Lecture on toxicosis in the last trimester of pregnancy
The kidneys are most sensitive to changes in blood flow and volume, increase the excretion of specialized products, make blood urea, uric acid decrease and creatinine excretion increases.
Pregnancy toxicity is a medical condition caused by pregnancy in the third trimester of pregnancy, consisting of three main symptoms: edema, hypertension and proteinuria. During the development of medicine, pregnancy poisoning was called by many different names: in 1928 Fabre called "Poisoning by the fetus". Germany calls Gestosis. Vietnam calls albuminuria during pregnancy. Recently the World Health Organization (WHO) recommended calling: Hypertension disorder caused by pregnancy. The rate of poisoning from pregnancy varies depending on region, country, in Vietnam, the rate of pregnant poisoning is 4-5% compared to the total number of pregnant people, if the blood pressure mark starts from 140 / 90 mmHg; and the rate of 10-11% if the blood pressure is from 135/85 mmHg according to WHO.
Causes and pathophysiology
Pathogenetic causes of fetal poisoning are currently under discussion, the clinical manifestations of pregnancy poisoning are kidney disease, cardiovascular system, liver, eye. In essence, this is a manifestation of disorders in the target organs caused by pregnancy.
Compare changes in normal pregnancy and toxicity in pregnancy
Physiological changes in pregnancy are usually in the heart, blood vessels, kidneys, and blood systems. Changes in pregnancy toxicity are summarized in the following table.
Table: pathophysiological changes
The volume of blood
Little or no increase
Increase ++ => + (physiological anemia)
Increase + + +
Increase from 40 - 50%
There is a change
Arterial blood pressure
Lower in the middle 3 months the last 3 months to normal.
Peripheral vascular resistance
Increased, increased vascular activity, blood vessel constriction.
Renal blood flow
Glomerular filtration rate in the middle trimester
Double blood transfusion
Creatinine clearance. Reduced uric acid
Blood urea increased
Increased blood creatinine
Blood uric acid increased
Angiotensin Aldosterone Renin System:
Active and appropriate
with posture and salt intake.
Renin activity and plasma concentrations are hindered by the loss of antagonism (vasodilation) with angiotensin.
Blood coagulation system:
• Weakness VII, VM, IX, and X
The ratio of von Wille Brand to factor IIX increased blood activity resulting in the consumption of factor IIX.
Normal or slightly increased
Vascular spasm: Vascular constriction from the pathophysiological basis of fetal toxicity - eclampsia. This concept was first described by Volhard based on direct observation of small blood vessels in the fundus, viscera. The constriction of blood vessels causes arterial hypertension. Hypertension damages blood vessels. The dilation and contraction of small artery segments can also damage the vascular lumen, reducing blood volume, also causing platelet deposition and endothelial fibrinogenesis. The vascular spasm causes a lack of oxygen in peri-vascular tissue, which can cause bleeding necrosis and other target organ disorders are seen in patients with severe pre-eclampsia.
The kidneys are most sensitive to changes in blood flow and volume, increase the excretion of specialized products, make blood urea, uric acid decrease, and creatinine excretion increases. Increased blood flow and glomerular filtration rate increase the excretion of metabolic products in the blood. That is in normal pregnancy.
In pregnancy toxicity: proteinuria, decreased blood Protide levels, and other abnormalities are indicative of kidney damage, due to decreased renal blood transfusion. Increased blood uric acid levels that herald a reduced glomerular filtration rate are considered important signs of serious disease development.
Theory of angiotensin-aldosterone-renin system or e applies to ch Land hypertension
In normal pregnancy: Components of the Renin-Angiotensin-Aldosterone System (Renin substance, Renin concentration, and plasma Renin activity, Angiotensin II and Aldosterone) increase.
