Conference Lectures

ANAESTHESIA FOR A HIGH RISK PDA LIGATION PROCEDURE
DR. V. KAMATCHI SELVAM
SrDMO,Southern Railway Head Quarters Hospital,Perambur, Chennai

 The Successful Perioperative Management of a high pressure, very large PATENT DUCTUS ARTERIOSUS is an anaesthetic challenge. ANESTHESIOLOGISTS have to operate under very narrow therapeutic index! In order to provide safe anaesthesia for children with congenital heart diseases, the anaesthesiologist must have a detailed understanding of the pathophysiology of the lesion(s), the pharmacology of the drugs being used and the intricate risks and dangers associated with the various surgical interventions.

PATENT DUCTUS ARTERIOSUS
ANATOMY
The isolated PDA arises from the anterior surface of the MPA (Main Pulmonary Artery) near its junction with the LPA (Left Pulmonary Artery)and joins the posterior descending aorta after the origin of the left subclavian artery
It is a normal and very essential fetal structure that becomes abnormal if it remains patent after the neonatal period (some authorities consider the patent ductus to be abnormal only after 3 months of age).

EMBRYOLOGY
In normal cardiovascular development, the proximal portions of the sixth pair of embryonic aortic arches persist as the proximal branch pulmonary arteries. The distal portion of the left sixth arch persists as the ductus arteriosus, connecting the left pulmonary artery with the left dorsal aorta. This transformation completes by 8 weeks of fetal life.

DA DURING FETAL LIFE - PURPOSE
Due to high resistance of fetal pulmonary circulation, only 5-10 % of the right ventricular output of the fetal heart passes through the lungs. Through DA most of the RV output passes to the descending aorta. Thus the Ductus Arteriosus is necessary to divert blood flow from the high resistance pulmonary vascular bed to the systemic circulation.

FACTORS FOR MAINTAINING PATENCY OF DA IN FETAL LIFE
HIGH PGE2 & PGI2 level ( due to)
Production by placenta & DA
Decreased metabolism in fetal lung
Interaction with ductal prostanoid receptors
Low PaO2

HOW DOES DUCTUS CLOSE AFTER BIRTH
1. Within few hours after birth, abrupt increase in arterial PaO2, inhibits ductal smooth muscle voltage dependant K channel, allowing influx of calcium in the ductal smooth muscle cells.
2. Decreased circulating PGE2 &  PGI2 levels due to elimination of placental source & increased metabolism in lung.
Due to 1 and 2 above, medial smooth muscle fibres in the DA contract, inner muscle wall of DA develops profound ischemia, leading to the formation and release of vascular endothelial growth factor, transforming growth factor beta and other inflammatory mediators and growth factors, ultimately transforming the DA into a non-contractile ligament.

TRANSITIONAL CIRCULATION IN PRETERM NEONATE
The reasons for persistent transitional circulation in preterm neonates are:

  1. Poor PG metabolism by immature lung
  2. High sensitivity to PG (premature ductus)
  3. Reduced Ca sensitivity to O2 in the immature ductal musculature

WHAT IS PATENT DUCTUS ARTERIOSUS?
PDA IS WHEN SPONTANEOUS CLOSURE OF A PDA DOES NOT USUALLY OCCUR IN FULL-TERM INFANTS AND CHILDREN !
PDA in term infants results from a structural abnormality of the ductal smooth muscle rather than decreased responsiveness of the premature ductus to oxygen. The absence of DA contraction in full term neonates might be due to failed PG metabolism most likely caused by infection, acidosis, hypothermia, asphyxia, meconium aspiration syndrome, pulmonary disease resulting in hypercapnia & hypoxia.

FEW WORDS ABOUT THE EXISTENCE OF PDA IN OUR PATIENTS
The incidence of this defect is 1 in 2000 live full-term births, accounting for approximately 5-10% of all congenital heart defects. Male to female ratio : 1:2
Aetiology:
Sporadic
Genetic factors: syndromes (trisomy 21, 4p- syndrome, Carpenter’s syndrome, Holt-Oram syndrome, incontinentia pigmenti)
Prenatal infection: Rubella in first trimester
Environmental: fetal valproate syndrome

