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Pregnancy Induced Hypertension Obstetric Complications. DR. PRAGATI NANDA. DR.LALITA SUBRAMANIUM. www.anaesthesia.co.in anaesthesia.co.in@gmail.com. Incidence. Most common medical complication of pregnancy 3rd leading cause of maternal mortality.
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Pregnancy Induced Hypertension Obstetric Complications DR. PRAGATI NANDA. DR.LALITA SUBRAMANIUM www.anaesthesia.co.inanaesthesia.co.in@gmail.com
Incidence • Most common medical complication of pregnancy • 3rd leading cause of maternal mortality.
Hypertensive Disorders of PregnancyACOG Criteria Chronic HT( 3-5%) HT existing before pregnancy, detected before 20 weeks gestation, or persisting after delivery (> 12 weeks) PIH Detected after 20 wk of gestation & resolves within 12 wks of delivery Gestational HT (6-7%) HT without proteinuria Preeclampsia (6-8%) HT with proteinuria Superimposed preeclampsia (25% of women with chronic HT) Chronic HT with signs of pre-eclampsia Eclampsia(0.05%) Convulsions during or within 24 hrs of delivery in preeclampsia
Gestational Hypertension • > 20 weeks gestation or during first 24 hrs postpartum Systolic BP > 140 mmHg Diastolic BP > 90 mmHg or both • on atleast 2 occasions • atleast 6 hours apart • Without proteinuria • Resolves by 12 weeks postpartum
Preeclampsia • SBP > 140 mmHg • DBP > 90 mmHg • PROTIENURIA > 0.3g/24hrs • DIPSTICK > 1+ • Severe • SBP > 160 mmHg • DBP > 110 mmHg • PROTIENURIA > 5gm/24 hrs • DIPSTICK > 3+ • Organ involvement • Oliguria, visual, epigastric pain, • IUGR, pulmonary oedema, • HELLP syndrome
Risk Factors Nulliparity • Age > 35 years • Multiple gestation • Family history • Past history of preeclampsia • Chronic HT • Chronic renal disease • Obesity • Protective factor • Cigarette smoking - ↓ sFlt 1
Aetiology - Preeclampsia • Genetic predisposition • Alterations • Immune response • Prostaglandin activity • Nitric oxide levels • Calcium metabolism • ↑ Oxygen free radicals • ↑ Oxidative stress • Tyrosine kinase 1 (sFlt 1) receptor
Aetiology - Preeclampsia • Imbalance of vasodilatory substances (Prostacyclin, Nitric oxide) • Vasoconstrictive substances (Thromboxane A2, Endothelin) • ↑ Vascular reactivity • ↑ Vasospasm
Pathogenesis of PIH • Markers of endothelial injury • e.g. ↑ levels of fibronectin & thromboxane • ↑ Vasoconstrictive substances (IL 1, TNF, • endothelin) • ↓ Endothelium derived relaxing factors (NO)
Hallmarks of PIH • Vasoconstriction • Reduced blood volume • Platelet aggregation • Uteroplacentalhypoperfusion • Leiden mutation in factor V gene • (Activated protein C resistance)
Predictors of Preeclampsia • ↑ Plasma homocysteine • ↑ S. sFlt 1 • ↓ S. Placental growth factor (↓PlGF) • ↓ Urinary PlGF • ↓ Vascular endothelial growth factor (VEGF)
Prevention • Low dose aspirin • Calcium supplementation • Magnesium supplementation • Fish oil supplementation • Antioxidant use – Vitamin C and E • Ketanserin • Experimental
Pathophysiology • Cardiovascular System. • Intravascular volume deficit (↓ preload) • High SVR (↑ afterload) • Hyperdynamicresponse to catecholamines & • Angiotensin II (↑ BP, ↑ HR) • ↓ COP • CVP does not correlate with PCWP
Respiratory System • Upper airway oedema • Swelling tongue & soft tissues • Friable mucosa • Pulmonary oedema Cardiogenic Noncardiogenic • 2-3 DPG ↓, shifts ODC left
Renal Vasospasm ↓ ↓ Renal perfusion ↓ ↓ GFR Glomerular capillary endotheliosis Abnormal RFT ↑ S. Uric Acid, ↑ BUN, ↓ Creatinine clearance ↓ ATN
Liver • Elevated enzyme levels • Subcapsular hematoma • Hepatic rupture • Periportalhaemorrhage • Ischaemiclesion • Fibrin deposition
Central Nervous System • Headache, visual disturbances, seizures Diffuse vasospasm ↓ Cerebral ischaemia • High BP ↓ Cerebral hyperperfusion • Severity of CNS symptoms do not necessarily correlate with degree of HT
Increase in Cerebral perfusion pressure • Usually cerebral antoregulationintact • Vasogenicoedema ↓ Failure of cerebral autoregulation ↓ Overperfusionof distal capillaries.
