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62 Cards in this Set
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Blood pressure during pregnancy ? Hypertension definition ? Classification of HTN during pregnancy ? Incidence of HTN during Pregnancy ? |
* During Pregnancy : There is a tendency towards a decrease in BP during 1st & 2nd TM with a return to pre-pregnancy levels at the begining of 3rd TM. * HTN : Eleavated BP > 140 /90 measured on two different occasions 6 hours apart * Classification : 1- Gestational HTN : HTN only + No proteinuria Occuring 1st time in pregnancy usually 2nd half. "Formerly called PIH" 2- Pre-eclampsia : Pregnancy specific syndrome of HTN + Proteinuria +/- edema Mostly in 2nd half of pregnancy 3- Eclampsia : Occurance of Siezures "fits or convulsions" in a patient with pre-eclampsia , which is not attributable to any other underlying cause / disease. 4- Chronic HTN : HTN presenting before pregnancy or < 20 weeks or persistant after 12 weeks postpartum * Incidence : - Complicates 5-10 % of all pregnancies - Serious effect on maternal & fetal mortality & morbidity The 2nd MC cause for maternal mortality in Egypt. |
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Pre-eclampsia ? Defintion Incidence Risk Factors |
* Definition : Acute Pregnancy specific syndrome of 1- HTN : Eleavated BP > 140 /90 measured on two different occasions 6 hours apart 2- Proteinuria : "Non-selective" Urinary PTN excreation > 300 mg/24 H "Fluctuate widely over 24 H" or persistant 30mg/dl "+1 Dipstick" 3- With or without edema : Not a diagnostic criterion & usually present in many normal pregnancies. - Occuring mostly in the 2nd half of pregnancy > 20 weeks - It is a mlutisystem disorder characterized by reduced organ perfusion 2ry to vasospasm & endothelial activation - If not treated it may induce fits "Eclampsia" * Incidence : - 3-7 % of all pregnancies - More in PG especially extremes of age. - Recurrence rate of 20% * Risk factors : 1- Age / Parity / Race : black race 2- Chorionic villi : - First time exposure in PG - Superabundance CV in MFP / Vesicular mole 3- Abnormal placentation : Hydrops fetalis / PHA 4- Pre-existing vascular disease : DM / HTN / Autoimmune vasulitis 5- Genetic PDF for HTN : PE in previous pregnancy / Chronic renal disease / Marked Obesity 6- Family Hx of PE or Eclampsia |
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Aetiology of Pre-eclampsia ? |
- Exact Aetilogy is unknown but theories postulates the following : A) Abnormal or Defective placentation (Zwefll theory) : Result in placental ischemia or hypoperfusion which result in release of unknown substance (May be cytokine / Oxygen free radical or prostanoids or endothelin ) that passes into maternal circulation leading to vascular endothelial damage with all its sequlae. B) Vascular endothelial damage & Generalized Vasospasm : - Role of endothelium : 1- Control Vascular tone by balance between VD = NO & Prostacycling VC = Thromboxane & endothlin 2- Control vascular permeability 3- Control Hemostasis - Effect of endothelial damage : 1- Inc. tone = VC 2- Inc. Permeability = edema & proteinuria 3- Platlet thrombosis & DIC in severe cases - This Leads to : Multisystem hypoperfusion state with ischemic effect on different organs especially in small capillaries & arterioles of : Placenta / Kidney / Liver / CNS But changes are non specific & evident only in severe cases. |
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Pathophysiology if Pre-eclampsia ? "Pathologic anatomy" |
1- CVS - Increased vascular responsiveness to VCs leading to generalized VC whcih increases PVR & causes HTN - Decreased plasma volume due to : VC / Increased capillary permeability / decreased plasma proteins 2- Renal - Glomerular endotheliosis : Charecterestic lesion where glomeruli are enlarged swollen bloodless with hypertrophy of intercapillary cells. - Decreased RBF & GFR : Oliguria - Glomerular & Tubular Dysfunction : Proteinuria : increased tubular permeability Hyperuricemia : decreased clearance by renal tubules. 3- Placenta A) Early = Failure of trophoblastic invasion of spiral arteries - Normaly Invasion of of spiral arteries with its replacement by trophoblastic tissue converts narrow muscular vessels into wide flacid vessels not responsicve to vasoactive compounds with decreased resistance & increased placental blood flow. - In PE : invasion is patchy & spiral arteries retain their muscular wall preventing increase in placnetal blood flow leading to placental ischemia. B) Late = Acute atherosis of spiral arteries Accumulation of fat -laden macrophages & perinuclear halo = narrowing of lumen = more placental ischemia C) Placental Infarctions Red infarcts is common in PE , maybe extensive leading to palcental insufficiency, IUGR & IUFD 4- Liver Periportal / Subcapsular Hge & Necrosis 5- CNS Vasospasm / Cerebral edema / Petechial Hge / Thrombosis |
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Clinical Picture of Pre-eclampsia ? A) Symptoms B) Signs C) Investigations D) Criteria of severity |
Symptoms : A) Asymptomatic : Early mild casses B) Symptomatic : Non-specific, late in severe complicated cases : 1- Persistant headache "not relieved by meds." 2- Visual disturbances : blurring / diplopia / scotoma / flashes / temporary blindness. 3- Persistant vomiting 4- Epigastric & Rt Upper abdominal pain 5- Diminished fetal movements 6- Oliguria "< 30 mg/hr" 7- Edema " LL - abdominal - generalized " Signs : - PE is a diseased of signs rather than symptoms ,Mainly HTN + Proteinuria +/- edema occuring in 2nd half of pregnancy - Regular ANC allow early detection of PE before symptoms are evident. 1- HTN - Earliest sign - Elevated BP = 140/90 or more on two or more occasions either 6 hours apart Or A rise of > 30 sytolic / > 15 Diastolic pressure "Only Close observation" - Labile from time to time - Resolves 6 weeks after delivery 2- Proteinuria - Late sign but essential criterion - Urinary PTN Excretion > 300 mg/24 H OR Reagent urine strips > +1 in at least 2 random urine samples without collection of 24 H urine as proteinuria is variable over 24 H 3- Edema - Common early feature but not a diagnostic criterion as it is a normal finding in pregnancy. - Early : Occult edema Abnormal rate of weight gain "> 1 kgm/Week" Precedes clinical edema - Late : Clinical edema Significant in non dependant areas +1 Ankle +2 Knee +3 Vulva +4 Lower abomen +5 Anasarca |
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Speceial investigations for Preeclampisa ? |
A) Evaluation of Severity : 1- Complete urine analysis 1- Proteinuria : - Dipstik random sample : rapid not accurate - 24 H urine collection for total protein : > 0.3 gm = Mild / > 5 gm = Severe 2- Others : Specific gravity / Epithelial casts / RBCs / Pus Cells 2- Serum Uric Acid For Hyperuricemia "N 3.5 - 5" it procede proteinuria but not specefic 3- KFT Serum Creatinine + Blood Urea = Normal except in late severe 4- LFT AST & ALT "N = 8-20 m.IU/ml" for detection of HELLP syndrome 5- CBC - Hb = low in anemia - HCT = elevated due to hemoconcentration - Platlets = low in help " N = 150000 - 250000" 6- Coagulation profile For diagnosis of DIC : PT "N = 11-12 S" & PTT "N = 24-36 S" Serum fibrinogen "N = 300-600 mg/dl" & FDP 7- Fundus examination For Retinal changes as : Vasospasm / Hge / Exaudates B) Evaluation of fetal well being : 1- DFMC 2- NST : if kick count is non reassuring 3- US : Detects IUGR / Oligohydramnios Performs BPPS test Doppler US : Umblical & Cerebral artery |
