Minimally Invasive Plate Osteosynthesis E-Book

Suthorn Bavonratanavech

• Herausgeber: Thieme
• Kategorie: Fachliteratur
• Serie: AO-Publishing
• Sprache: Englisch

Seitenzahl: 1318

Veröffentlichungsjahr: 2023

Beschreibung

A practical hands-on manual for surgeons of all levels, the Minimally Invasive Plate Osteosynthesis, Third Edition is a crucial guide to managing fractures using the minimally invasive plate osteosynthesis technique. Expanding on the foundations set by the previous editions, this new issue will be of substantial value to any surgeon, boosting excellent fracture healing and functional outcomes, while minimizing complications.

The minimally invasive surgical techniques are presented in a systematic, case-based format covering fractures of the upper and lower extremity and pelvic/acetabular injuries. This new third edition provides step-by-step coverage on managing a broad spectrum of injuries from acute fractures to nonunion/malunion. While a single case can be approached through various methods, this new book seeks to impart fundamental guidelines and indications for applying minimally invasive procedures.

New third edition focuses on:

• General principles in minimally invasive plate osteosynthesis
• Clinical and radiographic evaluation
• Decision-making and options
• Preoperative planning
• Surgical approaches
• Tips and pitfalls to avoid complications
• Postoperative rehabilitation

Key features include:

• Contributions from 68 expert surgeons from 14 countries
• More than 50 cases on a comprehensive range of fractures
• More than 487 high-quality illustrations and 2647 images

www.aotrauma.org

Leseprobe

Suthorn Bavonratanavech, Reto Babst, Chang-Wug Oh

Minimally Invasive Plate Osteosynthesis

Third Edition

Hazards

Great care has been taken to maintain the accuracy of the information contained in this publication. However, the publisher, and/or the distributor, and/or the editors, and/or the authors cannot be held responsible for errors or any consequences arising from the use of the information contained in this publication. Contributions published under the name of individual authors are statements and opinions solely of said authors and not of the publisher, and/or the distributor, and/or the AO Group.

The products, procedures, and therapies described in this work are hazardous and are therefore only to be applied by certified and trained medical professionals in environments specially designed for such procedures. No suggested test or procedure should be carried out unless, in the user‘s professional judgment, its risk is justified. Whoever applies products, procedures, and therapies shown or described in this work will do this at their own risk. Because of rapid advances in the medical sciences, AO recommends that independent verification of diagnosis, therapies, drugs, dosages, and operation methods should be made before any action is taken.

Although all advertising material which may be inserted into the work is expected to conform to ethical (medical) standards, inclusion in this publication does not constitute a guarantee or endorsement by the publisher regarding quality or value of such product or of the claims made of it by its manufacturer.

Legal restrictions

This work was produced by AO Foundation, Switzerland. All rights reserved by AO Foundation. This publication, including all parts thereof, is legally protected by copyright.

Any use, exploitation or commercialization outside the narrow limits set forth by copyright legislation and the restrictions on use laid out below, without the publisher‘s consent, is illegal and liable to prosecution. This applies in particular to photostat reproduction, copying, scanning or duplication of any kind, translation, preparation of microfilms, electronic data processing, and storage such as making this publication available on Intranet or Internet.

Some of the products, names, instruments, treatments, logos, designs, etc referred to in this publication are also protected by patents, trademarks or by other intellectual property protection laws (eg, “AO” and the AO logo are subject to trademark applications/registrations) even though specific reference to this fact is not always made in the text. Therefore, the appearance of a name, instrument, etc without designation as proprietary is not to be construed as a representation by the publisher that it is in the public domain.

Restrictions on use: The rightful owner of an authorized copy of this work may use it for educational and research purposes only. Single images or illustrations may be copied for research or educational purposes only. The images or illustrations may not be altered in any way and need to carry the following statement of origin ”Copyright by AO Foundation, Switzerland”.

Check hazards and legal restrictions on www.aofoundation.org/legal

Copyright © 2022 by AO Foundation, Clavadelerstrasse 8, 7270 Davos Platz, Switzerland

Table of contents

Foreword

Preface

Acknowledgment

Contributors

1

History and evolution of minimally invasive plate osteosynthesis

2.1

Basic mechanobiology of bone healing and biomechanics of fracture fixation

2.2

Cerclage wiring as a reduction technique

3

Instruments

4

Implants

5

Intraoperative imaging

6

Reduction techniques

7

Decision making and preoperative planning

8

Preoperative and postoperative management

9

Complications and solutions

10

Minimally invasive plate osteosynthesis and evidence-based medicine

11.1

Clavicle: introduction

11.2

Clavicle: bilateral comminuted diaphyseal fractures—15.2C

11.3

Clavicle, shaft: fragmentary spiral fracture—15.2C

11.4

Clavicular fracture—15.2C

11.5

Clavicle, shaft: long oblique fracture—15.2A

12.1

Scapula: introduction

12.2

Scapula: MIPO case

12.3

Scapula: minimal invasive scapula fixation

13.1

Humerus, proximal: introduction

13.2

Humerus, proximal: extraarticular fracture—11A3

13.3

Proximal humeral shaft fracture with extension into the humeral head—12B2.1

13.4

Humerus, proximal fracture 4-part, valgus malalignment—11C

14.1

Humerus, shaft: introduction

14.2

Humerus, shaft: wedge fracture, bending wedge—12B2

14.3

Distal one-third fracture of humerus: multifragmentatry fracture—12B3

14.4

Humerus, shaft: complex fracture, irregular—12B3

14.5

Humerus, shaft: lower third—12B

15.1

Forearm: introduction

15.2

Forearm—multifragmentary proximal one-third ulnar fracture (Monteggia fracture)— 2U2B3.a

15.3

Forearm: diaphyseal fractures

15.4

Forearm: comminuted distal one-third radial fracture (Galeazzi fracture)—2R2B3 (g)

15.5

Forearm: distal radial fracture with dislocation—2R3B2.3

16

Pelvis and acetabulum: introduction

16.1A

Pelvic ring fractures

6.1B

Acetabular fractures

16.2

Unstable 61C pelvic ring injury in an elderly patient with complete and bilateral posterior and anterior fractures

16.3

Pelvis, acetabulum: a displaced high anterior column fracture of the left acetabulum—62A3

16.4

Pelvis, acetabulum: minimally displaced left anterior column posterior hemitransverse acetabular fracture—62B2, and associated right pelvic ring injury with right sacral fracture and bilateral superior and inferior rami fractures—61B2

16.5

Pelvis, acetabulum: both-column acetabular fracture—62C1

17.1

Femur, proximal: introduction

17.2

Femur, proximal: extraarticular fracture, intertrochanteric—31A3

17.3

Femur, proximal: extraarticular fracture, trochanteric area pertrochanteric simple—31A1

17.4

Femur, subtrochanteric, multifragmentary—32B3.1

17.5

Femur, proximal: extraarticular fracture, intertrochanteric—31A3 and wedge subtrochanteric fracture—32B2.1

18.1

Femur, shaft: introduction

18.2

Femur, shaft: wedge fracture, fragmented wedge—32B3

18.3

Femur, shaft: wedge fracture, comminuted wedge—32B3

18.4

Femur, shaft: segmental fracture—32C2

19.1

Femur, distal: introduction

19.2

Femur, distal: periprosthetic fracture—V.3-B1

19.3

Femur, distal: intraarticular fracture—33C2

19.4

Femur, distal: intraarticular simple fracture—33C1

19.5

Femur, distal: intraarticular fracture—33C3

19.6

Femur, distal—33C3

20.1

Tibia and fibula, proximal: introduction

20.2

Tibia and fibula, proximal: metaphyseal simple fracture—42A2

20.3

Tibia and fibula, proximal: intraarticular bicondylar fracture with a nonimpacted, metaphyseal component—41C3 with diaphyseal involvement

20.4

Tibia and fibula, proximal: intraarticular bicondylar fracture, no metadiaphyseal involvement—41C3

