Intravenous Lipid Emulsion Therapy Research Articles

Clinical effects and adverse effects of intravenous lipid emulsion treatment in dogs and cats with suspected poisoning.

This retrospective study aimed to evaluate the effects on the clinical signs of poisoning and adverse effects of intravenous lipid emulsion treatment in 82 animals (dogs and cats) with suspected poisonings over 18 months. Physical examination parameters and state of consciousness were documented every hour after the intravenous administration of a bolus of 2 ml/kg and 0.25 ml/kg/min over 60 minutes of a 20% intravenous lipid emulsion. The modified Glasgow coma scale and laboratory findings (blood gas analysis, triglyceride, lactate) were evaluated initially and three hours after discontinuing intravenous lipid emulsion administration. A statistical evaluation of the occurrence of adverse effects and the development of laboratory values was performed. A decrease in respiratory rate in the second control (8-12 hours) after ILE was observed. Three hours after completing of the intravenous lipid emulsion, triglyceride concentration increased about 10 times (p <0.001). Venous carbon dioxide partial pressure, bicarbonate, base excess, as well as the electrolytes sodium, potassium and ionized calcium decreased significantly (p <0.001). Patients who experienced a worsening of the modified Glasgow coma scale had a higher increase in triglyceride concentrations (p = 0.041) and plasma lactate (p = 0.034) and a larger decrease in bicarbonate concentrations (p = 0.053) compared to others. About 54% (n = 44) of the patients showed adverse effects which could be attributed to the administration of intravenous lipid emulsion and may be associated with a higher triglyceride increase. All of them were completely reversible within 33 hours. Adverse effects associated with intravenous lipid emulsion therapy were observed in half of the patients and were associated with a higher increase in triglycerides.

Emerging Insights into Brevetoxicosis in Sea Turtles.

This review summarizes the current understanding of how brevetoxins, produced by Karenia brevis during harmful algal blooms, impact sea turtle health. Sea turtles may be exposed to brevetoxins through ingestion, inhalation, maternal transfer, and potentially absorption through the skin. Brevetoxins bind to voltage-gated sodium channels in the central nervous system, disrupting cellular function and inducing neurological symptoms in affected sea turtles. Moreover, the current evidence suggests a broader and longer-term impact on sea turtle health beyond what is seen during stranding events. Diagnosis relies on the detection of brevetoxins in tissues and plasma from stranded turtles. The current treatment of choice, intravenous lipid emulsion therapy, may rapidly reduce symptoms and brevetoxin concentrations, improving survival rates. Monitoring, prevention, and control strategies for harmful algal blooms are discussed. However, as the frequency and severity of blooms are expected to increase due to climate change and increased environmental pollution, continued research is needed to better understand the sublethal effects of brevetoxins on sea turtles and the impact on hatchlings, as well as the pharmacokinetic mechanisms underlying brevetoxicosis. Moreover, research into the optimization of treatments may help to protect endangered sea turtle populations in the face of this growing threat.

Effect of intravenous lipid therapy in critically ill pediatric patients with calcium channel blocker toxicity.

Overdose with calcium-channel blockers (CCBs) still maintain their importance with a high lethality rate after exposure. We report the intravenous lipid emulsion therapy (ILE) therapy in our CCB overdose patients. We retrospectively analyzed the records of 6 patients with CCB intoxication from Batman Training and Research Hospital PICU between March 2021 and September 2022. Patients aged 0-18 years who received ILE treatment for CCB poisoning were included. All six patients ingested CCB with the intention of committing suicide and were followed up in the pediatric intensive care unit (PICU). All patients received ILE therapy due to hemodynamic instability despite intravenous fluid boluses, calcium, glucagon, insulin-dextrose, and vasoactive agents. Vasoactive-Inotropic Score (VIS) decreased after ILE treatment. All patients were transferred from the PICU after recovery. ILE therapy should be kept in mind as a salvage therapy in hemodynamically unstable CCB poisoning cases that do not respond to initial and advanced options.

