| Glynis Hawkins is a registered nurse at St. Vincent's Hospital Sydney. Glynis studied this case while undertaking the Intensive Care Course. |
Muscle injury causing rhabdomyolysis involves a complex sequence of events that can potentially affect most major body systems. As the incidence of rhabdomyolysis from drug-related causes increases, nurses need to maintain familiarity with the progression and treatment of this clinical syndrome. With efficient medical and nursing management, the mortality from complications can be reduced and patient recovery enhanced.
This case study examines the sequence of rhabdomyolysis as experienced by a patient in the intensive care unit and the subsequent treatment that enhanced his recovery.
[top]
James (pseudonym), a 25 year-old audio engineer, presented at a small city hospital in early 1994. He was pale, hypotensive (BP 70/40 mmHg), hypothermic (temperature 34°C), tachycardic (pulse 110) and complaining of a painful, swollen, right leg. James 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.
Based on serum chemistry results and the clinical picture, a provisional diagnosis of rhabdomyolysis of the right leg and acute renal failure was made. As impending surgery and haemodialysis were anticipated, preparation was made to transfer James to a larger teaching hospital in the area. Prior to transfer he was resuscitated with intravenous fluids and given Narcan, an antagonist to heroin.
On arrival at the teaching hospital, two hours later, the provisional diagnosis was confirmed. Following a surgical consultation, preparation was made for transfer to theatre for a multi-compartmental fasciotomy of the right leg that afternoon.
Following theatre, James was admitted to the Intensive Therapy Unit (ITU) for postoperative management and ventilation. His main problems were identified as:
[top]
Rhabdomyolysis literally means the breakdown of striated muscle fibres that results in the release of muscle cell contents into the blood (Harper, 1990: 32). The breakdown in the muscle cell membrane is a consequence of hypoxic damage to the muscle. Lysis, necrosis and death of the muscle (Burr, 1991: 29). In James's case, his rhabdomyolysis can be attributed to his cocaine and heroin use. Cocaine, a potent vasoconstrictor, causes rhabdomyolysis (McCrea, Rust, Cook et al., 1992: 2923) 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, Bandi & Baghaie, 1992: 932). When a patient is in a drug-induced coma, compression of the vascular network from the weight of the body increases pressure in muscle compartments, restricting the blood supply to the compressed muscle and causing rhabdomyolysis. The ischaemic and oedematous muscle further raises intra-compartmental pressure potentiating a vicious cycle of continuing ischaemia (Gabrow, Kaehney & Kelleher, 1982: 146). Muscle cell contents released into the bloodstream results in damage to major organs and systems, potentiating acute renal failure, electrolyte imbalances, metabolic changes and cardiac arrhythmias (Better, 1990: 98). Extracellular fluids will also move into the damaged muscle cell, raising the intra-compartmental pressure of the enclosed muscle (Burr, 1991: 29). This results in gross muscle swelling, weak pulses and diminished sensation and movement of the affected limb (Vucak, 1991: 533). The influx of extracellular fluids also produces a 'third space' effect and as fluid is lost from the circulation, hypovolaemia and haemodynamic shock develop (Better, 1990: 99).
Acute renal failure occurs in rhabdomyolysis as a result of two processes:
This is particularly evident when aciduria is present (Burr, 1991: 30). Renal hypoperfusion and the nephrotoxic effect of myoglobin potentiate acute tubular necrosis, a form of acute renal failure (Humes, 1993: 1260).
Acute tubular necrosis (ATN) is a potentially reversible renal failure (Hoffart, 1986: 776) that results from either ischaemic or toxic processes (Humes, 1993: 1260). If treated early, the tubular damage is reversible due to the regenerative ability of the surviving renal epithelial cells. Necrotic areas are replaced with new cells and renal function returns to normal in most cases (Humes, 1993: 1260).
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: 778). 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: 763). Uraemia also decreases platelet aggregation predisposing the patient to excessive bleeding (Uldall, 1988: 107), especially from the mucous membranes and gastrointestinal tract. Anaemia may be present as a result of altered coagulopathy or blood loss from the rhabdomyolytic injury. Uraemia compromises both the cellular and humoral immune systems (Hoffart, 1986: 778), making the patient more susceptible to infections.
