5 Fingers Flashcards
History for multiple myeloma
> 50 yo, low back pain, anemia of chronic illness
Has not responded to conservative care for at least 1 month
Failure of bed rest to relieve pain, or bed rest makes pain worse
What is multiple myeloma?
Most common 1˚ bone cancer, though <1% all cancers
Red flags for multiple myeloma
- Previous history of cancer
- Unexplained weight loss of >10lbs over 3 months
- Does not respond to conservative care for at least 1+ months
Physical exam clues for multiple myeloma
Neurological deficits especially in female, pediatric, geriatric
Spinal percussion has poor sensitivity and specificity for dx cancer
Special studies for multiple myeloma
Radiograph and then MRI
ESR/CRP
CBC
Blood chemistry panel
Note: bone scans will be normal
How is multiple myeloma diagnosed?
Serum protein electrophoresis
And confirm with marrow aspiration
What is abdominal aortic aneurysm?
Permanent focal dilation of abdominal aorta >3cm most commonly occurring between branches of renal and common iliac arteries
Most occur in white males >60yo
M:F prevalence is 2:1 and death is 11:1
Strong risk factors for AAA
Older Cigarette smoking Male Family history of AAA Caucasian Increased diastolic pressure
History of abdominal aortic aneurysm
20-30% pts have symptoms
Pain: back, abdomen, groin, flank, testicles—generally left sided
Pulsation in abdomen with a quality that changes based on position
Pt may report early satiety, nausea, weight loss (all from GI compression), urinary urgency, sx of intermittent claudication, blue toe syndrome
Physical findings in AAA patient (4+additional)
1-Diastolic HTN
2-Absent pulses in LE
3-Bruit heard with abdominal auscultation
4-Exaggerated abdominal pulsation and widened aorta seen with abdominal palpation +LR 2.7-7.6
Additional: trash foot where tissue in toes breaks down and color changes from infarcts despite good pulses
What special studies would you do for suspected AAA?
Abdominal aortic ultrasound (92% sen, 100% spec)
CT and MRI are accurate too
How do you manage AAA?
Discovery AAA requires immediate referral for surgery
A-emergent referral if >7cm with pain, pulsating mass, hypotension, sudden increase of sx
B-urgent referral if >6cm, found on x-ray, acute LBP
Manipulation is contraindicated in active AAA
What is the prognosis for someone with AAA?
Mortality rate 75-90% after rupture
Long term is related to comorbidities
Most pts die due to coronary artery disease before they meet surgical criteria rather than dying from AAA
50% AAA pts show classic triad (in rupture). What is the classic triad
1-hypotension
2-back pain
3-pulsatile abdominal mass
What is cauda equina syndrome?
Multiple nerve roots are simultaneously compressed below the level of the conus medularis leading to neuromuscular and urogenital symptoms
3 most common causes of CES
1-Midline disc herniation
2-Spinal stenosis
3-Tumor
Main signs and symptoms for CES other than LBP. List them in orderstarting with the most common finding
1-Urinary retention +LR 18 2-Overflow incontinence 3-Saddle paresthesia 4-Diminished sexual fxn 5-Diminished anal sphincter tone and loss of anal wink reflex
Also: possible bilateral/unilateral sciatica
These signs and sx occur <24 hours after neurological compromise in 90% of patients
What will you see in physical exam with a CES pt?
+SLR
Sensory and motor deficits in dermatomal pattern S2-4
What specials studies would you order for suspected CES
MRI is gold standard for initial evaluation of patients with CES.
Plain films are not helpful.
Dx is usually made from history and physical
How do you manage pt with CES?
Urgent (same day) referral to neurologist.
If rapid onset of sx, referral is emergent (within hours).
Decompressive surgery must be done to relieve pressure on nerves. Pt must be monitored post surgery for progressive enervation of bowel and bladder even if back, leg or other peripheral sx improve.
Manipulation is contraindicated.
What is the prognosis for pt with CES
Prognosis improves if cause is identified and treated quickly
What is diabetic amotrophy/neuropathy?
A disabling illness that is distinct from other forms of diabetic neuropathy. It is characterized by weakness followed by muscle weakness and wasting, either unilaterally or bilaterally, with associated pain.
Diabetic neuropathy: multiple nerves are affected. more common
Diabetic amotrophy: only the femoral nerve is affected.