Treatment Modalities in Calcium Channel Blocker Overdose: A Systematic Review.

Calcium channel blocker poisoning is one of the most common poisonings encountered which presents with life-threatening complications. However, there is no unified approach for treating these patients in the existing literature. This study aimed to assess the effects of different treatment modalities used in calcium channel blocker poisoning, as reported by previous studies. The primary outcomes studied were mortality and hemodynamic parameters after treatment. The secondary outcomes were the length of hospital stay, length of intensive care unit stay, duration of vasopressor use, functional outcomes, and serum calcium channel blocker concentrations. A thorough literature search was performed through Ovid, PubMed, Cochrane Library, and Google Scholar from January 2014 to December 31, 2022, to identify all studies analyzing the effects of the treatment of calcium channel blocker poisoning on the desired outcomes. Two reviewers reviewed 607 published articles from January 2014 to December 2022 to identify studies analyzing the effects of the treatment of calcium channel blocker poisoning on desired outcomes. In this review, 18 case reports, one case series, and one cohort study were included. Most patients were treated with an injection of calcium gluconate or calcium chloride. The use of calcium along with dopamine and norepinephrine was found to have lower mortality rates. A few patients were also treated with injection atropine for bradycardia. High-dose insulin therapy was used in 14 patients, of whom two did not survive. In the cohort study, 66 calcium channel blocker toxicity patients were included. These patients were treated with high-dose insulin therapy. A total of 11 patients with calcium channel blocker toxicity succumbed. Although it was found to be associated with improved hemodynamic parameters and lower mortality, side effects such as hypokalemia and hypoglycemia were noted. Intravenous lipid emulsion therapy (administered to eight patients), extracorporeal life support (used in three patients with refractory shock or cardiac arrest), injection glucagon, methylene blue, albumin infusion, and terlipressin were associated with a lower mortality rate as well as improvement in hemodynamic parameters. None of the case reports provided any information on end-organ damage on long-term follow-up.

Successful management of minoxidil 5% toxicosis in 2 cats from the same household.

To describe the successful management of 2 cats following ingestion of minoxidil 5%. Two 2-year-old neutered male Savannah cats were presented following suspected minoxidil 5% ingestion. Both cats developed significant myocardial injury, and clinical signs were consistent with congestive heart failure, supported by cardiac troponin I concentrations, echocardiogram, and thoracic radiographs. They required vasopressor therapy and were decontaminated with intravenous lipid emulsion therapy. Following decontamination, both cats were successfully discontinued from vasopressor therapy, and their clinical signs resolved within 24hours. The cats were successfully discharged without long-lasting cardiac compromise. Their echocardiograms and cardiac troponin concentration 7weeks after discharge were within reference intervals. This is the first detailed report of the successful management of cats following minoxidil 5% ingestion.

Intralipid Emulsion Therapy for the Treatment of Suspected Toxicity in 2 Avian Species.

Intravenous lipid emulsion (ILE) therapy has shown promise as a treatment option for a variety of lipophilic toxins. Two birds presented for suspected ingestion of a toxic substance. A blue-and-gold macaw (Ara ararauna) presented after chewing a block of bromethalin rodenticide without overt clinical signs at the time of presentation. Additionally, a free-ranging bald eagle (Haliaeetus leucocephalus) was found weak and depressed near a municipal landfill after presumptive ingestion of pentobarbital. Both birds were treated with ILE therapy for potential intoxication without any adverse events. The macaw was clinically normal after 3 days of hospitalization and at a 1-week reevaluation. The eagle was transferred to a rehabilitation center after markedly improved mentation and strength and was released 7 days later. Clinicians should consider ILE therapy for the treatment of lipophilic toxicities; however, monitoring is recommended for persistent lipemia and other adverse effects that have been reported in the veterinary literature.

Antidepressant Poisoning Trends in Pediatric Intensive Care: A Comparative Study of New- and Old-Generation Antidepressants.

