eMedicine Specialties > Orthopedic Surgery > Pediatrics

Poliomyelitis

Author: S Vidyadhara, MBBS, MD, MS(Ortho), DNB(Ortho), FNB(Spine Surgery), MNAMS, Consultant, Department of Spine Surgery, Manipal Hospital, India
Coauthor(s): Sharath K Rao, MBBS, MS, D'Ortho, Professor and Head of Unit V, Department of Orthopedics, Kasturba Medical College Hospital, India; Mundkur Sudhakar Shetty, MBBS, MS, MCh, Senior Professor and Head Orthopedic Department, Yenapoya Medical College and Hospitals, Mangalore; James J Gnanadoss, MBBS, MS(Ortho), Professor and Head of Unit, Director, Department of Orthopedics and Spine Surgery, Mahatma Gandhi Medical College Hospital, India
Contributor Information and Disclosures

Updated: Nov 20, 2008

Introduction

The images below show surgically corrected deformities of the knee, hip, and foot associated with poliomyelitis.

History of the Procedure

Poliomyelitis first occurred nearly 6000 years ago in the time of the ancient Egyptians. The evidence for this is in the withered and deformed limbs of certain Egyptian mummies.

Following is a timeline of the recorded history of this disease:

• 3700 BC: An Egyptian mummy with probable polio.
• 1580–1350 BC: Priest Ruma with a withered leg and equinus foot—shown on a plaque; probably poliomyelitis.
• 1209 BC: Mummy Giptah with an equinus foot.
• 1559: A painting by Pieter Bruegel shows a crippled beggar. This may not be polio, although it probably did occur during this period in England.
• 1789: First known description of poliomyelitis by Underwood.
• 1834: First epidemic of poliomyelitis on the island of St. Helena.
• 1855: First description by Duchenne of the pathologic process in poliomyelitis involving the anterior horn cells of the spinal cord.
• 1908: Transmission of poliomyelitis to a monkey by Landsteiner.
• 1909: Passage of the virus through a monkey by Flexner.
• 1949: Growth of the virus on tissue culture.
• 1951: Three types of polio virus isolated and identified.
• 1954: First large-scale trial of Salk (dead vaccine) by injection.
• 1958: First general use of Sabin (live attenuated vaccine) by mouth.

Problem

Since the World Health Assembly in May 1988 resolved to eradicate poliomyelitis, the estimated global incidence of polio has decreased by more than 99%, and 3 World Health Organization (WHO) regions (the Americas, the Western Pacific, and Europe) have been certified as polio-free.

Since 1994, when the countries of the WHO South-East Asia Region (SEAR) began accelerating polio-eradication activities, substantial progress toward that goal has been made.

Problems remain due to the difficulties involved in extending immunization coverage to some regions (especially Africa), integrating new vaccines into routine immunization schedules, and securing sufficient funding for programs. Injection safety is also a major problem that should be resolved by utilization and proper disposal of single-use auto-disabling syringes. The forthcoming availability of new vaccines and the action of the Global Alliance for Vaccines and Immunization hold reasonable hope for the future. Other problems remain, such as new conditions resembling polio paralysis caused by viral infection other than by poliovirus 2 and post-polio syndrome (PPS).

It is safe to assume that acute and residual poliomyelitis is still encountered in the developing world. In developed countries, on the other hand, residual poliomyelitis is still occasionally seen in the elderly and immigrants.^{1,2,3,4,5,6,7}

Related eMedicine topics:

Poliomyelitis  (Pediatrics)

Acute Poliomyelitis

Postpolio Syndrome

Etiology

Acute poliomyelitis is caused by small RNA viruses of the enterovirus group of the Picornavirus family. The single-stranded RNA core is surrounded by a protein capsid without a lipid envelope, which makes poliovirus resistant to lipid solvents and makes it stable at a low pH. Three antigenically distinct strains are known, with type I accounting for 85% of cases of paralytic illnesses. Infection with one type does not protect from the other types; however, immunity to each of the 3 strains is lifelong.

Pathophysiology

• Poliovirus is spread by the fecal-oral route and by aerosol droplets.
• The poliovirus is shed in oral secretions for several weeks and in the feces for several months. 
• The poliovirus destroys the anterior horn cells in the spinal cord.

Presentation

Acute stage 

Poliovirus is primarily spread by fecal–hand–oral transmission from one host to another. The virus is shed in oral secretions for several weeks and in the feces for several months. It destroys the anterior horn cells in the spinal cord. Poliovirus infections can be divided into minor and major forms.⁸

Clinical findings

The clinical findings associated with an attack of polio are as follows:

• Fever, neck stiffness (nuchal rigidity), and a pleocytosis in the CSF
• Profound asymmetrical muscle weakness
• The initial phase is typically followed by some recovery of muscle strength, but permanent weakness results from necrosis of anterior horn cells
• Rarely, a transverse myelitis with paraparesis, urinary retention, sensory symptoms and signs, autonomic dysfunction (including hyperhidrosis or hypohidrosis), and decreased limb temperature may occur

Treatment

Treatment in the acute stage is mainly medical, involving the pediatricians. General supportive treatment for the pyrexia and irritation, for the prevention of secondary respiratory infection, and for any respiratory paralysis are the main aspects of treatment.

