Intravenous Immunoglobulin G Modulates the Expression of Sepsis-Induced Coagulopathy Factors and Increases Serum IgM Levels: A Prospective, Single-Center Intervention Study.

Sepsis and sepsis-related multiple organ failure are major causes of mortality in intensive care unit (ICU) settings. This study aimed to determine the effect of intravenous immunoglobulin G (IVIgG) on different types of immunoglobulin and anti-coagulant factor types in sepsis patients. A single-center observational study of patients with sepsis, severe sepsis, or septic shock was conducted from August 2008 to March 2013. Patients were divided into the IVIgG (immunoglobulin G [IgG] <870 mg/dL; lower normal range) and non-IVIgG (IgG ≥870 mg/dL) groups. The IVIgG group received IVIgG for three days, and other standard medications. Serial measurements were taken of serum IgG, immunoglobulin A (IgA), immunoglobulin M (IgM), total plasminogen activator inhibitor 1 (tPAI-1), and protein C. Patients in the IVIgG treatment group had significantly higher serum IgM level on Days 4 and 7 than on Day 1, but no significant changes in IgM levels were observed in patients in the non-IVIgG group. Patients in the IVIgG treatment had lower tPAI-1 levels on Days 4 and 7 than on Day 1 and increased protein C levels on Day 7 compared to those on Days 1 and 4. There were no significant differences in tPAI-1 levels or protein C levels in the non-IVIgG group, although a similar trend was observed. IVIgG administration increased patients' serum IgM and protein C levels and decreased their serum tPAI-1 levels. IVIgG has potential application for preventing sepsis-induced coagulopathy and disseminated intravascular coagulation.

Feasibility study of immediate pharyngeal cooling initiation in cardiac arrest patients after arrival at the emergency room.

AIM: Cooling the pharynx and upper oesophagus would be more advantageous for rapid induction of therapeutic hypothermia since the carotid arteries run in their vicinity. The aim of this study was to determine the effects of pharyngeal cooling on brain temperature and the safety and feasibility for patients under resuscitation. METHODS: Witnessed non-traumatic cardiac arrest patients (n=108) were randomized to receive standard care with (n=53) or without pharyngeal cooling (n=55). In the emergency room, pharyngeal cooling was initiated before or shortly after return of spontaneous circulation by perfusing physiological saline (5 °C) into a pharyngeal cuff for 120 min. RESULTS: There was a significant decrease in tympanic temperature at 40 min after arrival (P=0.02) with a maximum difference between the groups at 120 min (32.9 ± 1.2°C, pharyngeal cooling group vs. 34.1 ± 1.3°C, control group; P<0.001). The return of spontaneous circulation (70% vs. 65%, P=0.63) and rearrest (38% vs. 47%, P=0.45) rates were not significantly different based on the initiation of pharyngeal cooling. No post-treatment mechanical or cold-related injury was observed on the pharyngeal epithelium by macroscopic observation. The thrombocytopaenia incidence was lower in the pharyngeal cooling group (P=0.001) during the 3-day period after arrival. The cumulative survival rate at 1 month was not significantly different between the two groups. CONCLUSIONS: Initiation of pharyngeal cooling before or immediately after the return of spontaneous circulation is safe and feasible. Pharyngeal cooling can rapidly decrease tympanic temperature without adverse effects on circulation or the pharyngeal epithelium.

Actual situation regarding cardiac etiology determined by clinical diagnosis of and medical examiner's postmortem findings on witnessed out-of-hospital cardiac arrest cases.

AIM: To examine indicators that may assist in the diagnosis of cardiac etiology using simple tests in witnessed cardiac etiology out-of-hospital cardiac arrest cases, which is emphasized in the Utstein Style. METHOD: The subjects were 165 witnessed cardiac etiology out-of-hospital cardiac arrest cases, which were transported to Kobe University Hospital during the five-year period between January 1, 2005 and December 31, 2009. A comparative study was conducted into whether there were any significant differences in the initial electrocardiogram (ECG) and the various early diagnostic markers of acute myocardial infarction between the group who were finally diagnosed as being of cardiac etiology and the group who were finally diagnosed as being of non-cardiac etiology. RESULTS: Of the 165 witnessed cardiac etiological cases, 69 cases were finally re-classified as non-cardiac etiological cases on the basis of scrutiny after admission or postmortem findings by the Medical Examiner. Ventricular fibrillation shown in the initial ECG and Qualitative cardiac troponin T test positive were significantly higher in the final diagnosis cardiac group than in the final diagnosis non-cardiac group. Ventricular fibrillation and troponin T positive can be seen as significant indicators in determining whether a case was cardiac or non-cardiac, and the model χ2 test result of p < 0.01 in the multiple logistic regression analysis was significant, and the determining predictive value was 65.4%. CONCLUSION: The indicators which should be noted in simple tests to improve the precision of discrimination of cardiac etiology in out-of-hospital cardiac arrests are ventricular fibrillation in the initial ECG and the qualitative test of cardiac troponin T.

[Case of chemical burns caused by hexavalent chromium].

