Immediate \201 rst aid \200 Maintain clear airway and adequate ventilation \200 Give 100% oxygen to all patients \200 Monitor pulse, blood pressure, respiratory rate, oxygen saturation, and cardiac rhythm Transfer all de \201 nite cases to hospital as rapidly as possible \200 Consider startin g treatment on site if transfer to hospital is likely to be prolonged, and depending on severity of exposure. Diagnosis In the absence of a blood cyanide concentration the following features suggest cy anide poisoning: \200 Lactate >7 mmol/L \200 Elevated anion gap acidosis \200 Reduced arteriovenous oxygen gradient. Mild poisoning \200 Observe asymptomatic and mildly symptomatic patients for at least 6 h ours after ingestion of cyanide salt and at least 12h after ingestion of acetonitrile Give 50mL of 25% sodium thiosulphate (12.5g) IV over 10min. Moderate and severe poisoning \200 Patients with moderate or severe poisoning should be m anaged in a critical care environment Treatment with antidote therapy is necessary in all cases \200 It is important that the a dmitting hospital is informed if any antidote therapy has been given in the pre-hospital setting since repeat doses of some antidotes can cause unwanted side effects 1 If treatment is started on site the doctor should accompany the casualties to the admitting hospital Give 20mL of 1.5% dicobalt edetate solution (300mg) IV over 1min followed immediately by 50 mL of 50% dextrose. If there is only a partial response to dicobalt edetate 300mg or the pa tient relapses after recovery, a further dose of dicobalt edetate 300mg should be given. If a second dose of dicobalt edetate is administered, there is a danger of inducing cobalt to xicity, if the diagnosis is not cyanide poisoning In addition, the administration of 50mL of 25% sodium thiosulphate (12.5g) IV over 10min may be bene \201 cial Or , if dicobalt edetate is not available, give 10mL of 3% sodium nitrite solution (300mg) IV over 5 \200\22320min and 50mL of 25% sodium thiosulphate (12.5g ) IV over 10min 39_Smedley_Chap39.indd 798 1/2/2013 1:36:07 PM CYANIDE 2: TREATMENT 799 A further dose of sodium thiosulphate 12.5g IV over 10min may be needed. A second dose of sodium nitrite should not be given because of the risk of excessiv e methaemoglobinaemia Response to treatment in the pre-hospital setting can be assessed by improved haemodynamic status Single brief convulsions do not require treatment. If frequent or prolonged, control with IV diazepam (10 \200\22320mg) or lorazepam (4mg) Correct hypotension by raising the legs of the patient and/or expanding the intravascular volume. 39_Smedley_Chap39.indd 799 1/2/2013 1:36:07 PM CHAPTER 39 Acute poisoning 800 Hydrogen sulfide poisoning Properties \200 Colorless gas with characteristic \200\230rot ten egg \200\231 smell \200 CAS Number 7783 \200\22306 \200\2234 \200 UN 1053. Synonyms \200 Sulphuretted hydrogen \200 Sulfur hydride \200 Hydrosulphuric acid. Toxicity \200 Irritant gas with systemic asphyxiant effects \200 Reversibly inhibits cy tochrome oxidase, which impairs cell respiration \200 Rapidly absorbed by inhalation \200 Little absorption occurs through the skin \200 Irritating to the eyes \200 Occupa tional short-term exposure limit is 10ppm (14mg/m 3 ) \200 Long-term exposure limit is 5p pm (7mg/m 3 ). 0.02 \200\2230.025ppm Odor threshold 10ppm Unpleasant smell, sore eyes 100ppm Loss of smell after 3 \200\22315min, eyes, and throat sting 250ppm Prolonged exposure \200\224pulmonary oedema 1000ppm Rapid collapse, respiratory paralysis, coma, and death within minutes Features Prolonged exposure causes: Respiratory tract irritation \200 Rhinitis \200 Pharyngitis Bronchitis \200 Dyspnoea \200 Pulmonary oedema Systemic effects \200 Vomiting \200 Diarrhea \200 Headache \200 Nystagmus \200 Di zziness \200 Agitation Drowsiness \200 Tremor \200 Muscular weakness \200 Seizures \200 Tachycardia \200 Hypotension 39_Smedley_Chap39.indd 800 1/2/2013 1:36:07 PM HYDROGEN sulfide POISONING 801 Inhalation of high concentrations Leads rapidly to: \200 Collapse \200 Respiratory para lysis \200 Cyanosis \200 Convulsions Coma \200 Cardiac arrhythmias \200 Death within minutes Eye effects May be delayed and include: \200 Irritation \200 In \202 ammation \200 L acrimation \200 Conjunctival hyperaemia Photophobia \200 Conjunctivitis \200 Keratitis \200 Blepharospasm Recovery is usually complete, but there may be permanent damage. Skin effects \200 Skin discoloration \200 Pain, itching, erythema \200 Local frostbit e. Management of H 2 S poisoning \200 Remove from exposure (rescuers must wear PPE) \200 O xygen in as high a concentration as possible, if necessary via an endotracheal tube Skin decontamination is usually not necessary because it is a gas. Removing patient \200\231s clothing and washing the skin with water and a mild detergent ma y reduce the risk of odor-related complaints in rescuers, but this is not a priority if dea ling with a critically ill patient Maintain a clear airway and adequate ventilation \200 Monitor pulse, blood pressure, and oxygen saturation \200 If the patient has clinical features of bronchospasm treat conventionally with nebulized bronchodilators and steroids Transfer to hospital \200 Correct hypotension with IV \202 uids \200 Convulsions are unlikely to require treatment by the time the patient reaches medical care but IV diazepam 10 \200\22320mg could be given if necessary. 