Week 9: Falls, Rheum, and MSK Flashcards
What red flags are important to assess in a patient with back pain?
Neurologic
Infection
Fracture
Tumor
Inflammation
(NIFTI)
When assessing for neurologic red flags in back pain, what are you looking for? What do you do if a red flag is identified?
-diffuse motor/ sensory loss
-progressive neurological deficits (progressive motor weakness or significant motor deficits not localized to single unilateral nerve root)
-cauda equina syndrome (saddles anesthesia, bladder or bowel incontinence)
-emergency MRI indicated with specialist consultation
When assessing for infectious red flags in back pain, what are you looking for? What do you do if a red flag is identified?
-fever
-IVDU
-immunosuppressed
-XR, MRI indicated
When assessing for red flags for fracture in back pain, what are you looking for? What do you do if a red flag is identified?
-hx trauma
-osteoporosis risk/ fragility fracture
-XR (and possibly CT) indicated
What red flags may suggest tumour in back pain? What do you do if a red flag is identified?
-hx of cancer
-unexplained weight loss
-significant unexpected night pain
-severe fatigue
-XR and MRI indicated
What red flags in your assessment of back pain suggest inflammation? What would you do if these were identified?
-chronic low back pain >3 months
-age of onset <45
-morning stiffness >30 minutes
-pain improves with exercise
-disproportionate night pain
-rheumatology consultation recommended (core back tool) (I would also suggest imaging/ labs to start inflammatory arthritis work up)
What are yellow flags in back pain?
psychosocial risk factors for developing chronic pain. They include
-belief that back pain is harmful or potentially severely disabling
-fear and avoidance of activity or movement
-tendency to low mood and withdrawal from social interaction
-expectation of passive treatment rather than a belief that active participation will help
What to do if yellow flags for back pain are identified?
education and reassurance to reduce risk of chronicity. Consider PHQ-4.
Sally, age 65, has constant, back dominant pain that is much worse when she bends over to tie her shoes. What pattern/ etiology of low back pain does this suggest?
Disc pain
Carlo, age 63, has been experiencing low back pain and pretty severe pain down his left upper leg that comes and goes. His pain is worse when he walks his dog or stands. His pain resolves with sitting or when he flexes forward. What pattern/ etiology of low back pain does this suggest?
Spinal stenosis
(neurogenic claudication)
Lily, age 70, has been experiencing intermittent low back pain that seems to be worse with reaching over head, or certain yoga poses, like bending backwards. What kind of patter/ etiology of back pain does this suggest?
Facet joint pain
Elvis, age 80, has been experiencing bad right leg pain that seems to start in his lower back. He states that it is always there and he just cant seem to get rid of it. Everything hurts. What pattern/ etiology of back pain do his symptoms suggest?
Compressed nerve pain
Sam has been experiencing low back pain associated with some numbness to their inner thighs. What pattern/ etiology of back pain do their symptoms suggest?
Red flag- ?cauda equina
Ask about urinary retention, overflow incontinence, fecal incontinence
May require ED- urgent MRI
82 year old Ellen has been experiencing constant mid/ low back pain for the last week that is just not going away. She denies any falls or acute injuries to her back. Phx- history of polymyalgia rheumatica, which her symptoms have been improving after being on prednisone for 6 months. Life long smoker. Ht 5’2 (last visit- 5’3). What pattern/ etiology of back pain do her symptoms suggest?
red flag- r/o fracture given osteoporosis risk (chronic glucocorticoid use, smoking hx, height loss)- send for XR
You are performing a physical exam on a patient with back pain. You do a straight leg raise test. Describe how this test is done and why you did it.
-patient supine, examining raises symptomatic leg at hip with knee extended and foot dorsiflexed.
-this increases dural tension in lower lumbar/ upper sacral spine
-if pain worsens or occurs during test, it suggess a radiculopathy (i.e., herniated disc with nerve root compression)
What are the minimum components of a back exam, per the core back tool?
-movement testing in flexion
-movement testing in extension
-patellar reflex (L3-L4)
-great toe extension power (L5)
-great toe flexion power (S1)
-plantar response (upper motor test)
-passive striaght leg raise
-saddle sensation testing (s2-3-4)
What parts of the spine does OA commonly affect?
c spine, l spine
facet joints in spine
Bonus question that might be helpful for reading XR in future-
What XR findings suggest OA?
-joint space narrowing
-subchondral sclerosis
-osteophytes
-subchondral cysts
What is spondylosis?
Arthritis of spine (disc space narrowing, arthritic changes of facet joint)
What is spondylolisthesis?
displacement of vertebral body relative to the one below (usually anterior displacement)
What is spinal stenosis?
Local, segmental, or generalized narrowing of the vertebral canal by bone or soft issue elements
Usually caused by bony hypertrophic changes in facet joints and thickening of ligamentum flavum
What is a radiculopathy?
impairment of nerve root, usually causing radiating pain, numbness, tinging, muscle weakness corresponding to specific nerve root
What actually is cauda equina syndrome?
Loss of bowel and bladder control and numbness in the groin and saddle area of the perineum, associated with weakness of the lower extremities.
Can be caused by abnormal pressure on the bottom-most portion of the spinal canal and spinal nerve roots, related to either bony stenosis or a large herniated disc.