Natural History and Clinical Manifestations

The natural history of PDA is similar to that of other lesions with a left to right shunt and augmented pulmonary blood flow, which, if left untreated, may lead to pulmonary HTN and CHF. In most patients, congestive heart failure, manifested by tachypnoea, tachycardia, diaphoresis, failure to thrive, fluid retention, hepato-splenomegaly and cardiomegaly are present. If pulmonary vascular obstructive disease develops, a right- to-left ductal shunt results in cyanosis only in the lower half of the body (i.e.) DIFFERENTIAL CYANOSIS).Children with PDA have a continuous, machinery-type murmur in the left first intercostal space. Because of the low resistance shunt through the pulmonary vasculature, the systemic arterial pulse pressure is often wide, giving the impression of bounding peripheral pulses.
CXR: normal or cardiomegaly with increased PA size and increased pulmonary vascular markings
ECG: Normal or LVH/RVH
ECHO: diagnostic: documents patency, evaluates left sided cardiac chamber sizes and aortic arch anatomy, and estimates size of the shunt
LAB:  CBC; others as indicated by hospital protocol.
There is always a risk of bacterial endocarditis and this is a primary indication for closure even of small asymptomatic PDA.  SBE prophylaxis is not needed beyond 6 months after surgery.

MEDICAL MANAGEMENT
Early administration of indomethacin may promote ductal closure in many premature infants, obviating surgical intervention; however, this mode of therapy generally is contraindicated in the setting of renal insufficiency or intracranial bleeding.
Indomethacin is ineffective in term infants with PDA and should not be used.
Digoxin and diuretics are indicated for CHF
SBE prophylaxis is indicated when  indications arise

TECHNIQUES FOR CLOSURE OF PDA
Techniques for closure of PDA have evolved since the first report of surgical ligation by Gross and Hubbard in 1939. Transcatheter methods, to avoid thoracotomy, were pioneered by Portsmann et al, who reported use of a conical Ivalon plug in 1967, and by Rashkind and Cuaso, who reported initial results of an umbrella-type device in 1979. These devices were rather large and cumbersome to use, requiring large introducer sheaths and frequently leaving residual shunting. In 1992,Cambier reported the use of Gianturco coils for transcatheter closure of PDA. Since then transcatheter coil occlusion  has become a widely used technique for closure of  small to moderate PDA’s of less than 4mm size. Some centers use the Amplatzer device for moderate to large PDA’s of 4 – 10 mm size.

ANESTHESIA FOR TRANSCATHETER PDA CLOSURE PROCEDURES
Transcatheter  PDA closure procedures can be safely carried out under IV sedation and monitored anesthesia care in the Cardiac Catheterization Lab.

PDA CLOSURE IN PRETERM INFANT IN NICU – ANESTHETIC CONCERNS
Closure of PDA in the preterm infant is done at the bedside in the NICU.
These patients are intubated, mechanically ventilated, hemodynamically unstable, and may require inotropic support. The premature infant requiring surgical closure of PDA typically presents because indomethacin Rx has failed or is contraindicated. They often have primary pulmonary disease and multisystem organ problems. In these infants, the symptoms of large L → R shunt and pulmonary overcirculation → cardiac and respiratory failure and ventilator dependence. The ductal runoff causes ↓ DBP and compromises coronary blood flow and other organ perfusion.

PDA CLOSURE IN PRETERM INFANT IN NICU – ANESTHETIC TECHNIQUE
At the bedside of the preterm infant, anaesthesia can be provided with ketamine (1-2 mg/kg) and muscle relaxant (eg. Rocuronium 1mg/kg). Small doses of fentanyl (2-5 mcg/kg) may be given for supplemental analgesia. During lateral decubitus positioning, careful attention to the airway and close monitoring of BP and oxygenation is necessary.

PDA CLOSURE IN TERM INFANTS AND CHILDREN – TREATMENT OPTIONS
Older patients may be eligible for endovascular closure in the cath lab. A small percentage of patients  are candidates for open surgical closure in the OR. Surgical closure may be performed with video-assisted thoracoscopy (VAT) or via thoracotomy/ median sternotomy +/- CPB+/-DHCA.

 

STANDARD SURGICAL INTERVENTIONS
The ductus is interrupted with a surgical clip in neonates; In older children, the ductus is double- or triple-ligated or divided between vascular clamps, and the ends are oversewn. A small thoracostomy tube is placed, and the thoracotomy is closed. The thoracostomy tube is removed in the OR immediately after the chest is closed or a few hours later. Robotic technique is being  performed  experimentally at present.

Surgical technical options - I
Most children presenting for elective closure of PDA via thoracotomy are candidates for thoracic epidural analgesia, while for those undergoing thoracoscopic closure, an epidural is not required. In patients > 25 kg, placement of a DLT for selective ventilation of the right lung will improve surgical access. In general these patients are candidates for early extubation in the OR  and fast tracking.

