Rhabdomyolysis: Dana Bartlett

RHABDOMYOLYSIS
DANA BARTLETT, BSN, MSN, MA, CSPI

Dana Bartlett is a professional nurse and author. His
clinical experience includes 16 years of ICU and ER
experience and over 20 years of as a poison control
center information specialist. Dana has published
numerous CE and journal articles, written NCLEX
material, written textbook chapters, and done editing
and reviewing for publishers such as Elsevier,
Lippincott, and Thieme. He has written widely on the
subject of toxicology and was recently named a
contributing editor, toxicology section, for Critical
Care Nurse journal. He is currently employed at the
Connecticut Poison Control Center and is actively involved in lecturing and mentoring
nurses, emergency medical residents and pharmacy students.
ABSTRACT
Rhabdomyolysis is often a self-limiting condition that involves the rapid

destruction of muscle tissue that affects the kidneys as muscle protein
passes through to the urine. It is a syndrome that responds well to
supportive care, but rhabdomyolysis can cause serious complications such as
acute kidney injury and compartment syndrome, as well as death. The
etiologies, pathophysiology, and complications of rhabdomyolysis are
complex and the incidence high enough that health clinicians at all levels of
experience would benefit from ongoing review of the research and case
studies supporting safe and appropriate care.
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only claim credit commensurate with the credit awarded for completion of
this course activity.
Statement of Learning Need
Because rhabdomyolysis is often a self-limiting condition that can range in

severity and outcomes, including serious complications such as acute kidney
injury and compartment syndrome, even death, health clinicians at all levels
of experience should be reviewing recommended diagnostic and treatment
approaches for early diagnosis. The risk of patient mortality in those
diagnosed with rhabdomyolysis varies depending on multiple factors, some
of which can be determined through laboratory and other diagnostic testing,
and careful review of patient history and physical signs and symptoms.
Course Purpose
To provide health clinicians with knowledge about rhabdomyolysis diagnosis,

treatment and prognosis with early detection of symptoms and appropriate
physical evaluation and work up.
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Target Audience
Advanced Practice Registered Nurses and Registered Nurses
(Interdisciplinary Health Team Members, including Vocational Nurses and

Medical Assistants may obtain a Certificate of Completion)
Course Author & Planning Team Conflict of Interest Disclosures
Dana Bartlett, BSN, MSN, MA, CSPI, William S. Cook, PhD, Douglas
Lawrence, MA, Susan DePasquale, MSN, FPMHNP-BC - all have no
disclosures
Acknowledgement of Commercial Support
There is no commercial support for this course.
Please take time to complete a self-assessment of knowledge, on

page 4, sample questions before reading the article.
Opportunity to complete a self-assessment of knowledge learned

will be provided at the end of the course.
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1. Rhabdomyolysis is a syndrome characterized by
a. a breakdown of skeletal muscle.

b. reduced serum levels of creatine kinase.
c. reduced excretion of myoglobin by the kidneys.
d. All of the above
2. With rhabdomyolysis, regardless of the cause of the condition

there is a common end-point, pathologic event called
a. skeletal muscle damage.

b. hepatic failure.
c. decreased urine output.
d. compartment syndrome.
3. Exertional rhabdomyolysis is caused by
a. intense voluntary skeletal muscle activity.

b. intense involuntary skeletal muscle activity.
c. normal levels of exercise in inclement weather.
d. All of the above
4. True or False: All forms of rhabdomyolysis are rare, uncommon

conditions that result from a traumatic event.
a. True
b. False
5. Alcohol-induced rhabdomyolysis
a. appears commonly with people who drink alcohol.

b. may be caused by the direct, toxic effects of alcohol on the
muscles.
c. only occurs due to alcohol withdrawal syndrome.
d. only occurs from acid-base imbalance caused by acute alcohol
intoxication.
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Introduction
Rhabdomyolysis is a syndrome characterized by a breakdown of skeletal

muscle, elevated serum levels of creatine kinase, and renal damage. It is
most often a self-limiting condition that responds well to supportive care,
but rhabdomyolysis can cause death and serious complications like acute
kidney injury and compartment syndrome. Rhabdomyolysis is a commonly
encountered condition, but the etiologies, pathophysiology, and
complications of rhabdomyolysis are complex and even for experienced
health clinicians a review of these can be useful.
Rhabdomyolysis: Etiology
There are three primary etiologies of rhabdomyolysis - traumatic, exertional,

and non-traumatic/non-exertional,1 but categorizing rhabdomyolysis in this
way, although useful for understanding the condition, is somewhat arbitrary.
Many of the specific initiating causes of rhabdomyolysis; i.e., cocaine
intoxication, may involve traumatic,
exertional, and non-traumatic/non- The prefix rhabdo means rod-shaped
and when examined closely, skeletal
exertional mechanisms, and for all
muscle has a rod-shaped appearance.
the causes of rhabdomyolysis there Myo means of or relating to muscles,
and lysis is defined as destruction,
is a common end-point, pathologic decomposition.
event – skeletal muscle damage.
The terms listed below are helpful for understanding rhabdomyolysis.
• Acute Kidney Injury:
A sudden decrease in renal function, characterized by an increase in

serum creatinine and decreased urine output.
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• Compartment Syndrome:
Increased tissue pressure in a confined anatomical space that causes

decreased blood flow and ischemia.
• Creatine Kinase (CK):
An intracellular enzyme that helps form adenosine diphosphate and

phosphocreatine. There are three isoenzymes of CK; CK1 (BB) is found
primarily in the brain, CK2 (MB) is found primarily in the heart, and CK3
(MM) is found primarily in the muscle.
• Myoglobin:
The primary intracellular oxygen-transporting molecule.
• Syndrome:
A set of signs and symptoms that occur together.
Traumatic Rhabdomyolysis
Traumatic rhabdomyolysis is a common pathology,2 and it is caused by direct

injury or when a muscle is subjected to prolonged compression.1,3 Direct
injury that causes rhabdomyolysis can be from blunt trauma, burns, a high-
voltage electrical shock, the prolonged use of mechanical restraints, or as a
complication of using a tourniquet during a surgical procedure.1,3-7
Prolonged compression to a muscle that leads to rhabdomyolysis is caused

by immobilization. This can be caused by a medical condition like coma, a
drug overdose, a stroke1,8 or from a surgical procedure that requires the
patient to be immobile for a lengthy period.1,7-9
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Exertional Rhabdomyolysis
Exertional rhabdomyolysis is caused by intense voluntary or involuntary