Electrolyte imbalances result from the net movement of solutes into and out of the damaged cell (Muther, 1992: 1591). Potassium and calcium, two electrolytes whose movement is quite dramatic, are potentially, lethally cardiotoxic, particularly in hypotensive patients (Better, 1990: 55). The high concentration of potassium normally contained intracellularly is released into the extracellular environment when cell lysis occurs, resulting in significant hyperkalaemia (Weisberg, 1993: 1180).
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 the ECG may first be seen as ventricular fibrillation or asystole (Weisberg, 1993: 1187). Serum potassium levels above 6.5 mmol/L must be treated as an emergency (Weisberg, 1993: 1188).
Hypocalcaemia, defined as a serum calcium less than 2.25 mmol/L, results from the deposition of calcium salts into injured or necrotic muscle (Farmer, 1992: 1788). Hypocalcaemia, exacerbated by hyperphosphataemia will further irritate the heart (Better, 1990: 98).
Normally, hyperkalaemia is controlled by the body by increasing the renal excretion of potassium, and moving potassium from the extracellular fluid to the intracellular fluid (Worthey, 1991: 508). When hyperkalaemia is exacerbated by acute renal failure, normal regulatory mechanisms fail. Metabolic acidosis occurs early in the course of ATN, as end-product acids of normal metabolism are unable to be excreted by the kidneys (Hoffart, 1986: 776). Acidosis that causes a serum pH below 7.00 is not compatible with life for very long and requires urgent treatment (Whiteside, 1988: 16). Metabolic acidosis will also present as a consequence of the lactic acidosis of rhabdomyolysis (Franklin & Klein, 1994: 1188) and will affect the contractility and conductivity of the heart.
From the hypoxic effects of a drug overdose to the metabolic consequence of muscle breakdown, each aspect of rhabdomyolysis has the potential to cause cardiac problems.
[top]
The management of James was based on a combination of physical assessment, biochemical analysis and close monitoring of all body systems. In the intensive care unit, medical, nursing and staff from other disciplines worked together to manage each of James's individual problems simultaneously.
On arrival in intensive care, James was intubated with an endotracheal tube (ETT). He was ventilated on a pressure-cycled ventilator with a breath rate of 12 breaths/min, a tidal volume of 800 mL (based on 1015 mL/kg; Hudak, Gallow & Benz, 1990: 356), inspired gas 40% oxygen and a positive end expiratory pressure (PEEP) of 5 cm H2O. His oxygen haemoglobin saturation (Sa02) measured via pulse oximetery was 98%. James was predisposed to hypoxia from his decreased level of consciousness, pneumonia and presence of an ETT; therefore, his Sa02 was measured continuously via pulse oximetery and maintained over 90% saturation. While James was intubated, it was the responsibility of the nurse to ensure that a clear airway was maintained and that the mechanical ventilation was adjusted to his requirements. The ETT was kept secure, in a correct position on X-ray and clear of secretions by regular suctioning, physiotherapy and humidifying inspired gases. Sedation and pain relief were ordered and administered to maintain comfort.
Arterial blood gases indicated a metabolic and respiratory acidosis. On the basis of these results the decision was made to leave James intubated and ventilated. This facilitated airway suctioning and removed the respiratory component to his acidosis by hyperventilation. The ventilator settings were adjusted accordingly. Sodium bicarbonate 8.4% was administered intravenously to assist in correction of his acidosis. Bicarbonate administration and hyperventilation are also used as methods of treating hyperkalaemia as bicarbonate helps to force potassium intracellularly (Franklin & Klein, 1994: 1187). Sodium bicarbonate also alkalises the urine making circulating myoglobin more soluble and less likely to damage the renal tubules (Muther, 1992: 1590). A routine postoperative chest X-ray was performed that showed correct positioning of the ETT, central venous catheter (CVC) and nasogastric (NG) tube. Bibasal pneumonia with consolidation was evident. As aspiration was a possibility due to the period of unconsciousness from the initial drug overdose, intravenous penicillin, ceftriaxone and metronidazole were commenced. It was imperative while James was being ventilated for the nurse to observe continuously for complications that can result from positive pressure ventilation. Auscultating for equal air entry and observing the rise and fall of the chest assists in excluding the presence of pneumothorax and barotrauma. Close attention to ventilator alarm settings and observation of the patient's response to the mechanical ventilation is necessary to maintain safety. A high volume/low pressure cuffed ETT was used to provide a tight seal to the airway while preventing tracheal irritation and necrosis.
