Why is this patient underweight for his age? What else would you like to know specific to his growth that would influence your anesthetic plan? Why does this happen? Is it more or less common for children with OSA to be underweight?

How do the other symptoms and signs influence your plan? What is the significance of his good behavior at naptime? Are headaches common in children with OSA? Why? Why is he hypertensive and tachycardiac? What is the significance of his respiratory rate? Do you think he has “white coat hypertension” or could this be something else? Does this patient need a preoperative echocardiogram? What specifically on the echo would be worrisome or reassuring to you as an anesthesiologist? Would a preoperative ECG suffice?

Would you premedicate this patient? What are your concerns? What are the advantages? What agent(s) would you consider? Would you modify your anesthetic technique as a result?

In contrast to the popular association of hypoventilation and airway obstruction with the Pickwickian syndrome, most pediatric sleep-disordered breathing is associated with either a normal body habitus or weight below normal, even to the point of failure to thrive. The reason for this is that often children with chronic airway obstruction are slow eaters because they are forced to chew and swallow between episodes of mouth breathing. For that reason, many will choose to avoid foods that require a lot of chewing, such as meats, and therefore they will limit their own diet. They may also have impaired taste and smell if they have substantial nasal obstruction.

Interestingly, following adenotonsillectomy, approximately 75 % exhibit an increase in growth hormone, insulin-like growth factor 1, and significant weight gain. Comorbidities that may be associated with prolonged upper airway obstruction involve effects on the cardiovascular system such as pulmonary hypertension, systemic hypertension, morphometric facial changes (“adenoid facies”), and sleep fragmentation.

Behavioral abnormalities typically reside on a spectrum of irritability to somnolence and are difficult to separate out from normal toddler development. The constellation of symptoms is more important, and chronic airway obstruction is often associated with parental nighttime complaints of fears that their child will stop breathing, loud snoring, gasping, choking, coughing, periods of apnea, restless sleep, and the child’s head extension in an effort to unconsciously resolve the airway obstruction. Morning or daytime headaches are a frequent complaint and may be a result of systemic hypertension, nighttime fragmented sleep, head and neck muscular pain, or various combinations. Hypertension in children may be associated with a visit to the doctor’s office, so-called white coat hypertension, but in this patient population, elevations in blood pressure, especially systolic pressure, are also associated with sleep-disordered breathing in direct relationship to the apnea-hypopnea index. Moreover, these patients may have biventricular dysfunction on echo – features of left ventricular hypertrophy, pulmonary hypertension, and impaired right ventricular performance. It would not be unreasonable to seek this kind of evaluation in patients with long-standing sleep-disordered breathing because of these possibilities.

Premedication would depend on assessment in the preoperative period; the strategy has to take into account the concerns of the parent about the child’s behavior, the judgement of the anesthesiologist with regard to the effects of immediate preoperative stress on the cardiopulmonary system, and the concerns about any abnormalities of ventilatory control being aggravated by the premedication. Benzodiazepines alone would not be likely to shift the CO² response curve much if at all, but residual effects may very well emerge in the immediate postoperative period following inhalation anesthetics and/or opioids, so this must be kept in mind.

Does this patient need any monitors beyond standard noninvasive monitoring? What monitors do you have available among your standard monitors that help you evaluate the pulmonary circulation and the right heart?

Mask vs. intravenous induction – are both acceptable? Mom insists on being present for induction – is this a good idea? As the patient enters stage II, he develops “seesaw” breathing with phonation and profuse salivation, is moving all extremities in a flexion pattern, and seems to be struggling. What’s happening and why? His SpO₂ is 94 %, but in 5 s it goes to 88 %. What is your next move? Choices of drugs? How and where would you deliver them? The child was given an adequate dose of intramuscular succinylcholine and atropine (40 and 0.4 mg), but his heart rate has slowed to 62 although you are now moving the chest with adequate ventilation. What is your next move? Should you begin CPR?

He now has an IV. How will you plan your anesthetic at this point? Do these events influence your plan? The surgeon suggests a deep extubation because he thinks the wake-ups are less problematic. Do you agree? Would you choose that strategy? Why?

Does this patient need to go to the ICU?

No further monitoring is needed beyond standard noninvasive monitors. That said, the available standard monitors should be regarded with an additional level of interpretation to reflect possible aggravation of pulmonary hypertension and biventricular performance. Oxygen saturation will depend to some extent on pulmonary artery pressures as well as right heart performance; blood pressure will be a reflection of this as well. Left ventricular dysfunction may also be reflected in abnormal blood pressure responses, but it will depend on the balance of chronically elevated catecholamines along with any myocardial contractility impairment, especially with propofol or higher doses of inhalation anesthetics. Because of the solubility of carbon dioxide, it is not likely that patients will exhibit significant alterations of ETCO₂ as a reflection of elevated pulmonary artery pressures. ECG findings in severe circumstances might include bradycardias, right heart strain patterns, or ectopy.

While both are acceptable, there is no doubt that a mask induction would be easier, unless there was a preexisting IV. That is not very likely, as this child is probably coming in from home. That said, an IV induction should not be completely ruled out, because it affords a more rapid induction, bypassing the likelihood of passing through an excitement stage during an inhalation induction and allowing the rapid administration of neuromuscular blocking agents to minimize the chance of laryngospasm, which is higher in this patient population, particularly with the diagnosis of airway obstruction. Mom can certainly be present for the induction, with careful discussion beforehand that the primary job of the anesthesiologist remains the care of the patient and not the parent and the use of the euphemism “falling asleep” is just that – it is, after all, not really “sleep.”

The excitement stage during an inhalation induction is associated with the increased elaboration of endogenous catecholamines, which may be associated with all of these signs of reactivity, and in addition will produce an increase in oxygen consumption and therefore carbon dioxide production as well. Some positive pressure in the circuit by closing the APL valve is a reasonable strategy as is the insertion of an oral airway to improve upper airway patency. Occasionally, laryngospasm can only be treated with neuromuscular blockade; a depolarizing agent such as succinylcholine can be co-administered with an anticholinergic intravenously or intramuscularly (if prior to IV insertion), or a nondepolarizing drug such as rocuronium can be used. If the heart rate continued to decrease for a few seconds following administration of neuromuscular blockade, and the chest was rising and adequate gas exchange was the result, I think I would wait a few more seconds to see if the saturation began to improve. There is a little bit of a delay in the display of the SpO₂ in relation to improvement in ventilation. If the heart rate continued to decrease and there was evidence of impaired gas exchange, worsening hypoxia, and bradycardia, then CPR should be quickly initiated to augment the circulation of further resuscitation drugs and augment cardiac output and cerebral blood flow.