CASE REPORT

Hyperemesis Gravidarum

Supervised by :
dr. Mutawakkil J. Paransa, Sp.OG

Presented by :
Citra Annabella Handoko 2016 – 061 – 129

DEPARTMENT OF OBSTETRICS AND GYNECOLOGY

RSUD R. SYAMSUDIN, S.H., KOTA SUKABUMI
ATMA JAYA FACULTY OF MEDICINE
PERIOD: FEBRUARY 12 TH 2018 – MARCH 10 TH 2017 2018
 CHAPTER I
INTRODUCTION

Nausea and vomiting in pregnancy (NVP), or “morning sickness,” is one of the

commonest symptoms of pregnancy affecting 50–85% of women during the first half of
pregnancy. Symptoms usually start between 6 and 8 weeks, and most resolve by 20 weeks. Most
women (65–70%) self-manage, but for the remainder symptoms are more severe. The most
severe form – hyperemesis gravidarum (HG) – affects 0.3–1.0% of pregnant women and is
characterised by persistent vomiting, weight loss of greater than 5% of prepregnancy body
weight, and ketonuria. There is no widely accepted point at which NVP becomes HG.1
Study criteria have not been homogeneous, thus reports of population incidences vary.
There does, however, appear to be an ethnic or familial predilection. In population-based studies
from California and Nova Scotia, the hospitalization rate for hyperemesis gravidarum was 0.5
to 0.8 percent. Up to 20 percent of those hospitalized in a previous pregnancy for hyperemesis
will again require hospitalization. In general, obese women are less likely to be hospitalized for
this.2
The etiopathogenesis of hyperemesis gravidarum is likely multifactorial and certainly is
enigmatic. It appears to be related to high or rapidly rising serum levels of pregnancy-related
hormones. Putative culprits include human chorionic gonadotropin (hCG), estrogens,
progesterone, leptin, placental growth hormone, prolactin, thyroxine, and adrenocortical
hormones.2 There seems to be a disordered motility of the upper gastrointestinal tract that
contributes to the problem. In particular, hyperemesis is common in the setting of molar
pregnancies (likely since HCG levels can be very high) and a viable IUP should always be
documented in patients with hyperemesis.3
Superimposed on this hormonal cornucopia are an imposing number of biological and
environmental factors. Other factors that increase the risk for admission include
hyperthyroidism, previous molar pregnancy, diabetes, gastrointestinal illnesses, some restrictive
diets, and asthma and other allergic disorders. The vestibular system has been implicated. An
association of Helicobacter pylori infection has also been proposed, but evidence is not
conclusive. And for unknown reasons perhaps estrogen-related a female fetus increases the risk
by 1.5-fold. Finally, Bolin and coworkers (2013) reported an association between hyperemesis
gravidarum and preterm labor, placental abruption, and preeclampsia. 2
 CHAPTER II
CASE REPORT

2.1 Patient’s Identity

 Name : Mrs. N
 Date of birth / Age : August 9th 1985/ 32 years-old
 Nationality : Indonesian
 Address : Jl. Pelda Suryanta No. 86 RT 01 RW 11 Kec. Citamiang,
Sukabumi
 Marital status : Married
 Occupation : Housewife
 Religion : Moslem
 Date of admission : February 19th, 2017
 Date of examination : February 19th, 2017

2.2 History Taking

Chief Complaint
Patient came to RSUD Syamsudin S.H’s obstetric and gynecology emergency room
due to intractable vomiting for two weeks.
History of Present Ilness
The patient, G2P1A0, was 13 week pregnant came to the RSUD R. Syamsudin, SH
Emergency Unit claimed to have nausea 2 weeks prior to admission. She complained
that she had persistent vomitus, about 7-10 times a day, contained food that she has eaten
with no blood. She got nausea and vomitus everytime she ate or drink. She felt sour and
bitter sensation in the mouth. She also complained she got upper abdominal pain. The
patient got fatigue and weakness. She lost her appetite and lost 3kg. She admitted that
these symptoms interfered her daily activities. Other complains, like palpitation, heat
intolerance, tremor, urination and defecation disturbance were denied. Her first day of
last menstrual period is 21st of Nophember 2017.
History of Past Ilness
History of gastritis : the patient suffered from gastritis when she was
in elementary school and never relapse after she
was 10 year old.
History of hyperpemesis grvidarum : she got persisten vomitus dan nausea when she
was in her first pregnancy 7 years ago. She was
hospitalized at that time.
History of thyroid disease : denied
History of hypertension : denied
History of asthma : denied
History of diabetes mellitus : denied
History of allergy : denied
History of trauma : denied
History of past surgery : denied
History of tuberculosis : denied
Family History
History of hypertension : denied
History of asthma : denied
History of diabetes mellitus : patient’s mother
History of allergy : denied

