Handbook of Clinical Anesthesia

Chapter 52

The Renal System and Anesthesia for Urologic Surgery

The kidney plays a central role in implementing and controlling a variety of homeostatic functions, including excreting metabolic waste products in the urine while keeping extracellular fluid (ECF) volume and composition constant (Stafford-Smith M, Shaw A, George R, Muir HL: Anesthesia for urologic surgery. In Clinical Anesthesia. Edited by Barash PG, Cullen BF, Stoelting RK, Cahalan MK, Stock MC. Philadelphia: Lippincott Williams & Wilkins, 2009, pp 1346–1374). Renal dysfunction may occur as a direct result of surgical or medical disease, prolonged reduction in renal oxygen delivery, nephrotoxin insult, or a combination of the three.

  1. Renal Anatomy and Physiology
  2. Gross Anatomy(Fig. 52-1A)
  3. Renal pain sensation is conveyed back to spinal cord segments T10–L1 by sympathetic fibers. Sympathetic innervation is supplied by preganglionic fibers from T8–L1. The vagus nerve provides parasympathetic innervation to the kidney, and the S2–S4 spinal segments supply the ureters.
  4. The bladder is located in the retropubic space and receives its innervation from sympathetic nerves originating from T11–L2, which conduct pain, touch, and temperature sensations. Bladder stretch sensation is transmitted via parasympathetic fibers from segments S2–S4. Parasympathetics also provide the bladder with most of its motor innervation.
  5. The prostate, penile urethra, and penis also receive sympathetic and parasympathetic fibers from the T11–L2 and S2–S4 segments. The pudendal nerve provides pain sensation to the penis via the dorsal nerve of the penis.

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Figure 52-1. The gross anatomy (A) and internal structure of the genitourinary system and kidney. Internal organization of the kidney includes the cortex and medulla regions and the vasculature (B). The nephron is the functional unit of the kidney (C). Plasma filtration occurs in the glomerulus (D); 20% of plasma that enters the glomerulus passes through the specialized capillary wall into Bowman's capsule and enters the tubule to be processed and generate urine.

  1. Ultrastructure (Fig. 52-1B-D)
  2. The parenchyma of each kidney contains approximately 1 ÷ 106tightly packed nephrons (structural units of the kidneys), each one consisting of a tuft of capillaries (glomerulus) invaginated into the blind, expanded end (glomerular corpuscle) of a long tubule that leaves the renal corpuscle to form the proximal convoluted tubule in the cortex.

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  1. The distal convoluted tubule comes into very close contact with the afferent glomerular arteriole, and the cells of each are modified to form the juxtaglomerular apparatus, a complex physiological feedback control mechanism contributing in part to the precise control of intra- and extrarenal hemodynamics that is a hallmark feature of normally functioning kidneys.
  2. Correlation of Structure and Function
  3. Renal tissue makes up only 0.4% of body weight but receives 25% of cardiac output, making the kidneys the most highly perfused major organs in the body, and this facilitates plasma filtration at rates as high as 125 to 140 mL/min in adults.
  4. The kidney fulfills its dual roles of waste excretion and body fluid management by filtering large amounts of fluid and solutes from the blood and secreting waste products into the tubular fluid.
  5. Glomerular Filtration
  6. Production of urine begins with water and solute filtration from plasma flowing into the glomerulus via the afferent arteriole. The glomerular filtration rate (GFR) is a measure of glomerular function expressed as milliliters of plasma filtered per minute and is heavily influenced by arteriolar tone at points upstream (afferent) and downstream (efferent) from the glomerulus.
  7. An increase in afferent arteriolar tone, as occurs with intense sympathetic or angiotensin II stimulation, causes filtration pressure and GFR to decrease.
  8. Autoregulation of Renal Blood Flow and Glomerular Filtration Rate
  9. Renal blood flow (RBF) autoregulation maintains relatively constant rates of RBF and glomerular filtration over a wide range of arterial blood pressure (Fig. 52-2).
  10. Autoregulation of urine flow does not occur, and above a mean arterial pressure (MAP) of 50 mm Hg, there is a linear relationship between and MAP and urine output.
  11. Tubular Reabsorption of Sodium and Water
  12. Active, energy-dependent reabsorption of sodium begins almost immediately as the glomerular filtrate enters the proximal tubule. (An adenosine

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triphosphatase pump drives the sodium into tubular cells while chloride ions passively follow.)

