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<rdf:RDF xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns="http://purl.org/rss/1.0/"><channel rdf:about="http://www.medicinejournal.co.uk/?rss=yes"><title>Medicine</title><description>Medicine RSS feed: Current Issue.    
 Medicine  is a continually updated, evidence based review journal covering internal medicine and its subspecialties. 
 
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group of 35 Chapter editors and over 750 authors, all of whom are recognized experts in their field.   </description><link>http://www.medicinejournal.co.uk/?rss=yes</link><dc:publisher>Elsevier Inc.</dc:publisher><dc:language>en</dc:language><dc:rights> © 2011 Published by Elsevier Inc. All rights reserved. </dc:rights><prism:publicationName>Medicine</prism:publicationName><prism:issn>1357-3039</prism:issn><prism:volume>40</prism:volume><prism:number>2</prism:number><prism:publicationDate>February 2012</prism:publicationDate><prism:copyright> © 2011 Published by Elsevier Inc. All rights reserved. </prism:copyright><prism:rightsAgent>healthpermissions@elsevier.com</prism:rightsAgent><items><rdf:Seq><rdf:li rdf:resource="http://www.medicinejournal.co.uk/article/PIIS1357303911003574/abstract?rss=yes"/><rdf:li rdf:resource="http://www.medicinejournal.co.uk/article/PIIS1357303911003598/abstract?rss=yes"/><rdf:li rdf:resource="http://www.medicinejournal.co.uk/article/PIIS135730391100288X/abstract?rss=yes"/><rdf:li rdf:resource="http://www.medicinejournal.co.uk/article/PIIS1357303911003008/abstract?rss=yes"/><rdf:li rdf:resource="http://www.medicinejournal.co.uk/article/PIIS1357303911002908/abstract?rss=yes"/><rdf:li rdf:resource="http://www.medicinejournal.co.uk/article/PIIS1357303911003021/abstract?rss=yes"/><rdf:li rdf:resource="http://www.medicinejournal.co.uk/article/PIIS1357303911002891/abstract?rss=yes"/><rdf:li rdf:resource="http://www.medicinejournal.co.uk/article/PIIS1357303911002957/abstract?rss=yes"/><rdf:li rdf:resource="http://www.medicinejournal.co.uk/article/PIIS1357303911002970/abstract?rss=yes"/><rdf:li rdf:resource="http://www.medicinejournal.co.uk/article/PIIS1357303911003069/abstract?rss=yes"/><rdf:li rdf:resource="http://www.medicinejournal.co.uk/article/PIIS135730391100291X/abstract?rss=yes"/><rdf:li rdf:resource="http://www.medicinejournal.co.uk/article/PIIS1357303911003057/abstract?rss=yes"/><rdf:li rdf:resource="http://www.medicinejournal.co.uk/article/PIIS1357303911003100/abstract?rss=yes"/><rdf:li rdf:resource="http://www.medicinejournal.co.uk/article/PIIS1357303911003094/abstract?rss=yes"/><rdf:li rdf:resource="http://www.medicinejournal.co.uk/article/PIIS1357303911002945/abstract?rss=yes"/><rdf:li rdf:resource="http://www.medicinejournal.co.uk/article/PIIS135730391100301X/abstract?rss=yes"/><rdf:li rdf:resource="http://www.medicinejournal.co.uk/article/PIIS1357303911003033/abstract?rss=yes"/><rdf:li rdf:resource="http://www.medicinejournal.co.uk/article/PIIS1357303911002982/abstract?rss=yes"/><rdf:li rdf:resource="http://www.medicinejournal.co.uk/article/PIIS1357303911002933/abstract?rss=yes"/><rdf:li rdf:resource="http://www.medicinejournal.co.uk/article/PIIS1357303911003045/abstract?rss=yes"/><rdf:li rdf:resource="http://www.medicinejournal.co.uk/article/PIIS1357303911002969/abstract?rss=yes"/><rdf:li rdf:resource="http://www.medicinejournal.co.uk/article/PIIS1357303911003112/abstract?rss=yes"/><rdf:li rdf:resource="http://www.medicinejournal.co.uk/article/PIIS1357303911002921/abstract?rss=yes"/><rdf:li rdf:resource="http://www.medicinejournal.co.uk/article/PIIS1357303911003082/abstract?rss=yes"/><rdf:li rdf:resource="http://www.medicinejournal.co.uk/article/PIIS1357303911003070/abstract?rss=yes"/><rdf:li rdf:resource="http://www.medicinejournal.co.uk/article/PIIS1357303911002994/abstract?rss=yes"/><rdf:li rdf:resource="http://www.medicinejournal.co.uk/article/PIIS1357303911003124/abstract?rss=yes"/></rdf:Seq></items></channel><item rdf:about="http://www.medicinejournal.co.uk/article/PIIS1357303911003574/abstract?rss=yes"><title>Contents</title><link>http://www.medicinejournal.co.uk/article/PIIS1357303911003574/abstract?rss=yes</link><description></description><dc:title>Contents</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S1357-3039(11)00357-4</dc:identifier><dc:source>Medicine 40, 2 (2012)</dc:source><dc:date>2012-02-01</dc:date><prism:publicationName>Medicine</prism:publicationName><prism:publicationDate>2012-02-01</prism:publicationDate><prism:volume>40</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1357-3039(11)X0014-2</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>OFC</prism:startingPage><prism:endingPage>OFC</prism:endingPage></item><item rdf:about="http://www.medicinejournal.co.uk/article/PIIS1357303911003598/abstract?rss=yes"><title>Editorial Board</title><link>http://www.medicinejournal.co.uk/article/PIIS1357303911003598/abstract?rss=yes</link><description></description><dc:title>Editorial Board</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S1357-3039(11)00359-8</dc:identifier><dc:source>Medicine 40, 2 (2012)</dc:source><dc:date>2012-02-01</dc:date><prism:publicationName>Medicine</prism:publicationName><prism:publicationDate>2012-02-01</prism:publicationDate><prism:volume>40</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1357-3039(11)X0014-2</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>i</prism:startingPage><prism:endingPage>i</prism:endingPage></item><item