The document discusses several concurrent diseases that can occur during pregnancy including cardiac diseases, hematologic disorders, diabetes mellitus, renal disease, and hypertensive disorders. It provides details on the pathophysiology, risk factors, signs and symptoms, and management for each condition. Pregnancy places additional strain on the cardiovascular system and can exacerbate preexisting cardiac issues. Several anemias are also discussed including iron deficiency, folic acid deficiency, and sickle cell anemia. Close monitoring and supplementation is important for management. Diabetes and gestational diabetes require strict glucose control to prevent complications. Hypertensive disorders in pregnancy like preeclampsia can threaten both mother and baby if not properly treated.

1. CONCURRENT DISEASES
IN PREGNANCY

2. 1- Cardiac diseases in pregnancy
2- Hematologic disorders
3- Diabetes Mellitus and gestational diabetes
4- Renal disease
5- Hypertensive disorders
6- Hyperemesis gravidarum

3. 1- Cardiac diseases in pregnancy
Cardiovascular disease complicates 1 % of all pregnancies, because
congenital anomalies are diagnosed and treated during infancy, as well
as rheumatic fever is more prevented and treated.
• The danger of pregnancy in a woman with cardiac disease occurs
primarily due to the increase in circulatory volume, because both
the blood volume and cardiac output increase more than 30 %. The
most dangerous time for a woman is in weeks 28-32 when the
blood volume peaks.

4. • The determination of whether a woman with cardiovascular disease
can complete a pregnancy depends on the type and extent of her
disease.
• A woman with class I or II heart disease can expect to experience a
normal pregnancy and birth.
• Women with class III can complete a pregnancy by maintaining almost
complete bed rest.
• Women with class IV heart disease are poor candidates for pregnancy

5. • Women with left sided heart failure:
Left-sided heart failure occurs in conditions such as mitral stenosis, mitral
insufficiency, and aortic coarctation.
The left ventricle cannot move the volume of blood forward that is
received by the left atrium from the pulmonary circulation.
The reason for the failure is often at the level of the mitral valve.
The inability of the mitral valve to push blood forward causes back-
pressure on the pulmonary circulation, causing decrease in systemic blood
pressure and pulmonary hypertension and edema.

6. Pulmonary edema interferes with oxygen-carbon dioxide exchange because
the fluid coats the alveolar exchange space.
Because oxygen exchange is limited, women with pulmonary hypertension
are at an extremely high risk for spontaneous miscarriage, preterm labor, and
maternal death during pregnancy.
As the oxygen saturation of the blood decreases from dysfunction of the
alveoli, respiratory rate increases. At first this is noticeable only on exertion,
then finally with rest also.
A woman experiences fatigue, weakness, and dizziness (specifically from
lack of oxygen in brain cells).

7. The heart rate increases and peripheral vasoconstriction occurs in an
attempt to increase the systemic blood pressure.
The fall in blood pressure, causes retention of both sodium and water.
• A woman may be prescribed diuretics to reduce blood volume, and
beta blockers to improve ventricular filling. A low-sodium diet also
may be indicated.
• If blood flow to the uterus is impaired by the blood flow constriction,
poor placental perfusion, intrauterine growth restriction, and fetal
mortality will occur.

8. • Women with right sided heart failure:
Caused by Congenital heart defects such as pulmonary valve stenosis
and atrial and ventricular septal defects.
Output of the right ventricle is less than the blood volume received by
the right atrium from the vena cava.
Back-pressure from this results in congestion of the systemic venous
circulation and decreased cardiac output to the lungs.
Systemic blood pressure decrease (low blood volume in aorta)
Portal hypertension and jugular venous distention

9. Liver and spleen becomes enlarged and causes pain and dyspnea
especially with uterus distention.
Distention of abdominal vessels can lead to a shift of fluid from the vessels
into the peritoneal cavity (ascites). Fluid also moves from the systemic
circulation into lower extremity interstitial spaces (peripheral edema).
• Women who have an uncorrected anomaly of this type, may be advised
not to become pregnant. If they do become pregnant, they can expect to
be hospitalized for the last part of pregnancy.

