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
