Is this patient premature? Why? The progress note by the neonatologist refers to this infant as ELGAN. What does this term mean? What organ systems are you concerned about as you plan your anesthetic for this child?

Does this patient have surfactant in his lungs? If not, when will it develop? Would the administration of artificial surfactant influence your anesthetic plan?

How can you evaluate the status of the central nervous system (CNS)? What signs and symptoms would you look for with regard to intraventricular hemorrhage? What factors contribute to the onset of intraventricular hemorrhage? How will it affect your anesthetic management?

How can you diagnose persistent patency of the ductus arteriosus? Is this significant for anesthetic management? Why/why not?

Does this patient need a work-up for D.I.C.? Why? Will an assessment of fibrin split products help? Why/why not?

Infants born before the 37th week of gestation are considered premature [1]. The term ELGAN means extremely low gestational age newborn and is replacing the term for birth weight used to classify preterm newborns (low birth weight (LBW), extremely low birth weight (ELBW), etc.). The Committee on Fetus and Newborn (COFN) of the AAP made this change since morbidity correlates with gestational age (GA) more closely than with birth weight [2]. This infant is ELGAN, with a GA of 27 weeks, a postnatal age of 2 weeks, and a postconceptual age of 29 weeks. The third trimester is the time when most organ systems mature. Of particular importance is the immaturity of the pulmonary, central nervous, renal, and hepatic systems. Gas exchange and management of mechanical ventilation require exquisite attention to detail in these tiny patients. CNS immaturity and the possible deleterious effects not only of hypoxia and metabolic derangements but also of the anesthetic, hypnotic, and analgesic agents themselves are an evolving issue. Preterm infants do not maintain fluid and electrolyte balance well, requiring care in the administration of IV fluids and electrolytes. Liver immaturity, both in synthetic and metabolic capacities, can result in much longer duration of action of IV agents.

An infant born at 27 weeks will almost certainly be deficient in pulmonary surfactant and develop respiratory distress syndrome (RDS) [3]. Surfactant is produced by type II pneumocytes. The amount and composition of the surfactant change throughout gestation. Lamellar bodies are first seen in type II pneumocytes 20–24 weeks’ gestation. There is progressive accumulation of saturated phosphatidylcholine in the lung tissue until term. The surfactant present in the lungs of term newborns is composed of 50 % saturated phosphatidylcholine, 20 % unsaturated phosphatidylcholine, 14 % other lipids, 8 % phosphatidylglycerol, and 8 % surfactant proteins (SP-A through SP-D). The immature lung has decreased surfactant function, much less phosphatidylglycerol, and more phosphatidylinositol. Administration of artificial surfactant following delivery is very beneficial, decreasing surface tension in the alveoli as natural surfactant does in the term newborn. Practice varies among neonatologists with regard to administration of surfactant prophylactically in the delivery room or when needed later in the ICN. Generally no more than two doses are administered. If surfactant were administered, it should be expected that the compliance of the lungs would increase to closer to that seen in term newborns. When ventilating for a newborn treated with surfactant, it is important to consider this improved compliance. There are several manufacturers of surfactant. The primary difference is whether or not the product is derived from another species or the product is synthetic. A Cochrane review concluded that there is “some evidence that animal derived surfactant extract leads to better outcomes in babies with respiratory distress syndrome compared to synthetic surfactants that do not contains proteins” [4].

Periventricular–intraventricular hemorrhage (IVH) is a common occurrence in the preterm newborn and the most serious CNS lesion encountered in the newborn period [5]. It is a major cause of death in preterm newborns. In at least 90 % of cases, the hemorrhage occurs in the first week of life. The incidence and severity of periventricular–intraventricular hemorrhage occurring vary inversely with gestational age. IVH grades of severity go from I to IV based upon the radiographic appearance of the extent of the hemorrhage, from an isolated germinal matrix hemorrhage to intraventricular and parenchymal hemorrhage:

PDA is nearly a normal finding in the preterm [6]. In the fetus, the ductus arteriosus is essential for adequate circulation and oxygen delivery. In postnatal life, as pulmonary vascular resistance decreases, a large PDA may lead to inadequate forward systemic flow and CHF from excessive pulmonary blood flow. Clinically, bounding pulses, tachypnea, cardiomegaly, and signs of pulmonary overcirculation are seen when the ductus is opened. The diagnosis can be confirmed with 2-D echo with color Doppler. A functionally closed ductus in a patient such as the one in this case can be reopened by excessive fluid administration. This makes fluid administration in these critically ill infants challenging. Excessive fluid administration can lead to significantly worsened gas exchange and also decreased systemic flow, whereas inadequate preload will also lead to decreased LV output.

NEC is often associated with a coagulopathy. Thrombocytopenia is commonly seen as NEC worsens. In patients suspected of having NEC, serial platelet counts are followed as a measure of disease severity. The laboratory diagnosis of DIC can be difficult since, in the newborn, several tests of coagulation may be outside of the reference range [7, 8]. For example, D-dimers are often found in preterm newborns without DIC. In the clinical setting of NEC, thrombocytopenia, microangiopathic hemolytic anemia, and prolonged PT are indicative of DIC. Treatment of this infant’s coagulopathy will involve transfusion of PRBCs, platelets, and also coagulation factors either in the form of FFP or cryoprecipitate. In the NICU, exchange transfusion may also be undertaken.

Does this patient need an arterial line? Why/why not? A central line? Why? What site will you use to monitor temperature? Why? Where does temperature change first? Last? Will you monitor glucose levels? Why? How often?

Should you give atropine prior to induction? If this infant arrived in the OR with an endotracheal tube in place, on nasal cannula O₂, would you give atropine prior to an “awake” intubation? Why/why not? Would pancuronium do just as well?

How would you ensure temperature homeostasis? What is your choice of fluid management? Why? What if hyperalimentation is running? Would you discontinue and change over to a D₂₀ solution? D₁₀ solution? Not change? What are the effects of narcotic anesthetic techniques in this age group? Is MAC different in this age group? In what way? Is ketamine a choice?

What muscle relaxant would you choose? Why? Is there any specific advantage to cisatracurium?

As the case progresses, the airway pressure suddenly rises, there is a diminution of breath sounds bilaterally, and the SpO₂ decreases steadily. What could be going on? What measures can you take to prevent this from occurring again?