Oxford Handbook of Expedition and Wilderness Medicine (2 edn)
Annotate
Cite
The collapsed patient
Management of injured patients follows a well-established sequence (see Chapter 7). However, when an individual suddenly becomes unwell (‘collapses’), their basic life functions must be supported, a diagnosis made, the appropriate treatment instituted, and the patient stabilized before evacuation can be considered.
Collapse in young adults is very rare, but is generally very serious; infectious disease or environmentally induced conditions are the most likely causes. Psychological causes must be considered, but only after medical ones have been excluded. In older travellers, the likelihood of cardiovascular disease increases.
Medical emergencies
Before attempting to examine any seriously ill person look for life-threatening hazards so as to avoid further injury to the patient and any danger to the rescuers. If absolutely necessary, rapidly and carefully move the casualty to a place of safety.
Rapid primary assessment and resuscitation
This is the simultaneous assessment, identification, and management of immediate life-threatening problems. Rapid primary assessment should follow the ABC model.
A Assessment whilst approaching the casualty.
A Airway (with neck control if there is a history of injury).
B Breathing.
C Circulation (control bleeding and manage shock).
D Disability of the nervous system.
E Exposure and environmental control.
Primary assessment should be repeated following any change in the patient’s condition.
Assessment and approach
When it is safe to approach, check the casualty’s level of responsiveness. Tap or gently shake the shoulders and say ‘Are you OK?’ If there is no response call for help and proceed to check the airway.
Airway
Assess without moving the neck more than necessary—particularly if the patient has fallen and might have injured the head or neck. Remember, airway takes precedence over neck control.
Open the airway using chin lift or jaw thrust (
Airway, p. 186).
Look for, and remove any obvious obstruction, consider the use of airway adjuncts such as nasopharyngeal or oropharyngeal airways ( Maintaining an open airway, p. 187). Remember that oropharyngeal airways can provoke vomiting, and nasopharyngeal airways cause nosebleeds.
Breathing
Once the airway has been checked and opened, assess breathing.
Look, listen, and feel for breathing (10 s); if the patient is hypothermic then extend this period to 30 s.
Give oxygen if available, particularly to those who are shocked, bleeding, or who have breathing difficulties.
If respiration is absent, impaired, or inadequate, commence CPR ( Resuscitation in the wilderness, p. 216).
Is the breathing rate normal?
Can the patient count to ten in one breath?
If you suspect a chest problem, examine the chest for movement and breath sounds; normal, crackles, wheeze, or absent?
Circulation care with haemorrhage control
The aim is to detect and treat shock. Look for and control any external bleeding (consider direct pressure and elevation). Consider the possibility of internal bleeding.
Look at the patient’s skin colour and assess the skin temperature.
Measure pulse rate and assess pulse character (normal, thready, or bounding).
Estimate the BP by feeling the pulse:
Carotid (neck): systolic BP >60 mmHg.
Femoral (groin): systolic BP >70 mmHg.
Radial (wrist): systolic BP >80 mmHg.
Capillary refill should be <2 s in a warm casualty ( Capillary refill time, p. 417).
Treat shock:
Lie the patient flat, elevate legs on pillow or rucksack.
Keep warm and reassure.
Consider IV fluids—replacement amounts and rate will depend upon the cause of the shock.
For management of other causes of shock see Shock, p. 228.
Disability
Assess the patient’s neurological status using the AVPU scale:
A Alert.
V Responds to verbal command.
P Responds to pain.
U Unresponsive.
Pupils—assess size and reaction to light.
Look for neck stiffness.
Check blood glucose levels if possible.
If the patient is fitting, place them in the recovery position.
Exposure and environmental control
Where possible, examine the patient in a warm, light environment such as a tent or group shelter. Be gentle; unnecessary roughness may aggravate the problem. Examine the patient carefully but always prevent the development of hypothermia which will worsen shock. Measure body temperature and look for a rash.
Rapid history
The patient or bystanders may be able to give brief details to aid diagnosis:
Events leading up to the illness, any history of injury.
Past history, particularly known cardiac or respiratory illness, diabetes, epilepsy, alcohol/drug abuse, head injury.
Medication taken on a regular or occasional basis.
Allergies.
Secondary assessment
(See also Secondary survey, p. 204.)
Secondary survey is a methodical search for all signs of disease which may be present. On an expedition this should be delayed until the casualty is in a warm, dry environment such as in a tent or building or under a group shelter, lying on a mattress, airbed, or sleeping bag.
History-taking and examination are covered in Chapter 6.
Resuscitation in the wilderness
Survival from a cardiac arrest depends upon the cause of the arrest, the previous health of the patient, the rapidity of the initial response, and the availability of medical and transport facilities to ensure the chain of survival (Fig. 8.1).
The basic life support (BLS) algorithm (Fig. 8.2) remains the default response for a collapsed, unresponsive patient. However, current BLS and ALS guidelines have been developed for the patient who has had a cardiac arrest, most likely due to a myocardial infarction, and who collapses in an environment where early defibrillation and timely transfer to a facility for post-resuscitation care are possible.
Adult basic life support algorithm.
Resuscitation in the wilderness presents issues that do not normally need to be considered in a conventional healthcare setting, and may require some difficult decision-making. Rescuers must consider their own safety both at the time of arrival on scene and for potential dangers arising during the resuscitation and rescue process, and be prepared to either not commence resuscitation, or abandon it. The expedition leader must consider not only the medical needs of the victim, but also recognize that there is a duty of care to other expedition members. A prolonged resuscitation and rescue may expose others to unacceptable environmental risks, especially if the other members are children. The physical location of the victim and the available rescue equipment may mean that it is not possible to rescue the victim and continue CPR effectively.
Special circumstances1
Rescuers must consider if the following circumstances apply and modify their approach accordingly:
Hypothermia ( Hypothermia, p. 622)—airway protection and CPR should be commenced as soon as possible. However, CPR must be continued until the patient is either ‘warm and dead’, or return of spontaneous circulation (ROSC) occurs. If this cannot be guaranteed then CPR should be withheld and the patient handled very carefully.
Snake bite or marine envenomation—prolonged CPR is sometimes successful.
Electrocution (lightning strike) ( Lightning, p. 208)—prolonged CPR is worthwhile, especially after lightning strike. Late defibrillation may be successful.
Drowning, including cold water immersion ( Immersion and drowning, p. 688)—commence CPR, but discontinue after 30 min unless timely evacuation to a medical facility is possible.
Cardiac arrest secondary to trauma/haemorrhage ( Hypovolaemic shock, p. 234)—mean survival rate in conventional practice is 5%. Survival in a wilderness setting is extremely unlikely.