Eyes Retinal arteriolar constriction ↓ Bilateral retinal detachment ↓ Blindness
Haematological Profile • Relative thrombocytopenia • Platelet function impaired • Platelet adherence → consumption coagulopathy • HELLP syndrome → DIC • Bleeding time not a reliable clotting test • TEG
Placenta • Acute atherosis of decidual arteries • Vasospasm • Fibrin deposition • Hypoperfusion ↓ Chronic foetal hypoxemia • IUGR
Criteria for Diagnosis of HELLP Syndrome Hemolysis • Abnormal peripheral smear • Lactate dehydrogenase > 600 U/L • Bilirubin ≥ 1.2 mg/dL Elevated Liver Enzyme Levels • Serum aspartateaminotransferase > 70 U/L • Lactate dehydrogenase > 600 U/L Low Platelets • Platelet count < 100,000/mm3
HELLP Syndrome • Should not be considered a variant of DIC • - Prothrombin time • - Partial thromboplastin time • - S. Fibrinogen Normal in HELLP • Clinical Features • Epigastric pain • Rt upper quadrant pain • N,V, jaundice, HT
Clinical Features ofSevere Preeclampsia • Symptoms of severe headache • Visual disturbance • Epigastric pain and vomiting • Papilloedema • Liver tenderness • Platelet count falling to below 100 Χ 10°/1 • Abnormal liver enzymes (ALT or AST rising to above 70iu/l) • HELLP syndrome
Principles of Management • Definitive • Delivery of foeto-placental unit • Criteria for expectant management • Controlled hypertension • Reassuring foetal status • Elevated LFT without symptoms • Oliguria resolving with fluid challenge
Management of Severe PET • Supportive • Hospital admission • Control of hypertension • Optimization of intravascular status • Prevention of convulsions • Corticosteroids • Daily monitoring of vitals & maternal well being
Management of Severe Preeclampsia • Antihypertensive treatment should be started • Systolic BP > 160 mmHg • Diastolic BP > 110 mmHg • Labetalol, given orally or intravenously • Nifedipine should be given orally not sublingually • Intravenous hydralazine • Atenolol, ACE inhibitors, ARB and diuretics should be avoided.
Acute Treatment of Hypertension • α methyl dopa250mg tds • Hydralazine5-10mg every 20 min (upto max 200mg/day) • Labetalolinfusion 1-2 mg/min ( max 220mg/day) • Nifedipine10 mg tds oral (max 120 mg/day) • Sodium nitroprusside0.2-5 μg/kg/min infusion
Optimization of Intravascular Status • Judicious hydration • Crystalloids 1-2 ml/kg/hr - assess clinical condition & urine output • Avoid 5% dextrose → neonatal hypogly & hyperbilirubinemia • Colloids • no improvement in outcome • ↑ CVP & pulmonary oedema • Blood, if red cell replacement, Hct < 27% • Blood products to correct abnormalities • CVP & pulmonary artery catheter - selected cases
Maintain Urine Output Oliguria ↓ Fluid challenge 250-500ml crystalloids ↓ No effect ↓ CVP or PCWP becomes mandatory
Prevention of Convulsions • Initiate therapy before onset of labour • Should continue 24-48 hrs after delivery • Magnesium sulphate – Relieves cerebral vasospasm
Monitoring of Treatment • Daily review of signs / symptoms • 4 hrly BP record • Fluid balance chart • Daily urinalysis • B/weekly CBC, Serum Electrolytes, BUN • Platelets > 1,00,000/mm3, no further tests required • Platelets < 1,00,000/mm3, then PT, APTT, TEG • Monitoring should continue 72 hr postpartum
Role of Anaesthesiologist inLabour Room • Labour analgesia • CSE • Control convulsions • Airway management
