acute renal failure in the hospital: diagnosis and … into 3 major categories based on...

cute renal failure (ARF) frequently compli-cates the course of hospitalized patients. Theincidence of hospital-acquired ARF is between4.9% and 7%.1,2 ARF occurs commonly in the

intensive care unit, with an incidence up to 20% in thissetting.3 In contrast, the incidence of community-acquired ARF is 0.9%.4 Despite technical advances inthe management of ARF over the past 50 years, mortali-ty rates remain unchanged at 50%.5 Hospital-basedclinicians should be familiar with the diagnosis andmanagement of this renal disorder.

DEFINITION AND CLASSIFICATION

The term acute renal failure describes an abrupt de-cline in kidney function. There is no consensus on thedefinition of ARF; most definitions are based on absoluteor relative changes in serum creatinine concentration.6

An absolute increase in serum creatinine concentrationby 0.5 or 1.0 mg/dL or a relative increase of 25% to100% occurring over 24 to 72 hours is considered consis-tent with ARF. A multidisciplinary group convened in aconsensus conference (the Acute Dialysis Quality Ini-tiative [ADQI]) used both evidence and expert opinionto define and classify ARF. Based on this meeting, theADQI group proposed the RIFLE system, which classifiesARF into 3 categories according to severity and 2 cate-

gories according to clinical outcome (Table 1).7 Al-though serum creatinine concentration is commonlyused to assess renal function and to estimate ARF severity,a precise correlation between changes in creatinine con-centration and glomerular filtration rate (GFR) does notexist. The non-steady state conditions that prevail in ARFmake estimation of GFR using standard formulas inaccu-rate, often overestimating true GFR.8

ARF is also classified based on urine output: anuric (< 100 mL/d), oliguric (100–399 mL/d), and nonolig-uric (> 400 mL/d). Anuria usually reflects either com-plete urinary tract obstruction or a vascular catastrophecomplicated by cortical necrosis.

ETIOLOGY

The causes of ARF traditionally have been dividedinto 3 major categories based on pathophysiology: pre-renal, intrinsic renal, and postrenal (Table 2). Prerenaletiologies are the most common, accounting for 30% to60% of all cases of ARF.4 Prerenal azotemia results fromeither an absolute or relative decrease in blood volume

Dr. Yarlagadda is a fellow in nephrology, and Dr. Perazella is an associateprofessor of medicine, and director of the Nephrology Fellowship Program;both are at the Yale University School of Medicine, New Haven, CT.

www.turner-white.com Hospital Physician March 2006 51

R e s i d e n t G r a n d R o u n d s

Series Editor: Mark A. Perazella, MD, FACP

Acute Renal Failure in the Hospital: Diagnosis and Management

Sri Yarlagadda, MDMark A. Perazella, MD, FACP

A 69-year-old man with a history of coronary artery disease, hypertension, and stage 3 chronic kidney disease presented tothe emergency department with acute onset of chest pain, dyspnea, and dizziness. The patient was hypotensive (68/36 mm Hg)with clinical evidence of pulmonary edema. Electrocardiogram revealed an acute anterior wall myocardial infarction. The patientunderwent emergent cardiac catheterization during which an intra-aortic balloon pump (IABP) was placed for management ofcardiogenic shock. Two coronary artery stents were placed and 380 mL of low-osmolar contrast were administered. Bloodpressure improved over the next 24 hours and the IABP was removed. Urine output declined to less than 400 mL/day and theserum creatinine concentration increased from a baseline of 1.5 mg/dL to 6.8 mg/dL over 4 days. Serum potassium concentra-tion increased to 6.8 mEq/L. The patient became anorexic with nausea and vomiting. Uremic symptoms and metabolic abnor-malities developed, and acute hemodialysis was initiated.

A

or altered intrarenal hemodynamics, decreasing renalperfusion without cellular injury. It is rapidly reversibleif the hemodynamic insult is corrected. If the insult issustained, overt cellular injury results (ie, acute tubularnecrosis [ATN]) with transition from prerenal to intrin-sic ARF. Postrenal ARF is less common in the hospitalsetting, accounting for between 1% and 10% of cases ofhospital-acquired ARF, and is characterized by structur-al or functional obstruction of the urinary tract. Ob-struction occurs at any level from the renal pelvis to theurethra; either complete or partial obstruction cancause ARF. Postrenal causes should be quickly recog-nized and treated because recovery of renal function isinversely related to the duration of obstruction.9

Intrinsic renal failure is considered after prerenal andpostrenal causes have been excluded and clinical datapoint to a structural problem within the kidneys. Intrinsicrenal diseases are characterized according to the primarysite of injury, including the vasculature, glomerulus,tubules, and interstitium. The most common form ofhospital-acquired intrinsic renal failure is ATN. Thisterm is misleading because there is a spectrum of tubulardysfunction that may or may not result in tubular necro-sis. The most common causes of ATN are ischemia, exo-genous toxins (drugs and radiocontrast agents), endoge-nous toxins (heme pigments and toxic light chains), andnatural or drug-induced urinary crystals.