If none of these circumstances apply then conventional BLS and ALS guidelines should be followed where possible. Recovery from a ventricular fibrillation arrest requires timely defibrillation. If defibrillation occurs in a pre-hospital setting within 4 min of arrest with subsequent transfer to hospital, then long-term survival is 60%, at 20 min it is <1%.
Automated external defibrillators
Automated external defibrillators (AEDs) are compact, light, and relatively inexpensive; they can be used by lay people with little additional training, and in theory could be carried on many types of expedition. However, there are two major potential breaks in the chain of survival that render this approach of little value in most expedition contexts. Firstly, it is unlikely that the victim will have their cardiac arrest close to the medical kit where the defibrillator is kept. Secondly, long-term survival is usually dependent on the ability to identify and correct secondary complications such as arrhythmias, acidosis, and electrolyte disturbance.
If there is danger to the rescuers.
Obvious lethal injury, e.g. decapitation.
Rigor mortis.
If spontaneous pulse and breathing return.
Rescuers become exhausted.
Rescuers are placed in danger.
Dangers of resuscitation
There is understandable concern about the possibility of transmission of blood-borne diseases during resuscitation—particularly HIV and hepatitis B and C. Although viruses can be isolated from the saliva of infected persons, transmission is rare and there are few cases of CPR-related infection in the literature. To minimize the risk of acquiring infection, rescuers should wear gloves and use barriers whenever possible, and great care must be taken with sharps.
Basic life support (CPR)
‘For any seriously ill or collapsed patient it is important to assess for level of response and to start cardiopulmonary resuscitation (CPR) if breathing is abnormal or there is no palpable pulse.’ (From the Resuscitation Guidelines 2010).2
Initial management of adult patients
(See Fig. 8.2.)
Check for a response:
Gently shake the shoulders. Ask loudly ‘Are you alright?’
If patient responds:
If the individual is able to speak the airway is open and maintained.
Leave him in the position you find him, provided there is no further danger.
Stabilize the head and neck if there is a possibility of injury (Fig. 5.3).
Find out what is wrong and get help (ideally via radio, telephone, or written message), if available.
Reassess regularly.
If patient is unresponsive:
Shout/call for help.
Turn the casualty on his back, whilst maintaining neck control.
Institute life support measures.
Assess, open, and manage the airway as described in Airway, p. 186. Check the airway for 10s.
If the casualty is not breathing normally start CPR (Fig. 8.3):
Start with 30 chest compressions at a rate of 100–120/min:
Kneel beside victim.
Place heel of one hand in centre of victim’s chest.
Place heel of other hand on top of the first hand.
Interlock fingers of your hands and ensure pressure is not applied over the victim’s ribs, upper abdomen, or bottom end of the bony sternum.
Position yourself vertically above the victim’s chest and, with straight arms, press down on sternum 5–6 cm.
Release pressure without losing contact between your hands and the sternum. Compression and release should take equal time.
After 30 compressions give two rescue breaths:
Open airway with chin lift and head tilt.
Pinch soft part of the victim’s nose closed with the index finger and thumb of your hand on his forehead.
Allow his mouth to open whilst maintaining chin lift.
Take a normal breath and place lips around his mouth. Ensure a good seal.
Blow steadily into his mouth for about 1 s and watch the chest rise.
Maintaining head tilt and chin lift take your mouth away and watch for the chest to fall as air comes out.
Take another normal breath and blow into the victim’s mouth to give two effective rescue breaths. Immediately return your hands to his sternum and give a further 30 compressions.
If rescue breaths do not make the chest rise and fall, before next attempt:
Check victim’s mouth and remove any visible obstruction.
Recheck there is adequate head tilt and chin lift.
Do not attempt more than two rescue breaths before returning to 30 chest compressions.
Chest compressions: rescue breath ratio 30:2.
Hand position for CPR.
Continue CPR until:
Normal breathing resumes.
You become exhausted.
A more experienced doctor tells you to stop.
Call for assistance.
Push hard (effective cardiac compressions).
Push fast (maintain regular cardiac compressions).
Breathe slowly (excessive ventilation is unnecessary).
Don’t stop (gaps in compression reduce survival).
Obey automated defibrillator (if available).
Choking
Recognition
Foreign bodies may cause either mild or severe airway obstruction. It is important to ask the conscious victim ‘Are you choking?’
General signs of choking
Attack occurs while eating.
Victim may clutch his neck.
Signs of mild airway obstruction
Response to question ‘Are you choking?’:
Victim is able to speak, cough, and breathe.
Signs of severe airway obstruction
Response to question ‘Are you choking?’:
Victim unable to speak.
Victim unable to breathe.
Breathing sounds wheezy.
Attempts at coughing are silent.
Victim may become unconscious.
Management
(See Fig. 8.4.)
Choking algorithm.
Mild airway obstruction
Encourage him to continue coughing, but do nothing else.
Severe airway obstruction
Give up to five back blows.
Stand to the side and slightly behind the victim.
Support the chest with one hand and lean the victim forwards.
Give up to five sharp blows between the shoulder blades with the heel of your other hand.
If five back blows fail to relieve the airway obstruction, give up to five abdominal thrusts:
Stand behind the victim and put both arms round the upper part of his abdomen.
Lean the victim forwards and clench your fist and place it between the umbilicus (navel) and the bottom end of the breastbone.
Grasp hand with your other hand and pull sharply inwards and upwards. Repeat up to five times.
If the obstruction is still not relieved, continue alternating five back blows with five abdominal thrusts.
If the victim becomes unconscious:
Recovery position
Remove the victim’s spectacles, if worn.
Kneel beside the victim and make sure that both his legs are straight.
Place the arm nearest to you out at right angles to his body, elbow bent with the hand palm uppermost.
Bring the far arm across the chest, and hold the back of the hand against the victim’s cheek nearest to you.
With your other hand, grasp the far leg just above the knee and pull it up, keeping the foot on the ground.
Keeping the hand pressed against the cheek, pull on the far leg to roll the victim towards you onto his side.
Adjust the upper leg so that both the hip and knee are bent at right angles.
Tilt the head back to make sure the airway remains open.
Adjust the hand under the cheek, if necessary, to keep the head tilted.
Check breathing regularly.
Turning into the recovery position.
The recovery position.
If the victim has to be kept in the recovery position for >30 min turn him to the opposite side to relieve the pressure on the lower arm. Ensure that there are no objects in the pockets that the casualty will be lying on—these may cause pressure areas.
Shock
Shock occurs when the circulation is inadequate to meet the metabolic demands of the body. When key organs such as the kidneys, heart, and brain are relatively under-perfused their function fails.
