Chapter 86

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1462 PART 5 ■ Anesthetic, Surgical, and Interventional Procedures: Considerations TABLE 86-17. Typical Management of a Neonate Presenting With Tracheoesophageal Cleft Symptoms Preoperative investigations Monitoring Suggested anesthetic and recommendations Recommended Examinations and Management Recurrent episodes of cyanosis, frequently associated with feeding. Repeated tracheal tube dislodgment 1. Nasogastric tube for continuous suction. Can be very difficult. Check x-ray for position 2. Chest radiograph 3. Echocardiography 4. Routine laboratory 5. Blood type and compatibility test 6. Order 1 unit blood and 1 unit plasma 1. Routine monitoring 2. Invasive blood pressure monitoring 1. No premedication, I.V. atropine (10 g/kg), preoxygenation 2. Inhalation induction and spontaneous ventilation. Keep the nasogastric tube on suction 3. If symptoms are mild and complete cleft unlikely, bronchoscopy can be handled as usual. In severe cases, ventilation and oxygenation may be difficult due to reduced lung compliance and repeated aspiration. This is accentuated if positive pressure ventilation is attempted 4. If cleft is complete (down to the carina), securing the airway with a tracheal tube is not possible. Selective bronchial intubation might become the only option available. If necessary, use a normal tracheal tube for each main bronchus and two separate ventilation circuits for each tube. This will avoid many problems hypoperfusion. Pharmacologic closure of the PDA (I.V. indo - methacin) is often successful but if this treatment has failed, in longstanding cases or if the size of the PDA is judged to be very large, surgical ligation of the PDA is required. The anesthesiologist should be aware that one of the cornerstones of the conservative treatment of a PDA is fluid restriction and the use of diuretics (usually furosemide). Thus, these patients are regularly on the border of hypovolemia and can also have significant potassium deficits, two conditions that have serious implications for the safe administration of anesthesia. Even if unsuccessful in accomplish - ing closure of the PDA, I.V. indomethacin will regularly cause transient renal dysfunction with a reduction in urine output and a fall in platelet number and activity due to the effects of indo - methacin on prostanoid synthesis in the kidney and the platelet. Thus, it is wise to wait until urine output has normalized and there is no clinical or laboratory signs of platelet dysfunction before accepting the neonate for surgery. The main steps of anesthetic management are summarized in Table 86–19. TABLE 86-18. Typical Management of a Neonate With Congenital Lobar Emphysema Symptoms Preoperative investigations Monitoring Suggested anesthetic and recommendations Recommended Examinations and Management Tachypnea. Moderate to severe respiratory distress. Tachycardia and/or hypotension. Cyanosis. Lateral shift of cardiac sounds. Accidental finding on chest radiograph 1. Chest radiograph 2. Echocardiography 3. Routine laboratory, arterial blood gas, blood type and compatibility test 4. Order 1 unit blood and 1 unit plasma 1. Routine monitoring 2. Invasive blood pressure monitoring 3. Foley catheterization 1. No premedication, I.V. atropine (10 g/kg), preoxygenation 2. Inhalational induction, maintain spontaneous ventilation to limit enlargement of the lobar emphysema by positive pressure ventilation while securing the airway. If the patient is in distress ketamine is preferred to thiopental to prevent hemodynamic deterioration 3. Selective bronchial intubation might be necessary if positive pressure ventilation needed. 100% O 2 helps reduce the size of the emphysema (resorption of the nitrogen) 4. Maintenance depends on severity. Total intravenous anesthesia or volatile techniques are suitable 5. Inotropic support may be needed and a dopamine infusion should be at hand 6. Re-expand the lungs before thoracic closure to limit postoperative atelectasis 7. If possible, the trachea should be extubated at the end of procedure. Spontaneous breathing reduces the strain on the bronchial stump and decrease the risk for significant air leak or development of a bronchopleural fistula. Regional anesthetic techniques are very helpful (e.g., continuous paravertebral or thoracic epidural blockade)
