Clinical features The incubation period is usually 7 \200\22314 days for P. falciparum and 12 \200\22340 days for other types of malaria, but occasionally it is much longer ( > 1 yea r), especially in P. malariae and P. vivax infections. There is malaise, fatigue, fever and head- ache followed by paroxysms lasting 8 \200\22312hr of rigors, vomiting and then sever e sweating. The fever may be periodic (classically 48hr in P. ovale or P. vivax, and 72hr i n P. malariae ). Haemolytic anemia, jaundice and splenomegaly may occur, but lymphadenopath y is not a feature. P. falciparum may cause cerebral malaria with coma, \201 ts and focal neurological signs. Diarrhea, cardiac failure, pulmonary oedema and shock may occur. Deter ioration can be rapid. Investigations Consider Lassa fever ( b p.250) in recent visitors to West Africa. In any ill patient who has been in a malarious area send blood for thin and t hick \201 lm examination for malaria. Repeated blood \201 lms may be needed. Also arran ge FBC (since malaria may cause anemia, thrombocytopenia and neutropenia), blood glucose (h ypoglycaemia may be severe), U&E (renal failure is possible), and test the urine for blood ( \200\230black water fever \200\231). Treatment of falciparum malaria 1 Careful monitoring is needed ICU. Obtain expert advice from a tropical disease specialist ( b p.246), espe cially if the patient is severely ill or has come from south-east Asia, where there is wide spread drug resistance. Give quinine, orally or IV depending on the severity of illness: or al quinine sulfate 600mg (adult) or 10mg/kg (child) every 8hr for 7 days, followed by doxyc ycline 200mg od for 7 days, clindamycin 450mg tds for 5 days or Fansidar 3 tablets. Alte rnative oral drugs are Malarone (proguanil with atovaquone) or Riamet (artemether wit h lumefantrine): for details see BNF. For algorithm 1 see www.britishinfectionsociety.org . Treatment of benign malarias ( P. vivax, ovale, malariae ) 1 The usual treatment is chloro quine (see BNF ). A course of primaquine is also needed to prevent relapse in vivax and ova le infections, but glucose- 6-phosphate dehydrogenase levels should be checked before prima quine is used, since it may cause haemolysis in G6PD de \201 cient patients. In the UK ref er to an Infectious Diseases unit for treatment and follow-up. 1 Lalloo DG et al . ( 2007 ) UK malaria treatment guidelines . Journal of Infection 54 : 11 1 \200\223 121 . 248 CHAPTER 5 Infectious diseases Typhoid ND and paratyphoid ND (enteric fever) These fevers, caused by Salmonella typhi and S. paratyphi A, B, or C, occur throughout the world, especially where hygiene is inadequate . They are spread by contamination of food or water by urine or feces from a patient or an asymptomatic carrier. Typhoid may occur despite immu- nization. Typhoid and malaria are the \201 rst diseases to consider if fever develops soon after a visit to the tropics. The i ncubation period is usually 7 \200\22314 days, but may range from 3 \200\22360 days. Initial symptoms Headache, fever, and a dry cough, with abdominal discomfort and anorexia. Constipation is common, but diarrhea may occur, especially in children. Confusion and hallu cinations may develop. Physical examination This may be normal except for fever. There may be a relative brady- ca rdia (ie less than the usual 15 beats/min i in pulse rate per C of fever). Splenomegaly and abdominal tenderness occur, but there is no lymphadenopathy. \200\230Rose spots \200 \231 are pink macular spots on the lower chest or upper abdomen which blanch on pressure. T here may be signs of pneumonia or dehydration. Intestinal perforation or hemorrhage occur o ccasionally. Investigations FBC (mild anemia is common, WBC usually normal), blood \201 lms for malari a, U&E, LFTs, blood cultures, CXR (for signs of TB or pneumonia). Treatment Isolate and barrier nurse. Admit suspected cases to an Infectious Diseases unit a nd notify the local consultant in Communicable Disease Control. The usual drug treatment is with cipro \202 oxacin or cefotaxime but other antibiotics may be needed for drug-resista nt infections. Dengue Dengue is a mosquito-borne viral infection which is common in southern Asia, the wes tern Paci \201 c, central Africa and central and south America. Most infections are asympt omatic. Symptoms start after an incubation period of 4 \200\2237 days with fever, malaise, nausea and vomiting, headache, severe muscle and bone pains ( \200\230break bone fever \200 \231). Some patients have a transient macular rash, petechiae, lymphadenopathy, hepatomegal y, d WCC and platelets and i liver enzymes. Most patients recover after 3 \200\2237 days wi th symptomatic treatment. A few develop dengue shock syndrome (DSS) with hypotension, pleur al effusions, ascites, d plasma protein and bleeding problems. Abdominal pain may be severe . Treatment is supportive, with careful \202 uid balance management and IV \202 uids in DSS. With expert care most patients with severe dengue eventually make a full recovery. 