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RHABDOMYOLYSIS AND
CRUSH SYNDROME
PRESENTER; DR. BAHATI JAMES
EM RESIDENT YR3
FACILITATOR; DR. PIUS NJINGO
EM SPECIALIST
LAYOUT
•BACKGROUND
•PATHOPHYSIOLOGY
•DIAGNOSIS
•TREATMENT
•COMPLICATION
•DISPOSITION
BACKGROUND
Crush
syndrome
•Crush injury vs crush syndrome
Epidemiology of rhabdomyolysis
In USA 25000 cases
per year
More common in
Adults, male
African American
race, above 60years
In children up to
30% due to
infection
Prevalence of AKI in
rhabdomyolysis is 5
to 30%
AKI from
rhabdomyolysis
constitute 15% of
all cases of AKI
Limited data in
Africa and Sub-
saharan Africa
CAUSES OF
RHABDOMYOLYSIS
Pathophysiology
of
rhabdomyolysis
Presentation
Differential diagnosis
Hypothermia.
Malignant hyperthermia.
Neuroleptic malignant syndrome.
Sepsis.
Inflammatory myositis.
Guillain- Barré syndrome.
Hyperosmolar conditions.
Diagnosis
Role of histopathology in Rhabdomyolysis
• Muscle biopsy is crucial for identifying metabolic myopathies
in rhabdomyolysis patients.
• It is recommended to be performed after complete recovery,
as excessive muscle fiber necrosis may miss underlying
myopathy.
• Specific stains, such as para-aortic acid Schiff, hematoxylin
and eosin, and SDH, can help identify glycogen storage
disorders, mitochondrial myopathies, and enzyme
deficiencies.
CPK ISOENZYMES
• Normal CPK levels are 20 to 200 IU/L.
• Elevated levels, usually at least five times the upper limit of normal, are considered
rhabdomyolysis.
• CPK exists in four significant iso-enzymes: CK-MM, CK-MB1 &2, and CK-BB.
• The CK-MM is specific for skeletal muscle, CK-MB 1 and 2 are specific for cardiac
muscle, and CK BB for the brain.
• Its half-life is 36 hours.
• Serum CPK levels begin to rise within 2 to 12 hours after the injury and peak within 1 to
5 days.
• It declines after 3 to 5 days in the absence of muscle injury.
• Suspect continued muscle injury and compartment syndrome in cases of Persistently
elevated CPK level
McMahon score
to predict death
or dialysis need in
rhabdomyolysis
Management
• Little differences between traumatic and non
traumatic
1. Early rehydration; 1Lt/hr in 2hrs then
500mls/hr
2. Urine alkalization; 50meq of NaHCO3 in half
saline infusion
3. Mannitol infusion in crush injury; 60mls in
5min then reassess urine output increase 30
to 50mls from baseline warrant additional
mannitol
4. Oral polystyrene and sorbitol potassium
binders; controversial
5. Hemodialysis; If all conservatives have failed
6. Hyperbaric oxygen therapy; controversial
Complication of Rhabdomyolysis
• Acute kidney injury
• Electrolyte abnormalities
• Arrhythmias
• Compartment syndrome
• Disseminated intravascular coagulation
• End-stage renal disease requiring renal replacement
therapy
• Infections from a prolonged hospital stay
Consultations and Disposition
Acute rhabdomyolysis patients, both traumatic and non traumatic, with AKI,
hyperkalemia, compartment syndrome, hypotension, and arrhythmias,
should be admitted to the ICU
May require ventilatory support.
Consulting critical care, nephrologist, trauma surgeon, vascular surgeon, or
orthopedic surgeon may be needed depending on the severity and cause of
rhabdomyolysis
PROGNOSIS
varies depending on
the underlying cause.
However, even with
AKI, most patients have
favorable outcomes
with complete recovery
of kidney function
Traumatic
rhabdomyolysis has
poor prognosis
Poor outcome if
admitted in ICU and
those with significant
elevated CPK
Without AKI
mortality is up to
20%
Concurrent with AKI
mortality is up to
50%
References
1.Rosen’s emergency medicine: concepts and clinical practice, tenth edition, Vol
2, July 2022
2. Tintinalli's Emergency Medicine A Comprehensive Study Guide, 9th edition
Tintinalli, Ma, Yealy, Meckler, Stapczynski, Cline, and Thomas ISBN: 1260019934,
Available October 2019
3. Stanley M, Chippa V, Aeddula NR, et al. Rhabdomyolysis. [Updated 2023 Apr
16]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-.
