Download to read offline
![H:\Gestational Hypertension Capp Moms Mess 2[1]](https://cdn.slidesharecdn.com/ss_thumbnails/hgestationalhypertensioncappmomsmess-21-100304134429-phpapp02-thumbnail.jpg?width=600ounds&width=560&fit=bounds)
1300 - 1430 - I am sharing _PIH_ causes effects anaesthesia
- 1.
- 2. INTRODUCTION • Hypertension isone of the most common complication during pregnancy • Leading cause of maternal and perinatal morbidity and mortality • Incidence – 6-8% of all pregnancies
- 4. GESTATIONAL HYPERTENSION • SystolicBP ≥140 mm Hg or diastolic BP ≥90 mm Hg or both for first time after 20 weeks • Resolves within 12 weeks postpartum • No proteinuria or other systemic findings • Final diagnosis made only postpartum • Out of 6-8%, 15-25% progress to preeclampsia
- 5. CHRONIC HYPERTENSION • SystolicBP ≥140 mm Hg or diastolic bp ≥90 mm Hg or both before pregnancy or diagnosed before 20 weeks gestation - not attributable to gestational trophoblastic disease • Hypertension persists beyond 12 weeks postpartum
- 6. CHRONIC HYPERTENSION WITH SUPERIMPOSEDPREECLAMPSIA • New onset proteinuria ≥ 300mg/24 hrs after 20 weeks gestation in previously hypertensive patient or • Sudden increase in proteinuria and/or hypertension or other manifestations of preeclampsia after 20 weeks gestation in women having chronic hypertension and proteinuria before 20 weeks
- 7. PRE-ECLAMPSIA • Systolic BP≥ 140 mm Hg or diastolic BP ≥ 90 mm Hg on 2 occasions at least 4 hours apart after 20 wks of gestation in a woman with a previously normal blood pressure • & • Proteinuria • 300 mg or more per 24 hour urine collection • Or protein/creatinine ratio of 0.3 or more • Or dipstick reading of +2
- 8. • Or inthe absence of proteinuria, new-onset hypertension with the new onset of any of the following: • Platelet counts < 1lakh/mm3 • Renal insufficiency: serum creatinine > 1.1.mg/dL or a doubling of the serum creatinine concentration in the absence of other renal disease • Impaired liver function: elevated blood concentrations of liver transaminases to twice the normal concentration • Pulmonary edema • New-onset headache unresponsive to medication and not accounted for by alternative diagnosis or visual symtoms
- 9. SEVERE PRE-ECLAMPSIA • Systolicbp 160 ≥ mmhg or diastolic bp 110 ≥ mmhg or both • Platelet counts < 1lakh/mm3 • Renal insufficiency: serum creatinine > 1.1.mg/dL or a doubling of the serum creatinine concentration in the absence of other renal disease • Impaired liver function: elevated blood concentrations of liver transaminases to twice the normal concentration • Pulmonary edema • New-onset headache unresponsive to medication and not accounted for by alternative diagnosis or visual symtoms
- 10.
