01Approach to the Critical Patient/attcp62

Immediate priorities

›Acute respiratory threats

›Respiratory failure in post-polio hypoventilation

›Declining SpO2 despite supplemental oxygen

›Rising PaCO2 with somnolence or confusion

›Paradoxical breathing pattern

›If acute ventilatory failure, initiate noninvasive ventilation (BiPAP) emergently

›Avoid intubation unless NIV fails; PPS patients may have prolonged ventilator dependence

›Class I recommendation for NIV in neuromuscular respiratory failure

›Bulbar emergency

›Acute aspiration with oxygen desaturation

›Inability to manage secretions

›Rapidly progressive dysphagia with silent aspiration risk

›Hemodynamic assessment

›Baseline vitals

›SpO2 supine and upright

›Respiratory rate and work of breathing

›BMI contribution to respiratory compromise

›Sepsis concern with aspiration pneumonia

›SBP < 90 mmHg or MAP < 65 mmHg

›Lactate >= 2 mmol/l

›Tachycardia > 100 bpm

›Rapid functional assessment

›Baseline ambulatory status and assistive devices

›Recent falls or injuries

›Change from functional baseline over weeks to months

›Acute versus chronic decline determination

›Rapid progression suggests ALS or CIDP rather than PPS

02History/hx83

Acute presentation

›New symptom characterization

›New weakness

›Affected limbs versus previously unaffected limbs

›Rate of progression (weeks to months is typical for PPS; days is atypical)