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Criteria of Severity of PE ? |
A) Mild : - BP < 160/110 - Mild Proteinuria 1+ - No or mild associated symptoms B) Severe : - Symptoms : 1- Persistant headache "not relieved by meds." 2- Visual disturbances : blurring / diplopia / scotoma / flashes / temporary blindness. 3- Persistant vomiting 4- Epigastric & Rt Upper abdominal pain 5- Diminished fetal movements 6- Oliguria "< 30 mg/hr" 7- Edema " LL - abdominal - generalized " - Signs : BP : 160/110 or more - Investigations : - Persistant Proteinuria : +2 or more / 5gm or more per 24 hour urine - Elevated liver enzyme : ALT / AST / Billirubin / ALP = HELLP - Thrombocytopenia : low platlets < 100000 - Complications : 1- Maternal : HELLP / DIC / HF or P.edema 2- Fetal : IUGR |
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Complications of PE ? |
A) Maternal : 1- Eclampsia : 1-2% of cases 2- Abruptio placenta : Severe HTN = RP clot 3- Acute renal failure : - Reversible : Acute tubular necrosis - Irreversible : Bilateral cortical necrosis 4- HELLP : 2-4% High fetal+maternal mortality - Hemolysis - Elevated liver enzymes - Low platlet count 5- DIC 6- Heart failure & Acute pulmonary edema 7- Intracranial Hge : ruptured vessels 8- Hepatic rupture : Subcapsular Hge = Internal bleeding & Shock 9- Retinal detachment & Cortical blindness 10- Remote : Residual HTN / Recurrence 11- Maternal Mortality : 2nd major cause B) Fetal : 1- IUGR : placental insufficiency 2- IUFD : IUGR or Accidental Hge 3- Prematurity : spontaneous or induced PTL |
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Differential Diagnosis of Pre-eclampsia ? |
A) Other Causes of HTN : 1- Gestational HTN : NO Albuminuria 2- Chronic HTN : - Essential : - Onset : before preg. or before 20 weeks or persistant > 6 weeks postpartum - +ve Hx - Ex : Cardiac enlargement + No edema - Inv : No albuminuria + Normal KFT + Sclerotic fundal changes - 2ry : - Pheochromocytoma : Intermittent & urinaty VMAs - Thyrotoxicosis : T3 & T4 - Coarctation of aorta : Differential HTN B) Other Causes of Proteinuria : 1- Contamination by vaginal discharge "Midstream sample or catheter specimen" 2- UTI : Complete urine analysis for Dx 3- Chronic kidney disease : Chronic nephritis, Dx by KFTs, Albuminuria precedes HTN C) Other Causes of Edema : 1- Unilateral : DVT / Cellulitis / Cancer ovary / Lymphedema / Varicose veins of LL 2- Bilateral : - Physiological : pressure by gravid uterus especially oversized " MFP / PHA" Improves with lifting feet - Pathological : Cardiac / Renal / Hepatic |
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Causes of Acute abdomen in PE ? |
1- Subcapsular Hge in liver 2- Accidental Hge 3- True labour pains |
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Managment of Preeclampsa ? |
1- Prediction Uterine artery doppler + Fibronectin 2- Prevention Low dose aspirin + Antioxidants 3- Treatment : Why ? Prevent complications esp. eclampsia When ? Timing depend on GA & Severity of PE How ? Only way is termination by delivery 1- Mild pre-eclampsia : A) Full term : Termination B) Preterm : Expectant 2- Severe Pre-eclampisa : |
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Prediction & Prevention of PE ? |
* Prediction : No Reliable tests but : - Uterine artery Doppler studies : At 18-24 Weeks revealing : High resistance index + diastolic notching may identify up to 80% of women who will subsequently develop PE. - Fibronectin : Elevated with endothelial damage Precedes clinical course of PE * Prevention : 1- Low Dose Aspirin Infantile Aspirin 75-100 mg daily from 2nd TM - Indications : High risk patients for PE : Hx of severe PE before 30 weeks in a previous pregnancy or those with IUGR - Action : Inhibit thrombosis by inhibiting pl.aggregation Promote VD by inhibiting release of TXA2 without impairing synthesis of VD prostacyclin prod. by endothelium 2- Antioxidants : - Vitamin C & E - High risk cases with uterine artery doppler showing high resistance index - Act by inhibition of endothelial cell activation |
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Treatment of Mild PE ? |
A) Mild PE : - Full term = 37 Weeks or more Delivery by induction of labour or CS - Preterm < 37 Weeks Expectant managment till fetal lung maturity is reassured 1- Rest Mental + Physical "Bed rest Lt lateral" 2- Diet PTN rich diet + Salt restriction 3- AntiHTN No documented benefit alpha methyl dopa : 250 mg t.d.s 4- Close follow up : Maternal - Warning Symptoms - Warning Signs : BP + Hyperreflexia at joints - Labs. : Urinary protein & output + Serum uric acid + LFT + Daily maternal weight Fetal DFMC / NST / BPPS / Doppler US for umblical & cerebral arteries 5- Outpatient managment For mild cases , twice weekly follow up visits till fetal lung maturity achieved or spontaneous labour pains start 6- Hospitalization If rapid prog. deterioration or development of complications = immediate termination 7- Termination VD : Whether spontaneous or induced allowed with strict fetal surveillance with Continuous Electronic FHRM CS : Is prefered |
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Treatment of Severe PE ? |
A) Urgent adequate control by : 1- Hospitalization 2- Antihypertensive drugs : Must be given by Parentral route to reduce maternal risk of cerebrovascular accident which is important cause of maternal mortality - Hydralazine - Direct VD - 5 mg IV "Diluted by glucose 1:1" then 5 mg every 20 Mins till diastole is 100 mmHg. - SE : tachycardia / flushing / headache - Labetalol - Combined alpha & beta adrenergic blocker = decreases BP by decreasing HR & contractility - 10-20 mg IV repeated every 10 mins - SE : Less than hydralazine - Nifedipine - Ca channel blocker - 10 mg orally repeated in 4-8 hours - SE : Better not used with Mg sulphate 3- Prophylactic anticonvulsants : Magnesium Sulphate to prevent developing convulsions in severe PE before termination NB : - Diuretics : Contraindicated except in HF / Acute PE as they worsen hemoconcentration & predispose thrombosis - Corticosteroids : In cases of PTL to decrease risks of neonatal RDS or Tx of cases complicated with HELLP B) Immediate delivery : Mode of delivery depend on urgency of termination & ripeness of cervix. 1- Vaginal Delivery - If favorable conditions for safe well monitored VD - By INDUCTION OF LABOUR : By : IV Oxytocin infusion or Vaginal PGs "with or without amniotomy" Prerequisites : Favourable conditions : Cervix : Soft - Ripe - Effaced Pelvis : adequate Precautions : - CEFHRM - Adequate control of BP & Pain relief - Avoid difficult prolonged labour & Shortening 2nd stage of labour - Avoid PP ergometrin = inc. BP & VR - Close Observation for PP eclampsia & PP Hge 2- Caesarean Section : 1- Unfavourable conditions 2- Extremely premature / LBW fetus 3- Non reassuring Ante/Intrapartum fetal surveillance tests 4- Other relative indications : PP / OHA / Prev.Scar / CP / IUGR |
