Placenta previa

 Obstetrics  Comments Off
Feb 082011
 
With placenta previa, the placenta is implanted in the lower uterine segment, where it encroaches on the internal cervical os. This disorder, one of the most common causes of bleeding during the second half of pregnancy, occurs in approximately 1 in 200 pregnancies, more commonly in multigravidas than in primigravidas. Generally, termination of pregnancy is necessary when placenta previa is diagnosed in the presence of heavy maternal bleeding. Maternal prognosis is good if hemorrhage can be controlled; fetal prognosis depends on gestational age and amount of blood lost.

Causes
With placenta previa, the placenta may cover all (total, complete, or central), part (partial or incomplete), or a fraction (margin or low-lying) of the internal cervical os. (See Three types of placenta previa.) The degree of placenta previa depends largely on the extent of cervical dilation at the time of examination because the dilating cervix gradually uncovers the placenta. Although the specific cause of placenta previa is unknown, factors that may affect the site of the placenta’s attachment to the uterine wall include:
  • defective vascularization of the decidua
  • multiple pregnancy (the placenta requires a larger surface for attachment)
  • previous uterine surgery
  • multiparity
  • advanced maternal age.
With placenta previa, the lower segment of the uterus fails to provide as much nourishment as the fundus. The placenta tends to spread out, seeking the blood supply it needs, and becomes larger and thinner than normal. For unknown reasons, eccentric insertion of the umbilical cord often develops. Hemorrhage occurs as the internal cervical os effaces and dilates, tearing the uterine vessels.

Signs and symptoms
Placenta previa usually produces painless third-trimester bleeding (typically the first complaint). Because of the placenta’s location, various malpresentations occur that interfere with proper descent of the fetal head. (However, the fetus remains active, with good heart tones.) Complications of placenta previa include shock or maternal and fetal death.

Diagnosis

Special diagnostic measures that confirm placenta previa include:
  • transvaginal ultrasound scanning for placental position
  • pelvic examination, performed only immediately before delivery. In most cases, only the cervix is visualized. Continue reading »
VN:F [1.9.20_1166]
Rating: 6.0/10 (2 votes cast)
VN:F [1.9.20_1166]
Rating: +1 (from 1 vote)

Social Share Toolbar

Jan 152011
 
Also called consumption coagulopathy and defibrination syndrome, disseminated intravascular coagulation (DIC) occurs as a complication of diseases and conditions that accelerate clotting. This accelerated clotting process causes small blood vessel occlusion, organ necrosis, depletion of circulating clotting factors and platelets, and activation of the fibrinolytic system—which, in turn, can provoke severe hemorrhage.
Clotting in the microcirculation usually affects the kidneys and extremities but may occur in the brain, lungs, pituitary and adrenal glands, and GI mucosa. Other conditions, such as vitamin K deficiency, hepatic disease, and anticoagulant therapy, may cause a similar hemorrhage.
DIC is generally an acute condition but may be chronic in cancer patients. The prognosis depends on early detection and treatment, the severity of the hemorrhage, and treatment of the underlying disease or condition.
Causes
DIC may result from:
  • infection (the most common cause of DIC), including gram-negative or gram-positive septicemia; viral, fungal, or rickettsial infection; and protozoal infection (falciparum malaria)
  • obstetric complications, such as abruptio placentae, amniotic fluid embolism, and retained dead fetus
  • neoplastic disease, including acute leukemia and metastatic carcinoma
  • disorders that produce necrosis, such as extensive burns and trauma, brain tissue destruction, transplant rejection, and hepatic necrosis.
Other causes include heatstroke, shock, poisonous snakebite, cirrhosis, fat embolism, incompatible blood transfusion, cardiac arrest, surgery necessitating cardiopulmonary bypass, giant hemangioma, severe venous thrombosis, and purpura fulminans.
It isn’t clear why such disorders lead to DIC; nor is it certain that they lead to it through a common mechanism. In many patients, the triggering mechanisms may be the entrance of foreign protein into the circulation and vascular endothelial injury.
Results of accelerated clotting
Regardless of how DIC begins, the typical accelerated clotting results in generalized activation of prothrombin and a consequent excess of thrombin. Excess thrombin converts fibrinogen to fibrin, producing fibrin clots in the microcirculation.
This process consumes exorbitant amounts of coagulation factors (especially fibrinogen, prothrombin, platelets, and factor V and factor VIII), causing hypofibrinogenemia, hypoprothrombinemia, thrombocytopenia, and deficiencies in factor V and factor VIII. Circulating thrombin activates the fibrinolytic system, which lyses fibrin clots into fibrin Continue reading »
VN:F [1.9.20_1166]
Rating: 10.0/10 (1 vote cast)
VN:F [1.9.20_1166]
Rating: +1 (from 1 vote)

Social Share Toolbar

Dec 262010
 
Mastitis (parenchymatous inflammation of the mammary glands) and breast engorgement (congestion) are disorders that may affect lactating females.

Mastitis occurs postpartum in about 1% of patients, mainly in primiparas who are breast-feeding. It occurs occasionally in nonlactating females and rarely in males. All breast-feeding mothers develop some degree of engorgement, but it’s especially likely to be severe in primiparas. The prognosis for both disorders is good.
Causes
Mastitis develops when a pathogen that typically originates in the nursing infant’s nose or pharynx invades breast tissue through a fissured or cracked nipple and disrupts normal lactation. The most common pathogen of this type is Staphylococcus aureus; less commonly, it’s Staphylococcus epidermidis or beta-hemolytic streptococci. Rarely, mastitis may result from disseminated tuberculosis or the mumps virus. Predisposing factors include a fissure or abrasion on the nipple; blocked milk ducts; and an incomplete let-down reflex, usually due to emotional trauma. Blocked milk ducts can result from a tight bra or prolonged intervals between breast-feedings.
Causes of breast engorgement include venous and lymphatic stasis and alveolar milk accumulation.
Signs and symptoms
Mastitis may develop anytime during lactation but usually begins 3 to 4 weeks postpartum with fever (101° F [38.3° C] or higher in those with acute mastitis), malaise, and flulike symptoms. The breasts (or, occasionally, one breast) become tender, hard, swollen, and warm. Unless mastitis is treated adequately, it may progress to breast abscess.
Breast engorgement generally starts with onset of lactation (day 2 to day 5 postpartum). The Continue reading »
VN:F [1.9.20_1166]
Rating: 0.0/10 (0 votes cast)
VN:F [1.9.20_1166]
Rating: 0 (from 0 votes)

Social Share Toolbar