What is kyphosis?
outward curve (convexity) of thoracic spine- can caused rounded/ hunched shoulders
What is lordosis?
inward curve (concavity) of lumbar spine- makes buttocks appear more prominent
What is polymyalgia rheumatica? (PMR)
A type of non-articular rheumatism (chronic inflammatory disease affecting soft tissues/ periarticular structures) characterized by pain and stiffness of the proximal extremities (girdle area)
Describe the epidemiology of PMR
-Typically presents after age 70 (almost exclusively a disease of adults 50+)
-F>M (2:1)
-Risk factors: advancing age, being of northern European descent, GCA, family hx (rare but recognized)
What disease frequently occurs with PMR?
Often co-exists with giant cell arteritis (15% of those with PMR develop GCA)
Describe the patho of PMR
-?environmental infectious trigger?
-primarily affects periarticular structures (bursa and tendons) and proximal articular structures
-inflammation of periarticular structures> pain and functional limitation
-NOT erosive, does not cause structural damage.
Describe the time course of PMR
Onset is typically recent, discrete change in MSK symptoms that prompts pt to seek medical attention; can also be abrupt/ seemingly occurring overnight.
A story of longstanding stiffness and aching does NOT suggest PMR.
Can relapse during treatment (i.e., during steroid taper) or after complete discontinuation of treatment (i.e., months to years later)
Describe clinical presentation of PMR
-Pain, aching, and stiffness of symmetric/ bilateral proximal extremities (shoulder and hip girdle area, neck, thighs)
-NO muscle weakness
-morning stiffness >45 minutes, worst in am
-gel phenomenon (stiffness after prolonged inactivity)
-Constitutional signs and symptoms prominent (fever, weight loss, malaise, depression)
-Absence of other joint involvement
-PE reveals tender muscles, but no true weakness or atrophy
-Can have mild distal symptoms (wrists, MCPS, knees, NOT feet or ankles. CTS in 10-15% of patients)
-Difficulties in ADLs- pulling on shirt, hooking bra in back, getting up
How is PMR diagnosed?
Diagnosis based on symptoms and laboratory evidence of increased inflammation (elevated ESR or CRP)
- Required criteria: age 50+, bilateral shoulder aching, abnormal ESR/CRP
- Confirmed by rapid resolution of symptoms with low dose glucocorticoids; the lack of response to initial therapy strongly suggests alternative dx
What labs should be done in suspected PMR?
- CBC- may see anemia of chronic disease, elevate platelets
- Elevated ESR, CRP
- Prior to initiation of treatment, get a baseline glucose, Cr, LFT, calcium
- Could consider getting TSH, CK (will b normal), vit D, RF (negative in PMR), anti-CCP
What imaging should be done in suspected PMR?
- US or MRI (assess for underlying bursitis or local pathology like rotator cuff disease))
- XR not indicated unless another dx is being considered
- Bilateral subdeltoid/ subacromial bursitis is an imaging hallmark of PMR
- Subdeltoid and/ or biceps tenosynovitis and/ or glenohumeral synovitis (either posterior or axillary
- Hip with synovitis and/ or trochanteric bursitis on US
You are assessing a patient for suspected PMR. You do a general inspection, VS, MSK/ neuro assessment of the affected areas/ extremities. What else must you assess for?
Symptoms of GCA! Commonly co-occurs with PMR, and a red flag diagnosis (can result in permanent vision loss)
Symptoms of GCA: new onset headache, abrupt onset visual impairment, jaw claudication, unexplained fever, anemia, or other constitutional symptoms
What differentials should you consider when diagnosing a patient with PMR? How would you differentiate them from PMR?
- Rheumatoid arthritis (most challenging to differentiate is seronegative RA)- symmetric polyarthritis of small joints of hands and feet. Presence of joint erosions differentiates RA from PMR.
- Multifocal local MSK disease
- Bone disease
-Multiple myeloma can present with bone pain and elevate ESR, simulating PMR- ID by presence of monoclonal protein in serum in urine.
-Hyperparathyroidism- will usually have elevated calcium, elevated parathyroid hormone
-Osteomalacia - Drug induced myalgias or myositis (i.e., secondary to statins- will not have prominent morning stiffness)
- Inflammatory myopathy- associated with muscle weakness, elevated muscle enzymes, abnormal electromyography, abnormal MRI, evidence of myositis on punch biopsy
- Fibromyalgia (long standing duration as opposed to acute/ subacute onset in PMR)
- Infection
- PD
- Malignancy
- Late onset spondyloarthropathy; differentiated from PMR by presence of enthesitis, dactylitis, anterior uveitis, sacroiliitis, high prevalence of HLA B27
What is the goal of therapy in PMR?
Symptom relief, restoration of function
What is the first line pharmacological therapy in PMR? How long do you treat for?
Steroids! Start with prednisone 12.5-25mg oral once daily, reconsider diagnosis if no response in several days.
Follow up with patient in 1-2 weeks to see if ssx are improving or steroid needs to be increased.
Maintain glucocorticoid dose that controls symptoms for 2-4 weeks after aching, stiffness have resolved.
In person reassessment in 4-8 weeks to confirm resolution of symptoms and start tapering (or start work up for alternative dx)
Tapering is SLOW and may need to continue for over a year.
What are some AE of prolonged systemic glucocorticoid therapy?
-Osteoporosis: screen for fracture risk, possible need for biphosphonate rx
-GI disorders: gastritis, PUD, upper GI bleeding
-Impaired glucose regulation/ hyperglycemia (increase screening for T2DM)
- weight gain, cushingoid features
-skin thinning, ecchymosis
-CV: fluid retention, HTN, atherosclerotic CVD, arrythmias, VTE
-Neuro: Cognitive dysfunction , insomnia (take in am), anxiety, depression, psychosis
-cataracts, glaucoma
-increased risk infection
Do any referrals need to be made for pmr?
