OSTEOMYELITIS

LATAR BELAKANG.Osteomyelitis adalah proses inflamasi akut atau kronik pada

tulang dan struktur sekundernya karena infeksi oleh bakteri piogenik.

PATHOPHYSIOLOGY.Infeksi pada osteomyelitis dapat terjadi lokal atau dapat

menyebar melalui periosteum, korteks, sumsum tulang, dan jaringan retikular. Jenis bakteri bevariasi berdasarkan pada umur pasien dan mekanisme dari infeksi itu sendiri.Terdapat dua kategori dari osteomyelitis akut:1. Hematogenous osteomyelitis, infeksi disebabkan bakteri melalui darah. Acute hematogenous osteomyelitis, infeksi akut pada tulang disebabkan bekteri yang berasal dari sumber infeksi lain. Kondisi ini biasanya terjadi pada anak-anak. Bagian yang sering terkena infeksi adalah bagian yang sedang bertumbuh pesat dan bagian yang kaya akan vaskularisasi dari metaphysis. Pembuluh darah yang membelok dengan sudut yang tajam pada distal metaphysis membuat aliran darah melambat dan menimbulkan endapan dan trombus, tulang itu sendiri akan mengalami nekrosis lokal dan akan menjadi tempat berkembang biaknya bakteri. Mula-mula terdapat fokus infeksi didaerah metafisis, lalu terjadi hiperemia dan udem. Karena tulang bukan jaringan yang bisa berekspansi maka tekanan dalam tulang ini menyebabkan nyeri lokal yang sangat hebat. Infeksi dapat pecah ke subperiost, kemudian menembus subkutis dan menyebar menjadi selulitis atau menjalar melalui rongga subperiost ke diafisis. Infeksi juga dapat pecah kebagian tulang diafisis melalui kanalis medularis.Penjalaran subperiostal kearah diafisis akan merusak pembuluh darah yang kearah diafisis, sehingga menyebabkan nekrosis tulang yang disebut sekuester. Periost akan membentuk tulang baru yang menyelubungi tulang baru yang disebut involukrum (pembungkus). Tulang yang sering terkena adalah tulang panjang yaitu tulang femur, diikuti oleh tibia, humerus ,radius , ulna, dan fibula. 2. Direct or contigous inoculation osteomyelitis disebabkan kontak langsung antara jaringan tulang dengan bakteri, biasa terjadi

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karena trauma terbuka dan tindakan pembedahan. Manisfestasinya terlokalisasi dari pada hematogenous osteomyelitis.Kategori tambahan lainnya adalah chronic osteomyelitis dan osteomyelitis sekunder yang disebabkan oleh penyakit vaskular perifer.Osteomyelitis sering menyertai penyakit lain seperti diabetes melitus, sickel cell disease, AIDS, IV drug abuse, alkoholism, penggunaan steroid yang berkepanjangan, immunosuppresan dan penyakit sendi yang kronik. Pemakaian prosthetic adalah salah satu faktor resiko, begitu juga dengan pembedahan ortopedi dan fraktur terbuka.Rasio antara pria dan wanita 2 :1.

RIWAYAT PENYAKIT SEKARANGGejala hematogenous osteomyelitis biasanya berajalan lambat

namun progresif. Direct ostoemyelitis umumnya lebih terlokalisasi dan jelas.

Gejala pada hematogenous osteomyelitis pada tulang panjang umumnya adalah:- Demam tinggi mendadak.- Kelelahan.- Iritabilitas.- Malaise.- Terbatasnya gerakan.- Edem lokal yang disertai dengan erytem dan nyeri pada penekanan.Pada Hematogenous osteomyelitis pada tulang belakang:- Onsetnya bertahap.- Riwayat episode bekteriemi akut.- Kemungkinan berhubungan dengan insufisiensi vaskular.- Edem lokal, eritem, dan nyeri pada penekanan.Pada Kronik osteomyelitis :- Ulkus yang tidak kunjung sembuh.- Drainase saluran sinus.- Kelelahan yang berkepanjangan.- Malaise.

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Pada pemeriksaan fisik ditemukan :- Demam ( timbul hanya pada 50 % neonatus ).- Edem.- Terasa hangat.- Berfluktuasi.- Nyeri pada palpasi.- Terbatanya gerakan ekstremitas.- Drainase saluran sinus.

