MSK Flashcards
(31 cards)
Define rhabdomyolysis
Rhabdomyolysis is a condition characterized by primary (mechanical) or secondary (metabolic) skeletal muscle injury, resulting in cell death and release of potentially toxic substances into circulation.
Primary - direct myocyte injury related to trauma
Metabolic - disturbances affecting
supply of ATP within the myocyte
What is the primary complication of rhabdomyolysis?
AKI
What population of patients are at risk for rhabdomyolysis?
- Large burden of traumatic injury involving muscular
- Vascular injuries or muscle
ischemia with subsequent reperfusion
Describe the pathophysiology of rhabdomyolysis.
Rhabdomyolysis is the result of skeletal muscle breakdown with release of potentially toxic substances such as electrolytes, myoglobin, and sarcoplasmic proteins into circulation.
Kodadek L, Carmichael II SP, Seshadri A, et al. Trauma Surg Acute Care Open 2022;7:e000836.
What are the urine output goals in patients with rhabdomyolysis?
The most commonly cited urine output goals for intravenous fluid rehydration are 1 mL/kg/hour to 3 mL/kg/hour.
What laboratory findings aid in the diagnosis of rhabdomyolysis?
- CK >5× the upper limit of normal or >1000 IU/L
- Myoglobinemia
- Elevated lactate dehydrogenase (LDH)
- Hyperkalemia
- Azotemia (creatinine)
- Elevated aspartate aminotransferase (AST)
- Myoglobininuria
What is the role of RRT in rhabdomyolysis?
There is no role for RRT in rhabdomyolysis to prevent AKI. The utilization of RRT in patients with rhabdomyolysis should be based on traditional indications for AKI and the degree of renal impairment.
What is the goal of early-volume resuscitation in rhabdomyolysis?
- To promote renal tubule flow
- Diluting nephrotoxins such as myoglobin, and
- Supplying adequate renal perfusion to prevent AKI
Describe the half-life of CK in rhabdomyolysis?
CK values may become elevated within 12 hours of injury, peak at 24 to 72 hours, and return to normal in roughly 5 days, depending on the degree of injury and appropriate therapy.
Describe the half-life of myoglobin in rhabdomyolysis?
Myoglobin has a shorter half-life (1-3 hours) than CK, and resolves prior to CK, depreciating its clinical utility.
What are the guideline recommendations for trending CK in rhabdomyolysis?
Interval CK values should be followed until a peak concentration is identified (typically at 24–72 hours), and discontinued once the CK is reliably downtrending.
What patients are at highest risk for rhabdomyolysis?
- Multisystem trauma
- Crush injuries involving the extremities or torso
- Compartment syndrome
What are two conditions that can lead to skeletal muscle injury?
- Ischemia
- Reperfusion injury
Define secondary or metabolic causes of rhabdomyolysis?
Medical conditions that cause increased metabolic demands on myocytes in excess of the available ATP supply.
What are some examples of “secondary” causes of rhabdomyolysis?
- Extreme exertional demands (exercise)
- Exogenous agents:
- Drugs or toxins
- Genetic defects
- Myopathies
- Infections
Is lactated Ringer’s solution or saline recommended for the treatment of rhabdomyolysis? What is the argument for and against their use.
Both are considered safe for the treatment of rhabdomyolysis.
Saline lacks potassium, which could avoid worsening the hyperkalemia associated with rhabdomyolysis. However, resuscitation with normal saline can lead to metabolic acidosis, which can be counterproductive if urine alkalinization is desired.
LRS contains a buffer which can increase urine and serum pH (significantly higher after 12 hours of aggressive resuscitation) leading to significantly less need for bicarbonate administration to achieve goal urine pH.
One study showed no difference between saline and LRS administration, and serum potassium levels. There was also no difference in median time to serum CK <200, which arguably is the most clinically relevant outcome in the study.
Are diuretics and/or bicarbonate administration beneficial?
There is no strong clinical evidence supporting the use of sodium bicarbonate administration and/or mannitol to prevent AKI in rhabdomyolysis.
What are two important contributors in the development of myoglobin-induced renal toxicity?
- Hypovolemia
- Aciduria
What is the hallmark diagnostic finding of rhabdomyolysis-associated AKI?
Pigmented casts, which arise as a result of an interaction between the Tamm-Horsfall protein and myoglobin in an acidic environment.
What are some proposed mechanisms for myoglobin-induced renal injury?
- Tubular obstruction - Pigmented casts formed from an interaction between the Tamm- Horsfall protein and myoglobin in an acidic environment.
- Vasoconstriction- Heme proteins can potentiate renal vasoconstriction, which may have been initiated by hypovolemia and can activate the cytokine cascade.
- Oxidant injury - Heme proteins generating free radicals at a low pH with resultant toxicity to the tubules is what may give way to cast formation.
All lead to decreased glomerular filtration.
Are loop diuretics recommended for the treatment/management of rhabdomyolysis?
There is not sufficient evidence to support the use of loop diuretics.
Pros: Can reduce metabolic demand and oxygen consumption by the proximal tubular cells.
Cons: Can worsen renal afferent arteriole vasoconstriction, acidify urine, promote aggregation of the Tamm- Horsfall protein within the tubular lumen, and cause hypokalemia.
What electrolyte abnormalities should be expected in rhabdomyolysis?
- Hyperkalemia
- Hyperphosphatemia
- Hypocalcemia
- +/- Hypomagnesemia
What are the consequences of hyperphosphatemia in rhabdomyolysis?
- Phosphate binds to calcium and this complex deposits in the soft tissues.
- Inhibits 1α-hydroxylase, which inhibits calcitriol formation and thus limits formation of the active form of vitamin D.
How do you treat hyperphsophatemia in rhabdomyolysis?
Typically decreases as it is excreted in urine. Can consider a calcium chelator, but that can increase precipitation of calcium phosphate in injured muscle.
