Test 3: Pathologies Related to the Knee Flashcards
what is deep vein thrombosis
partial or complete occlusion of a vein by a clot
etiology of DVT
50% is unknown
other half involve conditions that have at least 2 of the following: venous stasis, hypercoagulability, or damage to the venous wall
conditions that may be more likely to produce DVT
prior DVT
hx of cancer/CHF/lupus
major infection/sx/trauma
chemotherapy
immobility
pregnancy
use of oral contraceptives/hormone therapy
genetic clotting disorder (i.e. Willebrand)
>60 years old
incidence and prevalence of DVT
3rd most common cardiovascular disease
most common in deep LE veins
most preventable cause of hospital related deaths
most common cause of readmissions and death after THA/TKA
common veins that develop DVT
popliteal
femoral
tibial
peroneal
pathogenesis of DVT
greater exposure of platelets and clitting factors to a damaged venous wall
fibrin, leukocytes, and erythrocytes adhere and form thrombosis
what could be done to prevent/treat DVT
early and regular exercise
anticoagulants
compression socks
intermittent pneumatic compression devices
avoid SAD
eliminate persistent smoking/drinking
caution with early and regular exercise for DVT
as a prevention it is great
be cautious/wait for anticoagulant therapy to take effect to avoid a PE from motion with treatment if a clot is already present; DO NOT WANT TO MOVE CLOT
what might be included in pt history if they have DVT
50% of individuals are asymptomatic in early stages
typically a gradual onset of a dull ache/tightness/calf pain
CDR for DVT include what factors
edema; possibly pitting in 70% of pts
increase calf girth
calf pain/tenderness in 50% of pts; worse with walking; relief lessens as condition worsens
possible redness/warmth
PT implications for DVT
referral to MD per CDR
urgent referral if <17% with less than 2 CDRs
emergency if 75% and 3 or more CDRs
do not want to miss
may lead to pulmonary embolism
etiology/pathogenesis of Pulmonary Embolism
DVT that moves and lodges into the smaller artery supplying the lungs
S&S of pulmonary embolism
often non specific… “the great masqueraders”
SOB/wheezing/rapid breathing may be only symptom
pleuritic chest pain; sudden/sharp chest pain that can be exacerbated by:
-deep inhale
-cough
-mechanical pain may occur due to lung fascia attachment to ribs/thoracic vertebrae (i.e. trunk, UE, or rib motion)
other/possibly less common S&S of pulmonary embolism
blood with cough
painful breathing at rest
fainting
tachycardia and palpitations
referral for PE
urgent of <2/6
emergency if greater than or equal to 2/6
what is peripheral artery disease
ischemia leading to symptoms in the most distal area from the blocked artery; most often on calf
where is peripheral artery disease most common
most often in LEs
risk factors for peripheral artery disease
over 45
family hx of MI or sudden death before 55
recent or current smoker
physical inactivity
metabolic syndrome
pathogenesis of peripheral artery disease
artherosclerosis or plaque build up in aa that also promotes vascular constriction thus further limiting circulation
symptoms begin once 50% of a is narrow
S&S of intermittent claudication with peripheral artery disease
LE pain; most often in calf with similar amount of activity and elevated positions
can be uni or bilateral depending on where blockage is
relief with rest and dependent position
often described as cramping but may be weakness/pressure/aching
S&S of peripheral artery disease distal to the ischemic area
loss of pulses
TTP
muscle atrophy/weakness
loss of hair
cool/bluish skin
bruit on auscultation
possible necrosis/wound
how might pain act in the presence of severe ischemia
pain at rest
can cause sleep interruptions
steps for ankle brachial test
take BP at posterior tibial a and brachial a (on both sides)
just looking at the ratio of the ankle systolic/brachial systolic
concerning levels for ankle brachial test
less than 0.9 is bad
the lower the worse the dieases
over 1.4 may indicate poorly compressed vv due to hardened aa from artherosclerosis
how to differentiate calf pain due to PAD vs stenosis
bicycle test
start in an upright position and then after a few minutes have them lean forward
if pain goes away with forward bend then it indicates stenosis
if it doesnt go away it can indicate the pain is from the muscles not getting enough bloodflow
referral for peripheral artery disease
urgent to vascular MD
what is osteochondritis dissecans
damage to subchondral bone
incidence/prevalence of osteochondritis dissecans
rare
most common in younger boys through early adulthood
males > females
most common in medial femoral condyle and talus
etiology of osteochondritis dissecans
mostly unknown
joint rotational or shearing trauma like a sprain
pathogenesis of osteochondritis dissecans
ischemia (AVN) then separation of subchondral bone from convex and WBing end bones
overlying articular cartilage can remain viable
clinical manifestations/S&S of osteochondritis dissecans
may be asymptomatic with incidental imaging
is symptomatic = persistent pain; not progressing as expected
may progress into severe pain if fragment displaces with joint locking/catching/swelling
S&S of hypermobility/instability of involved ligament but with persistent ARJC-like symptoms
what specific S&S may occur that mimic hypermobility/instability/ARJC with osteochondritis dissecans
ROM limited and painful especially with ext
resisted MMT = weak/painful especially at end range ext
compression likely +
TTP over femoral condyle
referral for osteochondritis dissecans
urgent
what is reactive arthritis (aka)
aka Reiter’s syndrome
acute infection that is at a site remote from the primary infection (septic arthritis is infection AT SITE of primary infection)
risk factors for reactive arthritis
IV drug use
high sexual activity
infrequent pelvic exams
weaker immune system
incidence/prevalence of reactive arthritis
targets larger joints in the LE and primarily the knee and ankle
etiology of reactive arthritis
most commonly from a respiratory infection
could also be from GI, genitourinary, and colon infections
pathogenesis of reactive arthritis
bacteria stimulates antibody and protein factor production that creates inflammation and tissue damage leading to an arthritic joint
clinical manifestations/S&S of reactive arthritis
begins 1-4 weeks after a recent infection
infection S&S
autoimmune S&S
may progress to incapacitating illness
osteochondritis dissecans can take up to 2-3 years to revascularize and heal due to these stresses/stability
higher BMI
deficient passive restraints
M imbalances
impaired proprioception
Why is it important to protect the joint after having osteochondritis dissecans
want to avoid separation of bone and articular cartilage into the joint
aka joint mouse
common at the knee
loss of joint surface congruency
how to treat a stable osteochondritis dissecans lesion vs non stable
stable = non operative; smae Rx as instability/ARJC
sx required for resurfacing or fixation that is needed for unstable lesions
observation / vitals of those with reactive arthritis
redness
swelling
fever
what might you find with scan anf BE exam for reactive arthritis
like ARJC
TTP and warm
swollen and tender lymph nodes
referral for reactive arthritis
urgent
