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«Official reprint from UpToDate ® ©2010 UpToDate ® Crush-related acute kidney injury (acute renal failure) Authors Section Editor ...»

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Crush-related acute kidney injury (acute renal failure) 21/11/10 18:58

Official reprint from UpToDate ® www.uptodate.com

©2010 UpToDate ®

Crush-related acute kidney injury (acute renal failure)

Authors Section Editor Deputy Editor

Raymond Vanholder, MD, PhD Paul M Palevsky, MD Alice M Sheridan, MD

Mehmet S Sever, MD Last literature review version 18.2: mayo 2010 | This topic last updated: junio 17, 2010 INTRODUCTION — High circulating plasma myoglobin levels secondary to rhabdomyolysis can cause heme pigment-associated acute tubular necrosis (ATN), which results in an abrupt rise in serum creatinine, or acute kidney injury (AKI) [1-5]. (See "Definition of acute kidney injury (acute renal failure)".) Rhabdomyolysis may be due to either traumatic or nontraumatic muscle injury. Much of our knowledge of rhabdomyolysis-associated ATN derives from observations of rhabdomyolysis that occurs as part of the crush syndrome resulting from large scale natural or man-made disasters.

The clinical features and prevention of AKI due to traumatic rhabdomyolysis will be reviewed here.

ATN due to nontraumatic rhabdomyolysis (due to exertion, coma-induced immobility, and toxins) and hemolysis and general overviews of rhabdomyolysis, hemolysis, and drug-induced myopathies are discussed in detail separately. (See "Clinical features and prevention of heme pigment-induced acute tubular necrosis" and "Clinical manifestations, diagnosis, and causes of rhabdomyolysis" and "Approach to the diagnosis of hemolytic anemia in the adult" and "Drug-induced myopathies".) DEFINITIONS AND EPIDEMIOLOGY — Crush injury complicated by AKI is often referred to as crush syndrome. Crush syndrome may include hypovolemic shock, sepsis, electrolyte disturbances (of which hyperkalemia is the most important), heart failure, arrhythmias, acute respiratory distress syndrome, disseminated intravascular coagulation, bleeding, psychological trauma, and heme pigment-induced ATN, although all of these components need not be present for the term crush syndrome to be used [6-8].

Crush syndrome develops in 30 to 50 percent of cases of traumatic rhabdomyolysis and is frequently seen after catastrophic earthquakes [6,7]. According to some estimates, the incidence of crush syndrome ranges between 2 and 5 percent of all injured victims of catastrophic earthquakes [9-11].

The following reports have analyzed the incidence of AKI as part of crush injury following

catastrophic earthquakes:

The frequency with which dialysis is required has varied widely in different studies. In a report from Bam, Iran, dialysis was required in 6.5 percent of 1975 patients admitted to the hospital [12]. The majority of victims were rescued in less than four hours, which may explain at least in part the lower rate of requiring dialysis than in other reports.

Much higher rates of requiring dialysis were noted in two other catastrophic earthquakes: 54 percent in the Kobe earthquake and 75 percent in the Marmara earthquake [11,13,14]. In the Kobe earthquake, the need for hemodialysis correlated directly with increased serum creatine kinase (CK) levels, as dialysis was required in 84 and 39 percent of patients with a CK level greater or less than 75,000 U/L, respectively [11].

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In the Kobe and Marmara earthquakes, the time under the rubble correlated inversely with both serum creatine kinase (CK) and the frequency of requiring dialysis. A possible explanation for these counterintuitive findings is that victims with more extensive muscle injury and higher CK levels died before they were transported to the hospital.

CLINICAL MANIFESTATIONS — The most typical local finding of rhabdomyolysis is compartment syndrome, due to swollen muscles. Patients suffer from severe pain, weakness, paresthesia, paresis or paralysis and pallor in the affected extremities. Distal pulses may be absent when intracompartmental pressure is very high, although increased intracompartmental pressure may be present even when distal pulses are palpable. In traumatic rhabdomyolysis, signs of blunt or penetrating trauma are also present.

AKI resulting from heme pigment-induced ATN is usually characterized by an initial oliguric period followed by polyuria, which usually starts within one to three weeks after the primary event. Some cases may present with a nonoliguric course.

