In addition to pathogen-associated molecular patterns (PAMPs) from invasive microorganisms, alarmins, which are major components of host defense mechanisms, are involved in the pathophysiology of sepsis. In fact, the magnitude of the insult is defined according to the damage-associated molecular pattern (DAMP), which is composed of alarmins as well as PAMPs, such as those involving the nucleosome, histones and DNA. Regarding the antimicrobial mechanism of neutrophils, an alternative non-phagocytic mechanism was first recognized as NETosis in 2004. In this mechanism, microorganisms are trapped and eliminated by neutrophil extracellular traps (NETs). NETs are composed of histones and DNA that have been expelled from the nucleus as well as antimicrobial proteases, including elastase and myeloperoxidase. NETosis, a cell-death pathway reported to be distinct from apoptosis, is an active area of recent research. Since NETs are composed of deleterious substances, they are extremely harmful to the host cells once they released into the circulating blood. Therefore, the meanings and putative roles of these components in sepsis has attracted much attention.

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We retrospectively reviewed the charts of 474 patients (627 visits) presenting with symptoms of hyperventilation syndrome at the emergency department of Kobe City Medical Center West Hospital between April 2004 and March 2010. The average age of the patients was 35 ± 16 years. The number of female patients (389 patients and 525 visits) was markedly higher than that of male patients (85 patients and 102 visits). Moreover, the number of visits in summer was higher than in winter, and the number of night visits was found to be higher. The patients often suffered from psychiatric disorders. F4 (neurotic, stress-related and somatoform disorders) in the International Classification of Disease 10 was confirmed in 104 patients (21.9%). Bronchial asthma was the most frequently observed physical complication and was confirmed in 64 patients (13.5%). In all, 348 patients required transportation by ambulance; these patients often developed psychiatric complications resulting in a longer stay at the emergency department. During the period of investigation, 15% of the patients revisited the emergency department for hyperventilation syndrome and developed psychiatric disorders more frequently than those who consulted the emergency department only once during this period. Furthermore, re-consultation for hyperventilation syndrome within a month was observed in 11.5% of the patients. For the purposes of treatment, paper bag rebreathing and sedative drugs were used in 19.5% and 51.4% of the patients, respectively. These patients required a significantly longer stay at the emergency department. Posthyperventilation apnea accompanied by significant decrease of SpO₂ levels was observed in 5.6% of the patients; however, only 7 patients (1.1%) were hospitalized. The prognosis of hyperventilation syndrome was very good. Nevertheless, other serious diseases presenting as hyperventilation should be carefully differentiated from hyperventilation syndrome, and hypoxemia caused by posthyperventilation apnea should also be considered when treating these patients.

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Background and Purpose: In recent years, malpractice litigations have steadily increased across all medical specialties. Claims arising from incidents in the emergency department are increasing as well, where a shortage of physicians is perceived as a high malpractice risk. An analysis of claims filed against emergency physicians has revealed certain disease process and case characteristics. In this study, we retrospectively analyzed the characteristics of medical malpractice claims stemming from emergency care.
Methods: This was a retrospective review of all Emergency Medicine malpractice claims filed between 1965 and 2011. The keywords used to search the databases of TKC Law Library and D1-Law.com were “medical lawsuit”, “medical malpractice”, “emergency outpatient department”, and “emergency medical center”. Results showed that emergency physicians were the primary defendants in 50 complaints made regarding emergency medical procedures. Variables such as diagnosis, claimant age, claimant sex, medical issue, clinical outcome, indemnity payment claimed by plaintiff, indemnity payment awarded to plaintiff, plaintiff’s claim, and legal outcome were analyzed.
Results: Characteristics of patients revealed that 80% (40/50) were men and 20% (10/50) were women whose average age was 46 (range, 8-84). Twelve percent of cases (6/50) involved adolescents under age 15. The disease processes associated with the highest number of claims included traumatic injury (11 deaths), ileus (6 deaths, 1 postsurgical sequela), acute epiglottitis (3 deaths, 3 severe brain dysfunction), subarachnoid hemorrhage (3 deaths, 1 severe brain dysfunction), acute myocardial infarction (3 deaths), and acute aortic dissection (3 deaths). Indemnity was paid in 76% of cases. Excluding the 12 dismissed cases, the average indemnity payment was 39.11 million yen, and over 100 million yen was settled in four cases.
Conclusion: Medical conditions associated with the highest number of malpractice claims are traumatic injury, subarachnoid hemorrhage, acute aortic dissection, epiglottitis and ileus. In any case, a misdiagnosis is all the biggest problem.

