Methamphetamine-Induced Keratitis Case Series.

ABSTRACT: Methamphetamine-induced keratitis is a recognized but not widely studied cause of corneal stromalysis and infections. These 2 cases describe the presentation and clinical course of keratitis in patients with preceding methamphetamine use.

Drugs of Abuse: Sympathomimetics.

Sympathomimetic drugs comprise a broad category of substances including both illicit and prescribed drugs that have deleterious effects when ingested or abused. The clinical syndromes that result from overstimulation of the sympathetic nervous system by reuptake inhibition of biogenic amines, such as norepinephrine and dopamine, carry significant morbidity. Recognition and awareness of the appropriate supportive measures are required to mitigate life-threatening complications of multiple organ systems. The sympathomimetic toxidrome is recognized by a constellation of symptoms including agitation, hyperthermia, tachycardia, and hypertension, and the primary treatment involves supportive care, including the liberal use of benzodiazepines.

Unilateral mydriasis following septoplasty with inferior turbinate reduction.

Nasal septoplasty and inferior turbinate reduction are common procedures performed in the treatment of nasal obstruction. These procedures are generally considered to be safe with minimal reported complications. Herein, we describe a case of a 43-year-old female who developed transient unilateral mydriasis following septoplasty with inferior turbinate reduction, likely due to the sympathomimetic agents used for vasoconstriction and mucosal decongestion.

Acute and chronic sympathomimetic effects of e-cigarette and tobacco cigarette smoking: role of nicotine and non-nicotine constituents.

Electronic cigarettes (ECs) and tobacco cigarettes (TCs) both release nicotine, a sympathomimetic drug. We hypothesized that baseline heart rate variability (HRV) and hemodynamics would be similar in chronic EC and TC smokers and that after acute EC use, changes in HRV and hemodynamics would be attributable to nicotine, not non-nicotine, constituents in EC aerosol. In 100 smokers, including 58 chronic EC users and 42 TC smokers, baseline HRV and hemodynamics [blood pressure (BP) and heart rate (HR)] were compared. To isolate the acute effects of nicotine vs. non-nicotine constituents in EC aerosol, we compared changes in HRV, BP, and HR in EC users after using an EC with nicotine (ECN), EC without nicotine (EC0), nicotine inhaler (NI), or sham vaping (control). Outcomes were also compared with TC smokers after smoking one TC. Baseline HRV and hemodynamics were not different in chronic EC users and TC smokers. In EC users, BP and HR, but not HRV outcomes, increased only after using the ECN, consistent with a nicotine effect on BP and HR. Similarly, in TC smokers, BP and HR but not HRV outcomes increased after smoking one TC. Despite a similar increase in nicotine, the hemodynamic increases were significantly greater after TC smokers smoked one TC compared with the increases after EC users used the ECN. In conclusion, chronic EC and TC smokers exhibit a similar pattern of baseline HRV. Acute increases in BP and HR in EC users are attributable to nicotine, not non-nicotine, constituents in EC aerosol. The greater acute pressor effects after TC compared with ECN may be attributable to non-nicotine, combusted constituents in TC smoke.NEW & NOTEWORTHY Chronic electronic cigarette (EC) users and tobacco cigarette (TC) smokers exhibit a similar level of sympathetic nerve activity as estimated by heart rate variability. Acute increases in blood pressure (BP) and heart rate in EC users are attribute to nicotine, not non-nicotine, constituents in EC aerosol. Acute TC smoking increased BP significantly more than acute EC use, despite similar increases in plasma nicotine, suggestive of additional adverse vascular effects attributable to combusted, non-nicotine constituents in TC smoke.

Safety of Intradermal/Subcutaneous Lidocaine With Epinephrine Use in Dermatologic Surgery.

BACKGROUND: Recently, the safety of lidocaine plus epinephrine use in outpatient surgery has come under scrutiny despite its long history of use in outpatient dermatologic procedures and surgeries. OBJECTIVE: To assess the frequency of crash cart and other emergency interventions during Mohs micrographic surgery when lidocaine plus epinephrine is used as a local anesthetic and evaluate patient comorbidities associated with these events. MATERIALS AND METHODS: A retrospective chart review was conducted in an outpatient Mohs micrographic surgery clinic. RESULTS: One thousand one hundred twenty-seven Mohs cases were reviewed from the period of March 2015 to June 2016 with 864 meeting the inclusion criteria of patient weight, medical history, and amount of lidocaine administered recorded. No adverse events requiring emergency intervention with a crash cart or transfer to the emergency department occurred despite a patient population with advanced age and a wide range of comorbidities. CONCLUSION: No serious adverse events requiring emergency intervention were associated with lidocaine with epinephrine doses administered below the Food and Drug Administration recommended maximum. The authors did not find evidence from this study or after a literature search to support the requirement for a crash cart and other emergency equipment to be present during procedures.

