2. 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.

C. Correlation of Structure and Function

1. 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.

2. Kidneys fulfill their 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.

D. Glomerular Filtration

1. 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.

2. An increase in afferent arteriolar tone, as occurs with intense sympathetic or angiotensin II stimulation, causes filtration pressure and GFR to decrease.

E. Autoregulation of Renal Blood Flow and Glomerular Filtration Rate

1. Renal blood flow (RBF) autoregulation maintains relatively constant rates of RBF and glomerular filtration over a wide range of arterial blood pressure (Fig. 49-2).

2. 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.

F. Tubular Reabsorption of Sodium and Water

1. Active, energy-dependent reabsorption of sodium begins almost immediately as the glomerular filtrate enters the proximal tubule. (An adenosine triphosphatase pump drives the sodium into tubular cells, and chloride ions passively follow.)

2. At the loop of Henle in the collecting duct, water reabsorption is controlled entirely by antidiuretic hormone secreted by the pituitary gland.

G. The Renin–Angiotensin–Aldosterone System

1. Renin release by the afferent arteriole may be triggered by hypotension, increased tubular chloride concentration, or sympathetic stimulation.

2. Aldosterone stimulates the distal tubule and collecting duct to reabsorb sodium (and water), resulting in intravascular volume expansion.

H. Renal Vasodilator Mechanisms

1. 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.

2. Nitric oxide produced in the kidney opposes the renal vasoconstrictor effects of angiotensin II and the sympathetic nervous system, promotes sodium and water excretion, and participates in tubuloglomerular feedback.

II. 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 49-1).

III. PERIOPERATIVE NEPHROLOGY

A. Pathophysiology. Altered renal function can be thought of as a clinical continuum ranging from normal compensatory changes seen during stress to frank renal failure.

1. 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.

2. 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.

B. Electrolyte Disorders (Table 49-2)

C. Acid–Base Disorders. Acid–base homeostasis involves tight regulation of HCO₃⁻ and PaCO₂ (Table 49-3).

D. Acute Kidney Conditions

1. 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%).

2. Prerenal azotemia is an increase in blood urea nitrogen associated with renal hypoperfusion or ischemia that has not yet caused renal parenchymal damage.

3. Intrinsic AKI includes injury caused by ischemia, nephrotoxins, and renal parenchymal diseases.

4. Postrenal AKI (Obstructive Uropathy). Downstream obstruction of the urinary collecting system is the least common pathway to established AKI, accounting for <5% of cases.

5. Nephrotoxins and Perioperative AKI (Table 49-4)

E. Chronic Kidney Disease (CKD). Patients with non–dialysis-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.

1. 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.

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

3. Patients with uremic syndrome often require frequent or continuous dialysis.

4. Life-threatening hyperkalemia may occur in patients with CKD because of slower-than-normal potassium clearance (Table 49-5). Derangements in calcium, magnesium, and phosphorus metabolism are also commonly seen in patients with CKD.

5. 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).

6. Complications of the Uremic Syndrome (Table 49-6)

F. Drug Prescribing in Renal Failure. Clearance of most medications involves a complex combination of both hepatic and renal function, and drug level measurement or algorithms for specific drugs are often recommended.

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

a. Ketamine is less extensively protein bound than thiopental, and renal failure appears to have less influence on its free fraction.

b. Propofol undergoes extensive, rapid hepatic biotransformation to inactive metabolites that are renally excreted.

c. AKI appears to slow the plasma clearance of midazolam.

4. Opioids

a. Chronic morphine administration results in accumulation of its 6-glucuronide metabolite, which has potent analgesic and sedative effects.

b. Meperidine is remarkable for its neurotoxic, renally excreted metabolite (normeperidine) and is not recommended for use in patients with poor renal function.

c. 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.

d. Codeine has the potential for causing prolonged narcosis in patients with renal failure and is not recommended for long-term use.

e. 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.

f. Remifentanil is rapidly metabolized by blood and tissue esterases, and renal failure has no effect on the clearance of remifentanil.

5. Muscle relaxants are the most likely group of drugs used in anesthetic practice to produce prolonged effects in ESRD because of their dependence on renal excretion (Table 49-7).

a. 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.

b. 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.