›Precipitant: overuse, weight gain, surgery, trauma, or intercurrent illness

›Fatigue pattern

›Generalized flu-like exhaustion worse as day progresses

›Focal muscle fatigability with repeated use

›Cognitive or postpolio wall fatigue

›Pain characterization

›Muscular aching and cramping in polio-affected limbs

›Activity-related and end-of-day worsening

›Joint pain from biomechanical overload

›Neuropathic pain quality

Classic presentation

›Diagnostic triad

›New or increasing muscle weakness after stable interval >= 15 years

›Affects previously polio-involved or clinically unaffected limbs

›Slow gradual onset distinguishes from ALS

›Generalized and focal fatigue

›Distinct from depression-related fatigue

›Worsens with activity; improves with rest

›Musculoskeletal pain

›Myalgia, joint pain, and myofascial pain patterns

Prior polio history

›Original illness documentation

›Age at polio onset and severity of paralysis

›Limbs involved and degree of permanent weakness

›Bulbar involvement with swallowing or respiratory compromise

›Hospitalization and ventilator use during acute illness

›Recovery history

›Duration and degree of functional recovery

›Greater initial recovery paradoxically increases PPS risk

›Stable interval

›Period of neurological stability before new symptoms emerged

›Minimum 15-year stable interval is a diagnostic criterion

Respiratory and bulbar symptoms

›Respiratory red flags

›Dyspnea on exertion and at rest

›Orthopnea and nocturnal dyspnea

›Morning headaches suggesting nocturnal hypoventilation

›Sleep-disordered breathing

›Excessive daytime somnolence

›Witnessed apneas or snoring

›Poor sleep quality with frequent arousals

›Chronic hypoventilation features

›Cor pulmonale signs: peripheral edema and JVD

›Polycythemia

›Bulbar symptoms

›Dysphagia to solids or liquids

›Choking episodes

›Up to 10-20% of PPS patients have swallowing dysfunction

›Dysphonia and voice changes

›Nasal voice quality

›Voice fatigue over the day

Risk factors

›Factors increasing PPS severity

›Severity of initial paralytic episode

›Greater initial paralysis predicts more severe PPS

›Paradoxically: greater recovery also increases risk due to motor unit overload

›Demographic risk

›Older age at acute polio onset

›Female sex has higher prevalence; male sex shows greater strength decline rate

›Lifestyle and biomechanical factors

›Physical overuse of weakened muscles over decades

›Weight gain and obesity

›Scoliosis contributing to respiratory compromise

›Comorbidities

›Sleep apnea, osteoporosis, osteoarthritis, depression

Past medical and surgical history

›Relevant history

›Prior orthopedic procedures

›Tendon transfers, arthrodesis, limb-lengthening procedures

›Spinal surgery for scoliosis

›Anesthesia history

›Prior complications: prolonged recovery or respiratory compromise

›Assistive device history

›Type and duration of brace, orthotic, cane, or wheelchair use

›Recent changes in device need indicating functional decline

Medications review

›Current medications

›Agents with respiratory risk

›Opioids: heightened respiratory depression sensitivity

›Sedative-hypnotics: may worsen nocturnal hypoventilation

›Medications tried for PPS

›Amantadine, prednisone, modafinil — evidence for fatigue benefit is negative

›Pyridostigmine — conflicting trial results; generally not recommended

›IVIg — reduces CSF cytokines; not recommended for routine use

›Lamotrigine — one controlled study showing benefit for pain and fatigue

03Physical Exam/exam57

Neurological examination

›Motor system

›Muscle strength testing using MRC grading scale

›Document all limb groups individually

›Compare polio-affected versus clinically unaffected limbs

›Specific attention to new atrophy in previously stronger muscles

›Reflexes

›Diminished or absent deep tendon reflexes in LMN pattern

›Hyperreflexia or Babinski sign raises concern for ALS or myelopathy

›Sensory examination

›Should be normal in PPS

›Dermatomal loss suggests superimposed radiculopathy or myelopathy

›Fasciculations

›May be present in PPS

›Widespread tongue fasciculations suggest bulbar ALS

Respiratory examination

›Ventilatory mechanics

›Chest wall excursion

›Reduced excursion from prior respiratory polio

›Scoliosis restricting expansion

›Breathing pattern

›Paradoxical abdominal movement suggesting diaphragm weakness

›Accessory muscle recruitment

›SpO2 supine versus upright

›Supine desaturation typical with diaphragm weakness

›Kyphoscoliosis assessment

›Degree of curvature

›Progression from prior measurements

04Differential Diagnosis/ddx59

Life-threatening and urgent mimics

›Amyotrophic lateral sclerosis (ALS)

›ICD-10 G12.21

›Upper AND lower motor neuron signs simultaneously

›Hyperreflexia, Babinski sign, spasticity distinguish from PPS

›More rapid progression — weeks to months rather than years

›Tongue fasciculations with atrophy in bulbar ALS

›Acute respiratory failure from neuromuscular cause

›Myasthenia gravis

›Fatigable weakness; ptosis and diplopia

›Positive acetylcholine receptor antibodies

›Edrophonium test or repetitive nerve stimulation

›Guillain-Barre syndrome

›Ascending weakness over days

›Albuminocytologic dissociation in CSF

Chronic neuromuscular mimics

›CIDP

›ICD-10 G61.81

›Sensory involvement distinguishes from PPS

›Elevated CSF protein typically > 0.45 g/l

›Demyelinating pattern on nerve conduction studies

›Treatment-responsive — important not to miss

›Inclusion body myositis

›ICD-10 G72.41

›Progressive finger flexor and quadriceps weakness

›CK elevated (often 2-15 times upper limit)

›Muscle biopsy shows rimmed vacuoles and p62 inclusions

›Spinal stenosis with myelopathy

05Laboratory Tests/lt58

Exclusionary workup

›Hematologic panel

›Complete blood count

›Anemia as cause of fatigue and exertional dyspnea

›Polycythemia in chronic hypoxemia

›Leukocytosis if aspiration pneumonia or infection

›Thyroid function

›TSH

›Hypothyroidism mimics proximal weakness and fatigue

›Free T4 if TSH abnormal

›Metabolic panel

›Comprehensive metabolic panel

›Electrolytes and renal function

›Hepatic profile

›Glucose

›Inflammatory markers

›ESR and CRP

›Elevated in polymyalgia rheumatica

›Nonspecific in PPS

›Nutritional markers

›Vitamin B12 and folate

›Neuropathy from B12 deficiency mimics superimposed pathology

›Vitamin D level

›Deficiency common with reduced outdoor activity and mobility

›Iron studies: serum iron, ferritin, TIBC

›Restless legs syndrome prevalence ~36% in PPS; iron deficiency exacerbates

Muscle and nerve injury markers

›Creatine kinase

06Diagnostic Tests/dt86

Scoring Systems

›PPS diagnostic criteria (Dalakas 1995 criteria)