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Eclampsia ? Definition Incidence Timing Pathogenesis |
- Definition : The Occurrence of Siezures / Convulsions / Fits in women with PE that cannot be attributed to any other underlying cause or pre-existing disease. - Incidence : 1 in every 2000 deliveries Complicate 1-2% of PE - Timing : A) Antepartum 65% B) Interpartum 20% C) Postpartum 15% Most dangerous = denotes brain insult - Pathogenesis : Unknown exactly, but maybe 2ry to : Cerebral edema & Vasospasm & Ischemia |
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Clinical Picture of Eclampsia ? |
1- Premonitory stage = 0.5 Min Twitches of face & hands + rolling up of eyes 2- Tonic stage = 0.5 Min Genealized tonic spasm + Opisthotonus position + Respiratory arrest = Cyanosis 3- Dome stage = 0.5 - 1 Min Bitten tongue + Stretous breathing 4- Coma stage Variable according to degree of acidosis so patient may recover or fit again NB : Death may occur due to : Aspiration Pneumonia |
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Differential Diagnosis of Eclampsia ? |
Epileptic Seizures : 1- Hx of previous fits antedating pregnancy 2- Hx of Tx with antiepileptic drugs 3- Preceded by aura of different stages 4- Not associated with HTN or Albuminuria |
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Prevention of Eclampsia ? |
- Eclampsia is a preventable complication of PE through early diagnosis & proper Mx. This can be achieved by : - Proper antenatal care assessment & follow up - Once PE develops it shoud be controlled & Managed - If the disease is progressive = termination of pregnancy - Post partum eclampsia is difficult to predict or prevent |
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Treatment of Eclampsia ? |
A) Emergency 1st Aid Measures : 1- Room : Semi dark + minimal noise 2- Nursing : on side with head down 3- Airway : Suction from mouth to avoid aspiration Ensure free airway + Oxygen mask = Perfusion Insert mouth gag = avoid tongue injury 4- IV line with good vein caliber & CVP monitor 5- Urinary catheter is inserted to record vol. 6- Initial IV dose of an anticonvulsant : MgSO4 20% = 4-6 gm over 20 mins IV drip Diazepam = 5-10 mg IV slowly B) Control of Epileptic Fits : 1- MgSO4 Action : - Inhibit Ms contractions by inhibition of NM transmission & decreasing Ca entry - CNS depressant Dose : Loading : 4-6 gm IV infusion over 20 mins Maintenance : 2 gm / hr by continuous IV infusion of 20% solution for 24 H 5 gm / 4 hrs by IM "buttocks" of 50% solution for 24 H " SE : convulsions or hematoma" Theraputic serum lvl : 4-7 m.Eq/L Precautions : before giving next dose : - Urine output > 30 ml/hr : toxicity with oliguria - RR > 16/min : Resp.center depression - +ve Knee jerk : diminished if severe NMJ Inhibtion Toxicity : Absent knee jerk / Respiratory distress / Cardiac arrest Antidote : Ca gluconate 10% 10 ml IV slowly over 3-5 Mins 2- Diazepam : Alternatice if MgSO4 is not available Less effective but more safe with less toxicity 5-10 mg IV slowly If quickly = sudden apnea + cardiac arrest C) Control of Hypertention : By IV Hydralazine or IV Labetalol D) Immediate termination of pregnancy : 1- VD : by Induction of labour by IV oxytocin or Vaginal PGs in favourable conditions as : Well controlled case + Cephalic pres. + engaged head + soft effaced cervix 2- CS : Rapid & Less traumatizing So Safer & Better if safe anaethesia is available E) Postpartum Care : Continue MgSO4 for 24 hours after delivery to gaurd against postpartum fits |
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Chronic HTN ? Definition Incidence Types |
Definition : Hypertension : - Antedating pregnancy - Detected before 20 weeks of gestation - Persistent after 12 Weeks Postpartum Incidence : 2-5% of all pregnancies Types : 1- Essential = 90% 2- 2ry = 10% due to : - Renal disease : Chronic nephritis / Renal artery stenosis - Coarctation of aorta - Hyperthyroidism - Pheochromocytoma |
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Chronic HTN ? Diagnosis Complications Treatment |
Diagnosis : A) Clinically = BP Measurment - On two or more different occasions each is 6 hours apart - in upper & lower limb - Difficult to Diagnose in 2nd TM : Physiological lowering of BP B) Investigations : For Cause : KFTs - Thyorid FTs - Urinary VMA - Blood glucose levels For Complications : Fundus Examination - ECG & ECHO * Complications : Superimposed Pre-eclampisa : aggregavation of HTN & appearance of proteinuria * Treatment : 1- Rule out & Treat causes for 2ry HTN 2- Anti-hypertensive drugs : If Diastole is 100 or more to reduce risk of ICH & HF 3- Obstetric managment : as PE |
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Diabetes Mellitus With Pregnancy ? Definition Incidence Classification |
- Definition : DM : Chronic metabolic disorder caused by relative or absolute insulin deficiency which primarily disturbs CHO metabolism with 2ry affection of lipid & protein metabolism Characterized by : hyperglycemia / glucosuria / microangiopathy. DM In pregnancy : May cause many serious maternal & fetal complications * Incidence : 1:350 pregnancies * Classification : A) Gestational DM : DM with onset or first recognition during pregnancy B) Established DM : DM existing before onset of pregnancy which may be : Insulin Dependant = Type 1 Insulin independant = Type 2 |
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Effect of Pregnancy on DM ? |
A) Effect of pregnancy on DM : - Pregnancy is diabetogenic : Due to Increased production of insulin antagonists during pregnancy as (( hPL - Placental insulinase - Cortisone - Estrogen - Progesterone )) - During Pregnancy the following occur : 1- Unmasking of latent DM : especially with repeated pregnancies & if the patient is predisposed 2- Established DM : becomes difficult to control due to increase in insulin requirements during pregnancy. - After labour Insulin Requirements decreases after delivery The patient is at risk for hypoglycemia : During labour : Utilization of glucose during uterine contractions After Labour : Utilization of glucose by breasts |
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Effect of DM on Pregnancy ( Complications of DM with pregnancy) ? |
