Antidote.
\\n\\n
Released this past November, the list is based on data collected from the Web of Science and highlights some of the world’s most influential scientific minds by naming the researchers whose publications over the previous decade have included a high number of Highly Cited Papers placing them among the top 1% most-cited.
\\n\\nWe wish to congratulate all of the researchers named and especially our authors on this amazing accomplishment! We are happy and proud to share in their success!
\\n"}]',published:!0,mainMedia:null},components:[{type:"htmlEditorComponent",content:'IntechOpen is proud to announce that 179 of our authors have made the Clarivate™ Highly Cited Researchers List for 2020, ranking them among the top 1% most-cited.
\n\nThroughout the years, the list has named a total of 252 IntechOpen authors as Highly Cited. Of those researchers, 69 have been featured on the list multiple times.
\n\n\n\nReleased this past November, the list is based on data collected from the Web of Science and highlights some of the world’s most influential scientific minds by naming the researchers whose publications over the previous decade have included a high number of Highly Cited Papers placing them among the top 1% most-cited.
\n\nWe wish to congratulate all of the researchers named and especially our authors on this amazing accomplishment! We are happy and proud to share in their success!
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This was paralleled by a dramatic decline in the morbidity and mortality of patients with MG secondary to evolving interventions in critical care and medical management. The advance in understanding the pathogenesis of MG resulted in the confirmation of the benefit of already used therapeutic interventions, a new US Food and Drug Administration-approved medication for MG including refractory MG and the development of several exciting new prospective drugs in the pipeline, which are in different stages of clinical trial testing. In this work, we reviewed the anatomy and physiology of neuromuscular junction as well as recent advances in the epidemiology, genetics, and pathogenesis of neuromuscular transmission dysfunction in MG. We also outlined the most important advancements in the diagnosis and management of MG and discuss new treatments in the pipeline. In addition, we included a separate chapter covering recent advances in the pathogenesis, diagnostic and treatment of pediatric MG.
\r\n\r\n\tOverall, this book intends to provide the reader with up-to-date information and a comprehensive overview of immunological mechanisms, diagnosis, and management of MG including pediatric MG.
",isbn:"978-1-83968-090-8",printIsbn:"978-1-83968-089-2",pdfIsbn:"978-1-83968-091-5",doi:null,price:0,priceEur:0,priceUsd:0,slug:null,numberOfPages:0,isOpenForSubmission:!0,hash:"db6c84e3aa58f3873e1298add7042c44",bookSignature:"Dr. Nizar Souayah",publishedDate:null,coverURL:"https://cdn.intechopen.com/books/images_new/9608.jpg",keywords:"Neuromuscular Junction, Acetylcholine Receptors, Incidence and Prevalence, Hla Alleles, Immune Pathogenesis, Postsynaptic Junction Dysfunction, Ocular Myasthenia, Generalized Myasthenia, Congenital Myasthenic Syndromes, Autoimmunity, Thymectomy, Immunosuppressive Medications",numberOfDownloads:null,numberOfWosCitations:0,numberOfCrossrefCitations:null,numberOfDimensionsCitations:null,numberOfTotalCitations:null,isAvailableForWebshopOrdering:!0,dateEndFirstStepPublish:"October 8th 2020",dateEndSecondStepPublish:"November 23rd 2020",dateEndThirdStepPublish:"January 22nd 2021",dateEndFourthStepPublish:"April 12th 2021",dateEndFifthStepPublish:"June 11th 2021",remainingDaysToSecondStep:"2 months",secondStepPassed:!0,currentStepOfPublishingProcess:4,editedByType:null,kuFlag:!1,biosketch:"Dr. Nizar Souayah is a leading researcher in neuromuscular disorders, appointed head of the neuromuscular program at New Jersey Medical School, Fellow of AAN and AANEM. He is board-certified in Neurology, Psychiatry, and Neuromuscular Disorders from the American Board of Psychiatry and Neurology. He published more than 300 peer-reviewed manuscripts, abstracts, poster presentations, and books in the neurology and neuromuscular disorders field, including the Myasthenia Gravis field.",coeditorOneBiosketch:null,coeditorTwoBiosketch:null,coeditorThreeBiosketch:null,coeditorFourBiosketch:null,coeditorFiveBiosketch:null,editors:[{id:"162634",title:"Dr.",name:"Nizar",middleName:null,surname:"Souayah",slug:"nizar-souayah",fullName:"Nizar Souayah",profilePictureURL:"https://mts.intechopen.com/storage/users/162634/images/system/162634.jpg",biography:"Dr Nizar Souayah is a neuromuscular program director and a faculty member at the University of Medicine and Dentistry of New Jersey. He is board certified in Neurology, Psychiatry and Neuromuscular Disorders from the American Board of Psychiatry and Neurology. He is also board certified in Electrodiagnostic Medicine from the American Board of Electrodiagnotic Medicine. He is an active member of the American Academy of Neurology and a fellow of the American Association of Neuromuscular & Electrodiagnostic Medicine. \r\nDr Souayah published extensively in the field of Neurology. He published more than 180 peer reviewed manuscripts, abstracts, poster presentations and books in the neurology and neuromuscular disorders field, including the peripheral neuropathy field. He contributed to several national and international neuroscience meetings. He is also directing a basic sciences laboratory focusing on translational research in inflammatory and neurodegenerative disease.",institutionString:"New Jersey Medical School",position:null,outsideEditionCount:0,totalCites:0,totalAuthoredChapters:"0",totalChapterViews:"0",totalEditedBooks:"1",institution:null}],coeditorOne:null,coeditorTwo:null,coeditorThree:null,coeditorFour:null,coeditorFive:null,topics:[{id:"16",title:"Medicine",slug:"medicine"}],chapters:null,productType:{id:"1",title:"Edited Volume",chapterContentType:"chapter",authoredCaption:"Edited by"},personalPublishingAssistant:{id:"247041",firstName:"Dolores",lastName:"Kuzelj",middleName:null,title:"Ms.",imageUrl:"https://mts.intechopen.com/storage/users/247041/images/7108_n.jpg",email:"dolores@intechopen.com",biography:"As an Author Service Manager my responsibilities include monitoring and facilitating all publishing activities for authors and editors. From chapter submission and review, to approval and revision, copyediting and design, until final publication, I work closely with authors and editors to ensure a simple and easy publishing process. I maintain constant and effective communication with authors, editors and reviewers, which allows for a level of personal support that enables contributors to fully commit and concentrate on the chapters they are writing, editing, or reviewing. I assist authors in the preparation of their full chapter submissions and track important deadlines and ensure they are met. I help to coordinate internal processes such as linguistic review, and monitor the technical aspects of the process. As an ASM I am also involved in the acquisition of editors. Whether that be identifying an exceptional author and proposing an editorship collaboration, or contacting researchers who would like the opportunity to work with IntechOpen, I establish and help manage author and editor acquisition and contact."}},relatedBooks:[{type:"book",id:"3464",title:"Peripheral Neuropathy",subtitle:"A New Insight into the Mechanism, Evaluation and Management of a Complex Disorder",isOpenForSubmission:!1,hash:"a46a3bbcb08cef678b7d4d22c776968f",slug:"peripheral-neuropathy-a-new-insight-into-the-mechanism-evaluation-and-management-of-a-complex-disorder",bookSignature:"Nizar Souayah",coverURL:"https://cdn.intechopen.com/books/images_new/3464.jpg",editedByType:"Edited by",editors:[{id:"162634",title:"Dr.",name:"Nizar",surname:"Souayah",slug:"nizar-souayah",fullName:"Nizar Souayah"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"6550",title:"Cohort Studies in Health Sciences",subtitle:null,isOpenForSubmission:!1,hash:"01df5aba4fff1a84b37a2fdafa809660",slug:"cohort-studies-in-health-sciences",bookSignature:"R. 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Venkateswarlu",coverURL:"https://cdn.intechopen.com/books/images_new/371.jpg",editedByType:"Edited by",editors:[{id:"58592",title:"Dr.",name:"Arun",surname:"Shanker",slug:"arun-shanker",fullName:"Arun Shanker"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"878",title:"Phytochemicals",subtitle:"A Global Perspective of Their Role in Nutrition and Health",isOpenForSubmission:!1,hash:"ec77671f63975ef2d16192897deb6835",slug:"phytochemicals-a-global-perspective-of-their-role-in-nutrition-and-health",bookSignature:"Venketeshwer Rao",coverURL:"https://cdn.intechopen.com/books/images_new/878.jpg",editedByType:"Edited by",editors:[{id:"82663",title:"Dr.",name:"Venketeshwer",surname:"Rao",slug:"venketeshwer-rao",fullName:"Venketeshwer Rao"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}}]},chapter:{item:{type:"chapter",id:"62069",title:"Toxicology in Emergency Medicine",doi:"10.5772/intechopen.77011",slug:"toxicology-in-emergency-medicine",body:'\nPoisoning is a serious worldwide public health problem. Based on World Health Organization (WHO) data in 2012, almost 190,000 people died worldwide and number of deaths due to poisoning in 2008 exceeded the number of deaths due to motor vehicular crashes; also, poisoning death rate nearly tripled worldwide. Number of patients presenting to the emergency departments with overdose, had been increased both intentionally and accidentally. All the previous facts make Toxicology an important field in emergency medicine [1, 2].
\nManagement of intoxicated patients has a unique approach because of the challenge in diagnosis and treatment of overdose cases. This chapter is focusing on general approaches for intoxicated patients and initial management and on how the history and physical examinations could help physicians to have what drug have been abused as well as review the mechanism of action, physical finding and treatment of the most common drugs-causing toxicity in addition to the drugs with high mortality morbidity rates.
\nApproach for the poisoned patients in emergency includes: resuscitation, history, physical examination and management.
