Pre eclampsia

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Pre eclampsia

  1. 1. PRE-ECLAMPSIA
  2. 2. Pre-Eclampsia  HYPERTENSION: Systolic BP > (or = to) 140 mmHg Diastolic BP > (or = to) 90 mmHg confirmed by repeated readings over several hours AND...
  3. 3. Pre-Eclampsia  RENAL INVOLVMENT: Protein > 0.3g / 24 hours Dipstick > 1 + PCR > 30mg / mmol OR...
  4. 4. Pre-Eclampsia  MULTI-ORGAN COMPLICATIONS: Haemtological - Coagulopathy - Haemolysis Liver - Dysfuntion - Rupture of capsule Neurological - Eclampsia - Stroke Pulmonary Oedema Fetal Growth Restriction Placental Abruption
  5. 5. Hypertensionin Pregnancy There are four major types of high blood pressure that may occur during pregnancy:  Pre-eclampsia  Chronic hypertension  Preeclampsia superimposed upon chronic hypertension  Gestational hypertension (also called transient hypertension)
  6. 6. Hypertensionin Pregnancy Chronic Hypertension:  Chronic hypertension is defined as a blood pressure ≥140/90 mmHg diagnosed either: - Before pregnancy - Before the 20th week of pregnancy - Or that persists more than 12 weeks after delivery.
  7. 7. Hypertensionin Pregnancy Pre-Eclampsia Superimposed Upon Chronic Hypertension:  This refers to a woman with chronic hypertension who develops signs of pre- eclampsia after the 20th week of pregnancy.
  8. 8. Hypertensionin Pregnancy Gestational Hypertension:  Women with gestational hypertension have all of the following: - Blood pressure ≥140/90 mmHg - No protein in the urine (proteinuria) - Are ≥20 weeks pregnant - No previous history of high blood pressure.
  9. 9. Hypertensionin Pregnancy Gestational Hypertension: Over time, some pregnant women with gestational hypertension will develop proteinuria and be considered preeclamptic, while others will be diagnosed with chronic hypertension because of persistently high blood pressure after delivery.
  10. 10. Pre-DisposingFactors  Age: <20 years / >35 years  Ethnicity: Indian, Pacific  Obesity  Diet: <2 servings of fruit per week, high fat  Lifestyle: Working in pregnancy, high stress  Booking BP >130/80: Predisposing hypertension  Miscarriage: 1 x lowers risk (immune response) 3 x increases risk (underlying)
  11. 11. Pre-DisposingFactors  Partner: Relationship < 3 months, Father previously involved in pre-eclamptic pregnancy  Woman born SGA  Family History: Pre-eclampsia, hypertension, diabetes, PCOS, underlying thrombophilias  Obstetric History: Previous pre-eclampsia, donated gamate  Multiple Pregnancy
  12. 12. Pathogenesis NORMAL PREGNANCY:  Fetal trophoblast invade walls of spiral arteries  This disrupts their smooth muscle layer and converts them into venous-like channels  Remodelling begins about 5-6 weeks and continues until around 20-22 weeks  This allows blood supply to uterus to increase from 10-15 mls (pre-pregnancy) to 600-800 mls per minute to meet placental blood flow requirements at term
  13. 13. Pathogenesis In pre-eclampsia, this process is DEFECTIVE 1. fewer of the arteries undergoing these changes 2. changes may not extend throughout the myometrium of the spiral arteries
  14. 14. Pathophysiology Renal  SYMPTOMS: Oliguria, Concentrated Urine Proteinuria PCR > 30mg/mmol Serum plasma creatinine > 90 umol/L  PATHOPHYSIOLOGY: Endothelial damage in glomeruli  GFR impaired Tubular necrosis and renal failure (rare)  EFFECTS: Reduced glomerular filtration rate, Reduced urea clearance and increased uric acid concentration, Proteinuria and hypoproteinaemia, Oliguria, Acute renal failure
  15. 15. Pathophysiology Liver  SYMPTOMS: Epigastric/Upper back pain, malaise, flu-like symptoms, nausea Raised SerumTransaminases (AST & ALT most significant): Aspartate transaminase (AST) > 60 U/L Alanine transaminase (ALT) > 40 U/L  PATHOPHYSIOLOGY: Endothelial damage  Impaired function  Capillary haemorrhage  Haemotoma  Ruptured capsule  EFFECTS: Abnormal liver function tests, Subcapsular haemorrhage and epigastric pain, Liver rupture
  16. 16. Pathophysiology CardiovascularSystem  SYMPTOMS: Oedema  PATHOPHYSIOLOGY: Endothelial damage Altered prostaglandin metabolism  Increased thromboxane and decreased prostacyclin concentration  vasoconstriction  EFFECTS: Widespread vasoconstriction, Normal or increased systemic vascular resistance, Left ventricular failure, Increased vascular permeability and oedema, Decreased circulating blood volume