6. Anticholinesterase and Anticholinergic Drugs

a. Anticholinesterases have a prolonged duration of action in patients with ESRD because of their heavy reliance on renal excretion.

b. Atropine and glycopyrrolate, used in conjunction with the anticholinesterases, are similarly excreted by the kidneys. Therefore, no dosage alteration of the anticholinesterases is required when antagonizing neuromuscular blockade in patients with reduced renal function.

IV. DIURETIC DRUGS: EFFECTS AND MECHANISMS

A. The Physiologic Basis of Diuretic Action (Fig. 49-3)

1. 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.

2. 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.

3. 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.

a. Loop diuretics are a first-line therapeutic modality for treatment of acute decompensated congestive heart failure.

b. 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.

4. Distal Convoluted Tubule Diuretics

a. 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.

b. Adverse reactions associated with distal tubule diuretics include electrolyte disturbances and volume depletion.

5. Distal- (collecting duct) acting diuretics inhibit 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).

a. These drugs are used primarily for potassium-sparing diuresis and in treating patients with disorders involving secondary hyperaldosteronism, such as cirrhosis with ascites.

b. Spironolactone treatment has been shown to improve survival with volume overload and left ventricular dysfunction or heart failure.

B. Dopaminergic Agonists

1. 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.

2. 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.

3. Renal-dose dopamine for the treatment of AKI, although widely used, has not been demonstrated to have significant renoprotective properties.

V. HIGH-RISK SURGICAL PROCEDURES

A. Cardiac Surgery

1. 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.

2. Numerous agents (mannitol, dopamine, dopexamine) have been used intraoperatively without success in attempts to protect the kidney during cardiac surgery.

B. Noncardiac Surgery

1. Several common noncardiac surgical procedures (emergency surgery, trauma surgery, multiple organ failure) can compromise previously normal renal function.

2. Preventing AKI in patients presenting for emergency surgery begins with restoring intravascular volume and managing shock.

a. 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.

b. 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.

c. Vascular surgery requiring aortic clamping has deleterious effects on renal function regardless of the level of clamp placement.

d. 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.

VI. COMMON UROLOGIC SURGICAL PROCEDURES

A. Nephrectomy

1. The approach and incision for nephrectomy are based on surgical priorities and surgeon preference. Retroperitoneal approaches require a flank incision and lateral decubitus positioning (simplifies procedures with prior abdominal surgery or obesity). Difficulties with the retroperitoneal approach include access to the vena cava, risk of unintentional pneumothorax, and the adverse effects of the lateral decubitus position on vital capacity.

2. Anterior approaches to nephrectomy involve supine positioning and breach of the peritoneal cavity through midline, subcostal, or thoracoabdominal incisions that provide direct access to both the kidney and major vascular structures.

3. Laparoscopic retro- and transperitoneal approaches to nephrectomy have surpassed their open equivalents in popularity, and other recent innovations include robotic-assisted, single port laparoscopic, and even transvaginal minimally invasive nephrectomies.

4. Preoperative Considerations

a. Protocols for assessment and management of perioperative cardiac risk are particularly relevant to nephrectomy surgery.

b. About 10% to 40% of patients presenting with renal cancer have associated paraneoplastic syndromes (fever, cachexia, weight loss, endocrine and nonendocrine categories).

c. Abdominal CT scans detail the tumor size, location, and invasion of the renal collecting system or perirenal fat, but MRI is most valuable to assess for vena caval or cardiac chamber involvement.

5. Intraoperative Considerations

a. If placement of a central venous catheter is deemed necessary, selection of the side ipsilateral to the nephrectomy surgery for subclavian or internal jugular central venous puncture should be considered to minimize the risk of bilateral pneumothorax.

b. Bladder catheter placement is essential for all nephrectomy procedures.

c. Standard preanesthesia induction considerations include administration of IV antibiotic prophylaxis within 1 hour before surgical incision.

d. Intraoperative and postoperative pain management can be accomplished by IV or other opioid therapies such as patient-controlled analgesia or neuraxial analgesia. Continuous epidural analgesia attenuates the neuroendocrine response but may also improve postoperative ventilatory mechanics and resolve ileus sooner and has been associated with improved survival in intermediate- to high-risk noncardiac surgery.

e. Potential intraoperative complications include injury to major blood vessels (inferior vena cava [IVC], aorta) or gastrointestinal organs (spleen, liver, pancreas) and unrecognized entry into the pleural space with resultant pneumothorax.

f. Unexplained changes in pulmonary mechanics or hypotension during a nephrectomy procedure may reflect diaphragmatic injury and pneumothorax.