20.5

Tibia and fibula, proximal—42A

21.1

Tibia and fibula, shaft: introduction

21.2

Tibia, shaft: complex fracture—42C3

21.3

Tibia and fibula, shaft: simple fracture, transverse—42A2

21.4

Tibia and fibula, shaft: wedge fracture, spiral wedge—42B3

21.5

Tibia, shaft: complex fracture—42C2

22.1

Tibia and fibula, distal: introduction

22.2

Tibia and fibula, distal: torsional wedge fracture of the distal tibia with posterolateral articular extension—42B2 in combination with a multifragmentary fracture of the distal fibula—44C2

22.3

Tibia and fibula, distal: intraarticular simple fracture of the distal tibia—43C1 with simple fracture of the distal fibula

22.4

Tibia and fibula, distal: intraarticular complex fracture of the distal tibia—43C3 with simple fracture of the distal fibula

22.5

Tibia and fibula, distal: extraarticular multifragmentary distal tibial fracture—43A3 in combination with a multifragmentary distal fibular fracture

23.1

Calcaneus: introduction

23.2

Bilateral calcaneal fracture—82B1 (tongue type), Sanders type II

23.3

Displaced, intraarticular calcaneal fracture—82C2: surgical treatment with minimally invasive plate osteosynthesis via sinus tarsi approach in Sanders type III fracture

24.1

Pediatric fractures: introduction

24.2

Tibia and fibula, shaft: simple fracture, oblique—42A3

24.3

Tibia and fibula, shaft: simple fracture, transverse—42A3

24.4

Femur, shaft: simple fracture, transverse—32A3

24.5

Femur, shaft: unstable fracture—32D5.1

25.1

Minimally invasive plate osteosynthesis in periprosthetic fracture management

25.2

Periprosthetic fracture: total knee replacement case, femur—3[V]B1

25.3

Periprosthetic fracture: total hip replacement case—32A1(c)

25.4

Periprosthetic fracture: interprosthetic case—32B1(c)

26

Special indications

26.1

Introduction

26.2

MIPO in open fractures

26.3

MIPO for deformity or malunion correction

26.4

MIPO in limb lengthening

26.5

Bone transport over a plate

26.6

Use of MIPO in the treatment of nonunion

27

Implant removal

Foreword

Minimally Invasive Plate Osteosynthesis, Third Edition Foreword

Pietro Regazzoni

Prof Pietro Regazzoni, Dr med

Foreword

In bone surgery, treatment with a minimum of additional tissue trauma has been accomplished already in the 19th century using external devices to treat fractures. Albin Lambotte used percutaneous wires in early 20th century.

In 1912, Severin Nordentoft spoke at a surgical congress in Berlin, Germany, of an endoscopy of the knee performed with a modified cystoscope and coined the term arthroscopy. It is not clear whether this was done on anatomical specimens or on living patients. From 1919 to 1924 Eugen Bircher in Aarau, Switzerland, performed 60 arthroscopies of the knee on patients. Another pioneer was Masaki Watanabe who performed around 800 arthroscopies until the 1950s.

Intramedullary nailing was another step forward, as fractures could be fixed without access to the fracture zone. Early uses by Konig and Bircher date back to the last years of the 19th century, but the real breakthrough was Gerhard Kuntscher presenting his nail in 1940.

Since its foundation in 1958 the Arbeitsgemeinschaft fur Osteosynthesefragen commonly called AO, a surgical working group, insisted on the biological argument of cautious soft-tissue handling to lower infection rates.

Over the years the concept of minimizing the additional trauma of surgical access, particularly to an already injured anatomical zone gained general acceptance.

Improvements in imaging technology were fundamental for a better understanding of the pathologies before surgery and for improved planning, which led to the acceptance of the concept of minimally invasive surgery (MIS).

To perform MIS safely, conventional instruments that were designed earlier for open surgery were replaced by a new generation of dedicated minimally invasive osteosynthesis (MIO) instruments. It was demonstrated that cerclages can be used with minimal additional damage when using special instruments. Thus, MIO cerclages in combination with both nails and minimally invasive plating became routine, eg, in the femur. Corresponding knowledge and correct use of these instruments must also be taught outside the operating room. The MIO skills and special anatomical knowledge must be acquired in courses and possibly by a mentor assisting in the operating room.

In the immediate future, modern high-tech optical and radiological imaging and navigation technology will help to perform certain highly specialized procedures as MIS, eg, percutaneous biopsies in tumors or percutaneous navigated sacroiliac joint fixation. In a first phase because of cost purposes, it is feasible that such a technology will be limited to specific facilities.

Unfortunately, even now it is still impossible to quantify the additional tissue damage (invasiveness) of surgical procedures. A biochemical marker will be extremely valuable, eg, to compare the same type of procedures performed by different surgeons or different techniques for the same pathology.

To date, and as long as a secondary analysis of the intraoperative technical performance quality by detailed intraoperative image documentation is not viable, only indirect signs can be used to judge invasiveness. This is disappointing because we know that enormous discrepancies in the quality of technical performance exist and there is a correlation to the frequency of complications; therefore, to costs.

The length of the skin incision is not a dependable measure of MIS, as significant tissue damage can be produced through small incisions. Minimally invasive surgery does not mean to perform conventional operations just with shorter incisions.

Adequate skin incisions followed by submuscular plate placement effectively diminish the surgical footprint; consequently, less or minimally invasive. After the introduction of anatomically preshaped locking plates, such as the less invasive stabilization system and the locking compression plate, minimally invasive plate osteosynthesis (MIPO) is increasingly prevalent. The implants can be slid under the muscles, hence improving biology by avoiding further vascular damage of the fracture zone.

Minimally invasive surgery cannot be a justification not to follow well-established rules and principles of treatment, such as joint congruity or adequate plate fixation constructs.

Using MIPO techniques should not generate higher risks than conventional open techniques. Limited vision might expand the risk of neurovascular damage, especially when combined with the surgeon's inadequate anatomical knowledge. The transdeltoid approach for proximal humeral fractures offers benefits, but lesions of the axillary nerve can eradicate such benefits. Therefore, adequate learning and “avoidance of occasional surgery” are needed.

Due to reduced anatomical exposure, MIPO can lead to enhanced use of image intensifier. Particular attention to the ALARA (as low as reasonably achievable) principles is mandatory.

When planning MIPO always remember that conversion to open surgery (ie, enlarged access) can become crucial at any stage of a MIS procedure, and the soft-tissue status must allow such a change.

Prof Pietro Regazzoni, Dr medEmeritus Head of Trauma SurgeryUniversity HospitalBaselSwitzerland

Preface

Why publish a third edition of the Minimally Invasive Plate Osteosynthesis book?

A group of AO surgeons from various parts of the world started to operate a fracture in a somewhat different approach from how we were trained, which was that every fracture needed open reduction with direct visualization and rigid internal fixation. While “all roads lead to Rome” eventually, new ideas or surgical techniques take time to prove their effectiveness and credibility to the surgeon community. Our group of surgeon-editors and surgeon-authors who contributed to this Minimally Invasive Plate Osteosynthesis, Third Edition are passionate, enthusiastic, and strongly believe that the minimally invasive plate osteosynthesis (MIPO) technique is an additional asset in the portfolio of modern fracture care.

In 2006, a group of surgeons from AO East Asia decided to publish a first edition to explain the concept and demonstrate the application with various types of fractures and bone locations. The editors and contributors acknowledged that this would be an eye-opening experience for trauma surgeons to start thinking of other methods to treat a fracture. The MIPO technique required a learning curve and we wanted to share our knowledge with surgeons who were interested in learning this new approach. Consequently, the MIPO technique became a part of AO education with a specific curriculum and adapted bone models for practical exercises by the AO MIO expert group.

The AO MIO course has been given globally and has caught the attention of an international audience of surgeons. After the first edition of the MIPO book, worldwide acceptance of this technique expanded. Surgeons utilizing this approach in the operating room wanted to share their expertise, thus leading to a second edition in 2012. The second expanded edition presented additional applications and successful results, which were encouraging and promising.

