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Rhabdomyolysis: A Case Study.


This educational activity is designed for nurses and other health care professionals who care for and educate patients regarding rhabdomyolysis. The multiple choice examination that follows is designed to test your achievement of the following educational objectives. After studying this offering, you will be able to:

1. Describe the pathophysiology of rhabdomyolysis.

2. Explain the process by which rhabdomyolysis can cause acute renal failure.

3. Identify laboratory and diagnostic studies used in assessing rhabdomyolysis.

4. Explain the rationale for interventions used in treating rhabdomyolysis.

Rhabdomyolysis, which may account for 25% of all cases of acute renal failure, results from injury to skeletal muscle causing the release of myoglobin into the urine. This case study presents' history and physical findings, nursing diagnoses, interventions, and research findings related to the disorder and its treatment.

On Tuesday afternoon, Mr. Daniels, a 48-year-old man with a history of excessive alcohol intake, is brought by ambulance to the emergency department. The manager at his apartment house called 911 after finding him unresponsive. Per a history obtained during a previous admission, the nurse notes that he usually consumes about a fifth of whiskey daily. The manager comments that the last time he saw Mr. Daniels was on Saturday evening when he seemed depressed and was drinking even more heavily than usual. His neighbors asked the manager to check on him because they had not seen him outside his apartment since Saturday.

The paramedics found him unresponsive but still breathing. There was a strong odor of urine. His clothes were slightly damp but not wet with urine. By his position on the floor it appeared that he may have had a seizure. There was a large amount of dried blood on his left forehead and face. An IV was started and he was transported to the hospital.

A CT scan is negative for a subdural hematoma, but a chest x-ray demonstrates right lower lobe infiltrate, probably due to aspiration. His mucous membranes are dry and his skin turgor is poor (tenting). His admitting labs are very remarkable: sodium (Na) = 150 mEq/l; potassium (K) = 6.4 mEq/l; calcium (Ca) = 6.8 mg/100 ml; phosphorus (P) = 6.0 mg/dl; albumin = 2.2 Gm/100 ml; blood urea nitrogen (BUN): 36 mg/100 ml; creatinine (Cr) = 6.5 mg/100 ml; bicarbonate (total [CO.sub.2]) = 14 mEq/l; Chloride (Cl) = 114 mEq/l; and creatine phosphokinase (CPK) = 1,200 U/L (normal = 150 U/L or less). His admitting diagnosis is rhabdomyolysis-induced acute renal failure.

A Foley catheter is placed and 120 cc of reddish-brown urine drained. The urine-specific gravity is 1.020. Urinalysis reveals a pH of 5, trace protein, 1+ ketones, trace bilirubin, 4+ blood, 1-2 RBCs, and 1-2 WBCs.

Mr. Daniels becomes septic from the pneumonia and has negligible urine output over the next 2 hours. His IV fluids have consisted of 1 liter of 0.45% saline with 50 mEq/L of sodium bicarbonate at 250 cc per hour. Dopamine therapy is started due to hypotension. In spite of therapy, the patient remains nearly anuric and dialysis is initiated.

Over the next 5 days, Mr. Daniels' condition stabilizes. He requires hemodialysis to maintain fluid and electrolyte balance. Fortunately, his hypotension only requires a few micrograms per kilogram per minute (mcg/kg/min) of dopamine, and he is weaned from this therapy over a 24-hour period. While the critical care physicians advocate maintaining "renal dose dopamine," the nephrologist advises against this because filtration will not be improved and the resultant urine will be free-water. By the 10th day, Mr. Daniels begins making urine; by the 14th day, his renal function is nearly normal, and he no longer needs dialysis. By the 21st day, he is discharged.


Acute renal failure (ARF) is a rapid decline in glomerular filtration rate (GFR) followed by the onset of the retention of metabolic waste products (azotemia) (Thelan, Davie, Urden, & Lough, 1994). In 1992, Baer and Lancaster predicted the incidence of ARF to rise from the then estimated level of 10,000 cases yearly. In 1997, Yucha and Shapiro reported an incidence of 5 to 14 cases per 100,000 people per year. This incidence is based on the following trends: the population is aging and will be more frail; more people will experience acute, complex, lengthy illnesses; and, scientific and health care knowledge is expanding along with the availability of newer technologic devices. ARF can result from a variety of direct and indirect insults on the kidney and an impaired renal system can adversely affect every other system of the body.