rdf:about="http://www.medicinejournal.co.uk/article/PIIS135730391100288X/abstract?rss=yes"><title>Poisoning: introduction</title><link>http://www.medicinejournal.co.uk/article/PIIS135730391100288X/abstract?rss=yes</link><description>In the minds of many doctors, exposure to a substance is equated with poisoning. However, systemic absorption is usually necessary for there to be a toxic effect and, even if this occurs, the amount absorbed may be too small to produce adverse effects or poisoning. Moreover, to many, the term poisoning suggests an acute event demanding immediate care and attention. This is often so, although the consequences of exposure are not always immediate. For example, distinctive sequelae may not appear until many years have elapsed, as is the case with hepatic haemangiosarcoma from vinyl chloride exposure. Alternatively, features may arise only after prolonged exposure, as with many heavy metals.</description><dc:title>Poisoning: introduction</dc:title><dc:creator>Allister Vale, D. Nicholas Bateman</dc:creator><dc:identifier>10.1016/j.mpmed.2011.11.002</dc:identifier><dc:source>Medicine 40, 2 (2012)</dc:source><dc:date>2012-02-01</dc:date><prism:publicationName>Medicine</prism:publicationName><prism:publicationDate>2012-02-01</prism:publicationDate><prism:volume>40</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1357-3039(11)X0014-2</prism:issueIdentifier><prism:section>Introduction</prism:section><prism:startingPage>41</prism:startingPage><prism:endingPage>41</prism:endingPage></item><item rdf:about="http://www.medicinejournal.co.uk/article/PIIS1357303911003008/abstract?rss=yes"><title>The epidemiology of poisoning</title><link>http://www.medicinejournal.co.uk/article/PIIS1357303911003008/abstract?rss=yes</link><description>Abstract: The epidemiology of poisoning can be studied from different perspectives. These include overall mortality, hospital admission rates, and enquiries to Poisons Information Services. Accidental poisoning is most common in children, but deliberate self-harm becomes predominant in teenage years and early adulthood. Understanding the patterns of poisoning assists in developing suicide prevention strategies and reducing the risks of accidental poisoning.</description><dc:title>The epidemiology of poisoning</dc:title><dc:creator>D. Nicholas Bateman</dc:creator><dc:identifier>10.1016/j.mpmed.2011.11.014</dc:identifier><dc:source>Medicine 40, 2 (2012)</dc:source><dc:date>2012-02-01</dc:date><prism:publicationName>Medicine</prism:publicationName><prism:publicationDate>2012-02-01</prism:publicationDate><prism:volume>40</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1357-3039(11)X0014-2</prism:issueIdentifier><prism:section>Epidemiology</prism:section><prism:startingPage>42</prism:startingPage><prism:endingPage>45</prism:endingPage></item><item rdf:about="http://www.medicinejournal.co.uk/article/PIIS1357303911002908/abstract?rss=yes"><title>Is the cause toxicological?</title><link>http://www.medicinejournal.co.uk/article/PIIS1357303911002908/abstract?rss=yes</link><description>Abstract: The diagnosis of poisoning is usually evident (e.g. in a patient presenting with drug overdose), but can occasionally be obscure. This article describes some clinical presentations where poisoning should be considered in the differential diagnosis. Examples are unexplained coma or confusion, hypoglycaemia, abnormal liver function, unexplained convulsions or acidosis or abnormal bleeding. Poisoning should also be suspected if several people present with similar symptoms or in children who have chronic, recurrent or unexplained symptoms.</description><dc:title>Is the cause toxicological?</dc:title><dc:creator>S.H.L. Thomas</dc:creator><dc:identifier>10.1016/j.mpmed.2011.11.004</dc:identifier><dc:source>Medicine 40, 2 (2012)</dc:source><dc:date>2012-02-01</dc:date><prism:publicationName>Medicine</prism:publicationName><prism:publicationDate>2012-02-01</prism:publicationDate><prism:volume>40</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1357-3039(11)X0014-2</prism:issueIdentifier><prism:section>Assessment</prism:section><prism:startingPage>46</prism:startingPage><prism:endingPage>47</prism:endingPage></item><item rdf:about="http://www.medicinejournal.co.uk/article/PIIS1357303911003021/abstract?rss=yes"><title>Assessment and diagnosis of the poisoned patient</title><link>http://www.medicinejournal.co.uk/article/PIIS1357303911003021/abstract?rss=yes</link><description>Abstract: Assessment of an acutely poisoned patient involves the taking of an appropriate history, assessment of the level of consciousness, ventilation and circulation, a physical examination, and requesting appropriate toxicological and non-toxicological investigations. Diagnosis is based on the history, circumstantial evidence (if available), a cluster of common features (if present) and, occasionally, the results of biochemical or toxicological analyses.