10. • Woman with peripartum heart disease:
- Extremely rare condition
- Peripheral cardiomyopathy occurs late in pregnancy
- Woman develops signs of myocardial failure (shortness of breath, chest
pain, and edema).
- Heart start to increase in size (cardiomyopathy)
- Women must decrease physical activity
- Diuretic and digitalis therapy to maintain heart action

11. If cardiomegaly persists past the postpartum period, it is generally
suggested that a woman not attempt any further pregnancies because the
condition tends to recur.
Oral contraceptives are contraindicated because of the danger of
thromboembolism they create.
The disease may progress to the point that following pregnancy, a
woman may need a heart transplant.

12. 2- HEMATOLOGIC DISORDERS
• Pseudoanemia
• Iron deficiency anemia
• Folic acid deficiency anemia
• Sickle cell anemia

13. • Iron deficiency anemia:
- The most common anemia of pregnancy
- Deficiency of iron stores resulting from a diet low in iron, heavy
menstrual periods, or unwise weight-reducing programs.
- Low serum iron level and an increased iron-binding capacity
- Iron-deficiency anemia is mildly associated with low birth-weight
and preterm birth.
- Woman experiences extreme fatigue and poor exercise tolerance
because she can not transport oxygen effectively.

14. • Women should take prenatal vitamins containing an iron
supplement .
• In addition they need to eat a diet high in iron and vitamins
(green leafy vegetables, meat, legumes, fruit).
• Iron is best absorbed from an acid medium. Therefore, advise
women to take iron supplements with orange juice or a vitamin C
supplement.

15. • Folic acid deficiency:
- One of the B vitamins
- Seen in 1-5% of pregnancies
- Occurs most often in multiple pregnancies, woman with secondary
hemolytic illness, women who are taking anticonvulsant agent (epilepsy)
- Megaloblastic anemia (enlarged red blood cells)
- Contributory factor in early miscarriage or premature separation of the
placenta

16. • Sickle cell anemia:
- Red blood cells are irregular or sickle-shaped so cannot carry as
much hemoglobin as normally shaped red blood cells
- At high altitudes or with dehydration the cells tend to clump because
of the irregular shape
- This clumping can result in vessel blockage with reduced blood flow
to organs
- The cells then will hemolyze, reducing the number available and
causing a severe anemia

17. - Blockage to the placental circulation can directly compromise the fetus,
causing low birthweight and possibly fetal death.
Prematurity, miscarriage, or perinatal mortality rates may be higher
Therapeutic Management:
- Interventions to prevent sickle cell crisis can include periodic exchange
transfusion throughout pregnancy to replace sickled cells with normal cells.
- During crisis: controlling pain, administering O2 as needed, and increasing
the fluid volume of the circulatory system to lower viscosity are important
interventions.
- Iron supplement is not given during pregnancy, cause cells cannot
incorporate iron in the usual manner that normal cells can, so excessive iron
buildup may result.
- Folic acid supplement keep the new cells produced from being
megaloblastic.

18. • Coagulation disorders in pregnancy:
- Von Willebrand disease, Hemophilia : women have normal
platelet counts, but bleeding time is prolonged, and are at risk for
hemorrhage with labor or a spontaneous miscarriage.
- Idiopathic Thrombocytopenic Purpura (ITP): there is decrease
in platelet (antiplatelet antibody that destroys platelets is apparently
released).
Women may suffer from minute petechiae or ecchymoses. Symptoms
are similar to pregnancy-induced hypertension with HELLP
syndrome. This could lead to increased bleeding at birth.

19. 3- Diabetes Mellitus and gestational diabetes
• Diabetes Mellitus (DM), an endocrine disorder of carbohydrate
metabolism, results from inadequate production or use of insulin.
• In early pregnancy the rise in serum levels of estrogen, progesterone,
and other hormones stimulates increased insulin production by the
maternal pancreas and increased tissue response to insulin. Thus an
anabolic (building up) state exists during the first half of pregnancy,
with storage of glycogen in the liver and other tissues.

20. • In the second half of pregnancy, placental secretion of human placental
lactogen (hPL) and prolactin (from the decidua), as well as elevated
cortisol and glycogen levels, cause increased resistance to insulin and
decreased glucose tolerance (Catabolic state).
• Due to the diabetogenic effect of pregnancy, any preexisting
disruption in carbohydrate metabolism is augmented by pregnancy,
and any diabetic potential may precipitate gestational diabetes
mellitus

21. • Influence of Pregnancy on Diabetes
• Pregnancy can affect diabetes significantly because the physiologic
changes of pregnancy can severely alter insulin requirements.
Pregnancy may also alter the progress of vascular disease secondary
to Diabetes Mellitus (DM).
• Influence of Diabetes on Pregnancy Outcome
• The pregnancy of a woman who has diabetes carries a higher risk of
complications, especially perinatal mortality and congenital
anomalies.