 

Figure 52-2. Renal blood flow (RBF) autoregulation. RBF and glomerular filtration rate (GFR) are relatively constant with changes in systolic blood pressure from about 80 to 200 mm Hg.

  1. At the loop of Henle in the collecting duct, water reabsorption is controlled entirely by antidiuretic hormone secreted by the pituitary gland.
  2. The Renin–Angiotensin–Aldosterone System
  3. Renin release by the afferent arteriole may be triggered by hypotension, increased tubular chloride concentration, or sympathetic stimulation.
  4. Aldosterone stimulates the distal tubule and collecting duct to reabsorb sodium (and water), resulting in intravascular volume expansion.
  5. Renal Vasodilator Mechanisms
  6. Opposing the saline retention and vasoconstriction observed in stress states are the actions of atrial natriuretic peptide (ANP), nitric oxide, and the renal prostaglandin system. ANP is released by the cardiac atria in response to increased stretch under conditions of volume expansion.
  7. Nitric oxide produced in the kidney opposes the renal vasoconstrictor effects of angiotensin II and the sympathetic nervous system, promotes sodium

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and water excretion, and participates in tubuloglomerular feedback.

Table 52-1 Clinical Assessment of the Kidney

Serum creatinine (GFR should be assessed)
BUN (not ideal as influenced by dehydration and postoperative catabolic states)
Urinalysis and urine characteristics (inspection for cloudiness, color, odors)
Urine specific gravity (>1.018 implies preserved renal concentrating ability)
Urine output (<400 mL urine/24 hr) may reflect hypovolemia or impending “prerenal” renal failure (perioperative renal failure often develops in the absence of oliguria

BUN = blood urea nitrogen; GFR = glomerular filtration rate.

  1. Clinical Assessment of the Kidney

Measures such as urine output correlate only poorly with perioperative renal function, but much about the kidneys can be learned from knowing how effectively they clear circulating substances and from inspection of the urine (Table 52-1).

III. Perioperative Nephrology

  1. Pathophysiology.Altered renal function can be thought of as a clinical continuum ranging from normal compensatory changes seen during stress to frank renal failure.
  2. The net result of modest activity of the stress response system is a shift of blood flow from the renal cortex to the medulla, avid sodium and water reabsorption, and decreased urine output.
  3. A more intense stress response may induce a decrease in RBF and GFR by causing afferent arteriolar constriction. If this extreme situation is not reversed, ischemic damage to the kidney may result, and acute renal failure (ARF) may become clinically manifest.
  4. Electrolyte Disorders(Table 52-2)

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Table 52-2 Electrolyte Disorders

Hyponatremia (most common electrolyte disorder; symptoms are rare unless sodium values are <125 mmol/L)
Hypernatremia (sodium gain or water loss; serum sodium >145 mmol/L)
Disorders of potassium balance (skeletal muscle weakness, ileus, myocardial depression)
Hypocalcemia (laryngospasm)
Hypercalcemia (primary hyperparathyroidism, malignancy)
Hypomagnesemia (<1.6 mg/dL)
Hypermagnesemia (>4 to 6 mg/dL)

  1. Acid–Base Disorders.Acid–base homeostasis involves tight regulation of HCO32 and PaCO2 (Table 52-3).
  2. Acute Kidney Conditions
  3. Acute kidney injury (AKI)is the preferred term for an acute deterioration in renal function. It is associated with a decline in glomerular filtration and results in an inability of the kidneys to excrete nitrogenous and other wastes. AKI frequently occurs in the setting of critical illness with multiple organ failure, and the mortality rate is alarmingly high (≤90%).
  4. Prerenal azotemiais an increase in blood urea nitrogen associated with renal hypoperfusion or ischemia that has not yet caused renal parenchymal damage.
  5. Intrinsic AKIincludes injury caused by ischemia, nephrotoxins, and renal parenchymal diseases.

