RHABDOMYOLYSIS

Introduction/Definition
It is a syndrome characterized by muscle necrosis and
release of intracellular muscle constituents into the
circulation.

It is characterized clinically by myalgias, muscle

weakness and red-brown urine due to myoglobinuria,
elevated serum muscle enzymes (creatinine Kinase-
CK)
Epidemiology
True incidence is unknown mainly due to high
variable presentation, under recognition and
reporting mild cases due to lack of formal clinical
definitions..
In the USA approximately 2600 cases of
rhabdomyolysis is reported every year.
It occurs in 85% of pts with traumatic injury.
It is estimated 10-40% of patients with
rhabdomyolysis develop AKI with 20% mortality rate.
The incidence of rhabdomyolysis is higher in males
than females.
Risk factors
• Male sex
• Black race
• Age<10 years and < 60 years
• Body mass index >40kg/m²
• Hx of prior heat injury
• Low premorbid physical fitness
• Chronic use of lipid lowering drugs
• Dehydration
Etiology of rhabdomyolysis
It is classified into three :
• Trauma or direct muscle injury causes

• Nontraumatic exertional causes

• Nontraumatic nonexertional causes

Trauma/direct muscle injury causes
• Crush syndrome -direct muscle trauma, injury or
compression
• Prolonged immobilization
• Compression of blood vessels
• Surgery
• Compartment syndrome
• Electrical injury
• Severe burn injury
• Physical restraint
2. Nontraumatic exertional causes
• It occurs when energy supply to the muscles is
insufficient to meet demands
• Physical exertion and excercise e.g hypokalemia
caused by K+ loss from sweating reduce vascular
perfusion of the muscles
• Seizures and hyperkinetic states
• Inherited disorders e.g lipid metabolism disorders,
muscular dystrophies and congenital myopathies.
• Thermal extremes and dysregulation e.g malignant
hyperthermia, hot environments, hypothermia.
• Neuroleptic malignant syndrome -high fever
develop after exposure to neuroleptic drugs.
3. Nontraumatic nonexertional causes
• Drugs e.g statins, antipsychotics, antihistamines
• Drugs of abuse e.g cocaine, heroin, methadone
• Toxins e.g metabolic poison-CO2, snake & insect
venoms, mushroom poisoning
• Infections eg viral ( HIV, CMV), Bacterial
(salmonella, streptococcus), others: malaria
• Electrolyte disorders e.g hypokalemia,
hypophosphatemia, hypocalcemia, hyponatremia
• Endocrine disorders e.g DKA
• Inflammatory myopathies
• Sickle cell trait.
Pathophysiology
The pathophysiology revolves around direct monocyte
injury, failure of energy supply within muscle cells,
muscle cell hypoxia, electrolyte imbalance which causes
perturbation of Na+/K+ pump.
During normal muscle physiology at rest,ion channels
including Na+/K+ pump and Na+/Ca²+ exchangers
located on the plasma membrane (sarcolemma),
maintain low intracellular Na+ and Ca²+ concentration
and high K+ concentration within the muscle fibre.
Muscle depolarization results in an influx of Ca²+ from
the reserves stores in the sarcoplasmic reticulum into
the cytoplasm through actin-myosin cross-linking.
Ctn
All theses process depends on the availability of
sufficient energy from adenosine triphosphate (ATP),
therefore any insult that damage ion channels
through myosite injury or depletes ATP will cause
disruption in proper balance of intracellular
electrolyte concentrations.
When muscle injury or ATP depletion occurs,it results
into excessive intracellular influx of Na+ and Ca²+
Increase in intracellular Na+ draws water into the cell
and disrupts integrity of intracellular space.
The prolonged presence of high Ca²+ levels
intracellularly leads to myofibrilar concentration
which depletes ATP.
Ctn
Also elevation of Ca²+ activates Ca²+dependent
