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Rhabdomyolysis
Rhabdomyolysis is a syndrome characterized by the breakdown of skeletal muscle fibers leading to the release of myoglobin into circulation, which can cause acute kidney injury and other complications. It has various causes, including trauma, exertion, infections, and medication use, and can present with symptoms like dark urine, muscle pain, and fatigue. Aggressive fluid resuscitation is crucial for treatment, along with monitoring for complications and implementing prevention strategies such as hydration, avoiding over-exertion, and being cautious with certain medications.
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Overview of Rhabdomyolysis, its definition, causes, and the potentially life-threatening nature.
Symptoms include tea-colored urine and oliguria indicating muscle breakdown and potential kidney injury.
Historical cases and significant events, including incidents from the 20th century related to crush injuries.
Clarifications of key terms and definitions related to muscle destruction and crush syndrome.
Major complications include Acute Renal Failure, Sudden Cardiac Death, and Acute Compartment Syndrome.Pathophysiological mechanisms leading to renal impairment and cardiac issues in Rhabdomyolysis.Details on acute compartment syndrome and critical management strategies to prevent long-term damage.
Anatomical insights into skeletal muscle, focusing on the sarcolemma and its functions.
Cellular events and electrolyte disturbances accompanying muscle breakdown and the resultant consequences.
Delineation of traumatic and non-traumatic causes leading to Rhabdomyolysis.
Chemical agents and medications that can induce muscle damage and increase Rhabdomyolysis risk.
Symptom triad of Rhabdomyolysis, potential complications and their management.
Key laboratory findings such as elevated CPK levels, myoglobinuria, and their implications.
Preventive measures for Rhabdomyolysis, emphasizing hydration, awareness of risks, and exercise guidelines.
Critical treatment strategies include fluid resuscitation, electrolyte management, and addressing complications.
Prognosis for Rhabdomyolysis, importance of early detection, and final preventive recommendations.
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Rhabdomyolysis
- 1. DR. FATHI NEANA CHIEFOF ORTHOPEDICS DR. FAKHRY & ALRAJHY HOSPITAL SAUDI ARABIA NOVEBER, 30 - 2016 Rhabdomyolysis Causes, Pathophysiology & Management Rhabdo •Striated Myo •Muscle Lysis •Breakdown
- 2. RhabdomyolysisRhabdo • Striated Myo • Muscle Lysis •Breakdown Breakdown of skeletal muscle fibers Potentially life-threatening syndrome Leakage of muscle contents into the circulation
- 3. • Tea orcoca cola like urine : breakdown of muscle fibers, specifically the sarcolemma resulting in release of myoglobin -> may cause acute kidney injury or renal failure • Oliguria : Shift of extracellular fluid into injured muscles -> hypovolaemia & under perfusion of the kidneys First clue 1- Tea or coca cola like urine 2- +ve urine myoglobin 3- Oliguria
- 4. History • First reportedin 1881, in the German literature . • In 1910 Myer-Betz Syndrome, (German physician) - Triad: Muscle Pain, Weakness, Brown Urine. • World War II – First described in the victims of crush injury . Dr Bywaters described patients during London Bombings (Battle of Britain 1941). – Oliguria, pigmented casts, limb oedema, shock & death. • In 1943, in animal models, Bywaters & Stead identified myoglobin as the offending agent, & formulated the first treatment plan. • In 1950 Korean War, dialysis reduces mortality rate from 84% to 53%. • Natural Disasters – Earthquakes – 1976 Tangshan (near Beijing): 20% of 242,000 deaths due to crush syndrome. – In 1995, British nephrologists introduced the Disaster Relief Task Force to prevent acute renal failure. – 1999 Marmara (Turkey): 7.2 Richter scale earthquake. 12% hospitalised patients had renal failure, 76% received dialysis, 19% fatality rate.