In pregnancy toxicity: Some of the components of this kit are lower than in normal pregnancy because Angiotensin II remains at the non-pregnancy range, which is lower than the level of normal pregnant women. Patients with fetal toxicity have low Angiotensin II levels, but an increased response to hypertension. In 1973, Gant et al. Demonstrated: Intravenous administration of Angiotensin II for pregnant women aged 28 - 32 weeks. If the infusion of Angiotensin II at a rate of over 8ng / Kg/min will cause a slight increase in diastolic blood pressure of 20mmHg, in normal pregnancy. Conversely, if the infusion of Angiotensin II to women of the same gestational age at a rate of less than 8ng / Kg/min has caused diastolic blood pressure to 20 mmHg, that person will develop fetal toxicity in the last 3 months of pregnancy.
It has been suggested that the Angiotensin II hypertensive response is decreased in pregnant women with normal blood pressure because of a decreased receptor for Angiotensin II in vascular smooth muscle cells (MacKanjee et al., 1991). Angiotensin II vascular resistance may be mediated by other factors, such as hyperaldosteronism. They believe that Angiotensin II acts on the coils of the adrenal cortex. Many studies believe that: smooth muscle in the arterioles inert with Angiotensin II is due to the presence of Prostaglandin, or Prostaglandin-like substances synthesized from endothelium. (Cunningham et al, 1975; Gant et al; 1974). This inertness is eliminated when using Prostaglandin inhibitors such as indomethacin, aspirin (Everette et al., 1978). There are some tissues, rapidly increasing Angiotensin synthesis or Prostaglandin release or both. It is believed that:
Currently not know the exact mechanism of Prostaglandin or related substances to necrosis on blood vessels during pregnancy. To elucidate the mechanism, Goodman et al. (1982) used vasodilator Prostaglandin in normal pregnancy; Everett et al. (1978) demonstrated that high doses of aspirin or Indomethacin would increase vascular susceptibility during Angiotensin II infusion, and they suggested that Prostaglandin synthesis was blocked. Sanchez - Ramos et al. (1978) noted a decreased vascular response after taking 40 mg of aspirin within 2 hours, similar to thromboxane vasoconstrictor blocker.
Prostacyclin theory and thromboxane A2
Prostaglandin is an acid whose precursor is arachidonic acid (eicosatetraenoic acid) metabolized in two ways: Lipoxygenase and Cyclooxygenase.
TxA2 was first synthesized from platelets, stroma, and cultured platelets of vegetable cakes. It is a substance that constricts vessels, concentrates platelets, reduces vegetable uterine circulation, and increases uterine activity. PGI2 is produced first from vascular endothelium and to a lesser extent from cultured leukocytes. It causes strong vasodilation, inhibits platelet concentration, promotes vegetable uterine circulation, and reduces uterine activity. PGI2 and TxA2 are equal in normal pregnancy, in pregnancy toxicity, preeclampsia (TSG), TxA2 are increased. Walsh (1988) reported increased progesterone production in preeclampsia and hypothesized that increased progesterone concentrations may inhibit PGI2 production.
Spitz et al. (1988) reported that women with high blood pressure taking 81 mg of aspirin daily were able to block TxA2 synthesis by about 75%, PGI2 synthesis decreased by 20%, PGE2 30% means that in TSG, the enzyme cyclooxygenase converts AA to PGI2. and PGE2 decreased while TxA2 gradually increased to vasoconstriction and susceptibility to Angiotensin II infusion.
Low-dose aspirin therapy drastically reduces TxA2 production, but only partially blocks PGI2 and PGE2 production, creating the vasodilator potential of PGI2.
In normal pregnancy, Prostacyclin can act to protect against thrombosis. Low-dose aspirin therapy has been shown to inhibit cyclooxygenase inhibiting the conversion of AA to TxA2, Prioritize the generation of PGI2 for clinical improvement to reduce the risk of pregnant women with pregnancy toxicity, as well as prevent pre-eclampsia. These observations support the role of Prostacyclin in the prevention of fetal toxicity, pre-eclampsia, and eclampsia.
