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Succinylcholine-Induced Hyperkalemia and Rhabdomyolysis in a Patient with Necrotizing Pancreatitis

Matthews, J. Mark MD

doi: 10.1097/00000539-200012000-00047

Implications Commonly used muscle relaxants may have serious side effects when used in critically ill patients. This case report relates some of these side effects and reviews the mechanisms by which they are thought to occur.

Department of Anesthesiology, Saint Luke’s Hospital, Kansas City, Missouri

August 11, 2000.

Address correspondence and reprint requests to J. MarkMatthews, MD, Department of Anesthesiology, St. Luke’s Hospital, 4400 Wornall Road, Kansas City, MO 64111.

Hyperkalemic responses to succinylcholine have been associated with many pathologic states, including burns, certain neuromuscular diseases, closed-head injury, malignancy, abdominal sepsis, hypovolemic shock, prolonged neuromuscular blockade, and prolonged immobilization (1–10). In the absence of malignant hyperthermia, rhabdomyolysis is a rare complication of succinylcholine administration. When identifiable risk factors are absent, succinylcholine-induced rhabdomyolysis may indicate an occult myopathy (11). We report a case of succinylcholine-induced hyperkalemic cardiac arrest and subsequent myoglobinuric renal failure occurring in a patient with severe necrotizing pancreatitis.

A 54-yr-old, 114 kg man presented to the hospital after the abrupt onset of abdominal pain accompanied by severe nausea and vomiting. A presumptive diagnosis of pancreatitis was confirmed by increased amylase and lipase. Abdominal computed tomography showed severe inflammation of the pancreas with probable necrosis. The pancreatitis was attributed to the presence of gallstones.

The past medical history was significant for a spinal cord injury sustained in a motor vehicle accident 14 mo before. A low-velocity collision caused cervical hyperextension with immediate tetraplegia. Cervical spine films failed to demonstrate fracture; however, subsequent magnetic resonance imaging showed cervical spondylosis with canal stenosis at the C 3–4 level and adjacent spinal cord contusion. After an uncomplicated anterior spinal fusion, the patient underwent rehabilitation and, over the next several months, regained almost full motor strength, although residual spasticity impaired his functional status. Implantation of a baclofen pump provided good control of his spasticity. Functional improvement was such that the patient was able to ambulate with the use of a cane.

Initial therapy of his pancreatitis consisted of fasting, total peripheral alimentation, and nasogastric tube decompression, along with narcotic analgesics. On the fifth day of admission, respiratory failure necessitated orotracheal intubation and mechanical ventilation. Midazolam infusion provided adequate conditions for ventilatory support, and nondepolarizing muscle relaxants were not administered. Ventilatory support continued for 1 wk before it was successfully terminated and the trachea extubated. On the 35th day of hospitalization, the patient again developed respiratory failure associated with large bilateral pleural effusions. Anesthesia personnel were summoned to the intensive care unit (ICU) to perform an endotracheal intubation.

Initial assessment revealed an obese man in obvious respiratory distress. Topical local anesthetic was applied to the oropharynx, and direct laryngoscopy was attempted. This was unsuccessful because of the patient’s confusion and inability to cooperate. Midazolam was titrated IV to a total dose of 8 mg without appreciable sedative effect. Because of the patient’s vigorous resistance to the procedure, his large body habitus with associated broad neck, his tolerance to standard sedatives, and the perceived need for expedient intubation, the decision was made to facilitate laryngoscopy with thiopental and succinylcholine. After breathing oxygen, thiopental 200 mg and succinylcholine 80 mg were given IV as cricoid pressure was applied. Successful endotracheal intubation was accomplished within 60 s, and the oxygen saturation increased to 96%. Approximately 2 min after intubation, the previously normal cardiac rhythm changed to a wide complex bradycardia. A presumptive diagnosis of hyperkalemia was made, and IV calcium chloride was given. The electrocardiographic complexes continued to widen to a sine-wave pattern followed by asystole. Cardiopulmonary resuscitation was performed. Epinephrine, sodium bicarbonate, and insulin/glucose were administered, and a blood sample was obtained to determine serum potassium. After 12 min of cardiopulmonary resuscitation, a narrow complex tachycardia resumed that was associated with good peripheral pulses. Defibrillation was not performed. Initial potassium level obtained during cardiopulmonary resuscitation was 9.8 mEq/L. Approximately 10 min after restoration of cardiac rhythm, the serum potassium had returned to a normal level of 4.1 mEq/L. Arterial blood gases obtained immediately postresuscitation showed a moderate metabolic and respiratory acidosis with pH 7.15, Paco2 58 mm Hg, Pao2 100 mm Hg, HCO3 19.2 mEq/L, and base excess −8.8 mEq/L. Infusions of phenylephrine and dopamine were required for the next several hours to maintain an adequate perfusion pressure.

