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Osteomyelitis is an infection of bone, usually caused by pyogenic bacteria or mycobacteria. It can be usefully subclassifed on the basis of the causative organism, the route, duration and anatomic location of the infection. more...

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Generally microorganisms may be disseminated to bone hematogenously (i.e., via the blood stream), spread contiguously to bone from local areas of infection, such as cellulitis, or be introduced by penetrating trauma including iatrogenic causes such as joint replacements or internal fixation of fractures. Leukocytes then enter the infected area, and in their attempt to engulf the infectious organisms, release enzymes that lyse bone. Pus spreads into the bone's blood vessels, impairing the flow, and areas of devitalized infected bone, known as sequestra, form the basis of a chronic infection. On histologic examination, these areas of necrotic bone are the basis for distinguishing between acute osteomyelitis and chronic osteomyelitis. Osteomyelitis is an infective process which encompasses all of the bone (osseous) components, including the bone marrow. When it is chronic it can lead to bone sclerosis and deformity.

Osteomyelitis often requires prolonged antibiotic therapy, lasting a matter of weeks or months, and may require surgical debridement. Severe cases may lead to the loss of a limb.

Because of the particulars of their blood supply, the tibia, the femur, the humerus, and the vertebral bodies are especially prone to osteomyelitis.

The vast predominance of hematogenously seeded osteomyelitis is caused by Staphylococcus aureus. Escherichia coli, and streptococci are other common pathogens. In some subpopulations, including intravenous drug users and splenectomized patients, Gram negative bacteria, including enteric bacilli, are significant pathogens.

Staphylococcus aureus is also the most common organism seen in osteomyelitis seeded from areas of contiguous infection, but here Gram negative organisms and anaerobes are somewhat more common, and mixed infections may be seen.

In osteomyelitis involving the vertebral bodies, about half the cases are due to Staphylococcus aureus, and the other half are due to tuberculosis (spread hematogenously from the lungs). Tubercular osteomyelitis of the spine was so common before the initiation of effective antitubercular therapy that it acquired a special name, Pott's disease, by which it is sometimes still known.


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Midfacial osteomyelitis in a chronic cocaine abuser: A case report - Brief Article
From Ear, Nose & Throat Journal, 10/1/01 by Jason F. Talbott


We describe the case of a 56-year-old man who was admitted for treatment of a progressive destruction of his hard palate, septum, nasal cartilage, and soft palate that had been caused by chronic cocaine inhalation. Biopsy of the bony septum revealed acute osteomyelitis and an extensive overgrowth of bacteria and Actinomyces-like organisms. There was no evidence of granuloma or neoplasm. The patient received intravenous ampicillin/ sulbactam for 6 weeks, followed by lifetime oral amoxicillin. When there was no further evidence that destruction was progressing, the patient underwent nasal reconstruction with a cranial bone graft. The surgery was completed with no complications. To our knowledge, this is the first reported case of midfacial osteomyelitis associated with chronic cocaine abuse. The severity of this patient's complications, coupled with the success of his reconstructive surgery, makes this case particularly interesting. We believe that it is important for physicians to understand that septal perfor ation in a cocaine abuser should not be underestimated because it could result in a secondary bone infection. Nasoseptal destruction secondary to intranasal cocaine abuse is a result of cocaine's vasoconstrictive properties, and a decrease in the oxygen tension of intranasal tissue can facilitate the growth of anaerobic pathogens.


