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MODERN PROBLEMS OF GESTOSES
Prepared by D.M.S., professor S.N.Heryak
Ternopol medical state univercityby I.Y. Gorbachevsky
Gestoses and hypertensive disorders are among the most common and yet serious conditions seen in obstetrics.
These disorders cause substantial morbidity and mortality for both mother and fetus, despite improved prenatal care.
CLASSIFICATIONGESTOSIS OF EARLY TERMS OF
PREGNANCY ptyalism in pregnancy vomiting nausea
RARE FORMS OF GESTOSIS IN PREGNANCY hyperemesis gravidarum acute fatty liver of pregnancy dermatosis gravidarum tetania gravidarum osteomalacia gravidarum bronchial asthma of pregnancy
PREGNANCY INDUCED HYPERTENSIONHELLP-syndrome
Ptyalism in pregnancy (or excessive salivation).
Ptyalism in pregnancy isespecially annoying for a small
number of patients,sometimes approaching 1 literproduction per day.
Treatment of ptyalism:
tincture of belladonna atropineMedical treatment only slightly so thatreassurance of the time-limited nature
ofthe problem is a mainstay ofmanagement.
Nausea and emesis.At least 66 % of women experiencenausea and 50 % emesis in the first trimester,with the frequency of these symptomslessening as the second and third trimesters
ensue.
Classically, symptoms are predominantly
present in the morning ("morning sickness"),
but they may occur throughout the day and evening.
The genesis of pregnancy-induced nausea and vomiting.
It may be that the hormonal changesof pregnancy are responsible.Chorionic gonadotropin, for instance,has been implicated on the basis thatits levels are rather high at the sametime that nausea and vomiting aremost common.
Light degree of vomiting.
It is accompanying with 2 - 4times per day episodes ofvomiting after taking meals,general state of the woman issatisfactory, light tachycardiamay be present.
Moderate degree of vomiting.
It is accompanying with 5-10 times
and more per day episodes ofvomiting which don't from takingmeals. Weight loss, ketosis,increased temperature arepresent.
Severe degree of vomiting.
It is also called as Hyperemesisgravidarum (intractable emesis during
pregnancy) is a more severe form of nauseaand vomiting, occurring in approximately 4 outof 1000 pregnancies. It is also associated with severe symptoms as
wellas weight loss, dehydratation, ketosis, andelectrolyte disturbances.
Hospitalization and treatment:
balanced crystalloid solutions and electrolytes to correct metabolic disturbances in a short time.
Diet can then be reinstituted slowly and progressively. Frequent small feedings and avoidance of foods that are unpleasant to the patient usually relieve symptoms to a manageable level.
Recurrences sometimes necessitate repeat hospitalizations.
Therapeutic abortion for management of this problem is rarely required.
A variety of antiemetics can be prescribed if the above measures fail to provide adequate relief (Metoclopramide, Meclizine, Promethazine).
Risk Factors for PIH
primigravid status, new paternity; family history of preeclampsia or eclampsia; previous preeclampsia or eclampsia; extremes of maternal age (younger than 20
y or older than 35 years of age); preexisting hypertensive vascular,
autoimmune, or renal disease; preexisting renal, pulmonary, thyroid
dysfunction; Diabetes mellitus; Multiple gestation; Nonimmune or alloimmune fetal hydrops; Hydatidiform Mole.
Theories of Pregnancy-Induced Hypertension
Immunological theory Genetic predisposition Dietary deficiency Vasoactive compounds Endothelial dysfunction
Aspects in pathogenesis of hypertensive disorders in pregnancy
1. Generalized vasospasm.2. Hypovolemia.3. Hemoconcentration.4. Disseminated intravascular coagulopathy.5. Metabolic impairment as result of
hypoxia.6.Organ dysfunction – renal, hepatic, cardiac
and pulmonary, hematological, cerebral problems.
