hyperemesis gravidarum 2

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Hyperemesis Gravidarum : 

Hyperemesis Gravidarum Mahmoud Zakherah Associate Prof Obstertris and Gynecology 2009-2010

Introduction : 

Introduction Nausea and vomiting in pregnancy is extremely common. Nausea and vomiting occurs in 50-90% of pregnancies Hyperemesis gravidarum (HEG) is the most severe form of nausea and vomiting in pregnancy

Introduction : 

Introduction Begins by 9-10 weeks of gestation, peaks at 11-13 weeks, resolves in most cases by 12-14 weeks. N&V In 1-10% of pregnancies, symptoms may continue beyond 20-22 weeks

Etymology : 

Etymology Morning sickness — some degree of nausea with or without vomiting occurs in 50 to 90 percent of all pregnancies five to six weeks of gestation, peaking at nine weeks, and usually abating by 16 to 18 weeks of gestation Hyperemesis gravidarum — Hyperemesis gravidarum is considered the severe end of the spectrum of nausea and vomiting persistent vomiting accompanied by weight loss exceeding 5 percent of prepregnancy body weight and ketonuria unrelated to other causes Hyperemesis tends to improve in the last half of pregnancy, but may persist until delivery

Etymology : 

Etymology Hyperemesis gravidarum Severe Nausea and Vomiting During Pregnancy) Greek hyper-, meaning excessive, and emesis, meaning vomiting, as well as the Latin gravida, meaning pregnant Hyperemesis Gravidarum means "excessive vomiting in pregnancy

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Race Hyperemesis patients are more likely to be nonwhite. Age Patients younger than 30 years are more likely to experience hyperemesis Incidence: HG seems to affect 1 - 2 % of all pregnancies

Etiology : 

Etiology Unknown (theories) Hormonal Hormonal changes Raised levels of beta HCG (Human Chorionic Gonadotrophin) High levels of estrogen and progesterone( hypersalivation; decreased gastric motility) Psychological------disproved Genetic component Infection Helicobacter pylori is a bacterium found in the stomach that may aggravate nausea and vomiting in pregnancy Subclinical vestibular disorders may account for some cases of hyperemesis gravidarum

Etiology : 

Etiology RISK FACTORS  Risk factors for hyperemesis gravidarum may include the following: Previous pregnancies with hyperemesis gravidarum Greater body weight Multiple gestations Trophoblastic disease ---- Nulliparity female fetuses Advanced maternal age (age >35) Cigarette smoking is associated with a decreased risk for hyperemesis gravidarum

Diagnosis : 

Diagnosis History Severe nausea and vomiting vomiting more than 3 or 4 times a day Food aversions Weight loss of 5% or more of pre-pregnancy weight Decrease in urination Dehydration Headaches Confusion Fainting Jaundice

Diagnosis : 

Diagnosis ptyalism (excessive salivation), fatigue, weakness, and dizziness. Patients may experience the following: Sleep disturbance Hyperolfaction Dysgeusia Decreased gustatory discernment Depression Anxiety Irritability Mood changes Decreased concentration

Diagnosis : 

Diagnosis Physical vital signs --blood pressure –pulse mucous membrane condition, skin turgor, neck veins, mental status. general appearance (eg, nutrition, weight), thyroid examination findings, abdominal examination f, cardiac examination and neurologic examination.

Diagnosis : 

Diagnosis Laboratory abnormalities  a) Urine analysis: there is decrease in specific gravity and urinary chloride, and appearance of ketonuria, and protinuria. b) Ultrasound examination: to exclude molar pregnancy or multiple pregnancy.   b) Fundus examination: to exclude hemorrhagic retinitis

Diagnosis : 

Diagnosis d) Blood analysis: there may be increase in hematocrit, impaired renal or liver functions, and electrolyte imbalance. Electrolyte derangements, such as hypokalemia and metabolic alkalosis increase in hematocrit, indicating hemoconcentration increase in serum aminotransferases. Alanine aminotransferase (ALT) is typically elevated to a greater degree than aspartate aminotransferase (AST) Hyperbilirubinemia also can occur, but rarely exceeds 4 mg/dL Mild hyperthyroidism

