UDK  616-001.32-083.98                        

ISSN 2466-2992 (Online) (2022) br. 2, p. 15-24

COBISS.SR-ID 110170889

TREATMENT OF PATIENTS WITH CRUSH INJURY

Biljana Stošić 1,2, Vesna Marjanović 1,2,  Marija Stošić 3, Jelena Živadinović2, Ivana Budić 1,2

1University of Niš, Faculty of Medicine, 2Clinic for Anesthesiology and Intensive Care, University Clinical center Niš, 3Clinic for Cardiac Surgery, University Clinical Center Niš

Summary:

It was observed that, in road traffic accidents extremities were the most affected parts of the body (41% lower extremity and 21% upper extremity). Superficial injuries were found to be most common (47%), followed by fractures (20%), crush injuries (14%) and concealed injuries (12.4%). Major reason of morbidity and prolonged hospital stay after traffic accidents is musculoskeletal injury. Victims who survive after the major traumatic injuries can succumb to the various life threatening complications. Most of these injuries are directly related to the bone and soft tissue injuries. Goal of an anesthesiologist is to address initial musculoskeletal insult and treat or avoid secondary complications. Every trauma patient has a possibility of crush injury and they should be searched for the same thoroughly. Early diagnosis and treatment of problems like hypovolemia, crush syndrome, rhabdomyolysis can avoid further metabolic, cardiovascular and renal complications. Thus early diagnosis and management of crush injury can modulate the overall outcome of a trauma patient. This management of crush injury patient is a multidisciplinary work and requires good interdepartmental coordination for successful outcome. More sophisticated biochemical studies and devices to measure intercompartmental pressures are required to avoid unnecessary fasciotomies.

Key words: Crush injury, treatment, hypovolemia, rhabdomyolysis

INTRODUCTION

It was observed that, in road traffic accidents extremities were the most affected parts of the body (41% lower extremity and 21% upper extremity). Superficial injuries were found to be most common (47%), followed by fractures (20%), crush injuries (14%) and concealed injuries (12.4%) [1]. Major reason of morbidity and prolonged hospital stay after traffic accidents is musculoskeletal injury. Victims who survive after the major traumatic injuries can succumb to the various life threatening complications. Most of these injuries are directly related to the bone and soft tissue inju­ries. Goal of an anesthesiologist is to address initial musculoskeletal insult and treat or avoid secondary complications. Every trauma patient has a possibility of crush injury and they should be searched for the same thoroughly. Early diagnosis and treatment of problems like hypo­volemia, crush syndrome, rhabdomyolysis can avoid further metabolic, cardiovascular and re­nal complications. Thus early diagnosis and management of crush injury can modulate the overall outcome of a trauma patient.

PATHOPHYSIOLOGY OF CRUSH INJURY

Crush injuries are caused by continuous pro­longed pressure on the body. It involves mainly lower and upper extremities. Chest, abdomen or face can also have crush injuries. The direct pressure after crush injury causes muscle cell to become ischemic. Continuous pressure causes muscle damage resulting in an influx of fluid into the muscles resulting in edema and eleva­tion in compartment pressure [2]. The cells then switch to anaerobic metabolism, generating large amounts of lactic acid. Prolonged ischemia then causes the cell membranes to leak. Continuous inflow of fluids (edema fluids, bleeding) or too little outflow (venous obstruction) can cause increased pressure in the compartment. This increased compartment pressure will cause tissue pressure to increase more than total capillary pressure and ultima­tely cause capillary collapse. All this will cause increased diffusion of fluid from the intravascu­lar space to the extravascular space and lead to further increase in compartmental pressure. This edema-outflow obstruction – more edema vicious cycle if continued will hamper oxygena­tion of muscle tissue. If not treated early this will proceed to tissue ischemia, muscle necrosis and nerve dysfunction, eventually irreversible cell damage/death [3].

TOXINS RELEASED IN CRUSH INJURY

The toxin leak may continue for as long as 60 hours after the crush injury [4,5]. Some of these substances and their consequences are listed in Table 1.

