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Obstetrics (SIMS) Dr Yovisha ST1 O&Gumar WinchesterTopics  History and assessment  Hyperemesis Gravidarum (Early pregnancy)  Hypertensive disorders in pregnancy  Diabetes in Pregnancy  Obstetric Cholestatis & Fatty Liver in pregnancy  Thrombosis  Ante-partum Haemorrhage  Post partum haemorrhageObstetric history  Gravida – How many pregnancies have they had  Parity – How many children do they have? o Any miscarriages, terminations, ectopics or Molar is a +1  Important to note how they were delivered  And how they were managed Why?Obstetric history ➢ Gravida – How many pregnancies have they had ➢ Parity – How many children do they have? o Any miscarriages, terminations, ectopics or Molar is a +1 ➢ Important to note how they were delivered ➢ And how they were managed Why? ➢ If they have had a previous C-section, the next mode of delivery could be a C-section or a VBAC (vaginal birth after C-section) ➢ They can be counselled on the risks ➢ If they need a surgical management of miscarriage, due to previous surgeries their risk of perforation is slightly higherExample Jamie has had 3 children, and no other pregnancies. She is not currently pregnant. Example Amy is currently 30 weeks pregnant. She has 2 children both delivered vaginally. She had 1 previous miscarriage that was managed medically Answers Example Jamie has had 3 children, and no other pregnancies. She is not currently pregnant. G3 P3 Example Amy is currently 30 weeks pregnant. She has 2 children both delivered vaginally. She had 1 previous miscarriage that was managed medically G4 P2+1 --> 2 alive children, 1x miscarriage (+1), and currently pregnant = 4 pregnancies Presenting complaint + History of presenting complaint  Systems review o Headaches – sign of pre-eclampsia, stroke, Venous thromboembolism o Fever - infection o Vomiting – infection, hyperemesis o Chest pain - Pulmonary embolism o SOB – Pulmonary embolism o Upper abdo pain / RUQ pain – Pre-eclampsia, Liver pathology o Lower abdo pain – Labour? o UTI symptoms – infection, Kidney stones o Bowels - constipation o Swelling (face, hands, legs) – Pre-eclampsia Current Antenatal history o Any problems – high blood pressure, gestational diabetes, fetal anomalies o Up to date with scans o Are they having any extra scans & why?  Gynae history o Any known gynae problems? o Smear history o Previous STI o If in early pregnancy more relevant to ask ▪ Planned pregnancy? ▪ On any contraception? ▪ Periods – cycle, heaviness, painful periods  PMH, PSH, Medications, Allergies  FH  Social history – smoking, alcohol, drugs Pregnant Abdomen Examination (a.k.a. Obstetric Abdominal Examination) - OSCE Guide | UKMLA | CPSA - YouTube Examination General examination - Hands: Capp refil, pulse, look for oedema - Face: Jaundice, oedema, conjunctiva pallor - In real practice: Auscultate heart and lungs Abdominal examination Linea Niagra Look Abdomen is distended, - ?Fetal movements seen - Umbilicus everted, - Linea niagra, - Striae Gravidarum – new stretch marks - Striae albicans – old stretch marksFEEL  Palpate upper border of uterus (Fundus) Measure symphysio fundal height (SFH)  Cover the measurement site so you are not biased  Measure from sysphysis pubis to Uterus fundus  Shouls be +2/-2 cm from actual dates FETAL LIE Longitudinal Oblique Transverse  FETAL PRESENTING PART Use one hand to stabilise the fetus & the other hand to palpate Then switch hands➢ Engagement o Is the Fetal head engaged in the pelvis? o How many fifth palpable is the head? o Usually you may expect head to be engaged from 38th weeks onward o Important during labour.Auscultate  Place Pinard stethoscope at the fetus's anterior shoulder  Don't hold the stethoscope while listening as it can interfere with the soundHyperemesis GravidarumHyperemesis Gravidarum  Nausea & Vomiting in pregnancy affects 90% of pregnant women  Hyperemesis gravidarum is a severe form of nausea & vomiting in pregnancy  Inability to eat and drink normally & strongly limits daily activities  10% of women will terminate the pregnancy due to HG  Stars prior to 16 weeks,  Peaks at 9th week  resolves by 20 weeks for most womenINVESTIGATIONS: Observations Urine dip: UTI, check ketones (marker for dehydration) Bloods: FBC, U+E, LFTs, Thyroid Function Tests ▪ Hyponatremia, hypokalemia, AKI Early pregnancy US scan: ?Viable pregnancy ▪ Molar pregnancies & Twin pregnancies may present with hyperemesis MANAGEMENT  Mild: Community  When 'flares up' - unable to keep food / fluid down: ambulatory inpatient management  Anti-sickness: o Doxylamine & pyridoxine, o Cyclizine, prochlorperazine, promethazine, chlorphenamine o Ondansetron (small increased risk of cleft palate  Others: Omeprazole, Thiamine & Folic acid supplementPre-EclampsiaBackground of HTN in pregnancy 20 weeks Pregnancy induced HTN Essential HTN Pre-eclampsia Normal pregnancy: will have a drop in BP Placenta is fully - Blood vessels expanding and formed at 20 weeks re-routed toward the fetus  Essential Hypertension –  Pregnancy induced HTN – HTN after 20 weeks without systemic features HTN before 20 weeks  Pre-eclampsia – HTN after 20 weeks + Proteinuria +/- systemic features Pre-Eclampsia • New onset of hypertension • after 20 weeks of pregnancy • and the coexistence of • Proteinuria , Other maternal organ dysfunction: • Renal insufficiency • Liver involvement • Neurological complications • Haematological complications • Uteroplacental dysfunction (Fetal growth restriction) 19Pathophysiology Abnormal placental development  Abnormal trophoblasts invasion into myometrium to meet with Spiral arteries  Spiral arteries are supposed to widen to become big arteries – but they don’t  Leads to a hypoxic placenta – releases placental hormones (Anti-angiogenic factors)  Higher resistance in arteries – HTN !Risk factors of pre-eclampsia  History of HTN in prev prgPre-existing HTN  Primigravida (1 pregnancy Diabetes  Multiple gestations  Obesity  Mothers >35 years old  Renal disease  Family history  Autoimmune (SLE, Anti-phospholipid)Signs and symptoms Systolic BP >140 Diastolic BP > 90 Headache, Visual disturbance Related to Cerebral irritation – hyper-reflexia Can lead to oedema & seizures Proteinuria – kidney damage RUQ pain / epigastric pain - Vasoconstriction & hypoxia - hepatic ischaemia Low abdominal pain – placental abruption Pulmonary & peripheral oedema - endothelial damage - fluid leaks out of vesselsRisks Risk to Mum Risk to baby HTN deterioration Intra-Uterine Growth Restriction - Eclampsia (compromised placenta blood flow) Pulmonary oedema Prematurity Renal failure Stillbirth Stroke HELLP syndrome – Haemolysis, Elevated liver enzymes, low platelets endothelial damage causes microthrombi, uses up platelets, causes hemolysisInvestigations Urine dipstick – look for proteinuria Urine Protein: Creatinine ratio (8mmol is diagnostic) Bloods – FBC (look at platelets), U+Es, LFTs Fetal assessments –  US: blood flow, fetal growth  CTG monitoringManagement Definitive management: delivery of the fetus! High-risk women - Refer for consultant-led care - Aspirin 75mg – 150mg OD from 12 weeks till birth - Aspirin suppresses prostaglandins – increases blood flow to the placenta Medication to control:  1 line: Labetalol (CI: Asthma) – Beta blocker  2nd line: Nifedipine / Amlodipine – Calcium channel blocker rd  3 line: Methyldopa - alpha-2 agonistic - reduces peripheral resistanceEclampsia Pre-eclampsia + seizures = Eclampsia ➢ Can happen post-partum - lining of placenta to shed ➢ monitored 72 hours after delivery Patho: abnormal cerebral blood flow in extreme hypertension Manage: ➢ Magnesium sulfate (protect the brain) – reduced acetylcholine release ➢ IV labetalol ➢ prompt delivery of babyHELLP syndrome • (H) Haemolysis – Anaemia, raised Bili & low haptoglobin • (EL) Elevated Liver enzymes (LDH >600), AST ALT x2 upper limit • (LP) Low Platelets ** Life threatening !  