7. Placental dysfunction because the vasospastic changes.
Classification of PIH (PREGNANCY INDUCED
HYPERTENSION)
1. Hypertensive disorders during pregnancy.
2. Edema during pregnancy.3. Proteinuria during pregnancy.4. Mild preeclampsia.5. Moderate preeclampsia.6. Severe preeclampsia.7. Eclampsia.
“Isolated” and “superimposed” hypertensive disorders are distinguished.
“Superimposed” hypertensive disorders develop on the underlying preexisting diseases, such as Diabetes Mellitus, Hypertensive disease, kidneys inflammatory diseases, thyroid and pulmonary dysfunction. They have such peculiarities as:
early beginning; severe duration; isolated symptoms only presenting (isolated
proteinuria, edema, or hypertension); presence of atypical clinical findings such as
paresthesia, insomnia, hypersalivation.
Chronic hypertension
Is defined as hypertension present before the twentieth week of gestation or beyond 6 weeks' postpartum.
Gestational hypertension
Occurs after 20 weeks of pregnancy and doesn’t accompanies with proteinuria.
Preeclampsia Is defined as the development
of hypertension with proteinuria or edema (or both), induced by pregnancy, generally in the second half of gestation.
1. Hypertension in pregnancy.
It is generally defined as a diastolic blood pressure of 90 mm Hg or greater, as a systolic blood pressure at or above 140 mm Hg at two estimations with the interval 4 hours
or 160/110 mm Hg at once or as an increase in the diastolic blood
pressure of at least 15 mm Hg or in the systolic blood pressure of 30 mm Hg or more when compared to previous blood pressures.
2. Weight gain.
It is a sudden increase in weight mayprecede the development of
preeclampsia. Weight increase of about much more
than400 g per week is abnormal.
3. Edema.
Peripheral edema is common in pregnancy, especially in the lower extremities;
however, persistent edema unresponsive to resting in the supine position is not normal, especially, when it also involves the upper extremities and face.
4. Headache.
It is unusual in milder cases but frequent
in more severe disease. It is often frontal but may be occipital,and it is resistant to relief from
ordinaryanalgetics.
5. Abdominal pain.
Epigactric or right upper quadrant pain. Often is a symptom of severe preeclampsia and may be indicated of imminent convulsions.
It may be the result of stretching of the Hepatic capsule, possibly by edema and hemorrhage. Tenderness over the liver should be presented.
6. Visual disturbances.
A spectrum of visual disturbances,ranging from slight blurring of vision toscotomas to partial or complete
blindness,may accompany preeclampsia. These develop as a result of vasospasm,ischemia, and petechial hemorrhageswithin the occipital cortex.
7. Hyperreflexia.
The patellar and achilles deeptendom reflexes should be
carefullyelicited and noted this symptom.The demonstration of clonus at
theankle is especially worrisome.
8. Loss of consciousness or seizures.
Any history of loss ofconsciousness or seizures,
evenin the patient with a known
seizuredisorder may be significant.
Laboratory findings of PIH. Maternal studies
Test or Procedure Rationale
Proteinuria Proteinuria is defined as 300 rng or more Urinary protein during a 24-hour period or 30-100 mg per dL or more in at least two random urine specimens collected 6 hours or more apart
Hematocrit in complete blood count / every 2 days
It increasing may signify worsening vasocanstriction and decreased intravascuiar volume.
Platelet count / every 2 days Thrombocytopenia and coagulopathy are associated
Coagulation profile (FT, PIT)
Fibrin split products
Liver function studies / weekly Hepaiocellular dysfunction is associated with worsening PIH
Serum creatinine / twice weekly Decreased renal function is associated
24-hour urine for creatinine clearance / twice weekly
24- hour for total protein / twice
Serum uric acid / twice weekly
Laboratory findings of PIH. Fetal studies
Test or Procedure Rationale
Ultrasound for fetal growth / every 2 weeks
To assess for pregnancy-associated hypertension effects on the fetus, intrauterine growth restriction.
