Vomiting in pregnancy


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done by Al Yaqdhan Al Atbi

Sultan Qaboos university- Oman

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  • HELLP syndrome is a life-threatening obstetric complication usually considered to be a variant or complication of pre-eclampsia.[1] Both conditions usually occur during the later stages of pregnancy, or sometimes after childbirth. "HELLP" is an abbreviation of the three main features of the syndrome:[2]Acute fatty liver of pregnancy is a rare life-threatening complication of pregnancy that occurs in the third trimester or the immediate period after delivery.[1] It is thought to be caused by a disordered metabolism of fatty acids by mitochondria in the mother, caused by deficiency in the LCHAD (long-chain 3-hydroxyacyl-coenzyme A dehydrogenase) enzyme.[2] The condition was previously thought to be universally fatal,[3] but aggressive treatment by stabilizing the mother with intravenous fluids and blood products in anticipation of early delivery has improved prognosis.[4]
  • Psychologic factors — Two general theories are that hyperemesis reflects (1) a conversion or somatization disorder or (2) a response to stress [28]. A feeling of ambivalence about the pregnancy has also been proposed as an etiologic or contributing factor. Although no study has definitively demonstrated that the psychologic makeup of patients with hyperemesis gravidarum differs from those without the disorder, the woman’s psychological response to persistent nausea and vomiting may exacerbate her symptoms as a result of conditioning [28,29].
  • Mallory–Weiss syndrome or gastro-esophageal laceration syndrome refers to bleeding from tears (a Mallory-Weiss tear) in the mucosa at the junction of the stomach and esophagus, usually caused by severe retching, coughing, or vomiting.Wernicke encephalopathy is a syndromecharacterised by ataxia, ophthalmoplegia, nystagmus, confusion, and impairment of short-term memory.[1][2] It is caused by lesions in the medial thalamic nuclei, mammillary bodies, periaqueductal and periventricular brainstem nuclei, and superior cerebellar vermis, often resulting from inadequate intake or absorption of thiamine (vitamin B1), especially in conjunction with carbohydrate ingestion. It is most commonly correlated with prolonged alcohol consumption resulting in thiamine deficiency. Alcoholics are therefore particularly at risk, but it may also occur with thiamine deficiency states arising from other causes, particularly in patients with such gastric disorders as carcinoid syndrome, chronic gastritis, Crohn's disease, and repetitive vomiting, particularly after bariatric surgery.[3][4][5][6]
  • Vomiting in pregnancy

    1. 1.  A case: Hx, PE, Investigations, management  Pregnancy in vomiting:  Introduction  Epidemiology  Risk factors  Pathogenesis  Clinical features  Investigation  Treatment  Prognosis
    2. 2.  28years old female , G3P2 on 12th week of gestation came to the hospital complaining of vomiting several times since few days.  She can not tolerate oral food, or drink immediately vomit any thing she eat  She denied any abdominal pain, diarrhea, or vaginal bleeding or leaking.  She had laparoscopic appendectomy in may/2012  Gynecological Hx: last menstrual period 23/11/2012. otherwise unremarkable  Obstetrical Hx: both pregnancies were uneventful
    3. 3. It is important to consider and exclude other causes of nausea and vomiting, including:  Hyperemesis gravidarum  cholecystitis  hydatiform mole  peptic ulcer disease  gestational hypertension  pyelonephritis     /HELLP syndrome pelvic inflammatory disease hyperthyroidism/thyrotoxico sis inflammatory bowel disease appendicitis  ovarian torsion  gastroenteritis  acute fatty liver disease of pregnancy  cerebral tumor  hepatitis  panreatitis
    4. 4.  O/E she is comfortable, alert, oriented, not in distress, but looks dehydrated.  Vitals: afibrile, tachycardiac 118/min, normal BP, O2 sat 99%  Chest examination: clear
    5. 5.  Important investigations for serious vomiting include:  electrolytes  urine ketones  Given other items on the differential, it is reasonable to consider:        CBC BUN, creatinine thyroid function liver enzymes, bilirubin amylase urinalysis acid-base disturbances  Diagnostic Imaging  A fetal doppler should be used to ascertain fetal viability.  If it is not able to be located, ultrasound surveillance is warranted to rule out hyadifirom mole.
    6. 6.  Urine dipstick:  Ketones +4, proteins +2, blood +4  Culture: normal  Blood tests:  CBC:  RBC: 5.93 (4.10- 5,40) 10^12/L  elevated  Hb : 15.1 (11.0- 14.5) g/dL  elevated  MCV : 73.5 (78.0- 95.0) fL  decreased  Haematocrits: 0.44 ( 0.34- 0.43) L/L elevated  Platelet: normal  WBC : 13.9 (2.40- 9.50) 10^9  elevated??
