Specialty Anesthesia
Genitourinary
GENITOURINARY PROCEDURES
1. What are the side effects of using a kidney rest?
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1. The kidney position may not only be uncomfortable but also cause serious cardiovascular (CV) and respiratory embarrassment when the kidney elevator is placed under the 12th rib.
2. What are the effects of using epidural/spinal anesthesia on the incidence of deep vein thrombosis (DVT) and why?
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2. Deep vein thrombosis (DVT) of the legs occurs more often in patients undergoing genitourinary (GU) surgery. Epidural/spinal anesthesia is thought to increase circulation and reduce blood loss, reducing the need for blood transfusion. These are both thought to reduce the occurrence of DVT.
3. What is the mechanism of postoperative urinary retention from regional anesthesia? How should this be managed?
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3. Regional anesthesia is associated with increased postoperative urinary retention. The mechanism is presumed to be delayed recovery of autonomic and somatic nerve function, eventually leading to overdistention and atony of the bladder under regional anesthesia. An indwelling catheter should be inserted prophylactically to minimize urinary retention from bladder dysfunction or vesical neck obstruction following surgery.
4. To what level should a regional block reach to prevent discomfort from bladder distention?
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4. Sensations aroused by bladder distention are mediated by sensory fibers accompanying the sympathetic and parasympathetic nerves that arise from the T9 to L2 segments of the spinal cord.
5. What is autonomic hyperreflexia? In which patients does this occur? How can this response be attenuated?
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5. If the injury is above T5, autonomic hyperreflexia develops in 66% to 85% of quadriplegics and paraplegics. It is manifested by acute generalized sympathetic hyperactivity (paroxysmal hypertension, bradycardia, cardiac dysrhythmias) in response to stimuli below the level of transection, such as catheterization or irrigation of the bladder. For full-blown paroxysmal hypertension to develop, the lesion must be above the splanchnic outflow (T4-6); T5-10 stimulation causes mild elevation of blood pressure (BP). General anesthesia or epidural/spinal anesthesia is effective in preventing this phenomenon.
6. Which factors affect testing for vesicoureteral reflux (VUR)? What problems are associated with VUR?
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6. Sedative and all inhalation anesthetics except nitrous oxide (N2O) decrease sphincter pressure to such a degree that they invalidate the results of urodynamic studies. Atropine sulfate relaxes the smooth muscle of the bladder and also invalidates urodynamic studies. Medical problems associated with vesicoureteric reflux (VUR) are renal damage, urinary tract infection, and hypertension.
7. What intraoperative problems are associated with bladder cancer surgery? Which anesthetic technique has been shown to decrease intraoperative blood loss in this procedure?
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7. Intraoperative problems associated with bladder cancer surgery include the following:
Dehydration from preoperative bowel preparations,
Bleeding,
Prolonged operative time,
Intravascular fluid loss to third-space compartment (with inability to measure urine output),
Heat loss.
Continuous epidural blockade combined with light general endotracheal anesthesia has been shown to reduce intraoperative blood loss and promote early extubation and continued postoperative analgesia.
8. To what level does testicular innervation occur? What postoperative problems are associated with orchiopexy?
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8. Testicular innervation can be traced to T10; therefore, this needs to be the height of regional anesthesia to prevent pain from testicular traction or manipulation. Orchiopexy is associated with considerable postoperative pain and a high incidence of nausea/vomiting.
9. Name two methods for performing a penile block.
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9. Methods of penile blockade are as follows:
Injection at the 2- and 10-o’clock positions at the penile base just through Buck’s fascia, plus a triangular subcutaneous ring of local at the penile base;
Blockade of penile dorsal nerves (0.25% bupivacaine, 1 to 4 mL) just superior to the pubic tubercle.
PROSTATIC SURGERY
1. What are the complications of using distilled water for continuous irrigation during transurethral prostatic resection (TURP)?
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1. Using distilled water as irrigation for transurethral prostatic resection (TURP) can lead to the following:
Water intoxication with hypo-osmolality,
Excessive dilutional hyponatremia → intravascular hemolysis,
Acute renal failure (ARF),
Central nervous system (CNS) symptoms ranging from confusion to convulsions and coma.
2. Which factors determine the amount of absorption of irrigating fluid?
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2. Amount of absorption of irrigating fluid is determined by the following:
Height of the container of irrigating fluid above the patient,
Duration of resection,
Number and size of venous sinuses opened during resection.
On average, 10 to 30 mL of fluid are absorbed per minute of resection time.
3. What has been the most common cause of death after TURP? What is the most common cause recently? What other diseases are common in these patients?
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3. CV complications were the most common cause of death after TURP, but more recently, it has been sepsis. Common findings in these elderly patients include pulmonary disease, hypertension, angina, congestive heart failure (CHF), cardiac conduction abnormalities, diabetes mellitus, infection, stroke, and renal insufficiency.
4. Which complications of TURP are particularly significant to anesthesiologists?
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4. TURP complications of particular concern to anesthesiologists include the following:
Intravascular fluid absorption: fluid overload, serum hypo-osmolality, hyponatremia, hyperglycinemia, hyperammonemia, hemolysis, hypothermia, and bacteremia;
Excessive bleeding and coagulopathy;
Perforation of bladder or urethra with extravasation (intra- or extraperitoneal).
5. What is TURP syndrome? What are the symptoms in the awake patient? How can regional anesthesia be beneficial for TURP?
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5. TURP syndrome describes increases in circulating blood volume and in dilution of serum electrolytes and increases in systolic, diastolic, and pulse pressure, with accompanying bradycardia. The awake patient may show symptoms of restlessness, nausea/vomiting, mental confusion, skeletal muscle twitching, and visual disturbance. Symptoms may progress to hypotension with cyanosis, dyspnea, cardiac dysrhythmias, lethargy, seizures, and occasionally death. A major component is severe hyponatremia.