TABLE 86-19. Typical Management of a Neonate With Patent Ductus Arteriosus Symptoms Preoperative investigations Monitoring Suggested anesthetic and recommendations CHAPTER 86 ■ Management of the Neonate: Anesthetic Considerations 1463 Recommended Examinations and Management Cardiac failure with fluid retention, poor weight gain, tachypnea, ventilator dependence. Bouncing femoral pulses or wide pulse pressure due to the left-to-right shunting (cf. aortic insufficiency). Echocardiography will give final diagnosis 1. Chest radiograph 2. Echocardiography (ask for signs of hypovolemia and degree of cardiac failure) 3. Ultrasonic head scan to document any pre-existing intracranial pathology 4. Routine laboratory including potassium 5. Blood type and compatibility test. Platelet count 7. Order 1 unit blood and 1 unit plasma 8. Check last 24 h urine output and diuretic use to judge body fluid status Routine monitoring; invasive blood pressure monitoring if patient is unstable 1. No premedication, IV atropine (10 g/kg), preoxygenation 2. Induction of anesthesia depends on the degree of cardiac failure. If moderate (failure to wean the patient from the ventilator), standard IV induction and maintenance with low dose sevoflurane (less myocardial depression than halothane); if severe (poor contractility on preoperative echocardiography or digitalization), opioid anesthetic and small doses of midazolam or a very low dose of sevoflurane 3. Nasal intubation is preferred to reduce the risk of dislodgment of the tube due to limited access to the patient, right lateral positioning and low weight 4. During surgery, lung compression is inevitable; periods of desaturation must be tolerated to allow progress of the surgery. If bradycardia develops, immediate re-expansion is needed 5. Hypotension occurs frequently; if not due to surgical impairment of venous return, this requires lightening anesthesia first, then give plasma expander (most patients are hypovolemic). If moderate expansion (10–15 mL/kg of 5% albumin solution) fails to restore the blood pressure, inotropic support is necessary (dopamine 5–10 g/kg/min) 6. Before closing the wound the surgeon should be encouraged to place either a multilevel intercostal block or a paravertebral block under direct vision 7. Weaning from the ventilator may requires several days despite the correction of the pathology due to edema and atelectasis of the right lung, necessity to administer fluids to stabilize hemodynamics and improve cardiac function Abdominal Surgery Congenital Diaphragmatic Hernia The incidence of congenital diaphragmatic hernia (CDH) is approximately 1/5000 live births. Most often it is left-sided, but right-sided cases do occur. The severity of the malformation depends on the amount of herniation of the abdominal contents that as occurred during fetal life. In minor herniation, the patient can be asymptomatic at birth and is only diagnosed by a chest radiograph often performed for other reasons. In severe cases, the baby has immediate symptoms of severe respiratory distress and hypoxic respiratory failure combined with life-threatening pulmo - nary hypertension. The ventilatory problems are not due solely to an intrathoracic mass lesion, as previously believed, but are instead also due to the associated pulmonary hypoplasia and pulmonary hypertension. Thus, there is no need for immediate reduction of the abdominal viscera as previously practiced. This can in fact be regarded as absolutely contraindicated and should be preceded by preoperative stabilization. In the case of more pro nounced intrauterine herniation not only will the ipsilateral lung be hypoplastic but the contralateral lung is also affected to some degree by hypoplasia. 197 Most of the children with CDH are term infants and normally developed regarding most organ systems except for the lungs. Not only are both lungs affected by varying degrees of hypoplasia depending on the severity of the intrauterine herniation, but they are also immature. Recent research has found CDH lungs in more severe cases to be surfactant deficient 198 and surfactant replacement has been reported to be successful in certain cases. 199 Thus, the CDH patient can be described as being term with the lungs of a premature. The associated pulmonary hypertension is due both to a reduction in the number of pulmonary vessels and also due to an exaggerated pulmonary vasoreactivity capable of causing life-threatening episodes of pulmonary vasospasm leading to profound extrapul monary right-to-left shunting. The vasoreactivity in CDH will occasionally produce what has been termed a “honeymoon period.” In these cases, the patient will have a period of acceptable gas exchange immediately after birth without the use of any more extreme ventilatory settings or adjuvant treatments. This is later followed by very severe pulmonary hypertension associated with profound hypoxic respiratory failure. Conventional treatment for the treatment of this situation has been prophylaxis consisting of deep analgo-sedation, inotropic support, moderate hyperventila tion if possible, and meticulous control of the patient’s acid-base status. Previous attempts to treat this situation with intravenous vasodilators has been abandoned due to the risk of hypotension, since systemic hypotension can be lifethreatening in this setting. More modern treatment consists of surfactant replacement, high frequency oscillatory ventilation, inhaled nitric oxide, and extracorporeal membrane oxygenation. The neonatal anesthesio logist might, thus, be faced with the situation of administering anesthesia to patients either on
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Chapter 86

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