Delayed Arterial Hemorrhage After Pancreaticoduodenectomy

Delayed arterial hemorrhage is a rare complication of pancreaticoduodenectomy that is associated with a high mortality and has no standard management. Between 2000 and 2011, 204 pancreaticoduodenectomies were performed, and there were 3 cases of delayed arterial hemorrhage. We reviewed the role of endoscopy, laparotomy, and interventional radiology the management of delayed hemorrhage. One patient presented with intraluminal bleeding and upper gastrointestinal endoscopy failed to identify the bleeding site. Two patients presented with bleeding from the drain tube. Laparotomy was performed in the patient with intraluminal bleeding and interventional radiology was employed for the other 2 patients. There was no hemorrhage-related mortality or rebleeding, but the patient who underwent laparotomy developed sepsis. Endoscopy may have no role in the initial management of delayed arterial hemorrhage after pancreaticoduodenectomy. Interventional radiology is less invasive compared with laparotomy, and may be considered as the first-line treatment for delayed arterial hemorrhage in pancreaticoduodenectomy patients.Key words: Pancreaticoduodenectomy, Postoperative hemorrhage, Interventional radiologyThe mortality rate of patients undergoing pancreaticoduodenectomy (PD) has decreased in recent decades, but complications still occur at a high rate of 30% to 50%.^1–5 Common complications of PD include pancreatic leakage, delayed gastric emptying, and intra-abdominal abscess. Hemorrhage only has an incidence of 2%–4%, but this complication is associated with a high mortality rate of 11% to 54%.^1–3 Because delayed hemorrhage is uncommon after PD, its management remains unclear. Here we present our experience with this complication and review the available therapeutic strategies.     

Effects of Collateral Vessel Occlusion on Oral Glucose Tolerance Test in Liver Cirrhosis

Alterations in carbohydrate metabolism associated with liver cirrhosis are characterized by a high serum insulin level and prolonged hyperglycemia on oral glucose tolerance test (OGTT). We measured plasma glucose, immunoreactive insulin (IRI), and C-peptide immunoreactivity (CPR) levels during a 75-g OGTT before and after varices obliteration in 10 cirrhotic patients with gastric varices. After obliteration, the indocyanine green retention rate was decreased and the portal flow velocity was increased. A significant decline in plasma glucose and IRI levels was also noted on OGTT. Moreover, the plasma glucose and IRI levels declined at 90 and 120 min in OGTT while they increased progressively by 120 min before obliteration. The levels of CPR were similar before and after treatment. These results indicate that decreased portal flow due to extrahepatic shunt and consequent impairment of insulin metabolism play a role in glucose intolerance observed in cirrhotic patients and that shunt occlusion improves glucose metabolism.     

Role of perfusion-weighted imaging at 3T in the histopathological differentiation between astrocytic and oligodendroglial tumors

Objective

The differentiation of oligodendroglial tumors from astrocytic tumors is important clinically, because oligodendroglial tumors are more chemosensitive than astrocytic tumors. This study was designed to clarify the usefulness of 3 T MR perfusion imaging (PWI) in the histopathological differentiation between astrocytic and oligodendroglial tumors. This is because there is a growing interest in the diagnostic performance of 3 T MR imaging, which has the advantages of a higher signal-to-noise ratio (SNR) and greater spatial and temporal resolution.

Materials and methods

This study retrospectively included 24 consecutive patients with supratentorial, WHO grade II and III astrocytic and oligodendroglial tumors (7 astrocytic, 10 oligoastrocytic, and 7 oligodendroglial tumors) that were newly diagnosed and resected between November 2006 and December 2009 at Hiroshima University Hospital. These patients underwent dynamic susceptibility contrast-enhanced (DSC) PWI relative cerebral blood volume (rCBV) measurements before treatment. Astrocytic tumors were designated as the astrocytic group, and oligoastrocytic and oligodendroglial tumors as the oligodendroglial group. The regions of interest with the maximum rCBV values within the tumors were normalized relative to the contra-lateral white matter (rCBVmax).

Results

The average rCBVmax of astrocytic tumors (2.01 ± 0.68) was significantly lower than that of the oligoastrocytic (4.60 ± 1.05) and oligodendroglial tumors (6.17 ± 0.867) (P < 0.0001). A cut-off value of 3.0 allowed to differentiate the oligodendroglial group from the astrocytic group at 100% sensitivity and 87.5% specificity.

Conclusion

The rCBVmax values obtained from 3 T MR PWI may be useful as an adjunct to the postoperative histopathological diagnosis of glioma patients.     

Microbial lipopolysaccharide-induced inflammation contributes to cognitive impairment and white matter lesion progression in diet-induced obese mice with chronic cerebral hypoperfusion

Aims

White matter lesions (WMLs) are involved in the pathological processes leading to cognitive decline and dementia. We examined the mechanisms underlying the exacerbation of ischemia-induced cognitive impairment and WMLs by diet-induced obesity, including lipopolysaccharide (LPS)-triggered neuroinflammation via toll-like receptor (TLR) 4.

Methods

Wild-type (WT) and TLR4-knockout (KO) C57BL/6 mice were fed a high-fat diet (HFD) or low-fat diet (LFD), and subjected to bilateral carotid artery stenosis (BCAS). Diet groups were compared for changes in gut microbiota, intestinal permeability, systemic inflammation, neuroinflammation, WML severity, and cognitive dysfunction.

Results

In WT mice, HFD induced obesity and increased cognitive impairment and WML severity compared with LFD-fed mice following BCAS. HFD caused gut dysbiosis and increased intestinal permeability, and plasma LPS and pro-inflammatory cytokine concentrations. Furthermore, HFD-fed mice had higher LPS levels and higher neuroinflammatory status, including increased TLR4 expression, in WMLs. In TLR4-KO mice, HFD also caused obesity and gut dysbiosis but did not increase cognitive impairment or WML severity after BCAS. No difference was found between HFD- and LFD-fed KO mice for LPS levels or inflammatory status in either plasma or WMLs.

Conclusion

Inflammation triggered by LPS–TLR4 signaling may mediate obesity-associated exacerbation of cognitive impairment and WMLs from brain ischemia.     

Potential efficacy of local therapy for progressive lesions after nivolumab in patients with recurrent or metastatic squamous cell carcinoma of the head and neck

International Journal of Clinical Oncology - In recurrent or metastatic squamous cell carcinoma of the head and neck (R/M SCCHN), local therapy (LT) such as surgery or radiotherapy can be treatment...