Ephedrine-Induced Increases in Blood Pressure and Heart Rate Due to Suspected Cardiac Sympathetic Denervation Supersensitivity in a Patient with Parkinson's Disease Under Spinal Anesthesia.

BACKGROUND Denervation supersensitivity to sympathomimetic drugs has been noted in patients with Parkinson's disease (PD) whose cardiac sympathetic nerves are denervated. This phenomenon is not as well recognized as other complications of PD patients, but anesthesiologists should be aware of it because sympathomimetic drugs can sometimes be dangerous to these patients. CASE REPORT A 60-year-old woman was scheduled for total hip joint replacement under combined spinal-epidural anesthesia and sedation. She had been diagnosed as PD (stage 4 on the Hoehn and Yahr scale) with a history of orthostatic hypotension. Her ¹²³I-metaiodobenzylguanidine (MIBG) scintigraphy revealed marked reduction of ¹²³I-MIBG accumulation in the heart. In the operating room, we placed an epidural catheter through the Th12-L1 space, and spinal anesthesia (2.6 mL of 0.5% normobaric bupivacaine) was administered. During the surgery, we infused propofol at 100 mg·hr⁻¹ for sedation. When 4 mg of ephedrine was administered intravenously because of marked decrease in patient's blood pressure, we observed unexpectedly large increases in the systolic blood pressure, from 78 mmHg to 168 mmHg, and the heart rate increased from 52 to 84 beats per minute (bpm). This phenomenon recurred each time 4 mg of ephedrine was administered. CONCLUSIONS We report a case in which ephedrine induced unexpectedly large increases in blood pressure and heart rate in a patient who suffered from PD with severe cardiac sympathetic nerve denervation. We speculate that this phenomenon was caused by denervation supersensitivity of the patient's heart.

Adrenaline can restart the heart, but is no good for the brain.

The studyA randomised trial of epinephrine in out-of-hospital cardiac arrestPerkins GD, Ji C, Deakin CD, Quinn T, Nolan JP, Scomparin C, Regan S, Long J, Slowther A, Pocock H, Black JJM, Moore F, Fothergill RT, Rees N, O'Shea L, Docherty M, Gunson I, Han K, Charlton K, Finn J, Petrou S, Stallard N, Gates S, Lall R for the PARAMEDIC2 CollaboratorsPublished on 18 July 2018 N Engl J Med 2018;379:711-21.This project was funded by the National Institute for Health Research HTA Programme (project number 12/127/126).To read the full NIHR Signal, go to: https://discover.dc.nihr.ac.uk/content/signal-000639/adrenaline-can-restart-the-heart-but-is-no-good-for-the-brain.

The sympathomimetic agonist mirabegron did not lower JAK2-V617F allele burden, but restored nestin-positive cells and reduced reticulin fibrosis in patients with myeloproliferative neoplasms: results of phase II study SAKK 33/14.

The ß-3 sympathomimetic agonist BRL37344 restored nestin-positive cells within the stem cell niche, and thereby normalized blood counts and improved myelofibrosis in a mouse model of JAK2-V617F-positive myeloproliferative neoplasms. We therefore tested the effectiveness of mirabegron, a ß-3 sympathomimetic agonist, in a phase II trial including 39 JAK2-V617F-positive patients with myeloproliferative neoplasms and a mutant allele burden more than 20%. Treatment consisted of mirabegron 50 mg daily for 24 weeks. The primary end point was reduction of JAK2-V617F allele burden of 50% or over, but this was not reached in any of the patients. One patient achieved a 25% reduction in JAK2-V617F allele burden by 24 weeks. A small subgroup of patients showed hematologic improvement. As a side study, bone marrow biopsies were evaluated in 20 patients. We found an increase in the nestin+ cells from a median of 1.09 (interquartile range 0.38-3.27)/mm2 to 3.95 (interquartile range 1.98-8.79)/mm2 (P<0.0001) and a slight decrease of reticulin fibrosis from a median grade of 1.0 (interquartile range 0-3) to 0.5 (interquartile range 0-2) (P=0.01) between start and end of mirabegron treatment. Despite the fact that the primary end point of reducing JAK2-V617F allele burden was not reached, the observed effects on nestin+ mesenchymal stem cells and reticulin fibrosis is encouraging, and shows that mirabegron can modify the microenvironment where the JAK2-mutant stem cells are maintained. (Registered at clinicaltrials.gov identifier: 02311569).

Myocardial hypertrophy associated with long-term phenylpropanolamine use in a dog.