- 11. ECLAMPSIA • New onsetof seizures or unexplained coma during pregnancy or postpartum period in patients with pre- existing preeclampsia and without a pre-existing neurological disorder • Most seizures intrapartum or within first 48 hrs post delivery
- 13. ETIOLOGY AND PATHOGENESIS • Exactcause is unknown - “the disease of theories.” Abnormal placentation Genetic factors Immunologic factors- uterine nk cells, trophoblastic hla- c, aa- at 1 Imbalance between thromboxanes and prostacyclines Antiangiogenic proteins- soluble endoglins, sflt 1, tk 1 receptor
- 14. Stage 1 Poor placentation (early) Stage 2 Placental oxidative stress(late) Fetal growth restriction Systemic release of placental factors Systemic inflammatory response, endothelial activation Preeclampsia syndrome
- 15. MARKERS OF PIH •↑ plasma Homocystiene • ↑ serum sFlt1(soluble fms-like tyosine kinase) • ↓serum and urinary Platelet Growth Factor • ↓ Vascular Endothelial Growth Factor
- 16. PREDICTION OF PIH Noscreening test is really helpful Various screening methods are: a. Doppler USG 1. Diastolic notch at 24weeks 2. Absence or reversal of end diastolic flow 3. Average mean arterial pressure ≥ 90 mmHg in 2nd trimester b. Infusion test: angiotensin infusion (8 ug/kg/ required to raise the blood pressure >20 mm Hg from baseline c. Roll-over test: rise in bp >20mmhg from baseline on turning supine at 28-32 weeks gestation
- 17. CLINICAL MANIFESTATIONS... CVS • Increasedvascular tone and sensitivity to vasoconstrictors → HT, vasospasm, end-organ ischaemia → ↑ BP and SVR • Intravascular volume depletion • Majority – hyperdynamic LV function • Smaller, high risk group – ↓LV function, markedly ↓ SVR, ↓ intravascular volume
- 18. Respiratory system • Pharyngolaryngeal edema •Increased risk of pulmonary edema due to lower colloid oncotic pressure, increased hydrostatic pressure and increased vascular permeability Haematologic system • Thrombocytopenia in severe disease (15-20%) • Hypercoagulability in disease without severe features, hypocoagulability in severe disease • DIC
- 19. Renal system • ↓GFR, proteinuria, ↑↑ uric acid • ↑ urine protein:creatinine ratio • Oliguria Hepatic system • Periportal hmg, fibrin deposition in hepatic sinusoids • ↑ serum transaminases • Hepatic edema/right upper quadrant abdominal pain; rupture of Glisson’s capsule with hepatic hmg
- 20. Endocrine system • Imbalanceof prostacyclin relative to thromboxane • Upregulation of systemic renin angiotensin aldosterone system Uteroplacental system • Persistence of a high-resistance circuit with ↓ blood flow •IUGR; oligohydramnios Eye • Retinal arteriolar constriction, retinal
- 21. Uteroplacental Circulation Uterine and intervillousblood flow is diminished by 50-70% due to hemoconcentration, increased blood viscosity and vasoconstriction leading to : • Decreased placental perfusion • Placental ischemia and infarction • Placental abruption • Preterm labour • IUGR • Fetal loss
- 22. COMPLICATIONS OF SEVEREPRE- ECLAMPSIA • APH • CVA • Eclampsia • Pulmonary edema • HELP/DIC • Hepatic failure • Renal failure Maternal Fetal • IUGR • Preterm birth • IUD
- 23. LAB INVESTIGATIONS Complete blood count Urine- routine & microscopy LFTs RFTs (BUN, Sr. creatinine , uric acid). Sr. electrolytes RBS BT, CT, Coagulation profile(PT, INR, PTTK, FDPs, D dimers, AT-3) Fundoscopy USG abdomen with doppler Blood grouping & cross matching 23
- 24. MANAGEMENT OF PRE-ECLAMPSIA •Maternal surveillance - Careful monitoring to detect progress of disease • Fetal surveillance • Induction beyond 37 weeks
- 25. MANAGEMENT OF SEVERE PRE-ECLAMPSIA • Hospital admission • Start antihypertensives • Optimize intravascular volume status • Monitoring – maternal , fetal • Administration of corticosteroids • Anti-Seizure prophylaxis • Vaginal delivery prefered • Timing – anytime after 34 weeks is ideal Expectant management till 34 weeks may improve fetal outcome Delay of 24-48 hrs after steroid for lung maturity Maternal and neonatal ICU facilities
- 26. CONTD… Expedite delivery regardlessof timing and steroid therapy in : 1. HELLP syndrome/DIC 2. Placental abruption 3. Pulmonary edema 4. Eclampsia 5. Refractory severe hypertension despite optimal medications 6. Persistent cerebral symptoms despite Mag. Sulphate 7. Non reassuring fetal status