›Required criteria for diagnosis

›Confirmed prior paralytic poliomyelitis by history, exam, and EMG

›Partial or complete neurological recovery after acute illness

›Stable neurological and functional status >= 15 years after acute polio

›New musculoskeletal symptoms: new weakness, fatigue, and/or pain

›Exclusion of other medical conditions explaining symptoms

›Severity classification

›Mild: fatigue and pain with preserved function

›Moderate: new weakness affecting ADLs

›Severe: progressive weakness with respiratory compromise or dysphagia

›MRC muscle grading scale

›Standardized strength documentation

›0: no contraction

›1: flicker of contraction

›2: movement with gravity eliminated

›3: movement against gravity only

›4: movement against some resistance

›5: normal strength

›Epworth Sleepiness Scale

›Sleep-disordered breathing screening

›Score >= 10 warrants polysomnography

›PPS patients have high prevalence of OSA and hypoventilation

›PHQ-9 depression screening

›Indicated in all PPS patients

›Score >= 10 warrants treatment intervention

›Depression worsens fatigue and pain outcomes

MRI

›Brain and spinal cord MRI

›Indications in PPS evaluation

›Upper motor neuron signs suggesting myelopathy or ALS

›Rapid weakness progression atypical for PPS

›Asymmetric reflex changes

›Spinal MRI for myelopathy

›Cervical and lumbar stenosis evaluation

›Disc herniation or cord compression

›Sensitivity ~90% for clinically significant stenosis

›Brain MRI in ALS differentiation

›Cortical thinning in motor cortex in ALS

›Normal in PPS

›PPS-specific MRI findings

›Anterior horn cell atrophy pattern in spinal cord

›No diagnostic sensitivity or specificity established for PPS specifically

CT

›CT chest for respiratory complications

›Indications

›Suspected aspiration pneumonia

›Suspected lung abscess or empyema

›Baseline scoliosis severity documentation

›CT findings in aspiration pneumonia

›Right lower lobe and right middle lobe predominance

›Ground glass opacification progressing to consolidation

›CT for scoliosis and chest deformity

›Rib cage restriction quantification

›Correlation with FVC restriction

›CT head

›Indications

›Altered mental status with respiratory failure

›Fall-related head injury in PPS patients

›Rule out intracranial pathology causing weakness

Ultrasound

›Diaphragm ultrasound

›Assessment of diaphragmatic function

›Diaphragm excursion < 10 mm during quiet breathing suggests dysfunction

›Thickening ratio < 1.2 indicates diaphragm paralysis

›Paradoxical cephalad movement with sniff suggests phrenic nerve involvement

›Bedside availability advantage

›No radiation; repeatable for monitoring

›Operator dependent; skill required for interpretation

›Musculoskeletal ultrasound

›Joint and tendon assessment

›Rotator cuff tears from compensatory upper extremity overuse

›Hip and knee joint effusions from osteoarthritis

›Tendinopathy from repetitive mechanical stress

›Cardiac ultrasound

›Echocardiography indications

›Cor pulmonale assessment in chronic hypoventilation

›Right ventricular hypertrophy and elevated RVSP

›Right atrial enlargement and tricuspid regurgitation

›Nerve conduction and EMG (performed by neurology)

›EMG findings in PPS

›Chronic denervation with reinnervation: large amplitude, long duration, polyphasic MUAPs