  17. 17. Pathophysiology Neurological  SYMPTOMS: Severe headache, convulsions, persistant visual disturbances  PATHOPHYSIOLOGY: Endothelial damage  Retinopathy  Cerebral oedema  CVA (rare)  EFFECTS: Headaches,Visual disturbances, Hyper-reflexia, Sustained clonus, Cerebral haemorrhage, Convulsions
  18. 18. Pathophysiology Haematological  SYMPTOMS: Feeling hot/burning (unusual) Thrombocytopenia Platelets <100 X 109/L Haemolysis Disseminated Intravascular Coagulation  PATHOPHYSIOLOGY: Endothelial damage  Leaky capillaries  Activated coagulation  Inflammatory Response  Haemolysis  DIC  EFFECTS: Increased turnover fibrinogen, fibrin and platelets, Thrombocytopaenia, Impaired platelet function, Disseminate Intravascular Coagulation, HELLP syndrome
  19. 19. Pathophysiology FetalSignsandSymptoms  SYMPTOMS: Slowed or slowing fetal growth, signs and symptoms related to abruption and/or preterm labour Abnormal biophysical profile score Slowed growth of the baby, based upon customised growth chart and/or an ultrasound Decreased amount of amniotic fluid around the baby, noted on ultrasound Decreased blood flow through the umbilical cord, noted on Doppler tests
  20. 20. Pathophysiology FetalSignsandSymptoms  PATHOPHYSIOLOGY: Reduced blood flow to the placenta  Decreased placental circulation  Placental ischaemia and infarction  EFFECTS: Intrauterine Growth Restriction, Placental Abruption, Preterm Labour
  21. 21. TestsandInvestigations  GPH Bloods: Full / Complete Blood Count + Liver Group + Renal + Coagulation
  22. 22. TestsandInvestigations: CompleteBloodCount HAEMOGLOBIN [Hb]: 100 – 140 g/L The iron-containing protein, which transports oxygen within the red blood cells  In normal pregnancy, there is a natural decrease in Hb, due to haemodilation  In pre-eclampsia, expected plasma volume increase is impaired, affecting Hb estimation  If at 28/40 bloods, Hb is not lower than booking bloods, this could be significant, and therefore need to be vigilant
  23. 23. TestsandInvestigations: CompleteBloodCount HAEMOGLOBIN [Hb]:  As the pregnancy progresses, and capillaries become more damaged, they begin to leak, causing fluid to shift from the blood vessels to extravascular spaces  Blood therefore becomes more concentrated, and a raised Hb may indicate reduced plasma (haemoconcentration)  Plasma volume normal with mild disease, but reduced with severe pre-eclampsia
  24. 24. TestsandInvestigations: CompleteBloodCount HAEMATOCRIT [PCV]: 0.28 – 0.41 (ratio) The proportion of total blood volume that is occupied by erythrocytes  High PCV is suggestive of hypovolaemia (low volume), which therefore may affect placental perfusion  No exact levels for Hb and PCV define significant haemoconcentration, serial measurements are more useful for monitoring the disease course
  25. 25. TestsandInvestigations: CompleteBloodCount PLATELETS: 150 – 400 109/L The total number of thrombocytes, which play an integral role in haemostasis  Platelet levels decrease as they aggregate following damage to the endothelial cells of the capillaries  Day-to day variations common so serial measurements are necessary and more informative
  26. 26. TestsandInvestigations: CompleteBloodCount MEAN PLATELETVOLUME [MPV]: 6.4 – 9.7 fl A measurement of the average size of platelets  The average lifespan of platelets is 5 – 9 days, and immature platelets are larger than mature ones
  27. 27. TestsandInvestigations: RenalFunctionInvestigations SERUM UREA: 2.0 – 4.0 mmol/L An organic chemical compound which essentially is the waste produced when the body metabolizes protein  A late sign of renal injury as a result of pre-eclampsia is impairment of glomerular filtration which causes an increase in serum urea
  28. 28. TestsandInvestigations: RenalFunctionInvestigations SERUM CREATININE: 0.04 – 0.08 mmol/L A breakdown product of creatine (muscle waste material), which is constantly produced and filtered by the kidneys  Creatinine is removed from the body entirely by the kidneys  If kidney function is abnormal, creatinine levels will increase in the blood