skeletal muscle activity,1,10-12 or by a normal level of exercise that is
performed in extreme weather conditions.1,12 Rhabdomyolysis from voluntary
muscular contractions is almost always associated with exercise, both
endurance and resistance exercise, and exercise-related exertional
rhabdomyolysis typically occurs when experienced athletes suddenly and
dramatically increase their level of training or when someone who has
previously been sedentary begins a fitness program.
Factors that increase the risk of developing exertional rhabdomyolysis

include (but are not limited to) dehydration, genetic susceptibility,
hot/humid weather, hypokalemia, male gender, and the type of exercise.10
People who have recurrent episodes of exertional rhabdomyolysis most likely
have a genetic susceptibility in the form of an undiagnosed metabolic
myopathy.10 Fortunately, although CK elevations caused by exercise are not
unusual,10 exertional rhabdomyolysis and serious complications of
rhabdomyolysis are uncommon.10,13,14
Involuntary muscular activity that causes rhabdomyolysis can be caused by

grand mal seizures, hyperthermia, psychiatric conditions like psychosis that
are associated with uncontrolled agitation, and by prescription and illicit
drugs like antipsychotics, amphetamines, cocaine, and 3,4
methylenedioxymethamphetamine, aka ecstasy.1
Non-traumatic/Non-exertional Rhabdomyolysis
Causes of non-traumatic/non-exertional rhabdomyolysis are discussed in this

section, and listed in Table 1.1,10,15
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Table 1: Non-Traumatic/Non-Exertional Rhabdomyolysis
Alcohol
Delirium tremens
Drug withdrawal
Electrolyte abnormalities
Endocrine disorders
Hyperthermia
Illicit drugs
Infections
Medical conditions
Metabolic myopathies
Near drowning and hypothermia
Shock
Prescription drugs
Toxins
Vascular thrombosis
This list is not all-inclusive and pathologies like the metabolic myopathies are
not common, and toxins like bee venom rarely cause rhabdomyolysis.
Several of the typically encountered etiologies of non-traumatic/non-
exertional rhabdomyolysis are highlighted below. Some of these, i.e.,
hyperthermia and stimulant intoxication are often accompanied by
rhabdomyolysis; conditions like alcohol use and electrolytes abnormalities
are very common, but rhabdomyolysis caused by them is not.
Alcohol Use
Alcohol use can cause rhabdomyolysis by one of the following mechanisms

or by a combination of them - a direct toxic effect of alcohol on the muscles,
immobilization subsequent to acute alcohol intoxication, and acid-base and
electrolyte abnormalities caused by chronic alcohol intake.15,16 Alcohol-
induced rhabdomyolysis does not appear to be common, but alcohol is a
frequent culprit when intoxication and/or drug use are examined as a cause
8
for rhabdomyolysis.17-19 Delirium tremens from alcohol withdrawal can be
complicated by rhabdomyolysis.
Electrolyte Abnormalities
Abnormally low levels of calcium, phosphate potassium, and sodium have

been implicated as causing rhabdomyolysis and/or contributing to its
development, as has hypernatremia,10 and these electrolyte disturbances are
associated with specific clinical conditions.10,20-22
Table 2: Electrolytes Disturbances and Rhabdomyolysis
Hypernatremia – Dehydration, diabetes

Hypocalcemia - Hypoparathyroidism
Hypokalemia - Diabetes, exertional rhabdomyolysis
Hyponatremia – Psychogenic polydipsia
Hypophosphatemia – Alcohol use, diabetes, hyperalimentation
Hyperthermia
Hyperthermia that causes rhabdomyolysis is a complication of stimulant

intoxication and deliberate overdose of anticholinergics and monoamine
oxidase (MAO) inhibitors. It is an adverse effect of prescription drugs like
antipsychotics, inhalational anesthetics, selective serotonin re-uptake
inhibitors (SSRIs),1,23,24 and rhabdomyolysis caused by high body
temperature can result from intense physical activity, high ambient
temperatures, exertional rhabdomyolysis, drug withdrawal, and sepsis.1,25
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Illicit Drugs
Rhabdomyolysis is a common complication of intoxication from the illicit

stimulants amphetamine, cocaine, ecstasy, phencyclidine (PCP), and
synthetic canthiones (commonly known as bath salts).1,26,27 These drugs are
directly toxic to the skeletal muscles and they increase circulating levels of
catecholamines and serotonin, causing agitation, hyperthermia, increased
skeletal muscle activity, increased body temperature, seizures, and
vasoconstriction that results in tissue hypoxia.1,26,27 Heroin and other opioids
can also be directly toxic to skeletal muscle, and intoxication with an opioid
is often accompanied by compartment syndrome, hypotension, hypoxia, and
prolonged immobilization, all risk factors for rhabdomyolysis.
Infections
Bacterial infections from E coli, Streptococcus, and other pathogens and viral
infections from influenza and herpes simplex have been associated with
rhabdomyolysis.1 Infections are a common cause of rhabdomyolysis in
children; this is less so in adults. The mechanism by which infection causes
rhabdomyolysis is not known.1
Prescription Drugs
There are many prescription and over-the-counter drugs that cause, or have
been associated with rhabdomyolysis.1,8,28 Some of the more common ones
are antipsychotics, antidepressants, antihistamines, benzodiazepines,
colchicine, corticosteroids, and the statin drugs.1,8,28 The statin drugs are
taken by millions of people but the risk of developing rhabdomyolysis from
the use of a statin is very small, and in most cases clearly identified risk
factors, particularly high doses and concurrent use of a drug that disrupts
statin metabolism, are involved.1,29-31
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Toxins
Carbon monoxide (CO) poisoning happens to millions of people each year,

and rhabdomyolysis is not unusual in serious cases of CO poisoning.32 Bee,
wasp, and other insect stings are an everyday occurrence, but
rhabdomyolysis after these events is rare and usually happens if the patient
has suffered a massive number of stings.32 Snake and spider venoms can
cause rhabdomyolysis, as well.
Pathophysiology Of Rhabdomyolysis
The different etiologies and the specific causes of rhabdomyolysis all result
in the same pathogenic pathway.1,3,8,34 The basics of this process are
illustrated below.
Regardless of the cause, muscle damage results in the influx of extracellular

calcium ions into the intracellular space. The end-result of the process
involved in rhabdomyolysis- necrosis of skeletal muscle- releases
intracellular enzymes and proteins into the bloodstream and the extracellular
space; and, for rhabdomyolysis, the most notable of these are creatine
kinase and myoglobin.
Creatine kinase is considered the most sensitive marker for the degree of
skeletal muscle damage and an elevated serum CK is diagnostic for
Rhabdomyolysis.1,8 Myoglobin is excreted by the kidneys, and excess levels of
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myoglobin caused by rhabdomyolysis precipitate in the glomeruli, they
occlude the renal tubules, and they are directly toxic to the kidneys.8,10
Other mechanisms of injury that complicate rhabdomyolysis and are