This study aimed to compare the frequency, clinical findings, treatment practices, and outcomes of toxicity to old-generation (OG) and new-generation (NG) antidepressants in our pediatric intensive care unit (PICU) by year-to-year. The study included patients hospitalized for antidepressant poisoning during the 11-year period of January 2010 through December 2020. Antidepressants were classified as OG and NG. The groups were compared in terms of patient demographic characteristics, type of poisoning (accidental/suicidal), clinical findings, supportive and extracorporeal treatments received, and outcomes. The study included 58 patients (NG, n = 30; OG, n = 28). The median age of the patients was 178 months (range, 13.6-215 months) and 47 patients (81%) were female. Patients admitted for only antidepressant poisoning constituted 13.3% of all poisoning cases (58/436). Of these, 22 cases (37.9%) were accidental and 36 (62.3%) were suicidal. The most common cause of poisoning was amitriptyline (24/28) in the OG group and sertraline (13/30) in the NG group. Neurological symptoms were significantly more common in the OG group (76.2% vs 23.8%), while gastrointestinal involvement was more common in the NG group (82% vs 18%; P = 0.001 and P = 0.026, respectively). Old-generation antidepressant poisoning was associated with more frequent intubation (4 vs 0 patients, P = 0.048) and longer length of PICU stay (median, 1 day [range, 1-8] vs 1 day [range, 1-4], P = 0.019). Rates of therapeutic plasma exchange and intravenous lipid emulsion therapy did not differ ( P = 0.483 and P = 0.229, respectively). In poisoned patients, proper evaluation and management of patients requiring PICU admission are vital for favorable patient outcomes.

Altered profile of plasma phospholipids in woman with recurrent pregnancy loss and recurrent implantation failure treated with lipid emulsion therapy.

Recurrent Pregnancy Loss (RPL) and Recurrent Implantation Failure (RIF) are highly heterogeneous condition and many of the mechanisms involved still require elucidation. The aim was to analyze the lipidomic profile in plasma of women with RPL and RIF before and after receiving the Lipid Emulsion Therapy (LET) containing 10% fish oil (SMOFlipid® 20%). This study included twenty-six women with RPL or RIF from immunological or inflammatory causes, with elevated natural killer cell levels and divided into a Pregnancy Loss or a Live Birth group according to the outcome. The women received intravenous LET and sample collecting was done before the first, third and fifth dose of LET in the pregnant women. Ultra-performance liquid chromatography quadrupole time of flight mass spectrometry (UPLC-QTOF MS) and multivariate statistical methods were performed to evaluate the profile of phospholipids present in the women's plasma. An increase of phosphatidylcholines (PC) 40:8 and 36:5 levels with predominance of n6 polyunsaturated fatty acids (PUFA) was observed in plasma lipids of the Pregnancy Loss Group compared to Live Birth Group. We also observed an increase in the relative abundance of n3 PUFA-PC species (42:10 and 36:6) and LysoPC 15:0 with the long term use of LET. The greater availability of n3 PUFA in plasma of the pregnant women stemming from LET use can be considered advantageous regarding the alteration of the phospholipid profile and its postulated anti-inflammatory and immunomodulatory role.

Use of Intravenous Lipid Emulsion Therapy to Prevent the Undesirable Effects of Midazolam

Use of Intravenous Lipid Emulsion Therapy to Prevent the Undesirable Effects of Midazolam

Low-dose lipid emulsion for pediatric vasoplegic shock due to quetiapine and fluvoxamine overdose: a case report

Background: Intravenous lipid emulsion (ILE) therapy was originally used for treatment of for local anesthetic systemic toxicity. Over the last decade, it has been successfully used to treat severe toxicity of numerous lipophilic substances. The mechanism by which ILE therapy treats lipophilic drug toxicity was originally purported to be due to the lipid sink mechanism; however, further research suggests that several other factors likely play more substantial roles, including free fatty acid provision to cardiomyocytes, positive inotropic effect, ion channel modulation, and nitric oxide synthase inhibition. No standardized dosing recommendation exists for ILE treatment of pediatric lipophilic drug toxicity. Several case reports have documented successful resuscitation of such overdoses using much lower dosages of ILE than are used for local anesthetic toxicity.

