RB: A Case of Tetraparesis

RB: A Case of Tetraparesis
Block Y. Tagomata. Talan. Tayag. Tolibas. Toledo. Uy. Wi. Yu. Zaldivar. Zamora.

General Data RB 25/M From Camarines Norte Roman Catholic
Married, with 1 child R handed

Chief Complaint Inability to walk

History of Present Illness
10 mos PTA, (+) intermittent pain on R medial arm, described as “parang binabanat ang ugat”, NPS 10/10, occurring 3x/wk, aggravated by exertion (e.g. reaching out or lifting an object) relieved by an unrecalled analgesic 0/10 (-) numbness, (-) tingling, (-) skin lesions, (-) hx of trauma 2 wks after, development of similar symptoms on L arm and both scapular areas, no consult was done

9 mos PTA, (+) weakness of R LE, (-) pain, (-) numbness, (-) tingling, (+) sensation of abdominal tightness, (+) dyspnea (-) hx of trauma consult was done at BHC, given vitamins and analgesic

A few days later, (+) weakness of R LE, admitted to LH; CXR, holoab UTZ, cranial CT scan and labs done were allegedly normal discharged and prescribed with unrecalled meds but stopped due to allergy (rashes on both thighs)

8 mos PTA, inability to walk/stand; assisted on ADLs (+) urinary/bowel incontinence (+) bedsore (approximately 1 cm, sacral) (-) fever

5 mos PTA, consult was done at V. Luna A> t/c Decompression sickness P> recompression x 10 session However, pt opted to discontinue after the third session due to fear of dyspnea inside the vessel

(+) consult at PGH OPD Ortho A> Pott’s disease P> workup and follow-up x 2 mos

3 mos PTA, admitted at Spine Unit, started on anti-TB meds co-managed by Rehab 1 mo PTA, s/p anterior decompression, debridement, fusion(C6-T2) with fibular strut graft (7/18/12) Day of admission, admitted at Rehab Ward for further therapy

Review of Systems (present)
(-) Cough, colds, fever (-) headache, blurring of vision, dizziness (-) chest pain, difficulty of breathing (-) changes in appetite (-) heat or cold intolerance, irritability (-) muscle or joint pain (-) penile pain, discomfort, erectile dysfunction

Past Medical History (-) HPN, DM, BA, CA, previous hosp (-) PTB/Primary Complex (?) drug allergy

Family Medical History
(+) HPN, father (+) BA, 5 siblings (+) DM, uncle (-) PTB

Personal and Social History
(-) smoking, alcohol intake, illicit drug use Breadwinner of the family Works as fisherman(diver) Married, with 1 daughter Finished 2nd yr HS

Functional History Previously independent on ADL Previously works as a fisherman (diving, swimming)

Environmental History
Lives in a 1-storey concrete house Safe from falls

Current Physical Exam General: awake, NICRD BP 110/60 HR 90 RR 18 T afebrile HEENT: AS, pink PC, (-) CLAD/NVE (+) surgical scar on L neck to anterior chest Chest/Lungs: DHS, (-) murmur/thrills/heaves ECE, clear BS (-) rales/wheeze/rhonchi Abdomen: Flat, normoactive BS, (-) masses/tenderness Skin/Extremities: FEP, pink NB, (-) edema/cyanosis/jaundice (+) sacral ulcer, healed

Current Physical Exam Motor: (R) (L) (R) (L) C5 5/5 5/5 L2 5/5 5/5 C6 5/5 5/5 L3 5/5 5/5 C7 5/5 5/5 L4 4/5 5/5 C8 5/5 5/5 L5 4/5 5/5 T1 5/5 5/5 S1 3/5 5/5 (Score 97) Sensory: ASIA Sensory: pin prick light touch C5-L3 2/2 2/2 2/2 2/2 L3 1/2 1/2 1/2 1/2 L4 1/2 2/2 1/2 2/2 L5-S4 S5 2/2 2/2 2/2 2/2