What does a history of someone with diabetic amotrophy/neuropathy look like?
Sudden severe LE pain and weakness
Pts typically have controlled Type II diabetes
Weight loss is a frequent accompanying sx
What will show up in a physical in a pt with diabetic amotrophy/neuropathy?
Sensory: burning pain in the pattern of femoral nerve (anteromedial thigh, knee and lower leg)
Muscle: weak hip flexors and knee extensors (iliacus, sartorius, rectus femoris, vastus medialis, vastus lateralis, vastus intermedius)
Reflex: patellar reflex may be reduced or absent
Other: loss of vibration
What special studies/how would you diagnose a pt with suspected diabetic amotrophy/neuropathy?
Fasting glucose (>126 mg/dL)
Glycosylated HgB or HgB-A1C (>6.5 or 7%)
An EMG or nerve conduction study may be necessary to DDX where the lesion is
CT should be done to rule out a mass compressing the femoral nerve
What is a common sensory loss pattern (and quality of sensation/pain) in pts with diabetic amotrophy/neuropathy
Begins in feet and hands in a glove and stocking distribution.
Tends to cause burning pain and allodynia
What is an internal disc derangement?
Tears in the inner laminae of the disc (are no pain fibers there) commonly occurring in posterior disc due to the daily flexion loading (or less commonly, extension) microtraumas of life. The nucleus pulposus migrates into the tears, which are usually posterior. With previous disc derangement, pain fibers can grow into the inner ring. The direction of herniation is opposite to the direction of the load.
What does the history of a disc derangement look like? What is the quality of pain? Onset is due to what? What is the chief complaint? What is a classic triad? Is there referred pain?
BACK PAIN: deep, achy, poorly localized and usually more midline or bilateral. Pain is constant or intermittent with varying degrees of severity. ACUTE: pain can be severe, sharp, stabbing with sudden movements aggravated by lumbar spine movement.
Onset may be associated with trauma (heavy lifting) but more often repetitive microtrauma.
CHEIF COMPLAINT: sitting intolerance. Sitting rapidly aggravates LBP and it may be relieved by standing.
Dejerine’s triad: straining with bowel movements, coughing or sneezing may induce LBP
Referred pain: unilateral or bilateral referral into buttock or LE, usually not below the knee. Back pain is greater than leg pain. Leg pain is non-dermatomal and there may be non-dermatomal paresthesia or weakness.
What is Dejerine’s triad?
LBP induced by
1-straining with bowel movements
2-Coughing
3-Sneezing
What would you notice with the physical in a disc derangement?
Pain centralization is key: usually into extension for a posterior disc derangement
Posture: normal or flexion antalgia, lateral pelvic shift
AROM: painful and reduced, usually into flexion for a posterior disc derangement
Minor’s sign
Valsalva and orthopedic tests promote spinal compression may be painful in acute phase
SMRs are NORMAL
Tension tests: negative for LE sx
Interspinous spaces tender to palpation
What special studies would you run on a pt with suspected disc derangement?
Imaging is NOT indicated unless as consideration for surgical tx.
A high intensity spot on MRI may suggest annular fissure that is inflamed or actively healing (+LR 1.5-5.9)
Presents of high intensity zone (HIZ) correlates with discography findings. Discography is considered to be gold standard, but this is controversial. Positive test must reproduce the pts CC and the dye must demonstrate internal derangement.
What is the gold standard for special studies in disc derangement? Tell me more
Discography is considered to be gold standard, but this is controversial.
Positive test must reproduce the pts CC and the dye must demonstrate internal derangement. And the HIZ from MRI correlates with discography findings.
How do you manage patient with disc derangement: (2x2 box) and what to do if conservative care fails?
Limit bed rest <2 days and return to activity
CMT: joint manipulation into pain centralizing or directional preference, flexion-distraction therapy.
STM: stretch hamstrings
Behavior Mod: hip hinging, abdominal bracing
Exercise: directional preferences exercises like McGill’s big 3
If conservative care fails:
- epidural injections
- spinal fusion
- IDET (Intradiscal Electrothermoplasty) or PIRFT (Percutaneous Intradiscal Radio-Frequency Thermocoagulation)
How does IDET (Intradiscal Electrothermoplasty) work?