</description><dc:title>Assessment and diagnosis of the poisoned patient</dc:title><dc:creator>Allister Vale, Sally Bradberry</dc:creator><dc:identifier>10.1016/j.mpmed.2011.11.016</dc:identifier><dc:source>Medicine 40, 2 (2012)</dc:source><dc:date>2012-02-01</dc:date><prism:publicationName>Medicine</prism:publicationName><prism:publicationDate>2012-02-01</prism:publicationDate><prism:volume>40</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1357-3039(11)X0014-2</prism:issueIdentifier><prism:section>Assessment</prism:section><prism:startingPage>48</prism:startingPage><prism:endingPage>52</prism:endingPage></item><item rdf:about="http://www.medicinejournal.co.uk/article/PIIS1357303911002891/abstract?rss=yes"><title>Low-toxicity ingestions</title><link>http://www.medicinejournal.co.uk/article/PIIS1357303911002891/abstract?rss=yes</link><description>Abstract: Accidental ingestion of products found in the environment is common. It particularly affects young children aged 1–4 years, especially boys. Fortunately, many substances that are taken by accident have low toxicity and further observation or treatment is unnecessary. This article includes information on substances found in the house or garden that are of low toxicity when taken by ingestion. Medicines that are of low toxicity when taken in overdose are also described.</description><dc:title>Low-toxicity ingestions</dc:title><dc:creator>S.H.L. Thomas</dc:creator><dc:identifier>10.1016/j.mpmed.2011.11.003</dc:identifier><dc:source>Medicine 40, 2 (2012)</dc:source><dc:date>2012-02-01</dc:date><prism:publicationName>Medicine</prism:publicationName><prism:publicationDate>2012-02-01</prism:publicationDate><prism:volume>40</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1357-3039(11)X0014-2</prism:issueIdentifier><prism:section>Assessment</prism:section><prism:startingPage>53</prism:startingPage><prism:endingPage>54</prism:endingPage></item><item rdf:about="http://www.medicinejournal.co.uk/article/PIIS1357303911002957/abstract?rss=yes"><title>Metabolic effects of poisoning</title><link>http://www.medicinejournal.co.uk/article/PIIS1357303911002957/abstract?rss=yes</link><description>Abstract: Biochemical abnormalities due to disturbed metabolic processes are common in severely poisoned patients. These may be of diagnostic value, but most importantly their recognition and treatment are important in the management of these patients. Acid–base abnormalites, particularly respiratory and metabolic acidoses, are common. Respiratory acidoses due to central nervous system depression or pulmonary toxicity, and metabolic acidoses due to lactic acidaemia or derangements of intermediary metabolism are particular features of poisoning. Plasma electrolyte abnormalities, particularly hyper- or hypokalaemia are found commonly in poisoned patients, most often due to redistribution of potassium across cell membranes. Hypoglycaemia is most frequently due to drug overdose.</description><dc:title>Metabolic effects of poisoning</dc:title><dc:creator>Alan Jones</dc:creator><dc:identifier>10.1016/j.mpmed.2011.11.009</dc:identifier><dc:source>Medicine 40, 2 (2012)</dc:source><dc:date>2012-02-01</dc:date><prism:publicationName>Medicine</prism:publicationName><prism:publicationDate>2012-02-01</prism:publicationDate><prism:volume>40</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1357-3039(11)X0014-2</prism:issueIdentifier><prism:section>Complications of poisoning</prism:section><prism:startingPage>55</prism:startingPage><prism:endingPage>58</prism:endingPage></item><item rdf:about="http://www.medicinejournal.co.uk/article/PIIS1357303911002970/abstract?rss=yes"><title>Methaemoglobinaemia</title><link>http://www.medicinejournal.co.uk/article/PIIS1357303911002970/abstract?rss=yes</link><description>Abstract: Methaemoglobin is formed when ferrous haemoglobin iron (II) is oxidized to ferric iron (III), which cannot participate in oxygen transport. Methaemoglobin-forming chemical groups of particular importance in poisoning are organic nitrites (e.g. amyl and isobutyl nitrite) and amino- or nitro-derivatives of benzene (e.g. aniline, dapsone and lidocaine). An asymptomatic, apparent ‘cyanosis’ is the earliest clinical feature, occurring when approximately 15% of total haemoglobin is replaced by methaemoglobin. Progressive manifestations of tissue hypoxia ensue at increasing methaemoglobin concentrations and concentrations approaching 80% may be fatal.</description><dc:title>Methaemoglobinaemia</dc:title><dc:creator>Sally Bradberry</dc:creator><dc:identifier>10.1016/j.mpmed.2011.11.011</dc:identifier><dc:source>Medicine 40, 2 (2012)</dc:source><dc:date>2012-02-01</dc:date><prism:publicationName>Medicine</prism:publicationName><prism:publicationDate>2012-02-01</prism:publicationDate><prism:volume>40</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1357-3039(11)X0014-2</prism:issueIdentifier><prism:section>Complications of poisoning</prism:section><prism:startingPage>59</prism:startingPage><prism:endingPage>60</prism:endingPage></item><item rdf:about="http://www.medicinejournal.co.uk/article/PIIS1357303911003069/abstract?rss=yes"><title>Rhabdomyolysis</title><link>http://www.medicinejournal.co.uk/article/PIIS1357303911003069/abstract?rss=yes</link><description>Abstract: Non-traumatic rhabdomyolysis may be caused by a direct insult to the cell membrane, affecting its ability to maintain ion gradients, or be secondary to local muscle compression as a result of coma or seizures. Acute renal failure and peripheral nerve damage are the two most common and important complications observed, though hyperkalaemia leading to a dysrhythmia is the main cause of death.