›Reduced motor unit recruitment

›Active denervation: fibrillations and positive sharp waves in some

›Normal sensory nerve conduction studies

›EMG role

›Confirms prior polio involvement in clinically unaffected limbs

›Distinguishes PPS from ALS and CIDP

›No single EMG finding is pathognomonic for PPS

07Disposition/dispo39

Admission criteria

›Indications for inpatient admission

›Acute respiratory failure

›Hypercapnic respiratory failure requiring ventilatory support initiation

›SpO2 < 90% not correcting with supplemental oxygen

›Vital capacity < 25% predicted acutely

›Aspiration pneumonia or aspiration event

›Hypoxemia, fever, and infiltrate on imaging

›High-grade aspiration with large volume or particulate matter

›Acute functional decline

›Inability to perform ADLs requiring inpatient rehabilitation

›New inability to walk safely with prior ambulatory status

›Perioperative management

›Significant respiratory compromise requiring postoperative monitoring

›Anticipated prolonged ventilatory support post-surgery

Observation indications

›Criteria for observation or short stay

›Borderline respiratory function

›New respiratory symptoms with FVC 40-55% predicted pending sleep study

›SpO2 mildly reduced with pending ABG results

›Acute pain crisis

›Uncontrolled musculoskeletal pain requiring IV analgesia

›Ruling out fracture or inflammatory arthritis

›Falls with injury

›Hip fracture evaluation in osteoporotic PPS patients

›Head CT if head injury

Discharge criteria

›Safe discharge indicators

08Treatment/t121

Energy conservation and pacing

›Activity modification

›Pacing strategies

›Scheduled rest periods throughout day

›Work simplification and task prioritization

›Avoid activity beyond 70% of maximum capacity to prevent overuse

›Lifestyle modifications

›Spread activities over full day rather than concentrating effort

›Morning activity prioritization when energy highest

›Delegate physically demanding tasks

Exercise prescription

›Exercise approach

›Moderate-intensity aerobic exercise

›Goal: 30 minutes of moderate aerobic activity 3-5 days per week

›Target heart rate 40-70% of maximum heart rate

›Supervised introduction with physiotherapist

›Strengthening exercise

›Nonfatiguing resistance training

›Avoid training to failure; stop at first sign of unusual fatigue or weakness

›Monitor for post-exercise weakness lasting > 30 minutes (indicates overuse)

›Aquatic therapy

›Preferred modality for weight-bearing limitation

›Reduces biomechanical joint stress

›Allows aerobic training at higher intensity without overloading weakened limbs

›Avoid complete inactivity

›Deconditioning worsens weakness and respiratory function

›Balance activity with rest is the therapeutic target

Respiratory management

›Noninvasive ventilation

›BiPAP indications

›Nocturnal hypoventilation: SpO2 < 90% for > 5% of night or PaCO2 > 45 mmHg

›FVC < 55% predicted with symptoms

›Morning headaches and daytime somnolence from CO2 retention

›BiPAP initiation

›IPAP 8-12 cmH2O starting, titrated to SpO2 and PCO2 normalization

›EPAP 4-5 cmH2O baseline

›Nocturnal use initially; daytime if progressive respiratory failure

›CPAP for obstructive sleep apnea

›Starting pressure 6-8 cmH2O titrated by sleep study

›Consider BiPAP if OSA coexists with hypoventilation

›Supplemental oxygen

›Caution in post-polio hypoventilation

›Hypercapnic drive preserved; supplemental O2 alone may mask CO2 retention

›Pair oxygen with NIV if CO2 retention present

›Target SpO2 92-96% in hypercapnic patients

Pain management

›Musculoskeletal pain

›First-line analgesics

›Acetaminophen 500-1000 mg orally every 6 hours; maximum 4000 mg/day

›NSAIDs: ibuprofen 400-600 mg orally every 6-8 hours with food

›Avoid chronic high-dose NSAID in elderly with renal impairment

›Physical modalities

›Heat application for muscular aching

›Physiotherapy with myofascial release and gentle stretching

›Transcutaneous electrical nerve stimulation for refractory pain

›Neuropathic and mixed pain

›Lamotrigine

›Starting dose 25 mg daily for 2 weeks

›Increase to 50 mg daily weeks 3-4

›Target dose 100-200 mg daily in divided doses

›One controlled study showing benefit for pain, fatigue, and quality of life

›Tricyclic antidepressants

›Amitriptyline 10-25 mg at bedtime; titrate to 75 mg maximum

›Benefit for neuropathic pain and comorbid depression

›Anticholinergic effects; avoid in urinary retention and cardiac conduction disease