Anesthetic techniques - concerns
Thoracotomy approach  involves issues associated with
lateral decubitus positioning,
One lung ventilation,
lack of proximal and distal control over the operated vascular structure with the risk of torrential hemorrhage which is potentially fatal and ensues rescue clamping of proximal & distal aorta and  main pulmonary artery.
Spinal cord ischemia and paraplegia
Surgical technical options - II
Most children presenting for elective closure of  large shunt, high pressure high risk PDA can be operated through elective median sternotomy, CPB and Deep Hypothermic Circulatory Arrest. This gives intraoperative safe proximal and distal control of vascular surgery. But exposes the patient to complications due to CPB and DHCA, which increases perioperative mortality and morbidity due to higher incidence of Pulmonary arterial Hypertensive Crisis.

PERIOPERATIVE ANESTHETIC CONSIDERATIONS
PRE OPERATIVE ANESTHETIC CONCERNS:
Paediatric patient : anatomical, physiological and pharmacological differences
PAH
CHF

INTRA OPERATIVE ANESTHETIC CONCERNS:
Positioning: V/Q mismatch, one lung ventilation, pressure points protection
Adequate surgical exposure
Injury to  the Vagus nerve, Phrenic nerve,  RLN, thoracic duct, lung, intercostal vessels
Hypotension, bleeding, rescue clamping of aorta & PA.
Spinal cord ischemia & paraplegia.

POST OPERATIVE ANESTHETIC CONCERNS:
Ventilation
PAH
CHF
Pain relief
Fast tracking
Complications & morbidities (see later).
A SAMPLE ANESTHETIC TECHNIQUE
PREOPERATIVE
PREMEDICATION: Not indicated for premature infants;
Midazolam 0.5-0.7 mg/kg PO 20 minutes prior to induction for children > 9 months having routine PDA closure.
INDUCTION
Children presenting in the OR for elective operation tolerate an inhalation induction with sevoflurane in 50% N2O + O2.
Once the patient is anesthetized, IV access is established, followed by oral intubation, with administration of a muscle relaxant (Rocuronium 1mg/kg).
MAINTENANCE and EMERGENCE
In patients for whom immediate postoperative extubation is planned, anesthesia is maintained with isoflurane in air + O2
An effective regional anesthetic  technique  by thoracic epidural  is helpful while practising  fast tracking by early extubation  of an awake patient  with post thoracotomy pain.
THORACIC EPIDURAL
Thoracic level T8-10 preferred
For neonates<10 kg, a caudal catheter can be advanced to thoracic levels.
Check coagulation parameters prior to placing epidural.
BLOOD AND FLUID REQUIRMENTS
IV: 22-24 g X 1-2. Blood loss may become significant if the ductus is torn during ligation.
Continue IV dextrose
Blood warmer
Type and cross match; have blood available for rapid transfusion
MONITORING
Standard monitors+/- Arterial line +/- CVP Line
In preterm infants monitoring of the preductal BP (right arm) and a postductal saturation monitor (usually lower extremity) are required because of possible inadvertent ligation of the descending aorta.
Place BP cuff on preductal (right arm) and pulse oximeter on the foot to monitor flow in the ascending and descending aorta.
Inadvertent aortic occlusion > decreased LE pulses/pressure/perfusion.
Inadvertent PA occlusion > decreased SpO2 + decreased ETCO2.
Bradycardia may occur during manipulation of the ductus.
The DBP will increase postligation
PATIENT CARE DURING ANESTHESIA
Watch for air bubbles: Clear air bubbles from IV tubing and stopcocks (potential bidirectional shunt > paradoxical embolism); Prevent hypothermia; Pad and protect pressure points, Protect eyes, Protect  a secure airway.
COMPLICATIONS
Occlusion of aorta or PA, Torn ductus > hemorrhage, Spinal cord ischemia and paraplegia, (hypotension, rescue clamping), Residual PDA, Lung truama +/_ pneumothorax, Chylothorax, Injury to vagus nerve, recurrent laryngeal nerve, Bleeding and infection

SUMMARY
Detailed understanding of the anatomy, pathophysiology of the congenital cardiac disease, physiological and pharmacological needs of the patient and the procedures to be carried out AND good communication and close interaction among the physicians, surgeons and anesthesiologists have made the surgical correction of a Large PDA with severe PAH (which is a  high risk surgery) to be carried out safely and successfully despite the narrow therapeutic index.
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