MSK (8%) Flashcards
NURSEMAID’S ELBOW
Nursemaid’s elbow is a partial dislocation of the elbow joint caused by a sudden pull on the extended pronated forearm, such as by an adult tugging on an uncooperative child or by swinging the child by the arms during play.
The technical term is “ radial head subluxation “
Nursemaid’s elbow is a dislocated elbow joint caused by a sudden pull on an extended pronated forearm.
The etiology of nursemaid’s elbow involves the radial head slipping under the ANNULAR LIGAMENT
Common upper extremity injury in infants and young children
Generally, occurs with a pulling upward type of motion while the child has an outstretched arm
MECHANISM: lifting / swinging / pulling a child while the forearm is pronated + extended ==> radial head wedges into stretched annular ligament***
MC in 2-5 y/o
CLINICAL MANIFESTATIONS
⦁ children presents with arm extended
⦁ refuse to move or use arm
⦁ Often has arm across abdomen, as if broken
⦁ usually no swelling
⦁ tenderness to palpation of radial head
On physical exam, the forearm of a child with nursemaid elbow will be in incomplete extension with the forearm partially pronated
(opposite of tx = supination + flexion)
- May have referred pain to wrist
Children with nursemaid elbow typically present with the complaint of refusal to use an arm.
DIAGNOSIS
⦁ clinical diagnosis
⦁ Xrays = typically normal
- dislocation is often reduced by radiology tech while they are trying to get xrays
TREATMENT ⦁ Manual reduction - The supination-flexion technique is the classic method of reducing a subluxated radial head - It has a success rate of 80-92% - another method of hyperpronation
- child often experiences immediate pain relief after manual reduction, and can resume normal activities shortly after
Always ensure the child spontaneously uses the arm after reduction before discharging to confirm success
- if child uses arm after 15 minutes = no xrays needed
- if child does not use arm after 15 minutes = may want to do xrays to rule out fracture, or reattempt reduction
Patient presents as → a 4-year-old boy with elbow pain. He was forcefully pulled onto the curb by his mother after a close call with an oncoming car. Since the incident, the child has presented with right elbow pain and has refused to move his right arm. Examination reveals an irritable child cradling his right upper limb with his left hand. The affected limb is pronated with the elbow slightly flexed. Radiographs reveal subluxation of the radial head but are otherwise negative for a fracture.
CAUDA EQUINA SYNDROME
CAUDA EQUINA = bundle of peripheral nerves protruding from the bottom of the spinal cord
(“horse tail”)
CAUDA EQUINA SYNDROME = - A condition in which damage occurs to the cauda equina, or the bundle of peripheral nerves protruding from the bottom of the spinal cord
CAUDA EQUINA SYNDROME = LOWER MOTOR NEURON LESION
- Emergency! - can lead to permanent paralysis / incontinence
ANATOMY
- vertebra are made up of the body and the vertebral arch
- between the body and the arch = vertebral foramen
Spinal column = 33 vertebrae ⦁ 7 cervical ⦁ 12 thoracic ⦁ 5 lumbar ⦁ 5 sacral ⦁ 4 coccygeal
Each cervical / thoracic / lumbar vertebrae are separated by intervertebral disc - which allows for slight movement of the vertebrae, and acts as a shock absorber
The 5 sacral vertebrae are fused together to form sacral bone, and 4 coccygeal vertebrae are fused together to form the coccyx (tailbone)
Spinal cord goes through the spinal canal (space between vertebral body and arch)
- the spinal cord is connected to the brain and travels down to the 2nd Lumbar vertebrae, where it ends in the CONUS MEDULLARIS, and then continues as the Cauda Equina
There are 31 pairs of spinal nerves branching off of spinal cord ⦁ 8 cervical ⦁ 12 thoracic ⦁ 5 lumbar ⦁ 5 sacral ⦁ 1 coccygeal
space between 2 vertebrae = intervertebral foramen
- spinal nerves branch out from spinal canal through intervertebral foramen
The Cauda Equina carries nerve innervation for
⦁ genitals
⦁ internal + external anal sphincter (bowel)
⦁ detrusor vesicae - muscle that relaxes during urination (bladder)
⦁ leg muscles
⦁ knee + ankle reflexes
⦁ skin sensation of legs + pelvis
CAUSE OF CAUDA EQUINA SYNDROME
- compression / trauma / damage to multiple nerves of the cauda equina
⦁ MC cause = ** Lumbar disc herniation **
- poor posture, trauma, physical activity, and strong rotational movement can cause disc herniation - compresses on nerves
