• Tuberculosis and Respiratory Diseases
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• v.59 no.6
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• pp.690-695
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• 2005

Nitric acid is an oxidizing agent used in metal refining and cleaning, electroplating, and other industrial applications. Its accidental spillage generates oxides of nitrogen, including nitric oxide (NO) and nitrogen dioxide ($NO_2$), which cause chemical pneumonitis when inhaled. The clinical presentation of a nitric acid inhalation injury depends on the duration and intensity of exposure. In mild cases, there may be no symptoms during the first few hours after exposure, or the typical symptoms of pulmonary edema can appear within 3-24 hours. However, in cases of prolonged exposure, progressive pulmonary edema develops instantaneously and patients may not survive for more than 24 hours. We report a case of a 44-year-old male who was presented with acute respiratory distress syndrome after nitric acid inhalation. He complained of cough and dyspnea of a sudden onset after inhaling nitric acid fumes at his workplace over a four-hour period. He required endotracheal intubation and mechanical ventilation due to fulminant respiratory failure. He was managed successfully with mechanical ventilation using positive end expiratory pressure and systemic corticosteroids, and recovered fully without any deterioration in his pulmonary function.

• Korean Journal of Clinical Pharmacy
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• v.22 no.4
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• pp.316-323
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• 2012

미숙아는 단백질 대사 속도가 빠르기 때문에 성장이 충분히 이루어질 수 있도록 ASPEN 가이드라인에서는 아미노산 초기용량을 1-2 g/kg/day로 투여하도록 권장하고 있다. 또한 최근 여러 연구에서 출생초기 고용량 (1.5-4 g/kg/day) 아미노산 투여에 대해 보고하고 있다. 이를 근거로 하여 삼성서울병원 신생아 중환자실에서도 2009년 6월부터 아미노산 초기용량을 0.5 g/kg/day에서 1.5~2 g/kg/day으로 증량하여 투여하고 있다. 본 연구에서는 신생아 중환자실에서 정맥영양요법을 받은 미숙아를 대상으로 고용량 아미노산 공급 효과를 평가하고자 하였다. 2009년 6월 기준으로 출생 후 48시간 이내에 0.5 g/kg/day로 아미노산을 투여 받은 저용량 환아군(38명: 대조군)과 1.5~2 g/kg/day로 투여 받은 고용량 환아군(38명: 시험군)의 전자의무기록을 후향적으로 검토하였다. 고용량 아미노산 공급 효과를 체중증가량 및 총 정맥영양기간, 경구 및 경장 영양 시작 시기, 재원기간으로 평가하였고, 안전성 평가를 위해 혈액화학검사 및 합병증을 조사하였다. 또한 두 군의 인구학적 및 주산기 인자, 영양 공급량 등에 대해 조사하였다. 두 군의 인구학적 및 주산기 인자는 재태기간에서만 차이를 보였으며, 시험군에서 재태기간이 길었다(p < 0.05). 초기 아미노산 용량만이 생후 28일간 일평균 체중증가량에 영향을 미치는 인자였으며 시험군의 일평균 체중증가량이 대조군보다 유의하게 큰 것으로 나타났다($12.6{\pm}4.5$ g/day vs $9.8{\pm}4.5$ g/day, p < 0.05). 목표 체중증가량에 도달한 비율도 시험군이 높았다(65.8% vs 47.4%). 총 공급열량, 총 정맥영양 공급 기간과 경구 및 경장 영양 시작 시기는 두 군간 차이가 없었으나 시험군에서 목표열량 도달시간, 신생아 중환자실 재원기간이 단축되었다(p < 0.05). 혈액화학검사 결과 및 대사성 산증, 호흡곤란증후군, 괴사성장염 발생은 두 군간 차이가 없었으며 고혈당 및 감염, 기관지폐이형증, 뇌실내출혈 발생률은 대조군에서 유의하게 높았다(p < 0.05). 연구 결과, 미숙아에서 출생 초기 고용량 아미노산 공급은 혈액화학검사 이상이나 합병증 없이 체중증가와 재원기간 감소에 효과가 있음을 확인하였다. 따라서 미숙아에 대한 출생초기 영양지원으로 1.5~2 g/kg/day 아미노산 공급은 안전하고 효과적이라고 사료된다.