22. • Maternal risks related to DM:
- Hydramnios: increase in the volume of amniotic fluid as a result of
excessive fetal urination because of fetal hyperglycemia. Premature
rupture of membranes and onset of labor may occasionally be a problem
with hydramnios.
- Preeclampsia and eclampsia
- Hyperglycemia: causing ketoacidosis, if untreated can lead to coma and
death.
- Increased risk of UTI and pyelonephritis

23. • Fetal and neonatal risks:
- Fetal death if untreated maternal ketoacidosis
- Congenital anomalies: heart, central nervous system and skeletal
system
- Sacral agenesis: sacrum and lumbar spine fail to develop and the lower
extremities develop incompletely
- Large for gestational age: macrosomia, increase risk of traumatic birth
injuries
- Post partum hypoglycemia
- IUGR in infants with advanced maternal diabetes (vascular
involvement)

24. - Respiratory Distress Syndrome: result from inhibition, by high levels
of fetal insulin, of some fetal enzymes necessary for surfactant
production.
- Hyperbilirubinemia: is a direct result of the inability of immature
liver enzymes to metabolize the increased bilirubin resulting from
polycythemia.

25. • Antepartum management of diabetes:
The aim is to:
1- to maintain a physiologic equilibrium of insulin availability and glucose use
during pregnancy.
2- to ensure an optimally healthy mother and newborn.
This is achieved by:
a.Dietary regulation: The pregnant woman with diabetes needs to increase her
caloric intake by about 300kcal/day.
b.Glucose monitoring: essential to determine the need for insulin and assess
glucose control.
c.Insulin administration

26. • Evaluation of Fetal Status
- Because pregnancies complicated by diabetes are at increased risk
of neural tube defects such as spina bifida in the fetus, maternal alpha
fetoprotein screening is offered at 16 to 20 weeks of gestation.
- Ultrasound is done at 18 weeks to detect anomalies, repeated at 28
weeks to monitor fetal growth for IUGR or macrosomia.
- Evaluation of fetal activity starting 28 weeks
- NST (Nonstress Test) done weekly starting the 28th week and twice
weekly at 32 weeks gestation.

27. • Intrapartal Management Of Diabetes
Medical therapy focuses on the following:
- Timing of birth: Some clinicians induce labor to avoid problems
related to an aging placenta. Birth before term may be indicated if
vascular changes occur with worsening hypertension or if evidence of
IUGR exists.
- Labor management: Maternal insulin requirements decrease
dramatically during labor. Consequently maternal glucose levels
are measured hourly to determine insulin need. The primary goal
in controlling maternal glucose level is to prevent neonatal
hypoglycemia.

28. • Postpartal Management of Diabetes Mellitus
- Maternal insulin requirements fall significantly during the
postpartum period for diabetic women, because with the placental
separation, hormones levels falls and the anti-insulin effect ceases.
- Antihyperglycemics are contraindicated during breastfeeding.
Consequently a nursing woman with diabetes that is not controlled
by diet alone may need insulin for a time postpartum.

29. 4- Renal disorders
1- Urinary tract infections:
In the pregnant woman, because the ureters dilates from the effect of
progesterone, stasis of urine occurs.
The minimal glucosuria that occurs with pregnancy allows more than the
usual number of organisms to grow.
Asymptomatic infections are dangerous because they can progress to
pyelonephritis (infection of the kidney) and are associated with preterm
labor and premature rupture of membranes.

30. Assessment:
UTI is manifested by frequency and pain on urination. In pyelonephritis ,
a woman develops pain in the lumbar region.
She may have accompanying nausea and vomiting, malaise, pain, and
frequency of urination.
Temperature may be elevated slightly or high. (chills)
• Therapeutic Management
Obtain a clean catch urine sample for culture and sensitivity to
determine which antibiotics needs to be prescribed to treat the
infection.

31. 2- Chronic kidney disease:
- Pregnancy does not appear to cause progressive deterioration of kidneys lesions
- May develop severe anemia during pregnancy because their diseased kidneys do
not produce erythropoietin
- Women with kidney disease who normally have a serum creatinine level of more
than 2.0mg/dL may be advised not to undertake a pregnancy
- Women with severe renal disease may require dialysis to aid kidney function during
pregnancy. This is associated with a risk of preterm labor, perhaps because
progesterone is removed with the dialysis.