Table 52-3 Acid–Base Disorders

Metabolic acidosis (to determine the cause, the anion gap should be calculated)
Metabolic alkalosis (gastrointestinal acid loss)
Respiratory acidosis (acute and chronic causes can be differentiated by examining arterial pH, PaCO2, and HCO3- values)
Respiratory alkalosis (increased minute ventilation)
Mixed acid–base disorders (common in intensive care unit patients)

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Table 52-4 Nephrotoxins Commonly Found in the Hospital Setting

Exogenous

Endogenous

Antibiotics (aminoglycosides, cephalosporins, amphotericin B, sulfonamide, tetracyclines, vancomycin)

Calcium (hypercalcemia)

Myoglobin (rhabdomyolysis)

Uric acid (hyperuricemia and hyperuricemia)

Anesthetic agents (methoxyflurane, enflurane)

Hemoglobin (hemolysis)

NSAIDs (aspirin, ibuprofen, naproxen, indomethacin, ketorolac)

Bilirubin (obstructive jaundice)

Chemotherapeutic–immunosuppressive agents (cisplatinum, cyclosporin A, methotrexate, mitomycin, nitrosoureas, tacrolimus)

Oxalate crystals

Contrast media

Paraproteins

NSAID = nonsteroidal anti-inflammatory drug.

  1. Postrenal AKI (Obstructive Uropathy).Downstream obstruction of the urinary collecting system is the least common pathway to established AKI, accounting for fewer than 5% of cases.
  2. Nephrotoxins and Perioperative AKI(Table 52-4)
  3. Chronic Kidney Disease (CKD).Patients with nondialysis-dependent CKD are at increased risk of developing end-stage renal disease (ESRD). These patients have GFRs below 25% of normal. Patients with decreased renal reserve are often asymptomatic and frequently do not have elevated blood levels of creatinine or urea.
  4. The uremic syndrome represents an extreme form of CRF, which occurs as the surviving nephron population and GFR decrease below 10% of normal. It results in an inability of the kidneys to perform their two major functions: regulation of the volume and composition of the ECF and excretion of waste products.
  5. Water balance in ESRD becomes difficult to manage because the number of functioning nephrons is too small either to concentrate or to fully dilute the

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urine. This results in failure both to conserve water and to excrete excess water.

Table 52-5 Factors Contributing to Hyperkalemia in Chronic Renal Failure

Potassium Intake
Increased dietary intake
Exogenous IV supplementation
Potassium salts of drugs
Sodium substitutes
Blood transfusion
GI hemorrhage
Potassium Release from Intracellular Stores
Increased catabolism or sepsis
Metabolic acidosis
β-Adrenergic blocking drugs
Digitalis intoxication
Insulin deficiency
Sch
Potassium Excretion
Acute decrease in GFR
Constipation
Potassium-sparing diuretics
ACE inhibitors (decreased aldosterone secretion)
Heparin (decreased aldosterone effect)

ACE = angiotensin-converting enzyme; GFR = glomerular filtration rate; GI = gastrointestinal; IV = intravenous; Sch = succinylcholine.

  1. Patients with uremic syndrome often require frequent or continuous dialysis.
  2. Life-threatening hyperkalemia may occur in patients with CKD because of slower-than-normal potassium clearance (Table 52-5). Derangements in calcium, magnesium, and phosphorus metabolism are also commonly seen in patients with CKD.
  3. Metabolic acidosis occurs in two forms in ESRD (hyperchloremic, normal anion gap acidosis and a high anion gap acidosis caused by an inability to excrete titratable acids).
  4. Complications of the Uremic Syndrome(Table 52-6)
  5. Drug Prescribing in Renal Failure.Clearance of most medications involves a complex combination of both hepatic and renal function, and drug level

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measurement or algorithms for specific drugs are often recommended.

