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Airway Obstruction and Flattening of Arterial Pressure Wave during Whole Lung Lavage: A Case Report
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Hyun Jung Koh, Sung Jin Hong, Ho Kyung Song, Ji Young Lee, Jin Young Chon, Ho Sik Moon, Yu Mi Ju, Hyung Mook Lee
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Korean J Crit Care Med. 2013;28(2):133-136.
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DOI: https://doi.org/10.4266/kjccm.2013.28.2.133
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- Whole lung lavage (WLL) is a challenging procedure; because lavage fluid may perturb the respiratory and hemodynamic systems. We observed severe airway obstruction and flattening arterial pressure wave during WLL for treatment of pulmonary alveolar proteinosis. The aim of this case report is to discuss the anesthetic requirement in order to prevent bronchospasm during WLL. Furthermore, we discuss the potential of lavage fluid to cause airway obstruction and decrease cardiac outflow through the mass effect.
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Muscle Relaxants in Critically Ill Patients with Renal Disease
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Jin Young Chon
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Korean J Crit Care Med. 2012;27(3):145-150.
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DOI: https://doi.org/10.4266/kjccm.2012.27.3.145
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- Critical illness often results in renal dysfunction. Renal disease includes acid base imbalance, electrolyte shift and neuromuscular disturbances in critically ill patients, who are influenced by the pharmacodynamics and pharmacokinetics of muscle relaxants, with kidney dependent metabolism and excretion. In terms of renal dysfunction, not only decreased circulating levels of normal cholinesterase, but also cholinesterase depletion after plasmapheresis and dialysis draw the attention of clinicians, when administering a muscle relaxant to critically ill patients who are compromised with renal function. These patients have a lower clearance of renal excreted drugs, changes of the volume of distribution, water retention, and pH changes that alter the protein bond and degree of ionization of the drugs.
Immobilization of the limb and respiratory muscles, leading to muscle atrophy and the up-regulation of nicotinic acetylcholine receptors, associated with critical illness, is observed in many patients hospitalized in the intensive care unit with renal dysfunction. Disease related conditions or iatrogenically induced factors, including sedation, lead to immobilization of skeletal muscles. Aside from systemic inflammation, immobilization is a key contributing factor to the development of critical illness myopathy. Physicians who care for critically ill patients with renal dysfunction should pay attention to the adequate choice of muscle relaxants and their antagonists.
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Nasogastric Tube Insertion using Savary-Gilliard Wire Guide(R) in a Comatose Patient : A Case Report
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Hae Jin Lee, Jin Young Chon, Jin Hwan Choi, He Jin Choi, Se Ho Moon
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Korean J Crit Care Med. 2006;21(2):135-139.
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- The insertion of nasogastric tubes in comatose, obtunded or anesthetized patients is often difficult, frustrating and time-consuming. A large variety of methods inserting nasogastric tubes in those uncooperative patients have been reported. As a new effective method, we used Savary-Gilliard Wire Guide(R), which is designed for introducing Savary-Gilliard Dilator(R) into a strictured esophagus, for inserting a nasogastric tube in a comatose patient who was intubated with a ballooned tracheostomy tube. The insertion was successful in the first attempt and no complication occurred.
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An Experience of Right Pneumonectomy in a Lung Cancer Patient with Poor Pulmonary Function Test within the Conventional Criteria of Contraindication to Surgery: Intraoperative Re-evaluation of Pulmonary Function: A case report
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Jin Young Chon, Sung Jin Hong, Ung Jin, Hae Jin Lee, Yong Woo Choi, Se Ho Moon, Sun Hee Lee, Man Seok Bae
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Korean J Crit Care Med. 1999;14(2):167-175.
