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Ovid: Oxford Handbook of Accident and Emergency Medicine

Editors: Wyatt, Jonathan P.; Illingworth, Robin N.; Clancy, Michael J.; Munro, Philip T.; Robertson, Colin E. Title: Oxford Handbook of Accident and Emergency Medicine, 2nd Edition Copyright ©2005 Oxford University Press > Table of Contents > Chapter 6 – Environmental emergencies Chapter 6 Environmental emergencies P.246
Near drowning and drowning Definitions Drowning is death by suffocation from submersion in any liquid. Drowning is a common cause of death in young people. 40% of drownings occur in children aged <4yrs. Near drowning is survival (at least temporarily). In adults, the commonest predisposing factor is alcohol, sometimes with other drugs. A significant proportion reflect attempted suicide. In the UK, marine near drowning is usually associated with hypothermia (p256). Pathophysiology Wet drowning Involves significant aspiration of fluid into the lungs. This causes pulmonary vasoconstriction and hypertension with ventilation/perfusion mismatch, aggravated by surfactant destruction and washout, ↓lung compliance and atelectasis. Acute respiratory failure is common. ABG shows hypoxia, hypercarbia and mixed respiratory/metabolic acidosis. The onset of symptoms can occur rapidly, but in lesser insults, symptoms may be delayed. Contamination Water contaminated with chemical waste, detergents etc, may induce further lung injury. Electrolytes Irrespective of whether aspirated water is salt, fresh or swimming pool, changes in serum electrolytes and blood volume are similar and are rarely immediately life-threatening. Gastric fluid Swallowing of fluid into the stomach, with gastric dilatation, vomiting and aspiration, is common. Dry drowning In ≈10-20% of deaths from drowning, a small amount of water entering the larynx causes persistent laryngospasm, which results in asphyxia and an immediate outpouring of thick mucus, froth and foam, but without significant aspiration—this is ‘dry drowning’. Secondary drowning A deterioration in a previously apparently well patient following successful resuscitation after submersion. It may occur in 5-10% of initial survivors. The diving reflex This is probably seen only in young children, but may explain why successful resuscitation without neurological deficit can occur after prolonged immersion. Cold water stimulates facial nerve afferents, while hypoxia stimulates the carotid body chemoreceptors. These effects reflexly ↓heart rate and vasoconstrict skin, GI tract and skeletal muscle vessels redistributing blood to brain and heart. Associated hypothermia results in ↓metabolic demands, delaying cerebral hypoxia. P.247

  • Consider associated injury (eg to the cervical spine from diving into a shallow pool or surfing), and treat appropriately.
  • Maintain the airway. Remove regurgitated fluid/debris by suction of the upper airway. It is crucial to ensure adequate ventilation and correction of hypoxia. If the patient does not have a gag reflex, or is apnoeic, ventilate with a bag and mask and proceed to early tracheal intubation with IPPV. In spontaneously breathing patients, give the highest FiO2 possible. IPPV will be required if hypoxia and/or hypercapnia are present despite O2 therapy, or there are signs of pulmonary oedema. PEEP ventilation may significantly improve oxygenation by ↓functional residual capacity, improving V/Q mismatch and enhancing fluid resorption from the pulmonary bed. However, PEEP may ↓venous return to the heart and this should be commenced under ITU guidance. Inhalation of mud/sand etc may require broncoscopy for clearance.
  • If the patient is in cardiac arrest, commence CPR (p46). Conventional CPR is appropriate, but defibrillation may not be successful until core T°>30°C (p258). Appropriate rapid core rewarming techniques are required.
  • Remove all wet/cold clothing.
  • Monitor core T° and start rewarming (p258).
  • Relieve gastric dilatation and water absorption from the stomach by NG tube.
  • Check U&E, blood glucose, ABG, FBC, CXR, ECG.
  • Consider the presence of alcohol, drugs of abuse or in the case of possible intentional overdose, other drugs. Alcohol and/or paracetamol blood levels may be appropriate.
  • Do not use ‘prophylactic’ steroids, or barbiturates.
  • Antibiotics may be warranted if contaminated water (eg sewage) is involved (see p229).

