Acute Kidney Injury In Adults Secondary to Rhabdomyolysis in Critical Care - Prevention of
|Publication: 04/01/2016 --|
|Last review: 02/04/2019|
|Next review: 02/04/2022|
|Approved By: Trust Clinical Guidelines Group|
|Copyright© Leeds Teaching Hospitals NHS Trust 2019|
This Clinical Guideline is intended for use by healthcare professionals within Leeds unless otherwise stated.
Prevention of Acute Kidney Injury In Adults Secondary to Rhabdomyolysis in Critical Care
This guideline is aimed at preventing acute kidney injury in adults secondary to rhabdomyolysis in the critical care setting. The guideline is aimed at healthcare professionals working in this environment. It is expected that any acutely ill patient in the critical care setting will have their care supervised by a consultant intensivist. The guideline outlines the common causes of rhabdomyolysis, the diagnosis, recommended investigations and management.
Rhabdomyolysis results from skeletal muscle injury and cell lysis with the release of myoglobin and other muscle breakdown products including potassium, phosphate and urate.
There are a number of causes including
- compartment syndrome
- drugs (ecstasy and statins)
Myoglobin is freely filtered by the kidneys and is directly toxic to the tubular epithelial cells (Blanco and Echeverria 2002), particularly in the setting of hypovolaemia and acidosis.
If the urine is acidic myoglobin is more likely to crystallise in the renal tubules contributing to the development of AKI (Block and Manning 2001). A rise in creatine kinase (CK) values may not necessarily have an associated rise in urinary myoglobin (Mikkelsen and Toft 2005).
Investigations supporting a diagnosis of rhabdomyolysis include
- an elevated CK (5x the upper limit of normal)
- an elevated aspartate transaminase (AST)
- presence of urinary myoglobin (urinary myoglobin can be difficult to detect and its absence does not exclude a diagnosis of rhabdomyolysis. It is not routine practice to measure urinary myoglobin in Leeds Teaching Hospitals Trust. It’s measurement is not routinely recommended)
Additional electrolyte abnormalities include
- Hypocalcaemia (binds to myoglobin)
These electrolytes should be monitored initially at least every 12-24 hours
Urea, electrolytes and creatinine
Liver Function Tests
Full blood count
CK level (daily testing until peaked and then three times weekly until returned to normal values).
The principles of management are correction of hypovolaemia and establishment of a good urine output (>100mls/hr) with aggressive fluid resuscitation.
- volume status must be assessed carefully.
- intravenous 0.9 % sodium chloride solution is recommended at a rate of 10-15 mls/kg/hour
- once a good urine output is established (>100mls/hr) and potassium < 5.5mmol/L switch to a balanced crystalloid (e.g. Hartmann’s - contains potassium 5 mmol/L), with continued monitoring of urea, electrolytes and creatinine.
There is additional weak evidence supporting the alkalisation of the urine to reduce the precipitation of myoglobin
- consider adding a separate infusion of intravenous 1.4% sodium bicarbonate at 50mls/hr to maintain a urinary pH >6.5. Increase rate to a maximum of 100mls/hr if the urinary pH fails to rise.
Careful monitoring (every 30 to 60 mins) is required of
- sodium, chloride and pH should be monitored as large volumes of rapidly infused 0.9% sodium chloride can lead to a hyperchloraemic metabolic acidosis.
Stop intravenous fluids if hypernatraemia or a hyperchloraemic metabolic alkalosis develops.
Careful monitoring of
- volume status must initially be performed continuously to assess response to intravenous fluid therapy and to avoid precipitatingpulmonary oedema developing.
If urine output is < 20mls/ hour consider the addition of
- 50 mls of intravenous 20% mannitol (discuss with consultant intensivist)
However there is no evidence that mannitol is superior to aggressive fluid resuscitation in preventing acute kidney injury in the setting of rhabdomyolysis.
Mannitol can be harmful due to the risk of rapid intravascular volume expansion leading to pulmonary oedema and resulting in hyperoncotic kidney injury. Its use should therefore be restricted to the high dependency unit/intensive care unit environment and only after careful evaluation of the patient's volume status and discussion with the consultant intensivist.
Avoid treating hypocalcaemia unless the patient is symptomatic (e.g. perioral/ peripheral paraesthesia, carpopedal spasms, seizures) due to risk of metastatic calcification and further tissue necrosis. Rebound hypercalaemia can occur later following the release of calcium from damaged muscle.
Seek senior medical advice if you are uncertain about management.
To improve the diagnosis and management of rhabdomyolysis in the critical care setting and prevent the development of acute kidney injury (AKI).
These guidelines do not give advice about the management of compartment syndrome; please seek advice from the relevant surgical team if you feel the patient has or is developing compartment syndrome and may require surgical intervention.
Patients with acute kidney injury (AKI) may also require referral to the Renal Team.
Prevention of Acute Kidney Injury In Adults Secondary to Rhabdomyolysis in a critical care setting
|Target patient group:||Applies to any adult patient with known or suspected rhabdomyolysis in a Critical Care setting (Comprehensive Critical Care Department of Health 2000).|
|Target professional group(s):||Secondary Care Doctors
Secondary Care Nurses
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The Scottish Intercollegiate Guidelines Network (SIGN) as recommended by The National Institute of Clinical Excellence (NICE) was used:
A=Meta analysis, randomised controlled trials/systematic reviews of RCT’s
B= Robust experimental or observational studies
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Trust Clinical Guidelines Group
LHP version 1.0
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