Penyebab: bakteri pada kasus direct osteomyelitis :Akut hematogenous osteonyelitis.Pada bayi baru lahir : S. aureus, Enterobacter Sp, dan Stretococcus Sp group A dan B.Pada anak umur 4 bulan sampai 4 tahun : S. aureus, Enterobacter Sp, Stretococcus Sp group A dan B dan H influenzae.

Pada anak-anak dan remaja muda : S. aureus ( 80 % ), Enterobacter Sp, Stretococcus Sp group A dan B dan H influenzae. Pada orang dewasa S. aureus, dan kadang-kadang Enterobacter Sp atau Stretococcus Sp group A dan B.

Differensial diagnosis :- Selulitis.- Gangren gas.- Gout dan Pseudogout.- Neoplasma, pada tulang belakang.- Kelumpuhan pada masa anak-anak.- Osteosarkoma.- Tumor Ewing.- Infeksi pada saraf spinal.

Lab.- Terjadi pergeseran shif kekiri.- CRP meningkat- Pada kultur hasil aspirasi dari tempat yang terinfeksi ditemukan normal pada 25 kasus, dan 50 % positif pada hematogenous osteomyelitis.- Peningkatan laju endap darah.

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Untuk menentukan diagnosis dapat ndigunakan aspirasi, pemeriksaan sintigrafi, biakan darah dan pemeriksaa pencitraan. Aspirasi dilakukan untuk memperoleh pus dari subkutis, subperiost, atau lokus radang dimetafisis. Untuk punksi tersebut digunakan jarum khusus untuk membor tulang.

Pada sintigrafi dipakai Thenectium 99. sensitivitas pemeriksaan ini terbatas pada minggu pertama, dan sama sekali tidak spesifik. Pada minggu kedua gambaran radiologi logis mulai menunjukkan dekstrusi tulang dan reaktif periostal pembentukkan tulang baru.

Therapi :Begitu diagnosis secara klinis ditegakkan, ekstremitas yang

terkena diistirahatkan dan segera berikan antibiotik. Bila dengan terapi intensif selama 24 jam tidak didapati perbaikan, dianjurkan untuk mengebor tulang yang terkena. Bila ada cairan yang keluar perlu dibor dibeberapa tampat untuk mengurang tekanan intraostal. Cairan tersbut perlu dibiakkan untuk menentuka jenis kuman dan resistensinya. Bila terdapat perbaikan, antibiotik parenteral diteruskan sampai 2 minggu, kemudian diteruskan secara oral paling sedikit empat minggu.

Penyulit berupa kekambuhan yang dapat mencapai 20%, cacat berupa dekstruksi sendi, gangguan pertumbuhan karena kerusakan cakram epifisis, dan osteomyelitis kronik.

Pada dasarnya penanganan yang dilakukan adalah :1. Perawatan dirumah sakit.2. pengobatan suportif dengan pemberian infus dan

antibiotika.3. Pemeriksaan biakan darah.4. antibiotika yang efektif terhadap gram negatif maupun

gram positif diberikan langsung tanpa menunggu hasil biakan darah, dan dilakukan secara parenteral selama 3-6 minggu.

5. Imobilisasi anggota gerak yang terkena.6. Tindakan pembedahan.

Indikasi dilakukannya pembedahan ialah :

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1. Adanaya sequester.2. Adanya abses.3. Rasa sakit yang hebat.4. Bila mencurigakan adanya perubahan kearah keganasan

(karsinoma Epidermoid).

PrognosisPrognosis bevariasi, tergantung pada kecepatan dalam

mendiagnosa dan melakukan penanganan

DAFTAR PUSTAKA

1. Sjamsuhidajat.R; De Jong.W, Editor. Buku Ajar Ilmu Bedah. Edisi Revisi, Cetakan Pertama, Penerbit EGC; Jakarta.1997. 1058-1064.

2. Sabiston. DC; alih bahasa: Andrianto.P; Editor Ronardy DH. Buku Ajar Bedah Bagian 2. Penerbit EGC; Jakarta.

3. Schwartz.SI; Shires.GT; Spencer.FC; alih bahasa: Laniyati; Kartini.A; Wijaya.C; Komala.S; Ronardy.DH; Editor Chandranata.L; Kumala.P. Intisari Prinsip Prinsip Ilmu Bedah. Penerbit EGC; Jakarta.2000.

4. Reksoprojo.S: Editor; Pusponegoro.AD; Kartono.D; Hutagalung.EU; Sumardi.R; Luthfia.C; Ramli.M; Rachmat. KB; Dachlan.M. Kumpulan Kuliah Ilmu Bedah. Penerbit Bagian Ilmu Bedah FKUI/RSCM; Jakarta.1995.

