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Late Onset of Respiratory Insufficiency After Poliomyelitis: A Preliminary Communication: A Preliminary Communication
... Cardiorespiratory complications associated with post-poliomyelitis sequelae and their assessment have been less well described than the neurological and musculoskeletal problems. These are important however, in that residual respiratory complications may be life-threatening (Fischer 1985, Hamilton et a11970, Lane 1974, Nichols etaI1972). The fact that patients may not have had respiratory complications at the initial onset of poliomyelitis does not preclude late-onset complications (Dean et aI1991). ...
Management of the late sequelae of poliomyelitis is based on their underlying pathophysiology and on a limited number of research reports. The key elements of management including the history, assessment and possible interventions are described in this article. The indications for intervention and its parameters are determined on an individual basis to maximise the benefit-to-risk ratio. Heavy resistive or exhaustive exercise, for example, cannot be supported physiologically as a means of preserving function in most patients. However rest, pacing of activities, lifestyle modification, orthotic fitting, weight control, use of aids and devices should be of value. Despite the importance of rest, inactivity is associated with detrimental side effects which can be accentuated in the patient with the sequelae of poliomyelitis. Research is needed to establish criteria for prescribing therapeutic interventions including rest and low-intensity exercise for the post-poliomyelitis population.
... Patients with PPS have reported respiratory symptoms that include exertional dyspnea and reduced physical endurance. (5)(6)(7) Respiratory problems can result from impairment of medullary centers, impairment of cranial nerves, impairment of respiratory muscles, or any combination of the three. (8) The World Health Organization estimates that there are 20 million polio survivors, (9) and new cases of poliomyelitis have been reported in certain African and Asian countries. ...
To compare lung function between patients with post-poliomyelitis syndrome and those with sequelae of paralytic poliomyelitis (without any signs or symptoms of post-poliomyelitis syndrome), as well as between patients with post-poliomyelitis syndrome and healthy controls.
Twenty-nine male participants were assigned to one of three groups: control; poliomyelitis (comprising patients who had had paralytic poliomyelitis but had not developed post-poliomyelitis syndrome); and post-poliomyelitis syndrome. Volunteers underwent lung function measurements (spirometry and respiratory muscle strength assessment).
The results of the spirometric assessment revealed no significant differences among the groups except for an approximately 27% lower mean maximal voluntary ventilation in the post-poliomyelitis syndrome group when compared with the control group (p = 0.0127). Nevertheless, the maximal voluntary ventilation values for the post-poliomyelitis group were compared with those for the Brazilian population and were found to be normal. No significant differences were observed in respiratory muscle strength among the groups.
With the exception of lower maximal voluntary ventilation, there was no significant lung function impairment in outpatients diagnosed with post-poliomyelitis syndrome when compared with healthy subjects and with patients with sequelae of poliomyelitis without post-poliomyelitis syndrome. This is an important clinical finding because it shows that patients with post-poliomyelitis syndrome can have preserved lung function.
... Nach der Extubation entwickel-Zwischen 1950 und 1961 erkrankten in Deutschland mehr als 80.000 Menschen an einer Poliomyelitis anterior acuta [3]. Über eine respiratorische Insuffizienz als Folge einer "alten" Poliomyelitiserkrankung wurde erstmals 1970 berichtet [10]. Da viele der Patienten, die während der großen Polioepidemien der 50er Jahre erkrankt waren, noch leben, werden immer wieder Patienten mit einer zurückliegenden Poliomyelitis anästhesiologisch zu betreuen sein. ...
About 80,000 polio survivors are still living 40 years after the last polio epidemics in Germany. Of these 40–70% have developed the so called post-polio syndrome (PPS) decades after the infection. The main symptoms of PPS are decreasing strength in voluntary muscles, pain and fatigue which occur spontaneously but may also be induced by physical stress and general illness.
We report the case of a 79-year-old male who developed hypercapnia due to ventilatory failure which necessitated reintubation several times after cholecystectomy.
The medical history revealed that he had had poliomyelitis at the age of 8 years. There was only a slight residual handicap from this infection which included mild pareses of the left limbs but had remained stable for about 70 years. Electromyography revealed signs of chronic neurogenic changes in muscles of the left upper limb as well as in the pectoralis major. The diagnostic criteria of a post-polio syndrome were fulfilled and other neuromuscular diseases were excluded. The patient could be discharged from intensive care only after treatment by intermittent positive pressure ventilation via a facial mask.