The previously normal creatine kinase subsequently peaked at more than 16,000 U/L, indicating significant rhabdomyolysis. Postresuscitation creatinine was 0.7 mEq/L, and blood urea nitrogen was 34 mg/dL. Mannitol and small-dose dopamine infusion was given for renal prophylaxis. Midazolam infusion was used to facilitate mechanical ventilation. By 30 h postresuscitation, the creatine kinase and creatinine were 11,692 U/L and 2.3 mg/dL, respectively. Oliguria developed and 48 h postresuscitation the urine was sampled for myoglobin with the result of 142 μg/mL (normal range 0.000–2.0 μg/mL). Renal function continued to deteriorate, and the midazolam infusion was discontinued to evaluate the neurologic status of the patient before initiation of hemodialysis. The electroencephalogram and neurologic evaluation were consistent with severe hypoxic encephalopathy. Seventy-two hours later, a repeat electroencephalogram continued to show diffuse slowing with no reactivity. Consultation with the patient’s family resulted in a decision to withdraw supportive measures, and the patient died on the 41st day after admission.

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The mechanism of potassium release after succinylcholine administration has been reviewed (12). Of most concern are pathophysiologic states that increase chemosensitivity of the muscle membrane because of development of receptor sites in extrajunctional areas. A theory of receptor-drug interaction featuring upregulation of skeletal muscle acetylcholine receptors has been proposed to explain this increased chemosensitivity (13). It is not clear how long this increased chemosensitivity exists with respect to denervation injury. Early estimates were three to six months (12). A review of anesthesia for chronic spinal cord lesions states, “Most authors agree that suxamethonium may be used safely in the first 72 hours after injury and few would deny that elective use of suxamethonium is safe after 9 months” (14). An earlier review suggested that the danger period with spinal cord trauma lasted for six to seven months (15). Gronert (16), in a recent letter, has questioned these recommendations, reporting two patients who developed hyperkalemic responses to succinylcholine 7 and 10 years, respectively, after the onset of progressive motor-related disease, although the exact nature of their disease was not specified.

The degree and duration of central nervous system injury sufficient to cause hyperkalemic responses to succinylcholine have also not been defined. One report describes a patient with transient paraplegia (4–6 hours’ duration) after repair of a traumatic aortic transection who subsequently suffered succinylcholine-induced hyperkalemic cardiac arrest two months after the injury, despite almost complete recovery of neuromuscular function (17). Martyn et al. (13) have noted that although the duration of aberrant responses is difficult to determine, there are modest increases in extrajunctional receptors observed even three years after spinal cord injury. They also observed that the associated lower motor neuron changes seen with denervation decrease with the onset of spasticity. This would suggest that hypersensitivity to succinylcholine would be less likely to occur when spastic motor tone returned to previously flaccid muscle. Although abnormal neuromuscular function may indicate abnormal response to succinylcholine, it is clear that a normal neuromuscular examination cannot guarantee that hypersensitivity to the drug does not exist. Bresland and Bodenham (18) argue against the use of succinylcholine in the ICU because of this unpredictable hyperkalemic response and the lack of reliable methods to determine who is at risk.

Reported mortality rates caused by succinylcholine-induced hyperkalemic cardiac arrest vary from 0% (14) to approximately 40% (11), although some have questioned the accuracy of these figures because of underreporting (16). We suspect that the poor outcome in this case report was primarily caused by the patient’s severely debilitated state.

Considering the increased use of intrathecal baclofen in the management of chronic spasticity, it is important to note the reports of patients who developed hyperthermia and rhabdomyolysis associated with intrathecal baclofen infusion interruption (19,20). Severe spasticity, hyperthermia, and respiratory failure requiring ventilatory support occurred in two cases despite conversion to oral baclofen therapy. In our case, it is difficult to assess what role, if any, intrathecal baclofen infusion may have played in the development of rhabdomyolysis. There was no known interruption of the baclofen infusion.

The use of succinylcholine in critically ill patients is controversial. A recent publication argues for the drug’s removal from clinical practice (21). In this case, the decision to use succinylcholine as an adjuvant to endotracheal intubation was made in response to the difficulties presented by a large, hypoxemic, uncooperative patient who had considerable tolerance to standard sedatives. Alternative methods routinely used in the ICU setting, such as blind nasal and fiberoptic intubation, were not attempted in this case because of the patient’s vigorous resistance and the perceived need to expedite ventilatory support. Likewise, titration of alternative sedative drugs, such as propofol, was felt to be too time consuming. Recognizing that the hyperkalemic response to succinylcholine is unpredictable and that there are currently no criteria to establish those definitively at risk, it is uncertain that alternative administration of a long-acting nondepolarizing muscle relaxant would result in less overall morbidity when administered to a series of patients under similar circumstances. Nondepolarizing muscle relaxants with similar pharmacokinetics to succinylcholine would be preferred to longer-acting drugs in the management of the potentially difficult airway. The recent availability of the nondepolarizing muscle relaxant rapacuronium represents a possible alternative, considering its rapid onset and brief duration.

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© 2000 International Anesthesia Research Society