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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
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.
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
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.
Deleterious = causing harm or damage
Progesterone retention of the gatric fluids due to impaired gastric motility
Psychogenic Becomes better after shifting from home environment, excessive perception of sensation
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
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
Depress labyrinthine function, CTZ stimulation and vestibular responses H1 receptor anatagonist
Metoclopramide Blocks D2 receptors in CTZ, increases gastric motility, ncreases LES tone
Tuna, turney, chicken,sundlower seeds, spinach, banana, potatoes, salmon vit B6
Intractable =hard to deal with