›Opioids

›Caution in PPS context

›Respiratory depression risk especially during sleep

›Reserve for severe refractory pain with specialist input

›Avoid in patients with uncontrolled sleep-disordered breathing

Orthotic and assistive device management

›Orthotic prescription

›Ankle foot orthoses

›Carbon-fiber AFOs preferred for reduced weight

›Reduce energy cost of walking by correcting foot drop

›Custom fit to prevent pressure injuries in insensate areas

›Knee ankle foot orthoses

›For combined quadriceps and ankle weakness

›Locking or free knee hinge based on functional requirement

›Mobility aids

›Prescribe to reduce overuse of weakened muscles

›Cane or forearm crutch for mild imbalance

›Rollator walker for moderate weakness

›Manual or power wheelchair for significant fatigue or weakness

›Mobility scooter for preserved upper limb strength with lower limb weakness

Sleep and fatigue management

›Restless legs syndrome treatment

›Dopamine agonist therapy

›Pramipexole 0.125 mg 2-3 hours before bedtime; titrate to 0.5 mg maximum

›Ropinirole 0.25 mg at bedtime; titrate to 4 mg maximum

›Iron supplementation if ferritin < 75 mcg/l

›Fatigue-specific management

›No pharmacotherapy has proven benefit for PPS fatigue

›Amantadine: two RCTs negative for fatigue

›Modafinil: two RCTs negative for fatigue

›Pyridostigmine: conflicting results; not recommended routinely

›Nonpharmacologic fatigue management

›Energy conservation program with occupational therapy

›Sleep hygiene optimization

›Treatment of underlying sleep-disordered breathing reduces daytime fatigue

Dysphagia management

›Swallowing intervention

›Speech-language pathology evaluation

›Modified barium swallow or FEES for objective aspiration risk assessment

›Videofluoroscopic swallow study preferred for anatomic detail

›Dietary modification

›Texture modification based on dysphagia severity

›Thickened liquids if liquid aspiration documented

›Small frequent meals to reduce fatigue

›Swallowing strategies

›Chin-tuck maneuver during swallowing

›Double swallow technique for residue clearance

›Upright position for all meals

Psychological support

›Mental health interventions

›Depression screening and treatment

›SSRIs first-line for comorbid depression

›Sertraline 50 mg daily; titrate to 200 mg over weeks

›Psychotherapy for adjustment difficulties

›Cognitive behavioral therapy

›Evidence-based for fatigue and pain management in chronic neurological conditions

›Targets illness beliefs and activity-avoidance behavior

Weight management

›Obesity management

›Weight reduction targets

›BMI < 25 kg/m2 target reduces respiratory load

›Every 10 kg weight reduction improves SpO2 by approximately 1-2%

›Dietary counseling

›Adequate protein intake 1.0-1.5 g/kg/day for muscle maintenance

›Calcium 1200 mg/day and vitamin D 800-2000 IU/day for osteoporosis prevention

09Special Populations/sp65

Pregnancy

›Maternal considerations in PPS

›Respiratory reserve in pregnancy

›Diaphragm elevation by gravid uterus reduces FRC by 20-30%

›PPS patients with borderline respiratory function at high risk of decompensation

›FVC monitoring each trimester mandatory

›Pulmonology co-management from first trimester

›Preconception counseling

›Spirometry and polysomnography before conception

›High-risk pregnancy if FVC < 50% predicted

›Labor and delivery considerations

›Regional anesthesia preferred over general anesthesia

›Succinylcholine absolutely contraindicated

›Multidisciplinary delivery planning: obstetrics, neurology, anesthesia, respirology