    7. 7.  Electrolytes profile:  Anion gap 21 mmol/L (5-13)  HCO3- 12 mmol/L (22-29)  K+ 3,4 mmol/L (3.5-5.1)  Na+ 131 mmol/L (135-145)  Cl- 104 mmol/L (98-107) elevated decrease decrease decrease normal Metabolic Alkalosis + hypokalemia  Amylase and lipase: normal
    8. 8.  TFT:  T4 22.4 pmol/L (7.9- 14.4)  TSH 0.19 mIU/L (0,34- 5.60)  LFT: elevated decrease unremarkable  Bed side scan: single intrauterine gestational sac and good cardiac activity
    9. 9.  Good hydration of patient  Regular antiemitics  KCl 20 unite with normal saline
    10. 10. Hyperemesis Gravidarum
    11. 11.  Nausea and vomiting in pregnancy (known as "morning sickness") are common complaints.  N/V in pregnancy can have a significant impact on jobs, activities, family relationships, and moods  Nausea and vomiting are common in pregnancy, affecting up to 70% to 85% of pregnant women.  Hyperemesis gravidarum:  is severe, debilitating nausea and vomiting in pregnancy that generally leads to more than 5 percent weight loss and may require fluid and nutritional supplement
    12. 12.  Nausea and vomiting in pregnancy are more common in:  Primigravidae.  Multiple pregnancy.  History of previous hyperemesis gravidarum.  It is less common with increasing maternal age.  It tends to be a disease of Western society and is less common in developing countries, especially in rural communities.  The incidence of women with severe symptoms is not well- documented; reports vary from 0.3 to 2 percent of pregnancies
    13. 13.  women with multiple gestations  women with hydatidiform mole  women who did not take multivitamins either prior to 6 weeks of gestation or during the peri-conceptional period  women with heartburn and acid reflux  genetic factors appear to play a role.  Women who are supertasters are also at increased risk; in contrast to anosmic women  Non-pregnant women who experience nausea and vomiting related to estrogen–based medication, motion, or migraine are more likely to experience pregnancy-related nausea and vomiting Alcohol use and cigarette smoking (perhaps due to the effect of nicotine) appear to be protective factors
    14. 14. The pathogenesis of nausea and vomiting in pregnancy is unknown Psychological Hormonal Gastrointestinal
    15. 15. Source Etiology Pathophysiology hCG •Distention of gastrointestinal tract •Crossover with TSH, causing gestational thyrotoxicosis Placenta •Estrogen •Progesterone •Decreased gut mobility •Elevated liver enzymes •Decreased LES pressure •Increased levels of sex steroids in hepatic portal system Gastrintestinal tract Helicobacter pylori Increased steroid levels in circulation •Placenta •Corpus luteum
    16. 16.  serum concentrations of human chorionic gonadotropin (hCG) peak during the first trimester  hyperemesis gravidarum is typically seen  serum hCG concentration is higher in women with hyperemesis than in other pregnant women  A causal association between hCG levels and hyperemesis gravidarum has not been firmly established
    17. 17.  Women with the common form of NVP maintain normal vital signs and have normal physical and laboratory examinations  Symptoms usually start between 4 and 7 weeks of gestation and resolve by 16 weeks in about 90% of women.  In contrast to women with mild disease, women with hyperemesis have orthostatic hypotension, laboratory abnormalities, and physical signs of dehydration, and often require hospitalization for stabilization.
    18. 18.  Severe nausea and vomiting  Loss of 5% or more of pre-pregnancy body weight  Dehydration symptoms  Difficulty with activities of daily living  Hyperolfcation: extremely sensitive to odors in their environment  Hypersalivation  some sufferers of HG will experience severe symptoms until they give birth to their baby, and sometimes even after giving birth.
    19. 19.  Laboratory evaluation  indicated in women with persistent nausea and vomiting to determine the severity of disease and to exclude other diagnoses that could account for the symptoms.  standard initial evaluation of pregnant women with persistent nausea and vomiting includes:       measurement of weight orthostatic blood pressures heart rate serum electrolytes urine ketones and specific gravity. An obstetrical ultrasound examination is performed to look for gestational trophoblastic disease and multiple gestation, both of which are associated with these symptoms  Tests to exclude other diagnoses: CBC, BUN, creatinin, LFT, TFT, amylase/lipase
    20. 20.  Electrolyte and acid-base derangements:  hypokalemia and hypochloremic metabolic alkalosis  Increase in hematocrit:  indicating hemoconcentration due to plasma volume depletion  elevated blood urea nitrogen and urine specific gravity.  Abnormal liver enzym:  Increase ALT>AST  Serum amylase and lipase  may increase as much as 5-fold and are of salivary rather than pancreatic origin
    21. 21.  Mild hyperthyroidism:  due to high serum concentrations of hCG which has thyroid-stimulating activity  To differentiate between HG induce hyperthyroidism and hyperthyroidism of other causes are:  the vomiting,  absence of goiter and ophthalmopathy  absence of the common symptoms and signs of hyperthyroidism (heat intolerance, muscle weakness, tremor).  serum free T4 concentrations are only minimally elevated
