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HYPEREMESIS GRAVIDARUM (HG)
SUBMITTED TO SUBMITTED BY
MRS. SNEHLATA PARASHAR MR. AKSHAY KUMAR MEENA
( LECTURER ) BSC.NURSING 4th YEAR
NAUSEA AND VOMITING IN PREGNANCY
(NVP)
INTRODUCTION- Nausea and vomiting in pregnancy is a
symptom which may be related to pregnancy or may be a
manifestation of some medical surgical gynecological
complication. Which can occur at any time during
pregnancy.
•NAUSEA- Nausea is defind as having discomfort in the
stomach usually accompained by an urge to vomit.
•VOMITING-Vomiting is the involuntary,forceful expulsion
of the contents of one’s stomach through the mouth and
sometime the nose.
•CLASSIFICATION -
• Depending upon the severity-It is clasified into two
types
•1.Simple vomiting of pregnancy or milder type
•2.Hyperemesis graviadrum or severe type
1.SIMPLE VOMITING (Sickness,Emesis Graviadrum)-
• Slight vomiting is so common in early pregnancy (about 80%)
that it is as a symptom of pregnancy the vomiting is small and
clear or bile stained.
• The feature disappears with or without treatment by 12-14
week of pregnancy.
•CAUSES-High level of serum human chorionic gonadotrophin,
estrogen and altred immunological status are considred
responsible for initiation of the menifestation
•2.HYPEREMESIS GRAVIDARUM [ HG ]
• Definition- It is a severe type of vomiting of pregnancy which has got
deleterious effect on the health of mother and /or incapacitates her in
day to day activities .
• The triad of adverse effect due to protracted NVP are :
{a} >5% loss of pregnancy weight.
{b} Dehydration
{c} Electrolyte imbalance
The other adverse effect are: Metabolic acidosis ,due to starvation or
alkalosis due to loss of hydrochloric acid from vomiting .
•INCIDENCE-There has been marked full in the incidence
during the Last 30 years. It is now rarity in hospital
practice{ >1 in 1000 pregnancies}
•Reason-(a) better application of family planning
knowledge which reduces the number of unplanned
pregnancies.
(b) early visit to the antenatal clinic
(c) potent antihistamine and antiemetics drug.
•Etiology-(1) It is mostly limited to the first trimester and
resolves by 20 week(90%)
•(2)It is more common in first pregnancy, with a tendency to
recure again in subsequent pregnancy(15%)
•(3)Younger age.
•(4)Low body weight.
•(5)History of motion sickness or migraine.
•(6)It has got a familial history-mother and sister also suffer
from the same manifestation
•(7)It is more commen in unplanned pregnancy but much less
amongst illegitimates ones. Women with hyperemesis
graviadarum, often sufer from treansient form of hyper
thyoidism (clinical or subclinical) .
•THEORIES-
(1)Hormonal -(a) Excess of chorionic gonadotrophin or higher
biological activity of HCG is assosiated. This is proved by the
frequency of vomiting at the peak level of hcg and also the
incerased assosiated with hydatiform mole or multiple
pregnancy when the hcg titer is very much raised.
•(b)High serum level of estrogen and progestroen excess leading
to relaxation of the cardiac sphincter and stimultaneous
retention of gastric fluids due to impaired gastric motility.
Other hormones involves are thyroxine prolactin leptin and
adrenocortical hormone.
(2)PSYCHOGENIC-It probably aggravates the nausea once it
begins but neurogenic element sometime plays a role as
evidenced by its subsidence after shifting the patient from the
home surrounding(biosocial)
(3)DIETETIC DEFICIENCY-Probably due to low carbohydrate
reserve as it happen after a night without food.deficiency of
vitamin B6 vitamin B1 and protein may be tha effects rather
that the causes.
(4)ALLERGIC OR IMMUNOLOGICAL BASIS
(5)DECREASE GASTRIC MOTILITY
•CAUSES- During early pregnancy
(a)Obstetric causes
-Molar pregnancy (vesicular mole]
-multiple pregnancy
-Hydraminos
(b)Non obstetric causes
(1)gastrointestinal causes
-Appendicitis
-pancreatitis
-peptic ulcers
-gastroenteritis
-intestinal obstruction
(2)Endocrine;DKA
(3)Cerebral tumor
(4)Infectious fever
(5)Drug induced N & V (iron ,opioid)
•Persistent vomiting late in pregnancy
-Acute fatty liver of pregnancy
-Pergnancy induced hyper tention severe preeclempsia,emitent
eclampsia.
-Abnormalplacenta
-Other non obstetric causes of vomiting.