- 27. MANAGEMENT OF HELLP SYNDROME •Immediate hospitalisation • Stabilise mother • Antihypertensives • Anti-seizure prophylaxis • Correct coagulation abnormalities • Assess foetal condition- FHR, BPP, Doppler ultrasound • GA for caesarean delivery
- 28. MANAGEMENT OF HELLP SYNDROME 1.Hospital admission 2. patient stabilization 3. Control and treat Hypertension 4. Improve intravascular volume 5. Seizure control and neurologic assessment 6. Treat and Prevent further complications 7. Fetal monitoring to Deliver viable fetus 8. Lab investigations
- 29. 1. CONTROL HYPERTENSION Generallyrequires invasive BP monitoring Target : SBP 120-159 mmhg and DBP 80-105 mmhg Lower map not more than 15-20% to avoid precipitous fall in placental perfusion and fetal oxygenation • Most commonly for acute control: hydralazine, labetalol • Nifedipine may be used, but unexpected hypotension may occur when given with MgSO4 • For refractory hypertension: nitroglycerin or nitroprusside may be used • Nitroprusside dose and duration should be limited to avoid fetal cyanide toxicity
- 30. 2. OPTIMIZE INTRAVASCULAR STATUS (CONTRACTED INTRAVASCULAR VOLUME VS LEAKY CAPILLARIES ) • Judicious hydration (prevent pulmonary edema) • Maintenance fluid : 1 mg/kg/hr • Urine output : 0.5 ml/kg/hr accepted minimum • Colloids : no improvement in outcome • Blood : if Hct. < 27 % • Blood products as needed
- 31. 3. SEIZURE PROPHYLAXIS Routinely in Preeclampsia with severe features Magnesium sulphate Initiated with onset of labor till 24h postpartum For caesarean, started at least 2hrs before the section till 24 hrs postpartum. MECHANISM OF ANTICONVULSANT EFFECT OF MAGNESIUM: 1.Reduces cerebral vasospasm by cerebral vasodilating properties 2.Vasodialation- decreases peripheral vascular resistance 3.Act on central NMDA receptor to raise seizure threshold
- 32. 32 RECOMMENDED REGIME Zuspan orsibai regime: 4-6 gm IV over 20-30min f/b infusion of 1-2 gm/hr Pritchard regime: 4 gm IV over 3-5 min f/b 5 gm in each buttock with maintenance of 5 gm IM in alternate buttock 4 hrly
- 33. 33 EFFECTS OF INCREASINGPLASMA MG LEVELS Plasma ( mEq/ level dl ) Plasma level ( mg/ dl ) EFFECTS 1.5 – 2.0 1.8 – 2.4 Normal plasma level 4.0 – 8.0 4.8 – 9.6 Therapeutic range 5.0 - 10 6.0 - 12 ECG Changes( prolonged PQ int., widened QRS complexes 10 12 Loss of deep tendon reflexes 15 15-20 Resp. arrest 25 30 Cardiac arrest
- 34. 34 EFFECTS OF MAGNESIUMSULFATE The primary anesthetic considerations for women receiving magnesium sulfate are (1) interaction with nondepolarizing muscle relaxants (2) effects on uterine tone, and (3) interaction with calcium channel blocking agent.
- 35. 1.Mg inhibits therelease of Ach at NMJ. - Sensitivity to acetylcholine. - Potency and duration of non depolarising muscle relaxants neuromuscular monitoring should be used and dose of non depolarizing muscle relaxants should be reduced. 2.As a tocolytic agent - Depresses smooth muscle contraction. - Risk for uterine atony and excessive blood loss. 35
- 36. 36 SIDE EFFECTS OFMAGNESIUM SULPHATE MATERNAL : flushing, chest pain, palpitation,headache, dizziness, drowsiness muscle weakness, pulmonary edema NEONATAL: lethargy, hypotonia, respiratory depression Eliminated by renal excretion, and serum levels may become dangerously high in the presence of renal insu ciency ffi .
- 37. • • Discontinuation ofmagnesium infusion and iv administration of calcium gluconate (1 g) over 10minutes. In case of respiratory compromise: tracheal intubation and mechanical ventilation until spontaneous ventilation returns. TREATMENT OF MAGNESIUM TOXICITY
- 38. 4. TREATMENT OFECLAMPSIA • Turn patient to left side , jaw thrust • Secure airway – bag mask, NPA, intubation as needed • Supplemental O2 • Pulse oximeter • Secure IV access • ECG monitoring • BP monitoring • Drugs Magnesium sulphate If necessary, small doses of barbiturate or benzodiazepine (STP 50 mg or midazolam 1-2 mg) • If seizure persists or patient is not breathing, rapid sequence induction with cricoid pressure and intubation should be performed. • Patient may be extubated once she is completely awake, recovered from neuromuscular blockade, and magnesium sulfate has been administered.