Outcome Resuscitation without cerebral deficit is possible after prolonged submersion (even >60mins), particularly if associated with hypothermia. 50% of children recovered ‘apparently lifeless’ will survive, and even adults GCS 3-4/15 with fixed dilated pupils can survive unimpaired. Respiratory effort is a sensitive prognostic sign, but in hypothermic patients its absence does not necessarily imply poor outcome. Note the time to the first spontaneous respiratory gasp. Poor prognostic factors include extremes of age, severe acidosis, immersion >5mins and coma on admission. Good prognostic signs are patients who are alert on admission, hypothermia, older children/adults, brief submersion time and those who receive rapid on-scene basic life support and respond to initial resuscitation measures. Asymptomatic patients who have no abnormality on repeated clinical examination, ABG and CXR require observation for at least 4-6h prior to considering discharge. Admit all others to ITU or general ward as appropriate. P.248
Electrical injuries An electric shock can cause cardiac and respiratory arrest. The heart often restarts spontaneously, but the respiratory arrest may be prolonged, causing fatal hypoxia. Thermal injury from the electric current produces burns and muscle damage. Muscle spasms from a shock may result in dislocations or fractures or precipitate a fall causing major trauma. Fatal electrocution can occur from domestic electricity (in the UK 230volts, alternating current at 50cycles/sec), but severe injury is more common with high voltage shocks (>1000volts). Lightning causes a direct current (DC) shock at a very high voltage (up to 100 million volts), but short duration (0.1-1milliseconds). Electrical flash and arc burns An electrical short-circuit near to a person may cause sudden vaporization of metal and deposition of a thin layer of hot metal on the skin, without any electricity passing through the casualty. Electrical flash burns may look dramatic because of discolouration of the skin, but are often superficial and heal uneventfully. In contrast, electrical arcing produces high temperatures and may cause deep dermal or full thickness burns, especially if clothing is set alight. Contact burns If electricity has passed through the patient there are usually two or more entry or exit wounds, which are full thickness burns with white or charred edges. Tissue damage is more extensive than the visible burns, especially with high voltage injuries. Deeper layers of skeletal muscle may be involved and muscle damage can cause myoglobinuria and renal failure. Myonecrosis and oedema of muscles may produce a compartment syndrome (p384). If current passes through the torso, cardiac arrhythmias are more likely than if only a single limb is involved. Myocardial damage may occur, often in association with vascular injuries. Neurological effects of electric shocks include coma, seizures, headaches, transient paralysis, peripheral neuropathy and mood disturbances. Ophthalmic injuries are common after electrical burns of the head. Cataracts and glaucoma may develop later. Electrocution in pregnancy has major risks for the fetus (spontaneous abortion has been reported). Obtain obstetric advice. Lightning The sudden vaporization of sweat and rain water caused by lightning may explode clothes and shoes off the victim and rupture ear drums. Lightning burns are superficial, often with a characteristic feathered or fern-like appearance. The limbs are often cold and mottled due to arterial spasm, which usually resolves over a few hours. Deep muscle damage and myoglobinuria are rare. Coma may result from direct brain injury, head injury due to a fall, or cardiac arrest. CPR, if indicated, may be successful even if required for prolonged periods. Survivors may be confused and amnesic for several days and may have fits and temporary paralysis. Cataracts are common. P.249

  • At the scene, make sure that the current is turned off before anyone approaches or touches the casualty. Remember that high voltage electricity can arc through the air or pass through the ground.
  • Check the airway, breathing and circulation. Electrical burns of the mouth and throat may cause oedema and airway obstruction.
  • Perform CPR (p46) if necessary, but minimize movement of the spine in case of trauma.
  • Examine thoroughly for head, chest, abdominal and skeletal injuries.
  • Examine all over for skin entry/exit burns and check pulses and sensation.
  • Check the ECG: there may be arrhythmias (eg AF), conduction defects, ST elevation and T wave changes.
  • Check FBC, U&E and creatine kinase (except in minor low-voltage burns).
  • Test the urine for blood. If the stick test is +ve for blood, but there are no RBC on microscopy, treat for myoglobinuria to prevent renal failure: obtain specialist advice and maintain a high urine output, consider using mannitol ± isotonic sodium bicarbonate.
  • Fluid loss into muscles results in hypovolaemia: IV fluids are often required. After high voltage injuries, widespread fasciotomies may be needed, with excision or amputation of non-viable tissues and inspection and further debridement after 48h.