</description><dc:title>Rhabdomyolysis</dc:title><dc:creator>Allister Vale</dc:creator><dc:identifier>10.1016/j.mpmed.2011.11.020</dc:identifier><dc:source>Medicine 40, 2 (2012)</dc:source><dc:date>2012-02-01</dc:date><prism:publicationName>Medicine</prism:publicationName><prism:publicationDate>2012-02-01</prism:publicationDate><prism:volume>40</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1357-3039(11)X0014-2</prism:issueIdentifier><prism:section>Complications of poisoning</prism:section><prism:startingPage>61</prism:startingPage><prism:endingPage>62</prism:endingPage></item><item rdf:about="http://www.medicinejournal.co.uk/article/PIIS135730391100291X/abstract?rss=yes"><title>Serotonin syndrome</title><link>http://www.medicinejournal.co.uk/article/PIIS135730391100291X/abstract?rss=yes</link><description>Abstract: The serotonin syndrome is the clinical manifestation of serotonin toxicity in patients taking one or more serotonergic agents. It is characterized by features of neuromuscular hyperactivity, autonomic instability and alteration of mental status. Management consists of discontinuation of the offending drug and supportive care. Cyproheptadine and chlorpromazine which have 5-HT2A antagonistic properties may be useful in severe cases.</description><dc:title>Serotonin syndrome</dc:title><dc:creator>Ruben Thanacoody</dc:creator><dc:identifier>10.1016/j.mpmed.2011.11.005</dc:identifier><dc:source>Medicine 40, 2 (2012)</dc:source><dc:date>2012-02-01</dc:date><prism:publicationName>Medicine</prism:publicationName><prism:publicationDate>2012-02-01</prism:publicationDate><prism:volume>40</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1357-3039(11)X0014-2</prism:issueIdentifier><prism:section>Complications of poisoning</prism:section><prism:startingPage>63</prism:startingPage><prism:endingPage>64</prism:endingPage></item><item rdf:about="http://www.medicinejournal.co.uk/article/PIIS1357303911003057/abstract?rss=yes"><title>Management of poisoning: initial management and need for admission</title><link>http://www.medicinejournal.co.uk/article/PIIS1357303911003057/abstract?rss=yes</link><description>Abstract: Initial management involves the treatment of any potentially life-threatening conditions, such as airway compromise, breathing difficulties, haemodynamic instability and serious dysrhythmias. Thereafter, convulsions should be treated, fluid, acid–base and electrolyte abnormalities corrected, and hypothermia managed by using a space blanket. Children under 5 years old who are suspected of having ingested paracetamol, salicylate, iron, an opioid, a tricyclic antidepressant or a substance of abuse require assessment in hospital and, possibly, admission. The need for admission of adult patients depends on the agent(s) ingested, features present, results of investigations and psychological state.</description><dc:title>Management of poisoning: initial management and need for admission</dc:title><dc:creator>Allister Vale, Sally Bradberry</dc:creator><dc:identifier>10.1016/j.mpmed.2011.11.019</dc:identifier><dc:source>Medicine 40, 2 (2012)</dc:source><dc:date>2012-02-01</dc:date><prism:publicationName>Medicine</prism:publicationName><prism:publicationDate>2012-02-01</prism:publicationDate><prism:volume>40</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1357-3039(11)X0014-2</prism:issueIdentifier><prism:section>Management</prism:section><prism:startingPage>65</prism:startingPage><prism:endingPage>66</prism:endingPage></item><item rdf:about="http://www.medicinejournal.co.uk/article/PIIS1357303911003100/abstract?rss=yes"><title>Reducing absorption and increasing elimination</title><link>http://www.medicinejournal.co.uk/article/PIIS1357303911003100/abstract?rss=yes</link><description>Abstract: There is no evidence that the use of single-dose activated charcoal, gastric lavage, syrup of ipecacuanha, cathartics or whole-bowel irrigation improves the clinical outcome in poisoned patients. However, activated charcoal and gastric lavage may be considered in patients who have ingested life-threatening amounts of a toxic agent up to 1 hour previously. To increase elimination, treatment with multiple-dose activated charcoal (in patients who have ingested a life-threatening amount of carbamazepine, dapsone, phenobarbital, quinine or theophylline) or urine alkalinization (in patients with moderately severe salicylate poisoning) should be employed. Haemodialysis and haemodialfiltration significantly increase the elimination of ethanol, ethylene glycol, isopropanol, lithium, methanol and salicylate, and should be considered in cases of severe poisoning from these agents.</description><dc:title>Reducing absorption and increasing elimination</dc:title><dc:creator>Allister Vale</dc:creator><dc:identifier>10.1016/j.mpmed.2011.11.024</dc:identifier><dc:source>Medicine 40, 2 (2012)</dc:source><dc:date>2012-02-01</dc:date><prism:publicationName>Medicine</prism:publicationName><prism:publicationDate>2012-02-01</prism:publicationDate><prism:volume>40</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1357-3039(11)X0014-2</prism:issueIdentifier><prism:section>Management</prism:section><prism:startingPage>67</prism:startingPage><prism:endingPage>68</prism:endingPage></item><item rdf:about="http://www.medicinejournal.co.uk/article/PIIS1357303911003094/abstract?rss=yes"><title>Management of poisoning: antidotes</title><link>http://www.medicinejournal.co.uk/article/PIIS1357303911003094/abstract?rss=yes</link><description>Abstract: Antidotes exert their beneficial effects by a variety of mechanisms, including forming an inert complex with the poison, accelerating detoxification of the poison, reducing the rate of conversion of the poison to a more toxic compound, competing with the poison for essential receptor sites, blocking essential receptors through which the toxic effects are mediated, and bypassing the effect of the poison. There are specific antidotes for only a small number of poisons and few antidotes are employed regularly in clinical practice. Those that are include acetylcysteine, naloxone and flumazenil.