    22. 22.  Goals of treatment:  Reduce symptoms through changes in diet/environment and by medication  Correct consequences or complications of nausea and vomiting (eg, fluid depletion, hypokalemia, and metabolic alkalosis)  Minimize the fetal effects of maternal nausea and vomiting and their treatment
    23. 23.  Treatment begins with advice about  diet  avoidance of triggers  non-pharmacologic interventions, such as acupressure  oral or rectal medications are added if symptoms do not improve
    24. 24.  Diet:  Meals and snacks  slowly and every 1-2 hr to avoid full stomach  Woman should figure out what foods they tolerate best and try to eat those foods  Fluids are better tolerated if cold, clear, and carbonated or sour (eg, ginger ale, lemonade), and if taken in small amounts between meals  Drinking peppermint tea or sucking peppermint candies can reduce postprandial nausea
    25. 25.  Nonpharmacologic interventions:  Avoidance of triggers  stuffy rooms, odors (eg, perfume, chemicals, food, smoke), heat, humidity, noise, and visual or physical motion (eg, flickering lights, driving)  Acupuncture and acupressure :  P6 acupressure wristbands do not require a prescription and have become a popular self-administered intervention  Hypnosis  Hypnosis has been reported to be helpful in some patients .  Psychotherapy
    26. 26.  Pharmacological treatment:  Complementary and alternative medications (CAM):  Ginger:  RCT studies suggest that powdered ginger is more effective than placebo, and equivalent to vitamin B6 (pyridoxine) for treatment of nausea and vomiting of pregnancy  safety of ginger in pregnancy has been questioned due to in vitro mutagenic properties
    27. 27.  Pyridoxine (vitamin B6):  Pyridoxine improves mild to moderate nausea, but does not significantly reduce vomiting  used as a single agent or in conjunction with doxylamine succinate  Antihistamines (H1 antagonists):  E.g.: doxylamine  Single agent or with vit B6  these agents significantly reduced pregnancy-related nausea and vomiting  In meta-analysis: found that H1-receptor blockers appeared to have a protective effect on risk of malformations  ADE: sedation, dry mouth, lightheadedness, and constipation.
    28. 28.  Without dehydration:  First-line therapy: Antihistamines (H1 antagonists)  E.g.: Diphenhydramine, Meclizine, Dimenhydrinate  Have good fetal and meternal safty  ADE: Sedation, urinary retention, blurred vision, exacerbation of narrow-angle glaucoma  Second-line therapy: Dopamine antagonists  E.g.: phenothiazines (promethazine and prochlorperazine), butyrophenones (droperidol), and benzamides (metoclopramide)  metoclopramide during the first trimester of pregnancy found no significant increase in risk of congenital malformations, low birth weight, preterm delivery, or perinatal death compared with nonexposed infants.  ADE: Sedation, extrapyramidal effects, QT prolongation, severe hypotension; rarely, seizures, agranulocytosis, neuroleptic malignant syndrome, blood dyscrasias  Third-line: Serotonin antagonists  E.g.: Ondansetron, granisetron, and dolasetron  ADE:QT prolongation, QRS widening, hypersensitivity reactions
    29. 29.  Adjunctive therapy:  Acid reducing agent:  E.g.: antacids, H2 blockers, PPI  Acid reducing agent + antiemetic's significant effect  Antacids containing aluminum or calcium are safe and preferable to those containing bismuth or bicarbonate
    30. 30.  With dehydration:  Indications for admition:  Failure of initial intervention  Women who have severe vomiting, weight loss, ketonuria,, poor skin turgor, dehydration, hypotension, alkalosis from hydrochloric acid loss, hypokalemia, or nutritional deficiencies are admitted to the hospital
    31. 31.  Fluids correction:  2 L intravenous Ringer’s lactate infused over 3-5Hr, supplemented with appropriate electrolytes and vitamins  Relief of symptoms is common within one to two days of rehydration  Vitamins and menirals:  provide thiamine (vitamin B1) supplementation Early administration of thiamine is important to prevent a rare maternal complication, Wernicke's encephalopathy  administer a multivitamin (MVI) intravenously pluse folic acid  IV fluid is usually dextrose 5% in 0.45% saline with 20 mEq KCl given at 150 mL/hour  Hypomagnesemia: magnesium sulfate
    32. 32.  Nausea and vomiting in pregnancy is generally mild and self- limiting  Almost 50% of cases resolve by week 14 gestation, and 90% by week 22  Maternal consequences include:      dehydration electrolyte or acid-base imbalances Mallory-Weiss tear Wernicke's encephalopathy Death  Fetal consequences are rare, but include Intra-Uterine Growth Restriction (IUGR)
    33. 33.  http://www.patient.co.uk/doctor/nausea-and- vomiting-in-pregnancy-including-hyperemesisgravidarum  http://ezproxy.squ.edu.om:2265/contents/clinicalfeatures-and-evaluation-of-nausea-and-vomiting-ofpregnancy?source=search_result&search=hyperemesis &selectedTitle=2%7E42  http://www.ncbi.nlm.nih.gov/pubmed/3341360
    34. 34.  THANK YOU