\nThe initial priorities for a poisoned patient presented emergency department are: securing the air-way and breathing and stabilizing the circulation. Inadequate ventilation may need intubation and mechanical ventilation. First-line treatment of hypotension is IV fluid bolus (10–20 mL/kg), if hypotension is not responding to fluid, it may be necessary to add specific antidote. If the patient presented with signs of opioid over dose (low Glasgow coma scale-GCS respiratory depression, meiosis), give him naloxone (0.1–2.0 mg I.V), check blood sugar and treat hypoglycaemia with 50% 50 mL dextrose [3].
\nHistory is very important and can be obtained from the patient, and in case the patient is comatose or cannot give his history, we may take collateral information from family, friends or medical records looking for past psychiatry illness, previous history of suicide or drugs abuse, chronic medication… History must include time, route of entry, quantity, intentional or accidental exposure, availability of drugs at home and if any member of the family has chronic diseases (hypertension, diabetic etc…), missing tablets or any empty pill bottles or other material was found around him [4].
\nPhysical examination of poisoned patients may give clues regarding the substance which has been abused and toxidromes. Physical examination includes: general appearance, mental status (agitated or confused), Skin (cyanosis, flashing, physical signs of intravenous drugs abuse (track marks), eyes: (pupil size reactivity lacrimation and nystagmus), odour (garlic, bitter almonds, glue, alcohol etc.…), Oropharynx hyper salivation or dryness, chest: breath sound, bronchorrhea, wheezing, heart rate, rhythm regularity), abdomen(bowel sound, tenderness, and rigidity), limbs(tremors and fasciculation), patient’s clothing (looking for any medications, illegal drugs) [3].
\nThe term toxidrome was coined in 1970 by Mofenson and Greensher. Toxidromes are group of abnormal physical examination and abnormal vital signs known to present with specific group of medications or substances. Most common toxidromes are Cholinergic, Anticholinergic, Sympathomimetic, opioids, and serotonin syndrome [4, 5].
\nPatients with cholinergic toxidrome present with wet manifestation. SLUDGE+3 killer B’s”or DUMBELLS are simple mnemonics for the common clinical symptoms.
\n“SLUDGE”: Salivation, Lacrimation, Urination, Defecation, GI cramping, Emesis + “Killer B’s”: Bronchorrhea, Bradycardia, and Bronchospasm.
\n“DUMBELLS”: Diarrhoea, Urination, Miosis (small pupils), Bradycardia, Emesis, Lacrimation, Lethargy, and Salivation.
\nMost common Causes: Organophosphate pesticides, Carbamates, Same type Mushrooms and Sarin (warfare agent) [4].
\nPatients with Anticholinergic toxidrome with dry manifestation, delirium, tachycardia, dry flushed skin, dilated pupils, clonus, elevated temperature, decreased bowl sounds, urinary retention. Simple mnemonics: “Hot as a Hare, Mad as a Hatter, Red as a Beet, Dry as a Bone, Blind as a Bat”.
\nMost common Causes: Antihistamines, antiparkinsonians, atropine, scopolamine, amantadine, antipsychotics, antidepressants, muscle relaxants and plants (Jimson weed) [4].
\nPatient present with CNS stimulation and psychomotor agitation, elevated blood pressure, tachycardia, dilated pupils, hyperthermia, diaphoresis and seizure in severe cases.
\nMost common causes: cocaine, amphetamine.
\nMost common clinical presentation of opioids toxidrome are: coma, respiratory depression and meiosis, hypotension, hypothermia, bradycardia and seizure may occur in propoxyphene overdose, but small pupils not always present may present with normal size pupils such in meperidine and, propoxyphene toxicities [4].
\nPatient present with altered mental status, hypertensive, and tachycardia, Myoclonus hyperreflexia, hyperthermia and increase muscles rigidity. Most common causes: SSRI interaction or overdose [4].
\nDecontamination of poisoned patient means remove the patient from the toxin and remove the toxin from patient, either outside patient’s body by gross washing or inside the body by gastrointestinal decontamination or enhance elimination.
\nPatient must be fully undressed and washed thoroughly with copious amount of water; all the clothing must be removed, and decontamination must be in isolated specific area. Gross decontamination used in chemical, biological and radiation exposure.
\nThere are multiple methods used for gastrointestinal decontamination including:
\nEmesis and gastric Lavage.
\nInduced vomiting by ipecac syrup and gastric lavage: those methods were used in the past and now rarely indicated because there is no evidence supporting them. They can decrease absorption and they may also increase the risk of complications. Syrup ipecac and gastric Lavage may be considered in conscious, alert patients with ingestion of potentially number of toxic drugs and present in a very short time after ingestion (<1 h). Contradictions includes: unprotected airway, Corrosive/hydrocarbon ingestion and unstable patient status (hypotensive-seizure) [6].
\nActivated charcoal is super-heating carbonaceous material. Activated charcoal works by reducing the absorption of substance in the gastrointestinal lumen but it is not effective in metal, alcohols, corrosive, and lithium. Most effective action can be achieved when activated charcoal is given within the first hour of ingestion. Contraindications: absent gut motility or perforation, caustic ingestion and unprotected airway (can be given through nasogastric tube if patient intubated).Complications: aspiration of activated charcoal led to pneumonitis, ARDS and other complications such as small bowel obstruction [7].
\nWhole-bowel irrigation is a mechanical cleansing of the whole gastrointestinal track reducing toxin absorption. The whole-bowel irrigation can be done by Polyethylene glycol solution. Indication includes: substance with a prolonged absorption phase like sustained released medication, potential toxin not absorbed by activated charcoal such—(metals, lithium) and Body packers or suffers. Adverse effects of whole bowel irrigation could be: vomiting, bloating and rectal irritation. Contradiction: absent bowel sound or perforation [8].
\nEnhanced elimination is a method used to increase the rate of toxic removal from the body so reducing the severity and duration of clinical intoxication.
\nEnhanced elimination methods are not routinely used in poisoned patients. The indications for Enhanced elimination include [4]:
Severe toxicity
Poor outcome despite supportive care/antidote
Slow endogenous rate of elimination
There are different techniques to enhance elimination:
\nMultiple dose activated charcoal (MDAC): it can be used in cases of carbamazepine, Phenobarbital, Dispone sever toxicities,
\nUrinary alkalinisation:
\nCan be used in cases of Salicylates Phenobarbitone.
\nExtracorporeal elimination (e.g. haemodialysis, hemofiltration, and haemoperfusion, plasmapheresis and exchange transfusion:
\nCan be used in cases of lithium, carbamazepine, salicylates, theophylline, and toxic.
\nAlcohols: ethylene glycol and methanol metformin.
\nAntidote is a substance that can prevent further poisoning from specific substances. The table below showing most common antidote used in emergency department (see Table 1) [4].
\nToxin | \nAntidote | \n
---|---|
Acetaminophen | \nN-acetylcysteine 150 mg/kg dextrose IV over 15–60 min then50 mg/kg NAC IV over 4 h. Then 100 mg/kg NAC IV over 16 h. | \n
Cholinergic (organophosphates, carbamates) | \nAtropine 1–2 mg every 2–3 mins, until there is drying of secretions Pralidoxime (2-PAM) 70 mg/kg IV then infusion at 500 mg/h | \n
Anticholinesterases | \nPhysostigmine 0.5–1 mg IV as a slow push over 5 min and repeat every 10 min | \n
Benzodiazepines | \nFlumazenil 0.2 Mg repeated max dose 2 mg | \n
β-Blockers | \nGlucagon 3–10 mg | \n
Calcium channel blockers | \nCalcium gluconate 10% 10–30 mL IV | \n
Cyanide | \nAmyl nitrite Sodium thiosulfate Sodium nitrite (3% solution) Vitamin B12 | \n
Digoxin | \nDigoxin Fab 5–10 vials | \n
Isoniazid | \nPyridoxine (vitamin B6) 70 mg/kg IV (maximum 5 gm) | \n
Methanol, ethylene glycol | \nEthanol Loading 8 mL/kg of 10% ethanol then 1–2 mL/kg/h of 10% ethanol Fomepizole Loading: 15 mg/kg in 100 mL IV over 30 min Maintenance: 10 mg/kg IV over 30 min every 12 h for 48 h | \n
Narcotics | \nNaloxone 0.1–0.4 mg, may repeated | \n
Tricyclic antidepressants | \nSodium bicarbonate 1–2 mEq/kg IV bolus followed by 2 mEq/kg per h IV infusion | \n
iron | \nDesferrioxamine IV infusion dose of 15 mg/kg/h | \n
methaemoglobinaemia | \nMethylene Blue 1–2 mg/kg (0.1–0.2 mL/kg of 1% solution) IV slowly over 5 min | \n
local anaesthetics | \nIntravenous lipid emulsion 1–1.5 mL/kg 20% IV bolus over 1 min Repeat bolus at 3–5 min Then Infuse 0.25 mL/kg/min | \n
Antidote.
First time acetaminophen had been clinically used was in 1950 and since that time acetaminophen become most common over-the-counter antipyretic and analgesic used in public. Acetaminophen is the most common cause of acute liver failure in the United States [9, 10].
\nAcetaminophen metabolized in the liver and converted to nontoxic metabolites via glucuronidation (40–67%) and sulfation (20–46%). In therapeutic doses of acetaminophen, the small amount of NAPQI formed which detoxified by conjugation with reduced glutathione (GSH). Glutathione is an important tripeptide which is reduced in a NADPH dependent reaction, and used to reduce oxidants (such as NAPQI).
\nIn large overdoses of APAP, the usual pharmacokinetic pathways are overwhelmed and saturation of the nontoxic pathways occurs. Endogenous glutathione is depleted and NAPQI cannot be detoxified. Leaving excess NAPQI to bind to intracellular proteins, cause cell death [11].
\nSymptoms are frequently nonspecific or absent in early Acetaminophen toxicity.
