The document discusses the relationship between vomiting and nausea during pregnancy, detailing physiological and pathological aspects such as hyperemesis gravidarum, which affects 1 in 200 pregnant women. It outlines causes, diagnostic investigations, and treatment options, emphasizing the role of vitamin B6 and ginger in managing symptoms. Additionally, the text highlights the importance of recognizing different types of vomiting to identify underlying conditions.

1. AMJAD IDREES MD OBGYN
MOH ,KUWAIT

2. Mala Arora
Vomiting and nausea are closely related and mediated by the same neural
pathways:
■ vomiting or emesis is forceful expulsion of gastric contents;
■ nausea is the imminent desire to vomit;
retching is the rhythmic contractions of abdominal and chest musculature■
that precedes or accompanies vomiting.
These often occur together and may be accompanied by hypersalivation
(ptyalism)
■ formerly know as pregnancy taxicosis.
■ Central Nervous system changes as confuion, Photo phobia and delirium.

3. Physiological vomiting
Physiological vomiting of pregnancy has been described by the Egyptians as early as 2000 BC.
It is most common in the first trimester and may recur in the third trimester in a milder form.
Historically, Fair weather proposed in the 1960s that nausea and vomiting of pregnancy was
an
allergic reaction to pregnancy, which today would be labeled as an immunological response.
However, there has been no substantiation of his theory. There are several reasons proposed
for physiological vomiting in the first trimester of pregnancy as outlined below.
■ Rising progesterone and beta-human chorionic gonadotrophin (?HCG) levels cause delayed
intestinal motility and gastric stasis. Physiological vomiting is exaggerated in cases of
multiple pregnancy and hydatidiform mole owing to higher ?HCG levels.
■ High levels of estrogen and progesterone, which accompany pregnancy, are potential
mediators of gastric slow-wave dysrhythmias in nausea of pregnancy.
■ Vitamin B6 deficiency, which occurs owing to a change in protein metabolism in
pregnancy, hence vitamin B6 is used for its treatment.
■ Relaxation of the gastro-esophageal sphincter and hyperacidity also contribute.
■ Few studies found a correlation between female fetal sex and hyperemesis gravidarum.
■ During the third trimester of pregnancy, the gravid uterus can mechanically reduce the
distensibility of the stomach as well as change the contour of the cardiac sphincter, leading to
an increased incidence of vomiting.

4. Types of vomiting
The most important clues to diagnosis lie in the history of vomiting and its
accompanying symptoms.
■ Vomiting occurring only in the early morning occurs in pregnancy, hyperacidity
and uraemia.
■ Vomiting occurring after food is more likely to point to peptic ulcer,
gastroparesis, pyloric obstruction and food poisoning.
■ Projectile vomiting without nausea occurs in raised intracranial tension. Silent
regurgitation of food occurs in esophageal diverticuli.
■ Vomiting accompanied by tinnitus and/or giddiness is seen in middle ear
disease
■ Vomiting accompanied with diarrhoea occurs in enteritis and food poisoning.
■ Vomiting with chest pain signifies myocardial infarction and, when
accompanied with abdominal pain, could signify appendicitis.

5. Pathological or hyperemesis gravidarum
If vomiting is excessive, develops or persists after 14 weeks of gestation and
leads to dehydration and/or ketosis, it is called hyperemesis gravidarum. It
affects 1 in 200 pregnant women. If vomiting is sustained over a period of time,
it will lead to maternal weight loss, oliguria, hypokalaemic alkalosis and
constipation. Fetal
intrauterine growth restriction is also reported
In such cases, a pathological cause should be excluded. The causes of
hyperemesis gravidarum In a recent study, occurs in chronic
infection with Helicobacter pylori was present in 61.8 per cent of pregnant
patients with hyperemesis in comparison with 27.6 per cent of
pregnant patients without hyperemesis. Other studies have confirmed this
correlation. A recent study from Turkey has shown higher levels of the hormone
leptin in 18 patients with hyperemesis compared to an equal number of
healthy pregnant women.

6. Acute systemic infections
■ For example, chorioamnionitis, and viral infections, such as influenza,
encephalitis, meningitis,
hepatitis, pancreatitis or generalized peritonitis

7. Central nervous system
■ Raised intracranial tension, as in benign intracranial hypertension,
neoplasms, meningitis and
encephalitis
■ Raised intracranial pressure can sometimes occur with pre-eclampsia and
eclampsia owing to cerebral oedema, which can cause vomiting in the third
trimester

8. Middle ear
■ Ménière’s disease
■ Acute viral labyrinthitis
■ Migraine
■ Motion sickness

9. Endocrinal
■ Diabetic ketoacidosis
■ Uraemia
■ Hyperthyroidism
■ Hyperparathyroidism
■ Adrenal insufficiency or Addison’s disease
■ Zollinger–Ellison syndrome

10. Surgical
■ Ovarian torsion, degenerating fibroids
■ Inflammations, such as appendicitis, diverticulitis, cholecystitis
■ Renal and biliary colic
■ Intestinal obstruction (refer to section on intestinal causes)
■ Gallstones