- similar to sciatica, but disc herniation is larger, and more nerves are compressed with herniation, and this includes the nerves that control the bladder and reproductive organs
⦁ Another cause = Spinal stenosis
- the narrowing of the vertebral foramen in the Lumbar vertebrae
- can be congenital, degenerative, Ankylosing spondylitis
⦁ Another cause = Spondylolisthesis
- vertebra gets displaced (trauma, surgery, degenerative spinal disease)
- MC = anterolisthesis (vertebra moves forward, narrowing the spinal canal and compressing nerves)
⦁ Another cause = any trauma to the spine (direct pressure on nerves, or bleeding into spinal canal –> hematoma –> nerve compression
⦁ Growths in spinal canal (tumors / cysts / abscesses)
** USUALLY AT L4-L5 LEVEL **
SYMPTOMS OF CAUDA EQUINA
⦁ severe back pain
⦁ sciatica - unilateral, or (usually) bilateral
⦁ decreased bowel + bladder control
⦁ decreased sexual function
⦁ “saddle anesthesia” = loss of sensation in saddle region (buttocks / inner thigh / perineum)
⦁ 1 or both legs may be impaired (muscle weakness)
⦁ loss of knee and/or ankle reflexes
⦁ may have paraplegia (no feeling / muscle control in legs)
⦁ may have sciatic pain = sharp pain going down back and leg
due to decreased tone of anal sphincter / bladder wall muscles
Cauda equina syndrome is characterized by severe back pain, saddle anesthesia, bowel / bladder incontinence, and sexual dysfunction.
*** NEW ONSET URINARY OR BOWEL RETENTION / INCONTINENCE with “ SADDLE ANESTHESIA “, unilateral or bilateral leg radiation
** DECREASED ANAL SPHINCTER TONE ON RECTAL EXAM = “ NO ANAL WINK “ **
DIAGNOSIS
⦁ clinical
⦁ confirmed by CT or MRI of spinal cord
- MRI with contrast* = gold standard
Diagnosis of cauda equina syndrome involves a pinprick pain sensation test that reveals leg anesthesia with perineal escape.
Treatment: This is a surgical emergency requiring immediate referral.
TREATMENT
- surgical emergency
⦁ surgical decompression if disc herniation, trauma, tumors or abscess (sudden symptoms)
will often immediately get surgical consultation prior to diagnosis - as cauda equina is an emergent diagnosis requiring immediate surgical consultation.
⦁ NSAIDS or Steroids to reduce inflammation
** LOWER MOTOR NEURON LESION ** = loss of reflexes / muscle flaccidity
(vs upper motor neuron lesion = hyperreflexia / spasticity
SCAPHOID FRACTURE
Scaphoid fractures are relatively uncommon in children but are at risk of nonunion, which can cause significant long-term pain
** INITIAL X-RAYS MAY BE NORMAL ** = so ALWAYS PLACE THUMB-SPICA SPLINT **
The arterial supply of the scaphoid bone enters distally leading to decreased blood and nutrient supply proximally
A fracture through the proximal or waist (central ⅓) of the bone can decrease blood supply further, especially if the artery is disrupted.
This causes poor healing conditions which can lead to nonunion or osteonecrosis
SYMPTOMS
⦁ tenderness at the anatomical snuffbox
⦁ dorsal radial wrist pain + decreased range of motion
With snuffbox tenderness = must rule out scaphoid fracture
DIAGNOSIS
⦁ X-ray
Most scaphoid fractures = at the waist or middle ⅓ of the bone
** In addition, many scaphoid fractures are extremely difficult to visualize on X-ray and swelling is not always present on exam **
Patients with a scaphoid fracture may only have pain at the anatomical snuffbox after a fall onto an outstretched hand (FOOSH)
TREATMENT
Current recommendations are to
⦁ place such patients in a THUMB-SPICA SPLINT
⦁ REFER to outpatient orthopedics to determine the need for further immobilization
⦁ REPEAT XRAYS in 2 weeks
SUMMARY
o Scaphoid Fracture
⦁ Patient with a history of fall on an outstretched hand (FOOSH)
⦁ Complaining of dorsal radial wrist pain with decreased range of motion
⦁ PE will show anatomical snuffbox tenderness
⦁ Treatment = thumb spica splint
RHABDOMYOLYSIS
a condition in which damaged skeletal striated muscle breaks down rapidly
- acute breakdown + necrosis of skeletal muscle
Breakdown products of damaged muscle cells are released into the bloodstream
some of these breakdown products, such as the protein MYOGLOBIN, are harmful to the kidneys and may lead to kidney failure
- myoglobin can also block conduits for urine release
The damaged muscle then becomes a reservoir for fluid, causing dehydration and further insult to the kidneys
Myoglobin can become lodged in the renal tubules –> obstruction –> can cause acute tubular necrosis, leading to acute kidney injury (which can lead to hyperkalemia) and increasing creatinine and BUN.