Clinical presentation and types of shock
All ‘shocked’ patients may exhibit:
Cerebral effects—irritable, drowsy, yawning.
GI effects—nausea, vomiting.
Renal effects—reduced urine output (>0.5 mL/kg/h being ‘normal’).
Other findings will depend on the type of shock. Shock is usually accompanied by hypotension (low BP). Arterial BP is governed by the combination of cardiac output driving the blood into the arteries and peripheral vascular resistance resisting its forward flow. Thus low BP may result either from a reduction in cardiac output or from a fall in peripheral resistance.
Shock caused by low cardiac output
A fall in cardiac output leads to a reflex increase in sympathetic activity—an increase in heart rate, respiratory rate, peripheral vasoconstriction, and sweating. Cold, clammy skin, fast pulse, and rapid breathing will be common to all underlying causes. Under-filling of the main pumping chamber of the heart, the left ventricle, may result from:
Loss of fluids from the body:
Diarrhoea.
Vomiting.
Haemorrhage.
Skin turgor (elasticity of the tissues) is low, the mouth is dry, and the patient is thirsty. If whole body water is low, sweating is limited (i.e. the skin isn’t ‘clammy’). With blood loss alone, sweating is expected.
Loss of fluids into tissue spaces:
Burns (including severe sunburn).
Anaphylaxis.
Profound hypoproteinaemia (as may occur in dysentery).
Obstruction to cardiac filling.
Pulmonary embolus.
Cardiac tamponade.
When fluids have been lost from the body or moved into tissue spaces, neck veins will be empty: when there is obstruction to blood flow from pulmonary embolism or cardiac tamponade, the neck veins will be full and jugular venous pressure will rise with inspiration. Breathlessness may be most profound with pulmonary embolism (as hypoxia contributes).
Shock caused by low peripheral resistance
This occurs in anaphylaxis, or any major systemic inflammatory response, including:
Severe infection (septic shock).
Toxins (stings, venom) and/or anaphylaxis.
Severe sunburn.
Blood vessels vasodilate, peripheral resistance decreases, and therefore BP falls. The inflammatory response directly affects the peripheral blood vessels and so the compensatory sympathetic response cannot cause the blood vessels to constrict; BP remains low. The skin may be warm, hot, or ‘patchy’. In sepsis, such ‘patchiness’ may alter with time (legs freezing one minute, and warm the next). Neck veins will be collapsed, and the skin may sweat due to fever but will not be ‘cold and shut down’ (i.e. clammy). Pulse rate and cardiac output will be high.
The young and fit can maintain BP for a very long time through sympathetic activity. In some cases BP may not fall until around 50% of the circulating volume has been lost.
Underlying dehydration may be common.
Urine output may already be low.
Sweating responses may be reduced—sweating thresholds are altered by acclimatization to ambient temperature and to exercise loads ( Acclimatization to heat, p. 754).
In the heat, most people are vasodilated. In ‘heat stroke’ ( Heat-related illnesses (HRIs), p. 748), severe inflammation coupled with volume loss may lead to a ‘shivering clammy’ patient, despite a very high central temperature.
In the cold, most are vasoconstricted.
Management of the shocked patient
Identify the type of shock.
As for all major emergencies—make sure that the environment is safe, summon help, and attend to Airway, Breathing and then Circulation (see Chapter 7).
Consider IV tranexamic acid, see Circulation, p. 194.
If the patient is more than mildly unwell, establish venous access at once. You may find it a lot harder later!
Stop the losses and treat the causes:
Stop all sources of loss (e.g. use antidiarrhoeals, antiemetics, cooling with sponging and fanning, keeping in the shade, light-reflective clothing if sun unavoidable).
If septic, seek the source (including the rare, but often missed, retained tampon) and treat at once with broad spectrum antibiotics.
Give fluids. Most wilderness victims will be depleted of intravascular volume, as will most with shock of any cause (see Types of shock, p. 234). The rate and route will be determined by a number of factors: if you have an uncontrolled source of blood loss, internal or external, give fluids cautiously until the source of bleeding is controlled. Raising pressure by rapid resuscitation will make bleeding worse. If fluid supplies are limited, use ‘permissive hypotension’ (maintain a just palpable radial pulse).
If the patient is conscious and able to swallow (without GI tract injury), let the patient drink as a means of conserving IV fluids.
No data, beyond anecdote, support the rectal administration of fluids in this context. However, this may be considered in the absence of other means of resuscitation.3
Consider intraosseous administration if oral or venous routes are unavailable, and you have the kit (and are trained to use it!).
During fluid resuscitation, give fluids by ‘bolus’ of 250 mL, and observe response, especially heart rate. For maintenance, calculate losses (blood loss, diarrhoea, vomiting, from skin in burns), including insensible losses (sweating and breathing, 10–20 mL/kg/day). Once resuscitated with boluses, spread this ‘maintenance’ over 24 h.
Treatment endpoints:
Control of fluid losses.
‘Organ survival and function’: urine output >0.5 mL/kg/h; patient is alert and orientated.
Improvements in observations—heart rate within normal range and respiratory rate falling, BP rising.
Allergy and anaphylaxis algorithm.
Additional specific treatments depending upon the type of shock are described in Fig. 8.9.
Shock algorithm.
Remember to put this treatment in the context of what is available to you. If you have only 2 L of IV fluids, then you must use them with care to resuscitate fast (e.g. if massive bleed now stopped) or gently (e.g. minor hypotension with continuing losses).
Remember, too, to call for help/evacuate fast. Prompt and sustained resuscitation is vital to survival.
Monitoring shock in the wilderness
BP may be well maintained at first. Look for trends over time and any postural drop (measured while lying then sitting or standing). If in doubt, use sitting BP as standing can provoke loss of consciousness.
Are heart rate and respiratory rate rising?
What is happening to:
Skin perfusion (skin colour/temperature)?
Brain (alert/orientated)?
Kidney function (urine output)? Consider a urinary catheter (if you have one) and measure hourly urine output. You can measure with a cup or Nalgene® bottle if no measuring jug.
Breathlessness (reflecting sympathetic activity, and clearance of lactic acidosis through respiratory compensation)?
Record the above on a chart to give a visual display of changes ( Documentation, p. 89).
Fig. 8.7 reproduces the NHS observations chart including the National Early Warning Score (NEWS). Patients whose observations fall outside the normal range require increased monitoring, and deterioration in the score will highlight the need for increased frequency of observations and may guide urgency of a medevac. Expeditions are recommended to obtain equivalent charts to these at full size and in colour as part of their medical stores. Online instruction of the use of NEWS can be found at: 
http://tfinews.ocbmedia.com/#home
Observations chart including National Early Warning Score (NEWS). https://www.rcplondon.ac.uk/projects/outputs/national-early-warning-score-news-2
You cannot prevent a fellow traveller becoming seriously ill. However, you can take appropriate equipment.