damaging to the kidneys include:8,10 1) Third-spacing of the intracellular
fluid from damaged muscle, 2) A reduction of intravascular volume,
3) Decreased blood flow to the kidneys, 4) Hypovolemia, 5) Free iron
released from myoglobin that generates reactive oxygen species that, in
turn, damage renal parenchyma, 6) Metabolic acidosis, a common feature of
rhabdomyolysis, and 7) Uric acid released from necrotic skeletal muscle, and
this can form obstructive crystals in the renal tubules.
What Does Rhabdomyolysis Look Like?
Muscle pain, muscle weakness, and red-brown urine have been described as
the classic signs of rhabdomyolysis, but the first two are somewhat
subjective in nature and in many cases all three may be, absent, mild in
intensity, or transient.1,8 Discolored urine is caused by renal excretion of
myoglobin, but this change only occurs when the myoglobin level is very
high. Myoglobin has a short half-life and it is cleared very quickly, and
excessive amounts of myoglobin in the urine, known as myoglobinuria, is
absent in 25% to 50% of patients who have rhabdomyolysis.1
The commonly used urine dipsticks do not distinguish between hemoglobin

and myoglobin.8 Other signs and symptoms that can occur, depending on
the initiating event, are abnormal blood pressure and heart rate, altered
mental status, fever, malaise, nausea, and vomiting.1,8
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Laboratory Testing to Diagnose Rhabdomyolysis
An acute elevation of serum CK is the hallmark of rhabdomyolysis.1 Serum

CK levels begin to rise 2-12 hours after skeletal muscle injury. The
maximum CK level is typically seen within 24-72 hours, and the level begins
to decline 3-5 days after the injury.1,8,35 Creatine kinase has a half-life of
approximately 1.5 days, and a serum level should decline 40%-50% from
the previous day’s level.1
There is no universally accepted level of CK that is used to establish a

diagnosis of rhabdomyolysis, but authoritative sources agree that a CK level
5-10 times the upper limit of normal, i.e., 500–1000 U/L, should be used to
define rhabdomyloysis.1,8,36 The peak level of CK will often be 10,000-25,000
U/L and levels of 100,000-200,000 U/L have occurred.15,37 Normal serum CK
levels are 9-171 and 9-195 for women and men, respectively.
The limitations of myoglobin for establishing the diagnosis of rhabdomyolysis

were previously discussed. However, myoglobin levels should be measured
as part of the diagnostic work-up, and there is evidence suggesting that the
initial and the peak levels of myoglobin can predict the risk of developing
AKI.38 Rhabdomyolysis can also cause an elevated lactate dehydrogenase
(LDH) hypocalcemia (initially) and hypercalcemia (several days after the
initiating event), hyperkalemia, hyperphosphatemia, hyperuricemia, and
metabolic acidosis.1
Complications of Rhabdomyolysis
Acute kidney injury occurs in 13% to >50% of all patients who have
rhabdomyolysis1,8 and it is a serious complication. In critically ill patients
who have rhabdomyolysis and AKI a mortality rate as high as 59% has been
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reported,39 and many patients who have rhabdomyolysis and AKI will need
renal replacement therapy.39
The risk of developing AKI from rhabdomyolysis increases if the myoglobin

level is very high, the patient has hypovolemia, a metabolic acidosis, or
sepsis,1,40 and when the CK level is > 20,000 U/L.41 The relationship between
the CK level and the development of AKI is weak however, and very high
levels do not always cause AKI.40 Risk prediction algorithms for identifying
patients that are likely to develop AKI from rhabdomyolysis are available,
but either they have not been validated or their clinical usefulness has been
questioned.40,42
Compartment syndrome is roughly defined as an abnormally high tissue

pressure within an anatomical compartment. Compartment syndrome is a
common complication of rhabdomyolysis, and compartment syndrome
associated with rhabdomyolysis can result from a traumatic or a non-
traumatic injury to a skeletal muscle. Skeletal muscles are arranged in
groups that are enclosed by fascial membranes. These membranes
effectively create a closed compartment and because they are quite stiff and
inflexible, the build-up of fluid and edema caused by an injury dramatically
increases tissue pressure, compromising local circulation, causing ischemia
and potentially leading to compartment syndrome.7,44,45 Pain out of
proportion to the injury, a tense swollen muscle compartment, and
paresthesias are commonly seen,44 and the signs and symptoms typically
progress rapidly over a few hours.
Trauma is the most common cause of compartment syndrome associated

with rhabdmyolysis;7 exertional rhabdomyolysis, 46,47 rhabdomyolysis that
complicates a medical condtion,23,45, 48 and rhabdomyolysis from prolonged
drug intoxication and immobilization can also cause compartment
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syndrome.1,45,49 Compartment syndrome is a very serious condition. If it is
not promptly diagnosed and treated, permanent muscle and nerve damage
can occur and amputation may be needed.
Hyperkalemia is the most immediate complication of rhabdomyolysis, and if

there is a metabolic acidosis, hypocalcemia, hypoxia, and/or hypovolemia
(all of which are commonly seen in cases of rhabdomyolysis), cardiac arrest
and dysrhythmias can occur.45,50 Other complications of rhabdomyolysis are
disseminated intravascular coagulation (DIC)41,45,50-53 and reversible hepatic
dysfunction.53,54 Cell destruction releases of pro-thrombotic substances41,45,50
can cause DIC, and temporary, reversible elevations of aspartate
aminotransferase (AST) or alanine aminotransferase (ALT) are a common
consequence of rhabdomyolysis.54,55
Treatment Of Rhabdomyolysis
Treatment of a patient who has rhabdomyolysis involves 1) Assessment and

stabilization, 2) Intravenous fluid resuscitation, and 3) Specific therapies.
Assessment and Stabilization
If a patient has, or is suspected to have rhabdomyolysis, certain laboratory

tests and diagnostic screening tests should be done. Tests marked by an
asterisk [] are mandatory; the need for the others can be determined by the
clinical situation and the underlying cause of the rhabdomyolysis. The
following list of laboratory testing is not all-inclusive.
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• Arterial or venous blood gas
• Blood urea nitrogen and serum creatinine
• Coagulation studies
• Compartment pressure measurements
• Liver function tests
• Myoglobin measurement
• Serum CK; this may or may not need to be fractionated
• Serum calcium, potassium, sodium, and phosphate
• Serum glucose
• Thyroid studies
• Toxicology screens, i.e., serum alcohol level, urine drug screen
• Uric acid level
• 12-lead ECG
Obtaining a detailed history is very important. This history should include

