• Herbal Formula Science
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• v.11 no.1
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• pp.57-90
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• 2003

The result of Bibliographic studies on the pathological mechanism of the sudden coma, we got the conclusion like this. 1. The sudden coma is an acute syndrome that refers to be a sudden fainting, an unconsciousness, an aphasia or a cold clammy limb, and immediately awakes or dies, and awakes in a short time, and if we awake, it doesn't leave over and above a sequela. 2. The clinical presentation of the sudden coma can be summarized as follows : The 1st is a disease raising the sudden death due to unconsciousness accompanied by wry mouth & sudden syncope with coma. The 2nd is simply the state of cold limbs. The 3rd is the meaning of the physique and symptomes of the six meridians. The last is the ancient method of expression in contrast of the beriberi. 3. The pathological mechanism of the sudden coma consists of the toxoid from outside, Qi and Xie, fatigue, damp phegm, the damage from seven emotions and the damage from five mental elements, especially the mental disorder due to the angry energy, causes the problems when the fleming-up of liver fire and the depressed of liver qi raise the physiological disorder. 4. Therapeutic methods of sudden coma are soothing the liver and remove stasis, soothing depression and circulating of the qi, calming the liver and suppressing yang. When that is early stage, at first, we must checking upward adverse flow of the qi after promoting the circulation of qi and awakening, and then, we must regulate excessive deficiency of yin yang by therapy that is based on differentiated in symptoms according to heat & cold, deficiency & excess, and use invigorating herb medicine for supporting vigour.

• Korean Journal of Veterinary Service
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• v.44 no.2
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• pp.113-117
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• 2021

Cocklebur poisoning in livestock can cause sudden death, with clinical signs include depression, inappetite, blindness, reluctance to move, hypersensitivity, ataxia and coma. The cause of cocklebur poisoning is ingestion of cocklebur sprout or seed, which contains carboxyatractyloside. In December 2020, a 47 month-old Hanwoo suddenly developed ataxia, and died after several hours. Hay mixed cocklebur seeds was fed to Hanwoo for 4 days before the symptoms. At autopsy, petechia and ecchymosis were seen on serous membrane of rumen and intestines. Peritoneal cavities contained a yellowish fluid and, hypoglycemia (Glu <20 mg/dL) was measured in blood test result. Microscopic lesions were karyolysis of centriloular hepatocyte and hemorrhage. Based on autopsy, blood and histopathological test, we diagnosed this case as cocklebur poisoning in Hanwoo.

• Korean Journal of Veterinary Research
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• v.33 no.1
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• pp.125-129
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• 1993

An acute fatal infectious disease in rabbits has been outbroken in Korea since 1985. This disease has been characterized as an acute hepatitis caused by viruses. However, viral pathogenesis in rabbit viral hepatitis leading to sudden death remain unclear. This report dealt with the electron microscopic findings on the spleen of experimentally infected rabbits, because spleen is one of the affected organs which have high titer of virus by a haemagglutination test. A typical crystalline array of virus was not found in the splenic cells of infected rabbits with acute hepatitis. Virus-like particles were seen within the phagosome of macrophages of the spleen. Ultrastructural changes in the spleen were severe with the lapse of time after inoculation. From these results, virus-like particles in the spleen were supposed to be phagocytosed by macrophage during viremia, while active replication of virus occurred in the liver. It was concluded that sudden death in this viral disease was caused by hepatic coma and/or circulatory disturbance.

• Journal of Korean Neurosurgical Society
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• v.65 no.5
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• pp.652-664
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• 2022

The Kernohan-Woltman notch phenomenon (KWNP) refers to an intracranial lesion causing massive side-to-side mass effect which leads to compression of the contralateral cerebral peduncle against the free edge of the cerebellar tentorium. Diagnosis is based on "paradoxical" motor deficit ipsilateral to the lesion associated with radiologic evidence of damage to the contralateral cerebral peduncle. To date, there is scarce evidence regarding KWNP associated neuroimaging patterns and motor function prognostic factors. A systematic review was conducted on Medline database from inception to July 2021 looking for English-language articles concerning KWNP, in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. The research yielded 45 articles for a total of 51 patients. The mean age was 40.7 years-old and the male/female sex ratio was 2/1. 63% of the patients (32/51) suffered from head trauma with a majority of acute subdural hematomas (57%, 29/51). 57% (29/51) of the patients were in the coma upon admission and 47% (24/51) presented pupil anomalies. KWNP presented the neuroimaging features of compression ischemic stroke located in the contralateral cerebral peduncle, with edema in the surrounding structures and sometimes compression stroke of the cerebral arteries passing nearby. 45% of the patients (23/51) presented a good motor functional outcome; nevertheless, no predisposing factor was identified. A Glasgow coma scale (GCS) of more than 3 showed a trend (p=0.1065) toward a better motor functional outcome. The KWNP is a regional compression syndrome oftentimes caused by sudden and massive uncal herniation and leading to contralateral cerebral peduncle ischemia. Even though patients suffering from KWNP usually present a good overall recovery, patients with a GCS of 3 may present a worse motor functional outcome. In order to better understand this syndrome, future studies will have to focus on more personalized criteria such as individual variation of tentorial notch width.

• Journal of The Korean Society of Clinical Toxicology
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• v.7 no.1
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• pp.26-31
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• 2009

Hydrogen sulfide is a by-product of decayed organic material and is ubiquitously found as an ingredient of manufacturing reagents or as an undesirable by-product of the manufacturing or industrial processing. Hydrogen sulfide is a chemical asphyxiant and interferes with cytochrome oxidase and aerobic metabolism. It has thus been deemed an important cause of work-related sudden death. This gas is particularly insidious due to the unpredictability of its presence and concentration and its neurotoxicity at relatively low concentrations, causing olfactory nerve paralysis and loss of the warning odor. Here, we report two cases of comatose patients presenting after accidental exposure to hydrogen sulfide gas.

• Journal of The Korean Society of Clinical Toxicology
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• v.13 no.1
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• pp.36-39
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• 2015

Copper sulfate is a copper compound used widely in the chemical and agriculture industries. Most intoxication occurs in developing countries of Southeast Asia particularly India, but rarely occurs in Western countries. The early symptoms of intoxication are nausea, vomiting, diarrhea, and abdominal cramps, and the most distinguishable clue is bluish vomiting. The clinical signs of copper sulfate intoxication can vary according to the amount ingested. A 75-year old man came to our emergency room because he had taken approximately 250 ml copper sulfate per oral. His Glasgow Coma Scale (GCS) score was 14 and vital signs were blood pressure 173/111 mmHg, pulse rate 24 bpm, respiration rate 24 bpm, and body temperature $36.1^{\circ}$ .... Arterial blood gas analysis (ABGa) showed mild hypoxemia and just improved after 2 L/min oxygen supply via nasal cannula. Other laboratory tests and chest CT scan showed no clinical significance. Three hours later, the patient's mental status showed sudden deterioration (GCS 11), and ABGa showed hypercarbia. He was arrested and his spontaneous circulation returned after 8 minutes CPR. However, 22 minutes later, he was arrested again and returned after 3 minutes CPR. The family did not want additional resuscitation, so that he died 5 hours after ED visit. In my knowledge, early deaths are the consequence of shock, while late mortality is related to renal and hepatic failure. However, as this case shows, consideration of early definite airway preservation is reasonable in a case of supposed copper sulfate intoxication, because the patients can show rapid deterioration even when serious clinical manifestation are not presented initially.