  29. 29. TestsandInvestigations: RenalFunctionInvestigations URATE (URIC ACID): 0.20 – 0.42 mmol/d End product of protein metabolism  Excreted by renal tubule, in preeclampsia this function is impaired by damage to kidney and blood levels rise  High levels associated with poor fetal outcome  Useful diagnostic feature of early preeclampsia  Diet may affect level
  30. 30. TestsandInvestigations: RenalFunctionInvestigations PROTEIN-CREATININE RATIO: 0 – 30 mg/mmol  Random (spot) urine protein-creatinine ratio collected during normal daytime activity  Provides an accurate and rapid quantitation of proteinuria in pregnant women with systemic arterial hypertension and increased risk of pre- eclampsia
  31. 31. TestsandInvestigations: RenalFunctionInvestigations CREATININE CLEARANCE: 120 – 160 ml/min The volume of plasma completely cleared of creatinine per unit of time  Assesses the glomerular filtration rate  Gives an indication of renal function  Creatinine clearance may be reduced in pre- eclampsia as a result of decreased GFR  Assessed via 24 hour specimen
  32. 32. TestsandInvestigations: LiverFunctionInvestigations ASPARTATETRANSAMINASE [AST]: < 45 U/L An enzyme, involved in cellular metabolism that has raised levels in acute liver damage  Also found in high concentrations in heart, muscle, kidney, pancreas and red blood cells  If any of these areas are damaged the blood levels of the enzyme will increase  Not specific for liver function
  33. 33. TestsandInvestigations: LiverFunctionInvestigations ALKALINE PHOSPHATASE [ALP]: 90 - 250 U/L An enzyme made in the liver, bone, and the placenta, released into the blood during injury and during such normal activities as bone growth and pregnancy  Involved in cell metabolism and present in nearly all tissues  Levels reach up to 3 times normal in pregnancy due to placental phosphatase  Exaggerated increases may point to placental and hepatic damage in preeclampsia
  34. 34. TestsandInvestigations: LiverFunctionInvestigations ALANINETRANSAMINASE [ALT]: 7 - 45 U/L An enzyme involved in cellular respiration, found in highest amounts in the liver. It is released into the blood through liver injury.  Found in low levels in other tissues  High levels are specific for hepatic damage In normal pregnancy AST and ALT usually remain unchanged. In severe preeclampsia they may be elevated
  35. 35. TestsandInvestigations: LiverFunctionInvestigations GAMMA GLUTAMYLTRANSPEPTIDASE [GGT]: < 50 U/L An enzyme that participates in the transfer of amino acids across the cell membrane, and in glutathione (an anti-oxidant) metabolism  Found almost entirely in the liver  Elevated in severe preeclampsia
  36. 36. TestsandInvestigations: LiverFunctionInvestigations LACTATE DEHYDROGENASE [LDH]: 120 – 250 U/L An enzyme that catalyzes the conversion of lactate to pyruvate  Found in liver, heart, skeletal muscle and red blood cells  As cells die, their LDH is released and finds its way into the blood
  37. 37. TestsandInvestigations: LiverFunctionInvestigations BILIRUBIN: 2 – 20 mmol/L Bilirubin is a product that results from the breakdown of hemoglobin  Serum bilirubin levels do not usually rise in pre-eclampsia, unless complicated by HELLP syndrome
  38. 38. TestsandInvestigations: LiverFunctionInvestigations SERUM ALBUMIN: 35 – 45 g/L Albumin transports many small molecules in the blood (for example, bilirubin, calcium, progesterone, and drugs). It is also of prime importance keeping the fluid from the blood from leaking out into the tissues.  Because albumin is made by the liver, decreased serum albumin may result from liver disease  In pre-eclampsia low levels of albumin may also be the result of protein lost through proteinuria
  39. 39. TestsandInvestigations: Coagulation ACTIVATED PARTIALTHROMBOPLASTINTIME [APTT]: 35 - 45 secs When you bleed, the body launches the coagulation cascade. There are three pathways to this event. The APTT test looks at special proteins, called factors, found in two of these pathways (intrinsic).  A blood test that looks at how long it takes for blood to clot  It can help tell if there are bleeding or clotting problems  A prolonged APTT time can be indicative of disorders such as DIC, haemophilia, lupus, etc.
