Transcript Rhabdomyolysis-3.ppt

Crush Injuries and
Rhabdomyolysis
Dr.M.Mortazavi
Nephrologist
INTRODUCTION
• Rhabdomyolysis is a syndrome characterized by
muscle necrosis and the release of intracellular
muscle constituents into the circulation.
• The severity of illness ranges from
asymptomatic elevations in serum muscle
enzymes to life-threatening cases associated
with extreme enzyme elevations, electrolyte
imbalances, and acute renal failure
• “Crush syndrome” first
recorded in bombing of
London during WWII: 5
people who were crushed
presented in shock with
swollen extremities, dark
urine.
• Later died from renal failure.
•5-35% of patients with rhabdomyolysis develop ARF
•mortality is 3-50%
Cause of Rhabdomyolysis
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Traumatic muscle injury
Drugs and toxins
Infections
Genetic disorders
Excessive muscle activity
Ischemia
Electrolyte and endocrine
Immunologic disease
Pathophysiology of
Rhabdomyolysis
Myocyte Injury
Tolerable-no
permanent
histological
changes
Hours of 0
ischemia
Muscle
necrosis
2
4
Irreversible
anatomic and
functional
changes
6
Cell Ion Physiology
intracellular
extracellular
Pathogenesis of Myocyte Injury
Ca++
compression
Protease activation
ischemia
Membrane degradation
Influx of Ca++, Na+ and fluids
Nuclease activation
Lipid peroxidation
Attraction of
PMN’s
Decreased ATP production
More Ca++ influx
cell lysis
Pathophysiology of ARF
CONTRIBUTORS:
Not reabsorbed
Binds TammHorsfell proteins
•Dehydration (hypovolemia)
•Aciduria
•Renal vasoconstriction
•Cast formation
•Heme-induced toxicity to
tubule cells
Myoglobin – 1-3% of
wet mm weight
Acute kidney injury
Prerenal
(60%-70%)
Intrinsic
25-40%
Postrenal
5-10%
Tubular cell injury
Acute interstisial
nephritis
Acute GN
Toxins
Ischemia and inflamation
Rhabdomyolysis
Myoglobinemia
Endotoxin
cascade
3,rd spacing
NO scavenging
Myoglobinuria
Volume depletion
Acidemia
Aciduria
Renal hypoperfusion/
Ischemia
Proxmial tubule
Fe loading
Cast formation
Luminal stasis
Synergistic tubular damage
ARF
ATN
Diagnosis
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)
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 (eg: hand)
• Laying on limb for long period of time –patient “found down”
• Long surgery
• Brown urine
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
upon reperfusion
Clinical and laboratory features of
rhabdomyolysis
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History and physical examination
Urinalysis
Serum potassium concentration
Creatine kinase
Acid –Base balance
Uric acid
BUN/Cr
Ca/Ph methabolism
DIC
Diagnosis
• Serum CKMM
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Correlates w/severity of rhabdo
sample UA
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
uric acid
crystals
• Ca++
• UA-myoglobinuria
– dipstick will be (+) for hemoglobin,
RBC’s and myoglobin
– Microscopy: no RBC’s, brown casts,
uric acid crystals
• Other measures: carbonic anhydrase III,
aldolase
(+) for blood
Approach to the patient with red or brown urine
Electrolyte abnormalities
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.
Electrolyte abnormalities
Prevention and
Treatment
MANAGEMENT
• 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.
• Monitoring with serial measurements of
serum potassium, calcium, phosphate,
and creatinine ,CPK is recommended.
MANAGEMENT
• The metabolic consequences of and renal
functional impairment due to
rhabdomyolysis should be anticipated,
particularly potentially life-threatening
hyperkalemia.
• Hypocalcemia? Should be treated?
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
• mannitol
– renal vasodilator
– free radical scavenger
Late Treatment
• Dialysis –
– intermitted preferred
to continuous
• Reduce use of
anticoagulants in
trauma patients