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March 2004

Transcutaneous monitoring: back to the future - An important adjunct to care during high frequency oscillatory ventilation

by Sherry E. Courtney
Neonatology Hemoglobins

High frequency oscillatory ventilation (HFOV) is often used in neonatal intensive care. HFOV has been shown to decrease bronchopulmonary dysplasia [1,2,3] in preterm infants and to be very effective in the treatment of persistent pulmonary hypertension of the newborn when used in conjunction with inhaled nitric oxide [4]. 

Other uses include pulmonary hypoplasia, air leak, and ventilation after abdominal surgeries such as gastroschisis closure.

Effective use of HFOV requires close attention to lung volume, with use of an “optimal volume” strategy to open the lung and maintain it open [5]. Mean airway pressure is adjusted to minimize FO2(I) requirement without evidence of under- or overdistention on chest X-ray. Continuous pulse oximetry assists with adjustments of mean airway pressure and FO2(I).

Continuous assessment of CO2 is also very important during HFOV. The oscillator is a powerful machine that can quickly drive arterial CO2 to unsafe levels. Evidence is accumulating that suggests cerebral damage may result from hypocarbia [6,7]. 

Many infants on HFOV have indwelling arterial lines; however, frequent blood draws may be necessary to appropriately monitor CO2 changes, leading to increased infection risk and/or anemia. A non-invasive, continuous estimate of pCO2 during HFOV would be safer and more effective. Transcutaneous monitoring can provide this estimate.

Transcutaneous (tc) monitoring is not new; it has been available for well over twenty years [8]. Early machines were cumbersome and difficult to use. Accurate tcpO2 assessment necessitated heating the skin to 43 °C, which often led to skin burns in small preterm infants. 

After the advent of pulse oximetry, use of tc monitoring faded in most NICUs. Unfortunately, this led to “throwing the baby out with the bathwater”, as tcpCO2 monitoring also dramatically decreased despite the lack of a replacement for CO2 monitoring such as pulse oximetry.

Currently available tc monitors are small and easy to use. Importantly, they can be used to monitor both tcpO2 and tcpCO2, or either one separately. 

Even more importantly, use of tcpCO2 alone can accurately be done at a monitor temperature of 40 °C, thus not causing skin burns [9], and site changes can be done as infrequently as every six to eight hours. The machine must simply be calibrated at the appropriate temperature.

The tcpCO2 will correlate with the pCO2(aB) – that is, as one goes up the other goes up; as one goes down the other goes down. The “closeness” of the numbers will depend on the thickness of the skin and the perfusion of the site. 

The numbers are seldom identical, as they measure different things: one measures the pCO2(aB) of arterial blood and the other the CO2 diffusing from the cutaneous tissue. The numbers, however, will correlate (trend together).

It is important to check tcpCO2 values with arterial blood gas samples or well-done capillary samples with each tc site change. Perfusion will vary somewhat from site to site, and thus the “closeness” of the numbers may also change. 

A rising tcpCO2 should always be considered a patient problem until proven otherwise. Something often forgotten is that an increasing tcpCO2 may of and by itself indicate decreasing perfusion in the patient – perhaps sepsis or impending shock. 

Though the tcpCO2 will still trend correctly, the tcpCO2 will be considerably higher than the pCO2(aB) in a patient with significant circulatory compromise. In these cases the underlying cause of the problem must be treated.

“Something is wrong with the machine” is unfortunately often heard before evaluation of the patient has been done. A recent article, for example, documented the value of a rising tcpCO2 in alerting staff to a pneumothorax well before acute decompensation of the patient [10]. 

A steadily rising or falling tcpCO2 should prompt careful attention to reasons for under- or overventilation, not an immediate recalibration of the monitor or, worse, turning a blind eye to the readouts because “the machine is not working”.

Troubleshooting the tc monitor is relatively easy. The calibration cylinder must contain sufficient gas and must be turned on during calibration. The cable must be intact. The sensor must be remembraned as per the manufacturer’s recommendations. 