Agent Effect

Amino acids and other organic acids Acidosis, Aciduria, Dysrhythmia

Creatinine phosphokinase (CPK) Laboratory marker for crush injury

Free radicals, superoxides, peroxides Secondary tissue damage

Histamine Vasodilation, Bronchoconstriction

Lactic acid Acidosis, Dysrhythmia

Leukotrienes Lung injury

Lysozymes Cellular injury

Myoglobin Renal failure

Potassium Renal failure, Dysrhythmia, Cardiac arrest

Thromboplastin Disseminated intravascular coagulation

Table 1: Toxins released after crush injury

CLINICAL PRESENTATION

 Pain is the main presenting symptom and it is deep and aching in nature and is worsened by passive stretching of the in­volved muscles. Pain can be out of propor­tion to the injury [2].

 Immediately following extrication, a severe neurologic deficiency, mainly flaccid paralysis of the injured limb, may be pre­sent. Sensory loss to pain and touch is seen in a patchy pattern.

 Pallor, pulselessness and poikilothermia (hypothermia) may be present but they are usually late signs [6].

 Limb edema is initially not present. Gross edema takes time to develop and can pro­gress to compartment syndrome.

 Distal pulses may be present even in the presence of gross edema. Investigation for additional injuries is warranted if pulses are not present.

 Uncontrolled bleeding in mangled extremi­ties may be present and it can lead to severe hypovolemic shock and death.

 Even if skin and subcutaneous layers are not injured still the underlying muscles can be severely damaged.

 Associated injuries elsewhere may be pre­sent.

 Unlike the adult, the signs of hypovolemia or significant hemorrhage in a child are subtle and difficult to identify. The best early sign of hypovolemia in pediatric victims is a weak pulse as opposed to tachycardia in adults.

PREHOSPITAL CARE

• Prehospital care begins with first assessing trauma scene safety by the care provider. It is important to move the victim away from the trauma scene and to get medical aid as early as possible.

• The primary focus for trauma resuscitation in the field is airway, breathing, circulation, (the ABCs of the primary survey) and spinal stabili­zation.

• Shock, respiratory distress, and altered men­tal status are associated with high mortality and must be rapidly identified in the field with sub­sequent rapid transport to the nearest appropriate trauma/medical center.

• For entrapped victims, venous access can so­metimes be established during extrication. For trauma victims in shock, venous access should be attempted during transport to the medical center [7].

• Resuscitation fluid of choice at trauma scene is Lactated Ringers solution. But if one suspects crush injuries then it is prudent to use isotonic saline for resuscitation fluid till victim reaches hospital as there are chances of fatal arrhythmias because of hyperkalemia.

• Tying of obviously bleeding vessels or applying direct pressure bandages on crushed or mangled extremities can stop ongoing hemorrhage

• Application of tourniquets above the injured extremity can itself cause limb ischemia hence routine use of tourniquets should be avoided. Tourniquet can be used temporarily in victim who is actively bleeding so that hypovolemic shock can be avoided before reaching hospital.

• Spinal stabilization, i.e. securing of a victim to a rigid spine support, of not only the cervical spine but whole spine is an important aspect of the prehospital care of trauma victims.

• Remember that the aim of primary resuscita­tion is not to treat the trauma but stabilization of the patient till transfer to hospital for treatment.

EMERGENCY MANAGEMENT

Emergency management is aimed at stabiliza­tion of hemodynamic status, treatment of crush injury and prevention of its complications. As patient arrives at EMS, airway, breathing, circu­lation and hemodynamic status should be checked. Secondary survey follows primary survey and associated injuries should be evaluated and treatment plan decided accordingly. Crush injury in more than one extremity should raise anticipation of crush syndrome. All routine investigations including serum electrolytes and urine for routine and myoglobin should be sent to laboratory after patient arrives at hospital.

