Intensive Care Med (2004) 30:1014–1016 DOI 10.1007/s00134-004-2216-6

Andrew C. Argent Brenda M. Morrow

EDITORIAL

What does chest physiotherapy do to sick infants and children?

Accepted: 28 January 2004 Published online: 5 March 2004
Springer-Verlag 2004 A. C. Argent ()) · B. M. Morrow Division of Paediatric Critical Care and Children’s Heart Disease, School of Child and Adolescent Health, University of Cape Town, Cape Town, South Africa e-mail: [email protected] A. C. Argent · B. M. Morrow Department of Paediatric Intensive Care, Red Cross War Memorial Children’s Hospital, Cape Town, South Africa

Endotracheal suctioning (ET) and chest physiotherapy (CP) are part of the accepted care of intubated children in many paediatric intensive care units in spite of a limited evidence-base [1, 2], largely because of the risks of endotracheal tube obstruction. A wide variety of deleterious effects of ET on children and infants have been reported including bacteraemia [3], lobar atelectasis [4, 5], hypoxia [6], decreased cerebral oxygenation [7, 8], hypertension and raised intracranial pressure [9, 10], pneumothoraces [11] and death. Some of the side effects may be minimised by reduction of suction pressure and limitation of the depth of insertion of the suction catheter [5], appropriate pre-oxygenation [12, 13], adequate sedation and analgesia [14] and muscle paralysis [9]. Chest physiotherapy has been associated with the development of severe brain damage in very low birth weight infants [15] and potentially severe hypoxaemia in neonates [16]. Following paediatric cardiac surgery, routine 4-hourly CP was related to the development of atelectasis and prolonged hospital stay [17], while another study showed that pre-extubation CP did not decrease the incidence of post-extubation atelectasis [18]. In this context Main et al. [19, 20] have accurately and reproducibly studied the effects of ET or CP on paralysed, sedated, mechanically ventilated children who had been

“deemed on assessment by the physiotherapist to require respiratory physiotherapy”, in a randomised cross-over trial. Fifteen minutes after CP there was a statistically significant drop in base excess (BE), bicarbonate and oxygen saturation, and a trend to a drop in respiratory resistance (Rrs). Thirty minutes after CP there was an increase in physiological deadspace (VDphys). Fifteen minutes after ET alone there was no change in expired tidal volume (VTE), compliance (Crs), Rrs blood gas parameters or physiological deadspace. When CP and ET were compared, at 15 min BE was higher in the CP group and, 30 min after intervention, VTE, VDphys, alveolar deadspace (VDalv) and Crs were higher in the CP group. There were no significant differences in pCO2, pO2 or pH. At an individual level, an apparent improvement in VTE, Crs and Rrs (exceeding the 95% limits of agreement) was observed in about twice as many subjects following CP as following ET. This reached statistical significance in VTE only. Improvements in VTE, Crs and Rrs were possibly offset by increases in dead space, although this specific data is not provided in the two papers. In up to a third of the patients, respiratory function deteriorated following both physiotherapy and suction procedures. Even in retrospect the authors were not able to identify groups of patients who were more or less likely to respond positively or negatively to therapy. As the authors suggest, more work is required to identify adequately the children who may benefit from or deteriorate following the procedure. These results were obtained following CP that took 8.5 minutes on average (range 1–33 min), used tracheal saline instillation in 98% of cases and consisted typically of pre-oxygenation, saline instillation, hyperinflation breaths with chest wall vibrations during expiration, tracheal suction and several re-inflation breaths. ET consisted of pre-oxygenation, saline instillation, manual hyperinflation breaths, suction and then manual re-inflation breaths, and took 5.6 min on average (range 1– 20 min). No details are given of the pre-oxygenation

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technique, pressures generated or rate during hyperinflation or re-inflation breaths. More than 1.5 ml/kg of saline was instilled in 20% of CP procedures and recommendations were made that suction pressure should not exceed 18–20 kpA, and the external diameter of suction catheters should approximate half the internal diameter of the tracheal tube during suctioning unless secretions were particularly tenacious. Chest physiotherapy and ET were “flexibly defined” in order to approximate clinical reality. Unfortunately this does undermine the generalizability and reproducibility of the study, as there appears to be considerable variation in the way in which these procedures are performed in different units [18]. The authors suggest that the greater drop in Rrs in the CP group could be explained by more effective removal of secretions. The suggestion that the increase in physiological deadspace could be attributed to the opening of poorly perfused alveoli to ventilation seems plausible. Both observations raise interesting questions about clinical relevance and show that careful monitoring of responses over time are required before we will begin to understand the processes set in motion by CP. The changes in BE, bicarbonate and oxygen saturation in the CP group were not clinically significant at 15 min. However they suggest that metabolic acidosis may have developed in the CP group during the procedure. Patients were monitored throughout the procedures, but haemo-

dynamics and other changes may be difficult to assess when patients are moved. One would expect different responses to these procedures depending on: the age and size of the patient; underlying respiratory system and cardiovascular pathology; nature of the ventilatory strategy that is employed; details of sedation and analgesia; nature of percussion and/or vibration used; pre- and post-oxygenation procedures (duration, FiO2 used); details of the hyperinflation and re-inflation procedures (pressures, duration, waveforms, pressures generated during expiratory vibration); use of saline installation; details of suctioning (duration, depth of insertion, size of suction catheters, relationship of endotracheal tube and suction catheter sizes, suction pressure) etc. Responses may affect the respiratory system [7, 8], cardiovascular system, metabolic demand and central nervous system [9, 11, 13]. Future studies will have to focus on the details of the procedures and their effects on organ systems. They must also be aimed at specific patient groups where clinical significance of changes may be more easily defined. Finally, the underlying issue is really: what effect do these procedures have on the clinical outcomes of individual patients? Any benefits must be balanced against the costs of the procedure: costs to the patient of undergoing potentially distressing procedures of significant duration and with well-documented side effects and costs of staff spending up to 33 min per patient performing the procedures.

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18. Bloomfield FH, Teele RL, Voss M, Knight DB, Harding JE (1998) The role of neonatal chest physiotherapy in preventing postextubation atelectasis. J Pediatr 133:269–271 19. Main E, Castle R, Newham D, Stocks J (2004) Respiratory physiotherapy versus suction: the effects on respiratory function in ventilated infants and children. Intensive Care Med (http:// dx.doi.org/10.1007/s00134-004-22620)

20. Main E, Stocks J (2004) The influence of physiotherapy and suction on respiratory deadspace in ventilated children. Intensive Care Med (http://dx.doi.org/ 10.1007/s00134-004-2261-1)