A 25-year-old man fell with his right lower limb into a pool of 40% hexavalent chromium at room temperature. At first, he showed no symptoms, but one hour later he felt itching along his right leg and went to a nearby hospital, where his left leg was washed with water. He was then referred to our hospital for further treatment. On the first day of hospitalization, only brownish areas of discoloration were noted around the inside of the right thigh and lower leg. In spite of our systemic treatment with N-acetylcystein and dimercaprol and local treatment with 10% ascorbic acid, the patient developed deep dermal chemical burns and those area increased from 1% to 5% . On the 12th day of hospitalization, skin transplantation was performed and the postoperative course was satisfactory. Even though injury to the skin caused by hexavalent chromium may seem minor at first, medical staff should be watchful with regard to such chemical burns since they can take a sudden turn for the worse.

[Can magnetic resonance imaging of the brain in the acute phase of carbon monoxide intoxication forecast delayed encephalopathy?].

We examined the usefulness of Magnetic Resonance Imaging (MRI) test in the acute phase of carbon monoxide intoxication for forecasting delayed encephalopathy (DE). [Case 1] 26-year-old female. COHb 12%. Takotsubo (Ampulla) cardiomyopathy was supervened. Pallidal disorder was recognized in MRI test in the early stage. Although Prophylactic HBO was performed, DE began. 36 days later, disorder was recognized in large area, such as, in cerebral white matter and callosum, and abnormality was found in WMS-R and MMSE. Since HBO was performed, DE subsided. In MRI test, on the other hand, high signal range in cerebral white matter and callosum were gradually decreased and WMS-R and MMSE were improved. [Case 2] 19-year-old female. COHb 9.4%. The state was considered to be mild but pallidal disorder was found in MRI test at the beginning. DE did not start, then the part of pallidal disorder was narrowed. WMS-R and MMSE showed slightly low level. [Case 3] 19-year-old female. COHb 7.3%. The state was considered to be mild and there was no abnormal findings in MRI test in the early stage. DE did not start. [Case 4] 48-year-old male. COHb 48.9%. Rhabdomylosis was supervened, then ischemic change in a left radiate crown was recognized in the early MRI test. Since the third day, disorientation and restlessness had been developed, so that the patient was transferred to psychiatric department, though it was still difficult to distinguish the case from DE. Although the case is relatively mild, pallidal disorder is recognized in the early MRI test. Pallidal disorder alone can cause memory disorder and cognitive impairment. Even if pallidal disorder alone is recognized in the early MRI test, white matter disorder is developed with time, and then DE begins. If there are no typical carbon monoxide intoxication findings, some cases can be suspected as DE. It is useful to perform serial MRI test in order to prepare for delayed encephalopathy in carbon monoxide intoxication.

Assessment of medical response capacity in the time of disaster: the estimated formula of Hospital Treatment Capacity (HTC), the maximum receivable number of patients in hospital.

INTRODUCTION For the assessment on medical response capacity for disaster in local area (such as rescue capacity, transport capacity and treatment capacity), it is necessary to assess it in peace time, and understand how many sufferers from disaster the hospital can respond to. Here the estimated formula of Hospital Treatment Capacity (hereinafter shortened to HTC), the maximum receivable number of patients in hospital (hereinafter shortened to MRN) was showed, which derived from the assessment on emergency medical response in Kobe University Hospital as an example. MATERIALS AND METHODS We treated a total of 12,032 patients transferred and admitted to Kobe University Hospital from April 2003 to January 2005. We calculated the required number of medical personnel, equipment and length of treatment time in order to respond to 410 severe traumas, 35 burn injuries, and 28 patients with blood purification, which were considered to be main clinical conditions in disaster. Beside, the occupation of emergency room and the operation room per hour were also investigated in our hospital. RESULTS HTC (MRN) for each clinical condition within H hours is expressed by following formula: (1) HTC (MRN) for burn injuries = The maximum integer of (< or =Doctors/2 intersection< or =Respirators/1 intersection< or =outpatient beds/1 intersection or =H/1.85) (2) HTC (MRN) for patients with blood purification = The maximum integer of (< or =doctors/2 intersection< or = blood purification systems/1 intersection< or = outpatient beds/1 intersection < or =inpatient beds/1 intersection< or =monitors/1) x the minimum integer of (> or =H/2.00) (3) HTC (MRN) for severe traumas =The maximum integer of (< or =doctors-a/2 intersection< or =surgeons/1 intersection< or =anesthetists/1 intersection< or =radiologists/1 intersection< or =respirators/1 intersection < or =outpatient beds/1 intersection< or =inpatient beds/1 intersection< or =monitors/1 intersection< or =operation rooms/1 intersection < or =angiography rooms/1) x the minimum integer of (> or =H/2.82+b) CONCLUSION The treatment capacity within local area is able to be assessed by adopting the estimated formula of HTC (MRN).

[A case of fatal chloropicrine poisoning induced by ingestion].

A case of fatal chloropicrine poisoning induced by suicidal ingestion was reported. The patient was found unconsciousness in his room with drinking about 100 ml of chloropicrine sodium at 8:55 in the morning and brought to a nearby hospital. He was transported to our ER at 10:17. 7 hours after ingestion, he died from metabolic acidosis and acute cardiac failure. It was difficult to detect chloropicrine in his serum and gastric content with GC/MS method. At the present, we must be severe to store and use chloropicrine as there is no specific treatment of chloropicrine poisoning. It is necessary to protect from exposure to volatile agricultural chemicals such as chloropicrine for prevention of secondary disaster.