39_Smedley_Chap39.indd 801 1/2/2013 1:36:07 PM CHAPTER 39 Acute poisoning 802 Organophosphate poisoning See also b p. 298. Immediate management and decontamination \200 1 Avoid contaminating yourself: organophosp hates are rapidly absorbed through skin Wear appropriate protective clothing \200 Supportive measures are vitally important. 2 Mo st products are dissolved in hydrocarbon solvents. Aspiration of these products will cause severe aspiration pneumonia with high mortality, and for this reason gastric aspiration sho uld be avoided. Management of organophosphate poisoning \200 Prevent further absorption according to rout e of exposure: \200 remove to fresh air \200 remove soiled clothing and wash contaminat ed skin with washing-up liquid in water (see b p. 803) \200 Consider hospital transfer early \200 Protect the a irway \200 Gain IV access \200 Monitor BP and pulse \200 In symptomatic patients esta blish intravenous access \200 Collect blood samples in an EDTA tube for measurement of erythrocyte and plasma cholinesterase activities to con \201 rm the diagnosis If bronchorrhoea develops, administer atropine 0.6 \200\2232mg IV every 10 \200\22315min until secretions are minimal and the patient is atropinized (dry skin and sinus tachycardia). In severe cases very large doses of atropine may be required if hospita l admission is likely to be delayed Moderately or severely poisoned patients should be given pralidoxime mesilate 2g IV over 4min to reactivate phosphorylated enzyme IV diazepam 5 \200\22310mg is useful in controlling apprehension, agitation, fasciculation, and convulsions. The dose may be repeated as required. 39_Smedley_Chap39.indd 802 1/2/2013 1:36:08 PM ORGANOPHOSPHATE POISONING 803 Skin decontamination: pesticides \200 1 Safety \201 rst \200 Avoid contaminating your self \200 Wear protective clothing \200 Do NOT allow smoking nearby. There may be a ris k of \201 re if a solvent is involved Carry out decontamination in a well-ventilated area, preferably with its own ventilation system The patient should remove soiled clothing and wash him/herself if possible Put soiled clothing in a sealed container to prevent escape of volatile substances Wash hair and all contaminated skin with liberal amounts of water (preferably warm) and soap Pay special attention to skin folds, \201 ngernails, and ears. Note: The intensity of the odor is not necessarily an indication of the toxicity of the pesticide. It may be due to t he solvent or have been added as a deterrent against ingestion. 39_Smedley_Chap39.indd 803 1/2/2013 1:36:08 PM CHAPTER 39 Acute poisoning 804 Mercury poisoning Properties Mercury occurs in three forms: \200 Elemental mercury: highl y mobile silvery liquid, volatile even at room temperatures. Rapidly absorbed by lungs. Usually only toxic by inhalation Inorganic mercurial salts or minerals: e.g. mercuric chloride, mercuric iodide, mercuric ox ide, mercuric sulfide, mercurous chloride \200 Organic mercury: e.g. ethylmercury, methyl mercury, merthiolate. Toxicity Can occur from ingestion, injection, inhalation, or dermal absorption. Acute inhalation of mercury vapor \200 Cough \200 Breathlessness \200 Chest tightness \200 Pulmonary irritation \200 Pneumonitis, pulmonary oedema, necrotizing bronchioliti s, and ARDS \200 \200\230In \202 uenza-like \200\231 symptoms with muscle pains, fever, and tachycardia \200 GI upset may occur within a few hours. Elemental mercury \200 Inhalation of elemental mercury globules may cause: pneumonitis \200 haemoptysis \200 respiratory distress Systemic mercury toxicity is unlikely to occur following ingestion. Management of elemental mercury poisoning \200 Remove from source of exposure \200 Give supplemental oxygen \200 Transfer to hospital if appropriate. Inorganic mercurial salts or minerals Toxicity \200 Inorganic salts are highly corrosive \200 Fatalities have occurred after ingestion of 0.5g of mercuric chloride. Features \200 GI mucosa and kidney are the main target sites \200 Burning of the mouth and throat \200 Abdominal pain \200 Nausea \200 Vomiting followed by haematemesis \200 Bloody diarrhea \200 Colitis \200 Intestinal mucosal necrosis. 