A) Maternal : 8Ps 1- Pregnancy loss "Abortion" 2- Preterm labour 3- Pre-eclampsia 4- Polyhydramnios 5- Pruritis vulva "Monilial vulvovaginitis" 6- Pyelonephritis "UTI" 7- Peurperal sepsis 8- Breast infection & Deficient lactation B) Fetal & Newborn : 1- Fetal Macrosomia : - Oversized fetus 4.5 Kgm or more - May occur even in prediabetic stage - Due to : 1- Maternal & consequently fetal hyperglycemia which stimulates hyperinsulinism in fetus, Both fetal hyperglycemia & Hyperinsulinism enhance synthesis of glycogen & Fat & PTN in fetus. 2- Insulin has GH action 3- Salt & Water retention = High Cortisol 2- Fetal congenital anomalies : - Higher incidence = 6-9% - Risk Increases with poorly controlled DM during early pregnancy due to disturbance of 2ry yolk salk in 1st TM - Anomalies : Most common : VSD & Neural tube defect Most specific : Caudal regression Syndrome "Sacral Agenesis" 3- Spontaneous abortion Especially with poor control 4- Tendency to IUFD : In last month, Unknown cause but maybe due to : - Congenital anomalies - Maternal hypoglycemia / ketosis - PE or Placental insufficiency 5- Neonatal complications : Infant of diabetic mother is at higher risk for neonatal morbidity & mortality due to : - Birth trauma : oversized with broad shoulder / premature - Congenital anomalies - RDS - Neonatal Hypoglycemia : Blood Glucose < 30 mg% Due to increased insulin production by hypertrophied fetal pancreas - Tendency to : Hypocalcemia = birth hypoxia Hyperviscosity Hyperbillirubinemia = immature liver NB : Uncontrolled DM : Early Pregnancy = Congenital anomalies Late Pregnancy = Fetal macrosomia |
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Cases at high risk for DM during pregnancy ? |
1- Family history of DM 2- Age = 35 years or more 3- Gross obesity > 90 Kgm 4- Hypertension 5- Bad obstetric Hx : - Previous unexplained intrauterine or neonatal deaths - Previous 2 or more unexplained abortions - Previous macrosomic babies - Presence or history of major FCA - Presence or history of polyhydramnios 6- Recurrent UTI / Moniliasis |
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Diagnosis of DM in pregnancy ? |
1- History : The patient is known diabetic or is at high risk for DM 2- Clinically : Symptoms suggesting DM ; Polyuria - Polydepsia - Polyphagia - Loss of weight - Parathesia - Recurrent UTI / Pruritis vulvae 3- Investigations : 1- Fasting & 2 Hrs Postprandial blood glucose = Hyperglycemia 2- Abnormal Glucose tolerance test : Raised FBG + Lagging GTT A) Screening for DM during Pregnancy : 50 gm oral glucose followed by estimation of blood glucose after 1 hour : IF < 140 mg% = Negative > 140 mg% = Do 100 gm GTT B) Dx of DM by GTT during Pregnancy : - Fasting Blood glucose = 90 mg/100ml - 100 gm oral glucose adminesteration test : * Normal levels : 165 mg% at 1 hour / 145 mg% at 2 hours / 125 mg% at 3 hours * If any 2 or more of these values are elevated = impaired glucose intolerance 3- Detection of complications |
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Managment of DM during Pregnancy ? |
1- During Pregnancy : A) Control DM : 1- More frequent ANC visits : adequate follow up of maternal diabetic state & fetal wellbeing 2- Repeated blood sugar estimation : For better control 3- Glycosylated Hemoglobin measurment: HbA1C = Glycosylayion of 1st carbon of alpha chain of hemoglobin during RBCs span - Used as an indicator of blood glucose levels in the preceding 2-3 months - Normally = 3-4 % of total Hb If > 10% = poor control of DM in preceding 2-3 months 4- Diet control : Total calories = 30-35 Kcal/kg/day 50% CHO - 30% PTN - 20% Fats 5- Insulin therapy : * Indications : 1- All cases of established DM 2- Cases of GDMwhenever diet control aloneis not reassuring in the control of diabetes * Dosage & Preparations : - Insulin requirements < 50 units/day : Single morning dose NPH/Regular insulin = 2:1 - Insulin requirement > 50 units/day : In 2 doses : 2/3 in the morning "NPH/regular = 2:1" 1/3 in the evening "NPH/regular = 1:1" NB : Oral Hypoglycemic Poorly control DM during pregnancy & may have a teratogenic effect B) Time & Mode of delivery : - Indications of termination : 1- Evidence of placental insufficiency as IUGR / Oligohydramnios / abnormal umblical doppler 2- Fetal lung maturity is achieved at 37 weeks to avoid IUFD & Macrosomia - Mode : 1- Induction of labour if favourable cervix + average fetal weight 2- CS is preferred if macrosomia or placental insufficiency 2- During labour : 40 grams of glucose "800 cc of glucose 5%" + 20 units of insulin to prevent ketosis 3- During Peurperium : 1- Reduction of insulin dose to prevent hypoglycemia 2- Proper antibiotic coverage to avoid peuroeral sepsis 3- If neonatal death, suppress lactation - control DM - avoid pregnancy for 1 year 4- Care of newly born infant : - Mx of RDS : IDM is more liable to develop Hyaline membrane disease leading to RDS - Hypoglycemia : 5% glucose IV solution given after delivery is needed to compact neonatal hypoglycemia due to overactive fetal pancreas |
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Priscilla white classification of DM ? |
A = Chemical diabetes B = Age > 20 years / Duration < 10 years C = Age 10-19 years / Duration 10-19 years D = Age < 10 years / Duration > 20 years / Benign retinopathy E = Nephropathy F = Cardiomyopathy G = Proliferative Nephropathy H = Diabetic after renal transplant |
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Differential Dx of Jaundice in pregnancy ? |
1- Infective Hepatitis : - Viral Hepatitis A / B / C - May lead to : Abortion / PTL / IUFD in pregnancy - > 50% of babies born to mothers with hepatitis B will have : Hepatitis B surface antigens in their blood and some will develop hepatic lesions 2- Hemolytic jaundice : Hemolytic diseases as : Thalassemia 3- Surgical causes : Obstructive Jaundice 4- Hepatic Degeneration : Severe HEG / Severe PIH "PE / Eclampsia" 5- Recurrent Cholestatic Jaundice of Pregnancy : Oestrogen induced cholestasis in women unduely sensetive to estrogen or with oral contraceptive intake 6- Others : 1- Mismatched blood transfusion 2- Infection with hemolytic organisms 3- Acute fatty liver "Acute yellow atrophy" 4- Congenital Hyperbillirubinemia |
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Vomiting - Definition - Physiology of vomiting |
Definition : - Reflex emptying of stomach content through mouth. - It may be preceded by sensation of nausea - It may lead to dehydration / weight loss / electrolyte & acid base imbalance & finally organ failure that endangers life. Physiology of Vomiting : A) Vomiting Act : - Reverse peristalsis empties small gut content into stomach - Abdominal wall muscles contract to increase intra-abdominal pressure - The gastric sphincter relaxes & gastric contents are ejected - Breath is held at midrespiration & cricopharyngeus closes the glottis to prevent aspiration B) Vomiting Center : 1- Vomiting Center - In Medulla - Acetyl choline transmitter - Stimulated by : tickling the back of tongue / stomach distension / vesitibular stimulation 2- CTZ - In 4th Ventricle - Dopamine transmitter - Stimulated by : emetics / uremia / hCG |
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Emesis Gravidarum "Simple Nausea & Vomiting of Pregnancy" ? Incidence Aetiology Clinical picture Managment |
