Tissue gas tensions in patients with necrotising fasciitis and healthy controls during treatment with hyperbaric oxygen: a clinical study

Objective: To investigate the effect of hyperbaric oxygen (HBO) treatment o n tissue oxygen and carbon dioxide tensions in patients with necrotising fa sciitis and healthy volunteers. Design: Clinical study in patients and healthy controls. Setting: University hospital, Finland. Subjects: 6 patients with necrotising fasciitis and 3 healthy volunteers. Interventions: Subcutaneous tissue PO2 and PCO2 tensions were measured dire ctly in patients with necrotising fasciitis and in healthy volunteers durin g normobaric and hyperbaric conditions. Arterial blood PO2 and PCO2 tension s were measured only in the patients. Tissue gas tensions were measured wit h a Silastic tube tonometer implanted in the brachial subcutaneous tissue o f both patients and controls as well as in the subcutaneous tissue of the p atients in the immediate vicinity of the necrotising process. The diagnosis of necrotising fasciitis was made on the basis of the presence of typical clinical signs and symptoms, intraoperative findings, and microbiological o bservations. Main outcome measures: Arterial and subcutaneous tissue PO2 an d PCO2 tensions. Results: In patients with necrotising fasciitis the arterial PO2 rose about 7-fold whereas the arterial PCO2 increased only slightly during exposure t o 2.5 absolute atmospheres (ATA) of oxygen. During HBO the subcutaneous tis sue PO2 increased four to five fold from the baseline and CO2 tensions also increased, but to a lesser degree, in both healthy and infected tissues. I n patients with necrotising fasciitis, the PO2 was higher, but not signific antly so, in the vicinity of the infected area than in the healthy tissue. Conclusion: Under hyperbaric conditions the subcutaneous PO2 in patients wi th necrotising fasciitis rose higher in the vicinity of the infected area t han in the healthy tissue, which may be the result of vasodilatation and in creased microcirculation induced by the inflammatory process associated wit h infection or it may be the result of decreased local tissue oxygen utilis ation, or both. The tissue PCO2 values tended to rise during HBO probably f rom hypoventilation or reduced CO2 washout from tissue because venous blood haemoglobin was fully saturated with oxygen.