Amniotic fluid volume Oligohydramnios
Fetal movement record /daily Chronic fetal distress.
Biophysical profile / twice weekly
Nonstress test / twice weekly
Placental status
Differential diagnosis of chronic hypertension and preeclampsia
Signs Hypertensive disease Preeclampsia
Onset of hypertension
Before pregnancy and in the first 20 weeks of gestation
After 20 weeks of gestation
Duration of hypertension
Constant, lasts during 3 months after delivery
It disappears after 6 weeks or 3 months after delivery
Hereditary anamnesis
Presence of hypertensive disease in the parents, family
Absent
Age 35-40 years old 20-25 years old
Retina Spasm of vessels, hemorrhages
Vasospasm, edema of retina
Proteinuria Absent Present
Assessment of different stages of PIH severity
Symptom of evaluation
Mildpreeclamp
sia
Moderate preeclampsia
Severepreeclam
psia
Systolic blood pressure 130-150 mm Hg
150-170 mm Hg
> 170 mm Hg
Diastolic blood pressure 90-99 mm Hg
100-110 mm Hg
> 110 mm Hg
Proteinuria in a 24hours collection sample
< 0,3 g / L 0,3-5 g / L 5 g/ L
Assessment of different stages of PIH severity
Diuresis per hour > 50 ml > 40 ml < 40 ml
Presence of edema In lower extremi-
ties
In lower extremities
and abdominal
wall
Generalized edema
Number of thrombocytes
> 150.000 150 - 80. 000 < 80.000
Hematocrit 36 – 38 39 – 42 > 42
Serum creatinine < 75 mkmoll/
L
75 – 120 mkmoll/L
> 120 mkmoll/
L
Clinical signs of severe preeclampsia
General edema weight gain exceeds more than 900 g in
a week cerebral or visual disturbances such as
headache and scotomata pulmonary edema or cyanosis epigastric or right upper quadrant pain,
evidence of hepatic dysfunction Oligouria (less than 500 ml/ day)
Complications of preeclapsia
Maternal – placenta abruption, cerebral hemorrhage, renal and liver insufficiency, disseminated intravascular coagulopathy, adrenal insufficiency, eclampsia.
Fetal – intrauterine growth retardation, intranatal fetal death, infant morbodity and mortality.
ECLAMPSIA
Is characterized typically by those same abnormalities as severe preeclampsia with the addition of convulsions.
The seizures are grand mal and may appear during pregnancy, during labor, or postpartum.
Principles of PIH treatment
Termination of the pregnancy with the least possible trauma to the mother and the fetus.
Birth of the infant. Complete restoration of the
health of the mother.
The severity of the preeclampsia and the maturity of the fetus are the primary considerations in the management of preeclampsia.
TREATMENT 1. Bed rest. Preferably with as much of
the time as possible spent in a lateral decubitus position. In this position, cardiac function and uterine blood flow are maximized and maternal blood pressures in most cases are normalized. This improves uteroplacental function, allowing normal fetal growth and metabolism.
Ambulatory treatment has no place in the management of PIH.
Bed-rest throughout the greater part of the day is essential.
Sedative drugs for normalization of status of central nervous system:
Droperidol – 2 ml IM, Seduxen – 2 ml IM. These drugs should be combined
with Droperidol – 0,25 % - 2ml IM or IV
Antihypertensive therapy eliminates vasospasm of macro- and microcirculation. It is started if BP > 150/100 mmHg
Methyldopa – a2 adrenoagonists, false neurotransmission in the dose 250-500 mg 3- 4 time a day – FIRST-LINE DRUG
Labetalol – a- and b- adrenergic blockers – in the dose 100-400 mg 2-3 times per day (10-20 mg IV every 10 minutes till 300 mg) –SECOND-LINE DRUG
Atenolol – b1- adrenergic blockers in the dose 25-100 mg once a day
Metoprolol - b1- adrenergic blockers in the dose 12,5-50 mg 2 times per day
Nifedipine – calcium-channel blocker – in the dose 10 mg po q 4-8 hours;
Hydralazine – miometrial vasodilator (if diastolic pressure is repeatedly above 110 mm Hg ) An initial dose of 5 mg given every 10 minutes till 20 mg until suitable blood pressure is achieved.