Acute renal failure carries a 45% to 75% mortality rate (Albright, 2001; Liano & Pascual, 1996; Lins et al., 2000). It can be classified as prerenal, postrenal, or intrarenal (parenchymal). Prerenal failure occurs when blood flow (perfusion) to the kidneys is reduced. Most often hypovolemia is the cause; however myocardial infarction, cardiac tamponade, vascular pooling from sepsis, or vascular occlusion from thrombi or emboli can also compromise renal perfusion. Postrenal failure results from ureteral, bladder, or urethral obstructions that prevent urine outflow. Outflow may be impeded sufficiently to cause backup pressure into the kidneys and subsequent damage to the kidneys themselves. Intrarenal failure results from damage to renal tissue. Damage may occur in the glomerulus (post-streptococcal infection, systemic lupus erythematosus, Good-pasture's syndrome, and bacterial endocarditis), renal vessels (inflammation or obstruction), nephrons (acute pyelonephritis, allergic reactions, hypercalcemia, uric acid nephropathy, myeloma of the kidney), and/or renal tubules (postischemia and nephrotoxins -- antibiotics, heme pigments, and radiocontrast media). The most common cause of acute renal failure is acute tubular necrosis, which causes 75% to 90% of all acute renal failure (Douglas, 1992). Mr. Daniels was stricken with rhabdomyolysis-induced acute tubular necrosis, a type of intrarenal acute renal failure.


Rhabdomyolysis, which may account for as much as 25% of all cases of ARF, results from an injury to skeletal muscle causing the release of an excess of myoglobin, an intracellular muscle protein, into the urine (Emadian, Caravati, & Herr, 1996). Rhabdomyolysis may be caused by strenuous exercise, convulsions, heat stroke, hypothermia, microbial infections, carbon monoxide poisoning, prolonged coma, hypokalemia, muscle trauma, Legionnaires' disease, drug overdose (for example, heroin, amphetamine, cocaine, phencyclidine, and alcohol), and following surgery (Huether & McCance, 1996; Richard, 1986). Other causes may include prolonged immobility, crushing injuries, sedatives, clofibrate, aminocaproate, and hypokalemia causing agents such as amphotericin B, licorice, azathioprine, and diphenhydramine overdose (Emadian et al., 1996; Huether & McCance, 1996). Rhabdomyolysis can be categorized as traumatic or nontraumatic. Contributing factors to Mr. Daniels' rhabdomyolysis include muscle necrosis from prolonged immobility and seizures.

Myoglobin, which is released into the bloodstream by injured muscles, may cause renal ischemia by clogging renal tubules (Douglas, 1992). Furthermore, myoglobin breaks down into ferrihemate and globin. Ferrihemate may be directly toxic to the renal tubules. The ability of ferrihemate to damage the renal tubules is enhanced by the acidic environment produced by the hypoxic muscle cells' use of anaerobic metabolism and by hypovolemia caused by fluid moving into injured muscles (Tierney, McPhee, & Papadakis, 1996). For example, in crush injuries of muscles, as many as 12 liters of fluid may be held within damaged muscle in the first 48 hours. Diminished renal perfusion may be exacerbated by hemoglobin and myoglobin inhibiting the vasodilator effect of nitric oxide, which is the major relaxing factor derived from the endothelium (Rose, 1994).

There are five phases of acute renal failure: onset, oliguric-anuric, early diuretic, late diuretic, and convalescent (Baer & Lancaster, 1992). Onset refers to the time from initial insult until the start of oliguria or anuria and lasts from 1 hour to 2 days. The oliguric-anuric phase is characterized by a urine output of below 400 ml/24 hours and lasts from 8 to 14 days. The early diuretic phase lasts approximately 10 days and refers to the time when urine output exceeds 400 ml/24 hours until laboratory values stop rising. During these first three phases the filtration clearance is approximately 10% of normal. The filtration clearance rises to 50% during the late diuretic phase during which laboratory values begin to decrease until they stabilize. Urine output during the diuretic phases is 150% to 200% of normal. The final stage is the convalescent phase. Laboratory values continue to stabilize, renal function returns to normal, and filtration clearance and urine output volume return to 97% to 100%. This phase may last from 4 to 6 months.