249 RABIESND Poliomyelitis ND Paralytic poliomyelitis is rare in developed countries where vaccination i s routine. Fever is followed by signs of meningitis, pain and spasm in limb muscles. Respir atory failure may be fatal. Resuscitate and ventilate if necessary and refer to ICU. The differential diagnosis include s Guillain \200\223Barr syndrome ( b p.142) and organophosphate poisoning ( b p.206). Rabies ND Rabies is a viral infection of mammals that occurs in most parts of the world, in cluding much of the Arctic, as well as tropical and temperate regions. At present it is not endemic in the UK, Norway, Sweden, Iceland, Australasia, or Japan. Human and animal rabies is most common in the Indian subcontinent, China, Thailand, the Philippines, and parts of South America. Most human infections result from dog bites, but rabies can be transmitted b y many other domesticated or wild animals, such as cats and foxes. Rabies virus in an anima l \200\231s saliva may cause infection by contamina- tion of a bite or scratch or by absorp tion through mucous membranes of the eye, mouth or nose. Rarely, infection occurs from inha lation of the virus in bat-infested caves. Prevention of rabies after a bite is described o n b p.415. Advice about post-exposure treatment and suspected cases of rabies is available in the UK from the Health Protection Agency. For details see www.hpa.org.uk/Topics/Infectio usDiseases/InfectionsAZ/Rabies Clinical features The incubation period of rabies is usually 3 \200\22312 weeks, but can va ry from a few days to > 2 years. The \201 rst symptoms are itching, tingling or pain at the site of the bite wound. Headac he, fever, and malaise occur, with spreading paralysis and episodes of confusion, hallucina tion and agitation. Hydrophobia is characteristic: attempts at drinking cause spasm of musc les involved in breathing and swallowing and also profound terror. In 8 20 % of cases there is \200\230dumb rabies \200\231 with increasing paralysis but no episodes of spasm or hyp eractivity. Rabies is almost always fatal, even with ICU treatment. Management If rabies is suspected, barrier nurse the patient in a quiet room with the minim um of staff, who must wear gowns, gloves, eye protection and masks. Obtain advice immediate ly from a specialist in Infectious Diseases. Anticipate press enquiries. Record the names o f all staff involved, so that they can be offered rabies immunization. 250 CHAPTER 5 Infectious diseases Viral haemorrhagic fevers ND Lassa fever Lassa fever occurs in many rural parts of West Afr ica. It is a viral infection acquired from infected blood or secretions, transmitted by ina dvertent innoculation (eg needlestick injuries) or contamination of mucous mem- branes or b roken skin. In Africa it is transmitted by multimammate rats. The incubation period is up t o 3 weeks. There is a high mortality. Early symptoms are non-speci \201 c with fever, malaise, headache, sore throat, retrostern al chest pain and backache. Periorbital oedema, swelling of the neck and conjunctival injec tion are common. Suspect Lassa fever in any pyrexial patient who has been in rural West Afr ica (south of the Sahara) in the previous 3 weeks. However, malaria and typhoid are much mo re common and need urgent diagnosis and treatment. Management If Lassa fever is possible, barrier nurse the patient in a cubicle by staff wear ing gloves, gowns, goggles and masks. Take special care to avoid needlestick injuries, whic h may cause fatal infection. Before taking any blood samples, discuss the case with a tropi cal diseases specialist and the local consultant in Communicable Disease Control. Start tre atment immediately for falciparum malaria ( b p.247). Warn the laboratory about Lassa fever and send blood for examination for malaria. The patient will be admitted to an isolation b ed, possibly in a high security Infectious Diseases unit. Ebola fever and Marburg fever These are viral haemorrhagic fevers which occur in West and C entral Africa (Zaire, Uganda, Kenya and Sudan), and have similar clinical features and a hi gh mortality. Transmission is usually by infected blood, but the viruses may be acquired fr om monkeys or apes. The incubation period is usually 4 \200\22310 days. Illness starts sudd enly with severe headache, high fever, and generalized pains, especially in the back, follo wed by severe diarrhea, abdominal pain, dry throat, a maculopapular rash, conjunctivitis, a nd gastrointestinal bleeding. Isolate and treat as for suspected Lassa fever. Other viral haemorrhagic fevers Diseases with similar features (plus in some cases jaundice ) include dengue (see b p.248), Crimean-Congo fever (central Africa, parts of Eastern Europ e, and Asia) and yellow fever (Africa and South America). The initial management is the sam e as for Lassa fever. 