INTRODUCTION
Necrotizing fasciitis is a progressive,
generally rapidly spreading, inflammatory
pro-cess located in the deep fascia with
secondary necrosis of subcutaneous tissues
and skin. The speed of skin involvement
is directly related and proportional to
the thickness of the subcutaneous layer.
This necrosis manifests itself as an extensive
undermining of the skin and subcutis. As
a rule, the patient is seriously ill, septic
with a high fever. Current recommendations
for the treatment of necrotizing fasciitis
in human patients include aggressive surgical
debridement, broad-spectrum multiple antibiotic
therapy and adjunctive hyperbaric oxygen.
Hyperbaric oxygen (HBO) therapy is defined
as therapy in which the patient breathes
100% oxygen at a pressure greater than that
at sea level, that is, greater than one
atmosphere absolute (ATA).
CLINICAL REPORT
An approximately 8-month-old female kitten
was admitted to the hospital with an apparent
traumatic hernia of the left abdominal
wall. She was also pregnant. Two students
found her in the parking lot of their
apartment complex. They reported that
she had been seen in the area for a few
weeks and appeared normal the day before.
That same afternoon, she was taken to
surgery. At laparotomy, an OVH was performed
on a large gravid uterus. A 2 cm tear
in the dorsolateral abdominal wall was
found with duodenum and greater omentum
in the SQ space. A 1 cm tear in the duodenum
was apparent. Ingesta contaminated the
SQ space and the abdomen. After repair
and closure of the abdomen, the SQ site
was lavaged with the Betadine and a penrose
drain placed. The kitten was unexpectedly
painful the first two days post-operatively,
but improved on SQ fluids and Cefazolin.
By day 3, she was eating and grooming.
Six days post-op a necrotic area became
apparent near the site of the hernia.
A 20cm by 10cm area of se-vere skin, fat
and muscle necrosis was extensively debrided,
flushed and bandaged. Closure was impossible
because of the size of the defect and
the degree of infection. For pain associated
with the wounds and bandage changes, a
25ug Fentanyl patch was employed. Enrofloxacin
and Cefazolin were given every 12 hours.
Bandage changes occurred daily. The wound
was lavaged with Betadine or Chlorhexiderm
at each bandage change. A topical cephalosporin
was applied during bandage changes. A
second debridement was performed 3 days
later. At that time, the margins of the
wound extended from the scapula distally
to the inguinal region and from the dorsum
ventrally beyond the midline to the other
side of the abdomen, approx. 23 by 20
cm. (Figure 1) This extent of this wound
was about 40% of the trunk or axial area.
She was not expected to survive. On the
tenth day of hospitalization, hyperbaric
therapy began." All other treatments
were continued as described. She was placed
in a small plexi-glass induction chamber
commonly used in veterinary medicine with
inflow and outflow connections. (Figure
2) Each session, called a "dive",
lasted over one hour and took place at
2.36 atmospheres within the diving chamber.
100% oxygen was delivered into the chamber
and expired air passively evacuated from
the chamber. After 2 dives, a granulation
bed began to form. Evidence of purulence
dramatically diminished. Emphysema appeared
in both back legs due to air leakage from
the caudal ingui-nal margin of the defect.
Both back legs were wrapped in a cruciate
pattern integrated with the abdominal
wrap. All other therapy contin-ued. The
emphysema in her legs resolved as wound
contracture proceeded and adhesion of
the skin and SQ to the body wall began.
. Healing continued rapidly. After eight
days, the wound bed appeared increasingly
vascular and became more painful as nerve
endings surfaced. The ventral margins
of the wound began to bleed during bandage
placement. After 2 weeks, the wound bed
had contracted to 9 by 10 cm, approx.
1/5 the original size. After four weeks
of hyperbaric sessions, the dorsal margins
of the wound were apposed. Ventrally the
wound measured 8 by 2 cm. (Figure 3) Bandaging
was discontinued after one month. In all,
she dove in 32 separate ses-sions for
a total of 2430 minutes. A scar appeared
at the most central aspect of the wound
where the two wound margins apposed. It
is a thin line that travels from the dorsal
lumbar area beyond the mid-line. It is
approx. 5 mm wide at its widest point
and is the only part of her body where
far re-growth has not occurred.
Discussion
It is highly characteristic of necrotizing
fasci-it is that the spread of the fascial
necrosis is more extensive than the visible
changes of the skin. The apparently normal
skin and subcuta-neous tissue are loosened
from the underlying necrotic fascia over
a great distance from the original wound.
Skin necrosis is secondary to thrombosis
of subcutaneous blood vessels. In this
case, the subcutaneous layer was thin
and the skin became involved within 5
days. The kitten was extremely painful,
became less so and then very painful during
the first weeks of hyperbaric therapy.
Hyperbaric oxygen therapy can be ad-ministered
in an individual pressurized deliv-ery
chamber or in a multi-position chamber.
In this case, a chamber large enough to
accomo-date at least six humans was used.
Treatment regimens vary according to the
disorder. De-livery of 100% oxygen at
2.0 to 2.4 ATA is standard for adult human
patients. 2 Oxygen was delivered at 2.36
ATA, usually for 50 minutes with 15 minute
com-pression (before) and decompression
(after) phases. Breathing oxygen at this
pressure in-creases oxygen tension in
the capillaries that surround ischemic
tissue and promotes oxy-gen diffusion
from the capillaries to the tissue. Hyperbaric
oxygen provides a signifi-cant increase
in tissue oxygenation in the hy-poperfused,
infected wound. This elevation in oxygen
tension induces powerful positive changes
in the wound repair process. HBO directly
enhances fibroblastic replication, col-lagen
synthesis and the process of neovascu-larization
in ischemic tissue. By providing mo-lecular
oxygen at the cellular level it also in-creases
leukocyte bactericidal activity. The hyperoxic
conditions increase the production of
intracellular and extracellular oxygen-derived
free radicals in leukocytes and phagocytes,
enhancing the bacteriocidal ef-fects on
strict anaerobic organisms and some microaerobic
organisms. This can be roughly summarized
as stimula-tion of the host defense and
repair mecha-nisms. Hyperbaric oxygen
therapy is a useful technique in the management
of problem wounds in which hypoxia and/or
infection are the underlying etiologic
factors.
References:
Bakker, Jan Dirk, SelectedAerobic and
Anaerobic Soft Tissue Infections, Diagnosis
and the Use of Hy-perbaric Oxygen as an
Adjunct, in Hyperbaric Medi-cine Practice,
p. 396-417.
Hosgood, Elkins and Hill, "Hyperbaric
Oxygen Ther-apy: Mechanism and Potential
Applications", The Compendium of
Continuing Education, Vol. 12 No. 11,
1990, p. 1589-1593
Inquiries about therapy may be made to
the author or:
Western Hyperbaric, L.L.C.
Mr. Mitch Hoggard, President
3880 Morrow Ln., Suite 4
Chico Ca. (530) 894-3288
Matos and Nunez, Enhancement of Healing
in Se-lected Problem Wounds, in Hyperbaric
Medicine Practice, p. 590-611.
ABOUT THE AUTHOR:
Elizabeth Colleran is a 1990 graduate
of Tufts University School of Veterinary
Medicine. She completed a one year in-ternship
at Southshore Veterinary Asso-ciates before
moving to California. In 1996, she was
awarded a Master of Sci-ence degree in
Animals and Public Policy from Tufts University
School of Veterinary Medicine. She owns
Chico Hospital for Cats, an AAHA hospital
in Chico.
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