Necrotizing Fasciitis and Gas Gangrene

Necrotizing Fasciitis and Gas Gangrene

Click on the publications below to view and close the abstracts

Not just full of hot air: hyperbaric oxygen therapy increases survival in cases of necrotizing soft tissue infections Shaw JJ, Psoinos C, Emhoff TA, Shah SA, Santry HP. Surg Infect (Larchmt). 2014 Jun;15(3):328-35. doi: 10.1089/sur.2012.135. Epub 2014 May 1.

ABSTRACT
BACKGROUND: The utility of hyperbaric oxygen therapy (HBOT) in the treatment of necrotizing soft tissue infections (NSTIs) has not been proved. Previous studies have been subject to substantial selection bias because HBOT is not available universally at all medical centers, and there is often considerable delay associated with its initiation. We examined the utility of HBOT for the treatment of NSTI in the modern era by isolating centers that have their own HBOT facilities.

METHODS: We queried all centers in the University Health Consortium (UHC) database from 2008 to 2010 that have their own HBOT facilities (n=14). Cases of NSTI were identified by International Classification of Diseases, Ninth Revision (ICD-9) diagnosis codes, which included Fournier gangrene (608.83), necrotizing fasciitis (728.86), and gas gangrene (040.0). Status of HBOT was identified by the presence (HBOT) or absence (control) of ICD-9 procedure code 93.95. Our cohort was risk-stratified and matched by UHC’s validated severity of illness (SOI) score. Comparisons were then made using univariate tests of association and multivariable logistic regression.

RESULTS: There were 1,583 NSTI cases at the 14 HBOT-capable centers. 117 (7%) cases were treated with HBOT. Univariate analysis showed that there was no difference between HBOT and control groups in hospital length of stay, direct cost, complications, and mortality across the three less severe SOI classes (minor, moderate, and major). However, for extreme SOI the HBOT group had fewer complications (45% vs. 66%; p<0.01) and fewer deaths (4% vs. 23%; p<0.01). Multivariable analysis showed that patients who did not receive HBOT were less likely to survive their index hospitalization (odds ratio, 10.6; 95% CI 5.2-25.1).

CONCLUSION: At HBOT-capable centers, receiving HBOT was associated with a significant survival benefit. Use of HBOT in conjunction with current practices for the treatment of NSTI can be both a cost-effective and life-saving therapy, in particular for the sickest patients.

http://www.ncbi.nlm.nih.gov/pubmed/24786980

Hyperbaric oxygen therapy in acute necrotizing infections with a special reference to the effects on tissue gas tensions
Korhonen K.
Department of Surgery, University of Turku, Turku, Finland.

ABSTRACT
Clostridial gas gangrene and perineal necrotizing fasciitis or Fournier’s gangrene are rare but serious infections with an acute onset, rapid progression, systemic toxemia and a high mortality rate.

The aim of this study was to investigate the efficacy of surgery, antibiotic treatment, surgical intensive care and in particular the role of hyperbaric oxygen (HBO) in the management of these infections.

An experimental rat model was used to investigate the possibilities for measuring tissue oxygen and carbon dioxide tensions during hyperbaric oxygen treatment. In addition to this preliminary experimental study, Silastic tube tonometer and capillary sampling techniques were tested to measure the effect of hyperbaric oxygen treatment on subcutaneous oxygen and carbon dioxide tensions in patients with necrotizing fasciitis and healthy controls.

Between January 1971 and April 1997, 53 patients with Clostridial gas gangrene were treated in the Department of Surgery, University of Turku. The patients underwent surgical debridement, broad spectrum antibiotic therapy and a series of hyperbaric oxygen treatments at 2.5 atmospheres absolute pressure (ATA). Twelve patients died (22.6%).

Hyperbaric oxygen therapy in gas gangrene seems to be life-, limb- and tissue saving. Early diagnosis remains essential. Patient survival can be improved if the disease is recognized early and appropriate therapy instituted promptly.

