Paralytic shellfish poisoning

Long, Randall R.; Sargent, Jane; Hammer, Kathryne

doi:10.1212/wnl.40.8.1310

Cited by 53 publications

(15 citation statements)

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“…STX has been shown to block voltagedependent sodium channels in nerve and muscle [35] and therefore block the propagation of nerve and muscle action potentials. Electrophysiologic studies demonstrate prolonged distal latencies, diminished conduction velocities, and a reduction in sensory and motor amplitudes in patients poisoned by STX [36], which are similar to that seen with tetrodotoxin (TTX) [35].…”

Section: Paralytic Shellfish Poisoningmentioning

confidence: 72%

Marine neurotoxins: Ingestible toxins

Stommel

Watters²

2004

Curr Treat Options Neurol

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Section: Paralytic Shellfish Poisoningmentioning

confidence: 72%

Marine neurotoxins: Ingestible toxins

Stommel

Watters²

2004

Curr Treat Options Neurol

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“…Propranolol is unique because of its Naþ channel blocking activity in overdose that can result in a prolonged QRS interval (O0.10 seconds) [58,[61][62][63]. Propranolol overdose has been associated with a higher mortality rate compared with other BBs [66]. These same investigators also found that a QRS interval O0.10 seconds in these patients was predictive of propranololinduced seizures.…”

Section: Electrocardiographic Manifestationsmentioning

confidence: 94%

“…Acebutolol preferentially blocks b 1 receptors and possesses partial agonist activity and membrane stabilizing activity similar to propranolol. QRS interval widening on ECG and ventricular tachycardia have been reported in several cases [59,65,66].…”

Section: Electrocardiographic Manifestationsmentioning

confidence: 99%

ECG Manifestations: The Poisoned Patient

Holstege

Eldridge

Rowden

2006

Emergency Medicine Clinics of North America

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Emergency physicians routinely evaluate and manage poisoned patients. In 2003, more than 2 million human exposure cases were reported to poison centers throughout the United States [1]. Of those cases, 22% were treated in a health care facility with most of those cases evaluated in the emergency department. Cardiovascular drugs were listed as the fifteenth most frequently encountered human exposure (66,401) and the fifth leading cause of poisoning deaths.Drug-induced changes and abnormalities on the 12-lead electrocardiogram (ECG) are common. There are numerous drugs that can cause ECG changes and lead to cardiac dysrhythmias. The diagnoses and subsequent management of patients manifesting ECG changes following poisonings can challenge even the most experienced physician. Drugs that are advocated in Advanced Coronary Life Support protocols for cardiac dysrhythmias may not apply or may even worsen the condition of overdose patients [2].Despite that drugs have widely varying indications for therapeutic use, many unrelated drugs share a common cardiac pharmacologic effect if taken in overdose. The purpose of this article is to group together agents that cause similar electrocardiographic effects, review their pharmacologic actions, and discuss the electrocardiographic findings reported in the medical literature. The five main categories reviewed include potassium (Kþ) efflux blockers, sodium (Naþ) channel blockers, sodium-potassium adenosine-triphosphatase (Naþ/Kþ ATPase) blockers, calcium channel blockers (CCB), and beta-adrenergic blockers (BB). It is important to keep in mind, however, that many medications have actions that involve more than one of these

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“…If the amount of PST is high enough, the intoxication can result in death. (Long et al, 1990;Montebruno, 1993;García et al, 2004a). Paralytic shellfish poisoning has the highest mortality rate (13%) of all marine toxins (Lagos, 1998).…”

Section: Introductionmentioning

confidence: 99%

Human intoxication with paralytic shellfish toxins: Clinical parameters and toxin analysis in plasma and urine

et al. 2005

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This study reports the data recorded from four patients intoxicated with shellfish during the summer 2002, after consuming ribbed mussels (Aulacomya ater) with paralytic shellfish toxin contents of 8,066 ± 61.37 µg/ 100 gr of tissue. Data associated with clinical variables and paralytic shellfish toxins analysis in plasma and urine of the intoxicated patients are shown. For this purpose, the evolution of respiratory frequency, arterial blood pressure and heart rate of the poisoned patients were followed and recorded. The clinical treatment to reach a clinically stable condition and return to normal physiological parameters was a combination of hydration with saline solution supplemented with Dobutamine (vasoactive drug), Furosemide (diuretic) and Ranitidine (inhibitor of acid secretion). The physiological condition of patients began to improve after four hours of clinical treatment, and a stable condition was reached between 12 to 24 hours. The HPLC-FLD analysis showed only the GTX3/GTX2 epimers in the blood and urine samples. Also, these epimers were the only paralytic shellfish toxins found in the shellfish extract sample.

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Paralytic shellfish poisoning

Cited by 53 publications

References 0 publications

Marine neurotoxins: Ingestible toxins

Marine neurotoxins: Ingestible toxins

ECG Manifestations: The Poisoned Patient

Human intoxication with paralytic shellfish toxins: Clinical parameters and toxin analysis in plasma and urine

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