Fractures with Soft Tissue Injuries

174 Pages·1984·10.16 MB·English

by  H.-J. Oestern, H. Tscherne (auth.), Prof. Dr. Harald Tscherne, Prof. Dr. Leo Gotzen (eds.)

Fractures with
Soft Tissue Injuries
Edited by
H. Tscheme and L. Gotzen
With 107 Figures
Springer-Verlag
Berlin Heidelberg New York Tokyo 1984
Prof. Dr. Harald Tscherne
Medizinische Hochschule, Unfallchirurgische Klinik
Postfach 610180, D-3000 Hannover 61
Prof. Dr. Leo Gotzen
Medizinische Hochschule, Unfallchirurgische Klinik
Postfach 610180, D-3000 Hannover 61
Translator: Terry C. Telger, 3054 Vaughan Avenue, Marina,
CA 93933/USA
Title of the original German edition: Fraktur und Weichteilschaden
© Springer-Verlag Berlin Heidelberg New York Tokyo 1984
ISBN-13 :978-3-540-13082-6 / 0-387-12095-5
ISBN -13: 978-3-540-13082-6 e-ISBN -13: 978-3-642-69499-8
001: 10.1007/978-3-642-69499-8
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Preface
Progress in medical science, and the deeping of physician experience in general, make
continuing education a fundamental obligation on the part of the practicing physician.
Besides academies of advanced medical training, we feel that medical schools and uni
versities offer a particularly good setting for continuing medical education.
When the Hannover Medical School established West Germany's fIrst Department of
Trauma Surgery in 1970, we committed ourselves to this goal and instituted the Hannover
Trauma Seminars as a regional forum for continuing physician education. Made up almost
entirely of our colleagues at the Trauma Surgery Clinic, the basic goal of the seminars is
to review new discoveries and techniques in the fIeld of traumatology and assess their
practical relevance to the physician who treats trauma victims. In addition to research, the
experience ofthe Hannover School of Trauma Surgery form an important basis for seminar
activities.
The fIrst Trauma Seminar was held on February 2, 1972. Initially, copies ofthe proceed
ings were simply distributed to all interested participants. But as attendance grew and
demand for the proceedings increased, it became necessary to seek a broader form of
publication. Henceforth, the Hannover Trauma Seminars will be published as part of the
Topics in Traumatology series. For this we are grateful to Springer Verlag and to series
editors Jorg Re~ and Leonhard Schweiberer.
The current issue deals with fractures and associated soft tissue injuries. These common
and often severe lesions are seen in a large percentage of multiple trauma patients, and they
can be quite troublesome in terms of management. A thorough understanding of indica
tions and therapy is needed in order to avoid infection and achieve a good end result.
The many problems posed by this type of injury are addressed in 11 papers, each of
which supplements the others in points emphasized, yet is distinct in terms of this content.
Clinical aspects are preceeded by a discussion of the pathophysiology of soft tissue trauma.
This forms the basis for a new, clinically-oriented classifIcation system which takes special
account of closed fractures with soft tissue injury.
The general management of open fractures is explained, drawing upon techniques that
have been successfully practiced at our center. The handling of open fractures at the
accident scene and in the hospital, diagnostic procedures, preparations for surgery, and
operative treatment are discussed in some detail. The special problems of closed fractures
with soft tissue injury are addressed in a separate paper.
Much space has been devoted to the tibial region on account of its peculiar anatomy,
the prevalence of tibial injuries, and the frequent severity of the trauma. The indications
for operative fIxation are outlined, and procedural details are given for various types and
localizations of osseous and soft tissue injury.
The compartment syndrome is one of the most frequent and severe complications of
fractures with soft tissue injury, yet its importance has not been fully appreciated in clinical
VI
practice. A separate paper is devoted to the etiology, pathophysiology, diagnosis and treat
ment of this condition so that the serious consequences of its neglect or delayed recognition
may be avoided.
