Medical Hypotheses 4: 1. 37-39, 1978.
MECHANISMS
THOMAS Texas
OF DECUBITUS
A. KROUSKOP,
Institute
ULCER
FORMATION
NARENDER
for Rehabilitation
- AN HYPOTHESIS
P. REDDY,
and Research,
WILLIAM
A. SPENCER
1333 Moursund
Avenue,
AND JOHN
Houston,
W. SECOR,
Texas 77030,
U.S.A.
SUMMARY Understanding
of the etiology
contains
experimental
much
extensively tissue
to depriving
can remain
applied
pressures
studies
done
a tissue
viable that
been
formulated
thesis
states
that a major
accumulation
of anaerobic
formation
region
of blood.
In fact,
lengths
of time,
on lymph
is consistent
with
contributing
and the existing
is substantial
up to 13 hours,
and pressure
the published
data
to pressure
waste products
there
in a region.
propulsion
factor
metabolic
is fragmentary
with the idea that pressure
the blood microvasculature
laboratory
that
ulcer
for very extended
collapse
in this
of decubitus
data that are inconsistent
data
that
is due
illustrate
when subjected
clinical
sores is the tissue
and on
an hypothesis
observations.
necrosis
of the lymph
that
to externally
Based on these observations sore prevention,
and with
due to occlusion
literature
sore formation
has
The hypo-
that is caused by the vessels.
INTRODUCTION Decubitus
ulcers,
compressive of the spinai tary
localized
or shear
cord injured
and incomplete.
It has been
observations
recognized,
(1).
arising
are a major
Understanding
in lymphatic
the effects
of prolonged
to the comprehensive
of the mechanisms is to offer
or excessive rehabilitation
of their formation an hypothesis
is fragmen-
for these
mechan-
physiology.
of years,
area. However,
from obstacle
of this communication
for a number
of functioning accumulation
necrosis
on tissue,
patient
in the affected
are capable known that
acting
The purpose
isms based on recent
to necrosis
areas of cellular
forces
that occlusion
it is known
of blood
flow tc) a region
of tissue
leads
that certain
cell types, such as the epidermal cells, (2). In addition, it is in-vivo, and in-vitro
in prolonged absence of oxygen of metabolic waste products in a tissue region leads to cellular
necrosis.
There-
fore, it is hypothesized that the application of mechanical loads impairs the function of the contractile lymphatic system. Impairment of lymphatic function combined with changes in the blood microvascular system ation.
causes accumulation
of metabolic
PRESSURE A number
of reported
is primarily
or solely
servations are analyzed mental results emerges. Several anoxia,
observations
to occlusion the lymphatic
investigators (3-6), believe which is then manifested reference
lymphatic
clogging
external
pressures
to the lymphatic are associated causing
70mm
in the tissue
which
in turn leads to ulcer-
AND LYMPHATICS with the hypothesis
of the blood hypothesis,
microvasculature.
a more
consistent
that decubitus However,
forrnation
when
interpretation
these
ob-
of the experi-
that external pressure leads to vascular ischemia and widespread tissue by tissue necrosis. Husain (3) recorded that a threshold pressure of
1OOmm Hg. had to exist for two hours He made
INJURY
products
seem to be inconsistent
attributable under
waste
to produce
system,
the first signs of typical
noting
with decubitus Hg. of pressure
that during
ulcer formation. subcutaneously
37
edema,
decubitus
poor lymph
Kosiak for two
(4) observed hours
tissue breakdown. return
and possible
on rats’ legs that
led to the first micro-
scopic such
changes effect.
cause
indicative
signs of ulcers, to the pathology
inences
to insure
not mention
damage.
of 60mm
edema,
associated
with a bruise.
pressure
the possibility with
hypothesis
that the lymph
the pressures
(5) measured
that
system
between
pressure
distribution
and extravasation:
during
closure,
involved
Hg. had no
these
of pressure
did not
changes
over bony
are
prom-
Kosiak also stated
the periods
of disturbance.