•PATHOLOGY-
•There are no specific morbid anatomical findings.the changes
in the various organ as described by sheehan are the
generalised manifestation of starvation and severe malnutrition
• LIVER-Liver enzyme are elevated.there is centrilobular fatty
infiltration without necrosis.
• KIDNEYS-Usually normal with occasional findings of fatty
changes in the cells of first convoluted tubule which may be
related to acidosis
• HEART-A small heart is a constant findings.there may be
subendocardial hemorrhage.
• BRAIN- Small hemorrhage in the hypothalamic region
giving the manifestation of wernickles encephalopathy
the leison may be related to vitaminB1 deficiency.
• METABOLIC ,BIOCHEMICAL AND CIRCULATORY
CHANGES-The changes are due to the combined effect
of dehydration and starvation due to protracted vomiting
METABOLIC-
Inadequate intake of food
Glycogen depletion
Fat reserve broken down
Low carbohydrate
Incomplete oxidation of fat
Accumulation of ketonebodies
Acetone excreted through kidney and in breath.
Excessive excretion of non protein nitrogen in urine
water &electrolyte imbalance .
BIOCHEMICAL CHANGES
Loss of water and salts
Fall in na+,k+,chloride.
Acidosis and ketosis
Increase in blood urea and uric acid,
Hypoglycemia,hypoproteinaemia,hypovitaminosis
and hyperbilirubinaemia.
•Circulatory-
There is hemoconcentration leading to rise in hemoglobin
percentage,RBC count and hematocrit values there is slight
increase in the white cell count with increase in eosinophills.
There is concomitant reduction of extracellular fluid.
•CLINICAL COURSE-
•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.
•EARLY-Vomiting occurs throughout the day. normal day to day
activities are curtailed.there is no evidance of dehydration or
starvation.
•LATE-Evidence of dehydration and starvation are present.
•SYMPTOMS-
• Vomiting is increased in frequency with retehing. Urine quantity is
diminised even to the stage of olliguria. Epigastric pain constipation
may occur. Complication may apper (discribed below) if not treated.
•SIGNS-
• Features of dehydration and keto acidosis dry coated tongue sunken
eye, acetone smell in breath , tachycardiya , hypotension, rise in
temprature may be noted, jaundice is a late feature. Seen late cases
are rarely seen These days. Veginal examination and ultrasonography
is done to confirm the diagnosis of pragnancy.
•INVESTIGATION-
•1.) Urinanalysis:
•I.Quantity-small,
•II.Dark colour,
•III.High specific gravity with acid reaction
•IV.Presence of acetone,occusional presense of protein and
rarely bile pigments
V.Dimnished or even absense of chloride.
•2.) Biochemical and circulatory changes-LFT’S are
abnormal in many patient (40%) with the rise in the level of
serum transaminases and billurubin. Jaundice may be present.
• Routine and periodic estimation of the serum electrolyte
(sodium potasium,and chloride) is helpful in the management
of cases.
•3.) Serum THS,T3 and Free T4-Women(60%) may suffre from
tranisient phase of thyroid dysfunction.
•4.) Ophthalmoscopic Examination- is required if the patient
is seriously ill. Retinal hemorrhage and detechement of the
retina are the most unfavorable sign.
•5.) ECG-When there is abnormal potasium level.
•COMPLICATION:-
• (1) Maternal-The majority of the clinical manifestation are due to
effects of dehydration and starvation with resultant ketoacidosis.
• Leaving aside those complication may occur which are fortunately rare
nowadays.
• Neurological complication-(a)wernickes encephalopathy,beri beri due
to thiamine deficiency
• (b)peripheral neuritis
• Stress ulcer in stomach
• Jaundice,hepatic failure
• Convulsion and coma
• Hypoprothrombinemia due to vitamin K deficiency.
• Renal failure.
•(2)Effects on the fetus-Fetal usually remain unaffected once the
problem is resolved.fetal risks may be due to low birth weight
and preterm birth.
•PREVENTION:-The only prevention is to impart effective
management to correct simple vomiting of pregnancy
•Common measure,managing nausea and vomiting in
pregnancy -
•(a)To take small amount and at frequent intervals
(b)To drink fluids in between measls and not after the
meals
(c)Not to lie down after meals.
(d)To avoid food that causes gastric irritation
(e)To avoid food(high fat) and odours that trigger nausea
and vomiting
•MANAGEMENT-
•Early causes with nausea vomiting in pregnancy at home with
oral antiemetics.
•The principles in the management are-
• Maintenance of hydration
• To control vomiting.
• To correct the fluid and electrolyte imbalance.