Labour Analgesia • Benefits of LEA • • Reduces stress response (catecholamines) • • Maintains uteroplacental blood flow • • Less requirement of systemic opioids • • Available option for operative delivery • Technique of LEA • • Hydration • • Monitors • • O2 facemask • • Bupivacaine 0.125% with fentanyl 2 μg/ml • 10-12 ml/hr • Risks • • Unmasks hypovolemia
Role of Anaesthesiologist in PIH • Vaginal delivery • Operative delivery • Control of convulsions (eclampsia) • ICU management
Technique of LEA • Hydration • Monitors • O2 facemask • Bupivacaine 0.125% with fentanyl 2 μg/ml 10-12 ml/hr
Combined Spinal Epidural • Intrathecalopioid • Fentanyl 20-25 μg Or • Sufentanil 2.5-5 μg • May add LA (0.5ml, 0.5% Bupivacaine)
Platelet Count & RA • > 1,00,000 / mm3 → Safe • 75,000 – 80,000 / mm3 → Perhaps safe • 50,000 – 75,000 / mm3 → Grey zone • < 50,000 / mm3 → Unsafe
Anaesthesia for LSCSPreanaesthetic Assessment • Volume status • Airway • Organ function – liver, kidneys, coagulation
Neuraxial Techniques • Continuous lumbar epidural Advantages • ↓ stress hormones • Gradual onset of sympathetic block • CVS stability • Avoids neonatal depression • Safeguards against risk associated with GA • Difficult intubation, ↑↑ BP, pulmonary aspiration • Ensure Normal coagulation profile Adequate circulating volume
Subarachnoid Block • Requires only a small volume of LA • Addition of opioids to reduce LA dose Precautions • Modest prehydration • Avoid sudden hypotension • Treat hypotension immediately • Combined Spinal Epidural (CSE)
General Anaesthesia for LSCS • Difficult airway management • ↑ Hypertensive response to TT • Drug interaction with Mg & NMBAs • Difficult airway cart • Titration of potent vasodilators • Peripheral nerve stimulator
Uterotonics • Ergometrine Not recommended ↑ BP Vomiting May precipitate eclampsia & hypertensive crisis • Oxytocin - cautiously Hypersensitive peripheral vasculature • 15 methyl prostaglandin F2α (prostidin)
Monitoring • Heart rate • NIBP • SpO2 • EtCO2 • ECG • Temperature • Urine output • Coagulation profile • CVP & PCWP optional • FHS monitoring • NM monitoring • Mg monitoring
Postoperative Care Continue • Monitoring in postpartum period • MgSO4 for 24 hrs • Antihypertensive • Analgesics • Epidural opioid • IV fluids • Oxygen therapy
ICU Care in PIH • Indications • Repeated convulsions • ↑ ↑ BP • Severe oliguria requires dialysis • Cerebral oedema / haemorrhage • Pulmonary oedema, CHF • Liver haematoma • HELLP, DIC, PPH
Indications for ICU Admission in Pre-eclampsia • Invasive haemodynamic monitoring – Severe hypertension – Guided fluid balance • Mechanical ventilation – Acute respiratory distress syndrome -Pulmonary oedema -Aspiration • Airway Protection - Seizures -Upper airway oedema • Disseminated intravascular coagulation • HELLP syndrome • Acute renal failure • Neurological – Severe convulsions – Stroke
Eclampsia • Major cause of maternal (4.2%) and perinatal morbidity and mortality (13-30%) • 0.05 – 0.1% USA • > 1% in India.
Incidence • Antepartum (50%) • Intrapartum (25%) • Postpartum (25%)
Course of Eclamptic Seizure • Seizure is self limited, 1-2 minutes • Abnormal foetal heart rate pattern • foetalbradycardia ↓ variability late decelerations Resolves within 5-10 mins of cessation of . seizure reflex tachycardia