Objective: To use weather data to predict the daily number of ambulance transports required for heat stroke cases.
Methods: We analyzed weather data and the number of ambulance transports for heat stroke cases in Tokyo, Kanagawa, and Osaka between July 1 and September 30, 2013. Weather data included daily temperature (average, maximum, and minimum), humidity, hours of daylight, wind velocity, and precipitation. The correlation between each parameter and the number of ambulance transports was analyzed, and we developed a prediction formula using these data.
Results: The daily average and maximum temperatures were strongly correlated with the number of transports for heat stroke (both, r = 0.73). Therefore, we created a formula using the daily average temperatures in Tokyo, and verified this formula in Tokyo, Osaka, and Kanagawa:
y_i ~ f (T_av,i) ≡ a exp (b T_av,i) + c = 0.3800 exp (0.00007 T_av,i)
This formula provided accurate predictions for August and September, although it underestimated the number of transports that occurred in July. Therefore, we created an adjusted formula that provided accurate predictions for July:
y_i ~ f (T_av,i) + Δf (x_i) ≡ (a exp (b T_av,i) + c) + (α T_*,i + β)
={0.3800 exp (0.00007 T_av,i) + 1.209 T_high,i − 33.47 (T_high)
={0.3800 exp (0.00007 T_av,i) + 1.416 T_low,i − 28.59 (T_low)
Conclusion: Accurately predicting the number of ambulance transports for heat stroke can facilitate better allocation of ambulance resources. Our revised formula provided accurate predictions in all 3 months and regions that we examined.

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Delayed diagnosis of traumatic duodenal injury raises the mortality rate and surgical treatment is usually performed. Here we report a case of duodenal injury that led to the diagnosis about three weeks after injury, and minimally invasive treatment, Histoacryl^® injection therapy, rather than surgical intervention was successful. A 56-year-old woman was injured while driving her car. After recognizing hemoperitoneum, free air, and liver injury etc. on computed tomography (CT), we performed an emergency laparotomy. The postoperative course was uneventful. But on the 23rd day, we recognized an increase of the inflammatory response.It showed a right retroperitoneal abscess due to duodenal injury on the CT and an opening of the fistula at the duodenum 3rd portion by duodenoscopy. We injected the Histoacryl^® into the fistula from the abscess cavity and into the inside of the duodenum. Then, closure of the fistula in the duodenoscopy was seen. She was discharged without any problems. In conclusion , the Histoacryl^® injection therapy is limited, but an easy and minimally invasive method. It can be considered as one of the treatments for duodenal injury.

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Abstract Hypertriglyceridemia (HTG) is one of the major causes of acute pancreatitis. When HTG is recognized, it thought that immediately lowering the triglyceride (TG) levels in the blood during treatment can improve the symptoms of pancreatitis. In this study, we experienced a case of severe acute pancreatitis accompanying HTG. A 30-year-old male presented with abdominal pain. The TG level at admission was 2,150mg/dL, and abdominal dynamic CT revealed severe acute pancreatitis. Fluid replacement/continuous regional arterial infusion (CRAI) was administered to treat the pancreatitis in addition to LDL (low-density lipoprotein) apheresis for the HTG. After the first cycle of LDL apheresis, the TG level declined to 974mg/dL; however, the patient's abdominal pain did not improve. Six hours later, we performed the second cycle of LDL apheresis, and the TG level subsequently declined to 317mg/dL, with improvements in abdominal symptoms. CRAI was terminated on the fourth hospital day, and the patient was discharged on the 16th hospital day. Acute pancreatitis accompanying HTG is thought to be caused by lipids interfering with pancreas microcirculation. As a result, CRAI may not show a sufficient effect under conditions of HTG. LDL apheresis may be safely carried out without any major side effects and with an immediate decline in TG. We therefore consider that LDL apheresis, used in combination with CRAI, may improve the symptoms of severe acute pancreatitis accompanying HTG.

