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Pregnancy: Medical Complications
By:DR.MALAK AL- HAKEEM ASSOCIAT PROF. & CONSULTANT OBSTETRICS &GYNECOLOGY.
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HYPERTENSIVE DISORDERS
Criteria for diagnosis Blood pressure (BP) elevation must be sustained, and one of the following conditions must be present: Absolute BP of ≥ 140/90 mm Hg, or An increase in baseline diastolic BP of ≥15 mm Hg, or An increase in baseline systolic BP of ≥ 30 mm Hg BP elevation must be confirmed on at least two occasions at least 6 hours apart and at bed rest
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Classification Mild preeclampsia. Criteria for diagnosis include:
BP of ≥ 140/90 mmHg or increase in diastolic BP of ≥ 15 mm Hg or increase in systolic BP of ≥ 30mmHg Proteinuria of 1-2+ on dipstick or ≥ 300 mg on 24 hour urine collection Edema of the face or upper extremities
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Severe Preeclampsia. Criteria for diagnosis include:
BP of ≥ 160/110 mm Hg Proteinuria of ≥ 3-4+ on dipstick or ≥ 5 g on 24-hour urine collection Symptoms Headaches resulting from cerebral edema Visual disturbances resulting from decreased cerebral perfusion of the occipital cortex Epigastric pain resulting from hepatocellular necrosis, edema, and ischemia stretching Glisson’s capsule
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Laboratory Findings Mild Preeclampsia – Relative increased dias
15 mmHg, or increased syst 30 mm Hg, or absolute 140/90 Proteinuria – 1-2+ on dipstick or ≥ 300 mg/24 hr Edema of face, hands - Variable Convulsions - None Symptoms - None DIC findings - None Hemoconcentration - Mild Cyanosis, Oliguria, pulmonary edema - None
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Severe Preeclampsia Blood pressure ≥ 160/110 mm Hg Proteinuria – 3-4+ on dipstick or ≥ 5 g/24 hr Edema of face, hands - Variable Convulsions - None Symptoms - Possible DIC findings - Possible Hemoconcentration - Marked Cyanosis, Oliguria, pulmonary edema - Possible
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Eclampsia Blood pressure - At least mild preeclampsia criteria Proteinuria - At least mild preeclampsia criteria Edema of face, hands - Variable Convulsions - Present Symptoms - Possible DIC findings - Possible Hemoconcentration - Marked Cyanosis, Oliguria, pulmonary edema - Possible
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Chronic HTN Blood pressure – Preexisting HTN or HTN < 20 weeks Proteinuria – Variable (may be none) Edema of face, hands - None Convulsions - None Symptoms - None DIC findings - None Hemoconcentration - None Cyanosis, Oliguria, pulmonary edema - None
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Chronic HTN with Superimposed Preeclampsia
Blood pressure – Increased over baseline Proteinuria – At least mild preeclampsia criteria or increased over baseline Edema of face, hands - Variable (may be none) Convulsions - None Symptoms - Possible DIC findings - Possible Hemoconcentration - Variable Cyanosis, Oliguria, pulmonary edema - Variable
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Transient HTN Blood pressure – At least mild preeclampsia criteria Proteinuria - None Edema of face, hands - None Convulsions - None Symptoms - None DIC findings - None Hemoconcentration - None Cyanosis, Oliguria, pulmonary edema - None
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Thrombocytopenia (<100,000/ml) resulting from vasospasm-induced macroangiopathic hemolysis
Elevated liver enzymes resulting from hepatocellular necrosis Clinical Findings Pulmonary edema resulting from increased capillary membrane permeability Oliguria resulting from intrarenal vasospasm Cyanosis resulting from right heart failure Eclampsia is diagnosed in the presence of unexplained convulsions with other criteria for preeclampsia. Approximately 25% occur antepartum (before labor) Approximately 50% occur intrapartum (during labor) Approximately 25% occur postpartum (most within first 24 hours)
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Chronic hypertension is diagnosed with a history of preexisting hypertension either before the onset of pregnancy or before 20 weeks’ gestation (without coexisting molar pregnancy) and persisting past 6 weeks postpartum. Chronic hypertension with superimposed preeclampsia has a worse outcome than either chronic or pregnancy – induced hypertension alone. Diagnosis requires all of the following criteria: Presence of chronic hypertension Increase in diastolic BP of ≥ 15mm Hg or systolic BP of ≥ 30 mm Hg Increase in proteinuria
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Transient hypertension, which is diagnosed with the development of hypertension without other findings of preeclampsia, is largely a retrospective diagnosis that is made after the pregnancy is over. HELLP syndrome is a subtype of preeclampsia. The five letters make characteristics by up a mnemonic device representing the unique disease findings: Hemolysis, Elevated Liver enzymes, and Low Platelets.
