Recommended
More Related Content
What's hot
What's hot (20)
Similar to Aki Rhabdomyolysis
Similar to Aki Rhabdomyolysis (20)
More from Adrianne Gabucan
More from Adrianne Gabucan (19)
Recently uploaded
Recently uploaded (20)
Aki Rhabdomyolysis
- 1. RHABDO GLENNIS FIONA JAVELOSA-TAN A TANGO with MYOLYSIS AN AKI CASE
- 2. And the people rose all that day and all night and all the next day, and gathered the quail⌠While the meat was yet between their teeth, before it was consumed, the anger of the LORD was kindled against the people, and the LORD struck down the people with a very great plague. -- Numbers 11:32-33 Shapiro, M, et al (2012). Rhabdomyolysis in the Intensive Care Unit. J Intensive Care Medicine 27:6, 335-342. Hemlock Herbs
- 5. RHABDOMYOLYSIS ⢠Leakage of muscle cell contents into the circulation ⢠Electrolytes ⢠Myoglobin ⢠Sarcoplasmic proteins (Creatine kinase, aldolase, LDH, AST, ALT) ⢠Massive necrosis manifests as: Limb weakness, Myalgia, Muscle swelling, Gross pigmenturia without hematuria Normal Muscle necrosis Bosch X, Poch E, Grau J (2009). Rhabdomyolysis and Acute Kidney Injury. N Eng J Med 36:1, 62-71
- 6. COMMONLY REPORTED CAUSES Trauma Exertion Muscle Hypoxia Genetic Defects Infection Body Temperature changes Metabolic and Electrolyte Disorders Drugs and Toxins Idiopathic (sometimes Recurrent) Bosch X, Poch E, Grau J (2009). Rhabdomyolysis and Acute Kidney Injury. N Eng J Med 36:1, 62-71
- 7. CASE ⢠B.O. ⢠28/M ⢠Single, Roman Catholic, from Caloocan City ⢠No known co-morbids ⢠No previous hospitalization or check-ups ⢠No regular exercise for the past 3 months
- 8. B.O., 28/M CC: Cramps of both lower extremities 1 day PTA 2 days PTA Admission 3.5 L of water 0.5 L gatorade 1 L water Dizziness Thigh pain Bureau of Fire Protection
- 9. B.O., 28/M 1 day PTA 2 days PTA Admission 3.5 L of water 0.5 L gatorade 1 L water Dizziness Thigh pain
- 10. B.O., 28/M 1 day PTA 2 days PTA Admission 3.5 L of water 0.5 L gatorade 1 L water IVF: PNSS 1 Liter Dizziness Thigh pain CBC Creatinine, BUN Na, K, Chloride Urinalysis KUB Ultrasound
- 11. LABORATORY RESULTS CBC 8/2/17 Hgb 15.4 WBC 16.5 Neutrophils 71.6 Platelet 270 Blood Chem 8/2/17 Creatinine 2.2 mg/dL BUN 17 mg/dL Sodium 134 meq/L Potassium 3.3 meq/L Chloride 100 meq/L Urinalysis 8/2/17 Color Light brown Clarity Cloudy Sp. gravity 1.025 pH 5.0 Protein 1+ Glucose 2+ Blood 2+ Ketone Negative WBC 0-2/hpf RBC 25-30/hpf Ultrasound, 8/2/17 Normal-sized kidneys with parenchymal disease and non-obstructing microlithiases
- 12. B.O., 28/M 1 day PTA 2 days PTA Admission 3.5 L of water 0.5 L gatorade 1 L water IVF: PNSS 1 Liter Dizziness Thigh pain Sent Home Advised Uro consult Admit
- 13. ROS ⢠No fever ⢠No headache ⢠No cough or colds ⢠No dysuria or flank pains ⢠No weight loss or easy fatigability
- 14. ⢠Past Medical History No known co-morbids No intake of any medications/herbal supplements/tea/coffee ⢠Family History Hypertension ⢠Social History Non-smoker, non-alcoholic beverage drinker Previously jogged daily but he has no routine exercise for the past 3 months
- 15. PHYSICAL EXAMINATION Awake, alert, ambulatory Vital Signs: BP 150/90, HR 71, RR 21, T 36.5 Dry oral mucosa, No cervicolymphadenopathies Equal chest expansion, Clear breath sounds Soft non-tender abdomen Tenderness over the lower extremities, more on the thighs Full equal pulses, No Edema
- 16. IMPRESSION Acute Kidney Injury secondary to 1. Rhabdomyolysis (Intrinsic) 2. Dehydration (Pre-renal)
- 17. LABORATORY RESULTS CBC 8/2/17, AM 8/2/17, PM Hgb 15.4 9.3 Hct 27.8 MCV (80-100) 80.1 Normal MCHC (31-35) 33.5 Normal WBC 16.5 10.8 Neutrophils 71.6 71.6 Lymphocytes 16.4 Platelet 270 222 Blood Chem 8/2/17 8/3/17 Creatinine 2.2 4.0 mg/dL Sodium 134 133 meq/L Potassium 3.3 3.4 meq/L
- 18. LABORATORY RESULTS Urinalysis 8/2/17, AM 8/2/17, PM Color Light brown Light brown Clarity Cloudy Clear Sp. gravity 1.025 1.004 pH 5.0 6.0 Protein 1+ 2+ Glucose 2+ Negative Blood 2+ 3+ Ketone Negative Trace L.E. Trace WBC 0-2/hpf 6/hpf RBC 25-30/hpf 4/hpf Ep cells 1/hpf Hyaline cast 0 Bacteria 7/hpf
- 19. Blood Chem 8/3/17 CPK (N 55-170iu/L) 44,820 iu/L CPK-MB (N 0-25iu/L) 25,521.4 iu/L LABORATORY RESULTS Acute Kidney Injury secondary to Rhabdomyolysis IMPRESSION
- 20. THE PATIENT HAD⌠⢠Inciting event ď Strenuous exercise ⢠Presenting symptoms: ďźMyalgia ďźLimb weakness ⢠Labs ďźCPK = 4,482 iu/L ďźUrine Color: Light Brown; ďźUrine Blood 4+; RBCs 4/hpf Efstratiadis G, Voulgaridou A, Nikiforou D, et al. Rhabdomyolysis updated. Hippokratia 2007; 11(3): 129-137
- 21. WHAT IS MYOGLOBIN? ⢠Myoglobin - A heme-containing respiratory protein, dark red - Freely filtered by the glomerulus - Renal threshold: 0.5 - 1.5mg/dL - >100mg/dL = Reddish-brown urine (tea-colored) * Not all cases of rhabdomyolysis will have myoglobinuria * Myoglobinuria occurs only in the context of rhabdomyolysis Bosch X, Poch E, Grau J (2009). Rhabdomyolysis and Acute Kidney Injury. N Eng J Med 36:1, 62-71.
