Pregnancy Induced Hypertension PDF

PREGNANCY INDUCED Blood pressure reach 140/90mmHg or greater for the first time after Midpregnancy but proteinuria is not identified. Half of...

PREGNANCY INDUCED Blood pressure reach 140/90mmHg or greater for the first time after Midpregnancy but proteinuria is not identified. Half of these patient subsequently develop preeclampsia syndrome. HYPERTENSION Gestational hypertension is reclassified by some as “transient Course Outline hypertension” if evidence for preeclampsia does not develop and blood pressure returns to normal by 12 weeks postpartum. ❖ TYPES OF PIH ❖ DIAGNOSIS OF HYPERTENSIVE DISORDERS PRE-ECLAMPSIA ❖ GESTATIONAL HYPERTENSION ❖ PRE-ECLAMPSIA Summary: ❖ PREECLAMPSIA SUPERIMPOSED ON CHRONIC HYPERTENSION ▪ Hypertension, proteinuria, edema ❖ RISK FACTORS ▪ The new onset of htn and proteinuria or htn and end- ❖ ETIPATHOGENESIS organ dysfunction with or without proteinuria. ❖ PHENOTYPIC EXPRESSION OF PREECLAMPSIA SYNDROME ▪ Caused by placental and maternal vascular and always ❖ ETIOLOGY resolves after delivery ❖ PATHOGENESIS ▪ Increase risk of cardiovascular disease ❖ PATHOPHYSIOLOGY ▪ Increases in systolic and diastolic blood pressure can ❖ PREDICTIVE TESTS be either normal physiological changes or signs of ❖ ECLAMPSIA developing pathology. ❖ OBSTETRIC MEASURE ❖ PREVENTION It is described as pregnancy-specific that can affect virtually ❖ EARLY DIAGNOSIS OF PREECLAMPSIA ❖ EVALUATION OF PREECLAMPSIA every organ system. Much more than gestational hypertension ❖ CLINICAL MANAGEMENT OF PREECLAMPSIA with proteinuria, appearance of proteinuria remains an ❖ MANAGEMENT CONSIDERATIONS OF important diagnostic criterion. Other diagnostic criteria are the PREECLAMPSIA following: thrombocytopenia, renal dysfunction, hepatocellular ❖ LONGTERM CONSEQUENCES necrosis, CNS perturbations, and pulmonary edema. TYPES OF PIH: INDICATORS OF PREECLAMPSIA SEVERITY (1) Preeclampsia and eclampsia syndrome ✓ Headaches or visual disturbances such as scotomata (2) Chronic hypertension of any etiology can precede eclampsia (3) Preeclampsia superimposed on chronic hypertension ✓ Epigastric pain or RUQ pain accompanies (4) Gestational hypertension hepatocellular necrosis, ischemia, and edema. Accompanied by elevated serum hepatic transaminase DIAGNOSIS OF HYPERTENSIVE DISORDERS levels. ✓ Thrombocytopenia. Represents platelet activation and Hypertension is diagnosed when blood pressure exceeds aggregation as well as microangiopathic hemolysis. 140mmHg systolic or 90mmHg diastolic. Eclamptic seizures ✓ Renal or cardiac involvement develop in some whose blood pressure have stayed below ✓ Obvious fetal-growth restriction 140/90mmHg. A sudden rise in mean arterial pressure but still ✓ Early-onset disease. in normotensive – “delta hypertension” – may signify preeclampsia PREECLAMPSIA SUPERIMPOSED ON CHRONIC HYPERTENSION Delta Hypertension is when there is an acute rise in blood pressure. Some women will go on to have obvious ▪ Chronic underlying hypertension is diagnosed in women preeclampsia, and some develop eclamptic seizures or HELLP with documented blood pressure > 140/90mmHg before while still in normotensive. pregnancy or before 20 weeks gestation or both ▪ Blood pressure normally drops during second and early GESTATIONAL HYPERTENSION third trimesters in both normotensive & chronically hypertensive women. Preeclampsia does not develop and hypertension resolves by 12th week postpartum. ▪ During third trimester BP return to their originally ETIOLOGY hypertensive levels, it may be difficult to determine whether hypertension is chronic or induced by pregnancy. (1) Placental implantation with abnormal trophoblastic ▪ Chronic hypertension, BP rises to abnormal levels typically invasion of uterine vessels after 24wks of gestation. If new-onset or worsening (2) Immunological maladaptive tolerance between baseline hypertension is accompanied by new-onset maternal, paternal, and fetal tissues. proteinuria, then superimposed preeclampsia is (3) Maternal maladaptation to cardiovascular or diagnosed. inflammatory changes