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Why a Paper on Anesthesia and Polio in 2016?

Calmes, Selma H. MD

doi: 10.1213/ANE.0000000000001333
Editorials: Editorial

From the Department of Anesthesiology and Perioperative Medicine, the David Geffen School of Medicine at UCLA, Los Angeles, California.

Accepted for publication March 2, 2016.

Funding: None.

The author declares no conflicts of interest.

Reprints will not be available from the author.

Address correspondence to Selma H.Calmes, MD, UCLA Department of Anesthesiology and Perioperative Medicine, Ronald Regan UCLA Medical Center, 757 Westwood Plaza, Suite 3325, Los Angeles, CA 90095. Address e-mail to

The article by Van Alstine et al.1 published in this issue has a story behind it. For years, postpolio friends kept asking me for information on anesthesia. They seemed to fear anesthesia, thinking they were at particular risk. But, each day at work, I saw desperately ill patients without polio surviving major procedures such as transplants. I wondered, “Why this perception of anesthesia and polio? Why would polio patients be at more risk than patients for a transplant?” Literature searches did not help, these found mostly single case reports. Then I heard Dr. Mark Warner of the Mayo Clinic talk on ulnar neuropathy possibly because of anesthesia. That study used Mayo Clinic’s electronic record system to identify patients to study for postoperative neuropathy. I realized suddenly that the Mayo Clinic system would be a place to do the needed study on anesthesia and polio. There was a record system with an ability to do complex searches (used in this article), and there should be lots of polio patients. Minnesota had many polio patients in the worst epidemic years (Ref. 1 in Table 1), the Sister Kenney Institute in nearby Minneapolis attracted many polio patients (Ref. 2 in Table 1), and the Mayo Clinic was a leader in determining whether the postpolio syndrome (PPS) really existed and in defining what it is. And so the idea for the study on polio and anesthesia published in this issue of Anesthesia & Analgesia came to be. The authors deserve a lot of credit for carrying this forward. A large amount of work was needed, as was persistence during both the study and the review process. This is the first article comparing postpolio patients with equivalent nonpolio patients having equivalent major operations and with a follow-up period of 30 days.

Table 1

Table 1

Anesthesiologists, especially younger ones who may not have seen polio cases, might ask why they should be interested in the possible anesthesia issues related to polio. The introduction of successful polio vaccines in the late 1950s and early 1960s eventually ended the frightening polio epidemics of the past. These epidemics left an estimated 15 to 20 million survivors worldwide.2 Immigration of these survivors to more developed countries occurs but has not been precisely documented, except in a poster presentation from a postpolio clinic (Ref. 3 in Table 1). Both wild polio virus (PV) type 1 and vaccine-derived PVs persist in the world today and continue to cause acute polio as recently as December 2015 and January 2016 in the polio-endemic countries of Afghanistan and Pakistan (Ref. 4 in Table 1). The World Health Organization monitors the presence of PVs in multiple countries and reports weekly on this, providing the needed surveillance. Polio vaccination efforts are supported by Rotary International and the Bill and Melinda Gates foundation. But, the difficulties of eliminating polio worldwide are hard to overcome, given the continuing social disruption in less-developed countries. Immigration can, then, easily bring polio survivors, and even acute cases, to the developed world and possibly to our operating rooms. Because population data on survivors and their immigration are difficult to get, it is not possible to estimate how long polio survivors might present for anesthesia in the future (Ref. 5 in Table 1).

Why might polio patients be at extra risk during anesthesia? Many think polio affects only the spinal cord’s anterior horn cells. Pathologic studies done in the 1940s,3,4 during efforts to develop a polio vaccine, documented widespread damage throughout the entire nervous system, from the brain (especially), spinal cord, and even neuromuscular junctions. Even patients without clinical signs of bulbar involvement in the acute disease show significant brain lesions. There is a predilection for the spinal cord’s gray matter, especially the anterior horn cells, but multiple areas of the central nervous system (CNS) are usually damaged. The intense scarring that results from PV infection can also disrupt neuronal function. This is an anatomically capricious disease. Pathologic lesions vary in number and locations, from the brain to various levels of the spinal cord and from right to left sides in individual patients. Each patient has unique pathologic lesions, making polio patients clinically heterogeneous and difficult to compare in studies.