This case report shows that even patients who have a mild handicap after poliomyelitis can develop weaning problems. A PPS can exacerbate with inclusion of respiratory muscles in critically ill patients.
... Patients may complain of difficulty in getting off to sleep, disturbed nights, and sudden awakening with a sensation of dyspnoea or morning headache. As the condition progresses, the patient may notice loss of concentration, daytime drowsiness, and exertional dyspnoea [2,34,52,53]. Many patients in our series had symptoms of nocturnal hypoventilation for a period before frank respiratory failure (often related to intercurrent infection) provoked investigation and treatment. ...
Progressive functional deterioration following poliomyelitis has been reported after a prolonged period of stability. We present follow up data on 209 patients; the period from the original illness to December 1985 or death was between two and 73 years (mean 33.9). One hundred and sixty-three (78 per cent) patients developed late functional deterioration. This was due to purely respiratory factors in 99 cases, new neurological signs in 20 cases, and orthopaedic problems in 17 cases; 31 patients deteriorated due to a combination of factors. The commonest cause of respiratory deterioration was the development of nocturnal alveolar hypoventilation, sometimes associated with late progressive scoliosis. Eighty-six patients needed respiratory support beginning between one year and 66 years (mean 28.5) after the acute illness. New neurological signs had a clearly defined cause in each of 20 patients. No cases of motor neurone disease or post-poliomyelitis muscular atrophy (PPMA) were identified. This series shows that late sequelae following poliomyelitis are common. There were no patients with functional deterioration after poliomyelitis in whom a clear underlying cause could not be shown. The major causes of deterioration may be treatable or avoidable, and in particular, those who develop chest infections or new respiratory symptoms should be treated with caution as respiratory failure may rapidly supervene.
... The need for ventilator management and the types of treatment available have increased in recent years. There may be a late respiratory decompensation in PPS with or without a history of ventilator dependence during the acute episode of polio [47] [48] [49]. Up to 42% of individuals with PPS report new breathing problems, and the need for ventilatory support among survivors of poliomyelitis is increasing because a number of previously ventilator-dependent survivors need ventilatory support [50]. ...
For a disease that was "conquered" some 40 years ago with the onset of effective vaccination, the issues of long-term survivors of paralytic polio as they age continue to present challenges to rehabilitation specialists. Aging with polio is a definition of PPS. There are over a million patients with PPS in the United States. Management has to include the appropriate use of exercises, appropriate bracing and support, and, in the case of bulbar and respiratory symptoms, the appropriate use of speech therapy services and ventilatory support. There are no prospective randomized trials studying the treatment of weakness and fatigue in PPS. Pharmacologic interventions are limited at this time but include anticholinergics for muscle weakness and dopaminergic agents or amantadine to control central fatigue. The pathophysiology of aging with polio is consistent with neuronal loss and denervation lying at the heart of the developing disorder, whereas the central nervous system components of the fatigue syndrome may be related to central changes with neuronal loss in the basal ganglia and reticular-activating system. Many of the survivors of the polio epidemics are in their later retirement years, and their needs will increase as they have other disabilities due to natural aging. Sensitivity to some of the special issues in PPS may help to avoid complications. Polio is an active infection in the third world. Although great strides have been made, the disease is endemic in eight nations and is threatening to spread. The lessons learned in treating PPS now will be useful in years to come as these individuals age and manifest PPS in the future.
A hypothesis is advanced concerning the relationship of poliomyelitis viruses and late developing neoplasia in the central nervous system. The literature is surveyed, and several experimental approaches based upon known evidence of viral and neoplastic behaviour are advanced. The present status of world polio incidence is discussed as it applies to this possible relationship.
