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Ann Thorac Surg 1996;61:1237-1239
© 1996 The Society of Thoracic Surgeons

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Case Report

Critical-Illness Polyneuropathy Complicating Cardiac Operation

H. Cem Alhan, MD, Cantürk Çakalaaolu, MD, Murat Hanci, MD, Fevzi Toraman, MD, Mustafa diz, MD, lyas Kayaciolu, MD, Sümer Tarcan, MD

Siyami Ersek Thoracic and Cardiovascular Surgery Center and Department of Neurosurgery, Cerrahpaa Medical Faculty, University of stanbul, stanbul, Turkey

Accepted for publication September 23, 1995.

	Abstract

Top Footnotes Abstract Introduction Comment Acknowledgments References

 
Critical-illness polyneuropathy is a complication of septic syndrome. However, this complication has been largely unrecognized in cardiac surgery units. Difficulty in weaning from the ventilator is an important early manifestation. Electromyography should be routinely performed to establish the diagnosis. Here we report a case of polyneuropathy complicating surgical repair of acute aortic dissection.

	Introduction

Top Footnotes Abstract Introduction Comment Acknowledgments References

 
The occurrence of sepsis and multiple organ failure in certain patients in critical care units has been recognized as a syndrome during the last two decades [1, 2]. The septic syndrome has been recently defined by Bone [3] as evidence of infection, increased respiratory rate, increased heart rate, elevated or reduced body temperature, and evidence of multiple organ failure. In recent years, critical illness polyneuropathy, characterized both electrophysiologically and morphologically by a primary axonal degeneration of motor and sensory fibers, has been reported [4] and has been shown to occur in the vast majority of patients with this syndrome [5]. This complication has been largely unrecognized especially in cardiac surgery units, perhaps due to difficulties in performing a clinical examination or electrophysiologic studies in the setting of a critical care unit. We report here a case of critical-illness polyneuropathy complicating a cardiac operation.

A 40-year-old man presented to the Siyami Ersek Thoracic and Cardiovascular Surgery Center emergency room with complaints of chest pain and shortness of breath. Physical examination revealed a 2/6 diastolic murmur at the second right intercostal space. Electrocardiography showed a sinus tachycardia of 120 beats/min with no ST or T wave changes. An admission chest x-ray study revealed the presence of mediastinal widening. The patient subsequently underwent transthoracic Doppler echocardiography, which revealed moderate aortic insufficiency and a linear echogenic density in the ascending aorta, a finding suggesting the presence of aortic dissection.

The patient was taken to the operating room without further examination due to the rapid deterioration of his clinical condition. The femoral artery was cannulated and, after separate cannulas were inserted into the superior and inferior venae cavae, the patient was placed on cardiopulmonary bypass. After systemic cooling to 18°C, total circulatory arrest, administration of cold blood cardioplegia, and retrograde cerebral perfusion, we evaluated the aorta and found an aortic dissection extending to the left common carotid artery. The ascending aorta and aortic arch were replaced with a 23-mm Dacron graft and the aortic valves were resuspensed. The patient was then weaned off cardiopulmonary bypass without difficulty. In the third postoperative hour he underwent resternotomy for excessive bleeding.

On the second postoperative day he was fully conscious without focal neurologic deficit and was extubated. He was able to eat and speak without any difficulty. However, 2 days later respiratory failure developed. At this time, chest roentgenography revealed diffuse bronchopneumonic infiltration. Four days later septicemia developed (hyperpyrexia; heart rate, 130 beats/min, plasma lactate level, 4 mmol/L; cardiac output, 10.5 L/min; pulmonary vascular resistance, 39 dynes•s•cm^-5; systemic vascular resistance, 453 dynes•s•cm^-5), and coagulase-positive staphylococcus (Staphylococcus aureus) was isolated from blood and tracheal secretion cultures. Antibiotic therapy (vancomycin and rifampin) and total parenteral nutrition was started. After being mechanically ventilated for 25 days he was extubated. Neurologic examination at this time revealed generalized muscular weakness that was more obvious at the proximal part of the right upper extremity. As oral feeding was started the patient aspirated all of the food into his trachea. A bronchoscopic examination revealed bilateral vocal cord paralysis while we were investigating a suspected tracheoesophageal fistula. Six weeks after the operation the patient was conscious and fully oriented, speaking hoarsely, with normal ocular, facial, and tongue movements. Neurologic examination showed symetrically reduced deep tendon reflexes, diffuse muscle weakness, and absence of gag reflex, with normal sensory examination.

At this time, electroneuromyographic study revealed fibrillation potentials and positive sharp waves, polyphasic motor unit potentials, poor recruitment, decreased conduction velocities of motor fibers predominantly in lower extremities, and diminished motor nerve action potential amplitudes consistent with primary axonal degeneration. As no evidence of albumino-cytologic dissociation was detected in cerebrospinal fluid examination, the diagnosis of Guillain-Barré syndrome was excluded.