Regional anesthesia produces sympathetic blockade and increases venous capacitance, which tends to reduce the likelihood of intraoperative fluid overload during TURP.
6. At what sodium level do significant problems develop?
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6. Hyponatremia contributes to negative inotropic effects and hypotension. Serum sodium levels and their effects are as follows:
120 mEq/L: borderline for the appearance of severe TURP syndrome;
<120 mEq/L: CNS symptoms (confusion and restlessness);
<115 mEq/L: electrocardiogram (ECG) changes characterized by a wide QRS complex and ST-segment elevation;
102 mEq/L: seizures, cardiac dysrhythmias, hypotension, and pulmonary edema;
<100 mEq/L: consciousness may be lost.
7. What are the unique complications from glycine and its metabolic byproduct?
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7. Glycine causes temporary visual disturbances (including transient blindness), mild depression, and confusion. It is an inhibitory neurotransmitter (like Gamma-aminobutyric acid [GABA] on chloride ion channels).
8. What are the treatments for TURP syndrome?
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8. Treatment for TURP syndrome:
Terminate surgery as soon as possible;
Optimize oxygenation;
Determine serum sodium, arterial blood gases (ABGs), and osmolality;
Institute invasive monitoring in patients with CV instability or pulmonary edema;
Administer diuretics and hypotonic saline.
In 66% of cases, the situation is corrected with furosemide (Lasix) and observation.
9. What signs/symptoms will occur with disseminated intravascular coagulation (DIC) after TURP? Which drug can be administered to produce a reduction of hematuria following TURP?
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9. Disseminated intravascular coagulation (DIC) is characterized by the following:
Thrombocytopenia,
Marked shedding of red blood cells (RBCs) from the blood clot,
Decreased fibrinogen,
High titer of fibrin degradation products (FDP),
Decreased Prothrombin time (PT),
Decreased concentration of clotting factors (V, VIII).
Successful treatment depends on rapid assessment of the degree and nature of the coagulation disorder. Epsilon-aminocaproic acid (plasminogen activator inhibitor) will decrease hematuria postoperatively in prostate resection patients.
PROSTATECTOMY AND UROLOGIC PROCEDURES
1. What are the signs/symptoms of bladder perforation?
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1. Most bladder perforations are extraperitoneal, with pain in the periumbilical, inguinal, or suprapubic region. In intraperitoneal perforation, pain may be generalized in the upper abdomen or referred from the diaphragm to the precordial region or the shoulder.
2. For which TURP patients is general anesthesia indicated? What are the benefits of using regional anesthesia for TURP?
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2. General anesthesia may be indicated for TURP patients under the following circumstances:
Needing pulmonary support,
Unable to tolerate IV infusion of fluids to compensate for the rapid loss of sympathetic tone from regional anesthesia,
Needing invasive monitoring.
Regional anesthesia techniques for TURP allow the awake patient to aid in early recognition of intravascular absorption of irrigating fluid, early signs of fluid overload, and water intoxication, as well as early diagnosis and treatment of urinary bladder perforation with extravasation of irrigating fluid. These techniques are also believed to reduce blood loss.
3. Which factors influence the choice of anesthetic technique for open prostatectomy?
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3. Factors influencing anesthetic technique for open prostatectomy include the following:
Status of cardiopulmonary system,
Patient position during surgery,
Mental status.
Uncooperative patients are more easily managed by general anesthesia.
4. What are the possible complications of percutaneous ultrasonic lithotripsy?
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4. Complications of percutaneous ultrasonic lithotripsy include the following:
Acute hyponatremia,
Acute hemolysis with hyperkalemia (sudden absorption of a bolus of water),
Air embolism.
5. What is the effect of immersion in a water bath for extracorporeal shock wave lithotripsy (ESWL)?
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5. Immersion in a water bath for extracorporeal shock wave lithotripsy (ESWL) has been shown to augment cardiac preload as a result of compression of peripheral vessels by hydrostatic pressure and a shift of blood volume into the central vascular compartment. Patients with dilated hearts, dilated left atrium, paroxysmal tachycardia, frequent extrasystoles, or syncope should be properly evaluated and treated preoperatively.
6. Which disease processes are contraindications to ESWL with immersion in a tub?
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6. Contraindications to ESWL with immersion include the following:
Aortic aneurysm,
Hemangioma in the vertebral canal,
Orthopedic implants in the lumbar region,
Pregnancy,
Morbid obesity,
Artificial cardiac pacemaker.
Coagulation defects may also be a contraindication.
7. Name some of the intraoperative complications of ESWL.
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7. Intraoperative complications of ESWL include the following:
Cardiac dysrhythmias (from the discharge of shock waves independent of the cardiac cycle),
Renal subcapsular hematoma,
Myocardial ischemia and infarction,
Cerebrovascular accident.
8. Which factors should be included for optimal anesthetic management of patients undergoing ESWL?
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8. Optimal anesthetic management of patients undergoing ESWL involves the following:
All equipment needed for airway control in the room;
Cardiac defibrillator and well stocked emergency cart;
Good-quality ECG tracing, waterproof ECG pads (for ESWL with immersion), and properly positioned leads;
Pulse oximeter;
Invasive lines for high-risk patients.
Renal
RENAL PHYSIOLOGY
1. From which segments do the vasomotor and pain fibers supplying the kidney arise?
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1. Vasomotor and pain fibers to the kidney arise from T4-12, cranial nerve X (through the celiac axis), and the splanchnic nerves.
2. What are the three functions of the kidney? Which factors alter the function of the kidney?
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2. The three functions of the kidney include the following:
Filtration,
Reabsorption,
Secretion.
Renal filtration and absorption may be altered by trauma, surgical stress, and anesthesia.
3. What is the normal glomerular filtration rate (GFR)?
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3. Normal glomerular filtration rate (GFR) is 125 mL/h in adults. The kidneys receive 20% to 25% of the total cardiac output (CO): 1000 to 1250 mL/min in adults.