Nasal inhalation is the most popular method of cocaine administration in the United States. [1] The adverse effects of intranasal cocaine abuse are well documented. Otolaryngologic complications are numerous, with one of the most common being nasal septal perforation. [2] Other complications include osteocartilaginous necrosis of the sinonasal tract, nasal septal necrosis mimicking Wegener's granulomatosis, and perforation of the hard palate. [2-4]

Nasopharyngeal destruction is a result of cocaine's vasoconstrictive properties. Cocaine produces sympathetic-nervous-system-mediated vasoconstriction by preventing the reuptake of presynaptic norepinephrine and dopamine. [5] The initial vasoconstriction is followed by a rebound vasodilation, which leads to atrophic changes in the mucosal lining. Mechanical destruction resulting from the forceful inhalation of powder or crystalline cocaine and the concomitant vasoconstrictive effect results in the formation of a nasal septal defect. [6] Such chronic intranasal abuse results in nasal crusting, epistaxis, and septal perforation. [7] A decrease in the oxygen tension of intranasal tissue can facilitate the growth of anaerobic pathogens and render the patient susceptible to infection. [8]

In this article, we describe the case of a chronic cocaine abuser who experienced a severe septal perforation. A complete loss of cartilage and bone of the midface was attributed to osteomyelitis. To our knowledge, this is the first documented case of midfacial osteomyelitis directly attributable to cocaine abuse.

Case report

A 56-year-old man with a conspicuous nasal defect and a history of chronic intranasal cocaine abuse had been admitted to the ENT clinic in 1994 for treatment of a hole in the roof of his mouth, which he said he had noticed 5 weeks earlier (figure 1). The man claimed to have been alcohol- and drug-free for 2 weeks.

Computed tomography (CT) of the paranasal sinuses without intravenous contrast showed a bilateral mucoperiosteal thickening of the sphenoid sinuses and what remained of the maxillary sinuses, along with evidence of a markedly erosive process that had destroyed the nasal septum, turbinates, and part of the antrum (figure 2). CT also showed a bilateral residual soft-tissue opacity in the inferior aspect of the frontal sinuses, ethmoid sinuses, and the entire maxillary sinuses. Analysis of biopsy specimens revealed some exposed bone and an absence of quadrangular cartilage. Extensive destruction of his maxillary walls was also noted. Physical examination revealed an oronasal fistula with black necrotic areas around the edges, accompanied by a foul odor. This pattern is unusual in cocaine-induced erosion.

The patient was given antibiotics and had a prosthesis plate constructed to cover the defect. The patient was dismissed as having a septal and palatal perforation that was caused by his cocaine abuse. Two months later, a palatal and left nasal cavity biopsy revealed no evidence of carcinoma or fungal growth.

The patient was not seen again until April 1996, when he was hospitalized for destructive midfacial osteomyelitis that was marked by a slow and progressive destruction of his midface. Upon physical examination, he was noted to have septal destruction with fistula between his oral and nasal cavity and a saddle-nose deformity with columellar and alar retraction secondary to total cartilage loss. In addition, he now had a complete palatal defect.

Nasal septal biopsy revealed acute osteomyelitis with an extensive overgrowth of bacteria, including Serratia, Streptococcus, and Staphylococcus spp. There was no evidence of granuloma or neoplasm. A peripherally inserted central catheter was placed on day 3 of hospitalization to provide long-term outpatient intravenous antibiotic delivery. The patient was treated with intravenous ampicillin/sulbactam for 6 weeks followed by lifetime oral amoxicillin. He was discharged on day 7.

Six months later, in October 1996, the patient underwent open surgery for nasal reconstruction with a cranial bone graft. The graft, which measured approximately 9 X 2 cm, was harvested in the anteroposterior direction along the flattest portion of the parietal bone (figure 3). Two glabellar furrows were used to camouflage the incision site. The incision was made in the shape of a teepee and used for placement of the bone graft. The nasal bones were dissected free, leaving the periosteum down. The periosteum was very carefully divided in the midline. With one finger in the nose and one finger on the skin of the nasal surface, the surgeon (R.J.K.) created a pocket in the nasal skin. A columellar strut, fashioned from calvarial bone, was placed via the glabellar incision. Next, the nasal tip of the dorsal graft was rounded to form an inverted shape. This graft was then placed in the pocket. A lag-screw technique was performed to enter the graft between 5 and 6 mm below the most superior cranial aspect of the gr aft. Once placement was determined to be adequate, the wound was closed and the patient was taken to the recovery room in stable condition.