Patients with chronic respiratory failure secondary to disorders which increase the work of breathing often benefit from assisted ventilation with body respirators. To test the hypothesis that body respirator therapy works by relieving the respiratory muscles of an excessive load, we recorded diaphragmatic and/or accessory inspiratory muscle electrical activity before and during assisted ventilation in 11 patients. All patients had chronic hypercapnia; seven had advanced obstructive pulmonary disease and four had severe thoracic cage restriction. When these patients used the tank respirator, their diaphragmatic activity fell to 9 ± SD 3 per cent of the level measured during spontaneous breathing. The reduction was highly significant in each patient (P < 0.001). Similar reductions of diaphragmatic activity occurred in the cuirass respirator. The body respirators also reduced accessory muscle activity (P < 0.02). Coincident with loss of diaphragmatic activity, the patients obtained relief from dyspnea. These results were independent of changes in arterial blood carbon dioxide tension (PaC02). Seven normal subjects were studied to further investigate the mechanism by which body respirators reduced inspiratory muscle activity. In the tank, these subjects displayed only minor reductions of diaphragmatic activity despite large decrements in end-tidal carbon dioxide pressure (PETCO2). However, when their upper airway resistance was increased, diaphragmatic activity promptly ceased in the tank. We conclude that capture of the ventilatory cycle by the body respirator is facilitated by loading the inspiratory muscles. We suggest that the beneficial effects of body respirator therapy for chronic respiratory failure are mediated in part through reduction of excessive inspiratory muscle contractile effort.
Two patients with traumatic high cervical cord injury are described. Both patients required long-term ventilatory support. Diaphragmatic pacing has been successful in meeting their ventilatory requirements and improving their quality of life. Both patients are now living in their own homes. Their medical, nursing and psychosocial needs have been met by multi-disciplinary team involvement and their ongoing support in the community.
We examined the relationship between the lung function of 74 individuals with a history of poliomyelitis and reports of shortness of breath during activities of daily living, and the presence of post-polio sequele risk factors. First, we studied the spirometry of 60 individuals (group 1) and second, we studied the relationship between the spirometry of an additional 14 individuals (group 2) and their respiratory muscle strength (PImax and PEmax). In both groups, we examined the relationship between factors associated with post-polio sequelae including ventilation at polio-onset, having contracted polio after the age of 10, and having had polio for over 35 years and lung function. In group 1, the FEV1 and FVC were lower for individuals with shortness of breath than individuals without (p < 0.01). With respect to risk factors, FEV1 and FVC were lower in individuals who were ventilated at polio-onset, in individuals who contracted polio over 10 years of age, and in individuals who had had polio for less, rather than more than 35 years (p < 0.05). The results for group 2 were comparable to group 1. In addition, the observed PImax and PEmax were significantly lower than predicted values (p < 0.05). Although FEV1 and FVC were positively correlated with both PImax and PEmax (p < 0.05), PEmax was disproportionately impaired compared to PImax (40 +/- 12.1 and 82 +/- 38.8 percent predicted respectively). We conclude that individuals with a history of poliomyelitis can have compromised lung function irrespective of shortness of breath, that risk factors such as ventilation at polio-onset and polio-onset after 10 years of age can help predict those at risk of respiratory compromise, and that the measurement of respiratory muscle strength and of PEmax in particular, can augment the assessment of lung function of these individuals. Such assessment may avert respiratory complications in the post poliomyelitis population including those secondary to health care interventions.
Lung volumes and spirometric flows, maximal respiratory pressures, lung diffusion capacity and blood gases were evaluated in 20 patients with prior poliomyelitis and compared with data from an age- and sex-matched control group. In the polio patients, static lung volumes and pulmonary flow capacity were significantly reduced to approximately 65% of the values of the control group. However, expiratory and inspiratory flows were normal in relation to lung volumes, while maximal respiratory pressures were significantly reduced in the polio patients. Static lung volumes and forced flows were correlated with the maximal respiratory pressures both in the polio patients and in the controls. However, when the muscle force in the polio patients decreased below a certain level, it became more important as a determinant of lung-flow capacity. The polio patients had a significantly increased Pco2 but a normal oxygen saturation and Pco2 was inversely correlated with the maximal respiratory pressures in the patients but not in the controls. The lung diffusion capacity was reduced in the polio patients compared to the controls, but less markedly than vital and total lung capacity.
The findings indicate a restrictive respiratory dysfunction and alveolar hypoventilation most probably due to weakness of the respiratory muscles.