Signs and Symptoms

In addition to the triad of skeletal muscle injury, pigmented urine, and acute renal failure (Emadian et al., 1996), patients may also experience the following signs and symptoms: fever, malaise, nausea/vomiting, pain, swelling, tenderness of affected extremities (Richard, 1986); fatigue, somnolence, lethargy, irritation, decreased concentration span, mental confusion, muscle hypersensitivity/pain, muscle cramps, asterixis (liver flap), clonicotonic seizure, coma, flaccid paralysis, generalized weakness, increased sensitivity of brain and muscle cells (Miller & Evans, 1987); peaked T-waves, flattening P waves, prolonged P-R interval, complete heart block, widened QRS, asystole, ventricular tachycardia, ventricular fibrillation, anemia, and high-minute volume (to compensate for metabolic acidosis) (Toto, 1992). A neurologic assessment should include deep tendon reflexes and sensory, motor, and cortical (memory and concentration) function.

History and Diagnostic Tests

The patient history is taken to identify ischemic or toxic insults, drug use, systemic diseases, and characteristics of urine and voiding. In the initial illness phase, vital signs are taken as needed to assess the patient's condition and to verify the effectiveness of therapy. Findings will depend on the underlying pathophysiology. Numerous laboratory studies are completed, which are depicted in Table 1.
Table 1.
Laboratory Studies

Serum                                       Findings

Myoglobin                           Myoglobinemia (2-3 times
                                    greater than upper normal
                                    test limit)

Creatinine                          Increased

Blood urea nitrogen (BUN)           Increased

BUN/Creatinine ratio                Decreased

Creatinine kinase (CK)              Increased

Lactate dehydrogenase (LDH)         Increased

Aspartate amino-transferase (AST)   Increased

Sodium (Na)                         Increased

Chloride (Cl)                       Increased

Potassium (K)                       Increased

Calcium (Ca)                        Decreased (initially)
                                    Increased (later)

Phosphorus (P)                      Increased

Uric acid                           Increased

Magnesium (Mg)                      Increased

Serum osmolarity                    Increased

Albumin                             Decreased

Arterial blood gases (ABGs)         Metabolic acidosis


Color                               Brownish

Orthotolidine                       Positive

Amount                              Oliguria in 75% of cases.
                                    Nonoliguria in 25% of cases.

Fractional Excretions of Sodium     <1% if prerenal disease.
(FENa)                              >2% if acute tubular necrosis.

Sodium (Na)                         Greater than 30 mEq/L

Specific gravity                    Fixed near 1.010

Osmolarity                          Fixed near 287 mOsm

Ammonium sulfate precipitate test   Supernate will be red-brown;
                                    reagent test strip will be
                                    positive for blood.

Miscellaneous                       Uric acid, calculi formation,
                                    casts, cellular debris

Serum                                         Comments

Myoglobin                           Not useful in determining severity
                                    of rhabdomyolysis in clients with
                                    acute pancreatitis (Pezzilli et
                                    al., 1999).

Creatinine                          Rises higher/faster than with most
                                    types of ARF and disproportionately
                                    to BUN due to release of creatinine
                                    from injured cells.

Blood urea nitrogen (BUN)           --

BUN/Creatinine ratio                As creatinine rises more than BUN;
                                    10-20 as opposed to >20 in

Creatinine kinase (CK)              MM isoenzyme of creatinine kinase
                                    released from injured skeletal

Lactate dehydrogenase (LDH)         Released from injured muscle cells.

Aspartate amino-transferase (AST)   Released from injured muscle cells.

Sodium (Na)                         Decreased in hypervolemia

Chloride (CI)                       In tubular acidosis.

Potassium (K)                       Due to potassium release from
                                    injured muscle cells and decreased
                                    ability of kidneys to remove
                                    potassium from serum.

Calcium (Ca)                        Due to precipitation with
                                    During the recovery phase when
                                    calcium that had been deposited in
                                    muscle is mobilized.

