Local Anesthetic Systemic Toxicity Joint Management in the Prehospital Environment: A Case Report.

Local anesthetic systemic toxicity (LAST) is a potentially life-threatening complication that may occur after local anesthetic injection. After reaching the systemic circulation, cardiovascular and central nervous system derangements may appear, with potentially fatal complications if left untreated. The pillars for LAST treatment are advanced life support measures, airway and seizure management, and a 20% lipid emulsion intravenous administration. When occurring in the prehospital setting, LAST is difficult to recognize, mostly because of its features overlapping with other acute conditions. Prompt treatment is also challenging because lipid emulsion may not be routinely carried on emergency vehicles. This article reports a case of LAST occurring in a dental ambulatory located in a remote location within the Italian Alps in which effective communication among different components of the same regional health care system (dispatch center, prehospital teams, and hospital network) led to fast lipid emulsion retrieval en route and on-site toxicity resolution. This case can inspire future operational changes, such as antidote networks available to prehospital emergency medicine crews, avoiding unnecessary deployment of antidotes on ambulances or helicopters, which is difficult to preserve without increasing management costs. However, to be established, such a network would need protocols to facilitate antidote retrieval, training focused on toxidromes recognition, and improved communication skills among different professionals involved in prehospital emergency medicine.

INTRAVENOUS LIPID EMULSION TREATMENT REDUCES SYMPTOMS OF BREVETOXICOSIS IN TURTLES (TRACHEMYS SCRIPTA).

Harmful algal blooms (HABs) occur when excess nutrients allow dinoflagellates to reproduce in large numbers. Marine animals are affected by blooms when algal toxins are ingested or inhaled. In the Gulf of Mexico, near annual blooms of Karenia brevis release a suite of compounds (brevetoxins) that cause sea turtle morbidity and mortality. The primary treatment at rehabilitation facilities for brevetoxin-exposed sea turtles is supportive care, and it has been difficult to design alternative treatment strategies without an understanding of the effects of brevetoxins in turtles in vivo. Previous studies using the freshwater turtle as a model species showed that brevetoxin-3 impacts the nervous and muscular systems, and is detoxified and eliminated primarily through the liver, bile, and feces. In this study, freshwater turtles (Trachemys scripta) were exposed to brevetoxin (PbTx-3) intratracheally at doses causing clear systemic effects, and treatment strategies aimed at reducing the postexposure neurological and muscular deficits were tested. Brevetoxin-exposed T. scripta displayed the same behaviors as animals admitted to rehabilitation centers for toxin exposure, ranging from muscle twitching and incoordination to paralysis and unresponsiveness. Two treatment regimes were tested: cholestyramine, a bile acid sequestrant; and an intravenous lipid emulsion treatment (Intralipidt) that provides an expanded circulating lipid volume. Cholestyramine was administered orally 1 hr and 6 hr post PbTx-3 exposure, but this regime failed to increase toxin clearance. Animals treated with Intralipid (100 mg/kg) 30 min after PbTx-3 exposure had greatly reduced symptoms of brevetoxicosis within the first 2 hr compared with animals that did not receive the treatment, and appeared fully recovered within 24 hr compared with toxin-exposed control animals that did not receive Intralipid. The results strongly suggest that Intralipid treatment for lipophilic toxins such as PbTx-3 has the potential to reduce morbidity and mortality in HAB-exposed sea turtles.

Dentists knowledge of lipid treatment of local anaesthetic systemic toxicity.

CONTEXT: : Local anesthetics (LAs) are in widespread use by dental practitioners, and erroneous administration, such as intravenously or exceeding the maximum dose, can cause the life-threatening condition of local anesthetic systemic toxicity (LAST). AIMS: The objective of the present study was evaluate the ability of dentists to recognize signs of LAST and quantify how often they have used lipids to treat LAST in dentistry patients. MATERIALS AND METHODS: The study administered 600 questionnaires that asked about the frequency with which dentists encountered LAST and the symptoms of LAST and its treatment, especially with lipids. RESULTS: The results showed that 520 (86.66%) respondents had never seen LAST, and 404 (67.3%) had no idea about lipid treatment. In addition, 128 (21.3%) had heard about lipid treatment but had inadequate knowledge of it and 59 (9.8%) had read an article about lipid treatment, but only 9 (1.5%) knew how to use lipid treatment. Finally, 80 (13.33%) participants had seen LAST but had used a treatment other than lipids. CONCLUSION: Dentists and all facilities using LA must be aware of LAST, and knowledge of lipid treatment must be increased by education. Twenty percent lipid solutions must be kept handy in their offices by dentists.

Intravenous lipid emulsion in treatment of cardiocirculatory disturbances caused by glyphosate-surfactant herbicide poisoning.

Introduction: Glyphosate is the first widely used herbicide against weed in genetically modified crops. Though glyphosate itself has a low toxicity, commercial products are more dangerous because of increased toxicity due to surfactants addition. There is no specific antidote for the poisoning with glyphosate-surfactant (Gly-SH). In recent times, the efficacy of intravenous lipid emulsion (ILE) administration for the treatment of acute poisoning caused by Gly- SH has been investigated. Case Report: A 50-year-old man was admitted 3 hours after self-poisoning with herbicide containing glyphosate and polyoxyethyleneamine, as a surfactant. On admission, the patient was in a coma, hypotensive (80/50 mmHg) and without spontaneous breathing. Electrocardiogram showed widecomplex tachycardia, and arterial blood gas (ABG) revealed acidosis (pH 7.07). Conventional treatment included mechanical ventilation, intravenous fluids, bicarbonate and dopamine. As there was no improvement, ILE was started. The patient received 100 mL of 20% Intralipid® bolus followed by infusion of 400 mL over 20 minutes. Prior to expiration of infusion, a gradual rise in blood pressure was noted, and within 2 hours sinus rhythm was restored. Conclusion: This case report suggests that the use of ILE may be an additional option for the treatment of cardiocirculatory disturbances caused by commercial products of glyphosate herbicide.

