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Dr. Priya M Bagade
MIMER TALEGAON(D)
INTRODUCTION
HYPER : EXCESSIVE
EMESIS : VOMIT
GRAVIDARUM : PREGNANCY
Nausea/vomit of moderate intensity are especially
common until about 16 week.
Hyperemesis gravidarum occurs when vomiting becomes
intractable in early pregnancy & cause fluid & electrolyte
imbalances & nutritional deficiency.
 Women usually needs to be hospitalized.
DEFINITION
HYPEREMESIS GRAVIDARUM IS DEFINED
VARIABLY AS VOMITING SUFFICIENTLY SEVERE
TO PRODUCE WEIGHT LOSS, DEHYDRATION,
ACIDOSIS FROM STARVATION, ALKALOSIS FROM
LOSS OF CHLORIDE IN VOMIT & HYPOKALAMIA.
SEVERE VOMITING IN PREGNANCY PARTICULARLY
DURING EARLY PREGNANCY CAUSING
DELETERIOUS AFFECTION ON MOTHER’S
HEALTH SUCH AS WEIGHT LOSS, DEHYDRATION,
ACIDOSIS OCCURING FROM STARVATION.
ETIOLOGY
 Unknown
 More common risk factors are-
o Trophoblastic disease
o Multiple pregnancy
o Nulliparity
o Female fetus
o Age > 30year
o Maternal obesity
o Smoking
o Those who had Hyperemesis in previous pregnancy
o Has got familial history.
THEORIES
 HORMONALTHEORY :
-excess of HCG & oestrogen → trigger vomiting centre
-progesterone excess → i)relaxation of cardiac sphincter →
retention of gastric fluid.
ii) decreased gastric and intestinal motility.
 INFECTION
-Helicobacter pylori, a gram negative bacteria, associated
with the development of peptic ulcer where similar symptoms
are seen.
-This organism has been isolated in severe hyperemesis
 PSYCHOGENIC THEORY:
It is associated with AGGRAVATED NAUSEA RELATED
NEUROGENIC ELEMENTS.
Theories
 DIETARY DEFICIENCY: Due to low Chloride reserve
-deficiency of vitamin B1, B6 & protein may be the effect
rather than cause.
 GENETIC
 ALLERGIC OR IMMUNOLOGICAL BASIS
 ANY PATHOLOGY OF :
Vestibular System
Liver
Kidney
Heart
Brain
CLINICAL FEATURE
SYMPTOMS
• Excess vomiting & retching day & night.
• Vomiting initially watery & bilious.(Weight loss seen)
• Oliguria
• Seldom mental symptoms
• Epigastric pain
• Constipation
• Ptyalism
• Spitting
• Fatigue
• Anorexia
CLINICAL FEATURE
SIGN:
• Dehydration
•Muscle wasting
•Ketosis
•Weight loss > 5% of pregnancy weight
•Tachycardia
•Postural hypotension
•Dry coated tongue
•Sunken eyes
•Acetone smell in breath
Pathology
 Metabolic changes
Glycogen depletion- incomplete oxidation of fat- ketone
bodies
 Biochemical- Loss of K, Na, Cl in the vomitus causes
acidosis and ketosis along with increase in blood urea,
uric acid
 Circulatory-
Haemoconcentration- rise in Hb,RBC count, haematocrit
INVESTIGATION
 URINE ANALYSIS
• dark coloured, oliguria, acidic PH
• high specific gravity with acid reaction
• presence of ketones
• Diminished or absent chlorides
 CBC: haemoconcentration- rise in Hb,RBC count, haematocrit
 LIVER FUNCTIONTEST(LFT)
 THYROID FUNCTIONTEST
 SERUM ELECTROLYTES
 ULTRASOUND SCAN
 ECG- when there is hypokalemia
 OPHTHALMOSCOPIC EXAMINATION -retinal haemorrhages &
detachment
MANAGEMENT
Principles of management:-
To control vomiting.
To correct fluid & electrolyte imbalance.
To correct metabolic disturbance.
To prevent serious complications of severe vomiting.
Care of pregnancy.
Cold meals reduce smell related nausea.
