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Prepared by: Maricar S.Feliciano,R.N.

Sometimes called


It is persistent vomiting typically in the first trimester that is severe enough to cause significant weight loss, dehydration, acidosis from starvation, alkalosis from vomiting, and hypokalemia

Occurance of nausea and vomiting in PREGNANCY

with HG

Pregnant women

with nausea and vomiting

The nausea and vomiting associated with pregnancy usually begins by 9-10 weeks of gestation, peaks at 11-13 weeks, and resolves in most cases by 12-14 weeks. In 1-10% of pregnancies, symptoms may continue beyond 20-22 weeks. HG usually extends beyond the first trimester and may resolve by 21 weeks; however, it can last the entire pregnancy in less than half of these women.

Morning Sickness
You lose little of any weight.
Nausea and vomiting do not interfere with your ability to eat or drink enough each day. You vomit infrequently and the nausea is episodic but not severe. It may cause discomfort and misery. Dietary and/or lifestyle changes are enough to help you feel better most of the time. You typically will improve gradually after the first trimester, but may be a little queasy at times during the remainder of your pregnancy. You will be able to work most days and care for your family.

Hyperemesis Gravidarum
You lose 5-20 pounds or more. (> 5% of prepregnancy weight)
Nausea and vomiting cause you to eat very little and get dehydrated from vomiting if not treated. You vomit often and may vomit bile or blood if not treated. Nausea is usually moderate to severe and constant. You will probably require fluid hydration through a vein and/or medications to stop the vomiting. You usually feel somewhat better by midpregnancy, but you may continue to be nauseous and/or vomit until late pregnancy. You will likely be unable to work for weeks or months, and may need help caring for yourself.

Loss of greater than 5% of pre-pregnancy body weight (usually over 10%) Dehydration and production of ketones Nutritional Deficiencies Metabolic Deficiencies Difficulty with daily activities Volume depletion Death


sense of taste Intra uterine growth restriction Sensitivity of the brain to motion Food leaving the stomach more slowly Rapidly changing hormone levels during pregnancy Stomach contents moving back up from the stomach Physical and emotional stress of pregnancy on the body Subconjunctival hemorrage (broken blood vessels in the eyes) Difficulty with daily activities Hallucinations

According to the severity of symptoms HG was divided into three levels, namely:
Tier I (mild)
* Nausea vomiting constantly affecting the general state of the patient * She felt weak * There is no appetite * Weight loss * Feeling pain in the epigastric * Nadi increased about 100 per minute * Blood pressure decreased * Reduced skin turgor * Tongue dry * Sunken eyes

Tier II (is being)

* People seem more weak and apathetic * Skin turgor started bad * The tongue was dry and dirty * Small and fast Nadi * Temp rises (dehydration) * Eyes start ikterik * Weight loss and sunken eyes * The tension down, hemokonsentrasi, oliguri and constipation * Acetone smell of air breathing and going asetonuria.

Tier III (severe)

* General situation is more severe (decreasing from somnolen consciousness until coma) * Dehydration great * Small Nadi, quick and smooth * Increased body temperature and blood pressure down * There was a fatal complications in the nervous system, known as Wernicke enselopati with nistagmus symptoms, diplopia and mental decline * Incurred jaundice which indicates a bad heart.

The physiologic basis of hyperemesis gravidarum is controversial. It appears to occur as a complex interaction of biological, psychological and socio-cultural factors. The following theories have been proposed:

Women with hyperemesis gravidarum often have high hCG levels that cause transient hyperthyroidism. hCG can physiologically stimulate the thyroid gland thyroidstimulating hormone (TSH) receptor. hCG levels peak in the first trimester. Some women with hyperemesis gravidarum appear to have clinical hyperthyroidism. However, in a larger portion (50-70%), TSH is transiently suppressed and the free thyroxine (T4) index is elevated (40-73%) with no clinical signs of hyperthyroidism, circulating thyroid antibodies, or enlargement of the thyroid. In transient hyperthyroidism of hyperemesis gravidarum, thyroid function normalizes by the middle of the second trimester without antithyroid treatment. Clinically overt hyperthyroidism and thyroid antibodies are usually absent. The severity of nausea appears to be related to the degree of thyroid stimulation. hCG may not be independently involved in the etiology of hyperemesis gravidarum but may be indirectly involved by its ability to stimulate the thyroid.

The stomach pacemaker causes rhythmic peristaltic contractions of the stomach. Abnormal myoelectric activity may cause a variety of gastric dysrhythmias, including tachygastrias and bradygastrias. Gastric dysrhythmias have been associated with morning sickness. The presence of dysrhythmias was associated with nausea while normal myoelectrical activity was present in the absence of nausea. Mechanisms that cause gastric dysrhythmias include elevated estrogen or progesterone levels, thyroid disorders, abnormalities in vagal and sympathetic tone, and vasopressin secretion in response to intravascular volume perturbation. Many of these factors are present in early pregnancy.

Liver disease, usually consisting of mild serum transaminase elevation, occurs in almost 50% of patients with hyperemesis gravidarum. Impairment of mitochondrial fatty acid oxidation (FAO) has been hypothesized to play a role in the pathogenesis of maternal liver disease associated with hyperemesis gravidarum.

Jarnfelt-Samsioe et al found higher levels of triglycerides, total cholesterol, and phospholipids in women with hyperemesis gravidarum compared with matched, nonvomiting, pregnant and nonpregnant controls. This may be related to the abnormalities in hepatic function in pregnant women.

