The Healthcare Effectiveness Data & Information Set

The Healthcare Effectiveness Data & Information Set ORDER NOW FOR CUSTOMIZED AND ORIGINAL ESSAY PAPERS ON The Healthcare Effectiveness Data & Information Set Help me study for my Health & Medical class. I’m stuck and don’t understand.The Healthcare Effectiveness Data & Information Set 1. Describe the pathophysiology of crush syndrome. What are the physical findings, lab findings, and EKG findings classically associated with it and how do they evolve? How do you treat them? 2. Using a recent earthquake (e.g. Haiti, China, and Chile) as an example, describe how medical, social, and environmental factors affect the morbidity and mortality of injured earthquake survivors? Use the resources on the attachment, Do not exceed 500 words for each question. co7xv_crush__clinics_.pdf a5lpem_crush_syndrome.pdf dgalvn_surviving_collapsed_structure_entrapment.pdf ikxkt1_earthquakes__clinics_.pdf management_of_crush_related_injuries_after_disasters.docx Crit Care Clin 20 (2004) 171 – 192 Crush injury and rhabdomyolysis Darren J. Malinoski, MDa,b,*, Matthew S. Slater, MDc, Richard J. Mullins, MDa,b,d a Department of Surgery, Oregon Health & Science University, 3181 Southwest Sam Jackson Park Road, Portland, OR 97201-3098, USA b Section of Trauma/Critical Care, Oregon Health & Science University, 3181 Southwest Sam Jackson Park Road, Portland, OR, 97201-3098, USA c Division of Cardiothoracic Surgery, Oregon Health & Science University, 3181 Southwest Sam Jackson Park Road, Portland, OR 97201-3098, USA d Division of General Surgery, Oregon Health & Science University, 3181 Southwest Sam Jackson Park Road, Portland, OR 97201-3098, USA Although clinical syndromes consistent with rhabdomyolysis were recognized in the late 19th and early 20th centuries, the modern history of the crush syndrome begins with Bywaters’ and Beal’s classic description of the entrapped bombing victims of London during World War II [1 –4]. They reported five cases of crush injury, in which victims had one or more of their extremities trapped under debris for prolonged periods of time. All five patients presented in shock, had swollen extremities, developed dark urine, progressed to renal failure, and eventually died. Histologic examination of the kidney revealed tubular necrosis and pigmented casts. In 1944, Bywaters and Stead identified myoglobin as the urinary pigment and proposed its role in the development of renal failure [5]. Large numbers of patients with crush injuries and rhabdomyolysis have been reported after the collapse of mines [6,7], severe beatings [8], and earthquakes [9 – 15]. In the United States, alcohol intoxication associated with prolonged muscle compression and seizures is the most common etiology of rhabdomyolysis [16]. Serum creatine kinase (CK) levels correlate with the degree of muscle injury The Healthcare Effectiveness Data & Information Set [14] and can be used to assess the severity of rhabdomyolysis. Acute renal failure (ARF) is one of the most serious consequences of rhabdomyolysis and occurs in 4% to 33% of cases, carrying with it a mortality rate of 3% to 50% [17]. Rhabdomyolysis accounts for 5% to 7% of all cases of ARF in the United States [18]. This article focuses on the pathophysiology and treatment of myoglobinuric renal failure caused by traumatic rhabdomyolysis and crush injuries. * Corresponding author. Department of Surgery, Oregon Health & Science University, 3181 Southwest Sam Jackson Park Road, Portland, OR 97201-3098. E-mail address: (D.J. Malinoski). 0749-0704/04/$ – see front matter D 2004 Elsevier Inc. All rights reserved. doi:10.1016/S0749-0704(03)00091-5 172 D.J. Malinoski et al / Crit Care Clin 20 (2004) 171–192 Etiologies Rhabdomyolysis is the liberation of components of injured skeletal muscle into the circulation [19]. There are many etiologies of rhabdomyolysis, but this article focuses on those most likely to be encountered in a trauma or surgical setting. Direct compression of muscle leading to a local crush injury is the most common mechanism of traumatic rhabdomyolysis. Compression causes muscle ischemia, as tissue pressure rises to a level that exceeds capillary perfusion pressure. When the compression is relieved, the muscle tissue