- 22. WHAT HAPPENS IN RHABDOMYOLYSIS? Calcium Influx Direct cell Membran e Damage ATP depletion Parekh R, Caro D, Tainter C (2012). Rhabdomyolysis: Advances in Diagnosis and Treatment. Emergency Medicine Practice 14:3.
- 23. Parekh R, Caro D, Tainter C (2012). Rhabdomyolysis: Advances in Diagnosis and Treatment. Emergency Medicine Practice 14:3. Reprinted from Critical Care Clinics, Vol. 20, issue 1, Darren Malinoski, Matthew Slater, Richard Mullins, Crush injury and
- 25. AKI SECONDARY TO MYOGLOBINURIA High incidence of AKI among Rhabdomyolysis patients if due to: - Illicit drug use or alcohol abuse - Trauma - Multiple causal factors Bosch X, Poch E, Grau J (2009). Rhabdomyolysis and Acute Kidney Injury. N Eng J Med 36:1, 62-71. Melli G, Chaudhry V, Cornblath DR (2005). Rhabdomyolysis: an evaluation of 475 hospitalized patients. Intensive Care Med 27:803- 11. 46% of 475 patients hospitalized for rhabdomyolysis
- 26. Intravascular volume depletion Deficit in nitric oxide Fluid sequestration within damaged muscle Scavenging effect of myoglobin Bosch X, Poch E, Grau J (2009). Rhabdomyolysis and Acute Kidney Injury. N Eng J Med 36:1, 62-71.
- 27. Bosch X, Poch E, Grau J (2009). Rhabdomyolysis and Acute Kidney Injury. N Eng J Med 36:1, 62-71. Hyperkalemia Hyperphosphatemia Hyperuricemia High anion gap acidosis Hypocalcemia 10 Liters of fluid per limb
- 28. Bosch X, Poch E, Grau J (2009). Rhabdomyolysis and Acute Kidney Injury. N Eng J Med 36:1, Acidic Urine Distal Tubule Obstruction Proximal tubule toxic & ischemic injury
- 29. RENAL MANIFESTATIONS ⢠Peak values are weakly correlated with kidney injuryâ Creatine Kinase ⢠Dipstick (+) for blood; no RBCs in sediment ⢠Sensitivity: 80% for rhabdomyolysis Myoglobinuria ⢠Reflecting primary preglomerular vasoconstriction & tubular occlusion rather than tubular necrosis Low FeNA (<1%) Bosch X, Poch E, Grau J (2009). Rhabdomyolysis and Acute Kidney Injury. N Eng J Med 36:1, Blood Chem 8/3/17 CPK (N 55-170iu/L) 44,820 iu/L CPK-MB (N 0-25iu/L) 25,521.4 iu/L
- 31. HOW TO PREVENT EXERTION RHABDOMYOLYSIS ďą Hydrate ďą Warm-up & Cool down ďą Pace ďąPeriodic repetition of eccentric exercises could reduce the level of muscle damage ďąConsider interval time between each exercise ďą Type of exercise that can prevent rhabdomyolysis? ďą Avoid: High-intensity, longer duration, and weight-bearing exercise Hot environment UNKOWN Kim J, et al (2015). Exercise-induced rhabdomyolysis mechanisms and prevention: A literature review. J Sport and Health Science 5: 324-333.
- 32. HANDLING ELECTROLYTES ⢠Correct Hyperkalemia ⢠Correction of hyperphosphatemia ⢠Do not use calcium-containing chelators ⢠Do not correct Hypocalcemia ⢠Unless symptomatic or with severe hyperkalemia ⢠Correction can increase precipitation of calcium phosphate in injured muscle HYPERCALCEMIA during recovery of renal function -- Mobilization of calcium deposited in muscle, normalization of Ph levels, increase in calcitriol Bosch X, Poch E, Grau J (2009). Rhabdomyolysis and Acute Kidney Injury. N Eng J Med 36:1,
- 33. 2003, magnitude 6.6 earthquake stuck the city of Bam in southeastern Iran At least 26,271 people were killed and 30,000 injured ⢠638 patients: 134 (21%) with AKI, and 110 of 134 needed dialysis ⢠â Intensity of trauma â Delay of fluid therapy ⢠â Volume of fluid therapy ď â AKI & need for dialysis (P = .005) ⢠Severe Rhabdomyolysis: > 6 L/day Moderate rhabdomyolysis: > 3 L/day Hydrate â AKI and need for dialysis (P < .001) Severe: CPK >15,000 IU/L Moderate: 1,000-14,999 IU/L
- 34. BICARBONATE ⢠Correct acidosis ⢠Prevent precipitation of myoglobin in tubules ⢠Reduce the risk of hyperkalemia MANNITOL ⢠Increases renal blood flow and GFR ⢠Reducing muscle swelling ⢠Prevents obstructive myoglobin casts ⢠Scavenges free radicals Mannit ol HCO3 Vanholder, R (2000). Rhabdomyolysis. JASN 11(8):1553-1561.
