Nephrology
Question 136 of 180
A 67 year old man presents to the Emergency Department after being found on the floor by his family after having no contact with him for 2 days. He has a past medical history of a stroke which has left him with a left sided weakness and he is prone to falls as a result. You receive a phone call from the biochemistry lab to inform you his creatine kinase level is over 30,000 U/L. You diagnose rhabdomyolysis secondary to a long lie. Which of the following is a proven cornerstone of management for rhabdomyolysis, along with saline hydration?
Answer:
Furosemide is somewhat contraindicated because of its tendency to acidify the urine. Mannitol and alkalinisation are not proven, although they are often used. Chelation therapy is under investigation.Rhabdomyolysis
Nephrology
Last Updated: 12th February 2021
Rhabdomyolysis, characterised by muscle cell lysis and necrosis, results in the leakage of potassium, phosphate, myoglobin and creatine kinase (CK) into the circulation and is a clinical syndrome ranging from isolated raised CK, to acute kidney injury, hyperkalaemia and death. CK levels rise in rhabdomyolysis within 12 hours of onset of muscle injury, peak in 1 - 3 days and decline after 3 - 5 days after the muscle injury. The measurement of serum CK levels at 5 times the upper limit of normal is used as diagnostic criterion.
Causes
Patients who have fallen are at risk of developing rhabdomyolysis secondary to prolonged muscle compression associated with a 'long lie'.
Other causes include:
- Trauma (particularly crush injuries), extensive burns, lightning and electrical injuries
- Compartment syndrome
- Status epilepticus
- Excessive exercise
- Alcohol abuse
- Prescribed drugs e.g. statins, colchicine, corticosteroids
- Illicit drugs e.g. cocaine, amphetamines, ecstasy
- Heat stroke
- Myositis and myocarditis
- Neuroleptic malignant syndrome
- Malignant hyperthermia
- Infections
- Tumour lysis syndrome
- Thyroid disease
Clinical features
- Muscle pain
- Muscle swelling
- Muscle tenderness
- Muscle weakness
- Malaise
- Dark urine
- Fever
- Anorexia, nausea and vomiting
- Anuria and dehydration
- Agitation
- Delirium
Complications
- Acute kidney injury (AKI) - occurs secondary to myoglobin causing renal tubular obstruction
- Hyperkalaemia
- Hyperphosphataemia
- Hypocalcaemia
- Metabolic acidosis
- Disseminated intravascular coagulation (DIC)
- Compartment syndrome
- Multisystem organ failure
Investigations
- Bloods
- Creatine kinase
- In the appropriate clinical setting, a measurement of the patient's serum creatine kinase (CK) level greater than 5 times the normal level will confirm the diagnosis.
- FBC and clotting
- Disseminated Intravascular Coagulation (DIC) can occur and serial coagulation and platelet studies with prothrombin time (PT) are required.
- Activated Partial Thromboplastin Time (APTT), fibrin degradation products and fibrinogen may need to be monitored to direct therapeutic intervention.
- Renal function
- Serum creatinine and urea will be elevated and the ratio of creatinine is increased relative to urea as large amounts are released from the damaged muscle.
- Hyperkalaemia can be life threatening in rhabdomyolysis. Early measurement and frequent monitoring are necessary. The high level of serums potassium released by necrosed muscle are further elevated by the development of acute kidney injury and acidosis.
- Calcium and phosphate
- Calcium levels may be low in serum initially as calcium is deposited in necrotic muscle tissue. This calcium is later released into the circulation and symptoms of hypercalcaemia may occur.
- When muscle damage occurs myocytes release phosphate which can bind with calcium forming calcium phosphate. This can exacerbate hypocalcaemia.
- Creatine kinase
- Urine dipstick and urinalysis
- Myoglobinuria is suggested if dipstick is positive for blood but with no red cells on urine microscopy (true myoglobinuria can be confirmed with lab testing).
- ECG
- Rhabdomyolysis can lead to cardiac arrhythmias as a consequence of metabolic acidosis and hyperkalaemia.
- Imaging
- Ultrasound shows decreased echogenicity compared with normal muscle imaging.
