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![Recommended activity
• Strenuous activities (eg, competitive sports) should be avoided if they cause
recurrent myalgias, myopathy, or rhabdomyolysis.
• Children and adolescents with recurrent rhabdomyolysis related to exertion require
further medical evaluation.
• High-school coaches and trainers must ensure proper hydration and maintain fluid
balance during practice sessions and games. Signs and symptoms of heat
exhaustion must be evaluated in a timely fashion during hot and humid
conditions.[53]](https://image.slidesharecdn.com/cf1de514-7bc2-4d17-af40-435cd156f87a-160330203122/75/rhabdomyolysis-2016-21-2048.jpg)
Uploaded byMuhamed Al Rohani
rhabdomyolysis 2016
Rhabdomyolysis is a condition characterized by the breakdown of skeletal muscle fibers and release of muscle contents into the bloodstream. It can be caused by trauma, exertion, medications, toxins, infections, and metabolic disorders. Symptoms may include muscle pain, weakness, and dark urine. Diagnosis is based on markedly elevated creatine kinase levels and presence of myoglobin in urine. Complications can include electrolyte abnormalities, acute kidney injury, compartment syndrome, and disseminated intravascular coagulation. Management involves fluid resuscitation and monitoring for complications.
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rhabdomyolysis 2016
- 1. Rhabdomyolysis Dr. Muhamed AlRohani, MD. FISN Consultant Nephrologist Dibba Hospital, Dibba UAE Associated Prof. UST hospital, Sanaa, Yemen
- 2. Hmmm…That’s weird... • “Rhabdomyolysiswas first reported in 1881, in the German literature” (Abbeele, Parker, 1985). • “Rhabdomyolysis was first described in the victims of crush injury during the 1940-1941 London, England, bombing raids of World War II” (Craig, 2006). • The overall mortality rate for patients with Rhabdomyolysis is approximately 5% • Rhabdomyolysis is more common in Males than in Females • May occur in infants, toddlers, and adolescents.
- 3. Case report: A19‐year young female experienced 2 episodes of rhabdomyolysis, while playing competitive ultimate Frisbee. The first episode occurred following a 5‐hr Frisbee tournament her playing time was to be 3 hours.at the end of this game she developed severe diffuse muscle soreness, she was unable to straight ten her elbows and knees, it was difficult to stand because of soreness in her back muscles. Her urine became brown-colored but she did not seek medical attention, the muscles soreness resolved after 3 days. Her second episode of rhabdomyolysis occurred 2 weeks later. This time she participated in a 2-hr Frisbee scrimmage followed by a 2-hr karate class. Shortly thereafter, she experienced severe muscle cramping, change in urine to black, and sought medical attention. The following day, her CK was 59,000 U/L and increase more in the following days and urine analysis showed heam and myoglobin by dipstick test. rise in s. crea, to 695 umol/l with anuria within 3 days the s. K was 6.3 and metabolic acidosis. The AKI and failure was established and hemodialysis done, after 2 weeks the urine output became normal and before that the CK fell to 266, after stabilization of her conditions she was discharged and she was advised to avoid that kind support or physical activities. She tolerated workouts of up to 2 hours without difficulty. She was a sprinter, but could ru n 2 miles with no problem. It was subsequently determined that she had a genetic predisp osition for rhabdomyolysis.
- 4. Case presentation: An 84-year-oldmale patient was admitted to the ED with: Generalized weakness and reduced consciousness for two days. He had a history of Alzheimer’s disease for one year and he had taken donepezil 5 mg daily for two months. He had no other diseases and he had not taken any other medications. He had no history of trauma, convulsion, previous fall, or alcohol intake. The physical examination revealed apathy, loss of cooperation, and decreased muscle strength. Temp. 36.8°C, BP140/90 mm/Hg, and pulse rate 88 bpm. He had bilateral moderate pretibial edema. Lab. studies: urea: 128 mg/dL; s. crea: 6.06 mg/dL; AST: 93 U/L; CK: 3613; Ca: 8.1 mg/dL; phos: 4.9 mg/dL; Na: 149 mmol/L; K: 4,3 mmol/L; albumin: 3.7 g/dL; LDH: 349 U/L; Hb: 14.2 g/dL; fT3: 3.5 (N: 1.71–3.71 pg/mL); fT4: 1.35 (N: 0.7–1.48 ng/dL); TSH: 2.04 (N: 0.35– 4.94 uIU/mL). Urinary test: 1+ protein and 3+ Haem. RBC, and 2-3 WBC. ABG: PH: 7.44, PCO2: 23 mmHg, PO2: 151 mmHg, SO2: 99.5%, and HCO3: 19 mmol/L. RFT was normal 2 months ago. The renal USG was normal. Echocardiography was performed and ejection fraction was 60%, left ventricle was concentric hypertrophic, and a minimal pericardial effusion was reported. The patient was diagnosed as ARF. Donepezil was discontinued. There was no indication for emergent hemodialysis. Intravenous hydration therapy was given. The patient’s renal function tests improved gradually and were normal after 12 days of the treatment. He was discharged with complete recovery.
