this PowerPoint presentation involves simplified explanation for emesis & hyperemesis with pregnancy and ways for their management. the difference between both

1. Hyperemesis Gravidarum
By
Dr. Ahmed Nasef
Assistant lecturer at
obstetrics& gynecology
department – Benha
university- Egypt

4. What is emesis
Emesis = vomiting
May be called morning sickness
It doesn’t affect general condition of the patient

6. When it happens?
Occurs in 1st trimester of pregnancy
Usually happens in the morning so the name
morning sickness

7. Is it one of the normal symptoms of
pregnancy?
Yes emesis is one of the frequently occurring
symptoms of pregnancy
About more than two thirds of pregnant women
present with emesis

9. What causes emesis with pregnancy?
The exact cause of morning sickness is
unknown. Hormonal changes are thought to
play a role in morning sickness especially rising
HCG levels in pregnancy 1st trimester

11. Management
Reassurance that with the advance of pregnancy it will disappear
general advice
Avoid immediate recumbency after meals
Iron therapy should be temporarily stopped (nauseating) till after 1st trimester
Drinking plenty of water
Drinking water before and after meals
Take naps
Assurance of ventilation of home and workspace to eliminate nauseating
odors
Avoiding spicy foods
Eating small meals
Avoiding nauseating fatty food
Avoiding cigarette smoke
If no response there is need for medications

12. So where is the problem?

13. The problem is not in emesis, its in
hyperemesis

15. But what is hyperemesis?

16. HEG
It is defined as severe recurrent vomiting to a
degree that affects the general condition

17. What is the incidence of HEG?
About 0.1 to 1% of pregnant women presented
by HEG

18. What are the causes of HEG?
Different theories explain HEG
Psychological theory
as it starts soon after knowing that she is pregnant
Only in front of her husband
Hormonal theory
Due to elevated levels of HCG (which occurs in
vesicular mole& in twins)
Increased levels of T3& T4 may play a role
Vitamin deficiency
B1& B6 deficiency

19. Who is at increased risk?
PG
Multiple gestations
Trophoblastic disease (as vesicular mole)
HEG in previous pregnancies
Overweight
Family history of HEG

20. Stages& clinical presentation of
HEG

21. 1st stage of HEG
Vomiting of food, fluids Which starts mild then
increase in frequency to
become severe intolerable
may be all the day, not
related to meals, not
controlled by usual drugs
Then may be blood tinged
due to injury of esophagus&
pharynx from recurrent
attacks of vomiting (Mallory
Weiss syndrome)

22. 2nd stage of HEG
Stage of starvation
Starvation
Dehydration
Electrolyte imbalance
(decreased Na, K, Cl)
Dry inelastic skin
Thirst sensation
Dry tongue
Drowsiness
Sunken eyes
Constipation
Oliguria
Hypotension
tachycardia

24. 3rd stage of HEG
Stage of organ affection Wernicke's encephalopathy
(degeneration of Wernicke's
area in basal ganglia in
brain)
Retinal detachment&
blindness
Starvation ketosis
Liver failure (fatty
infiltration& necrosis)
Kidney failure (tubular
necrosis)
Heart failure

25. What is ketosis?
Normally body uses glucose to meet energy
needs& major source for glucose is coming from
diet
But in case of HEG there is decrease in glucose
levels in diet so body use lipids to obtain energy
needs which will develop ketones which will be
elevated in blood and then passes out of the
body in urine

26. Management of HEG
Admission to hospital
Full history taking
Examination
Investigations
Observation
Treatment

27. Admission to hospital
Reassurance of the patient
Isolation in single room
Behave with sympathy with the patient
Speak with relatives especially husband to
decrease any psychological stress on the patient

29. Investigations
CBC
Increased Hct (due to hypovolemia)
Electrolyte levels
Decreased Na& K levels in blood
Urine analysis
Increased ketones in urine& no glucose
Thyroid profile
T3& T4 may be increased
Liver function tests (ALT& AST)
Kidney function tests (serum creatinine)
Fundus examination

30. Diet
NPO
Iv fluids (till 24-48 hrs after stoppage of
vomiting)
Then restart gradually by clear fluids&
carbohydrate meals with no fats or spices

31. Drugs
1st line (histamine receptor blockers) which act on both CTZ&
VC in brain so decrease vomiting as meclizine& cyclizine
(Navidoxine)
2nd line (dopamine receptor blockers) which act on CTZ
AS metoclopramide (Primperan)& chlorpromazine (Neurazine)
3rd line (serotonin receptor blockers)
Which act on both CTZ& VC as ondanesteron& granisetron
(Zofran)
Vitamin B6 may be added
Corticosteroids may be added if no response to the above
drugs

32. observation
Mother
Frequency of vomiting
Vital data
Laboratory results
Fundus examination
Any symptoms suggestive of
organ affection
Fetus
Ultrasound (US)

33. When to do TOP?
Deterioration of the general condition in spite of
treatment
Deterioration of organs affected
Methods:
By use of ecbolics, D&C or suction evacuation in
1st trimester
Or may be hysterotomy if in 2nd trimester

35. Take home messages
Emesis is normal association with pregnancy
but hyperemesis is abnormal
Hyperemesis is like starvation but is worse than
starvation because in HEG there is added
vomiting which worsen the condition
HEG may be a cause for TOP
HEG may cause blindness& organs failure