of normal pregnancy ▪ Superimposed preeclampsia is commonly diagnosed (4) Genetic factors including inherited predisposing genes earlier in pregnancy. It tends to be more severe and more and epigenetic influences. often accompanied by fetal-growth restriction. PATHOGENESIS RISK FACTORS VASOSPASMS. Caused by systemic endothelial activation that ❖ Older women are at greater risk for chronic increase resistance to produce hypertension subsequently. hypertension with superimposed preeclampsia Systemic endothelial cell injury promotes interstitial leakage, & ❖ African-American women [black women have greater blood constituents, including platelets & fibrinogen are morbidity] deposited subendothelially. With diminished blood flow due to ❖ Multiparas maldistribution from vasospasm and interstitial leakage, ❖ Pregnancies with male fetus. ischemia to the surrounding tissues can lead to necrosis, ❖ Smoking during pregnancy hemorrhage, and other end-organ disturbances characteristics. ❖ HIV ENDOTHELIAL CELL INJURY. Centerpiece of preeclampsia ❖ Seropositivity pathogenesis. Protein factor(s), secreted into maternal ❖ Sleep-disordered breathing circulation & produce activation & dysfunction of systemic vascular endothelium. Activated or injured endothelial cells ETIOPATHOGENESIS produce less nitric oxide & may secrete substances that Exposed to chorionic villi for the first time promote coagulation & greater sensitivity vasopressors. Exposed to superabundance of chorionic villi, as with Endothelial activation includes characteristics alteration in twins or hydatidiform mole glomerular capillary endothelial morphology, greater capillary Preexisting conditions associated with endothelial cell permeability, and elevated blood concentrations of substances activation or inflammation associated with endothelial activation. Genetically predisposed to hypertension developing during pregnancy. INCREASED PRESSOR RESPONSES. Pregnant women Regardless of those precipitating etiology, normally develop refractoriness to infused vasopressors. During preeclampsia is characterized by abnormalities early preeclampsia, women have enhanced vascular reactivity resulting in systemic vascular endothelial damage with to infused norepinephrine and angiotensin II. Increased in resultant vasospasms, transudation of plasma, and sensitivity in angiotensin II precedes the onset of gestational ischemic and thrombotic sequelae. hypertension. Nitric oxide is a vasodilator synthesized from l- arginine by endothelial cells. Inhibition of nitric oxide raises PHENOTYPIC EXPRESSION OF PREECLAMPSIA arterial pressure, lowers HR, and reverses the pregnancy- induced refractoriness to vasopressors. Endothelins are 21- SYNDROME amino-acid peptides & potent vasoconstrictors. ET-1 are TWO-STAGE DISORDER THEORY OF PREECLAMPSIA elevated in normotensive while highly elevated serum levels to women with preeclampsia. They likely arise from systemic Stage 1: caused by endovascular trophoblastic remodeling that endothelial activation. Magnesium sulfate lowers the levels of downstream causes the stage 2 clinical syndrome. ET-1 Stage 2: modified by preexisting maternal conditions that are ANGIOGENIC & ANTIGIOGENIC PROTEINS. Placental also manifest endothelial cell activation or inflammation and vasculogenesis is evident by 21 days after conception. are listed in the third prior bullet. Angiogenic imbalance describes excessive amounts if antigiogenic factors that are thought to be stimulated by worsening hypoxia at the uteroplacental interface. Soluble fins- like tyrosine kinase 1 (sFlt-1) is a receptor for VEGF. elevated reduce haptoglobin levels. Microangiopathic hemolysis is maternal sFlt- 1 levels inactivate and reduce circulating free caused by endothelial disruption with platelet adherence and placental growth factor (PIGF) and VEGF concentrations, fibrin disposition. leading to endothelial dysfunction. sFlt-1 levels begin to rise maternal serum months before preeclampsia is evident. High Hemolysis + thrombocytopenia = Abnormally elevated serum levels in 2nd trimester are associated