Decide on the volume of fluids you will carry, depending on logistic constraints (weight, bulk), duration of trip, evacuation times.
Take antibiotics for infections and adrenaline (epinephrine), steroids, and antihistamines for anaphylaxis.
Find out how safe or dangerous local blood sources may be.
Avoid GI tract infection if possible ( Camp health and hygiene, p. 22), and all the other recognized environmental causes.
Know the arterial pressure points.
Make sure your cannulation skills are updated.
Types of shock
Hypovolaemic shock
Causes
Blood loss:
External and visible (e.g. external wound).
Internal and invisible (e.g. into gut, into muscle around a fractured bone, into chest or abdominal cavity, into tissues behind abdominal contents).
Low fluid intake (usually when combined with high losses).
Loss of fluid from the body:
Gut (diarrhoea, vomiting).
Skin (extensive grazes, burns).
Sweat (fever, environmental heat).
Breathing (dry air, high respiratory rates).
Loss of fluid into tissues:
Anaphylaxis.
Crush injury.
Severe systemic inflammation and sepsis.
Signs
Those of ‘low cardiac output shock’ (
Cardiogenic shock, p. 235).
Specific treatment
Stop losses, fluid challenges of 250 mL IV, calculate daily maintenance and administer over 24 h.
NB Crush injury leads to loss of volume into the tissues, and low output shock. Tissue damage may worsen the inflammatory state and the muscle damage worsens kidney function. Maintain a high urine output if possible. Do not use diuretics (as this will worsen volume depletion). Check for compartment syndrome (as this may be causing low perfusion every bit as much as a fall in systemic perfusion pressure). Fasciotomies ( Compartment syndrome, p. 443; Crush injuries, p. 277) may be needed but beware: fluid losses will be massive. Have you enough IV fluids to keep up?
Septic shock
Causes
Infection in the bloodstream. Sometimes this may be from a wound that is hard to see. In women, ask about possible retained and infected tampon. Urine infection may be a source.
Signs
Those of ‘low peripheral resistance shock’: tachycardia, high volume pulse, warm skin (or patchy skin temperature distribution which changes), low BP, sweating/sweats. Rigors (severe ‘bone-shaking’ shivers) may occur.
Specific treatment
IV fluid challenges of 250 mL IV to resuscitate; calculate daily maintenance and administer over 24 h
Administer IV broad-spectrum antibiotics (e.g. ceftriaxone 1–2 g IV twice daily)
Evacuate as soon as possible.
Cardiogenic shock
Causes
Acute impairment of heart contractile function. In expedition teams, most commonly an acute myocardial infarction.
Signs
Generally preceded by history of classic cardiac pain (tight across chest, to shoulders, jaw, or down arm(s).
Signs are those of ‘low cardiac output shock’: tachycardia, low volume pulse, cold clammy skin, and low BP. Breathlessness. Inspiratory crackles at bases, spreading throughout lungs. (NB At altitude, consider high-altitude pulmonary oedema.) Neck veins may be elevated if right side of heart involved. (NB Consider pulmonary embolus.)
Specific treatment
This is life-threatening. Arrange evacuation at once. Give oxygen if available.
Sitting upright may help relieve breathlessness.
Fluids only if jugular venous pressure not elevated and chest clear (suggesting isolated right heart infarct). Unguided IV fluids may make matters worse.
If stabilizes over time, may need cautious fluids (100 mL challenges maximum).
Powerful analgesics to relieve chest pain.
Aspirin 300 mg to reduce progression of infarct.
A diuretic may relieve breathlessness if the jugular venous pressure is raised.
Pulmonary embolus
Blood clot impacts in pulmonary arterial circulation. Most commonly originates in leg veins, often after prolonged flight/coach journey/immobility. The risk rises when blood viscosity is high (dehydration, altitude).
Signs
Those of ‘low cardiac output shock’: tachycardia, low volume pulse, cold clammy skin, low BP. Neck veins may be distended. Look for unilateral (occasionally bilateral) lower limb swelling—may be confined to calf.
Specific treatment
IV fluid challenges of 250 mL IV to resuscitate.
Low molecular weight heparin (e.g. enoxaparin) 1.5 mg/kg subcutaneously once daily.
Neurogenic shock
Neurogenic shock is a very rare situation, in which severe damage to the spinal cord disrupts the transmission of ‘tightening up’ nerve impulses to the small arteries. The blood vessels therefore dilate, and ‘low resistance shock’ results.
Causes
Spinal cord injury (usually trauma, although inflammatory/infective causes are possible).
Signs
Those of ‘low peripheral resistance shock’: tachycardia, high volume pulse, warm skin, low BP. Casualty may develop priapism—an involuntary erection of the penis in males (seen with high spinal cord injuries above T6). Other signs of spinal cord injury (sensory loss, weakness or paralysis).
Specific treatment
IV fluids (as the intestines usually stop moving with high spinal cord injury) using 250 mL fluid challenges. Calculate daily maintenance and administer over 24 h. Evacuate as soon as possible. May need a nasogastric tube. Remember pressure area care and immobilization of the entire spine.
Anaphylaxis and anaphylactic shock
Anaphylaxis is a rapidly evolving and often dramatic clinical syndrome, usually precipitated by recent exposure to a substance (allergen) to which the patient is allergic, e.g.:
Drugs: any, especially penicillins.
Foods: any, especially nuts, fruits, sea food.
Environmental factors: animal venoms (e.g. wasp, hornet, bee, ant, or snake), plant substances (latex).
Examination
Anaphylaxis is characterized by one or more of the following features in any combination:
Rash and/or mucous membrane involvement: urticaria (‘hives’, ‘weals’, ‘welts’), flushing, itching, generalized erythema and swelling owing to massive extravasation of fluid and swelling of the lips, tongue, gums, and uvula.
Life-threatening circulatory collapse (‘anaphylactic shock’) caused by vasodilatation and/or hypovolaemia: premonitory features include dizziness, loss of vision, tachycardia, falling BP, and loss of consciousness.
Life-threatening airway obstruction: lower airways—bronchoconstriction/ asthma or, less often, upper airway—angio-oedema of the larynx. The signs include wheeze, tachypnoea, stridor (‘croup’), and cyanosis.
GI symptoms (vomiting, diarrhoea, retrosternal pain, abdominal colic).
Patients look and feel severely unwell, are usually anxious, and may have a feeling of impending doom. In extreme cases, they may collapse and lose consciousness within minutes of allergen exposure. Some present with shock and hypotension alone.