Sound postoperative management is an integral part of total patient care. Early compli
cations are frequent and require prompt, judicious intervention. The successful treatment
of fractures with soft tissue injury depends largely on the nature and extent ofthe damage
to soft tissue structures. Isolated bone fragments, even if securely fIxed, will eventually
succomb to necrosis and predispose to infection. In this situation, plastic procedures to
achieve soft tissue coverage are mandatory. Another paper addresses the currently accepted
indications for the replantation of amputated and partially amputated members, the tech
niques utilized, and the results that can be achieved.
It is hoped that, given the necessarily limited scope of this booklet, we have provided a
useful addition to the trauma literature that will aid the physician in solving the many
problems that arise in the treatment of fractures with associated soft tissue injury.
Hannover, February, 1983 H. Tscherne and L. Gotzen
Table of Contents
H.-J. Oestern and H. Tscherne
Pathophysiology and Classification of Soft Tissue Injuries Associated
with Fractures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1
H. Tscherne
The Management of Open Fractures. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 10
M. Rojczyk
Results of the Treatment of Open Fractures, Aspects of Antibiotic Therapy 33
H. Tscherne and M. Rojczyk
The Treatment of Closed Fractures with Soft Tissue Injuries. . . . . . . . . . . . . . . . 39
L. Gotzen and N. Haas
The Operative Treatment of Tibial Shaft Fractures with Soft Tissue Injuries 46
V. Echtermeyer, H. Tscherne, H.-J. Oestern, and E. van der Zypen
Compartment Syndrome: Etiology, Pathophysiology, Anatomy, Localization,
Diagnosis and Treatment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 75
D.Rogge
External Articular TransflXation for Joint Injuries with Severe Soft
Tissue Damage . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 103
E.G. Suren
Guidelines for the Postoperative Management of Fractures with Severe
Soft Tissue Injuries . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 118
G.Muhr
Early Complications of Fractures with Soft Tissue Injuries . . . . . . . . . . . . . . . . . 131
A. Berger
The Plastic Repair of Large Soft Tissue Defects 139
A. Berger
Replantation Surgery: Indications and Limitations 149
Subject Index ....................•......................... 163
List of Contributors
Prof. Dr. A. Berger, Klinik fur Hand-, Plastische- und Wiederherstellungschirurgie im
Krankenhaus Oststadt, Medizinische Hochschule, D-3000 Hannover 51
Dr. V. Echtenneyer, Unfallchirurgische Klinik, Medizinische Hochschule,
D-3000 Hannover 61
Priv.-Doz. Dr. N. Haas, Unfa1lchirurgische Klinik, Medizinische Hochschule,
D-3000 Hannover 61
Prof. Dr. G. Muhr, Chirurgische Klinik, Berufsgenossenschaftliche Krankenanstalten
"Bergmannsheil", D-4630 Bochum
Priv.-Doz. Dr. H.-J. Oestern, Unfallchirurgische Klinik, Medizinische Hochschule,
D-3000 Hannover 61
Dr. D. Rogge, Unfa11chirurgische Klinik, Medizinische Hochschule, D-3000 Hannover 61
Dr. M. Rojczyk, Chirurgische Abteilung, Agnes-Karll-Krankenhaus, D-3011 Laatzen
Priv.-Doz. Dr. E.-G. Suren, Unfa1lchirurgische Klinik, Medizinische Hochschule, D-3000
Hannover 61
Prof. Dr. E. Van der Zypen, Anatomisches Institut der Universitat, CH-3012 Bern
Pathophysiology and Classification of Soft Tissue Injuries
Associated with Fractures
H.-J. Oestem and H. Tscheme
I. Pathophysiology of Soft Tissue Injuries
The local response to a soft tissue injury has two basic aims:
1. closure of the wound to avoid excessive water and heat loss, and
2. prevention of infection.
1. Local Response to Hemorrhage
All injuries are characterized by some degree of tissue damage and extravasation. Immedi
ately following injury to a blood vessel, platelets bind to collagen and release their phopho
lipids, which stimulate the intrinsic coagulation mechanism. Injured tissue cells release
thromboplastin, which activates the extrinsic coagulation mechanism.