32. 5- Hypertensive disorders
Pregnancy-induced hypertension (PIH)
• Gestational Hypertension
• Mild Preeclampsia
• Severe Preeclampsia
• Eclampsia

33. • PIH is a condition in which vasospasm occurs during pregnancy in
both small and large arteries. Signs of hypertension, proteinuria, and
edema develops.
• The vascular spasm may be caused by increased cardiac output that
injures endothelial cells of the arteries.
• It tends to occur in women with multiple pregnancy, primiparas
younger than 20 years of age or older than 40 years, women from low
socioeconomic backgrounds (poor nutrition), those who have had five
or more pregnancies, those who have hydramnios, those with
underlying disease such as heart disease, diabetes with vascular or
renal involvement and essential hypertension.

34. • Gestational hypertension
A woman is said to have gestational hypertension when she develops
an elevated blood pressure (140/90mmHg) but has no proteinuria or
edema. Perinatal mortality is not increased with simple gestational
hypertension, so no drug therapy is necessary.

35. Pre eclampsia:
• Characterized by elevation in BP , protienuria & edema
after 20th wk of pregnancy.
• Hypertension occur suddenly or gradual.
• Sudden excessive wt gain ~ 1kg/wk.
• Protein urea +3 +4.
• Severs continuous headache often frontal or occipital.
• Swelling of the face or the fingers.
• Dimness or blurring of vision.
• Persistent vomiting.
• u/o BUN, Cr, uric acid.
• Signs of pulmonary edema.
• Epigastric pain due to vascular engorgement in the liver (often impending
convulsion)

36. Mild preeclampsia:
• Blood pressure more than 140/90mmHg after
20 wks gestation.
• Proteinuria : 300mg/24hrs or greater than +
1protein on dipstick urine sample.
• No seizures, no hyper reflexia.
• S&S: Mild facial or hand edema, wt gain.

37. Severe preeclampsia: Bp more than
160/110mmHg.
• Protein urea more than 500mg/24hrs, greater
than 3+ on urine dipstick.
• There is hyper reflexia , no seizures.
• S&S: Headache, oliguria, blurred vision,
pulmonary edema, thrombo cytopenea,
cerebral disturbances, epigastric or RUQ pain
HELLP
.

38. Medical Management:
• At home: Restrict activity , protein intake, Avoid sexual
intercourse.
• In hospital:
a. Protect patient from the effect of BP
cerebral bleeding.
b. Preventing the occurrence of eclamptic seizures.
c. Improving utero placental blood flow to  fetal risk.
d. Delivering the fetus as close to maturity.

39. Medical TX: Sedation to prevent convulsions.ex,
1- Mgso4:
- competing with calcium to block the reuptake of
acetylcholine in the CNS therefore number of impulses
through the ganglia
- the exacitability of the muscle fiber to direct stimulation &
relax smooth muscle.
2 - Anti hypertensive drugs:
❑ Hydralizine hydrochloride( Vascular smooth muscle
relaxant)
❑ Labetalol ( alpha 1 & beta blocker)
❑ Nifedipine(calcium channel blocker)

40. ❑Sodium nitroprusside( rapid vasodilation arterial & veinus)
❑Furosemide ( Lasix )

41. Nursing interventions(Pre eclampsia)
▪ Maintaining a well-balanced diet high in protein.
▪ Restrict activity & position in left lateral position.
▪ Monitor Bp.
▪ Watch for side effects of drug administered.
▪ Relieve anxiety.
▪ Keep oral airway or padded tongue blade beside the patient.
▪ Accurate I/O.
▪ Padded side rail.
▪ Observe S&S of Mgso4 toxicity, keep calcium gluconate IV available
(Antidote for Mgso4).
▪ Continuous monitoring FHR.
▪ Watch for vaginal bleeding & uterine rigidity ( signs of placental
separation)

42. ▪ Monitor BUN, Cr, uric acid , electrolyte, clotting time.
▪ Delivery according to patient condition& fetus maturity.
▪ Monitor deep tendon reflexes.
▪ Monitor V/SQ 1 hr
.
▪ Monitor urine for albumin & S.G.
▪ Monitor signs of edema.
▪ Keep O2 & suction bottle beside the patient.
▪ Delivery induced by oxytocin or C/S.
▪ S&S abate rapidly post partum.