A retrospective study was performed to identify symptoms and clinical findings in postpolio patients seen in a postpolio clinic. Charts of 79 consecutive patients (28 men and 51 women) with histories and examinations compatible with the diagnosis of poliomyelitis were reviewed. The average current age of our patients was 47.3 +/- 10.4 years; the average age at onset of acute polio was 10.4 +/- 9.4 years; and the average number of years since function was first noticed to decline was 7.8 +/- 6.4 years. The most common symptoms acknowledged were progressive weakness (87%), muscle pain (86%), fatigue (86%), decreased activity level (78%), joint pain (77%), and back pain (70%). The clinical impression in most of these patients was arthritis/arthralgia (71% of the patients) or muscle overuse or myofascial pain (71%). Eleven (14%) had evidence of nerve compression, although 39% complained of sensory loss. Five patients had respiratory problems that required evaluation. Recommendations proved helpful for 78% of those seen at follow-up. These recommendations included pacing, energy conservation (planning, use of wheelchair or motorized scooter), gentle stretching or strengthening exercise, use of orthotic devices, weight loss or nutritional counseling, gentle aerobic exercise, use of a cane, and use of adaptive equipment.
The relationship between spirometry and daytime blood gases on the one hand and hypoxaemia during sleep on the other was studied in 13 patients with severe thoracic scoliosis. Eight patients had hypoxaemia (mean Sao2 less than 90%) during sleep. They were characterized by a lower vital capacity (30 versus 50% of predicted, P less than 0.01) and by a greater fall in vital capacity from sitting to supine (26 versus 7% of sitting VC, P less than 0.05). All patients with hypoxaemia during sleep were hypercapnic during the daytime. The fall in Sao2 with sleep was related to the increase in transcutaneous PCO2, indicating hypoventilation as the main mechanism behind hypoxaemia during sleep in scoliosis patients.
One hundred forty-six respiratory polios have been reviewed for complications and current respiratory aids. One hundred thirty-eight of these people required respirator assistance at the onset of their poliomyelitis infection. Fifteen patients have kyphoscoliosis. Seventy-five percent of the total patients require some assisted ventilation. Fifty-two percent have tracheostomies. Most of these people have been followed at Rancho Los Amigos Medical Center for many years. The literature regarding late respiratory complications of polio is reviewed.
The diseases which are commonly complicated by hypercapnic respiratory failure also compromise the respiratory muscles in several ways. Increased work of breathing, mechanical disadvantage, neuromuscular disease, impaired nutritional status, shock, hypoxemia, acidosis, and deficiency of potassium, magnesium, and inorganic phosphorus are the major non-neurologic factors which contribute to respiratory muscle fatigue and failure. Respiratory muscle fatigue has two components. High frequency fatigue occurs rapidly with intense contractile efforts but is usually not severe. It also recovers rapidly with rest. Low frequency fatigue develops more slowly but is severe and requires hours for recovery. Since the spontaneous rate of neural stimulation is predominantly in the low frequency range, this component of fatigue is of particular clinical importance. Fatigue of the inspiratory muscles leads to acute respiratory acidosis, but before carbon dioxide retention occurs, it can be recognized from characteristic symptoms and signs. These include dyspnea which responds to mechanical ventilation, rapid shallow breathing, and asynchronous movements of the chest and abdomen. Inspiratory muscle fatigue must be treated by putting these muscles to rest, by mechanically supporting ventilation. In addition, underlying metabolic nutritional and circulatory abnormalities must be corrected and infection treated. Aminophylline and isoproterenol can restore inspiratory muscle contractility, but controlled clinical trials remain to be done regarding their application in acute and chronic respiratory failure. Inspiratory muscle training improves strength and endurance in patients with obstructive lung disease, cystic fibrosis, and spinal cord injury, but does not always improve physical exercise performance. Again, more work is needed to develop the indications for inspiratory muscle training and to determine the optimum type and duration of the training regimen.
Described in this study are eight patients with alveolar hypoventilation syndromes who presented with carbon dioxide narcosis and coma. After reversal of severe hypercapnia, all patients were discharged and maintained at home for an average period of 10 years utilizing "noninvasive" nocturnal mechanical ventilation. The use of "noninvasive" mechanical ventilation at home attempted to void the hazards of tracheostomy and the difficulties inherent in continuous daytime use of oxygen. This form of treatment has allowed these patients to continue their previously productive lives. This study represents the first published long-term follow-up regarding this mode of treatment in patients with alveolar hypoventilation.
