Approach to paraplegia
Presenter:- Dr. Abel A (R1)
Moderator:- Dr. Nebiyu B (Consultant Neurologist)
Contents
• Introduction
• Localization
• Approach to a patient
• Complications
• Management
• Reference
Introduction
• Paraplegia:- impairment in motor and or sensory functions of
the lower extremities
• Paraplegia
– Spastic paraplegia
– Flaccid paraplegia
• It affects not only the motor system, sensation, and autonomic
functioning of a patient but also have serious psychosocial
squeal
Localization of paraplegia
• Can be caused by a lesion at
– Cerebral cortex, brain stem, Spinal cord, peripheral nerves, muscles
• Lesions causing paraplegia can be localized by using
– Sensory, motor, reflex and autonomic dysfunctions
• Sensory level can be determined by assessment of pinprick or
cold from the legs bilaterally.
UMN Vs LMN lesion
• presence of cerebral
symptoms & signs
– Headache
– Confusion
– Seizures
– Personality changes
Cortical lesions
Brain stem lesions
• Fibers of the lower limb located in the medial part of the
brainstem
• Presence of associated cranial nerve deficit used for
localization
– Palatal or vocal cord paralysis, dysarthria, horizontal or vertical
nystagmus
– Episodic dizziness or vertigo
– Tongue weakness with atrophy
Spinal cord lesions
• Spinal cord lesions can be localized by determining
– Sensory
– Motor
– Reflex
– Pain
– Autonomic function level
• C3 Neck
• T4 Nipples
• T10 Umbilicus
• L1 Inguinal
• S5 Perianal
• L4 Knees
• L5 anterior
ankles & foot
Segment-Pointer Muscles
Muscle Spinal root Function
Diaphragm C3. C4 Respiration
Deltoid C5 Arm abduction
Biceps C5 Forearm flexion
Brachioradialis C6 Forearm flexion
Triceps C7 Forearm extension
Quadriceps femoris L3, L4 Knee extension
Tibialis anterior L4 Foot dorsiflexion
Gastrocnemius S1 Plantaflexion
• Achilles reflex = S1, S2
• Patellar reflex = L3, L4
• Biceps and brachioradialis
reflexes = C5, C6
• Triceps reflex = C6, C7
• Cremasteric reflex = L1, L2
• Anal wink reflex = S3, S4
• bulbocavernosus = S2-S4
Foramen magnum and upper cervical
lesion
• Brainstem signs may occur
– Dysarthria, dysphonia, dysphagia
• Long-tract signs:- spastic quadriparesis
– Due injury of the corticospinal tract
• Weakness with around the clock pattern
– Ipsilateral arm ipsilateral leg contralateral leg contralateral
arm
• Lesion at C2:- pain at the posterior scalp
• C3-C4:- pain projected to the neck or shoulder
• C3–C5:- diaphragmatic paralysis
Lower cervical and upper thoracic
lesion
• C4–C6 lesion
– Radicular pain and sensory symptoms over radial side of the arm,
forearm, and hand
– Weakness in elbow flexion
– Depressed or absent biceps and brachioradialis reflexes
• C7–T1 lesion
– Pain and sensory impairments over the ulnar side of the upper
extremity
– Weakness of elbow extension & intrinsic hand muscles
– Depressed or absent triceps reflex
• Horner syndrome
Thoracic Lesions
• Useful clinical landmarks are
– The nipple line for T4 dermatome and
– The umbilicus for T10 dermatome
• Sensory testing may determine the most caudal dermatome of
normal sensation
• Beevor’s sign:-
– Lesions at T9-T10 resulting in upward movement of the umbilicus
Lumbar lesion
• L2-L4 lesion:-
– Weakness of flexion and adduction of the thigh
