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J. L. Johnson and R. Golden
Fractures oftheTibial Plateau
Tibial plateau fractures involve the intra-articular surface of the proximal aspect of the tibia. They can involve the lateral side in isolation, the medial side in isolation, or a combination of both. Frequently, they are the result of “bumper inju­ries” after a valgus load when a pedestrian is struck by the bumper of a car. They can result, however, from any type of traumatic loading of the knee joint. A well-established classication system named after the orthopedic surgeon Joseph Schatzker is widely used to describe these fractures. Treatment depends on the degree of displacement and comminution. Nondisplaced fractures may be treated by restricting weight bearing and initiating early motion. Displaced fractures are best treated surgically, including anatomic reduction of the articular surface and stable xation to the shaft of the tibia.
Early motion is begun after denitive xation, but full weight bearing should be delayed for 8–12weeks. The most important distinctions for tibial plateau fractures are whether the fracture is unicondylar or bicondylar, and if the medial aspect of the plateau is affected. Unicondylar plateau
fractures typically affect the lateral plateau, are more commonly low energy mechanisms, and often do not require urgent surgical treatment if the knee is otherwise stable. A tibial plateau fracture with a fracture line through the medial plateau is typically due to a higher energy mechanism. These fracture patterns are considered to be a knee dislo­cation equivalent with higher risk of neurovascular injury and compartment syndrome. If a medial component is seen on imaging, ankle brachial indices should be obtained in the emergency department, and the fracture would be immobi­lized with an external xator to allow for soft tis­sues to become amenable to denitive xation. After external xation, a CT scan should be obtained for preoperative planning (Fig.4.29).
Fractures ofthePatella
The patella is a sesamoid bone that gives the quadriceps mechanism a mechanical advantage in knee extension. If the fracture is nondisplaced, or does not affect the extensor mechanism, closed treatment with immobilization for up to 6weeks can be performed. However, for displaced frac-
Fig. 4.29 Tibial plateau fractures—the top image is a Schatzker II tibial plateau fracture. The red arrow on the left image is the split and blue arrow is the articular
depression. On the right image the red arrow shows the medial piece and the blue shows the lateral piece
4 Skeletal Trauma
81
tures open reduction and internal xation is the treatment of choice. As in the fracture of the olec­ranon, a tension-banding procedure can achieve reliable xation, but many other constructs involving screws and plates can also be effective. In extremely comminuted fractures, a patellec­tomy may be the only option to avoid an irregular patellar surface that would result in painful trau­matic arthritis of the patellofemoral joint.
Dislocation oftheKnee
This injury is often the result of very severe trauma, although can sometimes occur in bariatric patients with otherwise relatively minor falls. When a patient gives a history that the “knee came out of place,” the injury is usually not a knee dislocation but rather a patella dislocation or anterior cruciate ligament tear. True dislocation of the knee is a very serious injury notable for a high risk of vascular injury to the pop­liteal vessels. The popliteal artery is xed anatomi­cally at the level of the proximal tibia by the interosseous membrane and, therefore, is at great risk when the knee dislocates. Careful physical exam should be performed including a full vascular exam with evaluation of pulses and ABIs. Arteriography can be performed following immedi­ate closed reduction of the dislocation if vascular compromise is suspected. The results of angiogra­phy will then determine whether consultation of the vascular surgery team and arterial repair is neces­sary. If gross instability is present following this injury, an external xator bridging the knee may be necessary until denitive ligament repair can be performed. Multiple ligament injuries are the norm after knee dislocations. Ligamentous repair/recon­struction is usually necessary after early emergent reduction, external xation, and vascular manage­ment have been accomplished.
Fracture oftheTibial Shaft
Fractures of the tibial shaft are one of the classic fractures in the treatment of long bone injuries and open fractures. Because of its vulnerable location just beneath the skin throughout its
