s-C5

Pathophysiology of infection - a theoretical approach

M. Hansis

Director, Klinik und Polikbnik fur Unfallchirurgie der Universitat Bonn, Sigmund-Freud-Str. 25, D-53103 Bonn

Summa+

The manifestation of postoperative wound infection the individual factors promoting infection, their
has a tri-factorial basis: the overall systemic trauma quantification, and their relative importance.
and the additional effects of premorbidity (age,
diabetes, etc.), the local host damage resulting from Keywords: postoperative wound infection, local host
both the accident and surgery, and the bacterial damage, bacterial inoculum, infection risk factors
contamination of the wound.
The first factor is only moderately open to
intervention, however, ,the amount of local host
Introduction
damage caused during the operation can be
influenced directly by the surgeon who must ensure
that his operating techniques are non-aggressive and The aim of this paper is on the one hand to summarize
in line with current knowledge. The factor of the current knowledge and generally accepted aspects of
intraoperative bacterial inoculum can be modified by the pathophysiology of posttraumatic infection and on
attention to hygiene. The latter two factors are in the other hand to articulate new, sometimes
direct relation to the following two hypotheses: provocative hypotheses and principles based on a
- Every wound is able to tolerate some local host theoretical model. The author is aware of the fact that
damage and some bacterial inocuhun without to some extent these hypotheses might lack correct
manifestation of infection. scientific evidence, although they are based on more
- The bacterial wound flora is the product of the than 15 years of infection assessment in the clinical
bacterial invasion force and the local wound traumatological setting. The intention of this initial
conditions. presentation during a “workshop” on “Implants and
The bacterial wound flora and the local condition of Infection” was to supply topics and material for a
the wound are interrelated. If either factor exceeds the controversial discussion on new approaches to
tolerable threshold, infection will become manifest, i.e. experimental research on the aetiology of implant
there will be an uncontrollable proliferation of related and posttraumatic infection.
bacteria. The level of this breaking point may depend
upon certain systemic host factors such as age,
diabetes, or immunodeficiency. Consequently, the The “imbalance” model
prevention of infection must focus simultaneously on Postoperative infections of bone and soft tissues are
minimizing the local bacterial inoculum and the result of both damage to the host and bacterial
optimizing local wound conditions. Future studies inoculation. Furthermore, systemic immunological
should concentrate on identifying the exact nature of defects, the presence of foreign bodies and possibly
allergic reactions to metal implants promote the
manifestation of infection (1-11). Fig. 1 shows a model
’ Abstracts in German, French, Italian, Spanish and to explain M-factorial infection genesis: Every wound
Japanese are printed at the end of this supplement.
 S-C6

is able to tolerate some local host damage and some
bacterial inoculum as well. As soon as one of these
factors or both of them become too great, this will
cause an imbalance and the threshold to manifestation
of an infection is exceeded. This threshold marks the
moment at which low grade, controlled contamination
changes to out of control, explosive, exponential
bacterial growth. But this model also leaves some
questions open:
- determining the breakpoint of uncontrolled
growth,
Principles of local host damage
The greater part of infections are not caused by lack
of hygiene but by severe local host damage
Infections in our clinic were followed up over a period
of 15 years in order to find out whether extensive local
host damage could be established as a major cause of
infection. In 51 of 74 cases, local host damage was
observed to be the main cause of infection. Lack of
bacterial hygiene, on the other hand, was the obvious main
cause of infection in only 13 of the 74 cases (Table 1).

Table 1: Main factors for genesis of postoperative

- when or whether this threshold shifts depending on
infection (n = 74 infections).
the age of the patient or pre-existing conditions, e.g.
diabetes, etc.,
Factor Infections (n) after
- how to grade such a scale: How can the local host
damage be measured (12,13)? CDC I* CDC II