Phosphorus (P)                      Due to phosphorus release from
                                    injured muscle cells.

Uric acid                           --

Magnesium (Mg)                      --

Serum osmolarity                    If hypovolemic.
                                    If hypervolemic.
                                    If kidney loses its ability to
                                    concentrate/dilute urine.

Albumin                             --

Arterial blood gases (ABGs)         Possibly respiratory alkalosis to
                                    compensate for metabolic acidosis.


Color                               --

Orthotolidine                       --

Amount                              --

Fractional Excretions of Sodium     May be falsely low with
(FENa)                              rhabdomyolysis for FENa.

Sodium (Na)                         --

Specific gravity                    If kidneys lose ability to

Osmolarity                          If kidneys lose ability to

Ammonium sulfate precipitate test   Differentiates hemoglobin and
                                    myoglobin in urine (Trainor &
                                    Solomon, 1997).

Miscellaneous                       --

Renal system impairment can adversely affect every body system. Table 2 provides a list of the most common nursing diagnoses, client outcomes, and nursing interventions seen in patients with rhabdomyolysis such as Mr. Daniels. Other pertinent nursing diagnoses include alteration in cardiac output, alteration in breathing pattern, alteration in comfort, fluid volume excess, anxiety/fear, potential for infection, knowledge deficit, alteration in thought processes, and alteration in oral mucous membranes (Baer & Lancaster, 1992).
Table 2.
Nursing Diagnoses, Outcomes, and Interventions
for Patients with Rhabdomyolysis

Nursing Diagnosis          Client Outcomes       Interventions

Fluid volume deficit    Fluid volume balance     Measure intake and
related to lack of      will be restored as      output every hour.
fluid intake while      evidenced by urine
unconscious,            output 800-1,500 ml/24   May require up to 12
vomiting/aspiration     hours According to       L/d of volume
and sepsis as           Cohen and Rao (1997),    replacement initially
evidenced by            this client will         (Cohen & Rao, 1997)
decreased urine         initially require
output and              urinary output above     Weigh daily.
hypotension.            200 mL/h, blood
(WARNING. THIS COULD    pressure within his      Assess skin turgor
CHANGE TO FLUID         normal range that        every 8 hours.
VOLUME EXCESS.          allows for adequate
MONITOR CAREFULLY.)     organ/tissue             Assess mental status
                        perfusion.               every 2 hours and

                                                 Monitor laboratory
                                                 studies; especially
                                                 Na, BUN, creatinine,
                                                 urine specific
                                                 gravity, urine
                                                 creatinine, and
                                                 urine Na.

                                                 Administer IV
                                                 fluids with
                                                 sodium bicarbonate
                                                 to increase
                                                 solubility of
                                                 myoglobin and
                                                 flush it out
                                                 in a forced
                                                 fluid intake to
                                                 decrease nephrotoxic
                                                 effects of myoglobin
                                                 and to decrease stone

                                                 While sodium
                                                 bicarbonate may be
                                                 beneficial, it may
                                                 also lead to fluid
                                                 retention and

                                                 Provide dialysis or
                                                 continuous filtration
                                                 (veno-venous or
                                                 arterial-venous) as
                                                 needed for fluid and
                                                 electrolyte balance.

                                                 Avoid overhydration;
                                                 monitor blood

Potential for injury    Client will have         Assess mental status
related to altered      adequate nutrition as    every 2 hours and
fluid/electrolyte       evidenced by serum       PRN.
balance, excess         albumin, sodium,
alcohol-ingestion       potassium, calcium,      Provide quiet, safe
pattern, and altered    phosphorus, BUN within   environment to avoid
mental status.          normal limits, and       overstimulation.
                        dry weight within 10%
                        of ideal body weight     Maintain bedrest to
                        (if achievable for       decrease muscle
                        this patient); no        metabolism.
                        signs of continued
                        tissue breakdown.        Assure seizure

                                                 Monitor laboratory
                                                 BUN, creatinine.