The muscle theory of endothelial damage
The theory focuses on vascular endothelial factors including Prostacyclin. This theory has been supported by Romeo & Cs (1988), Walsh & Cs (1990), Friedman & Cs (1991). They looked at the effect of low-dose aspirin therapy showing an imbalance between TxA2 and PGI2 in pre-eclampsia.
It has a role in regulating the general blood vessels and uterine-vegetable blood flow, which is mainly local blood transfusion in the uterus - vegetable cake.
To maintain vasodilation, endothelial dilatation factor (EDRF = Endothelium-derived relaxing lector), and PGI2 (Prostacyclin) are required. Pregnancy phase (between 10-16 weeks): EDRF is directed towards the uterine muscle and the torsary endothelium. Phase 2: occurring from weeks 16-22, EDRF directed at a part of the torsal artery in the uterine muscle.
The result: Dilated blood vessels cannot constrict.
In fetal toxicity, pre-eclampsia has no invasive presence of cultured cells, leading to local vasoconstriction and less blood transfusion, albeit with hypertension. When the endothelium is damaged causing: Proteinuria, systemic edema.
It is well known that endothelial cells are damaged, often secreting vasoconstrictors such as Endothelin, and others from endothelial cells. They also inhibit blood clotting and activate the thrombolytic tissue plasminogen. When endothelial cells are damaged, they not only lose their normal function, but also the production of precursors (replacing anticoagulants) and blood vessel constants. Therefore, endothelial damage, fibroblasts in early pregnancy easily cause disorders of the subsequent endothelial cell functions. Therefore, it is possible to explain many of the physiological changes of this disease.
Table: Clinical and physiological manifestations of pregnancy toxicity
• Unusual vegetable cake; Invasive fibroblasts are not enough, especially in the second phase.
• Prostacyclin deficiency; and redundant Thromboxane A2.
• Vascular spasm, (systemic).
• Damage to the endothelium of blood vessels.
• Reduced blood volume.
• Fetal growth is damaged secondary, high resistance, reduced blood-cake transfusion leading to fetal failure.
• Activate hemostatic system, platelet concentration; the constriction of blood vessels increases. Increased blood pressure.
• Hypertension; decreased organ blood transfusion (such as: decreased filtration rate, renal blood flow decreased, creatinine clearance decreased).
• Proteinuria. Coagulation disease; thrombocytopenia (normal above 100,000 / cc).
• Concentrated blood (increased hematocrit).
In summary, the pathogenesis of pregnancy-induced hypertensive disorders is now localized in the Renin - Aldosterone - Angiotensin system; Prostacyclin and Thromboxane A2 systems; endothelial damage; Less related to Catecholamine and ADH.
Risk factors influence the onset of the disease
Weather: The rate of pregnancy poisoning in the cold, wet season is higher than in the hot and humid season.
Age: The rate of fetal poisoning at 35 years old is nearly double that of pregnant women under 20 years old.
The number of pregnancies: The rate of pregnancy poisoning among pregnant women is higher than that of children.
The number of pregnancies: Twins, multiple pregnancies.
Poor economic life and low educational level, higher rates of pregnancy poisoning.
Geography: We have not had the work to verify the rate of pregnancy poisoning in each region.
Diet: The rate of fetal poisoning is high in the undernourished, folic acid deficiency and trace elements: Ca, Mg, p, Zn ...
Working regime: Heavy work regime, mental stress.
History of pregnancy toxicity, preeclampsia, eclampsia, premature peeling vegetables.
Pregnancy history: The fetus is underdeveloped and the fetus dies.
Medical history: diabetes, high blood pressure, kidney, colloid disorder, hypothyroidism.
Abnormal uterine artery Doppler flow rate:
Systolic / diastolic ratio> 2.6.
Resistance index (Resistance Index = RI)> 0.58.
A V-shaped notch appears.
Sensitivity to Angiotensin II increases at 28 weeks gestation.
Roll-over test: positive (+) blood pressure test.
Damage to blood vessels is common in organs such as:
Brain: Capillary constriction, tissue deficiencies, and brain cell damage, and brain edema.