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- Usually FEV1 lower than 1 liter is considered as a contraindication to pneumonectomy. Therefore sometimes, the curative operations of the resectable lung cancer can not be performed in case of poor pulmonary functions. The usual criteria on the performance of pneumonectomy on high risk patients based on the preoperative assessment of pulmonary function may not predict the operative outcome with accuracy in the postoperative period. Nowadays, there are some arguing points about applying the values of preoperative PFTs to pulmonary resection surgery. We performed a right pneumonectomy for stage IIIb lung cancer in a patient with poor lung function test; FVC 2.17 L, FEV1 0.97 L, FEV1/FVC 44%, FEF 25~75% 0.42 L/sec, MVV 28 L/min, TLC 5.18 L, RV 2.99, DLCO 13.46. After the temporary ligation of right main pulmonary artery during 30 minutes, arterial blood gas and percutaneous oxygen saturation with the controlled ventilation with room air (FiO2=0.21) confirmed the hemodynamic and oxygenation stabilities, twice. After successful surgery, the patient was tolerated for 4 months.
And the follow up PFTs at postoperative 3 months and 18 days showed as follows; FVC 1.20 L, FEV1 0.63 L, FEV1/FVC 53%, FEF 25~75% 0.31 L/sec, MVV 25 L/min, TLC 3.80 L, RV 2.33 L, DLCO 8.04. Through the intraoperative re-evaluation of pulmonary function in a patient with poor preoperative PFTs,had been conventionally considered as a contraindication to pneumonectomy, we report a successful surgery and anesthetic management with the literatures reviewed.
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The Effect of Clonidine Pretreatment on Bupivacaine-induced Cardiac Toxicity in Rabbit
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Eun Ju Lee, Jin Young Chon, Yong Woo Choi, Se Ho Moon
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Korean J Crit Care Med. 1998;13(2):205-211.
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- BACKGOUND: Bupivacaine, an amide type local anesthetic, is frequently used for regional anesthesia. Bupivacaine overdose induces cardiac toxicity and directly depresses both cardiac electrophysiology and hemodynamic status.
Clonidine, an imidazolin alpha-2-adrenoreceptor agonist, given prophylactically may delay the toxic manifestation of bupivacaine overdose and does not accentuate the subsequent hypotension. We studied the effect of clonidine pretreatment on bupivacaine induced cardiac toxicity.
METHODS
Fourteen rabbits (seven in each group) were anesthetized with ketamine and rompun, and tracheostomy was performed. Spontaneous ventilation with room air was continued throughout the experiment. Electrocardiogram, heart rate, and invasive arterial blood pressure were continuously recorded. Clonidine 5 microgram/kg (clonidine group) or saline (control group) was injected intravenously in randomized fashion. After 15 minutes, an intravenous infusion of bupivacaine was started at 0.3 mg/kg/min. The time of occurrence of the bupivacaine-induced toxic events: first dysrhythmia, 25% and 50% reduction in basal heart rate and mean arterial pressure, and asystole were recorded. At 5, 10, 15, and 20 minutes after bupivacaine infusion, 2 ml of whole blood were withdrawn via femoral arterial catheter for determination of bupivacaine concentration.
RESULTS
The threshold time at the first dysrhythmia was significantly greater in the clonidine group (27.2+/-4.5 min) than control group (19.9+/-1.2 min). The threshold times at the 25 and 50% reduction in basal heart rate were significantly greater in the clonidine group (23.7+/-5.8 min, 33.2+/-5.1 min) than control group (16.6+/-2.9 min, 22.9+/-2.8 min) and in basal mean arterial pressure were significantly greater in the clonidine group (15.6+/-2.6 min, 25.3+/-3.7 min) than control group (9.7+/-2.7 min, 16.3+/-5.8 min). The threshold time at the asystole was significantly greater in the clonidine group (38.2+/-7.7 min) than control group (28.7+/-3.4 min). At 5, 10, 15, and 20 minutes after bupivacaine infusion, there was no significant difference in the plasma bupivacaine concentration between two groups.
CONCLUSION
This study demonstrates that clonidine pretreatment delays the cardiac toxic manifestations of bupivacaine overdose. And plasma bupivacaine concentration was not influenced by clonidine pretreatment.
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