- 5. The incidence of rhabdomyolysisvaries with the underlying cause Levels increase with disasters - eg, earthquakes & in war zones Rhabdomyolysis account for ~7- 8% of all new cases of acute kidney injury Epidemiology
- 7. Definitions • Rhabdomyolysis -destruction of striated muscle (multiple causes) • A crush injury is direct injury resulting from a crush • A crush syndrome is the systemic manifestation of muscle cell damage Resulting from 3 criteria Crushing, Prolonged pressure, Devascularization Also known as Traumatic rhabdomyolysis
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- 9. 1- Acute RenalFailure ARF 2- Sudden Cardiac Death among young athletes SCD 3- Acute compartment syndrome ACS Sequelae of ACS -> contractures, deformities, long life disability & even amputation ex. Volkmann contracture Why all the worry? Devastating consequences is the answer (ASA)
- 10. Mechanisms of ARFin rhabdomyolysis • Hypovlemia -> renal vasoconstriction -> diminished renal perfusion • Cast formation leads to tubular obstruction • Direct Myoglobin nephrotoxicity • Haeme produced free radicles -Oxidants • When muscle is damaged, a protein pigment called myoglobin is released into the bloodstream and filtered out of the body by the kidneys. • The broken down myoglobin may block the structures of the kidney, causing damage such as acute tubular necrosis or kidney failure. • Dead muscle tissue may cause a large amount of fluid to move from the blood into the muscle, leading to Hypovolemic shock. Causing reduced blood flow to the kidneys.
- 11. Rhabdomyolysis after aninjury can be a cause of Sudden Cardiac Death among young athletes Usually in athletes, skeletal muscles are prone to injury either due to over exercises or any sports related injury Sudden Cardiac Death among young athletes
- 12. Sarcolemma damage releasethe content of sarcoplasm of muscle cells including potassium ions (K+) -> Electrolyte imbalance ->> Cardiac electrical activity changes may precipitate Sudden Cardiac Arrest Sudden efflux of potassium ions in the blood stream + High catecholamine level (exercises) Mechanisms of SCD in rhabdomyolysis
- 13. Acute compartment syndrome ACS= Critical increase of interstitial pressure within a confined closed fascial compartment ->> decline in the perfusion pressure to the compartment tissue Without timely diagnosis & treatment ->> microvascular compromise , ischaemia & cellular necrosis Ultimately permanent disability of the affected region.
- 14. Acute compartment syndrome •Immediate fasciotomy & decompression of all tissues within the affected compartment • Normal resting ICP is around 0 - 8 mmHg in adults & slightly higher (13 to 16 mmHg) in children • DBP – ICP = >30mmhg –> surgical assessment -> conservative -> normal muscle function at follow up - (McQueen and Court-Brown) • DBP – ICP = < 30 -> (fasciotomy) NB: Differential pressure = ( DBP) diastolic BP – (ICP) Intra compartment Pressure
- 15. Acute compartment syndrome •DBP - ICP = >30mmhg –> Non- operative techniques to delay the onset of ischemia & preserve soft tissues. • All restrictive dressings , tight pop cast should be loosened and removed. • Extremity elevation to maximize venous return and minimize edema. • Fracture reduction to limit ongoing soft tissue damage. • AVI System
- 16. Severe deformity, chronicpain, paralysis & even amputation. The best treatment is immediate Decompression Fasciotomies & prevention of late contractures Deformities depend on the most fibrotic & ischemic muscles Complications of A. compartment syndrome late sequelae of A. compartment syndrome
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- 19. Skeletal Muscle Cell Thesarcolemma is the cell membrane of a muscle cell. The membrane is designed to receive and conduct stimuli and surround The sarcoplasm
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- 21. Pathogenesis of Rhabdomyolysis1 • Compressive forces cellular hypoperfusion hypoxia • Decrease in ATPase failure of ATPase pump & sacrolemma leakage • Lysed cell release inflammatory mediators • platelet aggregation • Vasoconstriction • increase vascular permeability
- 22. Electrolyte disturbances Hyperkalaemia Hypocalcaemia Hyperphosphatemia Hyperuricaemia Metabolic acidosis Pathogenesisof Rhabdomyolysis 2 Revascularization • Fluids trapped in damaged tissue • Oedema of affected limb • Haemoconcentration and shock (hypovolaemia) • Myoglobin, potassium, phosphate enter venous circulation Lysed cell release Potassium Phospate Creatine kinase Myoglobin Lysed cell retain Ca water
