• Journal of Dental Anesthesia and Pain Medicine
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• v.17 no.3
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• pp.235-240
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• 2017

Pulseless electrical activity (PEA) is a clinical condition characterized by unresponsiveness and lack of palpable pulse in the presence of organized cardiac electrical activity and is caused by a profound cardiovascular insult (e.g., severe prolonged hypoxia or acidosis, extreme hypovolemia, or flow-restricting pulmonary embolus). Amyotrophic lateral sclerosis (ALS) is a disease that is characterized by progressive degeneration of all levels of the motor nervous system. Damage to the respiratory system and weakness of the muscles may increase the likelihood of an emergency situation occurring in patients with ALS while under general anesthesia. We report a case of PEA during the induction of general anesthesia in a patient with ALS who presented for dental treatment and discuss the causes of PEA and necessary considerations for general anesthesia in patients with ALS.

• Journal of Chest Surgery
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• v.3 no.2
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• pp.139-142
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• 1970

A Case of thoraco-abdominal aortic aneurysm involving from the lower descending- thoracic aorta to bifurcation of abdominal aorta into both common iliac artery is presented in special view-point of its surgical technic and postoperative complication. Operative technic is the most popular method of Dr. De Bakey's shunt of Dacron which is bridging thoracic aorta to terminal abdominal aorta primarily as temporary shunt but after anastomosing the individual hranch of left Renal, Celiac, Sup. meseateric and right Renal artery to corresponding part of the Dacron tube, the Dacroa graft is fixed as permanent graft in stead of excised thoraco-abdominal aorta. The patient died of acute renal failure and increasing evidence of CNS damage due to respiratory acidosis on 6th postoperative day hut this report will he a good experience in respect of further progress of aortic surgery in Korea.

• Journal of The Korean Society of Clinical Toxicology
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• v.2 no.1
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• pp.7-11
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• 2004

Purpose: We would evaluate the cardiovascular manifestations of the patients with acute organophosphate and carbamate poisoning in the emergency department. Methods: This was retrospectively studied with the review of patient's charts, included total 38 patients were admitted during the past two years in the emergency department of Yeungnam university hospital with the diagnosis of organophosphate or carbamate poisoning. Results: Cardiovascular complications were variously developed in many patients. Electrocardiographic findings were as follows; 4 ($10.5\%$) cardiac arrhythmias included 1 cardiac arrest caused by ventricular fibrillation, 14 ($36.8\%$) sinus tachycardias, 3 ($7.9\%$) sinus bradycardias, and 17 ($44.7\%$) normal sinus rhythms. Conduction disturbances were 23 ($60.5\%$) like as prolonged QTc, 4 ($10.5\%$) ST-T changes, 2 (5.3%) first degree AV block, and 3 ($7.9\%$) right bundle branch block were shown. Other cardiovascular complications were 22 ($57.9\%$) hypertensives, 4 ($10.5\%$) hypotensives, 15 ($39.5\%$) tachycardias, 2 ($5.3\%$) bradycardias, 18 ($47.4\%$) hypoxemics, 12 ($31.6\%$) metabolic acidosis, and 9 ($23.7\%$) pulmonary edemas. Sixteen patients ($42.1\%$) needed ventilatory support because of respiratory paralysis. No patients died in hospital and 36 ($94.7\%$) patients were alive-discharged. Conclusion: Cardiovascular complications are variously in patients with acute organophosphate and carbamate poisoning. Especially, some findings included ventricular arrhythmias, QTc prolongation, hypoxemia, acidosis, and blood pressure changes are known as major precipitating factors to increase the mortality. So, intensive support and aggressive treatment are needed in patients shown various cardiovascular manifestations in the emergency department.

• Parasites, Hosts and Diseases
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• v.51 no.5
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• pp.551-555
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• 2013

Complicated malaria is mainly caused by Plasmodium falciparum, but, increasingly, Plasmodium vivax is also being reported as a cause. Since the reemergence of indigenous vivax malaria in 1993, cases of severe malaria have been steadily reported in Korea. Herein, we report a case of vivax malaria complicated by adult respiratory distress syndrome (ARDS) that was successfully managed with extracorporeal membrane oxygenation (ECMO). A 59-year-old man presented at our hospital with fever and abdominal pain, which had persisted for 10 days. On admission, the patient had impaired consciousness, shock, hypoxia and haziness in both lungs, jaundice, thrombocytopenia and disseminated intravascular coagulation, metabolic acidosis, and acute kidney injury. A peripheral blood smear and a rapid diagnostic test verified P. vivax mono-infection. Ten hours after admission, hypoxia became more severe, despite providing maximal ventilatory support. The administration of antimalarial agents, ECMO, and continuous venovenous hemofiltration resulted in an improvement of his vital signs and laboratory findings. He was discharged from the hospital 7 weeks later, without any sequelae.