Sufficient contact fluid must be placed between the skin and the sensor. Recalibration should be done every six to eight hours if only tcpCO2 is being used. We have found every six hours to be best in this circumstance; towards eight hours the contact fluid tends to evaporate, leading to spurious values. 

The sensor site should be changed every three to four hours if both tcpO2 and tcpCO2 are utilized. Heating of the sensor to 43 °C is needed if the tcpO2 is employed, and the site must be changed more frequently to avoid skin burns. 

A tcpCO2 value of 0 or tcpO2 of about 150 means the sensor has dislodged or an air bubble is under the sensor. These are the values expected for room air. tcpCO2 values that jump about wildly indicate need for recalibration/remembraning. Steadily rising or falling values reflect patient status.

Though pulse oximetry has largely replaced the need for tcpO2 monitoring, tcpO2 monitoring can provide useful and complimentary information should the practitioner choose to use it. High pO2(aB) should be avoided in most cases [11,12]. 

Because of the shape of the oxygen-hemoglobin dissociation curve, an oxygen saturation in an acceptable range could be associated with a pO2(aB) that is unnecessarily high. By the same token, a low or borderline saturation might be associated with an acceptable pO2(aB) because of shifts in the oxygen-hemoglobin dissociation curve and varying amounts of fetal hemoglobin. 

tcpO2 monitoring can be very useful in titrating the FO2(I). Use of tcpO2 monitoring requires more frequent site changes and close attention to the baby’s skin to avoid burns.

In most cases, however, the “burn” is a reddened area just under the sensor that heals without residua. Occasionally, tiny scars can result if the sensor temperature is too high or the sensor is left on the skin for too long.

For a patient being started on HFOV, the tcpCO2 monitor should be placed on the patient prior to instituting HFOV. Once the tcpCO2 is stable and a correlating ABG has been obtained, HFOV can be started and the amplitude adjusted using the tc monitor.

Severe hypocapnia, such as can occur with an inadvertently high amplitude or postsurfactant can thus be entirely avoided. Hypercapnia from tube secretions, tube malposition, accidental extubation, pneumothorax or insufficient amplitude can also be quickly noted and appropriate interventions given.

The tcpCO2 monitor is also very valuable as the patient begins to wean, avoiding hypocarbia and allowing the staff to pace the wean appropriately.

Optimal use of HFOV should include concurrent use of tcpCO2 monitoring to ensure prevention of hypo- and hypercarbia and timely interventions for both complications of therapy and patient weaning.