- MRI is more sensitive at detecting muscle damage than ultrasound or CT but there are clear logistical problems in obtaining MRI.
- Muscle biopsy
- Muscle biopsy is only indicated if genetic aetiology is suspected.
Management
- The condition leading to rhabdomyolysis must be managed. Particular caution must be directed towards compartment syndromes that are commonly present in patients with rhabdomyolysis.
- Fluid resuscitation
- The cornerstone of management is aggressive intravascular fluid rehydration. The sooner this commences the lower the risk of developing acute kidney injury. No specific fluid algorithms exist and attention must be paid to strict fluid balance, urine output and serial monitoring of renal function and acid base status. Typically, this is initiated with normal saline or lactated Ringer's solution with the goal of maintaining a urine output of 200 to 300 mL/hour.
- Intravenous sodium bicarbonate
- Myoglobin is toxic to renal tubules in acidic urine, and some specialists recommend concurrent use of intravenous sodium bicarbonate to alkalinise the urine and prevent crystallisation of uric acid. Some evidence suggests that a urine pH >6.0 is protective. This is difficult to achieve without the use of large amounts of bicarbonate and, although many specialists may recommend urine alkalinisation, benefits of its use lack robust evidence-based support.
- Diuretic therapy
- The use of diuretic therapy to promote diuresis is unclear. The benefits of diuretic therapies (e.g. mannitol, furosemide) and at what point to administer them have not been prospectively studied. Reports have been spurious and anecdotal. European literature does not support their use. Some specialists advocate the use of mannitol and furosemide to prevent non-oliguric renal failure during aggressive rehydration. However, this approach may have only limited benefit in select patient populations.
- Renal replacement therapy
- If patients do not respond to rehydration, haemodialysis may be required. Haemodialysis corrects metabolic acidosis and electrolyte abnormalities, and removes plasma myonecrotic toxins. Dialysis is indicated in renal failure if the patient is anuric with severe acidosis and hyperkalaemia.
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- Biochemistry
- Blood Gases
- Haematology
| Biochemistry | Normal Value |
|---|---|
| Sodium | 135 – 145 mmol/l |
| Potassium | 3.0 – 4.5 mmol/l |
| Urea | 2.5 – 7.5 mmol/l |
| Glucose | 3.5 – 5.0 mmol/l |
| Creatinine | 35 – 135 μmol/l |
| Alanine Aminotransferase (ALT) | 5 – 35 U/l |
| Gamma-glutamyl Transferase (GGT) | < 65 U/l |
| Alkaline Phosphatase (ALP) | 30 – 135 U/l |
| Aspartate Aminotransferase (AST) | < 40 U/l |
| Total Protein | 60 – 80 g/l |
| Albumin | 35 – 50 g/l |
| Globulin | 2.4 – 3.5 g/dl |
| Amylase | < 70 U/l |
| Total Bilirubin | 3 – 17 μmol/l |
| Calcium | 2.1 – 2.5 mmol/l |
| Chloride | 95 – 105 mmol/l |
| Phosphate | 0.8 – 1.4 mmol/l |
| Haematology | Normal Value |
|---|---|
| Haemoglobin | 11.5 – 16.6 g/dl |
| White Blood Cells | 4.0 – 11.0 x 109/l |
| Platelets | 150 – 450 x 109/l |
| MCV | 80 – 96 fl |
| MCHC | 32 – 36 g/dl |
| Neutrophils | 2.0 – 7.5 x 109/l |
| Lymphocytes | 1.5 – 4.0 x 109/l |
| Monocytes | 0.3 – 1.0 x 109/l |
| Eosinophils | 0.1 – 0.5 x 109/l |
| Basophils | < 0.2 x 109/l |
| Reticulocytes | < 2% |
| Haematocrit | 0.35 – 0.49 |
| Red Cell Distribution Width | 11 – 15% |
| Blood Gases | Normal Value |
|---|---|
| pH | 7.35 – 7.45 |
| pO2 | 11 – 14 kPa |
| pCO2 | 4.5 – 6.0 kPa |
| Base Excess | -2 – +2 mmol/l |
| Bicarbonate | 24 – 30 mmol/l |
| Lactate | < 2 mmol/l |