PMR is co-managed with a rheumatologist
Review the clinical features of PMR
Proximal joint and neck symptoms are worst with inactivity, resulting in nocturnal pain and prominent morning stiffness. Morning stiffness, which can be severe and protracted, is invariable. Symptomatology involving the shoulders and upper arms is especially common and can produce a characteristic clinical finding, that of restricted active range of motion at the shoulders, especially abduction.
Physical examination can demonstrate decreased passive range of motion of the shoulders, neck, and hips. Muscle strength is normal when carefully tested.
Describe the patho of osteoarthritis.
It involves degeneration of joint cartilage and can progress to an inflammatory process with altered joint function and is associated with characteristic pathologic changes in the joint tissue and destruction of the articular cartilage.
Which joints are commonly affected in OA?
Large weight-bearing joints (hips/knees/spine) and the hands. Commonly asymmetrical.
What are classic S&S of OA?
-Insidious onset
-More common in middle age or older adults
-Early morning joint pain and stiffness with inactivity and motor restriction.
-Shorter duration of joint stiffness (<30 minutes) compared to RA
-During exarcebations, involved joint may be swolleen and tender to palpation (no warmth)/
-Absence of systemic symptoms
-Crepitus and reduced ROM may be noted during PE
-Heberden nodes-bony nodules on the DIP joints
-Bouchard nodes-bony nodules on the PIP joints.
Name non-pharm interventions for OA?
-Physio and excercise at least 3x week, lose weight, stop smoking.
-Do isometric excercises to strenghten quadriceps muscles in knee OA.
-weight-bearing exercise (walking, lifting weights), resistance band exercises.
-Avoid aggravating activities. Use cold or warm packs and ultrasound tx.
-Use walking aids, patellar taping by physio.
Tai-chi, acupuncture.
What are pharm treatments available in OA?
-In pt with one or a few joints affected, start with topical NSAIDs.
Diclofenac
e.g -knee OA-Dose: 50 drops per knee TID or 40 drops per knee qid
-Hand OA Diclofenac diethylamine (1.16%, 2.32% ) Dose: 2-4g applied tid-qid
-Acetaminophen
-Oral NSAID/COX-2 inhibitors in those without contraindications.
-Duloxetine for those with OA in many joints and have contraindications to NSAIDs.
-Topical capsaicin is for those with a few joints affected, but not recommended for hip or knee OA
-Intraarticular glucocorticoid injections for some candidates. Con is its short duration of effects.
-Tramadol may recommended for hip and knee OA.
-Opioids not recommended
You should exercise caution or entirely avoid prescribing oral NSAIDs for pts with the following conditions:
-Kidney dysfunction
-CV dx
-PUD
-High bleeding risk
Define Osteoporosis.
According to WHO: spinal or hip bone mineral density of 2.4 standard deviations or more below the mean (T-score of -2.5 or below). BMD is performed on the lumbar spine, hip, and or forearm.
What is an OP fracture?
Occurs from a fall while standing at normal height or less without any type of trauma and/or while performing daily activities. Vertebral # is the most common.
Can OP be diagnosed clinically?
Yes, in the event of a fragility fracture of the spine, hip, wrist, pelvis, rib, and/or humerus you can diagnose them with OP without evidence of a BMD.
Common findings: Loss of height, kyphosis (dowager’s hump), back pain from compression fracture, cervical lordosis, fracture with little or no trauma, crush fracture or vertebra, pain.
What is the peak incidence of fractures in men?
About 70 years, 10 more years than for women.
Name some causes of OP.
Primary causes:
Menopause, small body frame/low weight, smoking, low Ca+ intake, lack of weight-bearing exercise, family hx of hip/pelvic fracture, ++ETOH use, low vit D intake, Asian/caucasian, advanced age, previous fracture.
Secondary causes:
Hyperparathyroidism, cushings, multiple myeloma, thyroid replacement, corticosteroid therapy, renal dx
Shelly comes in for her annual physical. She is postmenopausal and is not on any resorptive medication. You decide to do a FRAX. Shelly asks you what that test is for. You say…
It estimates your risk of having a hip or other major fracture in the next 10 years, especially if you have osteoporosis.
<10% is low risk
10%-19.9% is moderate risk.
20% or more is high risk.
Who should get a BMD?
-are aged 50–64 yr with a previous osteoporosis-related fracture or ≥ 2 clinical risk factors OR
-are aged ≥ 65 yr with 1 clinical risk factor for fracture OR
-are aged ≥ 70 yr
What patients are recommended to initiate pharmacotherapy (if postmenopausal female and male aged ≥ 50 yr) to manage OP:
-have had previous hip, vertebra or ≥ 2 osteoporosis-related fractures OR
-have a 10-yr major osteoporotic fracture risk ≥ 20% OR
-are aged ≥ 70 yr and have a T-score ≤ −2.5 (femoral neck, total hip or lumbar spine).
What are some risk factors listed on the FRAX tool?
Previous fracture, parent fractured hip, current smoking, glucocorticoids, rheumatoid arthritis, secondary OP, ETOH >3 units/day, femoral beck BMD (optional).
Shelly is a candidate for antiresorptive medication and asks if BMD and FRAX need to be repeated.
You tell her that they need to be repeated in 3 years.
True or false?
True!
What is first line treatment for OP?
What important teaching points would provide?
What are adverse effects and contraindications?
