11/14/24, 10\:45 AM Rhabdomyolysis

Rhabdomyolysis

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Rhabdomyolysis\: characterised by breakdown of skeletal muscle cells (myocytes) and release of intracellular contents into
circulation, potentially causing acute kidney injury (AKI) and life-threatening electrolyte disturbances.
Aetiology\: Traumatic (crush injuries, prolonged immobilisation) and non-traumatic (extreme exertion, surgery, drugs like
statins, infections, inherited disorders like muscular dystrophy).
Pathophysiology\: Myocyte necrosis releases creatine kinase (CK), myoglobin, urate, and electrolytes (potassium,
phosphate). Myoglobin in blood can lead to AKI by causing tubular obstruction in kidneys.
Risk factors\: male sex, BMI >40, chronic use of lipid-lowering medications (e.g., statins).
Clinical features\: variable and non-speci
(myoglobinuria). Important to identify potential triggers like falls, extreme exercise, new medications.
Investigations\:
Bedside\: urinalysis (false positive for haematuria), ECG (assess for hyperkalaemia), blood gas (metabolic acidosis).
Laboratory\: serum creatine kinase (CK >5x normal), U&E (assess for AKI, hyperkalaemia), liver function tests (elevated
AST/ALT), bone pro
Management\:
IV
urine output.
Electrolyte management\: initial acute management of hyperkalaemia (IV calcium, insulin-glucose infusion), withholding
drugs that increase serum potassium.
Other\: severe cases may require IV sodium bicarbonate and emergency renal replacement therapy.
Complications\: AKI (may require renal replacement therapy), electrolyte disturbances, disseminated intravascular
coagulation (DIC).
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Introduction

Rhabdomyolysis is a clinical syndrome characterised by the breakdown of skeletal muscle cells (myocytes) and the
1
subsequent release of intracellular contents into the circulation. This can result in acute kidney injury (AKI) and life-
threatening electrolyte disturbances.

Aetiology

A variety of factors can trigger skeletal muscle breakdown.
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Traumatic factors include\:
Crush injuries
Prolonged immobilisation
Non-traumatic factors include\:
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Extreme exertion\: including prolonged seizures (status epilepticus)
Surgery\: due to prolonged immobilisation or direct muscle ischemia
Drugs\: statins, antipsychotic medications, illicit drugs
Infections
Inherited disorders\: muscular dystrophy
Pathophysiology
bloodstream.
Regardless of the underlying cause, myocyte cell death (necrosis) releases previously intracellular material into the
Key intracellular components released include creatine kinase (CK), myoglobin, urate and electrolytes (potassium,
phosphate).
Release of myoglobin into the bloodstream is particularly important, as this is the mechanism by which acute kidney injury
(AKI) can develop. The kidneys
within the renal tubules, causing tubular obstruction.
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When the kidney's
homeostatic functions of the kidney are impaired.

Risk factors

Risk factors for rhabdomyolysis include\:
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Male sex
Body mass index (BMI) >40
Chronic use of lipid-lowering medications (e.g. statins)

Clinical features

History
The history of rhabdomyolysis is variable and non-speci
Malaise
Myalgias
Muscle weakness
It is important to identify any potential triggers of rhabdomyolysis, including\:
Fall with a 'long lie' (common in elderly populations)
Extreme recent exercise
Initiation of new medications / illicit drugs
Clinical examination
There are few speci
trauma.
Patients may develop ‘tea-coloured urine’ caused by myoglobin in the urine (myoglobinuria).
Figure 1. Tea-coloured urine in
rhabdomyolysis due to myoglobinuria.
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Investigations

Bedside investigations
Relevant bedside investigations include\:
Urinalysis\: myoglobin in the urine produces a false positive result for haematuria. Although the dipstick will show
haematuria, no red blood cells will be present on high-powered microscopy when the laboratory examines the urine.
ECG\: to assess for signs of life-threatening complications, such as hyperkalaemia.
Blood gas (ABG/VBG)\: metabolic acidosis with a raised anion gap.
Laboratory investigations
Relevant laboratory investigations include\:
Serum creatine kinase\: essential for diagnosing rhabdomyolysis, usually >5x normal limits.
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U&E\: assess for the presence of AKI and identify hyperkalaemia.
Liver function tests\: elevated transaminases (AST/ALT) are a non-speci
Bone pro
associated with signi

Management

Initial management of rhabdomyolysis involves rehydration with intravenous
and close monitoring of electrolytes.
Intravenous
IV
and kidney toxicity.
5
Prompt administration of IV
high urine output.
Management of electrolyte disturbances
The most acute, life-threatening complication of rhabdomyolysis is hyperkalaemia.
Initial acute management of hyperkalaemia involves\:
Stabilising the myocardium (intravenous calcium)
Shifting potassium intracellularly (insulin-glucose infusion)
Drugs which can increase serum potassium should be withheld. For more information, see the Geeky Medics guide to
managing hyperkalaemia.
Hyperphosphataemia and hypocalcemia usually will not require speci
falls.
Other management
In severe cases, specialist treatments include IV sodium bicarbonate to alkalinise the urinary
myoglobin precipitation. 6
Occasionally, patients with severe acute kidney injury require emergency renal replacement
therapy.

Complications

Complications of rhabdomyolysis include\:
Acute kidney injury (may require renal replacement therapy if severe)
Electrolyte disturbances
Disseminated intravascular coagulation
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References

Patient.info Torres PA, from [LINK]
Professional. Helmstetter JA, R h a b d o m y o l y s i s a n d M y o g l o b i n u r i a . September Kaye AM, et al; R h a b d o m y o l y s i s \: p a t h o g e n e s i s , 2021. Available from\: [LINK]
d i a g n o s i s , a n d t r e a t m e n t . Spring 2015. Available
UpToDate. [LINK].
C l i n i c a l f e a t u r e s a n d d i a g n o s i s o f h e m e p i g m e n t-i n d u c e d a c u t e k i d n e y i n j u r y . November 2021. Available from
UpToDate. R h a b d o m y o l y s i s \: E p i d e m i o l o g y a n d e t i o l o g y . January 2023. Available from [LINK].
BMJ Best Practice. R h a b d o m y o l y s i s . November 2022. Available from\: [LINK].
UpToDate. P r e v e n t i o n a n d t r e a t m e n t o f h e m e p i gm e n t-i n d u c e d a c u t e k i d n e y i n j u r y ( i n c l u d i n g r h a b d o m y o l y s i s ) . January
2023. Available from\: [LINK].

Related notes

Acute Kidney Injury (AKI)
Chronic Kidney Disease (CKD)
Glomerular Disease (Glomerulonephropathies)
Haemodialysis
Henoch-Schönlein Purpura (IgA Vasculitis)

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Contents

Introduction
Aetiology
Risk factors
Clinical features
Investigations
Management
Complications
Source\: geekymedics.com
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