• Pediatric Infection and Vaccine
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• v.25 no.2
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• pp.101-106
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• 2018

A 6-year-old boy with underlying hemolytic anemia of unknown etiology, atopic dermatitis, and recurrent urticaria visited our hospital because of acute respiratory failure induced by influenza A. Despite mechanical ventilation after endotracheal intubation along with inhalation of nitric oxide, respiratory acidosis and hypoxemia persisted. Veno-venous extracorporeal membrane oxygenation (VV ECMO) insertion was performed to provide respiratory support. After performing flexible bronchoscopy, we found that thick mucus plugs were obstructing the right bronchus intermedius and the upper lobe orifice. After bronchial washing and removal of the plugs, we were able to wean the patient off VV ECMO and transfer him to the general ward. He was discharged without any neurologic or pulmonary sequelae.

• Journal of Yeungnam Medical Science
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• v.31 no.2
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• pp.89-93
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• 2014

Background: This study was conducted to investigate the epidemiological features, clinical courses, and diagnoses of neonates who are transferred to neonatal intensive care unit of Yeungnam University Hospital due to tachypnea soon after birth. Methods: Based on medical records, we performed a retrospective study of neonatal intensive care unit admissions due to tachypnea from January 2010 to December 2013. Results: A total of 311 neonates were included in this study. The patient characteristics showed male predominance at 2.65:1. Among the 311 neonates with tachypnea, 127 (40.8%) neonates needed oxygen supply, and 54 (17.4%) neonates needed assisted mechanical ventilation. Transient tachypnea of the newborns (TTN) (158, 50.8%) showed the highest incidence, followed by pneumonia (63, 20.3%), extrapulmonary infection (37, 11.9%), respiratory distress syndrome (21, 6.8%), air leak (16, 5.1%), meconium aspiration syndrome (12, 3.9%), congenital heart disease (5, 1.6%), metabolic acidosis (3, 1%), primary pulmonary hypertension of newborns (2, 0.6%) and anemia (2, 0.6%). Conclusion: Although the neonates with tachypnea showed no other respiratory distress symptom, clinicians should be aware of the possibility of other pulmonary diseases as well as TTN and their extra-pulmonary causes. If tachypnea does not improve within a few hours, the clinician should consider further evaluation and management as soon as possible.

• Journal of The Korean Society of Inherited Metabolic disease
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• v.16 no.2
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• pp.102-108
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• 2016

Mitochondrial encephalopathy, lactic acidosis, and stroke-like episode (MELAS) syndrome is one of mitochondrial encephalopathy. As the early clinical manifestations can be variable, it is important to suspect the disease, especially in patients with multiple organ dysfunctions. A boy was diagnosed with epilepsy when he was 9 years old. Two years later, severe headache and blurred vision developed suddenly. On examination, left homonymous hemianopsia was detected with corresponding cerebral parenchymal lesions in right temporo-occipito-parietal areas. MELAS syndrome was confirmed by genetic test, which showed m.3243 A>G mitochondrial DNA mutation. Multivitamins including coenzyme Q10 were added to anticonvulsant. He experienced 4 more events of stroke-like episodes over 5 years, but he is able to perform normal daily activities. A 13-year-old boy was brought to the hospital due to suddenly developed respiratory arrest and asystole associated with pneumonia. Past medical history revealed that he had multiple medical problems such as epilepsy, failure-to-thrive, optic atrophy, and deafness. He has been on valproic acid as an anticonvulsant which was prescribed from local clinic. He recovered after the resuscitation, but his cognition and motor function were severely damaged. He became bed-ridden. He was diagnosed with MELAS syndrome by brain MRI, muscle biopsy, and clinical features. Genetic test did not reveal any mitochondrial gene mutation. Four years later, he expired due to suddenly developed severe metabolic acidosis combined with hyperglycemic hyperosmolar nonketotic coma. The clinical features of MELAS syndrome are variable. Early diagnosis before the presentation to the grave clinical course may be important for the better clinical outcome.