251 SEVERE ACUTE RESPIRATORY SYNDROME Severe acute respiratory syndrome Background Severe acute respiratory syndrome (SARS) is a viral respiratory illness caused by a coronavirus. SARS was \201 rst recognized in March 2003, but probably originated in November 2002 in the Guangdong province of China, where th e virus has been found in wild animals. SARS spread to several countries, causing deaths in south-east Asia and Canada in March to May 2003. Few cases have occurred since then. No ca ses are known at the time of writing, but there is concern that SARS may re-emerge from Chi na. Spread SARS is spread by respiratory droplets produced when an infected person coughs, snee zes, or uses a nebulizer. The virus can also spread when someone touches an object contamin ated by infectious droplets and then touches his/her mouth, nose, or eyes. Features The incubation period of SARS is usually 2 \200\2237 days, but may be up to 10 day s. The illness starts with fever ( > 38 C), usually associated with rigors, head- ache, muscle pains and malaise. Diarrhea may occur. Some patients have mild respiratory symptoms initially. A dry cough develops after 2 \200\2237 days, with increasing breathlessness from hypoxia caused by pneumonia. Consider the possibility of SARS in a patient with these symp toms who, within 10 days of the onset of illness, has visited an area where SARS may occur (especially China) or worked in a laboratory holding SARS virus samples. CXR may be normal or may show patchy in \201 ltrates, and later areas of consolidation. WC C is usually normal or d initially (lymphopenia). Management If SARS is suspected, get expert help (ED consultant, Infectious Diseases specia list, and infection control staff) and isolate the patient (if possible in a negative press ure room). Ensure that the minimum number of staff have contact with the patient. Staff who do have contact must wear masks or respirators (of FFP3 standard), goggles, gowns and glov es, with strict handwashing and careful disposal of all items. Provide the patient with an N95 mask or a surgical mask. Record SpO 2 and give O 2 if necessary, but avoid \202 ow ra tes of > 6L/min, to minimize virus aerolization. If bronchodila- tors are needed, use a spa cer inhaler rather than a nebulizer. Maintain a list of all contacts. Expect press enquirie s. An expert will help to assess to decide about admission. Those admitted should ideally be p laced in a negative pressure isolation room with full infection control measures. Treat as for community-acquired pneumonia ( b p.110). Further information about SARS is available fr om: \200 www.hpa.org.uk/Topics/InfectiousDiseases/InfectionsAZ/ SevereAcuteRespiratorySyndrome/ (Health Protection Agency, UK). www.who.int/csr/sars/en/index.html (World Health Organization). 252 CHAPTER 5 Infectious diseases In \202 uenza pandemics, avian \202 u, and swine \202 u Background In \202 uenza is c ommon in the UK and many other countries, particularly during winter. Most people are ill f or only a few days with fever, muscle aches, coughing and nausea, but there are some deaths , especially in elderly people. Pandemic in \202 uenza occurs when a new subtype of in \202 uenza A emerges, which can sp read easily from person to person and which is different from previous strains (so there is no pre-existing immunity). In \202 uenza pandemics occurred in 1918 \200\2231919 (with 40 \200\22350 million deaths worldwide, including many children and young adults), and also i n 1957 and 1968. Another pandemic could develop at any time. There was concern about in \202 uenza A subtype H5N1, which infected poultry in Hong Kong in 1997 and 2003 and spread to birds across south-east Asia, with carriage by migrating birds across Asia and to Europe and Africa. This avian \202 u infected many millions of birds and some people in south-e ast Asia and Turkey who had been in close contact with infected chickens. The mortality in these cases was high. In 2009 in \202 uenza A subtype H1N1 caused a pandemic of swine \202 u which started in Mexico and spread to many other countries. Most patients with swine \202 u had only mild illness but a minority developed severe infection, and some died. Human-to-human spread of H1N1 or H5N1 \202 u is rare, at the time of writing, but another pandemic could develop if the virus mutates again. Spread Like SARS (see b p.251) \202 u is spread by droplets coughed or sneezed into the a ir, or by direct contact with hands contaminated with the virus. Features Consider the possibility of avian \202 u or swine \202 u in a patient with fev er (cid:116) 38 C and cough or breathlessness, who in the last 7 days has been in an are a affected by H1N1 or H5N1 in \202 uenza. Laboratory staff and health care workers in cont act with cases of severe unexplained respiratory illness could also be at risk. Management Isolate the patient and