Leanna R. Miller, RN, MN, CCRN-CSC, PCCN-CMC, CEN, CNRN, CMSRN, NP
Education Specialist
LRM Consulting
Nashville, TN
Objectives
Identify the causes of rhabdomyolysis.
Describe signs and symptoms of
rhabdomyolysis.
Utilizing a case study, identify
management strategies of a patient with
renal dysfunction resulting from
rhabdomyolysis.
“Rhabdomyolysis was first reported in
1881, in the German literature” (Abbeele,
Parker, 1985).
“Rhabdomyolysis was first described in the
victims of crush injury during the 19401941 London, England, bombing raids of
World War II” (Craig, 2006).
Rhabdomyolysis accounts for an estimated
8-15% of cases of acute renal failure.
the overall mortality rate for patients with
Rhabdomyolysis is approximately 5%
Rhabdomyolysis is more common in males
than in females
may occur in infants, toddlers, and
adolescents
disintegration of striated muscle
results in the release of muscular cell
constituents into the extracellular fluid
and the circulation
major component released is
myoglobin
massive amounts of myoglobin are
released  the binding capacity of the
plasma protein is exceeded
myoglobin is then filtered by the glomeruli
and reaches the tubules, where it may
cause obstruction and renal dysfunction
syndrome characterized by muscle
necrosis and the release of intracellular
muscle constituents into the circulation
creatine kinase (CK) levels are typically
markedly elevated, and muscle pain and
myoglobinuria may be present
severity of illness ranges from
asymptomatic elevations in serum muscle
enzymes to life-threatening disease
associated with:
extreme enzyme elevations
electrolyte imbalances
acute kidney injury
Rhabdomyolysis is the breakdown of
muscle fibers, specifically of the
sarcolemma of skeletal muscle, resulting
in the release of muscle fiber contents
(myoglobin) into the bloodstream.
Source: (Muscle Anatomy
& Structure, 2007)
The sarcolemma is the cell membrane of a muscle cell.
The membrane is designed to receive and conduct stimuli
when muscle is damaged, a protein pigment myoglobin is released into the bloodstream and
filtered out of the body by the kidneys.
broken down myoglobin may block the structures of
the kidney, causing damage such as acute tubular
necrosis or kidney failure.
dead muscle tissue may cause a large amount of fluid
to move from the blood into the muscle, leading to
hypovolemic shock  reduced blood flow to the
kidneys.
may result from a large variety of
diseases, TRAUMA, or toxic insults to
skeletal muscle
hereditary myopathies
 Causes







trauma
burns
compression syndrome
infection
seizures
heat intolerance
heat stroke
 Causes




vascular occlusion
prolonged shock
electrolyte disorders
drugs (cocaine, alcohol,
statins, amphetamine)
 low phosphate levels
 shaking chills
 Clinical Manifestations
 muscle tenderness
 myalgias
 muscle swelling &
weakness
 DIC
 color of urine
• Additionally some possible
symptoms include:
− Overall fatigue
− Joint pain
− Seizures
− Weight gain
Diagnosis
an examination reveals tender or
damaged skeletal muscles
Creatine Phosphokinase (CK) levels are
very high
serum myoglobin test is positive
serum potassium may be very high
serum CK begins to rise within 2 to 12
hours following the onset of muscle
injury and reaches its maximum within
24 to 72 hours
decline is usually seen within three to
five days of cessation of muscle injury
CK has a serum half-life of about 1.5 days
and declines at a relatively constant rate of
about 40 to 50 percent of the previous
day’s value
patients whose CK does not decline as
expected, continued muscle injury or the
development of a compartment syndrome
may be present
Diagnosis
Urinalysis may reveal protein and be
positive for hemoglobin without
evidence of red blood cells on
microscopic examination
Urine myoglobin test is positive
Urine Myoglobin
visible changes in the urine only occur once
urine levels exceed from about 100 to 300
mg/dL
can be detected by the urine dipstick at
concentrations of only 0.5 to 1 mg/dL
half-life of only two to three hours, much
shorter than that of CK.
rapidly excreted and metabolized to
bilirubin, serum levels may return to normal
within six to eight hours
 Lab Values
 elevated muscle
enzymes (CK)
 hyperkalemia
 hyperphosphatemia
 hypocalcemia
Complications
Kidney damage
Acute renal failure
Hyperkalemia
Cardiac arrest
Disseminated Intravascular Coagulation
Compartment syndrome
 Treatment
 volume replacement
 treat electrolyte
abnormalities
 protect renal
perfusion
 alkalinization of urine
 fasciotomy
• early and aggressive fluids (hydration)
may prevent complications by rapidly
remove myoglobin out of the kidneys.