Table 52-6 The Uremic Syndrome

Water Homeostasis
ECF expansion
Electrolyte and Acid–Base
Hyponatremia
Hyperkalemia
Hypercalcemia or hypocalcemia
Hyperphosphatemia
Hypermagnesemia
Metabolic acidosis
Cardiovascular
Heart failure
Hypertension
Pericarditis
Myocardial dysfunction
Dysrhythmias
Respiratory
Pulmonary edema
Central hyperventilation
Hematologic
Anemia
Platelet hemostatic defect
Immunologic
Cell-mediated and humoral immunity defects
Gastrointestinal
Delayed gastric emptying, anorexia, nausea, vomiting, hiccups, upper GI tract inflammation or hemorrhage
Neuromuscular
Encephalopathy, seizures, tremors, myoclonus
Sensory and motor polyneuropathy
Autonomic dysfunction, decreased baroreceptor responsiveness, dialysis-associated hypotension
Endocrine-Metabolism
Renal osteodystrophy
Glucose intolerance
Hypertriglyceridemia

ECF = extracellular fluid; GI = gastrointestinal.

  1. Anesthetic Agents in Renal Failure.With the possible exception of enflurane, anesthetic agents do not directly cause renal dysfunction or interfere with the

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normal compensatory mechanisms activated by the stress response.

  1. If the chosen anesthetic technique causes a protracted reduction in cardiac output or sustained hypotension that coincides with a period of intense renal vasoconstriction, renal dysfunction or failure may result.
  2. Significant renal impairment may affect the disposition, metabolism, and excretion of commonly used anesthetic agents (with the exception of the inhalational anesthetics).
  3. Induction Agents and Sedatives
  4. Ketamine is less extensively protein bound than thiopental, and renal failure appears to have less influence on its free fraction.
  5. Propofol undergoes extensive, rapid hepatic biotransformation to inactive metabolites that are renally excreted.
  6. AKI appears to slow the plasma clearance of midazolam.
  7. Opioids
  8. Chronic morphine administration results in accumulation of its 6-glucuronide metabolite, which has potent analgesic and sedative effects.
  9. Meperidine is remarkable for its neurotoxic, renally excreted metabolite (normeperidine) and is not recommended for use in patients with poor renal function.
  10. Hydromorphone is metabolized to hydromorphone-3-glucuronide, which is excreted by the kidneys. This active metabolite accumulates in patients with renal failure and may cause cognitive dysfunction and myoclonus.
  11. Codeine has the potential for causing prolonged narcosis in patients with renal failure and is not recommended for long-term use.
  12. Fentanyl appears to be an acceptable choice in patients with ESRD because of its lack of active metabolites, unchanged free fraction, and short redistribution phase. Small to moderate doses, titrated to effect, are well tolerated by uremic patients.
  13. Remifentanil is rapidly metabolized by blood and tissue esterases, and renal failure has no effect on the clearance of remifentanil.

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Table 52-7 Nondepolarizing Muscle Relaxants in Renal Failure

Drug

% Renal Excretion

Half-Life (hr) Normal/ESRD

Renally Excreted Active Metabolite

Use in ESRD

Pancuronium

30

2.3/4–8

+

Avoid

Pipecuronium

37

1.8–2.3/4.4

+

Avoid

Doxacurium

30

1.7/3.7

Avoid

Vecuronium

30

0.9/1.4

+

Avoid infusion

Rocuronium

30

1.2–1.6/1.6–1.7

Variable duration

Atracurium/cis-atracurium

<5

0.3/0.4

Normal

ESRD = end-stage renal disease.

  1. Muscle relaxantsare the most likely group of drugs used in anesthetic practice to produce prolonged effects in ESRD because of their dependence on renal excretion (Table 52-7).
  2. Provided the serum potassium concentration is not dangerously elevated, succinylcholine (Sch) use can be justified as part of a rapid sequence induction technique because its duration of action in patients with ESRD is not significantly prolonged.
  3. Concern about the increase in serum potassium levels after Sch administration (0.5 mEq/L in normal subjects) implies that the serum potassium level should be normalized to the extent possible in patients with renal failure, but clinical experience has shown that the acute, small increase in potassium after administration of Sch is generally well tolerated in patients with chronically elevated serum potassium levels.
  4. Anticholinesterase and Anticholinergic Drugs
  5. Anticholinesterases have a prolonged duration of action in patients with ESRD because of their heavy reliance on renal excretion.
  6. Atropine and glycopyrrolate, used in conjunction with the anticholinesterases, are similarly excreted by the kidney. Therefore, no dosage alteration

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of the anticholinesterases is required when antagonizing neuromuscular blockade in patients with reduced renal function.