STABILIZATION OF HEMODYNAMIC

STATUS

Intravenous Fluids

The mainstay of treatment for crush injury is administration of intravenous fluids. At least two 14 or 16 G intravenous access should be established as soon as patient arrives at emergency area and fluid resuscitation should be started immediately. Initially a colloid or crystalloid such as normal saline is used. Potassium containing fluid, e.g. lactated Rin­ger’s solution should be avoided in suspected crush injury patients as it may worsen hyperka­lemia [8]. Once the patient is rescued from tra­uma site, it is critical to maintain a high urine output. Foley catheter placement is very impor­tant as it allows more accurate measurements of urine output as well as urine pH.

Treatment of Hyperkalemia

Mode of treatment used to treat hyperkalemia depends upon its severity. Administration of calcium gluconate is one of the fastest method to decrease blood potassium, but it will act only for a short period of time. Usual dose is 10 ml of 10 percent solution infused over 3 to 5 minutes. Insulin will shift extracellular K+ to intracellular side. Infusion of 50 g of dextrose combined with 10 units of insulin will decrease blood K+ immediately and effect will last for some hours. Sodium bicarbonate can be used in cases with severe hyperkalemia associated with metabolic acidosis. Other modalities which can be used are β2 agonists, loop diuretics, cation exchange resins like sodium polystyrene sulfonate and ultimately hemodialysis as last resort [9].

Alkaline Diuresis

Alkalinization of urine will increase solubility of myoglobin and promote its excretion. It also prevents oxidative damage resulting from cycling of myoglobin by stabilizing the more reactive ferryl form. Sodium bicarbonate will reverse the pre-existing acidosis that is often present and also treat hyperkalemia. It will also increase the urine pH, thus decreasing the amount of myoglobin precipitated in the kidneys. Ion trapping via alteration of urine pH

may prevent the renal reabsorption of poisons that undergo excretion by glomerular filtration and active tubular secretion. Since membranes are more permeable to nonionized molecules than to their ionized counterparts, acidic (low-pH) poisons are ionized and trapped in alkaline urine, whereas basic ones become ionized and trapped in acid urine. Urine output of 3-6 ml/kg/hr and urinary alkalinization by adding sodium bicarbonate to an IV solution enhances the excretion of acidic toxins. Infusion of 12 L/day of normal saline with 50 mEq of sodium bicarbonate per liter of fluid will maintain an alkaline urine output of 8 L/day [8]. This can be achieved with intravenous fluids, mannitol, and sodium bicarbonate and furosemide at 1 mg/kg. Acetazolamide, 250 to 500 mg, may be used if the patient becomes too alkalotic. Alkalinization of urine is contraindicated in pa­tients with congestive heart failure, renal failure, and cerebral edema. Acid-base, fluid, and electrolyte parameters should be monito­red carefully. The patient with crush injury syndrome should maintain a urine output of at least 300 ml/h with a pH higher than 6.5.

Mannitol

Intravenous mannitol has several beneficial actions for the victim of crush injury. It protects the kidneys from the effects of rhabdomyolysis, increases extracellular fluid volume, and increases cardiac contractility. Mannitol can be given in doses of 1 gm/kg added to the patient’s intravenous fluid as a continuous infusion. The maximum dose is 200 gr/24h; doses higher than this can cause renal failure. Mannitol should be given only after good urine flow has been established with IV fluids. Mannitol should be avoided in patients with congestive heart failure and pulmonary congestion as it may cause frank pulmonary edema. It is contraindi­cated in patients with active cranial bleeding and in patients with anuria. Electrolyte monito­ring is essential during mannitol administration as it will cause excretion of many electrolytes including Na+, K+, Ca++, Mg++, Cl–, HCO3 and phosphate [10].

SURGICAL MANAGEMENT OF CRUSH INJURY

Wounds should be cleaned, debrided, and co­vered with sterile dressings in the usual fashion. Splinting the limb at heart level will help to limit edema and maintain perfusion. Application of the pneumatic anti-shock gar­ment (PASG) should be avoided. The use of PASG has been reported to cause compartment syndrome and crush injury syndrome [11]. There are case reports of hyperbaric oxygen improving the outcome of victims of crush injury [12]. Treatment of closed crush injuries is conservative. They should not be routinely explored since the intact skin acts as a barrier against infection. The use of fasciotomies is controversial. Routine use is not to be advoca­ted. Fasciotomies will not reverse muscle necrosis in the absence of compartment syndrome.