Menstruation History
Menarche : 13 years old
Menstrual cycle : 28 days, regularly, with duration of 7 days,
dysmenorrhea (-).
Total pads : 2-3 pads/day (40 – 60 cc)
First day of last menstrual cycle : Nophember 21st 2017

Contraception History
She used oral contraception for a year and had no adverse effect. She stopped using the
contraception due to planned pregnancy.
 Antenatal Care
Patient has a routine antenatal care at puskesmas nanggeleng during this pregnancy.
There was no abnormality detected during the visit.
Marital History
Married once, been married for 8 years now.
Gestational History
No Date Gestational Labor Sex Birth Breast
Age History Weight Feeding
1 2011 9 months vaginal male 3800g 6 months

2 This pregnancy

2.3 Physical Examination

General condition : moderately ill
Consciousness : compos mentis
Blood pressure : 110/70 mmHg
Heart rate : 96 bpm
Respiratory rate : 22 x/minute
Temperature : 36,2°C
Weight : 50 kg
Height : 158 cm
BMI : 20.02 kg/m2  normal
General Examination
Eyes : anemic conjunctiva -/-, icteric sclera -/-, sunken eyes +/+
Mouth : dry oral mucosa membrane, smell of ketones (+)
Neck : thyroid enlargement (-), trachea is in the middle
Thorax
 Heart : regular 1st and 2nd heart sounds, murmur -, gallop -
 Lung
 Inspection : symmetric chest expansion in both static and dynamic
breathing
 Percussion : sonor on both lungs
 Auscultation : vesicular breath sounds +/+ regular, rhonchi -/-, wheezing
-/-
  Mammae : hyperpigmentation of areola +/+
nipple retraction -/-
breast milk -/-
Abdomen
 Inspection : convex, striae gravidarum -, linea nigra -
 Auscultation : bowel sound +, 6x/minute
 Palpation : supple in all abdominal region, tenderness -
Extremities : warm, edema -/-/-/-
physiological reflex ++/++/++/++
pathological reflex --/--

2.4 Laboratory Examination

Hematology
Examination Result Units Normal value
Hemoglobin 12.9 g/dL 12-14

Hematocrit 38 % 37-47
Leukocyte 9,300 /µL 4,000-10,000
Eritrocyte 4.2 Juta/µL 3.8-5.2
Trombocyte 258,000 /µL 150,000-450,000
MCV 90 fL 80-100
MCH 31 pg 26-34
MCHC 34 g/dL 32-36
 Urinalysis
Examination Result Units Normal value

Color Yellow Yellow

Clarity Turbid Clear
pH 6.0 4.6-8.0

Specific gravity 1.025 1.005-1.030

Leukocyte - Cell/ µL -
Nitrite - -
Protein - mg/dL -
Glucose - mg/dL -
Keton Positive (+++/150) mg/dL Negative
Urobilinogen - mg/dL -
Bilirubin - -
Eritrocyte - Cell/ µL -

Urine microscopic
Examination Result Units Normal value
Leukocyte 1-2 HPF <6
Eritrocyte 1-2 HPF <3
Epithel + LPF 1-15
cylinder - HPF -

crystal - HPF -
bacteria - LPF -

Ultrasonography
Gestasional age 13-14 weeks, fetal heart rate (+)

CTG Examination
Not performed

2.5 Working Diagnosis

G2P1A0, 32 years old, 13-14 weeks of gestation with hyperemesis gravidarum.
2.6 Management
• IVFD futrolit 500 cc + 1 amp neurobion 20 tpm
• Ranitidin 2x1 amp
• Ondansetron 3x8 mg IV

