Surgical complications in neuromuscular scoliosis operated with posterior- only approach using pedicle screw fixation

<p>Abstract</p> <p>Background</p> <p>There are no reports describing complications with posterior spinal fusion (PSF) with segmental spinal instrumentation (SSI) using pedicle screw fixation in patients with neuromuscular scoliosis.</p> <p>Methods</p> <p>Fifty neuromuscular patients (18 cerebral palsy, 18 Duchenne muscular dystrophy, 8 spinal muscular atrophy and 6 others) were divided in two groups according to severity of curves; group I (< 90°) and group II (> 90°). All underwent PSF and SSI with pedicle screw fixation. There were no anterior procedures. Perioperative (within three months of surgery) and postoperative (after three months of surgery) complications were retrospectively reviewed.</p> <p>Results</p> <p>There were fifty (37 perioperative, 13 postoperative) complications. Hemo/pneumothorax, pleural effusion, pulmonary edema requiring ICU care, complete spinal cord injury, deep wound infection and death were major complications; while atelectesis, pneumonia, mild pleural effusion, UTI, ileus, vomiting, gastritis, tingling sensation or radiating pain in lower limb, superficial infection and wound dehiscence were minor complications. Regarding perioperative complications, 34(68%) patients had at least one major or one minor complication. There were 16 patients with pulmonary, 14 with abdominal, 3 with wound related, 2 with neurological and 1 cardiovascular complications, respectively. There were two deaths, one due to cardiac arrest and other due to hypovolemic shock. Regarding postoperative complications 7 patients had coccygodynia, 3 had screw head prominence, 2 had bed sore and 1 had implant loosening, respectively. There was a significant relationship between age and increased intraoperative blood loss (p = 0.024). However it did not increased complications or need for ICU care. Similarly intraoperative blood loss > 3500 ml, severity of curve or need of pelvic fixation did not increase the complication rate or need for ICU. DMD patients had higher chances of coccygodynia postoperatively.</p> <p>Conclusion</p> <p>Although posterior-only approach using pedicle screw fixation had good correction rate, complications were similar to previous reports. There were few unusual complications like coccygodynia.</p

Listeria pathogenesis and molecular virulence determinants

The gram-positive bacterium Listeria monocytogenes is the causative agent of listeriosis, a highly fatal opportunistic foodborne infection. Pregnant women, neonates, the elderly, and debilitated or immunocompromised patients in general are predominantly affected, although the disease can also develop in normal individuals. Clinical manifestations of invasive listeriosis are usually severe and include abortion, sepsis, and meningoencephalitis. Listeriosis can also manifest as a febrile gastroenteritis syndrome. In addition to humans, L. monocytogenes affects many vertebrate species, including birds. Listeria ivanovii, a second pathogenic species of the genus, is specific for ruminants. Our current view of the pathophysiology of listeriosis derives largely from studies with the mouse infection model. Pathogenic listeriae enter the host primarily through the intestine. The liver is thought to be their first target organ after intestinal translocation. In the liver, listeriae actively multiply until the infection is controlled by a cell-mediated immune response. This initial, subclinical step of listeriosis is thought to be common due to the frequent presence of pathogenic L. monocytogenes in food. In normal indivuals, the continual exposure to listerial antigens probably contributes to the maintenance of anti-Listeria memory T cells. However, in debilitated and immunocompromised patients, the unrestricted proliferation of listeriae in the liver may result in prolonged low-level bacteremia, leading to invasion of the preferred secondary target organs (the brain and the gravid uterus) and to overt clinical disease. L. monocytogenes and L. ivanovii are facultative intracellular parasites able to survive in macrophages and to invade a variety of normally nonphagocytic cells, such as epithelial cells, hepatocytes, and endothelial cells. In all these cell types, pathogenic listeriae go through an intracellular life cycle involving early escape from the phagocytic vacuole, rapid intracytoplasmic multiplication, bacterially induced actin-based motility, and direct spread to neighboring cells, in which they reinitiate the cycle. In this way, listeriae disseminate in host tissues sheltered from the humoral arm of the immune system. Over the last 15 years, a number of virulence factors involved in key steps of this intracellular life cycle have been identified. This review describes in detail the molecular determinants of Listeria virulence and their mechanism of action and summarizes the current knowledge on the pathophysiology of listeriosis and the cell biology and host cell responses to Listeria infection. This article provides an updated perspective of the development of our understanding of Listeria pathogenesis from the first molecular genetic analyses of virulence mechanisms reported in 1985 until the start of the genomic era of Listeria research