NOTES FOR UNDERGRADUATES AND POSTGRADUATES IN GYNE

1. DR.PRIYA SAXENA

2.  DEFINITION:
 Hyperemesis gravidarum is characterized by severe nausea and
intractable vomiting sufficient to interfere with maternal nutrition
causing deleterious effect on her health.

3.  Multiple pregnancy
 Molar pregnancy
 Family history
 History of hyperemesis in previous pregnancy

4.  Hormonal changes implicated in hyperemesis:
Elevated levels of-
 Estrogen
 Progesterone
 Human chorionic gonadotropin
 Thyroxine
 Placental growth hormone
 Adrenocortical hormones
 Prolactin

5.  Upper gastrointestinal dysmotility:
 During pregnancy esophageal,gastric and small bowel motility are
impaired as a result of smooth muscle relaxation induced by high
levels of progesterone.
 This dysmotility could be a factor contributing to nausea and
vomiting in pregnancy
 Dietary deficiency:
 Low carbohydrate intake, vitamins B1 and B6 deficiency have
been blamed
 Genetic:
 There is a familial tendency in daughters and sisters

6.  Psychological factors:
 Psychological factors are thought to play a major role
 Hyperemesis may be a response to stress or a somatization
disorder
 The woman’s attitude toward the pregnancy, environment and lack
of emotional support may also be underlying factors.
 Allergic or Immunological basis
 Infection:
 Helicobacter pylori has been blamed in some cases of severe
hyperemesis but it is not conclusive
 Vestibular system dysfunction
 Liver dysfunction: can also cause hyperemesis gravidarum

7.  There are no specific morbid anatomical findings.
 The changes in the various organs as described by Sheehan are the
generalized manifestations of starvation and severe malnutrition.
 Liver: Liver enzymes are elevated. There is centrilobular fatty
infiltration without necrosis.
 Kidneys: Usually normal with occasional findings of fatty change
in the cells of first convoluted tubule,which may be related to
acidosis.
 Heart: A small heart is a constant finding. There may be
subendocardial hemorrhage.
 Brain: Small hemorrhages in the hypothalamic region giving the
manifestation of Wernicke’s encephalopathy. The lesion may be
related to vitamin B1 deficiency.

8.  Metabolic: Inadequate intake of food results in glycogen
depletion. For the energy supply, the fat reserve is broken down.
o Due to low carbohydrate, there is incomplete oxidation of fat and
accumulation of ketone bodies in the blood.
o The acetone is ultimately excreted through the kidneys and in the
breath.
o There is also increase in endogenous tissue protein metabolism
resulting in excessive excretion of nonprotein nitrogen in the
urine.
o Water and electrolyte metabolism are seriously affected leading to
biochemical and circulatory changes.

9.  Biochemical:
o Patients develop acidosis (due to starvation) and alkalosis from
loss of hydrochloric acid and hyokalemia.
o Loss of water and salts in the vomitus results in fall in plasma
sodium, potassium and chlorides.
o The urinary chloride may be well below the normal 5 g/L or may
even be absent.
o Hepatic dysfunction results in ketosis with rise in blood urea and
uric acid.
o Patient suffers from hypoglycemia,hypoproteinemia and
hypovitaminosis.

10.  Circulatory:
o There is hemoconcentration leading to rise in hemoglobin
percentage, RBC count and hematocrit values.
o There is slight increase in the white cell count with increase in
eosinophils.
o There is concomitant reduction of extracellular fluid.

11.  From the management and prognostic point of view, the cases are
grouped into:
 Early
 Late (moderate to severe)
The patient is usually a nullipara, in early pregnancy. The onset is
insidious.
 EARLY: Vomiting occurs throughout the day. Normal day-to-day
activities are curtailed. There is no evidence of dehydration or
starvation.
 LATE: (Evidences of dehydration and starvation are present).

12.  Vomiting is increased in frequency with retching.
 Urine quantity is diminished even to the stage of oliguria.
 Epigastric pain, constipation may occur.
 Complications may appear if not treated.

