Rhabdomyloysis

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Certain situations warrant the use of diuretics early in acute renal failure after restoration of intravascular volume. These are rhabdomyolysis and poisoning (for example, lithium, theophylline and salicylates). Rhabdomyolysis is an important cause of acute renal failure. It occurs when there is massive breakdown of muscle. Myoglobin is released into the circulation along with other toxins, which leads to kidney dysfunction and general metabolic upset. Unlike many other causes of acute renal failure, prognosis is good in rhabdomyolysis and the kidneys usually recover. This makes it an important condition not to miss. Causes include:

• crush injury/reperfusion after compartment syndrome

• prolonged immobility following a fall or overdose especially with hypothermia

• drug overdose, for example Ecstasy and carbon monoxide poisoning

• extreme exertion

• myositis (caused by illnesses like influenza, severe hypokalaemia or drugs like statins)

• malignant hyperthermia (triggered by some anaesthetic agents)

• neuroleptic malignant syndrome

Myoglobin and urate from muscle breakdown are said to obstruct the tubules. Yet tubular obstruction is probably not what causes acute renal failure in rhabdomyolysis, because studies show that intratubular pressures are normal. More likely is free radical mediated injury. Renal vasoconstriction also occurs, partly because of the underlying cause and partly because myoglobin itself causes vasoconstriction.

Fluid resuscitation remains the most important aspect of management in rhabdomyolysis. Early and aggressive intravenous fluid has dramatic benefits on outcome when compared with historical controls. Guidelines go as far as 12 litres of fluid a day to "flush" the kidneys and achieve a urine output of 200-300 ml h-1. Alkalinisation of the urine significantly improves renal function, probably by inhibiting free radical mediated damage. The urine is dipsticked every hour and sodium bicarbonate is given intravenously to raise the urine pH to 7 0. Mannitol is the first-line diuretic in rhabdomyolysis, but it has not been shown to be better than volume diuresis alone. Frusemide acidifies the urine but is sometimes administered after a trial of mannitol. Plasmapheresis is not an established therapy in rhabdomyolysis, although myoglobin can be removed from the circulation this way.

Self-assessment - case histories

1. A 30-year-old man was admitted after being found lying on the floor of his apartment. He had taken intravenous heroin the night before. His admission blood results showed a normal full blood count, sodium 130 mmol litre-1, potassium 6 mmol litre-1, urea 64 mmol litre-1 (blood urea nitrogen [BUN] 177 mg dl-1) and creatinine 500 ^mol litre-1 (6 mg dl-1). His vital signs were: drowsiness, blood pressure 90/60 mmHg, pulse 100 per minute, respiratory rate 8 per minute and oxygen saturations 95% on air. What is your management?

2. A 60-year-old man was admitted with a general deterioration in health. He is treated for heart failure and is taking the following medication: ramipril 10 mg, frusemide 80 mg, and allopurinol 300 mg at night. He had been treated for a chest infection and pleurisy the week before admission with antibiotics (amoxycillin) and a NSAID. On examination he was drowsy and appeared dehydrated. His blood pressure was 70/40 mmHg, pulse 90 per minute, and regular, respiratory rate 25 per minute. His blood results showed: sodium 133 mmol litre-1, potassium 5-0 mmol litre-1, urea 50 mmol litre-1 (BUN 138 mg dl-1), creatinine 600 |imol litre-1 (7-2 mg dl-1). His last blood tests in hospital were a year ago, which showed a urea of 7 mmol litre-1 (BUN 19-4 mg dl-1), and creatinine 100 ^mol litre-1 (1-2 mg dl-1). Discuss your management.

3. A 34-year-old lady was admitted with breathlessness, which had started one week ago. The chest x ray film showed bilateral patchy shadowing and she reported coughing up blood the day before admission. Her blood results showed a normal full blood count, sodium 135 mmol litre-1, potassium 4-2 mmol litre-1, urea 40 mmol litre-1 (BUN 111 mg dl-1), and creatinine 450 ^mol litre-1 (5-4 mg dl-1). Her vital signs were: alert, blood pressure 180/85 mmHg, pulse 80 per minute, respiratory rate 20 per minute, and oxygen saturations 95% on air. What is your management?