Worrying features
Upper airway obstruction.
Wheeze.
Systolic BP <90 mmHg.
Differential diagnosis
Asthma.
Heart attack or pulmonary embolism (chest pain, shock, respiratory distress).
Faint, panic attack.
Vasovagal attack precipitated by injections, stings or sharp trauma (but this will be associated with bradycardia).
Prevention and risk management
Those with known allergy should carry an adrenaline (epinephrine) auto-injector such as EpiPen®, Jext®, or Emerade®.
Companions should know the location of the auto-injector and how to use it (Fig. 8.8).
Ensure cooks are aware of food allergies.
Further treatment
(See Fig. 8.9.)
Maintain BP >90 mmHg systolic. Give IV fluids as required.
If bronchospasm is severe/persistent despite adrenaline, give bronchodilator by inhalation (salbutamol, ipratropium).
If cardiac arrest occurs: follow guidelines for cardiopulmonary resuscitation. Early advanced life support is essential. IM adrenaline is unlikely to be beneficial in this setting so try an IV route or intraoral/intra-airway.
Monitor urine output.
Continue chlorphenamine 4 mg/8 h PO.
Consider a short course of steroids—prednisolone 40 mg/24 h for 5 days to prevent recurrent anaphylaxis.
The patient may require evacuation for further investigation.
Resources
Association of Anaesthetists of Great Britain and Ireland: 
http://www.aagbi.org
British Society for Allergy and Clinical Immunology: http://www.bsaci.org
European Academy of Allergy and Clinical Immunology: http://www.eaaci.net
European Resuscitation Council: http://www.erc.edu
Resuscitation Council UK: http://www.resus.org.uk
Heat injury
Remember, severe hyperthermia may present with a shivering ‘shut-down’ patient. They need active cooling and sometimes a lot of fluid (see Heat-related illnesses (HRIs), p. 748).
Environmental fluid loss: dehydration is common in all wilderness environments, owing to the effects of the heat, exercise, and sweating, high breathing rates (particularly in cold, dry air).
Summary
Unless appropriately treated, shock of any cause is a very dangerous condition. Identification of the cause and rapid appropriate treatment are crucial. In every case, rapid evacuation is indicated. This should be considered even if anaphylaxis rapidly resolves: it is hard to know that the environmental challenge (whatever it was) won’t occur again; avoidance is the best option.
Chest pain
History
Site of main pain and any radiation to arms, neck, jaw, or back.
Character of pain—heavy, sharp, tight, pleuritic (worse on inspiration).
Severity—out of ten.
Onset—at rest or during exertion.
Nature—whether constant and aggravated by exertion, position, eating, breathing, or relieved by analgesics, antacids, or GTN.
Associated symptoms—sweating, breathlessness, nausea, palpitations.
Trauma—nature of any injury.
Past history—cardiac or respiratory problems, acid indigestion.
Drugs—cardiac or respiratory drugs, antacids.
Social and environmental factors—alcohol/drugs, smoking status, recent stressors.
Cardiac disease risk factors
Previous ischaemic heart disease (IHD).
Smoking.
Hypertension.
Obesity.
Diabetes.
Family history of IHD.
Hypercholesterolaemia.
Venous thrombosis or pulmonary embolism risk factors
Previous thromboembolic disease (DVT or pulmonary embolism).
Smoking.
Immobility.
Dehydration.
Pro-thrombotic conditions.
Oestrogen containing medication—HRT/OCP.
Recent surgery/long travel/leg injuries.
Gastrointestinal risk factors
Gastro-oesophageal reflux disease (GORD).
Previous peptic ulceration.
Alcohol excess.
Examination
Temperature, pulse, respiration rate, BP in both arms, GCS score.
General condition—cyanosis, pallor, sweating.
Pulse rate, rhythm, character, BP, look for elevation and dilatation of the neck veins, listen to the heart sounds (any murmurs?), look for signs of cardiac failure (basal crackles in the lungs and swelling of the ankles), look for calf swelling or redness/tenderness.
Feel for position of windpipe, and assess for chest wall tenderness.
Feel the abdomen for localized tenderness or a pulsatile mass (abdominal aortic aneurysm).
Check blood glucose.
See Fig. 8.10 for management.
Management of chest pain.
Differential diagnosis
Originating from the chest
Myocardial infarction/angina.
Tension pneumothorax.
Pulmonary embolism.
Pneumonia.
Pleurisy.
High altitude pulmonary oedema.
Chest wall pain.
Gastro-oesophageal reflux disease (GORD).
Pericarditis.
Herpes zoster.
Originating from the abdomen
Aortic aneurysm.
Cholecystitis.
Peptic ulceration.
Pancreatitis.
Sickle cell crisis.
Make a ‘best guess’ diagnosis and treat accordingly. Observe the patient closely, record the details on a TPR chart, and monitor urine output.
Worrying features
Urgent evacuation for investigation and treatment is indicated if any of the following develop:
Tachycardia—heart rate >100 bpm persistently or irregular rhythm.
Bradycardia—heart rate persistently <50 bpm.
Hypotension—systolic BP <90 mmHg.
Elevated respiration rate.
Reduced GCS.
Sweating.
Vomiting.
Pain radiating to jaw, arms, or back.
Assess ABC. If the patient is unresponsive and there is no respiratory effort and/or no palpable pulse, commence CPR.
If the patient is conscious:
Sit patient up.
Give high-flow oxygen if available.
Consider aspirin, GTN, and IV analgesia if cardiac cause seems likely (Fig. 8.10).
Monitor pulse, BP, and respiratory rate.
Shortness of breath (dyspnoea)
(See Fig. 8.11.)
Shortness of breath algorithm.
History
Dyspnoea—speed of onset, cough, wheeze.
Sputum (colour, quantity, any blood).
Chest pain—characterize any pain (see Chest pain, p. 242).
Associated symptoms—sweating, nausea, palpitations.
Trauma—nature of injury if present.
Past history—cardiac or respiratory problems.
Drugs—inhalers, respiratory or cardiac drugs.
Allergies—medication and environmental, food, other allergens.
Social/environmental—smoking status, travel history ( Fever, p. 262).
Risk factors for pulmonary embolism/DVT—previous thromboembolic disease, smoking, obesity, immobility, dehydration, high altitude, pro-thrombotic conditions, HRT/OCP, recent surgery/long travel, leg injuries.
Examination
Temperature, pulse, respiratory rate, BP, GCS score.
General condition—confusion, cyanosis, pallor, cool peripheries, sweating, tremor, use of accessory muscles. Can the patient count to ten in one breath?
