HYPEREMESIS GRAVIDARUM

HYPEREMESIS GRAVIDARUM

Presented by: Reviewed by:

Mrs. Vinaya Kumary T Mrs. Janet Prima Miranda
Asst. professor HOD
Dept of OBG Nursing Dept of OBG Nursing
Yenepoya Nursing Yenepoya Nursing college,
college, mangalore mangalore 2
 LEARNING OBJECTIVES

At the end of the class, students will be able to;

• Understand the causes of vomiting
• Management of vomiting in pregnancy
• Define hyperemesis gravidarum
• Enumerate the risk factors of hyperemesis gravidarum
• Explain the theories behind hyperemesis gravidarum
• Describe the pathology of hyperemesis gravidarum
• Explain the clinical features of hyperemesis gravidarum
• Describe the different measures of management of
hyperemesis gravidarum
• Enumerate the complications of hyperemesis
gravidarum 3
 Causes of Vomiting in Pregnancy
• Early Pregnancy:
Associated with Pregnancy

Related to Pregnancy: Medical: UTI, Hepatitis, Intestinal

infestations, Uraemia, Ketoacidosis
-Simple Vomiting of DM

Surgical: Appendicitis, Peptic Ulcer,

-Hyperemesis Intestinal obstruction, Cholecystitis
gravidarum
(Pernicious vomiting) Gynecological: Twisted ovarian
tumor, Fibroid

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 Causes of Vomiting in Pregnancy

• Late pregnancy:

Related to Pregnancy Associated with

Pregnancy
-Continuation or
reappearance of simple -Medical, surgical,
vomiting gynaecological causes as
in early pregnancy
-Acute fulminating pre-
eclampsia -Hiatus hernia
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 Vomiting of Pregnancy
• Simple vomiting of pregnancy or mild typeor
morning sickness
• Hyperemesis gravidarum or severetype

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 Morning Sickness
• Nausea and occasional sickness in the
morning
• Slight vomiting is common in early pregnancy
• Considered as a symptom of pregnancy
• Vomitus small, clear or bile stained
• Does not impair health or restrictactivities

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 Morning Sickness
• Disappears with/out treatment in the12-14th
week of pregnancy
• Human chorionic gonadotrophin and estrogen
• Aggravated by psychogenic factors

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 Management of Morning
Sickness
• Assurance
• Dry toast or biscuit
• Avoid fatty and spicy foods
• Plenty of fluids (2.5 Lin 24 hrs)
• Fruit juice
• The smell of certain foodsaggravates
symptoms and should be avoided
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 Management of Morning
Sickness
• If simple measures fail, then try anti-emetics
• Vitamin B6or Vitamin B6 plus Doxylamine is
safe and effective and should be considered
first-line pharmacotherapy (American College
of Obstetricians and Gynecologists,2004)
• Antihistaminics, D2 Antagonists, etc. can also
be considered

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 Hyperemesis Gravidarum
• It is a severe type of vomiting of pregnancy which has
got deleterious effect on health of the patient and/or
incapacitates her day-to-dayactivities
• Defined variably as “Vomiting sufficiently severeto
produce
 weight loss
 Dehydration
 acidosis from starvation
 alkalosis from loss of hydrochloric acid invomitus
 hypokalemia”
• It is the vomiting which is severe enough to lead to
hospitalization of the lady
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 Risk factors
• Limited to 1st trimester
• More common in 1st pregnancy
• Tendency to recur again in subsequent
pregnancies
• Familial history: Mother and sisters alsosuffer
from the samemanifestation
• More prevalent in hydatiform mole andmultiple
pregnancy
• Common in unplanned pregnancies

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 Theories Behind Hyperemesis
Gravidarum
B.PSYCHOGENIC
A. HORMONAL
C.DIETARY DEFICIENCY: Low
•High hCG carbohydrate reserve, Vit B6,
Vit B1
•High Estrogen
•High progesterone D. Allergic or Immunologic
•Other hormones involved: E. Decreased gastric motility
-thyroxine
-prolactin F.Liver Theory: Liver can’t
adapt to the high level of
-leptin hormones in pregnancy
-adrenocortical hormones
G. H.pylori infection
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 Pathology
• Liver: Fatty infiltration without necrosis
• Kidney: Occasionally shows fatty degeneration
• Brain: Small hemorrhagic spots in
hypothalamus (may be due to Vit B1
deficiency)
• Blood: Mild leucocytosis andhaemo-
concentration due to dehydration

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 Pathology
• Metabolic
Due to less intake of food
Leads to depletion of glycogen  increases
metabolism of fat  accumulation of ketone
bodies  excreted through breath/urine
Leads to excessive breakdown of proteins in
the body  excessive accumulation of
Nitrogen

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 Pathology
• Biochemical Changes
 Occurs due to vomiting dehydration
 Decreased Na+, K+, Cl-
 Raised blood urea, creatinine, uric acid,ketone
bodies Fetal vulnerability to
 Hypoglycemia toxins peaks at around 3
 Hypoproteinemia months, which is time of
 Hypovitaminosis peak susceptibility to
morning sickness.
 Rare: Hyperbilirubinemia
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 Clinical Features
•Electrolyte imbalances
•Signs of dehydration: like hypokalemia,
dry coated tongue, hypocalcemia
sunken eyes, oligouria,
loss of skin elasticity , •Starvation related
increased pulse rate ketoacidosis that can
lead to acetone smell in
•Weight loss >5% ofTotal the breath
Body Weight
•Rise in temperature may
occur
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 Investigations
1. Complete Blood Count
 Haemoconcentration leads to rise Hb,RBC
count, and Hematocrit
 Slight increase in WBCcount