– Weakness of leg extension at the knee
– Loss of patellar reflex
• L5-S1 lesion:-
– Weakness of extension at the thigh
– Weakness of flexion at the knee
– Weakness of movements of the foot and ankle
– Loss of ankle jerk
Conus medullaris and Cauda equina
• Conus medullaris lesion:-
– Bilateral saddle anesthesia
– Prominent bladder bowel dysfunction
– Impotence
– Absent bulbocavernosus and anal reflexes
• Cauda equina lesion:-
– Low back and radicular pain
– Asymmetric leg weakness and sensory loss
– Variable areflexia in the lower extremities
– Relative sparing of bowel and bladder function
Myopathies
• Symmetric proximal weakness
• Malaise
• Fatigue
• No sensory complaints or paresthesia
• Preserved bowel bladder function
• Atrophy and areflexia are late finding
• Associated sign and symptoms
Patient approach- History
• Body weakness
• Onset
– Acute
– Sub-acute
– Chronic
• Bilateral/Unilateral
• Symmetrical/Asymmetrical
• Proximal /Distal muscle
weakness
• Progressive/ Static weakness
• Sensory symptoms
– Numbness, tingling
– Symmetrical/ asymmetrical
– Sacral sparing /sacral involved
• Any bladder/bowel
involvement
– Urinary Retention / incontinence
– Constipation/ Bowel
incontinence
– Early/Late involvement
History…
• History of back pain
– total duration
– site of maximum intensity
– history of spinal surgery
– any history of trauma to the back
• Types of pain
– Radicular pain:
• usually unilateral, sharp, aggravated by movements, cough, sneezing, straining
– Central (Funicular) pain
• deep and ill defined radiates to whole or part of leg and not affected by
movement
– Vertebral pain:
• Localized, may or may not be aggravated by movement
• May be worsened with palpation or percussion
History…
• History of recent
vaccination
– Anti Rabies, Polio, Tetanus,
COVID 19
• History of infections
– Recent Fever
– Cough, Rx for TB
– Skin lesion/rash
– HIV status
– Previous syphilis
– Preceding GI symptoms
• Dietary history
– Dietary habits – Vegetarian /
non veg
– Alcohol intake in excess or
not
– History of ingestion of
grasspeas(Guaya)
• Decrease vision, headache,
loss of consciousness ,or
Seizure
• History of Malignancy
– Swellings or bone tenderness
– Surgery for tumors
– Chemotherapy or radiation
– Weight loss
• Family history (of similar illness)
• Bleeding tendency/anticoagulant use
• History of DM
• History of other symptoms
Patient approach- Physical examination
• V/S :
– look for signs of Dysautonomia,
fever
• HEENT: Pale conjunctiva,
dryness of mouth and eyes
• LGS: for any LAP, Thyroid
mass or Breast mass
• Chest: any clue for chest
infection
• Abdomen:
– Intraabdominal mass,
Organomegally
• GUS: Distended bladder,
CVAT, Suprapubic tenderness
• IGS: look for any skin rash,
pallor
• MSS: check for vertebral
tenderness, gibbus deformity,
scoliosis
Physical examination…
Neurologic examination
• Mental status
• Cranial nerve examinations
– Concomitant optic nerve involvement
– Look for Argyll Robertson(AR) pupils
– Facial numbness and sensory loss from damage to the descending
tract of the trigeminal nerve
– Palatal or vocal cord paralysis, dysarthria, horizontal or vertical
nystagmus, episodic dizziness or vertigo, and tongue weakness
with atrophy
Physical examination….