Pulse rate, rhythm, BP, look for elevation and dilatation of the neck veins. Measure peak expiratory flow rate if possible, look for tracheal tug/deviation, percuss the chest, listen for air entry and breath sounds—normal, crackles, wheezes or absent. Look for calf swelling/redness/tenderness or ankle swelling (DVT)
Feel the abdomen for localized tenderness or a pulsatile mass (abdominal aortic aneurysm).
Differential diagnosis
Wheeze present:
No clinical signs:
Crackles audible:
Stridor present:
Foreign body ( Shortness of breath (dyspnoea), p. 246).
Absent breath sounds:
Pneumothorax ( Pneumothorax, p. 190).
Make a ‘best guess’ diagnosis and treat accordingly. Observe the patient closely; record the details on a TPR chart.
Worrying features
Urgent evacuation for investigation and treatment are indicated if any of the following develop:
Respiratory rate >30 breaths/min.
Tachycardia or bradycardia.
Core temperature >39°C.
Hypotension.
Reduced GCS (see Box 7.1).
Exhaustion.
Assess ABC. If the patient is unresponsive and there is no respiratory effort and/or no palpable pulse, commence CPR ( Basic Life support (CPR), p. 220).
If the patient is conscious:
Sit patient up.
Give high flow oxygen if available.
Monitor pulse, BP, and respiratory rate.
Coma
Unrousable unresponsiveness. (See Fig. 8.12.)
Loss of consciousness algorithm.
History (from bystanders)
How/where found.
Sudden or gradual onset.
Seizure.
Any trauma.
Recent illness—headache, chest pain, breathlessness, palpitations, fever, confusion, depression, sinusitis, seizures, vomiting.
Past history—cardiac, respiratory, diabetes, hypertension, psychiatric illness.
Drugs—overdose? Sedative or hypnotic medication.
Social/environmental—alcohol, illicit drugs, travel to malarial area.
Examination
GCS score.
Check pupil responses frequently.
Smell the breath—alcohol, ketones.
Rashes, signs of dehydration, cyanosis, pallor, needle injection marks.
Signs of external head injury—bruising, haematoma, CSF from ears/nose.
Fever and neck stiffness.
Localizing signs such as increased tone in limbs, asymmetrical reflexes.
Heart/lung for murmurs, rubs, wheeze, crackles.
Abdomen for organomegaly, aortic aneurysm, bruising, melaena.
Differential diagnosis
Hypoxia.
Hypotension.
Overdose.
Epilepsy ( Blackouts, syncope, and epilepsy, p. 316).
High-altitude cerebral oedema ( High-altitude cerebral oedema, p. 664).
Sepsis (pneumonia, uro-sepsis, toxic shock).
Meningitis/encephalitis ( Meningitis, p. 473).
Malaria ( Malaria, p. 480).
Carbon monoxide poisoning ( Carbon monoxide poisoning, p. 735).
Subdural/ subarachnoid haemorrhage, stroke.
Decompression sickness ( Decompression sickness, p. 736).
Diabetic emergencies.
Treatment
Treat any identifiable cause. Monitor vital signs and urine output. If full recovery does not occur, evacuate for further investigation and treatment. Remember pressure area care, maintenance fluids, and temperature control during evacuation. Catheterize the bladder if possible.
ABC.
Consider oropharyngeal or nasopharyngeal airway.
Give high-flow oxygen, if available.
Stabilize the cervical spine if there is a history of trauma.
Measure blood glucose and body temperature.
Obtain venous access and consider IV fluids.
Control seizures, treat hypoglycaemia (BM <4).
Treat life-threatening infection if suspected.
Monitor vital signs: pulse, BP, respiration rate, GCS.
Headache
(See Fig. 8.13.)
Headache algorithm.
History
Headache—severity, location, character, speed of onset, nausea/vomiting, head injury?
Direct questions—dizziness, blackouts/fits, visual changes.
Past history—previous headaches, migraine.
Drugs—recent change in medication.
Social/environmental—alcohol/drugs, recent stressors, post-diving or change in elevation.
Examination
Temperature, pulse, BP, blood sugar, GCS score.
Evidence of head injury? Neck stiffness, photophobia, Kernig’s (fully flex hip and passively extend knee. Positive if painful in head or neck). Look for any focal neurology—weakness/paralysis or changes in sensation.
Check whole body for purpuric rash.
Look for signs of URTI, including ear infection or sinus tenderness.
Differential diagnosis
Tension headache.
Migraine ( Migraine, p. 320).
Dehydration.
Acute mountain sickness ( High-altitude illness, p. 656).
High-altitude cerebral oedema ( High-altitude cerebral oedema, p. 664).
Carbon monoxide poisoning ( Carbon monoxide poisoning, p. 735).
Sinusitis.
Dengue fever ( Dengue fever (‘break bone’ fever), p. 465).
Malaria and other febrile illnesses ( Fever, p. 262).
If signs of meningism:
Meningitis/encephalitis ( Meningitis, p. 473).
Subarachnoid haemorrhage.
Decreased conscious level/localizing signs:
Treatment
If reduced GCS, see Coma, p. 248.
Focal neurology or possibility of meningitis/encephalitis: give oxygen, broad-spectrum antibiotics such as IV ceftriaxone or oral ciprofloxacin, evacuate urgently.
Give fluids and regular analgesia. Advise rest. Observe closely.
Delirium/confusion
(See Fig. 8.14.)
Delirium: an acute onset of confusion with hallucinations.
Confusion: a deficit in orientation, thinking, and short-term memory with reduced awareness.
Delirium/confusion algorithm.
History (from bystanders)
Sudden or gradual onset.
Any trauma.
Recent illness—headache, chest or abdominal pain, dysuria, cough, fever, seizures, vomiting, dizziness, diarrhoea, incontinence.
Past history—diabetes, cardiac, respiratory, epilepsy, psychiatric illness.
Drugs—overdose, sedatives/hypnotics, mefloquine, steroids, psychiatric medication.
Social/environmental—alcohol, recreational drugs, usual state.
Examination
GCS score.
Check pupil responses frequently.
Smell the breath—alcohol, ketones.
Rashes, signs of dehydration, cyanosis, pallor, needle injection marks.
Signs of external head injury—bruising, haematoma, CSF from ears/nose.
Neck stiffness.
Localizing signs such as increased tone in limbs, asymmetrical reflexes.
Abbreviated mental state score (see Box 8.1).
Check temperature.
Heart/lung for murmurs, rubs, wheeze, crackles, or injuries.
Abdomen for tenderness, signs of injury, melaena, organomegaly.
Test the urine and check blood glucose.