\nClinical presentation of Acetaminophen toxicity divided into four stages:
Stage I (first 24 h): Patients may present nausea, vomiting, malaise, anorexia, or may be asymptomatic. Also hypokalaemia and metabolic acidosis can be found in blood test.
-Stage II (Days 2–3): patients develop nausea, vomiting, right upper quadrant abdominal pain and laboratory evidence of hepatotoxicity. Aminotransferases (AST and ALT) elevate into thousands.
-Stage III (3–4 days) defined by maximum hepatotoxicity, Patients exhibit coma, encephalopathy, coagulopathy, renal failure, Jaundice, acute respiratory distress syndrome (ARDS), sepsis and cerebral oedema.
-Stage IV (7–8 d): recovery or deterioration to multi-organ failure and death [12, 13].
After initial support of airway, breathing and circulation, the clinician should consider gastrointestinal (GI) decontamination by activated charcoal. The cornerstone of acetaminophen overdose is N-acetylcysteine (NAC). NAC serves as a precursor to glutathione and may also directly reduce NAPQI. Clinical data suggest that if therapy is initiated within 8 h of ingestion, NAC is completely effective in preventing hepatotoxicity. Although NAC decreases in efficacy after 8 h, the drug has a benefit at all points in time, even for patients with fulminant hepatic failure.
\nN-acetylcysteine should only be given to patients with hepatotoxicity or risk of developing hepatotoxicity. The Rumack-Matthew nomogram is a tool for determining potential hepatotoxicity based on Acetaminophen level and time after ingestion. The nomogram is used to determine the risk for APAP hepatotoxicity for patients who present within 24 h of an acute ingestion. Risk determination of hepatotoxicity becomes more difficult when the nomogram is not applicable. Examples of such cases would be when the time of ingestion is unknown, when patients present more than 24 h after the ingestion and following ingestions that occur over many hours. In all of these cases NAC should be administered immediately. If aminotransferases (ALT, AST) are normal and APAP concentration is undetectable, the NAC may be discontinued. Otherwise, treatment with NAC should be continued.
\nN-acetylcysteine dose Oral 140 mg/kg loading dose 70 mg/kg q4 h × 17 doses or Intravenous 150 mg/kg loading dose 50 mg/kg over 4 h 100 mg/kg over 16 h [14, 15, 16] (Figures 1 and 2).
\nRumack-Matthew nomogram.
ECG changes in TCA toxicity.
Cyclic antidepressants were used to depression, but now their use has reduced greatly because of the presences of more safe agents. Cyclic antidepressants were most common antidepressants associated with overdose-related deaths in 2013 [17].
\nCA has multiple pharmacologic effects.
\nCyclic antidepressants are inhibiting postsynaptic histamine receptors, causing sedation, decrease level of conscious and coma.
\nAntimuscarinic effects are divided to central and peripheral. Inhibition central acetylcholine receptors cause agitation, delirium, confusion, hallucinations, slurred speech, ataxia and coma. Inhibition Peripheral acetylcholine receptors inhibition cause dilated pupils, tachycardia, hyperthermia, hypertension, dry skin, ileus, urinary retention, increased muscle tone and tremor [18].
\nThis effects cause sedation, orthostatic hypotension, tachycardia and pupillary constriction, but because of the antimuscarinic effects, this action usually offsets pupillary dilatation [18].
\nThis effect produces mydriasis, diaphoresis, tachycardia, early hypertension, myoclonus and hyperreflexia.
\nThis effect produces decreased conduction velocity, increases the duration of repolarization and depressed myocardial contractility which lead to heart blocks, bradycardia and widening of the QRS complex [19].
\nThis effect produces QT interval prolongation and rarely torsades de pointes can be seen [19].
\nSymptoms occur typically within 2 h of ingestion, which varies from mild antimuscarinic symptoms to severe cardio-toxicity. Patient may present with drowsiness, confusion, slurred speech, ataxia, sinus tachycardia, urinary retention, myoclonus and hyperreflexia. Serious toxicity is almost seen within 6 h of ingestion and patient present with: coma, cardiac conduction delays, supraventricular tachycardia, hypotension, respiratory depression, ventricular tachycardia and seizures [20, 21].
\n\n
Sinus tachycardia, most common
Right axis deviation of the terminal 40 milliseconds positive terminal R wave in lead aVR and a negative S wave in lead I)
Prolongation of QRS,(risk of seizures increases if the QRS complex is >100 milliseconds)
Prolongation QT, PR
Brugada pattern is seen 10–15%
Treatment starts with supportive management securing airway, bolus i.v fluid in case of hypotension, GI decontamination with activated charcoal within 1 h of ingestion.
\nAdd vasopressors if hypotensive refractory to IV normal saline. Cardiac conduction abnormalities, ventricular dysrhythmias, or hypotension refractory to IV fluid are indicated to start blood alkalization by Sodium bicarbonate Keep blood pH 7.50–7.55. Seizures, treat with Benzodiazepines if seizure refractory use Phenobarbital 10–15 mg/kg, The medication contraindication in CA toxicity are: Class I antiarrhythmic (lidocaine, phenytoin, and flecainide), Class III antiarrhythmic (amiodarone, sotalol), Β-blockers, Ca channel blockers, Physostigmine and Flumazenil [22, 23].
\nAspirin is the most common analgesic antiplatelet therapy used in cardiovascular and cerebrovascular disease. Aspirin is over-the-counter drugs and widespread used lead to accidental and intentional toxicity [24].
\nSalicylate Inhibit cyclooxygenase leads to decreased synthesis of prostaglandins; prostacyclin and thromboxane. It also leads to platelet dysfunction and gastric mucosal injury. Salicylate Stimulate the chemoreceptor trigger zone in the medulla which causes nausea and vomiting. Also activate respiratory centre of the medulla leading to hyperventilation and respiratory alkalosis. Uncoupling of oxidative and Inhibit the Krebs which lead to metabolic acidosis [25].
\nSalicylate toxicity divided to acute and chronic toxicities.
\nAcute salicylate toxicity manifests initially through GI, CNS effects and metabolic effects. Gastric irritation, vomiting and nausea may predominate early in the course and are more predominant in the acute poisoning. Rising CNS salicylate concentrations produce tinnitus, diminished auditory acuity, vertigo and hyperventilation. As the poisoning continues, the CNS effects may progress to agitation, hallucinations, delirium, seizure and lethargy. The metabolic effects of salicylate toxicity cause uncoupling of oxidative phosphorylation leading to temperature elevation (an indicator of severe toxicity) and a large anion gap metabolic acidosis. Subsequent squeal of salicylate toxicity include renal failure, acute lung injury and platelet dysfunction.
\nIn contrast, chronic poisoning occurs over a longer period of time, when patients ingest more drug than they can eliminate over a prolonged period. These patients tend to be older and the overdose is unintentional. The initial presenting signs and symptoms include those of acute toxicity although with slower onset and lesser severity. Chronic toxicity may easily be confused in the elderly for sepsis, ketoacidosis, delirium, dementia, CHF or respiratory failure. Diagnostic delay in the chronically poisoned patient has been shown to cause increased morbidity and mortality.
\nStabilization of the airway, breathing and circulation are the first steps in management. Intubation may increases the severity of the aspirin toxicity, so it is better to be avoided, but if intubation is necessary patients need appropriately high minute ventilation sitting. In case of volume depleted and acidosis, start treatment with I. V fluid. Gastrointestinal decontamination with Activated charcoal may help in early ingestion. Whole bowel irrigation (WBI) is useful in case of massive ingestions or sustained preparation or enteric-coated. Sever Salicylate toxicity treated with serum Alkalinisation by sodium bicarbonate with a aim of a serum pH of ~7.5.Patients may need haemodialysis and the indications for haemodialysis are clinical deterioration, severe acid-base disturbance, altered mental status, and acute lung injury, failure of serum and urine alkalinisation and renal failure [26, 27, 28].
\nOpioid abuse is a significant medical and social problem in the world. In the past 10 years, the number of abuses and deaths from opioid overdoses had been increased. Opioids are all substances related to opium. They have analgesic and sedative effects. Opiate is extracted from the poppy plants [29].
\nThere are three main opioid receptors: μ (mu), κ (kappa), and δ (delta), and Opioids have agonists effect on this receptors. Stimulation of opioids receptors will cause miosis, respiratory depression, cough suppression, euphoria and decreased GI motility.
\nClassic signs of opioid intoxication toxidrome, depressed mental status, decreased respiratory rate miosis, (constricted) pupils. Other finding includes: decreased bowel sounds orthostatic hypotension, urinary retention and localized urticaria. Normal pupil examination can be seen, meperidine diphenoxylate, propoxyphene toxicity and co-ingestion of other toxin such as sympathomimetic or anticholinergic.
\nSame opioids have specific clinical feature (Table 2) [30, 32]:
\nOpioids agent | \nSpecific clinical feature | \n
---|---|
Dextromethorphan | \nSerotonin toxicity; at high doses | \n
Loperamide | \nQRS and QT prolongation; Wide-complex tachycardia | \n
Meperidine | \nSeizure, normal pupils size Serotonin syndrome (in combination with other agents) | \n
Methadone | \nlong-acting; QT prolongation, Torsade de Pointes | \n
Oxycodone | \nQT interval prolongation | \n
Tramadol | \nSeizure | \n
Heroin | \nAcute lung injury | \n
Opioids with specific clinical feature.
Body packing: swallowing packets or containers of drug for the purposes of smuggling.
Body stuffing: swallowing of a smaller quantity of drug because of fear of arrest.
