Transcript Rhabdomyolysis

Rhabdomyolysis
MINI LECTURE
RICHARD JIN
PGY-2
2/23/15
Case Presentation
 47 y/o M with pmh HTN, ETOH dependency
complains of passing out, feeling lethargic, and
muscle aches. Upon further questioning the pt
admits to doing a large dose of crystal meth and
losing consciousness.
 Vitals: Afebrile, hemodynamically stable.
 Labs (pertinent):
BMP:Creatinine 2.9 (baseline 0.8), potassium 5.1, otherwise normal.
CBC: normal
Serum CK: 28,000
U/A: Myoglobin present
Objectives
 Identify causes of rhabdomyolysis
 Describe signs and symptoms
 How make the diagnosis
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 Review medical management strategies for
rhabdomyolysis
Rhabdomyolysis
 Breakdown of muscle fibers, specifically of the
sarcolemma of skeletal muscle, resulting in release of
myoglobin.
 Released myoglobin may cause acute kidney injury
or ultimately renal failure.
 Shift of extracellular fluid into injured muscles
resulting in underperfusion of the kidneys.
Rhabdomyolysis
Causes (Muscle Breakdown)
RHABDOMYOLYSIS
Nontraumatic
Traumatic/Compression
-Multiple Trauma
-Crush Injury
-Surgery
-Coma
-Immobilization
Exertional
-Exertion
-Heat illness
-Seizures
-Metabolic myopathies
-Malignant hyperthermia
-Neuroleptic Malignant
Syndrome
Nonexertional
-ETOH
-Drugs
-Infection
-Electrolytes
Causes (Metabolic)
Clinical Signs and Symptoms
 “Triad”: Muscle pain, weakness, dark urine
 Fatigue
 Joint pain
 Seizures
 AKI
 Compartment syndrome
 Disseminated intravascular coagulation
Laboratory Findings
 Creatine kinase: >5x ULN (1500-100,000)
Rises within 2 to 12 hours following the onset of muscle injury and reaches its
maximum within 24 to 72 hours. A decline is usually seen within three to five
days of cessation of muscle injury1,2.
 Myoglobinuria
 Hyperkalemia
 Hyperphosphatemia
 Hypocalcemia
 Hyperuricemia
Diagnosis
Elevation in serum creatine kinase (> 5x ULN)
+ acute neuromuscular illness or dark urine without any
other symptoms.
Generally not required:
 Muscle biopsy
 Electromyography
 Magnetic resonance imaging
Management
 Treat underlying cause.
 Early aggressive fluid resuscitation.
 Electrolyte replacement.
 Alkalinization of urine?
 Fasciotomy.
Fluid Resuscitation
 Optimal fluid and rate of repletion are unclear.
 No studies comparing efficacy/safety of different
types and rate of fluid administration.
Algorithm
CK>5000
Isotonic Saline
Titrate IVF
-Initial Resuscitation: 1-2 L/hr
-100-200 ml/hr (if hemolysis
induced injury)
-Correct electrolyte abnormalities
UOP goal: 200-300ml/hr
Serial CK measurements
CK<5000
Stop Treatment
Bicarbonate
Bicarbonate: Forced alkaline diuresis
 May reduce renal heme toxicity
 May also decrease the release of free iron from myoglobin, the
formation of vasoconstricting F2-isoprostanes, and the risk for
tubular precipitation of uric acid3,4
 No clear clinical evidence that an alkaline diuresis is more
effective than a saline diuresis in preventing AKI5.
Mannitol, Dialysis
Mannitol: Forced diuresis
 May minimize intratubular heme pigment deposition and cast
formation, and/or by acting as a free radical scavenger, thereby
minimizing cell injury6,7.
 Net clinical benefit of remains uncertain, and, therefore, not
routinely administered.
Dialysis
 Use of dialysis to remove myoglobin, hemoglobin, or uric acid in
order to prevent the development of renal injury has not been
demonstrated8.
Back to the Patient
 Aggressive fluid resuscitation started. Bolused
normal saline x 3 Liters in the ED.
 Maintained on normal saline 200cc/hr with
matching urine output of 200cc/hr.
 Serial CK measurements (8 hrs apart: 28k  33k 
38k 30k  24k  18k 5k).
 After 4 days in the hospital pt’s renal function
recovered and was discharged home.
Conclusion
 When rhabdomyolysis is suspected aggressive fluid
resuscitation should started to prevent pigment
nephropathy.
 Titrate to UOP 200-300cc/hr.
 The use of bicarbonate, mannitol, and dialysis: net
clinical benefit has not been shown.
References
1. Huerta-Alardín AL, Varon J, Marik PE. Bench-to-bedside review: Rhabdomyolysis -- an
overview for clinicians. Crit Care 2005; 9:158.
2. Khan FY. Rhabdomyolysis: a review of the literature. Neth J Med 2009; 67:272.
3. Melli G, Chaudhry V, Cornblath DR. Rhabdomyolysis: an evaluation of 475 hospitalized
patients. Medicine (Baltimore) 2005; 84:377.
4. Vanholder R, Sever MS, Erek E, Lameire N. Rhabdomyolysis. J Am Soc Nephrol 2000;
11:1553.
5. Huerta-Alardín AL, Varon J, Marik PE. Bench-to-bedside review: Rhabdomyolysis -- an
overview for clinicians. Crit Care 2005; 9:158.
6. Zager RA. Combined mannitol and deferoxamine therapy for myohemoglobinuric renal
injury and oxidant tubular stress. Mechanistic and therapeutic implications. J Clin Invest
1992; 90:711.
7. Odeh M. The role of reperfusion-induced injury in the pathogenesis of the crush
syndrome. N Engl J Med 1991; 324:1417.
8. Holt S, Moore K. Pathogenesis of renal failure in rhabdomyolysis: the role of myoglobin.
Exp Nephrol 2000; 8:72.