Clinical recovery from the acute infection is by reinnervation of remaining muscles by nearby surviving neurons, which then carry a heavier metabolic load.5 Patients can achieve close to normal status when recovered because of this reinnervation process. As aging occurs and surviving healthy neurons innervating larger-than-normal motor units grow old and die, there can be significant decreases in muscle function. New muscle weakness can appear in areas unaffected clinically in the original disease.

In the 1970s, many polio survivors began to experience more problems: new muscle weakness (often causing new respiratory insufficiency and pharyngeal and laryngeal neuropathy), atrophy of previously unaffected muscles, debilitating fatigue (central and muscular), musculoskeletal pain, and sleep-disordered breathing. This progression of symptoms is now recognized as the PPS. Criteria for the diagnosis of PPS, which was first named in 1991,6 were established by consensus of experts in 2001. These criteria are a history of polio, partial or complete functional recovery for at least 15 years, onset of progressive muscle weakness lasting at least 1 year, and exclusion of other possible neurologic causes (Ref. 6 in Table 1). Pathologic studies in this period revealed evidence of chronic inflammation in the nervous system, including cranial nuclei and neuromuscular junctions.7,8 Many therapies for PPS have been explored but none has been found to be conclusively effective in a recent Cochrane review.9

Research on PPS revealed inflammatory proteins in the cerebrospinal fluid of some PPS patients. Virologists also demonstrated the presence of PV fragments in the cerebrospinal fluid of some PPS patients. These findings suggest a chronic, ongoing inflammatory response, persistent PV infection, or, perhaps, an autoimmune attack to the CNS. There is no firm evidence yet to tie these experimental findings to the cause of PPS. Research in this area continues.2 Based on the early virology research, trials of IV immunoglobin began in Sweden.10 The recent Cochrane Review found that there was insufficient evidence that IV immunoglobin had a beneficial effect in PPS patients on activity and muscle strength.9 However, a multicenter, multicountry study of this therapy is beginning (Ref. 7 in Table 1).

In this situation of widespread CNS damage, we could anticipate several anesthesia problems: sensitivity to our centrally acting anesthetic drugs, prolonged wakening, autonomic nervous system issues such as low blood pressure in response to drugs and regional blocks, sensitivity to neuromuscular-blocking drugs (NMBDs), and respiratory failure after surgery. Does the Van Alstine et al.’s1 article add to our limited knowledge about polio and anesthesia? Unfortunately, this article does not conclusively answer these questions. The study’s patient matching and measures for anesthesia complications and, especially postoperative measures (postanesthesia care unit, pain scores, cardiac arrest, and need for a rapid response team), were well chosen. However, because of the low number of polio patients, especially the low number of severely affected ones, and because of the heterogeneity of these patients, it is difficult to statistically document differences. A larger number of patients is needed. The low number of polio patients is quite surprising and is unexpected. As the article’s authors suggest, postpolio patients may choose to avoid major surgery. Another possible explanation is that many Mayo Clinic patients came from the upper Midwest region of the United States, an area with severe winter weather. Postpolio patients are commonly cold intolerant, and they may have moved to warmer states, such as Florida and California.

To better answer the question of how postpolio patients do during anesthesia, another study is needed. A future study of polio and anesthesia might be prospective and multicenter. A prospective study could document preoperative respiratory function to try to confirm the clinical impression that those with worse pulmonary function preoperatively are at greater risk for postoperative respiratory failure. A multicenter study, including centers located in warmer climate states, could probably get more postpolio patients and hopefully give greater statistical power. The patients could be separated into groups such as “had polio, no physical sequelae; had polio, have physical sequelae but no PPS; and had polio, have physical sequelae, have PPS.” This would help define whether those with PPS are different during anesthesia from those without PPS. We also need to study the newer NMBDs, vecuronium and rorcuronium, in postpolio patients (compared with controls) to confirm whether postpolio patients are also sensitive to these newer NMBDs. A previous study11 documented that postpolio children were twice as sensitive as controls to NMBDs, but the drugs studied (curare, gallamine, and pancuronium) are no longer used. The study by van Alstine et al.1 compared total NMBD doses, and there was no difference between groups. But, once again, more polio patients are needed. We also need more sophisticated studies in the NMBD area. What about the effect of repeated electrical stimulation for neuromuscular monitoring in these patients, some of whom have clearly abnormal neuromuscular junctions?

