pre-eclampsia & severe pre-eclampsia

중증 전자간증의 진단기준이 뭐냐?! 라고 물어보시기에... 찾아봤습니다. 만?! 음... 명확하게 이게 severe pre-eclampsia다! 라고 말해주지는 않는군요... 아래 indication중 하나만이라도 있으면 되는걸까요...

Mild preeclampsia is diagnosed when:

• Pregnancy is greater than 20 weeks
• Blood pressure is greater than 140 systolic or 90 diastolic
• 0.3g of protein is collected in a 24-hour urine sample, or persistent 1+ protein measurement on urine dipstick
• There are no other signs of problems with the mother or the baby

Severe preeclampsia is a more serious problem. Diagnosis of severe preeclampsia requires the basic features of mild preeclampsia as well as some indication of additional problems with either the mother or the baby. Thus, one of the following findings is also necessary for a diagnosis of severe preeclampsia:

• Signs of central nervous system problems (severe headache, blurry vision, altered mental status)
• Signs of liver problems (nausea and/or vomiting with abdominal pain)
• At least twice the normal measurements of certain liver enzymes on blood test
• Very high blood pressure ( greater than 160 systolic or 110 diastolic)
• Thrombocytopenia (low platelet count)
• Greater than 5g of protein in a 24-hour sample
• Very low urine output (less than 500mL in 24 hours)
• Signs of respiratory problems (pulmonary edema, bluish tint to the skin)
• Severe fetal growth restriction
• Stroke

*Williams Obstetrics

 Preeclampsia

As shown throughout this chapter, preeclampsia is best described as a pregnancy-specific syndrome that can affect virtually every organ system. As discussed, although preeclampsia is much more than

simply gestational hypertension with proteinuria, appearance of proteinuria remains an important objective diagnostic criterion. Proteinuria is defined by 24-hour urinary protein excretion exceeding

300 mg, a urine protein:creatinine ratio of /0.3, or persistent 30 mg/dL (1& dipstick) protein in random urine samples(Lindheimer and colleagues, 2008a). None of these values are sacrosanct. Urine concentrations vary widely during the day, and so too will dipstick readings. Thus, assessment may even show a 1&to 2&value from concentrated urine specimens from women who excrete 300 mg/day. As discussed on page 719, it is likely that determination of a spot urine:creatinine ratio will be a suitable replacement for a 24-hour measurement. As emphasized in Table 34-1, the more severe the hypertension or proteinuria, the more certain is the diagnosis of preeclampsia as well as its adverse outcomes. Similarly, abnormal laboratory findings in tests of renal, hepatic, and hematological

function increase the certainty of preeclampsia. Persistent premonitory symptoms of eclampsia, such as headache and epigastric pain, also increase the certainty. That said, some women may have atypical preeclampsia with all aspects of the syndrome, but without hypertension or proteinuria, or both (Sibai and Stella, 2009).

Indicators of Severity of Preeclampsia

The markers listed in Table 34-1 are also used to classify the severity of the preeclampsia syndrome. Many use the American College of Obstetricians and Gynecologists dichotomous “mild” and “severe.” Thus, in many classifications, criteria are given for the diagnosis of “severe” preeclampsia, and the alternate classification is either implied or specifically termed “mild,” “less severe,” or “nonsevere” (Alexander and associates,2003; Lindheimer and co-workers, 2008b). These are used because

there are no generally agreed-upon criteria for “moderate”preeclampsia—an elusive third category. Criteria listed in Table 34-2 are categorized as “severe” versus “nonsevere.” Parenthetically,

the latter includes “moderate” and “mild,” although they are not specifically defined. 

Headaches or visual disturbances such as scotomata can be premonitory symptoms of eclampsia. Epigastric or right upper quadrant pain frequently accompanies hepatocellular necrosis, ischemia, and edema that stretch Glisson capsule. This characteristic pain is frequently accompanied by elevated serum hepatic transaminase levels. Thrombocytopenia is also characteristic of worsening preeclampsia. It probably is caused by platelet activation and aggregation as well as microangiopathic hemolysis induced by severe vasospasm. Other factors indicative of severe preeclampsia include renal or cardiac involvement as well as obvious fetal-growth restriction, which attest to its duration. The more profound these signs and symptoms, the less likely it is that they can be temporized, and the more likely it is that delivery will be indicated. The differentiation between nonsevere and severe gestational hypertension or preeclampsia can be misleading because what might be apparently mild

disease may progress rapidly to severe disease.