treat with precautions against transmission of the virus , as for SARS ( b p.251). Antiviral treatment with oseltamivir or zanimivir may be consider ed, depending on current guidelines. Further information Clinical guidelines about the assessment of suspected cases and the man - agement of in \202 uenza patients will be updated as the situation changes and if anothe r pandemic develops. Information is available from the UK Health Protection Agency: www.hpa .org.uk/infections/topics_az/in \202 uenza/pandemic 253 Chapter 6 Environmental emergencies Hypothermia Frostbite and non-freezing cold injury Drowning and near drowning Diving emerge ncies Heat illness Electrical injuries Radiation incidents 254 257 258 260 264 266 268 254 CHAPTER 6 Environmental emergencies Hypothermia: presentation De \201 nitions Hypothermia exists when the core temperature (T )<35 C. Hypothermia may be classi \201 ed as follows: Mild hypothermia = 32 \200\22335 C Moderate hypothermia = 30 \200\22332 C Severe hypothermia = <30 C Background Infants and the elderly are at particular risk. In young adults hypothermia is u sually due to environmental exposure (eg hill-walking or cold water immersion), or to immob ility and impaired conscious level from alcohol or drugs. In the elderly, it is more often a prolonged state of multifactorial origin: common precipitants include unsatisfactory hous ing, poverty, immobility, lack of cold awareness (autonomic neuropathy, dementia), drugs (s edatives, antidepressants), alcohol, acute confusion, hypothyroidism and infections. Clinical features Severe hypothermia may mimic death. Wide variations occur, but as core T d , cerebral and cardiovascular function deteriorate. At 32 \200\22335 C, apathy, amn esia, ataxia and dysarthria are common. At <32 C, conscious- ness falls progressively, l eading to coma, d BP, arrhythmias (check pulse for at least 1min before diagnosing cardiac arrest), respiratory depression and muscular rigidity. Shivering is an unreliable sign. VF may occur sponta- neously when T falls <28 C and may be provoked by limb movement or invasive procedures (especially in the presence of hypoxia). Diagnosis Check tympanic T (or rectal T with an electronic probe or low-reading therm ometer). Tympanic and rectal T may lag behind core (cardiac) T during rewarming. Oeso phageal T re \202 ects core levels more accurately, but requires special equipment. Investigations \200 U&E. \200 FBC, toxicology and clotting screens. Note that hypotherm ia can cause or aggravate coagulation disturbances. Blood glucose (BMG reading may be falsely d ). \200 Amylase ( i levels common, but do not necessarily imply pancreatitis). \200 Blood cultures. \200 ABG. \200 ECG: look for p rolongation of elements in the PQRST complex, J-waves, and arrhythmias (AF and bradycardias are the commonest) (Fig. 6.1 ). \200 CXR: look for pneumonia, aspiration, left ventricul ar failure. Other X-rays may be required after rewarming (eg for suspected fractured neck o f femur). CT scan may be indicated if head injury or stroke is suspected. 255 HYPOTHERMIA: PRESENTATION I v1 v4 avR avL II v5 v2 avF v3 III v6 RHYTHM STRIP II Fig. 6.1 ECG in hypothermia. Notes on this ECG \200 Rhythm disturbance: atrial \201 brillation with slow ventricular response. \200 Prolongation of QRS. \200 Delayed repolarization \200\230J-waves \200 \231 (arrowed). \200 ST \200\223T wave abnormalities. 256 CHAPTER 6 Environmental emergencies Hypothermia: management Principles \200 Treat in a warm room ( > 21 C). \200 Handle the patient gently (to d risk of VF). \200 Remove wet clothes and dry the skin. \200 Mo nitor ECG. \200 Give warmed, humidi \201 ed O 2 by mask. \200 Intubation, if needed, s hould be preceded by oxygenation and must be performed expertly to avoid precipitating arrhythmias. Secure IV access. IV \202 uid is rarely required unless there is loss of volume from anot her cause. If BP d during rewarming, give 300 \200\223500mL of warmed 0.9 % saline or collo id. In unstable patients, consider CVP and urinary catheter. Warm IV \202 uid administrat ion is an inef \201 cient rewarming method and runs the risks of \202 uid overload and p recipitating arrhythmias. Correct hypoglycaemia if present with IV glucose. \200 If CPR is required, give chest com pressions and ventilations at standard rates. In hypothermic cardiac arrest, the heart may be unresponsive to de \201 brillation, pacing and drug therapy. Drug metabolism is d and unpredictable: avoid drugs until core T > 30 C. De \201 brillation is appropriate at normal energy levels if VF/VT occurs. If 3 shocks are unsuccessful, defer further shocks until core T > 30 C. Rewarming methods The choice depends upon the severity and duration of the condition, avail able facilities and the individual patient: Passive rewarming Easy, non-invasive, and suita ble for mild cases (T > 32 C). d evaporative and conductive losses by wrapping