Muscoskeletal Flashcards
GOUT
Metabolic disease, in which an abnormal amount of urate deposits in the tissues and characterized by a recurring acute arthritis. Urate deposits occur when uric acid level is >6.8mg/dl. Hyperuricemia occurs with overproduction or under excretion of uric acid.
ETIOLOGY of Gout
Primary Gout- is common in Pacific islanders, men, over the age of 30. There is a hereditary component and genome research found linked risk of gout to several genes whose products regulate urate handling by the kidneys. In women, onset occurs after menopause.
Secondary Gout- may have hereditary component, but is related to acquired causes of hyperuricemia (medications, disease process such as myeloma, CKD, and hypothyroidism).
SIGNS AND SYMPTOMS of GOUT
Tophi found in the external ears, feet, hands, olecranon, and prepatellar bursae
Intense pain
Fever
Pruritus
LABORATORY AND DIAGNOSTIC FINDINGS of GOUT
Serial serum uric acid tests
Leukocytosis
Sodium urate crystals in joint fluid or material aspirated from a tophus
X-ray -negative early in disease process, later punched-out erosions with overhanging rim of bone (rat bite appearance) develop
DIFFERENTIAL DIAGNOSIS of GOUT
Cellulitis
Pyogenic arthritis
Rheumatoid arthritis
Sarcoidosis
Multiple myeloma
Hyperparathyroidism
TREATMENT of GOUT
Asymptomatic hyperuricemia should not be treated.
Medications should not be prescribed until arthritis, renal calculi, or tophi occur
ACUTE ATTACK
NSAIDs unless contraindicated (naproxen, indomethacin)
Colchicine-for acute gout, duration <36 hours
Corticosteroids-helpful in patients with contraindication to NSAIDs (methylprednisolone, prednisone)
Interleukin-1 inhibitors (anakinra, canakinumab, rilonacept)
CHRONIC MANAGEMENT
Diet (avoid alcohol particularly BEER, high purine food like organ meats)
Avoid hyperuricemic medications- thiazide and loop diuretics, ASA
Colchicine- to prevent attacks in patients who have mild hyperuricemia and when urate-lowering therapy has been started….DO NOT prescribe if patient has CKD
Xanthine oxidase inhibitors (allopurinol or febuxostat)
Uricosuria agents (pegloticase)
With rigorous medical compliance, allopurinol or febuxostat or pegloticase can shrink tophi and lead to their disappearance
Pseudo-gout occurs with calcium pyrosphosphate deposition in fibrocartilage and hyaline cartilage.
Pseudo-gout can be asymptomatic found incidentally on x-ray.
Prevalence increases with age.
Pseudo-gout is usually seen in patients over 60 years of age.
It is characterized by acute, recurrent, and rarely chronic arthritis of the large joints.
What food would you tell your gout patient to avoid? food high in uric acid -liver, kidney meat, mushrooms, asparagus, sardines
What medication would the NP NOT prescribe for CKD patient with gout and why? NSAIDS-cause worse , nephrotoxicity
Key points of GOut
Although increased purine intake and increased production can contribute to hyperuricemia, the most common cause of gout is decreased urate excretion secondary to kidney disorders or genetic variability in uric acid transporter efficiency.
Suspect gout in patients with sudden, unexplained acute monoarticular or oligoarticular arthritis, particularly if the great toe or midfoot is affected or there is a prior history of sudden, unexplained episodes of acute arthritis with spontaneous remission in 7 to 10 days.
Confirm the diagnosis by finding needle-shaped, strongly negatively birefringent urate crystals in joint fluid; or by dual-energy CT scans or ultrasound imaging.
Documentation of hyperuricemia is insufficient to confirm the diagnosis of gouty arthritis.
Treat acute flares of gout with oral colchicine, an NSAID, a corticosteroid, a combination of colchicine with an NSAID or a corticosteroid, or an interleukin-1 (IL-1) antagonist.