with doubling risk for liver transaminase levels that indicate hepatocellular necrosis. preeclampsia.These factors are also operative in pregnancies complicated by fetal-growth restriction. Soluble endogline COAGULATION CHANGES (sENG), inhibits transforming growth factor beta. Decreased There is a subtle change in coagulation and less often binding to endoglin diminishes endothelial nitric oxide- erythrocyte destruction is commonly found with preeclampsia dependent vasodilatation. It begin to rise months before and especially eclampsia. Abnormal coagulations are generally clinical preeclampsia develops, metformin reduces angiogenic mild and seldom clinically significant. Routine laboratory secretion from human tissue. assessments of coagulation, such as prothrombin time (PT) , activated partial thromboplastin time (aPTT) , and plasma PATHOPHYSIOLOGY fibrinogen level, are not required in the management of These are thought to consequence of endothelial dysfunction, pregnancy-associated hypertensive disorders. vasospasms, and ischemia. ENDOCRINE & HORMONAL ALTERATIONS CARDIOVASCULAR SYSTEM Renin, angiotensin II, angiotensin 1-, aldosterone, Common with preeclampsia syndrome related to: deoxycorticosterone, and atrial natriuretic peptide (ANP) are substantively augmented during normal pregnancy. (1) Greater cardiac afterload caused by hypertension. (2) Cardiac preload ▪ ANP released during atrial wall stretching from (3) Endothelial activation leading to interendothelial expansion of blood volume and it responds to cardiac extravasation of intravascular fluid into extracellular contractility. It rise in pregnancy and further enhanced space. in preeclampsia. ▪ Proatrial natriuretic peptide, precursor, also increased. ▪ Vasopressin levels are still similar in nonpregnant, HEMODYNAMIC CHANGES AND CARDIAC FUNCTION normal pregnant, and preeclamptic women. Cardiac output declines, due at least in part to greater peripheral resistance. When assessing cardiac function in FLUID AND ELECTROLYTE ALTERATIONS preeclampsia, consideration is given to echo cardiographic measures of myocardial function and to clinically relevant The volume of extracellular fluid, manifest as edema, usually ventricular function. blood loss incurred at delivery. Anemia much greater than normal pregnant women. Generalized may also partially result from greater erythrocyte destruction edema & proteinuria have reduced plasma oncotic pressure as subsequently described. that create filtration imbalance. This displaces intravascular fluid into the surrounding interstitial. MATERNAL THROMBOCYTOPENIA Eclamptic convulsion. The serum pH and bicarbonate Platelet count hemorrhage or fluid loss from vomiting or fever. Uric acid is endothelial activation + leakage of plasma into interstitial typically elevated that attributes to the reduction of GFR and space. In preeclamptic, depending on its severity, due to enhanced tubular reabsorption. Preeclampsia is also hemoconcentration is usually not as marked. associated with diminished urinary excretion of calcium. LIVER PROTEINURIA. Proteinuria aids the establishment of diagnosis of preeclampsia. 24-hour urinary excretion exceeding 300mmg Hepatic lesions with eclampsia are regions or periportal protein or 1+ dipstick. In urine dipstick assessment, the value hemorrhage in the liver periphery. Some degree of hepatic may show 1+ or 2+ from concentrated urine specimens from infarction accompanied hemorrhage in almost half of women women who excrete seizure NEUROLOGICAL MANIFESTATIONS ▪ Can happen up to 2 days postpartum ▪ Cerebral edema (acute) = coma ▪ Headache & scotomata – arise from cerebrovascular ▪ 20% maternal mortality rate perfusion. Don’t usually respond to traditional ▪ Poor fetal prognosis: hypoxia = fetal acidosis analgesia but improve after magnesium sulfate ▪ Before seizure: increase BP and increase temperature infusion. due to cerebral pressure. ▪ Convulsions – caused by excessive release of excitatory neurotransmitters. Extended seizures can Tonic Phase: approximately 20 seconds and may bite tongue cause significant