Commentary: Case report: Successful intravenous lipid emulsion therapy for canine amphetamine toxicosis.

Commentary: Case report: Successful intravenous lipid emulsion therapy for canine amphetamine toxicosis.

Use of intravenous lipid emulsion therapy as a novel treatment for brevetoxicosis in sea turtles

The southwest coast of Florida experiences annual red tides, a type of harmful algal bloom that results from high concentrations of Karenia brevis. These dinoflagellates release lipophilic neurotoxins, known as brevetoxins, that bind to sodium channels and inhibit their inactivation, resulting in a variety of symptoms that can lead to mass sea turtle strandings. Traditional therapies for brevetoxicosis include standard and supportive care (SSC) and/or dehydration therapy; however, these treatments are slow-acting and often ineffective. Because red tide events occur annually in Florida, our objective was to test intravenous lipid emulsion (ILE) as a rapid treatment for brevetoxicosis in sea turtles and examine potential impacts on toxin clearance rates, symptom reduction, rehabilitation time, and survival rates. Sea turtles exhibiting neurological symptoms related to brevetoxicosis were brought to rehabilitation from 2018–2019. Upon admission, blood samples were collected, followed by immediate administration of 25 mg ILE/kg body mass (Intralipid® 20%) at 1 mL/min using infusion pumps. Blood samples were collected at numerous intervals post-ILE delivery and analyzed for brevetoxins using enzyme-linked immunosorbent assays. In total, nine (four subadults, one adult female, four adult males) loggerheads (Caretta caretta), five (four juvenile, one adult female) Kemp’s ridleys (Lepidochelys kempii), and four juvenile green turtles (Chelonia mydas) were included in this study. We found that plasma brevetoxins declined faster compared to turtles that received only SSC. Additionally, survival rate of these patients was 94% (17/18), which is significantly higher than previous studies that used SSC and/or dehydration therapy (47%; 46/99). Nearly all symptoms were eliminated within 24–48 h, whereas using SSC, symptom elimination could take up to seven days or more. The dosage given here (25 mg/kg) was sufficient for turtles in this study, but the use of a higher dosage (50–100 mg/kg) for those animals experiencing severe symptoms may be considered. These types of fast-acting treatment plans are necessary for rehabilitation facilities that are already resource-limited. Intravenous lipid emulsion therapy has the potential to reduce rehabilitation time, save resources, and increase survival of sea turtles and other marine animals experiencing brevetoxicosis.

Is soybean therapy better than ClinOleic for reducing recovery time in cats with permethrin toxicosis?

PICO question&#x0D; Is soybean oil-based intravenous lipid emulsion (IVLE) therapy more effective than olive oil-based (ClinOleic IVLE therapy) for reducing time to recovery in cats with permethrin toxicosis?&#x0D; &#x0D; Clinical bottom line&#x0D; Category of research question&#x0D; Treatment&#x0D; The number and type of study designs reviewed&#x0D; Five case reports and one randomised clinical trial&#x0D; Strength of evidence&#x0D; Weak&#x0D; Outcomes reported&#x0D; Soybean oil-based and ClinOleic IVLE therapies can be used safely as adjuvant treatments to reduce time to recovery in cats with permethrin intoxication. However, the evidence collected suggests that soybean oil-based IVLE therapy is better in reducing the recovery time after permethrin toxicosis as compared to ClinOleic IVLE therapy&#x0D; Conclusion&#x0D; The overall findings showed that the average recovery time after soybean oil-based IVLE therapy across patients with permethrin intoxication was 8.5 hours and the average time to recovery after olive oil-based emulsions (ClinOleic therapy) was 39 hours. This may suggest that soybean oil-based formulations are a better option for reducing the recovery time in cats after permethrin toxicity. Dermal decontamination, supportive care, muscle relaxers, and anticonvulsant drugs are examples of recommended treatments before the administration of any intralipid therapies and must be used based on the clinical signs of each patient&#x0D; &#x0D; How to apply this evidence in practice&#x0D; The application of evidence into practice should take into account multiple factors, not limited to: individual clinical expertise, patient’s circumstances and owners’ values, country, location or clinic where you work, the individual case in front of you, the availability of therapies and resources.&#x0D; Knowledge Summaries are a resource to help reinforce or inform decision making. They do not override the responsibility or judgement of the practitioner to do what is best for the animal in their care.&#x0D; &#x0D;