DIAGNOSIS

A comprehensive history with detailed review of thehospital medical record, physical examination, and basiclaboratory tests correctly identifies hospital-acquiredARF. Diagnosis requires knowledge of the natural histo-ry of various causes of ARF and a systematic approach toevaluating renal insufficiency by excluding and correct-ing both prerenal and postrenal causes.

History

In the hospital, patients develop excessive fluid loss-es from diarrhea, ostomy losses, or high urine output.These losses are compounded by limited fluid intakeprior to the recognition of ARF. Obstruction, especiallyfrom urinary retention, is common and reduces urineoutput. The presence of urine output does not ex-clude partial urinary tract obstruction as a cause ofARF. Bone pain in an elderly patient might suggestmultiple myeloma as a cause of ARF.

Review of the hospital record for recent intake/out-put data, trends in body weights, episodes of hypo-tension (especially requiring vasopressors), evidence ofsepsis, use of radiocontrast for procedures, and admin-istration of any number of nephrotoxic medications iscritical. Invasive vascular procedures, including bothpercutaneous and open operative interventions, shouldbe assessed for their temporal relationship to ARF. Theoperative report of any surgical procedure should bescrutinized to identify hypotension, blood loss, and ad-ministration of potential nephrotoxins.

Physical Examination

Evaluation of intravascular volume status in hospital-ized patients is important to assess for prerenal ARF. Theexamination should include measurement of blood pres-sure and heart rate, including orthostatic readings, and

52 Hospital Physician March 2006 www.turner-white.com

Y a r l a g a d d a & P e r a z e l l a : R e s i d e n t G r a n d R o u n d s : p p . 5 1 – 5 8

Table 1. RIFLE Classification of Acute Renal Failure (ARF)

Glomerular Urine Output Filtration Rate Criteria

Risk SCr increased 1.5 times < 0.5 mL/kg/h for 6 h

Injury SCr increased 2.0 times < 0.5 mL/h for 12 h

Failure SCr increased 3.0 times < 0.3 mL/kg/h for 24 h or anuria for 12 h

Loss Persistent ARF; complete loss of kidney function for longer than 4 wk

End stage ESRD persisting longer than 3 mo

ESRD = end stage renal disease; SCr = serum creatinine.

TAKE HOME POINTS

• The causes of acute renal failure (ARF) are classi-fied as prerenal, intrinsic renal, and postrenal.

• Prerenal azotemia results from an absolute or rela-tive decrease in blood volume or altered intrarenalhemodynamics, decreasing renal perfusion withoutcausing cellular injury.

• The most common form of intrinsic renal failure isacute tubular necrosis, which most frequently iscaused by ischemia, toxins, and urinary crystals.

• Diagnosis of ARF requires thorough review of thehospital record, evaluation of volume status, and per-formance of pertinent laboratory and imaging tests.

• Intrinsic renal failure is considered after prerenaland postrenal causes have been excluded and clinicaldata point to a structural problem within the kidneys.

• Management of ARF entails correction of prerenaland postrenal diseases; optimal therapy of metabolic,uremic, and volume-related complications; and renalreplacement therapy for severe renal insufficiency.

assessment for pulsus paradoxus. Other required evalua-tions include assessment of mucosal hydration and skinturgor and assessment for the presence of edema (pretib-ial in ambulatory patients, sacral in bedridden patients),jugular venous distension, lung crackles, and an S3 cardi-ac gallop. Equally important are signs of coexistent co-morbidities, such as congestive heart failure, cirrhosis,nephrosis, and vascular disease. The presence of a diffuserash, livedo reticularis with skin mottling, or palpablepurpura suggest renal and vascular injury. Suprapubicfullness indicates a postrenal cause of ARF. Limb ischem-ia suggests the possibility of underlying rhabdomyolysis.