Alteration in           Client will remain       Provide high-calorie,
nutrition related to    free of further          low-protein (but high
chronic excessive       injury.                  in essential amino
alcohol intake,                                  acids) diet.
limitations, and                                 Monitor sodium,
emotional stress                                 potassium, and fluid
(depression) as                                  levels to identify
evidenced by (not                                excess/depletion
enough data given                                and treat accordingly
in the case study                                (will depend on
given to                                         phase; oliguria,
substantiate;                                    polyuria).
however, this is a
major nursing                                    Monitor phosphorous
diagnosis in general                             levels and supplement
for persons in renal                             as needed (alcoholics
failure and/or are                               frequently become
chronic alcoholics).                             HYPOphosphatemic
BUN is relatively low                            initially).
(36) in spite of a
high serum creatinine                            If HYPERphosphatemic
which may indicate                               administer phosphate
liver disease and/or                             binders (aluminum
poor nutrition.                                  hydroxide, calcium
                                                 carbonate, or calcium
                                                 acetate) with food.

Altered tissue          Client will have         Prevent further
perfusion (renal        clear, normal volume     tissue breakdown
and muscle) related     urine output.            through proper
to prolonged                                     positioning and
immobility and                                   maintaining a safe
tissue damage during                             environment.
leading to myoglobin                             Treat hyperkalemia
release from muscles                             with calcium
and movement to renal                            gluconate, glucose,
tubules evidenced by                             insulin, Kayexalate
crimson-colored                                  and if needed
urine; decreased                                 dialysis. Sodium
urine output; urine                              bicarbonate may also
pH of 5; trace                                   be useful.
protein, 1+ ketones,
trace bilirubin,                                 Administer sodium
4+ blood and 1-2                                 bicarbonate if
WBCs in urine.                                   needed for acid-base
                                                 control; may decrease
                                                 damage to tubules by
                                                 increasing urine pH
                                                 above 6. Sodium
                                                 bicarbonate may also
                                                 increase the
                                                 solubility of
                                                 myoglobin thus
                                                 expediting its

                                                 Administer low-dose
                                                 (0.5 to 3 mcg/kg/
                                                 min) dopamine to
                                                 increase renal
                                                 perfusion through
                                                 vasodilation by

                                                 The long-term
                                                 benefits of dopamine
                                                 therapy remain
                                                 controversial (Ichai
                                                 et al., 2000).

                                                 Consider using
                                                 dopamine is first
                                                 choice. Epinephrine
                                                 and norepinephrine
                                                 to increase cardiac
                                                 output if unable to
                                                 maintain B/P with

                                                 Administer diuretics
                                                 ethacrynic acid) in
                                                 the oliguric patient
                                                 (to flush out
                                                 cellular debris,
                                                 increase urine
                                                 output, and decrease
                                                 backleak of filtrate
                                                 across the damaged

                                                 Avoid mannitol in
                                                 oliguria because if
                                                 the patient does not
                                                 urinate mannitol
                                                 will circulate and
                                                 cause pulmonary
                                                 edema andother

                                                 Monitor patients
                                                 exposed to
                                                 nephrotoxins; monitor
                                                 renal function in
                                                 patients receiving
                                                 nephrotoxic drugs.

                                                 Avoid giving
                                                 cephalothin and
                                                 concurrently, both of
                                                 which may be
                                                 nephrotoxic (better
                                                 to use oxacillin in
                                                 place of cephalothin;
                                                 however must
                                                 administer gentamicin
                                                 and oxacillin at
                                                 least 1 hour apart
                                                 since oxacillin,
                                                 a penicillin,
                                                 an aminoglycoside
                                                 [Spencer, et. al.,

Implications for Research

Several investigators have studied the incidence and prevalence of rhabdomyolysis, recommended treatments, and client outcomes. Hojs, Ekart, Sinkovic, and Hojs-Fabjan (1999) studied 73 patients in acute renal failure cared for in one medical intensive care unit. Ten of the 49 who had multi-system failure also had a diagnosis of rhabdomyolysis. Patients with rhabdomyolysis had a significantly higher (p [is less than] 0.027) number of failing organs and had a significantly higher (p [is less than] 0.05) mortality than patients without rhabdomyolysis. No difference was found between the two groups in terms of age or gender.