Background

Osteomyelitis is an acute or chronic inflammatory process of the bone and its structures secondary to infection with pyogenic organisms.

Pathophysiology

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Osteomyelitis may be localized or it may spread through the periosteum, cortex, marrow, and cancellous tissue. The bacterial pathogen varies on the basis of the patient's age and the mechanism of infection.

The following are the 2 primary categories of acute osteomyelitis: hematogenous osteomyelitis and direct or contiguous inoculation osteomyelitis.

Hematogenous osteomyelitis is an infection caused by bacterial seeding from the blood. Acute hematogenous osteomyelitis is characterized by an acute infection of the bone caused by the seeding of the bacteria within the bone from a remote source. This condition primarily occurs in children. The most common site is the rapidly growing and highly vascular metaphysis of growing bones. The apparent slowing or sludging of blood flow as the vessels make sharp angles at the distal metaphysis predisposes the vessels to thrombosis and the bone itself to localized necrosis and bacterial seeding.

Vertebral osteomyelitis at any age is most often a secondary complication of a remote infection with hematogenous seeding. In approximately one half of vertebral osteomyelitis cases, a source can be identified such as urinary tract or skin, and approximately one third may be diagnosed with endocarditis.[1] Acute hematogenous osteomyelitis, despite its name, may have a slow clinical development and insidious onset.

Direct or contiguous inoculation osteomyelitis is caused by direct contact of the tissue and bacteria during trauma or surgery. Direct inoculation (contiguous-focus) osteomyelitis is an infection in the bone secondary to the inoculation of organisms from direct trauma, spread from a contiguous focus of infection, or sepsis after a surgical procedure. Clinical manifestations of direct inoculation osteomyelitis are more localized than those of hematogenous osteomyelitis and tend to involve multiple organisms.

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Additional categories include chronic osteomyelitis and osteomyelitis secondary to peripheral vascular disease. Chronic osteomyelitis persists or recurs, regardless of its initial cause and/or mechanism and despite aggressive intervention. Although listed as an etiology, peripheral vascular disease is actually a predisposing factor rather than a true cause of infection.

Disease states known to predispose patients to osteomyelitis include diabetes mellitus,[2] sickle cell disease , acquired immune deficiency syndrome (AIDS), intravenous (IV) drug abuse, alcoholism, chronic steroid use, immunosuppression, and chronic joint disease. In addition, the presence of a prosthetic orthopedic device is an independent risk factor, as is any recent orthopedic surgery or open fracture.

For the radiologic perspective, see Osteomyelitis, Acute Pyogenic and Osteomyelitis, Chronic.

Epidemiology

Frequency

United States

The overall prevalence is 1 case per 5,000 children. Neonatal prevalence is approximately 1 case per 1,000. The annual incidence in patients with sickle cell anemia is approximately 0.36%. The prevalence of osteomyelitis after foot puncture (as is seen in the image below) may be as high as 16% (30-40% in patients with diabetes). The incidence of vertebral osteomyelitis is approximately 2.4 cases per 100,000 population.[1]

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Osteomyelitis of diabetic foot. Photography by David Effron MD, FACEP.

International

The overall incidence is higher in developing countries.

Mortality/Morbidity

Morbidity can be significant and can include localized spread of infection to associated soft tissues or joints; evolution to chronic infection, with pain and disability; amputation of the involved extremity; generalized infection; or sepsis. As many as 10-15% of patients with vertebral osteomyelitis develop neurologic findings or frank spinal-cord compression. As many as 30% of pediatric patients with long-bone osteomyelitis may develop deep venous thrombosis (DVT). The development of DVT may also be a marker for disseminated infection.[3] Vascular complications appear to be more common with community-acquired methicillin-resistant Staphylococcus aureus (CA-MRSA) than was previously recognized.[4]

Mortality rates are low, unless associated sepsis or an underlying serious medical condition is present.

Race

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No increased incidence of osteomyelitis is noted based on race.

Sex

Males are at increased relative risk, which increases through childhood, peaking in adolescence and falling to a low ratio in adults.[5]

Age

In general, osteomyelitis has a bimodal age distribution. Acute hematogenous osteomyelitis is primarily a disease in children. Direct trauma and contiguous focus osteomyelitis are more common among adults and adolescents than in children. Vertebral osteomyelitis is more common in persons older than 45 years.