4. How is sodium reabsorbed in the kidney?
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4. The kidney filters >25,000 mEq of sodium per day, of which 65% is reabsorbed by the proximal renal tubule. An additional 25% of filtered sodium is actively reabsorbed as the filtrate passes through the ascending loop of Henle. Therefore, only 10% of the original sodium enters the distal tubule. The reabsorption of this small amount is influenced by aldosterone. Only approximately 1% of filtered sodium is ultimately excreted in the urine.
5. How is water reabsorbed in the kidney?
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5. Water is reabsorbed to a variable extent in the distal tubule, cortical collecting tubules, and the medullary collecting ducts. Antidiuretic hormone (ADH) regulates the amount of water reabsorbed in the collecting ducts. Reabsorption of sodium and water depends on the countercurrent multiplier system in the loop of Henle (a hypertonic medullary interstitium).
6. Which factors affect the reabsorption of sodium and water?
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6. Sodium and water reabsorption are affected by the following:
Hormonal factors,
Aldosterone,
ADH,
Atrial natriuretic factor (ANF),
Renal prostaglandins.
7. What is involved in the release of aldosterone?
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7. Aldosterone regulates sodium-potassium balance and BP. It is produced by the adrenal cortex in response to a chain of humoral mediators as follows:
Renin is released by the juxtaglomerular cells of the kidney (in response to the sympathetic nervous system [SNS], stimulation of intrarenal baroreceptors, or reduced delivery of sodium chloride to the macula densa);
Renin catalyzes the release of angiotensin I from angiotensinogen;
Angiotensin I is converted to angiotensin II in the lung;
Angiotensin II stimulates the cells of the adrenal cortex to produce aldosterone.
8. What is involved in the release of antidiuretic hormone (ADH)?
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8. ADH is released from the posterior pituitary gland in response to changes in both volume and osmolarity as follows:
Increased blood osmolarity is sensed or stimulated by the osmoreceptors of the hypothalamus;
It is inhibited by increased stretch of atrial baroreceptors when atrial volume is increased.
9. What stimulates the release of atrial natriuretic factor (ANF)? What is the effect of ANF?
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9. ANF is secreted by the cardiac atria. It reduces BP by the following:
Relaxation of vascular smooth muscle,
Reduction of sympathetic vascular stimulation,
Extravasation of intravascular fluid into the interstitial space.
Atrial natriuretic peptide (ANP) antagonizes sodium retention by inhibiting renin and aldosterone secretion.
10. What is the neuroendocrine response to trauma?
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10. The neuroendocrine response to trauma (decreased circulating volume) involves the release of ADH, aldosterone, and catecholamines → decreased urinary excretion of sodium and water.
RENAL PHARMACOLOGY
1. How does surgery and anesthesia alter autonomic and neuroendocrine function?
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1. The effects of surgery and anesthesia on autonomic and neuroendocrine function are as follows:
Epinephrine and norepinephrine are released in response to either noxious stimuli or hypovolemia, causing renal vasoconstriction and release of renin;
Anesthetics may cause increased secretion of ADH and aldosterone either directly or as a result of changes in BP or CO.
2. What is the effect of positive-pressure ventilation on urine output?
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2. Positive-pressure ventilation causes decreased urinary output associated with a decrease in CO, increased sympathetic flow, and release of renin.
3. Which inhalation anesthetics may have the greatest renal effects?
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3. Methoxyflurane causes the greatest nephrotoxicity with metabolism to an inorganic fluoride ion. Clinically, this is manifested by hyposmotic diuresis, azotemia, hypernatremia, and hyperosmolality.
4. What is the etiology of inhalation anesthetic effects on the kidney? How does this correspond clinically?
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4. The volatile anesthetics may be metabolized to different extents by the liver. The inorganic fluoride ion metabolite can cause renal dysfunction that manifests clinically as a decreased urinary concentrating ability and decreased responsiveness to vasopressin (Pitressin).
5. Which factors influence the effects of inhalation anesthetics on the kidney?
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5. The inhalation anesthetics may directly influence renal function: renal blood flow (RBF), sodium excretion, osmolal clearance, and urinary volume. They may also affect sympathetic innervation, the renin-angiotensin system, release of ADH, and release of catecholamines.
6. What are the effects of regional anesthesia on renal physiology?
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6. Effects of regional anesthesia on the kidney:
Spinal: only slight decreases in GFR and RBF despite anesthetized levels to T-1; these lead to parallel decreases in mean arterial pressure (MAP);
Epidural: minimal changes in GFR and RBF due to minimal change in systemic hemodynamics.
7. Which electrolyte abnormalities may be seen with the thiazide diuretics?
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7. The thiazide diuretics may produce the following:
Hypokalemia,
Metabolic alkalosis,
Hyperuricemia,
Hyperglycemia.
CHRONIC RENAL FAILURE
1. What percentage of the kidney may be destroyed before clinical symptoms develop?
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1. There are no signs/symptoms or laboratory abnormalities until 60% of functioning nephrons have been destroyed. With 10% to 40% of functioning nephrons, there are only mild signs of renal failure, such as nocturia (decreased concentrating ability). These patients may function well but have little or no renal reserve. Loss of 95% of functioning nephrons leads to uremic syndrome. This includes all of the problems of overt renal failure requiring dialysis: fluid overload, CHF, and electrolyte, hematologic, and acid-base disturbances.
2. What are the characteristics of dialysis-dependent renal failure?
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2. The characteristics of dialysis-dependent renal failure include metabolic acidosis, platelet dysfunction, fluid overload, electrolyte disorders, central and peripheral nervous system abnormalities, autonomic dysfunction, gastrointestinal (GI) disorders, anemia, and immunologic dysfunction. These manifest as follows:
CHF (sodium and water retention),
Hypertension,
Left ventricular hypertrophy,
Hyperkalemia (fatal cardiac arrhythmias),
Uremic encephalopathy,
Nausea/vomiting,
GI bleeding.