in war m blankets (remember to cover the back and sides of the head) polythene sheets. Avoid sp ace blankets which are noisy and have no advantages over polythene sheets. Endogenous metab olism and shivering usually generate enough heat to allow spontaneous rewarming. Aim for a rate of 0.5 \200\2232 C/hr, but do not rewarm the elderly with prolonged hypothermia too rapidly ( > 0.6 C/hr), as hypotension or cerebral/pulmonary oedema may develop. Active rewarming A water bath at 8 41 C is rapid and useful for immersion hypothermia, but cann ot be used in injured patients or if CPR is required. Airway care, ventilation and monitori ng are dif \201 cult, and hazards include core T after- drop and BP d due to peripheral vasodilation. Hot water bottles and heat pads are less ef \201 cient and can cause burns. A hot air blanket is more con- venient than a water bath, provides some heat and reduces h eat loss. Core rewarming \200 Airway warming with heated (40 \200\22345 C) humidi \201 ed O 2 provides some additional heat and reduces heat loss. It can be combined with ot her rewarming methods. It may reduce the risk of cardiac arrhythmias. \200 Peritoneal lav age is simple, and quick to set up. Saline at 45 C is run in via a DPL catheter ( b p.34 7), left for 10 \200\22320mins and replaced with a fresh warm supply. The \202 uid direct ly heats the liver and retroperitoneal structures including blood in the IVC. Extracorporeal rewarming with cardiopulmonary bypass maintains brain and organ perfusion an d, if available, is the method of choice in patients with severe hypothermia or cardiac arr est. Cardiopulmonary bypass can result in rapid rewarming with core T i at 1 \210\222 2 C/5min. 257 FROSTBITE AND NON-FREEZING COLD INJURY Frostbite and non-freezing cold injury Frostbite 1, 2 Frostbite occurs when tissues freeze at sub-zero temperatures. Predisposing factors include inadequate clothing/footwear, hypoth ermia, exhaustion, alcohol (which impairs judgment), drugs (eg beta-blockers), peripheral v ascular disease, smoking, and previous cold injury. Frostbite usually involves extremities, especially \201 ngers, toes, nose and ears. Frostnip may precede frostbite. The skin of the nose, face or \201 ngers goes white and numb, but recovers rapidly on protection from the cold, with transient paraesthesiae but no tissue loss and no permanent damage. Super \201 cial frostbite involves skin and subcutaneous tissues. The frozen area is numb, and lo oks white and waxy. Tissues feel \201 rm or hard but are still pliable. Rewarming is pain ful. Oedematous hyperaemic skin becomes mottled or purple, with serum- \201 lled blisters. A hard black eschar forms, and after 8 3 weeks this separates, revealing sensitive red shi ny skin. Deep frostbite involves muscles, nerves and sometimes bone, as well as skin and su per \201 cial tissues. The damaged area is hard and remains gray or white after rewarming. Blood- \201 lled blisters develop. The dead tissue mummi \201 es and then separates afte r several weeks or months. Treatment of frostbite varies with the situation and facilities. Only frostnip should be treated in the \201 eld. Frostbitten tissues need rewarming as s oon as possible but further damage must be avoided: it is better to walk out on frozen feet than on partially thawed feet. Treat hypothermia before frostbite. Rewarm frostbitten limb s in water at 37 \210\222 39 C until skin circulation returns (usually 830min). Give an algesia and ibuprofen (which inhibits prostaglandins). After rewarming let the area dry in warm air (do not towel dry). Elevate the limb. Expose the area, with a bed cradle to avoid pressure of bedclothes. Clean the area daily in a whirlpool bath and encourage movement. If necessary split eschar to relieve stiffness, but avoid surgical debridement and amputation s and allow the eschar to separate spontaneously: premature surgery causes avoidable tissue loss. Expert advice is helpful in severe frostbite: the British Mountaineerng Council ( ww w.thebmc.co.uk ) has a frostbite advice service. Bone scans or MRI/MRA may help to de \201 ne deep tissue injury. In severe frostbite early thrombolysis with tPA may reduce the risk of eventual amputations. Non-freezing cold injury 1, 2 Trench foot (immersion foot) is caused by prolonged immersion in cold water or wet boots at temperatures just above freezing. Vasoconstriction causes ti ssue ischaemia and nerve damage. The feet are initially cold, numb and pale or mottled. On rewarming they become red, swollen and very painful. Blisters may develop. Treatment : keep the feet clean, warm and dry, elevated to reduce oedema. Outcome : most patients recover fully, but some have continued pain, paraesthesiae and sens itivity to cold. 1 State of Alaska Cold Injury Guidelines . www.chems.alaska.gov/EMS/documents/AKColdInj2005 . pdf 2 Imray C et al . ( 2009 ) Cold damage to the extremities: frostbite and non-freezing cold injuries . Postgraduate Medical Journal 85 : 481 \200\223 8 . 