Using fluoroscopic guidance (real time x-ray), your surgeon inserts a hollow needle with a catheter (flexible tube) and electrode into the intervertebral disc. The catheter encircles the disc’s annulus fibrosis. The electrode is sufficiently heated to destroy small nerve fibers that have grown into the damaged disc and cause pain. The heat also seals small tears or cracks called fissures and stimulates the body’s production of proteins to strengthen the disc.
Complications are rare and may include infection, nerve damage, or disc damage.
Ref: https://www.coloradospineinstitute.com/treatment/surgical/idet/
How does PIRFT (Percutaneous Intradiscal Radio-Frequency Thermocoagulation) work?
The radiofrequency probe is placed into the center of the disc rather than around the annulus, and the device is activated for only 90 seconds at a temperature of 70 degrees centigrade. The mechanism of action is not precisely understood, but is thought to be related to reducing the nocioceptive pain input from the free nerve ending in the outer annulus fibrosis.
Ref: https://www.excellusbcbs.com/wps/wcm/connect/568f0e53-3f2a-4cf5-995b-b358879fc3c9/perc_idet+tac+18+%232.pdf?MOD=AJPERES&CACHEID=568f0e53-3f2a-4cf5-995b-b358879fc3c9
What is the prognosis for someone with internal disc derangement?
Conservative care may take 2+ months for healing.
Aggressive treatment shows mixed prognosis results
What is lumbar facet syndrome?
Pain originating from facets, their capsules, and adjacent soft tissues. It includes a spectrum of structural changes such as osteoarthritis, capsular tears, synovial cysts, and/or articular cartilage.
Lifetime prevalence with rigorous dual block criteria is ~15%. In older population of patients referred from rheumatologists, the prevalence rises to 40%.
What is a history for lumbar facet syndrome. Quality of pain, location, what aggravates it, MOI, pain referral pattern.
Deep achy back pain localized in paravertebral area (not midline). ACUTE phase: may be sharp with sudden movements
Pain is aggravated by hyperextension, rotation, lat flexion, walking downhill.
Least painful: walking and sitting
MOI: trauma, secondary to degeneration, or more commonly due to chronic postural or repetitive loads
Pain referral: anterior hip and thigh, posterior leg. Non-dermatomal, may not be contiguous, may refer as far as the foot.
What will you notice in a physical with suspected lumbar facet syndrome?
Pain is aggravated with:
- extending up from flexion (standing up from a forward bend)
- active hyperextension
- passive extension
- extension + rotation
(-) Kemp’s Test is pertinent negative against facet syndrome diagnosis.
(+) Kemp’s Test creates leg pain, suspect radiculopathy (nerve root) lesion
Static palp over facets is tender.
Motion palp reveals restricted joints
These tests are always negative:
- pain centralization (strong pertinent negative)
- valsalva
- flexion based loading tests
- SLR
What is a pertinent negative for lumbar facet syndrome?
(-) Kemp’s Test
(+) pain centralization
For a lumbar facet syndrome, what special studies should you order?
Imaging is NOT indicated.
Diagnostic facet block can be used to diagnose facet syndrome-this must be done prior to more aggressive Tx options
How is a diagnostic facet block performed?
It’s performed by anesthesiologist.
Intra-articular anesthetic injections with a double block or triple block protocol:
- inject the facet with short acting anesthetic and have patient note when pain returns
- repeat with longer lasting anesthetic injection
- for triple block, repeat a 3rd time with saline injection
What is the management plan with a pt with lumbar facet syndrome? 2x2 box
CMT: Spinal manipulation applied to painful joint restrictions, flexion-distraction therapy
STM: manual therapy for impaired thoracic extension, tight hip external rotators, tight hip anterior joint capsule or hip flexors, tight latissimus dorsi
BM: modify activities that promote extension
Exercise: prescribe core stability exercise program McGill’s big 3: side bridge, quadruped, curl up
If conservative care fails:
- therapeutic facet blocks
- radio frequency ablation (destroy the nerves)
What is the theory of acute locked low back?
Due to entrapped meniscoid or disc fragment lodged in the end plate
What is the history for acute locked low back?
Sudden onset (or slower onset over a few hours) of agonizing pain and inability to stand erect
May be triggered by forward flexion or sudden unguarded movement
Pain is slightly off midline with possible referral to ipsilateral thigh
Pt must brace with:
- walking, coughing, sneezing 🤧
What would you observe in a physical exam with acute locked low back?
