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Hypertensive disorder of pregnancy

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Hypertensive disorder of pregnancy

  2. 2. Outline Diagnosis of HTN Introduction Classification Pathophysiology and risk factor Clinical presentation Management
  3. 3. Introduction  Most common medical complication  Incidence 7-10% all pregnancies 70 % Preeclampsia- Eclampsia 30 % Chronic HTN 0.05 Eclamosia  Major cause of maternal and perinatal mortality & morbidity.
  4. 4. Classification 1) Gestational HTN( transient HTN) 2) Preeclampsia- Eclampsia syndrome 3) Chronic HTN 4) Preeclampsia superimposed on chronic HTN
  5. 5. Diagnosis Hypertension: Systolic BP > 140 or DBP > 90 mmHg. Measured on any two occasions > 6hrs apart or One DBP> 110 mmHg
  6. 6. Proteinuria Urine protein > 300mg/24hr or 30mg/dl(1+dipstick) or 0.1gm/L in at least two random urine sample Urine protein : creatinine ratio > 0.3 Edema No longer part of diagnosis * wt gain >1kg/ week & pathological edema are↑ warning sign
  7. 7. Gestational Hypertension Definition B/P > 140/90 mmHg for first time during pregnancy after 20 wks G.A or first 24 hrs post partum.  No proteinuia  Mild HPN & must return with in 12 weeks postpartum  It is a diagnosis of exclusion  Final dx made only postpartum. Pregnancy outcome similar to normotensive pregn
  8. 8.  At risk of progression to PE or eclampsia  Close observation of maternal & fetal condition  In absence of severe HPN or PE can continue pregnancy till term
  9. 9. Preeclampsia Definition  new onset of hypertension after 20 weeks of gestation and 1. Proteinuria 2.Trombocytopenia(<100,000/ml) 3.Renal insuficiency….cr>1.2 mg/dl or doubling of base line 4.Liver involvement….transaminase elivation 5.Cerebral symptoms…headache, visual disturbance, convulsion 6.Pulmonary edema
  10. 10.  pregnancy specific syndrome of reduced organ perfusion secondary to vasospasm and endothelial activation. incidence nullipara = 3-7% multipara 0.8-5%
  11. 11. Superimposed upon chronic HTN HTN and no proteinuria <20 weeks:  New onset proteinuria after 20 weeks of GA HTN and protienuria <20 weeks: Sudden increase in proteinuria Sudden increase in BP in woman whose BP was well controlled Thrombocytopenia ( <100,000/ml) Increase in ALT or AST to abnormal levels
  12. 12. Chronic HTN BP > 140/90 mmhg before px or diagnosed before 20 weeks of GA or diagnosed after 20 weeks of GA and persists after 12 weeks postpartum Other associated findings  Retinal change  Cardiac  Renal diseaese  Other medical illness
  13. 13. Risk factors for PE • Nulliparity • Obesity • Age <20 or > 35 yrs(chronic HTN and superimposed PE) • Multiple gestation • Low socioeconomic status • GTD • Poor outcome of previous pregnancy (IUGR, SB ,abruption) • ART( assisted reproductive technology) • Race , ethinicity, genetics
  14. 14. Pre-existing medical conditions  Chronic HTN  Renal disease  DM (type I)  Thrombophilias (APA, protein C,S deficiency ) Smoking is it a risk factor or protective?