258 CHAPTER 6 Environmental emergencies Drowning and near drowning De \201 nitions Drowning is death by suffocation from submersio n in any liquid. Drowning is a common cause of death in young people. 40 % of drownings occ ur in children aged <4 years. Near drowning is survival (at least temporarily). In adults, the commonest predisposing fac tor is alcohol, sometimes with other drugs. A signi \201 cant proportion re \202 ect atte mpted suicide. In the UK, marine near drowning is usually associated with hypothermia ( b p .254). Pathophysiology Wet drowning Involves signi \201 cant aspiration of \202 uid into the lu ngs. This causes pulmonary vasoconstriction and hypertension with ventilation/ perfusion mi smatch, aggravated by surfactant destruction and washout, d lung compliance and atelectasis . Acute respiratory failure is common. ABG shows hypoxia, hypercarbia, and mixed respirator y/metabolic acidosis. The onset of symptoms can occur rapidly, but in lesser insults, sympt oms may be delayed. Contamination Water contaminated with chemical waste, detergents etc., may induce further l ung injury. Electrolytes Irrespective of whether aspirated water is salt, fresh, or swimming pool, chan ges in serum electrolytes and blood volume are similar, and are rarely immediately life-thr eatening. Gastric \202 uid Swallowing of \202 uid into the stomach, with gastric dilatation, vomi ting, and aspiration, is common. Dry drowning In 810 \200\22320 % of deaths from drowning, a small amount of water entering the larynx causes persistent laryngospasm, which results i n asphyxia and an immediate outpouring of thick mucus, froth, and foam, but without signi \201 cant aspiration \200\224 this is \200\230dry drowning \200\231. Secondary drowning A deterioration in a previously apparently well patient following succes sful resuscitation after submersion. It may occur in 5 \200\22310 % of initial survivors. The mammalian diving re \202 ex This is probably seen only in young children, but may expl ain why successful resuscitation without neurological de \201 cit can occur after prolonge d immersion. Cold water stimulates facial nerve afferents, while hypoxia stimulates the car otid body chemoreceptors. These effects re \202 exively d heart rate and vasoconstrict ski n, GI tract and skeletal muscle vessels, redistributing blood to the brain and heart. Assoc iated hypothermia results in d metabolic demands, delaying cerebral hypoxia. 259 DROWNING AND NEAR DROWNING Management \200 Consider associated injury (eg to the cervical spine from diving into a shallow pool or sur \201 ng), and treat appropriately. Maintain the airway. Remove regurgitated \202 uid/debris by suction of the upper airway. Ensure adequate ventilation and correction of hypoxia. If the patient does not have a gag r e \202 ex or is apnoeic, ventilate with a bag and mask and proceed to early tracheal intub ation and IPPV. In possible. IPPV spontaneously breathing patients, give the highest FiO 2 will be required if hypoxia and/or hypercapnia are present despite O 2 therapy, or if there are signs of pulmonary oedema. Ventilation with PEEP may signi \201 cantly improve oxygen ation by i functional residual capacity, improving V/Q mismatch and enhancing \202 uid re sorption from the pulmonary bed. However, PEEP may d venous return to the heart. \200 If the patient is in cardiac arrest, commence CPR ( b p.46). De \201 brillation may not be su ccessful until core T > 30 C ( b p.256). Appropriate rapid core rewarming techniques are required. Remove all wet/cold clothing. \200 Monitor core T and start rewarming ( b p.256). \200 NG tube to relieve gastric dilatation. \200 Check U&E, blood glucose, ABG, FBC, CXR , ECG. \200 Consider the possibility of alcohol, illegal drugs or drug overdose. Keep urine and blood samples and test if appropriate, eg paracetamol. Do not use \200\230prophylactic \200\231 steroids or barbiturates. \200 Antibiotics may be warranted if contaminated water (eg sewage) is involved (see b Leptospirosis, p.239). Inhalation of mud/sand etc may require bronchoscopy for clearance. Outcome Resuscitation without cerebral de \201 cit is possible after prolonged submer- sio n (even > 60min), particularly if associated with hypothermia. 50 % of children recovered a pparently lifeless will survive, and even adults with GCS 3 _ 4 / 15 and \201 xed dilated pupils can survive unimpaired. Respiratory effort is a sensitive prognostic sign, but in h ypothermic patients its absence does not necessarily imply poor outcome. Note the time to t he \201 rst spontaneous inspiratory gasp. Poor prognostic factors include extremes of age, severe acidosis, immersion > 5 min, and co ma on admission. Good prognostic factors include patients who are alert on admission, hypothermia, older chi ldren/adults, brief submersion time, and those who receive rapid on-scene basic life suppor t and respond to initial resuscitation measures. Asymptomatic patients who have no abnormality on repeated clinical examination, ABG and CXR require observation for at least 4 \200\2236 hours prior to considering discharge. Admit a ll others to ICU or general ward as appropriate. 