Kidney: Constriction of kidney blood vessels reduces renal blood flow, reduces the rate of glomerular dialysis, damages kidney cells: protein urine, low urine output, urinary cylinder appearance; and increased blood urea, uric acid, and creatinine.
Heart: Myocardial anemia, causing arrhythmia, heart failure.
Lungs: Constriction of pulmonary blood vessels, pulmonary stasis causing pulmonary edema.
Eyes: Capillary constriction of the eye mainly capillaries (Gunn's sign) causes retinal edema, retinal secretion, and hemorrhage causing mild disease.
Damage to the coagulation system: Capable of causing blood clots scattered in the lumen of the vessel, causing a decrease in fibrinolysis, hemolysis causing bleeding in organs, young vegetables, and thrombosis in vegetable cakes. Bleeding in: lungs, kidneys, heart, brain, under the liver capsule, bleeding out after delivery due to blood clotting disorders. decreased platelet count.
Necrotic lesions: During surgery, necrotic lesions are often found scattered in vegetable cakes, kidneys, liver, around the small artery, portal vein.
Edema lesions: Common in intercellular edema, pulmonary edema causes pulmonary edema, cerebral edema causing eclampsia.
Damage deposition of degenerative products: From Fibrin - Fibrinogen, Globulin, AgG immunity, AgM, complement in tissues and capillary membranes. This damage is common in glomerular capillary bundles, liver tissue, sinus vessels in the liver.
The main symptoms:
Hypertension: Hypertension of the arteries is an important sign, because it is the earliest sign, the most common rate (87.5%), has prognostic value for both mother and child. There are three ways to evaluate arterial hypertension:
Evaluation of physiological constants: For those who have not had blood pressure measurements. If the blood pressure is at or above 140/90 mmHg, it is considered hypertension.
Comparative assessment with pre-and post-pregnancy blood pressure readings, if;
Systolic blood pressure increased by over 30mHg compared with pre-pregnancy systolic blood pressure.
Diastolic blood pressure increased over 15mHg compared with pre-pregnancy diastolic pressure.
If comparing with the post-pregnancy blood pressure increase, depending on the time when compared with gestational age, we can distinguish between high blood pressure or pregnancy poisoning.
Mean Blood Pressure: Evaluate both systolic and diastolic blood pressure readings, using the following formula at the same time:
Average blood pressure = (maximum blood pressure + 2 x minimum blood pressure) / 3
If the average blood pressure increases 20mmHg compared to before pregnancy, it is increased blood pressure.
Note: Measure is to record blood pressure in both hands, then take measurements on the hand with higher blood pressure to evaluate and monitor. Say high blood pressure when next time higher than last reading. Conditions at diagnosis: two high blood pressure readings 6 hours apart are called true hypertension. During labor, only 2 hours is needed enough to assess the increase in blood pressure.
Features of hypertension in pregnancy toxicity:
The systolic and diastolic blood pressure increased or decreased in harmony, the systolic blood pressure increased, the diastolic blood pressure was normal or vice versa. Usually increases both systolic and diastolic blood pressure. If diastolic blood pressure rises more rapidly leading to congestion, there is a worse prognosis.
Hypertension can fluctuate with the circadian rhythm of the day, or increase steadily. Therefore, before treatment, it is necessary to determine how high blood pressure is.
In pregnancy toxicity, hypertension usually begins at 32 weeks of pregnancy, increases earlier than the prognosis worsens, and returns to normal by the end of the postpartum period.
If six weeks after delivery, blood pressure remains high, usually chronic hypertension.
Proteinuria: Proteinuria appears later than signs of hypertension. Determined by the amount of Protein in the urine, called positive (+) when:
- Proteinuria above 0.3g / l in urine sample for 24 hours.
- Proteinuria is over 0.5g / l in a randomized sample of water.
Determination of proteinuria by semi-quantitative method, the value (+) => 3 (+). Kidney damage. The excretion of proteinuria during the day is not uniform, so the 24-hour urine sample is more valuable for diagnosis and monitoring. As a sign of blood pressure, the higher the proteinuria, the more severe the disease.