• Motor Examinations
– Muscle bulk, fasciculation, Tone, Power, DTR, plantar response
• Superficial reflexes
• Sensory examination
– Sensory level
– Assess all sensory modalities
• Sweat level
• Coordination and Gait
• Meningeal signs
Patient approach- Investigation
Laboratory
• CBC, ESR, Peripheral
Morphology, FBS
• HIV test, VDRL, Stool exam,
U/A
• Serum Vit B12, MMA,
Homocystien, Cu
• Autoantibodies
• Serum ACE, serum Ca
• Tumor markers
• Blood culture
• EMG, NCS, Evoked potentials
• CSF analysis
– Cell count, protein, Ig, OCB
– Viral PCR
– Cytology, Culture
– Gene xpert, VDRL
Investigation…
Imaging
• X-ray of the spine
• CXRS
• CT Myelography
• MRI
– Spine
– Brain
• Spinal angiography
Complications
• Autonomic dysreflexia
• Pain
• Spasticity
• Bladder and bowel dysfunction
• Sexual dysfunction
• Venous thromboembolism
• Respiratory failure
• Pressure ulcer
• Psychological problems
Management
• Treatment of the underlying cause
• Treatment of complications
Autonomic dysreflexia
• Lesion above T6 may impair autonomic control
• Caused by excessive and uncontrolled sympathetic output
from the spinal cord
• Result in episodes of severe hypertension or hypotension and
bradycardia
• SBP elevations of 20 to 30 mm Hg signify a dysreflexic
episode
• Associated symptoms include
– Headache, blurring of vision, flushed & sweaty skin above the level
of lesion, pale & cool skin below it
• Triggered by noxious stimulation below the level of injury
– Bladder distension, constipation,
– Rectal fissures, joint injury, and urinary tract infection
• Treatment is algorism based with measurement of BP and
pulse rate at each step
– 1st place the patient in a sitting position
– 2nd inspected for areas of constriction like clothing
– 3rd indwelling catheter
• Fast-acting short-duration antihypertensive agents
– Nifedipine, nitrates, and captopril
• Once BP is within an acceptable range
– Begin fecal disimpaction, follow for 2hrs
Pain
• Pain syndromes may develop as a result of compression,
inflammation, or injury to
– Vertebral column, ligaments, the dura mater, nerve roots,
– Dorsal horn, and ascending spinal cord sensory tracts
• Pain syndromes include
– Local pain, Radicular pain or Neuropathic pain
• Central neuropathic Pain include
– Paresthesia, dysesthesia, allodynia, and hyperalgesia
– They can occur at level, below level or above level
Pain treatment
• Pharmacologic agents
– 1st line
• Gabapentin, pregabalin, lamotrigine and topiramate
– 2nd line
• TCAs, valproate and carbamazepine
– 3rd line
• Opioids, intrathecal baclofen and morphine, SSRIs, clonidine
• Surgical options
– Decompressing nervous tissue, untethering the spinal cord
• Electrophysiological techniques
Spasticity
• Is one of common cause disability which will be obvious over
time.
• It may create enough intensity to expel a patient from
wheelchair.
• Occasionally, spasticity provides support for the body weight
during ambulation
Treatment of spasticity
• Physical therapy and rehabilitation
– Passive muscle stretching
– Orthoses
• Pharmacological methods:- Oral
– GABA ergic agents
– α2-adrenergic agents
– Peripheral-acting drugs
– Others
• Pharmacological methods:- Intrathecal
– Phenol, ethanol, botulinum toxin
• Surgical methods
– Selective rhizotomy
– Tenotomy
– Electrical stimulation
Bladder Dysfunction
• It can be caused by lesion at the cerebral cortex, brain stem or
any level of the spinal cord
• Lesion above T12 cause detrusor–sphincter dyssynergia
• Lesion at and below T12 will cause urinary retention
• Important diagnostic history includes
– Frequency of micturition, nocturia,
– Urgency and urgency incontinence
– Bladder diary supplements the history taking
• Important investigations include
– Screening for urinary tract infections
– Bladder scan
– Urodynamic studies
• urine flow rate, residual volume, cystometry
– EMG
• Complication of bladder dysfunction
– Bladder wall trabeculations and diverticula
– Vesico-ureteric reflux, hydronephrosis, renal impairment
– Genitourinary tract infections, bladder stones
Treatment-Bladder Dysfunction
• General measures
– Fluid intake, Caffeine reduction, Bladder retraining
• Voiding dysfunction
– Intermittent self-catheterization
– Triggered reflex voiding
– Crede maneuver
– Supra pubic vibration
– Alpha-blockers relax the internal urethral sphincter
– Botulinum toxin injections
• Storage dysfunction
– Anti-muscarinic agents
– Desmopressin
– Botulinum Toxin
– Peripheral nerve stimulation
– Sacral neuromodulation
– Percutaneous tibial nerve stimulation
– Surgery
– Permanent Indwelling Catheters
Stepwise approach
Bowel dysfunction
• Less common than bladder dysfunction
• It can be fecal incontinence or constipation
• Fecal incontinence can be treated with anticholinergics
• Constipation can be treated with
– Optimization of fiber and fluid intake
– Bulk laxatives or stool softeners
Sexual dysfunction
• Sexual dysfunction in neurologic patient can be
– Primary sexual dysfunction
– Secondary sexual dysfunction
– Tertiary sexual dysfunction
• Treatments
– Open discussion with partner
– PDE5 inhibitors for erectile dysfunction
– MAOI:- Yohimbine for ejaculatory dysfunction
– Sexual dysfunction in women is not well studied.