• administer isotonic crystalloid fluids
(Normal Saline or Lactated Ringer’s)
• give as much fluid as you would
give a severely burned patient.
studies of patients with severe crush
injuries resulting in Rhabdomyolysis
suggest that the prognosis is better
when prehospital personnel provide
FLUID RESUCITATION!
medicines that may be prescribed include
diuretics and sodium bicarbonate.
hyperkalemia should be treated if present
kidney failure should be treated as
appropriate
if urinary flow is >20 mL/hour add
mannitol to the intravenous alkaline
solution providing an increase in urine
output is demonstrated following a test
dose
suggested test dose is 60 mL of a 20
percent solution of mannitol
administered intravenously over three to
five minutes
if urine output increases by at least 30 to
50 mL/h above baseline levels in response
to the test dose, 50 mL of 20 percent
mannitol (1 to 2 g/kg per day [total, 120 g],
may be given at a rate of 5 g/hour.
mannitol is contraindicated in patients
with oliguria
The outcome varies depending on the
extent of kidney damage.
Source: Silberber, 2007
Renal Failure Index (RFI)
RFI = UNa x SCr/UCr
Intrepretation
RFI < 1 (prerenal failure)
RFI > 1 (intrarenal failure)
Fraction Excreted Sodium
(FENa)
FENa = Una X PCr / Pna X Ucr x 100
Intrepretation
FENa < 1 (prerenal failure)
FENa > 1 (intrarenal failure)
Renal Failure Index (RFI)
RFI = UNa x SCr/UCr
Example
RFI > 1
UNa>40 mEq/L
FENa > 2-3%
UCr/SCr<20
Renal Biomarkers
Urine interleukin – 18 (IL – 18)
Urine or blood NGAL
neutrophil gelatinase – associated lipocalin
Increase 24 to 48 hours earlier than creatinine
Intrinsic
Diagnostics
BUN/Creatinine ratio
RFI/FENa
urinalysis
Treatment
underlying cause
prevention on injury
high risk patient
hydration
limit exposure
Management Principles
maintain fluid balance
manage hyperkalemia
•
•
•
•
glucose & insulin
sodium bicarbonate
calcium gluconate
albuterol
Clinical Manifestations
hyperkalemia
hypocalcemia
hypermagnesemia
hyperphosphatemia
acid – base imbalance
hypocalcemia occurs in up to twothirds of patients with significant
rhabdomyolysis
increase in serum phosphate
deposition of calcium phosphate into
injured muscle
decreased bone responsiveness to
parathyroid hormone
Management Principles
control hypertension in
presence of
encephalopathy
bicarbonate for severe
acidosis (pH < 7.2)
manage anemia
Renal Replacement
Therapies
Treatment
Replacement Therapies
acidosis
HCO3 < 10 mEq/L
K+ > 6.5 mEq/L
need high protein diet
deteriorating
Treatment:
Types
hemodialysis
continuous renal replacement
therapy
Treatment
fluid balance
anticoagulation
prevent clotting
prevent blood loss
ultrafiltration
Case Study
 20 – year old male with friends “doing
drugs – cocaine”
 police break up party – male runs from
police but collaspes – states legs
became so weak that he fell
 admitted to ED – lower extremity
weakness and severe pain in legs
Case Study
Serum Electrolytes
ABGs
Na
K
Cl
CO2
Creatinine
BUN
Ca
Mg
PO4
pH
PaCO2
PaO2
SaO2
HCO3
141
6.7
104
7
4.5
20
5.0
2.0
11.2
7.11
27
97
98%
7
Case Study
Serum Enzymes
CK
LDH
4,780
812
Hematology Values
Hct
WBC
30
18,400
Clotting Profile
PT
PTT
Platelets
28
>180
80,000
Case Study
Urinalysis
Color
SG
pH
Reddish brown
1.008
5.0
Sediment
RBC
WBC
Casts
0-1
4-5
granular
& epithelial
Urine Chemistries
Urine Na
Urine Osm
42
280
wide variety of situations that cause
rhabdomyolysis
focus is fluid resuscitation and surgical
intervention if compartment syndrome
develops
ARF is a common consequence – treat as
you would any type of intrinsic ARF