Complications after crush injury

• Hemorrhage and shock

• Hypothermia

• Hyperkalemia

• Acute compartment syndrome

• Rhabdomyolysis

• Acute renal failure

• Hepatic dysfunction

• DIC.

COMPARTMENT SYNDROME

Richard von Volkmann in 1872 was first to describe compartment syndrome. He proposed that “The paralysis is caused by too long conti­nued isolation of the arterial blood” [13]. Com­partment syndrome may occur in the abdomen, chest and face but the majority of cases are diagnosed within the extremities. The majority of cases of compartment syndrome (roughly 45%) are due to tibial fractures. These fractures generally involve high levels of energy with many being open fractures [3]. Compartment syndrome develops when increased tissue pressure in a myofascial compartment increases to a point that blood flow to the muscles and nerves is impaired. The resultant ischemia cau­ses tissue and nerve damage leading to cellular death. Symptoms worsen acutely, and if the condition is not quickly reversed, individuals develop irreversible damage to nerves and muscles leading to permanent deficits. Tre­atment of compartment syndrome is emergency fasciotomy. Ideally it should be done before appearance of painlessness or pa­ralysis in extremity [4].

MEASUREMENT OF

INTRACOMPARTMENTAL PRESSURES

Mainly Stryker STIC Device (Stryker Corpora­tion, Kalamazoo, Michigan) is used to measure the intracompartmental pressures [3]. The nor­mal pressures within a compartment range from 0 to 4 mm Hg when muscle is at rest but during exertion it can rise up to 8 to 10 mm Hg. In normotensive patients cut off point for emergency fasciotomy is taken generally as 30 mm Hg. In hypotensive or hypertensive pati­ents comparison with diastolic pressures is more justified. Whitesides postulated that a pa­tient could be hypotensive and have a value less than 30 mm Hg but still have an elevated com­partment pressure being within 20 mm Hg from the diastolic number [14]. Some authorities con­sider that field fasciotomy can increase chances of infection, bleeding and sepsis. It converts a closed injury to an open one, risking infection and sepsis. Several studies indicate a worse out­come in patients who received fasciotomy com­pared with those who did not. Hence it is advo­cated that fasciotomies should be done only in patients not responding to conservative and medical line of treatment [2,8,15].

RHABDOMYOLYSIS

Crush syndrome is a form of traumatic rhabdomyolysis that occurs after prolonged continuous pressure and characterized by systemic involvement [16]. Rhabdomyolysis is the breakdown of muscle fibers with leakage of potentially toxic cellular contents, e.g. in Table 1 into the systemic circulation [17].

PATHOPHYSIOLOGY

In rhabdomyolysis, there is extensive muscle breakdown and release of toxins in systemic circulation, mainly myoglobin. Two crucial factors for development of myoglobinuric renal failure are hypovolemia and aciduria. Renal va­soconstriction with diminished renal circula­tion, intraluminal cast formation and direct heme protein induced cytotoxicity are main mechanisms behind heme protein induced re­nal toxicity [18]. It has been suggested that ARF is caused by tubular obstruction causing increased intraluminal pressures and thus opposing glomerular filtration. Other mechanism suggested is heme protein precipi­tated in kidneys itself providing substrate for generating toxic free radicals. The propensity for cast formation is determined by the pH, the filtered load of myoglobin and the flow through the renal tubules [19-20]. Heme causes free ra­dical induced oxidative damage to the renal tu­bule. It has been suggested that myoglobin is central to the oxidative injury manifested as li­pid peroxidation, and that this may be inhibited by an alkaline pH. Other reasons implicated in acute renal failure are, renal vasoconstriction secondary to circulatory shock and pigment nephrotoxicity [8].

CLINICAL FEATURES

• General: Malaise, fever, tachycardia, nausea and vomitings.

