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Featured researches published by Eike Blohm.


Clinical Toxicology | 2017

Resolution of cannabis hyperemesis syndrome with topical capsaicin in the emergency department: a case series

Laurel Dezieck; Zachary Hafez; Albert Conicella; Eike Blohm; Mark J. O’Connor; Evan S. Schwarz; Michael E. Mullins

Abstract Background: Cannabinoid hyperemesis syndrome (CHS) is characterized by symptoms of cyclic abdominal pain, nausea, and vomiting in the setting of prolonged cannabis use. The transient receptor potential vanilloid 1 (TRPV1) receptor may be involved in this syndrome. Topical capsaicin is a proposed treatment for CHS; it binds TRPV1 with high specificity, impairing substance P signaling in the area postrema and nucleus tractus solitarius via overstimulation of TRPV1. This may explain its apparent antiemetic effect in this syndrome. Purpose: We describe a series of thirteen cases of suspected cannabis hyperemesis syndrome treated with capsaicin in the emergency departments of two academic medical centers. Methods: A query of the electronic health record at both centers identified thirteen patients with documented daily cannabis use and symptoms consistent with CHS who were administered topical capsaicin cream for symptom management. Results: All 13 patients experienced symptom relief after administration of capsaicin cream. Conclusion: Topical capsaicin was associated with improvement in symptoms of CHS after other treatments failed.


Clinical Toxicology | 2017

Drug-induced hyperlactatemia

Eike Blohm; Jeffrey T. Lai; Mark J. Neavyn

Abstract Background: Hyperlactatemia is common in critically ill patients and has a variety of etiologies. Medication toxicity remains an uncommon cause that providers often fail to recognize. In this article, we review several medications that cause hyperlactatemia in either therapeutic or supratherapeutic dosing. When known, the incidence, mortality, pathophysiology, and treatment options are discussed. Methods: We performed a literature search using PUBMED and Google Scholar for English language articles published after 1980 regarding medication induced hyperlactatemia and its management. Our search string resulted in 798 articles of which 138 articles met inclusion criteria and were relevant to the topic of our review. Conclusions: Hyperlactatemia is a relatively rare but life-threatening toxicity of various medication classes. Discontinuation of the drug is always advised, and some toxicities are subject to specific antidotal treatment. If there is no apparent medical cause for hyperlactatemia (sepsis, hypotension, hypoxia), clinicians should consider a toxicological etiology.


Toxicology Communications | 2017

Canagliflozin-associated diabetic ketoacidosis: a case report

Peter R. Chai; Caitlin Bonney; Eike Blohm; Edward W. Boyer; Kavita M. Babu

ABSTRACT Canagliflozin is a novel sodium-glucose cotransporter-2 (SGLT-2) inhibitor approved for the management of diabetes. We report the presentation and management of two cases of canagliflozin associated diabetic ketoacidosis (DKA) and discuss the mechanism of canagliflozin associated DKA. Patient 1, a 55 year old woman maintained on canagliflozin for diabetes mellitus II presented to the emergency department (ED) with 24 hours of nausea and vomiting. She was diagnosed with DKA featuring hypotension, hyperglycemia, ketosis and acidosis. A second 54 year old man also maintained on canagliflozin for diabetes mellitus I presented to the ED with 24 hours of nausea and vomiting. He was diagnosed with DKA with similar manifestations as patient 1. Both patients underwent massive volume resuscitation and intravenous insulin therapy with resolution of ketosis and acidosis. By inhibiting SGLT-2, canagliflozin promotes glucosuria, which in turn can produce up to a 10% decrease in total plasma volume rendering patients maintained on canagliflozin susceptible to dehydration. Inhibition of SGLT-2 also leads to glucagon secretion, which in the volume deplete individual, can exacerbate DKA. Physicians should be aware of the rapid onset of DKA in patients maintained on canagliflozin after just minor additional fluid losses.