The educational goal and challenge for teaching MIPO was to create a curriculum that allowed applying this technique in a safe and reproducible way. The development of the internal fixator, anatomical plates, and numerous new instruments developed by the AO MIO expert group helped to achieve this goal. The MIPO teaching has now been integrated in all AO Trauma curricula as a valuable facet in the armamentarium of orthopedic trauma surgery. Since this technique has a flat learning curve it is essential to share the knowledge of its application in the different regions through clinical examples from experts in the field, as it is demonstrated in this third edition. Even though there are different ways to achieve stabilization in various areas of the body, there remain some common principles when applying this technique, like indirect reduction techniques and implant insertion remote from the fracture site as well as leaving small surgical footprints at the fracture site, when direct reduction is needed for better fracture alignment.

Meanwhile evidence for the biological advantages of this technique has been proven in different areas of the locomotor system as well as its mechanical advantages and its benefit in respect to soft-tissue compromise including neurovascular structures. Even in shaft fractures, where nailing is not possible or in periprosthetic fractures with poor and limited anchorage, the MIPO technique can limit the intervention impact specially in frail patients.

After almost 20 years applying the concept of biological fixation, indirect reduction, bridging plate, etc, it is time to consolidate the achieved knowledge and expertise from surgeons worldwide. In this third edition we present known and new potential indications for MIPO, which we hope will continue to be an important aspect in the decision-making process of biology-preserving fracture care.

This new book used the updated AO Foundation/Orthopae- dic Trauma Association (AO/OTA) Fracture and Dislocation Classification.

Not only the surgical techniques but also the anatomically designed locking plates help to improve the radiological and functional results after MIPO in fracture treatment. Minimally invasive techniques are also an important and valuable approach to solving problems like malunion, nonunion, limb shortening, or bone defect. As these complications may already include soft-tissue injury or limited capacity for bone healing, it is crucial to avoid further damage when performing a salvage procedure with another operation. For pediatric patients MIPO is an excellent tool to achieve a satisfactory outcome, since the small medullary canal and the physeal plate do not allow a nailing procedure. Minimally invasive osteotomy, minimally invasive plate augmentation, and limb lengthening or bone transport with MIPO techniques are other useful extensions that benefited from the original lessons learned with the previous editions of this book.

Prof Suthorn Bavonratanavech, MDProf Reto Babst, MDProf Chang-Wug Oh, MD

Acknowledgment

We the editors and authors acknowledge and express our sincere appreciation to AO Education Institute, and especially to Vidula H Bhoyroo, Project Manager/Medical Editor; Carl Lau, Manager Publishing; Marcel Erismann, Senior Medical Illustrator, and Roman Kellenberger, Graphic Designer.

Contributors

Editors

Suthorn Bavonratanavech, MD

Past President of AO Foundation

Chief of Orthopedic and Trauma Network, BDMS Senior Director of Bangkok Orthopedic Center Bangkok Medical Center

2 Soi Soonvijai 7

New Petchaburi Road

Bangkok, 10310

Thailand

Reto Babst, Dr med

Professor

Senior Consultant Trauma Surgery Clinic for Orthopedics and Trauma Luzerner Kantonsspital Full Professor and Head of Medical Science University of Lucerne

Spitalstrasse 16 6000 Luzern

Switzerland

Chang-Wug Oh, MD

Professor

Department of Orthopedic Surgery

School of Medicine, Kyungpook National University

Kyungpook National University Hospital

130 Dongdeokro, Jung-gu

Daegu 41944

Korea

Authors

Theerachai Apivatthakakul, MD

Professor

Department of Orthopaedics

Faculty of Medicine

110 Intavarorot

Mueang Chiang Mai

Chiang Mai University

Chiang Mai 50200

Thailand

Frank JP Beeres, MD, PhD

Specialist for Surgery

Trauma Surgery

ESBQ Trauma Surgery

Luzerner Kantonsspital

Spitalstrasse 16

6000 Luzern

Switzerland

William Belangero, MD

The State University of Campinas UNICAMP

Faculty of Medical Science

Department of Orthopaedic and Traumatology

Rua Tessalia Vieira de Camargo

126 Cidade Universitaria

Campinas, Sao Paulo

CEP 13083-887

Brazil

Pongsakorn Bupparenoo, MD Orthopaedic Trauma Instructor Department of Orthopaedic Rajavithi Hospital

2 Phyathai Road Rajathevi Bangkok 10400

Thailand

Peter A Cole, MD

Regions Hospital 640 Jackson Street

Saint Paul, MN 55101 USA

Jae-Woo Cho, MD

Assistant Professor Department of Orthopedics Korea University Guro Hospital 148, Gurodong-ro, Guro-gu 08308 Seoul

Korea

Juan Manuel Concha, MD

Professor

Orthopedic/Trauma Surgeon Universidad del Cauca

Calle 5 N° 4-70 Popayan Colombia

Alberto Fernandez Dell’Oca, MD

Chief of Orthopedic Department

British Hospital

Avenida Italia 2364 (Edificio Palma de Malaga)

Apto. 803

Montevideo, 11200

Uruguay

Pornpanit Dissaneewate, MD

Department of Orthopaedics

Faculty of Medicine

Prince of Songkla University

Hat Yai, Songkhla 90110

Thailand

Klaus Dresing, MD

University Medicine Gottingen Georg-August-

Universitat

Wilhelmsplatz 1

37073 Gottingen

Germany

Devakar Epari, MD

Assistant Professor

School of Mechanical, Medical and Process Engineering

Science and Engineering Faculty Queensland University of Technology

O Block, Level 4 Room O-408

Gardens Point Campus

Brisbane, QLD 4000

Australia

Jonathan Eastman, MD

Associate Professor

Orthopaedic Trauma, Department of Orthopaedic Surgery

University of Texas, Health Science Center at Houston

McGovern Medical School, Memorial Hermann Medical Center

Suite 1700

6400 Fannin Street Houston, TX 77030 USA

Christian Fang, MBBS (HK), FHKCOS, FHKAM

Orthopeadic Surgery, FRCSEd(Ortho) Clinical Assistant Professor

Department of Orthopaedics&Traumatology The University of Hong Kong

Queen Mary Hospital

5/F, Professional Block

102 Pokfulam Road

Hong Kong

Chris Finkemeier, MD

Department of Trauma

Acute Care Orthopedic Service Sutter Roseville Medical Center

1 Medical Plaza Drive Roseville, CA 95661 USA

Andrew L Foster, MBBS, BMedSci (Hons I)

Principal House Officer Department of Orthopaedics Jamieson Trauma Institute

Royal Brisbane and Women’s Hospital Corner of Bowen Bridge Rd and Butterfield St Herston QLD 4029

Australia

Fernando Garcia, MD

Calle Manzanillo #73 entre Tlaxcala y Aguascalientes

Col.Roma Sur

C.P 06760

Cuauhtemoc Ciudad de Mexico Mexico

Lucas F Heilmann, MD

University Clinic Munster

Department of Trauma, Hand and Reconstructive Surgery

Waldeyerstrasse 1 48149 Munster Germany

Dankward Hontzsch, Dr med

Cranachweg 9 72076 Tubingen Germany

Ladina Hofmann-Fliri, MSc

Project Manager Technology Transfer

AO Innovation Translation Center, Technology Transfer

Clavadelerstrasse 8 7270 Davos Switzerland

Chittawee Jiamton, MD

Institute of Orthopaedics, Lerdsin Hospital 9th floor, Karnchanaphisek Building Silom Road

Silom, Bangrak

Bangkok 10500 Thailand

Jochen Franke, Dr med

Head, Division of Trauma

Head, MINTOS Research Group

Department for Trauma and Orthopaedic Surgery BG Trauma Centre Ludwigshafen

Heidelberg University Hospital

BG Klinik Ludwigshafen Ludwig-Guttmann-Strasse 13 67071 Ludwigshafen

Germany

Surasak Jitprapaikulsam, MD

Buddhachinaraj Hospital 90 Srithamtraipidok Road Nai Mueang Subdistrict Mueang Phitsanulok District Phitsanulok 65000 Thailand

Joon-Woo Kim, MD, PhD

Associate Professor

Department of Orthopedic Surgery

School of Medicine, Kyungpook National University Kyungpook National University Hospital 130 Dongdeokro, Jung-gu