39_Smedley_Chap39.indd 804 1/2/2013 1:36:08 PM MERCURY POISONING 805 Management of inorganic mercury poisoning \200 Remove from source of exposure \200 Give supplemental oxygen \200 Give pain relief if necessary \200 Transfer to hospital as so on as possible Organomercury compounds Toxicity Systemic mercury poisoning results typically from acute in halational expo- sure or chronic/repeated ingestion of contaminated foods. Features \200 Ingestion causes: retching, coughing and choking \200 ingestion of aryl mercury salts causes nausea, vomiti ng and abdominal pain systemic mercury poisoning may ensue Inhalation may cause: mucous membrane irritation \200 repeated or substantial exposures can result in systemic toxicity. Skin exposure Mucous membrane irritant at high concentrations. Management of organomercury poisoning Ingestion \200 Supportive measures provide the mainstay of therapy \200 Save blood and urine for mercury concentration determination in symptomatic patients Specialist referral is indicated in patients with systemic features of mercury poisoning. Chelation therapy with DMPS may be required in these cases. Inhalation \200 Remove from exposure \200 Oxygen/bronchodilators may be required \200 Symptomatic and supportive measures dictated by patient \200\231s condition. Skin exposure Decontamination priority: use standard decontamination procedures. 39_Smedley_Chap39.indd 805 1/2/2013 1:36:08 PM CHAPTER 39 Acute poisoning 806 Phenol poisoning Properties Phenols are industrial chemicals, used in disinfectants, which have a char- acteristic sweet odor: \200 CAS 108 \200\22395 \200\2232 \200 UN 2821 phen ol (solutions) \200 UN 2312 phenol (molten) \200 UN 1671 phenol (solid). Synonyms Carbolic acid \200 Hydroxybenzene \200 Phenic acid \200 Phenylic acid Phenolum \200 Phenyl hydrate \200 Tar oils \200 Tar acids Toxicity \200 Corrosive to body tissues \200 Rapidly absorbed following skin contact, l eading to systemic toxicity \200 Inhalation is not the normal route of exposure \200 In gestion is very toxic . Occupational exposure limits Long-term exposure limit: 2ppm. Phenols and cresols: features and management \200 Exposure by any route can cause irritat ion, burns, and systemic effects. \200 Ingestion: causes irritation of mucous membranes and the GI tract. \200 signi \201 cant ingestion c auses white/brown skin and mucosal burns which may be painless laryngeal oedema can occur, and oesophageal stricture may be a late complication Skin contact : even dilute solutions (1%) can cause irritation, dermatitis, and burns to th e skin following prolonged contact. Often presents as relatively painless white or brown ne crotic lesions. The brown discoloration may remain after healing Eye contact: causes irritation, conjunctival and corneal oedema, and blindness. Systemic features \200 Nausea \200 Vomiting \200 Diarrhea \200 Hypotension \200 T achycardia 39_Smedley_Chap39.indd 806 1/2/2013 1:36:08 PM PHENOL POISONING 807 Cardiac arrhythmias \200 Metabolic acidosis \200 Pallor \200 Sweating \200 Shock. 2 CNS stimulation is followed by drowsiness, respiratory depression, cya- nosis, convulsions , coma, bronchospasm, rapid-onset pulmonary oedema, and death. Management of acute poisoning with phenols \200 Remove patient from exposure \200 Ensur e a clear airway and adequate ventilation \200 Give oxygen if clinically indicated \200 Monitor pulse, BP, and cardiac rhythm \200 Transfer to hospital \200 Single brief conv ulsions do not require treatment. If frequent or prolonged control with IV diazepam 10 \200 \22320mg or lorazepam 4mg. Phenol: skin contamination Wash all contaminated areas of the skin with copious quantities of water. Phenol splashed or sprayed into the eyes See b p. 792, General principles of acute poisonin g and contact details for specialist advice for eye decontamination procedures. 39_Smedley_Chap39.indd 807 1/2/2013 1:36:08 PM CHAPTER 39 Acute poisoning 808 Methaemoglobinaemia (acute treatment) Characterized by increased quantities of hemoglobin i n which the iron of haem is oxidized to the ferric (Fe 3+ ) form, i.e. leads to oxidation o f hemoglobin. Methaemoglobin causes a variable degree of cyanosis. See b p. 328, Methaemogl obinaemia for clinical features and causal exposures. Exposure to a large amount of these a gents can lead to the development of 50 \200\22360% methaemoglobin. The symptoms of acute a nemia develop because methaemoglobin lacks the capacity to transportation oxygen. Treatment of acute methaemoglobinaemia Acute toxic methaemoglobinaemia presents a serious medical emergency: \200 Remove from th e toxic agent \200 Arrange for immediate admission to hospital \200 Assessment with ABC s \200 Methylene blue (methylthioninium chloride) should be administered in a dose of 1 \200\2232mg/kg IV over 5min. Repeated doses may be needed Methylene blue (methylthioninium chloride) should not be used if the methaemoglobinaemia is due to chlorate poisoning as it may convert the chlorate to hypochlorite which is an even more toxic compound In cases of acute methaemoglobinaemia with intravascular haemolysis, haemodialysis with exchange transfusion is the treatment of choice. 