Rhabdomyolysis Im Morning
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Rhabdomyolysis Im Morning Presentation Transcript

  • 1. IM Morning ConferencesRenal Section
    Antonio L. Diaz-Hernandez, MD
    PGY-5 Renal section
  • 2. Reason for consult:
    “Please evaluate pt with rhabdomyolysis related to statin/gemfibrozil combination”
  • 3. History of present illness
    Patient is a 72 year old man, with pertinent medical Hx of hypertension and hypercholeterolemia who was in his usual state of health consisting of free ambulation and self care until the day before admission when he was unable to even stand up. Patient was referring this progressive weakness since last April. He use to walk long distance from his home and had been felling more tired needing to take breaks every few blocks or so. The Monday before admission he started to have muscular pain in his extremities, more prominent in legs, and reproduce with palpation.
  • 4. History of present illness
    The symptoms keep getting worse until yesterday when he felt extreme weakness. Patient also complains of tiredness and dizziness. As per interview reveals, signs and symptoms correlate in time with recent optimization of simvastatin treatment, form 40 mg to 80 mg day.
  • 5. Active medical problems
    Active medication
    Atenolol 50 mg day
    Gemfibrozil 600 mg BID
    Simvastatin 80 mg day
    ASA 81 mg day
    HCTZ12.5/
    irbesartan150 mg day
    Active Medical Problems
    Hyperlipidemia
    Hypertension
    Arthritis
    BPH
  • 6. Past Medical History
    Occupation - pension
    Habits
    Alcohol:1 liter of alcohol for 20 years, quit 18 years ago
    Tobacco: 40 packs/years, quit 18 years ago
    Drugs: marijuana
    Family history
    Father: HBP
    Allergies: NKA
    Transfusions: denies
    Travels: EEUU, Las Vegas, Oct 2007
    Surgeries: tonsilectomy
  • 7. Active Medications
    0.9% sodium chloride inj, 150 ml/hr@0 IV
    sodium bicarbonate 150 meq in 5% dextrose/water 100 ml/hr@0 IV
    Ceftriaxone/azythromycin; suspected CAP
  • 8. Physical exam:
    Vital Signs:
    DATE/TIME TEMP PULSE RESP BP PAIN
    8/30/08 @ 1528 98.6 82 20 110/75 0
    General: Alert and oriented times three. Free of chest pain, no in acute distress.
    HEENT: Atraumatic, No JVD at 45*, no carotid bruits.
    Heart: RRR, S4(-), S3(-) no murmur.
    Chest/lungs: bilateral clean auscultation
    Abd: Bowel sounds audible. Soft and depressible, no rebound, no tenderness.
    Extremities: +1 bilateral pitting edema no cyanosis. Bilateral lower extremities pain to palpation, bilateral extremities weakness, more evident lower extremities.
  • 9. Admission Labs
    CBC
    HGB 12.2
    Htc 35.6
    WBC 15.5
    Plat 253
    Serum Chemistry
    BUN 47
    Creat2.4 (1.1; 2007)
    Na 140
    K 5.2
    Cl 103
    HCO3 20
    Glu 106
    Ca 9.3
    PO4 XX
    CPK >20,000
  • 10. Admission Labs
    U/A
    Sg 1.015
    Blood large
    pH 5.5
    RBC 0-5
    WBC 0-5
    Protein 100
    Cast none
    Bacteria none
  • 11. Initial Clinical Impression
    AKI
    Rhabdomyolysis; statin induces
  • 12. Rhabdomyolysis
  • 13. Rhabdomyolysis
    Backgrounds:
    First describe 1940-1941 during WW II
    Commonly to the victims of crush injury in London during blitzkrieg  bombing raids
    Bywaters and Beall describe pathologic change of four patient who die during blitz operations, change were similar to the previews describe in mismatch blood transfusion
  • 14. Rhabdomyolysis
    Epidemiology