1) a complete medication profile, including the use of over-the-counter
medications, herbal/natural supplements, illicit substances, and any
medications a patient has used previously, 2) a review of the patient’s
physical activity and exercise habits, 3) any recent insect envenomations,
4) exposure to high ambient temperatures, 5) any recent accidents or
injuries, 6) any recent infections, and 6) the patient’s past medical and
surgical history.
Aside for examining the patient for the presence of compartment syndrome,
the physical examination does not need to be specifically focused. The
clinical signs and symptoms of rhabdomyolysis are non-specific and although
experienced clinicians will be familiar with the common causes of
rhabdomyolysis, the etiology of rhabdomyolysis is very diverse and
heterogenous and mild cases often go undetected.3 Health clinicians should
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consider the potential for rhabdomyolysis in any situation that can directly or
indirectly cause damage to skeletal muscles.
Intravenous Fluid Resuscitation
Intravenous fluid resuscitation with a high rate of infusion, which is often

called forced diuresis, is the most important therapy for a patient who has
rhabdomyolysis.3,8,45,56,57 Fluid resuscitation helps preserve renal function, it
treats hypotension, and it prevents complications. Recommendations for the
type of intravenous (IV) fluid and the rate of infusion differ depending on the
source, but recent reviews (2016, 2017) agree on several very basic
principles.8,36,45,56,57
• The optimal infusion rate of IV fluids is not known.

• The standard recommendation for initiating IV fluid therapy is 1-2
L/hour.
• The goal of IV fluid resuscitation is a urine output of 200-300 mL/hour.
• Use 0.9% sodium chloride solution (commonly called normal saline).
• There is no agreed up end-point of therapy.
A 0.9% sodium chloride solution is universally recommended, but the type of

IV fluid that is used should be determined by the specifics of the case, the
patient’s needs, and the risks and benefits of each fluid. For example, a
large amount of 0.9% sodium chloride could cause an iatrogenic
hyperchloremic metabolic acidosis, IV solutions containing lactate would be
problematic if the patient has a lactic acidosis, hyperkalemia is common in
rhabdomyolysis and IV solution that contains potassium could exacerbate
this, and a 0.9% sodium chloride solution could cause fluid overload and in
certain situations, acute respiratory distress, abdominal compartment
17
system, or interstitial or pulmonary edema, or abdominal compartment
syndrome.8,45,58
Many patients need several days of vigorous IV fluid resuscitation and in the
first 24-48 hours patients may require 12-24 liters of IV fluid.8,59 The goal of
this therapy is for the urine output to be greater than the rate of IV fluid
infusion,56 and treatment can be stopped when myoglobinuria has cleared
and the CK level is clearly decreasing to below a level that is desired by the
treating physician. This can be 1000 U/L,45 5000 U/L,57 and there is no
universally agreed upon CK level at which IV fluid resuscitation should be
stopped.
Specific Therapies
Alkaline diuresis with bicarbonate has theoretical advantages for preventing

AKI and in cases of rhabdomyolysis caused by a massive crush injury, it has
been used.56 However, this therapy is not recommended. It has potential
risks (a worsening of hypocalcemia), it has not been well-studied in clinical
or laboratory settings, and the clinical studies have shown that it has little or
no advantage over forced diuresis with 0.9% sodium chloride.8,56,60,61
Mannitol is an osmotic diuretic that inhibits the reabsorption of water and

electrolytes and increases urinary output. Mannitol has been used to treat
rhabdomyolysis,45,60-62 but there is no evidence that it is superior to forced
diuresis, it can cause serious side effects that this patient population is
susceptible to, and compared to forced diuresis its use in this situation is
somewhat complex.45,56,57,61
Loop diuretics should not be routinely used to treat rhabdomyolysis.45,56,57
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Electrolyte abnormalities are a common complication of rhabdomyolysis and
hyperkalemia is particularly dangerous. Hyperkalemia should be treated
promptly and aggressively using standard therapies, i.e., glucose and
insulin.45,57 Calcium supplementation for treating hyperkalemia should be
used cautiously as hypo- and hypercalcemia often accompanies
rhabdomyolysis.
Key Points of Treatment8
• Rhabdomyolysis is a syndrome characterized by a breakdown of skeletal

muscle, elevated serum levels of CK, and renal damage.
• It is usually a self-limiting condition, but rhabdomyolysis can cause death
and serious complications like acute kidney injury (AKI), compartment
syndrome, and electrolyte abnormalities.
• Rhabdomyolysis is caused by direct or indirect injury to skeletal muscle.
• Because of the heterogeneity of the etiologies of rhabdomyolysis and
because mild cases often go undetected, the true incidence of
rhabdomyolysis is not known.
• The etiologies of rhabdomyolysis are traumatic, exertional, and non-
traumatic/non-exertional. Some causes of rhabdomyolysis can feature all
three.
• A significant extent and a long duration of trauma is not required to
cause rhabdomyolysis. Immobility for as little as 20-60 minutes and
injury involving a small amount of skeletal muscle can cause
rhabdomyolysis.
• Exertional rhabdomyolysis can be caused by resistance and aerobic
exercise, it can happen to experienced and inexperienced athletes, and it
may occur after only one or two exercise sessions.
• The causes of non-traumatic/non-exertional rhabdomyolysis are diverse
and heterogenous; clinicians should consider the potential for
19
rhabdomyolysis in any situation that can directly or indirectly cause
damage to skeletal muscles.
• Rhabdomyolysis is diagnosed when the serum CK level is 5-10 times
above the upper limit of normal. The serum CK level does not correlate
well with the risk for developing AKI.
• Myoglobinuria and discolored urine are common signs of rhabdomyolysis
but in many patients these signs are absent or temporary.
• The clinical signs and symptoms of rhabdomyolysis are non-specific; in
many cases the index of suspicion for rhabdomyolysis is more useful for
its detection than a physical examination.
• The primary treatment for rhabdomyolysis is forced diuresis with IV
infusion of 0.9% sodium chloride. Several days of this therapy are often
needed, and patients may require 12-24 liters of IV fluid.
• Early recognition and prompt treatment can ensure a good outcome and
help prevent complications.
• Acute kidney injury is a common complication of rhabdomyolysis and it is
associated with a high mortality rate. There is no reliable way to predict
which cases of rhabdomyolysis will progress to AKI.
Case History Of Rhabdomyolysis
The patient is a 29-year-old male with

