Diagnosis
Differential diagnosis
Many conditions mimic or may be mistaken for warfarin necrosis, including pyoderma gangrenosum or necrotizing fasciitis. Warfarin necrosis is also different from another drug eruption associated with warfarin, purple toe syndrome, which usually occurs three to eight weeks after the start of anticoagulation therapy. No report has described this disorder in the immediate postpartum period in patients with protein S deficiency. Prevention
Vitamin K1 can be used to reverse the effects of warfarin, and heparin or its low molecular weight heparin (LMWH) can be used in an attempt to prevent further clotting. None of these suggested therapies have been studied in clinical trials. Heparin and LMWH act by a different mechanism than warfarin, so these drugs can also be used to prevent clotting during the first few days of warfarin therapy and thus prevent warfarin necrosis (this is called bridging). Treatment
The first element of treatment is usually to discontinue the offending drug, although there have been reports describing how the eruption evolved little after it had established in spite of continuing the medication.Based on the assumption that low levels of protein C are involved in the underlying mechanism, common treatments in this setting include fresh frozen plasma or pure activated protein C.Since the clot-promoting effects of starting administration of 4-hydroxycoumarins are transitory, patients with protein C deficiency or previous warfarin necrosis can still be restarted on these drugs if appropriate measures are taken.
Rates in various medical conditions
Fetal entities:
First twin 17–30%
Second twin 28–39%
Stillborn 26%
Prader–Willi syndrome 50%, Werdnig–Hoffman syndrome 10%
Smith–Lemli–Opitz syndrome 40%
Fetal alcohol syndrome 40%
Potter anomaly 36%
Zellweger syndrome 27%
Myotonic dystrophy 21%, 13 trisomy syndrome 12%
18 trisomy syndrome 43%
21 trisomy syndrome 5%
de Lange syndrome 10%
Anencephalus 6–18%, Spina bifida 20–30%
Congenital hydrocephalus 24–37%
Osteogenesis imperfecta 33.3%
Amyoplasia 33.3%
Achondrogenesis 33.3%
Amelia 50%
Craniosynostosis 8%
Sacral agenesis 30.4%
Arthrogriposis multiplex congenita 33.3
Congenital dislocation of the hip 33.3%
Hereditary sensory neuropathy type III 25%
Centronuclear myopathy 16.7%
Multiple pituitary hormone deficiency 50%
Isolated pituitary hormone deficiency 20%
Ectopic posterior pituitary gland 33.3%
Congenital bilateral perisilvian syndrome 33.3
Symmetric fetal growth restriction 40%
Asymmetric fetal growth restriction 40%
Nonimmune hydrops fetalis 15%
Atresia ani 18.2%
Microcephalus 15.4%
Omphalocele 12.5%
Prematurity 40%
Placental and amniotic fluid entities:
Amniotic sheet perpendicular to the placenta 50%
Cornual–fundal implantation of the placenta 30%
Placenta previa 12.5%
Oligohydramnios 17%
Polyhydramnios 15.8%
Maternal entities:
Uterus arcuatus 22.6%
Uterus unicornuatus 33.3%
Uterus bicornuatus 34.8%
Uterus didelphys 30–41%
Uterus septus 45.8%
Leiomyoma uteri 9–20%
Spinal cord injury 10%
Carriers of Duchenne muscular dystrophy 17%
Combination of two medical entities:
First twin in uterus with two bodies 14.29%
Second twin in uterus with two bodies 18.52%.Also, women with previous Caesarean deliveries have a risk of breech presentation at term twice that of women with previous vaginal deliveries.The highest possible probability of breech presentation of 50% indicates that breech presentation is a consequence of random filling of the intrauterine space, with the same probability of breech and cephalic presentation in a longitudinally elongated uterus. Types
Types of breech depend on how the babys legs are lying.