vomiting_during_pregnancy1 - By Tarek A Shokeir M.D...

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Unformatted text preview: By Tarek A. Shokeir, M.D. Lecturer in OB/GYN Mansoura Faculty of Medicine Classification Due to pregnancy (early pregnancy): Emesis gravidarum. Hyperemisis gravidarum. Associated with pregnancy (late pregnancy): Obstetric causes. Non-obstetric causes. Emesis Gravidarum Common (50% of gravid women). Starts about the time or soon after the 1st missed period. Commonly confined to the morning (morning sickness). Improves after the 12th week with or without simple measures. Does not affect the general condition of the mother. Treatment: Assurance, dietetic advice & vit. B. Hyperemesis Gravidarum Definition. Incidence: Rare, about 1:500 pregnancies. Aetiology: Unknown. Theories. A-Allergic Theory:- Againist hCG. ed frequency in vesicular mole & multiple pregnancy Response to antihistaminics. B-Neurosis Theory: Acts as agrevating factor. History of functional complaints. Response to assurance, sedation & even placebo. C-Deficiency Theory: CHO deficiency. Vitamin B1 & B6 deficiency. D-Hormonal Theory: Adrenocortical insufficiency. Deficiency of progesterone. Relative excess of E2. E-Toxemic Theory:- Toxin of unknown nature in early pregnancy: Trophoblastic toxin. Menotoxin. Intestinal toxin. Metabolic toxin. PATHOLOGY (Dehydration + Starvation) Biochemical changes. Metabolic changes. Organic changes. Vicious circle of vomiting. 1-Biochemical changes: ed extracellular fluids. ed serum Na & Cl. ed plasma volume (Hemoconcentration). ed blood urea. 2-Metabolic changes: Depletion of glycogen from the liver. consumption of fat Ketoacidosis. deamination of aminoacids by the liver Toxemia. Oliguria & the urine shows sp. Gr., Cl, ketonuria, protinuria and even bile salts. 3-Organic changes: Liver:- fatty degeneration starts in the centre & spreads to the periphery. Kidney:- toxic nephrosis with tubular degeneration. Heart:- subendocardial Hge with brown atrophy. Brain:- congestion & peticheal Hge in the brain stem (Wernicke's encephalopathy). Retina:- retinal Hge. Peripheral nerves:- degeneration. 4-Vicious circle of vomiting: Cause Neurosis Vomiting Diet Acidosis Starvation + Liver necrosis Degeneration Contipation + Dehydration Toxic state Clinical picture A-Symptoms Vomiting: Excessive and progressive. Vomitus is bile-stained and may contain altered blood. Starvation leads to subsequent symptoms e.g conistipation, oliguria, easy fatigability...etc. Later on, the patient becomes drowsy & confused. B-Signs: Progressive loss of wt. Patient becomes apathetic, emaciated & dehydrated. Sunken eyes, dry tongue & wrinkeled skin. Rapid pulse, low B.P. & temperature. Signs of vitamin deficiency. Finally: Jundice. Manifestations of peripheral neuritis. Manifestations of Wernicke's encephalopathy e.g drowsness, nystagmus & even vision. Coma. loss of C-Investigations:A-Urine analysis: Important for management, follow-up & prognosis. Changes encountred..... B-Blood examination:- Hemoconcentration (HCT value). bl. Urea & potassium. bl. Glucose & Chlorides. Impaired liver function. C-Fundus examination:- Late stages. Picture similar to optic neuritis. Retinal Hge. Indicate immediate termination. TREATMENT Factors concerned with the toxemia are:1-Neurosis. 2-Dehydration. 3-Constipation. 4-Diet = CHO. = proteins & fats. You have to combat these factors:- Isolation, assurance & sedation. Open bowels. Proper diet (excess cho, no fat, no proteins. Supportive therapy (antiemetics, antihistaminics, vitamins & corticosteroids). Treatment is divided into:A-Conservative treatment: * Moderate case. * Severe case. B-Termination of pregnancy. A-Conservative treatment 1-Moderate cases: Allow home treatment along the previous lines. If no improvement within few days treat as severe case. 2-Severe cases: Hospitalisationessential. Isolation, assurance & bed rest. Nothing by mouth for 48 hs. 3-Parenteral feeding: Fluids (3 L/day + losses in the vomitus). Normal saline + Glucose 5%. Good replacement urine output + presence of Cl in urine. 4-Correction of electrolyte imbalance:- Kcl low serum K (<3mEq/dL). Na bicarbonate low serum Na (<120mEq/dL). 5-Drugs: Anti-emetics. Anti-histaminics. Vitamins (B complex). Sedatives. Corticosteroids. 6- OBSERVATION: Vomitus. Fluid chart. Vital signs. Serum electrolytes. Liver function tests. Fundus examination. Serial U.S. After lapse of 24-48 hs. and/or if the patient asks for food, she is allowed a dry, small, sugary meal. If it is retained the diet is gradually built-up to a normal one. B-Termination of pregnancy: Indications: Persistent, severe vomiting after 2 ws. of therapy. Jundice, anuria, shock. Retinal Hge. Wernicke's encephalopathy. Mode of termination: If <12 ws. suction evacuation. If > 12 ws. hysterotomy. Vomiting in late pregnancy Obstetric causes: Pre-eclampsia. Impending eclampsia. Accidental Hge. Acute yellow atrophy of the liver. Complicated ovarian cyst or fibroids with pregnancy. Non-obstetric causes: UTI. Viral hepatitis. Cholecystitis. Appendicitis. Gastroenteritis. Cerebral tumours. ...
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This note was uploaded on 04/22/2008 for the course GYN 000 taught by Professor Khaledahmedanter during the Spring '08 term at Eastern Virginia Medical School.

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