Six hours after admission to ITU, arterial blood gas results showed a reduction in James's acidosis. Successful weaning off the mechanical ventilation was commenced and James was extubated 35 hours after his initial ITU admission. Oxygen therapy continued via a Puritan nebuliser and was titrated to maintain a Sa02 greater than 90%. It was important at this time to observe that James was able to protect his own airway and he was encouraged to participate in deep breathing and coughing exercises.
Antibiotic therapy to prevent wound infection and treat the aspiration pneumonia continued until Day 5 of admission.
James's clinical picture predisposed him to haemodynamic instability. Positive pressure ventilation decreased his cardiac output, acute renal failure can lead to fluid overload and he was losing fluid from 'third spacing' in his leg, ooze from the fasciotomy site and insensible losses from his gut, skin and lungs. An accurate fluid balance chart was maintained to monitor his fluid status. Blood pressure, central venous pressure, skin turgor and urine output were examined closely. Fluids were administered as required with care to avoid fluid overload. As a result of this close monitoring, James remained normotensive during his admission to ITU.
In an attempt to promote diuresis, and prevent the progression of renal failure (Harper, 1990: 34), intravenous sodium chloride (0.9% NACl) was ordered at 120 mL/hour. Packed cells were given when his serum haemoglobin dropped to 75 g/L (normal 130-180 g/L).
The nurse performed hourly limb observations on James's right leg to assess blood supply and innervation to the injured area. Throughout his admission, femoral, popliteal and pedal pulses were palpable, capillary return was brisk and his toes were warm indicating adequate circulation and perfusion. Movement and sensation remained absent to the day of discharge from hospital. It was necessary to protect the leg from the hazards of heat and sharp objects as sensation was impaired.
James was attached to an ECG monitor that showed sinus rhythm of 100 beats/min. Metabolic acidosis, hyperkalaemia, acute renal failure and James's cocaine use all had the potential to cause cardiac arrhythmias, so his ECG was monitored continuously. A 12 lead ECG on admission showed peaked T waves indicative of hyperkalaemia. Aggressive treatment for hyperkalaemia was continued as his serum potassium at this time was dangerously high at 7.1 mmol/L (normal 3.5-5.0 mmol/L).
Resonium, a cation exchange resin (Badewitz-Dodd, 1991: 523) was given rectally every four hours until serum potassium was less than 4.5 mmol/L. A glucose and insulin infusion was commenced to further decrease the serum potassium by forcing extracellular potassium into the cells (Franklin & Klein, 1994: 1187). Insulin stimulates potassium uptake by the muscles and liver leading to a rapid decrease in serum potassium levels (Weisberg, 1993: 1192). Glucose is given concomitantly to prevent hypoglycaemia. Bicarbonate therapy, as earlier explained, contributes to controlling hyperkalaemia in the same way (Franklin & Klein, 1994: 1187).
Intravenous calcium chloride was given on admission to decrease the effect of potassium on the heart (Franklin & Klein, 1994: 1187). Calcium therapy was not continued in ITU as studies have shown that infused calcium deposits in the injured muscles, and may aggravate metastatic calcification.
Within six hours of therapy, James's serum potassium dropped to an acceptable level of 4.2 mmol/L and the resonium and insulin therapy was ceased. Throughout the remainder of his admission, James's potassium remained stable until dialysis was commenced. At this stage, levels dropped to 2.9 mmol/L necessitating potassium supplements until a level of 3.5 mmol/L was reached. A Gated Heart Pool Scan (GHPS) on Day 3 of admission showed a left ventricular ejection fraction (LVEF) of 30%. A cardiology review concluded that the decreased LVEF may have been due to the myocardial depressive effects of heroin or an acute inferior myocardial infarction. Cardiac enzyme tests were shown to be normal. Creatinine kinase (CK) an enzyme found in cardiac and skeletal muscles, rises when damage to tissue occurs (Byrne, Saxton, Pelikan et al., 1986: 185). CKMB is a specific marker for cardiac muscle injury but is also found in small amounts in skeletal muscle (Goe, 1989: 282). A rise in CKMB of more than 5% of the total CK is significant of myocardial injury (Bryne et al., 1986: 187). Although James's CK peaked at 84,000 U/L (normal < 130 U/L) his CKMB was equally elevated at 1295 U/L (normal < 5 U/L); thereby, producing a percentage rise of 1.5%, ruling out the possibility of myocardial damage. The elevated levels can be directly attributed to the rhabdomyolytic injury (Goe, 1989: 281).
