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Hyperemesis Gravidarum
Sunil Kumar Daha
Causes of Vomiting in Pregnancy
• Early Pregnancy:
Related to Pregnancy:
-Simple Vomiting
-Hyperemesis
gravidarum
(Pernicious vomiting)
Associated with Pregnancy
Medical: UTI, Hepatitis, Intestinal
infestations, Uraemia, Ketoacidosis
of DM
Surgical: Appendicitis, Peptic Ulcer,
Intestinal obstruction, Cholecystitis
Gynecological: Twisted ovarian
tumor, Fibroid
Causes of Vomiting in Pregnancy
• Late pregnancy:
Related to Pregnancy
-Continuation or
reappearance of simple
vomiting
-Acute fulminating pre-
eclampsia
Associated with
Pregnancy
-Medical, surgical,
gynaecological causes as
in early pregnancy
-Hiatus hernia
Vomiting of Pregnancy
• Simple vomiting of pregnancy or mild type or
morning sickness
• Hyperemesis gravidarum or severe type
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 restrict activities
Morning Sickness
• Disappears with/out treatment in the 12-14th
week of pregnancy
• Human chorionic gonadotrophin and estrogen
• Aggravated by psychogenic factors
Management of Morning Sickness
• Assurance
• Dry toast or biscuit
• Avoid fatty and spicy foods
• Plenty of fluids (2.5 L in 24 hrs)
• Fruit juice
• The smell of certain foods aggravates
symptoms and should be avoided
Management of Morning Sickness
• If simple measures fail, then try anti-emetics
• Vitamin B6 or 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
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-day activities
• Defined variably as “Vomiting sufficiently severe to
produce
 weight loss
 Dehydration
 acidosis from starvation
 alkalosis from loss of hydrochloric acid in vomitus
 hypokalemia”
• It is the vomiting which is severe enough to lead to
hospitalization of the lady
Risk factors
• Limited to 1st trimester
• More common in 1st pregnancy
• Tendency to recur again in subsequent
pregnancies
• Familial history: Mother and sisters also suffer
from the same manifestation
• More prevalent in hydatiform mole and multiple
pregnancy
• Common in unplanned pregnancies
Theories Behind Hyperemesis
Gravidarum
A. HORMONAL
•High hCG
•High Estrogen
•High progesterone
•Other hormones involved:
-thyroxine
-prolactin
-leptin
-adrenocortical hormones
B. PSYCHOGENIC
C. DIETARY DEFICIENCY: Low
carbohydrate reserve, Vit B6,
Vit B1
D. Allergic or Immunologic
E. Decreased gastric motility
F. Liver Theory: Liver can’t
adapt to the high level of
hormones in pregnancy
G. H.pylori infection
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 and haemo-
concentration due to dehydration
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
Pathology
• Biochemical Changes
Occurs due to vomiting dehydration
Decreased Na+, K+, Cl-
Raised blood urea, creatinine, uric acid, ketone
bodies
Hypoglycemia
Hypoproteinemia
Hypovitaminosis
Rare: Hyperbilirubinemia
Fetal vulnerability to
toxins peaks at around 3
months, which is time of
peak susceptibility to
morning sickness.
Clinical Features
•Signs of dehydration:
dry coated tongue,
sunken eyes, oligouria,
loss of skin elasticity ,
increased pulse rate
•Weight loss >5% of Total
Body Weight
•Electrolyte imbalances
like hypokalemia,
hypocalcemia
•Starvation related
ketoacidosis that can
lead to acetone smell in
the breath
•Rise in temperature may
occur
Complications
NEUROLOGICAL
1. Wernicke’s
encephalopathy due
to thiamine deficiency
2. Pontine myelinolysis
3. Peripheral neuritis
4. Korsakoff’s psychosis
5. Ophthalmic: Retinal
haemorrhage
6. Convulsions
7. Coma
OTHER
1. Stress ulcer in the
stomach
2. Esophageal tears
(Mallory-Weiss
Syndrome)
3. Jaundice due to liver
damage
4. Renal failure
5. Vit K deficiency:
bleeding manifestations
Investigations
1. Complete Blood Count
 Haemoconcentration leads to rise Hb, RBC
count, and Hematocrit
 Slight increase in WBC count
2. Electrolytes: Na+, K+, Cl- decreased due to loss in
vomitus
3. Random Blood Glucose: Hypoglycemia
Investigations
4. Urinalysis:
Quantity (too see for oligouria)
Dark color (due to concentration)
High specific gravity with acid reaction
Presence of acetone, occasional presence of
protein and bile pigments
Diminished or even absence of chloride
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
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
Management
PRINCIPLES
•To correct vomiting
•To correct the fluids and electrolytes imbalance
•To correct metabolic disturbances (acidosis and
alkalosis)
•To prevent the serious complications of severe
vomiting
Management
1. Hospitalization
2. Fluids
3. Drugs
4. Nursing Care
5. Diet
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 and oligouria
When there is presence of ketone bodies in
the urine (Rothera’s Test Positive)
1. Hospitalization
Admit the patient
Open IV line and correct fluids
 Send for relevant investigations
Maintain an intake-output chart
Monitor urine output (catheterize the patient)
Monitor the vitals
Test the urine periodically for ketone bodies
2. Fluids
 Oral feeding is withheld for at least 24 hours after the
cessation of vomiting
 During this period, fluid given through IV drip method
 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.