- how important the external bacterial inoculum Local host damage 24 27

(from the accident) is in relation to the hospital Lack of hygiene 13 10
bacterial inoculum (perhaps due to hygienic
deficiencies). The same questions have to be * CDC - Center of Disease Control
addressed with reference to the local host damage Classification of initial bacterial contamination of wounds:
directly due to the trauma, - CDC I - clean; no bacterial contamination
- CDC II - contaminated, but not infected
- and especially, the relative importance of these two
parameters to each other: Is the two-fold bacterial
Reduction of local host damage will lower the
inoculum as important as two-fold local host
infection rate even under less than optimal hygienic
damage? Or should the inoculum be recorded
conditions
logarithmically and the host damage linearly? Or
vice versa? In the 1960s and 7Os, infection occurred after open
fracture in about 40% of cases. Nowadays the
infection rate after open fracture is down to about 5 -
A 7% (14-16). There have not been particular
improvements in hygienic techniques or antibiotic
regimes, but operating techniques have changed.
These include, for example, a change from closed
wound treatment to open wound treatment, from late
soft tissue reconstruction to early soft tissue
reconstruction, and especially from primary internal
fixation to primary external fixation.
The same can be seen in the plating of closed tibia1
Preexisting morbidity
systemic host damage fractures. For these fractures, there was an infection
rate of about 15% or more in the early 1980s which can
Quantity and virulence of bacteria
be compared with the present rate of about 2%. The
advantage here was gained by a departure from
anatomical reconstruction and the subsequent
Fig. 1: Pathophysiology of infection: The multifactorial development of biological bridging techniques.
aetiology depends on the local host damage, i.e.
reduction of defence capacity due to accident or
surgery (y-axis) and the bacterial inoculum (x-axis). If Principles of bacterial wound flora
either factor exceeds the threshold, uncontrolled
Most aseptic wounds will be contaminated
bacterial growth will cause the manifestation of
infection. The systemic condition of the organism (e.g. Theoretically, the so-called aseptic wounds are
premorbidity, age, diabetes, etc.) influences the contaminated. In the aseptic wounds, the bacterial
threshold level as an additional, third factor. density might only be so low that it cannot be proven
with normal techniques. This would mean that, in
principle, there is only a quantitative difference
Hansis: Pathophysiology of infection s-C7

between wounds classified as CDC I and CDC II. c. The evaluation of the microbiological monitoring of
Asymptomatic contamination in aseptic wounds our own patients (18) revealed two particular types
seems to increase the risk of an infection becoming of bacterial flora: Those associated with the
manifest. endoprosthesis (predominantly coagulase negative
staphylococci) and those in wounds to the hands
(predominantly i3-haemolytic streptococci).
Primary bacterial inoculum and infectious flora after
According to the literature, the preference of
open fractures are usually not identical
coagulase negative staphylococci for
A follow-up of 105 open fractures indicated that the endoprostheses can not only be explained by the
flora of the so-called complication wound inevitably phenomenon of special bacterial adherence (20).
alters in the hospital within the first 10 days. (17,18). Our endoprostheses only have a small plastic
In 60% of these wounds the primary inoculum surface and these special flora were not found on
consisted of multiple pathogenic and non-pathogenic other plastic implants. The preference of
germs. In 90% (n=55) of these initially contaminated streptococci for hand wounds can probably be
wounds the initial bacterial flora changed within the understood with reference to the anatomy of the
first 10 days to a bacterial flora typical for the hospital. hand which does not permit the formation of
Only in 3 out of 9 patients of this group, who became abscesses but rather phlegmonas.
infected, were the infectious flora identical to the
germs isolated initially on the day of injury. Patients d. Most interesting are the coagulase negative
normally seem to acquire the typical hospital flora. If staphylococci, especially S. epidermidis (21). Their
an infection becomes manifest later, it will generally variable pathogenicity might not alone be explained
be the result of infectious agents from within the by reference to the adherence theory or by different
hospital and not of those brought in from outside. biochemical classification and characteristics of the
sub-types (22). A reliable differentiation between
pathogenic and non-pathogenic strains so far seems
Interaction between local bacterial flora and local
to be impossible. The idea that the local host
wound quality
conditions and the quality of a wound might induce
From clinical experience those cases can be recognized the conversion of coagulase negative staphylococci
in which the wound itself seems to determine or from non-pathogenic to pathogenic characteristics
influence its bacterial flora and the virulence of the has at least to be considered.
microorganisms. Is it in consequence justified to state
that the quality of the wound and the type of
inoculum influence each other or that they exist in a
fluid balance or, more simply, “every wound gets the Conclusions
flora it deserves”? Some of our own observations
seem to underline this hypothesis: Postoperative wound infections have a t&factorial
basis; local host damage due to surgical technique can
a. In infected wounds usually the bacterial flora be influenced immediately by the physician, i.e. by
remains constant over the whole course of placing great emphasis on good operating technique.
treatment and does not change in spite of local The intraoperative bacterial inoculum is also easily
decontamination or systemic antibiotics. The influenced by good hygienic technique. Both these
microbiological situation does not change even if factors correlate with the following two hypothesis:
the patient is moved to another hospital or in the
outpatient environment. In 25 patients with chronic - Every wound is able to tolerate some local host
bone or soft tissue infections we only documented a damage and some bacterial inoculum without
change of the microbiological flora after improving manifestation of infection.
the local host conditions by surgical debridement
and excision of necrotic tissue (18). Without any - The bacterial wound flora is the product of bacterial
further antibiotic measures the improved vitality of invasion forces as well as local wound conditions.
the wound caused a change or even the
disappearance of germs. Knowledge is still lacking on the following points:

b. Anaerobics (Clostridium, bacteroides and - details of the individual influencing factors

peptostreptococci) are usually only found, except - the possibility for their quantification and
for fresh open wounds immediately after the - exact knowledge about their relative importance
accident, in old, dirty and surgically insufficiently
treated wounds. Anaerobics in an infected wound
are, in our opinion, always a sign of inadequate
wound treatment and surgical debridement (19).