Biphosphonates are first line. They increase BMD and inhibit bone resorption.
Treatment is for 3-6 years. Then stop therapy, reassess in 3 years.
Names:
Risedronate-weekly, monthly, or daily
Alendronate-weekly or daily
Zoledronic acid-IV yearly
Inform patient:
-Take med with a full glass of water
-Avoid food or drinks other than water at least 30 minutes -60 minutes after ingesting it.
-Needs to stand upright for 30 minutes after ingestion, as it can cause esophageal irritation.
-Do not crush/chew
-A potent esophageal irritant, ask pts to report: sore throat, dysphagia, midsternal pain), esophagitis, esophageal perforation, gastric ulcers, PUD
-Can cause MSK discomfort/GI discomfort or renal dyfx (Zoledronic acid).
-Contraindications: inability to sit upright, esophageal mobility disorders, hx of PUD, hx GI bleeding, CKD, certain types of bypass sx.
-Serious A/E: osteonecrosis of jaw/mandible/atypical femur fracture.
You determine that Shelly is not a candidate for biphosphonates for treating OP, because of hx of GI bleed. What would be your next option?
What are some side effects?
What is something Shelly would need to be aware of?
What kind of monitoring would you need to do is Shelly had kidney dx?
You can try denosunab (PROLIA), a RANK ligand inhibitor.
It acts by inhibiting osteoclast formation decreasing bone resorption, reducing bone fracture and increasing BMD.
Given SC every 6 months.
A/E: hypocalcemia, dermatitis, infections, MSK discomfort.
Serious: osteonecrosis of jaw/mandible, atypical femur fracture
Must be on it for long term. If discontinued, it can cause rebound bone turnover and fractures. She should switch to another agent if she is not tolerating prolia.
Those with CKD or risk of hypocalcemia should have serum ca level checked 10 days after administration.
In what instances would you prescribe anabolic therapy (teriparatide or romosozumab) in someone with OP?
What are contraindications and A/E?
If recent severe vertebral fracture or 2 or more vertebral fractures AND T-score 2.5 or more.
Very expensive!
Teriparatide- Subcutaneous: 20 μg daily for 24 mo
Check ca and renal fx before prescribing
Contraindicated in pt with hx kidney stones and prior hx of radiation therapy, CrCl < 30 mL/min, bone malignancy, Paget disease, previous skeletal radiation, hypercalcemia disorder, unexplained elevated ALP.
A/E: Orthostatic hypotension, nausea
Hypercalcemia, hypercalciuria
MSK discomfort
Romosozumab-Subcutaneous: 210 mg monthly for 12 mo
Inadequate vitamin D increases risk for hypocalcemia
Caution warranted in severe renal impairment.
Contraindicated Previous myocardial infarction or stroke, Hypocalcemia.
A/E: Myocardial infarction, stroke, Hypocalcemia
MSK discomfort. Rare: AFF, ONJ
A patient finished their anabolic therapy (teriparatide or romosozumab) for OP. What is next?
They are to continue with an antiresorptive medication-biphosphonates.
What are some non-pharm interventions for OP?
-For people initiating pharmacotherapy, it is good practice to individualize intake of calcium and vitamin D. Although participants in most pharmacotherapy trials received a minimum of 400 IU/d of vitamin D and up to 1000 mg/d of calcium supplements, food sources or supplementation should be individualized according to risk factors for insufficiency. https://www.cmaj.ca/content/195/39/E1333#T2
-Encourage to stop smoking or ETOH or caffeine
-Fall prevention strategies-can refer to fall clinic or PT/OT
-Balance and functional training ≥ twice weekly to reduce the risk of falls.
-Progressive resistance training ≥ twice weekly, including exercises targeting abdominal and back extensor muscles.
*Fun fact-Swimming, biking, and isometric exercises are not considered weight-bearing exercises.
Resistance training involves exercises in which major muscle groups (e.g., upper and lower extremities, chest, shoulders, back) work against resistance (e.g., squats, lunges and push-ups). Increase volume (e.g., sets, reps, weight), frequency or difficulty to achieve progressive overload. Many resistance-training exercises would be considered functional exercises.
https://www.cmaj.ca/content/195/39/E1333#T2
What is the most common form of arthritis?
OA - affects 13.9% of adults
Joint pain can be viewed as being articular (arthritic) and non-articular.
What are some non-articular differentials for joint pain?
Non-articular causes of joint pain:
Localized: bursitis, tendinitis, capsulitis, muscle sprain
Generalized: PMR, fibromyalgia, myofascial pain syndrome
Articular joint pain can be either degenerative or inflammatory. What are some differentials for degenerative joint pain?
Articular joint pain - degenerative:
Primary = OA
Secondary = Metabolic, hemophilic, neuropathic, trauma
Inflammatory arthritis can be further classified into seropositive, seronegative, crystal and infectious/septic.
List differentials for seropositive inflammatory causes of joint pain
- Rheumatoid arthritis
- Systemic Lupus Erythematosus
-Scleroderma
-Dermatomyositis/ polymyositis
-Sjogren’s syndrome
Inflammatory arthritis can be further classified into seropositive, seronegative, crystal and infectious/septic.
List differentials for seronegative inflammatory causes of joint pain
Symmetrical:
Ankylosing Spondylitis
Enteropathic Arthritis
Asymmetrical:
Reactive arthritis
Psoriatic arthritis
Inflammatory arthritis can be further classified into seropositive, seronegative, crystal and infectious/septic.