Secure Airway and maintain adequate oxygenation and ventilation by using bag-valve mask are the first important steps in treatment; serum glucose should be checked. After that administer naloxone 0.4 mg IV, in non-opioid-dependent with minimal respiratory depression abut if patient is opioid-dependent present with minimal respiratory depression, administer small dose of naloxone, 0.1 mg IV, because larger doses can induce opioid withdrawal symptoms. Patients presenting with apnea or near-apnea and cyanosis, start naloxone, 2 mg IV regardless of drug use history, can be repeated IV every 3 min [30, 31, 32].
\nCocaine is one of the most potent Sympathomimetic, extracted from the leaves of the coca by indigenous to South America; therapeutically, first time Cocaine was used in 1884 as a local anaesthetic for ophthalmologic procedures. In the United States Cocaine is one of the most common causes of acute drug-related emergency department visits.
\nCocaine stimulates alpha and adrenergic receptors by increasing levels of norepinephrine, causing vasoconstriction in cardiovascular system, also inhibits neuronal serotonin reuptake which lead to euphoria. Cocaine blocks Sodium (Na+) channel causing QRS interval prolongation [33, 34].
\nCocaine toxicity may cause sympathomimetic and vasoconstrictive effects on variety systems (cardiovascular, CNS …etc.).
\nCardiovascular: patients with cocaine toxicity present with high blood pressure and dysrhythmias include tachycardia, such as sinus tachycardia, SVT, and AF. ECG changes include rightward shift of the terminal portion of the QRS complex and prolongation the QT interval. Patients may present with acute coronary syndromes (cocaine-associated acute coronary syndrome), aortic and coronary artery dissection, myocarditis and cardiomyopathy. CNS: patients with Cocaine present with a variety CNS clinical features including: agitation, seizures, and coma. Pulmonary: mainly seen in patients who smoke crack cocaine includes pulmonary haemorrhage, barotrauma, pneumonitis and asthma.
\nGastrointestinal: Cocaine may cause intestinal ischemia, bowel necrosis and ischemic colitis, also increase risk for bleeding and ulcer perforation. Renal: acute kidney failure may occur because of rhabdomyolysis [35, 36, 37].
\nSecuring the airway and adequate breathing are initial steps in treatment. CNS manifestation (agitation, seizure) treated with sedation by Benzodiazepines, patient with Hyperthermia should be cooled rapidly, severe hypertension not responding to sedation can be treated with a sodium nitroprusside infusion or phentolamine; (avoid Β-ac blockers). Cocaine toxicity with acute coronary syndrome are treated with aspirin and nitroglycerin also may add calcium channel blockers, wide-complex tachycardia with cocaine toxicity treated with serum alkalinisation by sodium bicarbonate, make sure serum Ph do not exceed 7.55. Intravenous lipid emulsion can be used in severe cocaine toxicity, with refractory cardiovascular instability or refractory wide-complex tachycardia [37].
\nCardiac glycosides were used in treatment of heart failure since long time. Since 1785 glycosides found in plants like lily of the valley foxglove and oleander. Digoxin is most common digitalis drug used today for treatment of atrial fibrillation and congestive heart failure [38].
\nDigoxin inhibits Na + -K + -ATPase during repolarization which leading to increase in intracellular sodium and a decrease in intracellular potassium leading to increase in the intracellular concentration of calcium causing Positive inotropic, also increase automaticity and shorten the repolarization intervals of the atria and ventricles [39].
\nDigoxin toxicity divided to acute and chronic toxicities.
\nThe cause of acute toxicity is usually intentional or accidental ingestion, symptoms usually abrupt in onset, patients present with nausea, vomiting, non-specific abdominal pain, headache and dizziness. Sever toxicity may cause confusion and coma, Bradydysrhythmia and atrioventricular block or supraventricular tachydysrhythmia and hyperkalaemia. Xanthopsia is a classic eye future in digoxin toxicity (viewing yellow-green halos around objects), but the most common finding is nonspecific changes in their colour vision. Serum digoxin level usually marked elevated [40, 41].
\nChronic toxicity is commonly and mainly seen in elderly patients and common causes are interaction with other medications (calcium channel antagonists, amiodarone, β-receptor antagonists, and diuretics) or renal insufficiency which causes decree the clearance of digoxin.
\nIn contract of acute toxicity, where Gastrointestinal symptoms are prominent in chronic toxicity CNS symptoms (weakness, fatigue, confusion, or delirium) are more prominent. Ventricular dysrhythmias are commonly seen in chronic toxicity. Serum potassium level can be normal or decreased, also serum digoxin level usually minimally elevated [40, 41].
\nGeneral supportive care is an Initial step in treatment of digoxin toxicity; it includes securing airway and adequate ventilation and boluses of fluid IV in case of hypotension. Activated charcoal helps in early acute ingestion [42], Atropine can be given in case of Symptomatic bradycardia). Digoxin-specific antibody fragments (digoxin-Fab) are antidotes for digoxin. The indication to use (digoxin- Fab) includes Life-threatening dysrhythmias unresponsive to standard therapy and hyperkalaemia excess 6 mEq/L. [43] Digoxin-Fab doses are based on the total-body load of digoxin, which can be calculated from either the estimated dose ingested or the serum digoxin level, each vial of Digoxin-Fab reverses approximately 0.5 mg of ingested digoxin. If the amount of ingested digitalis is unknown, digoxin Fab 10 vials for adults empirically can be given. Hyperkalaemia is treated with insulin, dextrose, sodium bicarbonate. The use of calcium salts in digoxin induced hyperkalaemia is controversial because old literature shows increase incidence of ventricular dysrhythmias and increase mortality [44].
\nBeta adrenergic antagonists (beta blockers) are groups of medications which have been used in treatment of different cardiovascular, neurological and ophthalmological diseases more than 30 years, Bête blockers toxicity has significant morbidity and mortality [17].
\nBeta receptors are divided by location and action to beta 1, beta 2, and beta 3 (see the Table 3).
\n\n | Location | \nAction | \nAntagonism | \n
---|---|---|---|
B1 | \nMyocardium Kidney Eye | \nIncreases inotropy Increases chronotropy Stimulates renin release | \nDecreases inotropy Decreases chronotropy Inhibits renin release | \n
B2 | \nBronchial smooth muscle Skeletal muscle Liver Vascular | \nbronchodilation Relaxes uterus Increases force of contraction Stimulates glycogenolysis and gluconeogenesis Vasodilation | \nCauses bronchospasm Inhibits glycogenolysis and gluconeogenesis Minimal vasoconstriction | \n
B3 | \nAdipose tissue Skeletal muscle | \nStimulates lipolysis Stimulates thermogenesis | \nInhibits lipolysis Inhibits thermogenesis | \n
Beta receptor: Locations and actions.
There are two groups of beta-blockers: selective and non-selective.
\nCompetitive antagonism of the beta receptor decreases cellular levels of cyclic adenosine monophosphate (cAMP). Beta-1 selective blocker causing in depressed myocardial contractility, decreased automaticity in pacemaker cells, and decreased conduction through the AV node. Non- selective beta blockade results in systemic effects including bronchoconstriction, impaired gluconeogenesis and decreased insulin release. Same Beta blockers (e.g., propranolol) have high lipid solubility leading to rapid cross of the blood brain barrier into the central nervous system, causing a neurological manifestation such as seizures and delirium [45, 47].
\nThe major system affected by β-blocker toxicity is the cardiovascular system; patients present with bradycardia and hypotensive. The cause of bradycardia is sinus node suppression or conduction abnormalities but ingestion of β-blockers with partial agonist activity may cause hypertension and tachycardia as early presentation. The β-blockers with sodium channel block affect may cause a wide-complex bradycardia.
\nSotalol causes potassium channels block leading to prolonging the QT interval.
\nΒ-Blockers also have effect on CNS and pulmonary system. Neurologic features include delirium, coma and seizures with more lipophilic. Β-blockers (propranolol) have more neurological manifestations. Bronchospasm and hypoglycaemia can be in β-blockers toxicity [47, 48].
\nGI decontamination can be done by giving Activated charcoal within 1 h of ingestion and air way is the main aim treatment in beta-blocker toxicity focusing on restore perfusion to critical organ systems by increasing cardiac output by: fluid resuscitation and glucagon (3–10 mg), vasopressor (e.g., epinephrine) and high dose Insulin- glucose (insulin 1 unit/kg IV bolus). Intravenous lipid emulsion therapy may be used in case of sever toxicity and refractory to treatment. In case of refractory to pharmacologic therapy, haemodialysis, haemoperfusion, cardiac pacing, placement of intra-aortic balloon pumps can be used. Wide QRS-interval dysrhythmias due to sodium channel blockade treated with sodium bicarbonate 2–3 mEq/kg over 1–2 min [49, 50].
\nCalcium channel blockers (CCBs) are mainly used in the treatment of cardiovascular diseases such as hypertension, coronary artery disseise- CAD and cardiac arrhythmias Calcium channel blockers one most prescribed cardiovascular drugs and can be immediate-release or extended-release [17].
\nThe calcium channel blockers (CCBs) can be divided into two major groups based upon their major physiologic effects: the dihydropyridines, group which mainly block the L-type calcium channels in the vasculature and the non-dihydropyridines, which selectively block L-type calcium channels in the myocardium such as verapamil. Dihydropyridine group toxicity causes arterial vasodilation and reflex tachycardia, whereas non-dihydropyridines toxicity cause peripheral vasodilation decreased cardiac inotropy, and bradycardia [46].
\nCardiovascular system is the most affected system in CCBs toxicity. Patient present with hypotension and bradycardia or reflex tachycardia. Verapamil or diltiazem toxicity usually patients present with sinus bradycardia, on the hand dihydropyridine overdoses cause peripheral vasodilatation causing reflex tachycardia [55]. CCBs have not primary effect on pulmonary and CNS System; CNS symptoms (seizures, delirium, and coma) occur secondary to decrease organ perfusion. Cardiogenic pulmonary oedema and acute lung injury (non-cardiogenic pulmonary oedema) have also been reported in severe toxicity [48].