4. You are asked to see a 55-year-old man on the ward. He is being treated for ascending cholangitis and had a failed endoscopic retrograde cholangiopancreatogram (ERCP) that day for treatment of a stone in the common bile duct. His vital signs are: alert, blood pressure 80/60 mmHg, pulse 80 per minute, respiratory rate 30 per minute, temperature 38°C, and oxygen saturations 96% on air. He has warm hands and feet. His medication chart shows a ß blocker, calcium channel blocker, and a nitrate for angina. He has been given gentamicin intravenously for his infection. He also has a left nephrectomy scar from 15 years ago. The nurse alerts you to his urine output, which has been 10 ml h-1 for the last 2 hours. What is your management?

5. A 60-year-old lady is admitted with diarrhoea and vomiting, which she has had for 4 days. She has been taking a NSAID for aches and pains during the course of this illness. Her usual medication includes bendrofluazide for hypertension. On admission her vital signs are: alert, blood pressure 90/60 mmHg, pulse 100 per minute, respiratory rate 28 per minute, and oxygen saturations 98% on air. She reports that she is passing less urine. Her blood results show: sodium 145 mmol litre-1, potassium 4-0 mmol litre-1, urea 25 mmol litre-1 (BUN 69 mg dl-1) and creatinine 300 ^mol litre-1 (3-6 mg dl-1). From her records, her urea and creatinine were normal one month ago. Discuss your management.

6. An 80-year-old lady is admitted after a fractured neck of femur. She receives non-steroidal anti-inflammatory analgesia in the perioperative period. On admission her urea is 6 mmol litre-1 (BUN 16-6 mg dl-1), and creatinine 55 ^mol litre-1 (0-66 mg dl-1). Two days postoperatively her blood results are as follows: sodium 130 mmol litre-1, potassium 3-8 mmol litre-1, urea 20 mmol litre-1 (BUN 55-5 mg dl-1), and creatinine 250 ^mol litre-1 (3 mg dl-1). Her vital signs are: alert, blood pressure 180/80 mmHg, pulse 75 per minute, respiratory rate 14 per minute, and oxygen saturations 95% on air. Can you explain the cause of her acute renal failure and discuss your management?

7. A 50-year-old man with mild diabetic nephropathy is admitted to the coronary care with a myocardial infarction. He suffers a ventricular fibrillation arrest and has no pulse for 5 minutes. He has a 2-hour episode of hypotension following this, which is treated with fluid and vasoactive drugs. Although his cardiac condition recovers, his renal function worsens. On admission his urea was 12 mmol litre-1 (33-3 mg dl-1), and creatinine 150 ^mol litre-1 (1-8 mg dl-1). Now his urea is 22 mmol litre-1 (61 mg dl-1) and creatinine 300 ^mol litre-1 (3-6 mg dl-1). What are the reasons for his deteriorating renal function and what is your management?

8. A 55-year-old lady undergoes an elective abdominal aortic aneurysm repair. The aneurysm was located above the renal arteries and the aorta was cross-clamped for 10 minutes. She returns to the ICU from theatre still intubated. Her vital signs are: pulse 100 per minute, blood pressure 120/60 mmHg, CVP 8 mmHg, temperature 34°C. Her arterial blood gases on 40% oxygen show: pH 7-2, PaCO2 4-0 (30-7 mmHg), bicarbonate 11-5 mmol/l, BE - 12 PaO2 25-0 kPa (192 mmHg). Her urine output has been 20 ml h-1 for the last 2 hours. Discuss your management.

Self-assessment - discussion

1. Any airway and breathing problems should be assessed and treated first. It may be that this patient requires naloxone to improve his conscious level and respiratory rate. Emergency treatment of hyperkalaemia is always indicated above 6-5 mmol litre-1 or if there are changes on the 12-lead ECG. The blood pressure of 90/60 and tachycardia could indicate volume depletion so fluid should be given to restore intravascular volume. Treatment with vasoactive drugs may be needed if perfusion is inadequate despite volume replacement. The patient should be catheterised to allow hourly measurements of urine. An urgent renal tract ultrasound should be arranged. Finally, one should look for a treatable underlying cause. In this case, creatinine kinase should be measured as the combination of a drug overdose and prolonged immobilisation is a classical cause of rhabdomyolysis.