Decrease the risk of future flares by prescribing colchicine, an NSAID, and life-long use of drugs to decrease the serum urate level.
Give drugs that decrease serum urate levels if patients have tophi, > 2 flares of gout per year, urolithiasis, or multiple comorbidities that contraindicate the drugs used to relieve acute flares; individualize the use of urate-lowering ongoing therapy in other patients.
Decrease urate levels usually by prescribing allopurinol or febuxostat alone or in combination with a uricosuric drug.
GOUT
Acute , mono, articular, arthritis, often of the first MTP joint; reoccurrence is common.
Poly articular involvement more common in patients with long-standing disease.
Identification of your urate crystals in joint fluid or tophi is diagnostic.
Dramatic therapeutic response to NSAIDs
With conicity, urate deposits, in subcutaneous tissue, bone, Cartlidge, joints, and other tissues.
Osteoporosis Definition: A skeletal disorder characterized by decreased bone osteoid that reduces bone integrity
ETIOLOGY
Hormone deficiency (estrogen-women) (androgen-men)
Hormone excess (thyrotoxicosis, hyperparathyroidism, Cushing syndrome, Corticosteroid use)
Alcoholism
Inflammatory bowel disease
Immobilization and microgravity
Tobacco use
Genetic disorders (Marfan syndrome, Osteogenesis imperfect, Hypophosphatasia, Homocystinuria, Aromatose deficiency, Collagen disease processes, Ehlers-Danlos syndrome)
Long-term medication use (heparin, aromatase inhibitors, SSRIs, Vitamin A, Vitamin D
Osteoporosis
SIGNS AND SYMPTOMS
Usually asymptomatic until fractures diagnosed,
Backache-depending on severity of fracture or collapse of vertebrae
LABORATORY AND DIAGNOSTIC FINDINGS
Serum calcium, phosphate and PTH are normal
Alkaline phosphatase may be normal or slightly elevated (ie after fracture)
Vitamin D is decreased
Assess serum determining of 25-hydroxyvitain D if low bone density
Assess for thyrotoxicosis and hypogonadism
Assess for celiac disease with serum tissue transglutaminase antibody determinants
DEXA (dual energy x-ray absorptiometry) determine bone density of lumbar spine, hip, and distal radius
T score is the simple manner of reporting DEXA
> -1.0: Normal
-1.0 to -2.5: Osteopenia
<-2.5: Osteoporosis
< -2.5 with fracture: severe Osteoporosis
People with T score -1.0 to -1.5 need DEXA every 5 years
People with T score -1.5 to -2.0 need DEXA every 3-5 years
People with T score <-2.0 need DEXA every 1-2 years
Osteoporosis
DIFFERENTIAL DIAGNOSIS
Osteomalacia
Myeloma
Metastatic bone disease
TREATMENT
Diet: adequate in protein, total calories, calcium, vitamin D
Reduce/discontinue use of corticosteroids
Smoking cessation
Reduce/stop alcohol consumption
Increase exercise
Fall prevention: adequate home lighting, handrails on stairs, handhold in bathrooms, use of can or walker, PT/OT
Discontinue medications causing dizziness, orthostasis, or hypotension
Pharmacologic treatment indicated for T score below -2.5 & for all patient with fragility fractures
Prophylactic medication treatment for T score -2.0 and -2.5
Vitamin D and calcium: recommend vitamin D intake of 600-800 units/day, 1000mg/day of calcium for all adults and 1200mg/day for postmenopausal women
Bisphosphates for patients with pathological spine fracture or low impact hip fracture and those with osteoporosis (DEXA T score of -2.5 or less)
Fosamax, Binosto, Actonel, Boniva
If cannot tolerate oral bisphosphonates IV bisphosphonates are indicated: Aredia, Zometa, Reclast
Denosumab-(monoclonal antibody ) increases bone mineral density by inhibiting the proliferation and maturation of pre osteoblasts into mature osteoclast bone-resorbing cells
Forteo, parathar-stimulate production of new collagenous bone matrix. When administered in 20mcg/day SC for 2 years, it was found to improve bone density particularly in distal radius
Consult orthopedic or neurosurgery- for vertebroplasty or kyphoplasty if patient has vertebral compression fracture and have failed conservative pain management
Sex hormones- can prevent osteoporosis but not effective therapy for diagnosis of osteoporosis
Selective estrogen receptor modulators (SERMs)- can prevent but not treat established diagnosis of osteoporosis.