that
He did
the pressures
he used to cause damage
about
Hg, and lend credence
in pressure
60mm
are
to the
sore formation.
in men in the prone
obtained from a calibrated bed of springs. the vicinity of 1OOmm Hg. and emphasized
of 30mmg
the skin and the bone.
however,
lymphatic
is directly
pressures
experiments
of metabolites
origins;
cause
infiltration,
He utilized
distribution
of lymphatic
Subcutaneous
Hg. for one hour on dog ischial tuberosities
cellular
is due to an accumulation
consistent
Lindan
did cause
a uniform
hyperemia
tissue
of pressures
but
similar reactive
of irreversible
The application
and sitting
positions,
using contour
maps
He established that the highest pressures at the skin are in the need for experimentation in this range. His animal ex-
periments with rabbit ears gave an initial breakdown pressure of approximately 60mm Hg. Rabbit ears have unusually large numbers of arteriovenous anastomoses and rich lymphatic beds. This anatomy explains the prolonged time periods, as long as 13 hours, needed to produce damage leading to necrosis in these ear tissues.
LYMPHATIC A growing
body
of evidence
a principal
factor
in lymph
sic contractions vestigators the
rhythms
of the smooth
(7-12)
frequency
muscle
of the contractions
of the concept
along the lymphatic
that
active contractility
network.
active
contractility
was found
investigations
(13-17)
of active contractility
and lymph
of the lymph
to be independent propulsion,
lymphatic
drainage
vessels
a theoretical
from
nodes.
A number
intestinal,
of in-
toward
and
and cardiac
basis for lymph
the periphery
is
is due to intrin-
in-viva and in-vitro,
of respiratory,
which establish
in lymph
of the lymphatics
Active contractility
in the walls of the lymphatics
have demonstrated
(7). In our recent
the importance
is supportive propulsion
CONTRACTILITY
propulsion,
the thoracic
duct
has been confirmed. Pressure
gradients
the capability inward
maintain
of actively
permeability
chemical
of the terminal
irritation
and this effect
cessive or prolonged that
are sufficient
pressure
muscle
amount
of metabolites
when
importance
for
periods
lymphatics diminishes
contractile exhausting
probably
of the
one considers
fluid materials
has been applied
to occlude
smooth
The
terminal transporting
lymph
occupy system
the complications
(7). Necrosis
contractile
increases
of metabolites
occurs
lymphatics
as high as 60mm
markedly
the concentration
which
have
Hg (7-18).
The
mechanical
or
in an area to which
ex-
only when surface
with
pressures
are applied
drainage
or to block the oxygenation of lymphatic Under these circumstances, toxic capabilities.
anaerobic
the intercellular in maintaining that
larger pressures
to metabolites
lymphatic their
into
against
can occur
space, and thus, the tissue poisons a viable during
tissue
edema.
environment There
itself.
is further
are many
types
affirmed of edema:
hydrostatic, proteinaemic, inflammatory or lymphedema, but in each of these conditions a relatively normal blood circulatory pattern exists, as well as a functional lymphatic system except for lymphedema. In this state the lymphatic system is no longer functional, and it is only in lymphedema that there is a tendency to develop tissue necrosis similar to that seen in decubitus ulcers.
CONCLUSION Thus, there is a broad spectrum of information supporting the notion that lymphatic insufficiency a major contribution to the formation of decubitus ulcers. In light of this, and as an example
38
makes of the
usefulness
of mathematical
modeling,
and agents
treatment
and prevention
of decubitus
ulcers.
of lymphedema
and other
pathological
treatment proteins
(19). Thus,
which
it is suggested
propulsion
break
it appears
down
that pharmacological
the interstitial Benzopyrones
of decubitus
ulcers,
understanding
of all the critical
parameters
involving
to study
and to continue
could
in decubitus
in the
used for the medical of interstitial
of benzo-pyrones
of models
lymphatic
be beneficial
high concentrations
the effectiveness
the development
involved
agents which enhance
metabolites
have been successfully
conditions
to be worthwhile
cal treatment
protein
in the clini-
which can provide
detailed
ulcer formation.
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