Avoid caffeine & alcohol as these can enhancer dehydration.
Meal high in Carbohydrates & low in fat is better.
General Consideration
 Oral Medications will not be effective if the woman is
dehydrated.
With severe Hyperemesis, the risk of using certain
medicines is less than the risk of malnutrition and
significant weight loss
Always ask a health care provider before taking any
medications.
MEDICAL MANAGEMENT
DRUGS:
Antihistaminics:
Meclizine 50 mg I/V, I/M or orally
Dimenhydrinate
Diphenhydramine
Doxylamine 10 mg BD or TDS
Phenothiazines
Promethazin(phenargan) 25mg IM bd or tds maximum 150mg/day
Prochlorperazine(stemetil) 50 mg/day in divided doses
Chlorpromazine
Trifluopromazine 10mg IM
Drug stimulating gastric and intestinal motility without stimulating the secretions
Metachlopromide 10mg IM TDS
Nutritional support:- Vitamin B1, vitamin B6, vitamin B12 & vitamin C
MEDICAL MANAGEMENT
Drugs decreasing stomach acid production and reflux
Ranitine
Famotidine
Lansoprazole
Drugs decreasing stimulation of the vomiting centre in the brain
Ondencetron
Granisetron
Dolasetron
Steriods
Hydrocortisone:- 100mg IV in drip or I/M (for hypotension or intractale vomiting)
Pridnisolone orally maximum 60mg/day.
OTHER MANAGEMENT
FLUID: (Oral Fluid restricted)
• 3 liters-5% dextrose & RL infusion in 24 hrs.
• K+ supplement fluid (Correct Serum Electrolytes)
NURSING MANAGEMENT:-
 Initiate measures to alleviate nausea including medication
therapy. If unsuccessful on weight loss & electrolyte
imbalances correction occur, IV administration of fluid &
electrolyte replacement or total parenteral nutrition may be
necessary.
 Monitor lab data & look for sign of dehydration & electrolyte
imbalances.
NURSING MANAGEMENT
 Monitor urine for ketone.
 Monitor fetal heart rate, fetal activity & fetal growth.
 Encourage intake of small proportion of food.
 Liquid should be taken b/w meals to avoid distending
stomach & triggering vomit.
 Encourage patient to sit upright after meal.
OBSTETRIC CARE
No therapeutic abortion is indicated if patient improve on
therapy.
Therapeutic abortion is seldom indicated on-
o Vomiting doesn’t stop on therapy
o if there is risk of complication.
COMPLICATIONS
Dehydration
electrolyte imbalance
renal failure
Neurological-
 Wernicke’s Encephalopathy
(Thiamine deficiency)
 Korsakoff’s psychosis
 Peripheral neuritis
 Pontine myelinolysis
Vitamin K deficiency : maternal coagulopathy or foetal
intracranial haemorrhage
COMPLICATIONS
 Mallory Weiss tears
Characterized by upper gastro-intestinal bleeding
secondary to longitudinal mucosal lacerations at the
gastroesophageal junction or gastric cardia.
 Stress ulcers in Stomach
COMPLICATIONS
 Boerhaave syndrome - characterized by upper
gastrointestinal bleeding secondary to transmural
perforation of the esophagus
 Renal Failure, Convulsions, Coma.
HYPEREMESIS GUIDELINES
 A doxylamine/pyridoxine combination should be the standard
of care, since it has the greatest evidence to support its efficacy
and safety. (I-A)
 H1 receptor antagonists should be considered in the
management of acute or breakthrough episodes of NVP. (I-A)
 Pyridoxine monotherapy supplementation may be considered
as an adjuvant measure. (I-A)
 Phenothiazines are safe and effective for severe NVP. (I-A)
SOGC 2002, ACOG 2010
HYPEREMESIS GUIDELINES
Metoclopramide is safe to be used for management of
NVP, although evidence for efficacy is more limited. (II-
2D)
Corticosteroids should be avoided during the first
trimester because of possible increased risk of oral clefting
and should be restricted to refractory cases. (I-B)
When NVP is refractory to initial pharmacotherapy,
investigation of other potential causes should be
undertaken. (III-A)
SOGC 2002, ACOG 2010
Hyperemesis Gravidarum.pptx

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Hyperemesis Gravidarum.pptx

  • 1. Dr. Priya M Bagade MIMER TALEGAON(D)
  • 2. INTRODUCTION HYPER : EXCESSIVE EMESIS : VOMIT GRAVIDARUM : PREGNANCY Nausea/vomit of moderate intensity are especially common until about 16 week. Hyperemesis gravidarum occurs when vomiting becomes intractable in early pregnancy & cause fluid & electrolyte imbalances & nutritional deficiency.  Women usually needs to be hospitalized.