Raloxifene
Bazedoxifene
Calcitonin- less effective but helps reduce pain of acute compression fractures, ineffective for chronic pain
SIDE EFFECTS OF BISPHOSPHONATES
Fever, chills, flushing, musculoskeletal pain, nausea, vomiting, diarrhea, fatigue, dyspnea, edema, headache, dizziness, ocular inflammation
IV bisphosphonates have caused seizure
Symptoms are usually transient, lasting a few days but resolving
If have a severe acute response they can receive corticosteroids and ondansetron before any other IV infusion
COMPLICATION OF BISPHOSPHONATES
Osteonecrosis of the jaw: particularly after tooth removal
Atypical low-impact “chalkstick” fractures of the femoral shaft
21 foods that may help with osteoporosis, blueberries, oranges, broccoli, cabbage, feta cheese, fish oil, apples, bananas, kiwis, spinach, watercress, salmon, pumpkin seeds, grapes, strawberries, kale, sardines, sunflower, seeds, papayas, walnuts, spurulina
OSTEOMYELITIS
Osteomyelitis is an infection of bone.
It is often difficult to diagnosis. Over 50% of cases are due to Staph Aureus.
Osteomyelitis can be the result of direct exposure from open fracture, the result of surgery, contiguous focus of infection, open wounds, or hematogenous spread.
The long bones and vertebrae are the most common sites of infection.
Complication: Epidural abscess. Abscess should be considered if fever, severe back/neck pain, radiculapothy, or signs of spinal cord compression (incontinence, weakness, pathologic extremity reflexes).
Osteomyelitis
SIGNS AND SYMPTOMS
Fever
Chills
Pain
Sensory loss
Motor loss
Malaise
Anorexia
Night sweats
Draining sinus tracts
Osteomyelitis
LABORATORY/DIAGNOSTIC FINDINGS
Blood cultures
Leukocytosis
X-ray usually normal early in the infectious process but will become abnormal
CT scan is more sensitive than X-ray and can help localize the abscess
MRI is indicated if suspect epidural abscess with vertebral osteomyelitis
MRI is the most sensitive diagnostic tool
Nuclear medicine bone scan most valuable when osteomyelitis is suspected but no site is obvious
Osteomyelitis
DIFFERENTIAL DIAGNOSIS
Arthritis
Rheumatic fever
Cellulitis
Tuberculosis
Ewing sarcoma
Metastatic cancer
Osteomyelitis
TREATMENT
ID consult
Ortho/Neurosurgery consult
Patient will require debridement of necrotic bone
Patient may need emergent neurosurgical decompression
Antibiotics: oral can be effective: quinolones (cipro) BUT IV preferred particularly in acute phase
IV antibiotics: 4-6 weeks of therapy.
Nafcillin or oxacillin.
Cefazolin is effective.
If MRSA patient should be prescribed Vancomycin.
Oral step down to rifampin may be effective
BACK PAIN
Low back pain is the most common cause of disability for people over age of 45. It is the second most common complaint at PCP office.
Back pain
SIGNS AND SYMPTOMS
PAIN
Alarming symptoms in addition to pain: fever, pain at rest
Cauda equine syndrome is suggested by urinary retention or incontinence, saddle anesthesia, decreased anal sphincter tone, fecal incontinence, bilateral lower extremity weakness, progressive neurologic deficit.
Cauda equina is a medical emergency
Upon physical exam NP may see: kyphosis, scoliosis, lumbar hyperlordosis
Assess for pain with one leg standing extension.