is reperfused. Muscle ischemia followed by reperfusion (ischemia– reperfusion injury) represents the fundamental pathophysiologic mechanism of rhabdomyolysis and is discussed extensively. Acute alcohol intoxication with subsequent collapse, immobility, and coma is the most common etiologic factor of direct muscle compression [16,18]. Improper operative positioning using the extended lithotomy and lateral decubitus positions [20 –26], blunt trauma to the extremities and torso caused by beatings or sudden automobile deceleration, and Pneumatic Antishock Garments (PASG) also lead to muscle compression and can cause varying degrees of rhabdomyolysis [8,17]. Earthquakes, landslides, and building collapse are catastrophes that produce large numbers of casualties with crush injuries and rhabdomyolysis. Vascular compromise of an extremity because of arterial thrombosis, embolus, traumatic interruption, or external compression is another common cause of ischemic muscle injury and rhabdomyolysis. Venous injuries or thromboses also can lead to venous hypertension, which further decreases the capillary perfusion pressure. The duration of ischemia determines the degree of muscle injury. Skeletal muscle can tolerate warm ischemia for up to 2 hours without permanent, histologic damage. Two to four hours of ischemia lead to irreversible anatomic and functional changes, and muscle necrosis usually occurs by 6 hours of ischemia. By 24 hours, histologic changes caused by ischemia – reperfusion injury are maximal [17,27,28]. The Healthcare Effectiveness Data & Information Set Soft-tissue infections also can cause rhabdomyolysis. Legionella and Streptococcus species are the most common bacterial agents, but tularemia, Staphylococcus species, and Salmonella species are also responsible. Influenza is the most common viral etiology of rhabdomyolysis, but HIV, Coxsackie virus, and Epstein– Barr virus also have been implicated. Direct invasion of muscle cells and toxin generation have been proposed as two possible mechanisms of muscle injury because of either viral or bacterial agents. The risk of acute renal failure secondary to severe rhabdomyolysis after an infection ranges from 25% to 100% [29]. Electrical injuries from lightning strikes or high-voltage power lines have the potential to produce enough rhabdomyolysis to cause myoglobinuric renal failure. Muscle is injured directly by the electrical current (electroporation) and by the high temperatures that are generated [30,31]. Blood vessels also may coagulate, resulting in additional ischemic damage to the muscle. Up to 10% of patients with severe electrical injuries can develop renal failure. Steroids and neuromuscular blockade have been associated with rhabdomyolysis, although the exact mechanism is unknown [32]. Cushing first described the association between steroid excess and muscular weakness in 1932 [33]. More D.J. Malinoski et al / Crit Care Clin 20 (2004) 171–192 173 recently, muscle weakness after long-term neuromuscular blockade with vecuronium has been reported [34]. CK levels were elevated in 76% of asthmatics who were treated with both high-dose steroids and vecuronium. [35] Pathogenesis of muscle injury A critical relationship exists between the intracellular concentrations of sodium (Na+) and calcium (Ca++) ions. A sarcolemmic sodium –potassium (Na/K) ATPase regulates the intracellular concentration of Na+, keeping it at approximately 10 mEq/L. A low Na+ level creates a concentration gradient between the intraand extracellular environments, which facilitates the efflux of Ca++ as it is exchanged for Na+ by way of a separate ion channel [36]. This maintains the intracellular Ca++ concentration at a level several orders of magnitude less than the extracellular fluid [17]. Calcium also is transported actively into the sarcolemmal reticulum and mitochondria [19]. Muscle compression leads to mechanical stress, which opens stretch-activated channels in the muscle cell membrane [37]. This results in the influx of fluid and electrolytes, including Na+ and Ca++. Cells swell, and their intracellular Ca++ concentration rises, resulting in several pathologic processes (Fig. 1). An increase in the activity of cytoplasmic neutral proteases leads to the degradation of myofibrillar proteins [38]; Ca++ -dependent phosphorylases are activated, and cell membranes are degraded [39]. Additionally, nucleases are activated, and mitochondrial ATP production is diminished because of an inhibition of cellular respiration The Healthcare Effectiveness Data & Information Set [40]. Muscle ischemia caused by prolonged compression or vascular injury results in anaerobic metabolism and a further decrease in ATP production. This diminishes the activity of the Na/K ATPase, which leads to the accumulation of intracellular Fig. 1. The pathogenesis of rhabdomyolysis. 