3. Which electrolyte abnormalities are common in chronic renal failure?
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3. Common electrolyte disturbances seen in chronic renal failure (CRF) include the following:
Hyperkalemia,
Hyponatremia,
Hyper- and hypocalcemia,
Hypermagnesemia,
Hypophosphatemia.
4. How is oxygenation improved despite anemia in patients with chronic renal failure?
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4. Patients with CRF are chronically anemic (hemoglobin: 5 to 7 g/dL) because of decreased levels of erythropoietin and decreased RBC survival time. This is usually well tolerated because of slow onset and cardiac compensation (increased stroke volume and decreased blood viscosity). Tissue oxygenation is improved by rightward shift of the oxyhemoglobin dissociation curve (metabolic acidosis and increased 2,3-diphosphoglycerate [DPG]).
5. How is the clotting cascade inhibited in dialysis patients as the blood contacts the dialysis tubing and machine? Is this process neutralized?
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5. Patients with CRF are systemically or regionally heparinized for dialysis to counteract the clotting cascade stimulated by blood contact with the foreign body, dialysis machine tubing. In regional heparinization, heparin is added to the arterial limb of the dialysis machine, which is then neutralized with protamine sulfate in the venous line.
6. What are the complications of dialysis?
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6. Complications of dialysis include the following:
CNS: Disequilibrium syndrome, dialysis dementia, and progressive intellectual dysfunction;
CV: Hypotension;
Respiratory: Hypoxemia;
Neuromuscular: Cramping;
Nutritional: Protein depletion, hyperglycemia, and peritonitis.
ANESTHETIC MANAGEMENT IN CHRONIC RENAL FAILURE
1. Under which situation will laboratory tests inaccurately reflect renal function?
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1. Laboratory tests fail to accurately reflect the status of the kidneys in a large percentage of patients, especially elderly, malnourished, or dehydrated patients.
2. Which laboratory tests are commonly used to evaluate renal function? Which factors can affect their value?
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2. Commonly used laboratory tests to evaluate renal function include the following:
Urinalysis
Blood urea nitrogen (BUN)
Creatinine
Creatinine clearance
Creatinine clearance is the best overall indicator of GFR. Hepatic dysfunction decreases urea production and therefore BUN. It may also be affected by dehydration, variable protein intake, GI bleeding, and a catabolic state. Creatinine is low in the elderly and those with muscle wasting. It may be high in those heavily muscled or acutely catabolic (rapid muscle breakdown). Creatinine clearance may be affected by weight, inaccurate urine volume measurement, advanced age, catabolic state, and muscle mass.
3. How do you calculate creatinine clearance?
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3. Creatinine clearance may be calculated in one of two ways:
GFR = (140 – age) × Wt/(72 × serum creatinine), or
GFR = urine creatinine × urine volume/plasma creatinine
Wt: weight in kg, but multiply by 0.8 for women;
Using either a 2- or 24-hour urine collection.
4. What are the unique anesthetic considerations for anephric patients?
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4. Anesthetic considerations for anephric patients:
Preoperative evaluation: Adequacy of dialysis (volume status, acid-base), hemoglobin concentration and CV status;
Monitoring: BP, HR, ECG, pulse oximeter, capnometer, peripheral nerve stimulator, and invasive CV monitors (as needed);
Fluid management: cautious, no contraindications to packed red blood cells PRBCs; the patient may be dialyzed postoperatively if needed.
5. Which intravenous (IV) agents require a reduction in dosage for patients with renal impairment and why?
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5. Anesthetic agents requiring a reduction in dosage for patients with renal impairment include the following:
Sodium thiopental (STP): requires lower induction dose;
Benzodiazepines: cause an exaggerated response;
Morphine and anticholinesterase: agents have prolonged effect;
Succinylcholine: avoid if serum potassium >6.0 mEq/L;
Pancuronium bromide and d-tubocurarine: have delayed excretion.
Use of some of these agents is prolonged because they have a greater amount of unbound, bioavailable drug owing to the acidic pH of renal failure. Uremia alters the blood-brain barrier, increasing the sensitivity to IV agents.
6. How are the neuromuscular blocking-reversal agents affected by renal failure?
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6. The anticholinesterases undergo elimination primarily through the kidney. Therefore, renal failure prolongs the duration of action of neuromuscular blocking-reversal agents by at least 100%.
7. Which other factors affect the reversal of neuromuscular blockade?
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7. Other factors affecting the reversal of neuromuscular blockade include the following:
Temperature,
Depth of blockade,
Acid-base status,
Use of potentiating drugs such as antibiotics or diuretics.
ACUTE RENAL FAILURE
1. What is the incidence of mild to moderate renal dysfunction postoperatively? Which procedure is most commonly associated with acute renal failure (ARF)?
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1. Mild to moderate renal dysfunction occurs in 23% of patients, especially those with preexisting hypertension or diabetes mellitus (DM). CV surgery is most commonly associated with postoperative ARF (due to extensive tissue manipulation, loss of plasma volume into the interstitium, and variable to massive hemorrhage).
2. Which factors are involved in the pathogenesis of ARF (including initiating and maintenance factors)?
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2. The primary factor involved in the initiation of ARF is renal hypoperfusion (hemodynamic factors and nephrotoxins). ARF is maintained by the following:
Tubular dysfunction,
Tubular obstruction,
Decreased GFR,
Decreased RBF.
Once maintenance begins, improving RBF will not reverse ARF.
3. Name three drugs commonly used to treat acute renal insults. Describe their benefits and deficiencies.
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3. Three drugs (with their benefits and deficiencies) commonly used to treat ARF include the following:
Mannitol Improves cortical RBF and may exert a renal protective effect; it is ineffective in reversing profound reductions in GFR and RBF produced by renal cross-clamping;
Dopamine Induces natriuresis, increases GFR, and improves urinary flow; it is ineffective in reducing the effects produced by renal cross-clamping. (Fenoldapam mesylate, a new dopamine1-receptor agonist, enhances urinary flow, sodium excretion, and creatinine clearance while decreasing systemic vascular resistance [SVR]. Its role in ARF is still to be proved.)