Complication of pre-eclampsia / eclampsia  Usually presents at 29-37 weeks, but can even be post-partum  Epigastric / RUQ pain Pathophysiology  High pressure – haemolysis of RBC  High BP can damage vascular endothelium - activating coagulation cascade – low platelets  Clots may deposit in liver vessels – increased pressure – liver congestion – liver damageHELLP syndrome • (H) Haemolysis – Anaemia, raised Bili & low haptoglobin • (EL) Elevated Liver enzymes (LDH >600), AST ALT x2 upper limit • (LP) Low Platelets Complications:  High BP o Placental abruption o AKI o Stroke  Low platelets – Bleeding! o DIC o Ante-partum haemorrhage, Postpartum haemorrhage Treat: Delivery!!! & supportive careDiabetes in pregnancy Diabetes in pregnancy Risk factors:  BMI >30,  previous gestational diabetes, previous macrosomic baby,  family history of diabetes,  ethnicity with high prevalence of diabetes  Testing: 75g 2 hour oral glucose tolerance test (OGTT) - 24 – 28 weeks  Diagnosis: o Fasting plasma glucose of 5.6 or above o 2 hour plasma glucose of 7.8 or above o HbA1c is always checked at booking. If raised (>48) they probably had underlying Type 2 diabetes TREATMENT o 1st line: Diet & exercise o 2nd line: Metformin o 3rd line: + Insulin  MONITORING Women with Type 1 or type 2 Diabetes – using insulin o Test their fasting, pre-meal, 1-hour post meal & bedtime glucose Women with Type 2 Diabetes – on tablets / diet control o Test blood glucose once a day Aim: Fasting below 5.3, 1 hour after: below 7.8, 2 hours after below: 6.4  US monitoring of growth at 28 weeks, 32 weeks and 36 weeksPOSTNATALL Y  Fasting plasma glucose 6-13 weeks after o <6.0 : no worries o 6 – 6.9 : high risk of T2DM o >7: T2DM – need further testing  If not done, at 12 weeks should have HbA1c tested o <39: no worries o 39 – 47: high risk of T2DM o >48: T2DM o ANNUAL HbA1c testing OC & Fatty Liver In pregnancy, gallbladder contractility decreases – cholestasis & gallstonesObstetric cholestasis  Diagnosed with: Itchy skin & Raised Bile Acids  Classified into : o Mild: Bile acids 19 - 30 o Moderate: 40 - 99 o Severe: >100  Risk of stillborn increased only in Severe OC  Background risk is 3.44% (background 0.28%) o ?Pathophysiology: Increased bile acids can case an Arrythmia --> Acute fetal hypoxia Further investigations & hepatologist referral should be done if LFTs are very high in 1st and 2nd trimester, features of acute infection, or no resolution after birth in 4 weeks  ALT & AST can be raised immediately postpartum - found in smooth muscles, breasts, RBC  Treatments are only to reduce maternal itching Antihistamine (ex. Chlorphenamine) When to deliver? Mild (19 – 39) - deliver at 40 weeks Moderate (40 – 99) - deliver at 38 – 19 weeks Severe (>100) - deliver at 35 – 36 weeksFatty liver in pregnancy  1 in 20,000 pregnancies  Occurs predominantly in 3rd trimester  Twin pregnancies have 14x more risk  Can be related to pre-eclampsia  Is dangerous !! - 60% needs ITU admission Presents as  Raised LFTs - especially , AL, GGT  Symptoms: Epigastric / RUQ pain, vomiting, encephalopathy  US liver: Inflammation / ascites Delivery should be expedited!Why is it so bad?  