Clinical Toxicology | 2018

Cannabinoid hyperemesis syndrome and topical capsaicin: treating smoke with fire? – the authors reply

Zachary Hafez; Michael E. Mullins; Eike Blohm; Mark J. O’Connor; Laurel Dezieck; Evan S. Schwarz; Albert Conicella

We thank Wang and colleagues for their comments and interest reflected in their letter. First, they take issue with the study design. We again acknowledge the limitations inherent to a retrospective case series. We selected patients who received capsaicin because this use was new at both the hospitals. The objective of the retrospective case series was to describe and evaluate the effects of capsaicin on symptoms and disposition of patients with cannabinoid hyperemesis syndrome (CHS). We hope that our findings stimulate new hypotheses for more rigorous research. Our colleagues challenge the use of the SImonetto criteria for CHS [1], specifically, “the absence of major illness that could explain the symptoms.” This is only one of the five “supportive” criteria which Simonetto et al. proposed in the diagnosis of CHS (Table 1). Simonetto et al. [1] did not define a minimum number of major and supportive criteria necessary to diagnose CHS. They also did not suggest specific testing to exclude other diagnoses. This criterion simply refers to lack of alternative diagnosis based upon available clinical information. However, all the patients in our series consistently met most or all of the Simonetto criteria. The rapid improvement following capsaicin and lack of further need for anti-emetics in most of these cases would argue against the need for further diagnostic work up in the emergency department. They suggest that opioids may have explained the symptoms for some of our patients. However, most of the patients in the retrospective case series had immunoassay urine drug screens that were positive only for marijuana and not opiates. In addition, the lack of improvement after receiving opiates such as morphine and hydromorphone would suggest that opiate withdrawal was not the underlying problem. Opiate withdrawal also does not improve with hot showers, something all the patients admitted to helping with their symptoms. Lastly, they suggest that patients may have left due to the discomfort of topical capsaicin. We acknowledge this possibility. Some patients did decline further applications of topical capsaicin due to discomfort. However, all the patients reported symptomatic improvement, no patients left while vomiting, and no patients left against medical advice.


Clinical Practice and Cases in Emergency Medicine | 2017

Unsuspected Clenbuterol Toxicity in a Patient Using Intramuscular Testosterone

Matthew K. Griswold; Eike Blohm; Roderick Cross; Edward W. Boyer; Jennifer L. Carey

Clenbuterol is a beta-agonist that has been abused by fitness-oriented individuals for muscle growth and weight loss. We report a case of a 46-year-old man who presented tachycardic, hypokalemic, and hyperglycemic after injecting testosterone obtained from Brazil. He developed refractory hypotension and was started on an esmolol infusion for suspected beta-agonist toxicity. Laboratory analysis showed a detectable clenbuterol serum concentration. Analysis of an unopened ampule contained boldenone undecylenate, clenbuterol, and vitamin E. This case illustrates a novel exposure that caused beta-agonist toxicity and was treated successfully with rapid-onset beta blocker.


Current Emergency and Hospital Medicine Reports | 2015

Management of Status Asthmaticus

Ameer F. Ibrahim; Eike Blohm; Hannah Hammad

Status asthmaticus (SA) is a severe and life-threatening asthma exacerbation that requires aggressive treatment. First-line treatment entails continuous treatment of nebulized short-acting β-receptor agonists and intravenous (IV) steroid administration. This review article focuses on the current literature supporting the use of these medications as well as other treatment modalities such as inhaled anticholinergics, parenteral β-agonists, IV magnesium, and IV ketamine. We also explore the utility methylxanthines, volatile anesthetics, nitric oxide, antibiotics, IV fluids, and mucolytics in treating SA. Finally, we explore the data pertaining to the use of Heliox, non-invasive positive pressure ventilation, and bronchoscopy, and discuss ventilator management for patients with SA requiring intubation.


Journal of Medical Toxicology | 2014

Medical Marijuana and Driving: a Review

Mark J. Neavyn; Eike Blohm; Kavita M. Babu; Steven B. Bird


Side Effects of Drugs Annual | 1986

Opioid analgesics and narcotic antagonists

Peter R. Chai; Eike Blohm; Edward W. Boyer


Pediatric Emergency Care | 2017

Recognition and Management of Pediatric Salt Toxicity

Eike Blohm; Amy P. Goldberg; Ann Salerno; Carole Jenny; Edward W. Boyer; Kavita M. Babu


Ciottone's Disaster Medicine (Second Edition) | 2016

Chapter 183 – Bus Accident

Eike Blohm; Kavita M. Babu

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Kavita M. Babu

University of Massachusetts Medical School

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Edward W. Boyer

Brigham and Women's Hospital

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Albert Conicella

University of Massachusetts Medical School

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Evan S. Schwarz

Washington University in St. Louis

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Laurel Dezieck

University of Massachusetts Medical School

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Mark J. Neavyn

University of Massachusetts Medical School

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Mark J. O’Connor

University of Massachusetts Medical School

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Michael E. Mullins

Washington University in St. Louis

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Peter R. Chai

Brigham and Women's Hospital

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Zachary Hafez

Washington University in St. Louis

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