Intravenous lipid emulsion - rescued at LAST.

The accidental overdose of local anaesthetics may prove fatal. The commonly used amide local anaesthetics have varying adverse effects on the myocardium and beyond a certain dose all are capable of causing death. Local anaesthetics are the most frequently used drugs in dentistry and although uncommon, local anaesthetic systemic toxicity (LAST) accounts for a high proportion of mortalities in the dental office, with local anaesthetic-induced cardiac arrest particularly resistant to standard resuscitation methods. Over the last decade there has been convincing evidence of using intravenous lipid emulsions as a rescue in local anaesthetic - cardiotoxicity and anaesthetic organisations over the globe have developed guidelines on the use of this drug. Despite this, however, awareness among practitioners appears to be lacking. All who use local anaesthetics in their practice should have an appreciation of patients at high risk of toxicity, early symptoms and signs of toxicity, preventative measures when using these drugs and the initial management of systemic toxicity with intravenous lipid emulsion. In this review we intend to discuss the pharmacology and pathophysiology of local anaesthetic toxicity, and the rationale for intravenous lipid emulsion therapy.

Local anesthetic systemic toxicity: prevention and treatment.

Anesthesia is a sine qua non for most surgeries. Like any medical advance, progress in regional anesthesia has not come without its share of complications, including a spectrum extending from localized nerve injury to systemic cardiovascular toxicity and death. This article discusses the mechanisms and clinical presentation, prevention, treatment, and future trends of local anesthetic systemic toxicity. The adverse effects of lipid emulsion therapy are also included.

Intravenous lipid emulsions combine extracorporeal blood purification: a novel therapeutic strategy for severe organophosphate poisoning.

Organophosphorus (OP) pesticide self-poisoning is a major clinical problem in rural Asia and it results in the death of 200,000 people every year. At present, it is lack of effective methods to treat severe organophosphate poisoning. The high mortality rate lies on the amount of toxic absorption. Intravenous lipid emulsions can be used as an antidote in fat-soluble drug poisoning. The detoxification mechanism of intravenous lipid emulsions is "lipid sink", which lipid emulsions can dissolve the fat-soluble drugs and separate poison away from the sites of toxicity. Most of organophosphorus pesticides are highly fat-soluble. So, intravenous lipid emulsions have the potentially clinical applications in treatment of OP poisoning. Extracorporeal blood purification especially charcoal hemoperfusion is an efficient way to eliminate the poison contents from the blood. We hypothesize that the combination of intravenous lipid emulsions and charcoal hemoperfusion can be used to cure severe organophosphate poisoning. This novel protocol of therapy comprises two steps: one is obtained intravenous access to infuse lipid emulsions as soon as possible; another is that charcoal hemoperfusion will be used to clear the OP substances before the distribution of OP compounds in tissue is not complete. The advantages of this strategy lie in three points. Firstly, it will alleviate the toxic effect of OP pesticide in the patients by isolation and removal the toxic contents. Secondly, the dosage of antidotes can be reduced and its side-effects will be eased. Thirdly, a large bolus of fatty acids provide energy substrate for the patients who are nil by mouth. We consider that it would become a feasible, safe and efficient detoxification intervention in the alleviation of severe organophosphate poisoning, which would also improve the outcome of the patients.

Oxidation of parenteral lipid emulsion by ambient and phototherapy lights: potential toxicity of routine parenteral feeding.

Vitamin E can be a prooxidant in isolated lipoprotein suspensions. Because lipid emulsions used in parenteral nutrition are lipoprotein-like suspensions rich in polyunsaturated fatty acids and vitamin E, we hypothesized that vitamin E may act as a prooxidant in lipid emulsions, as it is in lipoprotein suspensions. We therefore exposed an intravenously administered lipid emulsion (Intralipid) to a single spotlight commonly used in the treatment of neonatal jaundice, and measured the formation of triglyceride hydroperoxides by using high-performance liquid chromatography with postcolumn chemiluminescence detection. Concentrations of these hydroperoxides in different batches of fresh intralipid were usually approximately 10 mumol/L but increased up to 60 times after exposure to phototherapy light for a period of 24 hours, even though significant amounts of vitamin E were present at the end of the exposure. Triglyceride hydroperoxides were formed during phototherapy light exposure whether the intralipid was in plastic tubing used routinely for infusion or in glass containers. Ambient light also caused significant peroxidation of the formula lipids, although to a much lesser extent than observed with phototherapy light. For infants in the neonatal intensive care unit who were receiving intralipid but not phototherapy, solutions being infused at the end of 24 hours contained a mean of 40 mumol/L hydroperoxides. For infants receiving phototherapy, the mean was 97 mumol/L. Phototherapy light-induced formation of triglyceride hydroperoxides was prevented by covering the intralipid with aluminum foil or supplementation with sodium ascorbate before light exposure. We conclude that intralipid is highly susceptible to oxidation and that elevated levels of oxidized lipids can be formed during its clinical use, especially when intralipid infusion is combined with phototherapy. Because lipid hydroperoxides are cytotoxic and can cause adverse effects, inadvertent infusion of rancid intralipid may add to the numerous problems encountered by premature neonates.