a past medical history of opioid use
disorder. He was transported to a local
ER after he was found unresponsive on
the ground in a public area. The
paramedics who provide initial care at
the scene reported that the patient did
not respond to verbal or vigorous
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physical stimulation, and his pupils were 2 mm and non-reactive, blood
pressure was 80/40 mm Hg and his respiratory rate was 6 breaths a minute,
and oxygen saturation measured by pulse oximetry was 83%.
A 2 mg dose of naloxone was administered intra-nasally and, after it was

given, the paramedics reported a temporal improvement in the patient’s
level of consciousness (spontaneous movement) and respiratory rate.
There was no information available about the events prior to the patient’s
discovery and it was not known how long he had been unconscious.
Laboratory test results were reported as:
ABG - 7.20/53/79/18
AST and ALT – 214 and 289 U/L, respectively
BUN - 28 mg/dL
Calcium – 8.0 mg/dL
CK - 13,545 U/L
Creatinine - 0.6 mg/dL
Electrolytes – 142/6.0/114/19
INR - 1.1
Uric acid – 8.2 mg/dL
Nothing was detected in the urine drug screen, the serum acetaminophen,
ethanol, and salicylate tests were negative, and a CT scan of the head and a
12-lead ECG were interpreted as normal. The urine sample tested positive
for myoglobin, and the urine was normal in appearance. The physical
examination was notable for a depressed level of consciousness with a
Glasgow Coma Scale score of 7, and ecchymosis, edema, and swelling of the
left arm.
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Supplemental oxygen via a nasal cannula was started, IV access was
obtained, and after a 0.4 mg IV bolus of naloxone the patient regained
consciousness (although described as being quite drowsy) and informed staff
that he had injected heroin earlier in the evening. Two liters of IV fluid were
infused and subsequent systolic blood pressure measurements were
consistently > 100 mm Hg and the pulse oximetry readings were
consistently ≥ 95%.
The patient was admitted to an intermediate care unit. Forced diuresis with
500 mL/hour of 0.9 sodium chloride was started. Three hours after arrival a
surgeon examined the patient. The patient was complaining of a mild level of
pain in his left arm (2 on a 1-10 scale), but there were no neuro-vascular
abnormalities or deficits. After 24 hours of IV therapy (500 mL/hour for 12
hours, 350 mL/hour for 12 hours) the serum CK level was 18,134 U/L, the
serum creatinine was 0.75 mg/dL, the coagulation studies were normal, the
LFTs had decreased, and no myoglobin was detected in the urine. The
patient’s urine output during that time was 11,250 mL.
Twenty-four hours later the serum CK had decreased to 9877 U/L, the serum
creatinine was 0.7 mg/dL, and the ecchymosis, edema, and swelling in the
left arm had all decreased significantly. A second examination by the
surgeon did not detect evidence of compartment syndrome. Laboratory
testing the next day showed continued improvement, the patient’s physical
examination was unremarkable, and he was discharged to home.
Summary
The classic signs of rhabdomyolysis have been reported as muscle pain and
weakness, and red-brown urine however in many cases all three signs range
from absent, mild intensity to transient. The renal excretion of myoglobin
22
can reach high levels, causing urinary symptoms, although myoglobinuria is
absent in a significant number affected individuals. Other signs and
symptoms, depending on the initiating event, are abnormal blood pressure
and heart rate, altered mental status, fever, malaise, nausea, and vomiting.
The key points of rhabdomyolysis have been raised and elucidated in the
case example above. Acute kidney injury is a common complication of
rhabdomyolysis that carries a high mortality rate. There is no reliable way to
predict which cases of rhabdomyolysis will progress to acute kidney injury.
Clinicians should be aware that with early recognition and prompt treatment,
prevention of complications and a good outcome can occur.
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23

b. reduced serum levels of creatine kinase.
c. reduced excretion of myoglobin by the kidneys.
d. All of the above


b. hepatic failure.
c. decreased urine output.
d. compartment syndrome.

d. All of the above

a. True
b. False
a. appears commonly with people who drink alcohol.

muscles.
c. only occurs due to alcohol withdrawal syndrome.
d. only occurs from acid-base imbalance caused by acute alcohol
intoxication.
24
6. ________________ that causes rhabdomyolysis is a complication
of stimulant intoxication and deliberate overdose of
anticholinergics and monoamine oxidase (MAO) inhibitors.
a. Hypothermia
b. Metabolic myopathies
c. Hyperthermia
d. Infection
7. True or False: Infections caused by rhabdomyolysis is more

common in children than in adults.
a. True
b. False
8. Which of the following signs is always present with

rhabdomyolysis?
a. Muscle pain
b. Muscle weakness
c. Red-brown urine
d. None of the above
9. Cardiac arrest and dysrhythmias can occur as an immediate

complication of rhabdomyolysis if
a. aspartate aminotransferase (AST) is elevated.

b. hypoxia develops.
c. alanine aminotransferase (ALT) is elevated.
d. hepatic dysfunction is present.
10. If a patient has, or is suspected to have rhabdomyolysis, which

of the following laboratory tests or diagnostic screening tests is
mandatory?
a. Arterial or venous blood gas

b. Compartment pressure measurements
c. Myoglobin measurement
d. Liver function tests
25
11. Intravenous fluid resuscitation with a high rate of infusion,
which is often called _______________, is the most important
therapy for a patient who has rhabdomyolysis.
a. rebound diuresis
b. optimal infusion
c. fluid overdose
d. forced diuresis
12. _______________ is defined as an abnormally high tissue

pressure within an anatomical closed space in the body.
a. Compartment syndrome
b. Paresthesia
c. Envenomation
d. Ischemia
13. Rhabdomyolysis, which leads to necrosis of skeletal muscle,

releases intracellular enzymes and proteins into the
bloodstream and the extracellular space, most notably of these
are
a. aspartate aminotransferase and alanine aminotransferase.

b. glycerol and fatty acids.
c. creatine kinase and myoglobin.
d. leucine and glycerol.
14. True or False: Myoglobinuria is present in over 90% of patients

who have rhabdomyolysis.
a. True
b. False
15. Hyperkalemia associated with rhabdomyolysis should be treated

promptly and aggressively by administering
a. alkaline diuresis with bicarbonate.

b. mannitol
c. glucose and insulin.
d. loop diuretics
26
CORRECT ANSWERS:
“Rhabdomyolysis is a syndrome characterized by a breakdown of

skeletal muscle, elevated serum levels of creatine kinase, and renal
damage.”