Edema: In the second half of pregnancy, there are two types of edema: compression-induced edema usually appears in the evening, when waking up in the morning with no edema. Edema caused by poisoning in pregnancy initially manifested in the morning and then throughout the day, increasing edema. These two types of edema are white edema, soft, concave. Edema due to fetal toxicity begins to swell from low (legs) to high (face) or total edema. There are two possibilities: clinical manifestations, as described above. The form does not show clinical manifestations, ie edema in the organs, difficult to find on clinical examination. These two edemas are expressed: pregnant women gain weight too quickly, increase over 500g / time, or over 2250g / month. Weight-based edema assessment is accurate.
Anemia: Fatigue, blue skin, pale mucosa, (hemolysis).
Lungs: Sometimes there is a triple syndrome due to the presence of water in the pleura.
Heart: Sometimes there is a mechanical blow due to anemia, blurred heartbeat, fluid retention, sometimes patients with mild dyspnea.
Abdominal: Free ascites may be present, due to peritoneal edema.
Eyes: Patients sometimes experience blurred vision due to retinal edema associated with severe fetal toxicity.
Kidney function tests: Urine: Protein intake. Urine residue: leukocytosis, leukocytes, urinary retention. Blood: quantitative substances such as creatinine (normal: 1.8mg); uric acid (normal: 4.5mg); urea (normally 0.3g / l), if they increase, kidney function is compromised.
Liver function tests: Quantitative SGOT, SGPT; reaction Gross, Mandaean, if increased, ie liver cells have shown signs of damage.
Blood cells: Number of red blood cells, hematocrit, hemoglobin; decreased platelets.
Quantification of blood Protide: If the decrease is edema due to reduced blood colloid pressure.
Fundoscopy: There are signs of Gunn, papillary edema, retinal hemorrhage, ... the eye has been damaged. Fibrotic ocular arteries are common in chronic hypertension.
Exploring the status of pregnancy: Test the chromosome, CT test, biological index during pregnancy, assess how much the fetus has been impaired, have the ability to live in the air environment.
According to the degree of lightweight :
Table: Clinical forms by severity
Edema after resting Increase weight
Proteinuria (g / L)
The amount of urine
Swelling in the legs
Over 0.5 kg / week
From 140 / 90mmHg
From 1 to 2
Over 800ml / 24 hours
Spread to the stomach, hands
Over lkg / week
From 150 / 100mmHG
From 3 to 4
Less than 800ml / 24 hours
Reduced or blurred
Spread the whole stomach
Over 2 kg/week
From 160 / 110mmHg
From 5.0 and up
Less than 400ml / hour
According to the symptom combination:
Type with a simple symptom: When there is only hypertension, or proteinuria, or just edema.
Type of hypertension: transient type of hypertension, easily mistaken for chronic high blood pressure.
Type that combines two symptoms:
Or increased blood pressure associated with edema.
Or increased blood pressure associated with proteinuria.
Or proteinuria combined with edema.
This is a diagnostic standard of HELLP syndrome of University of Tennessee, Memphis, USA: H (Hemolyze = hemolysis): blurred mark in blood sample. Total bilirubin> 1.2mg / dL. Lactic dehydrogenase> 600U / L. EL (Elevated Liver enzyme = elevated liver enzymes): SGOT> 70U / L. Lactic dehydrogenase increased. LP (Low Platelets = thrombocytopenia): <100,000 / mm. This is a severe syndrome that requires immediate suspension of pregnancy.
Got e resentment determine e Estimate
Based on the three main million of them: Blood pressure, proteinuria, and edema are not or accompanied by side signs and subclinical signs.
Diagnostics e resentment ph gifts special
Chronic hypertension and pregnancy: High blood pressure exists before pregnancy or increases from the moment of pregnancy, but proteinuria (-). It is easy to mistake a symptom of pregnancy poisoning. If proteinuria (+) was added to pre-eclampsia, there is a bad prognosis for mother and baby.