In another study of critically ill patients with ARF, approximately 70% of those requiring dialysis died in the hospital (Chertow, Christiansen, Cleary, Munro, & Lazarus, 1995). These researchers developed a model for predicting death among these patients. Factors associated with in-hospital deaths included mechanical ventilation, malignancy, and nonrespiratory organ failure.

The patient, Mr. Daniels, required hemodialysis but did not have any of the other factors associated with in-hospital death. He was discharged from the hospital in stable condition.

Determining the fractional excretion of sodium (FENa) is valuable in differentiating between acute tubular injury and prerenal azotemia (the presence of increased amounts of nitrogenous substances in the blood, consistent with renal failure) (Corwin, Schreiber, & Fang, 1984). In prerenal azotemia, including situations such as the initial phase of acute obstruction and contrast media-induced acute renal failure, the FENa is below 1% because the kidneys sense a decreased circulating blood volume and compensate by retaining sodium. In acute tubular injury the FENa is greater than 1% because the kidneys are unable, because of the injury, to retain sodium. The FENa in myoglobinuric and hemoglobinuric acute renal failures is less than 1% (see Figure 1).

Figure 1. Determining Fractional Exretion of Sodium (FENa)

FENa = (urine sodium/plasma sodium)/ (urine creatine/plasma creatine) x 100

During the oliguric phase of both pure myoglobinuric and hemoglobinuric acute renal failure, patients may retain their ability to reabsorb sodium, which is reflected in FENa values of less than 1% (Corwin et al., 1984). These FENa values are consistent with observations in decreased renal perfusion and acute tubular obstruction but not with acute tubular injury. Based on this, these researchers suggest that ARF secondary to finding hemoglobinuria and myoglobinuria is more likely due to acute tubular obstruction and/or diminished renal perfusion than to direct tubular nephrotoxicity. The initial insult may be obstruction which progresses to acute tubular necrosis especially in dehydrated patients. Unfortunately, inadequate data were available on Mr. Daniels to determine whether his FENa value was less than 1%.

In another study, the indicators of fluid volume deficit were validated (Gershan et al., 1990). Of the 72 clinical indicators initially examined, 17 were ultimately classified as critical indicators (major defining characteristics), and 29 were cited as minor defining characteristics. Consistent with this study's findings, Mr. Daniels exhibited the following defining characteristics of fluid volume deficit: negative intake and output, decreased urine output, decreased blood pressure, increased blood urea nitrogen, increased serum creatinine concentration, and lethargy (unconscious).


Mr. Daniels is a fortunate man. He survived an episode of acute renal failure sufficiently severe to warrant dialysis. It appears at least for now that he does not have any signs of chronic renal failure. However, the unfortunate reality is that he is an alcoholic who seems to lack an effective support system. If he continues to drink, he will likely insult his kidneys and other body systems again. He must be informed of the danger he faces if he continues to drink. To quit drinking he will need help establishing a support system. Encouragement to participate in Alcoholics Anonymous or rehabilitation on an inpatient or outpatient chemical dependency unit are suggested. Furthermore, the patient will need dietary instruction and access to appropriate foods to improve his overall health status. Nurses can make the difference in enhancing this possibility. Ultimately, the choice for improved health is his.


Albright, R. (2001). Acute renal failure: A practical update. Mayo Clinic Proceedings, 77(1), 67-74.

Baer, C.L., & Lancaster, L.E. (1992). Acute renal failure. Critical Care Nursing Quarterly, 14(4), 1-21.

Carpenito, L.J. (1995). Nursing care plans & documentation: Nursing diagnoses and collaborative problems (2nd ed.). Philadelphia: J.B. Lippincott.

Chertow, G.M., Christiansen, C.L., Cleary, P.D., Mundo, C., & Lazarus, J.M. (1995). Prognostic stratification in critically ill patients with acute renal failure requiring dialysis. Archives of Internal Medicine, 155(14), 1505-1511.

Cohen, R.I., & Rao, R. (1997). Pulmonary and critical care pearls: A 41-year old man with thigh pain and loss of sensation in the toes. Chest, 111, 810-812.

Corwin, H.L., Schreiber, M.J., & Fang, L.S. (1984). Low fractional excretion of sodium: Occurrence with hemoglobinuric- and myoglobinuric-induced acute renal failure. Archives of Internal Medicine, 144, 981-982.