P.E. on Admission & Course

Physical Examination on Admission
General Survey: Awake, coherent, not in cardiorespiratory distress Vital signs: BP 100/70 HR 87 RR T afebrile HEENT: Anicteric sclerae, pink palpebral conjunctivae, no cervical lymph nodes, no tonsillopharyngeal congestion

Chest/Respiratory: Equal chest expansion, clear breath sounds, no thoracic spine deformity Cardiovascular: Adynamic precordium, normal rate regular rhythm, distinct S1 & S2, no murmurs Gastrointestinal: Flat abdomen, normoactive bowel sounds, no tenderness Genitourinary: (+) weak sphincteric tone, (+) BCR

Extremities: Full and equal pulses, no edema, (+) multiple pressure ulcers - sacral area, grade 2 with undermining (+) well healing pressure ulcer on right posterior auricular area, right shoulder (+) grade 1 ulcer on heel, bilateral; medial knee, bilateral; lateral malleolus, bilateral

Right Left C5 5/5 C6 C7 4/5 C8 3/5 T1 L2 2/5 L3 L4 L5 S1 ASIA Motor

ASIA Sensory Pin Prick Light Touch Right Left C5-C7 2/2 C8 1/2 T1-L2 L3-S3 S4-S5 Right Left C5-C7 2/2 C8 1/2 T1-L2 L3-S3 S4-S5

Tone: (+) grade 1 – 1+ spasticity on both lower extremities DTRs: hyporeflexia on both lower extremities, (+) flexor spasm on both lower extremities (+) clonus (-) Babinski (-) Hoffman’s DTRs: hyporeflexia on both lower extremities, (+) flexor spasm on both lower extremities when patient tries to stroke both lower extremities.

Laboratory Tests ESR and CRP: elevated Sputum AFB x 3: all negative
All else normal

Imaging

Differential Diagnoses for Tetraparesis
Trauma Tumors Infection Inflammatory Vascular Vertebral Disease Others

Radiographic differentiation

Trauma Most common cause of tetraparesis
Ruled out because the patient has no history of trauma

Tumors Usual presentation is pain, often worse when in supine position, which can be axial (skeletal structures affected) or radicular (nerve roots affected) Usually presents with constitutional symptoms (night sweats, fever, unexplained weight loss, and anorexia) Radiographic examination is vital Can be metastatic (from lungs, breast, prostate and kidney) or primary (multiple myeloma, osteogenic sarcoma, vertebral hemangioma, chondrosarcoma, chordoma, ependymoma, astrocytoma, meningioma, schwannoma, neurofibroma)

Infection Bacterial osteomyelitis Spinal abscess HIV infection
a differential if the patient uses IV drugs, immunosuppressed, or undergoing dialysis usual etiology is Staphylococcus aureus Check via culture and inflammatory markers Spinal abscess Usually epidural; commonly presents with fever HIV infection Can present as primary HIV myelitis, vacuolar myelopathy, or as a result of opportunistic infection

Inflammatory Transverse myelitis Multiple sclerosis
Myelopathic process of unknown cause from inflammation of spinal cord May start as pain or paresthesia in localized body parts and can progress to paresis and plegia Multiple sclerosis Immune-mediated demyelinating disorder which may also initially present as pain and progress to weakness of limbs Systemic lupus erythematosus Autoimmune illness which usually presents with other systemic symptoms such as pleuritis, hematologic, immunologic or neurologic alterations, and dermatologic signs

Vascular Ischemia of spinal cord not very common; usually associated with anterior cord syndrome; often from: Anterior spinal artery occlusion Angioma AV malformation

Vertebral Disease Vertebral disk prolapse Spondylosis Paget’s disease
Usually due to a tear in the outer fibrous ring (annulus fibrosus) May initially present as pain of extremities and progress to paresis depending on the level of herniation Spondylosis Degenerative odteoarthritis of the spine Presents as pain, paresthesia or muscle weakness Paget’s disease Due to excessive breakdown and formation of bone, followed by disorganized bone remodeling Causes bone pain but very rarely presents as tetraparesis

