Loss of sagittal plane correction after removal of spinal implants.

STUDY DESIGN: A retrospective review of a clinical series was performed. OBJECTIVES: To evaluate the incidence of adult patients who experienced spinal collapse after spinal implant removal after a long spinal arthrodesis, and to assess the various factors that may influence the likelihood of collapse after implant removal. SUMMARY OF BACKGROUND DATA: Published reports describing the benefits or complications of spinal implant removal do not exist. Spinal implant removal, often considered a benign procedure, is even required by the Food and Drug Administration (FDA) for certain implants. METHODS: The medical records and radiographs of 116 consecutive adult patients with long posterior instrumented fusions (>5 segments) were reviewed. The information obtained included original diagnosis, patient age, number of previous surgeries before implant removal, levels of anterior and posterior fusion, time from fusion to implant removal, time from implant removal to failure, and reason for hardware removal. Radiographs also were assessed including scoliosis, lordosis, and kyphosis measurements before implant removal, after hardware removal, after failure, and after revision surgery. RESULTS: Of 116 patients, 14 underwent spinal implant removal. Most of these patients reported prominent implants either proximally in the thoracic spine or distally in the ilium (Galveston technique). Of these 14 patients, 4 experienced increased pain and collapse after implant removal despite thorough intraoperative explorations demonstrating solid fusion. CONCLUSIONS: Spinal implant removal after long posterior fusion in adults may lead to spinal collapse and further surgery. Removal of instrumentation should be avoided or should involve partial removal of the prominent implant.

Eikenella corrodens vertebral osteomyelitis secondary to direct inoculation: a case report.

STUDY DESIGN: A case report. OBJECTIVE: To present a unique method of inoculation with an unusual bacterial organism, Eikenella corrodens, which led to vertebral osteomyelitis and to heighten awareness of different bacterial organisms that may cause orthopedic infections. SUMMARY OF BACKGROUND DATA: E. corrodens has been known to cause orthopedic infections for more than 20 years. The usual mechanism is from "Fight bite" injuries to the hand or metacarpal phalangeal joint. Eikenella osteomyelitis of the vertebral body is extremely rare. METHODS: A 65-year-old man from Indonesia developed slowly progressive vertebral collapse and worsening neck pain. History suggested a previous pharyngeal injury while eating fish. Work up for malignancy was negative, and imaging studies were suggestive of osteomyelitis. An open biopsy and culture as well as fusion were performed for treatment of the osteomyelitis. RESULTS: After a complete work up was undertaken, cultures grew out E. corrodens as the causative organism of this patient's osteomyelitis. Computed tomography scan and history were consistent with inoculation of the paravertebral space with E. corrodens secondary to a fish bone transgressing the patient's pharynx. The patient was treated with surgery and the appropriate antibiotics and healed without any significant sequela. CONCLUSION: Vertebral osteomyelitis due to E. corrodens is extremely rare. Direct inoculation as a cause of vertebral osteomyelitis with Eikenella has never been reported. If diagnosed properly with appropriate cultures and antibiotic sensitivities, Eikenella osteomyelitis can be treated successfully according to standard orthopedic practices including debridement, fusion, and appropriate antibiotics. Awareness of unusual bacteria as potential causative organisms of osteomyelitis is imperative for appropriate treatment.

Analysis of pulsatile secretion of thyrotropin and growth hormone in the hypothyroid rat.

To characterize the role of TRH in the generation of TSH pulsatility as well as the effect of hypothyroidism on episodic GH secretion, blood was constantly withdrawn (30-60 microliters/min) from rats treated with 0.02% methimazole in the drinking water for 8-10 days. This treatment significantly reduced circulating levels of both T3 and T4 and elevated plasma TSH; however, since thyroid hormone titers were still detectable (T3, 39.6 +/- 5.3 vs. 89.8 +/- 5.3 ng/dl in euthyroid animals), methimazole-treated rats were referred to as being mildly hypothyroid. TSH was found to be secreted in secretory bursts, consisting of one to several peaks in these rats. Pulsar analysis of TSH secretory profiles revealed a mean pulse frequency of 2.8 pulses/h, a mean pulse amplitude of 10 ng/pulse, and a mean pulse duration of 0.2 h. Euthyroid rats exhibited similar fluctuations of circulating TSH levels; however, due to the variability of the TSH RIA in the range of euthyroid TSH titers, no significant pulsatility was detected by Pulsar. Mean plasma TSH levels in eu- and hypothyroid rats were 2.3 +/- 0.3 and 14.6 +/- 1.8 ng/ml, respectively. To confirm that the TRH antiserum (TRH-AS) used in the present study for passive immunization had sufficient binding capacity to absorb endogenous TRH release, euthyroid rats were pretreated with either normal rabbit serum or TRH-AS, followed by the injection of clonidine (100 micrograms/kg BW, iv). This alpha 2-adrenergic agonist caused a significant (P < 0.01) 12.7-fold rise in plasma TSH levels in normal rabbit serum-treated animals, which was completely abolished by TRH-AS pretreatment, indicating that clonidine stimulates TSH secretion via activation of hypothalamic TRH release. When TRH-AS was slowly infused into hypothyroid rats that were sampled frequently for the detection of TSH pulsatility, it caused a significant (60.3%; P < 0.01) decrease in mean TSH levels, with TSH titers approaching euthyroid concentrations 1 h after the infusion of TRH-AS. The antiserum treatment also caused the disappearance of statistically significant (Pulsar) TSH secretory pulses. Mild hypothyroidism shifted the GH secretory profiles from a low frequency, high amplitude in euthyroid animals to a high frequency, low amplitude pattern in hypothyroid rats. Mean GH levels in hypothyroid rats were 76% lower than those in euthyroid controls. These findings show that TSH is secreted in a pulsatile fashion in the hypothyroid rat and that TRH is predominantly responsible for the generation of TSH pulsatility.(ABSTRACT TRUNCATED AT 400 WORDS)