As perhaps expected, perinatal outcomes are also poor and are inversely related to the maternal cardiac arrest-to-delivery interval. Even so, neonatal survival rate is 70 percent, but unfortunately, up to half of survivors sufer residual neurological impairment. In the Canadian study, 28 percent of infants were considered to be asphyxiated at birth (Kramer, 2012).
Various infections that are accompanied by endo-or exotoxin release can lead to sepsis syndrome. Although a feature of this syndrome includes activation of coagulation, seldom does sepsis alone cause massive procoagulant consumption. Escherichia coli bacteremia is frequently seen with antepartum pyelonephritis and puerperal infections, however, accompanying consumptive coagulopathy is usually not severe. Some notable exceptions are septicemia associated with puerperal infection or septic abortion caused by exoroxins released from infecting organisms such as group A Streptococcus pyogenes, Staphylococcus aureus, or Clostridium peringens, C sordelii, or C noyi (Herrera, 2016). Treatment of sepsis syndrome and septic shock is discussed in Chapter 47 (p. 921).
his severe-often lethal-form of consumptive coagulopathy is caused by micro thrombi in small blood vessels leading to skin necrosis and sometimes vasculitis. Debridement of large areas of skin over the extremities and buttocks frequently requires treatment in a burn unit. Purpura fulminans usually complicates sepsis in women with heterozygous protein C deiciencies and low protein C serum levels (Levi, 2010b). Note that homozygous protein C or S deiciency results in fatal neonatal purpurafulminans (Chap. 52, p. 1007).
Septic abortion-especially associated with the organisms just discussed-can incite coagulation and worsen hemorrhage, especially with midtrimester abortions. Indeed, sepsis syn 25 percent of abortion-related deaths (Saraiya, 1999). In the past, especially with illegal abortions, infections with C perin gens were a frequent cause of intense intravascular hemolysis at
Parkland Hospital (Pritchard, 1971). More recently, however, septic abortions from infection with C sordelii have emerged as important causes (Chap. 18, p. 351).
cular coagulation even in the absence of sepsis. Ben-Ami and associates (2012) described a 1.6-percent incidence in 1249 evacuation. Two thirds were done for fetal demise, which may have been contributory to coagulopathy. Another source of intense coagulation is from instillation of hypertonic solutions to efect mid trimester abortions. These are not commonly used currently for pregnancy terminations. he mechanism is thought to initiate coagulation by thromboplastin release into maternal circulation from the placenta, fetus, and decidua by the necrobiotic efect of hypertonic solutions (Burkman, 1977).
Recognition of obstetrical hemorrhage severity is crucial to its management. Visual estimation of blood loss, especially when excessive, is notoriously inaccurate, and true blood loss is often two to three times the clinical estimate. Consider also that in obstetrics, part and sometimes even all of the lost blood may be concealed. Estimation is further complicated in that peripartum hemorrhage also includes the pregnancy-induced augmented blood volume. After pregnancy hypevolemia is lost at delivery, blood loss can be estimated by calculating 500 mL loss for each 3 volume percent drop in hematocrit. he hematocrit nadir depends on the speed of resuscitation with intravenous crystalloids. ith acute blood loss, the real-time hematocrit is at its maximum whenever measured in the delivey, operating, or recovey room.