39_Smedley_Chap39.indd 808 1/2/2013 1:36:08 PM This page intentionally left blank CHAPTER 39 Acute poisoning 810 Hydro \202 uoric acid exposure Properties A colorless fuming liquid used in metal extracti ng, re \201 ning, polishing, and glass etching. An industrial chemical but also present in some household rust removers. A solution of hydrogen \202 uoride in water. Synonyms Hydrogen \202 uoride. Toxicity See Table 39.1: \200 Corrosive (acid): readily penetrates intact skin, nails, an d deep tissue layers Skin exposure or ingestion of any quantity can be dangerous and can result in severe hypocalcaemia Ingestion or skin contact alone or with inhalation has led to death \200 There may be sud den deterioration and fatal arrhythmias can occur within 90min. Concentration Time to symptom onset Anhydrous or > 50% Immediate 20 \200\22350% Up to 8h < 20% Up to 24h 1 Solutions with concentrations as low as 2% may cause burns if they remain in contact with the skin for long enough. Further information True B-L, Dreisbach RH (eds) (2002). Dreisbach \200\231s handbook of po isoning prevention, diagnosis and treatment , 13th edn. Parthenon Publishing, Lancaster. Warrell DA, Cox TM, Firth JD, Benz EJ (2005). Oxford textbook of medicine , 4th edn. Oxford University Press, Oxford. 39_Smedley_Chap39.indd 810 1/2/2013 1:36:08 PM 3 9 _ S m e d l e y _ C h a p 3 9 . i n d d 8 1 1 Table 39.1 Toxicity of hydro \202 uoric acid Mode of entry Signs/symptoms Management (all transfer to hospital) Possible systemic effects to be aware of Urgent assessment of airway, intubation/ tracheostomy may be needed Transfer to hospital Tr eat hypocalcaemia Calcium gluconate 10 \200\22330mL of 10% sol IV Treat hypovolaemia Opiate s may be needed Hypocalcaemia Hypomagnesaemia Hyperkalaemia Metabolic acidosis Myoclonus Tetany Convulsions CNS depression Ingestion Burning of mouth, throat Retrosternal/abdominal pain Laryngeal burns Hypersalivation Vomiti ng 9 haematemesis Hypotension Oesophageal/gastric perforation H Y D R O F L U O R C Inhalation Irritation upper airway Cough Chest tightness Headache Ataxia Confusion Dyspnoea 9 stridor Haemorrhagic pulmonary oedema \200\224late sign As above Cardiac arrthymias: Prolonged QT VT/VF I A C D I E X P O S U R E 1 / 2 8 1 1 / 2 0 1 3 1 : 3 6 : 0 9 P M 3 9 _ S m e d l e y _ C h 8 1 2 a p 3 9 . i n d d C H A P T E R 8 1 2 Table 39.1 (Cont \200\231d) Mode of entry Signs/symptoms Management (all transfer to hospital) Possible systemic effects to be aware of 3 9 A c u t e Skin contact Severe and deep burns Pain disproportionate Blue-gray discoloration in severe cases Time fo r burn to develop: Remove clothing Irrigate with water for 15 \200\22330min Opiates may be needed Apply calciu m gluconate gel in surgical glove for hand burns See ingestion p o i s o n n g Anhydrous or >50% immediate 20 \200\22350% up to 8h <20% up to 24h i Eye contact Conjunctivitis Chemosis Corneal epithelium coagulation necrosis Remove contact lenses Irrigate with water or 0.9% saline for at least 30min Calcium glucona te solution should not be used Local anesthetics (e.g. amethocaine) may help decontaminatio n Mydriatic and cycloplegic agents (e.g. tropicamide), may help (avoid in glaucoma) See ingestion 1 / 2 / 2 0 1 3 1 : 3 6 : 0 9 P M 813 Chapter 40 Non-chemical emergencies Management of anaphylaxis (cid:2) 814 Management of needlestick and contamination incidents 1 816 Management of needlestick and contamination incidents 2: hepatitis B virus post-exposure prophylaxis 820 Management of needlestick and contamination incidents 3: human immunode \201 ciency virus post-exposure prophylaxis 822 Psychiatric emergencies 824 40_Smedley_Chap40.indd 813 1/2/2013 1:06:20 PM CHAPTER 40 Non-chemical emergencies 814 Management of anaphylaxis General considerations In OH practice, anaphylaxis can occur in a ssociation with the administra- tion of immunizations. All OH departments that administer v accines must have adequate facilities for resuscitation. Resuscitation equipment should be latex free, particularly in the health care industry where the incidence of type 1 hypersen sitivity to latex among employees is signi \201 cant. OH staffs who administer vaccines sh ould be retrained in resuscitation pro- tocols annually. Prevention of anaphylaxis \200 Seek history of known allergy to vaccine components prior to immunization Vigilance in individuals who have a strong history of atopy, although immunization is not contraindicated. Diagnosis of anaphylaxis Rapid onset (variable, but usually within minutes of immunization) of: \200 Generalized itching, urticaria \200 Peri-orbital oedema \200 Peri-oral