Admission It is reasonable to allow home asymptomatic patients with domestic and minor low voltage burns, a normal ECG, no history suggestive of arrhythmia (eg palpitations) and no myoglobinuria, but review if any problem develops. Admit children who bite electric flexes for observation because of the risk of delayed bleeding from labial blood vessels. Many patients with electrical injuries will need admission for observation and monitoring. Admit all patients with high voltage conduction injuries, cardiac arrhythmias, chest pain or ECG abnormalities, vascular injury or myoglobinuria. P.250
Radiation accidents In the UK, 24hr advice/assistance is available via NAIR (National Arrangements for Incidents involving Radioactivity) on telephone 0800 834153 or via the police. It is important to distinguish between external irradiation of a person and contamination with radioactive material. Someone exposed to X-rays or to gamma rays in a radiation sterilizing unit receives no further radiation after removal from the source and there is no risk of contaminating anyone else. However, a person contaminated with radioactive material is still exposed to radiation and needs urgent but careful decontamination to minimize the risks to himself and to other people. Some hospitals are officially designated for the care of casualties contaminated with radioactive substances, but in an emergency a patient may be taken to any A&E department, where a plan for such events should exist. Anticipation of a radiation accident

  • Inform the A&E consultant on duty immediately if a patient from a radiation accident arrives or is expected.
  • Get advice and help from a radiation physicist (from Medical Physics or radiotherapy department).
  • Implement the appropriate Radiation Incident Plan to deal with the patient.
  • Expect media enquiries.

Treatment of contaminated casualties Where possible, treatment should take place in a designated decontamination room. This room should have a separate entrance, ventilation arrangements, decontamination facilities with shower and contaminated water collection facilities. Cover the floor of this room and entrance/exit corridors with disposable sheeting. All staff must themselves be decontaminated and checked before leaving this area.

  • Turn off air conditioning.
  • Pregnant and potentially pregnant staff should not be involved.
  • Provide any necessary life-saving treatment, but avoid spreading contamination.
  • ‘Barrier nurse’, as for an infectious disease.
  • Assume patients are contaminated until they have been checked by the radiation physicist.
  • Instruct patients and staff not to eat, drink or smoke.
  • Involve the minimum number of staff, who should wear facemasks, theatre clothing with impermeable gowns or plastic aprons, two pairs of gloves and overshoes or rubber boots.
  • Restrict and record movements of people in and out of the room.
  • Ensure that the ambulance crew wait for monitoring of themselves and their vehicle.
  • Keep everything that may be contaminated for radiation testing.
  • Collect the patient’s clothes, dressings, swabs and any equipment used in plastic bags and keep them in the decontamination room.
  • All blood/urine samples must be specially labelled and the labs informed of the radiation risk.
  • Life-threatening injuries may take precedence over all of the above, such that patients need to be managed in the resuscitation room.

Decontamination of the patient The radiation physicist should determine the sites of contamination and monitor the effectiveness of treatment. The object is to remove any contaminating substance and minimize absorption into the body, especially via the mouth, nose and wounds.

  • Cover any wounds prior to decontamination.
  • Avoid splashing.
  • Radioactive material can usually be removed from intact skin by washing with soap and water. Gentle scrubbing may be needed, but it is important to avoid damaging the skin. Carefully clean wounds and irrigate with water or saline.
  • Clean the mouth using a mouthwash and a soft toothbrush, with care to avoid swallowing any fluid.
  • Instruct the patient to blow his nose into paper handkerchiefs. If the nose is still contaminated irrigate it with small amounts of water.
  • Irrigate each eye from the medial side outwards to avoid draining contaminated water into the nasolacrimal duct.
  • Clean the hair by washing with shampoo and by clipping if contamination persists, but do not shave the scalp.
  • If monitoring shows that all contamination has been removed, treat the patient as for an irradiated, but uncontaminated patient. However, if contamination persists, or if radioactive material has been ingested/inhaled, further treatment will be needed after discussion with a radiation specialist.
  • Check all staff involved in treating the patient for radioactive contamination before they leave the treatment area.