• To correct metabollic disturbance(acidosis and alkalosis).
• To prevent the serious complication of severe vomiting.
• To correct vitamin deficincies.
• Care of pregnancy.
•HOSPITALISATION:-Indication are
• (a) Protracted nausea and vomiting despite use of oral antiemetics
• (b)continued NVP with ketonuria andor weight loss >5%
• FLUIDS-Oral feedings is withheld for at least 24 hours after the
cessation of vomiting.during this period fluid is given through
intravenous drip method.the amount of fluid to be infused in 24
hours,calculated as folows.the total amount of fluid approximately 3
liters of which half is 5% dextrose and half is ringer solution.
• Extra amount of crystallois equal to the amount of vomitus and urine
in 24 hours is to be added. potasium chloride may be given additionally
.serum electrolyte should be estimated and correct if there is any
abnormally.enternal nutrition through nasogastric tube may also be
given.
•DRUGS-(a) Antiemetics drug promethazine(phenargan)25mg
or prochloperazine (stemetil)5mg may be administred twice
daily intramuscularly.
• Vitamin B6 (pyridoxin-25mg) amd doxylamine 25 mg are also
safe and effective combination.
• Metoclopramide stimulates gastric and intestinal motility
without stimulating the secretion. It is found usefull and used
as a second line drug.
•(b) Nutrional supplementation- with vitamin B1 (100mg daily)
vitamin B6 vitamin C and vitamin B12 are given.
•(c) ondasterone-is safe and effective and use as a second line
theraphy.
•NURSING CARE-Sympathetic but firm handling of the patient
is essential. Social and psychological support should be
extended.
• Parentral thiamine should be given to prevent wernickes
encephalopathy.
• Woman with NVP and HG need to be multidisciplinary team
management involving physician psychiatric nutrionist and the
midwife.
•HYPEREMESIS PROGRESS CHART is helpfull to asses the
progress of patient while in hospital. Daily record of pulse,
temprature , blood pressure at least twice daily intake output
urine for acetone protien,bile,blood biochemistry and ECG
•(when serum potassium is abnormal) are important .
•DIET-
•Before the intravenous fluid is ommited the foods are
given orally.at first dry carbohydrate food like
biscuit,bread and toast are given small but frequent
feeds are recommended.
NAUSEA_AND_VOMITING_IN_PREGNANCY_side_share[1] (1).pptx

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NAUSEA_AND_VOMITING_IN_PREGNANCY_side_share[1] (1).pptx

  • 1. HYPEREMESIS GRAVIDARUM (HG) SUBMITTED TO SUBMITTED BY MRS. SNEHLATA PARASHAR MR. AKSHAY KUMAR MEENA ( LECTURER ) BSC.NURSING 4th YEAR
  • 2. NAUSEA AND VOMITING IN PREGNANCY (NVP) INTRODUCTION- Nausea and vomiting in pregnancy is a symptom which may be related to pregnancy or may be a manifestation of some medical surgical gynecological complication. Which can occur at any time during pregnancy.
  • 3. •NAUSEA- Nausea is defind as having discomfort in the stomach usually accompained by an urge to vomit. •VOMITING-Vomiting is the involuntary,forceful expulsion of the contents of one’s stomach through the mouth and sometime the nose.
  • 4. •CLASSIFICATION - • Depending upon the severity-It is clasified into two types •1.Simple vomiting of pregnancy or milder type •2.Hyperemesis graviadrum or severe type
  • 5. 1.SIMPLE VOMITING (Sickness,Emesis Graviadrum)- • Slight vomiting is so common in early pregnancy (about 80%) that it is as a symptom of pregnancy the vomiting is small and clear or bile stained. • The feature disappears with or without treatment by 12-14 week of pregnancy. •CAUSES-High level of serum human chorionic gonadotrophin, estrogen and altred immunological status are considred responsible for initiation of the menifestation
  • 6. •2.HYPEREMESIS GRAVIDARUM [ HG ] • Definition- It is a severe type of vomiting of pregnancy which has got deleterious effect on the health of mother and /or incapacitates her in day to day activities . • The triad of adverse effect due to protracted NVP are : {a} >5% loss of pregnancy weight. {b} Dehydration {c} Electrolyte imbalance The other adverse effect are: Metabolic acidosis ,due to starvation or alkalosis due to loss of hydrochloric acid from vomiting .
  • 7. •INCIDENCE-There has been marked full in the incidence during the Last 30 years. It is now rarity in hospital practice{ >1 in 1000 pregnancies} •Reason-(a) better application of family planning knowledge which reduces the number of unplanned pregnancies. (b) early visit to the antenatal clinic (c) potent antihistamine and antiemetics drug.