Available from: https://www.ncbi.nlm.nih.gov/books/NBK448168
NDILUMBA HILO

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RHABDOMYOLYSIS BY DR BAHATI JAMES MSIGE.pptx

  • 1. RHABDOMYOLYSIS AND CRUSH SYNDROME PRESENTER; DR. BAHATI JAMES EM RESIDENT YR3 FACILITATOR; DR. PIUS NJINGO EM SPECIALIST
  • 5. Epidemiology of rhabdomyolysis In USA 25000 cases per year More common in Adults, male African American race, above 60years In children up to 30% due to infection Prevalence of AKI in rhabdomyolysis is 5 to 30% AKI from rhabdomyolysis constitute 15% of all cases of AKI Limited data in Africa and Sub- saharan Africa
  • 9. Differential diagnosis Hypothermia. Malignant hyperthermia. Neuroleptic malignant syndrome. Sepsis. Inflammatory myositis. Guillain- Barré syndrome. Hyperosmolar conditions.
  • 11. Role of histopathology in Rhabdomyolysis • Muscle biopsy is crucial for identifying metabolic myopathies in rhabdomyolysis patients. • It is recommended to be performed after complete recovery, as excessive muscle fiber necrosis may miss underlying myopathy. • Specific stains, such as para-aortic acid Schiff, hematoxylin and eosin, and SDH, can help identify glycogen storage disorders, mitochondrial myopathies, and enzyme deficiencies.
  • 12. CPK ISOENZYMES • Normal CPK levels are 20 to 200 IU/L. • Elevated levels, usually at least five times the upper limit of normal, are considered rhabdomyolysis. • CPK exists in four significant iso-enzymes: CK-MM, CK-MB1 &2, and CK-BB. • The CK-MM is specific for skeletal muscle, CK-MB 1 and 2 are specific for cardiac muscle, and CK BB for the brain. • Its half-life is 36 hours. • Serum CPK levels begin to rise within 2 to 12 hours after the injury and peak within 1 to 5 days. • It declines after 3 to 5 days in the absence of muscle injury. • Suspect continued muscle injury and compartment syndrome in cases of Persistently elevated CPK level
  • 13.
  • 14. McMahon score to predict death or dialysis need in rhabdomyolysis
  • 15. Management • Little differences between traumatic and non traumatic 1. Early rehydration; 1Lt/hr in 2hrs then 500mls/hr 2. Urine alkalization; 50meq of NaHCO3 in half saline infusion 3. Mannitol infusion in crush injury; 60mls in 5min then reassess urine output increase 30 to 50mls from baseline warrant additional mannitol 4. Oral polystyrene and sorbitol potassium binders; controversial 5. Hemodialysis; If all conservatives have failed 6. Hyperbaric oxygen therapy; controversial
  • 16. Complication of Rhabdomyolysis • Acute kidney injury • Electrolyte abnormalities • Arrhythmias • Compartment syndrome • Disseminated intravascular coagulation • End-stage renal disease requiring renal replacement therapy • Infections from a prolonged hospital stay
  • 17. Consultations and Disposition Acute rhabdomyolysis patients, both traumatic and non traumatic, with AKI, hyperkalemia, compartment syndrome, hypotension, and arrhythmias, should be admitted to the ICU May require ventilatory support. Consulting critical care, nephrologist, trauma surgeon, vascular surgeon, or orthopedic surgeon may be needed depending on the severity and cause of rhabdomyolysis
  • 18. PROGNOSIS varies depending on the underlying cause. However, even with AKI, most patients have favorable outcomes with complete recovery of kidney function Traumatic rhabdomyolysis has poor prognosis Poor outcome if admitted in ICU and those with significant elevated CPK Without AKI mortality is up to 20% Concurrent with AKI mortality is up to 50%
  • 19. References 1.Rosen’s emergency medicine: concepts and clinical practice, tenth edition, Vol 2, July 2022 2. Tintinalli's Emergency Medicine A Comprehensive Study Guide, 9th edition Tintinalli, Ma, Yealy, Meckler, Stapczynski, Cline, and Thomas ISBN: 1260019934, Available October 2019 3. Stanley M, Chippa V, Aeddula NR, et al. Rhabdomyolysis. [Updated 2023 Apr 16]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK448168

Editor's Notes