Antalgic posture: slight flexion and lateral flexion
ROM decreased globally and segmentally with many joint levels often locked up
Typically increased pain with flexion and lateral flexion toward involved side
Muscle spasm and tenderness with no point tenderness over facets
NORMAL SMRs
How would you manage a pt with acute locked low back?
Close the pain gate and control inflammation. Stop the pain-spasm cycle via cryotherapy (cold therapy) and electro therapy. Analgesics or short term anti-inflammatory meds may help
CMT: gap the joint to release entrapped meniscoid
STM: reduce muscle spasm
What is spinal canal stenosis?
Degenerative condition resulting in decreased cross sectional area of the spinal cord.
More common in pts 60-70+yo
14% of pts with LBP will have stenosis
Radiographic stenosis vs clinical stenosis
Radiographic stenosis: Symmetrical disc bulging, facet enlargement, thickened ligamentum flavor
Clinical stenosis: neurogenic claudication, radicular syndrome or both
What is the history with a pt with spinal canal stenosis
> 65 yo with unilateral or bilateral LE sx
Findings:
- No pain when sitting +LR 7.4
- CES Sx +LR 7.2
- Unexplained urinary problems
- Flexion improves sx +LR 6.2
- Bilateral but or leg pain +LR 6.3
- Neurogenic claudication (non dermatomal pain) +LR 3.7
Diagnostic prediction tool can be used to confirm. Score >7 has a +LR of 3.31 for clinical stenosis
What is a physical exam findings for a pt with spinal canal stenosis
- wide based cate +LR 13
- abnormal Romberg test +LR 4.2
Pertinent negative
- provocation of pain with forward flexion -LR 0.48
Additional clues may increase the likelihood of clinical stenosis
- LE weakness
- absent Achilles reflex
- loss of vibration sense in the LE
- loss of pinprick in LE
- sustained extension increases pain
What is a pertinent negative for spinal canal stenosis? And what is the LR?
Provocation of pain with forward flexion
-LR 0.48
What special studies would you run on a pt with suspected spinal canal stenosis?
Plain film radiographs
CT/MRI if suspicious remains high after xray
Rule out peripheral arterial disease:
US or MRA
How would you manage a pt with spinal canal stenosis?
CMT: Normalize joint fxn with mobilization, manipulation, flexion-distraction.
STM: MFTP therapy.
BM: modify standing posture to have 1 foot elevated or lean over the desk, practice posterior pelvic tilt.
Exercise: Rehab program with stabilization exercises, walking program, double knee to chest exercises that promote lumbar flexion.
If conservative care is not effective, surgery is an option:
- epidural injections
- surgical decompression
What is the prognosis for spinal canal stenosis?
10-12 weeks
Improvement should be seen in 3-4 weeks and maint or exceeded by the week 6.
Pt should be monitored for signs of CES (6% chance).
Motor and sensory fxn should be monitored, if sig deficit occurs they should be referred out for surgery.
What could a walking program for someone with spinal canal stenosis be like?
First week, start walking every day or doing some kind of aerobic activity. Eventually get to 20-60 minutes each day. Later, walking on uneven, sloping, sandy/moving ground.
Proprioception: wear a low back pack with 22 lbs.
What is lumbar sprain? Lumbar strain?
Sprain: painful injury of lumbar ligaments
Strain: painful traumatic tear of large posterior muscles of the back
Sprain/strain combined are associated with higher loads or higher reps aka “lumbalgia”
Most common lumbar sprains?
Supraspinous
Interspinous
Most common lumbar strains?
QL
Erector spinae
What is a common history for pts with lumbar sPrain?
Pain midline to unilateral with or without referral to buttocks/extremity
History of trauma or overuse
History does not support vectors that could injure large back muscles
What is a common history for pts with lumbar sTrain?
Dull, achy back pain commonly bilateral, referral to the legs is uncommon.
Initiated by trauma.
What is a common physical exam for pts with lumbar sPrain?
