Patent ductus arteriosus

Patent ductus arteriosus and anesthesia

1. PATENT DUCTUS ARTERIOSUS MODERATOR : Dr.Prashant PRESENTER: Dr. Richa

2. INTRODUCTION FETAL CIRCULATION: SPO2 = 40% Po2=12-14mmHg SPO2 =80% Po2=32-35mmHg SPO2 =70% Po2=28-30% SPO2 =55-60% Po2=20-22 SPO2 =65 Po2=26-28

3. Normal transition of circulation after birth:

4. AT birth…. Placenta removed  portal blood pressure falls  DV closes Blood is oxygenated in lungs  DA exposed to oxygenated blood VC First breath Pulmonary vascular resistance decreases now SVR>PVR  LAP> RAP  closure of foramen ovale

5. Although closure of DA occurs primarily by increased oxygen tension, successful complete closure requires arterial muscular tissue. DA begins to close within first 24 hours after delivery Completed sealed off in FIRST MONTH During this critical period, infant can readily revert from adult circulation to fetal circulation (FLIP-FLOP CIRCULATION) If shunt persists (preterm babies/maternal rubella) it leads to shunting of blood from left  right (ACYANOTIC CHD)

6. Diagnosis of persistent fetal circulation can be confirmed by measuring PaO2 in blood samples obtained simultaneously from preductal (right radial) and postductal ( umblical , posterior tibial or dorsalis pedis) arteries The presence of PaO2 differences of > 20 mmHg confirms the diagnosis

7. ANATOMY DA has diameter of 5-15mm Length of 2-15mm Relations: Posteriorly: left main bronchus Anteriorly: Vagus nerve Recurrent laryngeal nerve encircles ductus and ascends into neck

8. During fetal development ductus arteriosus connects the left pulmonary artery and descending aorta Distal to left subclavian artery. Right  left shunt in fetus (PVR>SVR) , bypassing the lungs F:M = 2:1

9. ASSOCIATED ANOMALIES EXTRACARDIAC Mental retardation Eye defects Deafness Sternal deformities Scoliosis clubfoot

10. CARDIAC PULMONARY ATRESIA, PULMONARY STENOSIS, TRICUSPID ATRESIA SYNDROMES CHARGE EDWARD PATAUS GOLDENHAR : oculoauriculovertebral dysplasia or hemifacial microsomia VATER: vertebral, anal, TEF, renal anomalies

11. RUBELLA SYNDROME

12. DUCTUS DEPENDENT CARDIAC LESIONS

13. CLOSURE OF DA The patency of PDA in fetal life is due to: low fetal oxygen tension and cyclooxygenase mediated products of arachidonic acid metabolism= PGE2 & PGI2  VD of DA High levels of PGE2 & PGI2 are due : Production by placenta Decreased metabolism by fetal lungs

14. At birth : abrupt increase in oxygen tension inhibits ductal smooth muscle potassium channels  calcium influx VC PGE2 & PGI2 levels falls due to their metabolism in lungs and decreased source of production (placenta removed) Functional closure : 24-48 hours Permanent closure within one month

15. INCIDENCE AND PATHOPHYSIOLOGY 50% infants weighing <1000gm 20.2% infants weighing <1750 gm have hemodynamically significant PDA In term infants, DA closes soon after birth in response to increased oxygen arterial tension In preterm infants, it has thinner and poorly contractile muscular layer with diminished response to increasing O2

16. Additionally , preterm infants often suffer hypoxemia due to RDS (not much stimulus for closure) Ultimately, preterm have both reduced stimulus to and reduced response to physiologic closure.

17. Pulmonary hypertension can present as: DYNAMIC: related to shunt flows that respond to reduction of the shunt REACTIVE: difficult variety, it is challenging to control in perioperative period SHUNT REVERSAL  Eisenmenger physiology ( central cyanosis, dyspnea , fatigue, hemoptysis , syncope and right sided heart failure)

18. The amount of shunting depends on : size of ductus pressure difference between aorta and pulmonary artery and ratio between pulmonary and systemic vascular resistance

19. HISTORY OF BABY WITH PDA Irritability ,feed poorly, failure to gain weight and sweat excessively Increased respiratory effort and rate (breathlessness) Prone to develop recurrent URTI and pneumonia Poor growth Easy fatiguability

20. H/O associated anomalies Drug history History of previous cardiac/other surgeries

21. EXAMINATION Tachycardia Increased respiratory rate Physical underdevelopment Wide pulse pressure- bounding peripheral pulses SYSTOLIC hypertension and low diastolic pressure On I & P: Hyperkinetic apex, continuous thrill in 2 nd ICS

22. Accentuated S1 or normal S2 narrow split or paradoxical split= masked by murmur continuous murmur (machinery murmur) **= upper left sternal border, radiating down the sternal border and into back GRAHAM steel murmur in Eisenmenger syndrome Differential cyanosis and clubbing in shunt reversal

23. S/S of congestive heart failure: failure to thrive, cough dyspnea , tachypnea , tachycardia, hepatosplenomegaly

24. INVESTIGATIONS CBC Electrolytes Coagulation profile Platelet count Serum proteins Calcium levels Arterial blood gas Urine analysis CXR ECG: sinus tachycardia , AF ECHO= doppler/ M-mode