* Incidence : 50% of PG but less in MP * Aetiology : Related to hCG levels but psychological conflicts & Avitaminosis "Thiamine deficiency" may worsen the condition & make it resistant. * C/P : Nausea & Vomiting - Starting early in pregnancy with a peak at 7-9 weeks & ameliorate by 12 weeks of gestation - Characters - Mild to moderate severety - Mostly confined to morning or related to food intake - Doesn't affect general conditions - Respond to treatment * Managment : A) Mild : No treatment , only reassurance as it is a sign of intact pregnancy B) Moderate : - Reassurance + Small frequent light meals - Limited use of Antiemetics may be allowed C) Severe : Known as Hyperemesis gravidarum Requires hospitalization + IV fluids + intense therapy |
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Hyperemesis Gravidarum "Pernicious Vomiting of Pregnancy " ? Definition Incidence Pathogenesis "Causes" |
* Definition : Severe nausea & vomiting in pregnancy that is : - Not confined to morning - Affects patient general condition - Not responding to regular medical treatment * Incidence : - Affect about 1% of all pregnancies - More common in PG - Deaths from HEG is rare nowadays * Pathogenesis "Causes" : 1- Neurosis theory : Psychological conflicts play a role as evidenced by rapid improvement on isolation 2- Avitaminosis theory : Therapy with vitamin B1 & B6 improvesmany cases of HEG - Vitamin B1 "Thiamine" Water soluble - Coenzyme for decarboxylases - Deficiency = HF "wet beriberi" neuritis "dry" - Vitamin B6 "Pyridoxine" Water soluble - NH2 carrier for De/transamination 3- Endocrine theory "Youssef Theory" - Severity correlates with levels of hCG - higher incidence of HEG in MFP & VM due to higher levels of hCG - hCG have TSH action = gestational thyrotoxicosis |
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Pathological changes in HEG ? |
A) Biochemical changes : - Dehydration & Hemoconcentration - Electrolytes imbalance : Hyponatremia Hypokalemia : renal loss Hypochloremia : Depletion of chloride from urine indicates poor prognosis "Fantous test" - Acid/Base imbalance : Metabolic alkalosis B) Circulatory changes : Hypovolemia & Circulatory collapse = lead to pre-renal failure C) Metabolic changes : - Starvation & Weight loss : Depletion of liver glycogen = in late stages liver shows cental lobular necrosis - Ketoacidosis : oxidation of fatty acids with production of ketone bodies D) Wernicke's Encephalopathy : - Degenerative changes in the brain due to thiamine deficiency - Manifested as : Delirium / ataxia / nystagmus / Neuritis : optic nerve & 6th nerve Late : Coma - Dx : MRI shows petechial Hge in Wernicke's area of brain "Basal ganglia" |
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Diagnosis of HEG ? Clinical Picture Criteria of diagnosis of HEG Investigations Differential Dx |
* Clinical Picture : A) Early : - As morning sickness but vomiting isn't confined to morning - No signs of dehydration / Ketosis B) Late : Symptoms 1- Vomiting becomes : - Frequent throuough the day - Apart from food intake - Bilious or nlood stained 2- Oliguria 3- Constipation Signs 1- Weigh loss : Patient is emaciated & lethargic 2- Dehydration : dry tongue / sunken globe / loss of skin turguros 3- Hypovolemic shock : Low BP / Rapid weak pulse 4- Ketosis : Acetone odour in breath C) End Stages : Jaundice - Hepatorenal failure - neuritis - Delirium - Coma * Diagnosis of HEG : A diagnosis of exclusion as no single confirmatory test available. Diagnosis should be based on he following : - Vomiting starting early in pregnancy "before 12 weeks" if after exclude other causes first. - Rapid progressive course - Not confined to morning - Affects patient general condition - Not responding to regular medical treatment * Investigations : A) US : Exclude VM & MFP B) Assess General condition : 1- Blood electrolytes & ABG : Fluids / Electrolytes / Acid-Base status 2- Urine analysis : Oliguria / Keturia / Depleted chloride 3- Fundus examination 4- Liver & Kidney Function tests * Differential Dx : Later |
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Differential Dx of Hyperemesis Gravidarum ? |
1- MFP & VM : Excluded in every case 2- Other Pregnancy Related Causes of Vomiting : - Severe Pre-eclampsia - HELLP syndrome - Acute fatty liver - Pregnancy cholestasis - Gestational Thyrotoxicosis 3- Other Associated Causes of Vomiting : A) Medical : Gastroenteritis / Pyelonephritis / Hepatitis / DKA / Uremia / Drug posioning B) Surgical : Appendicitis / Chloecystits / Perforated Peptic ulcer / IO C) Gynecological : Red degeneration of fibroid / Complicated ovarian cyst or tumor 4- Rare conditions : Brain tumors / Mismatched blood transfusion |
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Management of HEG ? |
A) General : - Hospitalization for early & aggressive treatment - Psychological support B) Fluid therapy : - Normal Saline is best option "Glucose worsens Wernicke's encephalopathy" - Initial loading dose till urine flow exceeds 30 ml/hr then maintenance dose with observation by fluid balance chart C) Feeding : NPO & Total Parentral nutrition - For severe cases at start of treatment till vomiting is controlled or ameliorated - Method : 1- Calculate : Daily caloric need = 30 Kcal/kgm/day & Daily fluid needs 30ml/kgm/day 2- IV Hyperalimenation via catheter in subclavian vein 3- Fluid should contain : lipid emulsion / dextrose / aminoacids / electrolytes / Vitamins & Should be kept in refrigerator - Troubles of Prolonged TPN : Line associated sepsis "Prolonged cathetrization - Circulatory troubles - Metabolic troubles D) Medication : 1- Antiemetics : IV / IM / Suppositories in severe cases Oral in mild cases - Metoclopramide "Primperan" - Class B : Promethazine "Phenergan" - Class C : Dopamine rec. blocker in CTZ - SE : Extrapyramidal & Hyperprolactinemia - Scopolamine "Hyosine" - Class B : Acetyl choline rec. blocker in VC- SE : Dry mouth - Meclozine "Navidoxine" - Class B : Histamine rec. blocker in Both VC & CTZ SE : Sedation, Advantage : Rectally - Ondansetron "Zofran" - Class C : Serotonin rec. Blocker in both VC & CTZ SE : Depression 2- Thiamine 100 mg IV diluted in saline 3- Prednisolone 40 mg/day E) Termination of Pregnancy : - Indication : Last choice, rarely resorted to, only in : Severe cases resistant to treatment with lifethreatening complications, including : 1- Drastic worsening of vital signs 2- Severe Dehydration / Anuria /Circulatory collapse with no response to IV Fluids. 3- Severly affected liver or kidney functions = Impending failure 4- Marked Fundus changes 5- Wernicke's Encephalopathy - Method : 1- Medically indued abortion using PG E1 2- Surgical evacuation may be needed |
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Significant Asymptomatic Bacturia ? Definition Incidince Clinical Picture Complications Investigations Treatment |
