Pih, by dr omer ajmal


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Pih, by dr omer ajmal

  2. 2. INTRODUCTION <ul><li>Hypertensive disorders of pregnancy are responsible for significant maternal and perinatal morbidity and are the second leading cause, after embolism, of maternal mortality. </li></ul><ul><li>Hypertensive disorders of pregnancy complicate approximately 12% to22% of all pregnancies and are directly responsible for 17.6% of maternal deaths in the united states. (high risk pregnancy 3 rd edi) </li></ul>
  3. 3. DEFINITIONS <ul><li>Hypertension – sustained systolic BP > 140mmHg or diastolic BP> 90mmHg </li></ul><ul><li>Chronic Hypertension – hypertension which predates pregnancy or is diagnosed before 20wks gestation </li></ul><ul><li>PIH – hypertension diagnosed after 20 weeks gestation in a patient without a history of chronic hypertension and is defined as a systolic BP greater than 140mmHg or diastolic BP greater than 90mmHg OR alternatively, as a consistent ↑in systolic or diastolic BP by 30mmHg and 15mmHg, respectively above the Pt,s normal base line. </li></ul><ul><li>Pre-eclampsia – PIH in association with renal involvement causing proteinuria (>300mg/24h or 2+ on dipstick </li></ul>
  4. 5. Preeclampsia <ul><li>A. Mild </li></ul><ul><li>B. severe (HELLP SYNDROME) </li></ul><ul><li>Multiorgan disease characterized by development of hypertension with Proteinuria after the 20 th week of gestation. </li></ul><ul><li>Disorder of unknown etiology with most cases occurring in the first pregnancy. </li></ul><ul><li>Proteinuria is defined as 300 mg or more of protein in a 24- hour urine collection. </li></ul><ul><li>Edema may manifest as a recent, rapid weight gain. </li></ul>
  5. 6. <ul><li>Severe Pre-eclampsia – pre-eclampsia in association with any of: </li></ul><ul><ul><li>Sustained BP > 160/110 </li></ul></ul><ul><ul><li>Proteinuria >5g/24hrs or 3+ on dipstick </li></ul></ul><ul><ul><li>Urine output <400ml/24hrs </li></ul></ul><ul><ul><li>Pulmonary oedema or evidence of pulmonary compromise </li></ul></ul><ul><ul><li>Epigastric or RUQ pain </li></ul></ul><ul><ul><li>Hepatic rupture </li></ul></ul><ul><ul><li>Platelet count <100 x 10 9 /L </li></ul></ul><ul><ul><li>Evidence of cerebral and visual complications </li></ul></ul><ul><ul><li>Intrauterine growth delay. (oligohydramnios?) </li></ul></ul>
  6. 7. What is HELLP syndrome? <ul><li>HELLP syndrome is a serious complication of severe pregnancy-induced hypertension (high blood pressure problems of pregnancy). It occurs in about 2 percent to 12 percent of women with high blood pressure of pregnancy. It usually develops before delivery, but may occur postpartum (after delivery) as well. HELLP syndrome consists of the following problems: </li></ul><ul><li>h emolysis - red blood cells break down. </li></ul><ul><li>e levated l iver enzymes - damage to liver cells cause changes in liver function lab tests. </li></ul><ul><li>l ow p latelets - cells found in the blood that are needed to help the blood to clot in order to control bleeding. </li></ul>
  7. 8. What causes HELLP syndrome? <ul><li>The cause of HELLP syndrome is unknown. Some conditions may increase the risk of developing HELLP syndrome, including the following: </li></ul><ul><li>preeclampsia during pregnancy </li></ul><ul><li>previous pregnancy with HELLP syndrome </li></ul>
  8. 9. What Is Eclampsia? <ul><li>Eclampsia is the final and most severe phase of preeclampsia and occurs when preeclampsia is left untreated. </li></ul><ul><li>In addition to the previously mentioned signs of preeclampsia, women with eclampsia often have seizures. </li></ul><ul><li>Eclampsia can cause coma and even death of the mother and baby and can occur before, during, or after childbirth. </li></ul>
