28 - Metabolic Disorders | Smiths General Urology, Seventeenth Edition (LANGE Clinical Medicine)

Authors: Macfarlane, Michael T.

Title: Urology, 4th Edition

> Table of Contents > Part Two - Selected Topics > Chapter 28 - Metabolic Disorders

Chapter 28

Metabolic Disorders

Normal Fluid and Electrolyte Requirements

Normal body homeostasis requires careful regulation of fluid volume and the concentration of electrolytes within the fluid. Volume regulation is primarily under the control of aldosterone, whereas tonicity is regulated by antidiuretic hormone (ADH). Volume has priority over tonicity when the protective mechanisms conflict.

Body Fluid Compartment	% Body Weight (kg)
Total body water	60
Intracellular fluid	40
Extracellular fluid	20
Blood (plasma 4% + RBCs 3%)	7

Maintenance Requirements

The normal daily maintenance requirements for fluid and electrolytes in an essentially healthy individual include the following.

Water	2 L/day
NaCl	75 mEq/day
K⁺	40 mEq/day

Minimum daily water requirement for the body is based on the following needs:

At least 600 mL urine is needed to keep the normal daily load of solutes in solution (1,000 mL in hypermetabolic, critically ill patients).
Approximately 1,000 mL is needed to replace daily insensible water loss (i.e., from the respiratory tract and skin). These losses will increase with fever.

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Abnormal water losses include fluid loss in nasogastric suction, vomiting, diarrhea, fistula drainage, and third-space sequestration (e.g., ascites, bowel obstruction, retroperitoneal edema, and operative trauma).

Saline Solutions	Na mEq/L
Normal saline (NS; 0.9% NaCl)	154
Half-normal saline (0.45% NaCl)	77

Maintenance carbohydrate replacement of 100 to 150 g/day is necessary; 5% dextrose in water (D5W) contains 50 g/L glucose. A reasonable intravenous maintenance fluid for the uncomplicated hospitalized patient who is taking nothing by mouth (NPO) would be D5 0.5 NS with 20 mEq KCl per liter at 100 mL/hour. Replacement of any abnormal fluid losses should be added to this maintenance.

Abnormal Fluid-loss Replacements

Gastric fluid is isotonic and high in K⁺. Replacement: 0.5 NS with 40 mEq KCl/L.
Fever or osmotic diuresis (as in diabetics or after hyperalimentation) results in hypotonic fluid loss (free water). Replacement: 0.5 NS.

Pediatric Intravenous Fluid Replacement

Weight	mL/kg/day
First 10 kg (0 10)	100+
Second 10 kg (10 20)	50+
Each additional kilogram	20

Abnormal Fluid Disturbances

Hypotonic Dehydration

Hypotonic dehydration occurs because of loss of isotonic fluid such as blood (hemorrhage), plasma (burns, pancreatitis, peritonitis), or gastrointestinal fluid (diarrhea) with secondary free-water retention, because of the increased ADH release with stress. Treatment use normal saline for all fluid needs for a few days.

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Hypotonic Overhydration

Hypotonic overhydration occurs because of inappropriate ADH secretion or acute renal failure. It most commonly occurs after the acute stress of surgery. Treatment water restriction.

Hypertonic Dehydration

Hypertonic dehydration occurs because of excessive free-water loss as from the lungs (mechanical ventilation), perspiration (fever), osmotic diuresis (diabetes, hyperalimentation), or diabetes insipidus. Treatment first correct hypovolemia with 0.5 NS, and then slowly correct tonicity with D5W (1 L D5W for each 3 mEq Na >140).