Nephritis and pregnancy: Patients with proteinuria before pregnancy and persist until delivery. Kidney disease that worsens during pregnancy, has a bad prognosis for both mother and baby.
Signs of edema due to other causes: Edema due to the heart, kidneys, oliguria, ... or pressure.
Protein markers: Heart or kidney.
Prognosis and progression
To make a prognosis, we must base on the main factors, subclinical, subclinical, the time to appear sooner or later according to gestational age and severity of the disease.
To the mother side:
Hypertension and other signs of hypertension
The three main symptoms worsen. Treatment is correct or not.
The sooner the illness occurs.
Late detection or late treatment and whether the disease responds to treatment.
Complications appear in the target organ of the disease such as: cerebral edema, edema or fundus hemorrhage, ...
Less urine output, kidney function gradually impaired.
There are other medical conditions such as heart disease, kidney disease, hemorrhagic rash (SLE), ...
About the child:
Based on gestational age, the smaller the gestational age, the worse the prognosis for the mother and child.
The less developed the fetus in the uterus, the more severe the disease.
Based on the volume of the fluid, the more severe the disease is reduced.
Based on diastolic hypertension:
At 110 mmHg high-risk pregnancy, chronic intrauterine failure.
At 120 mmHg the fetus is at risk of intrauterine death.
In general, if fetal toxicity is diagnosed early, well-treated, and the patient responds to treatment, one will be able to maintain the pregnancy until full term. When treatment is necessary and should always evaluate the results of treatment daily for prognosis. Since the mild form of fetal toxicity is very easy to progress to a severe form, pre-eclampsia and eclampsia, if not treated well, it can easily lead to maternal and child mortality.
Quiz with mom: Prevent the progression of the disease. Avoid complications. Hope to improve morbidity and reduce maternal mortality and complications.
The problem with the baby: Try to ensure the normal development of the fetus in the uterus, limit the possible risks to the fetus: underdevelopment in the uterus, malnutrition, stillbirth ... and reducing the rate of pregnancy. maternal morbidity and mortality.
During treatment, the physician needs to firmly grasp the motto: To protect the mother is the main, with consideration to the child; and the origin of the disease comes from the fetus. Medicines to treat symptoms for mothers and can affect the fetus should be considered carefully before using drugs to treat mothers.
Treatment content included
General nursing for clinical forms:
Care: Patients need bed rest, lying on their left side to increase uterine circulation beneficial vegetables for the fetus. The patient's room is warm, light is soft, low noise creates a sense of comfort, causes confidence in the expertise.
Diet: If blood Protide decrease and swelling should advise patients to increase dietary protein and salt restriction, especially in the presence of proteinuria.
About drinking: Advise patients to drink water every day as usual, (1.5-2L / day), not to drink water with salt.
Daily monitoring and evaluation of clinical signs, urine output / 24 hours, tests, ... about the progression of drug-responsive disease during treatment. Monitor the patient's weight every day.
When pregnancy is not enough months of treatment here is t stainless symptoms:
With blood pressure: The purpose of controlling blood pressure is not to increase, not to lower the pyramid so that it is safe for both mother and child, that is, it does not affect uterine circulation. The following drugs are currently selected for a safe treatment for mothers and children:
Alpha methyldopa (Aldomel, Dopegyt ...). It stimulates the inhibition of the alpha receptor center and reduces renin activity in plasma. 0.25g tablets; the maximum dose should not exceed 3g / 24hours. Low to high doses should be used evenly throughout the day to have a high concentration of inhibiting blood pressure.
Hydralazine hydrochloride (Dehydroalanine, Depressant, ...). It has a vasodilating effect and reduces peripheral resistance. 10mg tablets; 20mg; the maximum dose should not exceed 200mg / 24 hours. Note side effects: When standing, it is easy to drop blood pressure. Aldomet and Hydralazine are safe for pregnancy because it has been in use for more than 50 years.
