Objective: To investigate the effect of hyperbaric oxygen (HBO) treatment on tissue oxygen and carbon dioxide tensions in patients with necrotising fasciitis 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 directly in patients with necrotising fasciitis and in healthy volunteers during normobaric and hyperbaric conditions. Arterial blood PO2 and PCO2 tensions were measured only in the patients. Tissue gas tensions were measured with a Silastic tube tonometer implanted in the brachial subcutaneous tissue of both patients and controls as well as in the subcutaneous tissue of the patients 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 observations.
Main outcome measures: Arterial and subcutaneous tissue PO2 and PCO2 tensions.
Results: In patients with necrotising fasciitis the arterial PO2 rose about 7-fold whereas the arterial PCO2 increased only slightly during exposure to 2.5 absolute atmospheres (ATA) of oxygen. During HBO the subcutaneous tissue 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. In patients with necrotising fasciitis, the PO2 was higher, but not significantly so, in the vicinity of the infected area than in the healthy tissue.
Conclusion: Under hyperbaric conditions the subcutaneous PO2 in patients with necrotising fasciitis rose higher in the vicinity of the infected area than in the healthy tissue, which may be the result of vasodilatation and increased microcirculation induced by the inflammatory process associated with infection or it may be the result of decreased local tissue oxygen utilisation, or both. The tissue PCO2 values tended to rise during HBO probably from hypoventilation or reduced CO2 washout from tissue because venous blood haemoglobin was fully saturated with oxygen.