  40. 40. TestsandInvestigations: Coagulation THROMBIN CLOTTINGTIME: 10-18 secs A test which measures time required for plasma fibrinogen to form thrombin. Exogenous thrombin is added to citrated plasma and the time to clot formation is measured.  TCT is prolonged with abnormalities of fibrinogen and in the presence of heparin or of fibrin/fibrinogen degradation products  Prolonged in DIC as clotting mechanism fails
  41. 41. Section88 MaternityNotice ReferralGuidelines Current Pregnancy - Pre-Eclampsia:  LEVEL 3 (Code 4022) - Blood Pressure >140/90 (or rise of >30/15) AND... - Proteinuria > 0.3g / 24 hours - Platelets < 150 x 109 / L - Abnormal renal or liver function - Imminent eclampsia / eclampsia
  42. 42. Section88 MaternityNotice ReferralGuidelines Current Pregnancy - Eclampsia:  LEVEL 3 (Code 4006)
  43. 43. Section88 MaternityNotice ReferralGuidelines Previous Obstetric History - Pre-Eclampsia:  LEVEL 1 (Code 3007)
  44. 44. Section88 MaternityNotice ReferralGuidelines Previous Obstetric History - Pre-Eclampsia:  LEVEL 2 (Code 3008) WITH... - Significant IUGR - Requiring delivery <34 weeks OR... - Multi-organ involvement
  45. 45. CLASPTrial CollaborativeLow-doseAspirinStudiesinPregnancy  Aspirin and Calcium thought to produce modest reductions in blood pressure in pregnant women who are at above-average risk for PE  Debate continues over gestation at which prophylactic treatment should begin, but earlier the better (approx. 6/40 gestation)  Aspirin may also be beneficial in the treatment of IUGR
  46. 46. CLASPTrial CollaborativeLow-doseAspirinStudiesinPregnancy  For women who are at high risk of pre- eclampsia (>20%)  Aspirin 100 mg daily  Calcium 1.5 g daily  For women who are at very high risk of pre- eclampsia or previous pregnancy had very early onset  Heparin 7500 u BD or enoxaparin 40mg daily  Aspirin 100 mg daily
  47. 47. Management Depends on many factors:  Gestational age of the pregnancy  Severity of the disease  Presence of complicating factors  Evidence of maternal compromise  Evidence of fetal compromise The definitive treatment for pre-eclampsia is delivery of the fetus and placenta
  48. 48. Management  Expectant Management:  No evidence that hospital admission for mild PE improves maternal or fetal outcomes  Admission to hospital is stressful, emotionally and financially costly  Women with mild PE without significant proteinuria may be treated as outpatient or admitted as a ‘day case’ for assessment and evaluation
  49. 49. Management  Expectant Management:  Expectant management at home or hospital requires:  Reduced activity  Woman may be advised to stop working  May be advised to go on bed rest – although this is logical it has not been proved to improve outcomes  Careful recording and daily checking of:  Fetal activity  Blood pressure  Urine protein  Any other signs and symptoms of PE
  50. 50. Management  Collaborative Management: The goal is to:  Recognise pre-eclampsia early  Monitor the woman for evidence of disease progression that would mandate either delivery of more intensive fetal surveillance
  51. 51. Management  Collaborative Management: Education for the family begins as soon as the diagnosis is confirmed:  Should include information about the disease process  Signs and symptoms  Proposed course of treatment  Physical and laboratory investigations  Medications  Potential complications to mother and baby  Plan for birthing  Baseline laboratory evaluations:  Should be performed early in pregnancy for all women known to be at high risk of PE
  52. 52. Management  Collaborative Management:  Blood pressure:  Should be recorded more frequently in women at high risk of PE  Rapid increases warrant closer observation  Fundal height:  Should be measured at each visit  A measurement less than expected may indicate IUGR or oligohydramnios  Presence of either IUGR or oligohydramnios may occur before any other diagnostic criteria for PE become apparent  Oedema:  Rapidly increasing generalised, facial and/or periorbital oedema requires further assessment