“Many of the specific initiating causes of rhabdomyolysis; i.e.,

cocaine intoxication, may involve traumatic, exertional, and non-
traumatic/non-exertional mechanisms, and for all the causes of
rhabdomyolysis there is a common end-point, pathologic event –
skeletal muscle damage.”

d. All of the above [correct answer]
“Exertional rhabdomyolysis is caused by intense voluntary or

involuntary skeletal muscle activity, or by a normal level of exercise
that is performed in extreme weather conditions.”

b. False
“Rhabdomyolysis is a commonly encountered condition, but the

etiologies, pathophysiology, and complications of rhabdomyolysis
are complex and even for experienced health clinicians a review of
these can be useful.”
27

muscles.
“Alcohol can cause rhabdomyolysis by one of the following

mechanisms or by a combination of them - a direct toxic effect of
alcohol on the muscles, immobilization subsequent to acute alcohol
intoxication, and acid-base and electrolyte abnormalities caused by
chronic alcohol intake.”
6. ________________ that causes rhabdomyolysis is a complication

of stimulant intoxication and deliberate overdose of
anticholinergics and monoamine oxidase (MAO) inhibitors.
c. Hyperthermia
“Hyperthermia that causes rhabdomyolysis is a complication of

stimulant intoxication and deliberate overdose of anticholinergics
and monoamine oxidase (MAO) inhibitors.”
7. True or False: Infections caused by rhabdomyolysis is more

common in children than in adults.
a. True
“Infections are a common cause of rhabdomyolysis in children; this

is less so in adults.”
8. Which of the following signs is always present with

rhabdomyolysis?
a. Muscle pain
b. Muscle weakness
c. Red-brown urine
d. None of the above [correct answer]
“Muscle pain, muscle weakness, and red-brown urine have been

described as the classic signs of rhabdomyolysis, but the first two
are somewhat subjective in nature and in many cases all three may
be, absent, mild in intensity, or transient.”
28
9. Cardiac arrest and dysrhythmias can occur as an immediate
complication of rhabdomyolysis if
b. hypoxia develops.
“Hyperkalemia is the most immediate complication of

rhabdomyolysis, and if there is a metabolic acidosis, hypocalcemia,
hypoxia, and/or hypovolemia (all of which are commonly seen in
cases of rhabdomyolysis), cardiac arrest and dysrhythmias can
occur. Other complications of rhabdomyolysis are disseminated
intravascular coagulation (DIC) and reversible hepatic dysfunction.
Cell destruction releases of pro-thrombotic substances can cause
DIC, and temporary, reversible elevations of aspartate
aminotransferase (AST) or alanine aminotransferase (ALT) are a
common consequence of rhabdomyolysis.”
10. If a patient has, or is suspected to have rhabdomyolysis, which

of the following laboratory tests or diagnostic screening tests is
mandatory?
c. Myoglobin measurement
“If a patient has, or is suspected to have rhabdomyolysis, certain

laboratory tests and diagnostic screening tests should be done.
Tests marked by an asterisk [] are mandatory; the need for the
others can be determined by the clinical situation and the
underlying cause of the rhabdomyolysis. The following list of
laboratory testing is not all-inclusive. Arterial or venous blood gas;
Blood urea nitrogen and serum creatinine; Coagulation studies;
Compartment pressure measurements; Liver function tests;
Myoglobin measurement....”
11. Intravenous fluid resuscitation with a high rate of infusion,

which is often called _______________, is the most important
therapy for a patient who has rhabdomyolysis.
d. forced diuresis
“Intravenous fluid resuscitation with a high rate of infusion, which is

often called forced diuresis, is the most important therapy for a
patient who has rhabdomyolysis.”
29
12. _______________ is defined as an abnormally high tissue
pressure within an anatomical closed space in the body.
a. Compartment syndrome
“Compartment syndrome is roughly defined as an abnormally high

tissue pressure within an anatomical compartment.”
13. Rhabdomyolysis, which leads to necrosis of skeletal muscle,

releases intracellular enzymes and proteins into the
bloodstream and the extracellular space, most notably of these
are
c. creatine kinase and myoglobin.
“Regardless of the cause, muscle damage results in the influx of

extracellular calcium ions into the intracellular space. The end-
result of the process involved in rhabdomyolysis- necrosis of
skeletal muscle- releases intracellular enzymes and proteins into
the bloodstream and the extracellular space; and, for
rhabdomyolysis, the most notable of these are creatine kinase and
myoglobin.”
14. True or False: Myoglobinuria is present in over 90% of patients

who have rhabdomyolysis.
b. False
“Myoglobin has a short half-life and it is cleared very quickly, and

excessive amounts of myoglobin in the urine, known as
myoglobinuria, is absent in 25% to 50% of patients who have
rhabdomyolysis.”
15. Hyperkalemia associated with rhabdomyolysis should be treated

promptly and aggressively by administering
c. glucose and insulin.
“Hyperkalemia should be treated promptly and aggressively using

standard therapies, i.e., glucose and insulin.”
30
References Section
The References below include published works and in-text citations of