History

Hematogenous osteomyelitis usually presents with a slow insidious progression of symptoms. Direct osteomyelitis generally is more localized, with prominent signs and symptoms. General symptoms of osteomyelitis include the following:

Hematogenous long-bone osteomyelitis o Abrupt onset of high fever (fever is present in only

50% of neonates with osteomyelitis)o Fatigueo Irritabilityo Malaiseo Restriction of movement (pseudoparalysis of limb in

neonates)o Local edema, erythema, and tenderness

Hematogenous vertebral osteomyelitis o Insidious onseto History of an acute bacteremic episodeo May be associated with contiguous vascular

insufficiency

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o Local edema, erythema, and tendernesso Failure of a young child to sit up normally[6]

Chronic osteomyelitis o Nonhealing ulcero Sinus tract drainageo Chronic fatigueo Malaise

Physical

Findings at physical examination may include the following:

Fever (present in only 50% of neonates) Edema Warmth Fluctuance Tenderness to palpation Reduction in the use of the extremity (eg, reluctance to

ambulate, if the lower extremity is involved or pseudoparalysis of limb in neonates)

Failure of a young child to sit up normally Sinus tract drainage (usually a late finding or one that occurs

with chronic infection)

Causes

Note that responsible pathogens may be isolated in only 35-40% of infections. Bacterial causes of acute and direct osteomyelitis include the following:

Acute hematogenous osteomyelitis (Note increasing reports of other pathogens in bone and joint infections including community-associated methicillin-resistant Staphylococcus aureus [MRSA],[7] Kingella kingae,[8] and others.)

o Newborns (younger than 4 mo): Saureus, Enterobacter species, and group A and B Streptococcus species

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o Children (aged 4 mo to 4 y): S aureus, group A Streptococcus species, Haemophilus influenzae, and Enterobacter species

o Children, adolescents (aged 4 y to adult): S aureus (80%), group A Streptococcus species, H influenzae, and Enterobacter species

o Adult - S aureus and occasionally Enterobacter or Streptococcus species

Direct osteomyelitis o General - S aureus, Enterobacter species, and

Pseudomonas specieso Puncture wound through an athletic shoe - S aureus

and Pseudomonas specieso Sickle cell disease -S aureus and Salmonellae species

Differential Diagnoses

Animal Bites Cellulitis Deep Venous Thrombosis and Thrombophlebitis Gas Gangrene Gout and Pseudogout Hand Infections Juvenile Rheumatoid Arthritis Lumbar (Intervertebral) Disk Disorders Neoplasms, Spinal Cord Pediatrics, Limp Pediatrics, Sickle Cell Disease Plantar Fasciitis Septic Arthritis Septic Arthritis, Pediatrics Spinal Cord Infections Transient Synovitis

Laboratory Studies

The following studies are indicated in patients with osteomyelitis:

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CBC count: The WBC count may be elevated, but it is frequently normal.

o A leftward shift is common with increased polymorphonuclear leukocyte counts.

o The C-reactive protein level is usually elevated and nonspecific; this study may be more useful than the erythrocyte sedimentation rate (ESR) because it reveals elevation earlier.

o The ESR is usually elevated (90%); however, this finding is clinically nonspecific.

o CRP and ESR have limited roles in the setting of chronic osteomyelitis and are often normal

Culture: Superficial wound or sinus tract cultures often do not correlate with the bacteria that is causing osteomyelitis and have limited use. Blood culture results are positive in approximately 50% of patients with hematogenous osteomyelitis. However, a positive blood culture may preclude the need for further invasive procedures to isolate the organism. Bone cultures from biopsy or aspiration have a diagnostic yield of approximately 77% across all studies.[1]

Imaging Studies

Radiography o Radiographic evidence of acute osteomyelitis is first

suggested by overlying soft-tissue edema at 3-5 days after infection. Examples of radiographic evidence of osteomyelitis are presented in the images below.

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Osteomyelitis of the elbow. Photography by David Effron MD, FACEP.

Osteomyelitis of index finger metacarpal head secondary to clenched fist injury. Photography by David Effron MD, FACEP.

Osteomyelitis of the great toe. Photography by David Effron MD, FACEP.