As the patient was unable to swallow, a feeding gastrostomy was performed and physiotherapy and active rehabilitation were initiated. Three weeks later, he started oral feeding. Signs of reinnervation were detected at a second electroneuromyographic study performed 11 weeks after the operation. The patient was discharged from the hospital 12 weeks after admission with minimal neurologic deficit (bilateral vocal cord paresis and motor weakness of the right deltoid muscle).

Nine weeks after discharge electroneuromyographic study disclosed axonal regeneration of peripheral nerves except the distal part of the right median nerve.

	Comment

Top Footnotes Abstract Introduction Comment Acknowledgments References

 
The precise cause of critical illness polyneuropathy remains obscure. Bolton and associates [6] have speculated that a disturbance of the microcirculation to the peripheral nerve may be a basic mechanism because blood vessels supplying peripheral nerve lack autoregulation, rendering them particularly susceptible to such disturbances. Moreover, cytokines that are secreted in sepsis have histamine-like properties that may increase microvascular permeability. The resulting endoneurial edema could induce hypoxia by capillary closure, an increase in intercapillary distance, and other mechanisms. The result would be a primary axonal degeneration, which is typical of that seen in critical-illness polyneuropathy.

The findings of primary axonal degeneration of motor and sensory fibers, without inflammatory change, and relatively normal cerebrospinal fluid distinguish the neuropathy from the Guillain-Barré syndrome in most cases [7]. Other causes to be considered include toxins, drugs (particularly antibiotics), and nutritional deficiency.

Although clinical evaluation of patients with polyneuropathy is often difficult because of the severe systemic illness, certain clinical signs strongly suggest the diagnosis [8]. Spontaneous limb movements become increasingly weak, and the muscles are flaccid on passive limb movement. Painful stimulation of the limbs produces weak grimacing of facial muscles, but the expected flexion movements of the limbs are inappropriately weak, both proximally and distally. Finally, the deep tendon reflexes that have previously been present become absent.

The electrophysiologic signs are those of a pure axonal degeneration, mainly of motor but also of sensory fibers. Conduction velocities and distal latencies are relatively preserved, but compound muscle and sensory action potentials are reduced. Fibrillation potentials and positive sharp waves appear in muscle as shown by needle electromyography. Reduction of the diaphragmatic compound muscle action potential and signs of denervation of the chest wall muscles establish the polyneuropathy as a cause of difficulty in weaning from the ventilator [5, 6]. In our patient, although it has not been clearly documented, the existence of laryngeal and pharyngeal disorders strengthens the possibility of lower cranial nerve involvement.

There is no specific treatment of critical-illness polyneuropathy. Recovery may occur relatively quickly, but active physiotherapy to avoid pressure sores and contractures and active rehabilitation are important in management [4]. In fact, all measures to prevent or treat the septic syndrome are the only current methods of dealing with polyneuropathy.

	Acknowledgments

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We gratefully acknowledge the technical assistance of Dr Turgut Adatepe.

	Footnotes

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Address reprint requests to Dr Alhan, Acibadem, ebboylu Sok, 2/8, Kadiköy, stanbul, Turkey 81010.

	References

Top Footnotes Abstract Introduction Comment Acknowledgments References

 

1. Baue AE. Multiple progressive or sequential systems failure: a syndrome of the 1970s. Arch Surg 1975;110:779–81.[Medline]
2. Pine RW, Wertz MJ, Lennard ES, Dellinger EP, Carrico CJ, Minshev BH. Determinants of organ malfunction or death in patients with intra-abdominal sepsis: a discriminant analysis. Arch Surg 1983;118:242–9.[Abstract]
3. Bone RC. Let's agree on terminology: definitions of sepsis. Crit Care Med 1991;19:973–6.[Medline]
4. Zochodne DW, Bolton CF, Wells GS, et al. Critical illness polyneuropathy: a complication of sepsis and multiple organ failure. Brain 1987;110:819–42.[Abstract/Free Full Text]
5. Witt NJ, Zochodne DW, Bolton CF, et al. Peripheral nerve function in sepsis and multiple organ failure. Chest 1991;99:176–84.[Abstract/Free Full Text]
6. Bolton CF, Young GB, Zochodne DW. The neurological complications of sepsis. Ann Neurol 1993;33:94–100.[Medline]
7. Bolton CF, Laverty DA, Brown JD, Witt NJ, Hahn AF, Sibbald WJ. Critically ill polyneuropathy: electrophysiological studies and differentiation from Guillain-Barre syndrome. J Neurol Neurosurg Psychiatry 1986;49:563–73.[Abstract/Free Full Text]
8. Bolton CF, Gilbert JJ, Hahn AF, Sibbald WJ. Polyneuropathy in critically ill patients. J Neurol Neurosurg Psychiatry 1984;47:1223–31.[Abstract/Free Full Text]

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This Article Abstract Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Personal Folders Download to citation manager Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Alhan, H. C. Articles by Tarcan, S. Search for Related Content PubMed PubMed Citation Articles by Alhan, H. C. Articles by Tarcan, S.