- 23. Causes of Rhabdomyolysis(Muscle Breakdown) Traumatic Nontraumatic -Multiple Trauma -Crush Injury -Surgery -Coma -Immobilization Exertional Non exertional -Exertion -Heat illness -Seizures -Metabolic myopathies -Malignant hyperthermia -Neuroleptic Malignant Syndrome -ETOH (ethyl alcohol Abuse) -Drugs ( statins, OTC, illicit) -Infection -Electrolytes
- 24. Causes • Trauma • Exertion •Infection – viral myositis • Body temperature change: heat stroke, hypothermia • Connective tissue diseases • Genetic defects: metabolic disorders • Drugs and toxins: statins, OTC, illicit drugs
- 25. TABLE 1 Medications andToxic Substances That Increase the Risk of Rhabdomyolysis HMG-CoA = 3-hydroxy-3-methylglutaryl coenzyme A; LSD = lysergic acid diethylamide; MDMA = 3,4-methylene dioxymethamphetamine. Direct myotoxicity HMG-CoA reductase inhibitors, especially in combination with fibrate-derived lipid-lowering agents such as niacin (nicotinic acid; Nicolar) Cyclosporine (Sandimmune) Itraconazole (Sporanox) Erythromycin Colchicine Zidovudine (Retrovir) Corticosteroids Indirect muscle damage Alcohol Central nervous system depressants Cocaine Amphetamine Ecstasy (MDMA) LSD Neuromuscular blocking agents
- 26. Statins act byinhibiting HMG-CoA reductase (3-hydroxy-3-methyl-glutaryl-CoA Reductase) All metabolic functions further down the pathway are affected (isoprenoids) HMG-CoA reductase inhibitors
- 27. Clinical Mmanifestations ofRhabdomyolysis ? Range from asymptomatic to acute renal failure and DIC Triad : muscle pain , weakness , dark urine Systemic features • Coca-cola coloured urine – Results from Myoglobinuria • General weakness • Confusion, unconsciousness • Fever, nausea/vomiting, Tachycardia • Less frequent urination • In severe cases: AKI (acute kidney injury) renal failure • Disseminated intravascular coagulation Additional symptoms Overall Malaise - Fatigue - Joint pain – Seizures - Weight gain Local features • Muscle pain, swelling, stiffness & tenderness • Bruising & compartment syndrome • Muscle & Limb weakness
- 28. Complications of Rhabdomyolysis Earlycomplications (< 12- 72 hrs) • Hypovolaemia • Hyperkalaemia • Hypocalcaemia • Cardiac arrhythmias • Cardiac arrest Late complications (< 12- 72 hrs) • Kidney damage • Acute tubular necrosis • Acute renal failure 15% • DIC • ARDS • sepsis Early or late complications Acute compartment syndrome
- 29. Laboratory Findings • Creatinekinase: >5x ULN (1500-100,000) (heart, brain, skeletal muscle) 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 three to five days of cessation of muscle injury1,2. • Myoglobinuria • Hyperkalemia • Hyperphosphatemia • Hypocalcemia • Hyperuricemia
- 30. Laboratory Findings High CPKlevels may be seen in people who have: Brain injury or stroke Convulsions Delirium tremens Dermatomyositis or polymyositis Electric shock Heart attack Inflammation of the heart muscle (myocarditis) Lung tissue death (pulmonary infarction) Creatine phosphokinase Creatine phosphokinase (CPK) an enzyme found mainly in heart, brain, skeletal muscle Muscular dystrophies Myopathy Rhabdomyolysis Other conditions that may give positive test results include: Hypothyroidism Hyperthyroidism Pericarditis following a heart attack
- 31. Prevention • Balanced diet& exercise • Risk: Antipsychotics, statin & fibrate medications for high cholesterol , Selective serotonin reuptake inhibitors, Zidovudine, Colchicine, lithium, Antihistamines, and several others • Don’t: Over exercising in extreme heat conditions, take drugs & alcohol • Keep: hydrated – electrolytes
- 32. How can Iprevent Rhabdomyolysis • Drink plenty of fluids after strenuous exercise to dilute the urine and flush the myoglobin out of the kidney • Proper hydration is also necessary after any condition or event that may involve damage to skeletal muscle
- 33. Treatment • A BC • Fluids Early aggressive fluid resuscitation. • Electrolyte replacement. • Alkalinization of urine? • Treat hyperkalaemia • Treat underlying cause. • Fasciotomy. • Free radical scavengers and antioxidants
- 34. EMS Treatment 1. Immediatelyobtain intravenous access with a large-bore catheter. 2. Administer isotonic crystalloid 500 mL/h and then titrate to maintain a urine output of 200- 300 mL/h.
- 35. Fluid Resuscitation • Giveas much fluid as you would give a severely burned patient. • Optimal fluid and rate of repletion are unclear. • No studies comparing efficacy/safety of different types and rate of fluid administration. • Early and aggressive fluids (hydration) may prevent complications by rapidly remove myoglobin out of the kidneys. Administer isotonic crystalloid fluids (Normal Saline or Lactated Ringer’s). • Studies of patients with severe crush injuries resulting in Rhabdomyolysis suggest that the prognosis is better when prehospital personnel provide FLUID RESUCITATION!