oede ma, oedema of the tongue and pharynx (with stridor) \200 Wheezing and dyspnoea \200 Col lapse with hypotension, tachycardia. Treatment of anaphylaxis \200 Mild (itching, but no features of angio-oedema or shock). O ral anti-histamines Moderate to severe: maintain airway and circulation if cardiovascular collapse (30 chest compressions to two ventilations if cardiorespiratory arrest) 100% oxygen, via mask, insert airway if unconscious \200 adrenaline 0.5 \200\2231mL of 1: 1000 (0.5 \200\2231mg) IM; can be repeated at 5min intervals according to pulse and blood pressure establish venous access and start IV colloids \200 give hydrocortisone 200mg by IM or slo w IV injection (can be repeated) and chlorpheniramine 10mg IM or slow IV injection \200 M oderate to severe cases will require admission because of risk of prolonged reactions and recurrence. Individuals who experience mild reactions can be discha rged with oral antihistamines. Reporting adverse reactions \200 Report to Committee on Safety of Medicines (CSM) using y ellow card scheme. M http://medicines.mhra.gov.uk/ Record in OH notes and counsel individual about avoidance \200 Report to GP with the indi vidual \200\231s consent. 40_Smedley_Chap40.indd 814 1/2/2013 1:06:20 PM MANAGEMENT OF ANAPHYLAXIS 815 Further information Resuscitation Council (UK). Available at: M http://www.resus.org.uk/ De partment of Health (2006). Immunization against infectious disease (The Green Book). DH, Lo ndon. Available at: M http://www.dh.gov.uk/prod_consum_dh/groups/dh_digitalassets/@ dh/@en/ documents/digitalasset/dh_128623.pdf 40_Smedley_Chap40.indd 815 1/2/2013 1:06:20 PM CHAPTER 40 Non-chemical emergencies 816 Management of needlestick and contamination incidents 1 Hazards associated with needlestick injury \200 Main hazards: HBV, HCV, HIV ( b p. 152, Hepatitis B; b p. 154, Hepatitis C; b p. 156, Human immunode \201 ciency virus) Any blood-borne infection (e.g. malaria) can be transmitted by needlestick injury (NSI) For prevention of NSIs see b p. 104, Human tissue and body \202 uids. Classi \201 cation of contamination incidents \200 Percutaneous: when a contaminated sha rp breaches intact skin \200 Mucocutaneous: when blood or body \202 uids splash onto mu cous membranes or non-intact skin 2 Intact normal skin is an effective barrier against BBV. Immediate \201 rst aid \200 Wash wound with soap and water; encourage bleeding gently \200 Irrigate exposed mucous membranes copiously with water. Risk assessment (see Tables 40.1 \200\22340.3) Table 40.1 Risk estimates derived from historical data on occupational transmissions Speci \201 c BBV Risk of transmission after percutaneous exposure to infected source material HBV Up to 30% for HBeAg positive source HCV 1.9% HIV 0.3% Source testing Source patients should generally be tested for HBV, HCV, and HIV: \200 Pre -test discussion and informed consent: are essential, and may be carried out by any appropriately trained and competent health care worker The unconscious source patient: should not normally be tested until consent has been obtained. If necessary, PEP should be commenced until the patient awakes. If a source patient has died, consent should normally be obtained from a relative. 40_Smedley_Chap40.indd 816 1/2/2013 1:06:21 PM MANAGEMENT OF NSI AND CONTAMINATION 1 817 Table 40.2 Risk estimates can be re \201 ned according to two aspects of the NSI Higher risk Lower risk Injury details Hollow needle Exposure to blood Puncture to ungloved hands Deep wound Sharp visibly blood-s tained Needle had been directly in the source \200\231s blood vessel Solid needle Exposure to other \202 uids * Puncture through gloves Super \201 cial wound Sharp not visibly blood-stained Mucocutaneous exposure Source infectivity HBeAg negative, anti-HBe positive Low/undetectable HIV viral load/ high CD4 count * There i s no evidence of transmission from non-blood-stained urine, saliva, feces, or tears. HBeAg positive High HIV viral load/ low CD4 count (terminal AIDS) Table 40.3 Follow-up of NSI recipients NSI (high risk or known +ve source) Baseline 6wks 12wks 24wks HbsAg HbsAg HBsAg HBsAg HCV HCV RNA HCV RNA Anti-HCV LFTs Anti-HCV HIV Anti-HIV All Store serum (for 2yrs) Follow-up highlighted in bold is quoted in published guidance from the Health Protection Ag ency or Expert Advisory Group on AIDS. Co-infection (HIV + HCV) in the source patient has been associated with late seroconversion s in the recipient HCW, so 24-wk follow-up should be considered in these cases. Post-exposure prophylaxis \200 HBV, HIV: see b p. 820, Management of needlestick injury 2 : hepatitis B virus post-exposure prophylaxis, b p. 822, Management of needlestick injury 3: human immu node \201 ciency virus post-exposure prophylaxis. HCV: at present there is no effective PEP against HCV, but follow-up aims to identify seroconversion early so that intervention with interferon can be offered. 