• Musculoskeletal: Pain, tenderness, paraesthe­sia, weakness

• Complications: Dark urine, oliguria, anuria, hepatic dysfunction, disseminated intravascu­lar coagulation. Hepatic dysfunction occurs in 25 percent of patients with rhabdomyolysis. Proteases released from injured muscle lead to hepatic injury. ARF and diffuse intravascular coagulation are late complications, developing 12 to 72 hours after the acute insult [21].

Investigations

• Serum myoglobin levels

• Serial serum creatinine kinase (CK) levels

• Blood urea nitrogen

• Serum K+ levels

• Blood coagulation profile

• Urinalysis to determine myoglobin and CK

Management

Early diagnosis and treatment can prevent com­plications due to crush injury and rhabdomyolysis. Fluid replacement should start at the site of extrication of the trapped vic­tim. Initial fluid should be preferably isotonic saline at the rate of 1.5 L/hr. It has been re­commended as a prophylactic treatment [15]. Immediately after arrival of victim at hospital, we send all routine blood investigations to la­boratory along with serum electrolytes. Hyper­kalemia can develop within hours of crush injury and renal failure may develop. Patients often die of hyperkalemia unless they are trea­ted rapidly. Other electrolyte imbalances which can be encountered are hypocalcemia and hyperphosphatemia. Arterial blood gases, blood and urine pH should be measured. Empi­rical 1 mEq/kg sodium bicarbonate can be given to decrease pre-existing acidosis; later alkaline diuresis can be instituted to avoid myoglobinu­ric renal failure. The patient with crush injury syndrome should maintain a urine output of at least 300 ml/h with a pH higher than 6.5 [8]. Mannitol can be given in doses of 1 gr/kg or added to the patient’s intravenous fluid as a continuous infusion. The maximum dose is 200 gr/24h with continuous monitoring of urine output, urine pH, ABG, and serum electrolytes. Following algorithm can be used for a suspected rhabdomyolysis patient [22,23]  (Fi­gure 1).

ANESTHESIA IN CRUSH INJURY PATIENTS

Emergency fasciotomy, debridement, refashioning and amputation of involved extre­mity are some of the common surgical procedu­res required in crush injury patients. Muscle ischemia from acute crush injury can cause muscle necrosis within the 3-hour post-trauma period that was previously considered safe and irreversible tissue damage ensues after 8 hours of injury [5]. Hence it is very important to give emergency medical help at the earliest. If com­partment pressures are elevated, fasciotomies should be performed. At the time of fasciotomy, extensive resection of all dead muscle should be performed at the first operation. Dead muscle cannot be identified by lack of bleeding.

Identi­fication of dead muscle is by its reaction to di­rect physical or electrical stimulation. During preoperative assessment, along with general examination, volume status should be assessed. All patients with crush injury are required to be resuscitated and optimized well, before any surgical procedure. All patients are to be investigated with hemogram to estimate blood loss, serum electrolytes and renal functions.Hyperkalemia if present may lead to arrhythmias, which should be diagnosed and treated. Adequate cross matched blood and blood products are to be kept ready in blood bank. Additional investigations may be needed as per patients’ medical status. Associated inju­ries should be noted. Regional anesthesia can be used for fasciotomy but patient may not coope­rate because of associated injuries or deranged mental status. It may also be difficult to execute a regional block because of edematous extre­mities. Regional or Neuraxial blockade can be used for amputation cases where patient is he­modynamically stable and has no associated major injuries. Different peripheral nerve blocks like sciatico-femoral, popliteal, brachial plexus block can be used for such procedures. Neuraxial blockade is not advocated in he­modynamically unstable patients for both amputation and fasciotomy. One should avoid using adjuvants and intense blockade for fasciotomies as it is a short procedure, and it may obscure signs of inadequate fasciotomy for a long time. Hemodynamically unstable patient and associated major injuries will mandate ge­neral anesthesia with or without endotracheal intubation or laryngeal mask airway. Thio­pentone sodium, propofol, ketamine can be used for induction of anesthesia before endo­tracheal intubation. These agents should be gi­ven in smaller titrated doses, in hypovolemic patients. One should avoid use of succinyl­choline in extensive crush injury provided there is no anticipated airway difficulty as it can exacerbate existing hyperkalemia to dangerous levels. A short acting agent like atracurium or mivacurium may be used. Atracurium, cisatra­curium, mivacurium are also beneficial in pa­tients in ARF as these are least excreted by renal route. Maintenance of anesthesia is commonly done with inhalational agents or propofol infu­sion with opioids. It should be remembered that fasciotomy is a short procedure and hence unnecessary long acting anesthetic agents should be avoided. Intraoperative monitoring includes continuous electrocardiogram, pulse oximetry, capnography, blood pressure and urine output. Central venous line helps in assessing adequacy of fluid status and also offers route for fluid and drugs administration, e.g. mannitol. Serum electrolytes and arterial blood gases estimations should be done during the procedure, if needed.