Platelet adhesion and aggregation lead to the deposition of platelet factor N and
vasoactive amines. Prostaglandin metabolites such as thromboxan A are also secreted, thus
augmenting the vasoconstriction produced by the increased amounts of glucocorticoids and
catecholamines that are released in response to the trauma.
The vasoconstriction combined with closure of the vessels by the coagulation mechanism
creates a hypoxic state in the wound area, leading to acidosis. The proteolytic enzymes
released by the aggregating platelets activate the complement system and liberate chemo
tactic substances which "attract" intlammatOlY cells, mainly granulocytes (and later mono
nuclear round cells), to the wound area.
2. Resistance to Infection, Phagocytosis
The function of the macrophages is to inhibit and kill contaminating bacteria, as well as
to remove cellular debris from damaged tissue.
Recent investigations suggest that local macrophages playa nutritional role by function
ing as the "digestive tract" of the wound. It is also reported (Leibovich, Ross 1975) that
macrophages (1) debride injured tissue, (2) process macromolecules to amino acids and
sugar, (3) attract other macrophages, (4) signal for further fibroblast replication, (5)
stimulate the formation of new blood vessels, and (6) secrete lactate.
Once a neutrophilic granulocyte reaches the damaged tissue, further steps in the phago
cytic defense mechanism are initiated. These processes are facilitated by humoral factors
called opsonins.
2
The main components of this system are immunoglobulin G antibodies, which bind to
the surface of the bacterium, as well as heat-labile factors which belong to the complement
and properdin system and further stimulate this process.
The heat-labile systems fIX fragments of complement 3 to the microbial surface via the
classic antigen-antibody activated Cl, C4, C 2 complement way or via the alternative C3
activation pathway (Gigli, Nelson 1968; Johnston et al. 1969). The opsonins ftx the
bacterium to the cell wall by combining with receptor molecules on the surface of the
phagocyte. Once the phagocyte has ftxed the microbe to its surface, it engulfs it with its
pseudopodia and digests it.
3. The Importance of Oxygen
Phagocytosis initiates several metabolic processes in the neutrophils that are necessary for
their function.
Within seconds after the material is ingested, oxygen consumption within the phagocyte
rises to 15-20 times the basal value (Baldridge 1933).
In normal phagocytes, some of the oxygen is enzymatically reduced to superoxide.
Superoxide is an unstable molecule that has shown bactericidal activity against clostridia
and other organisms which lack the superoxide dismutase that converts superoxide to
hydrogen peroxide (Babior 1973). Superoxide is quickly reduced to hydrogen peroxide
in the phagosome. Hydrogen peroxide directly kills certain organisms (Kamovsky 1963),
and in the presence ofmyoloperoxidase (MPO and chlorine ions), its antimicrobial activity
is greatly increased.
Fibroblast and leukocyte function are depressed by hypoxia (Hunt, Pai 1972; Hunt
1974; Mandell 1974; Hunt et al. 1975). Studies by Hohn et al. (1976) have shown that the
number of Staphylococcus aureus organisms killed by leukocytes in vitro and in experi
mental animal wounds increases as the local oxygen tension is raised. From this and other
research, it has become clear that soft tissue injuries in hypoxic areas heal poorly. Ischemic,
dessicated tissue cannot be adequately perfused and so is exceedingly susceptible to infection.
Moreover, granulocytes and macrophages have only a limited capacity for phagocytosis.
If they exhaust that capacity by ingesting too much necrotic tissues, their microbicidal
capacity is markedly reduced. Hence, extensive debridement with removal of all necrotic
tissue is a highly effective means of preventing infection.
4. Humoral Mechanisms of Wound Heating
Other substances released in response to tissue injury are mitogenic substances, hydrolases,
chemotactic agents, histamine and prostaglandins.
The mitogenic substances released by the platelets and damaged tissue promote ftbro
blast replication and protein biosynthesis.
The hydro lases break down cell debris to soluble and diffusible substances. This enzym
atic breakdown in tum yields mitogenic and chemotactically active substances which
stimulate phagocytosis. However, these materials are rapidly degraded and inactivated by
progression of the enzymatic reaction.