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Rhabdomyolysis - Form Pathogenesis to Bedside - Dr. Gawad
The document discusses the pathogenesis and management of rhabdomyolysis, emphasizing both traumatic and non-traumatic causes. Key points include the clinical presentation, laboratory evaluations, and treatment options such as hydration and bicarbonate infusion, along with the prognosis for affected patients. It highlights the importance of timely identification and management to prevent acute kidney injury from muscle cell breakdown.
In this document
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Overview of Rhabdomyolysis, its pathogenesis, and the historical context during WWII.
Explains traumatic and non-traumatic causes, focusing on biochemical and cellular processes.
Details on cellular damage during Rhabdomyolysis, including electrolyte imbalances and mitochondrial effects.
Clinical indicators for suspecting AKI in Rhabdomyolysis, emphasizing CK levels and urine analysis.
Treatment strategies for managing Rhabdomyolysis, including hydration and biochemical corrections.
Concluding remarks on treatment efficacy, prognosis, and acknowledgments.
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Rhabdomyolysis - Form Pathogenesis to Bedside - Dr. Gawad
- 1. Rhabdomyolysis Form Pathogenesis toBedside Mohammed Abdel Gawad Nephrology Specialist Kidney & Urology Center (KUC) Alexandria - EGY [email protected] AKI Workshop – Ras El Bar – Feb 2015
- 2. To download thelecture with full animation please contact me on [email protected]
- 3. Bywaters EG, BeallD. Br Med J. 1941;1:427-432. During bombing of London in World War II
- 4. Pathogenesis / Causes Rhabdomyolysis TraumaticNon Traumatic
- 5. Pathogenesis / Causes Rhabdomyolysis TraumaticNon Traumatic
- 6. Traumatic - Rhabdomyolysis Myoglobin Na Ca MyocyteCell CK,LDH Purines Electrolytes (esp. K + and PO4) Aminotransferase enzymes Lactate Serum Bosch X, Poch E, Grau JM. N Engl J Med. 2009;361:62-72.
- 7. Traumatic - Rhabdomyolysis Myoglobin Na Ca MyocyteCell CK,LDH Purines Electrolytes (esp. K + and PO4) Aminotransferase enzymes Lactate Serum Bosch X, Poch E, Grau JM. N Engl J Med. 2009;361:62-72.
- 8. Traumatic - Rhabdomyolysis Myoglobin Na Ca MyocyteCell CK,LDH Purines Electrolytes (esp. K + and PO4) Aminotransferase enzymes Lactate Serum Bosch X, Poch E, Grau JM. N Engl J Med. 2009;361:62-72.
- 9. Traumatic - Rhabdomyolysis Myoglobin Na Ca MyocyteCell CK,LDH Purines Electrolytes (esp. K + and PO4) Aminotransferase enzymes Lactate Serum Bosch X, Poch E, Grau JM. N Engl J Med. 2009;361:62-72.
- 10. → Uric Acid MyocyteCellSerum BoschX, Poch E, Grau JM. N Engl J Med. 2009;361:62-72.
- 11. → Uric Acid MyocyteCellSerum H2O BoschX, Poch E, Grau JM. N Engl J Med. 2009;361:62-72.
- 12. Bosch X, PochE, Grau JM. N Engl J Med. 2009;361:62-72.