  • 8. •Etiology-(1) It is mostly limited to the first trimester and resolves by 20 week(90%) •(2)It is more common in first pregnancy, with a tendency to recure again in subsequent pregnancy(15%) •(3)Younger age. •(4)Low body weight. •(5)History of motion sickness or migraine. •(6)It has got a familial history-mother and sister also suffer from the same manifestation •(7)It is more commen in unplanned pregnancy but much less amongst illegitimates ones. Women with hyperemesis graviadarum, often sufer from treansient form of hyper thyoidism (clinical or subclinical) .
  • 9. •THEORIES- (1)Hormonal -(a) Excess of chorionic gonadotrophin or higher biological activity of HCG is assosiated. This is proved by the frequency of vomiting at the peak level of hcg and also the incerased assosiated with hydatiform mole or multiple pregnancy when the hcg titer is very much raised. •(b)High serum level of estrogen and progestroen excess leading to relaxation of the cardiac sphincter and stimultaneous retention of gastric fluids due to impaired gastric motility. Other hormones involves are thyroxine prolactin leptin and adrenocortical hormone.
  • 10. (2)PSYCHOGENIC-It probably aggravates the nausea once it begins but neurogenic element sometime plays a role as evidenced by its subsidence after shifting the patient from the home surrounding(biosocial) (3)DIETETIC DEFICIENCY-Probably due to low carbohydrate reserve as it happen after a night without food.deficiency of vitamin B6 vitamin B1 and protein may be tha effects rather that the causes. (4)ALLERGIC OR IMMUNOLOGICAL BASIS (5)DECREASE GASTRIC MOTILITY
  • 11. •CAUSES- During early pregnancy (a)Obstetric causes -Molar pregnancy (vesicular mole] -multiple pregnancy -Hydraminos (b)Non obstetric causes (1)gastrointestinal causes -Appendicitis -pancreatitis -peptic ulcers -gastroenteritis -intestinal obstruction
  • 12. (2)Endocrine;DKA (3)Cerebral tumor (4)Infectious fever (5)Drug induced N & V (iron ,opioid) •Persistent vomiting late in pregnancy -Acute fatty liver of pregnancy -Pergnancy induced hyper tention severe preeclempsia,emitent eclampsia. -Abnormalplacenta -Other non obstetric causes of vomiting.
  • 13. •PATHOLOGY- •There are no specific morbid anatomical findings.the changes in the various organ as described by sheehan are the generalised manifestation of starvation and severe malnutrition • LIVER-Liver enzyme are elevated.there is centrilobular fatty infiltration without necrosis. • KIDNEYS-Usually normal with occasional findings of fatty changes in the cells of first convoluted tubule which may be related to acidosis • HEART-A small heart is a constant findings.there may be subendocardial hemorrhage.
  • 14. • BRAIN- Small hemorrhage in the hypothalamic region giving the manifestation of wernickles encephalopathy the leison may be related to vitaminB1 deficiency. • METABOLIC ,BIOCHEMICAL AND CIRCULATORY CHANGES-The changes are due to the combined effect of dehydration and starvation due to protracted vomiting
  • 15. METABOLIC- Inadequate intake of food Glycogen depletion Fat reserve broken down Low carbohydrate Incomplete oxidation of fat
  • 16. Accumulation of ketonebodies Acetone excreted through kidney and in breath. Excessive excretion of non protein nitrogen in urine water &electrolyte imbalance .
  • 17. BIOCHEMICAL CHANGES Loss of water and salts Fall in na+,k+,chloride. Acidosis and ketosis Increase in blood urea and uric acid, Hypoglycemia,hypoproteinaemia,hypovitaminosis and hyperbilirubinaemia.
  • 18. •Circulatory- There is hemoconcentration leading to rise in hemoglobin percentage,RBC count and hematocrit values there is slight increase in the white cell count with increase in eosinophills. There is concomitant reduction of extracellular fluid.
  • 19.
  • 20. •CLINICAL COURSE- •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. •EARLY-Vomiting occurs throughout the day. normal day to day activities are curtailed.there is no evidance of dehydration or starvation. •LATE-Evidence of dehydration and starvation are present.
  • 21. •SYMPTOMS- • Vomiting is increased in frequency with retehing. Urine quantity is diminised even to the stage of olliguria. Epigastric pain constipation may occur. Complication may apper (discribed below) if not treated. •SIGNS- • Features of dehydration and keto acidosis dry coated tongue sunken eye, acetone smell in breath , tachycardiya , hypotension, rise in temprature may be noted, jaundice is a late feature. Seen late cases are rarely seen These days. Veginal examination and ultrasonography is done to confirm the diagnosis of pragnancy.