- Myoglobin, CK, LDH, K+, PO4, urate, etc all released with muscle breakdown
- hyperkalemia can lead to cardiac arrhythmias / arrest
CAUSES OF RHABDOMYOLYSIS ⦁ crush / blunt injury or trauma = MC ⦁ immobility ⦁ medications = statins (MC), fibrates, niacin, salicylates ⦁ strenuous exercise / weight-lifting ⦁ drug / alcohol abuse ⦁ infections ⦁ ischemia ⦁ electrocution ⦁ hyperthermia ⦁ seizures ⦁ burns
- Rhabdomyolysis is an adverse effect of STATINS when administered with FIBRATES + NIACIN
- statin alone, or fibrate alone may cause it too, but the combination is most likely
Statins can inhibit the electron transport chain, causing destruction of myocytes and leading to rhabdomyolysis
When there is no history of extreme exertion, alcohol consumption, or trauma, HYPERTHERMIA is a cause of muscle weakness. Geriatric population is more susceptible to heat stroke and is related to reduced mobility, capacity for independent living, compromised end organ function (e.g. renal, hepatic), or abuse by neglect (leading to inadequate hydration, among others). Hereditary muscle condition increases risk of rhabdomyolysis.
SYMPTOMS ⦁ severe muscle pains - usually proximal muscles ⦁ muscle weakness ⦁ vomiting ⦁ confusion ⦁ red / brown colored urine ⦁ muscle tenderness to palpation
CLASSIC TRIAD
o Myalgia + generalized weakness + dark urine
Moderate to severe rhabdomyolysis may present with red -brown colored urine due to myoglobin in the urine
severity depends on the extent of muscle damage and renal impairment
DIAGNOSIS
⦁ elevated creatine kinase (CPK or CK) = best marker for rhabdomyolysis
- (normal = 10-120 mcg/L), rhabdo = CPK in thousands
- normal = < 200; CK > 1000 = indicative of rhabdo
- CK > 5000 = should check for other complications, such as AKI, hyperkalemia, and DIC
⦁ may have elevated LDH (tissue damage)
⦁ elevated AST / LFTs (nothing actually wrong with liver; proteins / enzymes found in the liver are also found in skeletal muscle)
⦁ renal dysfunction = increased creatinine, BUN
⦁ hyperkalemia (intracellular K+ released from damaged muscle)
⦁ hypocalcemia (calcium binds to damaged muscle, also binds to phosphate that is released from muscle)
⦁ UA - myoglobin shows up positive for blood
(+ for heme, but - for blood)
- blood +
- protein +
⦁ may do EKG - signs of hyperkalemia / arrhythmias
TREATMENT
⦁ IV fluids - start quickly after a diagnosis of rhabdomyolysis to prevent further kidney injury (4-6L/day)
⦁ Mannitol = induce osmotic diuresis
⦁ Bicarbonate = alkalinize the urine
⦁ calcium gluconate if hyperkalemia with significant EKG changes
⦁ dialysis or hemofiltration if severe / already have renal dysfunction
COMPLICATION ⦁ Acute Kidney Injury ⦁ multi-organ failure ⦁ Hyperkalemia ⦁ DIC
SEPTIC ARTHRITIS
Infectious Arthritis
Septic arthritis = Infectious arthritis = joint inflammation secondary to infection
- usually due to bacterial infection of the joint
- considered a medical emergency due to high risk of joint destruction
All joint types (fibrous, cartilaginous, synovial) can get infected
** MC CAUSE = STAPH **
ex: in synovial joints
- synovial fluid - helps to lubricate the joint and to absorb shock
- the synovial membrane has vessels that supply the joint with nutrients + oxygen
- the 2 bones that form at that joint are covered in articular cartilage - also absorbs shock + reduces friction during movement
HOW DOES A JOINT BECOME INFECTED?
