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Dive into the research topics where Larissa I. Velez is active.

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Featured researches published by Larissa I. Velez.


Resuscitation | 2009

Intravenous fat emulsion therapy for intentional sustained-release verapamil overdose

Amy Young; Larissa I. Velez; Kurt Kleinschmidt

We report the first case of sustained-release verapamil toxicity treated with Intralipid fat emulsion (IFE). Toxicity was confirmed by elevated serial serum verapamil and metabolite, norverapamil, levels. Most previously reported cases of IFE therapy involve local anaesthetic toxicity and cardiac arrest. Our patient was in shock despite standard therapy. No adverse events were noted and the patient fully recovered.


Annals of Pharmacotherapy | 2008

Role of Hydroxocobalamin in Acute Cyanide Poisoning

Greene Shepherd; Larissa I. Velez

Objective: To review the recently approved cyanide antidote, hydroxocobalamin, and describe its role in therapy. Data Sources: Relevant publications were identified through a systematic search of PubMed using the MeSH terms and key words hydroxocobalamin and cyanide. This search was then limited to human studies published since 2000. Systematic searches were conducted through January 2008. References from identified articles were reviewed for additional pertinent human studies. Study Selection and Data Extraction: The literature search retrieved 7 studies on the safety and/or efficacy of hydroxocobalamin in humans. Four new studies were identified by the search and 3 studies were identified from the references. Data Synthesis: Studies of antidote efficacy in humans are ethically and logistically difficult. A preclinical study demonstrated that intravenous doses of hydroxocobalamin 5 g are well tolerated by volunteer subjects. Hydroxocobalamin has been shown to reduce cyanide concentrations in controlled studies of nitroprusside therapy and in heavy smokers. A retrospective study of 14 acute cyanide poisonings also demonstrated hydroxocobalamins safety and efficacy. Two studies examining hydroxocobalamin for smoke inhalation-associated cyanide poisoning indicated a possible benefit, but they are insufficient to establish definitive criteria for use in this setting. Randomized controlled trials of hydroxocobalamin and traditional cyanide antidotes (nitrites/thiosulfate) are lacking. Conclusions: Cyanide poisoning can rapidly cause death. Having an effective antidote readily available is essential for facilities that provide emergency care. In cases of cyanide ingestion, both the nitrite/thiosulfate combination and hydroxocobalamin are effective antidotes. Hydroxocobalamin offers an improved safety profile lor children and pregnant women. Hydroxocobalamin also appears to have a better safety profile in the setting of cyanide poisoning in conjunction with smoke inhalation. However, current data are insufficient to recommend the empiric administration of hydroxocobalamin to all victims of smoke inhalation.


Family & Community Health | 2002

Elemental mercury poisoning in a family of seven

Debra C. Cherry; Larry K. Lowry; Larissa I. Velez; Cindy Cotrell; D. Christopher Keyes

Mercury poisoning in children is rare but may have devastating health consequences when exposure is unrecognized. Mercury occurs in three forms: elemental, inorganic, and organic. Elemental mercury (Hg0) vapor may volatilize following an accidental spill and may be readily absorbed from the lungs. The following case study describes how the poison center, health department, physicians, and others worked together to treat a family with long-term exposure to elemental mercury vapor in the home. Identification and prevention of this type of exposure in the community are discussed.


American Journal of Emergency Medicine | 2013

Two cases of disseminated intravascular coagulation due to "bath salts" resulting in fatalities, with laboratory confirmation.

Amy Young; Evan S. Schwarz; Larissa I. Velez; Melody Gardner

Synthetic cathinones are phenylalkylamines developed for both medicinal use and as substances of abuse referred to as “bath salts.” The rapid emergence of these bath salts over the recent years has been concerning to the medical community and law enforcement. Widespread availability, legality, and desired amphetamine-like effects have dramatically increased sales of these compounds. Only recently has regulations on specific derivatives been enacted in the United States. The acute sympathomimetic toxidrome associated with bath salts by virtually any route can result in harmful effects. The mechanism of action of these various derivatives is not well understood. There is no specific antidote for these agents. Aggressive supportive care, including sedation with benzodiazepines, fluid administration, and cooling measures, should be provided early in the toxidrome. The media and poison centers have tracked similarities in the acute toxicity from these agents, including neurologic, cardiovascular, and psychiatric effects. Multiorgan failure and deaths have recently been reported with both mephedrone and methylenedioxypyrovalerone. We report 2 fatalities presenting with hyperthermia, delirium, and disseminated intravascular coagulation. Both patients had laboratory confirmation of recent exposure to methylenedioxypyrovalerone. Cathinone is a naturally occurring amphetamine analogue found in the leaves of the Catha edulis plant [1]. The leaves are chewed for their stimulant effects, which primarily include increased alertness, insomnia, and hyperactivity. Synthetic cathinone derivatives were developed for both medicinal use and as substances of abuse. Bupropion is a clinically used synthetic cathinone. Other derivatives such as methcathinone and pyrovalerone were investigated for medicinal purposes before being used recreationally. Recently, ☆ This article has never been presented. 0735-6757/