Magnesium sulfate 15% solution intravenously or intramuscularly both have the effect of dilating the capillaries as the two drugs above. Average dose from 3 to 4g / day. It has a hypotensive effect. It is recommended to use a low dose and then increase it gradually until the treatment goal is reached. You can use 1 or a combination of 2 - 3 drugs above by injection or oral so that there is always enough drug concentration in the blood to control the patient's blood pressure as required by treatment.
Beta-blockers: Labetalol, Trandate, .... are rarely used in pregnancy infection.
Regarding aspirin: Hauth et al. Randomized 604 pregnant women with healthy babies at 24 weeks gestation: 302 women took aspirin at 60 mg/day, and 302 women took fake pills. Results: The incidence of pre-eclampsia was significantly lower in the aspirin group. There was no difference between the two groups: gestational age at birth, weight at birth, or rate of developmental delay or preterm birth.
The authors found no difference in: rates of preeclampsia; developmental delay, or mother's complications. However, they concluded: Low-dose aspirin should not be routinely used to reduce pre-eclampsia and fetal growth retardation because:
There are at least two possible mechanisms in pregnant women with fetal toxicity. Arachidonic acid is changed by the enzyme cyclooxygenase to TxA2, PGI2, PGE2; This pathway responds to low-dose aspirin therapy. The second pathway of arachidonic acid metabolism by lipoxygenase causes vegetable cakes to increase production of 15 - dhydroxyeicoxatelraenoic - acid (15 - HETE); It inhibits prostacyclin production leading to vascular constriction.
There is a relationship between calcium supplementation and pregnancy toxicity. The author has observed a decreased urinary calcium excretion during pre-eclampsia, and several weeks before the onset of pre-eclampsia. Belizan (1988) reported an inverse association between dietary calcium supplementation, maternal blood pressure, and incidence of pre-eclampsia and eclampsia.
With proteinuria: In addition to nursing, limit sodium chloride; beta lactamin antibiotics should be used to fight glomerulonephritis during pregnancy.
With edema: Need to find the cause of edema. If sodium is in the bloodstream, sodium chloride must be limited in the body. If blood Protide is reduced, it is advisable to raise the intravascular colloid pressure by protein infusion or by the gastrointestinal tract, depending on the specific case.
When the amount of urine is below 800ml / 24hours: Should use more diuretics such as Lasix. When using diuretics should accompany potassium chloride to prevent potassium lowering due to diuretics. Do not use diuretics for a long time, easily causing danger of amniotic fluid for the fetus.
Sedation: Diazepam 5mgj Rotadda 30 mg; Tranxene 5mg; ...
Should use additional trace elements: Calcium, Magne-B6, zinc, folic acid. During treatment, it is necessary to evaluate the results of the treatment daily. When pregnancy toxicity responds to treatment, it is possible to keep the pregnancy for full months. The past term can cause labor if the Bishop is favorable, or wait for labor, the pregnancy should not exceed the due date. If pregnancy toxicity does not respond to treatment, pregnancy should be suspended to save the mother or treat the cause.
When diagnosing fetal toxicity at full maturity: We should assess the state of the degree of fetal toxicity. Proceed to implement medical measures accordingly. Simultaneously evaluate the Bishop index and other related preparation issues to determine whether to terminate a pregnancy by either the lower or upper line and choose an appropriate time to conduct a suspension.
When diagnosing fetal toxicity during labor: It is necessary to assess the status of fetal toxicity in order to implement appropriate medical and obstetric measures. If subjective, there are events that are difficult to foresee.
The cause of pregnancy poisoning is unknown, so there is no specific preventive measure. Related diseases such as high blood pressure and kidney disease should be treated before trying to conceive.
Because pregnancy makes the disease crutch and can easily lead to severe pregnancy infection.
When pregnant, pregnant women need to register, check up periodically at specialized clinics, to be able to detect early pregnancy abnormalities, for prompt treatment; you will be able to limit morbidity and mortality from fetal poisoning.