A full neurological assessment was conducted on admission and no deficits were detected except motor movement and sensation to the right leg. Although James's scrum urea and creatinine were raised (urea 20.8 mmol/L: normal 3.0-8.5 mmol/L; creatinine 0.56 mmol/L: normal 0.06-0.12 mmol/L) dialysis was initiated before uraemic toxicity affected his level of consciousness (Hoffart, 1986: 778). When sedation was ceased and James was extubated, the nurse observed that he scored maximum points on the Glasgow Coma Score (GCS); thus, he exhibited normal power in both arms, orientation and spontaneous eye opening (Frisby, 1991: 262). Neurological observations were continued hourly until ceased by the medical team.
On admission to ITU, James remained nil by mouth until he was extubated on Day 2. James was predisposed to decreased GIT integrity related to his nil by mouth order, acute renal failure and the stress placed on his body at this time. Gastric aspiration was performed every six hours via the NG tube and the pH of the aspirate tested to determine the acidity of the stomach contents. Gastric aspirates revealed a pH of 1 (normal pH = 6) so intravenous ranitidine was commenced. Histamine H2 receptor blockers, such as ranitidine, are the treatment of choice for hyperacidity related to renal failure (Franklin & Klein, 1994: 1192). Sucralfate was given via the NG to provide a cytoprotective barrier to the stomach (Badewitz-Dodd, 1991: 3). Folate, Intravite and vitamin K were given prophylactically while James was not eating to prevent vitamin deficiencies. By Day 3 of admission James was tolerating an oral diet. He was advised to commence high calorie, low sodium and low potassium diet. Auscultated bowel sounds were present by Day 2 and normal bowel function commenced on Day 3 of admission. A daily bowel chart was kept and stools were observed for the presence of blood. Fluid was restricted to 2000 mL/day to prevent fluid overload. Despite noncompliance with his food and fluid regimen James exhibited no adverse effects.
On admission to ITU James was oliguric with no palpable bladder. Urinalysis on admission to the Emergency Centre had shown a large amount of protein and blood and a pH of 5. Blood urea at 12.3 mmol/L (normal 3.0-8.5 mmol/L) and creatinine at 0.23 mmol/L (normal 0.06-0.12 mmol/L) were raised. The instigation of early large volume replacement in rhabdomyolysis has been shown by Better (1990: 101) to produce a forced solute diuresis that may protect the kidneys against acute renal failure. In James's case, fluid replacement was delayed and consequently renal failure resulted. Vasoconstriction of the renal vessels may also have been a contributing factor due to cocaine intake (Taylor et al., 1992: 930).
Mannitol, an osmotic diuretic, has the potential for reducing the level of toxin in the renal tubules by excretion of water and sodium (Humes, 1993: 1263). Frusemide was also trialled to produce a diuresis as recommended (Humes, 1993: 1263) but failed in this case. Definitive studies validating the use of mannitol or frusemide are lacking (Farmer, 1992: 1789). Renal dose doparnine at 51Ogg/kg/minute was commenced for renal vasodilation (Lee & Branch, 1991: 114). Despite this aggressive therapy, urine output failed to rise above oliguric levels.
Haemodialysis, via a subclavian vascular catheter, was commenced on Day 3 when serum urea peaked at 20.8 mmol/L. It was successful in reducing the serum urea to 14.4 mmol/L and removing 2000 mL of fluid. Haemodialysis removes waste products and water from the circulating blood by diffusion across an artificial membrane into a dialysis fluid. Dialysis continued after discharge from intensive care every two days until urine output resumed on Day 14. By Day 20, urea and creatinine levels had returned to normal and his indwelling urinary catheter was removed.
Initially sedation and analgesia were administered via a continuous infusion to maintain comfort. After James was extubated his pain was well controlled with patient controlled analgesia (PCA). Effective pain relief was monitored using a PCA assessment chart. This provides information concerning the amount of analgesia administered compared to the patient demand, level of sedation and the patient's interpretation of his pain relief. The PCA was ceased after he was transferred to a surgical ward. Morphine, 10 mg IMI, was given daily before dressings as well as two Panadol Forte every four hours. This regime failed to provide adequate pain relief and James became noncompliant with all aspects of his care. Rationale for the cessation of the PCA was unclear. Hobbes (1993) in his experience found that PCA is particularly effective for pain relief in heroin addicts.