</description><dc:title>Management of poisoning: antidotes</dc:title><dc:creator>Sally Bradberry, Allister Vale</dc:creator><dc:identifier>10.1016/j.mpmed.2011.11.023</dc:identifier><dc:source>Medicine 40, 2 (2012)</dc:source><dc:date>2012-02-01</dc:date><prism:publicationName>Medicine</prism:publicationName><prism:publicationDate>2012-02-01</prism:publicationDate><prism:volume>40</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1357-3039(11)X0014-2</prism:issueIdentifier><prism:section>Management</prism:section><prism:startingPage>69</prism:startingPage><prism:endingPage>70</prism:endingPage></item><item rdf:about="http://www.medicinejournal.co.uk/article/PIIS1357303911002945/abstract?rss=yes"><title>Psychiatric assessment and management of deliberate self-poisoning patients</title><link>http://www.medicinejournal.co.uk/article/PIIS1357303911002945/abstract?rss=yes</link><description>Abstract: Deliberate self-poisoning is one of the most common for general hospital presentation. The majority of the individuals involved are young, with females outnumbering males. Self-poisoning occurs in people from a variety of social backgrounds, but is associated with socio-economic deprivation and social fragmentation. Common precipitants include relationship problems, often in the context of depression and alcohol abuse. The risks of repetition of self-harm and of suicide following self-poisoning are substantial. Psychosocial assessment of patients should include investigation of the events and problems preceding the act, suicidal intent and other motives for the act, psychiatric disorder, personality traits and disorder, family and personal history, psychiatric history, including of self-harm, risk of further self-harm and suicide, and coping resources and support. Aftercare should be arranged according to the patient’s needs and risk.</description><dc:title>Psychiatric assessment and management of deliberate self-poisoning patients</dc:title><dc:creator>Keith Hawton</dc:creator><dc:identifier>10.1016/j.mpmed.2011.11.008</dc:identifier><dc:source>Medicine 40, 2 (2012)</dc:source><dc:date>2012-02-01</dc:date><prism:publicationName>Medicine</prism:publicationName><prism:publicationDate>2012-02-01</prism:publicationDate><prism:volume>40</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1357-3039(11)X0014-2</prism:issueIdentifier><prism:section>Management</prism:section><prism:startingPage>71</prism:startingPage><prism:endingPage>73</prism:endingPage></item><item rdf:about="http://www.medicinejournal.co.uk/article/PIIS135730391100301X/abstract?rss=yes"><title>Substance abuse: routes, hazards and body packing</title><link>http://www.medicinejournal.co.uk/article/PIIS135730391100301X/abstract?rss=yes</link><description>Abstract: Substances taken to alter the mental state may be ingested, inhaled, absorbed through mucous membranes or injected. Accidental overdose is common. Complications result either from the presence of contaminants or from the pharmacological actions of the substance(s) involved; these include respiratory, neurological, renal and metabolic complications. Body packers often swallow large numbers of packages in the hope of financial gain. Acute intestinal obstruction may result and overdose is a hazard if a packet bursts. Immediate surgery is indicated if acute intestinal obstruction develops, or when packets can be seen radiologically and there is clinical or analytical evidence to suggest leakage, particularly if the drug involved is a central nervous system stimulant (e.g. cocaine).</description><dc:title>Substance abuse: routes, hazards and body packing</dc:title><dc:creator>Allister Vale</dc:creator><dc:identifier>10.1016/j.mpmed.2011.11.015</dc:identifier><dc:source>Medicine 40, 2 (2012)</dc:source><dc:date>2012-02-01</dc:date><prism:publicationName>Medicine</prism:publicationName><prism:publicationDate>2012-02-01</prism:publicationDate><prism:volume>40</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1357-3039(11)X0014-2</prism:issueIdentifier><prism:section>Substance abuse</prism:section><prism:startingPage>74</prism:startingPage><prism:endingPage>76</prism:endingPage></item><item rdf:about="http://www.medicinejournal.co.uk/article/PIIS1357303911003033/abstract?rss=yes"><title>Chemical terrorism and nerve agents</title><link>http://www.medicinejournal.co.uk/article/PIIS1357303911003033/abstract?rss=yes</link><description>Abstract: Sarin and VX were released on civilians in Japan on 11 occasions in the period 1994 to 1995. Clinicians must be prepared, therefore, to treat casualties from nerve agent exposure. This requires an understanding of the mechanisms of nerve agent toxicity and the factors that influence their clinical impact. Clinicians need to be able to make a rapid and accurate diagnosis and use atropine, an oxime and diazepam optimally.