Furosemide Less effective than mannitol in complete renal ischemia but useful in combination with dopamine.
Other drugs have been used experimentally to reduce the incidence and severity of ARF caused by the depletion of high-energy phosphate bonds and the production of high intracellular calcium (adenine nucleotides and calcium channel blockers) and O2 free radicals (superoxide dismutase and O2 free radical scavengers), as well as leukotrienes and neutrophils. Sodium bicarbonate has also been shown to attenuate a serum chromium rise when given before renal ischemia.
4. What are the three patterns of ARF?
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4. Three patterns of ARF have been described:
ARF: Abrupt decline in creatinine clearance followed by a steady improvement in renal function (low mortality);
Overt ARF: Sustained prerenal insult, recovery of which is dependent on hemodynamic improvement;
Protracted ARF: The net effect of multiple ischemic insults (high mortality).
5. At what pulmonary microvascular pressure does pulmonary edema occur? In what percentage of patients with ARF do pulmonary complications develop? What are the mortality rates for ARF and adult respiratory distress syndrome (ARDS)?
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5. In normal patients, the pulmonary microvascular pressure associated with the development of pulmonary edema is 25 mm Hg. It may be decreased in patients with decreased serum oncotic pressure or increased capillary permeability. Pulmonary complications develop in 40% of patients with ARF, and ARF develops in 50% of patients with adult respiratory distress syndrome ARDS. The mortality of ARDS or ARF is 50% to 70%.
6. Which factors must be considered in managing patients with ARF?
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6. Factors in the management of patients with ARF include the following:
Timing and selection of renal replacement techniques;
Pharmacologic management: decreased drug doses in ARF;
Careful monitoring of:
Fluid and electrolyte therapy;
Nutritional support;
Infection (the most common cause of death in ARF);
Maintenance of appropriate hemodynamic monitoring.
7. What are the indications for acute dialysis therapy?
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7. Indications for acute dialysis:
Fluid overload,
Azotemia,
Hyperkalemia,
Severe acid-base disturbances.
Organ Transplant
TRANSPLANT—I
1. What are the four common physiologic derangements seen after brain death? What are their causes?
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1. The common physiologic derangements (and their causes) following brain death are as follows:
Hypotension: Hypovolemia due to diabetes insipidus or hemorrhage, or neurogenic shock;
Hypoxemia: Neurogenic pulmonary edema, pulmonary contusion, pneumonia, gastric aspiration, or fluid overload;
Hypothermia: Hypothalamic infarction or exposure;
Dysrhythmias (especially bradycardia): Intracranial injury or hematoma, hypothermia, hypoxia, electrolyte abnormality, or myocardial contusion or ischemia.
2. What are the anesthetic goals for the donor?
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2. Anesthetic goals for the donor include the following:
Maintenance of donor organ perfusion and oxygenation,
Suppression of reflex neuromuscular activity (mediated by spinal somatic reflexes) with relaxants.
3. When is heparin given?
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3. Heparin is administered after the liver is flushed with cold preservative solution. After this, the abdominal aorta is cross-clamped and perfused with cold preservative. Cardiectomy is performed once in situ preservation of the abdominal viscera is begun.
4. What is the action of cyclosporine (Sandimmune)?
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4. Cyclosporine is an antibiotic isolated from a soil fungus. It prevents helper T-cell activation by antigen and inhibits elaboration of T cell-derived factors, particularly interleukin-2.
5. What are the effects of transfusion on graft survival (particularly the kidney) and why?
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5. Blood transfusion before renal transplant has been shown to have a significant beneficial effect on graft survival. It is thought to be because of the induction of specific immunologic nonreactivity to the transfused histocompatibility antigens.
6. Which factors should be ascertained when dialysis precedes surgery?
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6. When dialysis precedes surgery, it is important to determine the net volume status of the following in the patient:
Final hematocrit,
Electrolyte (K+, Ca2+) and bicarbonate levels,
Any residual heparin effect.
7. Which of the nondepolarizing muscle relaxants (NDMRs) have an active metabolite? What is the metabolite? What are its effects?
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7. Atracurium besylate (Tracrium) is metabolized to laudanosine, which is excreted through the kidneys. Laudanosine increases the minimal alveolar concentration (MAC) of halothane in experimental animals, but not humans. It may also cause seizures at high levels.
8. Why does coagulopathy develop in patients with end-stage liver disease?
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8. A coagulopathy develops in patients with end-stage liver disease because of decreased synthesis of hepatically derived factors: I (fibrinogen), II (prothrombin), V, VII, IX, and X. Clearance of fibrinolytic factors is also decreased. Hypersplenism may diminish the platelet count.
TRANSPLANT—II
1. What is the absolute contraindication to heart transplantation?
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1. Heart transplantation is absolutely contraindicated if the recipient has irreversible pulmonary hypertension. The donor right ventricle will be unable to cope with the fixed elevated pulmonary vascular resistance (PVR) and will rapidly decompensate.
2. Which factors jeopardize the donor lungs for transplant?
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2. Donor lungs may be jeopardized by the following:
Massive fluid resuscitation,
Aspiration,
Pulmonary contusion,
Exposure to nonphysiologic O2 tensions.
3. What is involved in the anesthetic management of the lung recipient?
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3. Anesthetic management in the lung recipient:
Placing a double-lumen endotracheal tube (ETT) or bronchial blocker (for surgical exposure);
Administering drugs that do not cause histamine release;
Avoiding N2O in patients with bullae or an elevated PVR or requiring 100% O2 to maintain acceptable arterial saturation;
Maintaining oxygenation during one-lung ventilation utilizing positive end-expiratory pressure (PEEP), continuous positive airway pressure (CPAP), or high-frequency ventilation, which may be needed in the dependent lung, as well as ligation of the nondependent pulmonary artery;
Avoiding “stress” doses of glucocorticoids (to protect from systemic sepsis or suture line dehiscence);
Minimizing fluid administration.