Positive test can be caused by pars interarticularis fractures or facet joint arthritis
With the patient sitting assess motor strength, reflexes, and sensation.
It is important to compare strength and reflexes bilaterally
In supine position hip should be evaluated for ROM.
Rectal examination is required if suspect cauda equine syndrome
Back pain
LABORATORY/DIAGNOSTIC FINDINGS
AP/lateral X-ray
MRI is the method of choice in evaluation of symptoms not responding to conservative treatment
Electromyography or nerve conduction studies for pain lasting longer than 6 weeks
Back pain
DIFFERENTIAL DIAGNOSIS
Cauda equina syndrome
Spondylosis
Compression fracture
Anterolisthesis
Spinal stenosis
Kyphosis
Back pain
TREATMENT
Conservative measures —unless present as cauda equina—-
Educate on proper lifting techniques, abdominal wall/core strengthening
Weight loss
Smoking cessation
PT
Back brace
TENS
Acupuncture
NSAIDs
Stat referral to neurosurgery/orthodpedic surgery if cauda equina syndrome: requires emergent decompression
Refer to surgeon for further evaluation of pain if no improvement with conservative measures.
Why is cauda equina a medical emergency? because can cause neurological issues
How long does most insurance companies require conservative treatment before approving an MRI? At least wait at least 6 weeks
DISLOCATION -DEFINITION
- Result of the displacement or separation of the bone from its position at the joint
- Total loss of articulation of ends of bones within a joint muscle
DISLOCATION-ETIOLOGY
- Pathologic in nature
- Congenital in nature
- Neuromuscular disease process: i.e. muscular dystrophy
- Inflammatory disease process: i.e. arthritis
- Ligamentous laxity: ligament structures are stretch or loose
- Blunt force trauma
DISLOCATION-SIGNS AND SYMPTOMS
- Pain over affected area
- Parasthesias distal to injury
- Joint deformity
- Edema
- Contusion or laceration over affected joint
- Decreased or absent peripheral pulses
- Decreased or absent ROM of joint
- Decreased or absent sensation distal to joint secondary to peripheral nerve damage
DISLOCATION -LABS AND IMAGING
- CBC: elevated WBC secondary to stress response
- Anemia: secondary to hematoma formation or bleeding
- X-rays reveal dislocation. ANTEROPOSTERIOR AND LATERAL FILMS SHOULD BE ORDERED - Oblique film may be needed for fractures
- CT scan indicated for pelvic trauma
- Ultrasound and/or arteriogram needed for posterior knee dislocation because of high probability of popliteal artery injury
DISLOCATION -TREATMENT
- ANATOMIC REDUCTION IS THE FIRST LINE FOR TREATMENT
- Closed manual reduction for dislocation without fracture
- Surgical reduction may be needed if fracture present
- Postreduction immobilization is important (splint, cast, slings, elevation of extremity with cold compress)
- Surgical repair of ligamentous injury
- Physical therapy
- Occupational therapy
- NSAIDs (unless contraindicated)
- Muscle relaxant for severe spasms (valium, flexiril, skelaxin, robaxin, baclofen, norflex)
- Narcotics for short-term use (least addictive 1st..start with ultram then move to norco and then Percocet…very addicting)
FRACTURE -DEFINITION
- Break or disruption in the bone
Classification - Closed: no apparent break in the skin over the fracture
- Open: variety of skin and/or soft tissue injury over the fracture
1. Type I: wound smaller than 1cm, little contamination
2. Type II: wound larger than 1 cm, moderate contamination, moderate soft tissue damage with bony comminution
3. Type III: high contamination, severe unstable fracture, severe soft tissue damage - Incomplete or complete