\nFirst step in management is secure airway, stabilize ventilation and circulation.
\nDecontamination can be done by oral activated charcoal if patient present within 1 h of ingestion also the whole-bowel irrigation is useful in case of extended-release CCBs. Hypotension treated with IV fluid, Calcium chloride or calcium gluconate, glucagon (3–10 mg), if not responding start Vasopressors (e.g., norepinephrine). If symptoms refractory to vasopressor therapy start, high dose Insulin -glucose. If patient still not responding, lipid emulsion can be started. Finally, circulatory support measures, such as the placement of intra-aortic balloon pumps may be used in case of sever toxicity not responding to standard therapy [49, 50, 51].
\nCarbon monoxide (CO) is an odourless, tasteless, colourless and non-irritating gas.
\nPotential sources of Carbon monoxide (CO) are automotive exhaust, fuelled heaters, Wood- or coal-burning stoves, Structure fires and gasoline-powered generators other than fires.
\nThe incidence of co -poisoning increases during winter time because the use of space heaters, wood-burning stoves and charcoal burning for heat.
\nCarbon monoxide (CO) diffuses fast in the pulmonary capillary membrane and because of his rapid binding affinity (more than oxygen by 200 times), carbon monoxide bind to haemoglobin, that cause impaired releasing oxygen to tissue leading to shift the oxyhaemoglobin dissociation curve to the left [51].
\nCarbon monoxide poisoning have variable clinical picture depend on severity of exposure ranging from non-specific symptoms like headache, nausea and dizziness in mild to moderate cases to confusion, seizure and coma in severe cases patients may present with mild fever, tachycardia, tachypnoea and hypertension. Acute myocardial injury and life-threatening dysrhythmias are the most cardiovascular complications in case of severe Carbon monoxide poisoning. Delayed neuropsychiatric syndrome is long term neurological complication in severe cases characterized with different symptoms including cognitive deficiency, movement disorders and focal neurologic deficit. The standard pulse oximetry cannot differentiate carboxyhaemoglobin from oxyhaemoglobin, so it is unreliable in the diagnosis or screen carbon monoxide poisoning, so measuring carboxyhaemoglobin level in an arterial blood gas helps in diagnosis [52, 53, 54, 55].
\nAfter securing the airway, the most important step in treatment is oxygen 100% via non-rebreathing mask or intubation and mechanically ventilation with 100% oxygen if the patient is comatose and cannot secure his air way, half-life of carboxyhaemoglobin in room air 250–320 min while via non-rebreathing with 100% oxygen decreased to 90 min. Hyperbaric oxygen therapy could be considered in certain cases, the indication for Hyperbaric oxygen includes Pregnancy with carboxyhaemoglobin level > 15%, Carboxyhaemoglobin >25%, evidence of acute myocardial ischemia, and severe metabolic acidosis [56].
\nIron tablets are usually available in homes with small children and young women especially pregnant women. Because of its colour, sugar taste and appearance like a candy make iron tablet more attractive for accidental ingestion for children [57].
\nIron exerts a direct corrosive effect on the gastrointestinal tract at high plasma concentrations; it also possesses cytotoxic actions, particularly on the liver, leading to hepatocellular necrosis. Additionally, iron has a direct cardio- toxic effect acting as a negative inotrope and inhibits thrombin leading to a coagulopathy independent of hepatotoxicity. The direct corrosive effects and cellular toxicity contribute to metabolic acidosis [58].
\nSerious iron poisoning usually causes symptoms within 6 h of the overdose and if the ingested elemental iron more than 20 mg/kg body, the symptoms of iron poisoning typically occur in 5 stages:
Stage 1 (within 6 h after the overdose): Symptoms include vomiting, vomiting blood, diarrhoea, abdominal pain, irritability and drowsiness. If poisoning is very serious, rapid breathing, a rapid heart rate, coma, unconsciousness, seizures, and low blood pressure may develop.
Stage 2 (6–48 h after the overdose): condition can appear to improve (there is often a latent phase with minimal symptoms which may last up to 24 h and may be misinterpreted as an apparent recovery).
Stage 3 (12–48 h after the overdose): Very low blood pressure (shock), fever, bleeding, jaundice, liver failure, metabolic acidosis and seizures can develop.
Stage 4 (2–5 days after the overdose): The liver fails and people may die from shock, bleeding, and blood-clotting abnormalities. Sugar levels in the blood can decrease. Confusion and sluggishness (lethargy) or coma may develop.
Stage 5 (2–5 weeks after the overdose): The stomach or intestines can become blocked by scars [59, 60].
First step stabilize the air way, breathing and circulation. An abdominal x-ray may be helpful to confirm the presence of iron tablets. Consider GI decontamination by whole bowel irrigation if the patient is stable and has no contraindications, especially for large ingestions of modified release products, providing the airway can be protected. Activated charcoal does not bind iron. Asymptomatic patients need observation for 6 h and serum iron levels less than 300–350 mcg/dL may be discharged.
\nChelation therapy with deferoxamine is indicated for patients with serum iron levels >350 mcg/dL and have evidence of toxicity, or levels of >500 mcg/dL regardless of signs or symptoms. In patients with significant clinical manifestations of toxicity persistent emesis, metabolic acidosis, chelation therapy should not be delayed while one awaits serum iron levels. Haemodialysis does not remove iron effectively but should be considered on a supportive basis for acute renal failure as this will facilitate removal of the iron-deferoxamine complex [61, 62].
\nThe term toxic alcohol has generally referred to isopropanol, methanol, and ethylene glycol (EG). Poisoning involving toxic alcohols are relatively uncommon, but remain important causes of suicide or epidemic poisonings; Mortality and morbidity of toxic alcohols are high if prompt diagnosis and treatment are not initiated rapidly [63, 64].
\nMethanol also called methyl alcohol is found in paint removers or photocopying fluid, de-icing products and windshield wiper fluid. Methanol metabolism in the liver by alcohol dehydrogenase to formaldehyde. Aldehyde dehydrogenase then rapidly converts formaldehyde to formic acid with no appreciable accumulation of formaldehyde in the blood.
\nThe formic acid inhibits cytochrome c in the mitochondria, shifting the cell to anaerobic glycolysis, leading to lactic acid accumulation. The clinical features of methanol poisoning are the triad of severe anion gap metabolic acidosis, visual changes, and mental status depression. Other methanol intoxication symptoms include headache, light-headedness, nausea, vomiting, abdominal pain and dyspnoea. Methanol may produce pancreatitis by direct toxic effect on the pancreas.
\nEthylene glycol is found in radiator antifreeze, metal cleaners, and degreasing agents. It has no smell or colour and tastes sweet. Ethylene glycol is metabolized in the liver to glycolaldehyde by alcohol dehydrogenase. Glycolaldehyde is then converted to glycolic acid which is then converted to oxalic acid. Oxalic acid combines with serum calcium to form the classic calcium oxalate crystals found in the urine of patients who have consumed ethylene glycol.
\nEthylene glycol causes an elevated anion gap metabolic acidosis. The neurologic effects of ethylene glycol are coma, seizures, meningism, muscle spasms, and paralysis of the extraocular muscles. It can also affect the heart and lungs, causing tachycardia, hyperventilation, ARDS, and heart failure. Hypocalcaemia and resulting QT prolongation are due to serum calcium combining with oxalic acid. Lastly, kidney failure is due to these calcium crystals depositing into renal tubules.
\nIsopropyl alcohol is found in solvents and disinfectants. It is also found in mouthwashes, lotions, as well as rubbing alcohol and hand sanitizers. It is also hepatically metabolized by alcohol dehydrogenase to acetone. Isopropanol produces an increased osmole gap; however, it normally does not produce a metabolic acidosis unless concomitant hypotension causes lactic acidosis. It can cause haemorrhagic gastritis and profound inebriation with cerebellar signs and coma [64, 65, 66, 67, 68, 69, 70].
\nAn osmolar gap more than 10 mOsm/kg is suggestive of ethylene glycol, methanol, isopropanol, ethylene oxide, or acetone toxicity. A high anion gap metabolic acidosis may be revealed at later stages of methanol and ethylene glycol poisoning. Hypoglycaemia may be detected with isopropanol, while hyperglycaemia and hypocalcaemia may be detected in methanol and ethylene glycol poisonings, respectively. Hyperkalaemia due to acidosis is observed in methanol and ethylene glycol poisoning, whereas hypokalaemia due to vomiting may occur in ethanol intoxication.
\nUrine calcium oxalate crystals can be seen in ethylene glycol intoxication. These findings should be evaluated together with the other manifestations and observations [71, 72].
\nAny patient with serious poisoning may present in a critical condition. As with all poisoned patients, initial stabilization must be instituted before other possible treatments can be employed Initial evaluation should be focused on the improvement of vital signs: airway, respiration and circulation.
\nConsider toxic alcohol poisoning in a patient with an unexplained elevated anion gap metabolic acidosis and elevated osmolar gap.
\nFomepizole competitively inhibits alcohol dehydrogenase, which is involved in the metabolism of all alcohols, including ethanol. It is given to prevent the build-up of toxic metabolites from ethylene glycol (glycolic acid, glyoxylic acid, and oxalic acid) and methanol (formic acid) whose deposition in tissues can cause irreparable damage.
\nFomepizole is indicated for methanol or ethylene glycol ingestion resulting in a metabolic acidosis with an elevated osmolar gap and a serum Methanol or ethylene glycol level of at least 20 mg/dL.
\nHaemodialysis is indicated for toxic alcohol poisoning with an elevated osmolar gap and/or severe metabolic acidosis refractory to standard therapy, refractory hypotension, or end organ damage (i.e. acute renal failure. Vitamin Supplementation: Give folic or folinic acid to patients with methanol toxicity to divert metabolism away from formic acid to carbon dioxide and water. Give folic acid, pyridoxine, and thiamine to patients with EG toxicity to divert metabolism to nontoxic metabolites [73, 74, 75, 76].