- 35. ⢠Oregon Health & Science University, USA ⢠77 rhabdomyolysis patients over a 10-year period (1993 to 2002) ⢠Diagnosed with rhabdomyolysis and Creatine kinase >2,000 U/L ⢠Rhabdomyolysis Protocol initiated for CK >10,000 U/L: ⢠Goals 1. Brisk flow of urine on the 1st hour (>2-3 mL/Kg/hr ) 2. Raise urine pH > 6.0 Mannit ol HCO3
- 36. Nielsen JS, et al (2017). Bicarbonate and mannitol treatment for traumatic rhabdomyolysis revisited. Am J Surg 213(1):73-79
- 37. Nielsen JS, et al (2017). Bicarbonate and mannitol treatment for traumatic rhabdomyolysis revisited. Am J Surg 213(1):73-79
- 38. Nielsen JS, et al (2017). Bicarbonate and mannitol treatment for traumatic rhabdomyolysis revisited. Am J Surg 213(1):73-79
- 39. Mannit ol HCO3 56 patients w/ CK > 10,000 IU/L Rhabdo Protocol N=46 12 (26%) needed dialysis No protocol N=10 7 (70%) needed dialysis p=0.008 Nielsen JS, et al (2017). Bicarbonate and mannitol treatment for traumatic rhabdomyolysis revisited. Am J Surg 213(1):73-79 IVF 2-3 mL/Kg/hr + HCO3 + Mannitol
- 40. ⢠Article ⢠Myoglobin has a very low diffusion coefficient, requiring transport by convection ⢠High-flux membranes should be used ⢠Naka et al (2005): ⢠Case report: 53/F with Severe rhabdomyolysis secondary to serotonin syndrome ⢠Use of a continuous RRT in conjunction with a hyperpermeable membrane ⢠â Myoglobin clearance with hyperpermeable membrane RRT
- 41. ⢠China; Quasi-RCT; Therapy duration not reported ⢠22 participants ⢠Treatment group (N = 10) ⢠CVVH therapy: 10 to 16 hours ⢠Conventional therapy (fasciotomy when necessary; ďŹuid resuscitation; therapy for shock, hyperkalemia, acidosis; diuresis; antibiotics) ⢠Control group (N = 12) ⢠Conventional therapy & intermittent hemodialysis when necessary RRT Zeng L, Mi X, Zhang J, Li C. The efďŹcacy of CVVH for acute kidney injury induced by rhabdomyolysis. Si Chuan Yi Xue [Sichuan Medical Journal]
- 42. CVVH ⢠Shorter hospital stay (21.8 vs 34.1 days) ⢠â serum myoglobin and creatine on day 10 of treatment (161 vs 502 g/L) ⢠â Serum Creatine kinase on day 10 (205 vs 1931 g/L) ⢠â Duration of oliguria phase on day 10 (12 vs 23 days) RRT Zeng X, Zhang L, Wu T, Fu P (2014). Continuous renal replacement therapy (CRRT) for rhabdomyolysis. Cochrane Database Syst Rev. 2014 Jun
- 43. OTHER SUGGESTED THERAPIES Allopurinol Pentoxifyllin e N-acetyl- cysteine Antioxidant s Vanholder, R (2000). Rhabdomyolysis. JASN 11(8):1553-1561.
- 44. B.O., 28/M DOA 4th HD 8th 12th 16th 18th OPD 2 4 7 8 1 0 9 5 11 8 CK 44,82 0 CK 5,81 7 Hemodialysis Creatinine (mg/dL) Thigh pain HA P Piperacillin-tazobactam UTI CRO CK- MB 25,521 CK- MB 133 HCO3 Cipro 1 CK 167 Hgb: 10.5 g/dL ? Sickle Cell Trait?
- 45. SUMMARY ⢠Rhabdomyolysis is preventable ⢠Hydration is not enough; Avoid high-intensity, long duration exercise routine ⢠With Rhabdomyolysis, hydrate with 2-3mL/Kg/hr saline to target urine output of 2-3 mL/Kg/hr ⢠Use of HCO3 and Mannitol may be considered especially in non- oliguric patients ⢠If RRT is needed, CRRT (CVVH) may provide best results
- 46. SOURCES ⢠Bosch X, Poch E, Grau J (2009). Rhabdomyolysis and Acute Kidney Injury. N Eng J Med 36:1, 62-71. ⢠Kim J, et al (2015). Exercise-induced rhabdomyolysis mechanisms and prevention: A literature review. J Sport and Health Science 5: 324-333. ⢠Maggi G, et al (2012). Renal Replacement Therapy in Acute Kidney Failure due to Rhabdomyolysis. Case Reports in Critical Care, Volume 2012 (2012), Article ID 603849, 3 pages. ⢠Melli G, Chaudhry V, Cornblath DR (2005). Rhabdomyolysis: an evaluation of 475 hospitalized patients. Intensive Care Med 27:803-11. ⢠Naka T, et al (2005). Myoglobin clearance by super high-flux hemofiltration in a case of severe rhabdomyolysis: a case report. Crit Care. 2005; 9(2): R90âR95. ⢠Nielsen JS, et al (2017). Bicarbonate and mannitol treatment for traumatic rhabdomyolysis revisited. Am J Surg 213(1):73-79. ⢠Parekh R, Caro D, Tainter C (2012). Rhabdomyolysis: Advances in Diagnosis and Treatment. Emergency Medicine Practice 14:3.
- 47. SOURCES ⢠Ronco, C (2005). Extracorporeal therapies in acute rhabdomyolysis and myoglobin clearance. Crit Care. 2005; 9(2): 141â142. ⢠Shapiro, M, et al (2012). Rhabdomyolysis in the Intensive Care Unit. J Intensive Care Medicine 27:6, 335-342. ⢠Szczepanik M, et al (2014). Exertional rhabdomyolysis: identification and evaluation of the athlete at risk for recurrence. Curr Sports Med Rep. 2014 Mar-Apr;13(2):113-9. ⢠Tietze D, Borchers J (2014). Exertional Rhabdomyolysis in the Athlete: a Clinical Review. Sports Health. Jul;6(4):336-9. ⢠Vanholder, R (2000). Rhabdomyolysis. JASN 11(8):1553-1561. ⢠Zeng X, Zhang L, Wu T, Fu P (2014). Continuous renal replacement therapy (CRRT) for rhabdomyolysis. Cochrane Database Syst Rev. 2014 Jun 15;(6):CD008566. ⢠Zeng L, Mi X, Zhang J, Li C. The efďŹcacy of CVVH for acute kidney injury induced by rhabdomyolysis. Si Chuan Yi Xue [Sichuan Medical Journal] 2008;29:307â8.