Dolleris, P.M. (1992). Diuretic and vasopressor usage in acute renal failure: A synopsis. Critical Care Nursing Quarterly, 14(4), 28-31.

Douglas, S. (1992). Acute tubular necrosis: Diagnosis, treatment, and nursing implications. AACN Clinical Issues, 3, 688-697.

Emadian, S.E., Caravati, E.M., & Herr, R.D. (1996). Rhabdomyolysis: A rare adverse effect of diphenhydramine overdose. American Journal of Emergency Medicine, 14, 574-576.

Gershan, J.A., Freeman, C.M., Ross, M.C., Greenless, K., Smejkal, C., Brukwitzki, G., Schneider, K., Jiricka, M.K., Johnson, D., & Anderson, C. (1990). Fluid volume deficit: Validating the indicators. Heart & Lung, 19, 152-156.

Gordon, M. (1995). Manual of nursing diagnosis 1995-1996 (7th ed.). St. Louis: Mosby.

Hojs, R., Ekart, R., Sinkovic, A., & Hojs-Fabjan, T. (1999). Rhabdomyolysis and acute renal failure in the intensive care unit. Renal Failure, 21(6), 675-684.

Huether, S.E., & McCance, K.L. (1996). Understanding pathophysiology. St. Louis: Mosby.

Ichai, C., Passeron, C., Carles, M., Bouregba, M., & Grimaud, D. (2000). Prolonged low-dose dopamine infusion induces a transient improvement in renal function in hemodynamically stable, critically ill patients: A single-blind, prospective, controlled study. Critical Care Medicine, 28(5), 1329-1335.

Liano, F., & Pascual, J. (1996). Epidemiology of acute renal failure: A perspective, multicenter, community-based study. Madrid Acute Renal Failure Study Group. Kidney International, 50(3), 811-818.

Lins, R., Elseviers, M., Daelemans, R., Zachee, P., Gheuens, E., Lens, S., & DeBroe, M. (2000). Prognostic value of a new scoring system for hospital mortality in acute renal failure. Clinical Nephrology, 53(1), 10-17.

Miller, C.A., & Evans, D. (1987). CNS manifestations of acute renal failure. Critical Care Nurse, 7(3), 94-95.

Pezzilli, R., Billi, P., Carppelletti, O., Barakat, B., & Miglio, F. (1999). Rhabdomyolysis and acute pancreatitis. Journal of Gastroenterology and Hepatology, 14(2), 168-171.

Richard, C.J. (1986). Comprehensive nephrology nursing. Boston: Little, Brown.

Rose, B.D. (1994, August 2). Treatment of heme pigment-induced acute tubular necrosis [4 pages]. Update in Medicine [On-line serial]. (800-998-6374 or 617-237-4788).

Spencer, R.T., Nichols, L.W., Lipkin, G.B., Henderson, H.S., & West, RM. (1993). Clinical pharmacology and nursing management (4th ed.). Philadelphia: Lippincott.

Thelan, L.A., Davie, J.K., Urden, L.D, & Lough, M.E. (1994). Critical care nursing: Diagnosis and management (2nd ed.). St. Louis: Mosby.

Tierney, L.M., McPhee, S.J., & Papadakis, M.A. (Eds.). (1996). Current: Medical diagnosis & treatment (35th ed.). Stanford, CT: Appleton & Lange.

Toto, K.H. (1992). Acute renal failure: A question of location. American Journal of Nursing, 92, 44-53.

Trainor, L.D., & Solomon, H.M. (1997). Clinical pathology rounds: Detecting myoglobinuria: A low-tech analysis. Laboratory Medicine, 28, 569-571.

Yucha, C., & Shapiro, J. (1997). Acute renal failure: Recognition and prevention. Lippincott's Primary Care Practice, 1(4), 388-398.


The Sun and Your Skin

* 90% of skin damage results from exposure to the sun's ultraviolet rays.

* 50% of all skin damage occurs before the age of 18.

* Sun damage can lead to premature aging, such as rough, saggy, wrinkled, and discolored skin.

* Even normal, everyday sun exposure can cause lines and wrinkles.

