By Paul Mazurek
Case Study
An air medical team is called to the bedside of a 33-year-old female brought in by EMS as high priority an hour earlier. She was found on her bathroom floor, unresponsive with agonal respirations. It was unknown how long she had been lying there. Prehospital care included endotracheal intubation, full spinal precautions, and intravenous naloxone, thiamine, and 50 percent dextrose per local protocol.
The patient is well known in the local emergency department. She has a history of depression and substance abuse including alcohol, cocaine and prescription pain medications. She has been hospitalized several times over the past year due to her drinking binges, and more recently spent four days in the intensive care unit recovering from a cocaine overdose.
She has no known medication allergies and takes Paxil (paroxetine) for depression and Oxycontin (oxycodone) for chronic back pain.
Upon the air medical team’s arrival, the patient was being mechanically ventilated, had received two liters of isotonic crystalloid and lorazepam for agitation. Bilateral breath sounds revealed coarse rhonchi. There were no obvious signs of trauma, but the patient remained in spinal precautions pending imaging results.
The air medical team notes her abdomen is soft but slightly distended, and her skin is warm, dry with no obvious abnormalities. She moves only her right-sided extremities. Current vital signs include a heart rate of 136 beats/minute, a blood pressure of 136/94, oxygen saturation of 94 percent, and temperature of 38.3 degrees Celsius. Urine output by foley catheter is 40 ml for the last hour and is very dark-colored.
Laboratory results thus far include a serum sodium of 135 mEq/L, serum potassium of 7.4 mEq/L, serum chloride of 94 mEq/L, bicarbonate of 15 mEq/L, anion gap of 24, blood urea nitrogen (BUN) of 52 mg/dl, serum creatinine of 2.2 mg/dl, troponin-T of 0.2 ng/ml and an absolute creatine kinase (CK) of 52,000 U/L. Results of an arterial blood gas obtained shortly after arrival include a pH of 7.08, PaCO2 of 48 mmHg, PaO2 of 86 mmHg and an oxygen saturation of 92 percent.
What are treatment and transport priorities? What possibilities could explain the derangement in laboratory values? What should the transport team anticipate?
The Problem and Resultant Pathophysiology
This patient is suffering from respiratory and acute renal failure with a metabolic acidosis and a large anion gap. Troponin-T value is normal while absolute CK value is markedly elevated. History of present illness, clinical presentation and abnormalities in laboratory studies are highly suggestive of rhabdomyolysis.
Rhabdomyolysis is a clinical syndrome caused by skeletal muscle injury and results in release of intracellular contents into the extracellular fluid. Diagnosis is usually made by measuring these released substances in either plasma or urine. Injury can be reversible or irreversible, potentially leading to significant morbidity including renal failure or death.2 Clinically, rhabdomyolysis is identified using creatine kinase (CK) levels and similar clinical indicators of acute renal failure, crush injuries, acidosis, electrolyte derangements or myoglobinuria.1
While there are many causes of rhabdomyolysis, the most common include direct muscle injury from trauma, drug abuse (including alcohol, cocaine and narcotics), excessive physical activity and toxic ingestions.3 Within this patient’s history of present illness, potential contributors to rhabdomyolysis include the possibility of alcohol or cocaine abuse; prescription medications; prolonged state of immobility; compression; and vascular occlusion to blood vessels supplying blood flow to skeletal muscle, thus causing cellular damage, or sepsis.
Diagnosis and Management
Rhabdomyolysis is a clinical syndrome, complicated by acute renal failure and metabolic derangements. Complications may include disseminated intravascular coagulation, compartment syndrome and peripheral neuropathies.1
CK levels are a sensitive indicator of myocyte injury in rhabdomyolysis. A CK level greater than five times normal is often diagnostic, and levels as high as several hundred thousand have been reported.4 Suspect rhabdomyolysis in any stuporous or comatose patient or one who is otherwise unable to provide a medical history and has one or more of the following:
- Muscle tenderness
- Evidence of pressure necrosis of the skin
- Signs of multiple trauma or crush injury
- Recent history of prolonged or continuous muscle contraction
- Darkened or discolored urine
- Blood chemistries suggestive of muscle cell breakdown:
— Hyperkalemia
— Hyperphosphatemia
— Hypocalcemia
Mainstay treatment goals for rhabdomyolysis include airway protection, volume resuscitation, and correction of metabolic derangements. While there is no solid evidence for target urine output for patients with rhabdomyolysis, the generally accepted goal is an hourly output of 200 ml/hr or greater. This mandates monitoring with placement of a foley catheter.
In the transport environment, maintenance of urine output should be achieved with volume resuscitation in the form of intravenous normal saline, as this particular isotonic crystalloid does not contribute significantly to hyperphosphatemia. Transport to a center capable of continuous renal replacement therapy or hemodialysis is usually the definitive destination for appropriate management of these patients.
Diuretics should be used cautiously during transport and central venous pressure monitoring should be in place to assess intravascular volume status. An osmotic diuretic such as mannitol is the agent of choice in rhabdomyolysis. Avoid loop diuretics such as furosemide, as this can contribute to urine acidification and tubular cast formation.1
The efficacy of urine alkalinization remains controversial. Myoglobin protein binding and subsequent cast precipitation is enhanced in acidic conditions. Urine alkalinization could theoretically enhance renal myoglobin clearance by increasing myoglobin’s solubility. Sodium bicarbonate could aid in this management goal. Patients with rhabdomyolysis who have been severely injured or who are profoundly hypotensive tend to be acidotic and may benefit from supplemental sodium bicarbonate.1
Hyperkalemia is the most dangerous electrolyte disturbance in patients with rhabdomyolysis because of its propensity to precipitate lethal cardiac arrhythmias, as well as diminish contractility. Continuous cardiac monitoring should be in place and hyperkalemia should be treated aggressively. If possible, avoid calcium, as supplemental calcium can exacerbate cytoplasmic injury.1
Conclusion
In the transport environment, rhabdomyolysis remains an often underappreciated phenomenon. As a consequence, the causes are treated while the syndrome remains overlooked. It can become challenging to put all of the pieces of the clinical puzzle together, especially in the critical care transport environment.
Fortunately, the diagnosis of rhabdomyolysis requires only a few laboratory results from tests typically drawn on emergency department patients accompanied by the clinical presentation and history. Targeting the syndrome as opposed to merely treating symptoms can significantly reduce morbidity and mortality in patients with rhabdomyolysis.
References
1. Adams JG et. al. James G. Adams: Emergency Medicine (1st ed.). Chapter 170, pp. 1809-1819. Elsevier, Philadelphia. 2008.
2. Bontempo, LJ. Rosen’s Emergency Medicine: Concepts and Clinical Practice (6th ed.). Chapter 125. Elsevier, Philadelphia, 2006.
3. Criddle, LM. Rhabdomyolysis: Pathophysiology, Recognition and Management. Critical Care Nurse 23:6, December 2003. pp. 14-32.
4. Malinoski DJ, Slater MS, Mullins RJ. Crush Injury and Rhabdomyolysis. Critical Care Clinics 20 (2004). pp. 171-192.