- 48. THANK YOU O give thanks unto the lord, for he is good; for his mercy endures forever. Psalms 136:1
- 49. CHAMP GUIDELINES FOR RETURN TO SPORT FOLLOWING EXERTIONAL RHABDOMYOLYSIS Phase 1 â˘Rest for 72 hours and encouragement of oral hydration â˘8 hours of sleep nightly â˘Remain in a thermally controlled environment if the episode of ER was in relation to heat illness â˘Follow-up after 72 hours with a repeat serum CK level and UA â˘If the CK has dropped to below 5 times the upper limit of normal and the UA is negative, the athlete can progress to phase 2; if not, reassessment in 72 additional hours is warranted â˘Should the UA remain abnormal or the CK remain elevated for 2 weeks, expert consultation is recommended Phase 2 â˘Begin light activities, no strenuous activity â˘Physical activity at own pace/distance â˘Follow-up with a care provider in 1 week â˘If there is no return of clinical symptoms, the athlete can progress to phase 3; if not, the athlete should remain in phase 2 checking with the health care professional every week for reassessment; if muscle pain persists beyond the fourth week, consider expert evaluation to include psychiatry Phase 3 â˘Gradual return to regular sport/physical training â˘Follow-up with care provider as needed CHAMP: Consortium for Health and Military Performance Tietze D, Borchers J (2014). Exertional Rhabdomyolysis in the Athlete: a Clinical Review. Sports Health. Jul;6(4):336-9.
- 50. B.O., 28/M DOA 4th HD 8th 12th 16th 18th OPD UO/day 3,050cc 1,050cc 1,900cc 1690cc 810cc 1,250cc 2 4 7 8 1 0 9 5 11 8 CK 5,81 7 Hemodialysis Creatinine (mg/dL) Thigh pain HA P Piperacillin-tazobactam UTI CRO CK- MB 25,521 CK- MB 133 HCO3 Cipro 1 CK 167 Hgb: 10.5 g/dL ? CK 44,82 0
- 51. COMPLETE BLOOD COUNT 8/2/17 Hgb 9.3 Hct 27.8 MCV (80-100) 80.1 Normal MCHC (31-35) 33.5 Normal WBC 10.8 Neutrophils 71.6 Lymphocytes 16.4 Platelet 222
- 52. BLOOD CHEMISTRY 8/3/17 8/4/17 8/5/17 8/7/1 7 8/9/1 7 8/10/17 Creatinine 4.0 mg/dL 7.3 8.7 10 11.5 CPK (N 55-170iu/L) 4,482 iu/L CPK-MB (N 0- 25iu/L) 25,521.4 iu/L 133.62 BUN 39 mg/dL 53 Sodium 133 meq/L 137 139 Potassium 3.4 meq/L 4.4 4.7 4.1 Calcium 6.8 mg/dL 7.8 9 Albumin 3.6 g/dL Uric Acid 7.3 PT; INR 13.4 vs 12.3; 1.12 PTT 31.9 vs 32.7
- 53. BLOOD CHEMISTRY 8/13/17 8/14/17 8/17/17 8/19/17 Creatinine 9.8 8.3 5.5 CPK (N 55-170iu/L) 5817.48 CPK-MB (N 0-25iu/L) BUN Sodium Potassium 3.8 3.7 3.7 4.4 Calcium 7.2 Albumin Phosphorus 6.1 Urine Uric acid (37- 92) 15.9 mg/dL
- 54. URINALYSIS 8/2/17 8/4/17 8/9/17 8/11/17 8/13/17 8/15/17 Color Light brown Light yellow Light yellow Colorless Light yellow Light yellow Clarity Clear Cloudy Clear hazy Sl. hazy Clear Sp. gravity 1.004 1.006 1.006 pH 6.0 6.0 6.0 6.0 6.5 6.5 Protein 2+ 1+ Trace Glucose Negative Trace Negative Blood 3+ 2+ 2+ Ketone Trace Negative Negative L.E. Trace 1+ Negative WBC 6/hpf 7 6 RBC 4/hpf 164 16 Ep cells 1/hpf 1 1 Hyaline cast 0 0 0 Bacteria 7/hpf 97 1
- 55. 8/3/17, 2 AM 8/3/17, 3 PM 8/10/17 8/12/17 pH 7.30 7.32 7.46 7.48 pCO2 34 33 30 35 HCO3 16.7 17 21.3 26.1 PO2 99 104 54 213 O2 sat 97% 97% 89% 100% Room Air Room air 6 lpm Bipap 100% ARTERIAL BLOOD GAS
- 56. Urine CS 8/9/17 ⢠Klebsiella pneumoniae ⢠Sensitive to: Amikacin, cefotaxime, Ceftriaxone, Ciprofloxacin, gentamicin, norfloxacin, co-trimoxazole, meropenem, piperacillin/tazobactam, aztreonam ⢠Resistant to: Nitrofurantoin, Co-amox, AmpiSul
- 58. 8/03/1 7
- 59. 8/14/1 7
- 60. 8/10/1 7
- 61. 8/12/1 7
- 62. PO 8/16/1 7
Editor's Notes
- Rhabdomyolysis was observed in ancient times. The old testament refers to a plague suffered by Israelites during their exodus from Egypt after abundant consumption of quail. Myolysis after consumption of quail is well known in the Mediterranean region. It is the result of intoxication by hemlock herbs, which are consumed by quails during their spring migration. Hemlock herbs are known to cause direct muscle toxicity
- swollen, deeply eosinophilic, homogeneous myofibers that lack cross striations (hyalinization) Renal Complication: Acute kidney injury --> Renal failure The major locus of CKâMB is myocardium. Exact amounts are disputed, ranging from 15 to 30% CKâMB and 70 to 85% CKâMM. Older reports have indicated that CKâMB was absent from skeletal muscle, but radioimmunoassay enzyme analysis reports levels of CKâMB of 5 to 7% in skeletal muscle
- Trauma: Crush syndrome Exertion: Strenuous exercise, seizures, alcohol withdrawal syndrome Muscle hypoxia: Limb compression by head or torso during prolonged immobilization or loss of consciousness,* major artery occlusion Genetic defects: Disorders of glycolysis or glycogenolysis, including myophosphorylase (glycogenosis type V), phosphofructokinase (glycogenosis type VII), phosphorylase kinase (glycogenosis type VIII), phosphoglycerate kinase (glycogenosis type IX), phosphoglycerate mutase (glycogenosis type X), lactate dehydrogenase (glycogenosis type XI) Disorders of lipid metabolism, including carnitine palmitoyl transferase II, longÂchain acylÂCoA dehydrogenase, shortÂchain LÂ3ÂhydroxyacylÂCoA dehydrogenase, mediumÂchain acylÂCoA dehydrogenase, veryÂlongÂchain acylÂCoA dehydrogenase, mediumÂchain 3ÂketoacylÂCoA, thiolaseâ Mitochondrial disorders, including succinate dehydrogenase, cytochrome c oxidase, coenzyme Q10 Pentose phosphate pathway: glucoseÂ6Âphosphate dehydrogenase \ Purine nucleotide cycle: myoadenylate deaminase InfectionsâĄ: Influenza A and B, coxsackievirus, EpsteinâBarr virus, primary human immunodeficiency virus, legionella species Streptococcus pyogenes, Staphylococcus aureus (pyomyositis), clostridium BodyÂtemperature changes: Heat stroke, malignant hyperthermia, malignant neuroleptic syndrome, hypothermia Metabolic and electrolyte disorders: Hypokalemia, hypophosphatemia, hypocalcemia, nonketotic hyperosmotic conditions, diabetic ketoacidosis Drugs and toxins: Lipid Âlowering drugs (fibrates, statins), alcohol, heroin, cocaine direct toxic effect of ethanol in skeletal muscles through disruption of adenosine triphosphatase pump function, breakdown of the muscle membrane, and alteration of the sarcoplasmic reticulum, or induction of cytochrome P450 may play a crucial role in the skeletal musclesâ disintegration