Transurethral Resection Syndrome

Transurethral resection (TUR) syndrome results from the sudden intravascular absorption of large volumes of hypotonic irrigating fluid, through the prostatic bed, during transurethral surgery. Clinical manifestations include hypertension, bradycardia, dyspnea, cyanosis, and mental confusion. Treatment fluid restriction, diuretics (furosemide), and rarely hypertonic saline to restore tonicity (3% saline contains 513 mEq Na/L). The formula to calculate sodium deficit is

[weight (kg) 0.2] serum Na (mEq/L)

Electrolyte Disorders

Hyperkalemia

The most common cause of hyperkalemia (K⁺ >5.5 mEq/L) is acute oliguric renal failure. Other causes include potassium-sparing diuretics (e.g., spironolactone, triamterene, and amiloride), hypoaldosteronism, acidosis, rhabdomyolysis, and excessive potassium intake in the setting of renal insufficiency. Patients may demonstrate a generalized weakness, loss of deep tendon reflexes, irritability, and confusion. Electrocardiogram (ECG) changes, including peaked T waves, S-T depressions, and prolongation of the QRS, indicate significant hyperkalemia and may result in ventricular tachyarrhythmia or asystole.

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Treatment

Shift potassium into cells with alkali or glucose (50 mEq NaHCO₃ IV bolus or 1 ampoule D50 glucose with 15 units of regular insulin).
Block effects of potassium on the heart with calcium (1 ampule calcium chloride or calcium gluconate given slowly).
Remove potassium from the body with potassium-binding resins (Kayexalate 10 30 g/100 mL as a retention enema for 15 20 minutes or 5 15 g PO qid).
Remove potassium from the body with dialysis (hemodialysis or peritoneal dialysis).
Eliminate underlying cause.

Hypokalemia

Hypokalemia (K⁺ <3.5 mEq/L) most commonly results from increased potassium loss in gastrointestinal fluid (e.g., nasogastric suction, vomiting, diarrhea, and ureterosigmoidostomy) or urine [e.g., postobstructive diuresis, renal tubular acidosis (RTA), diuretics, hyperaldosteronism, and Cushing's syndrome]. Patients may demonstrate skeletal muscle weakness, ileus, abdominal distention, nausea, vomiting, and depressed sensorium. ECG changes include depressed T waves, sagging ST segments, and prominent U waves.

Treatment

Severe hypokalemia (K⁺ <3.0 mEq/L) can be managed with intravenous KCl boluses not to exceed 20 mEq/hour or 240 mEq/day.
Oral potassium supplementation can be used for chronic potassium deficiencies.
Eliminate underlying cause.

Hyperchloremic Metabolic Acidosis

Hyperchloremic metabolic acidosis is a common complication of urinary diversions with intestines, especially when the urine remains in contact with the intestinal mucosa for prolonged periods as with ureterosigmoidostomies. Active chloride transport across the intestinal mucosa into the systemic circulation with an obligate cation is thought to be the mechanism. Hydrochloric acid or ammonium chloride accumulation or both result in the hyperchloremic metabolic acidosis.

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Treatment

Restrict oral chloride and replace bicarbonate (e.g., sodium bicarbonate or potassium citrate).
Drain intestinal urinary reservoir.
Chlorpromazine (Thorazine) and nicotinic acid are drugs that block chloride transport via cyclic adenosine monophosphate (cAMP). Their use for treatment of chronic hyperchloremic metabolic acidosis has been suggested.

Hypercalcemia

Common causes of hypercalcemia include metastatic cancer to bone, hydrochlorothiazide therapy, and hyperparathyroidism. Patients may demonstrate weakness, somnolence, anorexia, polyuria, and coma. A history of stones, nephrocalcinosis, and hypophosphatemia suggests hyperparathyroidism as the etiology (measure serum parathyroid hormone). Patients with renal cell carcinoma may present with symptoms of hypercalcemia in fewer than 10% of cases. Production of a parathyroid-like hormone by the primary tumor has been suggested as a possible cause, in addition to hypercalcemia secondary to skeletal metastases with osteolysis.

Treatment

Initial therapy is to establish a sodium diuresis with intravenous saline administration followed by furosemide (Lasix).
Pamidronate (Aredia), 30 to 90 mg IV over a 24-hour period once will usually cause serum calcium to decrease within 12 to 24 hours and has been used for cases of severe hypercalcemia.