published works that are intended as helpful material for your further
reading.
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2. Stewart IJ, Faulk TI, Sosnov JA, et al. (2016). Rhabdomyolysis among
critically ill combat casualties: Associations with acute kidney injury
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3. Chavez LO, Leon M, Einav S, Varon J. (2016). Beyond muscle
destruction: a systematic review of rhabdomyolysis for clinical
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factors in electrical burns: a review of 101 patients. Burns.
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6. Coban YK. (2014). Rhabdomyolysis, compartment syndrome and
thermal injury. World J Crit Care Med. 2014;3(1):1-7.
7. Tsai WH, Huang ST, Liu WC, et al. (2015). High risk of rhabdomyolysis
and acute kidney injury after traumatic limb compartment syndrome.
Ann Plast Surg. 2015;74 Suppl 2: S158-61.
8. Cervellin G, Comelli I, Benatti M, Sanchis-Gomar F, Bassi A, Lippi G.
(2017). Non-traumatic rhabdomyolysis: Background, laboratory
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9. Karaoren G, Bakan N, Kucuk EV, Gumus E. (2017). Is rhabdomyolysis
an anaesthetic complication in patients undergoing robot-assisted
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10. Rawson ES, Clarkson PM, Tarnopolsky MA. (2017). Perspectives on
exertional rhabdomyolysis. Sports Med. 2017;47(Suppl 1):33-49.
11. Tietze DC, Borchers J. (2014). Exertional rhabdomyolysis in the
athlete: a clinical review. Sports Health. 2014;6(4):336-339.
12. Scalco RS, Snoeck M, Quinlivan R, et al. (2016). Exertional
rhabdomyolysis: physiological response or manifestation of an
underlying myopathy? BMJ Open Sport Exerc Med. 2016 Sep 7;2(1):
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13. Armed Forces Health Surveillance Bureau. Update: Exertional
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31
14. Stanfa MR, Silles NN, Cooper A, et al. (2017). Risk factors for
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15. Luckoor P, Salehi M, Kunadu A. (2017). Exceptionally high creatine
kinase (CK) levels in multi-causal and complicated rhabdomyolysis: A
case report. Am J Case Rep. 2017; 18:746-749.
16. Papadatos SS, Deligiannis G, Bazoukis G, et al. (2015). Nontraumatic
rhabdomyolysis with short-term alcohol intoxication - a case report.
Clin Case Rep. 2015;3(10):769-772.
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Rhabdomyolysis and acute renal failure resulting from alcohol and drug
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18. Janković SR, Stosić JJ, Vucinić S, Vukcević NP, Ercegović GV. (2013).
Causes of rhabdomyolysis in acute poisonings. Vojnosanit Pregl.
2013;70(11):1039-1045.
19. Koubar SH, Estrella MM, Warrier R, et al. (2017). Rhabdomyolysis in
an HIV cohort: epidemiology, causes and outcomes. BMC Nephrol.
2017 Jul 17;18(1):242. doi: 10.1186/s12882-017-0656-9.
20. Mercer S, Hanks L, Ashraf A. (2016). Rhabdomyolysis in pediatric
patients with diabetic ketoacidosis or hyperglycemic hyperosmolar
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2007;187(9):527-528.
22. Shenoi AN, Stockwell J. (2015). Recurrent rhabdomyolysis in a
teenager with psychosis-intermittent hyponatremia-polydipsia
syndrome. Pediatr Emerg Care. 2015;31(4):274-276.
23. Bartlett D. (2017). Drug-induced serotonin syndrome. Crit Care Nurs.
2017;37(1):49-54.
24. Gray RM. (2017). Anesthesia-induced rhabdomyolysis or malignant
hyperthermia: is defining the crisis important? Paediatr Anaesth.
2017;27(5):490-493.
25. Pomerantz WJ, Weiss SL. (2016). Systemic inflammatory response
syndrome (SIRS) and sepsis in children: Definitions, epidemiology,
clinical manifestations, and diagnosis. UpToDate. Retrieved online at
http://www.uptodate.com/contents/systemic-inflammatory-response-
syndrome-sirs-and-sepsis-in-children-definitions-epidemiology-clinical-
manifestations-and-diagnosis.
26. O’Conner, A.D., et al. (2015). Prevalence of rhabdomyolysis in
sympathomimetic toxicity: a comparison of stimulants. J Med Toxicol.
2015;11(2):195-200.
27. Goel N, Pullman JM, Coco M. (2014). Cocaine and kidney injury: a
kaleidoscope of pathology. Clin Kidney J. 2014;7(6):513-517.
32
28. Gannoum M. Goldfarb DS. Renal principles. In: Hoffman RS, Howland
MA, Lewin NP, Nelson LS, Goldfrank L, Flomenbaum NE, eds.
Goldfrank’s Toxicologic Emergencies. 10th ed. New York, NY: McGraw-
Hill Education;2015:356-365.
29. Ramachandran R, Wierzbicki AS. (2017). Statins, muscle disease and
mitochondria. J Clin Med. 2017 Jul 25;6(8). pii: E75. doi:
10.3390/jcm6080075.
30. Nelson KL, Stenehjem D, Driscoll M, Gilcrease GW. (2017). Fatal
statin-induced rhabdomyolysis by possible interaction with palbociclib.
Front Oncol. 2017 Jul 17;7:150. doi: 10.3389/fonc.2017.00150.
eCollection 2017.
31. Rosenson RS, Baker SK. (2016). Statin myopathy. UpToDate. March
11, 2016. https://www.uptodate.com/contents/statin-myopathy.
32. Kim YS, Cha YS, Kim MS, et al. (2017). The usefulness of diffusion-
weighted magnetic resonance imaging performed in the acute phase
as an early predictor of delayed neuropsychiatric sequelae in acute
carbon monoxide poisoning. Hum Exp Toxicol. 2017 Jan
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33. Silva GBD Jr, Vasconcelos AG Jr, Rocha AMT, et al. Acute kidney injury
complicating bee stings - a review. Rev Inst Med Trop Sao Paulo. 2017
Jun 1;59: e25. doi: 10.1590/S1678-9946201759025.
34. Kuzmanovska B, Cvetkovska E, Kuzmanovski I, et al. Rhabdomyolysis
in critically ill surgical patients. Med Arch. 2016;70(4):308-310.
35. Martin HA. Exertional rhabdomyolysis in the pediatric emergency
department: A case review. J Emerg Nurs. 2016;42(6):524-526.
36. Khatri M. (2016). Rhabdomyolysis. DynaMed Plus.
http://www.dynamed.com.online.uchc.edu/topics/dmp~AN~T114269/
Rhabdomyolysis#Diagnosis.
37. Melli, G., et al. (2005). Rhabdomyolysis: an evaluation of 475
hospitalized patients. Medicine (Baltimore). 2005;84(6):377-385.
38. Chen CY, Lin YR, Zhao LL, Yang WC, Chang YJ, Wu HP. Clinical factors
in predicting acute renal failure caused by rhabdomyolysis in the ED.
Am J Emerg Med. 2013;31(7):1062-1066.
39. McMahon GM, Zeng X, Waikar SS. A risk prediction score for kidney
failure or mortality in rhabdomyolysis. JAMA Intern Med.
2013;173(19):1821-1828.
40. Perazella MA. and Rosner MH. (2017). Clinical features and diagnosis
of heme pigment-induced acute kidney injury. UpToDate. August 2,
2017. https://www.uptodate.com/contents/clinical-features-and-
diagnosis-of-heme-pigment-induced-acute-kidney-injury.
41. Miller ML. (2016). Clinical manifestations and diagnosis of
rhabdomyolysis. UpToDate. October 13, 2016.
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http://www.uptodate.com/contents/clinical-manifestations-and-
diagnosis-of-rhabdomyolysis.
42. Safari, S., et al. (2016). The role of scoring systems and urine dipstick
in prediction of rhabdomyolysis-induced acute kidney injury: a
systematic review. Iran J Kidney Dis. 2016;10(3):101-106.
43. Palevesky PM. (2017). Definition and staging criteria of acute kidney
injury in adults. UpToDate. April 7, 2017.
https://www.uptodate.com/contents/definition-and-staging-criteria-of-
acute-kidney-injury-in-adults.
44. Stracciolini A, Hammerberg EM. Acute compartment syndrome of the
extremities. UpToDate. May 23, 2016.
https://www.uptodate.com/contents/acute-compartment-syndrome-
of-the-extremities.
45. Kruger, D. and Han, J. (2017). Assessing acquired rhabdomyolysis in
adults. JAAPA. 2017;30(1):20-26.
46. DeFilippis EM, Kleiman DA, Derman PB, DiFelice GS, Eachempati SR.
[Primary care] Spinning-induced rhabdomyolysis and the risk of
compartment syndrome and acute kidney injury: Two cases and a
review of the literature. Sports Health. 2014;6(4):333–335
47. Aynardi MC, Jones CM. Bilateral upper arm compartment syndrome
after a vigorous cross-training workout. J Shoulder Elbow Surg.
2016;25(3):e 65-e67.
48. Ridha A, Khan A, Al-Abayechi S, Puthenveetil V. Acute compartment
syndrome secondary to rhabdomyolysis in a sickle cell trait patient.
Lancet. 2014 Dec 13;384(9960):2172. doi: 10.1016/S0140-
6736(14)61944-9.
49. Clarissa Samara V, Warner J. Rare case of severe serotonin syndrome
leading to bilateral compartment syndrome. BMJ Case Rep. 2017 Mar
3;2017. pii: bcr2016218842. doi: 10.1136/bcr-2016-218842.
50. Criddle LM. Rhabdomyolysis: pathophysiology, recognition, and
management. Crit Care Nurse. 2003;23(6):14-22, 24-26.
51. Chatzizisis YS, Misirli G, Hatzitolios AI, Giannoglou GD. The syndrome
of rhabdomyolysis: complications and treatment. Eur J Intern Med.
2008; 19(8):568-574.
52. Huerta-Alardín AL, Varon J, Marik PE. Bench-to-bedside review:
Rhabdomyolysis -- an overview for clinicians. Crit Care.
2005;9(2):158-169.
53. Riggs J, Schochet S, Parmar J. Rhabdomyolysis with acute renal failure
and disseminated intravascular coagulation: association with
acetaminophen and ethanol. Mil Med. 1996;161(11):708–709.
54. Weibrecht K, Dayno M, Darling C, Bird SB. Liver aminotransferases are
elevated with rhabdomyolysis in the absence of significant liver injury.
J Med Toxicol. 2010;6(3):294-300.Akmal M, Massry S. Akmal M,
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Massry S. Reversible hepatic dysfunction associated with
rhabdomyolysis. Am J Nephrol. 1990;10(1):49–52
55. Vanholder R, Sever MS. Crush-related acute kidney injury (acute renal
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acute-renal-failure.
56. Perazella MA, Rosner MH. Prevention and treatment of heme pigment-
induced acute kidney injury. UpToDate. August 4, 2017.
https://www.uptodate.com/contents/prevention-and-treatment-of-
heme-pigment-induced-acute-kidney-injury.
57. Petejova N, Martinek A. Acute kidney injury due to rhabdomyolysis and
renal replacement therapy: a critical review. Crit Care. 2014 May
28;18(3):224. doi: 10.1186/cc13897. Review.
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Molecular mechanisms and novel therapeutic approaches to
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RHABDOMYOLYSIS