- direct toxic effect of ethanol in skeletal muscles through disruption of adenosine triphosphatase pump function, breakdown of the muscle membrane, and alteration of the sarcoplasmic reticulum, or induction of cytochrome P450 may play a crucial role in the skeletal musclesâ disintegration immobilization and ischemic compression of muscle statins and colchicine, are direct myotoxins Drug-induced agitation states, drug-induced seizures, dystonic reactions, and cocaine-induced hyperthermia are associated with excess muscle energy demands
- Jan â April 2017: Jogged 7km every day, no rice dietm lost 16 kg â biggest loser May- July: no exercise; accepted at the Bureau of Fire protection Aug 1: âReceptionâ â intense 1-2hr exercise routine: squats, etc, non-stop Drank 3.5L of water and 0.5L of gatorade prior to start @ 9am; had normal UO Next drink was 1L of water @ 1:30pm, no UO; noted bilateral thigh pain Had moderate exercise afterwards with breaks @ night he urinated ~400cc brown urine Aug 2: Woke up and urinated brown urine, 200cc? â last urine output Ate breakfast and Came in for 4 AM exercise Px had dizziness, worsening of thigh pains Brought to EAMC: noted elevated crea â Hydrated with PNSS 1L & sent home; advised hydration & KUB utz Px was still generally weak, no UO Sought 2nd opnion @ Delos Santos MC with urologist â advised admission Opted to transfer to NKTI
- Jan â April 2017: Jogged 7km every day, no rice dietm lost 16 kg â biggest loser May- July: no exercise; accepted at the Bureau of Fire protection Aug 1: âReceptionâ â intense 1-2hr exercise routine: squats, etc, non-stop Drank 3.5L of water and 0.5L of gatorade prior to start @ 9am; had normal UO Next drink was 1L of water @ 1:30pm, no UO; noted bilateral thigh pain Had moderate exercise afterwards with breaks @ night he urinated ~400cc brown urine Aug 2: Woke up and urinated brown urine, 200cc? â last urine output Ate breakfast and Came in for 4 AM exercise Px had dizziness, worsening of thigh pains Brought to EAMC: noted elevated crea â Hydrated with PNSS 1L & sent home; advised hydration & KUB utz Px was still generally weak, no UO Sought 2nd opnion @ Delos Santos MC with urologist â advised admission Opted to transfer to NKTI
- Jan â April 2017: Jogged 7km every day, no rice dietm lost 16 kg â biggest loser May- July: no exercise; accepted at the Bureau of Fire protection Aug 1: âReceptionâ â intense 1-2hr exercise routine: squats, etc, non-stop Drank 3.5L of water and 0.5L of gatorade prior to start @ 9am; had normal UO Next drink was 1L of water @ 1:30pm, no UO; noted bilateral thigh pain Had moderate exercise afterwards with breaks @ night he urinated ~400cc brown urine Aug 2: Woke up and urinated brown urine, 200cc? â last urine output Ate breakfast and Came in for 4 AM exercise Px had dizziness, worsening of thigh pains Brought to EAMC: noted elevated crea â Hydrated with PNSS 1L & sent home; advised hydration & KUB utz Px was still generally weak, no UO Sought 2nd opnion @ Delos Santos MC with urologist â advised admission Opted to transfer to NKTI
- Jan â April 2017: Jogged 7km every day, no rice dietm lost 16 kg â biggest loser May- July: no exercise; accepted at the Bureau of Fire protection Aug 1: âReceptionâ â intense 1-2hr exercise routine: squats, etc, non-stop Drank 3.5L of water and 0.5L of gatorade prior to start @ 9am; had normal UO Next drink was 1L of water @ 1:30pm, no UO; noted bilateral thigh pain Had moderate exercise afterwards with breaks @ night he urinated ~400cc brown urine Aug 2: Woke up and urinated brown urine, 200cc? â last urine output Ate breakfast and Came in for 4 AM exercise Px had dizziness, worsening of thigh pains Brought to EAMC: noted elevated crea â Hydrated with PNSS 1L & sent home; advised hydration & KUB utz Px was still generally weak, no UO Sought 2nd opnion @ Delos Santos MC with urologist â advised admission Opted to transfer to NKTI
- The major locus of CKâMB is myocardium. Exact amounts are disputed, ranging from 15 to 30% CKâMB and 70 to 85% CKâMM. Older reports have indicated that CKâMB was absent from skeletal muscle, but radioimmunoassay enzyme analysis reports levels of CKâMB of 5 to 7% in skeletal muscle
- Freely filtered by the glomerulus, Endocytosed in the tubule epithelial cell & is metabolized Detected if in excess of Renal threshold: 0.5 - 1.5mg/dL Myoglobinuria lacks sensitivity as a test for rhabdomyolysis; it may be absent in 25 to 50 percent of patients with rhabdomyolysis due to the more rapid clearance of myoglobin, compared with CK, following muscle injury. Myoglobin also decreases rapidly i
- The Primary mechanisms involved in RM are direct sarcolemmic injury (as in trauma), or depletion of ATP within the myocyte Both leads to unregulated increase in intracellular calcium Sarcoplasmic calcium is strictly regulated by a series of pumps, channels and exchangers which maintain low calcium levels when the muscle is at rest, and allows necessary increase for contraction Cell membrane damage directly leads to Ca2+ influx. ATP depletion, on the other hand, leads to increased intracellular Ca2+ concentrations in a more indirect fashion. disrupts proper functioning of the Na+/ K+/ATPase, causing an increase in intracellular Na+ concentrations, which results in increased Na+/Ca2+ ion exchanger function (also ATP-dependent) and increased cytosolic calcium concentrations. This temporary hyperactivity of the ATP-dependent Na+/ Ca2+ ion exchanger further deprives the cell of ATP and its ability to maintain low calcium concentrations. Once ATP debt reaches critical levels, the cellâs ability to keep calcium out and maintain the appropriate membrane potential for proper functioning is compromised.
