Rhabdomyolysis and spine surgery: A systematic review of the literature

Highlights

• The best evidence points out to the prognosis depend on the extension of surgery.

• The peak elevation of serum CPK usually occurs on the first postoperative day.

• About one week after surgery, serum CPK returns to normal levels.

Abstract

Rhabdomyolysis is characterized by the rupture of skeletal muscles due to a lot of reasons such as exercise, drug addiction, toxins, infections, trauma and some medications. The etiology of postoperative rhabdomyolysis is potentially multifactorial and has been documented in several types of surgery. The lysis of cell membrane releases organic and inorganic intracellular components that can be toxic and life threatening. Creatinephosphokinase (CPK) is one of the components and it is the most sensitive indicator of myocyte injury. The classic triad of symptoms is characterized by myalgia, weakness and brown-red urine. There is not a clearly agreed level of serum CPK that is evident for diagnosis of rhabdomyolysis. However, a CPK level higher than 5 times of its normal value is accepted by many authors as diagnostic criteria. Acute kidney injury is the most serious complication of rhabdomyolysis in the days following initial presentation and develops in 33% of patients. The objective of this study was to perform a review of the literature, aiming at a better understanding about the changes in CPK levels and the frequency of rhabdomyolysis in spine surgery, with special attention in posterior lumbar fusion. Nineteen studies were selected for analysis. The studies had different characteristics considering patients age, body mass index, comorbidities and type of surgery. The best available evidence points out to the prognosis depend on the extension and clinical severity of rhabdomyolysis, as well as on the early and prompt medical intervention.

Introduction

Rhabdomyolysis was first reported in Germany in 1881, but the syndrome was described in detail by Bywaters and Beall during 2nd World War, in the Battle of London [1], [2].

The syndrome is characterized by the rupture (lysis) of skeletal muscles due to a lot of reasons such as strenuous physical exercise, drug addiction, toxins, inherited disorders, infections, trauma, compression and some medications as statins, other antilipid agents, psychiatric agents, antihistamines and anesthetics (halothane, naltrexone, quinidine, propofol, succinylcholine, thiazides) [2], [3], [4], [5], [6].

The cell membrane lysis releases organic and inorganic intracellular components, such as myoglobin, creatinephophokinase (CPK), potassium, lactic acid, purines, aldolase, phosphate as well as electrolytes which can be toxic and life threatening when entering the circulation, after the restoration of blood flow. [1], [2], [4], [6], [7], [8]. CPK levels are the most sensitive indicators of myocyte injury [2], [4], [9].

CPK is a major cytoplasmatic enzyme of muscle, and it is present in three isoenzymic forms, MM (skeletal muscle), BB (brain) and MB (cardiac muscle). The isoenzym MM constitutes more than 90% of total CPK [9], [10].

Conditions of generalized ischemia and hypoxemia, such as shock, are associated with insufficient adenosine triphosphate (ATP) production and sarcolemma dysfunction. The cellular energy supplies are gradually reduced and more than 4 h of ischemia can provoke irreversible damage to skeletal muscle. However, rhabdomyolysis occurs mainly after muscle reperfusion, therefore the reperfusion injury is considered more deleterious than extended ischemia. When reperfusion starts, leukocytes migrate into the damaged area, cytokines and prostaglandins increase whereas free radicals are produced in oxygen’s presence [6].

Clinically, rhabdomyolysis ranges from an asymptomatic illness with elevation of CPK levels to a life-threatening condition with electrolyte imbalances, acute renal failure and disseminated intravascular coagulation [6].The classic triad of symptoms is characterized by myalgia, weakness and brown-red urine because of the myoglobin. In some patients, swollen muscle can appear [3], [4], [5]. The triad is observed in less than 10% of patients, and more than 50% of patients do not complain of muscle pain or weakness [1], [6].

Systemic manifestations may include tachycardia, hypothension, delirium general malaise, fever, nausea and vomiting [1], [4], [6].

There is not a clearly agreed level of serum CPK evident of rhabdomyolysis diagnosis. However, a CPK level higher 5 times than its normal value is accepted by many authors as diagnostic criteria [1], [2]. A CPK concentration more than 5.000 IU/L is closely related to the development of kidney damage. CPK has a half-life of 1.5 days, as a consequence, CPK blood levels remain increased longer than the concentration of myoglobin that has a half-life of 2–4 h [6].

Myoglobinuria does not occur without rhabdomyolysis, but rhabdomyolysis does not necessarily lead to visible myoglobinuria [1]. Plasma myoglobin is elevated early but these findings are not reliable index, because myoglobin is quickly removed through kidneys [4].

Acute kidney injury is the most serious complication of rhabdomyolysis in the days following initial presentation and develops in 33% of patients with a mortality rate between 20% and 50% as a result of myoglobin nephrotoxicity [6], [11]. Thus, the objective of this study was to perform a review of the literature, aiming at a better understanding about the changes in CPK levels and the frequency of rhabdomyolysis in spine surgery, with special attention in posterior lumbar fusion.