Daegu 41944

Korea

Christian Kammerlander, Dr med

Professor

Vice Director

Department of General, Trauma and Reconstructive

Surgery

Ludwig Maximilian University Munich NussbaumstraBe 20

80336 Munich

Germany

Michael D Kraus, Dr med

Professor

Orthix Zentrum

StadtbergerstraBe 21

86157 Augsburg

Germany

Apipop Kritsaneephaiboon, MD

Department of Orthopaedics

Faculty of Medicine

Prince of Songkla University

Hat Yai, Songkhla 90110

Thailand

Santiago Lasa, MD

Hospital Britanico

Av. Italia 2420

PA 11600-Montevideo

Uruguay

Michael C LaRoque, BSME

Regions Hospital

640 Jackson Street

Saint Paul, MN 55101

USA

Bruno Livani, MD, PhD

R. Vital Brasil

251 - Cidade Universitaria

Campinas - SP, 13083-888

Campinas, Sao Paulo

Brazil

Frankie KL Leung, MD, FRCS

Department of Orthopaedics and Traumatology

5th floor, Professorial Block

Queen Mary Hospital

102 Pokfulam Road

Pokfulam

Hong Kong

Bjorn C Link, PD Dr med

Chairman, Department of Orthopaedic and

Trauma Surgery

Luzerner Kantonsspital

Spitalstrasse 16

6000 Luzern

Switzerland

Cong-Feng Luo, MD

Professor

Chief, Division of Orthopaedic Trauma III Department of Orthopaedic Surgery

6th floor, Orthopaedic Building

Shanghai 6th People’s Hospital

No. 600 YiShan Road

Shanghai 200233

Republic of China

Peter Matter, Dr med

Professor Emeritius

Ortstrasse 6

7270 Davos Platz

Switzerland

Chatchanin Mayurasakorn, MD

Orthopaedic Trauma Surgeon

Bangkok International Hospital

2 Soi Soonvijai 7

New Phetchaburi Road

Huaikhwang

Bangkok 10320

Thailand

Christian Michelitsch, Dr med

Kantonsspital Graubunden

Department of Surgery

Loestrasse 170

7000 Chur

Switzerland

Hyoung-Keun, MD

Associate Professor

Department of Orthopedic Surgery

Inje University, Ilsan Paik Hospital

2240 Daehwa-dong, Ilsanseo-gu

Goyang-si, Gyeonggi-do

Korea

Jong-Keon Oh, MD

Professor

Head of Trauma Division

Department of Orthopedics

Korea University Guro Hospital

148, Gurodong-ro, Guro-gu

Seoul 08308

Korea

Kyeong-Hyeon Park, MD, PhD

Assistant Professor

Department of Orthopedic Surgery

School of Medicine, Kyungpook National University

Kyungpook National University Hospital

130 Dongdeokro, Jung-gu

Daegu 41944

Korea

Thomas Z Paull, MD

Regions Hospital 640 Jackson Street

Saint Paul, MN 55101

USA

Vajara Phiphobmongkol, MD

Chief Orthopaedic Trauma

Bangkok International Hospital

2 Soi Soonvijai 7

New Phetchaburi Road

Huaikhwang

Bangkok 10320

Thailand

Rodrigo Pesantez, MD

Department of Orthopedics

Fundacion Santa Fe de Bogota

Facultad de Medicina Universidad de Los Andes

Avenida 9 116-20 Consultorio 820

Bogota

Colombia

Stefan Rammelt, Dr med

Professor

Sektionsleiter Sprunggelenk, FuB und Kinderor- thopadie

UniversitatsCentrum fur Orthopadie &

Unfallchirurgie

Universitatsklinikum Carl Gustav Carus

FetscherstraBe 74

01307 Dresden

Germany

Michael J Raschke, Dr med

Professor

Direktor der Klinik fur

Unfall-, Hand- und Wiederherstellungschirurgie

Albert-Schweitzer-Campus 1, Gebaude W1

WaldeyerstraBe 1

48149 Munster

Germany

Pietro Regazzoni, Dr med

Professor

Emeritius, Head of Trauma Surgery

University Hospital

Basel

Switzerland

R Geoff Richards, FBSE, FIOR

Director

AO Research Institute Davos (ARI)

AO Foundation

Clavadelerstrasse 8

7270 Davos

Switzerland

Mark Rickman, MD

Associate Professor of Orthopaedics & Trauma

Department of Orthopaedics, 5G587

Royal Adelaide Hospital

Port Road

Adelaide SA 5000

Australia

Julian Salavarrieta, MD, MEd

Orthopaedic Trauma Surgeon

Fundacion Santa Fe de Bogota University Hospital

Calle 127A # 18b, 62 ap 305

Bogota 110111

Colombia

Paphon Sa-ngasoongsong, MD, FRCOST

Associate Professor, Orthopaedics

Department of Orthopaedics

Faculty of Medicine Ramathibodi Hospital

Mahidol University

270, Rama VI Road

Ratchathewi 10400

Bangkok

Thailand

Michael Schutz, FRACS, FaOrth, Dr med (RWTH

Aachen), Dr med habil (HU Berlin), Dr hc (QUT

Brisbane)

Director

Jamieson Trauma Institute

L11, Block 7

Royal Brisbane and Women’s Hospital

Brisbane Herston QLD 4029

Australia

Jamil Soni, MD, PhD

Professor Pontificia Universidade Catolica do

PR - PUCPR

Consultant of Paediatric Orthopedic Hospital

University Cajuru - PUCPR

and Hospital do Trabalhador-UFPR

Av Silva Jardim 1502

Zip 80250-200

Curitiba

Brazil

Inger Schipper, MD, PhD, FACS

Trauma Surgeon

Head, Department of Trauma Surgery

Director of Trauma Center West

Leiden University Medical Center

D6-39

Albinusdreef 2

2333 ZA Leiden

Netherlands

Eakachit Sikarinkul, MD

Trauma Unit

Department of Orthopedic Surgery Bangkok International Hospital 2 Soi Soonvijai 7 New Phetchaburi Road

Huaikhwang

Bangkok 10320

Thailand

Pongtorn Sirithianchai, MD

Bangkok International Hospital 2 Soi Soonvijai 7 New Phetchaburi Road

Huaikhwang

Bangkok 10320

Thailand

Christoph Sommer, MD

Kantonsspital Graubunden Department of Surgery Loestrasse 170

7000 Chur

Switzerland

Michael Swords, DO

Michigan Orthopedic Center

Chair, Department of Orthopedic Surgery

Sparrow Hospital

2815 S Pennsylvania Ave #204

Lansing, MI 48910

USA

Philipp Stillhard, MD

Kantonsspital Graubunden

Department of Surgery

Loestrasse 170

7000 Chur

Switzerland

Bryan JM van de Wall, MD, PhD

Consultant Surgeon Orthopedic Trauma

Clinic of Orthopedics and Trauma Luzerner Kantonsspital

Spitalstrasse 16

6003 Luzern

Switzerland

Weverley Valenza, MD

Hospital do Trabalhador

Av Republica Argentina No. 4406

Curitiba, Parana 81050-000

Brazil

Markus Windolf, PhD

Focus Area Leader Concept Development

AO Research Institute Davos

Clavadelerstrasse 8

7270 Davos

Switzerland

Hou Zhiyong, MD

Third Hospital of Hebei Medical University 139 Ziqiang Road Shijiazhuang, Hebei

Republic of China

Hans Zwipp, Dr med

Professor Emeritius

Dresden, Germany

1

History and evolution of minimally invasive plate osteosynthesis

Reto Babst, Peter Matter, Suthorn Bavonratanavech

1History and evolution 2References3Acknowledgment

1 History and evolution

In 1958 a small group of Swiss general and orthopedic surgeons established the Arbeitsgemeinschaft fur Osteosynthesefragen (AO) or the Association for the Study of Internal Fixation (ASIF) in an attempt to transform the contemporary treatment of fractures in Switzerland. The group of surgeons were Maurice E Muller, Hans Willenegger, Martin Allgower, Robert Schneider, and Walter Bandi. This association was revolutionary in the development of instruments and implants for operative fracture treatment. The first instructional course for teaching the use of these instruments and implants occurred in Davos, Switzerland, in the newly founded Laboratory of Experimental Surgery in 1960. Through a process of internal quality control by AO Documentation, the clinical success of these new techniques and implants became evident. Operative fracture treatment gained acceptance throughout Europe, and finally worldwide. AO International (AOI) was founded in 1972 to expand education and teaching programs for surgeons and operating personnel on an international basis.