Venous thrombosis
• Anticoagulation with LMW-heparin is recommended.
• In cases of persistent paralysis, anticoagulation should be
continued for 3 months
Respiratory failure
• Risk is higher in upper cervical complete lesions
• Patients with lesion above C3 and between C3-C5
– May not survive with out mechanical ventilation
• Mechanical ventilation
– Tidal volume:- 10-15ml/kg of PBW
– PEEP 5cm H2O
• Weaning
– ????
Prevention and treatment of pressure
ulcer
• Prevention is a lifelong requirement
• Prevention strategies include:
– Frequent changes in position in a chair or bed
– Avoiding excess moisture in susceptible regions
– Daily skin inspection
– Using special mattresses, and cushioning
– A well-balanced diet
• Early treatment of ulcers with
– Careful cleansing, surgical debridement of necrotic tissue
Addressing Psychosocial problems
• In patients with paraplegia following conditions are prevalent
– Clinically significant anxiety
– Depression
• Treatment:-
– Family support
– Peer support groups
– Psychologic counseling
– Proper pain management
– Pharmacologic intervention
References
THANK YOU

abel paraplegia.pptx

  • 1.
    Approach to paraplegia Presenter:-Dr. Abel A (R1) Moderator:- Dr. Nebiyu B (Consultant Neurologist)
  • 2.
    Contents • Introduction • Localization •Approach to a patient • Complications • Management • Reference
  • 3.
    Introduction • Paraplegia:- impairmentin motor and or sensory functions of the lower extremities • Paraplegia – Spastic paraplegia – Flaccid paraplegia • It affects not only the motor system, sensation, and autonomic functioning of a patient but also have serious psychosocial squeal
  • 4.
    Localization of paraplegia •Can be caused by a lesion at – Cerebral cortex, brain stem, Spinal cord, peripheral nerves, muscles • Lesions causing paraplegia can be localized by using – Sensory, motor, reflex and autonomic dysfunctions • Sensory level can be determined by assessment of pinprick or cold from the legs bilaterally.
  • 5.
    UMN Vs LMNlesion
  • 6.
    • presence ofcerebral symptoms & signs – Headache – Confusion – Seizures – Personality changes Cortical lesions
  • 7.
    Brain stem lesions •Fibers of the lower limb located in the medial part of the brainstem • Presence of associated cranial nerve deficit used for localization – Palatal or vocal cord paralysis, dysarthria, horizontal or vertical nystagmus – Episodic dizziness or vertigo – Tongue weakness with atrophy
  • 8.
    Spinal cord lesions •Spinal cord lesions can be localized by determining – Sensory – Motor – Reflex – Pain – Autonomic function level
  • 9.
    • C3 Neck •T4 Nipples • T10 Umbilicus • L1 Inguinal • S5 Perianal • L4 Knees • L5 anterior ankles & foot
  • 11.
    Segment-Pointer Muscles Muscle Spinalroot Function Diaphragm C3. C4 Respiration Deltoid C5 Arm abduction Biceps C5 Forearm flexion Brachioradialis C6 Forearm flexion Triceps C7 Forearm extension Quadriceps femoris L3, L4 Knee extension Tibialis anterior L4 Foot dorsiflexion Gastrocnemius S1 Plantaflexion
  • 12.
