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Case ReportA 34 year-old man with unremarkable past medical and family histories was referred by his GP with a one-day history of pain and weakness affecting the lower back and thighs, andtea-coloured urine. Earlier that day, he had performed a strenuous weight training session to which he was unaccustomed. He denied use of steroids, supplements, or statins.Examination was unremarkable aside from marked palpation tenderness in the quadriceps and lumbar para-spinal muscles, with 4+/5 weakness of hip flexion and knee extension bilaterally (limited by pain). There was no evidence of compartment syndrome.The full blood count, coagulation screen, routine biochemistry and thyroid function were normal except for elevated creatine kinase (CK) of >14,000 U/L (60-220 U/L) and mildly elevated serum lactate of 1.6mmol/L (0.3-1.3mmol/L). His urine was tea coloured (Figure 1) and was strongly positive for blood on dipstick testing. However, urinary creatinine and protein was normal and the urine was acellular upon microscopy. These changes are suggestive of myoglobinuria due to the cross-reactivity of urine dipstick testing with myoglobin/haemoglobin.Figure 1: Tea-coloured urine specimen from patient with exercise-induced rhabdomyolysis.The findings were consistent with exercise-induced rhabdomyolysis. Aggressive intravenous fluids were given and he was monitored daily for electrolyte disturbances and other sequelae. Electrolytes remained normal aside from transient asymptomatic hypocalcaemia 2.05 mmol/L (2.10-2.55mmol/L). CK remained >14,000 U/L for five days before falling. Symptoms improved over the same time-frame and he was discharged with GP follow-up.DiscussionRhabdomyolysis may be triggered by numerous insults (Table 1). Complications are less frequent in exercise-induced rhabdomyolysis than in other forms of rhabdomyolysis. Resolution is expected within one-two weeks. Severe exercise-induced rhabdomyolysis can cause acute kidney injury, electrolyte disturbances, disseminated intravascular coagulopathy, compartment syndrome and death.2,4Table 1: The major categories of rhabdomyolysis and common causes for each category. Type of Rhabdomyolysis Common causes Trauma Crush syndrome, major trauma Exertional Strenuous or unaccustomed exercise, seizures (epilepsy, alcohol withdrawal) Muscle hypoxia Acute limb ischaemia/major artery occlusion, prolonged compression of limb during immobilisation or unconsciousness Genetic Disorders of glycolysis or glycogenolysis, disorders of lipid metabolism Infection-related Influenza A and B, Cocksackievirus, EBV, HIV, staph aureus pyomyositis, clostridium Temperature-related Heat stroke, malignant hyperthermia, malignant neuroleptic syndrome, hypothermia Metabolic and electrolyte disorders Hypokalaemia, hypophosphataemia, hypocalcaemia, DKA, hyperosmolar hyperketotic state Drugs/toxins Fibrate, statins, alcohol, heroin, cocaine Idiopathic Unknown Excessive muscle activity induces rhabdomyolysis when myocyte energy demand exceeds production. Intracellular glycogen stores are exhausted and myocellular membranes become disrupted. The resulting release of intracellular skeletal muscle constituents into the circulation is responsible for complications observed.13 Exercise-induced rhabdomyolysis is most commonly seen following strenuous physical activity but can sometimes occur after low-intensity exercise, especially in dehydrated individuals.4 Risk factors include: male sex, being physically untrained, coexistent heat stroke, impaired sweating, sickle-cell trait, hypokalaemia and inherited muscle enzyme defects.1,3-4Clinically, exercise-induced rhabdomyolysis is characterised by:1 muscle tenderness, stiffness, cramping weakness in affected muscle groups tea-coloured urine other urinary symptoms: oliguria, anuria non-specific symptoms: malaise, fever, nausea, vomiting. Baseline investigations include: urine dipstick, serum CK, electrolytes (including calcium), full blood count, coagulation screen, lactate, blood gas, TFTs and ECG.1 The urine dipstick may be false-positive for blood due to cross-reactivity of myoglobin and haemoglobin (as in this case).1-2 In recurrent cases, or if there is a family history of exercise-induced rhabdomyolysis, investigation for a predisposing genetic cause is suggested.6 The conditions that predispose or cause rhabdomyolysis are varied and include disorders of lipid and carbohydrate metabolism, mitochondrial disease and myopathies.1,3 Investigations should be targeted to the specific conditions of concern and may include skin and/or muscle biopsy, tissue histochemistry, muscle-exercise testing, biochemical tests and formal genetic testing.The initial treatment of rhabdomyolysis is aggressive intravenous fluid resuscitation.1-2,4 Normal saline is most commonly used. Care should be taken with fluid resuscitation, particularly in the context of prolonged anuria where patients are at greater risk of iatrogenic overload. Electrolyte disturbances should be corrected promptly, aside from hypocalcaemia which should only be treated if symptomatic or if concurrent severe hyperkalaemia is present due to risk of arrhythmia.2 Sodium bicarbonate or mannitol may be considered under specialist guidance only.2 Renal-replacement therapy may be used for refractory complications, although this does not facilitate myoglobin elimination.2 Plasmapheresis or haemofiltration with super-high-flux dialysers may have a role in severe cases.7,8ConclusionExercise-induced rhabdomyolysis is an under-recognised phenomenon with potentially serious complications. The presentation, complications, investigations and management of exercise-induced rhabdomyolysis are summarised (Table 2). The most critical facet of making a diagnosis remains retaining a high-index of suspicion due to the uncommon nature of the presentation and its significant potential complications.Table 2:Exercise-induced rhabdomyolysis: key points. Summary of Exercise-induced Rhabdomyolysis Clinical features Muscle stiffness, tenderness, cramping Weakness in affected muscles Dark \"tea-coloured\" urine Non-specific: malaise, fever, nausea, vomiting, fever Risk factors Male sex, unaccustomed exercise, heat stroke/hot weather, impaired sweating, hypokalaemia, inherited muscle enzyme defects, sickle cell trait Investigations Urine dipstick and microscopy Bloods: FBC, UEs, creatine kinase, lactate, calcium, phosphate, TFTs, clotting Blood gas ECG May require specialist genetic testing if concerns about underlying cause Management Early IV fluids (0.9% saline), large volumes may be required Monitor: - Fluid input/output: may require catheter - Close electrolytes monitoring - Signs of compartment syndrome/coagulopathy Correct hypocalcaemia only if symptomatic or concurrent severe hyperkalaemia Treat other electrolyte disturbances especially hyperkalaemia Consider: - Early involvement of intensive care/renal-services - Consider use of Mannitol or Sodium Bicarbonate under specialist guideance - Renal replacement therapy if resistant hyperkalaemia or other sequaelae of renal failure Complications Acute kidney injury Electrolyte disturbance: hyperkalaemia, hypocalcaemia, hyper/hypophosphataemia Disseminated intravascular coagulopathy Compartment syndrome Death Prognosis Generally very good