</description><dc:title>Chemical terrorism and nerve agents</dc:title><dc:creator>Allister Vale, Timothy C. Marrs, Paul Rice</dc:creator><dc:identifier>10.1016/j.mpmed.2011.11.017</dc:identifier><dc:source>Medicine 40, 2 (2012)</dc:source><dc:date>2012-02-01</dc:date><prism:publicationName>Medicine</prism:publicationName><prism:publicationDate>2012-02-01</prism:publicationDate><prism:volume>40</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1357-3039(11)X0014-2</prism:issueIdentifier><prism:section>Chemical terrorism</prism:section><prism:startingPage>77</prism:startingPage><prism:endingPage>79</prism:endingPage></item><item rdf:about="http://www.medicinejournal.co.uk/article/PIIS1357303911002982/abstract?rss=yes"><title>Ricin and abrin</title><link>http://www.medicinejournal.co.uk/article/PIIS1357303911002982/abstract?rss=yes</link><description>Abstract: Ricin is derived from the beans of the castor oil plant, Ricinus communis. Many of the features seen in poisoning can be explained by ricin-induced endothelial cell damage, which leads to fluid and protein leakage and tissue oedema, causing so-called ‘vascular leak syndrome’. Ricin’s use as a potential bioterrorism agent makes inhalational exposure the primary concern. Both vaccination (prophylaxis) and antitoxin (therapeutic) approaches against ricin intoxication are being developed. Abrin is a plant toxin obtained from the seeds of Abrus precatorius; its structure and chemical properties are closely related to ricin.</description><dc:title>Ricin and abrin</dc:title><dc:creator>Sally Bradberry</dc:creator><dc:identifier>10.1016/j.mpmed.2011.11.012</dc:identifier><dc:source>Medicine 40, 2 (2012)</dc:source><dc:date>2012-02-01</dc:date><prism:publicationName>Medicine</prism:publicationName><prism:publicationDate>2012-02-01</prism:publicationDate><prism:volume>40</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1357-3039(11)X0014-2</prism:issueIdentifier><prism:section>Chemical terrorism</prism:section><prism:startingPage>80</prism:startingPage><prism:endingPage>81</prism:endingPage></item><item rdf:about="http://www.medicinejournal.co.uk/article/PIIS1357303911002933/abstract?rss=yes"><title>Sulphur mustard</title><link>http://www.medicinejournal.co.uk/article/PIIS1357303911002933/abstract?rss=yes</link><description>Abstract: Sulphur mustard is a powerful vesicant (blistering agent) which was used extensively in World War I and in the Iran–Iraq conflict (1984–1987). In addition to causing characteristic blistering burns to the skin, exposure may also result in severe conjuctivitis, ulcerative necrosis throughout the respiratory tract and systemic toxicity including bone marrow suppression. There is no specific therapy for sulphur mustard poisoning, but procedures such as laser debridement of established burns have been shown to increase the rate of burn resolution in animal models and may, therefore, be of benefit clinically.</description><dc:title>Sulphur mustard</dc:title><dc:creator>Paul Rice</dc:creator><dc:identifier>10.1016/j.mpmed.2011.11.007</dc:identifier><dc:source>Medicine 40, 2 (2012)</dc:source><dc:date>2012-02-01</dc:date><prism:publicationName>Medicine</prism:publicationName><prism:publicationDate>2012-02-01</prism:publicationDate><prism:volume>40</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1357-3039(11)X0014-2</prism:issueIdentifier><prism:section>Chemical terrorism</prism:section><prism:startingPage>82</prism:startingPage><prism:endingPage>83</prism:endingPage></item><item rdf:about="http://www.medicinejournal.co.uk/article/PIIS1357303911003045/abstract?rss=yes"><title>Drugs of abuse (amfetamines, BZP, cannabis, cocaine, GHB, LSD)</title><link>http://www.medicinejournal.co.uk/article/PIIS1357303911003045/abstract?rss=yes</link><description>Abstract: The features of amfetamine poisoning are related predominantly to stimulation of central and peripheral adrenergic receptors, and in severe cases, excitability, agitation, paranoid delusions, hallucinations with violent behaviour, hypertonia and hyperreflexia develop. Convulsions, rhabdomyolysis, hyperthermia, intracerebral haemorrhage and cardiac arrhythmias are less common. In addition, hyperthermia and hyponatraemia are features of severe MDMA toxicity.Benzylpiperazine (BZP) has stimulant and amfetamine-like properties. Those severely poisoned may develop seizures, collapse, hyperthermia, myoclonic jerks, extrapyramidal features and respiratory failure.Features of cannabis use include euphoria, distorted and heightened images, colours and sounds, altered tactile sensations, impairment of memory, sinus tachycardia, hypotension and ataxia. Visual and auditory hallucinations, depersonalization and acute psychosis are particularly likely to occur after substantial ingestion in naive cannabis users. Heavy chronic users suffer impairment of memory and attention, and have an increased risk of psychotic episodes and later schizophrenia.Cocaine is a psychomotor stimulant that inhibits re-uptake of monoamines into presynaptic terminals, thereby prolonging and augmenting their effects. Cocaine is also a powerful local anaesthetic and vasoconstrictor. In addition to euphoria, ventricular arrhythmias, acute myocardial infarction, stroke, acute dissection of the aorta, renal and intestinal infarction occur. Chronic intranasal use may cause perforation of the nasal septum and cerebrospinal rhinorrhoea as a result of thinning of the cribriform plate.After ingestion of a substantial amount of GHB, bradycardia, hypotension, myoclonus, respiratory depression and deep coma occur rapidly but usually resolve spontaneously within 12 hours, though deaths have been reported.Lysergic acid diethylamide (LSD) acts as an antagonist at peripheral 5-HT receptor subtypes, but as a 5-HT2A receptor agonist in the CNS. In severe poisoning, hyperreflexia, tremor, muscle twitching, coma, seizures, hypotension and respiratory arrest have been reported. In addition, changes in perception, mood and behaviour, panic, agitation and excitement, visual hallucinations, delusions and psychosis are observed. Hallucinogen persisting perception disorder (‘flashbacks’) may persist for several years after exposure has ceased.