The irradiated patient A patient who has been irradiated or contaminated with radiation may be at risk of radiation sickness or other ill effects. Admit to a designated unit for assessment and follow-up by a radiotherapist or other specialist. Initial symptoms of radiation sickness are malaise, nausea, vomiting and diarrhoea, starting a few hours after exposure. There is then a latent period before the main effects of radiation sickness appear. Record any symptoms and the time of onset. The effects of anxiety and stress may be similar to the early features of radiation sickness. Take blood for FBC, U&E and blood group, recording the time on the blood tubes and in the notes. Measurement of the lymphocyte count and analysis of chromosomes at known times after exposure are helpful in assessing the amount of radiation received and determining the prognosis. A low (<1.0 × 109/litre) or falling lymphocyte count indicates serious radiation exposure. Further Information http://www.nrpt.org/radiation-incidents/nair.htm(NAIR) http://www.hpa.org.uk (Health Protection Agency) P.252
Diving emergencies 1 Consider any symptom developing within 48h of a dive as related to the dive until proven otherwise. On suspicion of a diving-related episode, seek specialist advice urgently (see below). Diving related emergencies fall into four main categories: drowning (p246), barotrauma, decompression illness, marine bites or stings (p402). Barotrauma May occur in any gas-containing body cavity during descent or ascent. Descent barotrauma (‘squeeze’) results from compression of gas in enclosed spaces as the ambient pressure↑. Commonly, the ears, sinuses and skin are affected. Middle ear squeeze may be precipitated by Eustachian tube congestion and leads to erythema, haemorrhage 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 inner ear and results in acute tinnitus, vertigo and deafness and a perilymphatic fistula. ENT opinion is urgently required if a perilymphatic fistula is suspected and for cases of severe or continuing symptoms. If tympanic membrane rupture has not occurred, middle ear squeeze can usually be managed with a decongestants/simple analgesics. If it has ruptured, give antibiotics (p527). Instruct the patient not to dive until the symptoms have resolved and the drum has completely healed. Sinus barotrauma has a similar aetiology to middle ear injury and is often associated with URTI, 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 ‘face mask squeeze’ (skin barotrauma). Erythema, bruising and petechial and conjunctival haemorrhages 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 with asthma or congenital lung bullae. Mediastinal emphysema is the commonest event and presents with ↑hoarseness, neck swelling and retrosternal chest discomfort. Symptoms usually resolve spontaneously with high concentrations of O2. Pneumothorax is a potentially life-threatening complication if it develops during the dive, as the intrapleural gas cannot be vented and increasing ascent will precipitate tension. Conventional treatment by needle decompression, aspiration/chest drain insertion (p326) is required. Dental pain may occur on ascent or descent in carious teeth or those which have had recent fillings. The affected tooth is tender on tapping. Treat symptomatically with analgesics and arrange dental referral. P.253
For advice on treatment, and use of hyperbaric chambers in the UK contact:

England, Wales, Northern Ireland
  • Duty Diving Medical Officer Institute of Naval Medicine based in Gosport, Hants
Telephone 07831 151523 (24hrs)
  • Diving Diseases Research Centre Plymouth
Telephone 01752 209999 (24hrs) Ask for the Duty Diving Doctor.
  • • National Hyperbaric Centre Aberdeen, Royal Infirmary
Telephone 01224 681818 State ‘diving emergency’. Give your name and number. Request Duty Hyperbaric Physician.