Guarded posture neutral to slightly flexed
AROM protective and restricted
PROM in the direction of injury or loading is painful
Palpation
- pain over joint
- pain with joint play
- focal muscle splinting
- end play not reached due to guarding
- isometric muscle contraction is pain free, or less painful
- repetitive loading does NOT centralize pain
**if pain is more clearly aggravated by RESISTED MM TESTING, think sTrain (not sprain).
What is a common physical exam for pts with lumbar sTrain?
Guarded posture, superficial bruising may be present
AROM protective and restricted
Palpation
- broad palpable mm tenderness and hypertonicity at iliac crest (enthuses)
- localized defect and swelling (uncommon)
- no or minimal pain with joint play
- pain provoked by lumbar flexion and especially resisted lumbar extension test
**if pain is more clearly aggravated by RESISTED MM TESTING, think sTrain (not sprain).
What are special studies you’d run for a lumbar sPrain?
Trauma: X-ray to rule out fracture
Flexion-extension dynamic x-ray to rule out instability or poor response to Tx
What are special studies you’d run for a lumbar sTrain?
MSK US (rarely needed)
How would you manage a pt with lumbar sPrain/sTrain?
CMT & STM:
- ACUTE: light massage, joint mobilization
- SUBACUTE: manipulation, PIR/CRAC/pin and stretch, IASTM
Exercise:
- ACUTE: light stretching, muscle relaxation exercises (PIR)
- SUBACUTE: strengthening, lumbar stab, core stab, endurance
In the acute phase, limit end range flexion, lifting, or activities requiring full ROM until pain free.
Other: ice, heat, electromodalities, shorter term use of lumbosacral corset
Prognosis for lumbar sprain/strain
Mild cases resolve in a couple days, more severe may take 2+ weeks with low level pain up to 6 weeks.
What is spondylolysis?
Unilateral or bilateral stress fracture of the bridge between upper and lower pars interarticularis. It can range from a defect in the pars to a full Fx with separation. Bilateral in 80% of symptomatic cases, most commonly at L5 and then L4.
Estimated prevalence 6-13% of general population. Often asymptomatic.
In young athlete, prevalence rises to 47% of LBP. M>F 2:1
What is a common history of spondylolysis?
Suspect in a teenager or young adult with LBP, especially if they are an athlete in sports requiring:
- repeated flexion and extension
- repeated hyperextension
- twisting and axial load activities
Gymnastics and footballs are the highest risk sports
75% of cases in athletes <20 yo that train >15 hours per week
Pain onset may be sudden (50%) or gradual, acute then dull and achy in chronic presentation. Difficulty falling asleep, pain worse with sitting and standing (75%).
Pain associated with hyperextension is a common finding. (Increased lordosis is provocative.)
What physical exam findings would you expect with a spondylolysis?
AROM is variable — normal to reduced, pain elicited with extending from a flexed position, rotation/lateral flexion to the side of lysis, or hyperextension. Flexion may be pain relieving. Psoas may be short and tight bilaterally.
Stork test — poor accuracy, but increases likelihood of bilateral fracture if positive on both sides.
In acute cases — focal tenderness over the lumbar spine and discomfort with deep palpation.
No neurological deficits (though may occur if the Fx is filled with fibrocartilage as it heals that may impinge NRs).
Special studies for spondylolysis?
Radiographs, though often inconclusive in early stages.
- AP & Lateral
- AP axial lumbosacral spot view and/or oblique view
MRI, CT, SPECT Scan can be done
- CT cannot differentiate between active and non-active fx
- SPECT is the gold standard and can differentiate between active and inactive fx, but has substantial false positives, high radiation, and cannot rule out facet arthritis, neoplasm, or infection that are also active
- MRI is as accurate as CT but with no radiation dose. This should be ordered in rare cases that present with neurological signs
What is the management and prognosis for spondylolysis?
Primary goal is to prevent slippage, conservative care is effective in 95% of cases
Pt should avoid sports or activities that require repetitive flexion and extension. Pt must stop the activity or sport that evokes pain for 2-4 weeks, if symptoms do not resolve refraining from activity may be required for 3-6 months
Bracing to immobilize the pelvis and prevent hyperextension may be required. Worn 20-23 hours per day for 3-6 months and then slowly weaned off.
Acute intervention - ice 20 minutes, 3-4x per day, pain free ROM, stretch hip flexors, hamstrings, and psoas
Rehabilitation should focus on stabilizing the low back and core.
Stopping sports activity >3 months is reported to have better outcomes.
