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  
Clinical Guideline
CURRENT 
ID: 4438 
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.
For healthcare professionals in other trusts, please ensure that you consult relevant local and national guidance.

Prevention of Acute Kidney Injury In Adults Secondary to Rhabdomyolysis in Critical Care

Summary

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.

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Background

Pathophysiology

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

  • trauma
  • burns
  • 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).

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Diagnosis

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

  • Hyperkalaemia
  • Hyperphosphataemia
  • Hyperuricaemia
  • Hypocalcaemia (binds to myoglobin)

These electrolytes should be monitored initially at least every 12-24 hours

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Investigation

Urea, electrolytes and creatinine
Bicarbonate
Calcium, phosphate
Liver Function Tests
Full blood count
Coagulation screen
CK level (daily testing until peaked and then three times weekly until returned to normal values).
Urinary pH

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Treatment / Management

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.

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Provenance

Record: 4438
Objective:

Aims

To improve the diagnosis and management of rhabdomyolysis in the critical care setting and prevent the development of acute kidney injury (AKI).

Objectives

  • To provide timely treatment of rhabdomyolysis to prevent AKI
  • To provide patients and practitioners with graded evidence based care
  • To enable management to be audited

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.

Clinical condition:

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
Adapted from:

Evidence base

Better O.S. Rubinstein, and Ries N. (2003). Muscle crush compartment syndrome; Fulminant local oedema with threatening systemic effects. Kidney International. 63, 1155-1157.  (c)

Blanco J.R. and Echeverria L. (2002). Rhabdomyolysis of infectious and non- infectious causes. South Medical Journal. 95 (5) 542-544.http://www.medscape.com/viewarticle/433872_1. accessed on 03/12/2002. (c)

Block, C.A. and Manning, H.L. (2002). Prevention of Acute Renal Failure in the Critically ill. American Journal of Respiratory and Critical Care Medicine. 165, 320- 324. ( c)

Chendrasekhar A. (2000). Incidence of myoglobinuria in prolonged entrapment. Emergenza.

Demirkiran O. Dikmen Y. Utku T. e al (2003). Crush syndrome patients after the Marmara earthquake. Emergency Medical Journal. 20, 247-250. (b) Elitok S. Kettritz U. Brasen J.H.et al (2003) Myoglobinuria; round up more than the usual suspects. Nephrology Dialysis Transplantation. 18 (3)  615-617. (b)

Erek E., Sever M.S. Serdengecti K. et al (2002) An overview of morbidity and mortality in patients with acute renal failure due to crush syndrome; the Marmara earthquake experience. Nephrology Dialysis Transplantation. 17 33-40.  (b)

National Institute of Clinical Excellence (2004) Pre hospital initiation of fluid replacement therapy in trauma.TA74 Guidance

Fernandez-Funez A. (1998). Acute renal failure in rhabdomyolysis. Revista Clinica Espanola. 198 758-764. (c)

Gunal A.I., Celker H. Dogukan. A et al  (2004) Early and vigorous fluid resuscitation prevents acute renal failure in the crush victims of catastrophic earthquakes. Journal of American Society of Nephrology. 15, 1862-1867. (b)

Haas C.E., Magram Y. and Mishra A. (2003). Rhabdomyolysis and acute renal failure following an ethanol and diphenhydramine overdose. The Annals of Pharmacotherapy. 37, p 538-542. (c)

Hunter J.D. (2002). Rhabdomyolysis. Care of the Critically Ill. 18, (21) 52-54. [c]

Kumar, P and Clark, M. (2002) Clinical Medicine. Fifth edition. W.B.Saunders. Edinburgh. [c]

Lane, R. and Phillips, M. (2003) Rhabdomyolysis. British Medical Journal.327,  115-116. [c]

Lappalainen, H. Tiula E., Uotila L. et al (2002). Elimination kinetics of myoglobin and creatine kinase in rhabdomyolysis; Implications for follow-up. Critical Care Medicine.  30 (10) 2212-2215. [c]

Mikkelsen T.S. and Toft P. (2005) Prognostic value, kinetics and effects of CVVHDF on serum of the myoglobin and creatine kinase in critically ill patients with rhabdomyolysis. Acta Anaesthesiologica Scandinavica. 49, 859-864. [b]

Najafi  I. Hatamizadeh P. Seyrafian S. et al (2005). Association of Acute Renal Failure with mortality and morbidity after the catastrophic earthquake in Bam.

Ochoa-Gomez J., Villar-Arias A., Aresti I. et al (2003). A case of sever Hyperkalaemia and compartment syndrome due to rhabdomyolysis after drug abuse. Resuscitation. 54, 103-105. [c].

Pesik N.T. and Otten E.J. (1996). Severe rhabdomyolysis following a viral illness; a case report and review of the literature. The Journal of Emergency Medicine. 14 (4) 425-428. [c]

Sauret J.M. Marinides G. and Wang G.K. (2002). Rhabdomyolysis. American Family Physician. 65 (5) 907- 912. [c]

Sharp L.S. Rozychi G.S. and Feliciano D.V. (2005) Rhabdomyolysis and secondary renal failure in critically ill surgical patients. The American Journal of Surgery.  188, 801-806.[b]

Sever M.S. Vanholder R. and Lameire R. (2006). Medical progress; Management of Crush-related Injuries after Disasters. The New England Journal of Medicine. 354 (10) 1052-1063. [b]

Skinner S. (2005) Understanding clinical investigations; a quick reference manual. Second edition. Elsevier; China. [c]

Vanholder, R., Sever, M.S., Erek, E.et al (2000) Acute renal failure related to crush syndrome; towards an era of seismo-nephrology. Nephrology Dialysis Transplantation. 15, 1517-1521. [c]

Evidence Levels

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
C=Expert consensus

Consensus group
Intensivists
Renal physicians
Senior Nursing Team
Pharmacist

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Approved By

Trust Clinical Guidelines Group

Document history

LHP version 1.0

Related information

Appendix 1

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Equity and Diversity

The Leeds Teaching Hospitals NHS Trust is committed to ensuring that the way that we provide services and the way we recruit and treat staff reflects individual needs, promotes equality and does not discriminate unfairly against any particular individual or group.