Laboratory Testing

Blood tests. Measurement of serum blood ureanitrogen (BUN) and creatinine concentration, electro-lytes, calcium, and phosphate is an integral part of thediagnosis of hospital-acquired ARF and managementof its associated complications. The trends in BUN andserum creatinine concentrations help define the severi-ty and course of ARF. Metabolic disturbances such ashyperkalemia and hyperphosphatemia accompanied byan elevated creatine kinase level suggest rhabdomyoly-sis. Hypercalcemia can point to a malignant conditionsuch as multiple myeloma; similarly, hyperuricemia in-dicates tumor lysis syndrome. Abnormal transaminaselevels suggest congestive heart failure or liver disease;elevated bilirubin levels may represent hemolysis orhepatic disease.

Anemia in the presence of schistocytes and throm-bocytopenia should raise suspicion for a thromboticmicroangiopathy (hemolytic uremic syndrome, throm-botic thrombocytopenic purpura, antiphospholipidantibody syndrome), endocarditis, and disseminatedintravascular coagulation. Eosinophilia may be seenwith acute interstitial nephritis (AIN) and atheroem-bolic renal disease. Finding a monoclonal protein inthe serum suggests multiple myeloma. Positive bloodcultures can point to an endovascular infection with anassociated acute immune complex–associated glomer-ulonephritis. The utility of serologic tests such as hep-atitis serology and measurement of antinuclear anti-body, complement, and antineutrophil cytoplasmicantibody levels depend upon clinical suspicion.

Urine studies. Routine urinalysis consists of dipsticktesting, which provides information about urine con-centration and detects protein, ketones, glucose, leuko-cyte esterase, bilirubin, and blood. In the absence ofred blood cells (RBC), heme-positive urine suggeststhe presence of heme protein from either myoglobin(rhabdomyolysis) or hemoglobin (hemolysis).

Microscopic examination of the spun urine sedi-

ment is essential in the evaluation of ARF. The sedi-ment should be closely inspected for cellular elements,casts, and crystals. RBCs indicate bleeding along theurogenital tract if the cells are monomorphic (normalappearing) or glomerular injury if the cells are dysmor-phic. Renal tubular epithelial (RTE) cells suggest tubu-lar injury, while white blood cells (WBC) suggest infec-tion or renal inflammation. RTE cell casts and granularcasts typically represent renal tubular injury (Figure 1).RBC casts confirm glomerular injury, while WBC castssuggest either intrarenal infection or AIN. Uric acidcrystals in the urine of a patient with ARF suggest thepossibility of tumor lysis syndrome. Urine crystals associ-ated with medications (acyclovir, indinavir, sulfadiazine)point to drug-associated crystal nephropathy.

Urine chemistries can also provide useful informa-tion to classify the cause of ARF (Table 3). These testsmust be interpreted in conjunction with clinical assess-ment of the patient and other serum and urine testresults.

Diagnostic Imaging

Renal ultrasound is both sensitive (90%) and specific(90%) in diagnosing urinary tract obstruction. Hydro-nephrosis, which reflects dilatation of the renal pelvis andureters, is readily seen on ultrasound (Figure 2). Ultra-sound also provides information about renal size andechogenicity and cortical thickness. The absence ofhydronephrosis does not always exclude obstruction,especially in the setting of acute obstruction (< 72 h),



Table 2. Common Causes of Hospital-Acquired Acute RenalFailure

Prerenal

True volume depletion: nausea/vomiting, hemorrhage, burns, diarrhea/ostomy output, diuretics

Effective volume depletion: congestive heart failure, hepatorenal syn-drome, sepsis/third spacing of fluids, pancreatitis

Intrinsic

Ischemic acute tubular necrosis: shock from any cause, vasopressors

Nephrotoxic acute tubular necrosis

Medications: aminoglycosides, amphotericin B, radiocontrast agents, osmotic agents, crystal-forming agents, acyclic nucleo-tide phosphonates, zoledronate/pamidronate, oral sodium phosphate solution

Endogenous toxins: light chains, heme pigments, uric acid

Vascular injury: renal cholesterol emboli (atheroemboli)

Postrenal

Retroperitoneal obstruction: hematoma, cancer

Bladder outlet obstruction: structural, functional

retroperitoneal fibrosis, or severe hypovolemia. Com-puted tomography scan without radiocontrast is also use-ful in the diagnosis of urinary obstruction (Figure 2). Itsadvantage over ultrasound is enhanced sensitivity in visu-alizing the various etiologies of obstruction, such asstones, retroperitoneal disease, and malignancy.