References
  1. Gerstmann DR, Minton SD, Stoddard RA et al: The Provo multicenter early high-frequency oscillatory ventilation trial: Improved pulmonary and clinical outcome in respiratory distress syndrome. Pediatrics 1996; 98: 1044-57.
  2. Courtney SE, Durand DJ, Asselin JM et al: High-frequency oscillatory ventilation versus conventional mechanical ventilation for very low birth weight infants. N Engl J Med 2002; 347: 643-52.
  3. Henderson-Smart DJ, Bhuta T, Cools F et al: Elective high frequency oscillatory ventilation versus conventional ventilation for acute pulmonary dysfunction in preterm infants. Cochrane Library 2002 (online at www.nichd.nih.gov/cochrane)
  4. Kinsella JP, Truog WE, Walsh WF et al: Randomized, multicenter trial of inhaled nitric oxide and high-frequency oscillatory ventilation in severe, persistent pulmonary hypertension of the newborn. J Pediatr 1997; 131: 55-62.
  5. Froese AB: Role of lung volume in lung injury: HFO in the atelectasis-prone lung. Acta Anaesthesiol Scand 1989; 33: Suppl. 90: 126-30.
  6. Fujimoto S, Togari H, Yamaguchi N et al: Hypocarbia and cystic periventricular leukomalacia in premature infants. Arch Dis Child 1994; 71: F107-110.
  7. Okumura A, Hayakawa F, Kato T et al: Hypocarbia in preterm infants with periventricular leukomalacia: The relation between hypocarbia and mechanical ventilation. Pediatrics 2001; 107: 469-75.
  8. Pollitzer MJ, Whitehead MD, Reynolds EOR et al: Effect of electrode temperature and in vivo calibration on accuracy of transcutaneous estimation of arterial oxygen tension in infants. Pediatrics 1980; 65: 515-20.
  9. Binder N, Atherton H, Thorkelsson T et al: Measurement of transcutaneous carbon dioxide in low birthweight infants during the first two weeks of life. Am J Perinatology 1994; 11: 237-41.
  10. McIntosh N, Becher JC, Cunningham S et al: Clinical diagnosis of pneumothorax is late: Use of trend data and decision support might allow preclinical detection. Pediatr Res 2000; 48: 408-15.
  11. Chow LC, Wright KW, Sola A et al: Can changes in clinical practice decrease the incidence of severe retinopathy of prematurity in very low birth weight infants? Pediatrics 2003; 111: 339-45.
  12. Askie LM, Henderson-Smart DJ, Irwig L et al: Oxygen-saturation targets and outcomes in extremely preterm infants. N Engl J Med 2003; 349: 959-67. 
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References
  1. Gerstmann DR, Minton SD, Stoddard RA et al: The Provo multicenter early high-frequency oscillatory ventilation trial: Improved pulmonary and clinical outcome in respiratory distress syndrome. Pediatrics 1996; 98: 1044-57.
  2. Courtney SE, Durand DJ, Asselin JM et al: High-frequency oscillatory ventilation versus conventional mechanical ventilation for very low birth weight infants. N Engl J Med 2002; 347: 643-52.
  3. Henderson-Smart DJ, Bhuta T, Cools F et al: Elective high frequency oscillatory ventilation versus conventional ventilation for acute pulmonary dysfunction in preterm infants. Cochrane Library 2002 (online at www.nichd.nih.gov/cochrane)
  4. Kinsella JP, Truog WE, Walsh WF et al: Randomized, multicenter trial of inhaled nitric oxide and high-frequency oscillatory ventilation in severe, persistent pulmonary hypertension of the newborn. J Pediatr 1997; 131: 55-62.
  5. Froese AB: Role of lung volume in lung injury: HFO in the atelectasis-prone lung. Acta Anaesthesiol Scand 1989; 33: Suppl. 90: 126-30.
  6. Fujimoto S, Togari H, Yamaguchi N et al: Hypocarbia and cystic periventricular leukomalacia in premature infants. Arch Dis Child 1994; 71: F107-110.
  7. Okumura A, Hayakawa F, Kato T et al: Hypocarbia in preterm infants with periventricular leukomalacia: The relation between hypocarbia and mechanical ventilation. Pediatrics 2001; 107: 469-75.
  8. Pollitzer MJ, Whitehead MD, Reynolds EOR et al: Effect of electrode temperature and in vivo calibration on accuracy of transcutaneous estimation of arterial oxygen tension in infants. Pediatrics 1980; 65: 515-20.
  9. Binder N, Atherton H, Thorkelsson T et al: Measurement of transcutaneous carbon dioxide in low birthweight infants during the first two weeks of life. Am J Perinatology 1994; 11: 237-41.
  10. McIntosh N, Becher JC, Cunningham S et al: Clinical diagnosis of pneumothorax is late: Use of trend data and decision support might allow preclinical detection. Pediatr Res 2000; 48: 408-15.
  11. Chow LC, Wright KW, Sola A et al: Can changes in clinical practice decrease the incidence of severe retinopathy of prematurity in very low birth weight infants? Pediatrics 2003; 111: 339-45.
  12. Askie LM, Henderson-Smart DJ, Irwig L et al: Oxygen-saturation targets and outcomes in extremely preterm infants. N Engl J Med 2003; 349: 959-67. 
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May contain information that is not supported by performance and intended use claims of Radiometer's products. See also Legal info.

Sherry E. Courtney

 

Division of Neonatology
Schneider Children's Hospital
North Shore Long Island Jewish Health System
New Hyde Park, New York 11040
USA

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