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C OPYRIGHT Ó 2012 BY T HE J OURNAL OF B ONE AND J OINT S URGERY, I NCORPORATED

Infection in Closed Fractures

A Case Report and Literature Review
Christopher Kim, MD, and Ted V. Tufescu, MD, FRCSC

Investigation performed at the Health Sciences Centre, Winnipeg, Manitoba, Canada

I
nfection after a closed fracture is rare. Whereas open frac- the anesthesiologist noted that the patient had a fever of 39°C.
tures are considered contaminated, closed fractures are as- Intraoperatively, a small amount of purulent liquid was discovered
sumed to be uncontaminated and have an extremely low risk in the medial suprapatellar area. The surrounding soft tissue also
of infection. We report on a previously healthy adult patient who
presented acutely with an infected, closed patellar fracture. The
patient was informed that data concerning her case would be
submitted for publication, and she provided consent.
Our review of the literature has identified several reports
of osteomyelitis in closed fractures1-12. These were generally pe-
diatric cases1,3,5,8,9-11 or cases in immunocompromised adults2,11,12.
Our patient was an immunocompetent adult. We found only five
cases of osteomyelitis after closed fractures in immunocompetent
adults4,6,7,9. In two of the cases, the patients presented with mul-
tiple severe injuries and associated complications that could have
served as a source for hematogenous spread of bacteria4,7. In all
five cases, it took several weeks to months for an infection to
present at the closed fracture site4,6,7,9. Our patient presented
acutely with an isolated closed injury with no apparent source
for infection.
The pathogenesis of an infection after a closed fracture is
an area of interest and research. First, it appears that healthy
tissue and body fluids are not bacteria-free, and that an open
wound is not the only source for a bacterial infection13-17. Second,
mechanisms have been described that allow such indwelling
bacteria to ‘‘home’’ to sites of closed injury16-18. Third, it has been
suggested that local changes after a closed injury can increase
susceptibility to infection13,19. The purpose of this report is to
briefly review these issues and increase awareness of this rare
event.

Case Report

A previously healthy thirty-one-year-old woman sustained an

isolated left patellar fracture (Fig. 1) after falling down a
flight of stairs. The patient was afebrile without symptoms of
infection. Physical examination revealed moderate swelling with-
out open wounds or abrasions. Two days after injury, the patient Fig. 1
was taken to the operating room for fracture fixation. At this time, Lateral knee radiograph of the closed transverse patellar fracture.

Disclosure: None of the authors received payments or services, either directly or indirectly (i.e., via his or her institution), from a third party in support of
any aspect of this work. None of the authors, or their institution(s), have had any financial relationship, in the thirty-six months prior to submission of this
work, with any entity in the biomedical arena that could be perceived to influence or have the potential to influence what is written in this work. Also, no
author has had any other relationships, or has engaged in any other activities, that could be perceived to influence or have the potential to influence what
is written in this work. The complete Disclosures of Potential Conflicts of Interest submitted by authors are always provided with the online version of the
article.

