Correlations between histopathological diagnosis of chemotherapy-induced hepatic injury, clinical features, and perioperative morbidity

Background

Chemotherapy has in some series been linked with increased morbidity after a hepatectomy. Hepatic injuries may result from the treatment with chemotherapy, but can also be secondary to co-morbid diseases. The aim of the present study was to draw correlations between clinical features, treatment with chemotherapy and injury phenotypes and assess the impact of each upon perioperative morbidity.

Patients and methods

Retrospective samples (n = 232) were scored grading steatosis, steatohepatitis and sinusoidal injury (SI). Clinical data were retrieved from medical records. Correlations were drawn between injury, clinical features and perioperative morbidity.

Results

Injury rates were 18%, 4% and 19% for steatosis, steatohepatitis and SI, respectively. High-grade steatosis was more common in patients with diabetes [odds ratio (OR) = 3.33, P = 0.01] and patients with a higher weight (OR/kg = 1.04, P = 0.02). Steatohepatitis was increased with metabolic syndrome (OR = 5.88, P = 0.02). Chemotherapy overall demonstrated a trend towards an approximately doubled risk of high-grade steatosis and steatohepatitis although not affecting SI. However, pre-operative chemotherapy was associated with an increased SI (OR = 2.18, P = 0.05). Operative morbidity was not increased with chemotherapy, but was increased with steatosis (OR = 2.38, P = 0.02).

Conclusions

Diabetes and higher weight significantly increased the risk of steatosis, whereas metabolic syndrome significantly increased risk of steatohepatitis. The presence of high-grade steatosis increases perioperative morbidity, not administration of chemotherapy per se.     

Extensive craniocervical pneumocranium

The authors report the first case of extensive craniocervical pneumocranium causing mass effect, without any associated extradural pneumatocele. The patient presented with frontal headaches and unusual sensations in his left ear. He was found to have large pneumocranium involving his left frontal, temporal, parietal, and occipital bones as well as the atlas. He underwent a craniectomy with replacement of the pneumatized bone with titanium mesh, and mastoidectomy with obliteration of the mastoid air cells. This case is discussed in the context of the literature to date. A review of the literature shows that trauma is not a common cause of pneumocranium, with most cases occurring spontaneously. The authors believe that a combined neurosurgical-otological approach is beneficial in such cases.     

Gallbladder Carcinoma as a Long-Term Complication of Cholecystojejunostomy

Introduction  

Development of gallbladder cancer following cholecystojejunostomy has not previously been described.     

Modulation of immune response by head injury

Despite the fact that traumatic brain injury (TBI) is a silently growing epidemic, we are yet to understand its multifaceted pathogenesis, where various cellular pathways are initiated in response to both the primary mechanical insult and secondary physiologically mediated injury. Although the brain has traditionally been considered an immunologically privileged site, evidence to the contrary exists in studies of central nervous system (CNS) pathology, in particular TBI. Transmigration of leukocytes following blood brain barrier (BBB) disruption results in activation of resident cells of the CNS, such as microglia and astrocytes, to possess immunological function. Both infiltrating peripheral immune cells and activated resident cells subsequently engage in the intrathecal production of cytokines, important indicators of the presence of neuroinflammation. Cytokines can either promote this neurotoxicity, by encouraging excitotoxicity and propagating the inflammatory response, or attenuate the damage through neuroprotective and neurotrophic mechanisms, including the induction of cell growth factors. Certain cytokines perform both functions, for example, interleukin-6 (IL-6). This review article discusses the notion that the inflammatory response to TBI is no longer a peripherally mediated phenomenon, and that the CNS significantly influences the immunological sequence of events in the aftermath of injury.