  9. 10. Predisposing factors for PE Syndrome <ul><ul><li>First pregnancy </li></ul></ul><ul><ul><li>New partner/paternity </li></ul></ul><ul><ul><li>Age younger than 18 years or older than 35 years </li></ul></ul><ul><ul><li>History of preeclampsia </li></ul></ul><ul><ul><li>Family history of preeclampsia in a first-degree relative </li></ul></ul><ul><ul><li>Black race </li></ul></ul><ul><ul><li>Obesity (BMI ³ 35) </li></ul></ul><ul><ul><li>Interpregnancy interval less than 2 years or more than 10 years </li></ul></ul>
  10. 11. <ul><ul><li>Chronic hypertension, especially secondary causes of chronic hypertension such as hypercortisolism, hyperaldosteronism, pheochromocytoma, or renal artery stenosis </li></ul></ul><ul><ul><li>Preexisting diabetes (type 1 or type 2), especially with microvascular disease </li></ul></ul><ul><ul><li>Renal disease </li></ul></ul><ul><ul><li>Systemic lupus erythematosus </li></ul></ul><ul><ul><li>Protein S deficiency. </li></ul></ul><ul><ul><li>Activated protein C resistance </li></ul></ul><ul><ul><li>Obesity </li></ul></ul><ul><ul><li>Thrombophilia </li></ul></ul>
  11. 12. <ul><li>Placental/fetal risk factors for preeclampsia </li></ul><ul><ul><li>Multiple gestations </li></ul></ul><ul><ul><li>Hydrops fetalis </li></ul></ul><ul><ul><li>Gestational trophoblastic disease </li></ul></ul><ul><ul><li>Triploidy </li></ul></ul>
  12. 13. Aetiology <ul><li>Unknown </li></ul><ul><li>Theories </li></ul><ul><ul><li>Toxaemia </li></ul></ul><ul><ul><li>Immunological and genetic factors </li></ul></ul><ul><ul><li>Reduced levels of nitric oxide </li></ul></ul><ul><ul><li>Imbalance of thromboxane and prostacyclin – favours vasoconstriction </li></ul></ul>
  13. 14. Aetiology <ul><li>􀂾 Pre-eclampsia is mainly a disease of primigravida • </li></ul><ul><li>Thus it seems that exposure to past pregnancy or paternal/fetal antigens has a protective effect </li></ul><ul><li>Theorize that previous exposure builds up antibodies that block placental antigenic sites hiding these fromattack by T-cells -> immunosuppression of fetoplacental unit </li></ul><ul><li>Failure of immunosuppression results in placental damage with release of trophoblasts and/or immune complexes to initiate a number of cascades </li></ul>
  14. 15. pathogenesis <ul><li>I mmunological Factors: </li></ul><ul><li>Immunological disorders may arise from an abnormal maternal-fetal antigen- antibody response or from the contents of seminal fluids. </li></ul><ul><li>Spermatozoa may cause antibody formation or prostaglandins may initiate uterine vasoconstriction. </li></ul><ul><li>Genetic Factors: </li></ul><ul><li>Familial tendency towards preeclampsia exists in some population. </li></ul><ul><li>It may result from a recessive genetic inheritance. </li></ul><ul><li>Endothelial factors: </li></ul><ul><li>Vascular endothelial damage or dysfunction is the common pathologic feature of preeclampsia and occurs in placental decidual vessels and renal microvasculature. </li></ul>
  15. 16. <ul><li>Endothelial cell dysfunction in response to unknown factors may cause a hormonal imbalance in women with preeclampsia. </li></ul><ul><li>Endothelial dysfunction lead to hyper reactivity. </li></ul><ul><li>Pt,s with PIH have elevated levels of thromboxane A2 and decrease prostacycline (PGI2) production. </li></ul><ul><li>TXA2 is a potent vasoconstrictor and promote platelet aggregation. </li></ul><ul><li>PGI2 is a potent vasodilator and inhibitor of platelet aggregation. </li></ul><ul><li>Endothelial dysfunction may reduce production of nitric oxide and increase production of endothelin-1, that is also a potent vasoconstrictor and activator of platelets. </li></ul><ul><li>Abnormal regulation of oxygen derived free radical and lipid peroxidation may also play an important role. </li></ul><ul><li>Marked vascular reactivity and endothelial injury reduce placental perfusion and lead to widespread systemic manifestations. </li></ul>