Renal failure, infections, fulminant hepatic failure, coagulopathy, GI haemorrhage, severe PPH & stillbirth Management  Early discussion with Haematology: as can result in coagulopathy - FFP , Cryo  Strict fluid balance – prevent pulmonary oedema  Hypoglycaemia : Fluids + glucose  Parenteral Abx early  Cerebral oedema: IV sedation, raising the bed, oral lactulose & hyperventiliation  Continuous monitoring after delivery - LFTs every 6 hours  Resolves after delivery – LFTs return to normal in 7-10 days VTE in pregnancy • Leading cause of direct maternal death during • 1 in 1000 pregnanciestpartum (MBRACE report)VTE in pregnancy Investigations:  DVT : Compression duplex ultrasound  PE: ECG (41% are abnormal – T wave inversion, S1Q3T3)  Chest X-ray – pleural effusion  CTPA – Increased radiation dose – increased risk of breast cancer by 13.6%  V/Q scan – slight increased risk of childhood cancer  Note: D-dimer is raised in pregnancy Treatment:  Low Molecular Weight Heparin – Ex. Enoxaparin, Dalteparin  3 months in total & at-least 6 weeks postpartum Ante-partum haemorrhage Placental Abruption Placenta Previa Painful hard uterus? Placental Abruption Placenta Previa Covers the lower segment of the uterus / cervix Placental Abruption Placenta Previa Haemorrhage, hypovolemic shock? Placental Abruption Placenta Previa Ante-partum haemorrhage PV bleeding from 24 weeks of pregnancy Complications : o Mother: Anaemia, Shock, PPH, blood transfusion, Psychological o Fetus: SGA, fetal hypoxia, prematurity, death Assessing CTG: Fetal heart rate & Observations, Bloods: FBC, Coag, activity History Taking Examination G&S, crossmatch, Speculum, Kleihauer test (Anti- US: Can diagnose p previa, VE (Not in p. previa) D) But NOT p abruptionPlacental Abruption  Seperation of placenta from endometrium  Presents: PAINFUL, HARD UTERUS RISK FACTORS o Previous placental abruption o Pre-eclampsia o maternal thrombophillia o Abdominal trauma (Dom violence) o Assisted reproduction, o Fetal growth restriction, o Intrauterine infection o Advanced age, o smoking & drug misuse Revealed – there Concealed – no is bleeding PV bleeding Risk factors Placental previa o Previous previa, o TOP , o nultiparity,  Placenta attached to the lower segment of the uterus o maternal age, o multiple pregnancy,  Avoid VE, PR exams, or penetrative sexual intercourse o Smoking o Assisted conception o Deficient endometrium: Uteri ne scar, endometritis, MROP, sub- mucous fibroid Most low lying placenta's in early pregnancy will eventually move as the uterus grows Grade 3 or Grade 4 Can't deliver vaginally- Needs C-section in a specialist unit! THANK YOU  FEEDBACK FORM  https://app.medall.org/feedback /feedback- flow?keyword=9f52134c8686c601a 06c77c1&organisation=yovisha-s- teaching  ANY QUESTIONS  Vishavijayakumar@hotmail.com Post-partum haemorrhage Loss of blood after birthClassification Post-Partum Haemorrhage = Losing > 500 ml of blood after delivery  Minor: 500 – 1000 ml  Moderate: >1000 ml  Severe: > 2000 ml  Primary: Within 24 hours  Secondary: More than 24 hoursCauses – 4 T’s  Tone – Uterine Atony  Trauma – Laceration, C-section, Episiotomy  Tissue – Retained placenta  Thrombin – CoagulopathiesRisk factors Multiple pregnancy Previous PPH Large baby  Tone – Uterine Atony General anaesthetic  Trauma – Laceration, C-section, Episiotomy  Tissue – Retained placenta Pre-eclampsia  Thrombin – CoagulopathiesManagement  Resuscitate as needed !  A-E assessment  Large cannula  Bloods (FBC, Group and save, Coagulation)  IV fluids / blood transfusion  Tranexamic Acid  ?Major haemorrhage protocol  Red cells,, Cryoprecipitatem platelets TREAT THE CAUSETREA T THE CAUSE Uterine Atony  Uterine Massage  Uterotonics – Oxytocin, Ergometrine  Intra-uterine Baloamponade Bakri Balloon  B-Lynch suture  Uterine Artery Ligation  Emergency Hysterectomy Trauma Very normal in a C-section, Make sure there are no bleeding vessels after C-section Or after a Tear – repair the tear If PPH, we check Hb the next day Hb 100 – Oral iron tablets, in between Iron IV, <70 Blood transfusion  Tissue Placental not removed -> Manual Removal of Placenta in theatre  Thrombin Women with coagulopathies go through strict antenatal haematology clinics and will have a plan in place of what to administer at what time