40_Smedley_Chap40.indd 817 1/2/2013 1:06:21 PM CHAPTER 40 Non-chemical emergencies 818 Counseling and psychological support Despite the generally low risk of infection, NSIs are extremely anxiety- inducing. Careful risk communication, counseling, and support are vital. Restrictions from work Recipients of high risk NSIs should not be restricted from work (or EPPs) during follow-up, but advised to practice safe sex and avoid blood dona- tion. Fitnes s for EPPs (if seroconversion occurs) is covered in Chapter 24. Reporting procedures Exposure incidents from sources that are positive for BBV are reportab le \200 To HSE under RIDDOR 1995 \200 To the HPA Center for Infections (or to Health Pr otection Scotland) \200 In England, as a serious untoward incident to the Strategic Healt h Authority. Further information and guidance HPA (2012). Bloodborne viruses (BBVs) and occupational exp osure . Available at: M http://www.hpa. org.uk/infections/topics_az/bbv/guidelines.htm GMC (2012). Guidance on issues regarding consent. GMC, London. Available at: M http://www. gmc-uk.org/guidance/ethical_guidance.asp 40_Smedley_Chap40.indd 818 1/2/2013 1:06:21 PM This page intentionally left blank CHAPTER 40 Non-chemical emergencies 820 Management of needlestick and contamination incidents 2: hepatitis B post-exposure prophyla xis Indications Signi \201 cant occupational exposure to HBV positive source material. Regime \200 Treatment depends on whether the recipient has been immunized against HBV and (if so) whether they have achieved adequate immunity. See Table 40.4. Hepatitis B speci \201 c immunoglobulin (HBIG) is usually provided by the local HPA laboratory. If you provide cover for managing NSIs, ensure that clear arrangement s are in place to access HBIG promptly if indicated. Further information and guidance Department of Health (2006). Hepatitis B. In: Immunization against infectious disease: The Green Book . DH, London. Available at: M http://www.dh.gov .uk/prod_consum_dh/groups/dh_ digitalassets/@ dh/@en/documents/digitalasset/dh_108820.pdf HPA. Immunoglobulin handbook . Available at: M http://www.hpa.org.uk/webc/HPAwebFile/ HPAweb_C/1194947401259 40_Smedley_Chap40.indd 820 1/2/2013 1:06:21 PM 4 0 _ S m e d l e y _ C h a p 4 0 . i n d Table 40.4 Summary of post-exposure treatment for hepatitis B d 8 2 HBV status of person exposed Signi \201 cant exposure Non-signi \201 cant exposure 1 HBsAg positive source Unknown source HBsAg negative source Continued risk No further risk \211 1 dose HB vaccine pre-exposure Accelerated course of HB vaccine* HBIG \227 1 Accelerated course of HB vaccine* Initiate course of HB vaccine Initiate course of HB vaccine No HBV prophylaxis Reassure M A N A G E M E N T O F N S I \211 2 doses HB vaccine pre-exposure (anti-HBs not known) One dose of HB vaccine followed by second dose 1mth later One dose of HB vaccine Finish course of HB vaccine Finish course of HB vaccine No HBV prophylaxis Reassure Known responder to HBV vaccine (anti-HBs >10mLU/mL) Consider booster dose of HB vaccine Consider booster dose of HB vaccine Consider booster dose of HB vaccine Consider booster of HB vaccine No HBV prophylaxis Reassure HBIG \227 1 Consider booster dose of HB vaccine. A second dose of HBIG should be given at 1mth HBIG \227 1 Consider booster dose of HB vaccine. A second dose of HBIG should be given at 1mth Known non-responder to HB vaccine (anti-HBs <10mIU/mL 2 \200\2234mths post-vaccination) No HBIG Consider booster dose of HB vaccine No HBIG Consider booster dose of HB vaccine No prophylaxis Reassure A N D C O N T A M N A T O N 2 An accelerated course of vaccine consists of doses spaced at 0, 1, and 2mths. A booster dos e may be given at 12mths to those at continuing risk of exposure to HBV. Reproduced from Pu blic Health Lab Service, Hepatitis Subcommittee, Communicable Disease Report. 1992: 2, R97 \200\223R101. Permission granted. (Further details and explanation of terms used are contai ned in this article.) I I 1 / 2 8 2 1 / 2 0 1 3 1 : 0 6 : 2 1 P M CHAPTER 40 Non-chemical emergencies 822 Management of needlestick and contamination incidents 3: human immunode \201 ciency virus post-exposure prophylaxis Indications Signi \201 cant occupational exposure to source mate rial that is known to be infected with HIV, or high risk of infection and HIV test is not o btainable. Drug regime A combination of at least three oral anti-retroviral agents for 4wks, includ- i ng both nucleoside analog reverse transcriptase inhibitors (NRTIs) and protease inhibitors (PIs). The Expert Advisory Group on AIDS (EAGA) recommends the following standard regime Truvada o ne tablet (245mg tenofovir and 200mg emtricitabine (FTC)) once daily (od) plus Kaletra two \201 lm-coated tablets (200mg lopinavir/50mg ritonavir) bd. Other