    • Achilles reflex= S1, S2 • Patellar reflex = L3, L4 • Biceps and brachioradialis reflexes = C5, C6 • Triceps reflex = C6, C7 • Cremasteric reflex = L1, L2 • Anal wink reflex = S3, S4 • bulbocavernosus = S2-S4
  • 13.
    Foramen magnum andupper cervical lesion • Brainstem signs may occur – Dysarthria, dysphonia, dysphagia • Long-tract signs:- spastic quadriparesis – Due injury of the corticospinal tract • Weakness with around the clock pattern – Ipsilateral arm ipsilateral leg contralateral leg contralateral arm • Lesion at C2:- pain at the posterior scalp
  • 14.
    • C3-C4:- painprojected to the neck or shoulder • C3–C5:- diaphragmatic paralysis
  • 15.
    Lower cervical andupper thoracic lesion • C4–C6 lesion – Radicular pain and sensory symptoms over radial side of the arm, forearm, and hand – Weakness in elbow flexion – Depressed or absent biceps and brachioradialis reflexes • C7–T1 lesion – Pain and sensory impairments over the ulnar side of the upper extremity – Weakness of elbow extension & intrinsic hand muscles – Depressed or absent triceps reflex • Horner syndrome
  • 16.
    Thoracic Lesions • Usefulclinical landmarks are – The nipple line for T4 dermatome and – The umbilicus for T10 dermatome • Sensory testing may determine the most caudal dermatome of normal sensation • Beevor’s sign:- – Lesions at T9-T10 resulting in upward movement of the umbilicus
  • 17.
    Lumbar lesion • L2-L4lesion:- – Weakness of flexion and adduction of the thigh – Weakness of leg extension at the knee – Loss of patellar reflex • L5-S1 lesion:- – Weakness of extension at the thigh – Weakness of flexion at the knee – Weakness of movements of the foot and ankle – Loss of ankle jerk
  • 18.
    Conus medullaris andCauda equina • Conus medullaris lesion:- – Bilateral saddle anesthesia – Prominent bladder bowel dysfunction – Impotence – Absent bulbocavernosus and anal reflexes • Cauda equina lesion:- – Low back and radicular pain – Asymmetric leg weakness and sensory loss – Variable areflexia in the lower extremities – Relative sparing of bowel and bladder function
  • 19.
    Myopathies • Symmetric proximalweakness • Malaise • Fatigue • No sensory complaints or paresthesia • Preserved bowel bladder function • Atrophy and areflexia are late finding • Associated sign and symptoms
  • 20.
    Patient approach- History •Body weakness • Onset – Acute – Sub-acute – Chronic • Bilateral/Unilateral • Symmetrical/Asymmetrical • Proximal /Distal muscle weakness • Progressive/ Static weakness • Sensory symptoms – Numbness, tingling – Symmetrical/ asymmetrical – Sacral sparing /sacral involved • Any bladder/bowel involvement – Urinary Retention / incontinence – Constipation/ Bowel incontinence – Early/Late involvement
  • 21.
    History… • History ofback pain – total duration – site of maximum intensity – history of spinal surgery – any history of trauma to the back • Types of pain – Radicular pain: • usually unilateral, sharp, aggravated by movements, cough, sneezing, straining – Central (Funicular) pain • deep and ill defined radiates to whole or part of leg and not affected by movement – Vertebral pain: • Localized, may or may not be aggravated by movement • May be worsened with palpation or percussion
  • 22.
    History… • History ofrecent vaccination – Anti Rabies, Polio, Tetanus, COVID 19 • History of infections – Recent Fever – Cough, Rx for TB – Skin lesion/rash – HIV status – Previous syphilis – Preceding GI symptoms • Dietary history – Dietary habits – Vegetarian / non veg – Alcohol intake in excess or not – History of ingestion of grasspeas(Guaya) • Decrease vision, headache, loss of consciousness ,or Seizure
  • 23.