• The Korean Journal of Physiology
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• v.24 no.1
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• pp.123-129
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• 1990

A comparative study of acid-base balance has been made between acidemia-induced hyperkalemia and hyperkalemia-induced acidemia. A group of rabbits was infused 0.1 N hydrochloric acid solution and metabolic acidosis was induced. Another group was administered 20 mM potassium chloride solution and hyperkalemia was induced. The third group was infused 0.1 N hydrochloric acid and 20 mM potassium chloride solution, simultaneously. Acid-base data and plasma potassium ion concentration were monitored every thirty minutes in these three groups of rabbits. Following results were obtained: 1 ) Along with the infusion of hydrochloric acid, acute metabolic acidosis was induced in the rabbits. Plasma bicarbonate ion concentration decreased primarily in this group. As a respiratory compensation, there was a tendency of reduction of arterial $Pco_{2}$. The alteration of data became larger along with the amount of administration and the time elapsed. However, hyperkalemia was not so severe compared with the second group. 2) In potassium chloride infused group, plasma potassium ion concentration increased along with the time elapsed and the amount of infusion. And the alteration of acid-base data was parrallel to the level of potassium ion concentration, above all depression of pH was prominent. 3) Above data suggest that when acute metabolic acidosis was induced, exchange of intracellular potassium ion with extracellular hydrogen ion seems significant for the regulation of extracellular acid-base balance. And when hyperkalemia was induced with the infusion of potassium chloride solution, the exchange of intracellular hydrogen ion with extracellular potassium ion also seems significant for the regulation of extracellular potassium balance. 4) In the group of rabbits infused hydrochloric acid and potassium simultaneously, disturbances of acid-base balance and potassium balance were much more severe than two other groups. In these mixed disturbances, the process of compensatory mechanism might be inhibited and one disturbance might aggregate each other. 5) Through above data it has been postulated that in acid-base disturbance potassium balance can be sacrificed as a compensatory mechanism, and vice versa in disturbance of potassium balance. And our data also suggest that hydrogen ion and potassium ion are compensatory pair, one another.

• 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.

• Journal of Chest Surgery
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• v.3 no.2
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• pp.73-90
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• 1970

Clinical perfusion data on 16 cases of cardiopulmonary bypass using Sigmamotor pump and RyggKyvsgaard Oxygenator which performed at Seoul National University Hospital during the period of Aug. 1968 to Aug. 1970 was analized. AIl cases were hemodiluted and the perfusion was carried out under the normothermic condition. The age of the patients ranged between 6 and 43 years. The b:dy weight varied between 18.3 and 54.0 kg and the body surface area between 0.78 and 1. 59$M^2$. The priming solution was consiste:I with fresh ACD blood. Hartmann solution and Mannitol. The average amount of priming was approximately 2242 ml. The average hemodilution rate was 17%. The flow rate ranged from 1.7L to 3.5L/Min/$M^2$ and averaged 2.4L/Min/$M^2$ or 78mI/Min/kg. The duration of perfusion varied from 22 to 110 min with average of 56.9 minutes. Some hemodynamic responses were observed. The arterial pressure dropped immediately after the initiation of partial perfusion and was more marked after the total perfusion foIlowed by gradual increase to the safety level. The central venous pressure reflected the reduced blood volume especially in the cases of prolonged perfusion which lasted over 60 min. In most of the cases, red blood cell count decreased and white blood ceIl count increased after the perfusion. Hemoglobin level was decreased, averaging of 12.5mg%, Hct 3.3% and platelets count of 18% postoperatively. Plasma hemoglobin increased mildly, from pre-perfusion average value of 4. 06mg% to postperfusion value of 22.5mg%. Serum potassium was 4.4mEq/L pre-operatively and was decreased to 3.7mEq/L postoperatively. Five cases showed definite hypopotassemia immediately after the operation. Sodium and chloride decreased mildly. These electrolyte changes are thought to be related with hemodilution. diuretics and reduced blood volume during and after the perfusion. Arterial blood pH value revealed minimal to moderate elevation from preperfusion average value of 7.376 to 7.461 during perfusion and then 7.365 after perfusion. The pC02 and hicarbonate showed minimal to moderately lowered values. The total CO2 was decreased. Buffer base decreased during perfusion (Av. 42.6mEq/L) and further decreased after the perfusion (Av. 40.8mEq/L). These arterial blood acid base changes suggested that the metabolic acidosis was accompanied by respiratory alkalosis during and immediately after the perfusion. Authors belived that the acidosis could more effectively be corrected with the more additional dose of bicarbonate than we used by this study. The chest tune drainage during the first 24 hours following operation was 1158 ml in average. One case (Case No. 15) showd definite bleeding tendency and it was believed that the cause might be due to the defect of heparin and protamine titration. The average urinary out put during 24 hours post-perfusion was 1291ml. One case (Case No. ]) showed definite post perfusion oliguria. As conclusion hemodilution using fresh ACD blood. Hartmann and Mannitol solution added with Bivon and high flow rate unler normothermia. was thought to amelioratc the severity of mctabolic acidosis during and after perfusion with relatively satisfactory effect on the diuresis and bleeding tendency.