Based on the four pillars of research, development, documentation, and teaching, this group formulated already in the first edition of the Technique ofInternal Fixation ofFractures published in 1965 [1], the following principles to improve fracture care:

•Rigid fixation of fragments (direct bone healing)

•Preservation of vascularized bone fragments

•Early mobilization

Fig 1-1a-b X-rays of a diaphyseal fracture fixed with lag screws and neutralization plate with rigid fixation showing signs of direct bone healing.

In their justification of these principles, the surgeon-authors stated that direct healing of bone was a desirable clinical and radiological concept. It was also called “fracture union without visible callus formation”. They believed that any excess callus should be considered detrimental, regarded as a form of “keloid” of the bone, indicating movement at the fracture site. Any radiologically visible callus formation during fracture healing and after internal fixation was seen as a warning that should initiate appropriate action. Union without radiologically visible callus, though, appeared to be the most desirable form of healing. The healing of a fracture without callus can be considered as radiological evidence of continuous rigid fixation. These views were further supported by the experimental demonstration of direct bone healing by Schenk and Willenegger [2]. The trend was for all fractures to be anatomically reduced and rigidly fixed, with direct bone healing without visible callus formation as the desired result (Fig 1-1). Subsequent editions of the Manual of Internal Fixation: Techniques Recommended by the AO-ASIF Group [3] reiterated the treatment principles as:

•Anatomical reduction

•Rigid internal fixation

•Preservation of blood supply

•Early pain-free mobilization of muscles and joints adjacent to the fracture

The principles most appealing to surgeons were those of anatomical reduction and stable internal fixation—possible explanations are that these were the more visible and tangible of the principles as the results could be seen on x-rays. Furthermore, practical exercises at AO courses were conducted using plastic bones stripped of soft tissues, thus giving the false impression that the soft tissues can be ignored. To be fair, in the many cases of fractures treated by anatomical reduction and stable fixation with successful outcomes the results were impressive—patients were regaining pain-free mobility and function of their injured limbs shortly after surgery. “Fracture disease” soon became a lesson of the past.

However, despite the inclusion of preservation of blood supply as one of the original treatment principles, and the emphasis on careful handling of soft tissue during surgery, these two elements of fracture management did not receive as much attention from the orthopedic community. During this time, research and development were directed at improving the rigidity of internal fixation. The concepts of inter- fragmentary compression with lag screws and compression plates, first with the articulating tension device and then with dynamic compression plates (DCPs), were introduced. However, it soon became apparent that rigid internal fixation of fractures did not always produce the desired result. Instances of sepsis, sequestrum formation, delayed union or nonunion, and refractures were observed.

Research into these failures led to the discovery of the phenomenon of temporary porosis around the footprint of the plate on bone. The cause of this was considerable damage to the periosteal circulation resulting at the interface between implant and bone (Fig 1-2).

Studies using special undercut plates showed that the grooves in the plates reduced vascular damage and mitigated bone porosis. This led to the development of a special undercut plate, the limited-contact-dynamic compression plate (LC- DCP) (see also chapter 4Implants) (Fig 1-3 and Fig 1-4).

Fig 1-2a-b

aPhenomenon of temporary porosis.

bPhotomicroangiograph of a transverse section of the femur from a mature dog 6 weeks after plate placement. The cortex at the 12 o’clock position that was directly under the plate is devoid of arterioles, whereas the remainder of the cortex is vascular and viable.

Fig 1-3a-d A 23-year-old man sustained a closed femoral fracture in a motor vehicle injury. A minimally invasive plate osteosynthesis procedure was chosen due to the narrow canal and the lung contusion.

aInitial x-ray.

bX-ray immediately postoperative showing a bridge plate concept with relative stability with correct functional anatomy.

cX-ray 5 months after the injury indicating indirect fracture healing with callus formation.

dFracture healing with callus formation 1 year after the injury.

Fig 1-4a-c

aIndirect reduction with the distractor using the blade plate as a reduction tool.

b“Biological osteosynthesis”, the “no-touch” technique, bridging the fracture zone without devascularizing the single fragments by leaving the soft-tissue envelope untouched. However, the skin incision is approximately the same length as the plate.

cClinical example of a bridged metaphyseal fracture zone with callus formation.

The first moves away from mechanical stability of internal fixation toward biological internal fixation were made. Further evidence that absolute rigidity was not always necessary for fracture union came from the observation that fractures with flexible fixation also heal, although with callus formation. Such examples of flexible fixation or splinting came from intramedullary nails, external fixators, bridging, and wave plates. In fact, indirect healing often led to early and reliable solid bone union. The development of indirect methods of fracture reduction for diaphyseal fractures using the principle of ligamentotaxis led to the avoidance of further damage to the blood supply of the fracture fragments, which accompanied direct manipulation of the fracture ends. Furthermore, it was shown that internal fixation based only on reducing the mobility of the fracture fragments without contact between the bone fragments could result in solid healing. Thus, multifragmentary fractures fixed with bridging plates demonstrated high union rates without the need for bone grafting (Fig 1-5). The explanation for this was based on the concept of interfragmentary strain.

Fig 1-5 Submuscular plating using the dynamic condylar screw.

The concept of interfragmentary strain asserts that fractures with a single, narrow gap are intolerant of even small amounts of displacement because of deformation of repair tissues, while multifragmentary fractures can tolerate a greater degree of instability as the overall displacement is shared among many fracture gaps.

Similarly, the strain in fractures with a larger gap width was also reduced. It became apparent that anatomical reduction and rigid internal fixation were not necessary to achieve union in multifragmentary diaphyseal fractures. Fracture reduction in multifragmentary diaphyseal fractures became simpler and consisted mainly of regaining length, rotation, and axial alignment.

These clinical observations lead to a modification of the initial classic principles stated in the first AO Manual [1] with the goal to further improve surgical outcomes.

•Functional anatomy: Anatomical reduction is only needed for articular fractures, whereas in the metadiaphyseal area anatomical alignment for multifragmentary patterns with respect to length, axis, and rotation is needed. For simple fracture types, anatomical reduction is still recommended also on the diaphysis, often demanding direct reduction.

•Stable fixation: Includes absolute stability for simple fractures and relative stability for multifragmentary fractures

•Preservation of vascularization of all bone fragments should be aimed for by avoiding extensive dissection of soft tissue and periosteum

•Early pain-free mobilization of all joints is recommended and partial weight bearing as tolerated by the patients is instituted

The modification of the surgical strategy has been controversial among surgeons for many years until there was enough solid evidence showing the reproducible positive outcomes.

Thus, the stage was set for the progression to more biological methods of fracture fixation, namely in the treatment of patients with multiple injuries from high-energy crashes where either plate or intramedullary fixation was applied according to the needs of the patient and personality of the fracture.

Minimally invasive osteosynthesis is not a new concept in orthopedic trauma surgery. Closed intramedullary nailing, application of external fixators, and percutaneous fixation of fractures using screws and K-wires had been performed with acceptable outcomes. Orthopedic trauma surgery has traditionally attempted to minimize further trauma to the damaged area. With this consideration, minimally invasive fracture fixation was introduced with the use of the external fixator by a French surgeon, Albin Lambotte, at the beginning of the 20th century, and with the intramedullary nail by a German surgeon, Gerhard Kuntscher, during World War II. Common to both techniques were minimal access to the bone through small skin incisions and an indirect reduction technique that did not involve direct manipulation of the fracture. The relative stability of both stabilization concepts resulted in indirect bone healing with callus formation. The appeal of this minimally invasive stabilization technique was not the small incisions but the biological advantages, such as minimal soft-tissue compromise. It enabled undisturbed fracture healing and fewer infection-related complications compared with open reduction and internal fixation using cerclage wires and plates during the early period of fracture fixation.