11. Intestinal
■ Enteritis
■ Intestinal inflammation as in ulcerative colitis or Crohn’s disease
■ Intestinal obstruction due to adhesions, hernia, mesenteric lymphadenitis,
adenomatous polyps,stricture, volvulus, Hirchsprung’s disease
■ Food poisoning
● bacterial due to Shigella , Salmonella , Staphylococcus , Clostridium
● viral due to rotavirus
● toxins, such as Clostridium botulinum
● allergy to foods, such as eggs, nuts or mushrooms
■ Intestinal ischaemia, as in mesenteric vein thrombosis, Henoch–Schönlein
purpura
■ Hepatitis viral hepatitis A, B, C, D and E, Epstein–Barr virus,
cytomegalovirus, leptospirosis
■ Pancreatitis due to a calculus in the common bile duct, viral or alcohol
induced

12. Gastrointestinal
Oesophageal
■ Gastro-oesophageal reflux disease
■ Hiatus hernia
■ Achalasia cardia
Gastric
■ Gastritis
■ Peptic ulcers due to Helicobacter pylori
■ Disordered gastrointestinal motility seen in diabetes or idiopathic gastroparesis
■ Pyloric stenosis – partial or complete
■ Fundoplication for obesity
■ Aerophagia syndrome
■ Gastric carcinoma

13. ■ Investigations
These should include the following.
■ Urine analysis : urine should be checked for specific gravity and the presence of
glucose and ketones. It may occasionally show the presence of bile pigments.
■ Complete blood count : this will show a rise in haematocrit and haemoglobin
percentage. There may be slight leucocytosis.
■ Serum electrolytes , such as sodium and potassium: this will show
hyponatraemia, hypokalaemia and, in severe cases, hypokalaemic metabolic
acidosis.
■ Blood sugar : hyperglycaemia may be present in diabetes, while hypoglycaemia
may be present in persistent vomiting, which requires correction with intra-
venous fluids.
■ Liver function tests : 20–30 per cent of women show mild elevation of liver
enzymes in hyperemesis. In cases of hepatitis, the enzymes are markedly raised
and it may be of value to check the hepatitis markers. Serum amylase and/or lipase
will be raised in pancreatitis. Liver function tests also provide an opportunity to
look at serum protein levels, an indication of the nutritional status of the mother.
■ Renal function tests , as renal failure is a complication of severe dehydration.
■ Thyroid function tests : 50–70 per cent of women have transient
hyperthyroidism. This is usually a self-limiting condition and does not require
antithyroid therapy.

14. ■ Parathyroid hormone , if clinically indicated: hyperparathyroidism is a rare
cause of hyperemesis, which may be intractable. High serum calcium levels
will point to the diagnosis. Both maternal and fetal morbidity is high and surgery
is the definitive cure.
■ An electrocardiogram will show widened QRS complexes and U waves in
hypokalaemia.
■ An ultrasound scan to confirm intrauterine pregnancy, to exclude multiple
pregnancy or hydatidiform mole. It will also show the presence of gallstones,
mesenteric adenitis, dilated loops of bowel in intestinal obstruction, the presence
of an appendicular lump and small contracted kidneys in uraemia.

15. Complication of vomiting
The most obvious complications are dehydration and malnutrition.
Loss of gastric fluid leads to dehydration, metabolic alkalosis and
hypokalaemia.
The patient will need fluid replacement to treat the dehydration. A general
examination will give some idea of the severity of dehydration.
The presence of ketones in the urine and a raised haematocrit will confirm the
severity of dehydration. The patient then needs to be admitted to hospital.

16. Treatment of NVP varies with the severity of the disease and can begin
with nonpharmacological choices including dietary/lifestyle modifica-
tion and vitamin/herbal supplementation, followed by pharmacological
antiemetic therapy. Nonpharmacological therapy includes increased rest
and avoidance of foods and odors that trigger symptoms (perfumes,
smoke, petroleum products). Adjustment in eating habits may include
small, frequent snacks with a focus on bland and dry foods or foods
high in protein. Spicy, fatty, and acidic foods may need to be eliminated.
High-protein meals have been shown to alleviate nausea and vomiting
better than carbohydrate or fatty meals.
Acupressure has been used to alleviate symptoms of nausea and vomit-
ing by applying pressure at the Neguian P6 acupoint. This point is located
approximately 2in. proximal to the wrist crease between the flexor carpi
radialis and palmaris longus tendons (Niebyl 2010). See band
Ginger root, a common spice and flavorer, has also been used for treat
ment.Ozgolietal. randomized women to ginger 2 50 mg four times a day for
4 days versus placebo with an improvement in nausea (85% versus 56%;
P=0.01) and a decrease in vomiting (50% versus 9%; P=0.05). Ginger
extracts at doses up to 1g/day have been shown to be more efficacious
at reducing nausea than vitamin B 6 (pyridoxine). ACOG recommends the
use of vitamin B 6 (10–25mg orally every 8hours) alone or in combination
with doxylamine succinate as first-line therapy (ACOG Practice Bulletin
52, 2004).