• Journal of The Korean Society of Inherited Metabolic disease
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• v.16 no.1
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• pp.47-51
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• 2016

Propionic acidemia (PA) is an autosomal recessively inherited disorder of the organic acid metabolism. It is caused by a deficiency of propionyl-CoA carboxylase (PCC). PCC is a heteropolymeric enzyme composed of ${\alpha}$- and ${\beta}$-subunits. The clinical symptoms of PA are heterogeneous and present vomiting, dehydration, hypotonia, and lethargy, and it can result in death. The typical presentations of neonatal onset PA are life-threatening metabolic acidosis and hyperammonemia. Here, we described a case of neonatal onset PA with mild clinical presentations. She was born to a healthy mother without complications. No significant illness was observed until nine days after birth. She started exhibiting poor oral feeding, vomiting, lethargy, and hypotonia at ten days old. Her laboratory results showed mild hyperammonemia and acidosis. The initial diagnosis was neonatal sepsis and she was treated with antibiotics. However, her clinical symptoms didn't improve. So we considered a metabolic disease. She was given nothing by mouth and intravenous hydration and nutrition support was performed. Propionylglycine and 3-hydroxypropionic acid were showed high concentrations in urine by gas chromatograph mass spectrometry (GC-MS). C3 level of acylcarnitine analysis elevated 10.4 uM/L (range, 0.200-5.00) in plasma. We took gene analysis for PA to be based on the symptoms and laboratory results. We detected PCCB gene mutation and diagnosed PA. She survived without severe neurologic defects and complications and was hospitalized only three times with upper respiratory tract infections for 7 years. We report a case of a ten days old neonate with PA presenting without severe metabolic acidosis and hyperammonemia who was effectively treated with early aggressive care and conventional methods.

• Clinical and Experimental Pediatrics
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• v.52 no.3
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• pp.376-379
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• 2009

We report a case of a premature newborn baby who presented with hyponatremia, hyperkalemia, and metabolic acidosis accompanied by severe polyhydramnios in utero. The baby was diagnosed with pseudohypoaldosteronism on the basis of normal 17-hydroxyprogesterone levels, elevated aldosterone, and clinical symptoms. His serum electrolyte levels were corrected with sodium chloride supplementation. Sodium supplementation was reduced gradually and discontinued at 5 months of age. At 5 months, the child was able to maintain normal serum electrolyte levels without oral sodium chloride supplementation, and showed normal physical and neurological development. This case illustrates that pseudohypoaldosteronism must be considered if a newborn infant with an antenatal history of severe polyhydramnios shows excessive salt loss with normal levels of 17-hydroxyprogesterone.

• Childhood Kidney Diseases
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• v.14 no.2
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• pp.132-142
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• 2010

Hypokalemia usually reflects total body potassium deficiency, but less commonly results from transcellular potassium redistribution with normal body potassium stores. The differential diagnosis of hypokalemia includes pseudohypokalemia, cellular potassium redistribution, inadequate potassium intake, excessive cutaneous or gastrointestinal potassium loss, and renal potassium wasting. To discriminate excessive renal from extrarenal potassium losses as a cause for hypokalemia, urine potassium concentration or TTKG should be measured. Decreased values are indicative of extrarenal losses or inadequate intake. In contrast, excessive renal potassium losses are expected with increased values. Renal potassium wasting with normal or low blood pressure suggests hypokalemia associated with acidosis, vomiting, tubular disorders or increased renal potassium secretion. In hypokalemia associated with hypertension, plasam renin and aldosterone should be measured to differentiated among hyperreninemic hyperaldosteronism, primary hyperaldosteronism, and mineralocorticoid excess other than aldosterone or target organ activation. Hypokalemia may manifest as weakness, seizure, myalgia, rhabdomyolysis, constipation, ileus, arrhythmia, paresthesias, etc. Therapy for hypokalemia consists of treatment of underlying disease and potassium supplementation. The evaluation of hyperkalemia is also a multistep process. The differential diagnosis of hyperkalemia includes pseudohypokalemia, redistribution, and true hyperkalemia. True hyperkalemia associated with decreased glomerular filtration rate is associated with renal failure or increased body potassium contents. When glomerular filtration rate is above 15 mL/min/$1.73m^2$, plasma renin and aldosterone must be measured to differentiate hyporeninemic hypoaldosteronism, primary aldosteronism, disturbance of aldosterone action or target organ dysfunction. Hyperkalemia can cause arrhythmia, paresthesias, fatigue, etc. Therapy for hyperkalemia consists of administration of calcium gluconate, insulin, beta2 agonist, bicarbonate, furosemide, resin and dialysis. Potassium intake must be restricted and associated drugs should be withdrawn.

• Pediatric Gastroenterology, Hepatology & Nutrition
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• v.9 no.2
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• pp.153-161
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• 2006

Purpose: This study was designed to investigate rotavirus infection by comparing the clinical characteristics in neonates and infants. Methods: We enrolled 104 neonates and 250 infants wiht gastroenteritis and a rotazyme test positive reaction at the Soonchunhyang University Bucheon Hospital from February 2001 to January 2003. Results: The seasonal peaks of infection in infants occurred from February to June. However, in neonates, it occurred from October to December due to nursery outbreaks. Diarrhea, vomiting, fever and convulsions were significant symptoms in infants; however, metabolic acidosis with dehydration, jaundice, irritability, apnea, bloody stool, gastric residual, grunting, poor oral intake, lethargy as well as fever and diarrhea were more common in the neonates. Upper respiratory infection, pneumonia and bronchitis were present in the infants; however, necrotizing enterocolitis was more commonly observed in the in neonates. Among the patients with rotaviral infection, formula feeding was more popular than breast milk feeding in both the neonates and infants; however, this finding was not statistically significant. Conclusion: Rotavirus can be a significant pathogen in neonates as well as infants. Neonates suffering from fever, poor oral intake, lethargy and apnea should be investigated for rotaviral infection. A new vaccine, rotaviral specific immunoglobulin and treatment guidelines are needed for eradicating rotavirus infection. Further studies on isolation, infection pathway, immune response and treatment of rotavirus are needed.

