Spinal osteotomies to treat post-traumatic thoracolumbar deformity.

Fractures of the thoracolumbar junction can lead to regional kyphosis, this being a significant cause of pain and disability for the patients. After a traumatic fracture of the thoracolumbar spine, early or late regional kyphosis can be observed. This post-traumatic deformity can, however, be corrected with appropriate surgical methods. Posterior tricolumnar osteotomies are some of the most powerful methods of correction and are particularly indicated when sagittal and coronal deformities have to be simultaneously corrected or when anterior surgery is not possible. Anterior corpectomy and lengthening with posterior instrumentation are, however, an alternative technique to restore the anterior column support and to correct the regional kyphotic deformity and an option for appropriate sagittal balance restoration and control of symptoms. Proper surgical technique, evaluation of the bone quality and identification of eventual extension of the deformity to the thoracic spine are key aspects in prevention of failures.

Standing lateral lumbar spine and pelvis (SLLP) radiograph: a screening, reduced radiation method, for sagittal imbalance.

INTRODUCTION: Sagittal imbalance is a predictor of failure after surgery for lumbar degenerative pathology. For this reason, specialists advocate correction of sagittal deformity and systematically perform preoperative standing whole spine films. Such diagnostic investigations expose patients to significant doses of radiation. The authors propose an easier radiographic investigation helpful as a screening test to identify patients likely to have sagittal imbalance. METHODS: Fifteen whole spine lateral films were evaluated, classifying subjects into three categories: balanced, compensating imbalanced or imbalanced. A second specialist evaluated the reduced SLLP versions of the film (from L1 to proximal femora), measuring spinopelvic parameters. RESULTS: In the SLLP film, the combination of two parameters (femoral inclination >10°, pelvic tilt >1/3 pelvic incidence +5°) identified 94 % of patients with altered sagittal balance. CONCLUSIONS: This study preliminarily suggests that the SLLP film can be a useful screening test for sagittal balance abnormalities.

Preoperative calculation of the necessary correction in sagittal imbalance surgery: validation of three predictive methods.

INTRODUCTION: Surgery for correction of sagittal imbalance has frequent adverse events and complications. The most frequent cause of failure is inadequate correction of imbalance. The aim of this study is to verify the accuracy of three published methods (exact method by Ondra, FBI method by Le Huec and spinofemoral angle method by Lamartina) to preoperatively calculate the needed correction. DESIGN: This is a retrospective cohort study. METHODS: Fifteen patients treated for correction of sagittal imbalance, with preoperative and postoperative lateral standing whole spine radiographs, were identified. Preoperative calculation of the amount of needed correction has been done using these methods. In postoperative X-rays, the amount of correction obtained with and the degree of correction of sagittal imbalance have been measured. RESULTS AND DISCUSSION: The FBI and SFA methods obtain equivalent calculations of the amount of needed correction. The estimated correction angle with both methods is higher than that calculated with the exact trigonometric method. The difference between the latter and the former methods is equivalent to the observed excess of pelvic tilt.

Cardiomyopathy in dystrophin-deficient hypertrophic feline muscular dystrophy.

A colony of cats affected with hypertrophic feline muscular dystrophy was used to study the occurrence of cardiomyopathy associated with dystrophin deficiency. Affected male and female cats, obligate carrier females, and unaffected healthy littermates were followed from 12 weeks of age into adulthood. Thoracic radiography, 2-D echocardiography, and 2-D-derived M-mode echocardiography were performed at 3-month intervals until 12 months of age and regularly thereafter. From 9 months of age, all affected cats had larger hearts than normal and carrier animals. Left ventricular wall thickness in systole and in diastole and interventricular septal thickness in systole were greater in affected cats 12 months and older when compared with normal or heterozygous animals (P < .05). The myocardium of affected cats was diffusely hypoechoic and thickened. Multiple hyperechoic foci were in the myocardium and papillary musculature. Shortening fraction was normal in all cats. Changes seen in carrier females included enlargement and hyperechogenicity of the papillary musculature after the age of 2 years. Gross and light microscopic examination revealed left ventricular wall thickening with multiple foci of mineralization in 2 of 5 hearts from dystrophin-deficient cats. Although approximately 10% of the normal dystrophin amount was present in the skeletal muscle, dystrophin could not be detected in the myocardium. Early onset concentric myocardial hypertrophy was present in all adult cats. Lesions were mainly localized in the myocardium of the left ventricular free wall and interventricular septum, papillary musculature, and the endocardium. Clinical signs of heart failure developed only infrequently in cats with hypertrophic feline muscular dystrophy.

Lethal peracute rhabdomyolysis associated with stress and general anesthesia in three dystrophin-deficient cats.

Three cats affected with dystrophin deficiency and hypertrophic muscular dystrophy developed peracute rhabdomyolysis with a fatal outcome. Two cats were anesthetized with isoflurane for routine procedures and did not recover properly from the anesthetic procedure. One cat was manually restrained for an echographic examination and started staggering after a short struggle; its condition worsened, and it died. Blood chemistry findings included severe hyperkalemia, hyperphosphatemia, hypocalcemia, massive increases in creatine kinase, aspartate aminotransferase, and alanine aminotransferase concentrations, and high ion gap metabolic acidosis. Light microscopic evaluation of skeletal muscle revealed severe acute rhabdomyolysis with marked extensive necrosis of large groups of fibers and endomysial edema. These lesions were observed in many skeletal muscles but particularly in the masseter and supraspinatus muscles and in the diaphragm. Typical changes associated with dystrophin deficiency in cats were also noted. Histochemical analysis revealed that the dystrophin deficiency was associated with a decrease in the percentage of type 1 myofibers in all three cats. This change was marked in the 20-month-old cat and milder in the younger cats (6.5 and 8.5 months of age). Percentages of type 2A fibers were markedly decreased and percentages of type 2X fibers were markedly increased in the younger cats. Rhabdomyolysis has been reported in dystrophinopathic humans but not in other animal models of dystrophin deficiency. An increased sensitivity of the dystrophin-deficient sarcolemmal membrane to volatile anesthetic agents, stress, or intense muscular activity is suspected.