Summary

Abstract

We report the case of a 34 year-old man who developed exercise-induced rhabdomyolysis after unaccustomed high-intensity exercise. Subclinical rhabdomyolysis is common after heavy exercise, yet it is uncommon for patients to seek medical advice. The presentation is variable and despite potentially life-threatening complications the diagnosis may be easily missed by patients and healthcare professionals. A high-index of suspicion is critical to avoid missing the diagnosis. We summarise the current knowledge, clinical course, complications and management of exercise-induced rhabdomyolysis.

Aim

Method

Results

Conclusion

Author Information

Joseph Hutton, General Medicine, North Shore Hospital, Auckland; Daniel Wellington, General Medicine, North Shore Hospital, Auckland; Steven Miller, Diabetes Centre, North Shore Hospital (WDHB), Auckland.

Acknowledgements

Correspondence

Joseph Hutton, General Medicine, North Shore Hospital, Shakespeare Road, Auckland.

Correspondence Email

jh7480@my.bristol.ac.uk

Competing Interests

- - Khan FY. Rhabdomyolysis: a review of the literature. Netherlands Journal of Medicine 2009; 67-272. Bosch X, Poch E, Grau JM. Rhabdomyolysis and acute kidney injury. New England Journal of Medicine 2009; 361-362. Kim J, Lee J, Kim S, Young Ryu H, Suk Cha K, Jun Sung D. Exercise-induced rhabomyolysis mechanisms and prevention: a literature review. Journal of Sport and Health Science xx 2015; 1-11. Lee G. Exercise-induced rhabdomyolysis. Rhode Island Medical Journal 2014; 97 (11): 22-24. Hill OT, Wahi MM, Carter R, Kay AB, McKinnon CJ, Wallace RF. Rhabdomyolysis in the US Active Duty Army, 2004-2006. Medicine and Science in Sports and Exercise 2012; 44 (3): 442-449. Landau ME, Kenney K, Deuster P, Campbell W. Exertional rhabdomyolysis: a clinical review with a focus on genetic influences. J Clin Neuromuscul Dis. 2012 Mar;13(3):122-36. Homsi E, Fernanda M, Barreiro L, Orlando J, Higa E. Prophylaxis of acute renal failure in patients with rhabdomyolysis. Renal Failure 1997; 19: 283-288. Ronco C. Extracorporeal therapies in acute rhabdomyolysis and myoglobin clearance. Critical Care 2005; 9: 141-142.- -