3. Drugs
• Antiemetics such as:
 Vitamin B6 + Doxylamine
 Promethazine
 Prochlorperazine
 Chlorpromazine
 Triflupromazine
 Meclozine HCl
 Metoclopramide  D2 Antagonist
• Given parenterally
H1
Antihistaminics
3. Drugs
• Vitamin supplements like Vitamin B1, Vitamin
B6, Vitamin C and Vitamin B12 may be given
• Hydrocortisone in cases of hypotension or
intractable (hard to heal) vomiting.
• Oral Prednisolone is also useful is severe
cases.
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
5. Diet
• Diet:
Before IV fluids are omitted, food is given
orally
Small and frequent dry meals without fat
Biscuit, bread and toast
Ginger is helpful
Gradually full diet is restored
References
1. Williams Obstetrics, 24th Edition
2. DC Dutta’s Textbook of Obstetrics, 7th Edition
Hyperemesis gravidarum and its management

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Hyperemesis gravidarum and its management

  • 2. Causes of Vomiting in Pregnancy • Early Pregnancy: Related to Pregnancy: -Simple Vomiting -Hyperemesis gravidarum (Pernicious vomiting) Associated with Pregnancy Medical: UTI, Hepatitis, Intestinal infestations, Uraemia, Ketoacidosis of DM Surgical: Appendicitis, Peptic Ulcer, Intestinal obstruction, Cholecystitis Gynecological: Twisted ovarian tumor, Fibroid
  • 3. Causes of Vomiting in Pregnancy • Late pregnancy: Related to Pregnancy -Continuation or reappearance of simple vomiting -Acute fulminating pre- eclampsia Associated with Pregnancy -Medical, surgical, gynaecological causes as in early pregnancy -Hiatus hernia
  • 4. Vomiting of Pregnancy • Simple vomiting of pregnancy or mild type or morning sickness • Hyperemesis gravidarum or severe type
  • 5. 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 restrict activities
  • 6. Morning Sickness • Disappears with/out treatment in the 12-14th week of pregnancy • Human chorionic gonadotrophin and estrogen • Aggravated by psychogenic factors
  • 7. Management of Morning Sickness • Assurance • Dry toast or biscuit • Avoid fatty and spicy foods • Plenty of fluids (2.5 L in 24 hrs) • Fruit juice • The smell of certain foods aggravates symptoms and should be avoided
  • 8. Management of Morning Sickness • If simple measures fail, then try anti-emetics • Vitamin B6 or 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
  • 9. 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-day activities • Defined variably as “Vomiting sufficiently severe to produce  weight loss  Dehydration  acidosis from starvation  alkalosis from loss of hydrochloric acid in vomitus  hypokalemia” • It is the vomiting which is severe enough to lead to hospitalization of the lady
  • 10. Risk factors • Limited to 1st trimester • More common in 1st pregnancy • Tendency to recur again in subsequent pregnancies • Familial history: Mother and sisters also suffer from the same manifestation • More prevalent in hydatiform mole and multiple pregnancy • Common in unplanned pregnancies
  • 11. Theories Behind Hyperemesis Gravidarum A. HORMONAL •High hCG •High Estrogen •High progesterone •Other hormones involved: -thyroxine -prolactin -leptin -adrenocortical hormones B. PSYCHOGENIC C. DIETARY DEFICIENCY: Low carbohydrate reserve, Vit B6, Vit B1 D. Allergic or Immunologic E. Decreased gastric motility F. Liver Theory: Liver can’t adapt to the high level of hormones in pregnancy G. H.pylori infection
  • 12. 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 and haemo- concentration due to dehydration
  • 13. 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
  • 14. Pathology • Biochemical Changes Occurs due to vomiting dehydration Decreased Na+, K+, Cl- Raised blood urea, creatinine, uric acid, ketone bodies Hypoglycemia Hypoproteinemia Hypovitaminosis Rare: Hyperbilirubinemia Fetal vulnerability to toxins peaks at around 3 months, which is time of peak susceptibility to morning sickness.