- Simple or comminuted
- Traumatic or pathologic
- Displaced or non-displaced
- Avulsion
- Buckle
- Stress
Type of fracture line
1. Transverse
2. Spiral
3. Oblique
4. Comminuted
5. Longitudinal
6. Butterfly
7. Segmental
8. Impacted
9. Stellate
FRACTURE -ETIOLOGY
- Trauma: crush, blunt, deceleration forces
- Rotational forces
- Osteoporosis, osteopenia
- Tumors
- Metabolic disease: i.e. Paget’s disease, rickets
- Drugs: Prednisone, Dilantin
- Congenital in nature
- Neuromuscular disease process: spinal cord injury, muscular dystrophy
- Nutritional deficit: malabsorption syndrome, vitamin D, alcoholism
FRACTURES-Signs and symptoms of fracture
- Moderate to severe pain
- Possible limb deformity
- Crepitus
- Edema
- Diminished or absent pulse
- Ecchymosis
- Bleeding
- Decreased or absent ROM
FRACTURES-LAB AND IMAGING
- Anteroposterior and lateral X-ray imaging
- Oblique x-ray for complex fractures
- 3 dimensional and coronal/sagittal CT scan for pelvic and spinal fractures on X-ray
- MRI if spinal cord injury suspected
FRACTURE-TREATMENT
- CBC: elevated WBC
- Serial H&H needed to assess for anemia
- Urinalysis to assess for myoglobinuria for crush injury
- PT/INR, PTT to assess for clotting
- Chem 13
- Lactic acid
- CPK
- Type and screen/crossmatch
- Remember ABC as 1st priority upon patient arrival
- Musculoskeletal exam
- Fluid resuscitation (NS or LR)
- Open wounds should be covered with saline dressing
- EARLY REDUCTION OF FRACTURE
- CONSULT FOR ORTHOPEDIC SURGERY
- Will need IV antibiotics for open fractures (cefazolin, vancomycin)
- Narcotics (PCA pump)
- Ultram, Norco, Percocet
- Tetanus toxoid
RHABDOMYOLYSIS
A syndrome of acute necrosis of skeletal muscle associated with myoglobinuria and elevated CK levels.
ACUTE TUBULAR NECROSIS IS THE MOST FREQUENT COMPLICATION and occurs secondary to toxic effects of filtering large amount of myoglobin during hypovolemia.
RHABDOMYOLYSIS SYMPTOMS, CAUSES, AND TREATMENT
Cocaine use and alcohol intoxication, in the setting of prolonged immobility and exposure hyperthermia are leading cause of hospital admission.
Using statins another cause.
Patients with CKD, DM, liver failure, and hypothyroidism have increased risk of rhabdomyolysis.
Statins use along with niacin and fibric acids increase the likelihood as well.
Rhabdomyolysis is also associated with crush injuries to muscles.
Recently there has been discussion on extreme exercise such as bodybuilding and CrossFit causing rhabdomyolysis. In addition, those working in extreme heat and training (i.e. firefighters and military service) have increased risk of diagnosis.
RHABDO-SIGNS AND SYMPTOMS
Classic triad: muscle pain in shoulder, thighs, and lower back, dark red or brown urine, muscle weakness
Half of all those diagnosed will NOT have muscle symptoms
Abdominal pain
Nausea
Vomiting
Fever
Tachycardia
Confusion
LABORATORY/DIAGNOSTIC FINDINGS
Chemistry : check electrolytes particularly for K+-(Transient hyperkalemia second to increase potassiunm from inside the cells to the extracellualr fluid)
Hypocalcemia
Hyperphyphophate, Hyperuricemia
Urinalysis: positive for blood in absence of RBC -as measuring myoglobin and not hemoglobin
Serum creatinine kinase level
AST, ALT elevated
Lactate dehydrogenase elevated
TREATMENT
Fluids, Fluids, Fluids with careful monitoring for volume overload
Mannitol has been recommend to decrease injury to the kidneys
If BUN/Creatinine maintain elevation and or decreased urine output nephrology consult is warranted.
Admit with levels greater than 15,000 or electriolyrte derangement or AKI