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Case ReportA 34 year-old man with unremarkable past medical and family histories was referred by his GP with a one-day history of pain and weakness affecting the lower back and thighs, andtea-coloured urine. Earlier that day, he had performed a strenuous weight training session to which he was unaccustomed. He denied use of steroids, supplements, or statins.Examination was unremarkable aside from marked palpation tenderness in the quadriceps and lumbar para-spinal muscles, with 4+/5 weakness of hip flexion and knee extension bilaterally (limited by pain). There was no evidence of compartment syndrome.The full blood count, coagulation screen, routine biochemistry and thyroid function were normal except for elevated creatine kinase (CK) of >14,000 U/L (60-220 U/L) and mildly elevated serum lactate of 1.6mmol/L (0.3-1.3mmol/L). His urine was tea coloured (Figure 1) and was strongly positive for blood on dipstick testing. However, urinary creatinine and protein was normal and the urine was acellular upon microscopy. These changes are suggestive of myoglobinuria due to the cross-reactivity of urine dipstick testing with myoglobin/haemoglobin.Figure 1: Tea-coloured urine specimen from patient with exercise-induced rhabdomyolysis.The findings were consistent with exercise-induced rhabdomyolysis. Aggressive intravenous fluids were given and he was monitored daily for electrolyte disturbances and other sequelae. Electrolytes remained normal aside from transient asymptomatic hypocalcaemia 2.05 mmol/L (2.10-2.55mmol/L). CK remained >14,000 U/L for five days before falling. Symptoms improved over the same time-frame and he was discharged with GP follow-up.DiscussionRhabdomyolysis may be triggered by numerous insults (Table 1). Complications are less frequent in exercise-induced rhabdomyolysis than in other forms of rhabdomyolysis. Resolution is expected within one-two weeks. Severe exercise-induced rhabdomyolysis can cause acute kidney injury, electrolyte disturbances, disseminated intravascular coagulopathy, compartment syndrome and death.2,4Table 1: The major categories of rhabdomyolysis and common causes for each category. Type of Rhabdomyolysis Common causes Trauma Crush syndrome, major trauma Exertional Strenuous or unaccustomed exercise, seizures (epilepsy, alcohol withdrawal) Muscle hypoxia Acute limb ischaemia/major artery occlusion, prolonged compression of limb during immobilisation or unconsciousness Genetic Disorders of glycolysis or glycogenolysis, disorders of lipid metabolism Infection-related Influenza A and B, Cocksackievirus, EBV, HIV, staph aureus pyomyositis, clostridium Temperature-related Heat stroke, malignant hyperthermia, malignant neuroleptic syndrome, hypothermia Metabolic and electrolyte disorders Hypokalaemia, hypophosphataemia, hypocalcaemia, DKA, hyperosmolar hyperketotic state Drugs/toxins Fibrate, statins, alcohol, heroin, cocaine Idiopathic Unknown Excessive muscle activity induces rhabdomyolysis when myocyte energy demand exceeds production. Intracellular glycogen stores are exhausted and myocellular membranes become disrupted. The resulting release of intracellular skeletal muscle constituents into the circulation is responsible for complications observed.13 Exercise-induced rhabdomyolysis is most commonly seen following strenuous physical activity but can sometimes occur after low-intensity exercise, especially in dehydrated individuals.4 Risk factors include: male sex, being physically untrained, coexistent heat stroke, impaired sweating, sickle-cell trait, hypokalaemia and inherited muscle enzyme defects.1,3-4Clinically, exercise-induced rhabdomyolysis is characterised by:1 muscle tenderness, stiffness, cramping weakness in affected muscle groups tea-coloured urine other urinary symptoms: oliguria, anuria non-specific symptoms: malaise, fever, nausea, vomiting. Baseline investigations include: urine dipstick, serum CK, electrolytes (including calcium), full blood count, coagulation screen, lactate, blood gas, TFTs and ECG.1 The urine dipstick may be false-positive for blood due to cross-reactivity of myoglobin and haemoglobin (as in this case).1-2 In recurrent cases, or if there is a family history of exercise-induced rhabdomyolysis, investigation for a predisposing genetic cause is suggested.6 The conditions that predispose or cause rhabdomyolysis are varied and include disorders of lipid and carbohydrate metabolism, mitochondrial disease and myopathies.1,3 Investigations should be targeted to the specific conditions of concern and may include skin and/or muscle biopsy, tissue histochemistry, muscle-exercise testing, biochemical tests and formal genetic testing.The initial treatment of rhabdomyolysis is aggressive intravenous fluid resuscitation.1-2,4 Normal saline is most commonly used. Care should be taken with fluid resuscitation, particularly in the context of prolonged anuria where patients are at greater risk of iatrogenic overload. Electrolyte disturbances should be corrected promptly, aside from hypocalcaemia which should only be treated if symptomatic or if concurrent severe hyperkalaemia is present due to risk of arrhythmia.2 Sodium bicarbonate or mannitol may be considered under specialist guidance only.2 Renal-replacement therapy may be used for refractory complications, although this does not facilitate myoglobin elimination.2 Plasmapheresis or haemofiltration with super-high-flux dialysers may have a role in severe cases.7,8ConclusionExercise-induced rhabdomyolysis is an under-recognised phenomenon with potentially serious complications. The presentation, complications, investigations and management of exercise-induced rhabdomyolysis are summarised (Table 2). The most critical facet of making a diagnosis remains retaining a high-index of suspicion due to the uncommon nature of the presentation and its significant potential complications.Table 2:Exercise-induced rhabdomyolysis: key points. Summary of Exercise-induced Rhabdomyolysis Clinical features Muscle stiffness, tenderness, cramping Weakness in affected muscles Dark \"tea-coloured\" urine Non-specific: malaise, fever, nausea, vomiting, fever Risk factors Male sex, unaccustomed exercise, heat stroke/hot weather, impaired sweating, hypokalaemia, inherited muscle enzyme defects, sickle cell trait Investigations Urine dipstick and microscopy Bloods: FBC, UEs, creatine kinase, lactate, calcium, phosphate, TFTs, clotting Blood gas ECG May require specialist genetic testing if concerns about underlying cause Management Early IV fluids (0.9% saline), large volumes may be required Monitor: - Fluid input/output: may require catheter - Close electrolytes monitoring - Signs of compartment syndrome/coagulopathy Correct hypocalcaemia only if symptomatic or concurrent severe hyperkalaemia Treat other electrolyte disturbances especially hyperkalaemia Consider: - Early involvement of intensive care/renal-services - Consider use of Mannitol or Sodium Bicarbonate under specialist guideance - Renal replacement therapy if resistant hyperkalaemia or other sequaelae of renal failure Complications Acute kidney injury Electrolyte disturbance: hyperkalaemia, hypocalcaemia, hyper/hypophosphataemia Disseminated intravascular coagulopathy Compartment syndrome Death Prognosis Generally very good