JBJS Case Connect 2012;2:e44 d http://dx.doi.org/10.2106/JBJS.CC.L.00008

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Fig. 2
Lateral knee radiograph following fixation of the patellar fracture with the
tension band wiring technique.
appeared to be infected on visual inspection. Wound swabs, tissue
samples, and blood were collected for Gram stain and cultures.
Thorough irrigation and debridement were performed. After
internal fixation of the patella (Fig. 2), a Hemovac drain was
placed in the medial suprapatellar region, and the incision was
closed surrounding the drain. The patient was placed on in-
travenous (IV) cefazolin therapy postoperatively.
On postoperative day three, the patient developed con-
siderable cellulitis over the left knee. She was afebrile and the
pain was controlled. Intraoperative cultures revealed b-hemolytic
group-A streptococci from both the wound swab and tissue
samples. Blood culture specimens remained negative. The pa-
tient was placed on IV ceftriaxone therapy for a total of six
weeks, followed by oral cefalexin therapy for another six weeks.
The infection subsided with this treatment, and the patient re-
gained full knee function. Implant removal was planned after full
fracture consolidation.
Discussion
W hen identifying infection in closed fractures with unper-
forated skin, we must consider the origin of the invading
bacteria. It has been reported that bacteria dwell in normal healthy
INFECTION IN CLO S E D FR AC T U R E S
tissues, including the soft tissues, tissue fluids, lymphatics, and
lymph nodes13-17. Skin microorganisms can penetrate the epi-
dermis to translocate and eventually reside in deeper tissues18.
For example, foot microorganisms may penetrate the skin
through microinjuries or skin fissuring. They may use the
lymphatics and blood circulation to eventually settle within the
perivascular spaces and lymph nodes18. The propensity of pre-
patellar bursitis to become infected is also well recognized. Ap-
proximately 80% of cases are caused by Staphylococcus aureus20.
It is believed that such factors as minor trauma, humidity, and
skin fissuring all contribute to the direct inoculation of normal
skin bacteria into the superficial bursa20. The fluid collection or
hematoma from a patellar fracture is in close proximity to the
skin, and it is reasonable to consider a similar mechanism of
infection in the setting of local trauma. In any case, healthy,
noninjured tissue and body fluids are not bacteria-free. These
bacteria do not evoke a host response, perhaps because the
bacterial load remains below the threshold of an inflammatory
response.
It has been suggested that the effects of closed trauma
allow such indwelling bacteria to ‘‘home’’ to the site of injury.
Szczesny et al. hypothesized that bacteria residing in local lymph
and lymph nodes may translocate to an acute closed fracture
site16,17. They suggested that a fracture results in the activation of
the local lymphoid tissue, resulting in dilated lymphatics, en-
larged lymph nodes, and mobilization of cells within the nodes17.
Although the nature of this response is unknown, it provides a
possible mechanism for the movement of bacteria to the fracture
site. It has also been suggested that bacteria that survive and
reside within host phagocytic cells may be transported to dam-
aged tissue during the inflammatory phase18. It is also possible
that damage to local soft tissue contributes to the direct inocu-
lation of indwelling bacteria to the fracture site.
Posttraumatic infection is related to the local changes
that occur to increase susceptibility to infection; local soft-
tissue trauma is a risk factor for posttraumatic infection13,19.
It is believed that soft-tissue damage and its pathophysio-
logical consequences result in decreased resistance to bacte-
rial load. Observations have shown that surgical treatment of
closed fractures with severe soft-tissue injuries is associated
with a higher risk of infection compared with closed fractures
without severe soft-tissue injury21,22.
Our review of the literature revealed two main groups of
patients who developed infections after closed fractures. These
were either pediatric patients or immunocompromised adults.
The pediatric cases involved children who sustained a closed
fracture and subsequently developed osteomyelitis after a short
period of nonoperative management1,3,5,8,9-11. These children
usually developed a remote infection shortly after their fracture,
such as an upper respiratory tract infection (URTI) or urinary
tract infection (UTI). These types of infections are described as
the possible source for spread of infection to the fracture site.
They were treated with antibiotics and had excellent outcomes.
This was not the case with immunocompromised adults2,11,12 who
had reduced resistance to infection because of chronic con-
ditions, including diabetes, prolonged steroid use, or cancer.
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Nonunion was not uncommon, and the outcome was generally
poor in these patients.
The diagnosis of infection at a closed fracture site is often
