Prolonged ventilatory failure and flaccid quadriparesis after ingestion of poison hemlock.

INTRODUCTION: A 28-year-old man presented with acute flaccid paralysis and respiratory failure that persisted for 2 weeks after suicidal ingestion of unknown substances. METHODS: Extensive clinical, nerve, laboratory, and neuroimaging testing excluded alternative causes of this neuromuscular syndrome. Prompted by clues provided by family members, liquid chromatography time-of-flight mass spectrometry was used to investigate for the presence of poison hemlock. RESULTS: Testing of the residue in a jar used for the ingestion of a poisonous concoction confirmed the presence of the nicotinic alkaloid coniine. Analysis of patient serum suggested the presence of conhydrine. Concentrations of amitriptyline and diazepam were also found to be supratherapeutic, but only through the first few days of hospitalization. CONCLUSIONS: Herein we describe a case of reversible coma, flaccid quadriparesis, and neuromuscular respiratory failure caused by intentional ingestion of poison hemlock.

Poison hemlock-induced respiratory failure in a toddler.

The ingestion of poison hemlock, or Conium maculatum, is described in a 2-year-old boy. He had the onset of abdominal pain and weakness after being fed C. maculatum picked by his sister from the roadside 2 hours earlier. He had a rapidly progressive muscular weakness and was intubated for respiratory failure. His symptoms completely resolved within 24 hours of the ingestion. Conium maculatum is a common weed that causes toxicity by its primary toxin, coniine, which stimulates nicotinic receptors and causes a syndrome of rapidly progressive muscle weakness and paralysis. We describe the course of a benign-appearing plant ingestion resulting in respiratory failure.

Conium maculatum intoxication: Literature review and case report on hemlock poisoning.

The aim of this paper is to highlight the symptomatology in three Conium maculatum intoxication incidents, one of which was fatal. A number of studies were reviewed in order to update and summarize the relevant literature on the incidence, sociodemographic variables, method of poisoning, pathophysiology, diagnosis, variables associated with survival and fatality, management, and treatment of C. maculatum intoxication as well as the biosynthesis and biological effects of poison hemlock alkaloids. Results show that hemlock poisoning is relatively rare, although incidence varies in different regions, despite its worldwide distribution. Hemlock poisoning is more common in European and especially Mediterranean countries. The majority of the patients are adult males over 38 years of age. The clinical course of hemlock poisoning includes neurotoxicosis, tremor, vomiting, muscle paralysis, respiratory paralysis/failure, rhabdomyolysis, and acute renal failure. The therapeutic management focuses on absorption reduction, close observation for complications, and supportive therapy (especially for respiration). Acute occurrence is severe and life-threatening, but the survival rate is high if treatment is provided promptly. Recovery is rapid, generally taking only a few days.

Intravenous Poison Hemlock Injection Resulting in Prolonged Respiratory Failure and Encephalopathy.

BACKGROUND: Poison hemlock (Conium maculatum) is a common plant with a significant toxicity. Data on this toxicity is sparse as there have been few case reports and never a documented poisoning after intravenous injection. OBJECTIVES: We present a case of intravenous poison hemlock injection encountered in the emergency department. CASE REPORT: We describe a 30-year-old male who presented to the emergency department after a brief cardiac arrest after injecting poison hemlock. The patient had return of spontaneous circulation in the emergency department but had prolonged muscular weakness and encephalopathy later requiring tracheostomy. CONCLUSION: Intravenous injection of poison hemlock alkaloids can result in significant toxicity, including cardiopulmonary arrest, prolonged weakness, and encephalopathy.

Successful transplantation of donor organs from a hemlock poisoning victim.

BACKGROUND: The poison hemlock plant (Conium maculatum) has been a known poison since early in human history, most notably as the agent used for the execution/suicide of Socrates in ancient Greece. No experience has been reported regarding the suitability of a hemlock victim's organs for transplantation. METHODS AND RESULTS: This report documents successful transplantation of the liver, kidney, and pancreas from a 14-year-old girl who died of anoxic encephalopathy from asphyxia after the accidental ingestion of fresh hemlock while on a nature hike. Predonation laboratory values were not remarkable, and liver and kidney biopsy results were normal. All organs in the three recipients had immediate function, and no recipient had any clinical evidence of transmitted toxin. All recipients are well, with functioning transplants at greater than 6 months after transplantation. CONCLUSIONS: Poison hemlock intoxication does not seem to be a contraindication to organ donation.

Poison hemlock (Conium maculatum L.).

One of the most poisonous species amongst higher plants is Conium maculatum. It is a very common nitrophile weed species, belonging to the Apiaceae (formerly Umbelliferae) family. It contains some piperidine alkaloids (coniine, N-methyl-coniine, conhydrine, pseudoconhydrine, gamma-coniceine), which are formed by the cyclisation of an eight-carbon chain derived from four acetate units. gamma-Coniceine is the precursor of the other hemlock alkaloids. All vegetative organs, flowers and fruits contain alkaloids. The concentrations (both absolute and relative) of the different alkaloids depend on plant varieties, on ecological conditions and on the age of the plant. The characteristic biological effects of the plants are summarised on cattle, sheep, goat, swine, rabbit, elk, birds and insects and the symptoms of the human toxicosis (some cases of poisonings) are discussed according to the literature data. The general symptoms of hemlock poisoning are effects on nervous system (stimulation followed by paralysis of motor nerve endings and CNS stimulation and later depression), vomiting, trembling, problems in movement, slow and weak later rapid pulse, rapid respiration, salivation, urination, nausea, convulsions, coma and death.