A CASE OF STATUS EPILEPTICUS SECONDARY TO BUPROPION OVERDOSE TREATED WITH IV LIPID EMULSION THERAPY

TOPIC: Critical Care TYPE: Medical Student/Resident Case Reports INTRODUCTION: Bupropion is a norepinephrine/dopamine reuptake inhibitor useful in depression and smoking cessation, with seizures being its most well-known adverse effect. Here, we present a case of status epilepticus secondary to Bupropion overdose (OD), successfully treated with intravenous lipid emulsion (ILE) therapy. CASE PRESENTATION: A 21-year-old female with a past medical history of depression, anxiety, PTSD, and polysubstance abuse, presented to the emergency room with bizarre behavior. Her roommate reported finding empty pill bottles of bupropion, gabapentin, and propranolol at her apartment. On arrival, vitals were HR: 140, BP: 119/59, RR: 18, SpO2: 98%, and GCS: 12. Soon after, the patient had a tonic-clonic seizure that initially subsided on administering 2mg of Lorazepam. Post-seizure, she was tachycardic, diaphoretic with dry oral mucosa, and had dilated pupils with conjunctival injection. Pertinent laboratory findings included an arterial blood gas analysis suggestive of severe high anion gap metabolic acidosis secondary to elevated lactate of 13.2 mmol/L. Her urine toxicology was positive for amphetamine. Salicylates, acetaminophen, and alcohol levels were undetectable. CT head was unremarkable. She was transferred to ICU and intubated for an increasing frequency of seizures and status epilepticus. Despite being on lorazepam drip, her seizures continued and were also resistant to phenobarbital, levetiracetam, valproate, fentanyl, and propofol. Ventricular tachycardias further complicated her course with hemodynamic instability, requiring electro cardioversion and multiple vasopressors. The history of empty bottles of bupropion, positive amphetamine in urine toxicology, along with seizures and ventricular tachycardias, led to a suspicion of bupropion overdose. Intravenous lipid emulsion (ILE) therapy was administered, consequently reversing bupropion toxicity evidenced by cessation of seizures, decreasing vasopressor requirement, improvement in mental status, and extubation. DISCUSSION: Seizures, ventricular tachycardias, and QT prolongation are well-known side effects of bupropion OD, which can occur at any dose with higher incidences noted at higher doses. Positive amphetamines on urine toxicology are expected with bupropion use as their metabolites have chemical structures similar to amphetamine. Intravenous lipid emulsion therapy (ILE) was used in our patient as salvage therapy for bupropion overdose in the setting of hemodynamic instability and status epilepticus with effective reversal of toxicity. The proposed mechanism of action involves ILE sequestering lipophilic drugs such as bupropion followed by its removal via biliary excretion into the gut. However, the use of ILE lacks high-powered evidence, and further investigation is warranted to expand and strengthen the antidotal uses of ILE. CONCLUSIONS: ILE therapy can be used as an antidote for severe bupropion toxicity. REFERENCE #1: Bornstein K, Montrief T, Anwar Parris M. Successful Management of Adolescent Bupropion Overdose with Intravenous Lipid Emulsion Therapy. J Pediatr Intensive Care. 2019;8(4):242-246. doi:10.1055/s-0039-1693483 REFERENCE #2: Stall N, Godwin J, Juurlink D. Bupropion abuse and overdose. CMAJ. 2014;186(13):1015. doi:10.1503/cmaj.131534 REFERENCE #3: Casey ER, Scott MG, Tang S, Mullins ME. Frequency of false positive amphetamine screens due to bupropion using the Syva EMIT II immunoassay. J Med Toxicol. 2011 Jun;7(2):105-8. doi: 10.1007/s13181-010-0131-5. PMID: 21191682; PMCID: PMC3724447. DISCLOSURES: No relevant relationships by Mubashir Ayaz Ahmed, source=Web Response No relevant relationships by Shayet Hossain Eshan, source=Web Response No relevant relationships by sami hussein, source=Web Response No relevant relationships by Sudha Misra, source=Web Response No relevant relationships by Chenyu Sun, source=Web Response