Intraoperatively, normovolemia and normal blood pressure should be maintained to opti­mize perfusion to ischemic tissues. Hypoten­sion should be avoided. Hypertension, on the other hand, is associated with increased bleeding from muscles being excised. Most often, surgeries with crush injuries do not involve use of intraoperative tourniquets. When a patient arrives in the theater with a limb tourniquet, sudden blood loss and hypotension should be anticipated when they are removed at the start of surgical procedure. To avoid myoglobinuric renal failure intraoperatively, it is important to maintain central venous pressu­res, maintain alkaline pH of urine by producing alkaline diuresis, use of diuretics and mannitol during surgery. It is very important to monitor hemoglobin, serum electrolytes, serum myoglo­bin, serum CPK (if found raised initially) and blood coagulation during intraoperative pe­riod. Some authors suggest that serum myoglo­bin rather than CK levels should be used to gu­ide therapy in such patients [23]. Thus early re­suscitation, hemodynamic stability, adequate diuresis and prompt treatment of complications will help in better management of crush injuries.

PREVENTION AND TREATMENT OF ARF

Adequate intravascular volume expansion is the cornerstone of treatment of rhabdo-myolysis. Exact amount of preloading is not known but it should be adequate to ensure good urine output. Alkalinization of as descri­bed above will prevent formation of pigmented casts in kidneys and thus prevent renal failure [22]. Diuretics can be used to maintain adequate urine flow as well mannitol can be used as described above. While using diuretics like mannitol patient should be adequately hydra­ted as these agents themselves can cause renal dysfunction otherwise. Early renal replacement therapy use in case of suspected acute renal fai­lure had good results. Hemodialysis and conti­nuous or intermittent peritoneal dialysis are modes available for renal replacement therapy [24].

SUMMARY

Thus management of crush injury patient is a multidisciplinary work and requires good interdepartmental coordination for successful outcome. More sophisticated biochemical stu­dies and devises to measure inter­compartmental pressures are required to avoid unnecessary fasciotomies.

REFERENCE

1. Verma PK, Tiwari KN. Epidemiology of Road Traffic­Injuries in Delhi: Result of Survey. Regional Health Fo­rum- Volume 8, Number 1, 2004.

2. Gail T. Tominaga. Crush Syndrome. In: Demetrios Demetriades, Juan A. Asensio, (Eds). Trauma Manage­ment, Texas; Landes Bioscience 2000;61;618-22.

3. John FD. Compartment Syndrome of the Lower Extremity: Blast Injuries in a Ranger Battalion Don’t Miss The Diagnosis. Journal of special operations medicine; ISSN 1553-9768;2006; Vol 6, Edition 2.

4. Darren J. Malinoski, Matthew S. Slater, Richard J. Mullins. Crush Injury and Rhabdomyolysis. Crit Care Clin 20 04;20: 171-92.

5. Christian Vaillancourt, Ian Shrier, Alain Vandal, Markus Falk, Michel Rossignol, Alan Vernec, Dan So­mogyi. Acute compartment syndrome: How long be­fore muscle necrosis occurs? CJEM 2004;6(3):147-54.

