Polio natural history, complications and prognosis: Difference between revisions
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== Complications== | == Complications== | ||
Potential complications of poliomyelitis may include: | Potential [[complications]] of poliomyelitis may include:<ref>{{cite book | last = Mandell | first = Gerald | title = Mandell, Douglas, and Bennett's principles and practice of infectious diseases | publisher = Churchill Livingstone/Elsevier | location = Philadelphia, PA | year = 2010 | isbn = 0443068399 }}</ref><ref name="pmid13427128">{{cite journal| author=WEINSTEIN L| title=Cardiovascular disturbances in poliomyelitis. | journal=Circulation | year= 1957 | volume= 15 | issue= 5 | pages= 735-56 | pmid=13427128 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=13427128 }} </ref><ref name="pmid13826196">{{cite journal| author=GALPINE JF, WILSON WC| title=Occurrence of myocarditis in paralytic poliomyelitis. | journal=Br Med J | year= 1959 | volume= 2 | issue= 5163 | pages= 1379-81 | pmid=13826196 | doi= | pmc=PMC1990933 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=13826196 }} </ref> | ||
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| style="padding: 5px 5px; background: #DCDCDC;" | '''''' | | style="padding: 5px 5px; background: #DCDCDC;" | '''Respiratory compromise''' | ||
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* Resulting from paralysis of respiratory muscles (diaphragm and intercostal muscles) | |||
* Airway obstruction | |||
* Lesions in: | |||
:* Cranial nerve nuclei | |||
:* Medullary respiratory center | |||
|- | |- | ||
| style="padding: 5px 5px; background: #DCDCDC;" | '''''' | | style="padding: 5px 5px; background: #DCDCDC;" | '''Myocarditis''' | ||
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* Inflammatory infiltration in cardiac muscle | |||
|- | |- | ||
| style="padding: 5px 5px; background: #DCDCDC;" | '''''' | | style="padding: 5px 5px; background: #DCDCDC;" | '''Gastrointestinal''' | ||
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* [[Hemorrhage]] | |||
* [[Paralytic ileus]] | |||
* [[Gastric dilatation]] | |||
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Revision as of 23:56, 3 September 2014
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Many cases of poliomyelitis result in only temporary paralysis. After an interval of 30–40 years, 25%–40% of persons who contracted paralytic poliomyelitis in childhood experience new muscle pain and exacerbation of existing weakness, or develop new weakness or paralysis. This disease entity is referred to as pos-tpolio syndrome. Patients with abortive polio infections recover completely. In those that develop only aseptic meningitis, the symptoms can be expected to persist for two to ten days, followed by complete recovery.
Natural History
Many cases of poliomyelitis result in only temporary paralysis.[1] Nerve impulses return to the formerly paralyzed muscle within a month, and recovery is usually complete in six to eight months. The neurophysiological processes involved in recovery following acute paralytic poliomyelitis are quite effective; muscles are able to retain normal strength even if half the original motor neurons have been lost.[2] Paralysis remaining after one year is likely to be permanent, although modest recoveries of muscle strength are possible 12 to 18 months after infection.
One mechanism involved in recovery is nerve terminal sprouting, in which remaining brainstem and spinal cord motor neurons develop new branches, or axonal sprouts.[3] These sprouts can reinnervate orphaned muscle fibers that have been denervated by acute polio infection,[4] restoring the fibers' capacity to contract and improving strength.[5] Terminal sprouting may generate a few significantly enlarged motor neurons doing work previously performed by as many as four or five units: [6] a single motor neuron that once controlled 200 muscle cells might control 800 to 1000 cells. Other mechanisms that occur during the rehabilitation phase, and contribute to muscle strength restoration, include myofiber hypertrophy—enlargement of muscle fibers through exercise and activity—and transformation of type II muscle fibers to type I muscle fibers.[4][7]
In addition to these physiological processes, the body possesses a number of compensatory mechanisms to maintain function in the presence of residual paralysis. These include the use of weaker muscles at a higher than usual intensity relative to the muscle's maximal capacity, enhancing athletic development of previously little-used muscles, and using ligaments for stability, which enables greater mobility.