length and association with high energy mecha­nisms, it is prone to open fractures. Because of its tenuous blood supply, open fractures of the tibia are at risk for nonunion. A particular area of con­cern is at the junction of the middle and distal thirds where a vascular watershed exists, and the muscle envelope is decient over the anterome­dial surface of the bone. The time to fracture union is prolonged, generally taking 16–20weeks. Nondisplaced or minimally displaced tibial frac­tures can be treated by the application of a long leg cast. When early healing has occurred, a shorter, the so-called patella tendon bearing cast may be applied. Operative treatment options include percutaneous or open plating, external xation, and intramedullary nailing. As with long bone fractures in other locations, intramedullary nailing allows relatively early weight bearing and functional return and is generally considered the surgical treatment of choice if the fracture pattern is amenable to its use (Fig.4.30).
Ankle andTibial Plafond Fractures
Fractures of the malleoli are termed “ankle” frac­tures by convention and involve the distal end of the bula (lateral malleolus), the medial malleo­lus, and the posterior malleolus of the tibia. The mechanism of injury for these fractures is a tor­sional force applied to the ankle. Radiographic evaluation of these fractures should include an AP, lateral, and mortise view of the ankle. The mortise view is an oblique view with 15° of inter­nal rotation which provides an en face view of the ankle joint (Fig.4.31).
A CT scan is typically not required for a sim­ple ankle fracture. A commonly used system for ankle fractures is the Lauge-Hansen classica­tion system which is specic to bi-malleolar frac­tures of the medial and lateral malleoli. The rst word in each category describes the position of foot at the time the force was applied. The second word denotes the anatomic direction of the load (Fig.4.32).
This system is based on cadaver study and likely does not apply adequately to all fractures. It also has limited value in directing treatment. A
82
Fig. 4.30 Tibial Shaft Fracture Treated with an intramedullary (IM) nail
J. L. Johnson and R. Golden
Fig. 4.31 Ankle X-rays-These X-rays are a typical ankle series with a normal appearance. The top left is an AP view, the top right is a mortise view, and the bottom is a lateral view
ubiquitous classication specic to bula frac­tures is the Weber classication which is strati­ed into A-a fracture distal to the syndesmosis, B-a fracture at the level of the syndesmosis, and C-a fracture proximal to the syndesmosis (Fig.4.33).
While a nondisplaced fracture of the lateral malleolus with a stable ankle joint may be treated by a simple below-the-knee cast or sometimes a fracture boot, displaced ankle fractures with an unstable ankle joint are typically treated with open reduction and internal xation. The primary
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83
Fig. 4.32 Diagram of the Lauge-Hansen classication of ankle fractures
Supination–Eversion
Supination–Adduction
Fracture
at level
of
joint
line
Pronation–Abduction
Pronation–Eversion
84
J. L. Johnson and R. Golden
Fig. 4.34 Pilon fracture—a mortise view and lateral view of a pilon fracture. Note the disruption of the tibial plafond marked by the arrow
Fig. 4.33 Weber fracture locations—this is a mortise view of the ankle. The blue dots show the approximate region of the syndesmosis. Fractures below this region are Weber A, fractures within the arrows represent Weber B, and fractures proximal are classied as Weber C
goal of treatment for ankle fractures is anatomic restoration and maintenance of reduction of the mortise of the ankle. Following operative xation and depending on the fracture pattern, patients may be kept non-weight bearing for 6weeks, fol­lowed by gradual return to weight bearing and initiation of range of motion and strengthening exercises.
Fractures of the distal articular surface of the tibia are categorized separately from common ankle fractures. They typically result from axial loading injuries, as opposed to rotational or tor­sional forces as with ankle fractures, and involve a signicant amount of articular cartilage dam­age. They are termed pilon (French for “pestle”) fractures and represent a difcult management problem. These fractures are often comminuted and length unstable. Furthermore, they have high risk associated with swelling, fracture blisters,
and open fractures. As a result, they are com­monly complicated by wound issues and infec­tion. To account for this the typical treatment is restoration of length alignment and rotation with external xation in the acute setting. After the ini­tial reduction with external xation, a CT scan should be obtained, and open reduction internal xation may be performed in a delayed fashion once the soft tissues are amenable. Because of the high energy nature of these fractures and the disruption of the articular cartilage of the tibial plafond, they are frequently complicated by post­traumatic arthritis of the ankle (Fig.4.34).