The paralyzed legs are supported by plaster splints or pillows and sandbags to keep the hip joints in 5° of flexion and in neutral rotation. The knee joint is held at 5° of flexion, and the foot is supported in a 90° position. Splinting relieves pain and spasm and prevents the development of deformities.

Recovery stage

In this stage, also known as the convalescent stage, the acute symptoms and muscle tenderness disappear and the paralyzed muscles begin to recover. This stage lasts for up to 2 years after the onset of the disease. During this entire period, there is gradual recovery of the muscles; the recovery is rapid in the first 6 months but is slower during the subsequent months.

Residual-paralysis stage

The period beyond 2 years after the onset of the disease is called the residual-paralysis stage. No recovery of muscle power occurs in this stage. Deformities are liable to occur due to imbalance of muscle power and poor posture. There is also disuse atrophy of muscles and shortening of the leg due to interference with growth. In neglected cases, gross fixed deformities of the hip, knee, and foot occur with severe wasting of muscles. Children with extensive paralysis and gross deformities have to crawl on all fours to move from place to place.

Post-polio syndrome

Post-polio syndrome is the term used for the newly occurring late manifestations of poliomyelitis that develop in patients 30 to 40 years after the occurrence of the acute illness. It has been estimated that 25–60% of the patients who had acute polio may experience these late effects of the disease.^9,10

The specific cause of post-polio syndrome is unknown; the etiology has been attributed to pathophysiologic and functional causes. Pathophysiologic causes include chronic poliovirus infection, death of the remaining motor neurons with ageing, premature ageing, damage to the remaining motor neurons caused by increased demands or secondary insults, and immune-mediated syndromes.

Functional etiologies for post-polio syndrome include greater energy expenditure as a result of weight gain and muscle weakness caused by overuse or disuse. Post-polio syndrome has been recognized for over 100 years, but it is more common at the present time because of the large epidemics of poliomyelitis that occurred in the 1940s and 1950s.
 
Post-polio syndrome is characterized by neurologic, musculoskeletal, and general manifestations. Musculoskeletal manifestations include muscle pain, joint pain, spinal changes such as spondylosis and scoliosis, and secondary root and peripheral nerve compression. General manifestations include generalized fatigue and cold intolerance. The slowly progressive muscle weakness occurs in those muscle groups already involved, such as the quadriceps and calf muscles.

Diagnostic criteria for post-polio syndrome

1. A prior episode of paralytic poliomyelitis with residual motor neuron loss (which can be confirmed through a typical patient history, a neurologic exam, and, if needed, an electrodiagnostic exam¹¹
2. A period of neurologic recovery followed by an interval (usually 15 years or more) of neurologic and functional stability.
3. A gradual or abrupt onset of new weakness or abnormal muscle fatigue (decreased endurance), muscle atrophy, or generalized fatigue.
4. Exclusion of medical, orthopedic, and neurologic conditions that may be causing the symptoms mentioned in item No. 3 above

Pattern of muscle weakness and deformities

Upper-limb involvement

Late functional deterioration is common in long-term poliomyelitis patients. While upper-limb pain in individual functional regions is common, its overall prevalence and pattern in long-term poliomyelitis is poorly documented.¹²

There are data in support of overuse due to greater mobility and independence as a cause of increasing upper-limb pain in long-term poliomyelitis, especially among severely paralyzed polio patients.

Lower-limb involvement

Typical osseous or soft-tissue abnormalities around the knees associated with poliomyelitis include external rotation of the tibia, excessive valgus alignment, ligamentous laxity, and genu recurvatum.

With localized wasting, the quadriceps can help compensate for a weak calf. With hamstring weakness, the ability to decelerate the tibia is lost, and therefore, flexion of the knee will persist throughout the stance phase. In order to prevent this, the patient may attempt to compensate with increased quadriceps activity for a longer portion of the stance phase of gait. In the case of a weak quadriceps and hamstrings, the occurrence of an equinus contracture or a hinged ankle-foot orthosis (AFO) with a dorsiflexion block will prevent excessive ankle dorsiflexion, as well as knee flexion during the stance phase. Lengthening of the Achilles tendon should be avoided in these patients. They may require an ischial bearing, double upright locked knee orthosis, which helps prevent the knee from buckling during gait.

Common foot and ankle deformities seen are pes cavovarus (hindfoot cavus) due to evertor paralysis (peroneus brevis and longus) and pronated everted foot due to invertor paralysis (tibialis anterior and posterior). Foot intrinsics are typically spared in poliomyelitis. Claw toes result from relative overactivity of the long toe flexors and extensors (to compensate for weakness of the triceps).

• Search for CME/CE on This Topic »

• Poliomyelitis (Pediatrics: General Medicine)
• Acute Poliomyelitis (Physical Medicine and Rehabilitation)
• Guillain-Barre Syndrome (Physical Medicine and Rehabilitation)
• Picornavirus-Overview (Infectious Diseases)

• ACIP Updates Recommendations for Routine Poliovirus Vaccination
• Polio Incidence on the Decline in India; Total Eradication a Strong Possibility

• The Case for Cooperation in Managing and Maintaining the End of Poliomyelitis: Stockpile Needs and Coordinated OPV Cessation
• Progress Toward Poliomyelitis Eradication -- India, January 2007-May 2009
• Laboratory Surveillance for Wild and Vaccine-derived Polioviruses â€â€� Worldwide, January 2008–June 2009