Approach To A Patient With Paraplegia
Approach To A Patient With Paraplegia
Approach To A Patient With Paraplegia
PARALYSIS OF LOWER PART OF BODY,COMMONLY AFFECTING BOTH LEGS AND OFTEN INTERNAL ORGANS BELOW WAIST.
ETIOLOGY
DIVIDED INTO 2 TYPES
DUE TO UPPER MOTOR NEURON LESION DUE TO LOWER MOTOR NEURON LESION
UMN LESIONS
SPINAL LESIONS (common)
Spinal cord compression( Potts disease,disc prolapse or fracture, tumors,epidural abscess,cervical spondylosis etc) VASCULAR Hemorrhage, Infarction SYSTEMIC DEGENERATION OF TRACTS Multiple sclerosis, MND, Sub acute combined degeneration of cord. INFECTION Transverse myelitis, Neurosyphilis
UMN LESIONS
CEREBRAL LESIONS (uncommon)
Thrombosis of superior sagital sinus Tumor of falx-cerebri Hydrocephalus
LMN LESIONS
Anterior horn cells Poliomyelitis, Motor neuron disease Peripheral nerve Peripheral neuropathy Neuromuscular junction Myasthenia gravis Muscles Muscular dystrophies
It may be acute with trauma,metastasis or Arterial occlusion or it may be slow developing over weeks as in Potts disease,cervical spondylosis etc.
POTTS DISEASE
TB of spine often involves two or more adjacent vertebral bodies. Lower thoracic and upper lumber vertebrae are commonly involved.Intervertebral disc is also destroyed. With advanced disease paravertebral cold abscess , gibbus formation and PARAPLEGIA occur.
TRANSVERSE MYELITIS
It is an acute or subacute inflammation of spinal cord occuring after infection or recent vaccination. Many agents like influenza,measles,CMV,EBV and mycoplasma have been implicated.
Acute inflammatory or post-infective demyelinating polyneuropathy. Develops 1-3 weeks after respiratoryinfection or diarrhea in >70% cases. Ascending polyneuropathy.
Syndrome of combined spinal cord and peripheral nerve damage cause: Vit.B12 deficinency Changes start in posterior columnn (affecting vibration and position sense) then involve lateral column(pyramidal tracts)
MYASTHENIA GRAVIS
Acquired autoimmune disorder of NMJ. Causes skeletal muscle fatigubility and weakness, esp of proximal limb muscles,ocular anb bulbar muscles.
X-linked recessive disorder Deficiency of protein dystrophin in muscles. Symptoms start in childhood,become severe in adolescence and death occurs by age 20 years.
MANAGEMENT OF PARAPLEGIA
HISTORY EXAMINATION INVESTIGATIONS TREATMENT
HISTORY
AGE AND SEX Young age: Inherited disorders,muscle dis.,infections Old age: malignancies r common. DURATION ACUTE:GBS,transverse myelitis, cord compression. CHRONIC:MND,polyneuropathies,muscle dis. SPHINCTER DISTURBANCES (INITIALLY URGENCY OR HESITENCY OF MICTURATION,THEN URINARY RETENTION) Seen in UMN lesions.
HISTORY
SENSORY SYMPTOMS
Numbness,tingling and hyperesthesias in neuropathy. ROOT PAIN In cord compression. BACKACHE In cord compression,transverse myelitis. HEADACHE,VOMITING Intracranial lesions PRECEDING FEVER,URTI In GBS
EXAMINATION
MOTOR SYSTEM FEATURES Muscle waisting Muscle tone Power Deep reflexes Superficial reflex Planters Fasciculations UMNL LMNL absent present
absent present
SENSORY SYSTEM
Sharp sensory level in transverse myelitis differentiates it from GBS. Neuropathy:glove and stocking distribution. Romberg sign +ve if posterior column is involved.
CERVICAL,ABOVE C5 UMN signs and sensory loss in all 4 limbs CERVICAL,C5 TO T1 LMNsigns and segmental sensory loss in arms,and UMN signs in legs THORACIC CORD Spastic paraplegia with a sensory level on trunk. CONUS MEDULLARIS Sensory loss in sacral area and extensor plantar response CAUDA EQUINA LMN signs in lower limbs.
EXAMINATION
EXAMINATION OF SPINE For deformity and tenderness. SPHINCTERS:Look for incontinence or retention of urine or faeces. OTHER FEATURES: Anemia-B12 deficiency Stiff neck in cervical spondylosis Site of malignancy.
INVESTIGATIONS
X-RAY SPINE: May show collapse or erosion of vertebrae,herniated interverteberal disc,mets.,# or dislocation of vertebra etc. MRI: Investigation of choice CT SCAN BLOOD CP: Megaloblastic anemia in subacute combined degeneration of spinal cord.
INVESTIGATIONS
CSF examination:
Inflammatory lesions, both cells and proteins are increased. In malignancy,malignant cells may be present. In transverse myelitis ,proteins are increased and upto 50 lymphocytes/cmm are present. In MS,monoclonal IgG is increased. In GBS,protein cell dissociation is seen.
INVESTIGATIONS
MYELOGRAPHY: Site of cord compression is demonstrated. NERVE CONDUCTION STUDIES: Helpful in diagnosis of neuropathies. FUNDOSCOPY: For papilloedema due to intracranial tumor or MS. BONE SCAN: Mets and inflammatory vertebral lesions r detected.
TREATMENT
GENERAL MEASURES SKIN CARE: Change posture every 2-4 hrly to avoid bed sores. Keep skin dry and clean. BLADDER CARE: CATHETERIZATION for urinary retention. BOWEL CARE: Avoid constipation by suitable diet and laxatives.
TREATMENT
PREVENTION OF CONTRACTURES By regular passive movements. REHABILITATION By using wheel chair,standing frames,vocational training etc.
SPECIFIC TREATMENT
POTTS DISEASE
Immobilization ATT Surgery:Anterior transthoracic decompression.
TRANSVERSE MYELITIS
Glucocorticiods are given.Initially I/V methylprednisolone,then oral prednisolone.
TREATMENT
MND Symptomatic T/M like physiotherapy,walking aids,splints and speech therapy. Glutamate antagonist,RILUZOLE ? SUBACUTE COMBINED SPINALCORD DEGENERATION Injection vit.B12 1000 ug I/M daily for 7-10 days,then weekly for a month and then monthly for whole life.
TREATMENT
GBS
Plasma pharesis(effective only in first 2 weeks) i/v immunoglobulins(2g/kg in 5 days) No role of steriods. SPINAL CORD TUMORS Radiotherapy Surgical decompression.
COMPLICATIONS
BEDSORES BOWEL AND BLADDER INCONTINENCE DVT PULMONARY EMBOLISM PSYCHIATRIC LAYOUT HYPOSTATIC PNEUMONIA DISEASE RELATED COMLICATIONS
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