- 5. What is Rhabdomyolysis •Rhabdomyolysis is the breakdown of muscle fibers, specifically of the sarcolemma of skeletal muscle, resulting in the release of muscle fiber contents (myoglobin) and other intercellular proteins and electrolytes into the circulation. • Typically; patient has muscle pain and creatine kinase (CK) levels are markedly elevated, the myoglubinuria my occur • The clinical conditions ranges from asymptomatic to life threatening hyperkalemia and AKI
- 6. Skeletal Muscle Cell Thesarcolemma is the cell membrane of a muscle cell. The membrane is designed to receive and conduct stimuli Source: (Muscle Anatomy & Structure, 2007)
- 7. General Mechanism ofRhabdomyolysis: • Source: Adapted from Landau et al. 2012.
- 8. Rhabdomyolysis Causes Traumatic Crush injuryand trauma earthquakes, collapsed buildings road traffic collisions Compartment syndrome alcohol – associated immobility poor perioperative positioning prolonged collapse Electrocution Non-traumatic Exertional (Strainful muscle exercise) Body temperature changes Drugs / toxins / alcohol/ cocaine Coma Infection: Bacteria (strep pyogenes, staph aureus) Virus (HIV, CMV, influenza A and B, …..) Metabolic and electrolytes disorders Genetic / idiopathic
- 9. Selected drugs thatcause rhabdomyolysis Acetaminophen Amoxapine Amphetamines Amphotericin B Anticholinergics Antidepressants Antihistamines Antipsychotics Baclofan Barbiturates Benzodiazepines Betamethasone Butyrophenones Caffeine Carbone monoxide Chloral hydrate Chlorpromazine Cocaine Dexamethasone Diazepam Diuretics Ecstasy Ethanol Fluoroacetate Glutethimide Heroin Hydrocarbons Hydrocortisone Hydroxyzine Inhalation anesthetics Isoniazid Isopropyl alcohol Ketamine hydrochloride Licorice Lithium Lorazepam Lysergic acid diethylamide Loxapine Marjuana Methaphetamine Methanol Mineralocoricoids Morphine Narcotics Neuroleptics Phencyclidine Phenonarbital Phenothiazides Phenytion Predisone Salicylate Statins Serotonin antagonists Strychnine Succinylcholine Sympathomimetics Theophyline Septrine Vasopressin Alcohol is associated with rhabdomyolysis, 24% of pts presented with cocaine-related disorders to ED, developed rhabdomyolysis 60% of pts with rhabdomyolysis has positive tests of cocaine or amphetamine Statins can lead to rhabdomyolysis secondary to myopathy meanly Cerivastatin, which was 16 – 80 times higher than other statins, and it was withdraw in 2001
- 11. How to diagnoserhabdomyolysis • Clinic Presentation: • Muscular weakness, myalgia, swelling tenderness, stiffness, • Fever, feeling of nausea, vomiting, tachycardia, dehydration • Oliguria or anuria, in connection with AKI • Laboratory findings: • CBC includine HB, Hct, and platelets • Serum: , creatine kinase, myoglobin, lactate dehydrogenase, creatinine, BUN, acid-base balance, coagulation factors , S. electrolytes: K, Phos, Ca. • Urine: myoglobin or positive dipstick test without any RBC, protein • Radiography: • Computed tomography (CT) of the head (altered sensorium, significant head trauma, seizure, neurologic deficits of unknown origin) • Magnetic resonance imaging (MRI; assessment of myopathy) • Electrocardiography (ECG) • Measurement of compartment pressures • Muscle biopsy • Immunoblotting, immunofluorescence, and genetic studies
- 13. Creatine kinase: >5xULN (5000-100,000) Rises within 2 to 12 hours following the onset of muscle injury and reaches its maximum within 24 to 72 hours. A decline is usually seen within 3 - 5 days of cessation of muscle injury. Elevation in serum creatine kinase (> 5x ULN) acute neuromuscular illness or dark urine without any other symptoms.