Summary

Abstract

We report the case of a 34 year-old man who developed exercise-induced rhabdomyolysis after unaccustomed high-intensity exercise. Subclinical rhabdomyolysis is common after heavy exercise, yet it is uncommon for patients to seek medical advice. The presentation is variable and despite potentially life-threatening complications the diagnosis may be easily missed by patients and healthcare professionals. A high-index of suspicion is critical to avoid missing the diagnosis. We summarise the current knowledge, clinical course, complications and management of exercise-induced rhabdomyolysis.

Aim

Method

Results

Conclusion

Author Information

Joseph Hutton, General Medicine, North Shore Hospital, Auckland; Daniel Wellington, General Medicine, North Shore Hospital, Auckland; Steven Miller, Diabetes Centre, North Shore Hospital (WDHB), Auckland.

Acknowledgements

Correspondence

Joseph Hutton, General Medicine, North Shore Hospital, Shakespeare Road, Auckland.

Correspondence Email

jh7480@my.bristol.ac.uk

Competing Interests

- - Khan FY. Rhabdomyolysis: a review of the literature. Netherlands Journal of Medicine 2009; 67-272. Bosch X, Poch E, Grau JM. Rhabdomyolysis and acute kidney injury. New England Journal of Medicine 2009; 361-362. Kim J, Lee J, Kim S, Young Ryu H, Suk Cha K, Jun Sung D. Exercise-induced rhabomyolysis mechanisms and prevention: a literature review. Journal of Sport and Health Science xx 2015; 1-11. Lee G. Exercise-induced rhabdomyolysis. Rhode Island Medical Journal 2014; 97 (11): 22-24. Hill OT, Wahi MM, Carter R, Kay AB, McKinnon CJ, Wallace RF. Rhabdomyolysis in the US Active Duty Army, 2004-2006. Medicine and Science in Sports and Exercise 2012; 44 (3): 442-449. Landau ME, Kenney K, Deuster P, Campbell W. Exertional rhabdomyolysis: a clinical review with a focus on genetic influences. J Clin Neuromuscul Dis. 2012 Mar;13(3):122-36. Homsi E, Fernanda M, Barreiro L, Orlando J, Higa E. Prophylaxis of acute renal failure in patients with rhabdomyolysis. Renal Failure 1997; 19: 283-288. Ronco C. Extracorporeal therapies in acute rhabdomyolysis and myoglobin clearance. Critical Care 2005; 9: 141-142.- -