protease and phosphalipases promoting lysis of the
cellular membrane damaging the ion channels.
The end result of these alterations within muscle cell
milieu is an inflammatory, self -sustaining myolytic
cascade that cause necrosis of muscle fibres and
release muscle cell content into extracellular space
and blood stream.
These contents include K+, Phosphate, CK and
myoglobin.
Exces Myoglobin may cause renal tubular obstruction,
direct nephrotoxicity (ischemia and tubular injury),
intrarenal vasoconstriction and AKI.
Clinical manifestation
The classic triad comprises the following;
• Myalgia
• Generalized weakness
• Dark urine
• Additional non specific symptoms
• Fever
• Nausea
• Vomiting
Hx of the patient
• Alcohol use and resultant unresponsiveness
• Illicit drug use
• Use of prescribed medications
• Heatstroke
• Infection
• Trauma
• Metabolic disorders
• Inflammatory myopathies
Physical findings
• Muscle pain and tenderness
• Decreased muscle strength
• Soft tissue swelling
• Skin changes consistent with pressure necrosis
• Hypothermia, hyperthermia and electrical injuries
• Crush injuries/ deformities of long bones.
Diagnosis
1. Laboratory tests
• CBC- Hb, hematocrit and platelets
• Prothrombin time (PT)
• Activated partial thromboplastin time (aPPT)
• Serum aldolase
• Lactate dehydrogenase (LDH)
• Cardiac troponin 1
• Creatinine Kinase-CK (most reliable and sensitive
indicator of muscle injury)
• Urine myoglobin
• Serum chemistries (UECS, Ca²+, K+,PO4 BUN, LFTs, uric
acid
Imaging studies ( has a minimal role)
• Radioly-suspected fracture
• CT scan of head - altered sensorium, significant
head trauma,seizure, neurologic deficit of
unknown origin
• MRI - assessment of myopathy
• Other tests;
• ECG- monitor effects of hyperkalemia
• Measurement of compartment pressures
• Muscle biopsy
• Immunoblotting and genetic studies
Differential diagnosis
• AKI
• Drug induced mtopy
• Infectious myositis
• Malignant hyperthermia
• Hypothyroidism
• Trauma/ crush injuries
• Metabolic myopathies
Management
1. Medical management
• Assessment of ABC
• Identification and correction of inciting cause
• Fluid resuscitation, monitor input output
• Institution of measures to prevent AKI i.e urinary
alkalization(sodium bicarbonate), loop diuretics,
mannitol.
• Correction of electrolyte, acid-base and metabolic
abnormalities.
Other medical measures
• Dialysis if indicated(AEIOU)
• Use of free radical scavengers and antioxidants
• Discontinuance of any inciting myotoxic agents.
• Mgx depending on the cause i.e;
• Intracompartmental pressure>30 mmHg
fasciotomy is advocated
• Limb fracture requires surgical and orthopedic
treatment
Prevention/ Lifestyle related treatment measures
• Avoidance of strenuous activities that cause
recurrent myalgias, myopathy or rhabdomyolysis
• Maintenance of proper hydration during athletic
exertion.
• Dietary modification helps address metabolic
disorders or inborn errors of metabolism.
• Prompt attention to indicators of heat exhaustion
during hot and humid conditions
• Alcohol be avoided and proper mental health drug
rehabilitation
• Compliance with seizure/ asthma drugs, reduce
status epilepticus and status asthmaticus.
Complications of Rhabdomyolysis
• AKI
• Compartment syndrome
• Disseminated intravascular coagulation
• Electrolyte abnormalities
• Hyperuricemia
• Hypoalbuminemia
• Hypovo
Prognosis
The overall mortality for patients with
rhabdomyolysis is approximately 5%, however the
risk of death is dependant on the underlying cause
and any existing cormobidities.
Rapid intervention and appropriate supportive
treatment of Rhabdomyolysis related kidney injury
and renal failure improves outcome in traumatic
crush injuries.
Thank you!!
By
Hellen Kadesa