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Uterine atony is the most common cause of PPH and occurs in one in every twenty deliveries.
The most common definition of PPH is an estimated blood loss of greater than or equal to 500 ml after vaginal birth, or greater than or equal to 1000 ml after Cesarean delivery.
Endometritis in the postpartum period is most closely related to the mode of delivery. Uterine fundal tenderness is commonly observed in patients with endometritis. Endometritis can be found in less than 3% of vaginal births and this is contrasted by a 5-10 times higher incidence after Cesarean deliveries. Bacterial isolates related to postpartum endometritis are usually polymicrobial resulting in a mix of aerobes and anaerobes in the genital tract. The most causative agents are Staphylococcus aureus and Streptococcus. Factors related to increased rates of infection with a vaginal birth include prolonged labor, prolonged rupture of membranes, multiple vaginal examinations, internal fetal monitoring, removal of the placenta manually and low socioeconomic status.
Hormonal interventions for preventing lactation appear to predispose to thromboembolic events, as well as a significant risk of rebound engorgement. Bromocriptine, in particular, is associated with hypertension, stroke and seizures. The safest method to suppress lactation is breast binding, ice packs and analgesics. The patient should avoid breast stimulation or other means of milk expression, so that the natural inhibition of prolactin secretion will result in breast involution.
Breastfeeding: Benefits to the mother include increased uterine contraction due to oxytocin release during milk let down and decreased blood loss. Breastfeeding is associated with a decreased incidence of ovarian cancer. Some studies have reported a decreased incidence of breast cancer.
The patient has a classic picture of mastitis that is usually caused by streptococcus bacteria from the baby’s mouth. Mastitis is easily treated with antibiotics. The initial choice of antimicrobial is influenced by the current experience with staphylococcal infections at the institution. Most are community-acquired organisms, and even staphylococcal infections are usually sensitive to penicillin or a cephalosporin. If the infection persists, an abscess may ensue which would require incision and drainage. However, this patient’s presentation is that of simple mastitis. There is no need for the mother to stop breastfeeding because of the mastitis.
With delivery, there is a rapid and profound decrease in the levels of progesterone and estrogen, which removes the inhibitory influence of progesterone on the production of alpha-lactalbumin by the rough endoplasmic reticulum. The increased alpha-lactalbumin serves to stimulate lactose synthase and ultimately to increase milk lactose. Progesterone withdrawal allows prolactin to act unopposed in its stimulation of alpha-lactalbumin production. This may take up to two days.
Candida of the nipple is associated with severe discomfort and pain. All the other above organisms are associated with classic mastitis and do not usually cause intense nipple pain. Localized candida of the nipple may be treated with an antifungal, topical medication such as clotrimazole or miconazole cream. The treatment plan may include a topical antibiotic ointment because nipple fissures can concurrently present with candida of the nipples, and S. aureus is significantly associated with nipple fissures. Either a triple antibiotic ointment or mupirocin can be prescribed. A topical steroid cream can be used to facilitate healing for cases in which the nipples that are very red and inflamed. Every treatment regimen must include the simultaneous treatment of the mother and baby. Oral nystatin is the most common treatment for the baby, followed by oral fluconazole.
While prolactin is responsible for milk production, oxytocin is responsible for milk ejection. Production of oxytocin is stimulated by suckling which works better than a breast pump for stimulating the secretion of milk.
     
 
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