And, we need to follow the research on the chronic inflammatory process that is now documented in some postpolio patients. What would this inflammatory process mean for our use of regional anesthesia in these patients? If PPS is conclusively proved to be a chronic inflammatory process, does this get worse after anesthesia? Another question is whether local anesthetics used for postoperative pain blocks possibly damage nerves in polio-affected limbs. These studies are all inherently difficult because of the pathology of polio. Because of the great variability in pathology, each patient seems to be unique.

Anesthesiology owes something to the disease polio: our specialty was greatly changed by the 1952 polio epidemic in Copenhagen, Denmark. This epidemic resulted in the concepts of intensive care units (ICUs) and anesthesiologists’ presence in and leadership of ICUs and also accelerated work in blood gas measurements and better understanding of acid-base physiology.12,13 This 1952 polio epidemic overwhelmed the Blegham Hospital, Copenhagen’s infectious disease hospital, with patients with severe bulbar polio, most needing ventilation. Mortality in the first weeks was 90%. There were not enough ventilators, and 6 of the 7 available ventilators were negative-pressure chest cuirasses. Patients’ airways were often obstructed by airway muscle weakness and inability to swallow secretions. There was little understanding of respiratory physiology at the time, and blood gas measurements as we know them today did not exist. The only blood gas measurement that could be done was total CO2, using the cumbersome and time-consuming van Slyke manometric technique. The hospital’s temporary anesthetist, Bjørn Ibsen (1915–2007), was consulted on possible causes of the mysterious “alkalosis” that was being found in total CO2 measurements in these patients. (Because pH and PCO2 could not be measured at this time, a high total CO2 value, as measured with the van Slyke manometric method, was then thought to be because of a metabolic alkalosis.) Ibsen had trained in anesthesiology from 1949 to 1950 at the Massachusetts General Hospital and promptly recognized that, in this situation of respiratory paralysis, the cause of the elevated CO2 was inadequate ventilation, not a mysterious alkalosis. These patients needed ventilation! He used the low-cost, easily portable Waters’ canister to-and-fro system (then in use in US operating rooms), established secure airways via cuffed tracheostomy tubes, and developed trained teams of medical and dental students to do the ventilation by hand. Also, Ibsen placed the patients together geographically and trained nursing staff to cope with possible problems. This was the first ICU, and an anesthesiologist was the leader of its development. This epidemic established the concepts of ICUs for the sickest patients and for anesthesiologists running the units.

Important also was the pressure this epidemic put on respiratory physiologists and laboratory scientists to develop better blood gas technology and better understanding of acid-base disorders. A then-experimental pH electrode, which needed only small blood samples, was used early on by Poul Astrup (1915–2000), then laboratory director at the Blegham Hospital, to confirm Ibsen’s postulate that the mysterious alkalosis was really respiratory acidosis. Technology for clinical measurements of PCO2 and PO2 developed rapidly in the next few years.12,13 All these tools are essential parts of the daily work of anesthesiologists in 2016, and anesthesiologists continue to be leaders in intensive care settings. We owe it to the remaining polio patients and those yet to come to study how they do during anesthesia.

Meanwhile, there will be postpolio patients to care for. Patients today often present with possible significant issues for anesthesia management. Because of their complexity, we need to commit to evaluate them adequately preoperatively, especially respiratory function. There is much to go wrong in this area14: all the respiratory muscles may be weak and fatigue easily, including the diaphragm. Diaphragmatic paralysis is not unusual, especially in those with paralyzed upper extremities; their polio lesions have reached the C3 to C5 levels of the spinal cord, which provide the motor nerves to each diaphragm. Scoliosis compounds the consequences of respiratory muscle weakness, adding ventilation/perfusion abnormalities. Central respiratory drive may be absent, and sleep-disordered breathing is increasingly recognized. Because it is difficult for postpolio patients to get help managing, or even identifying, their respiratory problems, they may not be optimally managed preoperatively. Most use older negative-pressure devices with an oral/nasal interface, and patients may not adjust well to hospitals’ endotracheal tubes and positive-pressure ventilators. Sleep-disordered breathing needs to be evaluated, and appropriate postoperative care planned. There should be a plan for postoperative pain. Pain seems to be an issue in postpolio patients,15 and the finding that 27% of the study’s postpolio group was receiving opiates preoperatively, compared with 14% of controls, illustrates this issue.