Spasmolytic agents – No-spani 2 % - 2-4 ml IM, Papaverine hydrochloride – 2 % - 2-4 ml IM, Plathyphillinum – 0,2 % - 2, 0 – twice a day, Dibasol – 1 % 2-4 ml IM or IV, Euphyllinum – 2,4 % 10, 0 IV.
Magnesium Sulfate
It is used when diastolic pressure is > 110 mm Hg
It is used to arrest and prevent the convulsions of eclampsia
It has spasmolytic, sedative, antihypertensive and anticonvulsant effects.
Schemes of magnesium administration in the case of severe preeclampsia and eclampsia
Intravenous administration of Magnesium Sulfate – 4 gram 16 ml 25 % during 5 minutes very slowly (it is dissolved in 34 ml isotonic solution).
Maintenance dose is 1g-2g/hour (7, 5 g – 30 ml 25 % solution is dissolved in 220 ml isotonic solution – 3, 33 % Magnesial solution)
The maximal dose of magnesium during a day in the case of severe preeclampsia is 50-80 ml
(12,5 –24 g).
During prescription of magnesium sulfate
a. The patellar reflex is present. b. Respirations are not depressed (>
14 respiratory act in a minute) . c. Urine output the previous 4 hours
exceeded 100 mL.
Reversal of the effects of excessive magnesium concentrations is accomplished by the slow intravenous administration of 10% calcium gluconate
Limitated intravenous fluid therapy under control of blood volume, hematocrit, diuresis.
Primarily saline (lactated Ringer’s, isotonic solution) should be given at a rate of 60-125 ml per hour
PROTOCOL FOR TREATING ECLAMPSIA
Turn patient on the side Establish airways and administer
oxygen Pulmonary ventilation – elimination
of hypoxia Magnesial therapy. Immediate
delivery within 3 to 6 hours. Continue to administer magnesium for at least 24 hours after delivery or last convulsion.
Hypotensive therapy – if DBP > 110 mm Hg
PROTOCOL FOR TREATING ECLAMPSIA
Attention! In the case if severe preeclampsia and eclampsia three catheters should be inserted obligatory:
1 – into central vein - v. subclavia for a fluid therapy and controlling of central venous pressure;
2 – into urinary bladder for controlling of diuresis per hour;
3 – transnasal catheterisation of stomach for prevention of Mendelson’s syndrome.
Duration of treatment
Mild preeclampsia – 7-10 days Moderate preeclampsia – 7-10
days Severe preeclampsia – 24 hours
and termination of pregnancy Eclampsia – 5 hours and
termination of pregnancy
HELLP SYNDROME HELLP is the acronym for a specific set of
hypertensive patients who have: Hemolysis - anemia Elevated Liver enzymes – liver dysfunction, Low Platelet count – hemorrages.
Treatment: cardiovascular stabilization, correction of coagulation abnormalities - Platelet
transfusion correction of liver dysfunction immediate delivery.
Acute fatty liver of pregnancy.
It is a rare complication of pregnancy, but its severity and maternal mortality rate of 30 % make its timely diagnosis and treatment of importance. It is usually occurs late in pregnancy in primagravidas and characterized by vague gastrointestinal symptoms becoming worse over several days' time. Thereafter headache, mental confusion, and epigastric pain may ensue, and if untreated, there may be rapid development of coagulopathy, corna, multiple organ failute and death. Laboratory findings include an initial modest elevation in bilirubin and an elevation of transaminase levels.
Treatment of this serious complication is correction of coagulopathy and electrolyte imbalances, cardiorespiratory support, and delivery as feasible by the vaginal route, if possible.