\nOrganophosphates (OP) are used in insecticides for domestic and agricultural use. They are also the main toxins in nerve gases like Sarin. OP pesticide self-poisoning is a major clinical and public-health problem across much of rural Asia [77].
\nThe most serious poisoning of OP occurs by ingestion; cutaneous absorption and inhalation of sprays rarely cause serious toxicity. OP is extremely toxic pesticides, which produce acetylcholine excess with muscarinic, nicotinic and CNS effects.
\nPatients present with degrees of cholinergic crisis, usually within 4 h of ingestion or exposure. Specific manifestations include: Muscarinic manifestations like bronchospasm, vomiting, pinpoint pupils, bradycardia and hypotension, excessive sweating, lacrimation, salivation, profuse diarrhoea and urination (Table 4).
\nDiarrhoea | \n
Urination | \n
Miosis | \n
Bronchospasm | \n
Emesis | \n
Lacrimation | \n
Salivation | \n
DUMBELS mnemonic for signs of cholinergic excess.
Over-stimulation of nicotinic receptors causes tachycardia, hypertension and sweating. Accumulation of acetylcholine at the neuromuscular junction causes initial stimulation followed by depolarization and paralysis. This appears first as fasciculations, cramps and muscle weakness. Central nervous system (CNS) effects include delirium, coma and seizures. Most deaths are due to respiratory failure. Toxicity from gradual, cumulative exposure may be much more subtle. These patients commonly exhibit vague confusion or other central nervous system complaints; mild visual disturbances; or chronic abdominal cramping, nausea, and diarrhoea. A unique effect of organophosphorus insecticides results from “aging,” the irreversible conformational change that occurs when the organophosphorus agent is bound to the cholinesterase enzyme for a prolonged time, causing clinical effects to persist for a prolonged time. On average, some aging for commercial organophosphorus agents will occur by 48 h but may take longer. The intermediate syndrome is distinct from OP in the following ways: start within 24–96 h after recovery from acute cholinergic crisis, cranial nerves INNERVATED muscle and proximal muscles weakness, and rapid clinical recovery over 4–18 days. Any patient with a clinically apparent cholinergic syndrome should be treated empirically without waiting for laboratory confirmation of decreased cholinesterase activity [78].
\nMedical management of OP pesticide poisoning demands close observation, timely institution of antidote in adequate doses and duration and good supportive. The Treating staff should wear protective clothing. The patient’s clothes should be removed and destroyed and the patient should be showered in a designated decontamination area.
\nTreatment includes: resuscitation of patients giving oxygen, a muscarinic antagonist (usually atropine), fluids and an acetylcholinesterase reactivator (an oxime that reactivates acetylcholinesterase by removal of the phosphate group).
\nRespiratory support is given as necessary. Patients must be carefully observed after stabilization for changes in atropine needs, worsening respiratory function because of intermediate syndrome, and recurrent cholinergic features occurring with fat-soluble OP [79].
\nPoisoned patient in emergency department have unique Approach because of difficulties in obtain history, poisoned patients need careful physical examination looking for toxidromes or sign of illegal drugs abuse. Intoxicated patient’s management started with resuscitation and stabilization of air way, breathing and circulation. Consider decontamination in early time post ingestion. Most of the patient need laboratory test includes full cell count and electrolytes and kidney functions, specific drug level. Paracetamol level must be send for every present with history intestinal over dose. Symptomatic treatment is cornerstone treatment for post intoxicated patient also antidotes need for specific substances in specific conditions. Finally physicians in emergency department need to call the local poisoning centre to help them in management.
\nAs more people settle in cities, the increased urbanization requires cities to become sustainable. Sustainable cities provide access to a wide range of basic services such as affordable and clean energy. Globally electricity consumption rates are increasing year on year. One way in which sustainability can be achieved is by providing an affordable range of technologies that enable the management and reduction of electricity consumption. By decreasing the demand for more electricity cities can avoid the construction of more power plants. This can be realized by adopting standards for a wider range technologies that address the reduction in electricity demand. Investment in technology, infrastructure, innovation, sustainable development and scientific research is paramount if this goal is to be achieved. Advanced tools such as information and communication technology (ICT) are able to assist the realization of sustainable cities by enabling urban dwellings to be transformed into smart homes and smart spaces. These technologies can contribute to the global efforts to provide urban citizens access to clean and affordable energy and also help the efforts to preserve the environment.
\nAs an assistive technology in smart cities, home automation is able to offer a high level of comfort, sophistication, data access, environmental controls, energy management and operational efficiency. Home automation provides an avenue for users to actively participate in accessing and controlling their environments. This is achieved by delivering to users tangible means of energy saving, perimeter security, data access and control of home appliances. As an energy management tool, home automation synchronizes the technology platform with practical benefits such as the ability to reduce home electric bills through control of home electrical loads. The capability is further enhanced by the provision of remote access and resource management. This is achievable if this user desirable features include access via a web application and mobile software application. Figure 1 indicates the typical elements of a home automation network. This represents the basic configuration encompassing sensors, actuators, controllable user loads, a main system controller and a remote user interface.
\nHome automation system elements.
Modern assistive technologies should offer users smart and innovative solutions. These solutions should rely on technology to make tasks easier to manage and complete [1, 2, 3]. The rapid improvement in electronic systems such as mobile phones and home appliances are not beneficial to everyone, especially average consumers in developing countries. Energy consumption can be determined through measuring energy usage. This is accomplished using energy meters employing electrical current sensors. In electrical terms, energy consumption is the measure of how much power is used by the load side of an electrical circuit. Consumers wish to enjoy the benefits offered by smart cities such as access to information, remote sensing and automation. Facilities such as home automation can offer users some of these benefits. Recent studies have found that when users have access to their home power usage statistics, they are more readily willing to act or intervene [4, 5]. The other problem that this intervention addresses is the integrated home automation systems with customized installation where the end users cannot make modifications for their own joy and comfort; mostly these systems are expensive and out of reach for average consumers. Inexpensive solutions are desired to address customer needs.
\nRecently there has been much progress made in the areas of home automation with focus on the Internet of Things (IoT) [6, 7, 8].
\nThere have been developments in solutions presented to address home automation. The embedded controller may be provided by a host of different families of microcontrollers such as affordable variants, which include the Atmel ATmega microcontrollers [9], the Arduino [10] or Raspberry Pi [11, 12]. The propriety-based microcontrollers offer a relatively more expensive solution, which is not open-source, nor user code reconfigurable.
\nThe communication channel has been one of the main foci. There have been solutions provided that incorporated the use of Bluetooth technology [13] as well as systems that used ZigBee communication [14]. Some of these include the use of Global System for Mobile communication or GSM network as the communication technology [15]. Such an application is presented in Figure 2.
\nMobile GSM-based home automation platform.
Another variation on the communication channel targets the use of an Ethernet based Internet solution [16]. Such a system is depicted in Figure 3.
\nAn Internet-Ethernet-based home automation platform.
The system designed for this low-cost implementation uses readily available off-the-shelf components. The control algorithm is housed in an Arduino microcontroller. It is based on an open-source electronic prototyping platform and designed for ease of use. Arduino provides both the hardware components through single-board microcontrollers and also offers a software interface through its Integrated Development Environment (IDE). It is a powerful and popular embedded control solution. This makes the platform affordable for the average home user.
\nThe solution provided here is indicated in Figure 4. A range of home appliances is interfaced with Arduino through its input/output terminals (I/O pins). The control and sensing actions are controlled from the microcontroller. The Arduino host the control architecture which includes the appliance database and the website server. Via the web server, users are able to access the web application on an Android device. User authentication provides added level of security allowing only authenticated users access to the system.
\nImplemented home automation system.
The program flowchart shown in Figure 5 depicts the decision-making capability inherent in the system solution. The user is prompted after system initialization to authenticate themselves. If the user is not previously registered in the system database, they will not be able to proceed to the next step. If authentication passes, the user enters the home interface page. From this page the user is able to make system requests for data access to enable the appliance monitoring function or request appliance control status change. This allows connected devices such as user loads to be switched ON or OFF. The status change is indicated here in real-time.
\nProgram flowchart.
A typical HTML document starts with a declaration defining the document type (see Figure 6), followed by the parent element of HTML document, the HTML tag. All HTML tags have an opening and a closing tag, tags are contained inside angle brackets <>. All visible contents of a web page are contained in the body tag between the opening <body> and closing </body> body tags. HTML documents are created using any text editing programs, mostly Notepad, Notepad++ and much more, and this document must be saved with a .htm or .html extensions. HTML document can be opened in any web browser, but each web browser responds differently to some HTML tags.
\nHTML document structure.
The example shown below is the HTML structure, the first line in the HTML document should be the document type declaration, <! Doctype html> defines the document type and this aids the browser to correctly display the web page.
\nThe HTML <html> tag is the root element of any HTML document, and it is the second line in the HTML document after the document type declaration. The HTML tag is closed last at the end of an HTML document. The head section in an HTML document is contained between the head opening tag <head> and the head closing tag </head>, the content of the head section is the style, title, and java scripts if any are used.
\nThe body section in an HTML document is contained between the body opening tag <body> and the body closing tag </tag>, the body section contains the visible or information that need be displayed in the web page.
\nAn HTML element is made up of an opening tag <tag_name>, content and a closing tag </tag_name>. If an HTML element does not contain any contain between the starting and end tag, it is called an empty element. The content portion of an HTML element can be another HTML element; in this case, the elements are said to be nested. All HTML documents are made of nested HTML elements, as shown below the HTML is an HTML element with opening tag <html> and closing tag </html>. The content of this element is another HTML element head which also has a starting <head> tag and a closing </head> tag. The head tag contains an element, the title tag with <title> and </title> starting and closing tags respectively. The title element contains content, Home Automation Control Panel. The HTML element also contains another element that is the body element that in turn contains an image tag. Thus the figure below is good representation HTML elements and nested elements.