Clinical Toxicology | 2008

Recurrent life-threatening ventricular dysrhythmias associated with acute hydrofluoric acid ingestion: Observations in one case and implications for mechanism of toxicity

Rais Vohra; Larissa I. Velez; Wilfredo Rivera; Fernando L. Benitez; Kathleen A. Delaney

– see front matter. Published by Elsevier Inc. substances sold under the name of “bath salts” have become popular among recreational drug users [2]. These drugs are injected, inhaled, ingested, or smoked. Bath salts in the United States were found to contain mephedrone, methylone, and methylenedioxypyrovalerone (MDPV), all of which are synthetic cathinones [3]. These synthetic cathinones also have the ability to modulate serotonin, which can result in psychoactive effects [1]. The media have devoted a lot of attention to this problem because the drugs are widely available in the United States, and the use of these agents seems to have exponentially increased in the past few years [1]. Both emergency department visits and poison center calls have grown significantly in the past 3 years [4,5]. In 2010, the American Association of Poison Control Centers reported 304 calls related to bath salts; the number increased to 6138 calls in 2011 [5]. Many of the patients presenting for emergency care have tachycardia, hypertension, and hallucinations. Multiorgan failure and deaths have recently been reported [4,6-8]. We report 2 deaths of patients who presented with hyperthermia, delirium, and disseminated intravascular coagulation (DIC) with laboratory confirmation of exposure to MDPV. A 20-year-old man was witnessed fleeing from the police after sniffing bath salts when he started seizing. When emergency medical services arrived on the scene, the patient was unresponsive. Emergency medical services administered naloxone 0.4 mg IV and adenosine 6 mg IV for narrow complex tachycardia, without effect. At the initial health care facility, the initial rhythm was narrow complex tachycardia with a heart rate (HR) of 165 beats per minute. The patient had spontaneous respirations at a rate of 24 per minute and an oxygen saturation of 100% on room air. He was intubated for airway protection using succinylcholine 90 mg IV and midazolam 2 mg IV. Rocuronium 50 mg IV, midazolam 4 mg IV, and ceftriaxone 1 g IV were given after intubation. The narrow complex tachycardia was again treated with 12 mg of adenosine IV without effect. Cardioversion at 150 J was also ineffective. Two liters of IV normal saline were infused. Despite this, the patient remained with an HR of 160 to 188 beats per minute for an hour at the initial hospital. During this period, the blood pressure (BP) was reported between 120/55 and 80/35 mm Hg. Acetaminophen 650 mg suppository was given for a temperature (T) of 39.6°C. The


Annals of Pharmacotherapy | 2004

Serotonin Syndrome with Elevated Paroxetine Concentrations

Larissa I. Velez; Greene Shepherd; Brett Roth; Fernando L. Benitez

Introduction. Hydrofluoric acid (HF) is a weak inorganic acid used for etching and as rust remover. Systemic toxicity is manifested as ventricular dysrhythmias. The mechanisms for these dysrhythmias are not well elucidated. Case report. An 82-year-old woman ingested 8 ounces of 7% HF. Shortly after emergency department (ED) arrival, she became pulseless, developing recurrent ventricular dysrhythmias. She was defibrillated 17 times and received several doses of calcium, magnesium, and lidocaine. After three hours, she returned to sustained NSR. She was discharged home after four days. Discussion. The electrocardiographic findings in this patient demonstrate hypocalcemia, which has been implicated as the culprit in HF-induced arrhythmias. However, despite correction of the hypocalcemia, the ventricular arrhythmias persisted. The proposed mechanisms of systemic HF toxicity and the relevant literature are discussed. Conclusion. Ventricular dysrhythmias due to HF toxicity seem to be independent of either hypocalcemia or hyperkalemia. Systemic toxicity after ingestions may be delayed and precipitous.