List differentials for crystal related causes
Gout
Pseudogout
Hydroxyapatite
Inflammatory arthritis can be further classified into seropositive, seronegative, crystal and infectious/septic.
List differentials for infectious/septic causes
Gonococcal
Non-gonococcal
Lyme disease
Viral
Mycobacterial
Fungal
Look at TN RH3 for the chart this all came from
Differentiate the aggravating and relieving factors of pain between inflammatory and degenerative arthritis
Inflammatory - pain at rest, relieved with activity
Degenerative - pain with motion, relieved with rest
Differentiate duration of morning stiffness between inflammatory and degenerative arthritis
Inflammatory - morning stiffness > 1 h
Degenerative - morning stiffness < 1 h
Differentiate physical exam findings between inflammatory and degenerative arthritis
Inflammatory - Cardinal signs of inflammation - warmth, swelling, erythema, tenderness, loss of function.
Extra-articular manifestations
Late findings - malalignment/deformities
Degenerative - joint instability, buckling, gelling.
Late findings - bony enlargement, malalignment/deformity
Differentiate the timing of pain between inflammatory and degenerative arthritis
Inflammatory - nighttime awakening due to pain
Degenerative - evening/end of day pain
Summarize the general presentation of an inflammatory arthritis
Pain occurs at rest and is relieved with activity
Morning stiffness >1 hour
Signs of inflammation, extra-articular manifestations
Nighttime awakening due to pain
Summarize the general presentation of a degenerative arthritis
Pain with motion, relieved by rest.
Morning stiffness < 1 hour.
Joint instability, bucking, gelling, bony enlargement.
Pain worse at end of day
What type of gait is seen in stroke?
a) ataxic gait
b) sensory gait
c) hemiplegic gait
d) frontal apraxic gait
Hemiplegic Gait or Spastic Hemiparetic Gait
*The patient stands with unilateral weakness on the affected side, arm flexed, adducted and internally rotated.
*The leg (on the same side) is slightly bent at the hip, the knee cannot be extended fully at the end of the stance phase and the foot is inverted and in a plantar flexed position.
What is the characteristic of the hemiparetic gait disorder?
*swings leg in a semicircle
During the swing phase, the paretic leg performs a lateral movement (circumduction) which is termed Wernicke-Mann gait.
-this is due to weakness of distal muscles (foot drop) and extensor hypertonia in lower limb.
With mild hemiparesis, loss of normal arm swing and slight circumduction may be the only abnormalities.
Describe the hemiplegic gait..is it fast or slow, have a wide base or narrow base gait, is it symmetrical or asymmetrical?
Gait is slow, with a wide base and asymmetrical with a shortened weight-bearing phase on the paretic side.
Do spastic gait problems worsen or improve on attempts to walk faster?
Worsen
People who have a history of cerebral pasly and have extreme tightness of their hip adductors, the base of their gait becomes more narrow and their legs cross the midline. What is the name of this gait?
Diplegic or spastic gait a.k.a scissor gait.
- The patient walks with an abnormally narrow base and scissoring, dragging both legs and scraping the toes. Toes do not clear the ground b/c hip flexors are weak.
- Characteristic extreme tightness of hip adductors which can cause legs to cross the midline referred to as a scissors gait.
- This gait is seen in bilateral periventricular lesions, such as those seen in cerebral palsy.
- In countries with adequate medical care, patients with cerebral palsy may have hip adductor release surgery to minimize scissoring.
- Circumduction at the hip helps with toe clearance.
You watch a person lift their leg high enough during walking so that the foot does not drag on the floor. What type of gait is this?
Why are people having to lift their leg high?
What conditions/diseases are associated with this type of gait?
Neuropathic Gait or Steppage Gait or Equine Gait
Foot drop
- If unilateral, causes include peroneal nerve palsy and L5 radiculopathy.
- If bilateral, causes include amyotrophic lateral sclerosis (ALS), Charcot-Marie-Tooth disease and other peripheral neuropathies including those associated with uncontrolled diabetes.
This type of Gait can be mistaken as a drunken stumble.
Cerebellar ataxic gait
What are the characteristics of a cerebellar gait?
stumbling, lurching, staggering, reeling, drunken, clumsy, or slow, with reduced step length and a wide or broad base gait that is irregular and variable.
Patients will not be able to walk from heel to toe or in a straight line
While standing still, the patient’s body may swagger back and forth and from side to side, known as titubation.
The patients attempt to compensate lateral body sway by walking cautiously, stooping slightly and steadying the stance foot by bending at the hip.
What are the possible causes related to cerebellar gait?
- Stroke, Tumor, Neoplastic
- Inflammatory (e.g. multiple sclerosis)
- Vitamin deficiencies
- Drug toxicity or Alcohol
- Hereditary and neurodegenerative ataxias
People who have cerebellar ataxia gait, do they have problems initiating their walk?
No, gait initiation is usually normal - but ataxia generally increases on turning and during complex gait tests, such as walking on uneven surfaces.
What gait is this when someone classically is high stepping and stamping their foot hard onto the ground?
Sensory Ataxic Gait
What gait is this when the stride is slightly shortened, broad base, cautious, slower, and markedly decreases in the dark?
Sensory Ataxic Gait
The patients use visual control to compensate for the loss of proprioception. Loss of visual function causes marked worsening of ataxia.
Your patient’s gait is ataxic and you decide to assess your patient’s balance via applying the Romberg’s test. The test was positive, which means your patient has what type of ataxic gait?