  15. 15. Classification of PE Non severe PE Severe PE BP >160/110 mmhg Proteinuria of >5g/24 hr Oliguria <500ml/24 hrs Thrombocytopenia Elivated liver function test with persistent epigastric or RUQ pain Pulmonary edema Persistent severe cerebral or visual disturbances Convulsion HELLP syndrome and DIC BP >140/90 mmhg Proteinuria of 300mg/ 24 hrs or 1+ on dipstich
  16. 16. Etiology & pathogenesis Etiology – Unknown Known as disease of theory Some of theories • Abnormal trophoblast invasion Coagulation Abnormalties Vascular endothelial damage Immunologic theory Placental toxin theory……toxemia of pregnancy Genetic predisposition Dietary deficiencies ….calcium and antioxidant deficiencies
  17. 17. Any theory has the following charactersitics 1. Exposed to chorionic villi for the first time….nulliparous 2.Exposed to superabundance of chorionic villi…twins and GTD 3.Preexisting condition of endothelial cell activation/inflammation….DM/renal/ cardiovascular disease 4.Genetically predisposed to HTN developing during pregnancy…family hx
  18. 18. Abnormal Trophoblast invasion Defective vascular response to placentation due to inhibition of 2nd wave of endovascular trophoblast occur often 16 week
  19. 19. Trophoblastic invasion of spiral arterioles leads to the destruction of the muscularis layer which is replaced by trophoblastic cells which do not respond to the autonomic stimulation of blood vessels; this ensures that there is a constant uninterrupted blood flow to the intervillous space
  20. 20. According to the immunological theory, there is sufficient similarity between paternal and maternal HLA antigens, which prevents early fetal antigens from detection by the maternal immune system This leads to failure of production of blocking antibodies early in gestation As fetal antigens increase in amount later in gestation, the maternal immune system responds by producing antibodies that destroy placental trophoblasts
  21. 21. SYSTEMIC ENDOTHELIAL DYSFUNCTION All of the clinical features of preeclampsia can be explained as maternal responses to generalized endothelial dysfunction Disturbed endothelial control of vascular tone causes hypertension, increased vascular permeability results in edema and proteinuria, and abnormal endothelial expression of procoagulants leads to coagulopathy. These changes also cause ischemia of target organs, such as the brain, liver, kidney, and placenta.
  22. 22. Laboratory evidence supporting generalized endothelial dysfunction in preeclamptic women - Decreased production of endothelial-derived vasodilators -nitric oxide and prostacyclin - increased production of vasoconstrictors -endothelins and thromboxanes. - Enhanced vascular reactivity to angiotensin II
  23. 23. Organ system Pathology complication CVS Generalized vasospasm; increased afterload; left ventricular strain and failure; microvascular endothelial damage and fluid and protein leakage •Hypertension •Congestive heart failure •Generalized edema •Pulmonary edema Hematolog ic Excessive consumption of platelets to repair endothelial damage; RBC damage as they pass through the spastic arterioles •Thrombocytopenia •Microangiopathic hemolytic anemia Renal Decreased glomerular filtration rate due to spasm; renal glomerulo endotheliosis; renal tubular necrosis; renal cortical necrosis in advanced •Acute renal failure •Proteinuria •Hyperuricemia Respirator y Pulmonary capillary endothelial damage and leakage ( in addition to hypoproteinemia due to proteinuria and left ventricular failure) Pulmonary edema
  24. 24. Organ system pathology complication Gastrointes tinal Hepatocellular injury distal to vascular spasm site; focal hemorrhages distal to spasm site; coalescing focal hemorrhages leading to large hematoma collection under the Glisson’s capsule •Hepatic failure •Sub capsular hematoma •Acute liver rupture CNS Cerebral hypoxia due to vasospasm; focal hemorrhages distal to the vasospasm; secondary cerebral edema; intracranial hemorrhages •Eclampsia •Hemorrhagic stroke •Cerebral edema and death due to coning •Transient blindness – retinal or cortical HELLP syndrome Concomitant occurrence of microangiopathic hemolysis; thrombocytopenia and liver damage features in a woman with preeclampsia
  25. 25. system pathology complication Blood volume Due to generalized vasospasm, there is contracture of the total vascular space. The normal increase in blood volume that occurs during normal pregnancy fails in preeclampsia. They tend to have a contracted and overall reduced blood volume •Less tolerant to blood loss at delivery with an easy propensity to post partum hemmorhage with small amount of blood loss •Less tolerant to fluid administration with a propensity to develop pulmonary edema
  26. 26. symptoms sign Diagnostic study •Non severe preeclampsia is asymptomatic •Symptoms are late features indicating severe disease or imminent risk of convulsions •These symptoms include headache, blurring of vision, epigastric pain, oliguria and generalized body swelling •Hypertension •Generalized edema/anasarca •Excessive weight gain •Exaggerated deep tendon reflexes •Proteinuria •24 hour urine for proteinuria •Liver and renal function tests •Hematocrit •Peripheral blood smear for shistocytes (fragmented RBC) •Platelet count •Serum uric acid measurement •Fetal well being studies As preeclampsia is asymptomatic until it progresses to severe stages, detection and diagnosis requires active screening of all pregnant women during antenatal care. Routine blood pressure measurements, weight gain surveillance and check for symptoms and proteinuria are performed to detect preeclampsia early.