- Abbreviations: ATP, adenosine triphosphate; Ca2+, calcium; K+, potassium; Na+, sodium; PMN, polymorphonuclear neutrophil. The end result of these alterations within the muscle cell milieu is an inflammatory, self-sustaining myolytic cascade that causes necrosis of the muscle fibers and releases the muscle contents into the extracellular space and the bloodstream. Results to Persistent contraction, energy depletion, activation of calcium-dependent neutral proteases and phospholipases Destruction of myofibrillar, cytoskeletal, & membrane proteins Reperfusion injury: Leukocytes migrate to the damaged tissues only after reperfusion has started, & production of free radicals starts only when oxygen supply is restored In cases of traumatic RM, muscles are initially compressed and ischemic, muscle dysfunction starts to develop when perfusion is restored
- Most serious complication of traumatic & nontraumatic rhabdomyolysis Melli et al (2005): Seen in 46% of 475 hospitalized patients with rhabdomyolysis Incidence higher among: Patients who used illicit drugs or abused alcohol Trauma > those w/ muscle disease Multiple causal factors direct toxic effect of ethanol in skeletal muscles through disruption of adenosine triphosphatase pump function, breakdown of the muscle membrane, and alteration of the sarcoplasmic reticulum, or induction of cytochrome P450 may play a crucial role in the skeletal musclesâ disintegration
- Renal Vasoconstriction Characteristic feature; due to: Intravascular volume depletion due to fluid sequestration within damaged muscle --> activation of RAAS, vasopresssin, sympathetic NS Vascular mediators a. Deficit in nitric oxide due to scavenging effect of myoglobin b. Oxidant injury & leukocyte-mediated inflammation: promote endothelin-1, thromboxane A2, TNF-a, F2-isoprostanes
- Necrosis & inflammation --- JASN (2000) Accumulation fluid in the affected limbs (of up to 10L per limb) Hyperalbuminemia High anion gap acidosis ď release of organic acids from dying muscles Hypocalcemia Hyperphosphatemia Hyperkalemia Nucleosides released ď xanthine, hypoxanthine, uric acid Myoglobin becomes concentrated along the renal tubules, a process that is enhanced by volume depletion and renal vasconstriction, and it precipitates when it interacts with Tamm -Horsfall protein, a process favored by acidic urine Tubule obstruction occurs principally at the level of distal tubules, and direct tubule cytotoxicity occurs mainly in the proximal tubules
- Myoglobin becomes concentrated along the renal tubules, a process that is enhanced by volume depletion and renal vasconstriction, and it precipitates when it interacts with Tamm -Horsfall protein, a process favored by acidic urine Alkaline conditions stabilize the ferryl species, making myoglobin considerably less reactive towards lipids and lipid hydroperoxides Tubule obstruction occurs principally at the level of distal tubules, and direct tubule cytotoxicity occurs mainly in the proximal tubules No nephrotoxic effect in the tubules unless in ACIDIC urine As a heme protein, myoglobin contains Ferrous oxide (Fe2+), which can be oxidized to ferric oxide (Fe3+), generating hydroxyl radicals Cellular release of myoglobin --> uncontrolled leakage of Reactive Oxygen species --> cellular injury Hence the protective effects of deferoxamine (an iron chelator) & glutathione
- Creatin kinase is a sensitive indicator of muscle injury; maximum within 24 to 72 hours CK levels typically peak within 48 to 96 h followed by resolution within 10 to 14 d CK is located on the inner mitochondrial membrane, on myofibrils, and in the muscle cytoplasm [2]. It is involved in cellular energy storage and transfer The major locus of CKâMB is myocardium. Exact amounts are disputed, ranging from 15 to 30% CKâMB and 70 to 85% CKâMM. Older reports have indicated that CKâMB was absent from skeletal muscle, but radioimmunoassay enzyme analysis reports levels of CKâMB of 5 to 7% in skeletal muscle HYPERCALCEMIA During recovery of renal function is unique to RM-induced AKI Results from the mobilization of calcium that was previously deposited in muscle, the normalization of hyperphosphatemia, and an increase in calcitriol (previously inhibited by hyperphosphatemia)
- HYPERCALCEMIA During recovery of renal function is unique to RM-induced AKI Results from the mobilization of calcium that was previously deposited in muscle, the normalization of hyperphosphatemia, and an increase in calcitriol (previously inhibited by hyperphosphatemia) Hypocalcemia Results from calcium entering ischemic and damaged muscle cells and from precipitation of calcium phosphate with calcification in necrotic muscle Hyperphosphatemia inhibits 1a-hydroxylase limiting the formation of calcitriol (1,25-dihydroxyvitamin D3)
- Direct and significant relation between the intensity of the trauma and delayed-onset fluid therapy with the occurrence of AKI and need for dialysis (P < .001) As the volume of IV fluids received per day increases, the occurrence of AKI and the need for dialysis significantly decrease (P = .005) Preventive role of IV hydration at more than 6 L/day in severe rhabdomyolysis patients and of at least 3 L/day in moderate rhabdomyolysis ** Initially given 1L of PNSS in the 1st hospital, then 4L/day at our ER BACKGROUND: Acute kidney injury (AKI) is a severe and preventable problem of crushed earthquake victims. Early hydration therapy started before fully removing earthquake rubbles has been claimed to play a decisive role in AKI prevention, which saves the necessity of later dialysis. However, the extent, quality, and appropriateness of its know-how are controversial. METHODS: Processing clinical and paraclinical data gathered from Bam earthquake victims older than 15 years, we tried to determine correlations between the time of being under the rubbles (TUR), the level of serum creatine phosphokinase (CPK), the delayed onset of fluid therapy (DFT), and finally the volume of intravenous fluid received per day (VFR) with the formation of AKI and the need for dialysis. RESULTS: There is a direct and significant relation between the intensity of the trauma (TUR and CPK) and DFT with the occurrence of AKI and need for dialysis (P < .001). However, as the VFR increases, the occurrence of AKI and the need for dialysis significantly decrease (P = .005). Based on multivariate analysis, the occurrence of AKI and the need for dialysis are primarily affected by CPK, TUR, and VFR; and DFT has been dropped out. The analysis showed the preventive role of VFR more than 6 L in severe rhabdomyolysis patients and of at least 3 L in moderate ones in development of AKI and dialysis. CONCLUSIONS: In the severely rhabdomyolized patients (CPK ⼠15,000), higher volumes of prophylactic fluid (VFR >6 L) are required, whereas in less-traumatized patients, lower volumes (3-6 L) would be effective. https://www.ncbi.nlm.nih.gov/pubmed/20825890?dopt=Abstract