4. What is the fluid management for renal transplant in children?
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4. In pediatric renal transplantation, fluid boluses and vasoactive infusions (dopamine) are used to maintain systemic BP in the high-normal range. Adult kidneys placed in children will initially produce adult-sized urine volumes. Maintenance fluid volumes must be adjusted accordingly.
5. What is the Kasai procedure?
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5. The Kasai procedure is a choledochojejunostomy performed for decompression in children with biliary atresia.
6. What are the limits of venovenous bypass?
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6. Venovenous bypass alleviates lower-body venous congestion during portal vein and inferior vena cava occlusion during liver transplantation. It is not feasible in patients weighing <20 kg, so oliguria and intestinal complications may develop in these children.
7. What are the side effects/toxicities of cyclosporine?
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7. Cyclosporine side effects and toxicities include the following:
Acute and chronic nephrotoxicity: interstitial renal fibrosis or tubular atrophy with elevated blood urea nitrogen (BUN) and creatinine levels;
Systolic and diastolic hypertension;
Hepatotoxicity;
Hyperuricemia;
Gingival hypertrophy;
Seizures or neurotoxicity.
8. What are the chronotropic/inotropic effects of a transplanted heart?
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8. The chronotropic/inotropic effects of a transplanted heart include the following:
Permanent autonomic denervation with a prolonged response to increases in demand (i.e., with exercise, an increase in HR will eventually develop, most likely because of the time required for the secretion and response to catecholamines),
Preload dependent on CO for increases,
Normal stroke volume and myocardial contractility.
Denervation generally does not alter the atrioventricular conduction time or affect ventricular conduction.
9. Which is the drug of choice for heart-transplant patients to increase contractility and heart rate and why?
View Answer
9. The drug of choice for increasing heart rate (HR) and contractility in the denervated transplanted heart is isoproterenol. It acts directly on the myocardium or cardiac conduction tissue to exert its effects.
Obesity
ANESTHESIA AND OBESITY
1. Define morbid obesity.
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1. Morbid obesity is defined as follows:
Weighing >45 kg above ideal body weight (IBW), or
Having a body mass index (BMI) >35.
BMI = Wt/Ht2.
Wt: weight in kg;
Ht: height in meters.
Obesity is classified as weighing 20% above IBW or having a BMI >28.
2. What are the characteristics of android obesity?
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2. Android obesity is primarily of truncal distribution. It is associated with increased O2 consumption and an increased incidence of CV disease.
3. What are the characteristics of gynecoid obesity?
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3. Gynecoid obesity describes a fat distribution primarily on the buttocks and thighs; the fat is metabolically less active and less closely associated with CV disease.
4. What effect does obesity have on the respiratory system?
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4. Obese people have the following conditions:
Increased: O2 consumption, carbon dioxide (CO2) production, and energy expenditure for locomotion, breathing, and maintaining normocarbia;
Decreased: Chest wall compliance, functional residual capacity (FRC), and expiratory reserve volume (ERV).
Lung compliance is normal, but there is respiratory muscle insufficiency.
5. What are the implications of changes in static lung volumes?
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5. When static lung volumes change (normal residual volume but decreased ERV and FRC in the upright position), tidal ventilation may fall in the range of closing capacity with ensuing ventilation—perfusion ([V with dot above]/[Q with dot above]) abnormalities or frank R → L shunt with ensuing hypoxemia. As mass loading is increased by the patient lying supine, FRC often falls further within the range of closing capacity, with worsening hypoxemia.
6. What is the obesity hypoventilation syndrome? Name some of the causes.
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6. Obesity hypoventilation syndrome includes a loss of hypercarbic drive, sleep apnea, hypersomnolence, and potential or overt airway difficulties.
7. What is Pickwickian syndrome?
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7. Pickwickian syndrome involves hypercarbia, hypoxemia, polycythemia, hypersomnolence, pulmonary hypertension, and biventricular failure.
8. What are the effects of obesity on the cardiovascular system?
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8. Effects of obesity on the CV system include increases in the following:
Circulating blood and plasma volume,
CO,
Stroke volume,
Left ventricular (LV) end-diastolic pressure and pulmonary capillary wedge pressure with exercise or stress,
Preload and afterload,
Pulmonary volume and flows.
HR is normal. Patients with any degree of CV compromise are particularly at risk in the perioperative period. Morbidly obese patients with increased LV wall thickness but without other demonstrable cardiac disease have been found to have normal ejection fractions, but they cannot mount an increase in ejection fraction in response to exercise.
PATHOPHYSIOLOGY OF OBESITY
1. What effect does morbid obesity have on the endocrine system?
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1. A major endocrine effect of morbid obesity is impaired glucose tolerance with pancreatic islet cell hypertrophy and hyperinsulinemia irrespective of the state of carbohydrate intolerance. This is reflected in a high prevalence of DM in the morbidly obese patients. Abnormal serum lipid profiles are often found and may be associated with an increased prevalence of ischemic heart disease.
2. Name four gastrointestinal (GI) effects of morbid obesity.
View Answer
2. GI effects of morbid obesity include increases in the following:
Prevalence of hiatal hernia,
Intra-abdominal pressure with increasing weight (linear increase),
Resting gastric volume (>25 mL),
Gastric acidity (pH <2.5).
3. How may morbid obesity affect hepatic function?
View Answer
3. Effects of morbid obesity on hepatic function include increased liver fat content in 90% of the morbidly obese, which appears to reflect duration rather than the degree of obesity. Hepatic dysfunction is high in patients who have undergone intestinal bypass operations.