Between February 1971 and September 1996, 33 patients with perineal necrotizing fasciitis were treated in the Department of Surgery, University of Turku. The management included surgical debridement of the necrotic tissue with incisions and drainage of the involved areas, antibiotic therapy, hyperbaric oxygen treatment at 2.5 ATA pressure and surgical intensive care. Three patients died giving a mortality rate of 9.1%. The survivors received hyperbaric oxygen therapy for 2-12 times.

Our results indicate that hyperbaric oxygenation is an important therapeutic adjunct in the treatment of Fournier’s gangrene. Electrical equipment should not be used unsheltered in a hyperbaric chamber due to the increased risk of fire. The subcutaneous tissue gas tensions of rats were therefore measured using a subcutaneously implanted Silastic tube tonometer and a capillary sampling technique. The method was successfully adapted to hyperbaric conditions.

The subcutaneous oxygen tension levels increased five fold and the carbon dioxide tension levels two fold compared to initial levels. The PO2 and PCO2 of subcutaneous tissue and arterial blood were measured directly in six patients with necrotizing fasciitis and three healthy volunteers in normobaric conditions and during hyperbaric oxygen exposure at 2.5 ATA pressure.

The measurements were carried out in healthy tissue and at the same time in the vicinity of the infected area of the patients. During HBO at 2.5 ATA subcutaneous oxygen tensions increased several fold from baseline values and carbon dioxide tensions also increased, but to a lesser degree in both healthy and infected tissues. When examining the subcutaneous PO2 levels measured from patients with necrotizing fasciitis, the PO2 was regularly higher in the vicinity of the infected area than in healthy tissue.

In general, HBO treatment resulted in a marked increase in tissue oxygenation in both healthy tissue and in the vicinity of infected tissue. The hyper-oxygenated tissue zone surrounding the infected area may be of significance in preventing the extension of invading microorganisms.

http://www.ncbi.nlm.nih.gov/pubmed/11199291

Management of clostridial gas gangrene and the role of hyperbaric oxygen Korhonen K, Klossner J, Hirn M, Niinikoski J. Ann Chir Gynaecol. 1999;88(2):139-42.

ABSTRACT
BACKGROUND AND AIMS: Clostridial gas gangrene is one of the most dreaded infections in surgery. The aim of this study was to investigate the efficacy of surgery, antibiotic treatment, surgical intensive care and especially the role of hyperbaric oxygen in the management of clostridial gas gangrene.

MATERIAL AND METHODS: 53 patients, 42 of them submitted from other hospitals in Finland. After the diagnosis had been made the patients underwent surgical debridement, broad spectrum antibiotic therapy and a series of hyperbaric oxygen (HBO) treatments at 2.5 ATA pressure. The necrotic tissue was excised and incisions were made in the affected areas. Amputations were performed when necessary.

RESULTS: Twelve patients died (22.6%). Hyperbaric oxygen therapy decreased the systemic toxicity and prevented further extension of the infection thereby improving the overall outcome of the patients.

CONCLUSION: Hyperbaric oxygen therapy of gas gangrene seems to be life-, limb- and tissue saving. Early diagnosis remains essential. Patient survival can be improved if the disease is recognized early and appropriate therapy applied promptly. Surgical and antibiotic therapy as well as HBO treatment combined with surgical intensive care must be started as soon as possible.

http://www.ncbi.nlm.nih.gov/pubmed/10392252

A personal observation from Robert L Sands:

(excerpt from private correspondence)

… to explore some of the myths regarding the timing of hyperbaric oxygen therapy: two of the most common ones are, how long the treatment should be and also the time in between treatments.

It is interesting that the common denominator on both of these comes from reimbursement issues – usually in hospitals – not science at all.

The science of how long the treatment should be is actually 90 minutes at depth.  Whilst this does not seem to make much difference with oxygen costs it does make a large difference to the oxygen uptake and also the disassociation of nitrogen.

It all stems back from the treatment for necrotizing fasciitis and gangrene.  With the first one of these – the flesh eating bacteria – the patient needs to be debrided before hyperbaric oxygen therapy. With gangrene you go first to the chamber and then surgery.  Remember that with the latter, gangrene can travel up a limb at 4 inches an hour. A single 2.6 atm treatment for 90 minutes at depth will stop it in its tracks.