Complications
Potential complications of poliomyelitis may include:[8][9][10]
| Complications | Description |
|---|---|
| Respiratory compromise |
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| Myocarditis |
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| Gastrointestinal | |
| ' | |
| ' | |
| ' | |
| ' |
Muscle paresis and paralysis can sometimes result in skeletal deformities, tightening of the joints and movement disability. Once the muscles in the limb become flaccid, they may interfere with the function of other muscles. A typical manifestation of this problem is equinus foot (similar to club foot). If the problem is left untreated, the Achilles tendons at the back of the foot retract and the foot cannot take on a normal position. Polio victims that develop equinus foot cannot walk properly because they cannot put their heel on the ground. A similar situation can develop if the arms become paralyzed.[11]
In some cases the growth of an affected leg is slowed by polio, while the other leg continues to grow normally. The result is that one leg is shorter than the other and the person limps and leans to one side, in turn leading to deformities of the spine (such as scoliosis). Osteoporosis and increased likelihood of bone fractures may occur. Extended use of braces or wheelchairs may cause compression neuropathy, as well as a loss of proper function of the veins in the legs, due to pooling of blood in paralyzed lower limbs.[12][13]
Post-polio syndrome
Around a quarter of individuals who survive paralytic polio in childhood develop additional symptoms decades after recovering from the acute infection, notably muscle weakness, extreme fatigue, or paralysis. This condition is known as post-polio syndrome (PPS).[14] The symptoms of PPS are thought to involve a failure of the over-sized motor units created during recovery from paralytic disease.[15][16] Factors that increase the risk of PPS include the length of time since acute poliovirus infection, the presence of permanent residual impairment after recovery from the acute illness, and both overuse and disuse of neurons. Post-polio syndrome is not an infectious process, and persons experiencing the syndrome do not shed poliovirus.
Prognosis
Patients with abortive polio infections recover completely. In those that develop only aseptic meningitis, the symptoms can be expected to persist for two to ten days, followed by complete recovery. In cases of spinal polio, if the affected nerve cells are completely destroyed, paralysis will be permanent; cells that are not destroyed but lose function temporarily may recover within four to six weeks after onset.[17] Half the patients with spinal polio recover fully, one quarter recover with mild disability and the remaining quarter are left with severe disability.[18] The degree of both acute paralysis and residual paralysis is likely to be proportional to the degree of viremia, and inversely proportional to the degree of immunity.[19]. Spinal polio is rarely fatal.[20]
Without respiratory support, consequences of poliomyelitis with respiratory involvement include suffocation or pneumonia from aspiration of secretions.[21] Overall, 5–10% of patients with paralytic polio die due to the paralysis of muscles used for breathing. The mortality rate varies by age: 2–5% of children and up to 15–30% of adults die. Bulbar polio often causes death if respiratory support is not provided;[13] with support, its mortality rate ranges from 25 to 75%, depending on the age of the patient.[22] When positive pressure ventilators are available, the mortality can be reduced to 15%.[23]
References
- ↑ Frauenthal HWA, Manning JVV (1914). Manual of infantile paralysis, with modern methods of treatment.. Philadelphia Davis, 79–101. OCLC 2078290
- ↑ Sandberg A, Hansson B, Stålberg E (1999). "Comparison between concentric needle EMG and macro EMG in patients with a history of polio". Clinical Neurophysiology. 110 (11): 1900–8. PMID 10576485.
- ↑ Cashman NR, Covault J, Wollman RL, Sanes JR (1987). "Neural cell adhesion molecule in normal, denervated, and myopathic human muscle". Ann. Neurol. 21 (5): 481–9. PMID 3296947.
- ↑ 4.0 4.1 Agre JC, Rodríquez AA, Tafel JA (1991). "Late effects of polio: critical review of the literature on neuromuscular function". Archives of physical medicine and rehabilitation. 72 (11): 923–31. PMID 1929813.