DANA BARTLETT, BSN, MSN, MA, CSPI

Rhabdomyolysis is often a self-limiting condition that involves the rapid

Continuing Education Credit Designation

Statement of Learning Need

Because rhabdomyolysis is often a self-limiting condition that can range in

To provide health clinicians with knowledge about rhabdomyolysis diagnosis,

Advanced Practice Registered Nurses and Registered Nurses

(Interdisciplinary Health Team Members, including Vocational Nurses and

Course Author & Planning Team Conflict of Interest Disclosures

Acknowledgement of Commercial Support

There is no commercial support for this course.

Please take time to complete a self-assessment of knowledge, on

Opportunity to complete a self-assessment of knowledge learned

a. a breakdown of skeletal muscle.

2. With rhabdomyolysis, regardless of the cause of the condition

a. skeletal muscle damage.

3. Exertional rhabdomyolysis is caused by

a. intense voluntary skeletal muscle activity.

4. True or False: All forms of rhabdomyolysis are rare, uncommon

a. appears commonly with people who drink alcohol.

Rhabdomyolysis is a syndrome characterized by a breakdown of skeletal

There are three primary etiologies of rhabdomyolysis - traumatic, exertional,

event – skeletal muscle damage.

The terms listed below are helpful for understanding rhabdomyolysis.

• Acute Kidney Injury:

A sudden decrease in renal function, characterized by an increase in

Increased tissue pressure in a confined anatomical space that causes

• Creatine Kinase (CK):

An intracellular enzyme that helps form adenosine diphosphate and

The primary intracellular oxygen-transporting molecule.

A set of signs and symptoms that occur together.

Traumatic rhabdomyolysis is a common pathology,2 and it is caused by direct

Prolonged compression to a muscle that leads to rhabdomyolysis is caused

Exertional rhabdomyolysis is caused by intense voluntary or involuntary

Factors that increase the risk of developing exertional rhabdomyolysis

Involuntary muscular activity that causes rhabdomyolysis can be caused by

Causes of non-traumatic/non-exertional rhabdomyolysis are discussed in this

Alcohol use can cause rhabdomyolysis by one of the following mechanisms

Abnormally low levels of calcium, phosphate potassium, and sodium have

Table 2: Electrolytes Disturbances and Rhabdomyolysis

Hypernatremia – Dehydration, diabetes

Hyperthermia that causes rhabdomyolysis is a complication of stimulant

Rhabdomyolysis is a common complication of intoxication from the illicit

Carbon monoxide (CO) poisoning happens to millions of people each year,

Regardless of the cause, muscle damage results in the influx of extracellular

Other mechanisms of injury that complicate rhabdomyolysis and are

What Does Rhabdomyolysis Look Like?

The commonly used urine dipsticks do not distinguish between hemoglobin

An acute elevation of serum CK is the hallmark of rhabdomyolysis.1 Serum

There is no universally accepted level of CK that is used to establish a

The limitations of myoglobin for establishing the diagnosis of rhabdomyolysis

The risk of developing AKI from rhabdomyolysis increases if the myoglobin

Compartment syndrome is roughly defined as an abnormally high tissue

Trauma is the most common cause of compartment syndrome associated

Hyperkalemia is the most immediate complication of rhabdomyolysis, and if

Treatment of a patient who has rhabdomyolysis involves 1) Assessment and

Assessment and Stabilization

If a patient has, or is suspected to have rhabdomyolysis, certain laboratory