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932 PART 8: Renal and Metabolic Disorders
infusions (10 units IV over 15 minutes) also may serve as a temporary
TABLE 97-10 Therapy of Hyperkalemia
expedient in patients with uremic bleeding. Conjugated estrogens (0.6 mg/
Drug Dose Onset Duration Mechanism kg IV daily for 5 days) have a delayed onset of action (3-5 days), but the
Calcium gluconate 10-20 mL IV 1-5 min 0.5 h Membrane duration of the therapeutic effect can be as long as 14 days. 173
antagonist
Sodium bicarbonate 1-2 ampules (IV 30 min 1-4 h Cellular shift KEY REFERENCES
50-100 mEq)
• Aspelin P, Aubry P, Fransson SG, et al. Nephrotoxic effects in high-
Glucose + insulin 500 mL D W with 10 U 30 min 1-4 h Cellular shift
10
regular insulin IV risk patients undergoing angiography. N Engl J Med. 2003;348:491.
• Bellomo R, Chapman M, Finfer S, et al. Low-dose dopamine in
Sodium polystyrene 30-50 g with sorbitol PO, 1-2 h 4-6 h Increased patients with early renal dysfunction: a placebo-controlled ran-
sulfonate or as retention enema excretion
domised trial. Australian and New Zealand Intensive Care Society
D W, 10% dextrose in water. (ANZICS) Clinical Trials Group. Lancet. 2000;356:2139.
10
• Brigouri C, Visconti G, Focaccio A, et al. For the REMEDIAL
part of the treatment of life-threatening hyperkalemia or if hypocalcemic
tetany develops. Hypercalcemia may be observed when rhabdomyolysis- II Investigators. Renal Insufficiency After Contrast Media
Administration Trial II (REMEDIAL II): RenalGuard system
induced AKI enters the diuretic phase, and Ca deposited in damaged
2+
muscle is released. It is usually self-limited. in high-risk patients for contrast-induced acute kidney injury.
Circulation. 2011;124:1260-1269.
Uric acid levels may rise by 1 to 2 mg/dL per day in cases of AKI not
due to rhabdomyolysis, but rarely does the level exceed 15 mg/dL. This • Finfer S, Bellomo R, Boyce N, et al. A comparison of albumin and
plateau is thought to result from enhanced metabolism of uric acid by gut saline for fluid resuscitation in the intensive care unit. N Engl J
bacteria. Extreme elevations in uric acid levels have been observed in cases Med. 2004;350:2247.
of exertional rhabdomyolysis and following treatment of some lymphomas. • Herget-Rosenthal S, Marggraf G, Husing G, et al. Early detection of
Metabolic acidosis occurs commonly in AKI, and in cases of trauma acute renal failure by serum cystatin C. Kidney Int. 2004;66:1115.
or sepsis the fall in plasma bicarbonate may exceed 15 mEq/L per • Linton AL, Clark WF, Driedger AA, et al. Acute interstitial nephri-
24 hours. In the catabolic patient with AKI, acid is released from metab- tis due to drugs: review of the literature with a report of nine cases.
olism of sulfur- and phosphorus-containing compounds, which con- Ann Intern Med. 1980;93:735.
tributes to a rise in the anion gap. Acidosis may be treated with sodium • Murray PT, Mehta RL, Shaw AD, et al. Current use of biomarkers
bicarbonate; however, the additional volume is hazardous in the patient in Acute Kidney Injury: report and summary of recommenda-
with compromised renal function, the buffering requires increased tions from the 10th Acute Dialysis Quality Initiative Consensus
ventilation, and adverse intracellular effects may result. Uncontrollable Conference. Kidney International, 2013; Oct 9, epub ahead of print.
acidosis may mandate dialysis therapy.
Metabolic alkalosis may complicate AKI in the patient with nasogas- • Newman DJ, Thakkar H, Edwards RG, et al. Serum cystatin C
tric suction, but is a less frequent acid-base disturbance in these patients. measured by automated immunoassay: a more sensitive marker
Although nasogastric suction–induced metabolic alkalosis normally of changes in GFR than serum creatinine. Kidney Int. 1995;47:312.
responds to saline supplementation, this maneuver is ineffective in AKI • Salerno F, Gerbes A, Gines P, et al. Diagnosis, prevention and treat-
and carries the hazard of potential volume overload. Severe metabolic ment of hepatorenal syndrome in cirrhosis. Gut. 2007;56:1310-1318.
alkalosis in AKI may require dialysis using a reduced concentration • Uriz J, Ginès P, Cardenas A, et al. Terlipressin plus albumin
of bicarbonate or acetate in the bath. Alternatively, 0.1 N hydrochloric infusion: an effective and safe therapy of hepatorenal syndrome.
acid may be administered by slow intravenous infusion. Development J Hepatol. 2000;33:43-48.
of metabolic alkalosis in the patient on nasogastric suction may be
prevented or attenuated by use of proton pump inhibitors
Infection continues to be a leading cause of death in the patient with
AKI, and pneumonia, urinary tract infection, and wound infection are REFERENCES
most common. Infection has been the cause of death in up to 70% of Complete references available online at www.mhprofessional.com/hall
cases of AKI and has contributed to 50% of deaths occurring during the
diuretic phase. In several large series of AKI, the incidence of sepsis
169
exceeds 50%, and intra-abdominal sepsis is known to be a particularly
important determinant of survival. In the septic patient without an CHAPTER Renal Replacement Therapy
obvious source, intra-abdominal sepsis must be vigorously excluded.
CT scanning and ultrasound, with CT the better of the two. The severity 98
Imaging procedures of value for detecting an abdominal source include in the Intensive Care Unit
of infection in AKI is undiminished despite the advent of new antibiotics Suneel M. Udani
and other advances in general medical care. Prophylactic antibiotics are Jay L. Koyner
not recommended for the patient with AKI and may be harmful. Patrick T. Murray
Prior to the use of prophylactic acid suppression to prevent gastric
stress ulceration in AKI, GI hemorrhage was the second leading cause of
death. Now many centers report a dramatic decline in GI hemorrhage in KEY POINTS
AKI patient. Recent advances in the therapy of uremic bleeding include
170
use of 1-deamino-8-d-arginine vasopressin (DDAVP), cryoprecipitate, • Indications for the initiation of renal replacement therapy (RRT)
and conjugated estrogens. These drugs are most useful in patients with remain reactive, often waiting until potentially life-threatening
171
clinically significant bleeding episodes who lack evidence of any other complications/thresholds have been met.
(nonuremic) coagulopathy. DDAVP is typically infused over 30 minutes • The goal of renal replacement therapy should be to provide “renal
in a dose of 0.3 µg/kg of body weight and is effective within minutes. support” to facilitate the other aspects of care of the critically ill
172
Unfortunately, because of the short duration of action of this compound patient (fluid balance, nutritional support, etc).
(1-4 hours), frequent dosing may be required. The use of cryoglobulin
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