›Medication safety in pregnancy

›Analgesics

›Acetaminophen safe throughout pregnancy

›NSAIDs avoid after 20 weeks; risk of premature ductus closure

›Lamotrigine: continue if clinically essential; Category C; folate supplementation

›NIV in pregnancy

›BiPAP safe in pregnancy; maintain SpO2 > 95% given fetal oxygen dependence

›Target PaCO2 30-35 mmHg in pregnancy (physiologic hyperventilation)

Geriatric

›Age-related considerations

›Compounding sarcopenia

›Age-related muscle loss (sarcopenia) additive to PPS denervation

›Accelerated functional decline after age 70

›Falls risk markedly elevated: balance, weakness, and polypharmacy combined

10Background/b68

Epidemiology

›Global polio survivor burden

›Historical prevalence

›Estimated 20 million polio survivors worldwide prior to eradication efforts

›Major epidemics: United States 1952 (57,879 cases); peak global burden 1950s

›Vaccination campaigns beginning 1955 (Salk IPV) and 1961 (Sabin OPV)

›PPS prevalence

›Estimated 29-42% of paralytic polio survivors develop PPS

›Global PPS prevalence estimated at 4-8 million individuals

›Demographic patterns

›Most current patients acquired polio in 1940s-1960s; now aged 60-80+ years

›Female sex has higher PPS prevalence

›Male sex shows greater annual rate of strength decline

›Annual decline rate

›Typical muscle strength loss 1-3% per year

›Decline over 8 years approximately 9-15%

›Accelerated loss 5-8%/year in severely affected patients

›~20% of PPS patients lose walking capacity over 20 years

Pathophysiology

›Motor unit decompensation mechanism

›Acute polio pathophysiology

›Poliovirus destroys anterior horn cells in spinal cord and brainstem

›Surviving neurons undergo compensatory reinnervation via axonal sprouting

›Enlarged motor units (one neuron innervating 5-10 times normal muscle fibers)

›Post-polio decompensation

›Decades of metabolic demand on enlarged motor units causes premature aging

›Distal axon dropout exceeds capacity for further reinnervation

›Progressive denervation without adequate compensatory reinnervation

›New atrophy and weakness emerge after decades of stability

›Neuroinflammatory hypothesis

›CSF markers in PPS

›Elevated proinflammatory cytokines: IL-1beta, TNF-alpha in CSF

›Oligoclonal bands present in some patients

›IVIg reduces CSF cytokines; variable clinical translation

›Viral persistence hypothesis

›Poliovirus RNA detected in CSF of some PPS patients

›Not consistently reproduced; clinical significance unclear

›Central fatigue mechanism

›Central nervous system changes

›Poliovirus involvement not limited to anterior horn cells; reticular activating system affected

›Accounts for cognitive fatigue and sleep disruption patterns

›Distinct from peripheral motor unit fatigue mechanism

Therapeutic Considerations

›Evidence base overview

›Pharmacotherapy evidence

›No disease-modifying drug with Level A evidence for PPS

›Cochrane review (2015): insufficient evidence to support any specific drug treatment

›IVIg: reduced CSF cytokines and some functional improvements in small RCTs; not recommended for routine use

›Lamotrigine: one controlled trial showing benefit for pain, fatigue, quality of life

›Rehabilitation evidence

›Moderate evidence for individualized exercise programs improving function

›Aquatic therapy consistently shows benefit in controlled trials

›Energy conservation programs reduce fatigue with good quality evidence

›Respiratory management evidence

›NIV evidence

›Class I recommendation for NIV in neuromuscular respiratory failure

›BiPAP reduces morning headaches, improves sleep quality, extends survival

›OSA prevalence in PPS estimated 30-50% in sleep study cohorts

›Respiratory muscle training

›Limited evidence; must be done cautiously to avoid overuse

›Prognosis

›Long-term functional outlook

›Most PPS patients experience gradual decline over decades rather than rapid progression