  1. Diuretic Drugs: Effects and Mechanisms
  2. The Physiologic Basis of Diuretic Action(Fig. 52-3)
  3. Proximal Tubule Diuretics.Carbonic anhydrase inhibitors are drugs that inhibit this enzyme; the net effect of these agents is that sodium and bicarbonate, which would otherwise have been reabsorbed, remain in the urine, resulting in an alkaline diuresis. Specific uses for carbonic anhydrase inhibitors include the treatment of mountain sickness and open-angle glaucoma and to increase respiratory drive in patients with central sleep apnea.
  4. Osmotic Diuretics.Substances such as mannitol that are freely filtered at the glomerulus but poorly reabsorbed by the renal tubule cause an osmotic diuresis. Mannitol also draws water from cells into the plasma and effectively increases RBF. Mannitol has been widely used, especially for the prophylaxis of ARF. There is no clear evidence that mannitol is effective either for the prevention or treatment of ARF.
  5. Loop Diuretics.Loop diuretics (furosemide, bumetanide, torsemide) directly inhibit the electroneutral transporter (Na+/K+ ATPase in the loop of Henle), preventing salt reabsorption from occurring.
  6. Loop diuretics are a first-line therapeutic modality for treatment of acute decompensated congestive heart failure.
  7. Adverse effects of loop diuretics include hypokalemia, hyponatremia, and acute kidney dysfunction. Loop diuretics, especially furosemide, may cause ototoxicity, particularly in patients with renal insufficiency.
  8. Distal Convoluted Tubule Diuretics
  9. Clinically, distal convoluted tubule diuretics are used for the treatment of hypertension (often as sole therapy) and volume overload disorders and to relieve the symptoms of edema in pregnancy.
  10. Adverse reactions associated with distal tubule diuretics include electrolyte disturbances and volume depletion.

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Figure 52-3. Site of action of commonly available diuretics.

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  2. Distal (collecting duct) acting diureticsinhibit luminal sodium entry with a resulting potassium-sparing effect. A second class of distal-acting potassium-sparing diuretics is the competitive aldosterone antagonists (spironolactone and eplerenone).
  3. These drugs are used primarily for potassium-sparing diuresis and in treating patients with disorders involving secondary hyperaldosteronism, such as cirrhosis with ascites.
  4. Spironolactone treatment has been shown to improve survival with volume overload and left ventricular dysfunction or heart failure.
  5. Dopaminergic Agonists
  6. Intravenous (IV) infusion of low-dose dopamine (1–3 µg/kg/min) is natriuretic owing primarily to a modest increase in the GFR and reduction in proximal sodium reabsorption mediated by dopamine type 1 (DA1) receptors. Fenoldopam is a selective DA1 receptor agonist with little cardiac stimulation.
  7. At higher doses, the pressor response to dopamine is beneficial in patients with hypotension, but it has little or no renal effect in critically ill or septic patients.
  8. Renal-dose dopamine for the treatment of AKI, although widely used, has not been demonstrated to have significant renoprotective properties.
  9. High-Risk Surgical Procedures
  10. Cardiac Surgery
  11. Cardiac operations requiring cardiopulmonary bypass can be expected to result in renal dysfunction or failure in up to 7% of patients. Renal ischemia–reperfusion and toxin exposure are considered to be the two primary pathogenetic mechanisms involved in AKI.
  12. Numerous agents (mannitol, dopamine, dopexamine) have been used intraoperatively without success in attempts to protect the kidney during cardiac surgery.
  13. Noncardiac Surgery
  14. Several common noncardiac surgical procedures (emergency surgery, trauma surgery, multiple organ failure) can compromise previously normal renal function.