- administered as sodium bicarbonate. This helps to correct the acidosis induced by the release of protons from damaged muscles, to prevent precipitation of myoglobin in the tubules, and to reduce the risk of hyperkalemia. It should be mentioned that alkaline rehydration was recommended already during World War II, as noted in the seminal paper of Bywaters and Beall (7). The only drawback of bicarbonate administration is the decrease of serum ionized calcium. The addition of mannitol to the fluid regimen serves several purposes: mannitol increases renal blood flow and GFR; (2) mannitol is an osmotic agent that attracts fluid from the interstitial compartment, thus counterbalancing hypovolemia and reducing muscular swelling and nerve compression; mannitol is an osmotic diuretic that increases urinary flow and prevents obstructive myoglobin casts; and mannitol scavenges free radicals. Loop diuretics (furosemide, bumetanide, and torsemide) increase tubular flow and decrease the risk of precipitation of myoglobin, while simultaneously acidifying urine and increasing calcium losses.
- BACKGROUND: A rhabdomyolysis protocol (RP) with mannitol and bicarbonate to prevent acute renal dysfunction (ARD, creatinine >2.0Â mg/dL) remains controversial. METHODS: Patients with creatine kinase (CK) greater than 2,000 U/L over a 10-year period were identified. Shock, Injury Severity Score, massive transfusion, intravenous contrast exposure, and RP use were evaluated. RP was initiated for a CK greater than 10,000 U/L (first half of the study) or greater than 20,000 U/L (second half). Multivariable analyses were used to identify predictors of ARD and the independent effect of the RP. RESULTS: Seventy-seven patients were identified, 24 (31%) developed ARD, and 4 (5%) required hemodialysis. After controlling for other risk factors, peak CK greater than 10,000 U/L (odds ratio 8.6, P = .016) and failure to implement RP (odds ratio 5.7, P = .030) were independent predictors of ARD. Among patients with CK greater than 10,000, ARD developed in 26% of patients with the RP versus 70% without it (P = .008). CONCLUSION: Reduced ARD was noted with RP. A prospective controlled study is still warranted.
- Goals: Urine Output >2-3 mL/Kg/hr and urin pH 6-7
- The addition of mannitol to the fluid regimen serves several purposes: mannitol increases renal blood flow and GFR; (2) mannitol is an osmotic agent that attracts fluid from the interstitial compartment, thus counterbalancing hypovolemia and reducing muscular swelling and nerve compression; mannitol is an osmotic diuretic that increases urinary flow and prevents obstructive myoglobin casts; and mannitol scavenges free radicals. Loop diuretics (furosemide, bumetanide, and torsemide) increase tubular flow and decrease the risk of precipitation of myoglobin, while simultaneously acidifying urine and increasing calcium losses.
- No protocol due to delay in presentation or diagnosis BACKGROUND: A rhabdomyolysis protocol (RP) with mannitol and bicarbonate to prevent acute renal dysfunction (ARD, creatinine >2.0Â mg/dL) remains controversial. METHODS: Patients with creatine kinase (CK) greater than 2,000 U/L over a 10-year period were identified. Shock, Injury Severity Score, massive transfusion, intravenous contrast exposure, and RP use were evaluated. RP was initiated for a CK greater than 10,000 U/L (first half of the study) or greater than 20,000 U/L (second half). Multivariable analyses were used to identify predictors of ARD and the independent effect of the RP. RESULTS: Seventy-seven patients were identified, 24 (31%) developed ARD, and 4 (5%) required hemodialysis. After controlling for other risk factors, peak CK greater than 10,000 U/L (odds ratio 8.6, P = .016) and failure to implement RP (odds ratio 5.7, P = .030) were independent predictors of ARD. Among patients with CK greater than 10,000, ARD developed in 26% of patients with the RP versus 70% without it (P = .008). CONCLUSION: Reduced ARD was noted with RP. A prospective controlled study is still warranted.
- Myoglobin is 17âkDa PM, caries an electrical charge, and can be considered as a solute with a radius larger than expected. In these circumstances, it has a very low diffusion coefficient, thus requiring transport by convection, but also has a spherical size so it is likely to be rejected by the membrane pores. The standard cellulosic membranes are virtually impermeable to the molecule; therefore, high-flux membranes should be used [20]. The limitation of the therapy as a high-flux hemofiltration is the presence of low sieving coefficient for myoglobin filtration; even a high-volume hemofiltration or pulse high-volume hemofiltration may be inefficient Naka et al (2005): seems to be feasible and effective. The use of a continuous technique in conjunction with a hyperpermeable membrane with a myoglobin sieving well beyond the classic values observed with high-flux membranes seems to provide clearance and removal values previously unobtainable Myoglobin clearance significantly greater with the hyperpermeable membrane than the control treatment with a standard high-flux membrane. five times greater than the clearance achieved with conventional hemofiltration (control) in the same patient myoglobin clearance was significantly greater with the hyperpermeable membrane than the control treatment with a standard high-flux membrane.