Differential DiagnosesDD : 

Differential DiagnosesDD Appendicitis Hyperthyroidism Biliary Disease Irritable Bowel Syndrome Diabetic Ketoacidosis Nephrolithiasis Esophagitis Pancreatitis, Acute Fatty Liver Paralytic Ileus/Bowel Obstruction Gastroenteritis Peptic Ulcer Disease Gastroesophageal Reflux Disease

Differential DiagnosesDD : 

Differential DiagnosesDD Porphyria, Acute Intermittent Hepatitis Preeclampsia Hyperparathyroidism Other Problems to Be Considered Drug toxicityEating disordersGastroparesisMigrainesOvarian torsionPseudotumor cerebriPsychological disordersTumors of the central nervous systemVestibular lesions

Complications : 

Complications Maternal Renal failure Toxic nephritis and tubules necrosis which may lead to renal failure Coagulopathy Mallory-Weiss syndrome Hemorrhagic retinitis. Liver derangement: This may lead to jaundice, coagulopathy, and acute fatty liver. Metabolic complications: as hypoglycemic coma, and metabolic acidosis Malnutrition Wernicke's encephalopathy : this may lead to diplopia, nystagmus, or confusion. It is caused by thiamine deficiency Splenic avulsion, vasospasms of cerebral arteries. Depression is a common secondary complication of HG.

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Brown atrophy of the heart. Muscloskeletal atrophy and dysfunction Fetal No greater risk of complications or birth defects than the general population

Treatment : 

Treatment According to the severity of the symptoms and signs

TREATMENT : 

TREATMENT Fluids and nutrition  Non pharmacologic interventions Pharmacologic treatment TOP

Fluids and nutrition : 

Fluids and nutrition Hospitalization and IV hydration fluids: it is indicated when: Pulse is >100 b/ m. Blood pressure < 90/60 mm/Hg. Temp > 38 Vomiting > 5 times / day Marked dehydration Ketonuria and protinuria Intravenous fluids (IV) – to restore hydration, electrolytes, vitamins, and nutrients Input and output

Nonpharmacologic interventions : 

Nonpharmacologic interventions 1- Dietary modifications: frequent small meals, shift to dry bland food, and avoid rich, fatty and spicy foods. Separate solid and liquid foods by at least 2 hours.   2- Lifestyle changes: Avoid aromas of cooking, perfumes, and smoke. Better isolation from noise, and family members. Avoid anxiety, nervousness, and fatigue because it exacerbates vomiting. 3-Avoidance of triggers   4-Acupuncture and acupressure  5-Ginger (الزنجبيل) and peppermint 6-Hypnosis 6- Bed Rest –This may provide comfort

Pharmacologic treatment : 

Pharmacologic treatment should be given only when necessary and at small doses with one drug at a time either class B or C except pyridoxine is class A in FDA classification of drugs use in pregnancy). The following groups could be used:   Antihistaminic: as Cyclizine and Meclizine (25 mg/ Tds). Anti emetics: Metaclopromide (10-20 mg/ Tds). Serotonin antagonist: Adansterone (8 mg/ IV or IM). Phenothiazines: as chlorpromazine and prochlorperazine (25 mg/ tds orally or rectal suppository) Vitamins: Pyridoxine (vit B6 50-200 mg/ IM daily) Thiamine (1mg/ IM daily). Antacids: H2 blocker as Ranitidine (150- 300 mg/ Bid orally). Steroids: in refractory cases as Prednisone or Methyl Prednisone

Termination of pregnancy(TOP) : 

Termination of pregnancy(TOP) It is indicated in sever complicated cases of HG with progressive weight loss and different organs impairment and not responding for above treatment lines

OUTCOME AND PROGNOSIS : 

OUTCOME AND PROGNOSIS Usually good

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Thank you السلام عليكم