CASE DESCRIPTION A 9-year-old spayed female Dalmatian was examined because of progressive pelvic limb paraparesis. CLINICAL FINDINGS The dog had a history of chronic urinary incontinence and had been treated with phenylpropanolamine (PPA) for almost 8.5 years. Intervertebral disk disease at T12-13 was diagnosed, and a hemilaminectomy was performed. Three days after surgery, the dog developed a ventricular tachyarrhythmia. Severe left and mild right ventricular hypertrophy were detected by echocardiography. TREATMENT AND OUTCOME The arrhythmia was controlled with sotalol. Phenylpropanolamine administration was discontinued immediately before surgery and was not resumed. Heart rate and rhythm and blood pressure were within reference limits, and the ventricular hypertrophy had almost completely resolved 5 months later. Sotalol administration was discontinued. Shortly after the 5-month recheck evaluation, PPA administration was resumed, albeit at a lower dosage than that before surgery, for control of urinary incontinence. At the 10-month recheck evaluation, the dog was hypertensive and ventricular hypertrophy had recurred. Discontinuation of PPA administration was recommended but not heeded. The dog developed marked azotemia 1.5 years after surgery, which was managed by the referring veterinarian, and was subsequently lost to follow-up. CLINICAL RELEVANCE The fact that the ventricular hypertrophy almost completely resolved when PPA administration was discontinued and then recurred after it was resumed strongly suggested the drug was an important contributing factor to the cardiac disease of this patient. Patients receiving PPA on a long-term basis should be frequently monitored for cardiac disease, and use of other adrenergic receptor agonists should be avoided in such patients.

Sympathomimetic Toxidromes and Other Pharmacological Causes of Acute Hypertension.

PURPOSE OF REVIEW: Acute drug-induced hypertension, sympathomimetic toxicity, and other hyperadrenergic states can be caused by both xenobiotic toxicity and withdrawal. This manuscript is a selective review of the recent literature regarding pharmacologic causes of hypertensive emergencies and other hyperadrenergic states. RECENT FINDINGS: We will discuss designer stimulants, alpha2 and baclofen agonist withdrawal, and the clinical entity known as posterior reversible encephalopathy syndrome (PRES). Additionally, we examine the controversial "unopposed alpha" phenomenon which may result from use of beta-adrenergic antagonist in the presence of stimulant toxicity. These topics encompass clinical situations and disease entities that are increasingly encountered and are often either unanticipated or under-recognized.

Severe Sympathomimetic Toxidrome in a French Soldier: How Caffeine Overdose Can Lead to Severe Consequences.

We report the case of a French soldier, 29-yr-old, hospitalized in intensive care unit at Begin Military Hospital for the management of a sympathomimetic syndrome associated with severe metabolic disorders. Diagnosis of voluntary caffeine overdose was made. The evolution was favorable after metabolic disorders correction, without the need for dialysis. Caffeine is a molecule free of serious adverse effects when consumed at low doses. However, when consumed at high doses, it can become toxic and lead to death. Caffeine consumption has increased in recent years and especially in French Army. This toxicity remains unknown by a large part of population. We must be vigilant because this substance misuse can lead to serious consequences.

Sympathomimetic Effects of Acute E-Cigarette Use: Role of Nicotine and Non-Nicotine Constituents.

BACKGROUND: Chronic electronic (e) cigarette users have increased resting cardiac sympathetic nerve activity and increased susceptibility to oxidative stress. The purpose of the present study is to determine the role of nicotine versus non-nicotine constituents in e-cigarette emissions in causing these pathologies in otherwise healthy humans. METHODS AND RESULTS: Thirty-three healthy volunteers who were not current e-cigarette or tobacco cigarette smokers were studied. On different days, each participant used an e-cigarette with nicotine, an e-cigarette without nicotine, or a sham control. Cardiac sympathetic nerve activity was determined by heart rate variability, and susceptibility to oxidative stress was determined by plasma paraoxonase activity. Following exposure to the e-cigarette with nicotine, but not to the e-cigarette without nicotine or the sham control, there was a significant and marked shift in cardiac sympathovagal balance towards sympathetic predominance. The decrease in high-frequency component and the increases in the low-frequency component and the low-frequency to high-frequency ratio were significantly greater following exposure to the e-cigarette with nicotine compared with exposure to the e-cigarette without nicotine or to sham control. Oxidative stress, as estimated by plasma paraoxonase, did not increase following any of the 3 exposures. CONCLUSIONS: The acute sympathomimetic effect of e-cigarettes is attributable to the inhaled nicotine, not to non-nicotine constituents in e-cigarette aerosol, recapitulating the same heart rate variability pattern associated with increased cardiac risk in multiple populations with and without known cardiac disease. Evidence of oxidative stress, as estimated by plasma paraoxonase activity, was not uncovered following acute e-cigarette exposure.