1) pre-existing infection in adjacent tissue (usually the bone = Osteomyelitis) –> spreads to articular cartilage –> spreads to joint
2) hematogenous spread = bacteria is somewhere else in the body (ex: lungs) –> travels via bloodstream –> joint
3) Trauma / puncture wound / surgery
ex: if nail pierces through knee and into joint
- septic arthritis could either be from the nail (ex: tetanus) or from the surface of the skin (ex: staph)
Once bacteria gets into synovial joint ==> starts destroying the articular cartilage via TOXINS (ex: chondrocyte protease - enzyme that digests collagen in cartilage)
Bacteria stimulates an immune response reaction
⦁ macrophages phagocytose the bacteria, and release cytokines (Interleukin - 1 + TNF-alpha) = signaling cytokines
⦁ IL-1 + TNF-alpha recruit more immune cells to site
⦁ mast cells release histamine –> vasodilation + increases vascular permeability
==> more blood comes into area –> INFLAMMATORY RESPONSE –> joint becomes red / swollen / warm
⦁ due to increased vascular permeability –> more fluid accumulates in joint space –> increased interarticular pressure –> compresses blood vessels supplying blood to joint –> necrosis of affected bones / cartilage –> joint destruction
RISK FACTORS ⦁ age ⦁ chronic debilitating disease ⦁ immunosuppressive drugs ⦁ IVDU ⦁ prosthetic joint / surgery ⦁ chronic arthropathies (RA / gout / osteoarthritis)
SYMPTOMS ⦁ joint pain ⦁ red ⦁ swollen ⦁ warm ⦁ impaired ROM ⦁ systemic = fever / chills / diaphoresis / myalgia / malaise
- symptoms may vary depending on pathogen
GONOCCOCAL ARTHRITIS
- due to Neisseria gonorrhea
- spreads hematogenously from cervix / urethra / pharynx
- affects multiple joints
- causes multiple SKIN LESIONS + TENOSYNOVITIS (inflammation of muscle tendons)
Neisseria gonorrhoeae is the most common cause of infectious septic arthritis in young sexually active adults.
BUT MAJORITY OF SEPTIC ARTHRITIS = NON-GONOCCOCAL ARTHRITIS = includes all other pathogens that cause septic arthritis
- typically only 1 joint is affected (MC a knee)
⦁ ** MC CAUSE = STAPH AUREUS **
- can completely destroy the joint within days unless treated
- Other causes:
⦁ Strep species (2nd most common)
⦁ mycobacterium tuberculosis
⦁ borrelia species (lyme dz)
⦁ * Group B strep *, H. flu in neonates
⦁ Pseudomonas in IVDU
⦁ staph epidermidis in prosthetics
DIAGNOSIS OF SEPTIC ARTHRITIS
⦁ joint aspiration - collect joint fluid
- purulent synovial fluid
- elevated WBC (> 50,000)
(>1100 = positive in prosthesis) - primarily PMNs (polymorphonuclear leukocytes = granulocytes = basophils + neutrophils + eosinophils)
- positive gram stain / positive culture
- lactate level > 10 (cell death –> release lactic acid)
- elevated ESR / CRP
IMAGING ⦁ Xray ⦁ Ultrasound ⦁ CT or MRI - can show bone erosion + joint effusion - especially useful for hip or sacroiliac joints where aspiration of fluid is difficult
When the hip is affected, the leg is characteristically held in abduction, external rotation and flexion; this position provides the most comfort because it maximizes the joint space.
TREATMENT - Antibiotic therapy + pain medication ⦁ Staph = Nafcillin (MRSA = Vancomycin) ⦁ Gonococcal arthritis = Ceftriaxone ⦁ IVDU (pseudomonas) = Cipro or Levofloxacin
- Arthrocentesis - joint aspiration + washout
- Arthrotomy + joint drainage - surgical
Empiric IV antibiotics should be started that cover S. aureus, the most common cause of septic arthritis.
- must be > 12 to have fluoroquinolones
If MRSA is suspected, clindamycin or vancomycin are better options
In neonates, antibiotics must also cover H. influenza, as this is a major cause of septic arthritis in those who are non-immunized.