  16. 18. Symptomatology <ul><li>Increasing oedema, particularly tibial pitting oedema, lumbosacral, and facial. </li></ul><ul><li>– A rise in Blood pressure is insidious and thus asymptomatic </li></ul><ul><li>– Possible symptoms of frontal headache, blurring of vision, epigastric pain -> impending Eclampsia </li></ul><ul><li>– Signs of cerebral irritation Brisk reflexes, clonus </li></ul><ul><li>– Placental insufficiency 􀃆 Manning score; Doppler studies </li></ul><ul><li>IUGR </li></ul>
  17. 19. investigations <ul><li>– Hypertension </li></ul><ul><ul><li>• MILD:- diastolic >= 90 mmHg </li></ul></ul><ul><ul><li>• MODERATE:- 95-110 mmHg </li></ul></ul><ul><ul><li>• SEVERE:- >110 mmHg </li></ul></ul><ul><li>– Albuminuria </li></ul><ul><ul><li>• Significant >=3.0 g/l </li></ul></ul><ul><li>– Renal function tests deteriorating </li></ul><ul><ul><li>• Urea, creatinine, uric acid, decreasing urine output </li></ul></ul><ul><li>– Liver function tests </li></ul><ul><ul><li>• Deteriorating enzymes </li></ul></ul><ul><li>– Haematological </li></ul><ul><ul><li>• Falling platelet count </li></ul></ul>
  18. 20. <ul><li>Rollover test </li></ul><ul><li>A positive rollover test result is defined as an increase in diastolic BP of 20mmHg or more when measured 5 minutes after a gravida is “rolled” from the lateral to the supine position b/w 28-32 weeks gestation. </li></ul><ul><li>93% of primigravid women with a positive rollover test result later had gestational hypertension and 91% of women who had a negative test result did not have hypertension during that pregnancy. </li></ul><ul><li>However the value of this test as a clinical screening tool is debatable because in some studies the false positive rate is high. </li></ul>
  19. 21. <ul><li>Angiotensin Test </li></ul><ul><li>A normal pregnant Pt requires mean Angiotensin II doses of 13.5 to 14.9 ng /kg/minute to increase diastolic BP by 20 mmHg. </li></ul><ul><li>91% of women who requires more than 8ng / kg/min to achieve this BP elevation remained normotensive through out pregnancy. </li></ul><ul><li>Conversely normotensive primigravidae who later had gestational hypertension responded at doses of less than 8ng /kg/min as early as 28-32 weeks, gestation. </li></ul><ul><li>90% of these pts later had overt gestational hypertension. </li></ul>
  20. 22. Complications <ul><li>MATERNAL </li></ul><ul><li>Neurological </li></ul><ul><li>Headache </li></ul><ul><li>Visual disturbances </li></ul><ul><li>Hyperexcitability </li></ul><ul><li>Seizures </li></ul><ul><li>Intracranial hemorrhage </li></ul><ul><li>Cerebral edema </li></ul><ul><li>Pulmonary </li></ul><ul><li>Upper airway edema </li></ul><ul><li>Pulmonary edema </li></ul>
  21. 23. <ul><li>Cardiovascular </li></ul><ul><li>↓ intravascular volume </li></ul><ul><li>↑ arteriolar resistance </li></ul><ul><li>Hypertension </li></ul><ul><li>Heart failure </li></ul><ul><li>Hepatic </li></ul><ul><li>Impaired function </li></ul><ul><li>Elevated enzymes </li></ul><ul><li>Hematoma </li></ul><ul><li>rupture </li></ul>
  22. 24. <ul><li>Renal </li></ul><ul><li>Proteinuria </li></ul><ul><li>Sodium retention </li></ul><ul><li>Decreased GFR </li></ul><ul><li>Renal failure </li></ul><ul><li>Hematological </li></ul><ul><li>Coagulopathy </li></ul><ul><ul><li>Thrombocytopenia </li></ul></ul><ul><ul><li>Platelet dysfunction </li></ul></ul><ul><ul><li>Prolonged PPT </li></ul></ul><ul><ul><li>Microangiopathic hemolysis </li></ul></ul>