Sensory - the Romberg test assesses for balance issues that are related to the function of the dorsal column (proprioception) by removing the visual and vestibular components that contribute to maintaining balance. Patient stands with feet together, eyes closed.
I have read that if you do a modified Romberg test, patient stands with the feet together and eyes open - is assessing balance.
T/F: complex clinical tests including tandem walk and walking on uneven surfaces increases difficulty for sensory gait?
True - increases insecurity of sensory gait
What are the causes of sensory ataxic gait?
- In diseases affecting the peripheral nerves (uncontrolled diabetes). Sensory neuropathy
- Vitamin B12 deficiency
- Compressive myelopathy
- Paraneoplastic disorder
This type of gait is seen in people with muscular dystrophy, myasthenia gravis, sarcopenia, or deconditioned individuals.
Myopathic Gait (Waddling Gait)
What muscles are weak when you see someone have a myopathic/waddling gait?
Hip girdle muscles
-responsible for keeping the pelvis level when walking.
- If you have weakness on one side, this will lead to a drop in the pelvis on the contra-lateral side of the pelvis while walking (Trendelenburg sign).
- With bilateral weakness, you will have dropping of the pelvis on both sides during walking leading to waddling.
- Waddling gait and abnormal pelvic tilt with each step because of limb girdle weakness.
What gait is this?
-may have difficulty initiating steps.
-body position is stooped with the head and neck forward, with flexion at the knees, arm swing reduced when walking
-Narrow-based gait with small little steps, feet barely clear the floor
-turning is taken by small steps versus pivoting
Parkinsonian Gait
What are the cardinal signs of Parkinson’s Disease?
bradykinesia, rigidity, rest tremor and impaired postural stability.
Parkinsonian Gait is a.k.a Festinating Gait or Propulsive Gait, why?
- The patient may show an involuntary inclination to take accelerating steps, known as festination.
- The forward center of gravity develops a propensity to lean forward while walking. This causes bent truncal posture and an increasingly faster, step to step variability, causing the gait cycle to increase like a hurrying shuffle. When asked to walk faster, patients increase the step frequency rather than step length and this impaired postural reflex causes the patient to be more at risk for forward falls which is apparent when performing the pull or push test.
Other than PD, what other diseases can this gait be present in?
Dementia with Lewy bodies. Vascular dementia.
What gait is this?
-The patient will display irregular, jerky, involuntary movements in all extremities.
Choreiform Gait (Hyperkinetic Gait)
This gait is seen with certain basal ganglia disorders including Sydenham’s chorea, Huntington’s Disease and other forms of chorea, athetosis or dystonia.
This type of gait is considered a higher level gait disorder.
It may appear cautious or “magnetic.”
There is difficulty initiating or maintaining walking.
There may be inappropriate or counterproductive postural responses, short shuffling steps, disequilibrium, and start and turn hesitation.
Frontal (apraxic) Gait
T/F: People who have a frontal apraxic gait can still remember the act of walking.
False, generally they have forgotten how to perform the act of walking.
-Some patients attempt to initiate gait by swaying the trunk laterally or performing exaggerated arm movements.
-After having walked a few meters, gait often improves.
What conditions related to frontal apraxic gait?
- NPH
- Small vessel disease/vascular dementia affecting bifrontal white matter
- Neurodegenerative dementias
- Advanced alzheimer’s disease, frontotemporal lobar degeneration and space occupying lesions of the frontal lobe
What is propioception affected by?
- peripheral neuropathy
- Aging
- Spinal cord or neural conditions
- Vestibular functioning which naturally decreases with age
- Disorders of the inner ear
- Decreased vision r/t aging (cataracts, macular degeneration, glaucoma, optic nerve compression)
- Motor pathway impairment (corticospinal and vestibulospinal tracts)
What does TUG stand for? Describe.
The Timed Up and Go Test
On hearing the word “Go”, the individual in chair gets up, walks to line 3 meters (10 feet) away, and returns to sit in the chair. Repeat exercise 3 times and average 2nd and
3rd times. An average of >12 seconds suggests higher risk of falls
Risk factors for Falling
- Increasing age
- Overarching Factor: History of falls, especially multiple falls
- Female sex
- Functional decline: limitations in any activities of daily living (ADLs) or instrumental activities of daily living (IADLs)
- Medication (psychotropics, antipsychotics, sedative/hypnotics, antidepressants
- Vision impairments
- Difficulties with gait and balance; slow gait speeds
- Lower body weakness
- Presence of vertigo
- Medical and/or psychiatric comorbidity
- Cognitive impairment; Depression; Fear of falling; Dementia
- Parkinsonism - PD; DM; CVS; orthostatic hypotension
- Frailty;
- Pain; Arthritic diseases (RA/OA); Osteoporosis
- Urinary incontinence/rushing to the bathroom
- living alone; malnutrition; excessive alcohol
- Environment: poor lighting, clutter, loose mats, cords, lack of necessary assistive devices
(e.g. walker), poor footwear (slipping while walking)
Whats the other name for TUG test?
The Tinetti Balance and Gait Evaluation
Whats another Tool to assess gait?
Gait Speed Test (4-meter)
*BC Guidelines: https://www2.gov.bc.ca/assets/gov/health/practitioner-pro/bc-guidelines/frailty-gaitspeed.pdf
The test can be performed with any patient able to walk 4 metres using the instructions below:
1. Instruct the patient to walk at their normal pace. Patients may use an assistive device, if needed.
2. Ask the patient to walk down a hallway through a 1-metre zone for acceleration, a central 4-metre “testing” zone, and a 1-metre zone for deceleration (the patient should not start to slow down before the 4-metre mark).