Hypovolemia — Some patients with rhabdomyolysis have been immobile or comatose for significant periods of time. As a result, hypovolemia due to absence of fluid intake plus ongoing losses may be observed. This is particularly important among patients with rhabdomyolysis due to crush injury, since they may have been immobilized for hours to days. In addition, third spacing at the site of muscle injury among such patients significantly worsens hypovolemia. The latter phenomenon typically starts only after decompression, due to reperfusion of the traumatized muscle.

Dark urine — The characteristic manifestation of heme pigment-induced ATN is discolored urine.

Marked release of myoglobin leads to red or brown (or even black) urine, unless pigment excretion is limited because of a low glomerular filtration rate, extreme dilution of the urine due to preventive fluid administration, or clearance from the plasma by the reticuloendothelial system [15]. Urinalysis also reveals pigmented granular casts.

The plasma is typically normal in color with myoglobinuria. This is in contrast to conditions resulting in hemoglobinuria-induced ATN, such as massive hemolysis, that are characterized by red-tinted plasma. (See "Clinical features and prevention of heme pigment-induced acute tubular necrosis".) Renal insufficiency — The severity of renal insufficiency ranges widely from a mild elevation in the serum creatinine concentration to oliguric AKI requiring immediate hemodialysis. This variability is due to differences in severity of injury to muscle and presence or absence of volume depletion and/or underlying additional comorbid conditions, particularly sepsis [16,17].

BIOCHEMICAL ABNORMALITIES — The biochemical abnormalities that characterize rhabdomyolysis-associated AKI include hyperkalemia that may be life-threatening, hyperphosphatemia, hypocalcemia (which is occasionally followed by hypercalcemia during the recovery stage), a high CK, and a low fractional excretion of sodium. These are discussed elsewhere. (See "Clinical features and prevention of heme pigment-induced acute tubular necrosis".) DIAGNOSIS — Patients with rhabdomyolysis-induced ATN typically present with the triad of pigmented granular casts in the urine, a red to brown color of the urine, varying severity of kidney dysfunction, and a marked elevation in the plasma CK level. (See "Clinical manifestations, diagnosis, and causes of rhabdomyolysis".) DIFFERENTIAL DIAGNOSIS — The intermittent excretion of red to brown urine can be seen in a variety of clinical settings, including heme pigment-induced ATN. The approach to this issue is discussed separately. (See "Red to brown urine: Hematuria; hemoglobinuria; myoglobinuria".) AKI can also be caused by conditions or abnormalities commonly observed in patients with

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traumatic rhabdomyolysis. These include drug-induced AKI (such as aminoglycosides), sepsis, severe hypotension due to marked hypovolemia, and others. This is also discussed elsewhere. (See "Etiology and diagnosis of acute tubular necrosis and prerenal disease".) PREVENTION — The general goals for preventive therapy in all cases of heme pigment-induced AKI are the correction of volume depletion, if present, and prevention of intratubular cast formation.

The approach to prevention of AKI in the patient with rhabdomyolysis due to crush syndrome varies based upon the location of the patient and ability to closely monitor the victim.

Prior to extrication — Aggressive fluid repletion should be started before the extrication of entrapped subjects prone to develop the crush syndrome, if possible. Third spacing at the site of muscle injury worsens hypovolemia. Thus, patients with rhabdomyolysis may require massive amounts of fluid to initiate and maintain a vigorous diuresis.

The goals of volume repletion are to both enhance renal perfusion (thereby minimizing ischemic injury) and increase the urine flow rate to wash out obstructing casts. Volume resuscitation should be initiated before the crush is relieved, or as soon as possible thereafter, before heme pigment and other intracellular elements have been released into the circulation and before third spacing at the site of muscle injury worsens hypovolemia [2,8,18,19].

Evidence — The rationale for this approach is based upon the observations that early adequate fluid resuscitation is very important to help prevent AKI in patients with rhabdomyolysis due to crush injury.

Practically all of the published experience with volume resuscitation in patients with heme pigmentinduced ATN has come from retrospective reports of rhabdomyolysis in subjects with crush injury [2-4,18-20]. The following studies serve as examples of the importance of early fluid repletion in

this setting [18,19]:

Seven patients with crush syndrome who were trapped under rubble (all with CK concentrations 30,000 U/L) were treated with alkaline diuresis immediately after extrication; none developed renal failure [19]. One patient who did not receive prophylactic volume repletion developed AKI and required hemodialysis [21]. These data were compared to historical data where patients with injuries of comparable severity all developed AKI [3].