Age | 1 |
Date of birth | 1 |
Repeat 42 West Street | 0 |
Year | 1 |
Time (nearest hour) | 1 |
Current location | 1 |
Recognize two people | 1 |
Year World War II ended | 1 |
Name of the monarch | 1 |
Count backward from 20 to 1 | 1 |
Recall 42 West Street | 1 |
Total | 10 |
Age | 1 |
Date of birth | 1 |
Repeat 42 West Street | 0 |
Year | 1 |
Time (nearest hour) | 1 |
Current location | 1 |
Recognize two people | 1 |
Year World War II ended | 1 |
Name of the monarch | 1 |
Count backward from 20 to 1 | 1 |
Recall 42 West Street | 1 |
Total | 10 |
Confusion—differential diagnosis
Hypoxia.
Head injury ( Head injury, p. 312).
Alcohol/illicit drugs ( Recreational drugs and alcohol, p. 538).
Sepsis (commonly chest or urine infection).
Meningitis/encephalitis ( Meningitis, p. 473).
Intracranial bleed.
Stroke (CVA) ( Coma, p. 248).
Drug toxicity.
Malaria ( Malaria, p. 480).
High-altitude cerebral oedema ( High-altitude cerebral oedema, p. 664).
Post-ictal ( Epilepsy, p. 318).
Treatment
Treat any identifiable cause. Do not leave patient alone. Sedate only with great caution: lorazepam 1–2 mg PO/IM/IV. This may allow more detailed examination if the patient is very agitated/confused. Observe closely and evacuate for further investigation/treatment if complete recovery is delayed.
Convulsions
(See Fig. 8.15.)
Convulsion algorithm.
Airway: roll patient into the recovery position, protect from further harm but do not restrain. Consider oxygen and a nasopharyngeal airway.
Breathing: if no respiratory effort commence CPR.
Circulation and drugs: attempt venous access. Measure blood glucose; if <3.5 mmol/L give 100 mL glucose 10% by infusion. Recheck levels subsequently. Give lorazepam 4 mg IV over 2 min or diazepam 10 mg PR if no IV access.
If fits continue for >20 min, consider diazepam by infusion 100 mg in 500 mL of 5% glucose; infuse 40 mL/h. Phenytoin is unlikely to be available.
If seizures continue, make arrangements for urgent evacuation.
History
Get a detailed description of the seizure or fit:
Onset—activity, position, warning, tonic, starting in one limb?
During fit—sounds, cyanosis, breathing, eye, facial and limb movements, incontinence, duration.
Post-fit—tongue injury, post-ictal state, limb weakness, muscle pain/injuries, headache.
Preceding illness—headache, chest pain, palpitations, dyspnoea.
Past history—previous seizures, diabetes, alcoholism, pregnancy, cardiac, respiratory or renal disease. Head injury.
Drugs—antiepileptics, oral hypoglycaemics, medication compliance.
Social/environmental—alcohol/drugs, recent feverish illness, post-diving, high altitude.
Examination
Temperature, pulse, BP, blood sugar, GCS score.
Evidence of head injury? Sweating, neck stiffness, photophobia. Look for any focal neurology—weakness/paralysis or changes in sensation.
Check whole body for injury—posterior dislocation of the shoulder is often missed (check for full, pain-free movements of both shoulders).
Convulsions—possible causes
Treatment after convulsion
If reduced GCS see Coma, p. 248.
Focal neurology or possibility of meningitis/encephalitis evacuate urgently.
Otherwise give fluids and regular analgesia. Advise rest. Observe closely. If a first fit, evacuate for hospital investigations.
Diabetic emergencies
Hypoglycaemia
Coma or low GCS with blood glucose <4 mmol/L.
Can occur in non-diabetics—sepsis, alcohol excess, liver failure, malaria, quinine therapy.
History
Sweating, hunger, anxiety, inappropriate behaviour, exercise, seizure, last meal, previous hypos, usual blood sugar levels.
Past history—diabetes, liver disease. Recent infection.
Drugs—insulin dose, oral hypoglycaemics.
Social/environmental—alcohol excess.
Examination
Pallor, sweating, tremor, slurred speech, confusion/aggression, focal neurology, poor coordination, convulsions.
Check observations: pulse, BP, respiratory rate.
GCS score.
Examine for cause of sepsis: see Fever, p. 262.
Consider card test for malaria such as Rapimal®.
See Fig. 8.16.
Treatment
Diabetes
Most likely cause is excess insulin, particularly if the patient has been undertaking unusually high levels of activity on the expedition. If hypos are recurrent reduce insulin doses. Monitor blood glucose regularly, preferably before each meal.
Alcohol
Hypoglycaemia may recur if further excess alcohol is taken. Monitor blood glucose until patient is sober and eating/drinking normally.
Other causes
Evacuate from the field for further investigations/treatment.
Diabetic ketoacidosis
High blood sugars in a diabetic patient with poor glycaemic control may be secondary to infection or steroids. The classical clinical description of diabetic ketoacidosis (DKA) is of a comatose or pre-comatose patient who is dehydrated and hyperventilating.
History
Tiredness, thirst, polyuria, frequency, dysuria, weight loss, vomiting, breathlessness, cough, sputum, fever, chest/abdominal pain, skin infections, teeth problems.
Past history—diabetes, date of diagnosis, complications such as neuropathy, ulceration.
Drugs—insulin dose, oral hypoglycaemics, steroids.
Social/environmental—alcohol consumption, change in usual diet—often a problem on expeditions, particularly while travelling.
Examination
Check blood glucose.
Check observations: pulse, BP, respiratory rate, and temperature. BP may be low. GCS score. Record on chart.
Look for facial flushing, dry mouth, and rapid breathing (Kussmaul respirations), ‘pear-drop’ smell of ketones on breath.
Examine chest, abdomen, and skin for signs of infection (see Fever, p. 262). Look for evidence of dental infection.
Test the urine for ketonuria or evidence for infection.
Ongoing treatment
Mild hyperglycaemia will not necessitate evacuation from the field, provided that the patient is eating and drinking and blood sugars normalize with increased doses of insulin and rehydration. If the patient does not respond rapidly to treatment, evacuate urgently; limited amounts of IV fluids will be available on most expeditions. Change to usual insulin when eating and ketonuria <1+. Continue to monitor blood glucose regularly, preferably before each meal.
Give high-flow oxygen, if available.
Obtain venous access.
Insulin: give 20 units soluble insulin IM followed by 10 units IM/h. When patient has improved and is eating change to insulin SC
Fluids: give 1L normal saline IV, then 250 mL/h for 4–6 h.
When blood glucose <15 mmol/L change to glucose 5% 250 mL/h for 4–6 h (continue insulin 10 units IM/h).
Start a fluid balance chart and measure urine output.