</description><dc:title>Drugs of abuse (amfetamines, BZP, cannabis, cocaine, GHB, LSD)</dc:title><dc:creator>Allister Vale</dc:creator><dc:identifier>10.1016/j.mpmed.2011.11.018</dc:identifier><dc:source>Medicine 40, 2 (2012)</dc:source><dc:date>2012-02-01</dc:date><prism:publicationName>Medicine</prism:publicationName><prism:publicationDate>2012-02-01</prism:publicationDate><prism:volume>40</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1357-3039(11)X0014-2</prism:issueIdentifier><prism:section>Drugs of abuse</prism:section><prism:startingPage>84</prism:startingPage><prism:endingPage>87</prism:endingPage></item><item rdf:about="http://www.medicinejournal.co.uk/article/PIIS1357303911002969/abstract?rss=yes"><title>Acetone</title><link>http://www.medicinejournal.co.uk/article/PIIS1357303911002969/abstract?rss=yes</link><description>Abstract: Acetone is a mucous membrane irritant, which can be absorbed by inhalation, ingestion and through the skin. Its metabolism leads to increased glucose production. At high concentrations it is a central nervous system depressant. Haemodialysis to enhance elimination may be indicated in severe poisoning.</description><dc:title>Acetone</dc:title><dc:creator>Sally Bradberry</dc:creator><dc:identifier>10.1016/j.mpmed.2011.11.010</dc:identifier><dc:source>Medicine 40, 2 (2012)</dc:source><dc:date>2012-02-01</dc:date><prism:publicationName>Medicine</prism:publicationName><prism:publicationDate>2012-02-01</prism:publicationDate><prism:volume>40</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1357-3039(11)X0014-2</prism:issueIdentifier><prism:section>Specific substances</prism:section><prism:startingPage>88</prism:startingPage><prism:endingPage>88</prism:endingPage></item><item rdf:about="http://www.medicinejournal.co.uk/article/PIIS1357303911003112/abstract?rss=yes"><title>Alcohols and glycols</title><link>http://www.medicinejournal.co.uk/article/PIIS1357303911003112/abstract?rss=yes</link><description>Abstract: Ethanol is a central nervous system depressant and a peripheral vasodilator, thereby causing coma, hypothermia and hypotension in severe poisoning. Hypoglycaemia, particularly in children, is observed together with acid–base disturbances, which are common (respiratory acidosis is observed more frequently than metabolic acidosis, and metabolic alkalosis may be observed in those vomiting and hypovolaemic). Lactic acidosis (usually mild) is an uncommon but potentially serious complication. Haemodialysis may be considered if the blood ethanol concentration exceeds 7500 mg/L and severe metabolic acidosis is present.The principal features of severe methanol poisoning are metabolic acidosis and blindness. The first priority of management is to inhibit methanol metabolism using either intravenous fomepizole or ethanol. In addition, sodium bicarbonate and folinic acid should be administered to correct acidosis and increase formate metabolism respectively. Haemodialysis will enhance methanol and formate elimination and correct acid−base disturbances.Diethylene and ethylene glycols are both metabolized by alcohol and aldehyde dehydrogenases to produce toxic metabolites. Both glycols produce coma, seizures, metabolic acidosis and renal failure, though by different mechanisms. Management involves the administration of fomepizole or ethanol to prevent metabolism of the glycol, correction of acidosis, and the use of haemodialysis to remove the glycol and metabolites.</description><dc:title>Alcohols and glycols</dc:title><dc:creator>Allister Vale</dc:creator><dc:identifier>10.1016/j.mpmed.2011.11.025</dc:identifier><dc:source>Medicine 40, 2 (2012)</dc:source><dc:date>2012-02-01</dc:date><prism:publicationName>Medicine</prism:publicationName><prism:publicationDate>2012-02-01</prism:publicationDate><prism:volume>40</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1357-3039(11)X0014-2</prism:issueIdentifier><prism:section>Specific substances</prism:section><prism:startingPage>89</prism:startingPage><prism:endingPage>93</prism:endingPage></item><item rdf:about="http://www.medicinejournal.co.uk/article/PIIS1357303911002921/abstract?rss=yes"><title>Ammonia</title><link>http://www.medicinejournal.co.uk/article/PIIS1357303911002921/abstract?rss=yes</link><description>Abstract: Ammonia is a frequently used industrial agent. Ammonia is highly soluble in water and has toxic and corrosive actions caused by its alkalinity. It is easily absorbed through mucous membranes. Ammonia affects the upper airways more than the peripheral airways. Following exposure to ammonia, the clinical symptoms appear instantly and may consist of nasal discharge, lacrimation, pain in the upper airways, dyspnoea, bronchospasm, bronchial oedema, glottic oedema, increased mucus production, haemoptysis and cyanosis. Ingestion of ammonia water induces caustic lesions in the oropharynx, oesophagus and stomach. Liquid ammonia is corrosive. Evaporation of liquid ammonia from the eye or skin may cause cold burns.