- 39. ANAESTHETIC MANAGEMENT Role of anaesthesiologist Provide labour analgesia Provide anaesthesia for caesarean section Resuscitation Intensive care management
- 40. LABOUR ANALGESIA • Lumbarneuraxial analgesia is appropriate for women with preeclampsia during labour – continuous epidural or CSE • Early administration of epidural analgesia : 1. Good analgesia attenuates hypertensive response to pain 2. To avoid GA and possibility of airway catastrophe 3. Catheter placement in the setting of declining platelet count 4. Beneficial effects on uteroplacental perfusion
- 41. WHEN TO DELIVER?? Maternal Indication •Recurrent Severe Hypertension • Recurrent symptoms of severe preeclampsia • Progressive renal insufficiency i.e. serum creatinine >1.1 mg/dL or a doubling of the serum creatinine concentration in the absence of other renal disease • Persistent thrombocytopenia or HELLP syndrome • Pulmonary oedema • Suspected abruption placenta • Progressive labour or rupture of membranes
- 42. FETAL INDICATION • Gestationalage of 34 0/7 weeks • Severe fetal growth restriction • Persistent Oligohydramnios • BPP of 4/10 or less on at least two occasions 6 hours apart • Reversed end-diastolic flow on umbilical artery Doppler studies • Recurrent variable or late deceleration during NST • Fetal death
- 43. PRE ANAESTHETIC CONSIDERATIONS •Condition of mother – stabilization • Hypertension, antihypertensives • Risk of seizures • Difficult airway • Reduced plasma volume • Risk of pulmonary edema • Coagulopathy • Renal dysfunction • Hypoproteinemia • Liver dysfunction • Increased sensitivity to NMBA with Mag. Sulph • Fetal status
- 44. INVESTIGATIONS • CBC withplatelet count +/- peripheral smear • Liver function tests • Renal function tests • Coagulation profile • Urine – albumin, sugar • Blood sugar • ABG • BGCM • Magnesium levels
- 45. MONITORIN G • Basic Parameters: Non-invasive BP ECG Urine output Pulse oximetry Capnography Fetal monitoring • Additional Parameters: Intra-arterial BP ? Cvp ?? PCWP
- 46. • Before Induction: -Patent 18 G IV cannula - Anti-hypertensive/Anti- convulsants - Aspiration prophylaxis - Adequate (pre)oxygenation
- 47. TYPE OF DELIVERYAND ANAESTHESIA • Vaginal delivery is prefered ( ?analgesia ) • Caesarean may be done if other obstetric indications • Not to prolong induction / 1st stage Caesarean Section
- 48. 1. NORMAL VAGINALDELIVERY: Main aim is - To establish & maintain hemodynamic stability (control hypertension and prevent hypotension ) - To provide excellent labor analgesia - To prevent/ treat complications of preeclampsia Intracerebral haemorrhage Renal failure Pulmonary Edema Eclampsia
- 49. a) Controlled IVanalgesia: Fentanyl - Loading dose: 1 mcg/kg - Maintenance dose: 25-50 mcg every 20 min b) Regional Anaesthesia: Epidural Block - CBC and Coagulation profile - Baseline BP - Continue anticonvulsive therapy - Crytalloid and albumin to increase CVP - Segmental Epidural block with dilute increments
- 50. ADVANTAGE OF EPIDURALBLOCK: • - Hypertensive response to pain is attenuated by epidural block - Decreased levels of catecholamine which facilitates BP control - May improve intervillous blood flow and stable cardiac output - Can also be used in Caesarean section
- 51. A. REGIONAL ANAESTHESIA: Neuraxialanaesthesia is preferred (single shot spinal/ epidural/ CSE ) • Give aspiration prophylaxis • Availability of blood and blood products • Pre-hydration • Oxygen administration: 6lt/min • Epidural Block: 8-10 ml of 1.5-2% lignocaine or 0.5% Bupivacaine with 25-50 mcg of Fentanyl and the block should be raised to a minimum level of T4
- 52. • Sub-arachnoid Block:5-10mg of 0.5% bupivacaine with 20 mcg of Fentanyl • If hypotension occurs treat with Inj phenylepinephrine • Avoid ergot alkaloids once baby is delivered • Post-op pain relief with epidural infusion
- 53. • Platelet countand regional anaesthesia: Prior to placing regional block in a preeclamptic it is recommended to check the platelet count. • No concrete evidence at to the lowest safe platelet count for regional anaesthesia in preeclampsia • Any clinical evidence of DIC would contraindicate regional anaesthesia.