ANTERIOR SHOULDER DISLOCATION
- ANTERIOR GLENOHUMORAL SHOULDER DISLOCATION
A dislocated shoulder occurs when the humerus separates from the scapula at the ** GLENOHUMORAL JOINT ** that connects humeral head to glenoid fossa
The shoulder joint has the greatest range of motion of any joint in the body, and is thus particularly susceptible to subluxation (partial dislocation) and dislocation.
Approximately half of major joint dislocations seen in emergency departments involve the shoulder.
MECHANISM:
⦁ blow to an ABDUCTED, EXTERNALLY rotated arm that is EXTENDED
- can also be due to FOOSA (fall onto outstretched arm)
- contact sports in younger patients
- falls in older patients
Dislocations can occur from a trauma (95%) or from laxity of the ligaments (5%)
⦁ Patients often report hearing or feeling a pop during the incident***
SYMPTOMS ⦁ significant pain ⦁ limited ROM ⦁ swelling ⦁ obvious deformity ⦁ arm is ABDUCTED + EXTERNALLY ROTATED ⦁ can palpate humeral head inferiorly ⦁ ** LOSS OF DELTOID CONTOUR** ⦁ => " SQUARED OFF SHOULDER " - appears box-like due to glenoid bone sticking out
humeral head can often be palpated anteriorly beneath the clavicle
remember that ABs are anterior and important for EXTERNAL appearance
(Anterior = ABduction + External rotation)
Anterior dislocation = MC type of shoulder dislocation
COMPLICATIONS
⦁ Axillary nerve injury (C5-C6 fibers)
⦁ Axillary artery injury
⦁ Rotator cuff damage
MC torn rotator cuff tendon = supraspinatus tendon
- is commonly torn with anterior shoulder dislocation
DIAGNOSIS
⦁ Xray - Axillary + Y view
- see humeral head ANTERIOR + INFERIOR to glenoid fossa
- may have
⦁ HILL-SACHS lesion = groove on humeral head = compression fracture from impact against glenoid
⦁ BANKART lesion = fracture of inferior rim of glenoid or injury to glenoid labrum - soft tissue injury
TREATMENT = * Manual Reduction *
- closed reduction followed by sling immobilization for 2-6 weeks
- PT
- but must rule out axillary nerve injury first (pinprick sensation over the deltoid)
Patient will present as → an 80-year-old woman arrives at the emergency room with severe right shoulder pain and immobility. She fell down the steps outside her house and landed on her right side two hours prior to presentation. On exam, her right arm is abducted and externally rotated. She has decreased sensation to touch over the lateral aspect of her right shoulder. Radiographs demonstrate an anterior shoulder dislocation.
POSTERIOR SHOULDER DISLOCATION
- POSTERIOR GLENOHUMORAL SHOULDER DISLOCATION
A dislocated shoulder occurs when the humerus separates from the scapula at the ** GLENOHUMORAL JOINT **
The shoulder joint has the greatest range of motion of any joint in the body, and is thus particularly susceptible to subluxation (partial dislocation) and dislocation.
Approximately half of major joint dislocations seen in emergency departments involve the shoulder.
MECHANISM:
⦁ forced ADDUCTION, + INTERNAL rotation
Posterior shoulder dislocations are rare and typically seen after ⦁ ** seizures ** = MC ⦁ ** electrocution ** ⦁ car accidents ⦁ trauma
SYMPTOMS ⦁ significant pain ⦁ limited ROM ⦁ swelling ⦁ obvious deformity ⦁ arm is held ADDUCTED + INTERNALLY rotated
Anterior shoulder = FLAT
Humeral head is prominent
the anterior shoulder will appear square with a flat coracoid process, and the humeral head may be palpated posteriorly beneath the acromion process.
DIAGNOSIS
⦁ Xray - Axillary + Y view
TREATMENT = * Manual Reduction *
- closed reduction followed by sling immobilization for 2-6 weeks
- PT
ANTERIOR HIP DISLOCATION
Dislocation occurs when the ball–shaped head of the femur comes out of the cup–shaped acetabulum set in the pelvis.
Dislocation of the hip is a common injury to the hip joint. This may happen to a varying degree.
MC in females
A dislocated hip is a condition that can either be congenital or acquired.
True orthopedic emergency!!