4. What are the anatomic changes in the airway of morbidly obese patients?
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4. Anatomic airway changes in the morbidly obese include the following:
Limitation of cervical spine and atlantoaxial joint flexion by numerous chins and thoracic wall and breast fat; extension of these joints may be limited by low cervical or upper thoracic fat pads;
Restricted mouth opening by submental fat;
Narrowing of the airway by fleshy cheeks, a large tongue, and copious flaps of palatal, pharyngeal, and supralaryngeal soft tissue;
High-and-anterior (infantile) position of the laryngeal aperture.
The morbidly obese have a high prevalence of obstructive apnea syndrome.
5. Which drugs have altered biotransformation in morbidly obese patients?
View Answer
5. Drug biotransformation may be altered in the morbidly obese by hepatic disease, DM, or changes in splanchnic blood flow. Lipophilic drugs such as benzodiazepines and thiopental sodium (Pentothal) have an increased volume of distribution, more selective distribution to fat stores, and a longer elimination half-life. Clearance is normal. The implication is that fat-soluble volatile anesthetics have a prolonged elimination time, with a consequent slow recovery. However, for prolonged recovery, these agents would have to be administered for periods >24 hours. Hydrophilic drugs in the obese have a similar volume of distribution, elimination half-life, and clearance, as they do in normal-weight patients.
6. What are the effects of morbid obesity on the degradation of succinylcholine and the NDMR vecuronium bromide (Norcuron)?
View Answer
6. Morbidly obese patients have higher pseudocholinesterase activity. Doses of succinylcholine of 1.2 to 1.5 mg/kg are advised. Recovery of vecuronium (in mg/kg doses) in morbidly obese patients is slower than in normal-weight subjects.
OBESITY AND PREOPERATIVE ASSESSMENT
1. Name four things you should look for during the preoperative evaluation of the cardiovascular system in obese patients.
View Answer
1. The CV system must be assessed for the following:
Hypertension,
Signs of left or right ventricular (RV) failure,
Signs of pulmonary hypertension.
Patients must also be assessed for venous access and arterial cannulation. (Intra-arterial cannulation is advised for all but the shortest and simplest cases because cuff BP monitoring may be both difficult and inaccurate in obese patients.)
2. What should you look for on the preoperative electrocardiogram (ECG) and chest x-ray?
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2. In the obese, preoperative ECG should be assessed for evidence of ischemic heart disease and LV or RV hypertrophy. Chest x-ray should be assessed for an increase in cardiac size and pulmonary congestion.
3. Which obese patients should definitely have a cardiology evaluation?
View Answer
3. Obese patients should be assessed by a cardiologist preoperatively if they have the following:
Any evidence of ischemic heart disease,
LV or RV hypertrophy,
Increase in cardiac size, or
Pulmonary congestion.
In addition, any obese person with evidence of obesity hypoventilation syndrome or Pickwickian syndrome should also be evaluated to best optimize the patient management before surgery.
4. Which laboratory tests should be performed preoperatively in obese patients and why?
View Answer
4. Preoperative laboratory tests in obese patients should include the following:
Fasting blood glucose,
Urine for ketones,
Routine liver function tests.
If gross carbohydrate intolerance, diabetes mellitus, or ketosis is found, it should be corrected before elective or emergency procedures are performed.
5. What should be included in the physical examination of the airway in obese patients?
View Answer
5. The physical examination of obese patients should include the following:
Range-of-motion testing of the atlantoaxial joint and cervical spine,
Degree to which the mouth can open,
Distance between the chin and the hyoid cartilage.
The interior of the mouth and pharynx should be scrutinized for excessive folds of tissue. The Mallampati classification, based on the ability to visualize the uvula, may help identify patients with potentially difficult laryngeal visualization.
6. What type of premedication is advised for obese patients?
View Answer
6. In the obese, premedication, if any, should be given IV or orally. Intramuscular injections will usually result in intrafat injections with unpredictable absorption. Because of the high incidence of respiratory disease in the morbidly obese, premedication should not be administered until the patient is in a safely monitored environment. Because the obese also have a high incidence of reflux, they should preoperatively receive a clear antacid, metoclopramide (Reglan), and histamine2 (H2) blockers to lower the volume and increase the pH of the stomach contents.
OBESITY AND PERIOPERATIVE MANAGEMENT
1. Name three reasons why obese patients should be intubated for general anesthesia procedures.
View Answer
1. General anesthesia through endotracheal intubation is recommended in the obese for three main reasons:
Difficulty maintaining a gas-tight fit with a mask,
High risk for aspiration of stomach contents,
Hypoventilation → hypoxia or hypercarbia if allowed to breathe spontaneously.
2. For which morbidly obese patients is awake tracheal intubation recommended?
View Answer
2. Awake tracheal intubation is recommended in all patients >75% above IBW. Many patients with a history of sleep apnea or those undergoing procedures for this condition may also require awake tracheal intubation because of difficulties in placing the ETT after these patients are under general anesthesia.
3. What is the effect of obesity on the metabolism of inhalation anesthetics? Which is the inhalation agent of choice?
View Answer
3. Obese patients metabolize volatile anesthetics to a greater extent than do normal patients. Isoflurane (Forane) is metabolized the least and is therefore the agent of choice.
4. Is there prolonged recovery from fat-soluble volatile anesthetics in obese patients?
View Answer
4. No. Obese patients do not have a prolonged recovery from fat-soluble volatile anesthetics.
5. What is the best method of ventilating obese patients? Spontaneous respiration? What may be the effect of hyperventilation?
View Answer
5. Intermittent positive-pressure ventilation (IPPV) is the recommended method of ventilating obese patients. Hyperventilating to a Paco2 <30 mm Hg should be avoided because it may result in a rise in shunt fraction. Spontaneous respiration is relatively contraindicated in the obese because the hypoventilation produced by general anesthesia may lead to hypoxia and hypercarbia in patients predisposed to respiratory compromise.
6. How does obesity affect the dose of subarachnoid and epidural local anesthetics?
View Answer
6. The dose requirements for subarachnoid and epidural anesthesia are 75% to 80% of those of normal-weight patients; they are also more variable than in normal-weight patients. However, postoperative epidural requirements for analgesia appear to be similar to those in normal-weight patients for both local anesthetics and opioids.