In multifragmentary epiphyseal and metaphyseal fractures where indirect reduction techniques using intramedullary fixation were not possible, an open and direct approach to the bone risking delayed bone healing and infection-related complications because of the additional operative trauma. Open reduction results in further devascularization of single fragments. To obtain a biomechanically stable construct, the individual bone fragments were left untouched—the so-called “notouch” technique—and their vascularity was maintained. The goal was not anatomical reduction but regaining length, rotation, and axial alignment. The healing pattern by secondary intention with callus formation enabled a more rapid progression to weight bearing and led to fewer secondary bone grafts and associated infections. In the late 1980s, Mast and Ganz [4, 5] invented the term “biological plating” to describe using indirect reduction techniques, mainly applying blade plates in the epiphysis/metaphysis as extramedullary splints (Fig 1-3).

In 1996, Krettek et al [6] proposed a minimally invasive percutaneous plating osteosynthesis for the distal femur using the dynamic condylar screw (Fig 1-4). In a small clinical series of distal femoral fractures, they proved the biological advantage of this technique which resulted in fewer infection-related complications, and fewer primary and secondary bone grafts compared with the traditional open-access surgery. The concept of anatomical reconstruction of the joint using an approach as large as necessary to obtain anatomical reconstruction, combined with a submuscular plating approach to limit additional trauma to the metaphyseal area, were important pillars for the evolution of the concept of minimally invasive plating. Several groups have since proven this concept by applying it to the epiphysis/metaphysis [7] and to the diaphysis when a nail was not appropriate due to a narrow medullary canal [8], an occupied femoral canal by a prosthesis, an open physis, or due to physiological reasons in a polytraumatized patient [9]. Multifragmentary fractures fixed with bridging plates demonstrate high-union rates without further need of bone grafts. In 2001 the first minimally invasive plate osteosynthesis (MIPO) approach using a helical bridge plate at the proximal humeral shaft was proposed by Fernandez Dell’Oca [10]. In 2004 Livani and Belangero [8] showed the anatomical basis for and clinical application of an anterior bridging plate for the humeral shaft. Further anatomical studies by Apivatthakakul et al [11] gave rise to a widespread application of the MIPO technique for the humerus.

The evolution of submuscular plating was accelerated by the invention of internal fixators, eg, the point-contact fixator (PC-Fix), less invasive stabilization system (LISS), and locking compression plate (LCP). Locking head screws (LHSs) had the benefit of preserving the periosteal blood supply and they were easy to apply due to their self-drilling and self-tapping properties. Furthermore, the principle of the PC-Fix acting as an internal fixator caused no loss of primary reduction when the plate was not anatomically shaped to the bone.

The introduction of the PC-Fix was the first step in the realization of the biological advantages of LHSs, which preserved both the periosteal and endosteal blood supplies. Furthermore, these self-drilling and self-tapping screws offered the advantage of simple handling. Following in the footsteps of the PC-Fix was the LISS, for details see chapter 4 Implants. It was designed for application in the metaphyseal and epiphyseal areas, first of the distal femur (Fig 1-6) and then of the proximal tibia. The LISS can be considered the first plate that was specifically designed and instrumented for insertion using a minimally invasive submuscular approach. It had a special insertion handle which facilitated the introduction of the implant submuscularly and, at the same time, acts as a drill guide for accurate insertion of the screws through separate small stab wounds. The LHSs that are used with this system also offer angular stability to the construct, helping to prevent secondary varus dislocation in the distal femur or the proximal tibia.

The next step which facilitated the widespread implementation of MIPO was the introduction of the LCP with its combination hole. These plates can be applied either as internal fixators using LHSs or as standard dynamic compression plates when using cortex screws. A multitude of new low profile anatomical plates for different anatomical regions and various specially designed reduction instruments have made MIPO a reliable and successful development in the treatment portfolio of orthopedic trauma surgery. In addition, the combination hole has allowed the cortex screw once inserted through the plate hole into the bone to perform indirect reduction of the bone to the plate.

However, this technique with its biological benefits has some problems, including a long learning curve and a potential for malunion because of the limited view using the C-arm for reduction control. Moreover, simple fracture patterns due to inadequate reduction in distraction or due to high strain when using a bridging plate concept treated by MIPO may result in nonunion or delayed union. In simple fracture patterns anatomical reduction with stable fixation to achieve absolute stability has been proposed using limited open access at the fracture site also in MIPO surgery [12, 13].

Fig 1-6a-b Less invasive stabilization system distal femur is indicated for the stabilization of the distal femur.

The technique of minimally invasive plating has been supported by the AO since its introduction through special minimally invasive osteosynthesis (MIO) courses with the aim of teaching this technique in a safe and reproducible way. A special workforce of the AO Technical Commission also supported this evolution by creating specific instruments to ease reduction and leaving just small surgical “footprints” behind at the fracture site (Fig 1-7). Since minimally invasive surgery is not determined by the length of the incisions but more by the reduction technique and soft-tissue handling, a definition of MIO/MIPO includes the following recommendations:

•Small soft-tissue windows are used to allow the insertion of implants and instruments remote from the fracture site.

•Minimal additional trauma to the soft tissue and fractured fragments results from performing mainly indirect reduction. Use direct reduction only when it is necessary to achieve fracture alignment.

•Special instruments are designed to be used at the fracture site that cause minimal additional trauma.

These special instruments have been developed to allow direct reduction of a fracture by percutaneous means where it is needed, for example, the collinear reduction clamp (Fig 1-7), percutaneous manipulators, and MIPO cerclage passer.

Fig 1-7a-c Percutaneous reduction clamp with different tips (a) which allows direct reduction technique through stab incisions resulting in minimal additional trauma at the fracture site (b-c).

Several clinical trials [14-17] emerging during the last 30 years have not only proven the feasibility of the MIPO technique and its biological advantages but also reduced rates of infection and less need for primary or secondary bone grafts. This technique has also demonstrated advantages in several prospective randomized studies and metaanalyses having less nerve compromise, eg, in clavicular and humeral shaft fractures, without increasing the time to heal or complications compared with open procedures [18]. The MIPO approach has developed into a safe and reproducible technique in simple and complex shaft fractures, where nailing is technically not feasible. Evidence suggests its ultimate benefit at the level of the humeral shaft and the calcaneus, whereas in other areas MIPO has shown its biological potential due to minimized surgical footprint that allows for undisturbed bone healing. Multiple low-profile anatomical plate designs in different anatomical regions have improved its application also in the epimetaphyseal region (Fig 1-8). The special reduction instruments for MIPO procedures allow standardized reduction leaving small surgical “footprints” enabling undisturbed bone healing.

The MIPO approach is now an important enhancement in the assets of the orthopedic trauma surgeon allowing for the same or better outcome in selected fracture situations.

Fig 1-8a-d A 39-year-old man sustained a monotrauma on his right lower leg during a ski injury.

aInitial x-rays reveal a distal spiral fracture with an anterolateral wedge fragment (AO/OTA 42B1.3).

bPostoperative x-ray with a minimally invasive plate osteosynthesis technique using low-profile anatomical plate (locking compression plate metaphyseal plate) on the tibia and a 1/3 tubular plate on the fibula.

cTibia with incisions 6 weeks after the operation.

dX-rays at 1 year after the injury revealed a healed fracture.

2 References

1.Muller ME, Allgower M, Willenegger H.Technique of Internal Fixation of Fractures. Berlin Heidelberg: Springer-Verlag; 1965.

2.Schenk R, Willenegger H. [On the histology of primary bone healing.] Langenbecks Arch Klin Chir Ver Dtsch Z Chir. 1984;308:440- 452. German.

3.Muller ME, Allgower M, Schneider R, et al.Manual of Internal Ffixation: Techniques Recommended by the AO-ASIF Group. 3rd ed. Berlin Heidelberg: Springer Verlag.

4.Mast J, Jakob R, Ganz R.Planning and Reduction Technique in Fracture Surgery. 1st ed. Berlin Heidelberg: Springer-Verlag; 1989.