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  • 4. DEFINITION HYPEREMESIS GRAVIDARUM IS DEFINED VARIABLY AS VOMITING SUFFICIENTLY SEVERE TO PRODUCE WEIGHT LOSS, DEHYDRATION, ACIDOSIS FROM STARVATION, ALKALOSIS FROM LOSS OF CHLORIDE IN VOMIT & HYPOKALAMIA. SEVERE VOMITING IN PREGNANCY PARTICULARLY DURING EARLY PREGNANCY CAUSING DELETERIOUS AFFECTION ON MOTHER’S HEALTH SUCH AS WEIGHT LOSS, DEHYDRATION, ACIDOSIS OCCURING FROM STARVATION.
  • 5. ETIOLOGY  Unknown  More common risk factors are- o Trophoblastic disease o Multiple pregnancy o Nulliparity o Female fetus o Age > 30year o Maternal obesity o Smoking o Those who had Hyperemesis in previous pregnancy o Has got familial history.
  • 6. THEORIES  HORMONALTHEORY : -excess of HCG & oestrogen → trigger vomiting centre -progesterone excess → i)relaxation of cardiac sphincter → retention of gastric fluid. ii) decreased gastric and intestinal motility.  INFECTION -Helicobacter pylori, a gram negative bacteria, associated with the development of peptic ulcer where similar symptoms are seen. -This organism has been isolated in severe hyperemesis  PSYCHOGENIC THEORY: It is associated with AGGRAVATED NAUSEA RELATED NEUROGENIC ELEMENTS.
  • 7. Theories  DIETARY DEFICIENCY: Due to low Chloride reserve -deficiency of vitamin B1, B6 & protein may be the effect rather than cause.  GENETIC  ALLERGIC OR IMMUNOLOGICAL BASIS  ANY PATHOLOGY OF : Vestibular System Liver Kidney Heart Brain
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  • 9. CLINICAL FEATURE SYMPTOMS • Excess vomiting & retching day & night. • Vomiting initially watery & bilious.(Weight loss seen) • Oliguria • Seldom mental symptoms • Epigastric pain • Constipation • Ptyalism • Spitting • Fatigue • Anorexia
  • 10. CLINICAL FEATURE SIGN: • Dehydration •Muscle wasting •Ketosis •Weight loss > 5% of pregnancy weight •Tachycardia •Postural hypotension •Dry coated tongue •Sunken eyes •Acetone smell in breath
  • 11. Pathology  Metabolic changes Glycogen depletion- incomplete oxidation of fat- ketone bodies  Biochemical- Loss of K, Na, Cl in the vomitus causes acidosis and ketosis along with increase in blood urea, uric acid  Circulatory- Haemoconcentration- rise in Hb,RBC count, haematocrit
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  • 13. INVESTIGATION  URINE ANALYSIS • dark coloured, oliguria, acidic PH • high specific gravity with acid reaction • presence of ketones • Diminished or absent chlorides  CBC: haemoconcentration- rise in Hb,RBC count, haematocrit  LIVER FUNCTIONTEST(LFT)  THYROID FUNCTIONTEST  SERUM ELECTROLYTES  ULTRASOUND SCAN  ECG- when there is hypokalemia  OPHTHALMOSCOPIC EXAMINATION -retinal haemorrhages & detachment
  • 14. MANAGEMENT Principles of management:- To control vomiting. To correct fluid & electrolyte imbalance. To correct metabolic disturbance. To prevent serious complications of severe vomiting. Care of pregnancy.