brain injury and later brain and respirations halt dysfunction. Clonic Phase: up to minute, bladder and bowel muscles ▪ Blindness – rare but it complicates eclamptic contract, and relax incontinence. convulsions in up to 15% of women. It may develop up to a week or more following a delivery. ▪ Generalized cerebral edema – vary from confusion to TREATMENT coma. Dangerous because it can develop fatal (1) Prophylactic transtentorial herniation. - Proper antenatal care ▪ Cognitive decline - Low dose aspirin (2) Curative VISUAL CHANGES AND BLINDNESS. Scotomata, blurry - Delivery of fetus & placenta vision, or diplopia are common with severe preeclampsia and eclampsia. Improves with magnesium sulfate therapy or !!MUST CONSIDER MATURATION OF THE FETUS BEFORE lowered blood pressure. Amaurosis [occipital blindness], lasted DELIVERY!! from 4 hours to 8 days but it resolved completely in all cases. !! LESS COMPLICATIONS = INCREASE MATURATION!! CARDIOVASCULAR DRUGS – diuretics, antihypertensive drugs MANAGEMENT CONSIDERATIONS ANTIOXIDANTS – ascorbic acid, alpha tocopherol [vitamin E], (i) Severe htn vitamin D (ii) Fluid therapy (iii) Plasma volume expansion ANTITHROMBOTIC DRUGS – low dose of aspirin, aspirin/ (iv) Neuroprophylaxis dipyridamole, aspirin + heparin, aspirin + ketanserin (v) Analgesia anesthesia (vi) Blood loss delivery EARLY DIAGNOSIS OF PREECLAMPSIA (vii) Persistent severe postpartum htn ▪ Prenatal visits aid the early detection of preeclampsia. (viii) Plasma exchange ▪ Women without overt hypertension, but in whom early developing preeclampsia is suspected during OBSTETRIC MEASURES routine prenatal visits, are seen more frequently. (1) Timing of Delivery ▪ Overt hypertension, proteinuria, headache, visual ▪ > 37 terminate disturbances, or epigastric pain supervenes. ▪ < 37 expectant management at least 34 ▪ New-onset hypertension-either diastolic pressures >90 weeks mm Hg or systolic pressures >1 40 mmHg-are admitted ▪ Unstable conditions: to determine if the increase is due to preeclampsia, - Stabilized > deliver > start seizure prophylaxis and and if so, to evaluate its severity steroids if < 34 weeks (2) Method of Delivery EVALUATION OF PREECLAMPSIA ▪ Vaginal birth = vertex  Clinical findings such as headache, visual disturbances, ▪ Amniotomy + oxytocin = induction cervix epigastric pain, and rapid weight gain. ▪ PGE2: cervix (x)  Daily weight measurement ▪ C.S.: fetal distress, late deceleration, failure  Quantification of proteinuria and creatinine ratio induction of labor, contracted pelvis,  Blood pressure readings malpresentations.  Measurement of plasma or serum creatinine and (Immediate Delivery) hepatic transaminase levels and a hemogram. ▪ ER setting: control BP and seizures Measurement of uric acid and lactate dehydrogenase ▪ Don’t wait, don’t hesitate and withing 6hr… levels and coagulation. terminate  Fetal size and well-being and amniotic fluid volume (3) Intrapartum Care evaluation ▪ Close monitoring of the fetus ▪ Proper analgesic to the mother ▪ Anti-htn prn CLINICAL MANAGEMENT OF MIDTRIMESTER ▪ 2nd stage of labor shortened thru forceps PREECLAMPSIA (4) Postpartum Care NURSING MANAGEMENT FOR SEVERE ECLAMPSIA ▪ NO methergine [SMDOA] ▪ Continue observation for 48 hours ▪ Anti-htn until 48hrs  Support bed rest ▪ Prophylactic treatment: Magnesium sulfate  Monitor maternal & fetal well being ▪ Lorazepam and phenytoin: 2nd line agents for  Diet moderate CHON & low Na refractory seizures.  O2 pn, large bore IV  Anti htn medications and Magnesium sulfate and PREVENTION calcium gluconate DIETARY MANIPULATION – low salt diet, calcium or fish oil MEDICAL MANAGEMENT FOR SEVERE PREECLAMPSIA supplementation FOR < 34 WEEKS EXERCISE – physical activity, stretching  Admit to L&D  Maternal and fetal assessment   Consider magnesium sulfate -Note: fetal response to diminished uterine  Treat dangerous hypertension perfusion and may result in unnecessary & CONTRAINDICATION TO CONSERVATIVE MANAGEMENT potentially dangerous emergency. o Persistent symptoms or severe hypertension ❖ Labetalol o Eclampsia, pulmonary