With the next one – necrotizing fasciitis  – it is such a terrible assault on the human body where the flesh eating bacteria infiltrates all the way into the fascia of the skin.  You might recently remember the young lady who had both hands cut off and also her legs amputated because of this bacteria.  Her father said to the press that “the Lord had answered his prayers and that she was in good spirits.” The obscene thing about his comment was the fact that the surgeons who did all of the amputations also had a multi-place hyperbaric chamber in that same hospital.

However, to put a bunch of wound-care patients on hold while they salvaged this young lady’s limbs would’ve cost the hospital a large amount of money, since they were full of people that were insured or on Medicare and the payment was $2000 for each person.

Another factor was the fact that a 10 place chamber needs one or two inside attendants – usually nurses.  There is a a reluctance to take the chamber steeper than 60 feet of seawater since you would end up giving your expensive staff decompression illness – if you check the dive tables you will find that you can stay 60 minutes at 60 feet. After that you have to do decompression.  This mythology all started down in Panama City Florida when they used the same nurse for three separate diving accidents in the one day.  When she did not show for work the next day, the neighbors went to her house and found that she was stiff and cold in her bed and had died during the night.

To get around this problem, multi-place chambers now make their inside attendants have mandatory oxygen breathing during the treatments. When I was working at the University of Adelaide 25-odd years ago, we always took a nurse from whatever department the patient was coming from.  Remember that nitrogen has sharp teeth and loves fat – and since females carry more fat than males, we only ever dived a nurse one time each day.

So it really was no contest on the necrotizing fasciitis with the physicians and surgeons amputating and amputating and probably paid in excess of $150,000 each in a two-week period.  I have no doubts that the parents of this young lady still have to make regular weekly payments or declare bankruptcy.

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Why 90 minutes in the chamber?  Over the years we found that patients in a multi-place chamber – remember it is compressed on air – do not put hoods on until they reach the 60 foot mark and then they start breathing oxygen.  When you have a bunch of people in a chamber, all have different issues about how quickly they can get to depth.  So from door closure to door opening it is 90 minutes.  Keep in mind that all of these patients are going to be coming back for 40 treatments.

Using the latest equipment to measure oxygen and nitrogen – oxiometry – we find that the patient being treated at 2.6 atm saturates with oxygen at 90 minutes. Using transcutaneous O2 measurements during the treatment, the patient is saturated with oxygen within five minutes of reaching pressure in a Sands chamber.  Whereas a lot of the acrylic tube chambers take up to 15 minutes to reach 100% saturation within the chamber to get rid of the ambient room air.  If you kept the patient in the chamber for two hours, that patient would not have any more oxygen than they had at 90 minutes.

If I were to draw a graph it would be a bell-shaped graph on the pressurization side and on the depressurization side it would be a ski slope.  I would thoroughly recommend having your staff review the hyperbaric oxygen presentation which will explain this (see weblink below).

When the patient reaches depth, the whole deal is about the free radicals that are produced as nitrogen (approximately 2% of our body weight) is released.  The nitrogen turns into a number of different chemical components and it is those that do the hard work.

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What about the break in between treatments? Going back to our first two maladies, gangrene and necrotizing fasciitis, it is once again an affair of the wallet and those that claim that eight hours are needed between treatments are following the wrong path entirely – the path of reimbursement.

What we have found is this: a two hour break (at the most) allows for oxygen values to come back to normal and nitrogen to quickly rush back in and take up its 2% of our body fluids.

A lot of this mythology was reinforced by the Pope of hyperbaric’s – Dr. Paul Harch who actually patented what he called the Harch Protocol.  One of the things that you must understand is that why you would get results at lower pressures – say 1.6 atm for children twice each day,  it takes a lot longer and keeps them coming back for at least 40 days.

With all of the above, we find that whether it it is a mouse, rabbit, human or a horse, 2.6 atm is the appropriate treatment pressure.  That is not what I say by myself but comes from medical school in Pennsylvania and Prof. Stephen Thom.

Again, if you are new to hyperbarics I would recommend watching the presentation below that I narrated.  It really is worth the time – and should be part of the school work and retraining of all new staff.

I do hope that this helps you.

Part 2 – HBOT Science