2.7 Follow Up
Date Subjective Objective Assessment Planning
February 20st The patiet felt Consciousness : G2P1A0, 32 The patient
2018 nauseous and CM year old, 13-14 planned to
06.00 fatigue. BP : 100/60 weeks of discharge
Vomitous (-) mmHg gestation with Take home
Pulse : hyperemesis medicine:
88x/minute gravidarum. -ranitidine
RR : 18x/minute 2x150 mg PO
T : 36.4˚C -ondansetron
Epigastric 3x8 mg PO
tenderness +

2.12 Prognosis
Quo ad vitam : bonam
Quo ad functionam : bonam
Quo ad sanationam : dubia ad bonam
 CHAPTER III
CASE ANALYSIS

3.1. Definition
Mild to moderate nausea and vomiting are especially common in pregnant women until
approximately 16 weeks. In a small proportion of these, however, it is severe and unresponsive
to simple dietary modi cation and antiemetics. Severe unrelenting nausea and vomiting—
hyperemesis gravidarum—is defined variably as being sufficiently severe to produce weight loss
>5%, dehydration, ketosis, alkalosis from loss of hydrochloric acid, and hypokalemia. 2 In this
case, the pasient had persistent vomiting, weight loss, dan ketonuria.
3.2. Epidemiology
NVP affects up to 80% of pregant women and is one of the most common indications for
hospital admission among pregnant women, with typical stays of between 3 and 4 days.
Hyperemesis gravidarum is the severe form of NVP, which affect about 0.3-3.6% of pregnant
women.1 In Indonesia, the prevalence is 1-3%.4 Hyperemesis patients are more likely to be
nonwhite. Patients younger than 30 years are more likely to experience hyperemesis.5
3.3. Risk factor
A number of risk factors associated with hyperemesis have been reported, including
nulliparity, familial predilection low maternal age, multiple gestation, fetal anomalies, a
previous pregnancy complicated by hyperemesis, female sex, psychiatric conditions, and both
high and low maternal prepregnancy weight. Smoking, on the other hand, has been associated
with a reduced risk of hyperemesis.6 In this case, the patient has history of previous pregnancy
complicated by hyperemesis.
3.4. Etiology
Genetic factors increase the risk of occurrence: results from a Norwegian study which
included over 500,000 women found that the risk of HG was 15.2% in the second pregnancy of
women who had a previous history of HG compared with 0.7% in women who did not. The risk
of developing HG is also increased threefold in the daughters of women who suffered from HG.
Endocrine factors, especially higher levels of human chorionic gonadotropin, as is the
case in multiple or molar pregnancies, have been associated with more severe forms of NVP/HG.
A recent observational study found that free human chorionic gonadotropin and pappalysin-1
(also known as pregnancy-associated plasma protein A) were higher in women suffering from
HG than in non-sufferers
 Gestasional transient thyrotoxicosis has been reported in 60% of women suffering from
HG and thyroid-stimulatig hormone levels are raised in women with HG. Certain human
chorionic gonadotropin subtypes can stimulate thyroid-stimulating hormone receptors and so
contribute to the hyperthyroidism. The degree of levels of oestrogen, progesterone and leptin,
and lower levels of adrenocorticotrophic hormone and prolactin have also been associated with
HG.
Delayed gastric emptying related to relaxation of smooth muscle during pregnancy may
influence NVP symptoms. Furthermore, higher rates of Helicobacter pylori infection have been
noted in women suffering from meta-analysis of 25 studies investigating the association of H.
pylori and HG, 14 studies demonstrated an increased risk of HG in infected women (with OR
between 2.42 and 109.3), and 11 studies found no association.
3.5. Pathophysiology
Hormonal factors: Although the exact pathogenesis of NVP and HG unknown, it is
widely accepted that gestational vomiting results from various metabolic and endocrine factors,
