Physical activity and sickle cell disease
Roy J. Shephard in Physical Activity and the Abdominal Viscera, 2017
Exertional rhabdomyolysis can develop in anyone who exercises at a high intensity relative to their physical condition. The release of myoglobin during the break down of muscle tissue causes an associated myoglobinuria. In 5-7% of cases, the ferrihaemate that is released from myoglobin in an acidic environment reaches a sufficient concentration to damage the renal tubules, leading to pro gressive renal failure.[99] Manifestations of renal damage include an increase in serum potassium that causes muscle weakness, abnormalities of cardiac rhythm and a possibility of cardiac arrest, and decreases of calcium ion concentrations that induce muscular tremors and weakness of cardiac contraction. Even if a fatal outcome can be avoided, prolonged dialysis is often needed until renal function recovers.[100]
Diseases of Muscle and the Neuromuscular Junction
John W. Scadding, Nicholas A. Losseff in Clinical Neurology, 2011
Muscle rigidity may begin shortly after infusion of the triggering agent. This makes intubation difficult as the rigidity of the masseter muscles is often intense, rendering it impossible to open the jaw. Cardiac dysrhythmias, labile systolic blood pressure, hyperventilation, fever and mottling cyanosis are all common features. A rise in pCO2 or core temperature are probably the earliest signs of MH. An increasing pCO2 and oxygen consumption, rising CK, calcium, magnesium, glucose and urea, as well as a lactic acidosis are common. Subsequent damage to the skeletal muscle membranes results in myoglobinuria. These changes are usually maximal 1–4 days after the start of the reaction. Late complications include renal failure, clotting disorders, cerebral and pulmonary oedema.
Burns
Professor Sir Norman Williams, Professor P. Ronan O’Connell, Professor Andrew W. McCaskie in Bailey & Love's Short Practice of Surgery, 2018
The damage to the underlying muscles in the affected limb can cause the rapid onset of compartment syndrome. The release of the myoglobins will cause myoglobinuria and subsequent renal dysfunction. Therefore, during the resuscitation of these patients, efforts must be made to maintain a high urine output of up to 2 mL/kg body weight per hour. Severe acidosis is common in large electrical burns and may require boluses of bicarbonate. These patients are also at risk of myocardial damage as a result of direct muscle damage, rather than by interference with cardiac pacing. This gives rise to significant electrocardiogram changes, with raised cardiac enzymes. If there is significant damage, there is rapid onset of heart failure. In the case of a severe injury through a limb, primary amputation is sometimes the most effective management (Figure41.13).
Statin-induced myalgia and myositis: an update on pathogenesis and clinical recommendations
Published in Expert Review of Clinical Immunology, 2018
Albert Selva-O’Callaghan, Marcelo Alvarado-Cardenas, Iago Pinal-Fernández, Ernesto Trallero-Araguás, José Cesar Milisenda, María Ángeles Martínez, Ana Marín, Moisés Labrador-Horrillo, Cándido Juárez, Josep María Grau-Junyent
Rhabdomyolysis, the most severe form of acute muscle disease associated with statins, is fortunately, very rare, affecting less than 1 patient per 100,000 treated per year with these drugs [13]. High CK concentrations (>100-fold the upper limit of normality) are characteristic of rhabdomyolysis, but what defines the syndrome is evidence of myoglobinuria and renal impairment, due to acute tubular necrosis caused by myoglobin precipitation in the renal tubules [14]. Rhabdomyolysis is a life-threatening condition; statins must be discontinued and in most cases, avoided in the future for safety reasons. Dark urine with a positive dipstick test may be mistaken for hematuria. The absence of red cells in the urine sediment supports the diagnosis of myoglobinuria. In severe cases of rhabdomyolysis, muscle weakness may be a cardinal manifestation, but it is usually transitory, disappearing a few days after stopping the drug. Muscle biopsy is not generally indicated, and when it is necessary for diagnostic purposes, it should be performed several weeks or months after the clinical event.
COVID-19 causing rhabdomyolysis requiring hemodialysis in a young adult
Published in Baylor University Medical Center Proceedings, 2022
Nitish Mittal, Gaspar Del Rio-Pertuz, Mostafa Abohelwa
SARS-CoV-2, the causative agent of COVID-19, continues to cause a worldwide pandemic. The most common symptoms are fever, myalgia, headache, dyspnea, and sore throat, with some patients presenting with end-organ failure and shock.1,2 In young adults, symptoms are likely milder; however, they can still develop severe symptoms. In mid-2020, the first cases of rhabdomyolysis causing myoglobinuria in post–COVID-19 patients were reported, and more cases have been reported since then.3 Rhabdomyolysis, a life-threatening disorder associated with myalgia, fatigue, and acute renal failure,4 is rare and was only reported in 0.2% of patients in a study of 1099 patients in China.5 It has been suggested that myoglobinuria occurs from an abnormal immune response to the virus. The inducing factors of rhabdomyolysis include autoimmune response, septicemia, electrolyte abnormalities, infection, and substance abuse.6 As time elapses, more cases will be studied to provide better understanding of post-COVID rhabdomyolysis and myoglobinuria.
Serum creatine kinase levels are not associated with an increased need for continuous renal replacement therapy in patients with acute kidney injury following rhabdomyolysis
Published in Renal Failure, 2022
Liuniu Xiao, Xiao Ran, Yanxia Zhong, Yue Le, Shusheng Li
The myoglobin released from damaged muscles plays a dominant role in the pathogenesis ofRM–induced AKI [10]. Myoglobin is an iron-containing small protein with a molecular weight of 17.8 kDa and exists at a low concentration in serum under physiological conditions [11]. However, for a skeletal muscle injury, serum myoglobin levels increase within one hour and return to a normal range within one to six hours after lesion resolution. Myoglobin is freely filtered by the glomerulus and absorbed in the proximal tubule by endocytosis [12]. Excess myoglobin released into the circulation will lead to myoglobinuria and renal insufficiency, which brings about renal tubular obstruction and oxidative injury. A persistently increased serum creatinine, as well as a decreased glomerular filtration rate (eGFR), predicts deterioration of renal functions, resulting in AKI.