  • 22. •INVESTIGATION- •1.) Urinanalysis: •I.Quantity-small, •II.Dark colour, •III.High specific gravity with acid reaction •IV.Presence of acetone,occusional presense of protein and rarely bile pigments V.Dimnished or even absense of chloride.
  • 23. •2.) Biochemical and circulatory changes-LFT’S are abnormal in many patient (40%) with the rise in the level of serum transaminases and billurubin. Jaundice may be present. • Routine and periodic estimation of the serum electrolyte (sodium potasium,and chloride) is helpful in the management of cases.
  • 24. •3.) Serum THS,T3 and Free T4-Women(60%) may suffre from tranisient phase of thyroid dysfunction. •4.) Ophthalmoscopic Examination- is required if the patient is seriously ill. Retinal hemorrhage and detechement of the retina are the most unfavorable sign. •5.) ECG-When there is abnormal potasium level.
  • 25. •COMPLICATION:- • (1) Maternal-The majority of the clinical manifestation are due to effects of dehydration and starvation with resultant ketoacidosis. • Leaving aside those complication may occur which are fortunately rare nowadays. • Neurological complication-(a)wernickes encephalopathy,beri beri due to thiamine deficiency • (b)peripheral neuritis • Stress ulcer in stomach • Jaundice,hepatic failure • Convulsion and coma • Hypoprothrombinemia due to vitamin K deficiency. • Renal failure.
  • 26. •(2)Effects on the fetus-Fetal usually remain unaffected once the problem is resolved.fetal risks may be due to low birth weight and preterm birth. •PREVENTION:-The only prevention is to impart effective management to correct simple vomiting of pregnancy •Common measure,managing nausea and vomiting in pregnancy - •(a)To take small amount and at frequent intervals
  • 27. (b)To drink fluids in between measls and not after the meals (c)Not to lie down after meals. (d)To avoid food that causes gastric irritation (e)To avoid food(high fat) and odours that trigger nausea and vomiting
  • 28. •MANAGEMENT- •Early causes with nausea vomiting in pregnancy at home with oral antiemetics. •The principles in the management are- • Maintenance of hydration • To control vomiting. • To correct the fluid and electrolyte imbalance. • To correct metabollic disturbance(acidosis and alkalosis). • To prevent the serious complication of severe vomiting. • To correct vitamin deficincies. • Care of pregnancy.
  • 29. •HOSPITALISATION:-Indication are • (a) Protracted nausea and vomiting despite use of oral antiemetics • (b)continued NVP with ketonuria andor weight loss >5% • FLUIDS-Oral feedings is withheld for at least 24 hours after the cessation of vomiting.during this period fluid is given through intravenous drip method.the amount of fluid to be infused in 24 hours,calculated as folows.the total amount of fluid approximately 3 liters of which half is 5% dextrose and half is ringer solution. • Extra amount of crystallois equal to the amount of vomitus and urine in 24 hours is to be added. potasium chloride may be given additionally .serum electrolyte should be estimated and correct if there is any abnormally.enternal nutrition through nasogastric tube may also be given.
  • 30. •DRUGS-(a) Antiemetics drug promethazine(phenargan)25mg or prochloperazine (stemetil)5mg may be administred twice daily intramuscularly. • Vitamin B6 (pyridoxin-25mg) amd doxylamine 25 mg are also safe and effective combination. • Metoclopramide stimulates gastric and intestinal motility without stimulating the secretion. It is found usefull and used as a second line drug. •(b) Nutrional supplementation- with vitamin B1 (100mg daily) vitamin B6 vitamin C and vitamin B12 are given. •(c) ondasterone-is safe and effective and use as a second line theraphy.
  • 31. •NURSING CARE-Sympathetic but firm handling of the patient is essential. Social and psychological support should be extended. • Parentral thiamine should be given to prevent wernickes encephalopathy. • Woman with NVP and HG need to be multidisciplinary team management involving physician psychiatric nutrionist and the midwife. •HYPEREMESIS PROGRESS CHART is helpfull to asses the progress of patient while in hospital. Daily record of pulse, temprature , blood pressure at least twice daily intake output urine for acetone protien,bile,blood biochemistry and ECG
  • 32. •(when serum potassium is abnormal) are important . •DIET- •Before the intravenous fluid is ommited the foods are given orally.at first dry carbohydrate food like biscuit,bread and toast are given small but frequent feeds are recommended.