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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







            section08.indd   932                                                                                       1/14/2015   8:27:58 AM
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