6. Postoperative Complications

a. The most common radical nephrectomy complications are adjacent organ (bowel, spleen, liver, diaphragm, or pancreas) and vascular injury. Overall complication rates are similar whether an open or laparoscopic approach is used.

b. The pain of nephrectomy, laparoscopic or open, is significant. (Analgesia can be achieved with epidural or spinal analgesia strategies or with systemic opioids for nephrectomy surgery.)

B. Specific Procedures

1. Simple and Donor Nephrectomy. Simple nephrectomy is sufficient intervention for irreversible nonmalignant disease such as untreatable infection, unsalvageable kidney trauma, or a nonfunctioning kidney caused by calculi or hypertensive disease. During donor procedures, several steps are added to simple nephrectomy, including administration of drugs intravenously just before explantation to achieve low-level anticoagulation (heparin) and forced diuresis (mannitol, furosemide).

2. Radical Nephrectomy. Renal cell carcinoma is the main indication for radical nephrectomy. Hematuria, a palpable mass, and flank pain is the classic triad at presentation.

a. Radical nephrectomy involves renal artery and vein ligation with subsequent removal en bloc of the kidney, perinephric fat, Gerota’s fascia, the proximal ureter, and often the adjacent adrenal gland.

b. Lymph node dissection is then performed from the diaphragm to the aortic bifurcation.

c. Blood loss during radical nephrectomy is highly dependent on the location and extent of the tumor. Laparoscopic innovations have reduced bleeding for all types of nephrectomy surgery.

3. Radical Nephrectomy with Inferior Vena Cava Tumor Thrombus. Between 4% and 10% of patients with renal cell carcinoma have so-called “tumor thrombus” extension beyond the kidney either limited to the renal vein or extending into the IVC. (Right atrial involvement is present in 1% of cases.)

a. There is a risk of sudden major bleeding and potential for acute hemodynamic instability (IVC clamping or tumor pulmonary embolism).

b. Because thrombus extends into the intrahepatic IVC or higher, isolating the vessel to extract the thrombus becomes more challenging and ultimately can only be achieved safely using cardiopulmonary bypass with or without aortic cross-clamping.

c. When a supradiaphragmatic tumor thrombus is present, advance placement of a pulmonary artery catheter before thrombus resection is contraindicated because of a risk of embolization of tumor fragments.

d. Despite the potential for significant blood loss, cell saver technology use is discouraged because of the potential for returning tumor cells to the circulation.

4. “Nephron-Sparing” Partial Nephrectomy. Partial nephrectomy is often sufficient for benign tumors and is becoming an alternate to radical nephrectomy for some cancerous renal cell tumors. Limitations of partial nephrectomy include a higher perioperative risk of bleeding and urine leak.

5. Laparoscopic and Robotic Nephrectomy

a. Insufflation of carbon dioxide into the peritoneal cavity or retroperitoneal space is used to separate structures and enhance visibility.

b. Laparoscopic radical nephrectomy for cancer involves smaller incisions, less blood loss, decreased postoperative analgesic requirement, shorter hospital stay and convalescent period, and similar long-term outcomes than open radical nephrectomy.

c. Laparoscopic donor nephrectomy has no adverse effects on the success of kidney transplant but is associated with less pain and analgesic requirement, faster hospital discharge, and better quality of life than open donor nephrectomy.

d. Traditional open nephrectomy is associated with a significant incidence of chronic pain. Compared to open nephrectomy, the reduced pain and shorter recovery times have meant that epidural anesthesia is less likely to be selected for laparoscopic approaches (postoperative pain control being provided by a multimodal strategy involving opiates and appropriate nonopioid adjuncts and continuous local anesthetic infusions via catheters placed in the operative area). Nonsteroidal anti-inflammatory drugs are rarely used to avoid their potential nephrotoxic effects.

e. Robotic approaches to nephrectomy surgery have similar considerations to laparoscopic nephrectomy in terms of issues such as pneumoperitoneum. Robotic nephrectomy has specific positioning requirements because of the robotic equipment, and care must be taken to ensure the robotic arms do not cause pressure injury to the patient.

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