- ↑ Trojan DA, Cashman NR (2005). "Post-poliomyelitis syndrome". Muscle Nerve. 31 (1): 6–19. PMID 15599928.
- ↑ Gawne AC, Halstead LS (1995). "Post-polio syndrome: pathophysiology and clinical management". Critical Review in Physical Medicine and Rehabilitation 7: 147–88. Reproduced online with permission by Lincolnshire Post-Polio Library; retrieved on 2007-11-10.
- ↑ Grimby G, Einarsson G, Hedberg M, Aniansson A (1989). "Muscle adaptive changes in post-polio subjects". Scandinavian journal of rehabilitation medicine. 21 (1): 19–26. PMID 2711135.
- ↑ Mandell, Gerald (2010). Mandell, Douglas, and Bennett's principles and practice of infectious diseases. Philadelphia, PA: Churchill Livingstone/Elsevier. ISBN 0443068399.
- ↑ WEINSTEIN L (1957). "Cardiovascular disturbances in poliomyelitis". Circulation. 15 (5): 735–56. PMID 13427128.
- ↑ GALPINE JF, WILSON WC (1959). "Occurrence of myocarditis in paralytic poliomyelitis". Br Med J. 2 (5163): 1379–81. PMC 1990933. PMID 13826196.
- ↑ Sanofi Pasteur. "Poliomyelitis virus (picornavirus, enterovirus), after-effects of the polio, paralysis, deformations". Polio Eradication. Retrieved 2007-07-31.
- ↑ Mayo Clinic Staff (2005-05-19). "Polio: Complications". Mayo Foundation for Medical Education and Research (MFMER). Retrieved 2007-02-26. Check date values in:
|date=(help) - ↑ 13.0 13.1 Hoyt, William Graves; Miller, Neil; Walsh, Frank (2005). Walsh and Hoyt's clinical neuro-ophthalmology. Hagerstown, MD: Lippincott Williams & Wilkins. pp. 3264–65. ISBN 0-7817-4814-3.
- ↑ Trojan D, Cashman N (2005). "Post-poliomyelitis syndrome". Muscle Nerve. 31 (1): 6–19. PMID 15599928.
- ↑ Ramlow J, Alexander M, LaPorte R, Kaufmann C, Kuller L (1992). "Epidemiology of the post-polio syndrome". Am. J. Epidemiol. 136 (7): 769–86. PMID 1442743.
- ↑ Lin K, Lim Y (2005). "Post-poliomyelitis syndrome: case report and review of the literature" (PDF). Ann Acad Med Singapore. 34 (7): 447–9. PMID 16123820.
- ↑ Neumann D (2004). "Polio: its impact on the people of the United States and the emerging profession of physical therapy" (PDF). The Journal of orthopaedic and sports physical therapy. 34 (8): 479–92. PMID 15373011. Reproduced online with permission by Post-Polio Health International; retrieved on 2007-11-10.
- ↑ Cuccurullo SJ (2004). Physical Medicine and Rehabilitation Board Review. Demos Medical Publishing. ISBN 1-888799-45-5.
- ↑ Mueller S, Wimmer E, Cello J (2005). "Poliovirus and poliomyelitis: a tale of guts, brains, and an accidental event". Virus Res 111 (2): 175–93. PMID 15885840
- ↑ Silverstein A, Silverstein V, Nunn LS (2001). Polio, Diseases and People. Berkeley Heights, NJ: Enslow Publishers, 12. ISBN 0-7660-1592-0.
- ↑ Goldberg A (2002). "Noninvasive mechanical ventilation at home: building upon the tradition". Chest. 121 (2): 321–4. PMID 11834636.
- ↑ Miller AH, Buck LS (1950). "Tracheotomy in bulbar poliomyelitis". California medicine. 72 (1): 34–6. PMID 15398892.
- ↑ Template:Cite paper