edema, HELLP syndrome - Some prefer this medication because of few side o Significant renal dysfunction, coagulopathy effects o Abruption - Intravenous o Previable fetus - Hydralazine causes more maternal tachycardia o Fetal compromise and palpitations while labetalol leads to maternal ABSENCE OF CONTRAINDICATIONS bradycardia and hypotension ▪ Corticosteroids for lung maturation - Contraindicated to asthmatic women ▪ Frequent evaluation: vital signs, UOP ❖ Nifedipine ▪ Daily lab evaluation for HELLP syndrome - Orally administered ONGOING INPATIENT MANAGEMENT - Popular due to efficacy to control acute ▪ Daily maternal assessment pregnancy-related hypertension. ▪ Serial lab evaluation of renal function and for - Sublingual is not recommended because of HELLP syndrome dangerous rapid and extensive effect ▪ Daily fetal assessment and evaluation of serial growth and amniotic fluid. DELIVER AT 34 WEEKS FLUID THERAPY ECLAMPSIA NURSING MANAGEMENT (MAKRA) Lactated ringer solution is administered routinely at rate of 60  Maintain patent airway to 120mL per hour. Controlled, conservative fluid  Administer O2 via mask administration is preferred for typical women with severe  Keep NPO preeclampsia who already has excessive extracellular fluid that  Rx: Magnesium sulfate, Diazepam is inappropriately distributed between intravascular and  Assess fetal well being extravascular spaces. Infusion of large fluid volumes enhances the maldistribution and thereby appreciably elevates the risk ECLAMPSIA MEDICAL MANAGEMENT for pulmonary and cerebral edema. For patient with anuria, small incremental boluses can be given to maintain urine o Magnesium sulfate to control convulsions output above 30mL. o Intermittent administration of antihypertensive drugs o Avoid diuretics unless pulmonary edema is present ❖ Pulmonary Edema o Limit IV fluid administration unless there’s fluid loss - Aspiration of gastric contents may be the result of o Delivery of fetus to resolve preeclampsia convulsions, anesthesia, or over sedation should be excluded. MANAGEMENT CONSIDERATIONS FOR ECLAMPSIA - Three common causes: (1) pulmonary capillary permeability edema (2) cardiogenic edema and/ or (3) combination of two SEVERE HYPERTENSION MANAGEMENT - If given vigorous fluid replacement – will have Severe hypertension can cause cerebral hemorrhage, mild pulmonary congestion secondary to hypertensive encephalopathy and can provoke convulsions. permeability. Placental abruption and congestive heart disease can also ❖ Invasive Hemodynamic Monitoring trigger. - Ironically, usually vigorous treatment of the former that results in most cases of the latter. ❖ Hydralazine - Such monitoring is best reserved for severely - Severe gestational hypertension preeclamptic women with accompanying cardiac - Intravenously disease, renal disease, or both or with refractory - Recommend labetalol if 2nd dose of hydralazine is hypertension, oliguria, and pulmonary edema. not working - Proven remarkably effective to prevent cerebral BLOOD VOLUME EXPANSION hemorrhage Due to association to hemoconcentration, infusion of various PLASMA EXCHANGE fluids, starch polymers, albumin concentrates, or combinations Severe preeclampsia-eclampsia persists despite delivery. They thereof to expand blood volume. It is not recommended due to advocate single or multiple plasma exchange for these women. serious maternal morbidity and substantive perinatal mortality rate accompanied their expectant management. REVERSIBLE CEREBRAL VASOCONSTRICTION SYNDROME NEUROPROPHYLAXIS Another cause of persistent hypertension, “thunderclap” headache, seizures, and central nervous system findings. Magnesium sulfate was reported to be superior to the Reversible cerebral vasoconstriction syndrome is characterized comparator agent to prevent eclampsia. Magnesium sulfate by diffuse segmental constriction of cerebral arteries and may was superior to phenytoin to prevent eclamptic women with be associated with ischemic and hemorrhagic strokes. It is gestational hypertension or preeclampsia. common in women and in some cases, if vasoconstriction