Others Hereditary spastic paraparesis
characterized by insidiously progressive bilateral lower-extremity weakness and spasticity, with family history of similarly affected individuals may be transmitted in an autosomal dominant, autosomal recessive, or X-linked recessive manner Degenerative motor neuron disease Usually presents in the 6th-7th decades of life heterogeneous group of neurologic diseases characterized by progressive degeneration of upper and lower motor neurons Usually presents with weakness, atrophy, fasciculations, and hypo/hyperreflexia

Others Decompression syndrome
caused by intravascular or extravascular bubbles that are formed as a result of reduction in environmental pressure can occur in divers, compressed air workers, aviators, and astronauts manifestations range from itching and minor pain to neurological symptoms, cardiac collapse, and death Presents acutely

Impression Tetraplegia secondary to multiple compression deformity secondary to Pott’s disease (Asia D) NL: C6, AL: C6-T2, ML: C7, SL: C7 Neurogenic bowel and bladder Nephrolithiasis, right Sacral decubitus ulcer, grade 2

Course in the Wards Upon Ward admission:
- noted (+) flexor spasm 1-3x/hr upon movement able to tolerate sitting > 1 hr. during OT fair sitting balance unsupported but cannot be totally challenged still dependent in transition with sitting and transfer from bed able to eat his dinner, can sit with brace on, independent with setup

Course in the Wards Underwent PT exercises during the 1st month:
Practiced transitions from supine to sitting sit to stand Table tilt at 30o increasing by 15o Standing with || bars with PKS on (B) knees, increasing in duration and number of reps || bars with one PKS || bars without PKS Ambulating using walker with PKSusing BAC with 4 pt gait3 pt gait(B) Axillary crutches

Course in the Wards 8/27 – ASIA MMT: (R) (L) (R) (L)
C5 5/ / L / /5 C6 5/ / L / /5 C7 4/ / L / /5 C8 3/ / L / /5 T1 3/ / S / /5 - ASIA Sensory: pin prick light touch C2-C / / / /2 C / / / /2 T1-L / / / /2 L3-S4 S5 1/ / / /2 DTR: hyporeflexia on (B) LE (+) flexor spasm (B) LE pathologic reflexes: (+) clonus (-) Babinski (-) Hoffman

Course in the Wards 9/18 – (R) (L) (R) (L) C5 5/5 5/5 L2 4/5 4/5
T1 4/ / S / /5 (Score 8375) - ASIA Sensory: maintained at Score of 97

Course in the Wards Underwent PT exercises during the 2nd month:
Started stepping exercises Ambulating using BAC with 3 pt gait2 pt gaitBAC/3 pt. gait on level surface up/down stairs using BAC using quad cane Quad cane/3 pt. gait with ramp, stairs(B) axillary crutches Using Walker

Course in the Wards 9/26 – Fall while ambulating in bathroom (+) pain (R) lateral aspect of foot maintain MMT Score of 87 - ASIA Sensory: pin prick light touch (R) (L) (R) (L) C2-C / / / /2 C / / / /2 C9-L / / / /2 L4-S4 S5 1/ / / /2 A> Quadparesis and SCC secondary to Pott’s disease ASIA D, NLC7 MLC7 SL C8 AL: C6-T1, T4 T5 T8 Sacral decubitus ulcer Gr 2 Cystitis

Course in the Wards 10/2 – increase in flexor spasm/ankle clonus ~ (R) LE (R) (L) (R) (L) C5 5/ / L / /5 C6 5/ / L / /5 C7 5/ / L / /5 C8 5/ / L / /5 T1 4/ / S / /5 (Score 9187) - ASIA Sensory: pin prick light touch C2-C / / / /2 C / / / /2 C9-L / / / /2 L4-L / / / /2 S1-S4 S5 2/ / / /2 (Score 10797)

Course in the Wards 10/8 – ambulate on level surface with ramp using quad cane. Not Stairs increase in flexor spasm/ankle clonus ~ (R) LE (R) (L) (R) (L) C5 5/ / L / /5 C6 5/ / L / /5 C7 5/ / L / /5 C8 5/ / L / /5 T1 5/ / S / /5 (Score 9791) - ASIA Sensory: pin prick light touch C5-L / / / /2 L / / / /2 L / / / /2 L5-S4 S5 2/ / / /2