    World wide
    5-20% of AKI
    United State
    8-15% of AKI
    Estimated 2 cases per 10,000 person-years 26,000 total cases per year
    85% of patients with major traumatic injuries will experience some degree of rhabdomyolysis
  • 15. Rhabdomyolysis
    Pathogenesis
    Three principal mechanism:
    ATP demand that outstrip ATP supply
    Sustained increase in sarcoplasmatic calcium concentration
    Sarcolema increase permeability
  • 16. Rhabdomyolysis
    Na+
    Ca+
    Ca+
    Ca+
    Na+
    Ca+
    Ca+
    Ca+
    Na+
    Na+
    Ca+
    Na+
    ATPase
    K+
    K+
    K+
    Na+
    Ca+
    Na+
    Na+
    K+
    K+
    K+
    K+
    Na+
    K+
    K+
    Ca+
    K+
    ATPase
    Na+
    K+
    K+
    Na+
    K+
    K+
    Na+
    K+
    K+
    Ca+
    K+
    K+
    K+
  • 17. Rhabdomyolysis
    ↓ATP
    Increase intracellular [Ca+]
    Activation proteolytic and cytotoxic enzymes
    Na+ with associate cellular swelling and injury
    ATP maintain [Ca+] by
    Sequestration sarcoplasmic reticulum
    Promote outflow to extracellular spaces
  • 18. Rhabdomyolysis
    • Cell swelling
    Swelling restricted by surrounding fascia
    Trauma or toxin
    Sarcoplasmatic permeability
    compartment pressure
    ischemia, necrosis and compartment syndrome
  • 19. Hereditary Etiologies
    Deficiencies of glyco(geno)lytic enzymes
    myophosphorylase (McArdle's disease)
    phosphorylasekinase
    phosphofructokinase (Tarui's disease)
    phosphoglyceratemutase
    phosphoglyceratekinase l
    actatedehydrogenase
    Abnormal Lipid Metabolism
    carnitinepalmitoyltranferase deficiency I and II
    carnitine deficiency
  • 20. Acquires Etiologies
    Excessive muscle exercise
    sports and military training
    status epilepticus
    status asthmaticus
    prolonged myoclonus
    Metabolic disorders
    diabetic ketoacidosis
    nonketotichyperosmolar coma
    hypothyroidism
    hypophosphatemia
    hyponatremia
    hypokalemia
    Ischemic injury
    compression
    vascular occlusion
    sickle cell trait
    Infections
    bacterial
    viral
    Heat-related syndromes
    heat stroke
    Inflammatory myopathies
    polymyositis
    dermatomyositis
    Direct muscle injury
    crush
    burning/ freezing
    electric shock
    lightning stroke
  • 21. Associate drugs
    Drug
    Barbiturates
    Amphetamines
    Heroin
    Methadone
    Phencyclidine (PCP)
    Phenylpropanolamine
    Chlorpromazine
    Morphine
    Diazepam
    Dihydrocodeine
    LSD
    Lithium
    Salicylates
    Amoxapine
    Clofibrate/Bezafibrate
    Phenelzine
    Isoniazid
    Loxapine
    Antihistamines
    Theophyllin
    Oxprenolol
    Pentamidine
    Ethanol
    Vasopressin
    Statins
  • 22. Statin Induce Myopathies
    Muscle injury by
    ↓sarcolema cholesterol
    ↓Ubiquinone (coenzyme Q10)
    Impairs oxidative phosphorilation
    Presentations
    Asymptomatic CPK elevations
    Myalgia with normal CPK
    Frank rhabdomyolysis
  • 23. Rhabdomyolysis
    Increase risk if:
    Large dose
    Kidney disease
    Hepatic disease
    Hypothyroidism
    Amiodarone
    Gemfibrozil
    Erythromycin
    Warfarin
    Cyclosporine
    Itraconazole
  • 24. Rhabdomyolysis
  • 25. Rhabdomyolysis
    Cocaine
    Direct myotoxicity
    Indirect effect
    Vasoconstriction
    Seizures
    Agitation
    Delirium
    Hyperthermia
    Muscle compression in obtunded patient
    Ethanol
    Direct myotoxicity
    Indirect effect
    Poor caloric intake