Renal Biopsy

Renal biopsy is rarely required in the work-up ofARF. When a primary renal disease other than is-chemic or toxic ATN is suspected, renal biopsy mayestablish the diagnosis. Common indications includeunexplained ARF, suspicion of acute glomerulonephri-tis or lupus nephritis, protracted renal dysfunction inpatients suspected for AIN, and ARF that fails to im-prove after 6 to 8 weeks (due to potentially irreversiblecauses such as cholesterol emboli [Figure 3] and corti-cal necrosis). In a prospective study of patients withARF, renal histology altered management in 75% ofcases.10 Because the risks associated with renal biopsyare low (< 1%), this diagnostic procedure should beused in the appropriate setting to evaluate ARF.11

MANAGEMENT

The initial care of patients with ARF should focuson reversing the underlying cause (prerenal and post-renal) and correcting fluid, electrolyte, and acid-baseimbalances (Table 4). Every effort should be made toprevent further kidney injury and to provide support-ive care (including dialysis), until recovery occurs.

Fluids

An important goal of patient management is main-taining euvolemia. Careful physical examination and,when appropriate, invasive monitoring is vital to thisprocess. Achieving appropriate fluid balance involves 2 conflicting goals: providing sufficient volume to ensureadequate renal perfusion and avoiding volume overloadwith resulting pulmonary congestion. Attention to allsources of fluid intake and output, including surgicaldrains, nasogastric suction, diarrhea, and insensible loss-es is required. There is no substitute for daily weights.

Rapid restoration of intravascular volume may re-verse prerenal azotemia and prevent ischemic damage.Crystalloid solutions are often the best fluid choice. Insituations of increased vascular permeability, colloidsolutions may provide enhanced restoration of intravas-cular volume. Albumin therapy should be restricted tosituations where synthetic colloids cannot be used.12 Ofthe synthetic colloids, hydroxyethyl starch (HES) solu-tions with low in vivo molecular weight (HES, 200/0.5)demonstrate the best risk/benefit ratio,13 but theseshould be avoided in patients with underlying kidneydisease due to enhanced risk of ARF.

Vasoactive Agents

If hypotension persists despite adequate fluid re-placement, vasopressors are indicated. However, intra-renal vasoconstriction develops with these drugs andmay negate the hemodynamic benefit of increasedblood pressure. Norepinephrine reduces renal bloodflow in normal humans but improves renal blood flowand augments urine output and GFR in patients withseptic shock.14 Vasopressin also increases urine outputand GFR in patients with septic shock.15 Inotropicagents such as dobutamine increase cardiac outputand augment renal blood flow in patients with systolicdysfunction and ARF.

Low-dose dopamine (0.5–0.2 µg/kg body weight) iscommonly used to increase urine output in oliguric pa-tients. Several studies have demonstrated that dopaminedoes not promote renal recovery or reduce mortali-ty16–18 and is associated with tachyarrhythmias, pul-monary shunting, and gut or digital necrosis.19 Dop-amine should not be employed in the treatment of ARF.

Diuretics

Diuretics are often required to treat ARF when vol-ume overload develops. Loop diuretics (furosemide,ethacrynic acid, torsemide) diminish active transportand energy requirements in the thick ascending limb.Although a favorable diuretic response occurs with these



Figure 1. A granular cast is noted in the urine of a patientwith acute tubular necrosis. This finding represents tubularinjury with sloughing of cells into the urine. (Image courtesyof Mark A. Perazella, MD.)

drugs when administered within the first 24 hours ofonset of oliguria, this effect does not translate intoenhanced renal recovery or a mortality benefit. In aprospective study of loop diuretics in ARF, no significantdifference in renal recovery, requirement for dialysis, ordeath was observed.20 In another study, diuretics wereassociated with nonrecovery of renal function andincreased risk of death in critically-ill patients.21 Otherdiuretics such as mannitol are used in limited clinical sit-uations such as rhabdomyolysis with myoglobinuric ARF.Thiazide diuretics may increase urine output when com-bined with loop diuretics. Thus, diuretics should be usedonly in ARF for management of volume with no expec-tation that these agents improve outcomes.