Clinical Toxicology | 2004

Iron Bezoar Retained in Colon Despite 3 Days of Whole Bowel Irrigation

Larissa I. Velez; Rebeca Gracia; Lisa Mills; Greene Shepherd; Sing Yi Feng

OBJECTIVE To describe a case of serotonin syndrome due to paroxetine and ethanol. CASE SUMMARY A 57-year-old white man was brought to the emergency department one day after ingesting paroxetine 3600 mg and a pint of hard liquor. He denied the use of any other drug or herbal products and regular use of alcohol. Upon arrival to the hospital, vital signs were blood pressure 188/103 mm Hg, heart rate 114 beats/min, respiratory rate 28 breaths/min, temperature 36.8 °C, and O2 saturation 96% on room air. Findings on physical examination included dilated pupils, facial flushing, diaphoresis, shivering, myoclonic jerks, tremors, and hyperreflexia. A tentative diagnosis of serotonin syndrome was made. Initially, cyproheptadine 8 mg was administered orally with no observable effect. An additional 12 mg was given in 3 doses over 24 hours. Symptoms abated slowly over the next 6 days, during which a thorough evaluation failed to reveal any other potential causes for the patients condition. Serum paroxetine concentrations at 27.5 and 40 hours after ingestion were 1800 and 1600 ng/mL, respectively (normal 20–200 ng/mL). DISCUSSION Serotonin syndrome is rarely reported in patients taking only one serotonergic medication. Although serum paroxetine concentrations have not been shown to correlate with efficacy or toxicity, our patients serum paroxetine concentration was 9 times the upper end of the therapeutic range. Cyproheptadine, which has been suggested as a therapy, did not appear beneficial in this patient. Use of the Naranjo probability scale indicated a probable relationship between the serotonin syndrome and the overdose of paroxetine taken by this patient. CONCLUSIONS More studies are needed to better assess the role of cyproheptadine and other serotonin antagonists in the management of the serotonin syndrome. Regardless of the use of cyproheptadine or other agents, attention should be paid to fluid status, decontamination, and management of hyperthermia, agitation, and seizures.


American Journal of Medical Quality | 2014

A Survey of Handoff Practices in Emergency Medicine

Chad S. Kessler; Faizan Shakeel; H. Gene Hern; Jonathan S. Jones; Jim Comes; Christine Kulstad; Fiona A. Gallahue; B. Burns; Barry J. Knapp; Maureen Gang; Moira Davenport; Ben Osborne; Larissa I. Velez

Concretion formation is a documented complication of large iron ingestions. The generally accepted treatment is supportive care, whole bowel irrigation, and intravenous deferoxamine for systemic toxicity. Laparotomy and gastrotomy have also been used in patients with a high iron burden and bezoar formation. Though experiments suggest that iron is poorly absorbed in the colon, there are no case reports of iron overdose without systemic toxicity, despite a retained colonic bezoar. We report the case of a 16‐month‐old who presented to an Emergency Department 19 h after an iron ingestion. Initial laboratory studies revealed an anion gap of 14 mEq/L, and a 20 h serum iron concentration of 429 mcg/dL. An abdominal radiograph revealed multiple pills throughout the stomach and small bowel; whole bowel irrigation was initiated. Deferoxamine was administered at 10 mg/kg/h and then stopped when the serum iron level reached 27 mcg/dL, 36 h later. At this time, the abdominal radiograph showed an iron bezoar remaining in the ascending colon despite a clear rectal effluent from whole bowel irrigation. Despite whole bowel irrigation over the next 36 h, the iron bezoar was not removed and actually migrated proximally in the colon. Treatment was stopped on the third day and a normal diet was instituted with prompt passage of the bezoar.


Annals of Emergency Medicine | 2013

Man With a Rash

Walter L. Green; Fernando L. Benitez; Larissa I. Velez; Drew S. Weiner

This study aimed to assess practices in emergency department (ED) handoffs as perceived by emergency medicine (EM) residency program directors and other senior-level faculty and to determine if there are deficits in resident handoff training. This cross-sectional survey study was guided by the Kern model for medical curriculum development. A 12-member Council of Emergency Medicine Residency Directors (CORD) Transitions in Care task force of EM physicians performed these steps and constructed a survey. The survey was distributed to the CORD listserv. There were 147 responses to the anonymous survey, which were collected using an online tool. At least 41% of the 158 American College of Graduate Medical Education EM residency programs were represented. More than half (56.6%) of responding EM physicians reported that their ED did not use a standardized handoff. There also exists a dearth of formal handoff training and handoff proficiency assessments for EM residents.


Clinical Pediatrics | 2010

A Dispensing Error Resulting in Possible Fluoxetine Overdose and Subsequent Discontinuation Syndrome in a Child

Larissa I. Velez; Sing Yi Feng; Michael F. Neerman

A 48-year-old man with a history of hypertension and medication noncompliance presented to the emergency department, complaining of a generalized pruritic rash for 2 weeks that began at both ankles and spread to his knees, back, and arms. He observed polydipsia but denied other medical problem or rashes, allergens, travel, infectious agents, medications, fever, or dysuria. On physical examination, he had a symmetric erythematous papular rash with firm centers that were creamy white but not pustular. No scaling or crust was present and there was sparing of the face, palms, and soles. The greatest concentration of lesions was on the extensor surfaces of the knees (Figures 1 and 2). A point-of-care glucose level was greater than 500 mg/dL. A laboratory test provided the diagnosis. Figure 1. The patient’s right knee. Figure 2. A close-up image of the patient’s left knee.

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Greene Shepherd

Georgia Regents University

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Fernando L. Benitez

University of Texas Southwestern Medical Center

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Wilfredo Rivera

University of Texas Southwestern Medical Center

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Amy Young

University of Texas Southwestern Medical Center

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B. Burns

University of Oklahoma

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Barry J. Knapp

Eastern Virginia Medical School

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Brett Roth

University of Texas Southwestern Medical Center

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Daniel C. Keyes

American Association of Poison Control Centers

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