Three months later, in January 1997, the patient underwent the second stage of his surgery. For external nasal valve reconstruction, a conchal graft was taken from the right conchal bowl by making a postauricular incision and elevating the flaps on either side of the conchal cartilage. The graft was obtained, and the wound was closed primarily in the postauricular region.

An incision was made in the right nasoalar crease, and a pocket was created anteriorly toward the nasal tip and posteriorly toward the piriform aperture. Then a conchal cartilage graft with the proper curvature and shape was fashioned and placed in this bed. The wound was irrigated and closed.

For premaxillary augmentation, a sublabial incision was made, and then a periosteal plane was elevated up to the anterior maxillary spine. A small hole was drilled through the anterior portion of the spine from left to right, allowing for an area of fixation. A piece of the calvarial bone graft from the previous harvest, which had been stored under the postauricular skin, was drilled with two holes as well, and 4-0 Ethilon suture was used to fix it in the anterior maxillary spine region. The sublabial wound was then irrigated with clindamycin solution and closed.

A small excisional wedge was made at the right alar base near the aperture, where the ala was seen to be rotated far medially, causing collapse of the nostril. This was then closed and lateralized, providing a much more adequate nasal aperture (figure 4).


Cocaine is an alkaloid obtained from the leaves of the coca plant. Used medicinally as an anesthetic, it is also widely abused as a drug. Early natives of the Incan Empire experienced mild euphoria, stimulation, and alertness by chewing the coca leaves. [1] Cocaine was first isolated in 1855. In 1912, Owens reported the first case of nasal septal perforation caused by cocaine abuse. [3] Since then, cocaine abuse has been implicated in multiple complications affecting almost every system in the human body.

According to estimates, 30 million Americans have experimented with cocaine, and 5 million use it on a regular basis. [1] Despite the tremendous number of individuals who use intranasal cocaine and the numerous reports of nasopharyngeal destruction attributed to its abuse, our case is unique. Noskin and Kalish also described a rare case of chronic cocaine abuse in which a patient developed Pott's puffy tumor, which is a subperiosteal abscess of the frontal bone that is associated with frontal osteomyelitis. [8]

To our knowledge, ours is the first reported case of midfacial osteomyelitis caused by chronic cocaine abuse. The devascularized nasal tissue served as a breeding ground for secondary bacterial infection. The severity of our patient's complications, coupled with the success of his reconstructive surgery, makes this case particularly interesting. We believe that it is important for physicians to understand that septal perforation in a cocaine abuser should not be underestimated, because midfacial osteomyelitis might result.


(1.) Cregler LL, Mark H. Medical complications of cocaine abuse. N Engl J Med 1986;315:1495-500.

(2.) Kuriloff DB, Kimmelman CP. Osteocartilaginous necrosis of the sinonasal tract following cocaine abuse. Laryngoscope 1989; 99:918-24.

(3.) Armstrong M, Jr., Shikani AH. Nasal septal necrosis mimicking Wegener's granulomatosis in a cocaine abuser. Ear Nose Throat J 1996;75:623-6.

(4.) Mattson-Gates G, Jabs AD, Hugo NE. Perforation of the hard palate associated with cocaine abuse. Ann Plast Surg 1991;26:466-8.

(5.) Daggelt RB, Haghighi P, Terkeltaub RA. Nasal cocaine abuse causing an aggressive midline intranasal and pharyngeal destructive process mimicking midline reticulosis and limited Wegener's granulomatosis. J Rheumatol 1990;17:838-40.

(6.) Sastry RC, Lee D, Har-EI G. Palate perforation from cocaine abuse, Otolaryngol Head Neck Surg 1997:116:565-6.

(7.) Schwartz RH, Grundfast KM. Nasal septal perforation from illicit drug use. Am Fam Physician 1956;34:187-8.

(8.) Noskin GA, Kalish SB. Pott's puffy tumor: A complication of intranasal cocaine abuse. Rev Infect Dis 1991;13:606-8.

COPYRIGHT 2001 Medquest Communications, Inc.
COPYRIGHT 2001 Gale Group

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