  • 15. Clinical Features •Signs of dehydration: dry coated tongue, sunken eyes, oligouria, loss of skin elasticity , increased pulse rate •Weight loss >5% of Total Body Weight •Electrolyte imbalances like hypokalemia, hypocalcemia •Starvation related ketoacidosis that can lead to acetone smell in the breath •Rise in temperature may occur
  • 16. Complications NEUROLOGICAL 1. Wernicke’s encephalopathy due to thiamine deficiency 2. Pontine myelinolysis 3. Peripheral neuritis 4. Korsakoff’s psychosis 5. Ophthalmic: Retinal haemorrhage 6. Convulsions 7. Coma OTHER 1. Stress ulcer in the stomach 2. Esophageal tears (Mallory-Weiss Syndrome) 3. Jaundice due to liver damage 4. Renal failure 5. Vit K deficiency: bleeding manifestations
  • 17. Investigations 1. Complete Blood Count  Haemoconcentration leads to rise Hb, RBC count, and Hematocrit  Slight increase in WBC count 2. Electrolytes: Na+, K+, Cl- decreased due to loss in vomitus 3. Random Blood Glucose: Hypoglycemia
  • 18. Investigations 4. Urinalysis: Quantity (too see for oligouria) Dark color (due to concentration) High specific gravity with acid reaction Presence of acetone, occasional presence of protein and bile pigments Diminished or even absence of chloride
  • 19. 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
  • 20. 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
  • 21. Management PRINCIPLES •To correct vomiting •To correct the fluids and electrolytes imbalance •To correct metabolic disturbances (acidosis and alkalosis) •To prevent the serious complications of severe vomiting
  • 22. Management 1. Hospitalization 2. Fluids 3. Drugs 4. Nursing Care 5. Diet
  • 23. 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 and oligouria When there is presence of ketone bodies in the urine (Rothera’s Test Positive)
  • 24. 1. Hospitalization Admit the patient Open IV line and correct fluids  Send for relevant investigations Maintain an intake-output chart Monitor urine output (catheterize the patient) Monitor the vitals Test the urine periodically for ketone bodies
  • 25. 2. Fluids  Oral feeding is withheld for at least 24 hours after the cessation of vomiting  During this period, fluid given through IV drip method  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.
  • 26. 3. Drugs • Antiemetics such as:  Vitamin B6 + Doxylamine  Promethazine  Prochlorperazine  Chlorpromazine  Triflupromazine  Meclozine HCl  Metoclopramide  D2 Antagonist • Given parenterally H1 Antihistaminics
  • 27. 3. Drugs • Vitamin supplements like Vitamin B1, Vitamin B6, Vitamin C and Vitamin B12 may be given • Hydrocortisone in cases of hypotension or intractable (hard to heal) vomiting. • Oral Prednisolone is also useful is severe cases.
  • 28. 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
  • 29. 5. Diet • Diet: Before IV fluids are omitted, food is given orally Small and frequent dry meals without fat Biscuit, bread and toast Ginger is helpful Gradually full diet is restored
  • 30. References 1. Williams Obstetrics, 24th Edition 2. DC Dutta’s Textbook of Obstetrics, 7th Edition

Editor's Notes

  1. Fulminant: any event or process that occurs suddenly and quickly, and is intense and severe to the point of lethality A hiatus hernia happens when part of the stomach squeezes through an opening in the diaphragm, called the hiatus, and into the chest.  This is also known as a hiatal hernia. Can cause GERD.
  2. Deleterious = causing harm or damage
  3. Progesterone  retention of the gatric fluids due to impaired gastric motility Psychogenic  Becomes better after shifting from home environment, excessive perception of sensation
  4. WE=encephalopathy, ataxic gait, occulomotor problem. Due to thiamine deficiency. When persistent learning and memory deficits are present in patients withWernicke encephalopathy (a clinical triad that classically, but not always, consists of confusion, ataxia, and nystagmus [or ophthalmoplegia]), the symptom complex is often called Wernicke-Korsakoff syndrome. Clinically, this term is best conceptualized as 2 distinct syndromes, with one being characterized by an acute/subacute confusional state and often reversible findings of Wernicke encephalopathy and the other by persistent and irreversible findings of Korsakoff dementia. Central pontine myelinolysis (CPM), also known as Osmotic demyelination syndrome, is a neurological disease caused by severe damage of the myelin sheath. Peripheral neuritis =tingling, numbness, weakness
  5. Wernicke’s : Nystagmus, vertical and horizontal Weakness or paralysis of lateral rectus muscles - Occurs bilaterally but can be asymmetrical and is accompanied by diplopia and internal strabismus Weakness or paralysis of conjugate gaze Nonreacting miotic pupils and complete loss of ocular movements (in advanced cases) Ptosis, small retinal hemorrhages, involvement of near-far focusing mechanism, and optic neuropathy (occasionally) Papilledema (very rare
  6. Depress labyrinthine function, CTZ stimulation and vestibular responses  H1 receptor anatagonist Metoclopramide  Blocks D2 receptors in CTZ, increases gastric motility, ncreases LES tone
  7. Tuna, turney, chicken,sundlower seeds, spinach, banana, potatoes, salmon  vit B6 Intractable =hard to deal with