Course in the Wards 10/21 – ambulate using walker
able to do vocational training (+) flexor and bladder spasm on CMG 10/24 – ambulate using walker still with weakness of (R) plantar flexion 10/27 – still with poor proprioception of (B) feet

Problem List Medical s/p ADDT SCC sec to Pott’s Disease C7-T1
Neurogenic Bladder Altered Body Function Tetraparesis Sensory impairment below C8 Grade I spasticity of bilateral LE Poor proprioception

Pott’s Disease Secondary to an extraspinal source of infection.
Osteomyelitis + arthritis. Anterior aspect of the vertebral body adjacent to the subchondral plate: usual site Spreads to adjacent intervertebral disks. Adults: spreads from the vertebral body. Children: primary site (disk highly vascuarized) Pott disease is usually secondary to an extraspinal source of infection. The basic lesion is a combination of osteomyelitis and arthritis. The area usually affected is the anterior aspect of the vertebral body adjacent to the subchondral plate. Tuberculosis may spread from that area to adjacent intervertebral disks. In adults, disk disease is secondary to the spread of infection from the vertebral body. In children, because the disk is vascularized, it can be a primary site.

Pott’s Disease Vertebral collapse and kyphosis, narrowed spinal canal, cord compression Kyphotic deformity: anterior spine collapse (thoracic > lumbar) Cervical: minimal collapse Healing: gradual fibrosis and granulomatous tuberculous tissue calcification Paravertebral abscess formation is common (Lumbar-psoas fascial sheath; Thoracic-anterior chest wall, parasternal area) Progressive bone destruction leads to vertebral collapse and kyphosis. The spinal canal can be narrowed by abscesses, granulation tissue, or direct dural invasion. This leads to spinal cord compression and neurologic deficits. Kyphotic deformity occurs as a consequence of collapse in the anterior spine. Lesions in the thoracic spine have a greater tendency for kyphosis than those in the lumbar spine. The collapse is minimal in cervical spine because most of the body weight is borne through the articular processes. Healing takes place by gradual fibrosis and calcification of the granulmatous tuberculous tissue. Eventually the fibrous tissue is ossified, with resulting bony ankylosis of the collapsed vertebrae. Paravertebral abscess formation occurs in almost every case. With collapse of the vertebral body, tuberculous granulation tissue, caseous matter, and necrotic bone and bone marrow are extruded through the bony cortex and accumulate beneath the anterior longitudinal ligament. These cold abscesses gravitate along the fascial planes and present externally at some distance from the site of the original lesion.

Lesion The lesion could be: Florid - invasive and destructive lesion
Non destructive Encysted disease Carries sicca Hypertrophied Periosteal lesion 2 Patterns Classic: spondylodiscitis (SPD) Atypical: spondylitis without disk involvement (SPwD); more common pattern of spinal TB The lesion could be: Florid - invasive and destructive lesion Non destructive - lesion suspected clinically but identifiable by modern investigations like CT scan or M.R.I. Encysted disease Carries sicca Hypertrophied Periosteal lesion Recently, two distinct patterns of spinal TB can be identified, the classic form, called spondylodiscitis (SPD) Atypical form characterized by spondylitis without disk involvement (SPwD) SPwD seems to be the most common pattern of spinal TB

Regional Distribution
1 Cervical 12% 2 Cervicodorsal 5% 3 Dorsal 42% 4 Dorsolumbar 5 Lumbar 26% 6 Lumbosacral 3%

Anatomical Paradiscal - destruction of adjacent end plates and diminution of disc space. Appendeceal (Posterior) - involvement of pedicles, laminae, spinous process. Central - Cystic or lytic, concertina collapse. Anterior –longitudinal lig, Aneurysmal phenomenon Synovitis in posterior facet

History Presentation depends on:
Stage of disease Site Presence of complications such as neurologic deficits, abscesses, or sinus tracts On diagnosis, already with the disease for 3-4 mos. Back pain- earliest and most common symptom, can be spinal or radicular Constitutional symptoms (fever and weight loss)

