Makindo Medical Notes.com

Related Subjects: Acute Kidney Injury |Acute Rhabdomyolysis

Rhabdomyolysis is caused by myoglobin in the tubules and is strongly suggested by the fact that urinalysis is strongly positive for blood, whereas urine microscopy is negative for red blood cells.

Initial Management
ABC, Get IV access and commence fluids. Check CK is at least 1000. A CK > 5000 is regarded as Moderate to severe. Discuss with HDU to optimise diuresis Send FBC, U&E, LFT, Group and hold +/- Lactate, Coagulation Consider Urinary catheter to measure urine output Treat Infection. IV Fluids++, Watch electrolytes. Antibiotics

Conversion

• Ca²⁺: 10 mg/dl = 2.5 umol/L
• Ca²⁺:12 mg/dl = 3.0 umol/L
• Ca²⁺:14 mg/dl = 3.5 umol/L
• Creatinine: 0.8 mg/dl = 70 umol/L
• Creatinine: 1.2 mg/dL = 106 umol/L
• Creatinine: 1.4 mg/dl = 123 umol/L

About

• Damage to striated muscle can lead to Myoglobinuria
• Myoglobin precipitating in the kidney can lead to acute renal failure (AKI)
• Acute Rhabdomyolysis can cause AKI, DIC, ARDS and multiorgan failure
• Damaged muscle also releases the enzyme CK

Aetiology

• Myoglobin (Mb) is a globular protein in skeletal muscle
• In 1958, Max Perutz and John Kendrew determined the 3D structure of Myoglobin by X-ray crystallography
• It is a monomeric protein that has 153 amino acid residues and acts a store of oxygen similar to Hb
• Destruction of 100 g of muscle tissue is capable of inducing Rhabdomyolysis
• Release of excessive myoglobin into the plasma overwhelms the capacity of the binding proteins (mainly haptoglobin)
• Myoglobin then gets filtered across the glomerulus, causing tubular damage
• Myoglobin exerts a direct cytotoxic effect through the enhancement of local oxidative stress in the tubular cells

Causes

• Trauma and crush injuries
• Falls and lying on the floor for prolonged periods
• Severe exercise, Generalised seizures
• Neuroleptic malignant syndrome (NMS), Malignant hyperthermia
• Cocaine and heroin, Alcohol, Methanol, Ethylene glycol
• Carbon Monoxide poisoning
• Ischaemic limb with muscle necrosis
• Polymyositis, Statins +/- Fibrates, Hypokalaemia
• Snake bites, Compartment syndrome
• Muscle genetic disorders - carnitine deficiency
• Caffeine, Aspirin, Hypokalaemia, Hypophosphatemia
• Diabetic ketoacidosis and HONK
• Sepsis with bacterial infections

Clinical

• Muscles can be tender and swollen and painful
• There can be skin changes indicating pressure necrosis.
• Muscle pain, weakness and dark urine, Cause may be apparent
• Evidence of trauma or falls, Family history
• Drug history - neuroleptics
• Fever, increased tone, fever - NMS
• Tea coloured brown urine usually correlates with a urine myoglobin level

Investigations

• Urinalysis: positive for blood. Positive urinalysis is caused by myoglobin, a muscle protein released during muscle damage; this appears in the urine and can cause acute renal failure.
• Urea/Creatinine high with AKI
• High CK x 5 upper limit of normal IU/L
  • Normal CK (CK ~40-200 U/L).
  • Mild rhabdomyolysis (CK 1,000-5,000 U/L) Low risk for AKI
  • Moderate rhabdomyolysis (CK 5,000-15,000 U/L). Risk of AKI. Treatment is indicated.
  • Severe rhabdomyolysis (CK >15,000 U/L) Risk of dialysis. Treatment is indicated
• Raised LDH, AST, Aldolase, Myoglobin and other muscle enzymes
• Creatinine and Myoglobin in urine
• Low Calcium Ca²⁺, Low Phosphate, Low Potassium
• Magnetic resonance imaging can be useful to identify muscle damage
• ECG and Troponin if myocardial injury suspected

McMahon Score (≧6 indicates risk of renal failure)

• Age:
  • <50 = zero points.
  • 51-70 = 1.5 point.
  • 71-80 = 2.5 points.
  • >80 = 3 points.
• Female sex: 1 point.
• Initial creatinine:
  • <1.4 mg/dL (<124 uM) = 0 points.
  • 1.4-2.2 mg/dL (124-195 uM) = 1.5 points.
  • >2.2 mg/dL (195 uM) = 3 points.
• Initial calcium <7.5 mg/dL (1.88 mM) = 2 points.
• Initial phosphate:
  • <4 mg/dL (1 mM) = zero points.
  • 4-5.4 mg/dL (1-1.4 mM) = 1.5 points.
  • >5.4 mg/dL (>1.4 mM) = 3 points.
• Initial bicarbonate <19 mM = 2 points.
• Initial CK >40,000 U/L = 2 points.
• Rhabdomyolysis NOT caused by seizure, syncope, exercise, statins, or myositis: 3 points.

Management

• ABC, treat any hyperkalaemia, hypovolaemia, analgesia.
• Early treatment (ideally<6 hours from onset) is needed with volume expansion to generate a diuresis of all non-overloaded patients along with avoidance of nephrotoxins. There is insufficient data to recommend any specific fluid. The mortality rate ranges from 10% to up to 50% with severe AKI. Myoglobin is normally bound to plasma globulins, and has a rapid renal clearance with a half-life of 2-3 hours. In RML, the level of myoglobin in the serum increases within 1–3 h, reaches its peak in 8–12 h, and then returns to normal within 24 h after the onset of the injury.
• Current guidelines suggest against the routine use of alkalinisation with sodium bicarbonate. The long-term fall in estimated glomerular filtration rate (eGFR) correlated to serum phosphate and myoglobin (>8,000U/L) at admission. Myoglobin which is compatible with convective removal, can be transported to the filtrate by continuous and haemofiltration
• Catheterisation may be needed if difficulty passing urine or measuring output or retention and establish a good diuresis (200-300 ml/hr) with IV fluids
• Bromocriptine or Dantrolene in the case of NMS
• Fasciotomy for any compartment syndrome
• Plastics review for any skin damage needing debridement or grafting
• Revascularization for limb ischaemia
• Nephrology consults for deteriorating renal function

References

• Review article