• Hypertensive states of pregnancy occur in 5% to 10% of all pregnancies and are examined in five groups:
Chronic Hypertension
• It can be diagnosed in two ways;
- Blood pressure => 140 / 90 mmHg before pregnancy or before 20 weeks of gestation not attributable to gestational trophoblastic disease
- Hypertension diagnosed after the 20th week for the first time and continuing after the postpartum 12th week
If the diastolic pressure is consistently above 100 mmHg in those who do not have other health problems, antihypertensive treatment should be started. The most reliable agent in the antihypertensive treatment of chronic hypertensive pregnant women is a-methyldopa.
• Low-dose aspirin is recommended for pregnant women with chronic hypertension. (from 12 weeks to birth).
e Women with chronic hypertension, with or without treatment, have an increased risk of fetal congenital anomalies (especially cardiac anomalies).
Gestational Hypertension
• Diagnostic criterion is 2!140 / 90 mmHg blood pressure two times after the 20th week of pregnancy; however, the definitive diagnosis can be made after the blood pressure returns to normal before the postpartum 12th week.
preeclampsia
Diagnostic criteria;
► Having a blood pressure >= 140 / 90 mmHg for the first time after the 20th week of pregnancy, and
► Any of the following criteria accompanying hypertension
0 Detection of new onset pathological proteinuria (>= 300 mg/day or >=1 in spot urine + protein/creatinine in dipstick or spot urine >= 0.3
0 Platelet count less than 100,000/l
0 Creatinine over 1.1 mg/dl
0 Serum transaminases exceeding 2 times normal
0 Headache, visual disturbances, convulsions
0 Pulmonary edema
Peripheral edema is not a diagnostic criterion.
Eclampsia
• Convulsions that cannot be explained by any other reason in a preeclamptic pregnant
is to accompany.
Preeclampsia Developing on the Background of Chronic Hypertension
• If new-onset pathological proteinuria or other preeclampsia diagnostic criteria are present in a chronic hypertensive patient, a diagnosis of superimposed preeclampsia is made.
• Typically, after the 24th week, blood pressure values begin to rise. It tends to occur earlier and progress worse than pure preeclampsia. It is usually accompanied by IUGR.
PREECAMPSIA
Risk factors
• Those exposed to chorionic villi for the first time (nulliparity)
• Those exposed to chorionic villi more than normal (multiple pregnancy, molar pregnancy)
• Those with previous vascular disease (chronic HT, collagen tissue diseases, DM, kidney diseases, CVS diseases)
• Race and ethnicity genetically predisposed to develop hypertension in pregnancy
• Those with a history of hypertensive disease in a previous pregnancy
• Obesity
• Maternal age > 35
• Hyperhomocystinemia
• Metabolic syndrome
• Antiphospholipid antibody syndrome
• Factor 5 leiden mutation
• Pregnancies of women born with SGA
Smoking reduces the risk of preeclampsia. (Increases placental adrenomedullin expression)
Trisomy 13 is the only aneuploidy with an increased risk of preeclampsia.
Preeclampsia does not increase the risk of fetal cardiac anomaly.
etiopathogenesis
• For the development of preeclampsia, chorionic villi, not the fetus, must be present (can be seen in complete moles). However, chorionic villi are not necessarily intrauterine. It can also be seen in ectopic pregnancies greater than 18 weeks.
• The cause of preeclampsia is not known exactly, but the factors that trigger preeclampsia cause ischemic and thrombotic sequelae affecting the whole system by causing two main pathologies regardless of etiology.
► Generalized Vasospasm: (E-98) Increased resistance as a result of vasospasm causes hypertension. In addition, due to decreased blood flow, ischemia, necrosis, bleeding and end-organ disorders occur in all surrounding tissues.
► Endothelial Cell Activation: Unknown but possibly placenta! These factors are secreted into the maternal circulation and cause vascular endothelial dysfunction. As a result of this;
0 Endothelial cell damage
0 Decreased nitric oxide production, increased endothelin-1 synthesis
0 Disruption of prostaglandin balance
0 Atherosis and lipid-laden macrophages (foam cell)
0 Microvascular coagulation (thrombocytopenia)
0 Increased capillary permeability (proteinuria and edema)
While prostacyclin decreases in preeclamptic pregnant women, thromboxan A2 increases, and vasospasm occurs when resistance to angiotensin II disappears.