Another preoperative concern should be postpolio patients’ fear of anesthesia. This fear has been created by a lot of misinformation and, more importantly, by postpolio patients’ experiences with anesthesia after their initial acute illness. After the acute phase of polio, long hospitalizations (months or even years) continued for many. This often included multiple orthopedic surgeries to improve function of paralyzed limbs, such as release of contractures, and attempts at scoliosis repair and leg lengthening. These surgeries were most often in the 1940s to 1950s, a time when open drop ether was the usual anesthetic for children, inductions were by mask, and postoperative pain in children was not treated. After months of hospitalization for this dreaded disease, and separated from their family and friends because of hospital visiting restrictions then in place, the experiences of painful surgery and anesthesia of that time left deep psychic trauma.16 It is highly stressful for nearly all of postpolio patients to come again for an operation. They need to be treated with concern and respect for what they have been through.

The article by Van Alstine et al.1 is important because it raises the neglected issue of postpolio patients and anesthesia, even though the number of polio patients in the study was small and the statistics could not prove a significant difference. Just because a difference could not be proved does not mean it does not exist. Hopefully, larger studies with more polio-disabled patients and matched controls will be done in the future. The article also serves to call attention to how little significant information now exists about postpolio patients having anesthesia and surgery and that more studies are needed. Polio persists in the world, there are an estimated 15 to 20 million survivors worldwide,2 and immigration will continue to bring these patients to more developed countries, where they may need anesthesia care.

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Name: Selma H. Calmes, MD.

Contribution: This author wrote the manuscript.

Attestation: Selma H. Calmes approved the final manuscript.

This manuscript was handled by: Sorin J. Brull, MD.

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1. Van Alstine LW, Gunn PW, Schroeder DR, Hanson AC, Sorenson EJ, Martin DP. Anesthesia and poliomyelitis: a matched cohort study. Anesth Analg 2016;122:1894–900.
2. Baj A, Colombo M, Headley JL, McFarlane JR, Liethof MA, Toniolo A. Post-poliomyelitis syndrome as a possible viral disease. Int J Infect Dis 2015;35:107–16.
3. Sabin AB. Pathology and pathogenesis of human poliomyelitis. JAMA 1942;120:506–11.
4. Bodian D. Poliomyelitis; neuropathologic observations in relation to motor symptoms. J Am Med Assoc 1947;134:1148–54.
5. Dalakas MC. Pro-inflammatory cytokines and motor neuron dysfunction: is there a connection in post-polio syndrome? J Neurol Sci 2002;205:5–8.
6. Halstead LS. Assessment and differential diagnosis for post-polio syndrome. Orthopedics 1991;14:1209–17.
7. Pezeshkpour GH, Dalakas MC. Long-term changes in the spinal cords of patients with old poliomyelitis. Signs of continuous disease activity. Arch Neurol 1988;45:505–8.
8. Maselli RA, Wollmann R, Roos R. Function and ultrastructure of the neuromuscular junction in post-polio syndrome. Ann N Y Acad Sci 1995;753:129–37.
9. Koopman FS, Beelen A, Gilhus NE, de Visser M, Nollet F. Treatment for post-polio syndrome (Review). The Cochrane Library 1995. Available at:
10. Gonzales H, Khadimi M, Andersson M, Wallström E, Borg K, Olsson T. Prior poliomyelitis-IVIg treatment reduces inflammatory cytokine production. J Neuroimmunology 2004;150:139–44.
11. Gyermek L. Increased potency of nondepolarizing relaxants after poliomyelitis. J Clin Pharmacol 1990;30:170–3.
12. Severinghaus JW, Astrup P, Murray JF. Blood gas analysis and critical care medicine. Am J Respir Crit Care Med 1998;157:S114–22.
13. West JB. The physiological challenges of the 1952 Copenhagen poliomyelitis epidemic and a renaissance in clinical respiratory physiology. J Appl Physiol (1985) 2005;99:424–32.
14. Bach JR, Alba AS. Pulmonary dysfunction and sleep disordered breathing as post-polio sequelae: evaluation and management. Orthopedics 1991;14:1329–37.
15. Stoelb BL, Carter GT, Abresch RT, Purekal S, McDonald CM, Jensen MP. Pain in persons with postpolio syndrome: frequency, intensity, and impact. Arch Phys Med Rehabil 2008;89:1933–40.
16. Wilson DJ. Psychological trauma and its treatment in the polio epidemics. Bull Hist Med 2008;82:848–77.
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