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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Krouskop patients.

TA, Harrison

JM, Leavitt

p 136 in Devices

University,

Philadelphia,

LA, Carter

and Systems

RE. Pressure

for the

Disabled.

Clark WA. The Tissues of the Body. Oxford

3. Husain

J. An experimental

study

of some pressure

J. Path. Bact. 66: 347-358,

4. Kosiak M. Etiology 5. Lindan

of decubitus

0. Etiology

6. Dinsdale

SM. Decubitus

7. Taylor

wheelchair

bound Temple

University effects

Press, London, on tissue,

1971.

with reference

to the bed-sore

1971.

ulcers. Arch. Phy. Med 42: 19-29, 1961.

of decubitus

Phys. Med. 54: 51-56,

under

and R. Zuckerman.

April 1975.

2. LeGros problem.

distribution

E. Kwatny

ulcers

ulcers:

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in swine:

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light and electron

Arch. Phys. Med. 42: 774-783,

microscopy

study

1961.

of pathogenesis

Arch.

1973.

GW. Contractility

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15. Reddy NP, Krouskop TA, Newell, Jr. PH. Development sion. Lymphology 8: 105-109, 1975. 16. Reddy NP, Krouskop TA, Newell, Jr. PH. A note terminal lymphatics. Micro. Res. 10: 214-216, 1975.

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JM. Lymphatics,

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model

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Complex.

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of a lymphatic

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occlu-

through

the

Comp.

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12:

in

1970.

Mechanisms of decubitus ulcer formation--an hypothesis.

Medical Hypotheses 4: 1. 37-39, 1978. MECHANISMS THOMAS Texas OF DECUBITUS A. KROUSKOP, Institute ULCER FORMATION NARENDER for Rehabilitation...
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