Conclusion

Fracture treatment is a foundational aspect of orthopedic care. Understanding the mechanism and timing of the injury combined with a thor­ough physical and radiographic exam provide the means to develop a clear plan for initial and denitive treatment. The basic tenets involve understanding bone healing principles, types of xation, and the appropriate application of the mode of xation that will provide the fracture
4 Skeletal Trauma
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pattern with stability for the desired type of frac­ture healing. Successful fracture care applies each of these principles throughout the body and is the basis of each type of fracture surgery.

Further Reading

Augat P, von Rüden C. Evolution of fracture treatment
with bone plates. Injury. 2018;49:S2. https://doi.
org/10.1016/S0020- 1383(18)30294- 8.
Bekos A, Sioutis S, Kostroglou A, Saranteas T,
Mavrogenis AF.The history of intramedullary nailing.
Int Orthop. 2021;45(5):1355. https://doi.org/10.1007/
s00264- 021- 04973- y.
Benders KEM, Leenen LPH. Management of hemo-
dynamically unstable pelvic ring fractures. Front
Surg. 2020;7:601321. https://doi.org/10.3389/
fsurg.2020.601321.
Bible JE, Mir HR.External xation: principles and appli-
cations. J Am Acad Orthop Surg. 2015;23(11):683.
https://doi.org/10.5435/JAAOS- D- 14- 00281.
Galbiatti JA, Cardoso FL, Ferro JAS, Godoy RCG, Belluci
SOB, Palacio EP.Terrible triad of the elbow: evaluation
of surgical treatment. Rev Bras Ortop. 2018;53(4):460.
https://doi.org/10.1016/j.rbo.2017.05.016.
Guerado E, Bertrand ML, Cano JR, Cerván AM, Galán
A. Damage control orthopaedics: state of the art.
World J Orthop. 2019;10(1):1. https://doi.org/10.5312/
wjo.v10.i1.1.
Hak DJ, Toker S, Yi C, Toreson J. The inuence of
fracture xation biomechanics on fracture heal-
ing. Orthopedics. 2010;33(10):752. https://doi.
org/10.3928/01477447- 20100826- 20.
Iyer KM, Khan WS. General principles of orthopedics
and trauma. 2nd ed. Cham: Springer; 2019. https://doi.
org/10.1007/978- 3- 030- 15089- 1.
Von Keudell AG, Weaver MJ, Appelton PT, et al.
Diagnosis and treatment of acute extremity compart-
ment syndrome. Lancet. 2015;386(10000):1299.
https://doi.org/10.1016/S0140- 6736(15)00277- 9.
Langford JR, Burgess AR, Liporace FA, Haidukewych
GJ. Pelvic fractures: part 1. Evaluation, clas­sication, and resuscitation. J Am Acad Orthop Surg. 2013;21(8):448. https://doi.org/10.5435/
JAAOS- 21- 08- 448.
Langford JR, Burgess AR, Liporace FA, Haidukewych
GJ.Pelvic fractures: part 2. Contemporary indications and techniques for denitive surgical management. J Am Acad Orthop Surg. 2013;21(8):458. https://doi.
org/10.5435/JAAOS- 21- 08- 458.
Miller MD, Thompson SR.Miller’s review of orthopae-
dics. J Chem Inf Model. 2016;53(9):53.
Mohanty K, Musso D, Powell JN, Kortbeek JB,
Kirkpatrick AW.Emergent management of pelvic ring injuries: an update. Can J Surg. 2005;48(1):49.
Morrey ME, Morrey BF, Sanchez-Sotelo J, Barlow
JD, O’Driscoll S. A review of the surgical man­agement of distal humerus fractures and non­unions: from xation to arthroplasty. J Clin Orthop Trauma. 2021;20:101477. https://doi.org/10.1016/j.
jcot.2021.101477.
Seligson D, Mauffrey C, Roberts CS. External xation
in orthopedic traumatology. London: Springer; 2012.
https://doi.org/10.1007/978- 1- 4471- 2197- 8.
Smith WR, Stahel PF. Management of musculoskeletal
injuries in the trauma patient. New York: Springer;
2013. https://doi.org/10.1007/978- 1- 4614- 8551- 3.
Tornetta P, Court-Brown CM, Heckman JD, et al.
Rockwood, Green, and Wilkins fractures in adults and children, vol. 1–2. 8th ed. Lippincott Williams and Wilkins; 2014.
Watts AC, Singh J, Elvey M, Hamoodi Z. Current
concepts in elbow fracture dislocation. Shoulder Elbow. 2021;13(4):451. https://doi.
org/10.1177/1758573219884010.
Zalavras CG, Patzakis MJ.Open fractures: evaluation and
management. J Am Acad Orthop Surg. 2003;11(3):212.
https://doi.org/10.5435/00124635- 200305000- 00008.