History 50% with neurologic abnormalities (spinal cord compression with paraplegia, paresis, impaired sensation, nerve root pain, or cauda equina syndrome) If cervical, can present with pain and stiffness, dysphagia or stridor, torticollis, hoarseness, and neurologic deficits. HIV positive > HIV negative patients

Pott’s on Imaging XRAY Signs of infection with lytic lucencies in anterior portion of vertebrae Disk space narrowing Erosions of the endplate Sclerosis resulting from chronic infection Compression fracture Continuous vertebral body collapse Kyphosis; gibbous (severe kyphosis) CT scan Soft tissue findings: abscess with calcification is diagnostic of spinal TB Pattern and severity: framentary, osteolytic, localized and sclerotic, and subperiosteal Atypical features Soft tissue swelling from paraspinal abscesses, +/‐ calcification Involvement of only one vertebral body Involvement of several vertebral bodies without intervertebral discitis Bowing of rib cage secondary to collapse of multiple vertebral bodies Destruction of lateral or posterior aspects of vertebral bodies CT scan Soft tissue findingsAbscess with calcification is diagnostic of spinal TB; CT is excellent modality to visualize soft tissue calcifications Pattern and severity of bony destruction Pattern of vertebral body destruction‐ framentary, osteolytic, localized and sclerotic, and subperiosteal Used to guide needle in percutaneous needle biopsy of paraspinal abscess

Complications of tuberculosis
Paraplegia Cold abscess Sinuses Secondary infection Amyloid disease Fatality

Surgical indications No sign of neurologic recovery after trial of 3-4 weeks therapy Neurologic complication during treatment Neurologic deficit becoming worse Recurrence of neurologic complication Prevertebral cervical abscesses, neurological signs, & difficulty in deglutition & respiration Advanced cases: sphincter involvement, flaccid paralysis, severe flexor spasms

Other indications Recurrent paraplegia
Painful paraplegia– d/t root compression, etc Posterior spinal disease--involving the post elements of vertebrae Spinal tumor syndrome resulting in cord compression Rapid onset paraplegia due to thrombosis, trauma, etc. Severe paraplegia econdary to cervical disease and cauda equina paralysis

1 Decompression +/- fusion Failed response,Too advanced 2 Debridement+/- fusion Failed response after 3-6 months, doubtful diagnosis, instability 3 Debridement +/-DECOMP+/- fusion Recrudescence of disease 4 Prevent severe kyphosis 5 Anterior transpostion Severe kyphosis + neural deficit 6 Laminectomy STS, secondary stenosis, posterior disease

Tuli’s recommended approach
Cervical spine –T1  Anterior approch Dorsal spine –DL junction  Antrolateral approch Lumbar spine &Lumboscral junction Extraperitoneal Transverse Vertebrotomy

Problem List

Medical Problems Spinal cord compression Neurogenic bowel
Neurogenic bladder Pressure ulcers

(Possible) Medical Problems
Cardiovascular complications Hypertension Deep vein thrombosis and Pulmonary embolism Orthostatic hypotension Cardiac arrhythmia Pulmonary complications Musculoskeletal complications Osteoporosis Fractures Heterotrophic Ossification

Altered Body Structure and Function
Bilateral LE paresis Bilateral LE loss of sensation Neurogenic bladder Neurogenic bowel Pressure sores Sexual dysfunction and possible loss of sexual desire Possible MSK, cardiovascular and pulmonary complications

Limitations in Activities of Daily Living
Independence in feeding Dependence in self-care ADLs Bathing Grooming Dressing up Dependence in ambulation and transfers Poor sexual activity

Limitations in Instrumental Activities
Independence Communication (cellphones, etc.) Entertainment (watching TV, etc.) Difficulty in child-rearing Cannot anymore drive his motorcycle

Limitations in Participation
Inability to return to previous job Difficulty in finding another job Difficulty in community ambulation

Long-term Goals To treat the underlying cause of the SCI Spinal TB
To implement acceptable bowel and bladder management programs To address pressure ulcers and maintain skin integrity