  27. 27. Management Objective Preserve health of mother & fetus Prevent progression to eclampsia Delivery of alive, mature fetus * Once Dx is made definitive Rx is delivery * Precise Knowledge G.A Important for Mx. Mx of Non severe PE Hospitalization  at time of Dx Purpose Evaluate maternal & fetal condition
  28. 28. Hospital Mx Maternal follow up  Weight on admn. & every other day  B/P  Q 4 hrly  Daily clinical Hx premonitory Sx  Urine protein every 48 hrs Hct, Plc, RFT, LFT, uric Acid, coagulation profile weekly or 2x/week.
  29. 29. Fetal evaluation Daily FHR Auscultation & fetal mov’t count Fetal growth: clinical & U/Sound Well being NST/BPP (2x/week) **Non sevre PE remote from term delivery at term but pregnancy should not pass 40 weeks. ** no need of antihypertensive or seizure prophylaxix
  30. 30. Mx of severe PE characterized by progressive deterioration of both maternal & fetal condition  All should be delivered if disease develope >34 week G.A or prior to 34 weeks if there is - Maternal (Fetal) distress - Labor or PROM - Severe IUGR **Delivery should be based on maternal and fetal conditions as well as GA
  31. 31. Mx of severe PE includes Maternal & fetal evaluation same Non PE but more frequent. Anticonvulsant to prevent convulsion Antihypertensive To control B/P in safe range Induction of labor Delivery  Admit to labor & delivery area.  Then Maternal & fetal evaluation 1st 24 hr  Anti-convulsant  parenteral route To prevent seizure
  32. 32. Indication Anti- convulsant drugs  Mg so4  Diazepam  Phenytoin
  33. 33. Antepartum mg't of severe PE Magnesium Sulfate (Mg So4) Mg so4 Agent of choice for seizure prophylaxis Dose: loading dose 4gm 20%soln  over 10-15min followed by 10 g of 50% solution half on each buttock maintenance dose: 5gmI.M/4 hr Make sure the following before giving next dose 1. Patellar reflex is present 2.RR at least 16 breaths/min 3. UOP of previous 4 hr exceeded 100 ml Side effect: Weakness, paralysis, cardiac toxicity Monitor: RR, DTR,Level of consciousness, UOP Antidote: Calcium gluconate 10 ml of 10% I.V
  34. 34. MgSO4 level (mg/dl) 4.8- 8.4 8- 10 12 -17 13- 17 19 -20 Effects Therapeutic level Loss of DTR Respiratory depression CNS depression, coma Cardiac arrest Clinical effects are related directly to plasma levels
  35. 35. Antihypertensive  If DBP > 110 mmHg Acute Rx Arteriolar dilators – Hydralazine 5mg iv then 5-10mg Q 20min. B- Blocker – labetalol Ca channel blocker – nifedipine
  36. 36. Maintenance Rx Centrally acting  Methyl dopa B- Blockers- labetalol Ca channel Blocker -nefidipine ACE inhibitors C/I in pregnancy
  37. 37. Delivery PE progressive disease Timely delivery  decreases maternal and fetal morbidity& mortality Stabilize maternal status before Delivery Route of delivery…vaginal delivery is preferable
  38. 38. Indication to Delivery in PE >37 wks with mild PE > 34 wks with severe PE < 34 wks with any of  maternal or fetal Distress  Severe IUGR  HELLP syndrome  Pulm. Edema  Deranged LFT/RFT  Uncontrolled B/P despite Appropriate drugs  Imminent eclampsia
