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Case Reports: Case Report

The Use of Sugammadex in a Patient With Guillain–Barre Syndrome: A Case Report

Tezcan, Büşra MD; Bölükbaşi, Demet MD; Kazanci, Dilek MD; Turan, Sema MD; Suer Kaya, Gülseren MD; Özgök, Ayşegül MD

Author Information
doi: 10.1213/XAA.0000000000000465
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Abstract

Sugammadex is a selective relaxant binding agent that encapsulates and inactivates rocuronium and vecuronium. It is used to reverse neuromuscular blockade from these nondepolarizing agents. Sugammadex–rocuronium and sugammadex–vecuronium complexes are inactive and eliminated from the body according to pharmacokinetic properties of sugammadex, not those of neuromuscular blocking agents. Sugammadex is well tolerated in most patient groups, but its efficacy and safety have yet to be determined in patients with neuromuscular disorders. The purpose of this case report is to present our experience in administering sugammadex to a patient with Guillain–Barre syndrome (GBS).

The patient and his family reviewed this case report and gave written permission for the authors to publish this report.

CASE DESCRIPTION

A 48-year-old, 180 cm, 102 kg male patient with a diagnosis of colon carcinoma was scheduled for hemicolectomy. His medical history was significant for hypertension, diabetes (controlled by diet), and GBS. He was diagnosed with GBS 34 years ago with symptoms of lower limb paresthesias. His preoperative neurological examination revealed abolished plantar cutaneous reflex and loss of strength in both legs. He presented with a 4 out of 5 score using the Medical Research Council Scale for muscle strength.1 Laboratory tests showed no hematological, biochemical, or coagulation abnormalities. Subcutaneous low molecular weight heparin (40 mg) was initiated for prophylaxis of thromboembolic events.

On the day of the surgery, after the patient’s arrival in the operating room, pulse oximeter, electrocardiogram monitoring with leads II and V5, noninvasive blood pressure (BP) monitoring, and capnography were applied as standard monitors. Because of technical problems, neuromuscular function was not monitored. Before receiving an anesthetic, his oxygen saturation, heart rate, and BP were 96%, 115 beats per minute, and 170/85 mm Hg, respectively. The patient preoxygenated for 5 minutes. Induction of anesthesia consisted of intravenous fentanyl (1 µg/kg) and propofol (2 mg/kg). After he was rendered unresponsive, rocuronium (0.3 mg/kg) was administered. His trachea was then intubated. Sevoflurane in a 60:40 nitrous oxide and oxygen mixture was used for maintenance of anesthesia. The surgery was uneventful. The patient remained hemodynamically stable throughout the procedure with a heart rate of 90 to 100 beats per minute, systolic BPs between 130 and 160 mm Hg, and diastolic BPs between 60 and 85 mm Hg. At the end of the surgery, the rocuronium was reversed with sugammadex (4 mg/kg). The patient was extubated after his tidal volume (273–324 mL), respiratory rate (13 breaths/min), Spo2, grip strength, and 5-second sustained head lift were deemed adequate. The injection of sugammadex did not cause significant changes in heart rate, electrocardiogram, or BP values. He was admitted to the postanesthesia care unit, and 1 mg·kg−1 intravenous tramadol was used for analgesia. After an uneventful postoperative recovery with no anesthesia complication or difference in neurological examination, he was discharged home 10 days after surgery. Postoperative physical examinations, including the assessment of motor, sensory, cerebellar, and reflex function at 1 and 6 months after surgery, revealed no new neurological deficits.

DISCUSSION

GBS is an acute-onset, immune-mediated polyradiculoneuropathy with a reported incidence rate of 1 to 2 per 100,000. A total of 60% to 65% patients with GBS report a history of viral infection. The most common viral infections include upper respiratory tract infections, influenza, and gastrointestinal infections. The syndrome starts with weakness of the extremities and muscles of the trunk, cervical area, and face. It can progress to involve respiratory muscles and may cause respiratory failure in severe cases.2

The usual presenting symptoms in GBS are progressive bilateral and symmetric weakness of the limbs. Patients may also have numbness and paresthesias. Widespread areflexia or hyporeflexia is most frequently observed. GBS often affects cranial and phrenic nerves. Patients can develop respiratory, diaphragmatic muscle, or oropharyngeal weakness and may require prolonged mechanical ventilation.3 Autonomic dysfunction is seen in >50% of patients diagnosed with GBS.4 Pulmonary embolism and venous thromboembolism from prolonged immobility and pain are the other related comorbidities.5

There is no consensus in literature regarding anesthetic management of patients with GBS. Both regional and general anesthesia have been used, and both carry significant risks in this patient group. Ultimately, the choice of regional and general anesthesia is made in consultation between the anesthesiologist and patient when the potential benefits and risks of either technique are carefully considered.