Long-term Goals To maintain socially acceptable bladder and fecal continence To prevent possible complications of neurogenic bladder and bowel To prevent and treat accordingly the complications that may arise from the thoracic-level SCI To minimize the functional limitations and allow the patient to complete ADLs independently or with assistive equipment

Management of Spinal Cord Injury and Its Various Complications

Indications for Surgery
1. Instability 2. Deformity 3. Neurologic symptoms

Neurogenic Bladder When pathologic CNS/PNS conditions cause disruption of the nerve control to the urinary bladder, causing urinary retention and/or urinary incontinence

Bladder Innervation Pelvic Nerves Hypogastric Nerves Pudendal Nerves
Parasympathetic signals from S2-S3 segments to the detrusor muscles for bladder emptying/voiding Hypogastric Nerves Sympathetic signals from T11-L2 segments for bladder filling/storage Pudendal Nerves Somatic nerve fibers from S3-4 segments to voluntary skeletal muscles & external sphincter

Management Goals To prevent urinary tract infections and other long-term urologic sequelae To maintain a socially acceptable bladder continence by developing and implementing a bladder management program that will allow patient to reintegrate back into the community

Medical/Pharmacologic Management
Targeting the autonomic receptors For urinary retention Cholinergics (for detrusor contraction) Alpha receptor antagonists (for sphincter relaxation) For urinary incontinence Anticholinergics ( for detrusor relaxation) Alpha receptor agonists (for sphincter contraction)

Behavioral/Non-Pharmacologic Management
Catheterization programs Independent intermittent catheterization every 4 to 6 hours, if the patient has preserved hand function and does not have UTI Limitation of fluid intake Timed voiding Schedule voiding Use of a voiding diary

Bladder training programs Maneuvers Valsalva maneuver, suprapubic application of pressure Use of appliances Condom, foley, straight catheters

Surgical Management Augmentation cystoplasty Artificial sphincter
When the mentioned medical and behavioral strategies fail… Augmentation cystoplasty Artificial sphincter Sphincterotomy Pudendal neurectomy Bladder outlet surgery Balloon dilatation Interruption of innervation Neurostimulation

Neurogenic Bowel When pathologic CNS/PNS conditions cause disruption of the bowel innervation, causing stool incontinence (lax anal sphincter) and constipation (disrupted parasympathetic supply)

Management Goals To achieve socially acceptable fecal incontinence
Prevention of gastrointestinal complications Fecal impaction (most common)

Medical/Pharmacologic Management
Stool softeners (e.g. docusate sodium) Colonic stimulants (e.g. senna) Colonic irritants (e.g. glycerin, bisacodyl) Prokinetic agents (e.g. metoclopramide) Rectal suppositories Oral medications

Timed/regular bowel movement Taking advantage of the gastrocolic reflex (about minutes after meal) Dietary modification High fiber diet Increased fluid intake Digital stimulation Manual extraction

Surgical Management Colostomy/ileostomy
Decreases time required for bowel management Increases independence

Pressure Sores Stages of pressure sores/ulcers (NPUAP)
Stage I : Nonblanchable erythema not resolved within 30 minutes (epidermis intact) Stage II : Partial thickness skin loss; blisters with erythema, abrasion, shallow ulcer (possibly into dermis) Stage III: Full-thickness destruction of the skin; deep crater (into subcutaneous tissue) Stage IV: Full-thickness skin loss with deep-tissue destruction (up to fascia, muscle, bone, joint)

Pressure Sores Management: Wound cleansing with plain NSS Debridement
Wound dressing Topical antibiotics (e.g. Flammazine) Wound Care Modalities Whirlpool therapy, UV light, ultrasound Surgery skin grafts and skin flaps

Pressure Sores Prevention: Egg mattress
Proper turning frequency (at least every 2 hours) Adequate cushioning (e.g. surgical gloves with water)

Others Osteoporosis Fractures Heterotopic ossification
Pulmonary complications Hypertension and coronary artery disease Deep vein thrombosis Orthostatic hypotension Cardiac arrhythmia Sexual dysfunction Depression