LIPID EMULSION THERAPY FOR LIFE-THREATENING FLECAINIDE TOXICITY

TOPIC: Critical Care TYPE: Medical Student/Resident Case Reports INTRODUCTION: We present a case of flecainide (FLC) toxicity secondary to renal failure treated with intravenous lipid emulsion (ILE) therapy. CASE PRESENTATION: The patient is a 63 year old female with a history of stage IVB uterine carcinosarcoma, chronic kidney disease and supraventricular tachycardia (SVT) on FLC. She was admitted with intra-abdominal hemorrhagic metastases. A rapid response was called due to hypotension, and she was noted to be oliguric for the previous 24 hours with a serum creatinine 2.5 mg/dL (baseline 1.3 mg/dL) and hyponatremic (126 mmol/L). EKG showed a new wide complex rhythm, at 78bpm, QRS widening to 280ms, and prolonged QTc of 631. She subsequently suffered a wide complex tachyarrhythmic cardiac arrest (CA), refractory to two shocks, with return of spontaneous circulation after treatment with sodium bicarbonate (NaHCO3). FLC was discontinued and the patient was started on a hypertonic NaHCO3 drip, but frequent NaHCO3 pushes were required to correct widening of the QRS complex. The hypotension progressed requiring high dose infusions of epinephrine (15 mcg/min) and norepinephrine (90 mcg/min). ILE infusion was started, 20% lipid 1.5 mL/kg administered over 5 minutes, followed by an infusion of 0.25 mL/kg/minute over two hours. A serum FLC level was drawn during ILE infusion and came back elevated at 1.35 mcg/mL (therapeutic level 0.20-1.0 mcg/mL). In the 48 hours following ILE, there was resolution of the wide complex arrhythmias, and vasopressor requirements were reduced by more than 50% DISCUSSION: FLC is a class 1C antiarrhythmic that inhibits Na+ channels and is used for prevention of SVT. It has a narrow therapeutic range and about 30% is renally excreted making acute kidney injury a risk for toxicity. Other risk factors for toxicity are hyponatremia and hypokalemia. Characteristic signs of toxicity include hypotension, lethargy and EKG changes such as QRS widening and PR prolongation. These changes can progress to wide complex brady or tachyarrhythmic CA as seen in our patient. Standard of care is administration of hypertonic NaHCO3 which acts both as a Na+ load to compete with FLC for binding at Na+ channels and as an alkalinizing agent which decreases the ionized receptor-binding form of FLC. However, when NaHCO3 treatment fails, there are few other well studied options. One is VA-ECMO for which our patient was not a candidate. The other is lipid emulsion therapy, which is hypothesized to work by creating a lipid sink to sequester the drug and also has some positive ionotropy. CONCLUSIONS: In our patient, administration of ILE resulted in significant clinical improvement. Unfortunately, the clinical improvement did not sustain after several days and due to overall poor prognosis, the patient was eventually transitioned to comfort measures. REFERENCE #1: Subedi R, Dean R, Chaudhary A. Flecainide toxicity in renal failure. Proc (Bayl Univ Med Cent). 2018 May 9;3(3):328-330. REFERENCE #2: Ghataoura R, Patil S. Flecainide toxicity: a presentation to the emergency department with literature review. BMJ Case Rep. 2020 Feb 28;13(2):e232691. doi: 10.1136/bcr-2019-232691. PMID: 32114494; PMCID: PMC7050315. REFERENCE #3: Valentino MA, Panakos A, Ragupathi L, Williams J, Pavri BB. Flecainide Toxicity: A Case Report and Systematic Review of its Electrocardiographic Patterns and Management. Cardiovasc Toxicol. 2017 Jul;17(3):260-266. doi: 10.1007/s12012-016-9380-0. PMID: 27435408. DISCLOSURES: No relevant relationships by Rebecca Fieles, source=Web Response No relevant relationships by David Gerber, source=Web Response No relevant relationships by Brian Park, source=Web Response No relevant relationships by Harry Rockower, source=Web Response No relevant relationships by Diana Solomon, source=Web Response No relevant relationships by Yanika Wolfe, source=Web Response