Orthopedic Infections

RAdamsCowley II, KevinW.Park, andKennethM.Vaz
5

Introduction

When analyzed against common infections, musculoskeletal infections can be challenging to diagnose and thus treat. Unrecognized infections can be both life and limb threatening if not rec­ognized and treated. The most important aspect of caring for patients with a musculoskeletal infection is to come to a timely diagnosis to per­mit swift appropriate treatment. In these scenar­ios, most musculoskeletal infections can be effectively treated, decreasing morbidity. Open fractures are an extremely common occurrence in orthopedics, and special attention is given to this topic. While general principles have remained constant, the specic recommenda­tions have evolved. In general, appropriately treated open fractures can typically prevent the establishment of any type of chronic musculo­skeletal infection or osteomyelitis.
R. A. Cowley II (*) · K. W. Park · K. M. Vaz MedStar Georgetown Orthopedic Institute, Georgetown University School of Medicine, Washington, DC, USA
Department of Orthopedics, MedStar Georgetown University Hospital, Washington, DC, USA e-mail: RAdams.Cowley@medstar.net;
Kevin.W.Park@medstar.net; Kenneth.M.Vaz@medstar.net
Pathophysiology ofOsteomyelitis
The pathogenesis of osteomyelitis has been well dened; yet the clinical course may vary depend­ing on host, organism, and duration of infection. Thus, osteomyelitis is often classied using these parameters, which aids in determining severity, treatment, and prognosis.
Duration of infections is often divided into either acute or chronic osteomyelitis; this also applies to infections involving the joints such as septic arthritis. Acute osteomyelitis is usually considered to occur within the rst 6weeks fol­lowing inoculation, with chronic osteomyelitis being greater than 6weeks.
Bone and joint infections take place via one of two basic mechanisms: exogenous or hematogenous pathways. Exogenous delivery involves direct inoc­ulation of the bone from either trauma, surgery or a contiguous focus of infection. Hematogenous spread is via the vascular system into either osseous or synovial tissue, producing a localized focus of infec­tion. Local tissue compromise (i.e., open fracture) or systemic pathology (i.e., diabetes, immunode­ciency) is often associated with an increased propen­sity for bone infection by either method.
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2024 W. F. Postma et al. (eds.), Essentials of Orthopedic Surgery,
https://doi.org/10.1007/978-3-031-66215-7_5
87
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R. A. Cowley et al.
Two patterns of response occur depending on
the infecting organism:
1. Pyogenic organisms: rapidly progressive course of pain, swelling, abscess formation, and aggressive bone destruction
(a) Example: gram-positive staphylococcus
2. Nonpyogenic: less aggressive insidious gran­ulomatous reaction
(a) Example: acid-fast bacilli
Age is important in that differences in bone vascular anatomy between adults and children slightly alter the mechanism of hematogenous delivery. In addition, children are susceptible to different organisms depending upon their age.
Exogenous osteomyelitis usually involves a demarcated isolated anatomic site that is inocu­lated with pyogenic organisms. Typically, these infections are polymicrobial, frequently in asso­ciation with foreign debris. The bacteria are inoc­ulated into a compromised local environment, with bone and soft tissue disruption providing copious amounts of necrotic and devascularized material favorable for bacterial growth. In addi­tion, tissue devascularization prevents host response mechanisms from reaching bacterial colonies permitting unregulated proliferation.
Once a bone infection is recognized by the host, several steps are unfold:
1. Initial host response to both the injury and
infection include activation of inammatory and immunologic pathways.
(a) Inammatory elements serve to destroy
bacteria and remove nonviable material.
(b) Humoral and cellular immunologic
mechanisms act to recognize specic bac­teria and subsequently confer immunity to prevent further bacterial dissemination.
2. The inammatory response is initiated with
increases in blood ow and vascular permea­bility, with the delivery of polymorphonuclear leukocytes.
(a) The leukocytes phagocytize and destroy
bacteria and nonviable tissue.
3. Mononuclear cells arrive within 24–48h and
assist in eradication of bacteria and removal
of necrotic bone. As a large number of these cells arrive and die, pus is formed, with an abscess often being clinically appreciable.
4. Granulation tissue surrounds the infected area in an attempt to wall off the infection.
5. Reactive bone formation can occur to further sequester the infection from the host.
Within the infected region, dead bone, the sequestrum, and reactive bone, the involucrum, are appreciated. The treatment of osteomyelitis becomes clear once an understanding of how bacteria gain traction in either damaged tissues or surgical implants. Adhesion to the surface of tis­sue cells and implants depends on the physical characteristics of the bacteria, the uid interface, and the substratum.
1. Attachment and Adhesion: anionic surface
initially repels anionic bacteria; however, over time, attractive forces (Van der Waals) with hydrophobic molecules on both substrate and bacteria form an irreversible cross link glyco­proteinaceous conditioning lm.
2. Aggregation: polysaccharide slime layer
composed of bacterial extracapsular exopoly­saccharides that bind to surfaces, promote cell-to-cell adhesion, microcolony formation, and layering of the microorganisms.
(a) Additional species of bacteria may attach
to the surface of the biolm.
3. Dispersion: Thriving bacterial colonies may
be dispersed by sheer force, enabling a local­ized colony to establish secondary sites of infection (Fig.5.1).
These biolms can lead to antibiotic resis­tance through decreased metabolic rates and phe­notypic changes in surface-adherent bacteria. Therefore, bacteria on surfaces or within micro­colonies appear to be physiologically different from free-oating organisms, which may, in part, convey antibiotic resistance.
Treatment of osteomyelitis involves the dis­ruption of these bacterial colonies, which is best achieved with aggressive debridement of nonvi­able tissues to remove an acceptable bacterial substrate and their associated biolm. In the
5 Orthopedic Infections
89
Fig. 5.1 Molecular sequence in bacterial (B) attachment, adhesion, aggregation, and dispersion at substratum sur­face. A number of possible interactions may occur
case of osteomyelitis involving a prosthesis or fracture implant, it is often necessary to remove either the prosthesis or implant to eradicate the infection.