43. Eclampsia:
Is almost preceded by S&S of pre- eclampsia.
• Risk for eclampsia in twin pregnancies is about 4x than in
single pregnancies.
• It is one of the gravest complication of pregnancy
• Maternal mortality is 1-17%.
• Fetal mortality 13-30% or more

44. S&S: Onset sudden beginning with:
Stage of invasion of the convulsion: Lasts few seconds eye roll to
one side & stare fixedly into space , twitching of the facial
muscle.
Stage of contraction: Lasts 15-20sec.
 Generalized tonic muscular contraction Face is
distortedeyes protrudearm flexedhand clenchedLegs
inverted.
 Suddenly the jaw begin to open & close violently facial muscles
& the body muscles alternately contract & relax in rapid
succession.
 Gradually muscular movements becomes milder & farther
apartclient lies motionless, coma last few minutes or several
hours.
 N:B Convulsions may start before the onset of labor, during or
any time within the 1st 48hrs after delivery.

45. S&S of eclampsia: BP ranges 180mmHg- 200mmHg
Protein urea 10-20g/l
Edema may or may not present.
Oliguria or anuria.
Fever
S&S of pulmonary edema.
Medical management:
Termination of pregnancy.
Control of seizures, hyper reflexia.
Anticonvulsant.
Initiate diuresis.
Hemodynamic monitoring.

46. Nursing Interventions:
▪ Mgso4 to control Bp
▪ Diazepam but it can cause neonatal depression, so Mgso4 is the
drug of choice.
▪ Hydralazine  Bp prevent cerebral hemorrhage
▪ Digitalis to treat CHF
▪ Observe signs of placental separation.
▪ Monitor FHR
▪ Monitor signs of labor
▪ Post partum :Continue hydralazin & Mgso4 for the 48hrs post –op.
▪ Monitor vaginal bleeding.
▪ Monitor U/O, Bp, Hb, Ht.
69

47.  Magnesium sulfate(Mgso4):
It acts as CNS depressant
IV allow for immediate onset of action & it must be given by an infusion
pump for accurate dosage..
Loading dose: 250ml D/W 5% with 4 g Mgso4 is administered over 20
minutes.
Maintenance dose: based on serum mgso4 level & deep tendon
reflexes 1-3 g/hr is administered.
Side effect: sweating, flushing, depression or absence of reflexes,
hypothermia, muscle weakness, Oliguria, confusion, circulatory
collapse, & respiratory paralysis.

48. Nursing consideration:
Monitor Bp Q 1 hr
.
Monitor RR, assess knee jerk for evidence of
diminish or absent.
Monitor U/O, & FHR.
Monitor Mgso4 level.
Antagonist of Mgso4 is calcium.

49. • Serum magnesium levels ranging from 4 to 7 meq/L are considered
therapeutic, whereas levels more than 8 mEq/dL are generally
considered toxic.
As levels increase, the woman is at risk for severe problems:
• 15 mEq/L: possible respiratory depression
• 25 mEq/L: possible cardiac arrest
If signs and symptoms of magnesium toxicity develop, expect to
administer calcium gluconate as the antidote.

50. • THE PATELLAR REFLEX
Purpose: To Evaluate for Nervous System Irritability
Related to Preeclampsia

51. • ANKLE CLONUS

52. HELLP: Is a laboratory diagnosis for a variant of severe
pre-eclampsia characterized by:
H: Hemolysis
EL: Elevated liver enzymes.
LP: Low platelet count.
Incidence: 2-12% of severely pre-eclamptic women or
about 1 in 1000 pregnancies.
Causes: Unknown, but may result from arteriolar
vasospasm , endothelial damage, & platelet aggregation
with resultant tissue hypoxia.
Prognosis: Maternal mortality 24%.

53. S&S:
• Epigastric or RUQ abdominal pain ( Hepatic ischemia, hematoma)
• Malaise.
• Nausea & vomiting.
• Platelet count less than 100,000/mm3.
• Elevated liver enzymes.
• PT
,PTT normal & bleeding time.
• Signs of DIC.
• Hypertension & proteinuria may be mild or absent.
• Thrombotic thrombocytopenia purpura.

54. Treatment:
a. Bed rest.
b. Corticosteroids.
c. Fluid replacement.
d. Mgso4.
e. Hydralazine ex, Labetolol or Nifedipin.
f. Blood transfusion, FFP
, or P
.C.
Complications: Renal Failure.
• Pulmonary edema.
• Ruptured liver hematomas.
• DIC.
• Abruptio placenta.