25. CXR

26. ECHO

27. DOPPLER ECHO : for confirmation of diagnosis COLOR DOPPLER: can visualise jet of abnormal flow M-MODE ECHO : Measure cardiac chambers= LA ,LV enlarged in moderate to large PDA Quantify LV and RV systolic function

28. COMPLICATIONS OF PDA CHF: moderate to large PDA due to pulm . overcirculation and left heart volume overload Atrial flutter and AF Hypertensive pulmonary vascular disease Endarteritis Anneurysm of DA Dissection/ rupture of DA: rarely

29. ASSESSMENT OF SEVERITY Heart size Diastolic murmur Pulse pressure

30. MANAGEMENT OF PDA

31. Medical management Patients with congestive cardiac failure: Fluid restriction Furosemide Dopamine Digitalis is not used in small preterm infants because it does not effectively improve stroke volume or ventricular emptying, It decreases HR  detrimental decrease in C.O. Furthermore , digitalis toxicity increases mortality in preterm infants.

32. Role of prostaglandins: PGE1 used to keep ductus patent in duct dependent lesions Ibuprofen, indomethacin is used for closure of duct Indomethacin inhibits cyclooxygenase  decreased production of Pg Dose : 0.1-0.2mg/kg 3 doses in every 12 hours closes duct within 24 hours A/E: mesenteric,renal and cerebral blood flow decreased

33. Anti- arrythmic drugs Vasodilators : PGI2, CCB, endothelin antagonist and PDE inhibitors Other drugs : Diuretics and digoxin (avoided in preterm)

34. Minimally invasive technique Transcatheter closure with intravascular coils for small PDA Catheter introduced sacs or umbrella like device in moderate to large PDA

35. SURGICAL CLOSURE Division or ligation of PDA via left thoractomy Thoracoscopic technique : less pain, faster recovery compared to thoracotomy

36. ANESTHESIA CONSIDERATIONS Avoid Hypothermia Hemodilution Hypoxia Hyperoxia Cross matched blood Left thoracotomy approach is used :position Postoperative ventilation

37. Anesthesia drugs cause changes in SVR and PVR resulting in unbalancing of PBF High PBF leads to pulmonary edema and desaturation Lower PBF leads to desaturation and acidosis

38. Preoperative preparation Informed consent Hydration Avoid fluid overload Inotropic support if required Good preoperative medication is important to reduce anxiety and smooth induction Pulse oximetery is monitored after giving premedication CHOICES of drugs: midazolam 0.5mg/kg oral, 0.05-0.2mg/kg IV (may not be required in neonate)

39. INDUCTION Preoxygenation Prolonged onset time of IV agents is expected due to L  R shunt No change in inhalational induction IV agents : Ketamine 1-2mg/kg with glycopyrrolate 20mcg/kg NMBA : vecuronium 0.1 mg/kg IV If no IV line: sevoflurane induction SUCCINYLVCHOLINE avoided (contracture of PDA)

40. Dexamethasone 0.2-0.5mg/kg Ondansetron 0.1mg/kg to avoid nausea and vomiting

41. MONITORING ECG Pulse oximetery in right hand Invasive BP in right side etCO2 Airway pressure Temperature monitoring ABG TEE Temperature Urine output

42. MAINTENANCE Sevoflurane+ air+ Oxygen Vecuronium Fentanyl (small doses) 1-2 mcg/kg to blunt hemodynamic changes during stimuli Increase in Oxygen concentration decreases PVR NITROUS OXIDE IS AVOIDED (pulmonary HTN) Prevention of hypothermia

43. HEMODYNAMICS Fluid therapy: isotonic fluids with BSL monitoring / 1-2.5% dextrose with BSS Maintenance fluid 4ml/kg/hr IV tubing should be bubble free to prevent embolization Hematocrit is maintained as hemodilution leads to increase in L  R shunt Blood loss is replaced with PRBC / 1:3 crytalloid , mainaining Hct >30%

44. Bradycardia is watched for while handing PDA (RLN vagus nerve) Systolic hypotension may occur at time of ligation of DA Increase in DBP abruptly may occur after ligation of duct This is due to elimination of PVR from circulation

45. VENTILATION Controlled Ventilatory goals: TV adjusted to keep PIP pressure between 15 to 25 cm Hg Fi02 adjusted to keep PaO2 between 50-70 mmHg SPo2 between 87% to 92% ( to avoid ROP in neonates) etCO2 30-35cm H2O Hypoventilation can reverse the shunt due to HPV Hyperventilation can increase L  R shunt due to reduction in pulmonary vascular resistance

46. Paracetamol and local infilteration adequate for postprocedural analgesia Nephrotoxic drugs are avoided as iodinated contrast given during procedure cause renal dysfunction and predisposes to nephrotoxicity Postoperative ventilation needed in preterm /premature babies

47. OTHER CONCERNS Blood loss if control of PDA is lost during ligation Hypoglycemia is frequent complication in neonates Hypothermia : preterm neonates have impaired thermoregulation Systemic hypertension in postoperative period  Mx SNP

48. INTRAOPERATIVE COMPLICATIONS Tear/ avulsion of DA with profuse bleeding Bradycardia Inadvertent left pulmonary artery/aortic ligation Phrenic nerve injury Recurrent laryngeal nerve injury Trauma to thoracic duct Residual shunt Postoperative aneurysm Postoperative hypertension * Bacterial endocarditis

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