The nurse recognizes that a woman is in true labor when she states…., and finds that her cervix has dilated and effaced on examination.

A. 2+ Deep Tendon Reflexes. A 2+ deep tendon reflex is considered normal and does not indicate worsening preeclampsia. Severe preeclampsia is often associated with hyperreflexia, typically 3+ or 4+, which can signal worsening central nervous system involvement and an increased risk for seizures.

B. Platelets of 20,000. A platelet count of 20,000 is dangerously low and suggests the development of HELLP syndrome, a severe complication of preeclampsia that includes hemolysis, elevated liver enzymes, and low platelets. This condition increases the risk of spontaneous bleeding and requires immediate medical intervention.

C. Urine output of 75 ml per hour. A urine output of 75 mL per hour is adequate and does not indicate worsening kidney function. In severe preeclampsia, oliguria (urine output less than 30 mL per hour) is a more concerning sign, as it suggests impaired renal perfusion and possible acute kidney injury.

D. 1+ Proteinuria. While proteinuria is a key feature of preeclampsia, a 1+ reading is mild and not necessarily indicative of worsening disease. Severe preeclampsia is typically associated with proteinuria of 3+ or higher, along with other symptoms such as hypertension, headache, and visual disturbances.

A. Maintaining euglycemia in labor reduces the need for insulin postpartum. While insulin requirements typically decrease after delivery due to the loss of placental hormones that cause insulin resistance, the primary reason for tight glucose control during labor is to prevent neonatal complications rather than reducing postpartum insulin needs.

B. A blood glucose level above 110 puts the client at risk for infection in labor. Poorly controlled diabetes can increase infection risk over time, but transient hyperglycemia in labor is not a direct cause of infection. The focus of glucose management during labor is to prevent neonatal hypoglycemia rather than maternal infection.

C. More insulin will be available for fetal use via placental transfer. Insulin does not cross the placenta, so maternal insulin therapy does not provide insulin to the fetus. However, maternal hyperglycemia leads to increased fetal insulin production, which can cause neonatal hypoglycemia after birth.

D. An elevated blood glucose in labor increases the risk of neonatal hypoglycemia. Maternal hyperglycemia causes the fetus to produce excessive insulin in utero. After birth, when the maternal glucose supply is suddenly cut off, the infant’s high insulin levels can cause a rapid drop in blood glucose, leading to neonatal hypoglycemia, which can be dangerous if not managed properly.