Chapter 153 - Compartment syndrome and venous gangrene Flashcards
Phlegmasia definition
Greek - phlegma = inflammation
Cerulea definition
Latin - caeruleus = dark blue
Dolens definition
Latin - dolens = hurting/suffering
Alba definition
White
Difference between Phlegmasia cerulea dolens and Phlegmasia alba dolens
PCD = IFDVT without adequate drainage PAD = IFDVT with some drainage allowing venous return before derm and subdermal blood cause cyanosis
Cause of cyanosis in PCD
Increase in deoxyhemoglobin in subdermal tissue
Cause of gangrene in PCD
Small and microvessel thrombosis leading to tissue hypoperfusion
Hemorrhagic bullae in PCD
poor prognosis
underlying tissue necrosis
associated with venous limb gangrene
Treatment for PAD and PCD
1) therapeutic anticoagulation
2) wrap limbs from toes to inguinal crease
3) TPA or open thrombectomy within 24 hr
Venous limb gangrene definition
soft tissue necrosis in a limb with DVT
Phases of venous limb gangrene as per Tagariello
1) Phlegmasia alba dolens
2) phlegmasia cerulea dolens
3) venous limb gangrene
Association of venous limb gangrene with other conditions
Almost all have either
1) cancer
2) serious conditions complicating proximal DVT
Serious conditions that precipitate venous gangrene
1) warfarin necrosis
2) HIT
3) DIC
4) sepsis
5) purpura fulminans
6) pressor use
7) acute hepatic dysfunction
Heparin induced thrombocytopenia epidemiology
2x in women than men
Mortality of HIT
20-30%
Types of HIT
Type I = innocuous benign 2 days after heparin occurs in 10-30%
Type II = antibody mediated disorder need to cut off heparin, warfarin and use others
Mechanism of HIT
IgG bind heparin to PF4 –> prothrombotic state
Timing of HITT
1) 5-10 days after UFH infusion
2) can be secondary response which is immediate
Delayed onset HIT
HIT sera activating platelets in absence of heparin
heparin-independent activation of platelets
Warfarin-induced skin necrosis targets
1) central skin
2) subcutaneous tissue over adipose tissue (breast, thigh)
INR in warfarin-induced skin necrosis
supra-therapeutic
due to rapid depletion of Factor VII
Thrombotic complication rate of HIT if untreated
50-89%
White clot syndrome
Fibrin thrombus causing large vessel occlusion
Half life of Protein C
9 hours
Half life of Factor VII
5 hours
Prothrombin half life
60 hours
Treatment of warfarin induced skin necrosis in HIT
1) vitamin K
2) DOAC
Cancer-associated DIC with venous limb gangrene key points
When patient with DVT gets a rise in platelet after heparin treatment, cancer DIC suspicious
Warfarin avoided
Disseminated intravascular coagulation mechanism
1) platelet aggregation
2) pathologic thrombin generation
3) intravascular deposition of fibrin
4) endogenous fibrinolysis and protein C and S malfunction
Diagnosis of DIC
1) underlying associated disease
2) prolonged thrombin time and partial thromboplastin time
3) plt < 100 or rapid fall
4) presence of fibrin/fibrinogen degradation product
5) low antiithrombin III
Diseases associated with DIC
1) bacterial endotoxin
2) tissue injury
3) shock
4) metabolic acidosis
5) tumor-derived procoagulant microparticles
Purpura fulminans define
Symmetric peripheral gangrene
1) no large vein thrombosis
2) skin and soft tissue necrosis
Causes of purpural fulminans
1) septicemia
2) heart failure
3) metabolic acidosis
4) shock
5) pressor support
Most common infectious cause of purpura fulminans
1) Neisseria meningitides 69% (children)
2) streptococcus 13% (elderly)
Fasciotomy in venous obstruction and disease key points
No clear evidence
may improve healing may worsen
Thrombus removal most important
Can lead to chronic venous insufficiency due to disrupted calf pump