Injury 2996, Vol. 27, Suppl. 3

 S-C8

References 20. Peters G, Locci R, Pulverer G. Adherence and growth of

coagulase-negative staphylococci on the surface of
intravenous catheters. J. Inf. Dis. 1982;146:479-482.
1. Arens St, Schlegel U, Printzen G, Perren SM, Hansis M. 21. Hansis M, Weller S. Staphylococcus epidermidis als
Infection resistance of implant materials for DCP: Infektionserreger in der Unfallchirurgie. Infection 1984;
Experimental study in the rabbit. J. Bone J. Surg. (Br.) 12~342-344.
1996;78-B:647-51
22. Hansis M. Die Bakteriologie in der Unfallchirurgie. Eine
2. Cruse PJE. Some Factors determining wound infection: umfassende Analyse mikrobiologischer Vorglnge in
A prospective study of 30,000 wounds. In: Polk HC, einer Unfallchirurgischen Klinik unter besonderer
Stone HH (eds). Hospital-acquired infections in surgery. Beriicksichtigung von Staphylococcus aureus und
Baltimore London Tokyo: University Park Press, 1977. koagulase-negativer Staphylokokken. Klinische und
3. Dillin L, Slabaugh I’. Delayed wound healing. J. Trauma mikrobiologische Studie. Postdoctoral thesis, Tubingen,
1986;26:1116. 1987.
4. Elek SD, Conen PE. The virulence of staphylococcus
pyogenes for man. Brit.J.Exp.Path. 1957;38:573-581.
5. Gil-Egea MJ et al. Surgical wound infections. Inf.
Control 1987;8:277-280.
6. Hierholzer S, Hierholzer G. Allergie gegen metallische
Implantate. Hefte Unfallheilk. 1984;164:498.
7. Hopfer F. Der EinfluB des Alters auf die Haufigkeit
postoperativer Wundinfektionen. Zentralbl. Chir. 1988;
113:968.
8. Lau WY et al. Influence of surgeons experience on
postoperative sepsis. Am. J. Surg. 1988;155:322-326.
9. Lilienfeld DE, Vlahov D, Tenney JH, MC Laughlin JS.
Obesity and diabetes as risk factors for postoperative
wound infections after cardiac surgery. Am. J. Infect.
Control. 1988;16:3.
10. Nagachinta T, Stephens M, Reitz B, Polk BF. Risk factors
for surgical wound infection following cardiac surgery.
J. Infect. Dis. 1987;156:967.
11. Simchen E, Raz R. Risk factors for infection in fracture
war wounds. Military Medicine 1991;156:520-527.
12. Hansis M, Siebert CH, Arens St. Versuch einer
Bewertung (“Scoring”) posttraumatischer bzw. post-
operativer Infektionen an Knochen und Weichteilen. In:
Kienzl et al. (ed.). Diagnostik und Therapie der
posttraumatischen Osteitis. Hefte zu “Der Unfall-
chirurg”, Berlin Heidelberg: Springer, 1995;255:249-254.
13. Siebert CH, Arens St, Hansis M. The role of surgical
trauma in the aetiology of postoperative wound
infections - Quantification of surgery-induced trauma.
Hyg. Med. 1995;20:474-480.
14. Hansis M, Arens St, Wingenfeld C. Infektionsraten in
der Unfallchirurgie - Eine Ubersicht anhand der neueren
deutschsprachigen Literatur (in press).
15. Hontzsch D, Weller S, Engels C, Kaiserauer S. Der
Verfahrenswechsel vom Fixateur exteme zur
Marknagelosteosynthese an Femur und Tibia. Akt.
traumatol. 1993;23 (Sonderheft):21.
16. Nast-Kolb D, Betz A, Schweiberer L. Der Wandel der
Unfallchirurgie der letzten 10 Jahre - ein Beitrag zur
Infektionsprophylaxe. Chirurg 1991;62:846.
17. Hansis M. Keimbesiedlung und Keimwechsel in der
Verletzungswunde bei frischen offenen Frakturen.
Langenbeck’s Archiv fur Chirurgie 1984;364:305-307.
18. Hansis M. Wundinfektionen in der Unfallchirurgie.
mhp: Wiesbaden, 1990.
19. Straub DAF. Anaerobierinfektionen in der Unfall-
chirurgie. Doctoral thesis, Tubingen, 1994.