- 54. Neuraxial procedures maybe initiated in pregnant women without other risk factors if the platelet count is higher than 80,000/mm3 There is general consensus among anesthesia providers that a platelet count less than 50,000/mm3 precludes the administration of neuraxial anesthesia For women with a platelet count between 50,000 and 80,000/ mm3, the risks and benefits of neuraxial anesthesia must be weighed against the risks of general anesthesia 54
- 55. B. GENERAL ANAESTHESIA: •When to Induce??? - Coagulopathy - Fetal distress requiring emergency LSCS - Patient refusal
- 56. HAZARDS OF GA: -Upper airway oedema: careful airway assessment - Difficulty in cord visualisation - Worsening of mallampatti grading -Difficulty in laryngoscopy and intubation: Maternal BP should be stabilized and seizure prophylaxis should be given in view of response to laryngoscopy and intubation. Labetalol & NTG are commonly used acutely
- 57. - MgSo4 therapyinterfering with DMR and NDMR - Impaired hepatic/renal blood flow affecting drug metabolism and clearance - High risk of Aspiration
- 58. HOW TO INDUCE?? •Prior to induction aspiration prophylaxis is administered: 30 ml of 0.3 M of Sodium Citrate 30 min before induction • IV lines • Monitors • Failed intubation kit • Working suctions •All drugs- GA, anti-hypertensives, anti-convulsive
- 59. • Pre-oxygenate thepatient • Pre-medicate • Induction: Rapid sequence induction using Thiopentone 4- 5mg/kg and Succinylcholine 1-1.5 mg/kg • Intubation: sellicks manuever is maintained till the cuff of endotracheal tube is inflated. Small size cuffed endotracheal tube is used 6.0-6.5 ID • Maintained With: N2O:O2 (50:50) and a volatile agent preferably Isoflurane.
- 60. •If the patientis on MgSo4 therapy then neuromuscular blocked must be monitored with peripheral nerve stimulator and dose should be titrated accordingly •Avoid ergot alkaloids •Extubtion response to be pre-treated with lignocaine or beta blockers like esmolol •Continue anti-convulsive therapy in post op period. •Semiconscious patient with cerebral lesions should be ventilated electively.
- 61. Regional Vs GeneralAnaesthesia: • Epidural anaesthesia would probably be preferred by many anaesthesiologists in a severely preeclamptic pt. in a non- urgent setting. • For urgent cases it is reassuring to know that spinal is also safe. • This allows us to avoid general anaesthesia with the potential for encountering a swollen, difficult airway and/or labile hypertension
- 62. • General anaesthesiais a well-known hazard in obstetric anaesthesia: • 16X more likely to result in aesthetic-related maternal mortality • Mostly due to airway/respiratory complications
- 63. Conclusion • PIH isa multisystem disorder. • Management is supportive, delivery is the only definitive. • PIH patients: High risk for difficult intubation. • Hypertensive response to laryngoscopy may lead to intracranial haemorrhage.
- 64. • Spinal Anaesthesianot contraindicated in severe Preeclampsia/Eclampsia • Eclampsia can be prevented by prophylactic MgSO4 therapy. • Eclamptic patients should be monitored for at least 24 hrs. Post- partum. • Magnesium sulfate is now proven as the best medication to prevent and treat eclampsia. • Epidural analgesia for labour pain management & regional
- 65.