Pre eclampsia

1. PRE-ECLAMPSIA

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. Pre-Eclampsia RENAL INVOLVMENT: Protein > 0.3g / 24 hours Dipstick > 1 + PCR > 30mg / mmol OR...

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. Hypertension in 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. Hypertension in 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. Hypertension in 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. Hypertension in 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. Hypertension in 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. Pre-Disposing Factors 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. Pre-Disposing Factors 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. 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. 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. 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 , O liguria , Acute renal failure

15. Pathophysiology Liver SYMPTOMS: Epigastric /Upper back pain, malaise, flu-like symptoms, nausea Raised Serum Transaminases (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. Pathophysiology Cardiovascular System 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. 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. Pathophysiology Haematological SYMPTOMS: Feeling hot/burning (unusual) Thrombocytopenia Platelets <100 X 10 9 /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. Pathophysiology Fetal Signs and Symptoms 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. Pathophysiology Fetal Signs and Symptoms PATHOPHYSIOLOGY: Re duced blood flow to the placenta  Decreased placental circulation  Placental ischaemia and infarction EFFECTS: Intrauterine Growth Restriction, Placental Abruption, Preterm Labour

21. Tests and Investigations GPH Bloods: Full / Complete Blood Count + Liver Group + Renal + Coagulation

22. Tests and Investigations: Complete Blood Count 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. Tests and Investigations: Complete Blood Count 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. Tests and Investigations: Complete Blood Count 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. Tests and Investigations: Complete Blood Count PLATELETS: 150 – 400 10 9 /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. Tests and Investigations: Complete Blood Count MEAN PLATELET VOLUME [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. Tests and Investigations: Renal Function Investigations 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. Tests and Investigations: Renal Function Investigations 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. Tests and Investigations: Renal Function Investigations 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. Tests and Investigations: Renal Function Investigations 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. Tests and Investigations: Renal Function Investigations 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. Tests and Investigations: Liver Function Investigations ASPARTATE TRANSAMINASE [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. Tests and Investigations: Liver Function Investigations 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. Tests and Investigations: Liver Function Investigations ALANINE TRANSAMINASE [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. Tests and Investigations: Liver Function Investigations GAMMA GLUTAMYL TRANSPEPTIDASE [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. Tests and Investigations: Liver Function Investigations 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. Tests and Investigations: Liver Function Investigations 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. Tests and Investigations: Liver Function Investigations 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. Tests and Investigations: Coagulation ACTIVATED PARTIAL THROMBOPLASTIN TIME [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. Tests and Investigations: Coagulation THROMBIN CLOTTING TIME: 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. Section 88 Maternity Notice Referral Guidelines 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 10 9 / L - Abnormal renal or liver function - Imminent eclampsia / eclampsia

42. Section 88 Maternity Notice Referral Guidelines Current Pregnancy - Eclampsia: LEVEL 3 (Code 4006)

43. Section 88 Maternity Notice Referral Guidelines Previous Obstetric History - Pre-Eclampsia: LEVEL 1 (Code 3007)

44. Section 88 Maternity Notice Referral Guidelines Previous Obstetric History - Pre-Eclampsia: LEVEL 2 (Code 3008) WITH... - Significant IUGR - Requiring delivery <34 weeks OR... - Multi-organ involvement

45. CLASP Trial Collaborative Low-dose Aspirin Studies in Pregnancy 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. CLASP Trial Collaborative Low-dose Aspirin Studies in Pregnancy 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. 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. 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. Management Expectant Management: Expectant management at home or hospital requires: Reduced activity W oman 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. 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. 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 P roposed course of treatment P hysical and laboratory investigations Medications P otential 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. 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. 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. 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. Management Hospital Management: May be necessary for woman who: F eel 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. Management Antihypertensive Therapy: 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. 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. 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. 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. Management Management After 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. Implications for Midwifery Care 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