    • History ofMalignancy – Swellings or bone tenderness – Surgery for tumors – Chemotherapy or radiation – Weight loss • Family history (of similar illness) • Bleeding tendency/anticoagulant use • History of DM • History of other symptoms
  • 24.
    Patient approach- Physicalexamination • V/S : – look for signs of Dysautonomia, fever • HEENT: Pale conjunctiva, dryness of mouth and eyes • LGS: for any LAP, Thyroid mass or Breast mass • Chest: any clue for chest infection • Abdomen: – Intraabdominal mass, Organomegally • GUS: Distended bladder, CVAT, Suprapubic tenderness • IGS: look for any skin rash, pallor • MSS: check for vertebral tenderness, gibbus deformity, scoliosis
  • 25.
    Physical examination… Neurologic examination •Mental status • Cranial nerve examinations – Concomitant optic nerve involvement – Look for Argyll Robertson(AR) pupils – Facial numbness and sensory loss from damage to the descending tract of the trigeminal nerve – Palatal or vocal cord paralysis, dysarthria, horizontal or vertical nystagmus, episodic dizziness or vertigo, and tongue weakness with atrophy
  • 26.
    Physical examination…. • MotorExaminations – Muscle bulk, fasciculation, Tone, Power, DTR, plantar response • Superficial reflexes • Sensory examination – Sensory level – Assess all sensory modalities • Sweat level • Coordination and Gait • Meningeal signs
  • 27.
    Patient approach- Investigation Laboratory •CBC, ESR, Peripheral Morphology, FBS • HIV test, VDRL, Stool exam, U/A • Serum Vit B12, MMA, Homocystien, Cu • Autoantibodies • Serum ACE, serum Ca • Tumor markers • Blood culture • EMG, NCS, Evoked potentials • CSF analysis – Cell count, protein, Ig, OCB – Viral PCR – Cytology, Culture – Gene xpert, VDRL
  • 28.
    Investigation… Imaging • X-ray ofthe spine • CXRS • CT Myelography • MRI – Spine – Brain • Spinal angiography
  • 31.
    Complications • Autonomic dysreflexia •Pain • Spasticity • Bladder and bowel dysfunction • Sexual dysfunction • Venous thromboembolism • Respiratory failure • Pressure ulcer • Psychological problems
  • 32.
    Management • Treatment ofthe underlying cause • Treatment of complications
  • 33.
    Autonomic dysreflexia • Lesionabove T6 may impair autonomic control • Caused by excessive and uncontrolled sympathetic output from the spinal cord • Result in episodes of severe hypertension or hypotension and bradycardia • SBP elevations of 20 to 30 mm Hg signify a dysreflexic episode
  • 34.
    • Associated symptomsinclude – Headache, blurring of vision, flushed & sweaty skin above the level of lesion, pale & cool skin below it • Triggered by noxious stimulation below the level of injury – Bladder distension, constipation, – Rectal fissures, joint injury, and urinary tract infection
  • 35.
    • Treatment isalgorism based with measurement of BP and pulse rate at each step – 1st place the patient in a sitting position – 2nd inspected for areas of constriction like clothing – 3rd indwelling catheter • Fast-acting short-duration antihypertensive agents – Nifedipine, nitrates, and captopril • Once BP is within an acceptable range – Begin fecal disimpaction, follow for 2hrs
  • 36.
    Pain • Pain syndromesmay develop as a result of compression, inflammation, or injury to – Vertebral column, ligaments, the dura mater, nerve roots, – Dorsal horn, and ascending spinal cord sensory tracts • Pain syndromes include – Local pain, Radicular pain or Neuropathic pain • Central neuropathic Pain include – Paresthesia, dysesthesia, allodynia, and hyperalgesia – They can occur at level, below level or above level
  • 37.