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Osteomyelitis of T10 secondary to streptococcal disease. Photography by David Effron

MD, FACEP. Osteomyelitis. Radiography of diabetic foot showing osteomyelitis with gas. Photography by David Effron MD, FACEP.

o Bony changes are not evident for 14-21 days and initially manifest as periosteal elevation followed by cortical or medullary lucencies. By 28 days, 90% of patients demonstrate some abnormality.

o Approximately 40-50% focal bone loss is necessary to cause detectable lucency on plain films.

MRI o The MRI is effective in the early detection and surgical

localization of osteomyelitis.[9, 10]

o Studies have shown its superiority compared with plain radiography, CT, and radionuclide scanning and is considered to be the imaging of choice.

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o Sensitivity ranges from 90-100%. Positron emission tomographic (PET) scanning has accuracy

similar to MRI. Radionuclide bone scanning

o Three phase bone scan, gallium scan and tagged WBC scan are considerations in patients who are unable to have MRI imaging. A three phase bone scan has high sensitivity and specificity in adults with normal findings on radiograph. Specificity is dramatically decreased in the setting of previous surgery or traumatized bone.

o In special circumstances, additional information can be obtained from further scanning with leukocytes labeled with gallium 67 and/or indium 111.

CT scanning o CT scans can depict abnormal calcification,

ossification, and intracortical abnormalities.o It is not recommended for routine use for diagnosing

osteomyelitis but is often the imaging of choice when MRI is not available

Ultrasonography o This simple and inexpensive technique has shown

promise, particularly in children with acute osteomyelitis.

o Ultrasonography may demonstrate changes as early as 1-2 days after onset of symptoms.

o Abnormalities include soft tissue abscess or fluid collection and periosteal elevation.

o Ultrasonography allows for ultrasound-guided aspiration.

o It does not allow for evaluation of bone cortex.

Emergency Department Care

Osteomyelitis rarely requires emergent stabilization or resuscitation. The primary challenge for ED physicians is considering the appropriate diagnosis in the face of subtle signs or symptoms.

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Treatment for osteomyelitis involves the following:

Initiation of intravenous antibiotics that penetrate bone and joint cavities

Referral of the patient to an orthopedist or general surgeon Possible medical infectious disease consultation

Select the appropriate antibiotics using direct culture results in samples from the infected site, whenever possible. Empiric therapy is often initiated on the basis of the patient's age and the clinical presentation. Empiric therapy should always include coverage for S aureus and consideration of CA-MRSA. Further surgical management may involve removal of the nidus of infection, implantation of antibiotic beads or pumps, hyperbaric oxygen therapy,[11, 12] or other modalities.

Diagnosis requires 2 of the 4 following criteria:

Purulent material on aspiration of affected bone Positive findings of bone tissue or blood culture Localized classic physical findings of bony tenderness, with

overlying soft-tissue erythema or edema Positive radiological imaging study

Consultations

Order an orthopedics, general surgery, or infectious disease consultation, as needed. Patients with diabetic foot osteomyelitis are best cared for by a multidisciplinary team.[13]

Medication Summary

The primary treatment for osteomyelitis is parenteral antibiotics that penetrate bone and joint cavities. Treatment is required for at least 4-6 weeks. After intravenous antibiotics are initiated on an inpatient basis, therapy may be continued with intravenous or oral antibiotics,

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depending on the type and location of the infection, on an outpatient basis.

The following are recommendations for the initiation of empiric antibiotic treatment based on the age of the patient and mechanism of infection:

With hematogenous osteomyelitis (newborn to adult), the infectious agents include S aureus, Enterobacteriaceae organisms, group A and B Streptococcus species, and H influenzae. Primary treatment is a combination of penicillinase-resistant synthetic penicillin and a third-generation cephalosporin. Alternate therapy is vancomycin or clindamycin and a third-generation cephalosporin, particularly if methicillin-resistant S aureus (MRSA) is considered likely. Linezolid is also used in these circumstances. In addition to these above-mentioned antibacterials, ciprofloxacin and rifampin may be an appropriate combination therapy for adult patients. If evidence of infection with gram-negative bacilli is observed, include a third-generation cephalosporin.

In patients with sickle cell anemia and osteomyelitis, the primary bacterial causes are S aureus and Salmonellae species. Thus, the primary choice for treatment is a fluoroquinolone antibiotic (not in children). A third-generation cephalosporin (eg, ceftriaxone) is an alternative choice.

When a nail puncture occurs through an athletic shoe, the infecting agents may include S aureus and Pseudomonas aeruginosa. The primary antibiotics in this scenario include ceftazidime or cefepime. Ciprofloxacin is an alternative treatment.

