A review of the complexity adjustment in the Korean Diagnosis-Related Group (KDRG).

BACKGROUND: The Korean Diagnosis-Related Groups (KDRG) was revised in 2003, modifying the complexity adjustment mechanism of the Australian Refined Diagnosis-Related Groups (AR-DRGs). In 2014, the Complication and Comorbidity Level (CCL) of the existing AR-DRG system was found to have very little correlation with cost. OBJECTIVE: Based on the Australian experience, the CCL for KDRG version 3.4 was reviewed. METHOD: Inpatient claim data for 2011 were used in this study. About 5,731,551 episodes, which had one or no complication and comorbidity (CC) and met the inclusion criteria, were selected. The differences of average hospital charges by the CCL were analysed in each Adjacent Diagnosis-Related Group (ADRG) using analysis of variance followed by Duncan's test. The patterns of differences were presented with R 2 in three patterns: The CCL reflected the complexity well (VALID); the average charge of CCL 2, 3, 4 was greater than CCL 0 (PARTIALLY VALID); the CCL did not reflect the complexity (NOT VALID). RESULTS: A total of 114 (19.03%), 190 (31.72%) and 295 (49.25%) ADRGs were included in VALID, PARTIALLY VALID and NOT VALID, respectively. The average R 2 for hospital charge of CCL was 4.94%. The average R 2 in VALID, PARTIALLY VALID and NOT VALID was 4.54%, 5.21%, and 4.93%, respectively. CONCLUSION: The CCL, the first step of complexity adjustment using secondary diagnoses, exhibited low performance. If highly accurate coding data and cost data become available, the performance of secondary diagnosis as a variable to reflect the case complexity should be re-evaluated. IMPLICATIONS: Lack of reviewing the complexity adjustment mechanism of the KDRG since 2003 has resulted in outdated CC lists and levels that no longer reflect the current Korean healthcare system. Reliable cost data (vs. charge) and accurate coding are essential for accuracy of reimbursement.

Frequency of unexpected antibody and consideration during transfusion.

BACKGROUND: In this retrospective study, we measured the frequency of unexpected antibodies in the blood. Specific considerations for preoperative preparations were kept in mind for the patients undergoing surgery positive for these antibodies. METHODS: After reviewing the results of antibody screening tests lasted for 2 years, the frequency of unexpected antibodies was determined. Surgical patients who were positive for unexpected antibodies were selected and divided into two groups based on their potential need for an intra-operative transfusion (groups with high versus low possibility of transfusion). Blood for the high possibility group was prepared before surgery. For the low possibility group for which preoperative blood preparation was not performed, cases of this group were reviewed whether a blood preparation was delayed or not in case of transfusion. RESULTS: Among a total 22,463 cases, 340 (1.52%) had positive results for antibody screening tests. Among the 243 patients who were positive for unexpected antibodies, Lewis, Rh, Xga, and mixed antibodies were found in 85, 25, five, and eight cases, respectively. Out of 243 patients, 117 patients, specificities of the unexpected antibodies were not determined and 125 (51.4%) had a history of pregnancy and delivery, and 49 (20.2%) had a history of transfusion. In the low probability group, transfusions were administered for nine patients; transfusion was delayed for two patients due to difficulties with obtaining matched blood. CONCLUSIONS: Patients with unexpected blood antibodies may be at increased risk for delayed transfusion. For rapid transfusion, it might be helpful to keep a record about blood antibodies and introduce a notification system such as medical alert cards. Preoperative blood preparation is needed for timely intraoperative transfusion.

General anesthesia activates BDNF-dependent neuroapoptosis in the developing rat brain.

Brain-derived neurotrophic factor (BDNF) is important in supporting neuronal development. BDNF imbalance due to excessive neuronal inhibition can result in the apoptotic degeneration of developing neurons. Since general anesthetics cause profound depression of neuronal activity and are known to induce widespread degeneration in the developing brain, we studied their potential to activate BDNF-mediated developmental neuroapoptosis. When P7 rats (at the peak of brain development) were exposed to a commonly-used and highly pro-apoptotic anesthesia protocol (midazolam, isoflurane, nitrous oxide) for a period of 2, 4 or 6 h, we found that anesthesia modulates the key steps in BDNF-activated apoptotic cascade in two of the most vulnerable brain regions--cerebral cortex and thalamus in time-dependent fashion by activating both Trk-dependent (in thalamus) and Trk-independent p75NTR dependent (in cerebral cortex) neurotrophic pathways. beta-estradiol, a sex hormone that upregulates the protein levels of the activated Akt, protects against anesthesia-induced neuroapoptosis.

Melatonin reduces the severity of anesthesia-induced apoptotic neurodegeneration in the developing rat brain.

General anesthetics cause widespread apoptotic neurodegeneration in many regions of the developing rat brain. The activation of mitochondria-dependent apoptotic pathway is important in the early stages of anesthesia-induced developmental neuroapoptosis. To investigate potential means of protecting against this type of damage, we studied melatonin, a sleep-promoting agent and antioxidant known to inhibit apoptotic-type neuronal damage by improving mitochondrial homeostasis and stabilizing the inner mitochondrial membrane. When 7-day-old rats (the peak of synaptogenesis) were exposed to a commonly used and highly pro-apoptotic anesthesia cocktail (midazolam, isoflurane, nitrous oxide) in combination with the escalating doses of melatonin (from 1 to 20 mg/kg, s.c.), the severity of anesthesia-induced damage was reduced in a dose-dependent manner in two most vulnerable brain regions--the cerebral cortex and anterior thalamus. Melatonin-induced neuroprotection was mediated, at least in part, via the inhibition of mitochondria-dependent apoptotic pathway since melatonin caused an up-regulation of the anti-apoptotic protein, bcl-X(L), reduction in anesthesia-induced cytochrome c release into the cytoplasm and a decrease in anesthesia-induced activation of caspase-3, an important step in the activation of DNAses and the formation of the apoptotic bodies.