Hypoxemia in Children

Hypoxemia in Children – Diagnosis and Treatment

How do you deal with these situations?

1.    A twenty-day-old infant with a hernia for repair. During the course of the procedure, the infant begins to desaturate. Weight is 3.5 kg. the TV is 35cc. Infant is breathing spontaneously. ETT is taped at 12 cm. Why is this patient hypoxemic?

2.    Ventilating pressures are 40 torr in an otherwise normal 15 year old. The SpO₂ is 90%. How do you determine why this is happening?

3.    The patient is a 9 month old that has had a portacath placement in the operating room. In the PACU, the infant’s lower extremities are mottled and the oxygen saturation is 80%. What is the most likely cause?

4.    The patient is a former premature infant that is recovering from significant BPD. During a surgical procedure for gastrostomy placement, the oxygen saturation drops precipitously when the anesthetic is switched from sevoflurane to desflurane. Why does this happen?

5.    A fifteen-month-old infant comes to the operating room for a hernia repair. Two weeks ago, the infant had a URI and was treated for wheezing in the local emergency room. During the procedure, the infant becomes hypoxemic while breathing spontaneously through an LMA. What is going on here?

6.    A twelve-year-old male has a complex femur fracture after a bicycle accident. During the course of the surgical repair, the patient has an acute drop in his SPO_2, associated with hypotension. Why is this happening and what will you do?

7.    A sixteen year old with sickle cell disease has been poorly controlled and comes to the operating room for a cholecystectomy. In the holding room the oxygen saturation is 90% on room air. Why is this? What do you need to do for this patient before taking him to the operating room?

8.    The patient is a five year old with a history of chronic pneumonia and bronchiectasis. Despite no change in his acute condition, he has an SPO₂ of 88% on room air. A chest x-ray shows chronic right middle lobe opacification. Is there anything that needs to be done for this child before he goes to the operating room?

9.    A four-year-old little girl was recently adopted from China. She has a large VSD and an O₂ saturation of 90% on room air. Why is this child hypoxemic? What can you do to improve the child’s clinical condition?

10. An 18-year-old male was treated for testicular cancer with surgery and chemotherapy, including bleomycin. He is hypoxemic at rest. Does his history explain this finding? How will you manage this patient during the course of this procedure?

Bonus question: The child in question eight is coming to the operating room for a thoracotomy. How will your intraoperative management of this child affect his postoperative recovery. How can you manage this anesthetic to reduce the risks of respiratory failure and prolonged ventilation during the postoperative period?

Discussion

The differential diagnosis of hypoxemia in an infant or child may be different than that for an adult. This is because of different disease processes, different caliber of the airway and the impact of the anatomy of an infant on the capacity to effectively ventilate. As examples, infants do not smoke, but they may be exposed to second hand smoke. Infants that breathe spontaneously while laying on their back will be much more likely to become hypoxemic because closing capacity is within the tidal ventilation of the infant. Bronchopulmonary dysplasia, still a possibility in premature infants, produces an increase in airway irritability and in pulmonary hypertension.

Many infants and children develop hypoxemia during the perioperative period for exactly the same reasons as adults. In the management of these patients, consideration must be given to all of the possibilities with more weight given to those issues that reflect the pathophysiology at hand.

Question 1: There are several reasons for this patient to desaturate. An infant breathing spontaneously through an endotracheal tube is likely to develop atelectasis producing intrapulmonary shunt. The work of breathing through an endotracheal tube is great and infants tire quickly. This is caused by the caliber of the endotracheal tube and the difference in the respiratory muscle type that predominates in infants. Muscles of ventilation expend their energy load rapidly and the infant will become hypercarbic and hypoxemic. In addition, this infant‘s endotracheal tube is taped at 12 CM at the lip. The tip of this tube is likely in the right mainstem bronchus and the infant is ventilating only one lung. For most infants the correct depth is ten cm at the lip.

Question 2. Defining the reasons for an acute change in ventilating pressures requires a studied approach. Obstruction of the circuit from the anesthesia machine to the end of the endotracheal tube must be investigated. Obstruction distal to the ETT must be considered and may involve large and small airways. Pneumothorax can produce an acute rise in PIP. Consideration must be given to the medical condition of the patient, (Does the patient have pneumonia?) as well as physical characteristics of the circuit, (Is the ETT kinked?). Consideration of the anesthetic that is being provided as a gaseous agent must be considered as well as the possibility of anaphylaxis.  Hypoxemia usually occurs coincident with elevations in ventilating pressures.  This occurs because of incomplete expansion of the lung and subsequent atelectasis. Management of this issue requires an increase in FiO₂ until a definitive diagnosis is made and the pressure is reduced.

Question 3. One must consider pneumothorax before one can diagnose and treat. Mottled lower extremities suggest low cardiac output.

Question 4. As above, infants with BPD have irritable airways and will often respond to Desflurane with bronchospasm and hypoxemia. In addition, the disease process often produces a state of chronic pulmonary hypertension that is exacerbated by agents that produce an increase in activity in the sympathetic nervous system (such as Desflurane). 