260 CHAPTER 6 Environmental emergencies Diving emergencies: 1 Consider any symptom developing within 48 hours of a dive as related to the dive until proven otherwise. On suspicion of a diving-related episode, seek speciali st advice urgently (see Table 6.1 ). Diving related emergencies fall into four main categories: drowning ( b p.258), barotrauma, decompression illness, and marine bites or stings ( b p.416). Barotrauma May occur in any gas-containing body cavity during descent or ascent. Descent barotrauma ( \200\230squeeze \200\231) results from compression of gas in enclosed spaces as the ambient pressure i . Commonly, the ears, sinuses and skin are affected. Middl e ear squeeze may be precipitated by Eustachian tube congestion and leads to erythema, hemo rrhage, or tympanic membrane perforation with conductive hearing loss. Round or oval window rupture (inner ear squeeze) occurs with sudden pressure changes between the middle and inn er ear and results in acute tinnitus, vertigo and deafness, and a perilymphatic \201 stul a. ENT opinion is urgently required if a perilymphatic \201 stula is suspected and for ca ses of severe or continuing symptoms. If tympanic membrane rupture has not occurred, middle ear squeeze can usually be managed with decongestants/simple analgesics. If it has rupture d, give antibiotics ( b p.551). Instruct the patient not to dive until the symptoms have re solved and the drum has completely healed. Sinus barotrauma has a similar etiology to middle ear injury and is often associated with U RTI, mucosal polyps and sinusitis. Treat similarly to ear barotrauma. Divers who fail to exhale periodically via the nose into their face mask during descent may develop \200\230face mask squeeze \200\231 (skin barotrauma). Erythema, bruising, and pet echial and conjunctival hemorrhages develop in the enclosed area. Skin tightly enclosed by parts of the diving suit can have similar appearances. Usually no treatment is required. Ascent barotrauma is the reverse of squeeze, and particularly affects the lungs. It may be caused by breath-holding during rapid uncontrolled ascent or by air trapping in patients wi th asthma or congenital lung bullae. Mediastinal emphysema is the commonest event and prese nts with i hoarseness, neck swelling, and retrosternal chest discomfort. Symptoms usually r esolve spontaneously with high concentrations of O 2 . Pneumothorax is a potentially life-t hreatening complication if it develops during the dive, as the intrapleural gas cannot be v ented and increasing ascent will precipitate tension. Conventional treatment by needle deco mpression, aspiration or chest drain insertion ( b p.336) is required. Dental pain may occur on ascent or descent in carious teeth or those which have had recent \201 llings. The affected tooth is tender on tapping. Treat symptomatically with analgesi cs and arrange dental referral. 261 DIVING EMERGENCIES: 1 Table 6.1 Sources of advice on diving emergencies and hyperbaric chambers England, Wales, Northern Ireland Diving Incident Telephone Advice Line, Institute of Naval Medicine Gosport, Hampshire Telephone 07831 151523 (24 hrs) Ask for Duty Diving Medical Of \201 cer Diving Diseases Research Center Telephone 01752 209999 (24 hrs) Ask for the Duty Diving Doctor Plymouth www.ddrc.org Scotland Hyperbaric Medicine Unit Aberdeen Royal In \201 rmary www.hyperchamber.com Telephone 0845 408 6008 State \200\230diving emergency \200\231. Give your name and teleph one number. Ask for the Duty Hyperbaric Doctor In the event of any dif \201 culties in contacting these agencies in the UK, telephone 999 and ask for COASTGUARD Other countries Divers Alert Network DAN Diving Emergency Hotline (USA) + 1 919 684 8111 www.diversalertnetwork.org This has links to diving emergency contact numbers throughout the world Further information Diving and Hyperbaric Medicine Division, Institute of Naval Medicine (G osport, Hampshire, England) . http://www.royalnavy.mod.uk/training-and-people/rn-life/medical-branch/institute -of- naval-medicine/diving-and-hyperbaric-medicine-division-dhmd/ Diving Diseases Research Center (Hyperbaric Medical Center, Plymouth, England) . www.ddrc.o rg British Hyperbaric Association . www.hyperbaric.org.uk/ Scottish Diving Medicine . www.s dm.scot.nhs.uk Divers Alert Network . www.diversalertnetwork.org 262 CHAPTER 6 Environmental emergencies Diving emergencies: 2 Decompression illness There are two forms of decompression illness. T he \201 rst occurs when dissolved nitrogen in blood and tissues is not expelled at a suf \201 cient rate