174 D.J. Malinoski et al / Crit Care Clin 20 (2004) 171–192 fluid and further increases the intracellular Ca++ concentration. In addition, increased concentrations of neutrophil chemoattractants are present in postischemic tissues, which results in a high local concentration of activated neutrophils once reperfusion is initiated. These neutrophils damage reperfused tissue by releasing proteolytic enzymes, generating free radicals [41], producing large amounts of hypochlorous acid, and by increasing microvascular resistance [42]. Reperfusion of ischemic tissue after the release of entrapped victims or the reestablishment of vascular flow results in an ischemia – reperfusion injury. In addition to delivering activated neutrophils to previously ischemic tissue, reperfusion leads to the conversion of oxygen and hypoxanthine to xanthine by xanthine oxidase, with the generation of superoxide anions, which are highly reactive oxygen-derived free radicals [43]. Free radicals are potent oxidizing agents that damage intracellular and extracellular molecules when their concentrations become excessive. Lipid peroxidation occurs when free radicals oxidize and damage the lipid bilayer of cell membranes. The ferrous –ferric ion pair provided by iron within the porphyrin ring in myoglobin catalyzes this process and facilitates widespread lipid peroxidation in muscle tissue [44]. Cell membrane degradation impairs the normal permeability of the cell and results in further cellular edema, Ca++ influx, and Na + influx. Cell lysis follows, and the intracellular contents of the muscle cells are released into the circulation. Lipid peroxidation leads to cellular membrane leakiness, and, when combined with a reduction in active ionic extrusion caused by the depletion of ATP, causes cellular swelling and an accumulation of fluid in the interstitial space [45,46]. Three hours of ischemia followed by reperfusion appear to be the minimum requisites for this effect [47 – 49]. In muscle groups confined in tight, fibrous sheaths with low compliance, such as the calf and forearm, intracompartmental pressure rises rapidly [50]. When this pressure exceeds the arteriolar– perfusion pressure, muscle tamponade and myoneuronal damage occur, resulting in compartment syndrome. Signs and symptoms of compartment syndrome include a tense, swollen muscle compartment, pain with passive stretch (the most sensitive finding), paresthesias or anesthesia, weakness or paralysis of the affected extremity, and, in late stages, diminished peripheral pulses. Palpable pulses, however, often are found in the presence of significantly elevated compartment pressures and should not lead one to dismiss the diagnosis of compartment syndrome. Crush syndrome After muscle compression is relieved or vascular interruption is corrected, the cellular contents of the affected muscle tissue are released into the circulation. The Healthcare Effectiveness Data & Information Set Large volumes of intravascular fluid also can be sequestered in the involved extremities because of increased capillary permeability. The systemic manifestations of rhabdomyolysis, caused by hypovolemia and toxin exposure, are the components of the crush syndrome. D.J. Malinoski et al / Crit Care Clin 20 (2004) 171–192 175 Hypovolemia is often the first manifestation of the crush syndrome. In 1931, Blalock was able to show that large volumes of plasma accumulated in traumatized extremities, depleting intravascular volume and resulting in shock [51]. Bywaters and Beall recognized shock as a component of the crush syndrome in 1941 [3]. In a landmark animal experiment, Bywaters and Popjak demonstrated that several hours