For patients with osteomyelitis due to trauma, the infecting agents include S aureus, coliform bacilli, and Pseudomonas aeruginosa. Primary antibiotics include nafcillin and ciprofloxacin. Alternatives include vancomycin and a third-generation cephalosporin with antipseudomonal activity.

Antibiotics

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Class Summary

Empiric antimicrobial therapy must be comprehensive and should cover all likely pathogens in the context of the clinical setting.

View full drug information

Nafcillin (Nafcil, Unipen)

 

Initial therapy for suspected penicillin G–resistant streptococcal or staphylococcal infections. Use parenteral therapy initially in severe infections. Change to oral therapy as condition warrants. Because of thrombophlebitis, particularly in elderly patients, administer parenterally for only the short term (1-2 d). Change to PO route as clinically indicated. Note: Administer in combination with a third-generation cephalosporin to treat osteomyelitis. Do not admix with aminoglycosides for IV administration.

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Ceftriaxone (Rocephin)

 

Third-generation cephalosporin with broad-spectrum gram-negative activity; lower efficacy against gram-positive organisms; higher efficacy against resistant organisms; arrests bacterial growth by binding to one or more penicillin-binding proteins. Note: Administer with a penicillinase-resistant synthetic penicillin, when treating osteomyelitis.

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Cefazolin (Ancef)

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First-generation semisynthetic cephalosporin that arrests bacterial cell wall synthesis, inhibiting bacterial growth; primarily active against skin flora, including S aureus; typically used alone for skin and skin-structure coverage.

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Ciprofloxacin (Cipro)

 

Fluoroquinolone with activity against pseudomonads, streptococci, MRSA, Staphylococcus epidermidis, and most gram-negative organisms, but no activity against anaerobes. Inhibits bacterial DNA synthesis and, consequently, growth. Continue treatment for at least 2 d (typical treatment, 7-14 d) after signs and symptoms disappear.

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Ceftazidime (Fortaz, Ceptaz)

 

Third-generation cephalosporin with broad-spectrum gram-negative activity; lower efficacy against gram-positive organisms; higher efficacy against resistant organisms; arrests bacterial growth by binding to one or more penicillin-binding proteins.

View full drug information

Clindamycin (Cleocin)

 

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Lincosamide for the treatment of serious skin and soft-tissue staphylococcal infections; also effective against aerobic and anaerobic streptococci (except enterococci); inhibits bacterial growth, possibly by blocking dissociation of peptidyl t-RNA from ribosomes, arresting RNA-dependent protein synthesis.

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Vancomycin (Vancocin)

 

Potent antibiotic directed against gram-positive organisms and active against Enterococcus species. Useful in the treatment of septicemia and skin structure infections. Indicated for patients who can not receive or have failed to respond to penicillins and cephalosporins or have infections with resistant staphylococci. For abdominal penetrating injuries, it is combined with an agent active against enteric flora and/or anaerobes.

To avoid toxicity, current recommendation is to assay vancomycin trough levels after third dose drawn 0.5 h prior to next dosing. Use creatinine clearance to adjust dose in patients with renal impairment.

Used in conjunction with gentamicin for prophylaxis in penicillin-allergic patients undergoing gastrointestinal or genitourinary procedures.

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Linezolid (Zyvox)

 

Prevents formation of functional 70S initiation complex, which is essential for bacterial translation process. Bacteriostatic against staphylococci.

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The FDA warns against the concurrent use of linezolid with serotonergic psychiatric drugs, unless indicated for life-threatening or urgent conditions. Linezolid may increase serotonin CNS levels as a result of MAO-A inhibition, increasing the risk of serotonin syndrome.[14]

Deterrence/Prevention

Acute hematogenous osteomyelitis can potentially be avoided by preventing bacterial seeding of bone from a remote site. This involves the appropriate diagnosis and treatment of primary bacterial infections.

Direct inoculation osteomyelitis can best be prevented with appropriate wound management and consideration of prophylactic antibiotic use at the time of injury.

Complications

Complications of osteomyelitis may include the following:

Bone abscess Paravertebral/epidural abscess Bacteremia Fracture Loosening of the prosthetic implant Overlying soft-tissue cellulitis Draining soft-tissue sinus tracts

Prognosis

The prognosis for osteomyelitis varies but is markedly improved with timely diagnosis and aggressive therapeutic intervention.

http://emedicine.medscape.com/article/785020-overview

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