›~20% will lose ambulation over 20 years of follow-up

›Respiratory failure is leading cause of PPS-related mortality

›Quality of life preserved in most patients with appropriate management

›Factors associated with better prognosis

›Lower initial paralysis severity

›Maintained healthy weight

›Participation in supervised exercise programs

›Early initiation of respiratory support when indicated

11Patient Discharge Instructions/pdi34

copy discharge instructions

›Discharge instructions for Poliomyelitis / Post-Polio Syndrome

›What is Post-Polio Syndrome

›Post-polio syndrome (PPS) causes new muscle weakness, fatigue, and pain many years after your original polio illness

›It typically begins 15 or more years after recovering from polio

›PPS progresses slowly over years; it is not the same as getting polio again

›Activity and energy management

›Pace your activities throughout the day and take planned rest breaks

›Stop activity before you feel exhausted — do not push through fatigue

›Light to moderate exercise is beneficial but avoid overexertion

›Aquatic therapy or pool exercise is an excellent low-impact option

›Breathing concerns

›If prescribed a BiPAP or CPAP machine, use it every night as directed

›Sleep on your side if possible to improve breathing during sleep

›Avoid sedatives, sleeping pills, or strong pain medications without telling your doctor

›Swallowing concerns

›Eat slowly and sit fully upright during all meals

›Follow texture and thickening recommendations from your speech therapist

›Do not eat when very tired — fatigue increases choking risk

›Medications

›Take acetaminophen or anti-inflammatory medications as prescribed for pain

›Do not take extra sedatives or sleeping pills without medical advice

›Inform any doctor or dentist that you have post-polio syndrome before any procedures or anesthesia

›Return to Emergency Department immediately for

›Difficulty breathing, worsening shortness of breath, or inability to lie flat

›Choking episode or coughing up food or vomit

›Sudden significant new weakness in any limb

›Confusion, severe morning headache, or difficulty waking up

12References/r31

Guidelines and key sources

›Primary references

›Lo JK, Robinson LR: Postpolio syndrome and the late effects of poliomyelitis Parts 1 and 2. Muscle and Nerve 2018

›Part 1: pathogenesis, biomechanical considerations, diagnosis, and investigations

›Part 2: treatment, management, and prognosis

›Gonzalez H, Olsson T, Borg K: Management of postpolio syndrome. Lancet Neurology 2010

›Comprehensive management review with evidence grading

›Koopman FS et al: Treatment for postpolio syndrome. Cochrane Database of Systematic Reviews 2015

›Systematic review: insufficient evidence for specific pharmacotherapy

›Trojan DA, Cashman NR: Post-poliomyelitis syndrome. Muscle and Nerve 2005

›Pathophysiology and clinical characterization

›Dalakas MC: The post-polio syndrome as an evolved clinical entity. Annals NY Academy of Sciences 1995

›Original clinical diagnostic criteria

›Anesthesia references

›Romero A, Joshi GP: Neuromuscular disease and anesthesia. Muscle and Nerve 2013

›Succinylcholine contraindication and relaxant dosing guidance

›Lambert DA, Giannouli E, Schmidt BJ: Postpolio syndrome and anesthesia. Anesthesiology 2005

›Perioperative risk stratification and drug sensitivity

›Tseng WC et al: A patient with postpolio syndrome developed cauda equina syndrome after neuraxial anesthesia. Journal of Clinical Anesthesia 2017

›Case report: cauda equina syndrome after spinal anesthesia

›Respiratory references

›Hsu AA, Staats BA: Postpolio sequelae and sleep-related disordered breathing. Mayo Clinic Proceedings 1998

›Sleep-disordered breathing prevalence and management

›Aboussouan LS, Mireles-Cabodevila E: Sleep-disordered breathing in neuromuscular disease. Chest 2017

›NIV indications and management framework for neuromuscular disease

›Ding Q et al: Obstructive sleep apnea in community-dwelling polio survivors. Frontiers in Neurology 2025

›5-year longitudinal follow-up confirming high OSA prevalence in polio survivors

›Additional sources

Evidence & Review