CAUSE
⦁ MC = Trauma
-MVA
- fall from height
Anterior hip dislocation = usually secondary to forced hip abduction
MC = ** POSTERIOR HIP DISLOCATION ** (90%)
CLINICAL MANIFESTATIONS
⦁ Anterior = may be externally rotated
COMPLICATIONS ⦁ ** Avascular Necrosis ** - reduced with early closed reduction < 6 hours ⦁ * Femoral nerve / artery injury * ⦁ DVT ⦁ Bleeding
FEMORAL NERVE INJURY
- loss of sensation over thigh
- weakness of quadriceps
- loss of knee DTR
FEMORAL ARTERY INJURY
- hematoma
- loss of pulses
- pallor
Vs Sciatic nerve injury (posterior hip dislocation complication) = loss of sensation in posterior leg/foot, loss of plantar flexion / dorsiflexion, loss of ankle DTR
DIAGNOSIS
⦁ Xray = 1st line!
- no fracture
- An anteriorly dislocated femoral head will appear LARGER than the contralateral side on AP film
TREATMENT
- emergent reduction under conscious sedation
⦁ Closed reduction within 6 hours (to prevent avascular necrosis)
CI to reduction = concurrent femoral neck fracture
⦁ PT
** If patient presents with hip pain, shortened leg, externally rotated + abducted = more likely hip fracture than anterior hip dislocation (not very common)
POSTERIOR HIP DISLOCATION
Dislocation occurs when the ball–shaped head of the femur comes out of the cup–shaped acetabulum set in the pelvis.
Dislocation of the hip is a common injury to the hip joint. This may happen to a varying degree.
MC in females
A dislocated hip is a condition that can either be congenital or acquired.
True orthopedic emergency!!
CAUSE
⦁ MC = Trauma
-MVA (ex: knee hits dashboard)
- fall from height
Posterior hip dislocations are most commonly associated with high-energy trauma such as motor vehicle collisions, falls from significant height, and high impact sports.
Artificial hips can dislocate with less force.
Posterior hip dislocations account for 90% of all hip dislocations.
Posterior dislocations occur when a large axial load is transmitted through a FLEXED KNEE
- ex: when the knee comes into contact with the dashboard in a crash
MC = ** POSTERIOR HIP DISLOCATION ** (90%)
Given the large amount of force needed to dislocate the femoral head, the majority of dislocations are associated with other injuries.
CLINICAL MANIFESTATIONS o Posterior ⦁ Severe hip pain ⦁ Inability to bear weight ⦁ hip deformity ⦁ limited ROM ⦁ ** Shortened leg ** ⦁ INTERNALLY ROTATED + ADDUCTED ⦁ with hip / knee slightly flexed
A detailed neurovascular exam should be conducted to rule out sciatic nerve injury.
COMPLICATIONS
⦁ ** Avascular Necrosis ** - reduced with early closed reduction < 6 hours
⦁ * Sciatic nerve injury * (or superior / inferior gluteal nerve injury)
⦁ DVT
⦁ Bleeding
⦁ Recurrent dislocations
⦁ Arthritis
SCIATIC NERVE INJURY
- loss of sensation in posterior leg + foot
- loss of plantar flexion + dorsiflexion
- loss of ankle DTR
DIAGNOSIS
⦁ Xray = 1st line!
- no fracture
- A posteriorly dislocated femoral head will appear SMALLER than the contralateral side on AP film
TREATMENT
- emergent reduction under conscious sedation
⦁ Closed reduction within 6 hours (to prevent avascular necrosis)
CI to reduction = concurrent femoral neck fracture
⦁ PT
BOXER’S FRACTURE
fracture of 5th metacarpal bone (may also include 4th metacarpal)
May have rotational deformity
May appear as if loss of knuckle
MECHANISM: usually occurs due to punching with clenched fist
If fracture is at the base of metacarpal bone, look for associated carpal injuries
TREATMENT
▪ Ulnar Gutter Splint
○ Any fracture > 25-30 degree angulation should be reduced
○ If remains > 40 degrees angulated = ORIF (surgery)
▪ Always check for bite wounds Augmentin
BENNET FRACTURE vs ROLANDO FRACTURE
fracture-dislocation of the base of the first metacarpal
Rolando fracture = comminuted fracture of first metacarpal base
COLLES vs SMITH FRACTURE
distal radius fracture
SMITH FRACTURE = caused by a direct blow to the dorsal forearm or falling onto FLEXED wrists
Smith = palmar (volar) angulation of distal radius bone fragment
- more dangerous due to more neurovascularity there!