* More than 90% of all skin cancers occur on parts of the body exposed to the sun.

* It takes about an ounce of sunscreen to protect exposed skin from the sun.

Staphylococcus Epidermidis Facts

* S. epidermidis is found in small stitch abscesses and other skin wounds, which occur on parasitic skin and mucous membranes.

* It is parasitic rather than pathogenic.

* It is the cause of bacteremia in premature infants and immunocompromised patients.

* S. epidermidis causes infections of vascular access devices, prosthetic heart valves, and can cause urinary tract infections in teenaged females.
Choose one correct answer for each question.
CE Questions

1. Rhabdomyolysis may account for as much as
   -- percent of all cases of acute renal failure.

   a. 10.
   b. 15.
   c. 25.
   d. 35.

2. The renal ischemia associated with rhabdomyolysis-induced
   renal failure may be due to:

   a. The clogging of tubules by myoglobin.
   b. Hyperperfusion of skeletal muscles.
   c. Renal artery occlusion.
   d. Vascular pooling.

3. The rhabdomyolysis Mr. Daniels experienced
   was likely related to:

   a. Hypothermia.
   b. Prolonged immobility and seizures.
   c. Hypokalemia.
   d. Infection and concussion.

4. The convalescent phase of acute renal failure
   usually lasts:

   a. 1-2 months.
   b. 2-3 months.
   c. 4-6 months.
   d. 10-12 months.

5. The triad of signs and symptoms associated
   with rhabdomyolysis includes:

   a. Skeletal muscle injury, pigmented urine,
      acute renal failure.
   b. Fever, malaise, pain.
   c. Tenderness of extremities, heart block,
      mental confusion.
   d. Asterixis, decreased concentration span,
      muscle, hypersensitivity.

6. In the study by Hojs et al. (1999), which of the
   following was true of patients with rhabdomyolysis
   when compared to patients with acute renal failure
   due to other causes? The patients with rhabdomyolysis

   a. Better response to therapy.
   b. Longer survival time.
   c. Higher mortality rates.
   d. Fewer number of failing organs.

7. The fractional excretion of sodium (FENa) is
   valuable in differentiating between:

   a. Prerenal and postrenal failure.
   b. Intrarenal and postrenal failure.
   c. Acute pyelonephritis and uric acid
   d. Acute tubular injury and prerenal azotemia.

8. What may be added to IV fluids to increase
   solubility of myoglobin and flush it out in forced

   a. Glucose.
   b. Insulin.
   c. Potassium.
   d. Sodium bicarbonate.

9. The ultimate goal for the unconscious patient
   with a fluid volume deficit related to lack of fluid
   intake is a 24-hour urine output of:

   a. 200-400 ml.
   b. 500-700 ml.
   c. 800-1500 ml.
   d. 1600-2000 ml.

10. Dietary recommendations for persons with
   renal failure and/or chronic alcoholism includes:

   a. High calorie, low protein.
   b. Low calorie, low fat.
   c. High calorie, low carbohydrate.
   d. Low calorie, restricted concentrated sweets.


This independent study activity for 1.0 contact hour(s) is provided by the Academy of Medical-Surgical Nurses, which is accredited as a provider and approver of continuing education in nursing by the American Nurses Credentialing Center's Commission on Accreditation (ANCC-COA).

This article was reviewed and formatted for contact hour credit by Catherine Todd Magel, EdD, RN, C, Assistant Professor, College of Nursing, Villanova University, Villanova, PA; Sally S. Russell, MN, RN,C, Medical-Surgical Course Chairperson/ Instructor/Staff Nurse, St. Elizabeth Hospital School of Nursing, Lafayette, IN; and Marilyn S. Fetter, PhD, RN, CS, Assistant Professor, College of Nursing, Villanova University, Villanova, PA.

Linda S. Wallace, EdD, RN, is Assistant Professor, School of Nursing, Indiana University, Kokomo, IN.

Acknowledgment: Special thanks to Nephrologist, Dawn M. Sabau, MD, Kokomo, IN, for providing this case study and for reviewing/critiquing this article.
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Author:Wallace, Linda S.
Publication:MedSurg Nursing
Geographic Code:1USA
Date:Jun 1, 2001
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