For the PDF of this article,
contact nzmj@nzma.org.nz

View Article PDF

Case ReportA 34 year-old man with unremarkable past medical and family histories was referred by his GP with a one-day history of pain and weakness affecting the lower back and thighs, andtea-coloured urine. Earlier that day, he had performed a strenuous weight training session to which he was unaccustomed. He denied use of steroids, supplements, or statins.Examination was unremarkable aside from marked palpation tenderness in the quadriceps and lumbar para-spinal muscles, with 4+/5 weakness of hip flexion and knee extension bilaterally (limited by pain). There was no evidence of compartment syndrome.The full blood count, coagulation screen, routine biochemistry and thyroid function were normal except for elevated creatine kinase (CK) of >14,000 U/L (60-220 U/L) and mildly elevated serum lactate of 1.6mmol/L (0.3-1.3mmol/L). His urine was tea coloured (Figure 1) and was strongly positive for blood on dipstick testing. However, urinary creatinine and protein was normal and the urine was acellular upon microscopy. These changes are suggestive of myoglobinuria due to the cross-reactivity of urine dipstick testing with myoglobin/haemoglobin.Figure 1: Tea-coloured urine specimen from patient with exercise-induced rhabdomyolysis.The findings were consistent with exercise-induced rhabdomyolysis. Aggressive intravenous fluids were given and he was monitored daily for electrolyte disturbances and other sequelae. Electrolytes remained normal aside from transient asymptomatic hypocalcaemia 2.05 mmol/L (2.10-2.55mmol/L). CK remained >14,000 U/L for five days before falling. Symptoms improved over the same time-frame and he was discharged with GP follow-up.DiscussionRhabdomyolysis may be triggered by numerous insults (Table 1). Complications are less frequent in exercise-induced rhabdomyolysis than in other forms of rhabdomyolysis. Resolution is expected within one-two weeks. Severe exercise-induced rhabdomyolysis can cause acute kidney injury, electrolyte disturbances, disseminated intravascular coagulopathy, compartment syndrome and death.2,4Table 1: The major categories of rhabdomyolysis and common causes for each category. Type of Rhabdomyolysis Common causes Trauma Crush syndrome, major trauma Exertional Strenuous or unaccustomed exercise, seizures (epilepsy, alcohol withdrawal) Muscle hypoxia Acute limb ischaemia/major artery occlusion, prolonged compression of limb during immobilisation or unconsciousness Genetic Disorders of glycolysis or glycogenolysis, disorders of lipid metabolism Infection-related Influenza A and B, Cocksackievirus, EBV, HIV, staph aureus pyomyositis, clostridium Temperature-related Heat stroke, malignant hyperthermia, malignant neuroleptic syndrome, hypothermia Metabolic and electrolyte disorders Hypokalaemia, hypophosphataemia, hypocalcaemia, DKA, hyperosmolar hyperketotic state Drugs/toxins Fibrate, statins, alcohol, heroin, cocaine Idiopathic Unknown Excessive muscle activity induces rhabdomyolysis when myocyte energy demand exceeds production. Intracellular glycogen stores are exhausted and myocellular membranes become disrupted. The resulting release of intracellular skeletal muscle constituents into the circulation is responsible for complications observed.13 Exercise-induced rhabdomyolysis is most commonly seen following strenuous physical activity but can sometimes occur after low-intensity exercise, especially in dehydrated individuals.4 Risk factors include: male sex, being physically untrained, coexistent heat stroke, impaired sweating, sickle-cell trait, hypokalaemia and inherited muscle enzyme defects.1,3-4Clinically, exercise-induced