2. Electrolytes: Na+, K+, Cl- decreased due to loss in

vomitus

3. Random Blood Glucose: Hypoglycemia

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 Investigations
4. Urinalysis:
Quantity (too see for oligouria)
Dark color (due to concentration)
High specific gravity with acidreaction
Presence of acetone, occasional presence of
protein and bile pigments
Diminished or even absence of chloride

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 Investigations
5.Liver Function Tests: Albumin, Prothrombin
time, ALT,AST,ALP,Bilirubin levels

6.Renal Function Test: Urea and Creatinine

levels

7. Ophthalmoscopic examination
Retinal hemorrhage
Detachment of retina

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 Investigations

8. ECG
 Abnormal serum potassium level can cause
arrythmias

9. USG
 Confirms pregnancy
 Excludes molar or twin pregnancy
 Excludes other gynaecological, surgical and medical
causes for the hyperemesis

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 Management
PRINCIPLES

•To correct vomiting

•To correct the fluids and electrolytesimbalance

•To correct metabolic disturbances (acidosis and

alkalosis)

•To prevent the serious complications of severe

vomiting
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Management

1. Hospitalization

2. Fluids

3.Drugs

4.Nursing Care

5. Diet

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 1. Hospitalization
When general measures like dietary advice,
rest and anti-emetics fail to control the
vomiting
When there is clinical evidence of dehydration
like sunken eyeballs, tachycardia, dry furred
tongue, loss of skin turgor andoligouria
When there is presence of ketone bodiesin
the urine (Rothera’s TestPositive)

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 1. Hospitalization
Admit the patient
Open IV line and correct fluids
 Send for relevant investigations
Maintain an intake-output chart
Monitor urine output (catheterize thepatient)
Monitor the vitals
Test the urine periodically for ketonebodies

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 2. Fluids
 Oral feeding is withheld for at least 24 hours after the
cessation of vomiting

 During this period, fluid given through IV dripmethod

 The amount of fluid to be infused in 24 hours is calculated

as: total amount of fluid approx. 3litres, of which half is 5%
is dextrose and half is Ringer’s solution.

 Extra amount of 5% dextrose equal to the amount of

vomitus and urine in 24 hours, is to be added.

 These measures help to correct dehydration, electrolyte

imbalance and keto-acidosis.
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 3. Drugs
• Antiemetics such as:

 Vitamin B6 +Doxylamine
 Promethazine
 Prochlorperazine
 Chlorpromazine
 Triflupromazine H1
 Meclozine HCl Antihistaminics
 Metoclopramide  D2Antagonist

• Given parenterally
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 3. Drugs
• Vitamin supplements like Vitamin B1,Vitamin
B6, Vitamin Cand Vitamin B12 may be given
• Hydrocortisone in cases of hypotension or
intractable (hard to heal)vomiting.
• Oral Prednisolone is also useful is severe
cases.

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 4. Nursing Care

• Sympathetic but firm handling of patient

• Daily monitoring of the patient
• Look for signs of improvement in the patient:
subsidence of vomiting, feeling hungry,better
look, disappearance of acetone from breath
and urine, normal pulse and blood pressure,
normal urine output
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 5. Diet
• Diet:
Before IV fluids are omitted, food isgiven
orally
Small and frequent dry meals without fat
Biscuit, bread and toast
Ginger is helpful
Gradually full diet isrestored

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 Complications
OTHER
NEUROLOGICAL
1. Stress ulcer in the
1. Wernicke’s
stomach
encephalopathy due
2. Esophageal tears
to thiamine deficiency
(Mallory-Weiss
2. Pontine myelinolysis
Syndrome)
3. Peripheral neuritis
3. Jaundice due to liver
4. Korsakoff’s psychosis
damage
5. Ophthalmic: Retinal
4. Renal failure
haemorrhage
5. Vit Kdeficiency:
6. Convulsions
bleeding manifestations
7. Coma 31
 CONCLUSION
Hyperemesis gravidarum is estimated to affect 0.3–
2.0% of pregnant women. While previously known as
a common cause of death in pregnancy, with proper
treatment this is now very rare. Those affected have a
lower risk of miscarriage but a higher risk
of premature birth. Some pregnant women choose to
have an abortion due to hg's symptoms

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 EVALUATION
• List down the causes of vomiting
• Explain the management of vomiting in pregnancy?
• Define hyperemesis gravidarum.
• Enumerate the risk factors of hyperemesis gravidarum?
• Explain the theories behind hyperemesis gravidarum?
• Describe the pathology of hyperemesis gravidarum?
• Explain the clinical features of hyperemesis
gravidarum?
• Describe the different measures of management of
hyperemesis gravidarum?
• Enumerate the complications of hyperemesis
gravidarum? 33
 REFERNCES
1. Jacob Annamma. A comprehensive textbook of Midwifery. 1ST
ed. Jaypee brothers medical publishers;2012
2. Dutta DC. Textbook of Obstetrics. 3ed ed. New Delhi. New
central book agency.2011
3. Fraser DM, Cooper MA. Text book for midwives. 14th ed.
Edinburgh. Churchill Livingstone.2013
4. Pilliteri Adele. Maternal Child health Nursing. 4th ed.
Philadelphia: J. B. Lippincot Company; 2004
5. Williams Obstetrics, 24th Edition

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THANK YOU…

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