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- 19. Non Traumatic -Rhabdomyolysis MyocyteCellSerum Sarcoplasmic Reticulum (Ca Store) Intracellular Contents Na Ca Khan FY. Neth J Med. 2009 Oct;67(9):272-83
- 20. Non Traumatic -Rhabdomyolysis MyocyteCellSerum Sarcoplasmic Reticulum (Ca Store) Na-K ATPase Pump Ca ATPase Pump Ca ATPase Pump Intracellular Contents Na Ca Khan FY. Neth J Med. 2009 Oct;67(9):272-83
- 21. Non Traumatic -Rhabdomyolysis MyocyteCellSerum Sarcoplasmic Reticulum (Ca Store) Na-K ATPase Pump Ca ATPase Pump Ca ATPase Pump Depletion of ATP Disturbance of ATPase function ↑ Intracellular & Mitochondrial Ca Intracellular Contents Na Ca Khan FY. Neth J Med. 2009 Oct;67(9):272-83
- 22. Non Traumatic -Rhabdomyolysis MyocyteCellSerum Sarcoplasmic Reticulum (Ca Store) Ca ATPase Pump Depletion of ATP Disturbance of ATPase function ↑ Intracellular & Mitochondrial Ca ↑ Intracellular Ca → increased skeletal muscle cell contractility and the production of ROS → skeletal muscle cell death Intracellular Contents Na Ca Khan FY. Neth J Med. 2009 Oct;67(9):272-83
- 23. Non Traumatic -Rhabdomyolysis MyocyteCellSerum Sarcoplasmic Reticulum (Ca Store) Ca ATPase Pump Depletion of ATP Disturbance of ATPase function ↑ Intracellular & Mitochondrial Ca ↑ Intracellular Ca → increased skeletal muscle cell contractility and the production of ROS → skeletal muscle cell death Intracellular Contents Na Ca Khan FY. Neth J Med. 2009 Oct;67(9):272-83
- 24. Non Traumatic -Rhabdomyolysis MyocyteCellSerum Sarcoplasmic Reticulum (Ca Store) Ca ATPase Pump Depletion of ATP Disturbance of ATPase function ↑ Intracellular & Mitochondrial Ca ↑ Intracellular Ca → increased skeletal muscle cell contractility and the production of ROS → skeletal muscle cell death Intracellular Contents Na Ca Khan FY. Neth J Med. 2009 Oct;67(9):272-83
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- 26. When to Suspect? ClinicalPresentation & Lab Ix ATN
- 27. ATN When to Suspect? ClinicalPresentation & Lab Ix • The reported frequency of AKI ranges from 15 to over 50 percent • CK < 20,000 U/l → lower risk of AKI • CK levels 5000 U/l + coexisting conditions (sepsis, intravascular volume contraction, acidosis) → AKI risk increases. Melli G. Medicine (Baltimore). 2005 Nov;84(6):377-85. Bosch X. N Engl J Med. 2009 Jul 2;361(1):62-72. Bosch X, Poch E, Grau JM. N Engl J Med. 2009;361:62-72.
- 28. When to Suspect? ClinicalPresentation & Lab Ix ATN
- 29. ATN When to Suspect? ClinicalPresentation & Lab Ix Myoglobin excreted in urine Dark, reddish-brown urine (+ve dipstick) -ve microscopic evaluation of the urine for RBCs (less than five per high-powered field) - Sanders PW, Agarwal A. In: Nabel EG, ed. ACP Medicine, A Textbook of Medicine. Hamilton, Canada: Decker Intellectual Properties; 2010. - Huerta-Alardín AL. Crit Care. 2005 Apr;9(2):158-69. Epub 2004 Oct 20 - Giannoglou GD. Eur J Intern Med. 2007 Mar;18(2):90-100.
- 30. ATN When to Suspect? ClinicalPresentation & Lab Ix Myoglobin excreted in urine Dark, reddish-brown urine (+ve dipstick) -ve microscopic evaluation of the urine for RBCs (less than five per high-powered field) Routine urine testing for myoglobin by urine dipstick evaluation may be negative in up to 50% of patients with rhabdomyolysis • Myoglobin appears in the urine when the plasma concentration exceeds 1.5 mg/dL • Myoglobin has a short half-life of only 2-3 hours • A suggested role for extrarenal metabolism and clearance of myoglobin Giannoglou GD. Eur J Intern Med. 2007 Mar;18(2):90-100. Khan FY. Neth J Med. 2009 Oct;67(9):272-83 Wakabayashi Y. Intensive Care Med. 1994;20(2):109-12.
- 31. When to Suspect? ClinicalPresentation & Lab Ix ATN
- 32. ATN When to Suspect? ClinicalPresentation & Lab Ix Giannoglou GD. Eur J Intern Med. 2007 Mar;18(2):90-100. Gabow PA. Medicine (Baltimore). 1982 May;61(3):141-52. However, more than half of patients may not report muscular symptoms Muscle pain, Weakness
- 33. When to Suspect? ClinicalPresentation & Lab Ix ATN
- 34. ATN When to Suspect? ClinicalPresentation & Lab Ix Khan FY. Neth J Med. 2009 Oct;67(9):272-83
- 35. ATN When to Suspect? ClinicalPresentation & Lab Ix Serum Level: 1500 to over 100,000 IU/L Type: Mainly CK-MM, Small amount CK-MB 2 -12 hours after injury 24 -72 hours after injury 3-5 days after injury cessation Khan FY. Neth J Med. 2009 Oct;67(9):272-83
- 36. ATN When to Suspect? ClinicalPresentation & Lab Ix Serum Level: 1500 to over 100,000 IU/L Type: Mainly CK-MM, Small amount CK-MB 2 -12 hours after injury 24 -72 hours after injury 3-5 days after injury cessation CK serum half-life = 1.5 days declines 40 to 50 % of the previous day’s value If CK does not decline as expected = continued muscle injury or the development of a compartment syndrome Khan FY. Neth J Med. 2009 Oct;67(9):272-83
- 37. MyocyteCell CK, LDH Purines Electrolytes (esp.K + and PO4) Aminotransferase enzymes Lactate Myoglobin Serum When to Suspect? Clinical Presentation & Lab Ix Thromboplastin + other prothrombotic substances Chatzizisis YS. Eur J Intern Med. 2008 Dec;19(8):568-74
- 38. MyocyteCell CK, LDH Purines Electrolytes (esp.K + and PO4) Aminotransferase enzymes Lactate Myoglobin Serum When to Suspect? Clinical Presentation & Lab Ix Thromboplastin + other prothrombotic substances DIC (infrequent complication) Chatzizisis YS. Eur J Intern Med. 2008 Dec;19(8):568-74
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- 41. Volume Replacement (Hydration) •What? Isotonic saline • Target? UOP should be maintained around 200-300 ml/h • Continued until –plasma CK levels decrease to <5000 unit/L –urine is dipstick negative for hematuria 1 Hatamizadeh P. Am J Kidney Dis. 2006 Mar;47(3):428-38. Sever MS, Vanholder R. Clin J Am Soc Nephrol.2013;8:328-335.