of hind limb ischemia created by a tourniquet, followed by restoration of blood flow, resulted in cold, firm, edematous, and paralyzed extremities. Although the extremities were ischemic, the rabbits did not experience any significant physiologic derangements. After reperfusion occurred, however, their blood became hemoconcentrated and their blood urea nitrogen levels rose. When both extremities were involved, the animals died from hypovolemic shock [52]. Clinical observations in human studies also have demonstrated that large volumes of fluid can leak into the interstitial space and cause hypotension [3,53]. In a series of 372 patients with crush syndrome, Oda [14] found that hypovolemic shock was the most common cause of death during the first 4 days after crush injury (23/35, 66%) (Fig. 2). In addition to intravascular depletion, patients with the crush syndrome are faced with a large toxin load and can develop life-threatening electrolyte abnormalities (Table 1). Hypocalcemia results from the influx of Ca++ into the affected muscle tissue. This becomes dangerous when combined with hyperkalemia and acidemia, both of which can occur upon reperfusion of ischemic tissue. Hyperkalemia and its associated cardiotoxicity represent the second most common cause of early deaths following crush injury [14]. Volume replacement is the mainstay of Fig. 2. The causes of death in 50 patients with the crush syndrome following the Hanshin – Awaji Earthquake. Deaths from hypovolemia and hyperkalemia were the most common in the early period, while sepsis leading to multiple organ failure was responsible for most of the late deaths. (Adapted from Oda J, Tanaka H, Yoshioka T, et al. Analysis of 372 patients with crush syndrome caused by the Hanshin – Awaji Earthquake. J Trauma 1997;(42):470 – 6; with permission.) 176 D.J. Malinoski et al / Crit Care Clin 20 (2004) 171–192. The Healthcare Effectiveness Data & Information Set Table 1 Intracellular contents released during rhabdomyolysis and their effects Agent Effect Potassium Hyperkalemia and cardiotoxicity, provoked by hypocalcemia and hypovolemia Hyperphosphatemia, worsening of hypocalcemia, and metastatic calcification Metabolic acidosis and aciduria Myoglobinuria and nephrotoxicity Elevation of serum CK levels Disseminated intravascular coagulation Phosphate Organic acids Myoglobin Creatine kinase (CK) Thromboplastin treatment for patients with crush injuries and rhabdomyolysis, because it addresses the two main early threats to survival, hypovolemic shock and hyperkalemia. Hyperphosphatemia also follows rhabdomyolysis and can worsen the aforementioned hypocalcemia by depressing levels of 1,25-dihydroxycholecalciferol (1,25-(OH2)-D). Tissue thromboplastin levels also increase and can lead to disseminated intravascular coagulation (DIC); patients often present with depressed platelet levels because of DIC-related consumption [53]. Large amounts of myoglobin also are released into the general circulation and represent a significant threat to the kidney. If intravenous fluid replacement is inadequate or delayed for more than 6 hours, patients are also at significant risk for developing renal failure [50]. Pathophysiology of renal injury Four percent to 33% of patients with rhabdomyolysis will develop ARF (a decline in renal function that requires some form of renal replacement therapy) with an associated mortality rate of 3% to 50% [17,18]. There are three main mechanisms by which rhabdomyolysis can lead to the development of renal failure: decreased renal perfusion, cast formation with tubular obstruction, and the direct toxic effects of myoglobin on the renal tubules. Decreased renal perfusion results from the inherent hypovolemia of the crush syndrome, the stimulation of the sympathetic nervous system and the renin – angiotensin – aldosterone axis and renal vasoconstriction in the presence of myoglobin. Vasoconstrictors released in the presence of myoglobin include plasma endothelin-1 and platelet activating factor (PAF) [54 – 56]. Endothelins reduce glomerular filtration by constricting the afferent and efferent arterioles. Administration of bosentan, an endothelin receptor antagonist, prevented renal failure in rats with myoglobinuria [57]. Platelet activating