- Definition : - Presence of 100,000 or more bacteria per ml in two freshly voided midstream specimen of urine without producing symptoms. - The Presence of bacteria only without pus cells in the urine of pregnant women doesn't signify urinary tract infection. NB : < 100,000 = Insignificant Asymptomatic bacturia * Incidence : 2-10% of all pregnancies "Average = 6%" * C/P : Asymptomatic * Complications : Pyelonephritis Risk increases to 25-30% of cases with untreated significant bacturia compared to 1% in patients without bacturia. * Investigations : 1- Complete Urine analysis : Presence of Pus Cells 2- Urine Culture & Sensetivity : Identify Pathogenic organisms * Treatment : The most common is E.Coli = Ampicillin 500 mg every 8 hours for 10 days If Recurrence in 1/3 of cases = Repeat course If Resistant / Recurrence again give antibiotics according to culture & sensetivity After Delivery : Resistant Recurrent cases should be offered full urological examination including Intravenous Pyelography NB : Cause of recurrence : Stones + Anomalies IVP in pregnancy : If indicated do 2 films only at 15 & 30 mins, each film is 0.1 rads "Maximum is 5 rads during pregnancy" |
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Acute Pyelonephritis in Pregnancy ? Definition Incindence Aetiology |
* Definition : Acute inflammation of renal pelvis & parynhema * Incidence : 1-2% of all pregnancies 25-30% in women with Sign. Asymp.Bacturia * Aetiology : - PDF : 1- Significant Asymptomatic Bacturia 2- Urinary stasis by dilatation of ureter due to : - Atony of ms by progesterone & relaxin - Compression by enlarging gravid uterus " It is more common in Rt Kidney due to more compression on Rt ureter due to dextro-roration of uterus in most of cases. - Hypertrophy of wall of lower end of ureter - Causative organism : E.Coli is the most common Others : Strept.fecalis / Staph / Klebsiella / Proteus - Route : 1- Blood borne is the most common 2- Lympthatic spread : Ascending infection along periureteric lymphatics or from colon |
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Diagnosis of Acute Pyelonephritis ? Symptoms Signs Investifations Differential Dx Complications |
* Clinical Picture : ِUsually after 16 weeks A) Symptoms : 1- High fevers & Rigors 2- Acute onset of loin pain : Associated usually with nausea & Vomiting, Preceded by recurrent attacks of burning micturition B) Signs : - General : High temp + Tachycardia - Local : Tenderness on one or both renal angle regions * Investigations : 1- Complete Urine analysis : - Diminished amount / acidic ph / fishy odour due to production of ammonia by E.Coli - Contain Albumin - Contain Pus cells > 10 per HPF 2- Urine Culture & Sensetivity 3- CBC : Leukocytosis with shift to the left in the ratio between staff/segmented RBCs 4- ESR Elevated / CRP +Ve * Differential Dx : 1- Appendicitis : Tender Rt Iliac fossa / Lower fever / Marked Leukocytisis / Free Urine 2- Twisted Ovarian Cyst 3- Other Causes of fever + Vomiting in pregnancy * Complications : 1- Chronic Pyelonephritis & Renal failure : Recurrent inadequetly treated cases 2- Abortion / PTL / IUFD in severe neglected cases or IUGR / PTL in less severe cases |
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Managment of Acute Pyelonephritis in Pregnancy ? |
A) General : 1- Rest / Light diet / Increase fluid intake 2- Alkalinzation of acidic urine 3- IV Fluids if there is excessive vomiting B) Antibiotics : Ampicillin 500 mg every 6 hours Alternatives : Augmentin = Amoxicillin + Clavulinic acid Unacyn = Ampicillin + Sulbactam then continue according to results of C&S C) Theraputic Abortion if : Solitary Kidney - Recurrent resistant infection |
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Anemia During Pregnancy ? Definition Incidince Classification |
* Definition : - WHO : Anemia in pregnancy is Hb concentration < 11 g/dl "7.45 m.mol/L" Hematocrite < 33% at any trimester of pregnancy - CDC : Proposed a cut off point of 10.5 g/dl during 2nd TM * Incidince : - Commonest Medical disorder in pregnancy - 50 % of pregnant women worldwide suffer from some degree of anemia * Classification : A) According to Cause : 1- Physiological Anemia of Pregnancy : Increase in plasma volume > Increase in RBCs volume "Hemodilutional anemia" 2- Nutritional Anemia : - Iron Deficiency Anemia : Most common nutritional anemia in pregnancy, either due to increased iron loss or decreased absorption. - Megaloblastic Anemia : Vitamin B12 or Folate deficiency affects DNA replication leading to derangement of RBC's with production of abnormal RBCs precursors "Megaloblasts" 3- Hemorrhagic Anemia : Severe recurrent blood loss as APH / GIT 4- Hemolytic Anemia : 1- Microangiopathic HA : In patients with severe PE / Eclampsia / ITTP 2- Acquired Immune HA : IgG Ab against red cell Ag found in collagen vascular diseases 3- Hemoglobinopathies : abnormal Hb as sickle cell anemia / Beta thalassemia 5- Aplastic Anemia : Rare with 30% mortality B) According to severity : Mild = 10 - 10.9 Moderate = 7 - 10 Severe = < 7 Decompensated = < 4 |
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Iron Requirements during pregnancy ? |
Basal iron requirements = 280 mg RBCs = 570 mg Placenta = 50 - 150 mg Fetus = 200 - 350 mg Blood loss at delivery = 100 - 250 mg After deduction of Iron conserved by amenorrhea ( 240 - 480 mg ) An additional 500 - 600 mg is required during pregnancy which means 4-6 mg of absorped iron per day Because absorped iron is only 10 % of ingested so 40-60 mg of iron should be available in diet which makes iron supplementation a necessity in all pregnancies |
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Effect of Pregnancy on anemia ? Effect of anemia on pregnancy ? |
Effect of Pregnancy on anemia : Pregnancy will aggravate any already existing anemia Effect of anemia on pregnancy : A) Maternal : Mild No effect on pregnancy or labour but mother show low iron stores Moderate Weakness / Fatigue / Lack of energy / Poor work performance Severe Poor pregnancy outcome as : PE / PTL / Prolonged labour / Post partum Hge / Peurperal sepsis / Failure of lactation B) Fetal : - Decreased fetal iron stores - PTL / SGA / Increased Perinatal morbidity & Mortality |
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Diagnosis of Anemia in Pregnancy ? |
A) Symptoms : 1- Mild / Moderate : Asymptomatic 2- Severe : Weakness / Exhaustion / loss of appetite Dyspnea & Palpitations CHF in severe cases B) Signs : 1- Mild / Moderate : Asymptomatic 2- Severe : Pallor Hyperdynamic circulation + Systolic murmur Glossitis & Stomatitis Koilonychia C) Investigations : - CBC : Decreased Hb & Hct -Serum iron : Decreased & Serum Ferritin : < 30 ug/L "Diagnostic" - Investigations for cause : Hb electrophoresis / Peripheral blood smear |
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Managment of Anemia with Pregnancy ? |
A) During Pregnancy : - Prevention : Proper ANC / Oral Iron Supplementation / Diet rich in iron & vitamin c - Treatment : 1- Oral iron therapy : Iron gluconate Hb rises about 0.3-1 g per week 2- Parentral iron therapy : Iron dextran Severe anemia in late 3rd TM or Poor compliance for oral therapy 3- Packed RBCs : Better than transfusion = avoid overload Severe anemia beyond 36 weeks / associated infections / Compensation of APH B) During Labour : 1st stage : Oxygen if dyspnea + Pro.Antibiotic 2nd stage : Shortened to avoid exhaustion 3rd stage : Active management except in very severe anemia for fear of cardiac failure + Prompt managment of PP Hge C) During Peurperium : 1- Adequate rest 2- Continue iron & folate therapy for at least 3 months 3- Any infecion is promptly treated |