2. The combination of dehydration from a chest infection and medication (ACE inhibitor and NSAIDs) has triggered acute renal failure. Hypotension is causing hypoperfusion of the kidneys and making the renal impairment worse. Oxygen should be given, followed by fluid challenges to expand intravascular volume. In a patient normally treated for heart failure, invasive monitoring may be considered earlier than in people with normal cardiac function. Once intravascular volume is adequately replaced, vasopressors may be necessary to treat ongoing hypotension. He should be catheterised and a renal tract ultrasound scan arranged. Nephrotoxic medication should be stopped. If renal function fails to improve with these measures, renal replacement therapy should be considered. As with all cases of acute renal failure, urine should be sent for microscopy and culture. More specialised tests may be recommended by a renal specialist to look for other possible causes.

3. Treatment starts with an assessment of airway and breathing followed by circulation. Intravenous fluid should be given to correct any volume depletion. There is unlikely to be hypoperfusion in this case as the blood pressure is 180/85 mmHg, but other signs of this should be assessed. She should be catheterised to allow accurate measurement of urine output and an urgent renal tract ultrasound arranged. The underlying cause should be investigated. Dipstick testing, microscopy, and culture of the urine should be requested. This gives clues in conditions such as glomerulonephritis (microscopic haematuria and proteinuria) and acute tubulo-interstitial nephritis (eosinophiluria), and diagnoses urinary tract infection, which is an important cause of acute renal failure, especially in the elderly. Although the combination of breathlessness with bilateral patchy shadowing and acute renal failure may be due to chest infection and dehydration/medication as in case 2, one should consider a pulmonary-renal syndrome, for example Goodpasture's (anti-GBM disease). A renal specialist should be contacted.

4. After assessing A and B, blood cultures may be taken at the same time as gaining intravenous access. Assuming there is no life-threatening hyperkalaemia, fluid challenges should be given to treat volume depletion. Invasive monitoring may be needed if there is any uncertainty as to when the patient is adequately filled in the presence of persisting hypotension/hypoperfusion. Any anti-hypertensive medication should be temporarily stopped (apart from p blockers, which can be reduced). This patient is at high risk of acute renal failure because of oliguria, cholestasis (which causes renal vasoconstriction), gentamicin therapy, and a previous nephrectomy - early action is essential to prevent irreversible damage to his remaining kidney. Persisting hypoperfusion despite adequate volume replacement requires vasoactive drug therapy in a high dependency area. He should be catheterised and an urgent renal ultrasound arranged. The cause of acute renal failure here is most likely to be acute tubular necrosis from hypoperfusion and sepsis.

5. The history and examination in this case point to volume depletion, which should be corrected with fluid challenges. If hypotension/ hypoperfusion persists despite this, invasive monitoring and vasoactive drug therapy may be required. Note she is normally hypertensive - her normal blood pressure should be ascertained to guide therapy. She should be catheterised to allow accurate measurements of urine output. The underlying cause in this case is likely to be dehydration exacerbated by NSAID use. Frusemide is often used to improve urine output after adequate filling and perfusion has been achieved. Frusemide does not affect outcome nor alter GFR but is useful when there is persisting oliguria and the patient still requires intravenous medications. Renal replacement therapy would be the next step if there is no improvement.

6. Surgery can be associated with episodes of hypoperfusion (because of volume depletion and hypotension due to anaesthesia). Perioperative NSAID use in addition, especially in the elderly, has caused acute renal failure in this case. There is no life-threatening hyperkalaemia. Volume depletion should be treated with intravenous fluid, a urinary catheter should be inserted and a renal tract ultrasound arranged. Urinary tract infection should be excluded and nephrotoxic drugs stopped.

7. This man is at risk of developing acute renal failure because he has pre-existing diabetic renal disease and has had a major cardiovascular upset. A period of hypoperfusion has caused acute renal failure. Management is the same as in the other cases: treat any life-threatening hyperkalaemia, then hypovolaemia, then any hypoperfusion, catheterise, exclude higher obstruction with an ultrasound scan, and treat the underlying cause. If renal function continues to deteriorate, renal replacement therapy should be considered.

8. The cause of acute renal failure in this case is the transient interruption of blood flow to the renal arteries. The patient is hypoperfused as indicated by the history, low temperature, and metabolic acidosis. She should be "warmed up and filled up". Dopexamine is often used in post-aneurysm repair patients because a few small studies have suggested a beneficial effect on creatinine clearance following major surgery - probably owing to increased cardiac output and systemic vasodilatation. However, the vast majority of clinical studies of dopamine and dopexamine following major surgery have not demonstrated a benefit.

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