VENOUS DISORDERS
Venous thrombosis/ DVT
= clotting in vein
Pathophysiology
Exact cause is unclear
genetics
hypercoagulability - Factor V
More common in lower extremities
Virchow Triad
Stasis of blood: cause by immobility (Bed rest, prolonged standing/sitting, extensive travel)
Vessel Wall injury (Endothelial injury): caused by trauma (Fractures, contusions), central venous catheterization, vascular devices (PICC, central lines, pacemaker wires), IV medications, cancer therapy (Hormonal, chemotherapy, or radiation)
Altered coagulation: caused by estrogen-containing oral contraceptive or hormone replacement, cancer (Secretes procoagulants), smoking, dehydration, hypercoagulable states, late stages of pregnancy, and the postpartum period
Clinical Manifestations
difference in leg circumference
Erythema
Warmth to extremity
tenderness to touch
Low-grade fever
Induration of vessel wall
Dilated veins
Assessment / Risks
history of varicose veins
hypercoagulable states (covid-19)
cancer
cardiovascular disease
recent major surgery or injury
BMI > 35
immobility
Old age
women taking oral contraceptives or hormone replacement therapy
Prevention
compression stocking (TEDs)
intermittent compression devices (SCDs)
exercise (walking)
Anticoagulation medications
Medical Management
Goal:
prevent clot growth
reduce risk of dislodgement
prevent reoccurrence
Pharmacology:
heparin
unfractionated
Low-molecular-weight (LMWH)
Direct thrombin inhibitor
thrombolytic therapy
oral anticoagulants
Surgical:
thrombectomy - take clot out
IVC filter
Nursing Management
Monitor labs based on drugs prescribed
mild analgesic for pain control
Monitor for spontaneous bleeding
Promote ambulation
Adminster reversal agent if appropriate
TEDS with ambulation
Active and passive exercise
Monitor for thrombocytopenia
compression therapy
Elevate extremity
Avoid sitting for long periods
Inferior Vena Cava (IVC) Filter
saves from heart attack
filter sits in inferior vena cava
looks like a scalp scratcher
Varicose Veins
= dilation of superficial veins
Varicosities
Pathophysiology
primary
DOes not involve deep vein
Pt. may be asymptomatic
image disturbance
Secondary
result of an obstructed deep vein
Who’s who at Risk
hereditary weak veins
pregnant women
Prior DVT
Old age
BMI . 30
Multigravida woman
Clinical Manifestations
Dull aches
muscle cramps
Lower extremity muscle
fatigue
Ankle edema
“heavy” legs
NIght-time leg cramps
Assessment/Diagnosis
Venous Duplex Scan: for deep veins
locates reflux + measures severity
Air plethysmography: progressive
Measures changes in venous blood volume
Prevention
Avoid activities that increase venous hypertension
tight cloths
crossing legs
sitting or standing for long periods of time
Frequent position changes
Elevate legs
Promote Circulation
walking (heel-toe stepping)
weight reduction
Surgical/Medical Management
Ligation & Strippping
Sclerotherapy - for superficial veins
Ablation
ECT in the vein - gets ride of diseased veins
Postoperative Nursing Management
mobility is best to promote circulation
walk, increase activity as tolerated
compression stockings X 1-2 weeks
elevated foot of bed
Avoid strenuous activity
analgesics for pain management
monitor surgical dressings
patient teaching on incision care
nurse alert: nerve damage
Chronic Venous Insufficiency
= Veins are chronically incompetent
Postphlebitic syndrome
venous valve injury results in an incompetent valve and reverse venous flow
fluid, plasma, and red blood cells leak inot the interstitial tissue
edema forms around ankles and/or lower legs
staining of skin occurs as red bloods cells break down, releasing hemosiderin
subcutaneous tissue becomes firm and fibrotic
loss of elasticity in the skin and subcutaneous tissue results
tissue becomes vulnerable to trauma and ulcer formation
Clinical Manifestations & NUrsing Assessment
edema
hemosiderosis
varicosities
telangiectasias (spider-veins)
warmth
post-thrombolyic syndrome
chronic edema
altered pigmentation
pain
dermatosclerosis
aches & heaviness in evening
Management
leg elevation
compression stocking use
provide symptom relief
encourage walking
Avoid prolonged sitting & standing
Vascular ulcers
Patho
most severe complication of CVI
treatment is dependent on type of ulcer
result of:
increased venous pressure
external trauma
ischemia secondary to atherosclerosis
Clinical Manifestations & assessment
venous ulcers
located in gaiter area
small to large
superficial
excessive drainage
damage to surrounding skin
Arterial Ulcers
located on toe tips and in toe webs
small lesions
digital gangrene
Management
pharmacology
infected = antibiotics
would cleaning & debridement
arterial - keep dry, Do not debride
Venous (with necrosis) - clean & Debride
Wound dressings
stimulated healing
tissue-engineered human skin
stimulates growth factor
painless
hyperbaric oxygenation
adjunctive therapy
used when wound is not responding to standard treatment is not responding to tandard treatment
decreases edema, kills bacteria, increases oxygen to hypoxic wounds
compression
promote edema reduction
unna boot/compression bandages
Lymphatic disorders
Lymphangitis
acute inflammation
secondary to infection in extremity
red streaks extending from wound
Lymphadenitis
enlarged, red, tender lymph nodes
can necrose and develop into abscesses
commonly in groin, axilla, cervical region
Lymphedema/Elephanntiasis
patho
classification:
Primary - congenital malformation
Secondary - Acquired obstruction
increase in lymph secondary to a obstructed lymph vessel
axillary node dissection
varicose veins
chronic thrombophlebitis
chronic lymphangitis
soft & pitting progresses to firm, nonpitting & resistant to treatment
Clinical Manifestations & Assessments
early stage
soft, pliable tissue
late stage
thick, firm tissue
stemmer sign
diagnosis is made through symptom evaluation
Early diagnosis prevents tissue damage
Stemmer Sign
how to assess
try to pinch and lift a skin fold at the base of the second toe (or finger)
positive stemmer sign
you cannot lift/pinch a thin fold of skin, only a thick “pad, because the skin is irdurated.
negative stemmer sign
you can pinch and lift a normal think skin fold.
What it indicates
dermal and subcutaneous fibrosis
Medical management
Medical
pharmacologic therapy
AVOID diuretics
exercise & compression
active & passive ROM exercises
external compression devices
lymphatic drainage massage
surgical management
excision & Skin grafting
relocation of lymphatic vessels
Nursing
management of skin graft & flap
extremity elevation
frequent monitoring for complications:
Flap necrosis
hematoma
abscess
cellulitis
Patient Education
Cellulitis
Patho
breakdown in normal skin protective barrier allowing for entry of bacteria
Clinical Manifestations & Assessment
acute swelling
locak erythema
pain
fever
chills
sweating
skin dimpling
lymph node swelling
Medical Management
mild -oral antibiotic therapy
severe - IV antibiotics
Proper identification of entry point on skin
Nursing Management
extremity above heart level
warm and moist heat to site
Pt education on episode recurrence prevention