When administering neuromuscular blockade, sensitivity to nondepolarizing muscle relaxants (NDMRs) may be variable in patients with GBS. Early in the disease process, denervation will lead to an induced resistance phase. Over time, this resistance may be gradually replaced by a second hypersensitivity phase with proliferation of extrajunctional acetylcholine receptors in response to the denervation.6,7 As a result, NMDRs should be used with caution, especially in chronic-phase patients, because they may result in prolonged neuromuscular block and the need for postoperative ventilation.8 Careful titration with small divided doses after starting with a lower dose of NDMRs and monitoring the effect of the drug with a nerve stimulator are appropriate.

Given that NDMRs may cause prolonged block and the need for postoperative mechanical ventilation in GBS patients, complete reversal of neuromuscular blockade is of paramount importance. Sugammadex reliably reverses rocuronium neuromuscular blockade in a manner that neostigmine could never achieve.

Autonomic dysfunction is an important consideration for anesthetic management of patients with GBS. Different patterns of autonomic outflow imbalance can be seen throughout the disease course in an individual patient. Common imbalances include sympathetic overactivity with parasympathetic underactivity.4 This manifests as tachycardia. Other adverse consequences include life-threatening arrhythmias, hypotension, hypertension, gastrointestinal dysmotility, and urinary retention.9 Determining the exact pattern of autonomic imbalance and physiologic repercussion of this imbalance may be difficult in the perioperative period. Of note, the administration of sugammadex did not have any apparent autonomic effects in our patient.

Anticholinesterases (neostigmine and pyridostigmine) have been used in treatment of GBS, particularly with symptoms of dysphagia, gastroparesis, and adynamic ileus.10,11 This approach is challenging because anticholinesterases can induce unexpected hemodynamic responses such as dangerous arrhythmias in GBS patients, especially with acute use during the perioperative period. Unpredictable physiologic repercussions of variable autonomic imbalance may be another reason to avoid anticholinesterases and anticholinergics. For this reason, reversal of neuromuscular blockade with sugammadex may be safer in this patient group.

Pain is also a common and often severe symptom of GBS. There are different kinds of pain involved in GBS, such as neuropathic, musculoskeletal, and visceral pain. This should be considered when determining an appropriate intraoperative and postoperative analgesic regimen. Pain may be severe in the acute denervation phase and can last up to 2 years. Perioperative pain management for GBS patients may require special attention by those trained in acute pain management.12 Poor pain control management may be another factor contributing to respiratory failure in GBS patients in the postoperative period. For our patient, postoperative pain was adequately controlled with tramadol with no adverse respiratory events.

Previous clinical trials have established that sugammadex is well tolerated in healthy volunteers, elderly and pediatric surgical patients, as well as patients with known renal impairment, cardiac disease, or pulmonary disease. In a pooled analysis, serious adverse events were infrequent. Procedural pain, nausea, and vomiting are the most commonly reported adverse events. The efficacy and safety of sugammadex in patients with poor health conditions or in those with neuromuscular disorders have not been formally determined. To date, several case reports suggest that sugammadex may in fact be safe and effective in these patient groups.13 In patients with chronic inflammatory demyelinating polyradiculoneuropathy (CIDP), there is only 1 report of sugammadex use. Maruyama et al14 used sugammadex in 2 patients with CIDP and reported that all patients rapidly regained muscular strength without any complications.

Sugammadex specifically encapsulates the aminosteroid nondepolarizing neuromuscular blocking agents rocuronium and vecuronium. The ability of sugammadex to form complexes with other steroidal and nonsteroidal compounds, such as cortisone, atropine, and verapamil, is probably clinically insignificant. Steroidal drugs and endogenous steroidal hormones form complexes with sugammadex, but with a much lower affinity.15 This may be an important issue for GBS patients because many of them are treated with steroids. The patient in this case report had no recent history of steroid treatment.