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Preeclampsia – eclampsia spectrum
Epidemiology of preeclampsia. Preeclampsia occurs only in humans and only in pregnant women beyond 20 weeks’ gestation. Incidence. Approximately 8% of the general obstetric population develop preeclampsia. Risks factors Nulliparity (most common risk factors; eight times than in multiparas) Age extremes (i.e., <20 years, >34 years) Multiple gestation Hydatidiform mole Diabetes mellitus (DM) Nonimmune fetal hydrops
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Chronic hypertension Preexisting renal disease Small vessel disease (e.g., systemic lupus erythematosus, longstanding type 1 DM) Characteristic pathology involves renal glomerular endotheliosis, which refers to swelling of the endothelial cells of the capillary loops in the glomerular tuft. Pathogenesis involves diffuse vasospasm and capillary wall endothelial injury. Diffuse vasospasm produces: Altered refractory state of pregnancy against the pressor effect of renin, angiotensin II, and aldosterone
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Systolic and diastolic hypertension
Increased capillary permeability, which results in: Hemoconcentration from decreased intravascular volume, which leads to increased blood urea nitrogen (BUN), creatinine, uric acid, hemoglobin, and hematocrit. Diuretics should be avoided, because they may exacerbate hemoconcentration by further reducing intravascular volume. Edema from loss of protein into extravascular space Excessive weight gain from fluid retention.
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Reduced systemic perfussion of the following organ systems:
Kidneys, resulting in increased BUN, creatinine, and uric acid Uteroplacental unit, resulting in placental insufficiency, which may decrease placental nutritional function and lead to intrauterine growth restriction (IUGR) as well as decrease placental respiratory function that leads to fetal hypoxia. Vasoactive prostaglandins imbalance, with levels of vasoconstricting thromboxane exceeding the vasodilating effect of prostacyclin
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Capillary wall endothelial injury results in:
Fibrin deposition in the capillary beds (microangiopathic hemolytic anemia) Platelet destruction Disseminated intravascular coagulation (DIC) Consumptive coagulopathy
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Evaluation of maternal – fetal status
Evaluation of maternal – fetal status. Management is based on type and severity of hypertensive disease as well as gestational age. Indicators of a decline in maternal well – being Increasing BP (systolic and/or diastolic) Worsening symptoms (i.e., headache, visual disturbances, epigastric pain) Increasing hemoconcentration (i.e., BUN, creatinine, uric acid, hemoglobin, hematocrit) Increasing proteinuria on 24-hour urine collection Worsening DIC laboratory tests (e.g., decreasing platelet count, lengthening prothrombin/partial thromboplastin times (PT/PTTs), decreasing fibrinogen)
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Indicators of a decline in fetal well-being
Nonreactive nonstress test (NST) Positive contraction stress test (CST) Declining biophysical profile (BPP) Serial sonographic growth parameters showing slowing or arrest of growth Decreasing fetal movements Clinical approach. Management is based on the type and severity of hypertensive disease as well as gestational age. Options include aggressive inpatient, conservative inpatient, and conservative outpatient.