many of placental origin. The most implicated factor is human chorionic gonadatropin (hCG).
This link between hCG and NVP is based largely on the temporal relationship between the peak
of NVP and the peak of hCG production, both of which occur between 12 and 14 weeks
gestation. In addition, nausea and vomiting are often worse in pregnant women with conditions
associated with elevated hCG levels such as molar pregnancies, multiple gestations, and Down’s
syndrome. Higher urinary hCG and serum hCG levels have also been found in women with NVP
compared to those who are asymptomatic. Furthermore, a study by Goodwin et al. found that
concentrations of hCG correlated positively with the severity of nausea and vomiting in women
with HG.
The ovarian hormones, estrogen and progesterone, have also been implicated in the
pathogenesis of NVP and HG. Estrogen is thought to contribute to HG by stimulating the
production of nitric oxide via nitrogen oxidase synthetase, leading to relaxation of the cardiac
sphincter and simultaneous retention of gastric fluids due to impaired gastric motility.
Progesterone decreases smooth muscle contractility and may alter gastric emptying and lead to
increased nausea and vomiting.
Metabolic: Inadequate intake of food results in glycogen depletion. For the energy
supply, the fat reserve is broken down. Due to low carbohydrate, there is incomplete oxidation
of fat and accumulation of ketone bodies in the blood. The acetone is ultimately excreted through
the kidneys and in the breath. There is also increase in endogenous tissue protein metabolism
resulting in excessive excretion of nonprotein nitrogen in the urine. Water and electrolyte
metabolism are seriously affected leading to biochemical and circulatory changes.
Biochemical: Patients develop acidosis (due to starvation) and alkalosis from loss of
hydrochloric acid and hyokalemia. Loss of water and salts in the vomitus results in fall in plasma
sodium, potassium and chlorides. The urinary chloride may be well below the normal 5 g/L or
may even be absent. Hepatic dysfunction results in ketosis with rise in blood urea and uric acid.
Patient suffers from hypoglycemia, hypoproteinemia and hypovitaminosis.
Circulatory: There is hemoconcentration leading to rise in hemoglobin percentage, RBC
count and hematocrit values. There is slight increase in the white cell count with increase in
eosinophils. There is concomitant reduction of extracellular fluid.
Whatever may be the cause of initiation of vomiting, it is probably aggravated by the
neurogenic element. Unless it is not quickly rectified, features of dehydration and carbohydrate
starvation supervene and a vicious cycle of vomiting appears — vomiting → carbohydrate
starvation → ketoacidosis → vomiting.
3.6 Clinical manifestation
Nausea and vomitus often begin within weeks of missing menses and thus is caricatured
across most cultures as the initial sign of pregnancy. Symptoms usually peak between 10 and 16
weeks gestation and usually resolve after 20 weeks. Up to 10% of women, however, continue to
be symptomatic beyond 22 weeks.6
The defining symptoms of hyperemesis gravidarum are gastrointestinal in nature and
include nausea and vomiting. Other common symptoms include ptyalism (excessive salivation),
fatigue, weakness, and dizziness.5
Patients may also experience the following:
 Sleep disturbance
 Hyperolfaction
 Dysgeusia
 Decreased gustatory discernment
 Depression
 Anxiety
 Irritability
 Mood changes
 Decreased concentration
This patient has persistent vomiting for 2 weeks, since 11 weeks of gestasional age. She
vomited everytime she ate and drank, about 7-10 times a day. She lost her appetite and
lost 3kg. She also complained about feeling fatigue and ptyalism.
 3.7. Physical examination
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.
Table 3.1. Physical examination in hyperemesis gravidarum