Metabolic Management

Acidosis. Metabolic acidosis in ARF can be explained

largely by (1) reduced renal excretion of acid and sever-al organic and inorganic anions and (2) excessive acidproduction via catabolism. Correction of metabolic aci-dosis enhances response to vasopressors, improves car-diac contractility, ameliorates bone injury due to acidbuffering, and reduces catabolism. Bicarbonate -containing intravenous fluids correct acidosis, but prop-er use is required to limit excess volume repletion andminimize symptoms of hypocalcemia. Depending onthe serum sodium concentration, sodium bicarbonate(50–150 mEq) can be added to a liter of either 5% dex-trose in water or 0.45% normal saline to make an iso-tonic solution. Oral bicarbonate or bicarbonate precur-sors (citrate) are preferable in patients able to take pillsor a liquid preparation. The goal is to correct the se-rum bicarbonate to approximately 22 mEq/L, de-pending on respiratory status and arterial pH.



Figure 2. (A) Dilated renal calyces on ultrasound scan indicative of hydrenephrosis. This ultrasound finding is highly specific forrenal obstruction. (B) Dilated renal calyces on computed tomography scan indicative of hydronephrosis. This finding is also high-ly specific for renal obstruction. (Images courtesy of Mark A. Perazella, MD.)

Table 3. Diagnostic Clues to the Etiology of Acute Renal Failure

Urine Osmolality, Urine BUN/ Cr Urine Urine Na,mOsm/kg Sediment Ratio Dipstick mmol/L FE Na, % FE Urea, %

Prerenal > 500 Bland or > 20 No proteinuria < 20 < 1 < 35hyaline casts

Intrinsic < 450 RBCs, WBCs, < 20 ++ Proteinuria > 40 > 1 > 50cellular casts

Postrenal < 450 Bland, RBCs, < 20 No proteinuria > 40 > 1 –crystals

BUN = blood urea nitrogen; Cr = creatinine; FE = fractional excretion; RBCs = red blood cells; WBCs = white blood cells.

BA

Hyponatremia. Hyponatremia is the most commonelectrolyte abnormality in oliguric renal failure and usu-ally is the result of excess water in the setting of reducedrenal free water clearance. Sources of free water in hos-pitalized patients are hypotonic solutions (5% dextrose,0.45% normal saline), parenteral medications adminis-tered in 5% dextrose, or excessive amounts of hypoton-ic fluid with enteral or parenteral feeds. Restriction ofthese types of fluid often minimizes worsening of hypo-natremia and allows slow correction.

Hyperkalemia. Hyperkalemia is the most seriouselectrolyte abnormality associated with ARF. Cardiactoxicity as manifested by several forms of arrhythmia isa life-threatening complication. Serum potassium con-centrations greater than 6.0 to 6.5 mEq/L requirerapid therapy. The electromechanical effects of hyper-kalemia are potentiated by hypocalcemia, acidosis, andcertain medications. The ECG, which measures thesummation of these effects, should be examined inconcert with serum potassium concentration. The ear-liest change is peaked T waves, followed by shorteningof the QT interval and flattening of P waves, whicheventually disappear. Later, QRS complex widening,prolongation of the QT interval, and ultimately a sinewave pattern develop.

Therapy is based on stabilization of excitable mem-branes, rapid reduction in serum potassium concentra-tion utilizing cellular shift, and removal of potassiumfrom the body (Table 5). Along with these interven-tions, limited potassium intake is an obvious therapy.

Hyperphosphatemia and hypocalcemia. Impairedrenal function limits phosphate excretion and pro-

motes hyperphosphatemia. Cell release of phosphate incertain settings (rhabdomyolysis, tumor lysis syndrome,and hemolysis) exacerbates hyperphosphatemia. Severehyperphosphatemia can cause hypocalcemia and softtissue calcium and phosphate deposition as well asimpair renal function. Hypocalcemia is often asympto-matic, although tetany can develop with overly aggres-sive correction of acidosis.

Treatment of hyperphosphatemia is based on re-ducing gastrointestinal absorption. Reduced dietaryphosphate (including parenteral nutrition) and oralphosphate binders with meals are the mainstay of treat-ment. Phosphate-containing bowel-cleansing regi-mens should be avoided. Hypocalcemia rarely requirestherapy in the absence of symptoms of tetany. If symp-toms develop, intravenous calcium gluconate shouldbe administered to acutely improve symptoms, fol-lowed by oral calcium carbonate to correct the calciumto the lower limit of normal.