13.  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.
 Vaginal examination and/or ultrasonography is done to confirm
the diagnosis of pregnancy.

14.  Urinalysis:
(1) Quantity—small, (2) Dark color, (3) High specific gravity with
acid reaction,(4) Presence of acetone, occasional presence of
protein and rarely bile pigments and (5) Diminished or even
absence of chloride.
 Biochemical and circulatory changes: The changes are
mentioned previously. Routine and periodic estimation of the
serum electrolytes (sodium, potassium and chloride) is helpful in
the management of the case.

15.  Serum TSH, T3 and Free T4: Women may suffer from transient
phase of thyroid dysfunction (clinical or subclinical).
 Ophthalmoscopic examination :is required if the patient is
seriously ill. Retinal hemorrhage and detachment of the retina are
the most unfavorable signs.
 ECG: when there is abnormal serum potassium level.

16.  Maternal: The majority of the clinical manifestations are due to
the effects of dehydration and starvation with resultant
ketoacidosis. Leaving aside those symptomatology, the following
complications may occur which are fortunately rare nowadays.
(1) Neurologic complications—
(a) Wernicke’s encephalopathy, beriberi due to thiamine deficiency;
(b) Pontine myelinolysis;
(c) Peripheral neuritis;
(d) Korsakoff’s psychosis.
(2) Stress ulcer in stomach;
(3) Esophageal tear (Mallory-Weiss syndrome);

17. (4) Jaundice, hepatic failure;
(5) Convulsions and coma;
(6) Hypoprothrombinemia due to vitamin K deficiency and
(7) Renal failure.
 Effects on the fetus: Fetus usually remains unaffected once the
problem is resolved. Fetal risks may be due to low birth weight.

18.  The principles in the management are:
 Maintenance of hydration
 To control vomiting
 To correct the fluids and electrolytes imbalance
 To correct metabolic disturbances (acidosis or alkalosis)
 To prevent the serious complications of severe vomiting
 Care of pregnancy.

19.  Diet:
 small meals at 2-3 hourly intervals
 Fluids with lime/mint and electrolytes
 Avoid oily,spicy, acidic and sweet foods
 Avoidance of triggers
 Supportive therapy
 Acupressure
 Medications: Pyridoxine 10mg+doxylamine 10mg is the first line
treatment of choice for nausea and vomiting in pregnancy.

20.  Women with hyperemesis not responding to general measures and those
who present with moderate to severe dehydration, ketosis and electrolyte
disturbances must be hospitalized.
 Other causes of vomiting should be excluded by clinical examination and
investigations.
 Intravenous thiamine 100mg should be considered before initiating IV
dextrose,if vitamin B deficiency is suspected.
 Fluids and electrolytes should be replaced
 If serum potassium is low, additional potassium is added to the IV
fluids(20 mmol of potassium to each bottle of IV fluid
 Ringer lactate can also be used initially and switched to dextrose saline
after 6 hours.
 Dextrose saline should be continued till urine is free of ketone bodies.

21.  Hypomagnesemia and hypocalcemia also should be looked for and
corrected
 Oral fluids should be introduced gradually.

22.  Drugs:
(a) 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.

23. (b) 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.
(c) Nutritional supplementation— with vitamin B1 (100 mg daily),
vitamin B6, vitamin C and vitamin B12 are given.
 Hyperemesis progress chart is helpful to assess the progress of
patient while in hospital.
 Daily record of pulse, temperature, blood pressure at least twice
daily, intake-output, urine for acetone, protein, bile,blood
biochemistry and ECG (when serum potassium is abnormal) are
important.

24.  Clinical features of improvement are evidenced by —
(a) subsidence of vomiting
(b) feeling of hunger
(c) better look
(d) normalization of blood biochemistry (electrolytes)
(e) disappearance of acetone from the breath and urine
(f) normal pulse and blood pressure and
(g) normal urine output.

25. THANK YOU