells. After metabolism, these drugs are excreted in the urine in a form that is 2usually pharmacologically inactive. Most drugs, including most narcotics and barbiturates, fall into this category. Drugs, such as muscle relaxants, cholinesterase inhibitors, thiazide diuretics, digoxin, and many antibiotics, are lipid insoluble and are eliminated unchanged in the urine. Their duration of action may be prolonged in patients with impaired renal function. Although 200/0-50% of a dose of atropine is excreted unchanged in the urine, a single dose will not cause clinical difficulties. Morphine is almost completely metabolized in the liver to an inactive glucuronide, which is excreted in the urine, thus its effect will not be prolonged by azotemia. More than 90% of the thiazides and 70% of furosemide are excreted by the kidney and have prolonged durations of action in patients with abnormal or absent renal function. Propranolol and the calcium channel blocking agents nifedipine, verapamil, and diltiazem are extensively metabolized in the liver and may be administered in usual doses to patients with renal insufficiency. Accelerated or malignant hypertension is common in patients with acute and chronic renal failure. Care must be taken not to decrease the blood pressure too rapidly because transient hypotension may aggravate renal dysfunction due to impaired autoregulative mechanisms. In patients with renal failure, especially in those with diabetes mellitus or reduced cardiac output, the amount of contrast material used must be kept to a bare minimum. If possible, the use of magnetic resonance (MR) angiography or ultrasound (US) should be substituted for angiographic procedures. If an angiogram is necessary, carbon dioxide should be substituted for iodinated contrast material whenever practical. If the use of contrast material is required, the smallest necessary amounts of a nonionic, low-osmolar agent should be used. Pressure gradients should be measured across areas of poorly defined stenosis rather than performing additional angiography. Azotemic patients also have an increased susceptibility to infection and bleeding complications. ~reoperative broad-spectrum antibiotics should be considered for patients who are un-

Salurday, March 2, 1996 dergoing a nonvascular interventional treatment and for azotemic patients who are undergoing vascular stenting, vena cava filter placement, embolotherapy, or intervascular thrombolysis. Postoperative Therapy Dialysis should be considered if fluid and electrolyte balance is difficult to attain. Special care should be exercised to diagnose infection or hemorrhagic complications as early as possible. SWlDmary

Treatment of the azotemic patient is complex and requires teamwork involving the interventional radiologist, nephrologist, urologist, and, occasionally, the anesthesiologist. All members of this team must understand that the risks of the interventional procedure are significantly increased by the patient's disease and that certain precautions or treatment modifications by all team members will be necessary. The nephrologist will supply the expertise necessary to optimize fluid and electrolyte balance. However, if these efforts prove inadequate, dialysis should be used preoperatively and postoperatively. Vascular diagnostic procedures have traditionally involved the use of contrast material, a substance that is especially dangerous to the azotemic patient. MR angiography and transcutaneous US should be substituted for procedures that require the use of contrast material. If intravascular information is needed, the use of contrast material should be limited to a nonionic, low-osmolar agent. Additionally, the volume of contrast material used should be as little as possible, substituting injections of carbon dioxide, intra-arterial vascular US, and intravascular determination of pressure gradients for angiographic images whenever possible. The patient's azotemic state and its effect on the possible prolongation of therapeutic effect must be considered when prescribing medications before, during, or after the interventional procedure.

References 1. Bastl CP, Rudnick MR, Narins RG.

Assessment of renal function: characteristics of the functional and organic forms of acute renal failure. In: Seldin DW, Giebisch G, eds. The Kidney: Physiology and Pathophysiology. New York: Raven Press, 1985; 1819-1836.

2. Blantz RC. Intrinsic renal failure: acute. In: Seldin OW, Giebisch G, eds. The Kidney: Physiology and Pathophysiology. New York: Raven Press, 1985; 1863-1884. 3. Bricker NS, Shapiro MS, Levine MM, Makoff RK. Physiology and pathology of electrolyte metabolism in chronic renal disease. In: Seldin OW, Giebisch G, eds. The Kidney: Physiology and Pathophysiology. New York: Raven Press, 1985; 1837-1862. 4. Lang GR, ]onasson O. Acute renal insufficiency complicating surgery and trauma. In: Hardy JO, ed. Complications in Surgery and Their Management. Philadelphia: WE Saunders, 1981; 8&-97. 5. Malhorta V. Anesthesia and renal and genitourinary systems. In: Miller RO, ed. Anesthesia. New York: Churchill Livingstone, 1994; 1947-1968. 6. Martin LG, Casarella W}, Gaylord GM. Azotemia caused by renal artery stenosis: treatment by percutaneous angioplasty. AJR 1988; 150:839-844. 7. Morrison G, Geheb MA, Earley LE. Chronic renal failure. In: Seldin OW, Giebisch G, eds. The Kidney: Physiology and Pathophysiology. New York: Raven Press, 1985; 1901-1943. 8. Moser M. Hypertension. In: Seldin OW, Giebisch G, eds. The Kidney: Physiology and Pathophysiology. New York: Raven Press, 1985; 263-280. 9. Saurina GR, Bonventre]V. Acute renal failure. In: Rakel RE, ed. Conn's Current Therapy. Philadelphia: WE Saunders, 1995; 635-642. 10. Smith MC, Dunn MJ. Chronic renal failure. In: Rakel RE, ed. Conn's Current Therapy. Philadelphia: WE Saunders, 1995; 642-648. 11. Thurau K, Mason J, Gstraunthaler G. Experimental acute renal failure. In: Seldin OW, Giebisch G, eds. The Kidney: Physiology and Pathophysiology. New York: Raven Press, 1985; 1885-1899.

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1:05 pm Management of the Diabetic Patient Irl B. Hirsch, MD Learning objective: To become familiar with the management of diabetes during interventional procedures. The type of diabetes a patient has must be determined before that patient undergoes an in-

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