</description><dc:title>Ammonia</dc:title><dc:creator>Jan Meulenbelt</dc:creator><dc:identifier>10.1016/j.mpmed.2011.11.006</dc:identifier><dc:source>Medicine 40, 2 (2012)</dc:source><dc:date>2012-02-01</dc:date><prism:publicationName>Medicine</prism:publicationName><prism:publicationDate>2012-02-01</prism:publicationDate><prism:volume>40</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1357-3039(11)X0014-2</prism:issueIdentifier><prism:section>Specific substances</prism:section><prism:startingPage>94</prism:startingPage><prism:endingPage>95</prism:endingPage></item><item rdf:about="http://www.medicinejournal.co.uk/article/PIIS1357303911003082/abstract?rss=yes"><title>Anticonvulsants</title><link>http://www.medicinejournal.co.uk/article/PIIS1357303911003082/abstract?rss=yes</link><description>Abstract: Generally, phenytoin and carbamazepine have greater toxicity in overdose than sodium valproate and the newer anticonvulsants, though case reports confirm that severe toxicity can occur uncommonly.</description><dc:title>Anticonvulsants</dc:title><dc:creator>Allister Vale</dc:creator><dc:identifier>10.1016/j.mpmed.2011.11.022</dc:identifier><dc:source>Medicine 40, 2 (2012)</dc:source><dc:date>2012-02-01</dc:date><prism:publicationName>Medicine</prism:publicationName><prism:publicationDate>2012-02-01</prism:publicationDate><prism:volume>40</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1357-3039(11)X0014-2</prism:issueIdentifier><prism:section>Specific substances</prism:section><prism:startingPage>96</prism:startingPage><prism:endingPage>97</prism:endingPage></item><item rdf:about="http://www.medicinejournal.co.uk/article/PIIS1357303911003070/abstract?rss=yes"><title>Antidiabetic drugs</title><link>http://www.medicinejournal.co.uk/article/PIIS1357303911003070/abstract?rss=yes</link><description>Abstract: Over recent years, there has been rapid expansion of different classes of antihyperglycaemic drugs. These drugs have diverse toxicological profiles because each possesses a unique pharmacological mechanism of action and, correspondingly,. Antidiabetic drugs have the potential to exert severe toxic effects, and patients normally require urgent medical assessment and treatment.</description><dc:title>Antidiabetic drugs</dc:title><dc:creator>W. Stephen Waring</dc:creator><dc:identifier>10.1016/j.mpmed.2011.11.021</dc:identifier><dc:source>Medicine 40, 2 (2012)</dc:source><dc:date>2012-02-01</dc:date><prism:publicationName>Medicine</prism:publicationName><prism:publicationDate>2012-02-01</prism:publicationDate><prism:volume>40</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1357-3039(11)X0014-2</prism:issueIdentifier><prism:section>Specific substances</prism:section><prism:startingPage>98</prism:startingPage><prism:endingPage>99</prism:endingPage></item><item rdf:about="http://www.medicinejournal.co.uk/article/PIIS1357303911002994/abstract?rss=yes"><title>Antidepressants</title><link>http://www.medicinejournal.co.uk/article/PIIS1357303911002994/abstract?rss=yes</link><description>Abstract: Antidepressant drugs differ in their relative toxicities. The most hazardous are tricyclics, citalopram, venlafaxine and the rarely used monamine oxidase inhibitors. Features include arrhythmias, convulsions and cardiovascular effects. Management should be as active as necessary to reduce arrhythmia risk by aggressive correction of acidosis and use of sodium bicarbonate to shorten QRS duration if prolonged.</description><dc:title>Antidepressants</dc:title><dc:creator>D. Nicholas Bateman</dc:creator><dc:identifier>10.1016/j.mpmed.2011.11.013</dc:identifier><dc:source>Medicine 40, 2 (2012)</dc:source><dc:date>2012-02-01</dc:date><prism:publicationName>Medicine</prism:publicationName><prism:publicationDate>2012-02-01</prism:publicationDate><prism:volume>40</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1357-3039(11)X0014-2</prism:issueIdentifier><prism:section>Specific substances</prism:section><prism:startingPage>100</prism:startingPage><prism:endingPage>102</prism:endingPage></item><item rdf:about="http://www.medicinejournal.co.uk/article/PIIS1357303911003124/abstract?rss=yes"><title>Self-assessment/CPD</title><link>http://www.medicinejournal.co.uk/article/PIIS1357303911003124/abstract?rss=yes</link><description>This CPD section was prepared by Eric Beck FRCP FRCP(Ed) FRCP(Gl)   We hope you enjoy the CPD section. Let us know your views by email to: medicine@medicinepublishing.co.uk</description><dc:title>Self-assessment/CPD</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/j.mpmed.2011.11.026</dc:identifier><dc:source>Medicine 40, 2 (2012)</dc:source><dc:date>2012-02-01</dc:date><prism:publicationName>Medicine</prism:publicationName><prism:publicationDate>2012-02-01</prism:publicationDate><prism:volume>40</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1357-3039(11)X0014-2</prism:issueIdentifier><prism:section>Self-assessment</prism:section><prism:startingPage>103</prism:startingPage><prism:endingPage>103</prism:endingPage></item></rdf:RDF>