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Cardiac disease with Pregnancy ? Incidence Aetiology Classification |
- Incidence : 0.5 - 1% of pregnancies - Aetiology : Most Common in developping countries is Rheumatic heard disease mostly "MS" In developped countries CHD is more common - NYHA grading "Assessment of cardiac disease " : Class 1 organic heart disease without limitation of house hold activities Class 2 Limitation "dyspnea-chest pain" at ordinary house duties / at end of stairs Class 3 Limitation of activity at less than ordinary house duties / during climbing stairs Class 4 Dyspnea at rest NB : Prgnancy worsen the condition by one grade 1&2 = compensated / 3&4 = Uncompensated |
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Changes in ( COP - Heart rate & Pulse - Apex beat variation - ECG ) with pregnancy ? |
A) COP : Increase gradually from 1st TM till reaching a peak of 40% increase above non-pregnant woman by 20 weeks & remain constant till full term, due to : 1- Increase SV by 40-50% 2- Incease pulse rate by 10-12 BPM B) Heart rate & Pulse : - Tachycardia - Occasional extrasystole - Water hammer pulse "Increased Sys - Dia" - Obvious capillary pulsation "nail bed" C) Apex beat variation : - Shift of apex up to 4th IC + laterally one inch - Soft systolic murmur - Split of 1st sound = Mitral closes earlier - Appearance of loud 3rd sound D) ECG : - Left axis deviation - Deep Q in lead 3 - Flat T & Inverted ST in V2-V4 |
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Factors affecting maternal cardiac condition ? |
1- History of recent reactivation of rheumatic fever 2- Associated cardiomyopathy & tight mitral stenosis 3- Associated Anemia 4- Infections : UTI & Dental caries = SAIE 5- Hypertensive disorders / Thyrotoxicosis in pregnancy |
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Management of cardiac diseases with pregnancy ? |
A) During Pregnancy : 1- ANC : - More frequent - Attended by both obstetrician & cardiologist - Examination : 1- Obstetric : maternal & fetal condition 2- Cardiac assessment & early detection of HF 3- Detection of Risk factors - Advice : 1- Rest : 9H by night + 2 by day "Semi-setting" 2- Diet : Salt restriction 2- Gaurd against risk factors : Weight gain / HTN / Anemia / Infections = SAIE by dental care + Antibiotics before procedures 2- Indications for Digitalis : - Already on it before pregnancy - Class II or more or Impending HF 3- Indication for hospitalization : - Class II : at 24-32 weeks & 1 week before EDD - Class III & IV : earlier & longer periods B) During Labour : - Proper pain relief : minimize anxiety & tachycardia NO Epidural in Rt-Lt shunt = Hypotension - No straining : minimze tachycardia & Inc. VR - Delivery : VD in semisetting position + adequate O2 CS if obstetrically indicated - Digitalis : if high risk for HF - Antibiotics : gaurd from SBE C) In Peurperium : High risk for HF due to : Increased VR due to reduced pressure on IVC + Mobilization of ECF 1- Monitoring : 2 weeks till COP normalization 2- Breast feeding : only CI if HF 3- Proper contraception : adequate spacing D) Termination of pregnancy : - Now : Only cases with pulmonary HTN or Rt to Lt shunt - Past : Class III & IV / Hx of HF in prev.pregnancy / Reactivation of RF But not encouraged now due to recent surgical treatments abailable & Proper medical control. |
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Rhesus Factor ? |
- It is a complex antigent which is a lipoprotein component of RBCs membrane. - Consists of 3 pairs of genes Cc / Dd / Ee The most important is D = Common C & E May cause incompitablity but are rare - D gene is dominant over d so : Rh +ve = DD & Dd = 85% Rh -ve = dd = 15% |
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Erythroblastosis Fetalis "Hemolytic Disease of newborn " ? Definition Aetiology |
- Definition : - Immunologic disorder charecterized by excessive hemolysis of fetal RBCs by antibodies that pass through the placenta from maternal blood. - It occurs due to RH allo-immunization & is an important cause of neonatal morbidity & mortality. - Aetiology : Formation of anti-Rh antibodies in an RH-negative female following : 1- Blood transfusion with Rh-positive blood immune system responds by production of antibodies against the D antigen. 2- Pregnancy with an Rh-positive baby Fetomaternal hge ( passage of fetal RBCs to maternal circulation ) may occur at : Time of delivery "3rd stage" / Abortion / Disturbance of an ectopic / APH / Amniocentesis / ECV The immune system produces antibodies against RH +ve antigens. |
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Incidence of Erythroplastosis fetalis ? |
Rh +ve : 85% of caucasians Rh -ve : 15% of caucasians Erythroblastosis fetalis : Only less than 1% : 1- Rh -ve female married to Rh -ve male 2- Rh -ve female married to heterozygous Rh +ve male will have 50% chance of having RH -ve baby 3- ABO incompitability between mother & fetus : destruction of fetal RBCs in maternal circulation before they induce antibody response 4- Immunological variation in response to Rh +ve Ag : Some Rh -ve females are Non / Poor responders. 5- 1st baby is unaffected : 1st exposure = IgM immune response "Large doesn't cross the placenta" But on following exposures = IgG immune response "Cross placenta affecting fetus" 1st baby maybe affected only if previous sensitization by blood transfusion or previous abortion, |
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Clinical Picture of Erythroblastosis fetalis ? |
Passage of anti-Rh antibodies from maternal into fetal circulation leads to hemolysis of fetal Rh +ve RBCs, Clincal types depend on degree of hemolysis : A) Congenital Hemolytic Anemia : Mildest - Fetal Hemolytic anemia : develops after 2 weeks of birth - Erythroblastosis : Increased production of immature nucluated RBCs "Erythroblasts" due to faster rate of erythropoiesis B) Icterus Gravis Neonatorum : Commonest - Fetal Hemoltic anemia : At birth - Jaundice : - Never at birth as placenta transfers unconjugated billirubin from fetal circulation to be conjugated by liver of mother. - Develops within 48 H after birth due to inability of fetal liver to conjugate high amount of billirubin produced by RBCs hemolysis - HSM : Inc. Extramedullary hematopoiesis - Kernicterus : When fetal billrubin exceeds 20 mg% it crosses brain barrier & become deposited in basal ganglia of brain stem = serious condition causing neonatal death irreversible brain damage & Mental retardation C) Hydrops Fetalis : Severest - IUFD : Severe hemolysis = Anemic HF - If born alive : death within few hours The fetus : accumulated fluid in body cavities Generalized edema / pleural effusion / ascites due heart failure + Hepatosplenomegaly The Placenta : Large & edematous US during pregnancy : Buddha attitude Flexion of thigh / Abdominal distension / halo around skull = scalp edema Diff.Dx : Parvo B19 / Organ failure : HF / RF / LF |