3. Start the timer with the first footfall after the 0-metre line.
4. Stop the timer with the first footfall after the 4-metre line.
SCORING: Gait speed of longer than 5 seconds to walk 4 metres (<0.8 m/s) suggests an increased risk of frailty and the need for further clinical review.
Risk factors for RA?
Genetics
F:M 3:1
Australasian, Western Europe, and North American regions
Lower socioeconomic & education
Cigarette smoking
poor diet quality
Obesity
physical inactivity
Occupational exposures to airborne inhalants
Infections
Stress, PTSD
Typical age of onset for RA?
20-40yrs
Joint involvement in RA is typically ______ (symmetric/assymetic)
Symmetric
Which joints are typically involved with RA? Which are affected first?
Initially involves small joints of hands and feet (MCP, PIP, MTP)
(**not DIPs like OA)
Then spreads to Wrist, elbow, shoulder, knee, ankle, MTP, c-spine
axial skeleton is usually spared, other than the cervical spine (particularly C1 to C2)
Does the pain in RA improve or worsen with activity & rest?
Pain improves with use, worsens with rest
How long does morning stiffness last with RA?
Longer, >1 hour
Worse after effort so may be described as evening stiffness
What lab results may indicate RA (in comparison to OA)
Positive RF
Positive anti-CCP antibody
Elevated ESR and CRP
(all of these typically negative in OA)
Patho of RA
Erosive synovitis of peripheral joints
Inflammatory disease +/- extra-articular features
***Autoimmune disorder attacking synovium of joint
Complex genetic and environment interactions lead to disruption of immune tolerance, ultimately resulting in synovial inflammation
Inflammatory process causes transformation of synovium into an invasive pannus tissue that degrades cartilage and bone with absence of repair
What kind of time course does RA follow?
Chronic
Variable course of exacerbations and remissions
What can indicate a poorer prognosis with RA?
Poor prognosis if: young age at onset, RF+/ high RF titre, elevated ESR, activity of >20 joints, presence of extra articular features
Typical S&S of RA
joint with definite clinical synovitis (swelling) not explained by another disease
Key early symptoms are pain and swelling of the affected joints
Common presentation:
Morning stiffness >1h, improves with use, worsens with rest
Symmetric joint involvement
Initially involves small joints of hands and feet (MCP, PIP, MTP) - Symmetrical effusions and soft tissue swelling around the MCP and proximal interphalangeal (PIP) joints typically occur
Constitutional symptoms (profound fatigue, depression, myalgia, weight loss)
Lots of extraarticular manifestations that will be talked about later
What MSK complications occur from chronic synovitis in RA
(Specific names of deformities)
Mechanical joint damage- loss of motion, instability, deformity, crepitus, joint deformities
Swan neck deformity, boutonniere deformity, ulnar deviation and subluxation of MCP, radial deviation of wrist joint, hammer toe, mallet tow, claw toe, flexion contractures
Axial subluxation- c-spine instability (neurologic impairment, difficult/ dangerous intubation due to risk to SC)
Limited shoulder mobility and tears of rotator cuff
Tenosynovitis may cause tendon rupture
Carpal tunnel
Ruptured Baker cyst (outpouching of synovium behind knee)- presentation similar to DVT
Are extraarticular features common in RA?
Common in RA and is associated with more severe and typically seropositive disease.
What systemic symptoms can be seen with RA?
Constitutional: generalized aching, stiffness, fevers, weight loss, and fatigue
Many with RA experience chronic widespread pain and may meet criteria for fibromyalgia – more strongly associated with seronegative RA
Common mental health symptoms with RA?
Depression common
Examples of neurologic disease assoc with RA?
Range of neurologic disease
Carpal tunnel most common
Myelopathy or radiculopathy
Neuropathies d/t vasculitis
T/F those with RA are more likely to develop osteoporosis
True! +++
Generalized bone loss d/t immobility & systemic inflammation, chronic steroid use (those with RA have 60-100x greater risk of osteoporotic # than general population)
How are muscle impacted in RA
Muscle weakness d/t synovial inflammation, drug-induced muscle disease, myositis, and vasculitis
How can body composition change with RA?
inc body fat mass, sarcopenia
(I’m assuming also related to immobility & medications such as steroids…)
Most common skin problem with RA?
Name some others if you can…
Most common = rheumatoid nodules
Skin ulcers
Neutrophilic dermatoses: Sweet syndrome, pyoderma gangrenosum, rheumatoid neutrophilic dermatitis
Are the eyes typically affected with RA?
Other than Sjögren’s disease, eye involvement is uncommon
Sjögren’s = ocular and/or oral dryness are the hallmarks of this disorder
Very rare: Scleritis, episcleritis, uveitis, iritis,
Are any other organs affected in RA?
Yes! Basically all of them.
Lung disease: pulmonary fibrosis, pleural effusion, pleuritis, pulomonary nodules
Cardiac disease: peri/myocarditis, valvular disease, CAD, HF, Afib
Vascular disease: vasculitis, PAD, VTE, stroke, lymphatic obstruction
Kidney disease – most often d/t drug toxicity (NSAIDs, cyclosporine)
Splenomegaly
T/F RA is considered a clinical diagnosis
Yes…. but supported by labs & imaging
Lab tests to do if you suspect RA
RF
Anti-CCP
CBC
ESR
CRP
T/F if someone has RA, their RF will always be positive
False - RF is 80% sensitive but nonspecific, and may not be present at onset of disease. Levels do not correlate with disease activity. RF+ can be associated with more erosions, more extra articular manifestations, and worse function.
