A newborn tolerated severe hypercapnia during general anesthesia: a case report

In this newborn, the main problem noted was severe hypercapnia. Infants are more likely to develop hypercapnia because of the age-related physiological changes in vital systems and a higher metabolic rate in relation to weight. The causes of hypercapnia include two aspects: the increase of CO₂ generation and the decrease of CO₂ discharge. Detailed factors include malignant hyperthermia, equipment and breathing circuit malfunction, patients’ preexisting pulmonary diseases, CO₂ pneumoperitoneum, improper ventilatory settings and invalidity of CO₂ absorber. However, in the present case, we failed to determine the real cause of the hypercapnia. Malignant hyperthermia was excluded as the neonate’s temperature decreased to normal level after the heating was switched off in the operating room and she did not show any sign of muscle rigidity, tachycardia, etc. CO₂ canisters as well as the anesthesia machine were working properly. Time-cycled, pressure-limited ventilation mode is the most widely used mechanical ventilation mode for neonates and ventilation parameters were appropriate for the newborn.

An important factor we ignored during anesthesia was that a heat and moisture exchanger (HEM) was used between the circle system Y-piece and endotracheal tube. A circuit containing HEM can increase the dead space by almost 70% compared with a circuit without HEM in a 24-month-old child undergoing general anesthesia [3]. We did not realize the HEM was there until the tracheal extubation. It is not certain whether the HEM caused hypercapnia in this neonate, but a HEM used in pediatric anesthesia can induce hypoventilation with subsequent hypercapnia [3].

Hypercapnia is a two-edged sword and it exerts multiple physiologic effects on different organs. The word “permissive hypercapnia” was first described by Hickling in 1990 who suggested that adoption of low-tidal-volume ventilation strategies with tolerance of elevation in PCO₂ was associated with lower hospital mortality [4]. Hypercapnia displaces the oxygen dissociation curve to the right, which improves tissue oxygenation and perfusion and may alleviate the injury to immature lung and brain [5]. Retrospective studies in premature neonates also concluded that higher PCO₂ contributed to less lung injury [6].

In spite of these protective effects, it is believed that severe hypercapnia leads to an increase of intracranial pressure (ICP) via acidosis-induced cerebral arteriolar dilation, which is thought to be related with well-known neurological complications such as cerebral edema, intraventricular hemorrhage and temporary neurological impairment [7]. Reduced skeletal muscle contractility and decreased myocardial contractility are also known to occur following hypercapnia [8]. However, no evidence of neurological sequelae was observed in this neonate.

A few cases of severe hypercapnia have been reported in the literature. Most cases of patients with severe hypercapnia are related to chronic obstructive pulmonary disease, exacerbation of bronchial asthma causing severe hypoxemia or defective apparatus used during general anesthesia [9, 10]. Compared with those patients, several unique characteristics in our case deserve further discussion. First, to the best of our knowledge, this is the first reported case of a neonate who developed severe hypercapnia during general anesthesia for unclear reasons. Second, the neonate regained full consciousness and no residual neurological deficit was observed.

The ability to tolerate hypercapnia varies among individuals for a broad spectrum of factors such as duration of hypercapnia, the speed at which high values are reached, maximal PCO₂ value, patient age and preexisting diseases. The threshold of PCO₂ above which neurological impairment occurs is unclear [11]. Hypercapnia coma has been observed in patients with PCO₂ values of 58mmHg. However, a sober patient with PCO₂ values of 160mmHg has also been reported [12].

Remarkable renal compensation enables patients with end-stage lung disease to tolerate severe chronic hypercapnia. But how to explain why the newborn can tolerate such severe hypercapnia? The first reason could be that the neonate is insensitive to elevation of CO_2. Central chemosensitivity in the newborn is not the same as that in the adult. In term neonates, the ventilatory handling of a hypercapnia challenge is fully functional on postnatal day 2. Then during the following 8 weeks, ventilatory response to CO₂ declines markedly and subsequently achieves adult level of responsiveness after the 9th week [13]. The altered CO₂ sensitivity of neurons, the loss of GABAergic excitation and changes in astrocytic function during development may account for the triphasic pattern of responsiveness to the CO₂ [14]. Both carotid and central chemoreceptors are important for a normal ventilatory of CO₂–H⁺ chemosensitivity. Nevertheless, carotid plays a greater role at low levels of hypercapnia, whereas intracranial chemoreceptors are more dominant at high levels [15]. In neonates, peripheral CO₂ chemoreceptors exert greater influence than central CO₂ chemoreceptors [13]. Therefore, we may infer that a nadir of ventilatory responsiveness to CO₂ in this 21-day-old newborn as well as the specificity of CO₂ chemoreceptors in neonates might make newborns insensitive to elevation of CO₂. This might be an important reason why the neonate can tolerate severe hypercapnia.

Clinical severe hypercapnia frequently occurred with tissue hypoxia or arterial hypoxemia. However, in this newborn, this is not the case. Oxygen saturation was continuously monitored and it never fell below 95% during the increase of P_ETCO₂. Hemodynamics remained stable during the anesthetic procedure, which also guaranteed tissue perfusion and oxygenation. Research has indicated that the central system has a potent ability to recover from nonhypoxic severe respiratory acidosis [9]. As long as tissue perfusion and oxygenation are preserved, effective transfer of HCO₃⁻ from extracellular space into cells by Na⁺/K⁺ changes or Na⁺/H⁺ changes will continuously occur when exposing to hypercapnia [10]. Consequently, the drop of pH in intracellular cells is far slower than that in extracellular cells. It is important to note that this regulation is energy-consumed, which requires the cells to be oxygenation and perfused [10]. The adequate oxygenation and strong chemical buffering capacity in intracellular cells enable important organs to tolerate extreme acidosis and that might contribute to the benign outcome of the newborn.