Question 5. RSV is common in the population of patients that come to the operating room. Some of the patients that have this virus in their airways are asymptomatic, but begin to develop an increase in mucous when the airway is instrumented. Because of this effect, children are at risk for atelectasis when breathing spontaneously even through an LMA.  It is often necessary to intubate these patients in order to suction the airway and provide recruitment breaths.

Question 6. A pulmonary embolus caused by a thrombus or by fat is common with long bone fractures, especially during the time that they are being manipulated. V/Q mismatch produced by small fat globules may be accompanied by hypoxemia, which may or may not be associated with hypotension or a significant change in ETCO_2. Large emboli may manifest with precipitous reductions in cardiac output causing secondary reduction in ETCO₂ and decreases in perfusion pressure and SPO_2.

Question 7. Acute chest syndrome represents widespread sickling within the microcirculation of the lung. Patients that have these episodes develop pulmonary infarcts, hypoxemia, and eventually pulmonary hypertension. This patient will show evidence of multiple past infarcts on a CT scan of the chest; thus the hypoxemia that is discovered in the holding room. Preparing patients such as these for safe general anesthesia will require eliminating the possibility of an acute infection and oxygen supplementation to reduce the risk of a sickle cell crisis during the perioperative period.

For patients that require chest procedures, judicious use of fluids to reduce the risk of postoperative respiratory failure is key. This must be balanced against the need to maintain sufficient intravascular volume reducing the risk of dehydration and a sub sequent crisis.

Question 8. Chronic atelectasis produces a respiratory shunt and subsequent hypoxemia. Often this anatomic finding has been present for such a long period of time that the lung segment is and never will be functional. Post obstructive pneumonias form in some of these segments. Surgical exenteration may be required in order to reduce the risk of further chest pathology or the development of widespread septicemia.

Perioperative treatment includes aggressive pulmonary toilet to remove foreign matter from as much of the lung as possible. In addition treatment of acute pneumonias based on bronchial washings reduces the risk of sepsis in the operating room or during the recovery phase.

Question 9. This child has a wide-open VSD. Because of the high flow through this defect the lungs are chronically flooded increasing the amount of interstitial water to a level that is greater than can be filtered and carried away. Interstitial water prevents effective movement of oxygen across the alveolar membrane leading to hypoxemia. In addition, the high flow causes anatomic changes in the muscular walls of pulmonary arteries producing increases in pulmonary artery pressures over time and eventually reversing flow to a rt. to lt. shunt. This is a late finding and is rarely encountered.

Early treatment includes the use of diuretics to reduce pulmonary interstitial edema and eventual pulmonary banding to substantially reduce pulmonary blood flow. As the heart grows, it becomes more appropriate to patch graft the VSD and remove the pulmonary band.

Question 10. Bleomycin is an antibiotic antitumor agent effective against germ cell tumors. Pulmonary toxicity has been reported with this compound since the 60s with attention being given to the effect of bolus dosing, age and total dose of the drug. In addition, exposure to oxygen has often been cited as a mechanism of toxicity thought the primary cause of this has yet to be elucidated. Recent studies have focused more attention on the renal function of the patient as a reason for elevations in the levels of the drug that can produce pulmonary interstitial fibrosis. In this patient, his young age and the fact that in the modern era drug is given as an infusion, and after verification of renal function, his hypoxemia is likely not secondary to bleomycin toxicity.

Bonus Question: Appropriate management of intraoperative fluids has been shown to affect significantly the length of stay as well as the risk for postoperative respiratory failure for patients having surgical procedures in the chest. While appropriate resuscitation is often required, excessive fluid administration is ill advised.

General Approach to Hypoxemia

If the patient’s oxygen saturation has decreased:

1. Ask the question “Is the patient at risk for injury?” if the answer is yes, then you must increase the flow of oxygen to the patient. This gives the clinician time to think and should virtually always be the first order of business.
2. Ask the question” Am I actually delivering oxygen to the patient?” Could this be a hypoxic mixture, a line swap, loss of pipeline flow with empty tanks?
3. Am I adequately ventilating the patient? Is the ETCO₂ waveform present and of normal configuration? Is the ventilating pressure reasonable? Does the patient have bronchospasm?
4. Is the endotracheal tube taped appropriately? Right main stem intubation is the most common cause of hypoxemia in other wise healthy patients.
5. Has the thorax been invaded – central line placement, retroperitoneal dissection, and laparoscopic cases? Is the risk of a pneumothorax elevated for any reason?
6. Has there been a catastrophic decrease in the cardiac output such as with a dissection of the aorta, a pericardial tamponade or profound anemia?
7. Is this a procedure that predisposes to hypoxemia – one lung ventilation?
8. Finally, after every other avenue has been exhausted, could this be a spurious reading? Occasionally caused by the compression of a blood pressure cuff, the administration of dye, or probe failure?

 

 Rae Brown, M.D.

February 19, 2015