    Malnutrition
    Potassium/phosphate depletion
    Hyperactivity
    Deliriums tremens
    Associate trauma
    Muscle compression due to coma
  • 26. Systemic Effects
  • 27. Rhabdomyolysis
    Possible kidney manifestation
    Asymtomatic normal renal function with discrepancy of blood vs RBC presence
    Ex: Blood= large/RBC=2-5
    Pigment nephropathy
    ATN
    Oliguric
    Non oliguric
  • 28. Kidney Vulnerability
    ↓renal vasodilatation
    Nitric oxide
    Heme proteins
    ↓[NO]
    +
     Heme proteins
    production of vasoconstrictors (endothelin, isoprostanes)
    Glomerular filtration/ ultrafiltration
    Concentrate and internalize heme proteins
    oxidizes
    Hydrogen peroxyde
    +
    urine heme protein
    Increasing toxicity
    denaturate heme
    protein
    Acidic urine pH
    interaction with Tamm-Horsfall protein
     urine cast formation
  • 29. Pigment Nephropathy
    Vasoconstriction
    Cytokines activity
    Heme toxic effect
    Cast formation
  • 30. Rhabdomyolysis
    Diagnosis
    Wide range of presentation
    Muscle pain
    Swelling weakness
    Bruising
    Compartment syndrome features
    Largely asymtomatic with dark urine, decrease urine output and abnormal electrolytes
  • 31. Rhabdomyolysis
    Laboratory evaluation
    Myoglobinuria
    Dark urine
    50% positive heme proteins with 0-5 RBC/hpf
    Acidic urine pH
    Tubular epithelial cells
    Granular cast
    Dark pigment cast
    Proteinuria 50% case
    May reach nephrotic range
    Myoglobinuria; transitory finding
  • 32. Rhabdomyolysis
    Patient serum
    CPK
    Peaks 48 hr after event
    ½ life 48 hr
    Range could vary from 1,000 to 100,000 IU/L
    Fivefold greater than upper limits or > 500 IU/L
    Second wave elevation rise suspicious of possible compartment syndrome
  • 33. Rhabdomyolysis
    Patient serum
    Hyperkalemia
    Hyperphosphatemia
    Hypocalemia
    Hyperuricemia
    Hypoalbuminemia?
    Low BUN/creatinine
  • 34. Rhabdomyolysis
    Treatment options:
    Crush syndrome:
    1-1.5 L 0.9 NSS 1 Hr
    +/- 10 L first 24 Hr
    Non traumatic:
    High rate 0.9 NSS infusion
    Correct intravascular volume depletion
  • 35. Rhabdomyolysis
    Treatment options:
    Urine alkalinization?
    May reduce risk of pigment nephropathy
    1L 0.45 NSS + NaHCO3 75 mmol
    Mannitol in isotonic solution
    100 meqq NaHCO3 + mannitol 100mL(25%) + D5% 800 mL; 1 L in 4 Hr, if no improve in urinary output (< 20mL/Hr) stop treatment
    May worse hypocalcemia
  • 36. Rhabdomyolysis
    Treatment options:
    Hemodialysis!
  • 37. Be carful of simvastatin 80 mg! (and also from alcohol + exercise)
  • 38. Clostridium septicum
  • 39.
  • 40. Human renal biopsy showing proximal tubule injury. This image is a representative sample of a kidney biopsy for ARF, kindly provided by Dr. James Hasbargen, following exercise-induced rhabdomyolysis. The biopsy, obtained within 24 hours of the event, revealed significant proximal tubule cell damage with intraluminal accumulation of apical membrane fragments and a detached cell (*), thinning of proximal tubular cells to maintain monolayer tubule integrity (arrowhead), and dividing cells and accumulation of white cells within the microvascular space in the peritubular area (arrow). The patient required renal replacement therapy but did regain complete renal function.
  • 41. Pathogenesis of Pigment Nephropathy
    Myoglobin Release
    Intravascular volume depletion
    Systemic acidosis