factor is produced in the mesangial and glomerular cells and causes vascular smooth muscle constriction [58]. Increased levels have been observed with myoglobinuria, and renal injury is lessened when PAF receptors are blocked in experimental models of myoglobin-induced renal failure [54,59 – 61].The Healthcare Effectiveness Data & Information Set D.J. Malinoski et al / Crit Care Clin 20 (2004) 171–192 177 Myoglobin is a respiratory pigment protein that comprises 1% to 3% of the wet weight of skeletal muscle [19]. It has a molecular weight of 17,800 d and is filtered readily by the kidney. At the center of the myoglobin molecule is a single heme prosthetic group with an iron atom that serves as an oxygen-binding site [17]. Low levels of circulating myoglobin are (50% to 85%) bound mostly to haptoglobin and a2 – globulin and are cleared from the circulation by the reticuloendothelial system [62]. When circulating levels of myoglobin are elevated, as occurs after rhabdomyolysis, the binding capacity of haptoglobin is saturated, and free plasma levels rise. Plasma levels greater than 0.5 to 1.5 mg/dL are filtered by the kidney, resulting in myoglobinuria. Normal urinary myoglobin levels are less than 5 ng/mL. Myoglobin is not reabsorbed in the renal tubules and increases in concentration as water is reabsorbed from the tubular filtrate, resulting in dark, teacolored urine. The presence of myoglobin in the urine can be confirmed with a positive urine dipstick, which reacts with the heme groups of both myoglobin and hemoglobin. The absence of red cells on microscopy confirms that the discolored urine is caused by myoglobin. Myoglobinuria and hemoglobinuria can occur simultaneously, however. Myoglobin cast formation and tubular obstruction occur in patients with acidic urine and a high concentration of myoglobin in the renal tubules. The myoglobin reacts with the Tamm – Horsfell (THP) protein and precipitates, forming casts. This binding is enhanced under acidic conditions, and urinary alkalinization with sodium bicarbonate has been shown to reduce cast formation [63]. Whether this effect is directly caused by the alkaline pH or the induced solute diuresis is not certain. The hypothesis that myoglobin casts obstruct urine flow [63,64] and cause a transtubular leakage of glomerular filtrate [65] has been promoted widely. Micropuncture experiments have shown that intratubular pressures are low, however, and that perfusion of the tubule with buffer at low pressures easily removes the casts [66]. The Healthcare Effectiveness Data & Information Set The direct toxic effect of myoglobin is likely the main component in the development of renal failure after rhabdomyolysis. There is an increasing body of evidence that supports free radical-mediated renal injury, especially to the proximal tubule. It has been shown that endogenous radical scavenging agents are depleted during myoglobinuria-induced renal failure, while antioxidant administration can improve renal function [67 – 70]. Myoglobin separates into protein and ferrihemate moieties in an acidic environment [71]. Iron catalyzes the formation of free radicals by ways of the Fenton reaction, which, in turn, leads to lipid peroxidation in the renal tubules [70]. The heme group of the myoglobin molecule itself also may promote lipid peroxidation during redox cycling between its different oxidation states. The reactivity of ferryl myoglobin, which is responsible for inducing lipid peroxidation, is attenuated markedly at alkaline pH [72]. This further supports the role of an induced alkaline diuresis in the treatment of patients with rhabdomyolysis. Additionally, desferrioxamine (DFO), an iron chelator, has been shown to protect against renal dysfunction in animal models of rhabdomyolysis [68,73]. This protects against the exposure to free iron and the redox cycling of myoglobin, and thus lipid peroxidation [74]. 178 D.J. Malinoski et al / Crit Care Clin 20 (2004) 171–192 Additional vasoconstrictors also are generated by the presence of myoglobinuria and contribute to the renal dysfunction following rhabdomyolysis. F2isoprost … Get a 10 % discount on an order above $ 100 Use the following coupon code : NURSING10

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