is severe it can be the cause of cerebral ischemia and infarction. ANALGESIA AND ANESTHESIA Use of conduction of analgesia for women with preeclampsia LONG-TERM CONSEQUENCES syndrome has proven ideal. The initial problem in this method includes hypotension and diminished uterine perfusion caused FUTURE PREGNANCIES by sympathetic blockade in preeclamptic women. Rapid Lack of deep placentation is linked with preeclampsia, placental infusion of large volume of crystalloids or colloid corrects abruption, fetal-growth restriction, and preterm birth. hypotension from neural blockage. Maternal hypotension Gestational hypertension or preeclampsia also contributes to resulting from regional analgesia was managed with judicious developing hypertension in the future. Recurrence of risk for IV fluid administration. Undergoing general anesthesia, preeclampsia is elevated further in women with metabolic maternal blood pressure was managed to avoid severe syndrome. Nulliparas diagnosed with preeclampsia before hypertension. 30wks had a recurrence risk as high as 4015 during subsequent pregnancy. BLOOD LOSS AT DELIVERY Fall in blood pressure soon after delivery most often means LONG TERM MORBIDITY AND MORTALITY excessive blood loss and not sudden resolution of vasospasm Preeclampsia is a marker for subsequent long-term and endothelial damage. Oliguria follows delivery, hematocrit cardiovascular and related morbidity and mortality. should be evaluated frequently to aid detection of excessive Hypertension attributable to pregnancy should resolve withing blood loss. If identified, hemorrhage should be treated 12 weeks of delivery. appropriately by crystalloid and blood transfusion. CARDIOVASCULAR MORBIDITY PERSISTENT SEVERE POSTPARTUM HYPERTENSION Any hypertension is a marker for morbidity and mortality in Severe PP hypertension usually follows labor and delivery later life. The prevalence of ischemic heart disease and stroke complicated by hypertension. If intravenous hydralazine or were increased in women who had gestational hypertension labetalol are being used repeatedly, oral regimens can be given. compared with normotensive controls. Diastolic dysfunction is Administration of NSAIDs may aggravate PP hypertension in also more common and preeclampsia is also a risk for coronary those with preeclampsia syndrome. Women with chronic artery calcification and idiopathic cardiomyopathy. Women hypertension and left-ventricular hypertrophy, severe PP with pregnancy-associated hypertension are at increased risk hypertension can cause pulmonary edema from cardiac failure. for type 2 diabetes. Preeclampsia is a risk factor for later Nifedipine plus furosemide or nifedipine alone can treat severe diabetic retinopathy and retinal detachment. postpartum eclampsia and significantly lowered the need for additional antihypertensive. Long term adverse outcomes: metabolic syndrome, diabetes, obesity, dyslipidemia, atherosclerosis. Women with severe preeclampsia often have immediate PP weight in excess of their last prenatal weight. If this weight In later life, patient who had preeclampsia will develop chronic increases and associated with severe persistent PP hypertension and have an increased ventricular mass before hypertension, diuresis with IV furosemide is helpful in becoming hypertensive. controlling blood pressure. RENAL SEQUELAE Preeclampsia is a marker for subsequent renal disease. 15% of previously preeclamptic patient have renal dysfunction. Women with recurrent preeclampsia have higher risk for renal sequelae. CENTRAL NERVOUS SYSTEM SEQUELAE Eclamptic seizures were believed to have no significant long- term sequelae. All eclamptic women have multifocal areas of perivascular edema and some areas have cerebral infarction. Temporal lobe white matter changes and reduced cortical volume in previously preeclamptic women. Formerly preeclamptic women at approximately 10 years had lower vision-related quality of life compared with control subjects, Elevated risk for retinopathy. A cause versus an effect of these white matter lesions remains unknown.