Our patient was slightly hypertensive and tachycardic before anesthesia induction, which may be a sign of autonomic imbalance. His body mass index was 31.5 (considered obese). The increased risk of residual neuromuscular blockade in an obese patient with GBS and problems with neuromuscular blockade monitoring motivated the use of sugammadex in our case.

CONCLUSIONS

The anesthetic technique used in GBS patients should be individualized to each patient based on their clinical condition and comorbidities. This patient group remains a challenge for anesthesiologists. Both the risk of autonomic instability potentially worsened by anticholinesterase and anticholinergic drugs and the increased risk of postoperative respiratory complications and residual neuromuscular blockade in GBS patients suggest that sugammadex reversal of rocuronium may be ideal in this patient group. In this case report, we describe the use of sugammadex without incident in a patient with GBS. More definitive work is warranted to explore the safety and efficacy of sugammadex in this patient group.

DISCLOSURES

Name: Büşra Tezcan, MD.

Contribution: This author helped write the manuscript and obtain the data about the patient.

Name: Demet Bölükbaşi, MD.

Contribution: This author helped obtain the data about the patient and with clinical management of the patient.

Name: Dilek Kazanci, MD.

Contribution: This author helped with clinical management of the patient.

Name: Sema Turan, MD.

Contribution: This author helped review the manuscript.

Name: Gülseren Suer Kaya, MD.

Contribution: This author helped with clinical management of the patient.

Name: Ayşegül Özgök, MD.

Contribution: This author helped review the manuscript.

This manuscript was handled by: Ken B. Johnson, MD.

REFERENCES

1. Medical Research Council. Aids to Examination of the Peripheral Nervous System. Memorandum No. 45. 1976.London: Her Majesty’s Stationary Office.
2. Van den Berg, Walgaard C, Drenthen J, et al. Guillain–Barré syndrome: pathogenesis, diagnosis, treatment and prognosis. Nat Rev Neurol. 2014;10:469482.
3. Ye Y, Li SL, Li YJ. Comparison on therapeutic effect of plasma exchange and intravenous immunoglobulin for Guillian-Barre syndrome. Transfus Med. 2015;25:7984.
4. Burns TM. Guillain-Barré syndrome. Semin Neurol. 2008;28:152167.
5. Gaber TA, Kirker SG, Jenner JR. Current practice of prophylactic anticoagulation in Guillain-Barré syndrome. Clin Rehabil. 2002;16:190193.
6. Fiacchino F, Gemma M, Bricchi M, Giudici D, Ciano C. Hypo- and hypersensitivity to vecuronium in a patient with Guillain-Barré syndrome. Anesth Analg. 1994;78:187189.
7. Brambrink AM, Kirsch JR. Perioperative care of patients with neuromuscular disease and dysfunction. Anesthesiol Clin. 2007;25:483509, viii–ix.
8. Brooks H, Christian AS, May AE. Pregnancy, anaesthesia and Guillain Barré syndrome. Anaesthesia. 2000;55:894898.
9. Miller RD. Sugammadex: an opportunity to change the practice of anesthesiology? Anesth Analg. 2007;104:477478.
10. Shaffer JO. The use of neostigmine in the treatment of the Guillain-Barré syndrome. J Am Med Assoc. 1946;131:285.
11. Lee KL, Lim OK, Lee JK, Park KD. Treatment of dysphagia with pyridostigmine bromide in a patient with the pharyngeal-cervical-brachial variant of Guillain-Barré syndrome. Ann Rehabil Med. 2012;36:148153.
12. Liu J, Wang LN, McNicol ED. Pharmacological treatment for pain in Guillain-Barré syndrome (Review). Cochrane Database Syst Rev. 2013:CD009950.
13. Yang LP, Keam SJ. Sugammadex: a review of its use in anaesthetic practice. Drugs. 2009;69:919942.
14. Maruyama N, Wakimoto M, Inamori N, Nishimura S, Mori T. [Anesthetic management of three patients with chronic inflammatory demyelinating polyradiculoneuropathy]. Masui. 2015;64:852855.
15. Naguib M. Sugammadex: another milestone in clinical neuromuscular pharmacology. Anesth Analg. 2007;104:575581.
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