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  1. Decrease in BP with positional changes due to blood pools in LE as result of decreased muscle tone in the abdomen on LEs
    Sign & symptoms: lightheaded, dizzy, pallor, unresponsive, sudden weakness
    Prevention: compression socks, abdominal binders, slow change in position
    Tx: recline patient immediately. Build up their tolerance to sitting up with elevating the bed a little at a time and let them adjust to that.
    Orthostatic (postural) hypotension
  2. An ANS function it can be disrupted making it difficult to regulate body temperature for those with injury above T6
    1st year- assumes temp of external environment. So if the room is 68 degrees their body will try to match that. (Poikilothermia)
    Later body adjusts a bit but cold weather can cause discomfort due to insufficient vessel constriction below level of injury to preserve body heat (hypothermia); in summer below level of injury does not sweat which hinders prevention of hyperthermia
    TX: teach how to dress warmer so the body temp doesn’t go to low. And dress cooler for warmer climates so they don’t over heat.
    Thermal regulation
  3. Occurs because of the UMN lesion; muscles below level of injury become spastic after spinal shock subsides
    Signs and symptoms: Spasms: all cervical, 75%thoracic, 58% lumbar
    Factors causing spasm: infection, positioning, pressure sores, emotions
    Advantages: build muscle mass, increased circulation which helps to prevent pressure sores, improved ADLs/ transfers
    Disadvantages (Precautions): Increase in spasticity can cause: contractures, pain, decreased function. Watch for fever, bladder infections, skin breakdown.
    TX: Medical = nerve blocks, medications, surgical release   OT =  Tell OTR if spasms have increased in frequency &/or duration. ROM, splinting in functional positions, positioning in chair or bed in patterns outside of spasticity pattern.
  4. a common cause of death in the SCI population
    Huge Concern. Major reason for hospital readmission. Usually can’t be felt due to the loss of sensation from SCI.Due to the Pressure in one area it causes Ischemia (no oxygen/ no blood flow) which causes Necrosis. Most common areas are the bony prominences.TX = PREVENTIONDiet: well-nourished; high in protein helps to restore function to the skinPositioning (cushions, mattresses)-use a time scheduleWeight shifting/ pressure reliefSelf -InspectionKeep skin clean & dry- dress in different clothesUse care during transfers to prevent shearing or skin tearsSigns & Symptoms: Levels of pressure sore:Level 1: red spot, blanches when pressed Level 2: red, almost a blister, doesn’t extend below all layers of skin, does not blanch- a sign of necrosis beginningLevel 3: Extends below all layers of skin just above muscleLevel 4: below muscleSkin breakdown can occur in about 30 mins.Treatment = “FLAPS” – reconstruct site by transferring skin from healthy “donor” site to wound site. Requires intact blood supply.
    Skin breakdown/ Decubitus ulcer/ pressure sores
  5. a medical condition in which the bones become brittle and fragile from loss of tissue, typically as a result of hormonal changes, or deficiency of calcium or vitamin D. Bones are not subjected to stress/torque due to not standing and disuse Vulnerable to pathological fractures… especially femur due to being brittle and fragile and not weight bearing
    Patients with spasticity may have lower risk because in essence the muscles have “tone” and this tone helps keep the bones strong
    TX = standing/weight bearing exercise using a standing frame, strengthening what muscles they have, ROM, maintain body weight, medication
    Heterotopic ossification: Abnormal formation of bony deposits on muscles, joints, tendons; 20% of SCI pts. Hips/knees are most common; shoulders/ elbows less frequently. Occurs below the level of injury.Signs & Symptoms: heat/warmth over joint, pain, edema, and decreases ROM due to pain
    TX:  PROM to prevent ankylosis (fusion of a joint), good positioning,anti-inflammatory meds; cortisone administered locally, surgery may be indicated but typically 1+ years after onset
  6. UTI due to residual urine in bladder
    Signs& symptoms: cloudy/excessive particles in urine, dark/foul smell, fever, chills, increase spasticity
    UMN= spastic bladder; involuntary emptying; need voiding schedule/ catheterization to prevent over distended bladder can cause Autonomic Reflexia (The ANS will increase BP which cause HR to increase. then the HR drops.)
    LMN= flaccid bladder; no reflexive emptying since reflex arc is destroyed; must have catheterization or apply external pressure to abdomen to empty
    RENAL FAILURE is a common cause of death in the SCI
    TX: catheter, voiding schedule, teach the coordination, fine motor control and cognition for self-catheterization.
    Bowel & bladder dysfunction
  7. Cauda equina (lumbar) =Males=Usually no reflex erections, Rare psychogenic erection, Ejaculation usually occurs
    Females=Vaginal secretions often absent, Generally fertile
    Female – menstrual cycle resumes within 1 year of injury.
    Male – fertility rates decrease
    MaleReflex erections predominate
    Psychogenic erections generally absent
    Ejaculation occasional
    FemaleVaginal secretions present as part of genital reflex
    Fertility preserved
    Sensation of labor pain absent
    TX: discussion about how to handle the dysfunction, meds, injections for men, vacuum pump, implant
    Sexual Dysfunction
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