Start antibiotics if any cause for infection identified.
Monitor blood glucose hourly.
See Fig 8.16: diabetic emergencies algorithm.
Gastrointestinal bleeding
History
Vomit—colour, quantity, blood mixed in, frequency, onset, pain on vomiting.
Stools—onset, quantity, colour (red, black, clots), pain on opening bowels, constipation, diarrhoea, change in bowel habit.
Other—appetite, dysphagia, weight loss, dyspnoea, palpitations, tiredness, dizziness, fainting, sweating, abdominal/chest pain.
Past history—previous bleeding, clotting problems, inflammatory bowel disease, liver disease (varices?), peptic ulceration, heartburn/indigestion.
Drugs—aspirin, NSAIDs, steroids, warfarin, clopidogrel, dabigatran, iron, PPIs/antacids.
Social/environmental—alcohol/drugs, smoking status, recent stressors.
Examination
Temperature, pulse, BP, blood sugar, GCS score.
Look for ongoing bleeding, evidence of shock, abdominal distension/ tenderness/rebound/masses. Bowel sounds. PR examination for fresh blood/melaena/palpable mass/haemorrhoids.
Gastrointestinal bleeding—differential diagnosis
Upper GI
Lower GI
Haemorrhoids/anal fissure ( Haemorrhoids, p. 397).
Inflammatory bowel disease.
Diverticular disease.
Treatment
Keep nil by mouth for 24 h. Maintain BP >90 mmHg systolic by cautious use of fluids. Give analgesia as required (not NSAIDs or aspirin!). Monitor urine output. Consider PPI/antacids. Avoid spicy food. Observe regularly and evacuate for further investigation.
See Fig. 8.17: GI bleeding algorithm.
Gastrointestinal bleed algorithm.
Place the patient supine with legs elevated. If vomiting, place in the recovery position.
Give high-flow oxygen.
Check observations: pulse, BP, respiratory rate, and temperature.
Obtain venous access.
Consider IV saline depending on pulse and BP.
Fever
History
Fever type—high swinging, low grade, periodic (i.e. every 2 or 3 days in malaria), association with rigors.
Respiratory/ENT—cough, wheeze, stridor or croup, sputum or nasal catarrh, haemoptysis, dyspnoea, chest pain, otalgia, sore throat, hoarse voice, facial pain, or tenderness (sinusitis), coryzal illness.
Urinogenital—frequency, dysuria, haematuria, loin pain, genital discharge/ulceration, suprapubic pain.
Neurological—headache, photophobia, neck stiffness, impaired consciousness.
Skin/mucous membranes/joints—rash, petechiae, skin infections such as bites/ulcers/sores, mucosal lesions, arthralgia, swollen joints.
Gastrointestinal—vomiting, haematemesis, abdominal pain, bloating, diarrhoea, blood in stools or melaena, foul/excessive flatus.
Other—changes in appetite, aching, night sweats, weight loss.
Past history—previous similar symptoms, immunocompromise, diabetes mellitus.
Drugs—steroids, antimalarials taken regularly, antipyretics, antibiotics.
Social/environmental—infectious disease contact, detailed travel history, adequacy of pre-travel vaccinations.
Travel history
Which countries and which parts of the countries?
When? Length of trip, date of arrival, and departure (estimate possible incubation period).
Purpose of travel—business, pleasure, family visit, military, airline crew, expedition, emigration?
Type of travel, hotels, safari, backpacking.
Special activities (climbing, diving, caving)?
Insect bites/stings (tsetse, ticks, fleas).
Animal contact.
Swimming in fresh water lakes.
Sexual or other infectious disease contact.
Antimalarials taken/immunizations received pre-travel.
Illness among other members of the family or party.
Examination
Temperature (chart if possible), pulse/respiratory rate, BP, GCS score, urine output.
Warm or cool peripheries, capillary refill time ( Capillary refill time, p. 417), sweating, rash, mucosal lesions, wounds, abscesses, insect bites, ulcers, eschar, buboes, cellulitis, or other focal skin infection (examine the entire body surface, including the scalp, axillae, and perineum). Look up the nose and at throat, tonsils, tongue, and buccal mucous membrane. Look in the ears with an auriscope. Examine chest for breath sounds and heart murmurs; abdominal tenderness, bowel sounds, lymphadenopathy; joint pain or swelling, external genitalia (retained tampon) and rectal examination if relevant.
Investigations
Usually impossible. The macroscopic appearance and odour of vomitus, stool, and urine may be helpful (e.g. obvious blood; cloudiness and foul fishy smell of urine suggest infection). Consider dip testing urine, microscopic examination of blood, sputum, urine, stool (experience required). Rapid antigen tests for malaria (see Malaria, p. 480).
Possible diagnoses
URTI—viral coryza, sinusitis, otitis media, tonsillitis, ‘strep’ throat.
Chest—bronchitis, pneumonia, tuberculosis.
Gut—gastroenteritis, dysentery.
Urinary—UTI, pyelonephritis.
Neurological—meningitis/encephalitis.
Tropical infections—malaria, dengue, typhoid, legionella, leptospirosis, hepatitis, rabies, typhus/other rickettsiae, viral haemorrhagic fevers.
Treatment
Focal neurology or possibility of life-threatening sepsis: give oxygen, broad-spectrum antibiotics, evacuate urgently.
If malaria is a possibility treat urgently ( Malaria, p. 480).
Reduce fever with regular paracetamol and/or ibuprofen.
Encourage oral fluids and monitor urine output; start a fluid balance chart.
Advise rest in a cool place. Observe closely, evacuate if not improving.
Empirical antibiotic therapy:
Urinary tract infection—trimethoprim 200 mg/12 h PO (or ciprofloxacin 250 mg/12 h PO) 5-day course.
Cellulitis—flucloxacillin 1 g/6 h IV + benzylpenicillin 1.2 g/6 h IV 7-day courses.
Wound infection—flucloxacillin 500 mg/6 h PO 7-day course.
Meningitis—ceftriaxone 2 g/12 h IV 5-day course.
Septic arthritis—flucloxacillin 2 g/6 h IV 7-day course.
Pneumonia—amoxicillin 500 mg/8 h PO or clarithromycin 500 mg/12 h PO 7-day course.
Intra-abdominal sepsis—ceftriaxone 2g/12 h IV + metronidazole 500 mg/8 h IV. 7-day courses.
Penicillin allergy
For many infections a penicillin is a sensible first-line antibiotic of choice. If an expedition member is known to be allergic to penicillins then the medical kit should contain additional quantities of a suitable alternative. Depending upon the nature of the infection, clarithromycin, metronidazole, or doxycycline may be appropriate; consult a pharmacopoeia.