\nThe style <style> tag is used to represent the information regarding the HTML document style. The specifications pertaining to how the web browser should display the HTML document is contained in this tag. In one HTML document, it is possible to have more than one style element.
\nThe style <style> element must be contained inside the head <head> section of the HTML document. If a “scope” attribute is specified in the style element, then that style setting will apply only to the parent and child elements that style [8].
\nHTML document style could also be defined in a style sheet external to the HTML document; in this case, a link tag should be used to reference the style sheet. In the example below, divBorder has defined a class with red style color. This means that any content contained within an element whose class is divBorder will have a red color.
\nFigure 5 below shows a microcontroller based home automation system. The user mobile application interacts with the microcontroller via the web server using the Internet protocol. The microcontroller receives commands from the user interface and performs the required tasks based on a controlling algorithm governing the controller. The controller reads devices status and updates this data into the server for the user mobile application. Also, refer to Figure 4 in the literature review for a typical Internet-based home automation system.
\nThe server handles the users and ensures secure communication between the user mobile application and the controlling unit. Once a user is identified, he will then be granted access to the controlling interface (web page).
\nThe advantages of using a microcontroller have reduced the size of circuitry, affordability, and increased flexibility. A microcontroller can be used as a substitute for other integrated circuits (IC’s). It can also be easily reprogrammed to modify its functionality. The Microcontroller that was used for this project is the Arduino MEGA 2560 R3.
\nThe Wattmeter graphic as shown in Figure 7, was created using the HTML platform and Java Script. The meter was designed to measure up to 30 kW of power. The green color represents the power consumption as below 10 kW. The yellow color on the gauge represents power consumption in the range above 10–20 kW. It is an indication that the user should become aware of high power consumption. The red color represents the range above 20 kW of power consumption. Here users are acutely aware that extremely high power consumption could cause severe outage. Users should immediately switch off all non-essential appliances or high power loads.
When the “Read Power” button is clicked, a “PowerControl()” function is called. The PowerControl function generates a random together with an HTTP “GET” request. The request buffer is made up of a “GET” method, “Power” command and a random number.
When the web server replies to the request, the “PowerControl ()” function reads the HTTP response and changes the reading the gauge with the one contained in the response from the server.
The random number is generated and attached to the request buffer every time the function is called to avoid caching of commands on the web browser.
The wattmeter user interface.
A range of home appliances can be controlled via this application. These appliances are interfaced to the application controller via relays. This functionality allows users full control over appliance ON/OFF status.
\nAppliance control as shown in Figure 8 below, this section of the user interface enables a person to turn ON/OFF appliances, in this case, a light bulb, a stove, a heater and a television. The system is designed in such a way that a picture representing the current state of the appliance is updated on the user interface.
When the Light “ON” button is clicked, the “BulbControlON()” function is called. This function generates a random number together with an HTTP “GET” request and sends it to the controller which is also the web server. The request buffer is made up of a “GET” method, “BulbON” command and a random number.
When web server replies to the request, the “BulbControlON()” function reads the HTTP response and changes the state picture of the bulb with the one contained in the response from the server.
When the Light “OFF” button is clicked, the “BulbControlOFF()” function is called. This function generates a random number together with an HTTP “GET” request. The request buffer is made up of a “GET” method, “BulbOFF” command and a random number.
When web server replies to the request, the “BulbControlOFF()” function reads the HTTP response and changes the state picture of the bulb with the one contained in the response from the server.
When the Stove “ON” button is clicked, the “StoveControlON()” function is called. This function generates a random number together with an HTTP “GET” request. The request buffer is made up of a “GET” method, “StoveON” command and a random number.
When web server replies to the request, the “StoveControlON()” function reads the HTTP response and changes the state picture of the stove with the one contained in the response from the server.
When the Stove “OFF” button is clicked, the “StoveControlOFF()” function is called. This function generates a random number together with an HTTP “GET” request. The request buffer is made up of a “GET” method, “StoveOFF” command and a random number.
When web server replies to the request, the “StoveControlOFF()” function reads the HTTP response and changes the state picture of the stove with the one contained in the response from the server.
When the Heater “ON” button is clicked, the “HeaterControlON()” function is called. This function generates a random number together with an HTTP “GET” request. The request buffer is made up of a “GET” method, “HeaterON” command and a random number.
When web server replies to the request, the “HeaterControlON()” function reads the HTTP response and changes the state picture of the heater with the one contained in the response from the server.
When the Heater “OFF” button is clicked, the “HeaterControlOFF()” function is called. This function generates a random number together with an HTTP “GET” request. The request buffer is made up of a “GET” method, “HeaterOFF” command and a random number.
When web server replies to the request, the “HeaterControlOFF()” function reads the HTTP response and changes the state picture of the heater with the one contained in the response from the server.
When the TV “ON” button is clicked, the “TvControlON()” function is called. This function generates a random number together with an HTTP “GET” request. The request buffer is made up of a “GET” method, “TvON” command and a random number.
When web server replies to the request, the “TvControlON()” function reads the HTTP response and changes the state picture of the tv with the one contained in the response from the server.
When the TV “OFF” button is clicked, the “TvControlOFF()” function is called. This function generates a random number together with an HTTP “GET” request. The request buffer is made up of a “GET” method, “TvOFF” command and a random number.
When web server replies to the request, the “TvControlOFF()” function reads the HTTP response and changes the state picture of the tv with the one contained in the response from the server.
Home appliance control panel.
This section of the user interface as shown in Figure 9 presents the user with means to adjust the position of a camera as well as adjust the brightness of a light. The adjustment is accomplished through two position sliders.
\nSecurity camera position and exterior light brightness control panel.
The camera position slider ranges from 0 to 100 with 0 representing the leftmost position of the camera or 0° position and 100 representing the rightmost position of the camera or 100° position. These positions represent the wide range of movement possible for the camera viewing postion. A camera placed on a flat wall would have 180° viewing angle. Similarly a camera placed in a corner position would either have a 90 or 270° viewing angle. See Figure 10 for illustration of camera position and possible viewing angles.
\nCamera position and possible viewing angles.
The light brightness position slider ranges from 0 to 100% with 0% representing the light OFF and 100% representing the light ON or bright.
\nWhen the camera position or light brightness slider thumb is moved, the “PositionBright-nessControl (DeviceName, Value)” function is called. This function generates a random number together with an HTTP “GET” request. The request buffer is made up of a “GET” method, “DeviceName” command, “Value” parameter containing the desired position or brightness depending on the DeviceName and finally a random number.
\nThis section of the user interface does not receive any response from the web server, it updates the current slider’s value as it changes on the inner HTML document.
\nThe intrusion detection section of the user interface as shown in Figure 11 consists of a “CheckEntrance” button, the entrance names and the entrance status fields.
\nSecurity camera position and exterior light brightness control panel.
When the “CheckEntrance” button is clicked, the “IntrusionDection()” function is called. This function generates a random number together with an HTTP “GET” request. The request buffer is made up of a “GET” method, “Intrusion” command and a random number.
\nWhen web server replies to the request, the “IntrusionDection()” function reads the HTTP response and changes every entrance status field with the current state of the entrance contained in the response from the server.
\nFinally, the complete user interface is a web page that can be accessed via a web browser or using the android web-enabled mobile application created using App Inventor. The android app will be discussed in the next section.
\nTo design the Android the web interface, the open-source Android application, APP Inventor, is used to create a simple android application that browses to a web user interface.
\nThis App presents the user with an input field where the user can enter the IP address or domain of the web interface server of the home automation system controller. There is also a clickable button labeled “Click Here.” Once this button is clicked, the app requests the web interface from the server.
\nThe app was designed using the layout components, that is the vertical components who’s width was set to fit the parent (fit the screen).
\nText elements from the user interface were used as text input field to enter the desired web server IP address. The name describing the designer and the app itself were designed using the label component also from the user interface section.
\nThe user clickable button component also found in the user interface section was used, its background color, size, and text were changed in the component editing section.
\nThe web component responsible for loading the web page is found under activity starter section and it is an invisible component, meaning it is not seen in the designer phase of the app.
\nOnce satisfied with the design and user interface of the app as shown in Figure 12, it is now time to move to the block section where blocks representing component’s functionalities are grouped to create the desired function.
\nDesigner blocks for Android app.
The user must enter the IP address assigned to the system to be controlled or its domain name, then the user must press the “CLICK HERE” button. As shown in Figure 7 below, in this case, once the “CLICK HERE” button is clicked, an activity starter blocks are called.
\nFirst the “set ActivityStarter1.DataUri to” block is called and to it is attached the “TextBox1.Text.”
\nSecondly the “set ActivityStarter1.Action to” block is called and to it is attached the “Text.”
\nFinally the “call ActivityStarter1.StartActivity” block is called and the App will load the web page specified in the text field if it exists and the phone has Internet connectivity, else the app will return an error.
\nThe Android mobile user interface landing page for user authentication is shown in Figure 13. User authentication is applied to all users of the web app. The web server checks the credentials entered by the user and compares them with the information on its database, if the username and the associated password correspond to the ones in the database then access is granted to the user, else the user is requested to try again. When a user clicks a certain button, or requests that the status of a certain device is change, a corresponding function is called which generates a specific request buffer to send to the server. The server interprets the request buffer and controls the devices accordingly while updating the web client on the current state on the devices.
\nAndroid application interface panel.
After successful user authentication, the user is directed to the home automation control interface. The fully completed and integrated user web interface monitoring and control panel is depicted in Figure 14. This interface houses all the various elements that encompass the total controller capability.
\nComplete user interface and control application.