Features of dehydration and ketoacidosis: Dry coated tongue, sunken eyes, acetone smell in
breath, tachycardia, hypotension, rise in temperature may be noted, jaundice is a late feature.
Such late cases are rarely seen these days.
This patient has normal vital sign with dry oral mucosa membrane, smell of ketones in breath,
and sunken eyes.
3.8. Investigations
Table 3.2. Investigations in hyperemesis gravidarum

Urinalysis: (1) Quantity—small, (2) Dark color, (3) High speci c gravity with acid reaction, (4)
Presence of acetone, occasional presence of protein and rarely bile pigments and (5) Diminished

or even absence of chloride. 


Serum TSH, T3 and Free T4: Women may su er from transient phase of thyroid dysfunction

(clinical or subclinical). 


ECG when there is abnormal serum potassium level. 


Ultrasonography is useful not only to confirm the pregnancy but also to exclude other, obstetric
(hydatidiform mole, multiple pregnancy), gynecological, surgical or medical causes of vomiting.
This patient has positive ketonuria (+++), other urinalysis and complete blood count are
unremarkable. Ultrasound examination confimed the singleton pregnancy and exclude
hydatidiform mole.
3.9. Treatment
3.9.1. Hospitalization
 Inpatient management should be considered if there is at least one of the following:
 Interfered her daily activities
 Continued nausea and vomiting and inability to keep down oral antiemetics
 Continued nausea and vomiting associated with ketonuria and/or weight loss (greater
than 5% of body weight), despite oral antiemetics
 Confirmed or suspected comorbidity (such as urinary tract infection and inability to
tolerate oral antibiotics).
3.9.2. Fluid
Administration of i.v. fluids treats the consequences of NVP/HG rather than the symptoms.
Women who are severely dehydrated and ketotic need hospital admission and i.v. fluid and
electrolyte replacement. This is routinely carried out in either a day care ‘outpatient’ setting or
on an inpatient ward.
 If significant ketonuria, 1000 ml 0.9% sodium chloride intravenously over 2 to 4 hours.
Hartmann’s can also be used.
 Thereafter fluids should be reduced to 500 ml 4–6 hourly, the regime being guided by
U&E results, which should be performed daily, particularly for monitoring potassium
levels.
 Avoid glucose initially as it contains insufficient sodium and especially as Wernicke’s
encephalopathy may be precipitated unless thiamine is given first.

3.9.3. Drugs
A. Antiemetic
Antiemetic drugs promethazine (Phenergan) 25 mg or prochlorperazine (Stemetil) 5 mg
or triflupromazine (Siquil) 10 mg may be administered twice or thrice daily
intramuscularly. Trifluoperazine (Espazine) 1 mg twice daily intramuscularly is a potent
antiemetic therapy. Vitamin B6 and doxylamine are also safe and effective.

Metoclopramide stimulates gastric and intestinal motility without stimulating the

secretions. It is found useful. 


B. Corticosteroid
Hydrocortisone 100 mg IV in the drip is given in a case with hypotension or in intractable

vomiting. Oral method prednisolone is also used in severe cases. 7

C. Nutritional supplementation—
 Vitamin B1 (100 mg daily), vitamin B6, vitamin C and vitamin B12 are given. 


3.9.4. Education
A. Diet: Modification of the amount and size of meals consumed throughout the day may
help relieve symptoms. Having smaller amounts of food and fluids more often can help
prevent mild cases of nausea and vomiting from worsening. The meals should contain
more carbohydrate than fat and acid.6 Protein-rich meals also decrease symptoms.
Lighter snacks, including nuts, dairy products, and beans, are often endorsed. Drinks that
contain electrolytes and other supplements are advised. If certain foods or food
preparations trigger nausea, they should be avoided.
B. Women who are affected by this illness should avoid stress and try to get as much rest as
possible. If emotional support is needed, the patient can see a psychologist to help address
the debilitating symptoms. Supportive counseling or crisis intervention may be
necessary. Sympathetic but firm handling of the patient is essential. Social and
psychological upport should be extended
3.10. Complication
Vomiting may be prolonged, frequent, and severe, and a list of potentially fatal
complications is given in Table 3.3.
Table 3 3. Complications of Hyperemesis gravidarum.
 REFERENCES

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Obstetrics. 24th ed. New York: McGraw-Hill Companies,Inc; 2014. 1448 p.
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and Gynecology. Malden, Mass., USA: Blackwell Science, 1998

4. Prawiharjo, Sarwono. 2014. Ilmu Kebidanan. Jakarta: Bina Pustaka. 


5. Ogunyemi DA. Hyperemesis gravidarum. Medscape. 2017. Available at
https://emedicine.medscape.com/article/254751-overview
6. Fell Db, Dodds L, et al. Risk Factors for Hyperemesis Gravidarum Requiring Hospital
Admission During Pregnancy. American College of Obstetricians and Gynecologust.
2006.
7. Dutta D. DC Dutta’s Textbook of Obstetrics including Perinatology and Contraception.
8th ed. New Delhi: Jaypee Brothers Medical Publishers (P) LTD; 2013.