Rhabdomyolysis Im Morning
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Rhabdomyolysis Im Morning

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    Rhabdomyolysis Im Morning Rhabdomyolysis Im Morning Presentation Transcript

    • IM Morning ConferencesRenal Section
      Antonio L. Diaz-Hernandez, MD
      PGY-5 Renal section
    • Reason for consult:
      “Please evaluate pt with rhabdomyolysis related to statin/gemfibrozil combination”
    • 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.
    • 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.
    • 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
    • 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
    • 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
    • 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.
    • 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
    • Admission Labs
      U/A
      Sg 1.015
      Blood large
      pH 5.5
      RBC 0-5
      WBC 0-5
      Protein 100
      Cast none
      Bacteria none
    • Initial Clinical Impression
      AKI
      Rhabdomyolysis; statin induces
    • Rhabdomyolysis
    • 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
    • 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
    • Rhabdomyolysis
      Pathogenesis
      Three principal mechanism:
      ATP demand that outstrip ATP supply
      Sustained increase in sarcoplasmatic calcium concentration
      Sarcolema increase permeability
    • 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+
    • 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
    • Rhabdomyolysis
      • Cell swelling
      Swelling restricted by surrounding fascia
      Trauma or toxin
      Sarcoplasmatic permeability
      compartment pressure
      ischemia, necrosis and compartment syndrome
    • 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
    • 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
    • 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
    • Statin Induce Myopathies
      Muscle injury by
      ↓sarcolema cholesterol
      ↓Ubiquinone (coenzyme Q10)
      Impairs oxidative phosphorilation
      Presentations
      Asymptomatic CPK elevations
      Myalgia with normal CPK
      Frank rhabdomyolysis
    • Rhabdomyolysis
      Increase risk if:
      Large dose
      Kidney disease
      Hepatic disease
      Hypothyroidism
      Amiodarone
      Gemfibrozil
      Erythromycin
      Warfarin
      Cyclosporine
      Itraconazole
    • Rhabdomyolysis
    • 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
    • Systemic Effects
    • 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
    • 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
    • Pigment Nephropathy
      Vasoconstriction
      Cytokines activity
      Heme toxic effect
      Cast formation
    • 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
    • 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
    • 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
    • Rhabdomyolysis
      Patient serum
      Hyperkalemia
      Hyperphosphatemia
      Hypocalemia
      Hyperuricemia
      Hypoalbuminemia?
      Low BUN/creatinine
    • 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
    • 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
    • Rhabdomyolysis
      Treatment options:
      Hemodialysis!
    • Be carful of simvastatin 80 mg! (and also from alcohol + exercise)
    • Clostridium septicum
    • 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.
    • Pathogenesis of Pigment Nephropathy
      Myoglobin Release
      Intravascular volume depletion
      Systemic acidosis