Home automation represents a big shift in user data access and system control. As an assistive technology for smart cities, it allows users the autonomy and flexibility to interact with their immediate environment. The solution presented, required the use of the ubiquitous and low cost Arduino microcontroller. This unit is a powerful and versatile embedded platform with which to structure an intervention as described here. The implementation provided here showcases a low-cost solution for home automation. It is an effective tool for all home inhabitants to exercise control and influence over their monthly electric bills. With the application of this affordable and functional user interface, a home can easily be transformed into a smart home. It is also a solution to transform any liveable space into a smart space by offering access to measured data and allowing users regulation of the electrical loads. This comprehensive home automation solution further provides lighting dimming control and access to perimeter security through features such as security camera control and intruder detection alerts.
\nAs an Open Access publisher, IntechOpen is dedicated to maintaining the highest ethical standards and principles in publishing. In addition, IntechOpen promotes the highest standards of integrity and ethical behavior in scientific research and peer-review. To maintain these principles IntechOpen has developed basic guidelines to facilitate the avoidance of Conflicts of Interest.
",metaTitle:"Conflicts of Interest Policy",metaDescription:"As an Open Access publisher, IntechOpen is dedicated to maintaining the highest ethical standards and principles in publishing. In addition, IntechOpen promotes the highest standards of integrity and ethical behavior in scientific research and peer-review.",metaKeywords:null,canonicalURL:"/page/conflicts-of-interest-policy",contentRaw:'[{"type":"htmlEditorComponent","content":"In each instance of a possible Conflict of Interest, IntechOpen aims to disclose the situation in as transparent a way as possible in order to allow readers to judge whether a particular potential Conflict of Interest has influenced the Work of any individual Author, Editor, or Reviewer. IntechOpen takes all possible Conflicts of Interest into account during the review process and ensures maximum transparency in implementing its policies.
\\n\\nA Conflict of Interest is a situation in which a person's professional judgment may be influenced by a range of factors, including financial gain, material interest, or some other personal or professional interest. For IntechOpen as a publisher, it is essential that all possible Conflicts of Interest are avoided. Each contributor, whether an Author, Editor, or Reviewer, who suspects they may have a Conflict of Interest, is obliged to declare that concern in order to make the publisher and the readership aware of any potential influence on the work being undertaken.
\\n\\nA Conflict of Interest can be identified at different phases of the publishing process.
\\n\\nIntechOpen requires:
\\n\\nCONFLICT OF INTEREST - AUTHOR
\\n\\nAll Authors are obliged to declare every existing or potential Conflict of Interest, including financial or personal factors, as well as any relationship which could influence their scientific work. Authors must declare Conflicts of Interest at the time of manuscript submission, although they may exceptionally do so at any point during manuscript review. For jointly prepared manuscripts, the corresponding Author is obliged to declare potential Conflicts of Interest of any other Authors who have contributed to the manuscript.
\\n\\nCONFLICT OF INTEREST – ACADEMIC EDITOR
\\n\\nEditors can also have Conflicts of Interest. Editors are expected to maintain the highest standards of conduct, which are outlined in our Best Practice Guidelines (templates for Best Practice Guidelines). Among other obligations, it is essential that Editors make transparent declarations of any possible Conflicts of Interest that they might have.
\\n\\nAvoidance Measures for Academic Editors of Conflicts of Interest:
\\n\\nFor manuscripts submitted by the Academic Editor (or a scientific advisor), an appropriate person will be appointed to handle and evaluate the manuscript. The appointed handling Editor's identity will not be disclosed to the Author in order to maintain impartiality and anonymity of the review.
\\n\\nIf a manuscript is submitted by an Author who is a member of an Academic Editor's family or is personally or professionally related to the Academic Editor in any way, either as a friend, colleague, student or mentor, the work will be handled by a different Academic Editor who is not in any way connected to the Author.
\\n\\nCONFLICT OF INTEREST - REVIEWER
\\n\\nAll Reviewers are required to declare possible Conflicts of Interest at the beginning of the evaluation process. If a Reviewer feels he or she might have any material, financial or any other conflict of interest with regards to the manuscript being reviewed, he or she is required to declare such concern and, if necessary, request exclusion from any further involvement in the evaluation process. A Reviewer's potential Conflicts of Interest are declared in the review report and presented to the Academic Editor, who then assesses whether or not the declared potential or actual Conflicts of Interest had, or could be perceived to have had, any significant impact on the review itself.
\\n\\nEXAMPLES OF CONFLICTS OF INTEREST:
\\n\\nFINANCIAL AND MATERIAL
\\n\\nNON-FINANCIAL
\\n\\nAuthors are required to declare all potentially relevant non-financial, financial and material Conflicts of Interest that may have had an influence on their scientific work.
\\n\\nAcademic Editors and Reviewers are required to declare any non-financial, financial and material Conflicts of Interest that could influence their fair and balanced evaluation of manuscripts. If such conflict exists with regards to a submitted manuscript, Academic Editors and Reviewers should exclude themselves from handling it.
\\n\\nAll Authors, Academic Editors, and Reviewers are required to declare all possible financial and material Conflicts of Interest in the last five years, although it is advisable to declare less recent Conflicts of Interest as well.
\\n\\nEXAMPLES:
\\n\\nAuthors should declare if they were or they still are Academic Editors of the publications in which they wish to publish their work.
\\n\\nAuthors should declare if they are board members of an organization that could benefit financially or materially from the publication of their work.
\\n\\nAcademic Editors should declare if they were coauthors or they have worked on the research project with the Author who has submitted a manuscript.
\\n\\nAcademic Editors should declare if the Author of a submitted manuscript is affiliated with the same department, faculty, institute, or company as they are.
\\n\\nPolicy last updated: 2016-06-09
\\n"}]'},components:[{type:"htmlEditorComponent",content:"In each instance of a possible Conflict of Interest, IntechOpen aims to disclose the situation in as transparent a way as possible in order to allow readers to judge whether a particular potential Conflict of Interest has influenced the Work of any individual Author, Editor, or Reviewer. IntechOpen takes all possible Conflicts of Interest into account during the review process and ensures maximum transparency in implementing its policies.
\n\nA Conflict of Interest is a situation in which a person's professional judgment may be influenced by a range of factors, including financial gain, material interest, or some other personal or professional interest. For IntechOpen as a publisher, it is essential that all possible Conflicts of Interest are avoided. Each contributor, whether an Author, Editor, or Reviewer, who suspects they may have a Conflict of Interest, is obliged to declare that concern in order to make the publisher and the readership aware of any potential influence on the work being undertaken.
\n\nA Conflict of Interest can be identified at different phases of the publishing process.
\n\nIntechOpen requires:
\n\nCONFLICT OF INTEREST - AUTHOR
\n\nAll Authors are obliged to declare every existing or potential Conflict of Interest, including financial or personal factors, as well as any relationship which could influence their scientific work. Authors must declare Conflicts of Interest at the time of manuscript submission, although they may exceptionally do so at any point during manuscript review. For jointly prepared manuscripts, the corresponding Author is obliged to declare potential Conflicts of Interest of any other Authors who have contributed to the manuscript.
\n\nCONFLICT OF INTEREST – ACADEMIC EDITOR
\n\nEditors can also have Conflicts of Interest. Editors are expected to maintain the highest standards of conduct, which are outlined in our Best Practice Guidelines (templates for Best Practice Guidelines). Among other obligations, it is essential that Editors make transparent declarations of any possible Conflicts of Interest that they might have.
\n\nAvoidance Measures for Academic Editors of Conflicts of Interest:
\n\nFor manuscripts submitted by the Academic Editor (or a scientific advisor), an appropriate person will be appointed to handle and evaluate the manuscript. The appointed handling Editor's identity will not be disclosed to the Author in order to maintain impartiality and anonymity of the review.
\n\nIf a manuscript is submitted by an Author who is a member of an Academic Editor's family or is personally or professionally related to the Academic Editor in any way, either as a friend, colleague, student or mentor, the work will be handled by a different Academic Editor who is not in any way connected to the Author.
\n\nCONFLICT OF INTEREST - REVIEWER
\n\nAll Reviewers are required to declare possible Conflicts of Interest at the beginning of the evaluation process. If a Reviewer feels he or she might have any material, financial or any other conflict of interest with regards to the manuscript being reviewed, he or she is required to declare such concern and, if necessary, request exclusion from any further involvement in the evaluation process. A Reviewer's potential Conflicts of Interest are declared in the review report and presented to the Academic Editor, who then assesses whether or not the declared potential or actual Conflicts of Interest had, or could be perceived to have had, any significant impact on the review itself.
\n\nEXAMPLES OF CONFLICTS OF INTEREST:
\n\nFINANCIAL AND MATERIAL
\n\nNON-FINANCIAL
\n\nAuthors are required to declare all potentially relevant non-financial, financial and material Conflicts of Interest that may have had an influence on their scientific work.
\n\nAcademic Editors and Reviewers are required to declare any non-financial, financial and material Conflicts of Interest that could influence their fair and balanced evaluation of manuscripts. If such conflict exists with regards to a submitted manuscript, Academic Editors and Reviewers should exclude themselves from handling it.
\n\nAll Authors, Academic Editors, and Reviewers are required to declare all possible financial and material Conflicts of Interest in the last five years, although it is advisable to declare less recent Conflicts of Interest as well.
\n\nEXAMPLES:
\n\nAuthors should declare if they were or they still are Academic Editors of the publications in which they wish to publish their work.
\n\nAuthors should declare if they are board members of an organization that could benefit financially or materially from the publication of their work.
\n\nAcademic Editors should declare if they were coauthors or they have worked on the research project with the Author who has submitted a manuscript.
\n\nAcademic Editors should declare if the Author of a submitted manuscript is affiliated with the same department, faculty, institute, or company as they are.
\n\nPolicy last updated: 2016-06-09
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