Hypocalcemia

Hypocalcemia is most commonly an artifact of hypoalbuminemia, which reduces the protein-bound fraction of total serum calcium. (Total calcium will decrease by 0.8 mg/dL for each decrement in serum albumin of 1 g/L.) Ionized calcium is normal, and the patient is asymptomatic in these cases. Causes of true hypocalcemia include hypoparathyroidism, hypomagnesemia, abnormalities in vitamin D metabolism, acute hyperphosphatemia or pancreatitis, blood transfusions, and osteoblastic metastases (e.g., breast, prostate, and lung). Acute hypocalcemia may be associated with tetany or latent tetany, as assessed by the Chvostek sign (tapping the facial nerve against the bone just anterior to the ear

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produces ipsilateral contraction of the facial muscles) or Trousseau's sign (induction of carpal spasm by occluding the brachial artery for 3 minutes) or both. Immediate treatment should be rendered because of the possibility of laryngeal spasms or seizures or both.

Treatment

Intravenous calcium gluconate is appropriate initial therapy for patients with tetany or latent tetany.
Chronic hypocalcemia is managed with oral calcium and vitamin D supplementation. (Remember first to reduce hyperphosphatemia in patients with renal failure.)

Hypermagnesemia

Hypermagnesemia rarely occurs in the setting of normal renal function. It can occur, however, when using Suby's solution G or magnesium carbonate (Renacidin) for irrigation of the urinary system to dissolve stones. The impaired neuromuscular transmission that results can produce mental confusion, drowsiness, muscular paralysis, and occasionally coma.

Treatment

A sodium diuresis with saline and furosemide (Lasix) is usually effective therapy.
When symptoms are severe, emergency treatment with calcium gluconate should be undertaken, followed by hemodialysis if the patient has decreased renal function.

Renal Tubular Acidosis

RTA refers to a disorder of urinary acidification. The inability to excrete acid into the urine results in a systemic metabolic acidosis and concurrent elevated serum chloride. The higher urinary pH increases urine phosphate levels. Three major types of renal tubular acidosis are recognized: types I, II, and IV. Type III RTA is now considered a variant of type I.

Type I Renal Tubular Acidosis (Distal)

Classic RTA is caused by an inability of the distal tubule to secrete hydrogen ion into the urine. Urinary wasting of calcium,

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phosphorus, and potassium also is noted in this syndrome. Nephrocalcinosis or nephrolithiasis will occur in about 70% of patients. The diagnosis is made in the setting of a systemic acidosis (serum bicarbonate <20 mEq/L) with an inappropriately high urinary pH (>5.5). In adults, the disorder is persistent and is found predominantly in women, whereas the infantile form is transient but can result in significant growth impairment. Treatment fluid and electrolyte replacement with potassium citrate.

Type II Renal Tubular Acidosis (Proximal)

Type II RTA is caused by a defect in the reabsorption of filtered bicarbonate in the proximal tubule. Initially, massive bicarbonaturia is found; however, as the plasma bicarbonate level decreases with consequent worsening systemic acidosis, the filtered load of bicarbonate also decreases, resulting in disappearance of bicarbonaturia and normal urinary pH. It is often associated with other proximal tubular defects such as Fanconi's syndrome, hereditary fructose intolerance, Wilson's disease, or multiple myeloma. However, vitamin D deficiency secondary to intestinal malabsorption is the most common cause in adults. Nephrolithiasis does not occur. Treatment vitamin D therapy will correct the acidification defect in patients with vitamin D deficiency; otherwise therapy is directed at treating the acidosis with alkali (e.g., potassium citrate or bicarbonate).

Type IV Renal Tubular Acidosis

Type IV hyperkalemic RTA occurs because of a defect in aldosterone-dependent potassium ion secretion. It most frequently is noted in elderly diabetics with hyporeninemic hypoaldosteronism. Mineralocorticoid replacement (fludrocortisone 0.1 mg/day) will reverse hyperkalemia and acidosis.

Renal Tubular Acidosis Syndromes

	Type I	Type II	Type IV
Site	Distal	Proximal	Distal
Defect	H⁺ secretion	HCO₃ reabsorption	Aldosterone
Serum K⁺	Low	Low	High
Other	Stones	Fanconi's syndrome