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  1. Preventing AKI in patients presenting for emergency surgery begins with restoring intravascular volume and managing shock.
  2. Invasive hemodynamic monitoring may be required to guide intraoperative management of ongoing cardiovascular instability caused by surgical manipulation, blood loss, fluid shifts, and anesthetic effects. Intraoperative transesophageal echocardiography provides excellent assessment of left and right ventricular function, as well as guidance of fluid resuscitation.
  3. There is no place for either furosemide or mannitol therapy in the early, resuscitative phase of trauma management, except in the case of head injury with elevated intracranial pressure or when massive rhabdomyolysis is suspected.
  4. Vascular surgery requiring aortic clamping has deleterious effects on renal function regardless of the level of clamp placement.
  5. Although hemodynamic changes during endovascular procedures on the aorta may be less dramatic than those accompanying open repair, the prevalence of renal complications appears to be similar. During endovascular procedures, patients may be exposed to substantial amounts of radiocontrast dye, which may exacerbate postoperative renal dysfunction, especially in those with pre-existing renal insufficiency.
  6. Anesthesia for Urinary Tract Disease
  7. Cystourethroscopy and Ureteral Procedures.Ureteroscopy, a simple extension of cystoscopy into the upper urinary tract using a flexible or rigid scope, can facilitate treatment of upper urinary tract malignancies and strictures and aid in diagnostic endoscopy and biopsy.
  8. Transurethral Resection of Bladder Tumors
  9. Superficial transitional cell carcinoma accounts for approximately 90% of bladder cancers.
  10. In diagnosing and treating this cancer, most patients undergo endoscopic transurethral resection. This procedure can be performed with topical, regional, or general anesthesia.

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Table 52-8 Safety Issues During Use of Lasers

Retinal or corneal damage (protective goggles or lenses should be used)
Thermal injuries
Inadvertent ignition of surgical drapes
Vaporization of Condyloma acuminatum tissue (plume of smoke that contains active human papilloma virus particles; a smoke evacuation system should be used in the operating room)

  1. If a neuraxial regional block is used, an anes-thetic level to T10 is required to prevent the pain associated with bladder distention.
  2. Patient movement caused by obturator nerve stimulation during resection of an inferior lateral tumor is associated with an increased likelihood of bladder perforation. A conscious patient who experiences bladder perforation often describes sudden abdominal pain with referred shoulder pain from diaphragmatic irritation.

VII. Lasers in Urology

(Table 52-8)

VIII. Extracorporeal Shock Wave Lithotripy (SWL)

Since 1980, when extracorporeal SWL became available, it has been the leading modality for the treatment of urinary calculi. SWL has the advantages of being a minimally invasive technique that is performed on an outpatient basis and is associated with minimal perioperative morbidity and a significant reduction in anesthetic needs.

  1. Complications of Shock Wave Lithotripsy(Table 52-9)
  2. Anesthetic Techniques for Shock Wave Lithotripsy.The majority of second- and third-generation lithotriptors require monitored anesthesia care with IV sedation and analgesia. The exception to this rule is pediatric patients, who usually require a general anesthetic.

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Table 52-9 Contraindications to Extracorporeal Shock Wave Lithotripsy

Absolute Contraindications
Bleeding disorder or anticoagulation
Pregnancy
Relative Contraindications
Large calcified aortic or renal artery aneurysms
Untreated UTI
Obstruction distal to the renal calculi
Pacemaker, AICD, or neurostimulation implant
Morbid obesity

AICD = automatic implantable cardioverter-defibrillator; UTI = urinary tract infection.

  1. Anesthesia for Prostatic Surgery
  2. Benign prostatic hyperplasia (BPH)is a frequent cause of lower urinary tract symptoms in older men. The clinical symptoms are not simply attributable to mechanical obstruction of urine flow because age-related detrusor dysfunction (an androgen-related phenomenon) plays an additional significant role. The hypertrophied prostate surrounds and compresses the prostatic (proximal) urethra, causing obstruction that often produces urinary retention.
  3. Transurethral resection of the prostate (TURP)is the surgical treatment for BPH. To facilitate clear vision of the surgical field, continuous irrigation is required. The irrigation fluid serves to distend the operative site and removes dissected tissue and blood. If the irrigating fluid infusion pressure exceeds venous pressure during a TURP procedure, the lush venous plexus of the prostate may allow intravascular absorption of irrigating fluid.
  4. Irrigating Solutions for Transurethral Resection of the Prostate(Table 52-10). Glycine has also been attributed a role in negative hemodynamic changes.
  5. Transurethral Resection of the Prostate Syndrome(Table 52-11)
  6. Factors that predict the amount of irrigation fluid absorption during a TURP procedure include the number and size of open venous sinuses (blood loss implies potential for irrigation absorption), duration

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of resection, hydrostatic pressure of the irrigating fluid, and venous pressure at the irrigant–blood interface.