Osteoporosis Occurs below the level of injury
Cause: reduction of bone mineral content Immobilization Lack of weight-loading activities Effect: Increased risk of lower extremity fracture Management: Ambulatory activities Medications (e.g. Vitamin D, calcitonin, biphosphonates) Functional electric stimulation

Fractures Occurs in chronic SCI Common causes: Osteoporosis Falls
Vigorous physical therapy Common in long bones of lower extremity Management: Patient and family education Training in proper transfer and ambulation techniques Fall prevention Avoidance of vigorous physical therapy

Heterotopic Ossification (HO)
Development of ectopic bone within soft tissues surrounding the joints Often seen in the first 6 months post-injury Incidence: 20-30% Common areas : Hip > Knee > Shoulder > Elbow Etiology is still unclear but may be due to metabolic, biochemical and circulatory factors Presentation: Heat and swelling over the joints Decrease in ROM Fever

Heterotopic Ossification (HO)
Complications: Peripheral nerve entrapment pressure sores Ankylosis increased risk of DVT Management: ROM Exercises Medications to limit ossification (e.g. disodium etidronate, indomethacin) Surgery for mature bone

Pulmonary Complications
Depend on the level of the lesion C4: highest level with spontaneous ventilation Above C8: loss of abdominal and intercostal muscles T1-T12: impairment of intercostal muscles, reduced cough, possible paradoxical retraction of chest wall during inspiration T8-T10: impairment of abdominal muscles Below T12: no impairment of respiratory function

Pulmonary Complications
Management: Position changes/postural drainage Deep breathing exercises Use of incentive spirometry Cough assist Glossopharyngeal breathing exercises. Pneumobelt Phrenic nerve pacing Non-invasive ventilatory support

CV complications: Hypertension and Coronary Artery disease
Inactivity causes: Increased cholesterol levels Increased risk of coronary artery disease Management: Exercise/ increased activity

CV complications: Deep Vein Thrombosis
3 important factors (Virchow’s triad) Venous stasis Hypercoagulability Vessel wall damage Highest risk period: 1st 2 weeks Serious complication: Pulmonary embolism Risk of death decreases over time 210 times greater in the acute phase 19.1 times 2-5 years post-injury 8.9 times beyond 5 years post-injury

CV complications: Deep Vein Thrombosis
Management Pharmacologic (e.g. heparin, coumadin) Prophylactic measures compression stockings, external pneumatic compression, continuous rotation beds Avoid ROM and strengthening exercises on the affected limb Bed rest until medications are given

CV Complications: Orthostatic Hypotension
Common in higher levels of SCI Causes: Ineffective vasoconstriction Pooling of blood in the lower extremities Treatment: Progressive elevation Use of compression stocking and abdominal binders Liberal salt and fluid intake Elevated leg rests Medications (e.g. NaCl tablets, ephedrine)

CV complications: Cardiac Arrhythmias
Common during the acute period (14 days post injury) Usually in cervical and complete injuries Cause: autonomic imbalance  sympathetic and  parasympathetic activity Prevention: Use of atropine Induced hyperventilation Usually resolved within 6 weeks after injury

Sexual Dysfunction Sexual desire is not necessarily affected but depression, poor body image and fears of inadequacy may alter sexual desire. Sexual function, however, may be affected. Erection (parasympathetic) Ejaculation (sympathetic) Lubrication (in women) Complete SCI (no sacral reflexes): more impairment

Sexual Dysfunction Addressing concerns on body image, maintenance of intimate relationships, etcetera Management options for erectile dysfunction: Oral medications (e.g. sildenafil) Vaccum devices Penile injection programs (papaverine) Surgically implanted prosthesis

Depression Management:
Consultation with appropriate mental health care professional Continued follow-up. Prevent and address suicidal tendencies Anti-depressants may be given

Functional Rehabilitation
Focuses on helping the patient to function at optimal levels Supervised PT and OT to improve strength in all active muscle groups and ROM in all joints Adaptive equipment Long-handled shoehorns Reachers Ambulation equipment Low-back wheelchairs are feasible because patients with lower-level SCIs have better truncal stability.

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RB: A Case of Tetraparesis

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