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Aggressive inpatient management includes:
Diagnostic criteria Mild or severe preeclampsia; ≥ 37 weeks’ gestation Severe preeclampsia; <26 weeks’ gestation Severe preeclampsia; weeks’ gestation, when associated with maternal jeopardy: Severe persistent headache Persistent visual changes Hepatocellular injury Thrombocytopenia or other evidence of DIC Pulmonary edema Abruptio placentae
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Severe preeclampsia; 26-34 weeks’ gestation, when associated with fetal jeopardy:
Repetitive severe variable decelerations Repetitive late decelarations Repetitive BPP ≤ 4 Oligohydramnios (amniotic fluid index (AFI) ≤ 4cm) IUGR (estimated fetal weight ≤ fifth percentile) Chronic hypertension with superimposed preeclampsia at any gestational age Eclampsia or HELLP syndrome at any gestational age
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Guidelines Maintenance of diastolic BP between 90 and 100 mm Hg. Further reduction of BP jeopardizes placental blood flow. Appropriate antihypertensive medications include: Hydralazine (direct arteriolar vasodilator), which causes baroreceptor sympathetic stimulation (increasing heart rate (HR) and cardiac output (CO), thus preserving placental blood flow> Labetalol (nonselective β-blocker), which preserves uteroplacental blood flow.
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Box 4-1 Clinical Findings for Parenteral Magnesium Sulfate Dose Effect
Prevention of convulsions with intravenous (IV) magnesium sulfate Administration of loading dose of 5g IV over 20 minutes, and maintenance infusion at 2g/hr. The maintenance IV infusion should be given for 24 hours after delivery. Watching for clinical evidence of magnesium toxicity (Box 4-1) Absence of toxicity is ensured as long as deep tendon reflexes are obtainable. Box 4-1 Clinical Findings for Parenteral Magnesium Sulfate Dose Effect 5-8 mg/dl Therapeutic level 10 mg/dl Loss of deep tendon reflexes 15 mg/dl Respiratory paralysis 25 mg/dl Cardiac arrest
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IV calcium gluconate is the antidote for magnesium toxicity.
Initiation of delivery. Labor can be induced anticipating vaginal delivery if the patient is stable and there are no contraindications. Otherwise, cesarean delivery is indicated. Conservative inpatient management is appropriate in the following cases: Mild preeclampsia that is remote from term (<37 weeks). Guidelines include: Monitoring BP every 4 hours Performing a daily urine dipstick for protein Performing twice-weekly 24-hour urine protein measurements
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Performing weekly liver function tests and electrolyte levels
Initiating delivery if criteria for severe preeclampsia are met Severe preeclampsia in carefully selected cases All of the following criteria must be met a) Gestational age >26 weeks but < weeks b) BP persistently ≥ 160/110 mmHg c) Absence of fetal jeopardy d) Absence of maternal jeopardy
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Guidelines include: a) Intensive maternal and fetal monitoring in a tertiary perinatal center b) Cautious volume expansion c) Aggressive antihypertensive therapy (e.g., hydralizine, labetalol) d) Anticonvulsant therapy (e.g. magnesium sulfate) e) Corticosteroids to enhance fetal lung maturity Initiation of delivery if maternal or fetal deterioration occurs
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Conservative outpatient management
Patient selection criteria include: 1) Transient hypertension (i.e., BP in the mildly elevated range, no proteinuria) 2) Uncomplicated chronic hypertension (without superimposed preeclampsia) Guidelines include: 1) Bed rest in the left lateral position 2) Home BP monitoring 3) Twice – weekly outpatient visits Initiation of delivery if maternal or fetal deterioration occurs
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Prevention. Large, prospective, randomized studies have shown that no prophylactic intervention for preeclampsia improves pregnancy outcome. This includes use of aspirin and supplemental calcium.
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