5.Kinast C, Bolhofner BR, Mast JW, et al. Subtrochanteric fractures of the femur: results of treatment with the 95 degrees condylar bladeplate. Clin Orthop Relat Res. 1989 Jan;(238):122-130.

6.Krettek C, Schandelmaier P, Tscherne H. [Distal femoral fractures. Transarticular reconstruction, percutaneous plate osteosynthesis and retrograde nailing.] Unfallchirurg. 1996;99:2-10. German.

7.Helfet DL, Shonnard PY, LevineD, et al. Minimally invasive plate osteosynthesis of distal fractures of the tibia. Injury. 1997;28(Suppl 1):A42-47; discussion A47-48.

8.Livani B, Belangero WD. Bridging plate osteosynthesis of humeral shaft fractures. Injury. 2004 Jun;35(6):587-595.

9.Pape HC. Effects of changing strategies of fracture fixation on immunologic changes and systemic complications after multiple trauma: damage control orthopedic surgery. J Orthop Res. 2008 Nov;26(11):1478-1484.

10.Fernandez Dell’Oca AA. The principle of helical implants. Unusual ideas worth considering. Injury. 2002 Apr;33 Suppl 1:SA1-21.

11.Apivatthakakul T, Arpornchayanon O, Bavornratanavech S. Minimally invasive plate osteosynthesis (MIPO) of the humeral shaft fracture. Is it possible? A cadaveric study and preliminary report. Injury. 2005 Apr;36(4):530-538.

12.Horn C, Dobele S, Vester H et al. Combination of interfragmentary screws in distal metaphyseal frac- trues of the tibia: a retrospective, single -center pilot study. Injury. 2011 Oct;42(10):1031-1037

13.Wenger R, Oehme F, Winkler J et al. Absolute or relative stability in minimal invasive plate osteosynthesis of simple distal meta or diaphyseal tibia fractures? Injury. 2017;48(6):1217-1223.

14.Zlowodzki M, Bhandari M, Marek DJ, et al. Operative treatment of acute distal femur fractures: systematic review of 2 comparative studies and 45 case series (1989 to 2005). J Orthop Trauma. 2006 May;20(5):366-371.

15.Hasenboehler E, Rikli D, Babst R. Locking compression plate with minimally invasive plate osteosynthesis in diaphyseal and distal tibial fracture: a retrospective study of 32 patients. Injury. 2007 Mar;38(3):365-370.

16.Kregor PJ, Stannard J, Zlowodzki M, et al. Distal femoral fracture fixation utilizing the Less Invasive Stabilization System (L.I.S.S.): the technique and early results. Injury. 2001 Dec;32 Suppl 3:SC32-47.

17.Schutz M, Muller M, RegazzoniP, et al. Use of the Less Invasive Stabilization System (LISS) in patients with distal femoral (AO33) fractures: a prospective multicenter study. Arch Orthop Trauma Surg. 2005 Mar;125:102-108.

18.van de Wall B, Beeres FJB, Knobe M, et al. Minimally invasive plate osteosynthesis: an update of practice. Injury. 2021 Jan;52(1):37-42.

3 Acknowledgment

We acknowledge the contribution of G On Tong, MD. In: Babst R, Bavonratanavech S, Pesantez R, eds. Minimally Invasive Plate Osteosynthesis, Second Edition. Stuttgart, Thieme Publishing; 2012:5-10.

2.1

Basic mechanobiology of bone healing and biomechanics of fracture fixation

Markus Windolf, Ladina Hofmann-Fliri, Devakar Epari

In memory of Prof Stephan Marcel Perren

1Introduction2Bone healing2.1Intact bone and fracture2.2Primary (direct) bone healing2.3Secondary (indirect) bone healing3Fracture treatment3.1General treatment goals3.2Absolute stability: compression osteosynthesis3.3Relative stability: installing flexibility with locking implants3.4Bone screws4Future trends4.1Dynamic implants4.2Fracture monitoring4.3Controlling fracture dynamics5Key points5References

1 Introduction

The rationale for mechanically stabilizing bone fractures is the need to restore the anatomy and the mechanical function of the bone. Optimal bone healing requires preservation of the biological healing potential and a suitable mechanical environment. This principle is aided by modern osteosynthesis.

A study of the evolution of fracture management reveals periodic shifting of priorities from biology to mechanics and vice versa. Before the advent of modern fixation techniques, the priority of treatment was to achieve solid union of the fracture. Traction and/or external splinting with rigorous longterm immobilization of joints and patient were the preferred treatments despite the shortcomings of these procedures. A high rate of devastating clinical results was the consequence. With the development of internal fixation, treatment priorities moved toward the opposite extreme. The main goal was recovering function by rigid mechanical stabilization of the fracture. This view neglected the potential of the body’s natural healing and intermediate stabilization capacities through callus formation. Furthermore, precise reduction and absolute stable fixation were achieved at the expense of extensive soft-tissue trauma from surgery.

Subsequent development in surgical treatment focused on improvements to the implants and procedures tailored to minimize the surgical trauma during reduction and fixation. The goal of minimally invasive osteosynthesis is preserving the biological environment and using natural healing competencies through relative stability and flexible fixation as opposed to suppressing them.

This chapter introduces the basic mechanobiological interactions that occur in bone healing and shows their practical implications on day-to-day surgery to allow the surgeon to optimize the procedure of fracture stabilization when applying minimally invasive osteosynthesis.

2 Bone healing

2.1 Intact bone and fracture

The human skeleton provides a protecting and supporting framework for the internal organs. It makes the mechanical functions of the limbs possible that require the skeleton to be rigid.

A fracture occurs when the applied force exceeds the strength of the bone. Neighboring elements that were solidly connected separate. Loss of function and pain develop. Mechanically, fracturing leads to local disruption of the bone rigidity and impairs the function of the bone.

A fractured bone is clinically healed when it has recovered its strength and stiffness, allowing unrestrained function like weight bearing. In addition, complete healing includes remodeling whereby the woven bone is replaced by lamellar bone. In this regard, bone is unique because it can regain its original structure and the same tissue without permanent scarring.

As an immediate response to a fracture, biological processes are triggered by inflammatory signals. With minimal or no intervention, the natural healing response involves the formation of callus (see section 2.3 Secondary [indirect] bone healing). While in some cases this response may be successful in restoring continuity of the injured bone, it involves a substantial period of temporary disability and potentially permanent functional impairment caused by malalignment and limb shortening which may further have consequences for degenerative diseases at neighboring joints. The goal of intervention is then to support the body’s natural healing potential and to ensure timely healing while maintaining anatomical reconstruction. Depending on the conditions provided by the intervention, bone healing may take one of two distinct pathways.

2.2 Primary (direct) bone healing

Reduction and absolute stabilization (no relative movement) of the fracture fragments results in bony union via a process termed primary bone healing. Healing occurs with marginal or no callus formation. Danis [1] named this healing through internal welding (soudure autogene). Union of the fracture is achieved by a continual process of renewal in bone, known as bone remodeling. Clusters of cells, bone resorbing osteoclasts and bone forming osteoblasts, which traverse healthy intact bone constantly repairing cracks can cross the fracture plane establishing new Haversian structures that restore continuity to the bone.

While the process of primary healing may be considered robust, it is reliant on absolute stability maintaining compression across the fracture planes by intervention with surgical implants. This compressive preload suppresses intermittent gapping and shear that may disturb healing by frictional locking and interdigitation of rough bony surfaces. Physiologically, the compressive preload is superimposed by functional loading (loads arising from limb movement). If these loads produce additional pressure, the compression of the fracture is amplified. However, in the case of superimposed tension, ie, due to an eccentric load, the compression may be locally diminished. The fracture surfaces are held closely together if the compression is greater than the tension. Should the opposite occur, and the tension becomes predominant, the fracture surfaces open (intermittent instability) and healing is interrupted. Furthermore, absolute stability and compression must be maintained for the duration of healing until bone strength is restored. Compromised stability that results in loss of compression may disturb bone healing.

As primary healing is a process internal to the bone that takes place without formation of an external callus, monitoring healing visually (x-rays) is neither possible nor the determination of bony union. Because the strength of the bone will approach the preoperative strength but not exceed it, the healing fracture is somewhat susceptible to refracture if implants are removed too early. However, primary healing may be well suited to clean fracture lines that lend themselves to reduction and where absolute stability can be maintained.

