The purpose of this case study is to evaluate and reflect upon the care given to a patient with acute renal failure and to evaluate the outcomes of the care given using the Roper-Logan and Tierney model of learning which looks at the activities of daily l

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COVENTRY UNIVERSITY SCHOOL OF HEALTH AND SOCIAL SCIENCES

Name: Lisa Gallard

Cohort: February 2008

Module code and title: 362CPD ACUTE RENAL CARE MANAGEMENT

Assignment Title: CASE STUDY – Rhabdomyolysis and acute renal failure

Module Leader: Richard Flemming

Word Allowance:  2500 +/- 10%

Word Count:  2476

Date for Submission:   5th SEPTEMBER 2008

The purpose of this case study is to evaluate and reflect upon the care given to a patient with acute renal failure and to evaluate the outcomes of the care given using the Roper-Logan and Tierney model of learning which looks at the activities of daily living.

Robert (pseudonym), a 35 year-old engineer, presented at the hospital. He was pale, hypotensive (BP 70/40 mmHg), hypothermic (temperature 34°C), tachycardic (pulse 110) and complaining of a painful, swollen, right leg. Robert admitted to a 10 year history of heroin, cocaine and amphetamine use. He was unsure of the events of the last 24 hours, but remembered injecting himself intravenously with a "usual" dose of heroin and cocaine the previous evening. On awakening the next morning he had a painful, right leg and was unable to move his right foot. He also has a history of smoking and alcohol abuse.

Based on serum chemistry results and the clinical picture, a provisional diagnosis of rhabdomyolysis of the right leg and acute renal failure was made.  He was resuscitated with intravenous fluids and given Narcan, an antagonist to heroin.

Following a surgical consultation, the provisional diagnosis was confirmed and preparation was made for transfer to theatre for a multi-compartmental fasciotomy of the right leg that afternoon.  After theatre, Robert was admitted to the Intensive Therapy Unit (ITU) for postoperative management and ventilation. His main problems were identified as: rhabdomyolysis secondary to drug overdose, acute renal failure, hyperkalaemia, metabolic acidosis and cardiac changes.

For the purpose of this case study I will look more closely at the management of rhabdomyolysis in acute renal failure. I will discuss the pathophysiology and look at the nursing interventions and outcomes for this patient.

Rhabdomyolysis literally means the breakdown of striated muscle fibres that result in the release of muscle cell contents into the blood (Harper, 1990). The breakdown in the muscle cell membrane is a consequence of hypoxic damage to the muscle. Lysis (destruction of cells), necrosis and death of the muscle (Burr, 1991). In Robert's case, his rhabdomyolysis can be attributed to his cocaine and heroin use. Cocaine, a potent vasoconstrictor, causes rhabdomyolysis (McCrea et al, 1992) by limiting the blood supply to the muscle. Diamorphine (heroin) belongs to the class of opiates that target receptors in the central nervous system producing effects of analgesia, ventilatory depression, bradycardia and sedation (Taylor, et al, 1992).  Muscle cell contents released into the bloodstream results in damage to major organs and systems, leading to acute renal failure, electrolyte imbalances, metabolic changes and cardiac arrhythmias.  Extracellular fluids will also move into the damaged muscle cell, raising the intra-compartmental pressure of the enclosed muscle (Burr, 1991). This results in gross muscle swelling, weak pulses and diminished sensation and movement of the affected limb (Vucak, 1991). The influx of extracellular fluids also produces a 'third space' effect and as fluid is lost from the circulation, hypovolaemia and haemodynamic shock develop.

Acute renal failure occurs in rhabdomyolysis as a result of two processes: decreased circulating plasma volume potentiates renal hypoperfusion and release of myoglobin from the muscle causes obstruction of the renal tubules.  This is particularly evident when aciduria is present (Burr, 1991). Renal hypoperfusion and the nephrotoxic effect of myoglobin may lead to acute tubular necrosis, (Humes, 1993).  

During the course of acute renal failure, waste products such as urea nitrogen and creatinine accumulate in the blood resulting in a uraemic syndrome (Hoffart, 1986). High concentrations of urea in the blood will cross the blood/brain barrier causing an osmotic effect that leads to abnormal amounts of water accumulating in the cells of the brain. As these cells swell, the patient is predisposed to seizures and neurological changes (MacGeorge & Bruno, 1986). Uraemia also decreases platelet aggregation which may lead to excessive bleeding (Uldall, 1988).  Anaemia may be present as a result of this and the patient may be more susceptible to infections due to the uraemic effect.

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Electrolyte imbalances result from the movement of solutes into and out of the damaged cell (Muther, 1992). Potassium and calcium, two electrolytes whose movement is quite dramatic, are potentially, lethally cardiotoxic, particularly in hypotensive patients. The high concentration of potassium normally contained intracellularly is released into the extracellular environment when cell lysis occurs, resulting in significant hyperkalaemia (Weisberg, 1993).

Hyperkalaemia is defined as a serum potassium greater than 5.0 mmol/L. Cardiac changes occur above this level due to the role of potassium in determining resting membrane potential. Normal ECGs may occur despite extreme hyperkalaemia and changes in ...

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