combinations of NRTIs and PIs are used in particular circumstances: \200 Where ther e is a suspicion of antiretroviral drug resistance in the source patient If the recipient is pregnant or has a medical condition \200 Where there is dif \201 cul ty in sourcing starter packs containing Truvada, Combivir plus Kaletra may be used. However, Truvada packs are now available from a number of sources. If the source patient has been treated with anti-retrovirals, OH profes- sionals are strong ly recommended to seek advice from an expert geni- tourinary physician with experience in t reating HIV disease. Timing of PEP The EAGA recommends that PEP is given as soon as possible after expo- sure an d certainly within 48 \200\22372h of exposure, and continued for at least 28 days. It is no t generally recommended to commence PEP beyond 72h post-exposure, but this is a matter for the judgment of local experienced clinicians. 40_Smedley_Chap40.indd 822 1/2/2013 1:06:21 PM MANAGEMENT OF NSI AND CONTAMINATION 3 823 Side effects of PEP \200 Serious side effects are rare, but one death has been reported w ith a previous PEP regime for an occupational exposure Unpleasant minor side effects (GI upset, headache) common; treatment with adjuvant anti-emetics and anti-diarrhoeals often required The newer PEP regime generally better tolerated than previous combination therapy, but there is still a high incidence of failure to adhere. Ef \201 cacy of PEP \200 Advice on HIV PEP is based on indirect evidence of ef \201 cac y in the prevention of vertical transmission of HIV, and on surveillance data following occ upational exposures PEP with Zidovudine has been shown (in a case control study) to reduce the risk of occupational transmission by 80% There have been documented cases of occupational transmission of HIV despite appropriate PEP. Further information and guidance Chief Medical Of \201 cers \200\231 Expert Advisory Group on AIDS (2008). HIV post-exposure prophylaxis: Guidance from the UK Chief Medical Of \201 cers \200\231 Expert Advisory Group on AIDS. Available at: M http://www.dh.gov.uk/en/Publi cationsandstatistics/Publications/PublicationsPolicyAndGuidance/ DH_088185 40_Smedley_Chap40.indd 823 1/2/2013 1:06:21 PM CHAPTER 40 Non-chemical emergencies 824 Psychiatric emergencies General points \200 Psychiatric emergencies are relatively common among people who have an established diagnosis of serious mental disorder, but unusual in the general workin g population A situation can be considered as an emergency when there is a serious and current risk to t he safety of the person and/or others. This danger may be: \200 a consequence of delibera te planning \200 or the risk can be unintentional. Immediate assessment of emergencies \200 Ensure the safety of the person \200 Try to sp eak with the person, recognizing that it is usually impractical to carry out a detailed psy chiatric assessment in these circumstances Ensure the safety of others (including yourself) while doing so 1 When there is an immediat e and serious risk of harm, there should be no delay in calling the police \200 If possib le, try to establish some dialog with the person. However, avoid confrontation and disagree ment. This may calm the situation, enable further evaluation of the problem, and perhaps gi ve an initial indication whether there is an underlying psychiatric disorder \200 A more detailed assessment of the person \200\231s mental state can be arranged thereafter in a more secure and specialist setting \200 When talking with the pe rson, it may be useful to ask about: what they are planning to do? \200 why they wish to harm themselves or others? \200 wha t, if anything, has happened very recently to them to prompt the crisis? whether they have had previous mental health problems? 1 Take any account of suicidal thoughts seriously. Particular concern is raised when a person makes clear statements of intent to kill themselves, particularly: \200 if they have made \201 rm plans of how to kill themselves \200 if they have curr ent signi \201 cant symptoms of depression and/or if they have experienced recent serious loss- Colleagues and management may have some knowledge, ask about: recent stress (whether or not work-related) \200 and any history of previous mental disor der. 2 A person whose behavior is considered dangerous as a result of a current mental disorder does not need to be detained using the Mental Health Act in order for them to be restrained in an emergency. This can be carried out under common law. Subsequent specialist assessmen t and treatment may require the person to be legally detained in hospital. 