Table 52-10 Properties of Commonly Used Irrigating Solutions for Transuretheral Resection Procedures

Solution

Osmolality (mOsm/L)

Advantages

Disadvantages

Distilled water

0

Improved visibility

Hemolysis
Hemoglobinemia
Hemoglobinuria
Hyponatremia

Glycine (1.5%)

200

Less likeli-hood of TURP syndrome

Transient postoperative visual syndrome
Hyperammonemia
Hyperoxaluria

Sorbitol (3.3%)

165

Same as glycine

Hyperglycemia, possible lactic acidosis
Osmotic diuresis

Mannitol (5%)

275

Isosmolar solution
Not metabolized

Osmotic diuresis
Possibility of acute intravascular volume expansion

TURP = transurethral resection of the prostate.

  1. When neurologic or cardiovascular complications of TURP procedures are recognized, prompt intervention is necessary (Table 52-12).

Table 52-11 Signs and Symptoms of Acute Hyponatremia

Serum Sodium (mEq/L)

Central Nervous System Changes

Electrocardiographic Changes

120

Confusion
Restlessness

Possible widening of QRS complex

115

Somnolence
Nausea

Widened QRS complex
Elevated ST segment

110

Seizures
Coma

Ventricular tachycardia or fibrillation

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Table 52-12 Treatment of the Transurethral Resection Syndrome

Ensure oxygenation and circulatory support.
Notify the surgeon and terminate the procedure as soon as possible.
Consider insertion of invasive monitors if cardiovascular instability occurs.
Send blood to the laboratory for electrolytes, creatinine, glucose, and ABG analysis.
Obtain a 12-lead electrocardiogram.
Treat mild symptoms (with serum sodium concentration >120 mEq/L) with fluid restriction and a loop diuretic (furosemide).
Treat severe symptoms (serum sodium <120 mEq/L) with 3% sodium chloride IV at a rate <100 mL/hr.
Discontinue 3% sodium chloride when serum sodium is >120 mEq/L.

ABG = arterial blood gas; IV = intravenous.

  1. Other complications of TURP include blood loss (2 mL/min) and abnormal bleeding after surgery (<1% of resections). Fever suggests bacteremia secondary to spread of bacteria through open prostatic venous sinuses and hypothermia.
  2. Anesthetic Techniques for Transurethral Resection of the Prostate
  3. Regional anesthesia, most commonly spinal block, has long been considered the anesthetic technique of choice for TURP.
  4. Because many patients having prostate surgery are elderly, consideration should be given to prevention of postoperative cognitive dysfunction. A prospective study comparing cognitive function after TURP using general versus spinal anesthesia found a significant impairment in both groups at 6 hours after surgery but no differences between approaches at any time in the first 30 days after surgery.
  5. The incidence of perioperative myocardial ischemia in patients undergoing TURP surgery, assessed by Holter monitoring, increases after surgery, but this also appears unaffected by the choice of anesthesia.
  6. Morbidity and Mortality after Transurethral Resection of the Prostate.The majority of patients undergoing TURP are elderly and have numerous comorbidities.

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Mortality after TURP surgery is most commonly related to cardiac and respiratory comorbidities.