Fluid Therapy During Cardiopulmonary Resuscitation

Cardiopulmonary arrest (CPA), the acute cessation of blood flow and ventilation, is fatal if left untreated. Cardiopulmonary resuscitation (CPR) is targeted at restoring oxygen delivery to tissues to mitigate ischemic injury and to provide energy substrate to the tissues in order to achieve return of spontaneous circulation (ROSC). In addition to basic life support (BLS), targeted at replacing the mechanical aspects of circulation and ventilation, adjunctive advanced life support (ALS) interventions, such as intravenous fluid therapy, can improve the likelihood of ROSC depending on the specific characteristics of the patient. In hypovolemic patients with CPA, intravenous fluid boluses to improve preload and cardiac output are likely beneficial, and the use of hypertonic saline may confer additional neuroprotective effects. However, in euvolemic patients, isotonic or hypertonic crystalloid boluses may be detrimental due to decreased tissue blood flow caused by compromised tissue perfusion pressures. Synthetic colloids have not been shown to be beneficial in patients in CPA, and given their documented potential for harm, they are not recommended. Patients with documented electrolyte abnormalities such as hypokalemia or hyperkalemia benefit from therapy targeted at those disturbances, and patients with CPA induced by lipid soluble toxins may benefit from intravenous lipid emulsion therapy. Patients with prolonged CPA that have developed significant acidemia may benefit from intravenous buffer therapy, but patients with acute CPA may be harmed by buffers. In general, ALS fluid therapies should be used only if specific indications are present in the individual patient.

A case of acute drug toxicity in a patient indicated for intravenous lipid emulsion therapy

A case of acute drug toxicity in a patient indicated for intravenous lipid emulsion therapy

Lamotrigine Toxicosis Treated with Intravenous Lipid Emulsion Therapy in a Dog

A female spayed dachshund/mixed-breed dog was evaluated following ingestion of lamotrigine tablets with subsequent rapid onset of vomiting, diarrhea, and generalized tremoring. On initial examination, the dog was moderately obtunded and nonambulatory with intermittent myoclonus and hyperesthesia. Electrocardiogram revealed sinus tachycardia with prolongation of the QT interval. Intravenous lipid emulsion (ILE) infusion was initiated, with reduction in tremoring and improved patient mentation being noted after ∼20 min of therapy. An elevated cardiac troponin I value measured at 1.02 ng/mL the day after presentation. Serum toxicological assay revealed marked reduction in serum lamotrigine levels following ILE and continued reduction during hospitalization. The dog's clinical signs resolved, corrected QT interval returned to normal, and the patient was discharged 38 hr after presentation. Individual cases of lamotrigine toxicosis have not been fully reported in veterinary literature. This case report documents the rapid onset of clinical signs including neurologic dysfunction, cardiac arrhythmias, and transient corrected QT prolongation. Serial serum concentrations of lamotrigine showed a rapid reduction with ILE therapy and corresponded with clinical recovery, suggesting efficacy of ILE treatment in this case.

Management of presumptive canine permethrin toxicosis using intravenous lipid emulsion as an adjunctive therapy

A seven-month-old Cavalier King Charles spaniel presented with generalised, coarse muscle tremors that progressed to seizure activity, after observed ingestion (licking) of a cleaning product containing permethrin. At the time...