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Diagnosis of Erythroblastosis fetalis ? |
A) During Pregnancy : - 1st ANC visit : All pregnant females should be checked for RH group, if -ve : Ask about previous blood transfusion , previous fetal anemia / neonatal jaundice / IUFD Test Husband for RH group , if +ve : 1- Indirect Coomb's test : Detect presence & titre of Anti-D IgG in maternal blood : > 1/16 : Amniocentesis is indicated < 1/16 : Repeat every 4 weeks 2- Amniocentesis : Detect amount of billirubin in amniotic fluid by spectrophotometry which reflects degree of hemolysis of fetal blood. 3- US : May show HSM / generalized edema / Buddha attitude B) After Labour : Cordocentesis : Cord is clamped at 20 cm & cord blood is obtained & tested for : - Rh group : If +ve procede with the following - Hb : Detect fetal anemia "N = 18 gm%" - Serum billirubin : Detect jaundice "N = 2mg" - Direct Coomb's test : Detect antibodies adsorbed to RBCs in fetal circulation. |
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Managmenet of Erythroblastosis Fetalis ? |
A) Prophylaxis : 1- Never tranfuse Rh +ve blood to Rh -ve femal 2-Anti-D Immunoglobulins : To all non-sensitized "Indirect Coombs -ve " Rh -ve females married to Rh +ve males in the following conditions : - After delivery of Rh +ve baby to destroy fetal RBCs before they induce maternal response ( 300 mcg Anti-D IM within 72 H of delivery ) - At time of Abortion / Disturbed ectopic / APH / Amniocentesis / Version : prevent sensitization during pregnancy ( 50-100 mcg Anti-D IM ) - If Rh +ve blood transfusion ( 300 mcg per 100 ml blood ) - Recently, Routinely at 28 weeks of pregnancy ( 300 mcg Anti D IM ) NB : Prophylaxis is contraindicated if : Already sensitized ( Coombs +ve ) or have a previously affected baby B) Managment during pregnancy : 1- IU Blood transfusion : - Indications : severly affected fetus before 34 Weeks of gestation - Method : Injection of RH -ve group O blood into the peritoneal cavity or umblical vein of fetus under LA & US guidance 2- Termination of pregnancy : - Indications : Severly affected fetus after 34 weeks of gestation - Method : Induction of labour or CS if indicated but only after lung maturity is demonstrated by L/S ratio C) Neonatal managment : Exchange Transfusion : 10-20 ml of blood are withdrawn from umblical vein & replaced with the same amount of Rh -ve group O antibodies & repeated till 80-90% of blood is replaced to Remove Ag & Ab + Corrcet anemia & jaundice |
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Venousthrombosis in pregnancy ? Incidence Etiology |
- Incidence : - 0.5-3 of every 1000 pregnancies are complicated by symptomatic DVT = 5 fold risk over the non-pregnant female. - If untreated 25% may develop pulmonary embolism - PE is fatal in 15% of cases - Etiology : Pregnancy is Hypercoaguable state due to the following changes of thrombotic & fibrinolytic activities : 1- Increased Coagulation factors 7 / 8 / 9 / 10 2- Increased fibrinogen levels 3- Increased platlet activation 4- Decreased PTN-S & Antithrombin III |
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Thrombophilias ? |
Tendency to thrombosis due to acuired / inherited disorders of coagulation & fibrinolytic systems. - Mostly Antiphospholipid syndrome : - Causing thrombosis & recurrent abortion B) Inherited : Protein S & C & Antithrombin III deficiency |
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Risk factor for DVT & PE during pregnancy ? |
1- Age : above 35 = atherosclerosis 2- Weight : Prepregnancy > 80 kgm 3- Previous DVT : Hypercoaguability 4- Pre-existing Thrombophilia : Hyper 5- Severe PE : Hemoconcentration 6- Severe Varicose veins : Stasis + Phleboitis 7- MFP : 8- Prolonged bed rest 9- Pelvic surgery : 10- Sepsis esp. pelvic : |
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Diagnosis of Deep Venous Thrombosis ? |
Symptoms : Painful calf muscles with unilateral redness / hotness / swelling "Edema" Signs : - Unilateral tenderness / edema / redness / hotness - Pressure on sole of the leg during extension = severe pain in calf muscles Investigations : 1- Colour doppler US : - Allow assessment of deep veins between knee & Iliac veins & dynamic assessment of femoral & illiac veins - Prefered first line for a suspected DVT during pregnancy accurate & non-invasive 2- Venography : - Allow excellent visualization of veins above & below the knee - Invasive procedure requiring injection of a contrast medium & use of x-ray = not prefered |
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Managment of Deep venous thrombosis ? |
A) Prophylactic anticoagulant : 1- History of DVT during or following a previous pregnancy : Prophylactic LMW Heparin in subsequent pregnancies at least in the last trimester till the end of peurperium 2- History of DVT in non pregnant state : - Screen for thrombophilias - Anticoagulant prophylaxis starting from 2nd Trimester 3- History of Artificial valve / APS with recurrent DVT / previous Pul.Embolism : Full anticoagulation throughout pregnancy B) Managment : 1- Suspected Cases : Anticoagulant therapy is started immediately with heparin / LMW heparin in treatment doses till Dx is confirmed 2- Established Cases : - Complete rest & immobilization for the 1st 24 hours - Avoid dehydration by oral fluid intake / IV fluid infusion - Continuation of already started anticoagulant theapy with maintenance doses NB : + Discuss Anticoagulants |
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Anticoagulant therapy in pregnancy ? |
A) Heparin & LMW heparin derivatives ( Calcium Heparin ) : Advantage : 1- Don't cross placent " Not Teratogenic" 2- Short action = stopped within hours used safely before & after delivery without increaseing risk of hge Action : Prolongs APTT+Decrease Factor X act. Side effects : 1- Daily Repeated S.C injection 2- If prolonged > 6 months : Idiosyncrasy - Thrombocytopenia - Osteoporosis B) Oral Anticoagulants : Advantage : Drug of choice 1- Convenient for long term use : easily monitored & adjusted by INR 2- Safe during lactation Action : Prolongs PT Side effects : Cross placenta "Teratogenic" Causing - Limb & face defects in 1st TM - Fetal ICH in 3rd TM NB : Recently Some centers use Heparin derivative in 1st trimester Oral anticoagulants in 2nd trimester Heparin derivativrs in 3rd trimester to be stopped only few hours during delivery / CS |
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Pulmonary embolism ? Cause C/P Managment |
* Cause : Undiagnosed or improperly managed DVT : already formed thrombus in LL or Pelvic vein fragments & small emboli will travel through venous circulation to be entrapped in lungs. * C/P : - Hx : Recent DVT or Prescence of clinical evidence of pelvic / lower limb DVT - Symptoms : Mild breathlessness Inspiratory chest pain - Signs : Tachycardia / Hyopxia / Pleural rub / ECG changes * Mx : - Suspected Cases : Full IV heparinization + Supportive O2 therapy - Definitive Dx : V/Q scan or pulmonary angiography If +ve = longterm anticoagulation |