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Aconite is a well-known toxic plant that contains highly toxic aconitines that cause aconite poisoning. We report an investigation of the clinical features and management of aconite poisoning induced-arrhythmia in cases of aconite poisoning. The subjects were 30 patients with aconite poisoning who were admitted to the Critical Care and Emergency Center at Iwate Medical University between 1984 and 2011. Medical charts were reviewed to obtain information on the background characteristics of the patients, including the cause, occurrence time, symptoms and treatment of intoxication; the ingested plant parts; and the outcome. The subjects comprised 22 males and 8 females, and ranged in age from 5 to 78 years old (mean age, 48.3 years old). The causes of intoxication were ingestion of aconite for suicide and attempted suicide in 15 cases, mistaken ingestion of the plant instead of edible wild plants in 14 cases, and ingestion of the plant as a folk remedy in 1 case. The suicide attempts and suicide cases tended to involve ingestion of aconite roots and occurred in seasons throughout the year. The mistaken ingestion cases tended to involve ingestion of aconite leaves and mainly occurred between April and June, in the season for collecting edible wild plants. The symptoms of intoxication were circumoral paresthesia (23 cases), numbness of the extremities (23 cases), paralysis (5 cases), weakness (11 cases), dizziness (9 cases), consciousness disorder (13 cases), nausea/vomiting (24 cases), abdominal pain (4 cases), palpitation (19 cases), chest pain/chest discomfort (17 cases), hypotension (18 cases), and arrhythmias (26 cases). The arrhythmias varied in type, but were mostly premature ventricular contractions (17/26 cases, 65.4%). Of the 26 cases that developed arrhythmia, 7 had fatal arrhythmia such as ventricular fibrillation (VF). Antiarrhythmic agents such as lidocaine were administered in cases with tachyarrhythmia. These agents were ineffective for patients with VF, but effective for other patients. Percutaneous cardiopulmonary support (PCPS) was effective in VF patients with unstable hemodynamics due to arrhythmia refractory to treatment with antiarrhythmic agents and defibrillation. Overall, antiarrhythmic therapy seems to have little effect on aconite poisoning-induced VF, and an episode of severe arrhythmia influences the outcome. Therefore, a severe case with VF refractory to antiarrhythmic therapy requires aggressive treatment with PCPS for stabilization of hemodynamics. These results provide useful information for future treatment of aconite poisoning.

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There have been reports on patients with symptoms of crush syndrome and peripheral nerve paralysis caused by limb compression on prolonged immobilization, after administration of a psychotropic drug. However this rare case involved pulmonary embolism in addition to the clinical condition mentioned above. A 73-year-old man was receiving outpatient treatment for manic depression. A change in his medication resulted in heavy sedation, and he fell asleep for approximately 10 h in the cross-legged position. On waking, he was paralyzed in the right leg. After arrival at our hospital, a physical examination was performed, which indicated a swelling and tenderness from the right hip to the thigh, as well as sciatic nerve palsy. During the examination, the patient developed respiratory distress. Computed tomography revealed a swelling in the muscles from the right gluteus medius to the quadriceps and pulmonary embolism. Blood test results showed elevated levels of creatine phosphokinase. The patient was diagnosed with the crush syndrome and pulmonary embolism. The possibility of complication with pulmonary embolism merits careful attention in patients who present with disturbance of consciousness following drug administration, especially in those with crush syndrome caused by prolonged compression of the legs.

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Poisoning with potassium cyanide is usually fatal because of the inhibition of cytochrome oxidase in tissue. It is known that patients exposed to a large-dose die after several minutes. We report a survival case of acute potassium cyanide poisoning likely due to a delayed severe symptomatic episode. A male in his 30’s took three capsules containing potassium cyanide. After approximately 15 minutes from the time of ingestion, the subject exhibited dilated pupils and tachycardia. Upon admission (approximately 38 minutes after ingestion), the subject began to show signs of tachypnea. More severe symptoms, such as circulatory failure, cyanosis and severe metabolic acidosis, appeared approximately 86 minutes after ingestion. We administered antidotes and observed that, the severe metabolic acidosis and circulatory failure improved rapidly. The whole blood cyanide concentration peaked at 3.1 μg/ml, and then gradually decreased. The patient was discharged after 10 days without any sequelae. The delayed development of symptoms is likely due to the slow digestion of the capsules. Therefore, it is imperative to determine, not only the name and quantity of an ingested poison, but also the form in which the poison was ingested. This information can aid in the prediction of symptomatic episode development and treatment.

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We report a case of pharyngolaryngeal thermal burn requiring emergency airway management and whose esophageal thermal burn caused delayed cicatricial strictures. A 28 year old male visited our hospital complaining of odynophagia and progressive dyspnea after having a 200ml of hot coffee at the temperature of around 90°C at a drinking party. At the emergency department, he required emergency tracheostomy because of upper airway obstruction. Even after the tracheostomy, prolonged epiglottic edema caused frequent aspirations. On day 25 he abruptly vomited blood, then an endoscopic examination revealed multiple erosions and ulcers along the full length of the esophagus. A repeated endoscopy done on day 40 and the esophagogram on day 48 revealed wide range of strictures. He improved to take solid foods without difficulties, so that he was discharged on day 53. But since esophageal strictures gradually became advanced and the patient no longer responded to endoscopic ballon dilatation, esophagectomy and reconstruction were performed on day 264 in another hospital. Severe thermal injuries on ingestion require not only acute airway care and prevention of aspiration from pharyngolaryngeal injuries, but also a long-term management for esophageal strictures.

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