Diving emergencies 2 Decompression illness There are two forms of decompression illness. The first occurs when dissolved nitrogen in blood and tissues is not expelled at a sufficient rate to prevent bubble formation. The second occurs when air bubbles are released 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 the heart to the systemic circulation. Cerebral air embolism usually causes symptoms as the diver surfaces with loss of consciousness, fits, cardiovascular collapse and chest pain. Clinically, differentiation between the two forms is difficult and initial management is the same. In general, the sooner the onset of symptoms, the greater the likely severity. Symptoms may be attributed by the patient (and the unwary doctor) to musculoskeletal sprains/strains or other minor injury. Decompression illness is more likely in divers who have not followed safe ascent recommendations, the obese, in cold water and when excessive exercise has occurred during the dive. It may be precipitated by air travel if insufficient time is left between diving and flying for residual nitrogen to leave the body in a controlled fashion. Bubbles have direct mechanical and local inflammatory effects, commonly involving joints, skin, CNS, lungs and ears. Joint pain, ‘the bends’, most often affects shoulders and elbows. A dull aching sensation, ↑by movement, but without localised tenderness is common. Pruritic rashes, local swelling and a peau d’orange effect may occur. Back pain, limb weakness, sensory abnormalities or urinary retention imply spinal cord involvement. Central effects include focal deficits, cerebellar disturbance and mood changes. Treatment for decompression illness is recompression. If delayed, risks of permanent damage to brain and spinal cord greatly↑. The diagnosis of decompression sickness may only follow the response to recompression. Pending this, give the highest possible concentration of O2. Analgesics/sedatives can mask recompression responses and should be used after obtaining specialist advice. Entonox is absolutely contraindicated. If intubation is required, inflate the ET tube cuff with sterile water, since during recompression an air-filled cuff will deflate. IV fluids (0.9% saline or a plasma expander) assist oxygenation of ischaemic tissues and facilitate discharge of excess tissue nitrogen load into the venous system by ensuring adequate circulating volume. Some centres may recommend aspirin and/or dextran solutions to ↓capillary sludging which accompanies severe decompression sickness. Despite dry or wet suits, hypothermia is common. Treat with appropriate passive or active rewarming (p258). Air evacuation If, after consultation with the diving medical centre, air evacuation is necessary, unpressurized aircraft should not fly above 300m. The diver should breathe 100% O2. On reaching the diving centre, recompression to a simulated depth of 18m with 100% O2 occurs interspersed with periods of air breathing to ↓ O2 toxicity risk. Slow decompression then follows standard treatment protocols. Divers usually dive in pairs. If a diver has symptoms of decompression sickness or pulmonary barotrauma, his ‘buddy’ will be at risk also. Although recompression may not be required in the buddy, transfer him along with the affected diver and their diving equipment to the recompression facility. P.255
Obtain the following information before referral, if possible:

  • The patient’s current condition, progression since onset and response to treatment.
  • Time of onset of symptoms related to the dive.
  • Dive profile and history (depth, duration, activity during the dive, speed of ascent including details of any stoppages, environmental conditions (water, temperature, currents etc), pre-dive exercise, alcohol, drugs 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.

Hypothermia—presentation Definitions Hypothermia exists when the core T°<35°C.

Hypothermia may be classified as follows:
mild hypothermia= 32-35°C
moderate hypothermia= 30-32°C
severe hypothermia= <30°C

Background Infants and the elderly are at particular risk. In young adults hypothermia is usually due to environmental exposure (eg cold water immersion, hill-walking) or to immobility and/or impaired conscious level from alcohol/ drugs. In the elderly, it is more often a prolonged state of multifactorial origin. Common precipitants include immobility (Parkinson’s disease, hypothyroidism), lack of cold awareness (dementia, autonomic neuropathy), unsatisfactory housing, poverty, drugs (sedatives, antidepressants), alcohol, acute confusion and infections. Clinical features Severe hypothermia may mimic death. Wide variations occur, but as core T°↓, cerebral and cardiovascular function deteriorate. At 32-35°C, apathy, amnesia, ataxia and dysarthria are common. At <32°C, consciousness falls progressively leading to coma, ↓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 spontaneously when T° falls <28°C and may be provoked by excessive movement or invasive procedures. Diagnosis Check rectal T° with an electronic probe or low-reading thermometer. Rectal T° may lag behind true core levels. Tympanic or oesophageal T° reflect core levels, but require special probes. Investigations

  • U&E
  • FBC, toxicology and clotting screens. Note that hypothermia can cause or aggravate coagulation disturbances
  • blood glucose (BMG reading may be falsely↓)
  • amylase (↑levels common, but do not necessarily imply pancreatitis)
  • blood cultures
  • ABG
  • ECG: look for prolongation of elements in the PQRST complex, J-waves, and arrhythmias (AF and bradycardias are the commonest)
  • CXR: look for pneumonia, aspiration, LVF, other X-rays may be required (eg for suspected fractured neck of femur, head injury)
  • CT scan may be indicated if head injury or CVA is suspected


Figure. ECG in hypothermia (with J-waves)

Notes on this ECG:

  • rhythm disturbance is atrial fibrillation with slow ventricular response
  • prolongation of QRS
  • delayed repolarisation ‘J-waves’ (arrowed)
  • ST-T wave abnormalities