Pediatric Infections

Acute Hematogenous Osteomyelitis

Hematogenous inoculation represents the most common etiology for acute osteomyelitis. Given the tortuous vascular anatomy of children’s long bones, the risk of hematogenous inoculation and proliferation of bacteria is increased.
The nutrient artery of long bones enters through the cortical bone to divide within the medullary canal, ending in small arterioles that ascend toward the physis (Fig.5.2). Just deep to the physis, these arterioles turn away from the physis and empty into venous pools within the medullary cavity. The acute bend in these arterial loops serve as points of diminished blood veloc­ity, promoting sludging of bacteria directly under
depending on the specicities of the bacteria or substra­tum system (graphics, nutrients, contaminants, macro­molecules, species, and materials)
Fig. 5.2 Microcirculation of the metaphysis predisposes it to sludging and infection
the physis. In addition, phagocytic capability and reticuloendothelial function may be depressed in these vascular loops, permitting the establish­ment of bacterial colonies. Trauma, often associ­ated with the emergence of osteomyelitis in children, may actually promote bacterial seeding and proliferation in metaphyseal sites (Fig.5.3).
90
If the immune system fails to eradicate the infection and/or appropriate treatment is not initi­ated, purulent material will be produced (Fig. 5.4). This pus can spread in one of three ways: through the physis, toward the diaphysis, or through the adjacent bony cortex (Fig.5.5).
This purulent material tends to seek the path of least resistance, through the metaphyseal cor­tex, to form a collection of subperiosteal pus. Although this is the most common route, younger children (less than 1year) with intact transphyseal vessels may demonstrate epiphyseal spread with the development of epiphyseal abscesses. In older children, the development of a subperios­teal abscess results in devascularization of the bone both from thrombosis of the endosteal blood supply and from the stripping away of the overly­ing periosteum. The periosteum, which is extremely thick and loosely adherent in children, is not easily penetrated. In the devascularization process, it is lifted off the bone, with the inner cambial layer producing a layer of new bone. In this case, the sequestrum and involucrum are formed (Fig.5.6).
The time frame of diagnosis plays a role in appropriate treatment. The cellulitic phase pre­cedes abscess formation. During this early phase, medical management alone is typically success­ful to cure the infection. However, once an abscess forms, surgical debridement is necessary for three critical reasons:
R. A. Cowley et al.
Fig. 5.3 Schematic representation of the blood supply to a long bone
1. Remove the nonviable bone
2. Reduce the bacterial population
3. Provide for a vascularized tissue bed for anti-
biotic delivery
As the majority of pediatric infections ema­nate via hematogenous seeding from other sites, the specic organisms may differ depending upon the child’s age. The vast majority of osteo­myelitis in children is secondary to Staphylococ- cus aureus (90%). In neonates, the most common organisms include Staphylococcus aureus, group B streptococci, and gram-negative organisms.
Fig. 5.4 A localized abscess develops, and the microen­vironment is altered