- 42. Volume Replacement (Hydration)1 PalettaCE. Ann Plast Surg. 1993 Mar;30(3):272-3. Carefully assess: Volume status, UOP (Take care of HYPERVOLEMIA) Compartment syndrome may develop after fluid resuscitation, with worsening edema of the limb and muscle
- 43. Bicarbonate Infusion2 To Whom? CK> 5000 / Sever injury, providing the following conditions are met: ●Severe hypocalcemia is not present ●Arterial pH is <7.5 ●Serum HCO3 < 30 mEq/L How? - Infuse 150 mL of 8.4 % NaHCO3 mixed with 1 L of 5 % dextrose (alternating with isotonic saline) - The initial rate of infusion is 200 mL/hour - the rate is adjusted to achieve a urine pH of >6.5. When to stop? 1- symptomatic hypocalcemia 2-arterial pH > 7.5 3-serum bicarbonate > 30 mEq/L. 4-urine pH does not rise above 6.5 after 3-4 hrs Monitor art pH & Ca / 2hrs Melli G. Medicine (Baltimore). 2005 Nov;84(6):377-85.
- 44. Mannitol Infusion3 To Whom? Urinaryflow is adequate (defined as >20 mL/hour) Patients with extremely high serum CK levels (greater than 30,000 unit/L) Brown CV. J Trauma. 2004 Jun;56(6):1191-6. How? given at a rate of 5 g/h added to each liter of infusate and not exceeding 1 to 2 g/kg/day. When to stop? 1- osmolal gap rises above 55 mosmol/kg 2- diuresis of 200 to 300 mL/hour cannot be achieved (increased risk of hyperosmolality, volume overload, and hyperkalemia ) Sever MS, Vanholder R, Lameire N. N Engl J Med. 2006;354:1052-1063.
- 45. Evidence !!! The evidencefor the effectiveness of NaHCO3 infusion & Mannitol is very weak
- 46. Hypocalcemia4 Give Ca supplementONLY IF: 1- Symptomatic hypocalcemia 2- Management of hyperkalemia Why? During the recovery phase: Release of calcium from injured muscle → serum Ca levels return to normal and may rebound to significantly elevated levels Akmal M. J Clin Endocrinol Metab. 1986 Jul;63(1):137-42.
- 47. Treat the cause •The specific cause is frequently evident from the history or from the immediate circumstances preceding the disorder. • Consider toxicology screen for drugs, viral screen, TSH if cause not apparent.
- 48. PROGNOSIS The overall prognosisfor patients with heme- induced AKI is favorable as most survivors recover sufficient kidney function to be dialysis independent, and many will recover to normal or near-normal kidney function Woodrow G. Ren Fail. 1995 Jul;17(4):467-74.
- 49. • Rhabdomyolysis maybe traumatic or non traumatic • Final common pathway of pathogenesis is the leak of intramuscular contents into circulation • Final common pathway is sequestration of Ca & H2O into muscles • Hallmark of AKI is ATN
- 50. • Dipstick maybe –ve for myglobinuria • Muscle pain may be absent • Re-rise of CK = Compartment syndrome or metabolic disorder • Corner stone of management is hydration
- 51. • NaHCO3 =Precautions = Weak evidence • Mannitol = Precautions = Weak evidence • Ca supplement = Precautions • Prognosis is good
- 52.