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 28,634 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Aggravating headache accompanied by nausea and epigastric discomfort suggesting a warning leak in a 39-year-old woman with a giant thrombosed intracranial aneurysm prompted us to undertake coiling of the aneurysm. After uneventful coil embolization of the aneurysm, collapse of the lung related to bronchospam developed, and was found to have a gastrointestinal pathology which had gone undetected before the procedure. Despite its rarity, gastrointestinal pathology mimicking warning leak should have been considered in a patient with a warning leak sign.
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PMID:Can a warning leak in a patient with unruptured aneurysm mask an underlying gastrointestinal pathology? A case report. 2425 18

Yellow phosphorus is a toxic substance used in the production of firework cracker, fireworks, ammunition and agricultural dung. When ingested, it shows its effects mainly in the liver, the kidneys, and the brain. A four-year-old girl had died as a result of acute hepatic failure caused by ingesting a firework cracker. The case showed high levels of hepatic enzymes, along with non-specific signs such as nausea, vomiting and diarrhea. Autopsy revealed diffuse microvesicular steatosis in the liver and disseminated degeneration in the proximal tubules of the kidneys. In cases with concomitant hepatorenal failure and cardiovascular collapse, death is inevitable. However, when only hepatic failure develops, hepatic transplantation may be lifesaving. Although intoxication from ingesting yellow phosphorus has a very high rate of mortality, forensic cases are extremely rare in the literature.
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PMID:Clinical and Pathological Findings on Intoxication by Yellow Phosphorus After Ingesting Firework Cracker: A Rare Case of Autopsy. 2427 31

Acute carbon monoxide (CO) poisoning is the most common cause of poisoning and poisoning-related death in the United States. It manifests as broad spectrum of symptoms ranging from mild headache, nausea, and fatigue to dizziness, syncope, coma, seizures resulting in cardiovascular collapse, respiratory failure, and death. Cardiovascular complications of CO poisoning has been well reported and include myocardial stunning, left ventricular dysfunction, pulmonary edema, and arrhythmias. Acute myocardial ischemia has also been reported from increased thrombogenicity due to CO poisoning. Myocardial toxicity from CO exposure is associated with increased short-term and long-term mortality. Carboxyhemoglobin (COHb) levels do not correlate well with the clinical severity of CO poisoning. Supplemental oxygen remains the cornerstone of therapy for CO poisoning. Hyperbaric oxygen therapy increases CO elimination and has been used with wide variability in patients with evidence of neurological and myocardial injury from CO poisoning, but its benefit in limiting or reversing cardiac injury is unknown. We present a comprehensive review of literature on cardiovascular manifestations of CO poisoning and propose a diagnostic algorithm for managing patients with CO poisoning.
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PMID:Cardiovascular Abnormalities in Carbon Monoxide Poisoning. 2451 73

Disulfiram treatment for alcohol dependence is used with acceptable outcomes. By inhibiting the aldehyde dehydrogenase enzyme, this treatment increases acetaldehyde concentration after the ingestion of alcohol causing an unpleasant disulfiram-alcohol reaction. Typical symptoms include flushing, headache, nausea, vomiting, sweating, vertigo, and lightheadedness. However, there have also been descriptions of more serious reactions including severe hypotension, arrhythmias, myocardial infarction, and cardiovascular collapse. We report a patient with a severe disulfiram-alcohol reaction marked by flushing, confusion, generalized malaise, epigastric pain, and hypotension. Cardiac biomarker and electrocardiographic changes were suggestive of non-ST-elevation myocardial infarction (NSTEMI). Left heart catheterization showed no angiographic evidence of coronary artery disease. Because of the frequency of alcohol dependence and its treatment with disulfiram, it is critical for physicians to be aware of these types of life-threatening complications.
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PMID:Disulfiram--alcohol reaction mimicking an acute coronary syndrome. 2474 56

Since the late 70s of the last century there were more than 700 incidents related to the use of the ricin toxin. For this reason, CDC (Center of Disease Control and Prevention) recognized toxin as a biological weapon category B. The lethal dose of ricin toxin after parenteral administration is 0.0001 mg/kg and after oral administration 0.2 mg. The first symptoms of poisoning occur within a few hours after application of toxin as a nausea, vomiting and abdominal pain. In the final stage there are observed: cardiac arrhythmia, collapse and symptoms suggestive of involvement of the central nervous system. Stage immediately preceding death is a state of coma. The ricin toxin is still the substance against which action has no optimal antidote. Developed a vaccine called RiVax is waiting for its registration. It should be pointed out that the availability of a ricin toxin makes it possible to use it for real bioterrorists.
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PMID:[Today's threat of ricin toxin]. 2644 79

Anaphylaxis is an acute, potentially lethal, multisystem syndrome resulting from the sudden release of mast-cell- and basophile-derived mediators into the circulation. Common manifestations of anaphylactic reactions include urticaria, angioedema, nausea, vomiting, hypotension and cardiovascular collapse. Cardiovascular collapse is the first detected manifestation in up to 50% of cases in perioperative anaphylaxis, because patients are anesthetized and unable to report symptoms. A 25-year-old male presented with severe hypotension and erythema after intravenous atropine administration during general anesthesia. Postoperative laboratory findings demonstrated elevated serum tryptase and total immunoglobulin E. An intradermal test showed atropine sensitivity. Although atropine is used widely as a perioperative anticholinergic agent, it is a potential risk factor for a severe anaphylactic reaction. Therefore, prompt recognition and adequate therapeutic measures are necessary to avoid fatal consequences.
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PMID:Anaphylaxis following atropine administration during general anesthesia: a case report. 2649 61