Hypothermia—management Principles

  • Treat in a warm room (>21°C).
  • Handle the patient gently.
  • Remove wet clothes and dry the skin.
  • Monitor ECG.
  • Give warmed, humidified O2 by mask.
  • Intubation, if needed, should be preceded by pre-oxygenation and must be performed expertly to avoid precipitating arrhythmias.
  • If gastric dilation is present pass an NG tube.
  • Secure IV access. IV fluid is rarely required unless volume loss from another cause is present. If BP↓ during rewarming, give 300-500mL of warmed 0.9% saline or colloid and consider CVP and urinary catheter in unstable patients. Warm IV fluid administration is an inefficient rewarming method and runs the risks of fluid overload and precipitating arrhythmias.
  • Correct hypoglycaemia if present with IV 50% glucose.
  • If CPR is required, give chest compressions and ventilations at standard rates.
  • In hypothermic cardiac arrest, the heart may be unresponsive to defibril-lation, pacing and drug therapy. Drug metabolism is ↓ and unpredictable: avoid drugs until core T°>30°C (then give with ↑dosage intervals).
  • Defibrillation is appropriate at normal energy levels if VF/VT is present. If the initial sequence of 3 shocks is unsuccessful, defer further attempts until core T°>30°C.

Rewarming methods The choice depends upon the severity and duration of the condition, available facilities and the individual patient: Passive rewarming Easy, non-invasive, and suitable for mild cases (T°>32°C). ↓evaporative and conductive losses by wrapping in warm blankets and polythene sheets (remember to cover the back and sides of the head). Endogenous metabolism and shivering generate heat allowing spontaneous rewarming. Aim for a rate of 0.5-2°C/h, but do not rewarm the elderly with prolonged hypothermia too rapidly (>0.6°C/h), as cerebral/pulmonary oedema may develop. Active rewarming Surface A water bath at 37-41°C is rapid and useful for acute immersion hypothermia. Hazards include core T° afterdrop with peripheral vasodilation. It cannot be used in injured patients, or if CPR is required. Airway care, ventilation and monitoring are difficult. Heat pads or hot-water bottles are less efficient and can cause burns. A hot air blanket is convenient and effective. Core rewarming

  • airway warming: in self-ventilating patients by inhalation of heated (40-45°C) humidified O2 or air is effective (T°i at 1-2.5°C/h), simple to use, and can be combined with other methods.
  • peritoneal lavage: simple, and quick to set up. Saline at 45°C is run in via DPL catheter (p336), left for 10-20mins and replaced with a fresh warm supply. The fluid directly heats the liver and retroperitoneal structures including blood in the IVC.
  • extracorporeal: cardiopulmonary bypass maintains brain and vital organ perfusion and if available, is the method of choice in patients with severe hypothermia or those in cardiac arrest. Core T°i at 1-2°C/5mins.

Heat illness Body T° is normally kept at 36-8°C by homeostatic mechanisms controlled by the hypothalamus. Hyperthermia occurs when these mechanisms are overwhelmed by factors acting individually, or (commonly) together. These conditions arise even in temperate climates. At-risk groups include the very young and elderly in conditions of ↑temperature/humidity and patients with unaccustomed or prolonged muscular activity (eg at ‘raves’, associated with ecstasy or other drugs), grand mal fitting, athletes, marathon runners and armed forces recruits. Predisposing medical factors include

  • alcohol use/withdrawal (including delerium tremens)
  • cardiac disease
  • any condition which may cause or aggravate Na+/H2O loss (eg gastroenteritis, cystic fibrosis)
  • drugs, including: alcohol, diuretics, salicylates, anticholinergics (antihistamines, tricyclic antidepressants), sympathomimetics (amphetamines, ecstasy, LSD, cocaine, phencyclidine, appetite suppressants), phenothiazines, antipsychotics, MAOI, SSRI.