► There may be incomplete trophoblastic invasion in preeclampsia. While invasion occurs in decidual spiral arterioles, invasion is not observed in myometrial spiral arterioles. Thus, high resistance and small diameter vessels
consists of. Incomplete invasion of spiral arterioles is associated with severe preeclampsia.
► Another theory is the absence or dysregulation of maternal immune tolerance to placental and fetal antigens of paternal origin. A decrease in the amount of HLA-G expressed by extravillous trophoblasts has been shown in preeclamptic pregnant women in the early period. This can cause abnormal trophoblastic invasion. While the Th1/Th2 ratio is in favor of Th2 in normal pregnancies, this ratio changes in favor of Th1 in preeclampsia. Thl causes an increase in inflammatory cytokines. Microparticles secreted from the placenta are also thought to initiate these inflammatory reactions.
► Preeclampsia risk doubles in pregnant women whose daily ascorbic acid intake is below 85 mg, since antioxidant production is reduced.
► It is recommended to use low-dose aspirin to reduce the recurrence of preeclampsia.
► Genetic predisposition: Preeclampsia is a multifactorial, polygenic disease. First-degree relatives are at increased risk.
► Changes in arteries at the implantation site in preeclampsia: Endothelial damage, penetration of plasma components into the vessel wall, proliferation of myointimal cells and medial necrosis. Fat accumulation in myointimal cells is called atherosis. An infarct can be seen in the placenta.
Clinic
• It can be in a spectrum ranging from symptoms that are difficult to notice clinically to multiorgan involvement that threatens the life of the mother and the baby. Therefore, gestational hypertensive diseases are clinically examined in two groups as mild and severe.
• Presence of one of the following findings makes the diagnosis of severe gestational hypertensive disease.
Mild to severe preeclampsia criteria | ||
| Light | Severe |
Diastolic pressure | < 110 mmHg | >= 110 mmHg |
systolic pressure | <160 mmHg | 160mmHg |
headache | no | There is |
Visual disturbances (scotoma) | no | There is |
epigastric pain | no | There is |
oliguria | no | There is |
Convulsion (eclampsia) | no | There is |
Serum creatinine | Normal | increased |
thrombocytopenia | no | There is |
Serum transaminase elevation | Very little | Evident |
Fetal growth restriction | no | Evident |
pulmonary edema | no | There is |
Onset of preeclampsia | start in the coming weeks | Early weeks start |
Presence or degree of proteinuria is NOT a criterion for severe preeclampsia.
Renal System
► Glomerulocapillary endotheliosis {classical pathological lesion)
► Decreased renal perfusion
► Decrease in glomerular filtration rate (GFR)
► Decreased uric acid clearance
► Increased plasma uric acid concentration (one of the earliest laboratory findings)
► Increase in creatinine level
► Proteinuria
► Sodium uptake increases
► Urine sodium concentration increases
► Decreased urinary calcium excretion
► Oliguria (Excessive fluid therapy should not be applied.)
► Acute renal failure (acute tubular necrosis); rare unless there is severe haemorrhage
► Renal cortical necrosis (rare)
Hematological System
► Thrombocytopenia (most common hematological finding)
► Microangiopathic hemolysis; LDH increases
► Reduction in coagulation factors
► Increase in fibrin degradation products
► Increase in D-Dimer, fibrinopeptide A and B levels
► Decrease in antithrombin, protein C and S levels
► Disseminated intravascular coagulation {DIC)
► HELLP syndrome
Induction of microangiopathic hemolysis of severe vasospasm and activation and aggregation of platelets leads to thrombocytopenia in cases, which is a sign of worsening preeclampsia.
In pregnant women with preeclampsia, the level of fibronectin, a glycoprotein associated with the endothelial basement membrane and indicating endothelial damage, is increased.
Cardiovascular System
► Increased peripheral vascular resistance results in increased cardiac afterload. In this case, cardiac output decreases.
► Hemoconcentration (especially in cases with severe preeclampsia and eclampsia) leads to a decrease in preload.
► Decreased blood volume (normal in gestational hypertension)
► In preeclampsia, ventricular remodeling (in response to increased afterload) occurs in the myocardium. Diastolic dysfunction is present in 40% of patients.
► Since there is no normal hypervolemia of pregnancy, even normal blood loss is less tolerated than normal pregnancies.
Endocrine Changes
► Renin, angiotensin and aldosterone decrease compared to normal pregnancy, but they are still above normal values compared to non-pregnant women.