Gastrointestinal
GI DISORDERS
1. Which circumstances are associated with reduced lower esophageal sphincter (LES) tone?
View Answer
1. Lower esophageal sphincter (LES) tone may be reduced by the following:
Pregnancy,
Obesity,
Hiatal hernia.
It may also be affected by a number of drugs.
4. Which patients have a high resting gastric content volume?
View Answer
4. Pregnant women, the obese, and patients who are bedridden or have experienced pain, stress, shock, and trauma have a high resting gastric content volume.
5. What volume of secretions is produced by the stomach and by the small intestine?
View Answer
5. Volume of secretions per day is as follows:
Gastric: 2000 mL; pH 1.0 to 3.5;
Small intestine: 2000 mL; pH 7.0 to 8.0.
The colon absorbs approximately 400 to 500 mL/d.
6. What is proposed to be the optimal hematocrit for healing?
7. What methods can be utilized to decrease the risk of regurgitation and pulmonary aspiration?
View Answer
7. The risk of regurgitation and pulmonary aspiration may be reduced by the following:
Reducing the volume of the stomach content: nasogastric tube, induced vomiting, accelerated gastric emptying with drugs (e.g., metoclopramide);
Raising the gastric content pH with clear antacids and H2 blocker,
Increasing LES tone (e.g., metoclopramide).
8. What problems may be encountered in patients with carcinoid syndrome?
View Answer
8. Likely problems in patients with carcinoid syndrome include the following:
Bronchospasm provoked by histamine-releasing drugs,
Hypotension secondary to innate fluid deficit and hormone release,
Hypertension, probably due to tumor release of serotonin.
Liver
ANESTHESIA AND THE LIVER
1. What is the primary cause of severe jaundice postoperatively? What percentage of asymptomatic surgical patients may have significant liver disease?
View Answer
1. The primary cause of severe jaundice postoperatively is bilirubin overload. This results primarily from blood transfusions combined with disturbances in hepatic cellular metabolism that compromise the ability of the liver to excrete bilirubin. Before anesthesia and surgery, 0.15% of completely asymptomatic patients actually have significant liver disease.
2. In the National Halothane Study, which factors were found to be the primary causes of jaundice? In what percentage of patients was hepatitis of unknown origin found to develop?
View Answer
2. The National Halothane Study (NHS) showed that extensive hepatic necrosis developed in 0.01% of 850,000 surgical cases. Most of these complications could be attributed to shock, prolonged use of vasopressors, infection, CHF, or existing hepatic disease. Only nine cases were of unknown origin.
3. What is the morbidity and mortality for patients with liver disease undergoing liver biopsy?
View Answer
3. At 30 days following laparotomy and liver biopsy, the morbidity rate is 31% and the mortality rate 61%. In the NHS, all patients with viral or alcoholic hepatitis died, as did those with ascites. Other studies have shown even higher figures for 30-day morbidity and mortality.
4. What is normal hepatic blood flow? What is normal portal pressure?
View Answer
4. Normal hepatic blood flow (HBF) is 100 mL/min (25%) of the CO. The hepatic artery accounts for 25% of total HBF but 45% to 50% of O2 supply. The portal vein provides 75% of total HBF but only 50% to 55% of O2 supply.
5. What regulates liver vasculature? How can this be important in hypovolemia and hemorrhage?
View Answer
5. The liver vasculature is controlled by sympathetic innervation mediated through alphaadrenoceptors. Changes in hepatic venous compliance play an important role in overall regulation of CO. The liver vasculature has a vital role as a blood reservoir mediated through the SNS.
During hemorrhage, the liver may squeeze 500 mL of blood into the systemic circulation. Anesthetics may impair this response if blood loss is not quickly replaced. Patients with liver disease have a decreased responsiveness to catecholamines → impaired ability to compensate for hemorrhage and hypovolemia by sympathetic mechanisms (i.e., vasoconstriction to divert blood to the heart and brain, expulsion of blood from the splanchnic reservoir, and constriction of the capacitance vasculature).
6. What is the arterial buffer response?
View Answer
6. In the arterial buffer response, local and intrinsic mechanisms adjust hepatic arterial flow to compensate for changes in portal blood flow. These mechanisms involve neural, myogenic, and metabolic controls.
7. What is the washout theory?
View Answer
7. The washout theory suggests that when portal blood flow decreases, a vasodilator produced in the liver (probably adenosine) accumulates → hepatic arterial dilation. The increased portal blood flow causes an effective washout of the substance and therefore a decrease in the vasodilating effect on the hepatic arterial vasculature.
HEPATIC STRUCTURE
1. Name five functions of hepatocytes.
View Answer
1. Functions of hepatocytes:
Absorb digestive material from the portal venous blood;
Store proteins, vitamins, carbohydrates, and lipids;
Excrete bile salts, facilitating the absorption of fat from the intestines;
Synthesize plasma proteins, glucose, cholesterol, fatty acids, and phospholipids;
Metabolize, detoxify, and inactivate exogenous and endogenous compounds, including drugs, some poisons, steroids, and most other hormones;
Play a role in the immune system.
2. What is the function of Kupffer cells?
3. What are the neurologic effects of hyperbilirubinemia?
View Answer
3. Unconjugated hyperbilirubinemia may cause severe neurologic dysfunction, including a rapidly fatal encephalopathy, whereas conjugated hyperbilirubinemia is not accompanied by neurologic sequelae.
4. What is the main function of the liver in carbohydrate metabolism?
View Answer
4. The main function of the liver in carbohydrate metabolism consists of the following:
Storing gylcogen,
Converting galactose to glucose,
Gluconeogenesis,
Forming many of the intermediate compounds of carbohydrate biotransformation.
5. Which factors affect hepatic elimination of drugs?
View Answer
5. The hepatic elimination
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