Apart from James's existing aspiration pneumonia, other factors regarding his general condition predisposed him to further infections. These included uraemia, decreased nutritional status, open fasciotomy wound and multiple invasive sites.
As the central line, urinary catheter and AV fistula were all potential ports for infection, aseptic technique was adhered to when attending to each site. The central line and AV fistula were dressed according to unit protocol. IV lines were changed second daily and new IV fluids commenced every 24 hours. As James's condition improved, unnecessary lines were removed.
The fasciotomy wound was dressed daily as per the surgeon's orders and remained free from infection. Haemodialysis prevented further rises in James's serum urea level.
James's core temperature was monitored continuously via a rectal thermometer while he remained in ITU. Routine sputum, urine and wound specimens were analysed twice a week and as necessary. If his temperature had risen above 38.5°C, blood cultures would have been taken. Triple antibiotics were ordered and administered to treat James's chest infection and prevent wound infection. Oral Nilstat was given every six hours as prophylaxis to oral candida while on broad antibiotic cover. Oral feeding was commenced as early as feasible.
James made a good recovery from his chest infection and as he acquired no further infections the antibiotics were ceased prior to transfer to the surgical ward.
Unfortunately James had a poor social network and had few visitors while he was in intensive care. Over the years he had lost contact with his family, and the majority of his close friends were connected with his fast-paced lifestyle.
There were many challenges for James concerning his upcoming recovery. He faced the possibility of not regaining the use of his leg and consequently it was uncertain if he would be able to return to his profession as an Audio Engineer. This placed his financial stability and lifestyle at risk. Physiotherapy was commenced in ITU by way of passive range of motion exercises and a leg splint to prevent foot-drop. On the ward he was encouraged to keep his leg elevated and rested as requested by the surgeon to promote healing and later skin grafting. He was uncompliant with these orders and insisted on mobilising to go outside for cigarettes. The social workers attempted to assist with his financial and social problems. As he was still receiving sick pay from his employer he did not see his financial situation as an immediate threat. James was not interested in discussing his social situation or the possibility of work retraining.
James was offered drug rehabilitation services by the medical and nursing staff. Despite his long history of drug use, he failed to identify that he had a problem. During his hospital admission he did not show signs of drug withdrawal. The risk of infectious diseases such as HIV and hepatitis from James's IV drug use was also discussed with him. He assured staff that he adhered to 'safe' needle practices; therefore, he did not see this as a problem. He did not recognise that by continuing his present lifestyle he was placing his life at risk.
While James was unable to care for himself his needs were attended by the nursing staff. Initially while he was intubated and sedated, mouth and eye care were performed every two hours. Pressure area care was attended second hourly and he was nursed side-to-side to promote lung drainage and maintain skin integrity. As James's condition improved and he regained his independence he was encouraged to attend to his own hygiene needs. For his own safety, bedrails were kept in place and his hands were restrained while the ETT was in situ to prevent accidental dislodgment. A nurse observed James at all times. He was continually orientated to his environment and all procedures explained prior to commencing. Environmental stressors such as excessive noise and light were kept to a minimum. These measures assisted to avoid unnecessary anxiety and consequently James was quite compliant with his personal care while in ITU.
[top]
The combined medical and nursing management of James's problems assisted him to achieve a relatively complication free admission. His ABG's returned to normal indicating a resolution of the metabolic acidosis, blood electrolyte results were within normal range, renal function returned and no permanent cardiac problems ensued. He remained normotensive for the majority of his stay.
On Day 29 skin grafts were successfully applied to the open fasciotomy wound. On Day 53 he was awaiting transfer to a rehabilitation facility.
Considering James's long history of drug abuse and his refusal of drug rehabilitation, there is a risk that he will return to his previous lifestyle when he is discharged from hospital. The rehabilitation process to regain the use of his leg will be extensive and it is still uncertain if he will be able to return to his previous employment. These factors combined with his poor social support network and noncompliant nature unfortunately jeopardise his long term prognosis.
[top]
James's admission to ITU with rhabdomyolysis was complicated by damage to numerous body systems. Although the damage to his leg may be permanent, death from organ failure was avoided. As a result of multidisciplinary support, James was able to make a good recovery.
By anticipating problems and providing quality nursing and medical care, the outcome from this complex syndrome can be favourable.
[top]
[top]