In brief: Athletes who compete in endurance sports may sustain exercise-associated collapse (EAC) during or after an event. A classification system was devised for EAC that can be used by physicians who cover endurance events. Symptoms and signs of EAC include exhaustion, nausea, cramps, abnormally high or low core body temperature, muscle spasms, and inability to walk unassisted. The three classes of EAC are hyperthermic, normothermic, and hypothermic; each class is subclassified as mild, moderate, or severe. Treatment of warm runners includes applying ice bags wrapped with wet towels to the major areas of heat loss (neck, axilla, groin) to lower the core body temperature. Treatment of cool runners involves removing wet clothing, drying the skin, and insulating with wool blankets.
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PMID:Exercise-Associated Collapse in Endurance Events: A Classification System. 2744 66

Cannabinoids are the most commonly used illegal substances in the world [1]. Synthetic Cannabinoids (SCB) are also known as "Spice", "K2", "Spike", "herbal incense", "Cloud 9", "Mojo" and many others are becoming a large public health concern due to their increasing use, unpredictable toxicity, and abuse potential [2]. The most common reported toxicities with SCB use based on studies using Texas Poison control record are tachycardia, agitation and irritability, drowsiness, hallucinations, delusions, hypertension, nausea, confusion, dizziness, vertigo, chest pain, acute kidney injury, seizures, heart attacks and both ischemic and hemorrhagic strokes [3]. The Emergency Department (ED) here at Lincoln Medical Center has certainly seen a sizeable volume of K2 abusers who present displaying a spectrum of symptoms as noted above. However, during a concentrated outbreak of K2 use in the summer of 2015, a large cohort of patients presented with a toxidrome not previously described in any published literature. This included marked bradycardia and hypotension while maintaining global neurologic function. Although these patients were drowsy and sleepy at presentation, tactile stimuli would arouse these patients to awaken and participate in an interview. The patients described in this case series, appeared to be on the brink of cardiovascular collapse. The vital signs however normalized with intravenous fluid (IVF) hydration only, over the course of 6 to 7h, allowing a safe discharge from the ED.
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PMID:Profound hypotension and bradycardia in the setting of synthetic cannabinoid intoxication - A case series. 2823 95

Spontaneous intracranial hypotension presents with many symptoms including orthostatic headache, dizziness, and nausea due to cerebrospinal-fluid (CSF) leakage from the spinal dural sac. Although CSF leakage can be estimated by radioisotope (RI) cisternography or computed tomography/magnetic resonance imaging myelography, it is not easy to detect the leakage point using these modalities. Here, we describe a patient with spontaneous intracranial hypotension in whom three-dimensional computed tomography (3D-CT) performed just after an epidural blood patch (EBP) containing contrast medium detected leakage point. The contrast medium injected into the epidural space at the L3/4 level migrated into the intradural space at the lower cervical spine level. RI cisternography performed before EBP did not show the CSF leakage point or any intracranial extension of the tracer. The rostral extension of the RI may be blocked by the collapse of the CSF space due to a large amount of CSF leakage, and due to the compression of the intradural CSF space by epidural CSF. 3D-CT epidurography may be useful to detect the fistula of a CSF leakage even in patients where other modalities including MRI, CT, or RI cisternography cannot specify the leakage point.
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PMID:3D-CT Epidurography Can Detect Cerebrospinal-Fluid Leakage in a Patient with Spontaneous Intracranial Hypotension: A Case Report. 2866 70

Ricin is a highly toxic agent derived from the castor bean plant (Ricinus communis). Poisoning occurs commonly by oral ingestion of the beans. Injection of ricin is believed to be more lethal. Ricin is a large glycosylated protein difficult to detect in clinical samples. Instead, ricinine, a small alkaloid found in the same beans, is used as surrogate marker for ricin exposure. We describe a simple LC-MS/MS method for the detection of ricinine in serum, blood and urine, validated according to EMA guidelines and successfully applied to patient samples of a suicidal death after injection of a castor bean extract. A 26-year-old man self-presented to the emergency department with severe abdominal cramps and nausea after injection of a castor bean extract. Due to rapid deterioration of his hemodynamic function despite early aggressive fluid resuscitation, he was transferred to ICU. Abdominal cramps worsened and a fulminant diarrhea developed, resulting in hypovolemic shock and cardiorespiratory collapse. Despite full supportive therapy, the patient died approximately 10 hours after injection due to multiple organ failure. Ricinine was quantified by LC-MS/MS after LLE with diethyl ether using ricinine-D3 as internal standard. Six hours after injection, ricinine concentrations in serum and blood were 16.5 and 12.9 ng/mL, respectively, which decreased to 12.4 and 10.6 ng/mL, 4 hours later. The urinary concentration was 81.1 ng/mL 7 hours after injection, which amply exceeded the levels previously reported in similar cases with lethal outcome. Concentrations of ricinine, compatible with a lethal exposure to castor beans, were detected in serum, blood and urine. Ricinine was also found in bile and liver tissue.
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PMID:Lethal Injection of a Castor Bean Extract: Ricinine Quantification as a Marker for Ricin Exposure Using a Validated LC-MS/MS Method. 3059 May 81


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