  1. Rhabdomyolysis means dissolution of skeletal muscle, and it is characterized by leakage of muscle cell contents, myoglobin, sarcoplasmic proteins (creatine kinase, lactate dehydrogenase, aldolase, alanine, and aspartate aminotransferase), and electrolytes into the extracellular fluid and the circulation Conclusion: At present, we recommend a clinical syndrome of acute muscle weakness, myalgia, and muscle swelling combined with a CK cut-off value of > 1000 IU/L/ or CK > 5 × ULN for the standard definition of a mild RML. Additionally measured myoglobinuria and AKI indicate a severe type of RML. Exclusion criteria as well as the chronological sequence need to be considered for a conclusive RML definition
  2. Crush Injury: Compression of extremities or other parts of the body that causes muscle swelling and/or neurological disturbances. Crush Syndrome: Crush injury with systemic manifestations. Systemic manifestations are caused by a traumatic rhabdomyolysis due to muscle reperfusion injury when compressive forces on the tissues are released cause local tissue injury, organ dysfunction, and metabolic abnormalities, including acidosis, hyperkalemia, and hypocalcemia Triad of diagnosis; muscle mass involvement, prolonged compression 4-6hrs and compromised local circulation Scapellato S, Maria S, Castorina G, Sciuto G. Sindrome da schiacciamento [Crush syndrome]. Minerva Chir. 2007 Aug;62(4):285-92. Italian. PMID: 17641588.
  3. The etiology of rhabdomyolysis can be classified as traumatic due to compressional injury and non traumatic due to oxygen supply demand mismatch. Important causes of traumatic rhabdomyolysis are crush syndrome from accidents, earthquakes, burns, and other natural and manufactured disasters. Not every muscle trauma leads to rhabdomyolysis and renal failure. Alternative causes for acute renal failure like dehydration, sepsis, should always be evaluated. Seizures, alcohol use, drugs, prolonged bedridden state are common causes of non traumatic rhabdomyolysis
  4. -Traumatic or non-traumatic breakdown of muscle cells causing injury results in increased calcium intracellularly as ATP is depleted. -Increased calcium levels activates proteases, skeletal muscle contractility, mitochondrial dysfunction and reactive oxidases which further cause muscular necrosis. -This results in release of intra-cellular constituents; myoglobin, electrolytes, proteins like creatinine kinase.
  5. Overall in the literature, symptoms of rhabdomyolysis are uncommon: -Muscle pain (23% of patients), swelling, or cramping. -Muscle weakness (12% of patients). -Muscle swelling -coca cola like urine Stahl K, Rastelli E, Schoser B. A systematic review on the definition of rhabdomyolysis. J Neurol. 2020 Apr;267(4):877-882. doi: 10.1007/s00415-019-09185-4. Epub 2019 Jan 7. PMID: 30617905.
  6. Lab clues to rhabdomyolysis; POC Electrolytes, Uric acid, Poc urinalysis, POC ABG, LFT, RFT, total CK, FBP, Coagulation profile , Poc Ecg; risk for dysrhythmias Performance of urinalysis for diagnosis of rhabdomyolysis: The sensitivity of a heme-positive urine is good (>90%)
  7. Conclusions: The findings of this systematic review showed that based on the available resources, using the prediction rules and urine dipstick could be considered as valuable screening tools for detection of patients at risk for AKI following rhabdomyolysis. Yet, the external validity of the mentioned tools should be assessed before their general application in routine practice
  8. Predicts mortality or acute kidney injury in rhabdomyolysis patients Used in patients with more than 18yrs old Mostly CPK >5000U/L within 72 hrs Not for use in preexisting ESRD,CPK raised to MI Sensitivity is 86% LOW CORE means low risk do serial cpk levels, perform Reno protective therapy Indication for dialysis Refractory hyperkalemia, uncontrolled metabolic acidosis, and uremia, anuria or oliguria despite volume expansion
  9. Fluid choice??, dns provide depleted ATP with source of energy, and minimize hyperkalemia, isotonic saline, stop when clear urine, CPK down trending Urine alkalization; prevents myoglobin precipitation to DCT, Decrease uric and potassium levels, correct metabolic acidosis Prerequisities; confirm absence of alkalosis, and should have good urine output., Goal ph 7.5 serum and urine 6.5, caution NaHCO3 cause decrease of Ca2+ levels may present with seizures and tetany Stop mannitol if AKI, Need of NaHCO3 because of pigment induced Kidney injury