Unlabelled:
The purpose of this study was to determine, in exercising patients, how much diaphragm force increases before electromyographical evidence of diaphragm fatigue occurs. The study was performed in ten male patients with complete cervical cord injury (CCI) at the C5 to C8 levels, and five male patients with prior poliomyelitis infection (PPI) requiring chronic treatment with intermittent positive pressure ventilation (IPPV) at night. We studied the time course of the diaphragmatic tension-time index (TTdi), the centre frequency (CFdi) of the diaphragm electromyogram (EMGdi) power spectrum, and the ventilatory parameters, during steady-state submaximal arm/leg exercise. During exercise, early signs of diaphragm fatigue were present in seven out of 10 CCI patients and in four out of five PPI patients, as indicated by a reduction in CFdi. The increase in TTdi achieved before reductions in CFdi occurred was twofold in both the CCI and PPI patients. All patients except for the PPI patients, who demonstrated a reduction in CFdi, showed an increase in minute ventilation (VE), achieved by increasing both their tidal volume (Vt) and the breathing frequency (fb). The PPI patients demonstrating reductions in CFdi during exercise also increased their VE however, this was achieved by increasing fb while Vt remained constant. Following the reductions in CFdi, the CCI patients further increased their TTdi throughout the exercise test, while the PPI patients reduced their TTdi values.
In conclusion:
(1) During exercise, electromyographical evidence for diaphragmatic fatigue frequently occurred in the CCI and PPI patients studied; (2) Compared to the eightfold increase in TTdi seen in healthy subjects before reductions in CFdi occur, the TTdi values increased only two-fold before electromyographical evidence of diaphragm fatigue was present in these patients; (3) There is a clear discrepancy between the CCI and PPI patients who demonstrate electromyographical evidence of diaphragm fatigue, in terms of their ventilatory and TTdi responses.
The object of this investigation was to prospectively study the annual decline in lung function in a cohort of postpolio patients, and to determine the usefulness of initial lung function tests in the prediction of a subsequent poor outcome. Cross-sectional data were analysed in 55 patients from the total cohort of 350 survivors of poliomyelitis in our admission area of 550,000 inhabitants. Longitudinal data (> 5 yrs, average 8.9 yrs) were available for 31 patients. Seventeen of the patients had a poor outcome (13 were started on domiciliary artificial ventilation and five died from respiratory failure; with one overlap). At the time of entry to the study (on average 4.3 years before the poor outcome), these patients had a lower vital capacity (VC) (43 vs 65% of predicted; p < 0.01) and arterial oxygen tension (Pa,O2) (9.9 vs 11 kPa; p < 0.05) and a higher arterial carbon dioxide tension (Pa,CO2) (6.0 vs 5.0 kPa; p < 0.01). They also had a more rapid increase in Pa,CO2 (0.3 vs 0.03 kPa.yr-1; p < 0.01), but the difference in decline in VC (40 vs 30 mL.yr-1) was not significant. Initial VC < 50% of predicted and/or Pa,CO2 > 6 kPa was associated with a poor prognosis. In conclusion, annual decline in vital capacity was not abnormally rapid but annual increase in arterial carbon dioxide tension was higher in patients with a poor outcome. Initial determination of vital capacity and initial and repeated blood gas analysis appear to be useful in identifying high-risk postpolio patients.
To evaluate the limiting factors of exercise performance and to analyze the respiratory strategies adopted during exercise in postpolio patients with severe inspiratory muscle dysfunction.
Five patients with prior poliomyelitis associated with scoliosis and with respiratory muscle dysfunction (mean vital capacity, 1.74L [range, 1.1 to 2.4]) were studied at rest and during leg or arm cycle exercise.
Gas exchange was examined by arterial blood gases and mass spectrometry of expired air. Ventilatory mechanics were studied by measurement of esophageal and gastric pressures.
Blood gases at rest were normal, except for subnormal PO2 levels in three patients. In all but one patient, ventilatory insufficiency was the limiting factor for exercise. A compensatory breathing pattern with abdominal muscle recruitment during expiration was present already at rest in three of the patients. The pressures generated by the diaphragm were below fatiguing margins, ie, levels that in healthy subjects can be sustained for at least 45 minutes.
The extent of ventilatory dysfunction was not evident in blood gas values at rest; however, it was revealed by blood gas values during the exercise test. Diaphragm fatigue seems to be avoided at the cost of impaired blood gases.
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