Renal Replacement Therapy

Multiple modalities of renal replacement therapy(RRT) are available to manage ARF, including intermit-tent hemodialysis (IHD), peritoneal dialysis (PD), con-tinuous renal replacement therapy (CRRT), and new“hybrid” therapies such as sustained low efficiency dialy-sis. Despite 4 decades of experience with RRT in ARF,there are no strict guidelines on the appropriate indica-tions for initiation of therapy, the most appropriatemodality, and the optimal dose of dialysis. Despite theabsence of solid evidence, there is general consensus



Figure 3. Kidney biopsy specimen showing atheroemboli andcholesterol clefts surrounded by fibrin within the blood ves-sel lumen. This histology explains the etiology of protractedrenal failure. (Image courtesy of Mark A. Perazella, MD.)

Table 4. Strategies for Management of Acute Renal Failure

Exclude urinary tract obstruction by utilizing clinical suspicion,assessment of postvoid urine residual, and renal ultrasonography

Evaluate for the presence of a prerenal state

If evidence of intravascular depletion is present, restore intravascularvolume

Always consider the possibility of intrarenal causes that require earlydiagnosis

Discontinue all potential nephrotoxins or drugs associated with acuteinterstitial nephritis

Search for and treat acute uremic complications such as hyperka-lemia, hyponatremia, acidosis, and volume overload

Optimize nutritional status and avoid foods high in potassium andphosphorus

Dose drugs appropriately according to estimated renal clearanceusing glomerular filtration rate estimation formulas, recognizingtheir limitations in the setting of acute renal failure

Initiate renal replacement therapy before uremic, metabolic, or volume-related complications develop

regarding some of these issues. Treatment should beinitiated before uremic, metabolic, and volume-relatedcomplications occur.22 Commencement of RRT isappropriate for volume overload that is unresponsive todiuretics, hyperkalemia and metabolic acidosis, refrac-tory to conservative measures, and pericarditis orencephalopathy due to uremia. Strict laboratory valuesper se are not an indication for initiation of RRT,although a low threshold develops when the BUN levelexceeds 100 mg/dL.

Until CRRT emerged as a form of therapy, IHD, andless commonly, acute PD were utilized for severe ARF.The advantages of CRRT over IHD include more pre-cise fluid, electrolyte, and metabolic control; increasedhemodynamic stability; and the ability to administerunlimited nutritional support. The disadvantages ofCRRT include requirements for prolonged anticoagula-tion, patient immobilization, and sophisticated nursingsurveillance. PD is utilized in hypotensive patients whereCRRT is unavailable. Although CRRT is often consid-ered to be superior to IHD, studies have not demonstrat-ed a significant difference in patient outcomes.23 How-ever, CRRT is preferable in patients with cerebraledema, liver failure, severe lactic acidosis, and profoundhypotension. Sustained low efficiency dialysis haspromise as a hybrid therapy that combines the advan-tages of both continuous and intermittent therapies.

PROGNOSIS

Given its diverse causes, the long-term effects ofARF are unknown. Progressive kidney dysfunction iscommonly observed after severe ARF.24 IrreversibleARF occurs in 5% of cases and approaches 16% in theelderly.25 When ARF is severe enough to necessitateRRT, hospital mortality exceeds 50%.26

CONCLUSION

Hospitalized patients may develop ARF from variousetiologies, although ATN is the most common cause.Rapid diagnosis utilizing history, chart review, physicalexamination, and laboratory data enhances the chancesfor renal recovery. Appropriate management of ARFand its complications is required to improve patient out-come. ARF that requires RRT is associated with in-creased mortality. HP

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Table 5. Treatment of Hyperkalemia

Stabilize excitable tissues (cardiac and neuromuscular):

Calcium gluconate (10% solution), 10 to 20 mL given as an intravenous bolus

Calcium chloride (10% solution), 5 mL given as an intravenous bolus

Each may be repeated every 5 min if the electrocardiogram appearance does not improve. Calcium gluconate should bemixed in 100 mL of 5% dextrose and infused over 10 to 20 minif the patient has been treated with digoxin.

Shift potassium into cells:

Regular insulin, 10 U plus 50 mL of 50% dextrose given as an intravenous bolus, followed by 10% dextrose at 50 mL/min untildefinitive therapy is instituted. Check glucose levels at 1 to 2 hintervals.

Albuterol (5 mg/mL concentration), 10 to 20 mg nebulized over approximately 10 min

Terbutaline, 7 µg/kg administered via subcutaneous injection

Combination therapy of insulin/dextrose and nebulized albuterol

Remove potassium from the body:

Acute hemodialysis (low potassium dialysate) to remove potassi-um in patients with severe renal insufficiency

Sodium polystyrene sulfonate, 15 to 30 g plus 15 to 30 mL of sorbitol administered orally or rectally (without sorbitol)

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