Helicobacter pylori is a bacterium found in the stomach that may aggravate nausea and vomiting in pregnancy. Studies have found conflicting evidence of the role of H pylori in hyperemesis gravidarum. Recent studies in the United States have not shown association with hyperemesis gravidarum. However, persistent nausea and vomiting beyond the second trimester may be due to an active peptic ulcer caused by H pylori infection.

Hyperacuity of the olfactory system may be a contributing factor to nausea and vomiting during pregnancy. Many pregnant women report the smell of cooking food, particularly meats, as triggers to nausea. Striking similarities between hyperemesis gravidarum and motion sickness suggest that unmasking of subclinical vestibular disorders may account for some cases of hyperemesis gravidarum.

Hyperemesis gravidarum is associated with overactivation of sympathetic nerves and enhanced production of tumor necrosis factor (TNF)[21]Increased adenosine levels have also been noted; alpha. since adenosine is an established suppressor of excessive sympathetic nerves activation and cytokine production, the increase in plasma adenosine in hyperemesis gravidarum may be modulatory. Increased fetal DNA has been found in the maternal plasma of women with hyperemesis gravidarum, and the increased DNA is speculated to be derived from trophoblasts that have been destroyed by the hyperactive maternal immune system. Thus, hyperemesis gravidarum may be mediated by immunologic aberrations in pregnancy.

Physiological changes associated with pregnancy interact with each woman's psychologic state and cultural values. Psychologic responses may interact with and exacerbate the physiology of nausea and vomiting during pregnancy. In very unusual instances, cases of hyperemesis gravidarum could represent psychiatric illness, including conversion or somatization disorder or major depression.


obtaining history from the patient, discuss present symptoms. Obtain information pertaining to the timing, onset, severity, pattern, and alleviating and exacerbating factors (eg, relationship to meals, medications, prenatal vitamins, stress, other triggers). A thorough review of systems for any symptoms that might suggest other gastrointestinal, renal, endocrine, and central nervous system disorders is vital. Review past medical history, placing emphasis on past medical conditions, surgeries, medications, allergies, adverse drug reactions, family history, social history (including support system), employment, habits, and diet.

Obtaining a thorough gynecologic history of symptoms, such as vaginal bleeding or spotting, past pregnancies, past use of oral contraceptives, and response to oral contraceptives used, is important. Pay attention to the vital signs, including standing and lying blood pressure and pulse, volume status (eg, mucous membrane condition, skin turgor, neck veins, mental status), general appearance (eg, nutrition, weight), thyroid examination findings, abdominal examination findings, cardiac examination findings, and neurologic examination findings. Laboratory work ups including: - Urinalysis for ketones and specific gravity - Serum electrolytes and ketones - Amylase/lipase - Liver enzymes and bilirubin - TSH, free thyroxine - Urine culture - Calcium level - Hepatitis panel - Hematocrit

Initial management should be conservative and may include reassurance, dietary recommendations, and support.
Suggestions for dietary modification in patients with nausea and vomiting associated with pregnancy include the following: -Eat when hungry, regardless of normal meal times. -Eat frequent small meals. -Avoid fatty and spicy foods and emetogenic foods or smells. Increase intake of bland or dry foods. -Eliminate pills with iron. -High protein snacks are helpful. -Crackers in the morning may be helpful. -Increase intake of carbonated beverages. -Other suggested foods include herbal teas containing peppermint or ginger, other ginger-containing beverages, broth, crackers, unbuttered toast, gelatin, or frozen desserts. -Preconception use of prenatal vitamins may decrease nausea and vomiting associated with pregnancy.

Women with hyperemesis gravdarum usually need to be hospitalized for 24 hours to monitor intake, output and blood chemistries and to prevent dehydration. All oral foods and fluids are withheld. Intravenous fluid (3,000 ml Ringers lactate with added vit. B, for example) may be administered to increase hydration. An antiemetic, such as metoclopramide (Reglan), may be prescribed to control vomiting. Throughout this period, carefully measure intake and output, including the amount of vomitus. If there is no vomiting after the first 24 hours of oral restriction, small amounts of clear fluid may begun and the woman may be discharged home. If she can continue to take clear fluid, small quantities of dry toast, crackers, or cereal may be added every 2-3 hours, then gradually advance to soft diet, then to normal diet. But if vomiting returns at any point, enteral or parenteral nutrition may be prescribed.

Risk for deficient fluid volume may be r/t excessive gastric losses and reduced intake possibly evidence by dry mucous membranes, decreased/concentrated urine, decreased pulse volume and pressure, thirst and hemoconcentration.

Maintain IV fluids, as ordered, until patient can tolerate oral feedings. Maintain NPO status until vomiting stops. Ice chips may be given. Monitor intake and out put, vital signs, weight, serum electrolytes, and urine for ketones. Medicate with antiemetics as prescribed.

Imbalanced nutrition less than body requirements may be r/t inability to ingest/digest/absorb nutrients(prolonged vomiting) possibly evidenced by reported inadequate food intake, lack of interest in food/aversion in eating, and wt. loss. Suggest to decrease fluid intake during meals. Advise woman that oral intake can be restarted when emesis stopped.

Company and diversionary conversation during meal time may be beneficial.

Instruct pt to remain upright for 45 minutes after eating to reduce reflux. Suggest that the patient eat 2-3 dry crackers on awakening in the morning before getting out of the bed to alleviate nausea.