Sixteen earthquake victims trapped for a mean of 10 hours (12 had CK concentrations 20,000 U/L) were treated initially with isotonic saline at 1 L/hour, then with an alkaline-mannitol solution [18]. The four patients who required dialysis were treated approximately nine hours after extrication and received significantly less fluids compared with 12 patients who did not require dialysis, who were treated four hours after extrication.

In other reports of earthquake-related crush injury, AKI occurred in over 50 percent of patients for whom therapy was instituted much later [20,22].

Thus, preventive therapy appears to be less effective after the first 6 to 12 hours, when the kidney injury may already be established.

The optimal fluid and rate of repletion are unclear. No studies have directly compared the efficacy and safety of different types and rates of fluid administration in this setting.

Prior to extrication, we and the International Society of Nephrology Renal Disaster Relief Task Force recommend isotonic saline rather than isotonic bicarbonate, because saline solutions are more readily available in disasters and have a well-described efficacy for volume replacement [8].

Isotonic saline should initially be given at a rate of 1 L/hour (10 to 15 mL/kg of body weight per

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hour) while the victim is still under the rubble. After 2 liters are given, the rate of administration should be decreased to 500 mL/hour to avoid volume overload. However, this volume should be individualized. Factors to consider are age (fluid administration should be performed more carefully in the elderly); body mass index (more fluids are needed for the victims with larger body surface area); trauma pattern (compartment syndrome is worse with more serious trauma); and amount of presumed fluid losses (more fluids are needed in hot climates and in victims who produce urine or have ongoing blood losses).

There is a role for isotonic bicarbonate therapy after extrication. (See 'Use of bicarbonate' below.) Fluid overload is defined by signs of pulmonary congestion. Limb swelling alone may not represent volume overload, since it may be due to third space sequestration (compartment syndrome).

Severe hyperkalemia is relatively frequent among patients with crush injuries. As a result, intravenous solutions containing potassium, such as Ringer's lactate, are contraindicated in such patients.

After extrication Use of bicarbonate — After the victim has been removed from the rubble, urine output has been documented, and overt alkalosis has been excluded, it is suggested to switch from isotonic saline to an alkaline solution that is approximately isotonic in an attempt to achieve a forced alkaline diuresis.

The rationale for this approach is that raising the urine pH above 6.5 may prevent heme-protein precipitation with Tamm-Horsfall protein, intratubular pigment cast formation, and uric acid precipitation [1,3,23]. Alkalinization may also decrease the release of free iron from myoglobin and the formation of F2-isoprostanes, which may enhance renal vasoconstriction. (See "Clinical features and prevention of heme pigment-induced acute tubular necrosis".) Despite these potential benefits, there is no clear clinical evidence that an alkaline diuresis is more effective than a saline diuresis in preventing acute kidney injury, as no direct comparative trial has been performed. The best data in support of an alkaline diuresis are derived from uncontrolled case series. In a study cited above, for example, renal failure did not develop in seven patients with crush syndrome who were trapped under rubble and were treated with alkaline diuresis immediately after extrication [19]. By comparison, one patient who did not receive prophylactic volume developed acute kidney injury and required hemodialysis [21].

The optimal regimen and rate of administration of bicarbonate are unknown. We generally

administer one of the following two fluid regimens after extrication:

One liter of isotonic saline alternating with 1 liter of half isotonic saline plus 50 mEq of sodium bicarbonate.

Isotonic saline for the first 2 liters, followed by 1 liter of half isotonic saline plus 50 mEq of sodium bicarbonate. This sequence is then repeated, as indicated.

The choice between these two regimens depends in part upon the general clinical and biochemical condition of the patient and the blood pH. As an example, if measured laboratory values reflect only a mild acidosis, more liters of isotonic saline and fewer liters of bicarbonate-containing solution are given.

The rate of fluid administration with either regimen is based upon the ability to attain urinary output goals, and assessment of volume status. In general, we administer the intravenous solution at 500 mL/hour for the first 24 hours as long as there is no evidence of fluid overload and the patient can

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