Traumatic diaphragmatic hernia: delayed presentation with tension viscerothorax--lessons to learn.

Diaphragmatic rupture is a serious complication of thoracoabdominal trauma. The condition may be missed initially. We describe the clinical course of a patient who sustained blunt abdominal trauma in a car accident. His diaphragmatic injury passed unnoticed, to present two years later with left tension viscerothorax, a rarely reported and hardly recognised entity. Nasogastric tube insertion aborted the emergency situation and the hernia was repaired successfully in a semielective setting.

Hepatitis C Virus Sero-status in Hemodialysis Patients Returning from Holiday: Another Risk Factor for HCV Transmission.

Hepatitis C virus (HCV) infection is an endemic disease in most hemodialysis (HD) units in Saudi Arabia. We observed that many of our HD patients seroconvert shortly after returning from "holiday dialysis" in other units. We investigated this issue together with other possible factors related to HCV transmission. During the study period, 56 patients were being dialyzed in our unit. Systematic screening was performed on all patients for anti-HCV antibody utilizing ELISA 2.0 and/or RIBA 3.0 and HBsAg every three months together with aminotransferases activity. The same tests were carried out on patients returning from "holiday dialysis" in other units. Test for HCV-RNA was performed in patients with elevated aminotransferases and negative HCV serology. HCV-antibody was positive in 32 patients (57%) of whom 15 (27%) were already positive at the time of starting HD and 17 (30%) seroconverted after starting HD. A total of 24 patients (43%) remained sero-negative. Comparing the sero-converters (SC) to the remained sero-negatives (RSN), the SC had been out for "holiday dialysis" more than the RSN with a mean number of such HD treatments of 16 versus 4 (P= 0.006). The SC had longer duration on dialysis, 38 versus 19 months for the RSN. The two groups did not have significant difference in their age, sex, number of blood transfusions or prior kidney transplantation. Fourteen out of 17 SC (82%) had seroconverted after a mean duration of 100 days from leaving our unit for "holiday dialysis". Eight out of 24 (33%) of the RSN had dialysis outside our unit and remained sero-negative; HCV-RNA confirmed infection in three of them, all of whom had high amino transferase levels. Our study suggests that patients who have "holiday dialysis" in units with high prevalence of HCV-antibody, run a high risk of sero-conversion and may play a role in unit to unit transmission of HCV.

Magnesium deficiency: pathophysiologic and clinical overview.

Magnesium is an essential cation, involved in many enzymatic reactions, as a cofactor to adenosine triphosphatases. It is critical in energy-requiring metabolic processes, as well as protein synthesis and anaerobic phosphorylation. Serum Mg concentration is maintained within a narrow range by the kidney and small intestine since under conditions of Mg deprivation both organs increase their fractional absorption of Mg. If Mg depletion continues, the bone store contributes by exchanging part of its content with extracellular fluid (ECF). The serum Mg can be normal in the presence of intracellular Mg depletion, and the occurrence of a low level usually indicates significant Mg deficiency. Hypomagnesemia is frequently encountered in hospitalized patients and is seen most often in patients admitted to intensive care units. The detection of Mg deficiency can be increased by measuring Mg concentration in the urine or using the parenteral Mg load test. Hypomagnesemia may arise from various disorders of the gastrointestinal tract, conditions affecting Mg renal handling, or cellular redistribution of Mg. The gastrointestinal causes include the following: protein-calorie malnutrition, the intravenous administration of Mg-free fluids and total parenteral nutrition, chronic watery diarrhea and steatorrhea, short bowel syndrome, bowel fistula, continuous nasogastric suctioning, and, rarely, primary familial Mg malabsorption. The renal causes include Bartter's and Gitelman's syndrome, post obstructive diuresis, post acute tubular necrosis, renal transplantation, and interstitial nephropathy. Many therapeutic agents cause renal Mg wasting and subsequent deficiency. These include loop and thiazide diuretics, aminoglycosides, cisplatin, pentamidine, and foscarnet. Magnesium deficiency is seen frequently in alcoholics and diabetic patients, in whom a combination of factors contributes to its pathogenesis. Hypomagnesemia is known to produce a wide variety of clinical presentations, including neuromuscular irritability, cardiac arrhythmias, and increased sensitivity to digoxin. Refractory hypokalemia and hypocalcemia can be caused by concomitant hypomagnesemia and can be corrected with Mg therapy. The dose and route of administration of Mg in the treatment of hypomagnesemia is dictated by the clinical presentation, the degree of Mg deficiency, and the renal function.