► Deoxycorticosterone (DOC) increases. This explains the sodium retention in preeclamptic pregnant women.
► Vasopressin levels do not change.
► Atrial natriuretic peptide (ANP) increases.
► So-called antiangiogenic soluble endolgin (sEng) and soluble Fms like tyrosine kinase 1 (sflt-1) increase in preeclampsia. While sflt-1 causes endothelial dysfunction; soluble endolgin reduces nitric oxide dependent vasodilation.
Fluid - Electrolyte Changes
► Extracellular fluid volume increases; Due to endothelial damage, proteinuria and decrease in plasma oncotic pressure, the passage of intravascular fluid into the interstitial space is increased. Thus, edema is seen.
► Electrolyte concentrations do not change.
► After an eclamptic convulsion, serum pH and bicarbonate concentration decrease.
Liver
► Periportal hemorrhage, infarction, necrosis, hepatic failure
► Increased transaminases
► Subcapsular hematoma and rupture (The risk increases especially in those with HELLP syndrome.)
► HELLP syndrome
0 Epigastric and right upper quadrant pain in patients occurs as a result of stretching Glisson's capsule due to hepatocellular necrosis, ischemia, and edema. These findings are preliminary signs of liver infarction or rupture of a subcapsular hematoma.
0 Hemolysis, elevated liver enzymes and thrombocytopenia are present in HELLP syndrome.
Neurology System
► Intracranial petechial hemorrhages (especially in eclampsia)
► Changes in cerebral perfusion and perivascular edema (reversible posterior leukoencephalopathy): The development of generalized edema in the brain is dangerous; because fatal transtentorial herniation can develop.
► Hyperreflexia
► Convulsions (grand mal type): excitatory neurotransmitter release increases (especially glutamate)
► Headache and scotoma
► Visual disturbances: Often, scotoma, blurred vision, diplopia occur due to edema in the occipital lobe and usually resolve spontaneously. Temporary blindness of 4-6 hours (amorosis) may occur. It may rarely be permanent blindness due to retinal ischemia, necrosis or detachment (Purtscher retinopathy).
► Neurocognitive sequelae are detected in eclamptic patients in the long term (comprehension decreases).
Theroplacental Perfusion
► Increases perinatal morbidity and mortality
► Uteroplacental insufficiency (IUGR and intrauterine fetal death)
► Detachment placenta
Screening and Prophylaxis
• There is no reliable and valid screening test. It has been shown that salt restriction in the diet, the use of diuretics, and the intake of antioxidants such as calcium, fish oil, vitamin C and E have no effect.
• It is recommended to use low-dose aspirin from the 12th week of pregnancy until delivery in high-risk pregnant women to reduce the recurrence of preeclampsia.
Treatment
• The only real treatment for preeclampsia is termination of pregnancy. Management varies according to mild or severe preeclampsia.
Mild Preeclampsia
► Inpatient treatment or outpatient follow-up is appropriate. Mild preeclampsia can be followed until lung maturation is achieved. Physical activity restriction is helpful; however, absolute bed rest is not necessary. Coagulation tests do not need to be routinely performed during follow-up.
► If diastolic blood pressure is >100 mgHg in mild preeclampsia, antihypertensive treatment
recommended.
► Mode and timing of delivery: Induction vaginal delivery is the first choice after lung maturity is achieved.
Severe Preeclampsia
The purpose of the treatment of severe preeclampsia;
Control of Maternal Blood Pressure (Antihypertensive Treatment):
0 Purpose; To prevent complications such as hypertension-related cerebrovascular hemorrhage, encephalopathy, convulsions, congestive heart failure and detachment without reducing uteroplacental blood flow. Most of these complications occur when blood pressure is above 160/110 mmHg.
0 Agents used in antihypertensive therapy:
- Oral nifedipine: Nifedipine sublingual is not recommended. The blood pressure lowering effect is faster. May cause headache and tachycardia. Increases renal blood flow.
- Hydralazine: Hydralazine is a direct-acting arteriolar vasodilator. Hydralazine is the most commonly used drug in gestational hypertension and significantly reduces cerebral hemorrhage. The aim is to bring the diastolic pressure to 90-110 mmHg. Placenta if dropped even more! perfusion is affected. May cause maternal tachycardia. Increases renal blood flow.
- Labetalol: May cause maternal hypotension and bradycardia.
- Nitroprusside or Nitroglycerin: It is a direct-acting arteriolar and venous vasodilator. If there is no response to the first group of drugs, it should be evaluated. Fetal cyanide toxicity should not be forgotten.
