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Rhabdomyolysis .-dr.-osama-2017

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Rhabdomyolysis

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Rhabdomyolysis .-dr.-osama-2017

  1. 1. Rhabdomyolysis Dr. Osama El-Shahat Head of Nephrology Department New Mansoura General Hospital (international) ISN Educational Ambassador
  2. 2. WEEKLY SCIENTIFIC MEETING Nephrology Department New Mansoura General Hospital (international)
  3. 3. Definition  Destruction or disintegration of striated muscle resulting in the leakage of the intracellular muscle constituents into the circulation and extracellular fluid
  4. 4. Cause s Exertional & Traumatic Inherited metabolic Miscellaneous Acquired metabolic Hypoxia / Ischemia Drugs
  5. 5. Etiology of rhabdomyolysis Physical Causes  Trauma & Compression • Traffic or working accidents • Disasters • Torture • Abuse • Long term confinement to the same position  Occlusion or hypo perfusion of muscular Vs • Thrombosis • Embolism • Vs clamping • Shock  Electric current • High voltage electric injury • Lightening • Cadioversion  Straining muscular exercise • Exercise • Epilepsy • Psychiatric agitation • Delirium tremens • Tetanus • Amphetamine overdose • Ecstasy • Status asthmatics  Temperature related • Exercise • High ambient temperature • Sepsis • Narcoleptic malignant syndrome • Malignant hyperthermia Critical care 2005 – 9,158-169
  6. 6. Non physical causes  Metabolic myopathies • McArdle disease • Mitochondrial respiratory chain enzyme deficiencies • Carnitine palmitoyl transferas deficiency • Myoadenlyate deaminase deficiency • Phosphofructokinase deficiency •  Drug & toxins • Regular & illegal drugs • Toxins • Snake & insect venom  Polymyositis/dermatomyositis  Infections • Local and metastatic infections  Endocrinolgic cause • Hyper/hypothyrodism  Systemic effect • Toxic shock syndrome • Influenza • HIV • Herpes viruses • Coxsackie virus  Electrolyte abnormalities • Hypokalemia • Hypocalcaemia • Hyponatremia & hypernatremia • Hypophosphatemia • Hyper osmotic conditions Critical care 2005 – 9,158-169
  7. 7. Drugs that may induce rhabdomyolysis
  8. 8. Statin related rhabdomyolysis  Directly or indirectly impairs the production or use of ATP by skeletal muscle  Increases energy requirements that exceed the rate of ATP production  Interfere with ATP production by reducing levels of coenzyme Q, chronic myositis syndrome  Risk factors: high dosages, increasing age, female, renal and hepatic insufficiency, DM and concomitant therapy with drugs such as fibrates
  9. 9. Exertional Rhabdomyolysis  Exercise beyond physical capabilities  ATP demand outweighs supply resulting in cellular membrane breakdown  Intense exercise in normal individuals  Grand mal seizure  Delirium tremens  Physical abuse  Contact sports  Crush injury  Compression
  10. 10. Factors in the development of Exertional Rhabdomyolysis  Fitness level  Experience with the type of exercise being Performed  Intensity of exercise  Type of exercise (eccentric vs concentric)  Ambient temperature  Hydration level  Fasting  Associated illness
  11. 11. Causes of Cellular Destruction in Rhabdomyolysis  Direct injury to cell membrane (ex. crushing, tearing, burning..)  Severe electrolyte disturbance disrupting sodium-potassium pump  Muscle cell hypoxia leading to depletion of ATP
  12. 12. Physical injury Compression Ischemia Excessive contractions Electric injury Hyperthermia Non physical injury •Metabolic myopathies •Drug & toxins •Infection •Electrolyte •Endocrine disorder Decrease intracellular ATP Sarcoplasmic Ca++ influx Reperfusion injury Compartment syndrome •Increase phospholipase A2 •Increase Ca++ dependent phosphorylases •Increase nucleases •Increase proteases •Increase free radicals •Increase local BMN cells R h a b d o m y o l y s i s Primary cellular injury inrcease intracellular Ca++ secondary injury Activation Goldman: Cecil Medicine 23rd ed Patho-physiology