rhabdomyolysis is characterised by:1 muscle tenderness, stiffness, cramping weakness in affected muscle groups tea-coloured urine other urinary symptoms: oliguria, anuria non-specific symptoms: malaise, fever, nausea, vomiting. Baseline investigations include: urine dipstick, serum CK, electrolytes (including calcium), full blood count, coagulation screen, lactate, blood gas, TFTs and ECG.1 The urine dipstick may be false-positive for blood due to cross-reactivity of myoglobin and haemoglobin (as in this case).1-2 In recurrent cases, or if there is a family history of exercise-induced rhabdomyolysis, investigation for a predisposing genetic cause is suggested.6 The conditions that predispose or cause rhabdomyolysis are varied and include disorders of lipid and carbohydrate metabolism, mitochondrial disease and myopathies.1,3 Investigations should be targeted to the specific conditions of concern and may include skin and/or muscle biopsy, tissue histochemistry, muscle-exercise testing, biochemical tests and formal genetic testing.The initial treatment of rhabdomyolysis is aggressive intravenous fluid resuscitation.1-2,4 Normal saline is most commonly used. Care should be taken with fluid resuscitation, particularly in the context of prolonged anuria where patients are at greater risk of iatrogenic overload. Electrolyte disturbances should be corrected promptly, aside from hypocalcaemia which should only be treated if symptomatic or if concurrent severe hyperkalaemia is present due to risk of arrhythmia.2 Sodium bicarbonate or mannitol may be considered under specialist guidance only.2 Renal-replacement therapy may be used for refractory complications, although this does not facilitate myoglobin elimination.2 Plasmapheresis or haemofiltration with super-high-flux dialysers may have a role in severe cases.7,8ConclusionExercise-induced rhabdomyolysis is an under-recognised phenomenon with potentially serious complications. The presentation, complications, investigations and management of exercise-induced rhabdomyolysis are summarised (Table 2). The most critical facet of making a diagnosis remains retaining a high-index of suspicion due to the uncommon nature of the presentation and its significant potential complications.Table 2:Exercise-induced rhabdomyolysis: key points. Summary of Exercise-induced Rhabdomyolysis Clinical features Muscle stiffness, tenderness, cramping Weakness in affected muscles Dark \"tea-coloured\" urine Non-specific: malaise, fever, nausea, vomiting, fever Risk factors Male sex, unaccustomed exercise, heat stroke/hot weather, impaired sweating, hypokalaemia, inherited muscle enzyme defects, sickle cell trait Investigations Urine dipstick and microscopy Bloods: FBC, UEs, creatine kinase, lactate, calcium, phosphate, TFTs, clotting Blood gas ECG May require specialist genetic testing if concerns about underlying cause Management Early IV fluids (0.9% saline), large volumes may be required Monitor: - Fluid input/output: may require catheter - Close electrolytes monitoring - Signs of compartment syndrome/coagulopathy Correct hypocalcaemia only if symptomatic or concurrent severe hyperkalaemia Treat other electrolyte disturbances especially hyperkalaemia Consider: - Early involvement of intensive care/renal-services - Consider use of Mannitol or Sodium Bicarbonate under specialist guideance - Renal replacement therapy if resistant hyperkalaemia or other sequaelae of renal failure Complications Acute kidney injury Electrolyte disturbance: hyperkalaemia, hypocalcaemia, hyper/hypophosphataemia Disseminated intravascular coagulopathy Compartment syndrome Death Prognosis Generally very good

