This document describes the case of a 28-year-old pregnant woman in her 12th week of gestation who is experiencing severe vomiting and inability to keep food or drink down. After examination, she is found to have signs of dehydration. Tests show electrolyte imbalances and ketones in her urine, consistent with hyperemesis gravidarum. She is treated with IV fluids, potassium supplementation, and antiemetics. The document then provides background information on hyperemesis gravidarum, including risk factors, pathogenesis, clinical presentation, diagnostic evaluation, and treatment approaches.

2.  A case: Hx, PE, Investigations, management
 Pregnancy in vomiting:
 Introduction
 Epidemiology
 Risk factors
 Pathogenesis
 Clinical features
 Investigation
 Treatment
 Prognosis

3.  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

5. 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

6.  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

9.  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.

10.  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??

11.  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

12.  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

13.  Good hydration of patient
 Regular antiemitics
 KCl 20 unite with normal saline

14. Hyperemesis Gravidarum

15.  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

16.  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

17.  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

18. The pathogenesis of nausea and vomiting in pregnancy is
unknown
Psychological
Hormonal
Gastrointestinal

19. 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

20.  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

21.  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.

22.  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.

24.  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

25.  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

26.  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

27.  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

28.  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

29.  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

30.  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

31.  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

32.  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.

33.  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

34.  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

35.  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

36.  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

38.  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)

39.  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

40.  THANK YOU