  23. 25. <ul><li>FETAL </li></ul><ul><li>Placental insufficiency -> 􀃆 IUGR -> 􀃆 Intrauterine death </li></ul><ul><li>Premature delivery [iatrogenic] -> 􀃆 Neonatal death </li></ul>
  24. 26. Management <ul><li>Domain of obstetricians </li></ul><ul><li>Bed rest. </li></ul><ul><li>Sedation </li></ul><ul><li>Improve intravascular volume </li></ul><ul><li>Control hypertension – prevent maternal morbidity </li></ul><ul><ul><li>B-blockers in third trimester (labetolol preferred) – prolonged use may decrease fetal growth(10-20 mg iv) </li></ul></ul><ul><ul><li>Hydralazine – for acute reduction(5-10 mg iv increments) </li></ul></ul><ul><ul><li>Methyldopa – safe in pregnancy(250-500mg) orally. </li></ul></ul>
  25. 27. <ul><ul><li>Nifedipine(10 mg) orally or sublingually ( tocolytic action) </li></ul></ul><ul><ul><li>Avoid ACE inhibitors – associated with oligohydramnios, still birth, neonatal renal failure </li></ul></ul><ul><ul><li>Nitroglycerine (50-100 ug iv or sublingually in a 400 ug metered spray) </li></ul></ul><ul><ul><li>Nitroprusside( cyanide toxicity more likely if infusion rate exceed 4 ug/kg/min over several hours to days) </li></ul></ul><ul><ul><li>Diuretics - NO PLACE [unless heart failure] SINCE PREECLAMPSIA IS ASSOCIATED WITH HYPOVOLAEMIA </li></ul></ul><ul><ul><li>Invasive arterial, central venous and pulmonary artery catheter is indicated in pts with severe hypertension, pulmonary edema, persistent oliguria and difficulty in fluid management therapy in ante partum and postpartum period. </li></ul></ul>
  26. 28. <ul><li>Treat seizures – magnesium sulphate (4-6g initial bolus over 20 min followed by 1-2g per hour).Also used to control BP. </li></ul><ul><li>Serum MgSo4 concentration should be measured atleast 4 Hrs after initiation of therapy. </li></ul><ul><li>Therapeutic range for serum MgSo4 concentration is b/w 4-6 mEq/L </li></ul><ul><li>Urine output, respiratory rate, patellar reflexes are monitored during magnesium therapy . </li></ul><ul><li>It also crosses placenta so may decreases fetal HR and beat-to-beat variability. Neonatal depression can also occur. </li></ul>
  27. 29. <ul><li>Severe pre-eclampsia /eclampsia </li></ul><ul><ul><li>A,B,C’s </li></ul></ul><ul><ul><li>Appropriate fetal and maternal monitoring etc.. </li></ul></ul><ul><li>Term delivery ideal – risk of morbidity associated with pre- eclampsia and risks of a pre-term delivery </li></ul><ul><li>Aim to stabilise symptoms long enough to mature fetal lungs </li></ul><ul><ul><li>In established pre-eclampsia the only definitive treatment is the delivery of the placenta. </li></ul></ul>
  28. 32. MgSo 4 Toxicity <ul><li>If MgSo4 toxicity is suspected, MgSo4 infusion should be immediately discontinued. </li></ul><ul><li>I/V calcium gluconate 1G or calcium chloride 300 mg to antagonize the effect of MgSo4. </li></ul><ul><li>If respiratory distress occur, the Pt may require ETT and mechanical ventilation. </li></ul>
  29. 34. Anaesthetic Implications <ul><li>Pain management during labour </li></ul><ul><li>Regional anaesthesia for surgical delivery </li></ul><ul><li>GA for surgical delivery </li></ul>
  30. 35. <ul><li>Initial laboratory studies should be evaluated. </li></ul><ul><li>Critically ill pts require stabilization before induction. </li></ul><ul><li>Hypertension should be controlled. </li></ul><ul><li>Hypovolemia should be corrected. </li></ul><ul><li>A platelet count and coagulation profile should be checked prior to regional anaesthesia in pts with severe PIH. </li></ul><ul><li>CVP line may be used to guide fluid therapy. </li></ul><ul><li>Intra arterial BP monitoring is indicated with severe hypertension. </li></ul>