2.3 Secondary (indirect) bone healing

2.3.1 Detour via callus healing

Where primary healing occurs by direct union of the bone fragments, secondary healing proceeds with the formation of an external callus under conditions where relative motion is not suppressed (relative stability). Callus prepares a suitable environment by stabilizing the fracture before solid bridging takes place.

Secondary healing is composed of complex biological events that cannot be distinctly separated from each other. However, according to generally accepted opinion, bone healing may be divided into sequential phases for a clearer understanding of the process [2].

1.Inflammatory phase (1-7 days postinjury). Traumatic failure of the bone structure is often accompanied by collateral soft-tissue damage. Periosteal and endosteal blood-vessel disruption results in necrotic bone tissue at the fractured bone ends. Chemotactic signals are triggered by platelet degranulation and cytokines are released to initiate invasion of cells (led by macrophages) and angiogenesis.

2.Repair phase (2 days to 6 months postinjury). As inflammation reduces, reparative tissue proliferates mechanically stabilizing the injured zone. Revascularization, considered a fundamental process for bone healing, takes place. Adjacent to the fracture site intramembranous ossification occurs to create hard fracture callus (Fig 2.1-1). Under conditions of oxygen deficiency, fibrocartilage and hyaline cartilage will differentiate. Osteogenic factors cause further differentiation of chondroid tissue into bone—a process comparable to the differentiation that occurs at the growth plate (endochondral ossification). If the fracture is adequately stabilized the opposing bony fronts unite and the fracture is bridged.

3.Bone remodeling phase (3 months to 1-year postinjury). After achieving “clinical union”, interaction of osteoclasts and osteoblasts leads to replacement (remodeling) of callus and conversion of woven bone to mechanically superior lamellar bone. This maturation of the bone tissue includes realignment of osteons. Cancellous bone remodels to form bone trabeculae whereas cortical bone remodels to form a Haversian structure.

Secondary healing can tolerate varying degrees of stability. However, too much stability can suppress callus formation altogether resulting in a delayed union or nonunion. On the other hand, too much movement from unstable fixation may result in a large external callus. But if the instability persists, healing may be delayed and result in what is termed a hypertrophic nonunion.

Fig 2.1-1a-f Sequence of secondary healing in an ovine tibia osteotomy. Calcified bone tissue is depicted in black. Only one cortex is shown with endosteal side left and periosteal side right. At 2 weeks (a) new bone formation is visible on the periosteal aspect of the bone and grows predominantly laterally at first till 3 weeks (a-c). Following bridging at around 6 weeks (d), the callus remodels and resorbs (d-f). Histological images are taken from 2, 3, 6, and 9 weeks postoperatively. (Images courtesy of Georg N Duda, Dr-Ing [3].)

Extensive research [4] has revealed that a certain magnitude of fracture gap motion supports timely secondary bone healing, which makes relative stability an important pillar of modern osteosynthesis. Figure 2.1-2 shows an exemplary progression of fracture gap motion over time measured in an experimental fracture (ovine tibia) under functional loading. The formation of callus in combination with fixation leads to increased stability; hence, to a characteristic decline of motion until a level is reached whereby the tissues can calcify and remodel into solid bone for restoration of the bone’s load-bearing function.

Fig 2.1-2 Continuous interfragmentary motion measurements in a 3 mm sheep tibia osteotomy under physiological loading over time. Average fracture motion decrease indicates temporary stabilization by fracture callus (see corresponding x-rays). When fracture motion drops below 2% interfragmentary strain, bone remodeling can occur in the gap (unpublished data, courtesy of AO Research Institute Davos).

2.3.2 Concept of interfragmentary strain

The macroscopic loading environment of a fracture is complex. The predominant compression force is often superimposed with bending, shear, and torsion leading to multi-directional deformation of the fracture gap. However, understanding the influence of load on bone healing requires a closer look at the tissue/cellular level. It is crucial to understand that the important parameter is not the macroscopic motion within the fracture (interfragmentary movement), but the deformation of the repair tissue. The mechanical macroenvironment has an immediate impact on the cell microenvironment and is influenced by two major factors:

1.Gap motion: the displacement of the fracture surfaces in relation to each other.

2.Gap width: the initial distance between the fracture surfaces.

Stephan Perren [5] proposed the concept of interfragmentary strain, gap motion divided by gap width, to capture the role of these two influencing factors. The term “strain” describes the deformation of a body in relation to its original dimension. Interfragmentary strain provides a framework to understand the appearance of different tissue types within a fracture callus and changes in tissue types as healing progresses. A given displacement within a fracture gap is shared by the cells in the tissue bridging that gap. With a decreasing number of cells (decreasing gap width), each cell experiences a larger individual deformation (increasing strain) (Fig 2.1-3a- b). According to Yamada [6], liver parenchyma, here assumed to offer similar properties to granulation tissue, fails at 100% elongation. Cartilage ruptures at 10% and cortical or cancellous bone at 2% elongation (Fig 2.1-3c).

It can be safely assumed that tissue cannot be formed under conditions where it would be disrupted. For example, bone cannot be generated when the local tissue strain exceeds 2%. The goal of flexible fixation is to create an environment where the deformation of the repair tissue currently present in the fracture remains tolerable when the fracture is loaded. For example, the strain in the gap in the exemplary healing case of Fig 2.1-2 peaks at approximately 8% on day 12, which is tolerable for callus tissue, and drops below the 2% mark at around day 25 to enable actual bone formation bridging the gap.

In cases when the gap mobility cannot be controlled, the gap width must be adjusted to obtain acceptable conditions for bone healing. Initial bone resorption at the fracture ends may be regarded as a natural response of the biological system to reduce tissue strain by enlarging the fracture gap width.

Fig 2.1-3a-c Principle of strain. The same fracture gap motion results in markedly different deformation of the interfragmentary tissue (b) depending on the width of the unloaded gap (a). According to its properties, a tissue tolerates different magnitudes of elongation in relation to its initial length L0 before failure occurs (c).

2.3.3 How much flexibility is needed?

Figure 2.1-4 shows results of an animal experiment limiting the amount of initial gap motion to different magnitudes resulting in low, medium, and high interfragmentary strain. Foremost, this experiment indicates that larger strain induces larger callus. It is notable that callus tends to grow predominantly radially toward the outside at higher strain magnitudes. This can be regarded as a natural attempt to reduce local tissue strain by creating a larger surface area of hard tissue pressing into the relatively soft early callus (much like a snowshoe prevents sinking deep into the snow) (Fig 2.1-4).

With recovery of the animals after surgery, the gap motion first rose to reach a maximum at around week 1 correlating with an increase in postoperative weight bearing. Even though the peak gap motion was different among the strain groups, at approximately week 5 gap motion had equalized among all animals (Fig 2.1-4). Hence, larger strain and callus magnitudes appear neither supportive for faster healing, nor does it seem to decelerate the consolidation. Secondary bone healing presents itself therefore as a robust process tolerating a variance of mechanical stimuli. This is good news for the surgeon because installing exact mechanical conditions at highly individual fracture and loading situations is not trivial. However, basic knowledge about the upper and lower limits of this window of strain where indirect bone healing can progress timely is important to identify and react on extreme cases ideally before healing complications occur.

Fig 2.1-4 Sheep experiment using an instrumented fixator with adjustable flexibility [7]. Top: average interfragmentary motion over time of three animal groups with different strain levels. Within 5 weeks, callus reduced the fracture gap motion in all strain groups to a level allowing fracture consolidation. Bottom: evolution of callus size measured from x-rays. Larger strain creates larger callus. X-rays are from exemplary animals of two strain groups indicating the different size in callus at week 7 (unpublished data, courtesy of AO Research Institute Davos, Switzerland).

The experiments of Hente and Perren [8] provide an interesting insight in this matter. By cutting out a wedge-shaped bone segment from a sheep tibia, a strain gradient was applied from 0% to 90% along a fracture plane by periodically tilting the bone wedge with an actuator (Fig 2.1-5