- Conventional: fasciotomy when necessary; ďŹuid resuscitation; therapy for shock, hyperkalemia, acidosis; diuresis; antibiotics conventional therapy (including surgical interventions and intermittent haemodialysis as appropriate) and conventional therapy pl us CVVH (10 to 24 h/d; replacement ďŹuid volume 2000 to 3000 mL/h; blood ďŹow volume 120 to 200 mL/min; with heparin/l ow molecul ar weight heparin as anticoagulant therapy). Diagnostic criteria: conditions that can le ad to rhabdomyolysis; dark urine and oliguria or anuria; positive urine occult blood test but no red blood ce lls; CK > 5 x normal range or CK > 1000 U/L; AKI ⢠Number of participants: 22 ⢠Mean age Âą SD: 37 14.47 years ⢠Sex (M/F): 15/7 ⢠Exclusion criteria: not reported Low quality: âPatients were randomised al located into study group and control groupâ. But according to the study authors, quasi-randomisation was performed and participants were al located by alternative admission IDs Allocation concealment not applied; Blinding not reported All data included Study protocol and prespeciďŹed outcomes not reported
- None of the studies indicated if conventional therapies were comparable between study and control groups. CVVH (10 to 24 h/d; replacement ďŹuid volume 2000 to 3000 mL/h; blood ďŹow volume 120 to 200 mL/min; with heparin/l ow molecul ar weight heparin as anticoagulant therapy). Shorter hospital stays MD -9.69 (days), 95% CI -14.16 to -5.22 Serum myoglobin : MD -341.87 (Âľg/L), 95% CI -626.15 to -57.59) and creatine kinase : MD -1726.42 (Âľg/L), 95% CI -3135.38 to -317.46) were signiďŹcantly decreased on day 10 of treatment Low quality: âPatients were randomised al located into study group and control groupâ. But according to the study authors, quasi-randomisation was performed and participants were al located by alternative admission IDs Allocation concealment not applied; Blinding not reported All data included Study protocol and prespeciďŹed outcomes not reported
- Antioxidants like glutathione Studies done in the 1990s found no hard evidence for their use in rhabdomyolysis
- Exercise-associated collapse with sickle cell trait (ECAST) can be catastrophic with a fulminant rhabdomyolysis requiring the emergent attention of the clinical medical staff. Although exercise intensity, hydration, and environmental conditions have been associated with ECAST events, the precise etiology remains undetermined Screening for sickle cell trait is done with isoelectric focusing (IEF), hemoglobin electrophoresis, or high pressure liquid chromatography (HPLC). Sickle cell trait cannot be detected by measuring hemoglobin level, hematocrit, reticulocyte count, red blood cell indices such as mean cell volume (MCV), or review of the peripheral blood smear, as these measures are all normal in individuals with sickle cell trait. Iso UF: 5th (8/12 partial), 6th (8/13), 7th partial (8/15), Sputum CS: A. baumani, Sens to amik, cipro, genta, ampisul, cefepime, piptazo Resistant to ceftri & cotri Urine CS: Kleb pneu; sens to amik, ceftri, cipro, genta, norflox, piptaz, imip Resistant to nitro, coamox, ampisul
- CHAMP: Consortium for Health and Military Performance
- Exercise-associated collapse with sickle cell trait (ECAST) can be catastrophic with a fulminant rhabdomyolysis requiring the emergent attention of the clinical medical staff. Although exercise intensity, hydration, and environmental conditions have been associated with ECAST events, the precise etiology remains undetermined Iso UF: 5th (8/12 partial), 6th (8/13), 7th partial (8/15), Sputum CS: A. baumani, Sens to amik, cipro, genta, ampisul, cefepime, piptazo Resistant to ceftri & cotri Urine CS: Kleb pneu; sens to amik, ceftri, cipro, genta, norflox, piptaz, imip Resistant to nitro, coamox, ampisul
- For severe RUQ pain
- Myoglobin becomes concentrated along the renal tubules, a process that is enhanced by volume depletion and renal vasconstriction, and it precipitates when it interacts with Tamm -Horsfall protein, a process favored by acidic urine Tubule obstruction occurs principally at the level of distal tubules, and direct tubule cytotoxicity occurs mainly in the proximal tubules
- Ferrous oxide (Fe2+) necessary for the binding of molecular oxygen
- BACKGROUND: The Wenchuan Earthquake resulted in calamitous destruction and massive death. We report the characteristics of crush syndrome (CS) and acute kidney injury (AKI) brought by the earthquake, which took place in a mountainous area. METHODS: We conducted a cross-section survey of total 2,316 consecutive admissions because of seismic trauma, of which 1,827 had complete data available after we excluded those victims with mild injuries. The characteristics of CS and AKI in the mountainous earthquake were analyzed. RESULTS: A total of 149 patients (8.2%) were diagnosed with CS. They had various complications, including different kinds of infection or sepsis, AKI, hematological abnormality, adult respiratory distress syndrome, congestive heart failure, multiple organs dysfunction syndrome, etc. The incidence of hyperkalemia was 15.9% in patients with CS. The hyperkalemia relapsed in five patients after hemodialysis in the first 3 days. AKI occurred in 62 patients (41.6% of CS patients) with CS and 33 of them received renal replacement therapy. In our hospital, 5 of them died. The overall mortality rate was 1.0% and mortality of patients with CS was 6.7%. Twelve patients (50%) died in the first 3 days. CONCLUSIONS: Although the mountains hampered rescue actions, causing more loss of life, CS and AKI were still common and life-threatening events in the Wenchuan Earthquake. Most patients with CS and/or AKI had severe complications, especially hyperkalemia.
- conventional therapy (including surgical interventions and intermittent haemodialysis as appropriate) and conventional therapy pl us CVVH (10 to 24 h/d; replacement ďŹuid volume 2000 to 3000 mL/h; blood ďŹow volume 120 to 200 mL/min; with heparin/l ow molecul ar weight heparin as anticoagulant therapy). Low quality: âPatients were randomised al located into study group and control groupâ. But according to the study authors, quasi-randomisation was performed and participants were al located by alternative admission IDs Allocation concealment not applied; Blinding not reported All data included Study protocol and prespeciďŹed outcomes not reported