  13. 13. Etiology of acute renal injury with rhabdomyolysis Acute kidney injury Direct toxicity of myoglobin in tubular cells Hypovolemia and decrease renal perfusion Cast formation decreasing tubular flow
  14. 14. Cellular Patho- physiology  Influx of extra cellular contents  (sodium, water, chloride, calcium)  Efflux from damaged muscle cells  (potassium, phosphates, lactic acid and other organic acids, purines, myoglobin,thromboplatin, creatinine, creatine kinase)
  15. 15. Influx and Efflux of Extra and Intra Cellular Fluids During Cellular Destruction Chemical composition Extracellular (mEq/L) Intracellular ( mEq/L) Sodium 142 10 Potassium 4 140 Calcium 2.4 0.0001 Magnesium 1.2 58 Chloride 103 4 Bicarbonate 28 10 Protein ( myoglobin, CKetc) 5 40
  16. 16. Myocyte Injury Hours of ischemia 0 2 4 6 Tolerable-no permanent histological changes Irreversible anatomic and functional changes Muscle necrosis
  17. 17. When to Suspect Rhabdo  Occurs in up to 85% of patients with traumatic injuries.  Those with severe injury who develop rhabdomyolysis- induced renal failure have a 20% mortality rate  Multiple orthopedic injuries  Crush injury to any part of the body (eg: hand)  Laying on limb for long period of time –patient “found down”  Long surgery  Brown urine
  18. 18. AXIOM Sudden collapse during physical exertion carried out under warm climatic conditions should be primarily diagnosed as rhabdomyolysis (unless and until proven otherwise)
  19. 19. What to Watch for if you suspect Rhabdo:  Clinical: Ms pain, weakness, dark urine  Hypovolemia, shock  Electrolyte abnormalities : ↑K+, ↓ Ca++ (sequestered in injured tissues)
  20. 20. Early Signs and Symptoms  weakness  fatigue  headache  slowed mentation  thirst  muscle cramps  nausea, vomiting  diarrhea
  21. 21. Causes of reddish-brown discoloration of the urine
  22. 22. Characteristics of urine and plasma in the different conditions that may cause red discoloration of the urine Characteristic Rhabdomyolysi s Haemolysis Hematuria Red discoloration plasma Positive benzidine dipstick Presence of erythrocyte by urine microscopy Elevated CK concentration in the blood
  23. 23. Approach to the patient with red or brown urine
  24. 24. Diagnosis  Serum CKMM  Correlates w/severity of rhabdo  Normally 145-260 U/L  100,000’s not uncommon  high t(1/2): 1.5 days  Rises within 12 hours of the onset  Peaks in 1–3 days, and declines 3–5 days  5000 U/l or greater is related to renal failure  Serum myoglobin t(1/2) 2-3 h Excreted in bile sample UA uric acid crystals
  25. 25. Creatine kinase(CK);CPK ( 38-174U/L for M 26-140 U/L for F )  CPK can be divided to 3 isoenzymes: 1-MM or CK3 96-100%(Skletal muscle and cardiac) is the isoenzyme that constitutes almost all the circulatory enz. In the healthy person 2-BB or CK1 0%(brain,GIT,Genitourinary) 3MB or CK2 0-6%
  26. 26. Creatine kinase(CK);CPK  CK levels rise within 12 hours of muscle injury, peak in 24-36 hours, and decrease at a rate of 30-40% per day.The serum half-life is 36 hours. CK levels decline 3-5 days after resolution of muscle injury ; failure of CK levels to decrease suggests ongoing muscle injury or development of a compartment syndrome. The peak CK level, especially when it is higher than 15,000 U/L, may be predictive of renal failure.
  27. 27. Myoglobin(5-70ng/ml)  Plasma myoglobin measurements are not reliable, because myoglobin has a half- life of 1-3 hours and is cleared from plasma in the urine within 6 hours. Urine myoglobin measurements are therefore preferable.