  39. 39. Steroid All pts with severe PE < 34 wks prevent RDS, treatment of thrombocytopenia Intrapartum care • Maternal – V/S Q 30min Avoid fluid overload  input/output every 1 hr FHR monitor Q 15min or EFM Shorten 2nd stage labor – Instrumental delivery Fluid –125ml/hr, U.O.P > 30ml/hr Active Mx of 3rd Stage
  40. 40. Postpartum Close follow up & monitor B/P Anticonvulsant for 24-48 hrs
  41. 41. Eclampsia Definitionn: Occurrence of seizure or coma in woman with PE that cannot be attributed to other cause Preventable complication of preeclampsia 50% intrapartum 25% antepartum 25% postpartum Atypical eclampsia Occurrence of eclampsia before 24 week of GA or after 7th postpartal day
  42. 42. Most common last trimester & wide spectrum of Sn & Sign and symptom ranging from: Extremely B/P <-- --> minimal B/P proteinuria 4+ <-- --> No proteinuria (14%) Generalized edema <-- -->No edema (26%) Patellar reflex 4+ <-- --> normal reflex ##1st warning sign may be excessive Wt gain
  43. 43. Diagnosis Features of preeclmpsia + Generalized tonic-clonic seizure Aura Tonic phase Clonic phase Post-ictal comavery brief or even not present
  44. 44. Complications of eclampsia Known complications of PE + • Aspiration and asphyxia • Trauma • Preterm seizure • Fetal distress and asphyxia • Crebral edema in prolonged or repititive seizure
  45. 45. Managem ent Description General •Airway and oxygenation- put in left lateral position; suction airway, insert airway to depress tongue and prevent injury, administer oxygen via face mask or endotracheal tube if in respiratory failure •Prevent trauma – tongue depressor ; fall accident etc •Fluid resuscitation if in hemodynamic instability- IV line and fluids Control convulsion Administer anticonvulsants – Magnesium sulphate (first line drug); diazepam ( if magnesium is not available); phenobarbitone; phenytoin… can also be used if the two are not available Control severe HTN If BP >160/110 mmHg, use fast acting antihypertensives (hydralazine; labetalol; diazoxide; sodium nitroprusside) to maintain BP between 140/90-160/110. Fluid mx Restrict fluid administration to 125ml/hr and monitor input-output including urine output Organ support If any evidence of organ failure; requires critical care and organ support to maintain homeostasis Delivery After the above measures are taken and patient is stabilized; pregnancy should be terminated by the most appropriate route. No conservative Mx !
  46. 46. Prognosis Reading assignment effect of preeclampsia-eclampsia syndrome for future pregnancy
  47. 47. DDX All pregnant women & convulsion should be considered Eclampsia till other cause R/O  Epilepsy - encephalitis, meningitis Cerebral malaria - cerebral tumor Hypertensive encephalopathy
  48. 48. References 1. Williams obstetrics, 24th edition 2. Normal and problematic pregnancy, Gabbe, 6th edition 3. Uptodate 21.6 4. Management protocol on sstetric case, FMOH, january, 2010
  49. 49. Quize 1. Define severe preeclampsia(2 points) 2. Mention at least four risk factors for preeclampsia. (2 points) 3. List the two common theories incriminated in preeclampsia(2 points) 4. How do you define proteinuria in preeclampsia(2 points) 5. What is the preferred drug for seizure prophylaxis(1 point) 6. What is the definative mx for preeclampsia(1 point)
  50. 50.  THANK YOU