Cases reported "Alcoholic Intoxication"

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1/10. Intoxication by cholinesterase inhibitors versus opioid intoxication.

    A 47 y-old male shopkeeper from a rural area ingested an unknown substance while under the effects of ethylic alcohol. He was admitted at the University Hospital of the Andes in generally poor condition with a cholinergic syndrome. An erroneous diagnosis of acute pulmonary edema and opioid intoxication was reached. The value of a patient's history (background) and careful evaluation of the physical examination findings without underestimating critical clinical signs are very important when handling a clinical intoxication.
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2/10. Homicidal cerebral artery aneurysm rupture.

    When a normally natural mechanism of death is induced by physical injury or intense emotional stress, it is appropriate to rule the manner of death as something other than natural. When the case-specific circumstances are such that the death occurs as a result of the criminal activity of another person, it is acceptable to rule such deaths as homicides. Presented herein is a case of homicidal cerebral artery aneurysm rupture occuring in an intoxicated, 46-year-old man who was punched in the face by another individual. The details of the case are presented, followed by a discussion of the controversies that exist when dealing with such cases. Guidelines for investigating similar deaths are presented, with emphasis on the timing of the trauma in relation to onset of symptoms due to aneurysm rupture.
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ranking = 0.21729447038186
keywords = physical
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3/10. Death due to positional asphyxia under severe alcoholisation: pathophysiologic and forensic considerations.

    In contrary to "physical restraint", describing a fixed body position due to external devices, "positional restraint" is defined as an abnormal body position, resulting from accidental fixation under unfortunate circumstances. We report on a remarkable case of positional asphyxia of an alcoholised young man after a fall down a staircase. On external examination, the body showed petechiae of the conjunctivae and oral mucosa, abrasions on the left zygomatic region and scratch marks, respectively. Neither broken fingernails, etc. nor signs of external violence against the neck were found. autopsy revealed haemorrhages in the praevertebral cervical musculature and Simon's sign. Haemorrhagic pulmonary edema and cerebral edema were observed; blood alcohol concentration: 2.60 g/l, urine alcohol concentration: 3.26 g/l. As cause of death, positional asphyxia after blunt head trauma has to be considered as well as lethal ethanol intoxication. To us, alcoholisation attributed to the fall and together with unconsciousness following blunt head trauma circumvented self-rescue efforts, and therefore, aggravated the potentially lethal impact of positional restraint.
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keywords = physical
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4/10. delirium and lactic acidosis caused by ethanol and niacin coingestion.

    A 44-year-old male presented to the emergency department with altered mental status. He was receiving niacin therapy for hypercholesterolemia, and 16 hours earlier had ingested a large quantity of wine. Past medical history was otherwise unremarkable; physical examination revealed paranoid ideation and asterixis. Laboratory evaluation was significant for metabolic acidosis with a calculated anion gap of 39. liver enzymes were elevated, and lactic acid level was 9.5 mmol/L (normal: 0.5 to 2.2 mmol/L). White blood cell count was 23,100, but all cultures were negative, and all other diagnostic studies, including bilirubin, prothrombin time, and ammonia were normal. The patient recovered rapidly with hydration and administration of thiamine and magnesium. After psychiatric evaluation, a diagnosis of toxic delirium due to niacin and ethanol coingestion was made. This is the first case reporting toxic delirium and lactic acidosis due to niacin and ethanol coingestion. This occurred in the absence of significant hepatic impairment. Possible mechanisms for the observed derangements are discussed.
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5/10. Substance abuse: clinical identification and management.

    Substance abuse is a significant health problem in the adolescent population. Prevention is a formidable challenge, but attempts at discouraging experimentation in early adolescence and the promotion of healthy adult role models may be effective strategies. Questions that may elicit a history suggestive of abuse should be a routine part of the adolescent medical history. Pediatricians should be familiar with the important clinical findings resulting from intoxication with the various substances of abuse and should be able to recognize the "telltale" signs of abuse. Effective management is based on attention to the basics of life support, careful attention to the physical findings, and judicious use of specific therapeutic agents. Above all, a compassionate attitude should prevail if acute-phase recovery and long-term rehabilitation are to be successful.
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keywords = physical
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6/10. The effects of acute alcohol intoxication on biophysical activities: a case report.

    A computer-assisted biophysical assessment was performed in a woman with chronic alcoholism at 37 weeks' gestation. She was first seen in a state of acute alcohol intoxication (322 mg/dl). Although fetal breathing movement incidence was normal (30%), fetal tachypnea (67 breaths per minute) and decreased fetal body movements (0.11%) were seen. Because these findings differ from those previously reported with regard to normal pregnancies exposed to lower levels of alcohol, their implications are discussed.
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ranking = 1.0864723519093
keywords = physical
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7/10. Acute alcohol intoxication in a two-month-old baby.

    A 2-month-old, well developed, healthy boy, weighing 5.55 kg, was fed 200 ml of bottle-milk containing 65 ml of sake. So-called kanzamashi (sake boiled in the evening and remaining in a bottle overnight,) was mistaken for yuzamashi (water boiled and left to cool), and used to prepare a 15% formula milk. About 10 minutes later, the baby became flushed, began to breath hard, and lose consciousness, and an alcoholic odor was noticed. He was brought to our clinic, where gastric lavage and parenteral fluid therapy were started. On admission, his main physical signs were, whole body had become red, unconsciousness, alcoholic odor, tachycardia and tachypnea, without low body temperature, while his remarked laboratory findings were metabolic acidosis, hyperglycemia, and high A/G ratio. Moreover, a transient proteinuria, alternately followed by a transient glycosuria, appeared within the course. About 10 hours later, he showed an obvious improvement in both physical and laboratory findings. As an explanation of these changes in his condition due to alcohol ingestion, we speculated that a metabolic acidosis with hyperglycemia caused the disturbed reabsorption in his renal tubulus, which revealed alternating proteinuria and glycosuria.
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ranking = 0.43458894076371
keywords = physical
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8/10. An unusual autoerotic death: asphyxia with an abdominal ligature.

    A case of accidental death resulting from an autoerotic episode involving a high abdominal ligature is reported. Pathologic findings, physical evidence, and the psychological investigation are discussed.
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keywords = physical
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9/10. Anesthetic management of the alcoholic patient.

    This article encompasses a brief background on the physical effects of alcohol-both in acute intoxication and in the chronic alcoholic. Also covered is an explanation of the process of intoxication, blood alcohol concentration and its pertinence in the anesthetic management of the acutely intoxicated. The author includes a section on the anesthetic management of both the chronic alcoholic and the patient who is acutely intoxicated.
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keywords = physical
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10/10. Decerebrate posturing in alcoholic coma.

    Two cases of alcoholic coma are presented where extensor responses to noxious stimuli are demonstrated. Decerebrate posturing normally indicates severe structural or functional depression of midbrain function but can be caused by depressant drugs. Blood alcohol measurements are a vital test in the comatose patient as the clinical picture may be caused, or temporarily significantly worsened, by severe alcohol intoxication. The preservation of pupillary light reflexes in the presence of deep coma with decerebrate posturing should alert the clinician to a possible metabolic cause for the coma, including alcohol. Nevertheless, a diagnosis of alcoholic coma should not be made unless the blood alcohol concentration is grossly elevated and other causes of coma have been excluded by careful physical examination, blood glucose and electrolyte measurement, skull radiography and, in the absence of a rapid improvement, computerized tomography.
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