    Pain treatment • Pharmacologicagents – 1st line • Gabapentin, pregabalin, lamotrigine and topiramate – 2nd line • TCAs, valproate and carbamazepine – 3rd line • Opioids, intrathecal baclofen and morphine, SSRIs, clonidine • Surgical options – Decompressing nervous tissue, untethering the spinal cord • Electrophysiological techniques
  • 38.
    Spasticity • Is oneof common cause disability which will be obvious over time. • It may create enough intensity to expel a patient from wheelchair. • Occasionally, spasticity provides support for the body weight during ambulation
  • 39.
    Treatment of spasticity •Physical therapy and rehabilitation – Passive muscle stretching – Orthoses • Pharmacological methods:- Oral – GABA ergic agents – α2-adrenergic agents – Peripheral-acting drugs – Others • Pharmacological methods:- Intrathecal – Phenol, ethanol, botulinum toxin
  • 40.
    • Surgical methods –Selective rhizotomy – Tenotomy – Electrical stimulation
  • 41.
    Bladder Dysfunction • Itcan be caused by lesion at the cerebral cortex, brain stem or any level of the spinal cord • Lesion above T12 cause detrusor–sphincter dyssynergia • Lesion at and below T12 will cause urinary retention • Important diagnostic history includes – Frequency of micturition, nocturia, – Urgency and urgency incontinence – Bladder diary supplements the history taking
  • 42.
    • Important investigationsinclude – Screening for urinary tract infections – Bladder scan – Urodynamic studies • urine flow rate, residual volume, cystometry – EMG • Complication of bladder dysfunction – Bladder wall trabeculations and diverticula – Vesico-ureteric reflux, hydronephrosis, renal impairment – Genitourinary tract infections, bladder stones
  • 43.
    Treatment-Bladder Dysfunction • Generalmeasures – Fluid intake, Caffeine reduction, Bladder retraining • Voiding dysfunction – Intermittent self-catheterization – Triggered reflex voiding – Crede maneuver – Supra pubic vibration – Alpha-blockers relax the internal urethral sphincter – Botulinum toxin injections
  • 44.
    • Storage dysfunction –Anti-muscarinic agents – Desmopressin – Botulinum Toxin – Peripheral nerve stimulation – Sacral neuromodulation – Percutaneous tibial nerve stimulation – Surgery – Permanent Indwelling Catheters
  • 45.
  • 46.
    Bowel dysfunction • Lesscommon than bladder dysfunction • It can be fecal incontinence or constipation • Fecal incontinence can be treated with anticholinergics • Constipation can be treated with – Optimization of fiber and fluid intake – Bulk laxatives or stool softeners
  • 47.
    Sexual dysfunction • Sexualdysfunction in neurologic patient can be – Primary sexual dysfunction – Secondary sexual dysfunction – Tertiary sexual dysfunction • Treatments – Open discussion with partner – PDE5 inhibitors for erectile dysfunction – MAOI:- Yohimbine for ejaculatory dysfunction – Sexual dysfunction in women is not well studied.
  • 48.
    Venous thrombosis • Anticoagulationwith LMW-heparin is recommended. • In cases of persistent paralysis, anticoagulation should be continued for 3 months
  • 49.
    Respiratory failure • Riskis higher in upper cervical complete lesions • Patients with lesion above C3 and between C3-C5 – May not survive with out mechanical ventilation • Mechanical ventilation – Tidal volume:- 10-15ml/kg of PBW – PEEP 5cm H2O • Weaning – ????
  • 50.
    Prevention and treatmentof pressure ulcer • Prevention is a lifelong requirement • Prevention strategies include: – Frequent changes in position in a chair or bed – Avoiding excess moisture in susceptible regions – Daily skin inspection – Using special mattresses, and cushioning – A well-balanced diet • Early treatment of ulcers with – Careful cleansing, surgical debridement of necrotic tissue
  • 51.
    Addressing Psychosocial problems •In patients with paraplegia following conditions are prevalent – Clinically significant anxiety – Depression • Treatment:- – Family support – Peer support groups – Psychologic counseling – Proper pain management – Pharmacologic intervention
  • 52.
  • 53.