Many patients develop a variety of bowel dysfunction after sphincter preserving surgeries (SPS) for rectal cancer. The bowel dysfunction usually manifests in the form of low anterior resection syndrome (LARS), which has a negative impact on the patients’ quality of life. This study reviewed the LARS after SPS, its mechanism, risk factors, diagnosis, prevention, and treatment based on previously published studies. Adequate history taking, physical examination of the patients, using validated questionnaires and other diagnostic tools are important for assessment of LARS severity. Treatment of LARS should be tailored to each patient. Multimodal therapy is usually needed for patients with major LARS with acceptable results. The treatment includes conservative management in the form of medical, pelvic floor rehabilitation and transanal irrigation and invasive procedures including neuromodulation. If this treatment failed, fecal diversion may be needed. In conclusion, Initial meticulous dissection with preservation of nerves and creation of a neorectal reservoir during anastomosis and proper Kegel exercise of the anal sphincter can minimize the occurrence of LARS. Pre-treatment counseling is an essential step for patients who have risk factors for developing LARS.

The clinical, biochemical, and neuroradiologic findings and clinical follow-up of seven patients with glutaric aciduria type II are reported. Three phenotypes of the disease are encountered: neonatal-onset form with congenital anomalies (two patients) or without congenital anomalies (three patients) and late-onset form (two patients). The neonatal-onset form presents as an overwhelming illness, with severe hypoglycemia and metabolic acidosis leading to rapid death. Frequently it is associated with perinatal energy deprivation, a neonate with low birth weight and prematurity. The late-onset form presents with intermittent episodes of vomiting, hypoglycemia, and acidosis especially after meals rich in fat and/or proteins. All parents are consanguineous and have a first- or second-degree relationship. Initially, in the two phenotypes with neonatal onset and during crisis in the late-onset phenotype, routine laboratory evaluation showed severe metabolic acidosis, with an increased anion gap, hypoglycemia without ketonuria, and disturbed liver function tests. In the majority of patients with neonatal-onset forms, the kidneys, liver, and at times the spleen are enlarged with an increased echogenic pattern; however, no hepatic or renal cysts are detected. Cardiomegaly is observed in most patients. The diagnosis can be easily and rapidly reached through tandem mass spectrometry study of the blood and can further be confirmed by gas chromatography/mass spectrometry analysis of the urine organic acids. In this report, the magnetic resonance imaging/computed tomography brain studies showed brain atrophy, white matter disease, and in one patient, fluid-filled cavities in the periventricular area and putamina. Fluorine-18-labeled 2-fluoro-2-deoxyglucose positron emission tomographic (FDG PET) brain studies in two patients with late-onset disease showed slightly decreased activity in the cerebral cortex in one and in the caudate nuclei in the other. Brain FDG PET scan and magnetic resonance spectroscopy were normal in one patient with neonatal-onset disease. All patients were treated with a diet low in fat and protein, oral riboflavin, and carnitine. The results were promising for the late-onset disease. Intravenous carnitine gave rewarding results in one patient with neonatal-onset disease.

In a patient with ESRD receiving intermittent hemodialysis, a ceftolozane-tazobactam loading dose of 1.5 g i.v. followed by a maintenance dosage of 300 mg every 8 hours appeared to be safe and effective in the treatment of nosocomial pneumonia caused by MDR .