Is anti-CCP sensitive or specific for RA?
Anti-CCP: 80% sensitive, 94-98% specific; may precede onset of symptoms
**more specific for RA than RF
How might a CBC be altered in someone with RA?
CBC- increased disease activity associated with decreased Hb (anemia of chronic disease) and increased platelets
What imaging might we do for RA?
XR: Bilateral hands/ wrists, ankles/ feet
C-spine XR (may be normal at onset)
US- changes of synovitis/ erosions noted before XR picks up
MRI- hands- to detect early synovitis and erosions
**I think I remember curbsiders talking about how changes won’t typically show up on xray early on in the disease
What is the goal of treatment of RA? Is early detection important?
Goal: Remission or lowest possible disease activity
Key is early diagnosis and intervention with DMARDs- window of opportunity (first 3 mo of disease may allow better control/ remission)
Nonpharm management of RA
Exercise (active gentle ROM and isometric exercise during flares; aquatic/ aerobic. Strengthening exercise between flares)
PT, OT
Job modification, assistive devices as necessary
Interventions to reduce CVD (smoking cessation, lipid control); screen for CVD
T/F RA is an independent risk factor for atherosclerosis and CVD.
TRUE! It is associated with an increased overall mortality/ morbidity from all causes: CVD, neoplasm (esp. lymphoma, infection)
You suspect your patient has RA. What are you going to do?
Refer to rheum!!!
First line treatment of RA
Tx should be started as soon as RA dx made, and should be aimed at reaching sustained remission
Methotrexate is the gold standard and is first line unless contraindicated
WHen are biologics used for RA
Use if inadequate response to DMARDS; should be combined with DMARD therapy
First line options are anti-TNF (i.e., infliximab)
Reassess q3-6mo and monitor disease activity
What other supportive therapies may be used for RA?
NSAIDS, acetaminophen
Corticosteroids- injection to control symptoms in specific joint; systemic or oral (low doses useful short term if NSAIDs are ineffective and to bridge gap until DMARDs take effect.
Important thing we need to remember if our patient is started on longterm corticosteroids for RA?
Do baseline DEXA bone density and consider supportive pharmacologic therapy (i.e., bisphosphonates) if using >3 mo.
Other A/E of steroids?
weight gain, OP, AVN, cataracts, glaucoma, PUD, susceptibility to infection, easy bruising, acne, HTN, hyperlipidemia, hypokalemia, hyperglycemia, mood swings.
T/F if RA has progressed within a joint, the person may need surgery
True
Indicated for structural joint damage
Synovectomy, joint replacement, joint fusions, reconstruction/ tendon repair
What does DMARDs stand for and what are they used for?
Disease modifying anti-rheumatic drugs
when used early, change the course of RA disease and are proven to reduce damage and associated disability
What are some examples of DMARDs?
methotrexate, leflunomide, sulfasalazine, hydroxychloroquine, cyclosporine, azathloprine
Are glucocorticoids considered first line therapy for RA?
Shouldn’t be. Trial NSAIDs first.
Glucocorticoids or NSAIDs are generally reserved for short-course management of flares and to control symptoms until DMARD takes effect.
DMARDs are 1st line for treatment.
If patient has been on steroids for long term, what condition should you screen for?
osteoporosis
What are the key things to monitor for when taking methotrexate (MTX)?
MTX is a sulfa drug - affects folic acid metabolism
-Monitor for leukopenia and liver dysfunction. Patients should take folic acid supplementation to reduce the occurence of associated side effects such as mucositis, mucosal ulcerations, hair thinning and alopecia.
*monitor WBC at initiation and in one week.
*MTX commonly causes a mild elevation in liver enzymes, but persistent elevations require further evaluation
*CBC, aminotransferases, and creatinine every 2 to 4 weeks for the first 3 months or after increasing the dose, every 8 to 12 weeks for months 3 to 6, then every 12 weeks.
Avoid alcohol (prevent hepatoxicity)
What should be monitored when taking hydroxychloroquine?
annual ophthalmology examination for retinal deposits
Older adults with macular degeneration should not take hydroxychloroquine
No BW required for monitoring
What are you monitoring when pt is taking Sulfasalazine?
sulfasalazine necessitates monitoring for leukopenia and liver dysfunction
*CBC, aminotransferases, and creatinine every 2 to 4 weeks for the first 3 months or after increasing the dose, every 8 to 12 weeks for months 3 to 6, then every 12 weeks.
Are DMARDs immunosuppressive?
Yes. Older adults should be monitored closely (risk for infection)
What is first-line treatment when using DMARDs?
Triple therapy: methotrexate, hydroxychloroquine, and sulfasalazine or leflunomide
Requires routine monitoring for toxicity every 8-12weeks
*CRP/ESR
*Hgb - anemia
*increased disease activity - albumin may be reduced
*ongoing inflammation - platelets may increase
*ALT/AST
If triple therapy is not effective, what step is next?
Biologic treatment - sometimes in combination with methotrexate or other nonbiological DMARDs
What is best to initiate before any DMARD or biological DMARD therapy begins?
Make sure vaccinations are up-to-date!
DMARD: herpes zoster, pneumococcal, influenza, human papillomavirus.
biological DMARD: TB, Hep B & C,
General side effects of DMARDs?
- Myelosuppression
- Hepatotoxicity
- GI side effects
General side effects of Biologics?
- Increased risk of infections
- Injection site reactions