  53. 53. Management  Collaborative Management:  Once hypertension is documented in second half of pregnancy, or onset of PE is suspected laboratory investigations to track progression:  Full blood count  Liver function tests  Renal tests  Coagulation screening  Urinanalysis
  54. 54. Management  Collaborative Management:  Fetal monitoring:  Antepartum surveillance (CTG’s)  Symphyseal-fundal height measurements  Record of fetal movements  Ultrasonography:  Amniotic fluid index  Fetal growth  Biophysical profiles  Umbilical artery Doppler studies Used to monitor fetal growth and to ascertain the most appropriate and safest time for delivery
  55. 55. Management  Hospital Management: May be necessary for woman who:  Feel safer in hospital  Hypertension worsens  Presence of significant proteinuria  Signs of end organ involvement  There are concerns about fetal wellbeing  Baseline laboratory evaluations as with Collaborative management to monitor progression of disease  Crucial that an accurate fluid-balance chart maintained to ensure that renal impairment detected early
  56. 56. Management  AntihypertensiveTherapy:  Indicated once the BP is persistently above >160/100 mmHg, with the aim of achieving a diastolic reading of 90 – 100 mmHg  This is to avoid ‘overcorrection’ and the risk of exacerbating placental hypoperfusion  Drugs used include methyldopa, atenolol and labetalol  ACE inhibitors contraindicated in pregnancy
  57. 57. Management  Timing of Delivery:  Delivery is the only cure for clinically diagnosed PE  Should be accomplished once the fetus is mature  Earlier if maternal condition deteriorates or if there is evidence of significant fetal compromise  Delivery should always take place in a level 2 hospital, where there are obstetric and paediatric facilities readily available  Timing and management of delivery requires close collaboration between the woman, midwifery, obstetric, paediatric and anaesthetic teams
  58. 58. Management  Timing of Delivery:  If fetus is between 24 -34 weeks gestation and urgent delivery is required, corticosteroids are administered to the mother  Vaginal birth preferable  Epidural anaesthesia preferred choice of pain relief as the maternal stress response releases catecholamines and increases BP, although contraindicated if there is evidence of coagulopathy  Continuous monitoring of fetus  Syntometrine to be avoided for third stage due to ergometrine component
  59. 59. Management  Timing of Delivery:  Fetal indications for immediate delivery:  Intrauterine Growth Restriction  Non-reassuring CTG  Oligohydramnios  Maternal indications for immediate delivery:  Progressive deterioration of liver function  Progressive deterioration of renal function  Suspected placental abruption  Persistent severe headache or visual changes  Persistent severe epigastric pain, nausea or vomiting
  60. 60. Management  ManagementAfter Delivery:  30% of cases of PE only diagnosed in postpartum period  Following initial improvement, 60% of women will worsen within 48 hours of delivery  Antihypertensive drugs usually continued for a further 48 hours  Close monitoring of BP should continue, as well as a meticulous fluid balance chart  Good analgesia cover to reduce maternal stress  Follow-up consultation and/or debrief
  61. 61. ImplicationsforMidwiferyCare  Must begin with an accurate record of a woman’s history to identify risk factors and establish baseline recordings of BP and laboratory values  Early recognition and diagnosis of physical signs rather than symptoms, as woman may feel well, yet have severe pre-eclampsia  Scope of care depends on severity of disease  Referral guidelines encompass a three-way discussion between the woman, her midwife, and specialist – therefore availability of the midwife paramount

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