55. 6- Hyperemesis gravidarum
Severe nausea and vomiting which results in pathological effects:
▪ Fluid & electrolyte imbalance.
▪ Marked Weight loss.
▪ Acetone urea.
▪ Nutritional deficits.
▪ Alkalosis from loss of hydrochloric acid in the gastric fluids.
▪ Hypokalemia.
▪ Short term hepatic dysfunction with elevated liver enzymes.
▪ Deficiency in vitamin K may cause coagulation disorders and
deficiency in thiamine may cause encephalopathy.

56. 29
Laboratory and Diagnostic Testing :
• Liver enzymes—elevations of aspartate aminotransferase
(AST) and alanine aminotransferase (ALT) are usually present
• CBC—elevated levels of red blood cells and hematocrit,
indicating dehydration
• Urine ketones—positive when the body breaks down fat to
provide energy in the absence of inadequate intake
• Blood urea nitrogen (BUN)—increased in the presence of salt
and water depletion
• Urine specific gravity—greater than 1.025, possibly indicating
concentrated urine linked to inadequate fluid intake or
excessive fluid loss
• Serum electrolytes—decreased levels of potassium, sodium,
and chloride resulting from excessive vomiting and loss of
hydrochloric acid in stomach

57. ▪ S&S:
Nausea early in the morning or at any time during the day. Persists for few
weeks then suddenly ceases.
▪ Persistent vomiting lasts 4-8 Wks or longer & unable to retain any liquid or
solid foods which leads to Dehydration + Starvation.
▪ Decrease U/O , hypovolemia, Wt loss, dry skin, hypotension, ketone in urine ,
starvation.
Causes: Unknown
 Endocrine imbalances created by high level of chorionic gonadotropins &
estrogens.
Metabolic changes.
Fragments of chorionic villi entering maternal circulation motility 
vomiting

58. Causes: (Countinued)
▪ Possible allergy to fetal protiens.
▪ Helicobacter pylori .
▪ Psychological factors.
▪ Treatment:
 Correct fluid & electrolyte (3liters/24h)
 Treating acidosis
Medication :
Pyridoxine 10 –30mg/ day.
promethazine ( phenergan)10-25 mgQ6hrs.
Methylprednisolone has been recently used to reduce nausea & vomiting.
 In severe cases NG feeding or Hyperalimentation.
 Psychological support.

59. 8/23/2021 Maternity Nursing Mrs. samara fadda 32
Medication Action/Indications Nursing Implications
Promethazine (Phenergan) Diminishes vestibular stimulation
and acts on the chemoreceptor
trigger zone (CTZ)
Symptomatic relief of nausea
and vomiting, and motion
sickness
Be alert for urinary retention,
dizziness, hypotension, and
involuntary movements.
Institute safety measures to prevent
injury secondary to sedative effects
Offer hard candy and frequent rinsing
of mouth for dryness.
Prochlorperazine (Compazine) Acts centrally to inhibit dopamine
receptors in the CTZ and
peripherally to block vagus nerve
stimulation in the GI tract Controls
severe nausea and vomiting
Be alert for abnormal movements and for
neuroleptic malignant syndrome such as
seizures, hyper-
/hypotension, tachycardia, and
dyspnea.
Assess mental status,
intake/output
Caution patient not to drive as a result of
drowsiness or dizziness Advise to change
position slowly to minimize effects of
orthostatic hypotension.
Ondansetron (Zofran) Blocks serotonin peripherally,
centrally, and in the small intestine
Prevents nausea and vomiting
Monitor for possible side effects such as
diarrhea, constipation, abdominal pain,
headache, dizziness, drowsiness, and
fatigue.

60. Teaching to Minimize Nausea and Vomiting
• Avoid noxious stimuli such as strong flavors, perfumes or strong odors that
might trigger nausea and vomiting.
• Avoid tight waistbands to minimize pressure on abdomen.
• Eat small, frequent meals throughout the day— six small meals.
• Separate fluids from solids by consuming fluids in between meals.
• Avoid lying down or reclining for at least 2 hours after eating.
• Use high-protein supplement drinks.
• Avoid foods high in fat.
• Increase intake of carbonated beverages.
• Increase exposure to fresh air to improve symptoms.
• Drinkherbal teas containing peppermint or ginger
• Eat foods that settle the stomach, such as dry crackers, toast

61. Thank you