Heat illness has a spectrum of severity: Heat cramps ⇔ Heat exhaustion ⇔ Heat stroke In heat cramps/exhaustion, homeostatic mechanisms still function, but are overwhelmed. In heat stroke, all thermoregulatory control is lost, body T°↑ rapidly to very high levels (>41°C) causing widespread severe tissue/organ damage. Mortality may exceed 10%. Heat cramps Core T° 37-39°C. Mental function is normal. Sweating during exercise and replacement with hypotonic fluid leads to Na+deficiency. Brief cramps occur in muscles used in heavy work, usually after exertion. Heat exhaustion Core T°<40°C. Mental function is normal. Characterized by mixed Na+/H2O depletion. Sweating and tachycardia are usually present. Symptoms of weakness, fatigue, headache, vertigo, nausea/vomiting, postural dizziness, syncope. Patients will recover with rest and fluids. In mild cases, remove from heat and use simple cooling techniques. Rehydrate with oral electrolyte solutions. More severe cases require IV 0.9% saline or 0.45% saline/5% dextrose. Use clinical assessment, U&E and Hct to guide infusion rate. Up to 4 litres may be required over 6-12h. Avoid over-rapid infusion which may cause pulmonary/cerebral oedema. Measurement of core T° Oesophageal, tympanic membrane and intravascular (Swan-Ganz) probes give the most accurate readings, but are rarely available or practical in A&E. Continuous monitoring by an electronic rectal probe is most applicable in A&E, but may underestimate core T°, and respond slowly to changes. P.261
Heat stroke Suspect in collapse during or after exercise and in high risk groups. Core T° is very high >41°C (but significant cooling can occur before arrival in A&E). There is multi-system damage especially to the CNS. Outcome depends upon the height and duration of ↑T°. Mortality is ≈10%. CNS—oedema and petechial haemorrhages cause focal/generalised damage. Muscle injury releases enzymes, myoglobin, urate, K+, PO43- Liver—cell injury releases liver enzymes. Jaundice commonly develops after 24h. Kidneys—ARF from hypovolaemia, muscle breakdown products, DIC, acidosis. Blood—DIC, thrombocytopenia, leucocytosis. Metabolic ↑ or ↓ K+, metabolic acidosis, respiratory alkalosis, hypoglycaemia. Features Sweating may be present. The skin surface may feel deceptively cool due to peripheral vasoconstriction. CNS—confusion, delirium, fitting, coma, oculogyric crisis, tremor, muscle rigidity, decerebrate posturing, cerebellar dysfunction, pupils may be dilated. CVS—tachycardia, hypotension, arrhythmias. Coagulopathy—purpura, conjunctival haemorrhages, melaena, haematuria. Investigations ABG, U&E, BMG, CK, clotting screen, LFTs, urate, Ca2+, PO43-, ECG, CXR. Treatment

  • Rapid therapy is vital. Do not wait for the results of investigations.
  • Remove all clothing and from hot environment.
  • Secure the airway (intubation and IPPV may be needed) and give high FiO2.
  • Cooling techniques depend upon facilities available and the clinical state of the patient. Do not give ‘antipyretics’ such as aspirin/paracetamol. Aim for cooling rate at least 0.1°C/min. When core T°<39°C stop active cooling as hypothermia may develop. Evaporative cooling is the most efficient and applicable treatment. Spray the naked patient with tepid tap water and blow air over the body with fans. Ice-packs can be applied to the axillae, groins, neck and scalp (but avoid prolonged contact). Consider cold gastric or peritoneal lavage, or cardiopulmonary bypass if these techniques fail.
  • IV Fluids — give 50mL 50% dextrose IV if BMG <3mmol/litre. Severe hypovolaemia is uncommon. If hypotension persists despite ↓T°, give IV 0.9% saline (1-1.5litres over 1-2h). Avoid overloading circulation with risk of pulmonary/cerebral oedema. CVP/Swan-Ganz monitoring may be needed. CVP may be initially ↑ due to peripheral vasoconstriction.
  • Insert a urinary catheter. If myoglobinuria is present, aim for ↑urine output and consider giving IV bicarbonate and/or mannitol.
  • If fits occur, give IV diazepam—but beware respiratory depression.

Neuroleptic malignant syndrome is an idiosyncratic reaction in patients on antipsychotics (esp haloperidol, thioridazine, chlorpromazine). Features are muscle rigidity, extrapyramidal signs, autonomic dysfunction, severe dyskinesia. Treat with dantrolene rapid IV (dose 1mg/kg, repeated up to 10mg/kg). Malignant hyperpyrexia is a rare autosomal dominant condition related to use of suxamethonium/halothane. Dantrolene (dose as above), prevents Ca2+release from skeletal muscle and is very effective.

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