We have located links that may give you full text access.
Clinical Trial
Journal Article
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 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.
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.
Full text links
Related Resources
Trending Papers
British Society of Gastroenterology guidelines for the management of hepatocellular carcinoma in adults.Gut 2024 April 17
Systemic lupus erythematosus.Lancet 2024 April 18
Should renin-angiotensin system inhibitors be held prior to major surgery?British Journal of Anaesthesia 2024 May
Ventilator Waveforms May Give Clues to Expiratory Muscle Activity.American Journal of Respiratory and Critical Care Medicine 2024 April 25
Acute Kidney Injury and Electrolyte Imbalances Caused by Dapagliflozin Short-Term Use.Pharmaceuticals 2024 March 27
Colorectal polypectomy and endoscopic mucosal resection: European Society of Gastrointestinal Endoscopy (ESGE) Guideline - Update 2024.Endoscopy 2024 April 27
Get seemless 1-tap access through your institution/university
For the best experience, use the Read mobile app
All material on this website is protected by copyright, Copyright © 1994-2024 by WebMD LLC.
This website also contains material copyrighted by 3rd parties.
By using this service, you agree to our terms of use and privacy policy.
Your Privacy Choices
You can now claim free CME credits for this literature searchClaim now
Get seemless 1-tap access through your institution/university
For the best experience, use the Read mobile app