delayed. It is not unreasonable to suspect infection in patients
who continue to have symptoms of pain and swelling to the
fracture site after several weeks of immobilization. This is es-
pecially true in the pediatric patient with a history of a recent
remote infection, such as a URTI or UTI. In many cases, pa-
tients are febrile and present with a warm, tender, and fluctuant
fracture site. The belief that infection does not occur with
closed fractures may prove too simplified, as perforated skin
may not be the only source for bacterial invasion. Bacteria re-
side in normal healthy tissue and fluids, including within the
callus of a healing fracture16. We must question what the risk
factors and mechanisms are for such bacteria to evoke an in-
References
1. Aalami-Harandi B. Acute osteomyelitis following a closed fracture. Injury. 1978
Feb;9(3):207-8.
2. Aluisio FV, Scully SP. Acute hematogenous osteomyelitis of a closed frac-
ture with chronic superinfection. Clin Orthop Relat Res. 1996 Apr;(325):
239-44.
3. Baharuddin M, Sharaf I. Acute haematogenous osteomyelitis: an unusual com-
plication following a closed fracture of the femur in a child. Med J Malaysia. 2001
Dec;56 Suppl D:54-6.
4. Baskaran S, Nahulan T, Kumar AS. Close fracture complicated by acute
haematogenous osteomyelitis. Med J Malaysia. 2004 Dec;59 Suppl F:72-4.
5. Canale ST, Puhl J, Watson FM, Gillespie R. Acute osteomyelitis following
closed fractures. Report of three cases. J Bone Joint Surg Am. 1975 Apr;57(3):
415-8.
6. Cozen L. Four unusual cases of osteomyelitis in adults. West J Surg Obstet
Gynecol. 1958 Jan-Feb;66(1):36-9.
7. Folberg C, Hardy AE, Isaacs RD, Ellis-Pegler RB. Osteomyelitis complicating a
closed fracture. N Z Med J. 1987 Jun 24;100(826):392-3.
8. Hardy AE, Nicol RO. Closed fractures complicated by acute hematogenous os-
teomyelitis. Clin Orthop Relat Res. 1985 Dec;(201):190-5.
9. Stuart D. Local osteo-articular tuberculosis complicating closed fractures: report
of two cases. J Bone Joint Surg Br. 1976 May;58(2):248-9.
10. Veranis N, Laliotis N, Vlachos E. Acute osteomyelitis complicating a closed
radial fracture in a child. A case report. Acta Orthop Scand. 1992 Jun;63(3):
341-2.
11. Watson FM, Whitesides TE Jr. Acute hematogenous osteomyelitis complicating
closed fractures. Clin Orthop Relat Res. 1976 Jun;(117):296-302.
12. Weidle PA, Brankamp J, Dedy N, Haenisch C, Windolf J, Jonas M. Compli-
cation of a closed Colles-fracture: necrotising fasciitis with lethal outcome.
A case report. Arch Orthop Trauma Surg. 2009 Jan;129(1):75-8. Epub 2008
Oct 18.
INFECTION IN CLO S E D FR AC T U R E S
flammatory response and cause an infection. It appears that
properties of the invading bacteria and local host factors both
play an important role. n
Christopher Kim, MD
University of Manitoba, AD 420 – 720 McDermot Avenue,
Winnipeg, Manitoba, R3E 0T3 Canada.
E-mail address: umkim88@cc.umanitoba.ca
Ted V. Tufescu, MD, FRCSC
Health Sciences Centre, AD4 – 820 Sherbrook Street,
Winnipeg, Manitoba, R3A 1R9 Canada.
E-mail address: ttufescu@exchange.hsc.mb.ca
13. Kälicke T, Schlegel U, Printzen G, Schneider E, Muhr G, Arens S. Influence of a
standardized closed soft tissue trauma on resistance to local infection. An experi-
mental study in rats. J Orthop Res. 2003 Mar;21(2):373-8.
14. Raasch W, Regunathan S, Li G, Reis DJ. Agmatine, the bacterial amine, is widely
distributed in mammalian tissues. Life Sci. 1995;56(26):2319-30.
15. Olszewski WL, Jamal S, Manokaran G, Pani S, Kumaraswami V, Kubicka U,
Lukomska B, Dworczynski A, Swoboda E, Meisel-Mikolajczyk F. Bacteriologic studies
of skin, tissue fluid, lymph, and lymph nodes in patients with filarial lymphedema.
Am J Trop Med Hyg. 1997 Jul;57(1):7-15.
16. Szczêsny G, Interewicz B, Swoboda-Kopeć E, Olszewski WL, G órecki A,
Wasilewski P. Bacteriology of callus of closed fractures of tibia and femur.
J Trauma. 2008 Oct;65(4):837-42.
17. Szczesny G, Olszewski WL, Gewartowska M, Zaleska M, Górecki A. The healing
of tibial fracture and response of the local lymphatic system. J Trauma. 2007
Oct;63(4):849-54.
18. Medina E, Goldmann O, Toppel AW, Chhatwal GS. Survival of Streptococcus
pyogenes within host phagocytic cells: a pathogenic mechanism for persistence and
systemic invasion. J Infect Dis. 2003 Feb 15;187(4):597-603. Epub 2003 Feb 7.
19. Nuwayhid ZB, Aronoff DM, Mulla ZD. Blunt trauma as a risk factor for group A
streptococcal necrotizing fasciitis. Ann Epidemiol. 2007 Nov;17(11):878-81. Epub
2007 Aug 13.
20. Cea-Pereiro JC, Garcia-Meijide J, Mera-Varela A, Gomez-Reino JJ. A comparison
between septic bursitis caused by Staphylococcus aureus and those caused by
other organisms. Clin Rheumatol. 2001;20(1):10-4.
21. Gustilo RB, Anderson JT. Prevention of infection in the treatment of one thou-
sand and twenty-five open fractures of long bones: retrospective and prospective
analyses. J Bone Joint Surg Am. 1976 Jun;58(4):453-8.
22. Siebert CH, Arens S, Hansis M. The role of surgical trauma in the aetiology of
postoperative wound infection-quantification of surgery induced trauma. Hyg Med
1995; 20:474-80.