Second Trimester Complications
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Complications affecting comfort, rest, mobility:
Incompetent cervix
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Pathophysiology - inability of
cervix to support growing weight of pregnancy; associated with repeated spontaneous second trimester
abortion.
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Etiology:
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Unknown; exposure to DES.
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Congenital defect in cervical musculature.
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Cervical trauma during previous birth, abortion; aggressive, deep, or repeated
dilation and curettage.
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Assessment:
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History of habitual, second trimester abortions.
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Painless, progressive cervical effacement and dilation during second
trimester.
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Signs of threatened abortion or (early third trimester) preterm labor.
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Analysis/nursing diagnosis:
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Pain related to early dilation.
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Fear related to possible pregnancy loss.
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Nursing care plan/implementation:
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Medical management
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Cerclage surgical procedure (Shirodkar, McDonald).
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Preoperative nursing
management
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Goal: reduce physical stress
on incompetent cervix. Bed rest, supportive care.
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Goal: emotional
support. Encourage verbalization of anxiety, fear, concerns.
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Goal: health (preoperative)
teaching. Explain procedure - purse-string suture encircles cervix and
reinforces musculature.
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Goal: preparation for
surgery.
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Postoperative nursing
management
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Goal: maximize surgical
result. Bed rest, supportive care.
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Goal: health
teaching.
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Avoid: strenuous physical activity; straining.
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Report promptly: signs of labor (vaginal bleeding, cramping).
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Need for continued, close health surveillance.
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Evaluation/outcome
criterion: woman carries pregnancy to successful termination.
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Complications affecting sensory/perceptual functions:
pregnancy-induced hypertension (PIH); preedampsia/eclampsia
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Pathophysiology
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Generalized arteriospasm —> increased peripheral resistance, decreased tissue
perfusion, and hypertension.
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Kidney:
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Reduced renal perfusion and vasospasm —> glomerular lesions.
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Damage to membrane —> loss of serum protein (albuminuria). Note: Reduced serum
albumin/globulin (A/G) ratio alters blood osmolarity —> edema.
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Increased tubular reabsorption of sodium —> increased water retention
(edema).
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Release of angiotensin contributes to vasospasm and hypertension.
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Brain: decreased oxygenation, cerebral edema, and vasospasm —> visual disturbances and
hyperirritability, convulsions, and coma.
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Uterus: decreased placental perfusion —> increased risk of SGA baby, abruptio placentae,
oligohydramnios.
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Etiology: unknown.
Risk factors:
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Pregnancy - occurs only when a functioning trophoblast is present; more common in
first pregnancies;
develops after week 20 of gestation.
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Coexisting conditions - diabetes, multifetal gestation, polyhydramnios, renal
disease.
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Angiotensin gene T235.
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Assessment - types:
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Preeclampsia - mild
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Hypertension - systolic increase of 30 mm Hg or more over baseline; diastolic
rise of 15 mm Hg or more.
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Proteinuria - 1 g/day.
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Edema - digital and periorbital; weight gain over 0.45 kg (1 lb)/wk.
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Preeclampsia - severe
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Increasing hypertension - systolic at or above 160 mm Hg or more than 50 mm Hg over
baseline; diastolic, 110 mm Hg or more
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Urine: proteinuria (5 grams or more in 24 hours); oliguria (400 mL or less in 24 hours).
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Hemoconcentration, hypoproteinemia, hypernatremia, hypovolemic condition.
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Nausea and vomiting.
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Epigastric pain - due to edema of liver capsule.
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Cerebral or visual disturbances (before convulsive state):
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Disorientation and somnolence.
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Severe frontal headache.
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Increased irritability; hyperreflexia.
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Blurred vision, halo vision, dimness, blind spots.
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HELLP Syndrome (Hemolysis, Elevated Liver enzymes, and Low Platelets).
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Eclampsia
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Tonic and clonic convulsions; coma.
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Renal shutdown - oliguria, anuria.