• Journal of The Korean Society of Inherited Metabolic disease
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• v.15 no.1
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• pp.18-24
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• 2015

Glycogen storage disease type Ib (GSD Ib) is one of the rare inherited metabolic disease caused by mutation of SLC37A4 gene. Clinical characteristics include hepatomegaly, hypoglycemia, lactic acidosis, hyperlipidemia and high serum uric acid concentration. The authors analyzed clinical and molecular characteristics of three Korean patients (one male and two females) with GSD Ib by retrospective review of medical records. Two patients were diagnosed in toddler period by hypoglycemia and hepatomegaly. One patient was diagnosed by growth retardation and short stature in puberty. c.412T>C (p.Trp138Arg) (3/6 alleles, 50.0%) was most frequently observed, following by p.Leu348Valfs*53 (1 allele), p.Pro191Leu (1 allele), p.Ala148Val (1 allele) in molecular analysis. Uncooked corn starch and allopurinol was administered. Because all three patients had neutropenia and recurrent infections, G-CSF was administered. Two patients had severe osteoporosis needing calcium supplement. The patient who diagnosed at puberty had relatively poor prognosis demonstrated by having severe infection and complications in liver and kidney.

• Journal of the Institute of Electronics Engineers of Korea SC
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• v.48 no.4
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• pp.1-9
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• 2011

Hemorrhagic shock is a clinically widespread syndrome characterized by inadequate oxygenation and supply. It is important to diagnose hemorrhagic shock in its early stage for improving treatment effects and survival rate. However, an accurate diagnosis and treatment could be delayed in the early stage of hemorrhagic shock by evaluating only vital signs such as heart rate and blood pressure. There have been many studies for the early diagnosis of hemorrhagic shock, reporting that lactate concentration and perfusion were useful variables for tissue hypoxia and metabolic acidosis. In this study, we measured both perfusion using a laser Doppler flowmeter and lactate concentration from the volume controlled hemorrhagic shock using rats. We also proposed a new shock index which was calculated by dividing lactate concentration by perfusion for early diagnosis. As a result of the survival prediction by the proposed index with the receiver operating characteristic curve method, the sensitivity, specificity, and accuracy of survival were 90.0, 96.7 and 94.0%, respectively. The proposed index showed the fastest significant difference among the other parameters such as blood pressure and heart rate. It could offer early diagnosis and effective treatment for human hemorrhagic shock if it is applicable to humans.

• Childhood Kidney Diseases
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• v.17 no.2
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• pp.137-142
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• 2013

Pseudohypoaldosteronism (PHA) is a condition characterized by renal salt wasting, hyperkalemia, and metabolic acidosis due to renal tubular resistance to aldosterone. Systemic PHA1 is a more severe condition caused by defective transepithelial sodium transport due to mutations in the genes encoding the ${\alpha}$ (SCNN1A), ${\beta}$ (SCNN1B), or ${\gamma}$ (SCNN1G) subunits of the epithelial sodium channel at the collecting duct, and involves the sweat glands, salivary glands, colon, and lung. Although systemic PHA1 is a rare disease, we believe that genetic studies should be performed in patients with normal renal function but with high plasma renin and aldosterone levels, without a history of potassium-sparing diuretic use or obstructive uropathy. In the present report, we describe a case of autosomal recessive PHA1 that was genetically diagnosed in a newborn after severe hyperkalemia was noted.

• Journal of the Korea Academia-Industrial cooperation Society
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• v.19 no.11
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• pp.421-425
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• 2018

Methanol is a clear, colorless, volatile, and poisonous liquid that is commonly used as an industrial solvent. Visual impairment is a common symptom of methanol poisoning; however, visual impairment rarely occurs after exposure through inhalation. Therefore, visual loss after methanol intoxication via respiration has rarely been reported. We report a case of visual damage associated with methanol poisoning via respiratory exposure in an industrial setting. In this case in South Korea, a 28-year-old woman who worked at a cell phone factory was admitted to the emergency department with mental changes. She had blurred vision that began two days prior, but she did not come to the hospital until she experienced mental changes. She ranked 9 on the Glasgow Coma Scale and presented with severe metabolic acidosis. So, she was admitted to intensive care, and continuous renal replacement therapy was performed. Finally, she was discharged after recovery of her mental state, but had to undergo rehabilitation for six months. Also, her visual impairment was permanent. Methanol intoxication can occur through inhalation, which is difficult to detect initially. However, treatment of methanol poisoning is time-critical. Therefore, doctors should always keep in mind that methanol intoxication may occur via respiration. If in doubt, treatment should be given as soon as possible.