Summary

Abstract

We report the case of a 34 year-old man who developed exercise-induced rhabdomyolysis after unaccustomed high-intensity exercise. Subclinical rhabdomyolysis is common after heavy exercise, yet it is uncommon for patients to seek medical advice. The presentation is variable and despite potentially life-threatening complications the diagnosis may be easily missed by patients and healthcare professionals. A high-index of suspicion is critical to avoid missing the diagnosis. We summarise the current knowledge, clinical course, complications and management of exercise-induced rhabdomyolysis.

Aim

Method

Results

Conclusion

Author Information

Joseph Hutton, General Medicine, North Shore Hospital, Auckland; Daniel Wellington, General Medicine, North Shore Hospital, Auckland; Steven Miller, Diabetes Centre, North Shore Hospital (WDHB), Auckland.

Acknowledgements

Correspondence

Joseph Hutton, General Medicine, North Shore Hospital, Shakespeare Road, Auckland.

Correspondence Email

jh7480@my.bristol.ac.uk

Competing Interests

- - Khan FY. Rhabdomyolysis: a review of the literature. Netherlands Journal of Medicine 2009; 67-272. Bosch X, Poch E, Grau JM. Rhabdomyolysis and acute kidney injury. New England Journal of Medicine 2009; 361-362. Kim J, Lee J, Kim S, Young Ryu H, Suk Cha K, Jun Sung D. Exercise-induced rhabomyolysis mechanisms and prevention: a literature review. Journal of Sport and Health Science xx 2015; 1-11. Lee G. Exercise-induced rhabdomyolysis. Rhode Island Medical Journal 2014; 97 (11): 22-24. Hill OT, Wahi MM, Carter R, Kay AB, McKinnon CJ, Wallace RF. Rhabdomyolysis in the US Active Duty Army, 2004-2006. Medicine and Science in Sports and Exercise 2012; 44 (3): 442-449. Landau ME, Kenney K, Deuster P, Campbell W. Exertional rhabdomyolysis: a clinical review with a focus on genetic influences. J Clin Neuromuscul Dis. 2012 Mar;13(3):122-36. Homsi E, Fernanda M, Barreiro L, Orlando J, Higa E. Prophylaxis of acute renal failure in patients with rhabdomyolysis. Renal Failure 1997; 19: 283-288. Ronco C. Extracorporeal therapies in acute rhabdomyolysis and myoglobin clearance. Critical Care 2005; 9: 141-142.- -

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