  31. 36. <ul><li>Epidural </li></ul><ul><ul><li>Traditionally considered anaesthetic of choice </li></ul></ul><ul><ul><li>Controls excessive surges in BP </li></ul></ul><ul><ul><li>Decreases circulating stress-induced catecholamines and uterine vascular resistance </li></ul></ul><ul><ul><li>Check platelet count </li></ul></ul><ul><ul><li>Beware of fluid preloading prior to insertion in patients with pulmonary oedema </li></ul></ul><ul><ul><li>Monitor BP and fetus carefully and treat BP promptly with ephedrine. </li></ul></ul><ul><ul><li>Avoids the increased risk of a failed intubation due to severe edema of upper airways. </li></ul></ul>
  32. 37. Anaesthetic Implications - Spinal <ul><li>Spinal Anaesthesia </li></ul><ul><ul><li>Evidence based studies limited </li></ul></ul><ul><ul><li>Use controversial – risk of profound maternal hypotension and uteroplacental hypoperfusion but a recent study noted that the risk of hypotension was almost six times less in severely preeclamptic woman than in healthy pregnant woman receiving spinal anesthesia for elective CS. </li></ul></ul><ul><ul><li>Theoretical advantage of epidural weighed against known benefits of spinal ie. greater reliability, less procedural time, less epidural vascular trauma </li></ul></ul><ul><ul><li>Check platelets, reduce preload volume, ephidrine etc </li></ul></ul>
  33. 38. Anaesthetic Implications - GA <ul><li>General Anaesthesia </li></ul><ul><ul><li>Only if regional anaesthesia cotraindicated or precluded by urgency of need for delivery </li></ul></ul><ul><ul><li>Endotracheal intubation more difficult in pregnant population, plus oedema of upper airway, therefore prepare for difficult intubation. </li></ul></ul><ul><ul><li>Aspiration prophylaxis. </li></ul></ul><ul><ul><li>Preoxygenation with 100% oxygen </li></ul></ul><ul><ul><li>Exaggerated hypertensive response to laryngoscopy – significant morbidity( Labetalol 5-10 mg). </li></ul></ul><ul><ul><li>RSI </li></ul></ul>
  34. 39. <ul><ul><li>Use a small ETT(6.0 or 6.5mm) because of airway edema. </li></ul></ul><ul><ul><li>Use two third of Mac of inhalational agent of non pregnant adult to insure an adequate depth of anesthesia. </li></ul></ul><ul><ul><li>If magnesium used – expect prolongatin of action of muscle relaxants (prepheral nerve stimulator used). </li></ul></ul><ul><ul><li>Normal dose of suxamethonium, titrate non-depolarising muscle relaxants </li></ul></ul><ul><ul><li>Avoid NSAIDs for post-op analgesia </li></ul></ul>
  35. 40. Postoperative Management <ul><li>Provide adequate analgesia. </li></ul><ul><li>Maintain strict intake/ output for at least 24 hours postpartum or until diuresis develops. </li></ul><ul><li>Continue MgSo 4 for at least 24 hours postpartum or until evidence of diuresis. </li></ul><ul><li>Maintain hemodynamic control with anti hypertensives if necessary. </li></ul>
  36. 41. Take Home Message <ul><li>Usually multi systemic involvement </li></ul><ul><li>Risk of significant obstetric and anaesthetic complications </li></ul><ul><li>Anaesthetic risks reduced by </li></ul><ul><ul><li>Early communication and preparation </li></ul></ul><ul><ul><li>Early placement of epidural catheter </li></ul></ul><ul><ul><li>Utilising spinal for urgent C-section if no epidural in place </li></ul></ul><ul><ul><li>GA only when regional anaesthesia contraindicated </li></ul></ul><ul><ul><li>Anticipate difficult airway </li></ul></ul><ul><ul><li>Emphasis on preoperative baseline BP reduction and blunting hypertensive response to laryngoscopy </li></ul></ul>