40_Smedley_Chap40.indd 824 1/2/2013 1:06:21 PM PSYCHIATRIC EMERGENCIES 825 Lower risk situations Some situations that cause alarm may not be regarded as medical emerg en- cies that require immediate and assertive intervention. However, they may make it impos sible for the person to continue working, and they would bene \201 t from early medical as sessment. Such situations may include: \200 Acts of self-harm without suicidal intent \200 Symptoms of mild or moderate mood disorder \200 Overwhelming symptoms of anxiety. I t will be useful to ensure the person agrees to be seen urgently by their GP, out-of-hours medical services or at the A&E department, and if neces- sary to make arrangements for them to be transported there. Particular psychiatric disorders \200 Behavior that is dangerous to self or others does n ot in itself indicate that a person is mentally ill. In many situations, such behavior aris es at times of crisis, and the person may well have behaved similarly in the past when face d with overwhelming dif \201 culties Current intoxication with alcohol and/or drugs may increase impulsivity and disinhibition In a minority of situations, current symptoms of an untreated serious mental disorder present a serious risk \200 people who have delirium may be disorientated , aroused, hallucinated, and irrational those who have acute schizophrenia may be violent as a result of command hallucinations, or because of their persecutory beliefs symptoms of acute mania may include irrational thinking and extreme excitement and irritability symptoms of severe depression may result in acts of serious self- harm It is very unlikely that a con \201 dent diagnosis can be made in the setting of an acute emergency. This will usually be possible only after further assessment and observation, phy sical examination and appropriate investigations, interviews with others who know the perso n, and knowledge of any previous psychiatric and medical history. 40_Smedley_Chap40.indd 825 1/2/2013 1:06:21 PM This page intentionally left blank 827 Chapter 41 Terrorism Terrorism (deliberate use of chemical, radiation or biological or nuclear weapons 828 Chemical weapons 829 Biological weapons 830 Radiation and nuclear weapo ns 832 41_Smedley_Chap41.indd 827 1/2/2013 1:07:04 PM CHAPTER 41 Terrorism 828 Terrorism (deliberate use of chemical or biological weapons, or radiation and nuclear weapo ns) Small groups of terrorists have the ability to cause massive damage and extensive human suffering with little or no warning. Emergency services must be able to respond rapidly an d appropriately to such scenarios. \200 Rescue and treatment of victims, and control and containment of \201 re or other hazards are complicated. Sites may be contaminated with n uclear, chemical, biological, or radiological substances The impact of weapons may stretch much further than the scene of disaster. Exposed personnel can spread contamination into other areas as they depart from t he scene As well as the physical injuries, there is major public fear over any use of such weapons, with the risk of signi \201 cant psychological casualties. Public reassurance and health r isk communication forms an essential part of the management of any incident Thorough contingency planning is necessary by all organizations likely to be involved. Routes of exposure \200 Radiation and chemical agents can enter the body by: inhalation \200 absorption through skin or eyes \200 injection by \202 ying glass or shrapnel \200 ingestion Biological agents are usually transmitted through inhalation. Other factors As well as the direct and indirect health effects from the terrorist agent, t he effect of risk controls on responding forces must be considered. Protective equipment li mits movement and carries risks of hyperthermia in its own right. Speci \201 c terrorist weapons Each main class of weapon is covered as a separate topic (s ee b p. 829, Chemical weapons; b p. 830, Biological weapons; b p. 832, Radiation and nuclea r weapons). Further information and guidance Guidance is available from the Health Protection Agency. A vailable at: M http://www.hpa.org.uk/ Topics/EmergencyResponse/CBRNAndDeliberateRelease/ 41_Smedley_Chap41.indd 828 1/2/2013 1:07:04 PM CHEMICAL WEAPONS 829 Chemical weapons Terrorists have used chemical weapons in the past, and it is likely to hap - pen again. There is the potential for large numbers of casualties. Numerous chemical agen ts exist, each with different symptoms and effects. Although some may require extensive lab oratory facilities to manufacture, others can be fabricated relatively simply. Much of the ef \201 cacy of such a weapon depends on its ability to disperse the material. Types of chemical weapons \200 Blood agent/cyanides: attack the capacity of the blood to hold and deliver oxygen, causing the victim to suffocate. Cyanide gasses and compounds are most common Nerve agents: affect the individual \200\231s nervous system. Most belong to the family of organophosphates, and have similarities to some pesticides