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To diagnose traumatic urinary extravasation, reexamination within 48 hours after initial excretory-phase computed tomography (CT) is recommended. We report a case of delayed traumatic urinary extravasation that was not detected on CT twice within 48 hours after injury. The patient was a 42-year-old female with blunt right renal injury. Initial CT showed a complex deep injury of the right lower kidney, no urinary extravasation, partial residual contrast medium in the injured renal parenchyma, and arterial extravasation that was not depicted on angiography. On the next day, excretory-phase CT images showed no urinary extravasation and partial residual contrast medium, and truncation of the right lower calyces was detected on maximum intensity projection (MIP) images. On the 8th day after injury, excretory-phase CT images depicted urinary extravasation at the right lower kidney and disappearance of partial residual contrast medium. On MIP images, urinary extravasation was detected at the right lower calyces. Urinary extravasation spontaneously disappeared on the 21st day after injury. In this patient, obstruction of injured calyces was regarded as the cause of delayed excretion of contrast medium in the injured renal parenchyma and delayed urinary extravasation. MIP images were useful to detect calyceal obstruction and to diagnose delayed urinary extravasation.

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Kounis syndrome (KS) occurs when acute coronary syndrome (ACS) is triggered by conditions associated with mast cell activation, such as allergic, hypersensitive, anaphylactic, or anaphylactoid insults. This case report shows KS after administration of gabexate mesilate (GM). A 72 y/o woman with a past medical history of chronic alcoholic pancreatitis presented with epigastric pain and was diagnosed with acute on chronic pancreatitis. After plain abdominal computed tomography, ulinastatin and intravenous GM were administered. Eight minutes later, however, she acutely developed shortness of breath, wheezing, facial flushing, and decreased level of consciousness. She went into shock, and electrocardiogram showed significant ST elevation in the inferior leads. Given her anaphylactic shock, two doses of intravenous epinephrine 0.1mg were given. Sublingual nitroglycerin was also administered given the left ventricular systolic motion abnormality on echocardiogram. Coronary angiography, however, showed no significant stenosis, thereby leading to a diagnosis of vasospastic angina. The patient eventually recovered and was discharged after two weeks. In patients such as the above, ACS is induced when chemical mediators are released from mast cells during allergic reactions. During treatment of patients with allergic reactions, therefore, the concurrence of ACS should be considered.

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A 70-year-old man was transported to our emergency department by ambulance after complaining of sudden chest and back pain. On arrival, his level of consciousness was 300 by the Japan Coma Scale, pulse rate 49 beats/min, and blood pressure 96/80 mmHg. We suspected cardiac tamponade due to acute type A aortic dissection (AADA), because emergency echocardiography revealed pericardial effusion. After endotracheal intubation, cardiopulmonary arrest occurred. Two minutes after cardiopulmonary resuscitation, spontaneous circulation was restored. Pericardiocentesis was performed, because he became hemodynamically unstable. After the aspiration of about 10 mL of blood, his blood pressure rapidly increased and circulatory dynamics then stabilized. Based on the results of CT, a diagnosis of AADA was established. The patient underwent emergency surgery (partial replacement of the ascending aortic arch). On hospital day 22, he left the ICU. However he experienced aspiration pneumonia and died on hospital day 177. Pericardiocentesis for cardiac tamponade complicating AADA should be considered when circulation cannot be maintained while waiting for surgery. At the time of pericardiocentesis, it is important to prevent an excessive increase in blood pressure with a minimum amount of drainage.

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Patient management after fires in confined spaces is often complicated by carbon monoxide (CO) poisoning and burn injuries. Furthermore, some patients develop cyanide poisoning due to hydrogen cyanide inhalation. In this study, we report a patient with cyanide and CO poisoning in whom we could measure the blood cyanide concentration. An 18-year-old man was admitted to our hospital after being recovered by a fire fighter following a fire at a bar. On admission, his Glasgow Coma Scale score was 3, and he had burns to 12% of his body surface area, including his face and hands. His blood lactate and carboxyhemoglobin levels were 13.5 mmol/L and 33.8%, respectively. Blood cyanide concentration 1 hour after admission was 4.3 µg/mL. Hydroxocobalamin as an antidote to cyanide poisoning was not administered to the patient because the drug was not prepared in our hospital. Computed tomography of the head performed 3 days after admission revealed severe brain edema and loss of the border between the cerebral cortex and the medulla. He died 6 days after his presentation, and the cause of death seemed to be hypoxic encephalopathy. Thus, hydroxocobalamin should always be available in patients who have been injured during fires in confined spaces.

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