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  • 18. Cold meals reduce smell related nausea. Avoid caffeine & alcohol as these can enhancer dehydration. Meal high in Carbohydrates & low in fat is better.
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  • 22. General Consideration  Oral Medications will not be effective if the woman is dehydrated. With severe Hyperemesis, the risk of using certain medicines is less than the risk of malnutrition and significant weight loss Always ask a health care provider before taking any medications.
  • 23. MEDICAL MANAGEMENT DRUGS: Antihistaminics: Meclizine 50 mg I/V, I/M or orally Dimenhydrinate Diphenhydramine Doxylamine 10 mg BD or TDS Phenothiazines Promethazin(phenargan) 25mg IM bd or tds maximum 150mg/day Prochlorperazine(stemetil) 50 mg/day in divided doses Chlorpromazine Trifluopromazine 10mg IM Drug stimulating gastric and intestinal motility without stimulating the secretions Metachlopromide 10mg IM TDS Nutritional support:- Vitamin B1, vitamin B6, vitamin B12 & vitamin C
  • 24. MEDICAL MANAGEMENT Drugs decreasing stomach acid production and reflux Ranitine Famotidine Lansoprazole Drugs decreasing stimulation of the vomiting centre in the brain Ondencetron Granisetron Dolasetron Steriods Hydrocortisone:- 100mg IV in drip or I/M (for hypotension or intractale vomiting) Pridnisolone orally maximum 60mg/day.
  • 25. OTHER MANAGEMENT FLUID: (Oral Fluid restricted) • 3 liters-5% dextrose & RL infusion in 24 hrs. • K+ supplement fluid (Correct Serum Electrolytes) NURSING MANAGEMENT:-  Initiate measures to alleviate nausea including medication therapy. If unsuccessful on weight loss & electrolyte imbalances correction occur, IV administration of fluid & electrolyte replacement or total parenteral nutrition may be necessary.  Monitor lab data & look for sign of dehydration & electrolyte imbalances.
  • 26. NURSING MANAGEMENT  Monitor urine for ketone.  Monitor fetal heart rate, fetal activity & fetal growth.  Encourage intake of small proportion of food.  Liquid should be taken b/w meals to avoid distending stomach & triggering vomit.  Encourage patient to sit upright after meal.
  • 27. OBSTETRIC CARE No therapeutic abortion is indicated if patient improve on therapy. Therapeutic abortion is seldom indicated on- o Vomiting doesn’t stop on therapy o if there is risk of complication.
  • 28. COMPLICATIONS Dehydration electrolyte imbalance renal failure Neurological-  Wernicke’s Encephalopathy (Thiamine deficiency)  Korsakoff’s psychosis  Peripheral neuritis  Pontine myelinolysis Vitamin K deficiency : maternal coagulopathy or foetal intracranial haemorrhage
  • 29. COMPLICATIONS  Mallory Weiss tears Characterized by upper gastro-intestinal bleeding secondary to longitudinal mucosal lacerations at the gastroesophageal junction or gastric cardia.  Stress ulcers in Stomach
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  • 31. COMPLICATIONS  Boerhaave syndrome - characterized by upper gastrointestinal bleeding secondary to transmural perforation of the esophagus  Renal Failure, Convulsions, Coma.
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  • 33. HYPEREMESIS GUIDELINES  A doxylamine/pyridoxine combination should be the standard of care, since it has the greatest evidence to support its efficacy and safety. (I-A)  H1 receptor antagonists should be considered in the management of acute or breakthrough episodes of NVP. (I-A)  Pyridoxine monotherapy supplementation may be considered as an adjuvant measure. (I-A)  Phenothiazines are safe and effective for severe NVP. (I-A) SOGC 2002, ACOG 2010
  • 34. HYPEREMESIS GUIDELINES Metoclopramide is safe to be used for management of NVP, although evidence for efficacy is more limited. (II- 2D) Corticosteroids should be avoided during the first trimester because of possible increased risk of oral clefting and should be restricted to refractory cases. (I-B) When NVP is refractory to initial pharmacotherapy, investigation of other potential causes should be undertaken. (III-A) SOGC 2002, ACOG 2010