  1. The Future of Transurethral Resection of the Prostate
  2. The rate of TURP procedures has declined, largely because of the development of non-operative strategies for BPH management (α1-adrenergic antagonists that reduce dynamic urethral obstruction or 5-α reductase inhibitors that block conversion of testosterone to reduce prostate hypertrophy).
  3. Less invasive surgical treatments for BPH have also been developed and include balloon dilatation, intraprostatic stents, transurethral incision, needle ablation, vaporization of the prostate, and laser prostatectomy.
  4. Despite these other surgical options, TURP has not been displaced as the best treatment for BPH, particularly in highly symptomatic patients and those with recurrent urinary tract infections related to incomplete bladder emptying.
  5. Surgery for Prostate Cancer
  6. Radical Retropubic Prostatectomy.Prostate cancer is the most common cancer in men. Advances in surgical techniques for radical prostatectomy continue to improve outcomes and reduce the complexity of the anesthetic care for these procedures.
  7. The traditional approach has been open radical retropubic prostatectomy (ORRP). This procedure, involving a transverse abdominal incision, is often associated with blood loss exceeding 1000 mL. Anesthetic technique and monitor selection need to be tailored toward intravascular volume assessment and using adjuncts that may help limit the volume of blood loss and reduce the need for blood transfusion.
  8. Monitoring for radical prostatectomy should be dictated by patient comorbidities and anticipated blood loss. Notably, urine flow, a traditional monitor of intravascular volume, is interrupted. Central venous pressure monitoring may be helpful, both to follow intravascular volume changes and to provide access for rapid transfusion. An arterial line provides continuous blood pressure monitoring and the possibility of serial hemoglobin assessment.

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  1. Optimal patient positioning for this procedure is a hyperextended supine position, which may theoretically increase the risk of nerve injury and rhabdomyolysis. The patient's iliac crests are positioned over the break in the operating table, which is then extended to create a maximal distance between the iliac crest and rib cage. The patient is then tilted to a head-down (Trendelenburg) position to achieve an operative field parallel to the floor.
  2. Improved postoperative pain management can also lead to better patient outcomes and overall satisfaction.
  3. Radical perineal prostatectomyis an alternate open surgical approach to prostatectomy. Positioning for this approach poses a significant anesthetic challenge because patients are in an exaggerated lithotomy position, so ventilatory mechanics may be compromised. Although the surgical site for this approach would be ideally amenable to spinal or epidural anesthesia, the position is so poorly tolerated by patients and the ventilatory alterations are so profound that general anesthesia is often indicated.
  4. Laparoscopic and Robotic Prostatectomy (LRP)
  5. A major impetus in the development of minimally invasive prostate cancer techniques has been patient satisfaction and quality of life. Shorter convalescence with a more rapid return to normal activity and shorter urinary catheter duration can be achieved with LRP.
  6. Anesthetic complications for LRP include extended surgical times coupled with high abdominal insufflation pressures and the head-down position can sometimes compromise ventilation. Because blood loss with LRP is minimal, monitoring decisions based on hemorrhage concerns with ORRP are replaced by selection of monitors focused primarily on patient comorbidities.
  7. Specific considerations include attention to temperature control (forced-air warming and warming insufflated gas to maintain normothermia), use of short-acting anesthetic agents, minimizing opioid administration, addressing postoperative nausea and vomiting, and reducing insufflation pressures from 15 to 12 mm Hg (to facilitate earlier return of bowel function).

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  1. Pain associated with the ORRP and LRP approaches to radical prostatectomy is similar, with the overall analgesic needs for both approaches being short lived.
  2. Anesthesia for Other Urologic Cancer Surgery
  3. Radical nephrectomyremains the mainstay of treatment for renal cell carcinoma. Surgery is associated with significant postoperative pain and specific risks (pneumothorax, tumor extension into the inferior vena cava and right atrium).
  4. A primary concernin the anesthetic management is attention to fluid management and the potential for significant blood loss.
  5. When planning for postoperative epidural analgesia, it is important to know what is planned for postoperative deep venous thrombosis (DVT) prophylaxis because all patients with cancer are at a high risk for DVT and pulmonary embolus.
  6. Radical cystectomywith pelvic node dissection is the “gold standard” for treatment of muscle-invasive bladder carcinoma.
  7. Anesthetic care for radical cystectomy should focus on preoperative assessment and patient optimization because these patients are often elderly and have multiple comorbidities. Significant blood loss and the need for transfusion are possible. An arterial line offers the advantage of easy blood pressure monitoring in high-risk patients and a method for obtaining serial samples for hematocrit measurement.
  8. Although there is no contraindication to the use of regional anesthesia, radical cystectomy is usually performed under general anesthesia because of the long duration of surgery.

Editors: Barash, Paul G.; Cullen, Bruce F.; Stoelting, Robert K.; Cahalan, Michael K.; Stock, M. Christine

Title: Handbook of Clinical Anesthesia, 6th Edition

Copyright ©2009 Lippincott Williams & Wilkins

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