- 36. 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
- 37. Bicarbonate, Mannitol, Dialysis Bicarbonate:Forced alkaline diuresis • May reduce renal heme toxicity • May also decrease the release of free iron from myoglobin, the formation of vasoconstricting F2-isoprostanes, and the risk for tubular precipitation of uric acid3,4 • No clear clinical evidence that an alkaline diuresis is more effective than a saline diuresis in preventing AKI. Mannitol: Forced diuresis • May minimize intratubular heme pigment deposition and cast formation, and/or by acting as a free radical scavenger, thereby minimizing cell injury6,7. • Net clinical benefit remains uncertain, therefore, not routinely administered. Dialysis • Use of dialysis to remove myoglobin, hemoglobin, or uric acid in order to prevent the development of renal injury has not been demonstrated.
- 38. Free radical scavengersand antioxidants • The magnitude of muscle necrosis caused by ischemia-reperfusion injury has been reduced in experimental models by the administration of free-radical scavengers . • Many of these agents have been used in the early treatment of crush syndrome to minimize the amount of nephrotoxic material released from the muscle • Pentoxyphylline is a xanthine derivative used to improve microvascular blood flow. In addition, pentoxyphylline acts to decrease neutrophil adhesion and cytokine release • Vitamin E , vitamin C , lazaroids (21-aminosteroids) and minerals such as zinc, manganese and selenium all have antioxidant activity and may have a role in the treatment of the patient with rhabdomyolysis
- 39. Prognosis of Rhabdomyolysis •The outcome varies depending on the extent of kidney damage. Source: Silberber, 2007 Automatic Positive Airway Pressure
- 40. Rhabdomyolysis is thebreakdown of skeletal muscles ATP depletion ->> increase in intracellular Ca2+ ->> triggering a series of proteolytic enzymes =>> myocyte destruction ->> leakage of cell components in blood stream (myoglobin, creatine kinase, K, P, electrolytes, etc.) Summary and Conclusions
- 41. Summary and Conclusions •Excess myoglobin —>> precipitate in glomerular filtrate —>> acute renal failure • Rhabdomyolysis accounts for an estimated 8-15% of cases of acute renal failure • 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
- 42. Summary and Conclusions •High index of suspicion (coca- cola coloured urine, muscle pain, nausea, confusion) • On scene treatment Aggressive fluid treatment Adequate monitoring • Recognition & early treatment of complications Laboratory tests: Plasma creatine kinase levels Plasma potassium levels urine myoglobin assay
- 43. Summary and Conclusions •When rhabdomyolysis is suspected aggressive fluid resuscitation should started to prevent pigment nephropathy. • Titrate to UOP 200-300cc/hr. • The use of bicarbonate, mannitol, and dialysis: net clinical benefit has not been shown.
- 44. Keep always hydrated Wellsupplemented with electrolytes & carbohydrates Avoid drugs, alcohol, excessive heat & over-exercising Summary and Conclusions Prevention strategies
Editor's Notes
- #24 There are several causes of rhabdomyolysis attributable to muscle breakdown. These can be broken down into traumatic and nontraumatic causes. Nontraumatic causes can be further broken down into exertional and nonexertional causes.
- #32 The risk of rhabdomyolysis exists for patients taking statin and fibrate medications for high cholesterol control. Exercise programs and routines need to be thoughtfully planned to prevent rhabdomyolysis. This includes avoiding exercising in extreme heat conditions and drinking adequate fluids. Your cells need a good balance of sodium and potassium to function. Without these essential electrolytes your body’s cell metabolism starts to malfunction. For vigorous exercise it’s important to hydrate with electrolytes before, during, and after. Carbohydrates are also essential to your body’s metabolism during intense activity. During intense bouts of physical activity, muscles can run out of their nutrients. Failure to provide the energy to for muscles to be able to contract can lead rhabdomyolysis. Water is great. Dehydration is your kidneys worst enemy. On the flip side, hydrating yourself with just water doesn’t do your body any good either. Too much water without electrolytes can actually dilute your blood, dropping your electrolyte levels and wreak havoc on your body Your body can be as a machine if the right factors are present. Your cells love a good balance of sodium and potassium to function. Without these essential electrolytes your body’s cell metabolism starts to malfunction. For vigorous exercise it’s important to hydrate with electrolytes before, during, and after. Carbohydrates are also essential to your body’s metabolism during intense activity
- #37 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.