  28. 28.  UA-myoglobinuria  dipstick will be (+) for hemoglobin, RBC’s and myoglobin  Microscopy: no RBC’s, brown casts, uric acid crystals  Other measures: carbonic anhydrase III, aldolase  Serum creatinine : disproportionate to BUN  Uric acid  Leucocytosis  Hypoalbuminemia  Haematocrite  Urine Na +  K +  Ca + +  Po4  Gluc.in urine  Pigment casts (+) for blood
  29. 29. Clinical Manifestations & Complications  Early signs: ɚ Hyperkalemia, ɚ Hypocalcemia, ɚ Hyperphosphatemia, ɚ Hyperuricemia, ɚ Acidosis Early complications: ɚ Cardiac arrhythmia up to cardiac arrest & death ɚ Hypovolemia  Late complications: ɚ Acute renal failure ɚ DIC ɚ Compartment syndrome ɚ Hypercalcemia ɚ Infection ɚ MOSF ɚ ARDS ɚ Fascial compartment compression syndrome American Family Physician (2002) 65:907-912
  30. 30. TREATMENT  Fluid Resuscitation Is the cornerstone of treatment and must be initiated as soon as possible. No randomized trials of fluid repletion regimens in any age group have been done.
  31. 31. Patients with a CK elevation in excess of 2-3 times the reference range, appropriate clinical history, and risk factors should be suspected of having rhabdomyolysis. For adults, 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 or 3 ml per kilogram
  32. 32.  Because injured myocytes can sequester large volumes of ECF, crystalloid requirements may be surprisingly large. Consider central venous pressure measurement or Swan- Ganz catheterization in patients with cardiac or renal disease. Repeat the CK assay every 6-12 hours to determine the peak CK level.
  33. 33.  The composition of repletion fluid is controversial and may also include sodium bicarbonate, esp. in NS is used.
  34. 34.  To prevent renal failure, many authorities advocate urinary alkalization, mannitol, and loop diuretics. Check urine pH. If it is less than 6.5, alternate each liter of normal saline with 1 liter of 5% dextrose plus 100 mmol of bicarbonate.
  35. 35.  Alkalinization of urine benefits:- 1-Decrease precipitationof the Tamm–Horsfall protein–myoglobin complex 2- Inhibits reduction–oxidation (redox)cycling of myoglobin and lipid peroxidation , thus ameliorating tubule injury. 3- Counteract VC
  36. 36. Dirutics  Remains controversial, but it is clear that it should be restricted to patients in whom the fluid repletion has been achieved.Mannitol may have several benefits: as an osmotic diuretic, it increases urinary flow and the flushing of nephrotoxic agents through the renal tubules; as an osmotic agent, it creates a gradient that extracts fluid that has accumulated in injured muscles and thus improves hypovolemia; finally,it is a free-radical scavenger
  37. 37.  During the time mannitol is being administered, plasma osmolality and the osmolal gap (i.e., the difference between the measured and calculated serum osmolality) should be monitored frequently and therapy discontinued if adequate diuresis is not achieved or if the osmolal gap rises above 55 mOsm per kilogram
  38. 38. Late Treatment  Dialysis – ◦ intermitted preferred to continuous  Reduce use of anticoagulants in trauma patients ◦ Peritoneal dialysis is inadequate ◦ The removal of myoglobin by plasma exchange has not demonstrated any benefit
  39. 39. Take Home Message  Impairment of the production or use of ATP is the basic cause.  Most useful laboratory findings are elevated CK(> 5000U/L related to ARF), initial detection of myglobolin.  Management: Aggressive hydration, diuresis, urine alkalinzation, free-radical scavengers, dialysis.  Do not treat hypocalcemia unless symptom developed.  Conditioning by regular exercise to prevent ″white-collar rhabdomyolysis ″ .
  40. 40. ‫الرحيم‬‫الرحمن‬‫هللا‬ ‫بسم‬
  41. 41. *‹‫حى‬ ‫شئ‬ ‫كل‬ ‫الماء‬ ‫من‬ ‫وجعلنا‬›* ‫األنبياء‬(30)
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