- 14. Complications of Rhabdomyolysis Compartment syndrome Muscle ischemia Fluidsequestration Hypovolemia Fluid sequestration Hypercalcemia Efflux from damaged muscles Hypocalcemia Inward flux and binding to phosphatidylinositol Avoid giving Calcium Hyperphosphatemia Muscle breakdown Hyperkalemia Release from cells Decrease of clearance (AKI) Disseminated intravascular coagulation (late) Thromboplastin release Thrombotic microangiopathy Acute Kidney Injury Direct effect of myoglobin Hypovolemia
- 15. Manifestations of rhabdomyolysis •Fluid and electrolyte abnormalities: With or without AKI or Hepatic Injury • Hyperkalemia: Cardiac dysrhythmias and cardiac arrest • Hypovolemia: results from “third-spacing” due to the influx of extracellular fluid into injured muscles. • Compartment Syndrome: when increased pressure in a closed anatomic space. may develop after fluid resuscitation, with worsening edema of the limb and muscle. Increased interstitial pressure in close fascial compartment leading to microvascular compromise and cellular death. Pressure measuring > 30 mmhg surgical assessment (dBP – compartment = < 30 fasciotomy • Disseminated intravascular coagulation: The release of thromboplastin and other prothrombotic substances from the damaged muscle .
- 16. Rhabdomyolysis accounts foran estimated 8-15% of cases of acute renal failure. ARF develops in 30-40% of patients with rhabdomyolysis.
- 17. Management General recommendations inICU: • Ensure adequate hydration; fluid resuscitation and prevention of AKI , • Record urine output. Insert a Foley catheter for careful monitoring of urine output. • Correction of electrolyte imbalances.Obtain an ECG to monitor effects of hyperkalemia and other electrolyte disturbances. • Compartment syndrome necessitates immediate orthopedic consultation for fasciotomy. • DIC should be treated with fresh frozen plasma, platelet transfusions and cryoprecipitate. • Monitor creatine kinase (CK) levels to show resolution of rhabdomyolysis. • Once the patient’s condition has been stabilized and life- and limb-threatening conditions have been addressed, he or she may be transferred to another facility if necessary. • Once they are well hydrated, patients with normal renal function, normal electrolyte levels, alkaline urine, and an isolated cause of muscle injury may be discharged and monitored as outpatients.
- 18. Algorithm Isotonic Saline -Initial Resuscitation:1-2 L/hr -100-200 ml/hr (if hemolysis induced injury) -Correct electrolyte abnormalities Titrate IVF UOP goal: 200-300ml/hr Serial CK measurements CK>5000 CK<5000 Stop Treatment
- 19. Fluid Resuscitation Dehydration: (hematocrit>50, serum sodium level >150 mEq/L, orthostasis, pulmonary wedge pressure < 5 mm Hg, urinary fractional excretion of sodium < 1%) CK elevation in excess of 2-3 times the reference range. Administer isotonic fluids at a rate of approximately 400 mL/h (may be up to 1000 mL/h based on type of condition and severity) and then titrate to maintain a urine output of at least 200 mL/h. In patients with CK levels of 15,000 IU/L or greater, higher volumes of fluid, on the order of at least 6 L in adults, are required. Remember: • Sepsis • Hyperkalemia, hypocalcemia or hyperphosphatemia • Hypoalbuminemia • urinary alkalization, mannitol, and loop diuretics.
- 20. Treatment (Cont.) Depending onthe cause of rhabdomyolysis, surgical care may be necessary, as follows: When intracompartmental pressure exceeds 30 mm Hg, a fasciotomy is advocated Limb fractures may call for surgical and orthopedic treatment Lifestyle-related treatment measures may be considered, as follows: Dietary modification to help address metabolic disorders or inborn errors of metabolism Avoidance of strenuous activities if such activities cause recurrent myalgias, myopathy, or rhabdomyolysis Maintenance of proper hydration during athletic exertion Prompt attention to indicators of heat exhaustion during hot and humid conditions
- 21. Recommended activity • Strenuousactivities (eg, competitive sports) should be avoided if they cause recurrent myalgias, myopathy, or rhabdomyolysis. • Children and adolescents with recurrent rhabdomyolysis related to exertion require further medical evaluation. • High-school coaches and trainers must ensure proper hydration and maintain fluid balance during practice sessions and games. Signs and symptoms of heat exhaustion must be evaluated in a timely fashion during hot and humid conditions.[53]
Editor's Notes
- #11 Often, when we think about rhabdomyolysis we think first and foremost about muscle breakdown. We need to keep in mind metabolic myopathies in our differential diagnosis to ensure we are not missing anything.
- #19 Keep in mind, volume status. Though initial volume resuscitation is warranted, maintaining volume status is equally important. The keys here that one wants to achieve are hemodynamic stability and adequate urine output.