COLLES FRACTURE = occurs as a result of falling onto wrists in EXTENSION
Colles = dorsal angulation of distal radius bone fragment
posterior fat pad sign or “sail sign” = occur in
humerus fractures
humerus fractures = most concerned about RADIAL nerve
TX = sugar tong splint (distal) coaptation splint (shaft) with ortho follow up in 24-48 hours
MONTEGGIA vs GALLEAZI FRACTURE
MUGGER
MUGR
Monteggia = ULNAR fracture with radial head dislocation
monteggiA = proximal (A) = near elbow
Galleazi = RADIAL fracture with ulnar dislocation
galleaZi = distal (Z) = near wrist
OSTEOARTHRITIS
OSTEOARTHRITIS = chronic disease due to ARTICULAR CARTILAGE DAMAGE + DEGENERATION
MC in weight bearing joints (knees / hips / cervical / lumbar spine v Narrowed joint space due to loss of articular cartilage v Sclerosis v Osteophyte formation v Chondrocyte inability to repair damaged cartilage ANATOMY - Joint = where 2 bones meet - Each bone at a joint is covered with its own articular cartilage - allows bone to glide over one another without damage / friction - Osteoarthritis = particular to synovial joints = which contain the synovium in addition to articular cartilage - Synovium = connective tissue / blood vessels / lymphatic vessels / type A cells (clear debris) / type B cells (create synovial fluid to help lubricate the 2 articular surfaces) OSTEOARTHRITIS = PROGRESSIVE LOSS OF ARTICULAR CARTILAGE ==> not much separating the 2 bones anymore ==> Friction ==> Inflammation ==> Pain Chondrocytes = maintains articular cartilage = especially important for weight-bearing joints (knees/hips) - provides elasticity and high-tensile strength Chondrocytes usually maintain a healthy balance between breaking down old cartilage (catabolic) and forming new cartilage (anabolic) With age / over time ==> increased breakdown of cartilage faster than build-up of cartilage Inflammation caused by friction, but also caused by increased cartilage debris that needs to be removed by type A cells ==> macrophages/lymphocytes that populate synovium ==> SYNOVITIS Eventually cartilage degrades away so much that it causes bone-on-bone friction. Bone starts to grow outward ==> BONE SPURS = ** OSTEOPHYTES ** § Heberden's nodes = DIP (HD) § Bouchard's nodes = PIP (BP)
RISK FACTORS FOR OSTEOARTHRITIS v **** AGE **** - Cartilage slowly degrades over a long period of time v Obesity v Trauma / previous joint injury v Inflammation v Mechanical stress
SYMPTOMS v *** ASYMMETRIC JOINT STIFFNESS *** (RA = symmetric) § Morning for < 1 hour (vs RA) § Then improves with motion, but worsens throughout the day v Pain § Sharp Ache or Burning sensation v Pain worse with prolonged activity v **CREPITUS** v **No Swelling** (unlike RA) - NO JOINT INFLAMMATION (unlike RA) The pain of OAworsens with useandimproves with rest. Versus rheumatoid arthritis which causes morning stiffness > 30 minutes and pain that improves with use. Commonly involves thehands, hips, and knees Pain is usually worsened by weight bearing and relieved by rest but can eventually become constant - As OA progresses, joint motion becomes restricted, and tenderness and crepitus or grating sensations develop - Osteophytes:bony projections that form along joints - Swelling of the distal interphalangeal (Heberden nodes) - Swelling of the proximal interphalangeal (Bouchard nodes) Osteoarthritis causes osteophytes, narrowing of the joint space, increased density of the subchondral bone, subchondral cyst formation, bony remodeling, and joint effusions - Knee OA commonly causes Baker's cyst
DIAGNOSIS v XRAY § Asymmetric joint space narrowing § Sclerosis § Osteophytes
- Synovial fluid analysis in OA reveals low levels of WBCs - Negative RF - Negative Anti-CCP Antibodies - Normal CRP / ESR - Medial knee cartilage loss OA ==> bow-legged stance or gait (valgus) - Lateral knee cartilage loss OA ==> varus stance or gait * ** OSTEOARTHRITIS DOES NOT AFFECT MCP JOINTS *** - Affects DIP, PIP and CMC (carpal-metacarpal) joints
TREATMENT v Lose weight v Exercise - avoid high impact exercises v Physical Therapy v NSAIDS / Acetaminophen § Acetaminophen = preferred initial tx for mild/mod OA in elderly due to bleeding risk § NSAIDS more effective v Steroid injections v Sodium hyaluronate v Glucosamine + Chondroitin v Surgery / replacement of joint
