Rhabdomyolysis is a syndrome characterized by muscle necrosis and the release of intracellular muscle constituents into the circulation. It can range from asymptomatic to life-threatening acute renal failure. It was first documented in victims of bombings in London during World War II who developed crush injuries, swollen extremities, and dark urine before dying of renal failure. Early and aggressive intravenous fluid therapy is the primary treatment to prevent acute kidney injury by maintaining adequate renal perfusion and dilution of myoglobin in the kidneys.
9. Pathogenesis of Myocyte Injury
compression
Influx of Ca++, Na+ and fluids
Ca++
Protease activation
Membrane degradation
Nuclease activation
Lipid peroxidation
ischemia
Decreased ATP production
More Ca++ influx
Attraction of
PMN’s
cell lysis
10. Pathophysiology of ARF
Not reabsorbed
Binds Tamm-
Horsfell proteins
CONTRIBUTORS:
•Dehydration (hypovolemia)
•Aciduria
•Renal vasoconstriction
•Cast formation
•Heme-induced toxicity to
tubule cells
Myoglobin – 1-3% of
wet mm weight
14. CLINICAL MANIFESTATIONS AND
DIAGNOSIS
• The classic presentation of
rhabdomyolysis includes myalgias, red to
brown urine due to myoglobinuria, and
elevated serum muscle enzymes
(including creatine kinase)
15. When to Suspect Rhabdo
• Occurs in up to 85% of patients with traumatic injuries.
Those with severe injury who develop rhabdomyolysis-
induced renal failure have a 20% mortality rate
• Multiple orthopedic injuries
• Crush injury to any part of the body
• Laying on limb for long period of time, patient “found down”
• Long surgery
• Red to Brown urine
16. What to Watch for if you suspect Rhabdo:
• Clinical: Mm pain, weakness, dark urine
• Hypovolemia, shock
• Electrolyte abnormalities : ↑K+, ↓ Ca++
(sequestered in injured tissues), acidemia
17. Clinical and laboratory features of
rhabdomyolysis
• History and physical examination
• Urinalysis
• Serum potassium concentration
• Creatine kinase
• Acid –Base balance
• Uric acid
• BUN/Cr
• Ca/Ph methabolism
• DIC
18. Diagnosis
• Serum CKMM
Correlates w/severity of rhabdo
Normally 145-260 U/L
Levels peak w/in 24h
>3000 high correlation with renal failure
#’s in 100,000’s not uncommon
high t(1/2): 1.5 days
• Serum myoglobin
t(1/2) 2-3 h
Excreted in bile
• Ca++
• UA-myoglobinuria
dipstick will be (+) for hemoglobin,
RBC’s and myoglobin
Microscopy: no RBC’s, brown casts,
uric acid crystals
sample UA
(+) for blood
uric acid
crystals
19. Muscle enzymes
• The hallmark of rhabdomyolysis is an
elevation in serum muscle enzymes.
Serum CK levels may be massively
elevated to above 100,000 IU/L.
• Elevations in serum aminotransferases
are common and can cause confusion if
attributed to liver disease.
21. Managment
• Plasma volume expansion with
intravenous isotonic saline should be
given as soon as possible, even while
trying to establish the cause of the
rhabdomyolysis.
• Treatment of the underlying cause of the
rhabdomyolysis.
22. • Monitoring with serial measurements of
serum potassium, calcium, phosphate,
and creatinine, CPK is recommended.
23. • The metabolic consequences and renal
functional impairment due to
rhabdomyolysis should be anticipated,
particularly potentially life-threatening
hyperkalemia.
• Hypocalcemia usually self-limited and
rarely requires therapy.
24. Early Treatment
FLUIDS
Begin early, even on the field
• Damaged muscles attract a lot of fluid
Up to 10L/day
• Ideally NS with bicarb
prevents tubular precipitation
reduces risk of hyperkalemia from
damaged mm
corrects academia
26. Treatment Summary
Do
Isotonic fluids
1-2 L/h
UOP 200-300 ml/h
Consider
Sodium bicarbonate to cause forced alkaline diuresis
Ph < 7.5
HCO3 < 30 mEq/L
Don’t
Loop diuretics
Mannitol
Ca supplementation
27. Conclusion
• Rhabdomyolysis is The result of muscle
breakdown secondary to traumatic &
nontraumatic causes
• CK 5 normal & history to make diagnosis
• Myoglobin is fleeting
• AKI if CK > 5000 IU/L
• Early IV fluids to perfuse the kidneys &
prevent tubular obstruction simply save
the kidneys.