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.
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Vomiting in pregnancy
1.
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
4.
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
7.
8.
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.
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.
23.
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
37.
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)
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]
CODEBREAKER
CODEBREAKER
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]