6. Wallace S, Goodman S. Compartment Syndrome, Lower Extremity. Emedicine 2005. Updated on Feb 9, 2009 http://www.emedicine.com/orthoped/topic596.htm

7. Samuel JS, Mark Eckstein. Prehospital Trauma Care; In: Demetrios Demetriades, Juan A. Asensio, (Eds). Trauma Management, Texas; Landes Bioscience 2000;1: 2-15.

8. Jason Smith, Tan Greaves. Crush Injury and Crush Syn­drome: A Review; The journal of trauma 2003;54: S226-30.

9. Gary GS, Barry MB. Fluid and Electrolyte Disturbances. In: Anthony S Fauci, Eugene Braunwald, Dennis L Kasper, Stephen L Hauser, Dan L Longo, J. Larry Jame­son, Joseph

10. Edwin K, Jackson Diuetics. In: Goodman LA, Gilman A, Hardman JG, Limbard LE (Eds). The Pharmacological Basis of Therapeutics, 10th edn. New York; The McGraw Hill 2006;29:757-87.

11. Godbout B, Burchard KW, Slotman GJ, Gann DS. Crush syndrome with death following pneumatic anti-shock garment application. J Trauma 1984;24:1052-6.

12. James PB. Hyperbaric oxygen treatment for crush injury. BMJ 1994;309(6967):1513.

13. Hatch W, Hatch V. Richard von Volkmann and surgical school of Halle from 1867 to 1889. Zentralbl Chir 2001;126: 822-7.

14. Whitesides TE, Heckman MM. Acute Compartment Syndrome: Update on Diagnosis and Treatment; J Am Acad Orthop Sueg 1996;4:209-18.

15. Demirkiran, Y Dikmen, T Utku, S Urkmez. Crush syn­drome patients after the Marmara earthquake. Emerg Med J 2003;20:247-50.

16. Hiraide A, Ohnishi M, Tanaka H, et al. Abdominal and lower extremity crush syndrome. Injury 1997;28:685-6.

17. Ana L Huerta-Alardín, Joseph Varon, Paul E Marik. Bedside review: Rhabdomyolysis—an overview for cli­nicians. Critical Care 2005;9:158-69.

18. Flamenbaum W, Gehr M, Gross M, Kaufman J, Ham­burger R. Acute renal failure associated with myoglo­binuria and hemoglobinuria. In: Brenner B, Lazarus J (Eds). Acute Renal Failure. Philadelphia: WB Saunders 1983;269-82.

19. Salahudeen A, Wang C, Bigler S, Dai Z, Tachikawa H. Synergistic renal protection by combining alkalinediuresis with lipid peroxidation inhibitors in rhabdomyolysis: possible interaction between oxidant and nonoxidant mechanisms. Nephrol Dial Transplant 1996; 11:635-42.

20. Zager R, Burkhart K. Differential effects of glutathione and cysteine on Fe2+, Fe3+, H2O2 and myoglobin-in­duced proximal tubule cell attack. Kidney Int 1998;53:1661-7.

21. Akmal M, Massry S. Reversible hepatic dysfunction associated with rhabdomyolysis. Am J Nephrol 1990;10: 49-52.

22. Brown, Carlos VR, Rhee, Peter , Chan, Linda, Evans, Kelly, Demetriades, Demetrios, Velmahos, George C. Preventing Renal Failure in Patients with Rhabdo­myolysis: Do

23. Bicarbonate and Mannitol Make a Difference? The Jour­nal of Trauma: Injury, Infection, and Critical Care 2004; 56:(6)1191-6.

24. Helena Lappalainen, Eero Tiula, Lasse Uotila, Matti Manttari. Elimination kinetics of myoglobin and creatine kinase in rhabdomyolysis: Implications for follow-up. Crit Care Med 2002;30:2212-5

/Correspondence

 

Biljana STOŠIĆ

Univerzitet u Nišu, Medicinski fakultet

Klinika za anesteziologiju i intenzivnu negu

E-mail:  b.stosic@yahoo.com

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