to prevent bubble formation. The second occurs when air bubbles are releas ed into the circulation because of pulmonary barotrauma. This follows if air bubbles enter the pulmonary capillaries from ruptured alveoli. The bubbles travel via the left side of th e heart to the systemic circulation. Cerebral air embolism usually causes symptoms as the d iver surfaces, with loss of consciousness, \201 ts, cardiovascular collapse and chest pai n. Clinically, differentiation between the two forms is dif \201 cult and initial manageme nt is the same. In general, the sooner the onset of symptoms, the greater the likely severi ty. Symptoms may be attributed by the patient (and the unwary doctor) to musculoskeletal sp rains/strains or other minor injury. Decompression illness is more likely in divers who have not followed safe ascent recommenda tions, the obese, in cold water, and when excessive exercise has occurred during the dive. It may be precipitated by air travel if insuf \201 cient time is left between diving and \202 ying for residual nitrogen to leave the body in a controlled fashion. Bubbles have di rect mechanical and local in \202 ammatory effects, commonly involving joints, skin, CNS, lungs and ears. Joint pain, \200\230the bends \200\231, most often affects shoulders and elbows. A dull ac hing sensation, i by movement but without localized tenderness is common. Pruritic rashes, local swelling and a peau d \200\231orange effect may occur. Back pain, limb weakness, sens ory abnormalities or urinary retention imply spinal cord involvement. Central effects inclu de focal de \201 cits, cerebellar disturbance and mood changes. Treatment for decompression illness is recompression. If delayed, risks of permanent damage to brain and spinal cord greatly i . The diagnosis of decompression sickness may only foll ow the response to recompression. Pending this, give the highest possible concentration of O 2 . Analgesics and sedatives can mask recompression responses and should only be used on specialist advice. Entonox is absolutely contraindicated. If intubation is required, in \202 ate the ET tube cuff with sterile water, since during r ecompression an air- \201 lled cuff will de \202 ate. IV \202 uids (0.9 % saline or a p lasma expander) assist oxygenation of ischaemic tissues and facilitate discharge of excess tissue nitrogen load into the venous system by ensuring adequate circulating volume. Some c enters may recommend aspirin and/or dextran solutions to d capillary sludging which accompa nies severe decompression sickness. Despite dry or wet suits, hypothermia is common. Treat with appropriate passive or active r ewarming ( b p.256). 263 DIVING EMERGENCIES: 2 Air evacuation If, after consultation with the diving medical center, air evacuation is nec essary, unpressurized aircraft should not \202 y above 300m. The diver should breathe 100 % O 2 . On reaching the diving center, recompression to a simulated depth of 18m with 100 % O 2 occurs, interspersed with periods of air breathing to d O 2 toxicity risk. Slow decom pression then follows standard treatment protocols. Divers usually dive in pairs. If a diver has symptoms of decompression sickness or pulmonar y barotrauma, his \200\230buddy \200\231 will be at risk also. Although recompression may not be required in the buddy, transfer him/her along with the affected diver and their divi ng equipment to the recompression facility. Obtain the following information before referral, if possible: \200 The patient \200\231s current condition, progression since onset, and response to treatment. Time of onset of symptoms related to the dive. \200 Dive pro \201 le and history (depth, duration, activity during the dive, speed of ascent including details of any stoppages, en vironmental conditions (water temperature, currents, etc.), pre-dive exercise, alcohol, dru gs and food, type and condition of diving equipment used, clothing worn, other recent dives ). Many divers store much of this information in a dive computer. Previous medical history, previous diving-related episodes, drug history. 264 CHAPTER 6 Environmental emergencies Heat illness Body T is normally kept at 36 \200\22338 C by homeostatic mechanisms whi ch are controlled by the hypothalamus. Hyperthermia occurs when these mechanisms are overwh elmed by factors acting individually, or (commonly) together. These conditions can occur ev en in temperate climates. At-risk groups include the young and the elderly in conditions of i temperature and humidity, and patients with unaccustomed or prolonged muscular activity (eg at \200\230raves \200\231, associated with ecstasy or other drugs), grand mal \201 t ting, athletes, marathon runners and armed forces recruits. Predisposing medical factors include \200 Alcohol use or withdrawal (including delirium t remens). \200 Cardiac disease. \200 Any condition which may cause or aggravate Na + /H 2 O loss