- Verapamil, Nimodipine
- Ketanserine
Diuretics are used only for antepartum pulmonary edema. Other than that, the placenta! They are not used because they reduce perfusion. ACE inhibitors are NOT to be used as they are teratogenic.
Prevention of Convulsions (Magnesium Prophylaxis)
0 Since it is excreted by the kidneys, they can be used in patients with normal kidney functions. Dose adjustment should be made in patients with impaired renal function. It should not be given in complete anuria:
0 The therapeutic dose range is 4-7 mEq/L or 4.8-8.4 mg/dl; however, routine measurement of magnesium level is not recommended. Clinical follow-up is performed by the follow-up of deep tendon reflexes and the first sign of magnesium toxicity is loss of DTR. Calcium gluconate should be used as an antidote.
0 Magnesium sulfate should be given during labor and 24 hours postpartum.
Magnesium sulfate is not used for antihypertensive therapy.
Initiation of Birth:
0 Severe preeclampsia requires immediate delivery. Steroids should be administered between 24-34 weeks.
0 Type and timing of birth; vaginal delivery is the first choice.
ECLAMPSY
• Convulsions that cannot be explained by another reason in a preeclamptic pregnant woman. The incidence is 1/2000 births. Seizures are tonic-clonic in character and can be seen antepartum, intrapartum or postpartum. Eclampsia is most common in the third trimester.
and the frequency increases as the term approaches. Postpartum convulsions are seen less than 10%
and usually occurs in the first 48 hours.
Complications
• Ablation placenta-------10%
• Neurological deficits-----7%
• Aspiration pneumonia--------- 7%
• Pulmonary edema-------5%
• Cardiopulmonary arrest------ 4%
• Acute renal failure--------4%
• Maternal death------ 1%
Clinic
• An aura that precedes the seizure is often absent and is in the form of a generalized tonic-clonic convulsion. Fever is rare; however, it is a poor prognostic factor in its presence (a sign of hemorrhage in CNS). Pulmonary edema may develop following the seizure, due to aspiration pneumonitis. Retinal detachment and visual loss due to occipital lobe ischemia-edema may develop in 10% of cases following the seizure. cases Persistent coma may develop in up to 5% of patients due to diffuse cerebral edema and transtentorial uncal herniation. In some severe cases of eclampsia, sudden death may occur due to massive cerebral hemorrhage developing during convulsions. Very rarely, psychosis and related aggression may be seen in the patient after the attacks.
• Sometimes, uterine contractions may begin or intensify during seizures. Maternal hypoxemia and lactic acidemia due to convulsions cause fetal bradycardia. This condition usually resolves in 3-5 minutes; however, if it lasts longer than 10 minutes, other factors should also be considered, such as detachment.
• Epilepsy, encephalitis, meningitis, cerebral tumor, cysticercosis and ruptured cerebral aneurysm should be considered in the differential diagnosis. However, all pregnant women with convulsions should be considered eclampsia until other causes are excluded.
Treatment
• Control of convulsions and prevention of recurrence: Magnesium sulfate is the most effective and safe. Other agents that can be preferred in the control of convulsions in eclampsia; amobarbital, thiopental, midazolam, lorazepam
• Antihypertensive treatment
• Initiation of labor: It is the definitive form of treatment. First of all, vaginal delivery should be preferred. Usually, labor begins spontaneously or labor can be successfully induced.
Prognosis
• Preeclampsia and eclampsia always improve after delivery (except for complications such as SVO). Diuresis (4 L/day) is the best indicator of recovery. Proteinuria and edema return to normal within 1 week after delivery in eclampsia. Fetal prognosis mostly depends on gestational age at birth and problems are related to prematurity.
• The risk of recurrence in subsequent pregnancies is increased (25%). The earlier it is diagnosed, the greater the risk of recurrence. If diagnosed before the 30th week, 40% will recur. The risk of recurrence is also significantly higher in those with HELLP syndrome and thrombophilia.
• Long-term risks of women who have had any hypertensive processes during pregnancy:
► Morbidity and mortality due to cardiovascular diseases increase: The risk of ischemic heart disease, stroke, venous thromboembolism, chronic hypertension and type II DM increases.
► Increased risk of kidney failure
► It has been determined that lesions in the white matter of the brain persist in those who have had eclamptic convulsions in the long term, and some cognitive functions may be impaired (impaired attention, decreased cognition).