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Dramatic improvement in oxygenation after sternotomy in a patient with acute respiratory distress syndrome.

Acute respiratory distress syndrome (ARDS) is a frequent complication of trauma and surgery with a high mortality rate between 30 and 50% (1). The search for effective treatments has been unsuccessful in decreasing mortality rate (2). We report a dramatic and intriguing increase in arterial saturation after sternotomy in an organ-donor patient suffering ARDS. This report represents the first clinical report of this phenomenon.

A 17-year-old female was admitted in the hospital after a car accident. The first radiographic and computed tomographic scan revealed multiple rib fractures, bilateral haemopneumothoraces and contusions in both lungs, as well as fractures of the hip and the femur. The patient initially underwent bilateral tube thoracostomy and an open reduction and fixation of the femoral fracture. On arrival in the intensive care unit, pressurecontrolled ventilation was instituted. Positive endexpiratory pressure of 5 cm was applied and the [FiO.sub.2] was elevated to 1.0 due to oxyhaemoglobin saturation (Sp[O.sub.2]) at 88%. The patient continued to deteriorate and adequate oxygenation could not be maintained with [FiO.sub.2] 1.0, positive end-expiratory pressure 15 cm[H.sub.2O] and nitric oxide 15 ppm. The chest radiograph showed diffuse opacities in both lungs leading to the diagnosis of ARDS. On the sixth day, brain death was confirmed following anoxic injury. After obtaining family approval, the patient was scheduled for organ donation (liver). On arrival in the operating theatre, controlled ventilation was applied with Fi[O.sub.2] 1.0, cm positive end-expiratory pressure 20 cm[H.sub.2O] and nitric oxide 15 ppm. Arterial saturation (Sp[O.sub.2]) was 67% and end-tidal C[O.sub.2] 3.6 kPa (ETC[O.sub.2]). Immediately after median sternotomy, Sp[O.sub.2] and ETC[O.sub.2] increased abruptly to 99% and 5.0 kPa respectively, although ventilatory parameters were unaltered. No pleurotomy occurred and peak airway pressure remained at the same level as previously, i.e. around 65 cm[H.sub.2O.] The oxygenation improvement remained stable until cardiac arrest 15 minutes later. All data were computerised using Recall-System[TM] (Drager, Germany) (Figure 1).


The mechanism involved in the dramatic increase in oxyhaemoglobin saturation observed after sternotomy is not entirely clear in the absence of more detailed information on pulmonary mechanics and haemodynamics. Sternotomy is associated with a reduction in chest wall elastance that affects lung mechanics, e.g. increasing the functional residual capacity, and improves gas exchange (3,4). Jonmarker et al (3) reported that functional residual capacity consistently increases by about 50% with median sternotomy if the pleurae are intact. Barnas et al (4) studied the mechanical properties, elastance and resistance of the respiratory system during mechanical ventilation in patients undergoing coronary artery bypass grafting surgery. They show that after median sternotomy, elastance of the respiratory system does not change but resistances decrease. The chest wall elastance is higher than in the closed chest while elastance and resistance of the lungs are lower, thus explaining the increase in functional residual capacity. The resistance of the chest wall does not change. These authors concluded that the chest wall/pleura compartment offers significant impedance to lung expansion after sternotomy.

The increase in [ETCO.sub.2] observed after sternotomy in our patient could be attributed to an improvement in venous return and thereby cardiac output. Changes in cardiac output have been reported to positively correlate with the intrapulmonary shunt fraction (5).

This brief clinical observation addresses the question of the mechanism involved in the dramatic increase in oxygenation after chest opening in a patient with refractory ARDS.



Charleroi, Belgium


(1.) Rubenfeld GD. Epidemiology of acute lung injury. Crit Care Med 2003; 31:S276-284.

(2.) Browner RG, Ware LB, Berthiaume Y, Matthay MA. Treatment of ARDS. Chest 2001; 120:1347-1367.

(3.) Jonmarker C, Nordstrom L, Werner O. Changes in functional residual capacity during cardiac surgery. Br J Anaesth 1986; 58:428-432.

(4.) Barnas GM, Gilbert TB, Watson RJ, Sequeira AJ, Roitman K, Nooroni RJ. Respiratory mechanics in the open chest: effects of parietal pleurae. Respir Physiol 1996; 104:63-70.

(5.) Lynch JP, Mhyre JG, Dantzker DR. Influence of cardiac output on intrapulmonary shunt. J Appl Physiol 1979; 46:315-321.
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Title Annotation:Correspondence
Author:Stadler, M.; Boogaerts, J.G.
Publication:Anaesthesia and Intensive Care
Article Type:Case study
Geographic Code:1USA
Date:Mar 1, 2012
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