A 41-year-old woman who was diagnosed with myocarditis presented eosinophilia. Since the antibody against Toxocara canis (T. canis) was positive, we diagnosed that she had visceral larva migrans due to T. canis associated with myocarditis. She was treated with oral albendazole and prednisolone for two weeks, eosinophil count and hepatic enzymes were normalized after completion of treatment. This is the first report of myocarditis caused by T. canis infection in Korea.

Background/AimsInadequacy of dialysis is associated with morbidity and mortality in chronic hemodialysis (HD) patients. Blood flow rate (BFR) during HD is one of the important determinants of increasing dialysis dose. However, the optimal BFR is unclear. In this study, we investigated the impact of the BFR on all-cause mortality in chronic HD patients.MethodsPrevalent HD patients were selected from Clinical Research Center registry for end-stage renal disease cohort in Korea. We categorized patients into two groups by BFR < 250 and ≥ 250 mL/min according to the median value of BFR 250 mL/min in this study. The primary outcome was all-cause mortality.ResultsA total of 1,129 prevalent HD patients were included. The number of patients in the BFR < 250 mL/min was 271 (24%) and in the BFR ≥ 250 mL/min was 858 (76%). The median follow-up period was 30 months. Kaplan-Meier analysis showed that the mortality rate was significantly higher in patients with BFR < 250 mL/min than those with BFR ≥ 250 mL/min (p = 0.042, log-rank). In the multivariate Cox regression analyses, patients with BFR < 250 mL/min had higher all-cause mortality than those with BFR ≥ 250 mL/min (hazard ratio, 1.66; 95% confidence interval, 1.00 to 2.73; p = 0.048).ConclusionsOur data showed that BFR < 250 mL/min during HD was associated with higher all-cause mortality in chronic HD patients.

BackgroundOsmotic demyelination syndrome (ODS) primarily occurs after rapid correction of severe hyponatremia. There are no proven effective therapies for ODS, but we describe the first case showing the successful treatment of central pontine myelinolysis (CPM) by plasma exchange, which occurred after rapid development of hypernatremia from intravenous sodium bicarbonate therapy.Case presentationA 40-year-old woman presented with general weakness, hypokalemia, and metabolic acidosis. The patient was treated with oral and intravenous potassium chloride, along with intravenous sodium bicarbonate. Although her bicarbonate deficit was 365 mEq, we treated her with an overdose of intravenous sodium bicarbonate, 480 mEq for 24 hours, due to the severity of her acidemia and her altered mental status. The next day, she developed hypernatremia with serum sodium levels rising from 142.8 mEq/L to 172.8 mEq/L. Six days after developing hypernatremia, she exhibited tetraparesis, drooling, difficulty swallowing, and dysarthria, and a brain MRI revealed high signal intensity in the central pons with sparing of the peripheral portion, suggesting CPM. We diagnosed her with CPM associated with the rapid development of hypernatremia after intravenous sodium bicarbonate therapy and treated her with plasma exchange. After two consecutive plasma exchange sessions, her neurologic symptoms were markedly improved except for mild diplopia. After the plasma exchange sessions, we examined the patient to determine the reason for her symptoms upon presentation to the hospital. She had normal anion gap metabolic acidosis, low blood bicarbonate levels, a urine pH of 6.5, and a calyceal stone in her left kidney. We performed a sodium bicarbonate loading test and diagnosed distal renal tubular acidosis (RTA). We also found that she had Sjögren’s syndrome after a positive screen for anti-Lo, anti-Ra, and after the results of Schirmer’s test and a lower lip biopsy. She was discharged and treated as an outpatient with oral sodium bicarbonate and potassium chloride.ConclusionThis case indicates that serum sodium concentrations should be carefully monitored in patients with distal RTA receiving intravenous sodium bicarbonate therapy. We should keep in mind that acute hypernatremia and CPM can be associated with intravenous sodium bicarbonate therapy, and that CPM due to acute hypernatremia may be effectively treated with plasma exchange.

A 61-year-old man presented with lower extremity paralysis and severe hypokalemia. His thyroid function test showed thyrotoxicosis. Despite attempts to correct his hypokalemia, he developed pulseless polymorphic ventricular tachycardia two hours later. He was successfully resuscitated after defibrillation. We performed continuous venovenous hemodiafiltration for 10 days due to acute kidney injury and rhabdomyolysis. We observed life-threatening polymorphic ventricular tachycardia requiring urgent defibrillation, as well as rhabdomyolysis requiring dialysis during the transient thyrotoxic phase of painless thyroiditis. Pay attention to the possibility of the development of life-threatening ventricular tachycardia associated with hypokalemia in the setting of thyroiditis and thyrotoxic paralysis.

Carbamazepine (CBZ) intoxication can be associated with severe toxicity, including neurological and cardio-respiratory abnormalities. Highly protein-bound, CBZ is not removed efficiently through conventional hemodialysis. Charcoal hemoperfusion is the most effective extracorporeal elimination therapy for CBZ intoxication. Recent reports have indicated that continuous venovenous hemodiafiltration (CVVHDF), albumin-enhanced continuous venovenous hemodialysis, high-flux hemodialysis and plasma exchange can be as effective as charcoal hemoperfusion. In contrast to recent reports, which demonstrated the effectiveness of CVVHDF with high dialysate flow in CBZ intoxication, we observed that serum CBZ level was decreased minimally by albumin-enhanced CVVHDF with low dialysate flow. Therefore, albumin-enhanced CVVHDF with high dialysate flow should be considered in severe CBZ intoxication, if hemoperfusion is unavailable because of the lack of facilities or if it cannot be performed.

Invasive aspergillosis (IA), generally considered an opportunistic infection in immunocompromised hosts, is associated with high morbidity and mortality. IA commonly occurs in the respiratory tract with isolated reports of aspergillosis infection in the nasal sinuses, central nervous system, skin, liver, and urinary tract. Extra-pulmonary aspergillosis is usually observed in disseminated disease. To date, there are a few studies regarding primary and disseminated gastrointestinal (GI) aspergillosis in immunocompromised hosts. Only a few cases of primary GI aspergillosis in non-immunocompromised hosts have been reported; of these, almost all of them involved the upper GI tract. We describe a very rare case of IA involving the lower GI tract in the patient without classical risk factors that presented as multiple colon perforations and was successfully treated by surgery and antifungal treatment. We also review related literature and discuss the characteristics and risk factors of IA in the immunocompetent hosts without classical risk factors. This case that shows IA should be considered in critically ill patients, and that primary lower GI aspergillosis may also occur in the immunocompetent hosts without classical risk factors.

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