Treatment of Bupropion Toxicity with Lipid Emulsion

We have read with interest the case report, “Successful Management of Adolescent Bupropion Overdose with Intravenous Lipid Emulsion Therapy,” recently published in the Journal of Pediatric Intensive Care.[1] Lipid emulsion is effective in the treatment of acute toxicity induced by local anesthetics or nonlocal anesthetic drugs, including amitriptyline, bupropion, and verapamil, in pediatric patients.[2] A previous in vitro study reported that the magnitude of the reduction of the serum concentration of bupropion, which is a highly lipid-soluble antidepressant (log [octanol/water partition coefficient]: 3.2), was 46 by 2% lipid emulsion (Intralipid).[3] In addition, the magnitude of the sequestration of drugs with varied lipid solubility by lipid emulsion is dependent mainly on the lipid partition coefficient and partially on the volume of distribution, which appears to account for 88% of variations in the reduction of drug serum concentration by lipid emulsion.[3] As suggested by Bornstein et al, the lipid sink theory, which is considered the mechanism underlying the effect of lipid emulsion as a nonspecific antidote, states that lipid emulsion absorbs highly lipid-soluble drugs, such as bupivacaine (log [octanol/water partition coefficient]: 3.41), from the heart.[1] [4] However, the following comments should be considered to understand this case report well. First, the first administration of lipid emulsion improved the mental status of the patient.[1] On day 3, the second administration of lipid emulsion was performed due to the recurrence of an altered mental status.[1] The elimination half-life of bupropion is 29 ± 9 hours.[5] In addition, the absorption of a toxic dose following oral administration (enteral route) is more prolonged than that following intravenous administration, leading to extended toxicity.[6] In contrast, Intralipid has a very short half-life (13.7 ± 5.2 minutes).[7] Considering previous reports, the lipid phase of lipid emulsion appears to absorb highly lipid-soluble bupropion from the heart and brain for a very short period following lipid emulsion administration.[3] [7] Furthermore, 1% of plasma triglyceride concentration, which provides lipemic plasma without fat overload, is sufficient to exert scavenging and cardiotonic effects on the toxicity induced by an enteral overdose.[6] Thus, the altered mental status on day 3 following a marked improvement after the first administration of lipid emulsion may be ascribed to a greatly reduced concentration of Intralipid.[1] A previous report recommends the following lipid emulsion regimen to treat toxicity induced by enteral overdose: bolus administration of Intralipid 1.5 mL/kg for 1 minute and subsequently 0.25 mL/kg/min for an additional 3 minutes, followed by intravenous infusion of 0.025 mL/kg/min (up to 6.5 hours) to theoretically maintain a 1% plasma triglyceride concentration.[6] This regimen, as an adjuvant, can be used with supportive care in cases of toxicity induced by oral overdose.[6] However, further research in an in vivo model on the optimal dosing regimen of lipid emulsion for the treatment of toxicity following oral overdose of bupropion is needed because the pharmacokinetics of an oral overdose are different from those of intravenous overdose (e.g., local anesthetic systemic toxicity). Second, initially, lipid sink was widely accepted as the underlying mechanism of lipid emulsion treatment.[4] However, a previous study using a physiologically based pharmacokinetic model reported that lipid emulsion decreased only 11 and 18% bupivacaine concentrations in the heart and brain, respectively.[8] The free bupivacaine concentration was not significantly different between the control and lipid emulsion groups in an in vivo study after administration of a nontoxic dose of bupivacaine in humans.[9] Thus, lipid shuttle has recently been widely accepted as the mechanism of lipid emulsion treatment; it states that lipid emulsion absorbs lipid-soluble drugs, such as bupivacaine, from the heart and then the lipid emulsion, containing the sequestered lipid-soluble drug (e.g., bupivacaine), is transported to the liver and muscle for detoxification and storage, leading to enhanced redistribution.[4] We believe that this case report contributes valuable data on the efficacy of lipid emulsion treatment in bupropion toxicity and emphasizes the need for continuous infusion of lipid emulsion following the initial bolus administration in lipid emulsion treatment.