Stephen Hearns, Annabel Nickol, Paul Cooper, Daniel Morris, and David Geddes
Minor injuries to head and neck [link]
Fractured facial bones [link]
Cervical spine injuries [link]
Head injury [link]
Blackouts, syncope, and epilepsy [link]
Sleep disturbances [link]
The eye [link]
Ear problems [link]
Nasal problems [link]
Upper respiratory tract [link]
The skull is a complex structure, initially comprising 29 bones, but these fuse during childhood, leaving mobile only the lower jaw and three pairs of tiny bones within the middle ears. Eight bones form the cranium that protects the brain, while another fourteen provide the supporting structure for the eyes, nose, and facial muscles. Areas of the head are described according to their underlying bony parts (Fig. 9.1). The eyes lie protected within the orbit, while the prominent nose is susceptible to injury.
The breathing and digestive passages cross in the oropharynx, requiring complex mechanisms to ensure correct routing (Fig. 9.2). The nose and upper airway form a humidification and filtering mechanism. The opening to the lower airway is the larynx, a complex cartilaginous structure hung from the hyoid bone, which in turn is slung from the base of the skull. When foods or fluids are swallowed, the epiglottis, a roof-like flap, closes over the glottis and protects the trachea. Inside the lower end of the larynx are the vocal cords, used both to provide a watertight seal to the airways and to phonate. These are fixed in the midline anteriorly, but attached to the arytenoid cartilages posteriorly. Movement of the arytenoids permits alterations both to the position and the tension of the vocal cords. The two prominent thyroid cartilages form the anterior border, the ‘Adam's apple’ of the larynx. Just below these cartilages is an obvious groove, the cricothyroid membrane—the safest location of emergency surgical access to the airway.
The swallowing mechanism primarily involves the tongue and oropharynx. Movement of a food or fluid bolus to the back of the mouth causes reflex closure of the larynx and a peristaltic wave to pass down the oesophagus. Tongue swelling or a sore throat will disrupt swallowing.
Head injuries such as bruises, black eyes, or lacerations are relatively common; more serious head injuries are fortunately rare, but are an ever-present risk during outdoor activities.
Scalp lacerations tend to bleed a lot initially and can look a lot worse than they really are. Apply firm pressure until the bleeding stops. Small wounds can be closed using cyanoacrylate tissue glue. Conventional superglue has been used for this purpose, but can provoke tissue reactions and is not recommended1. The area around larger lacerations should be shaved and cleaned, and the edges of the laceration sutured ( [link]). If appropriate medical kit is not available, it may be possible to approximate the wound by tying the patient's hair across it.
Facial lacerations usually heal well, but it is important to minimize scarring. Clean the wounds and, where possible, use glue or skin fixers (Steri-Strips™, etc.) to bring the edges together. If wounds are deep, try to remove tension from the surface by placing subcutaneous sutures to approximate the edges and then suture the skin itself using as fine a suture material as possible (ideally ‘6/0’) to finish the job. Ensure that tension is even throughout the wound and that the edges are aligned. When a lip has been cut, make every effort to realign the vermilion edges, as even small deviations are very obvious and may require subsequent corrective plastic surgery.
Injured noses tend to bleed a lot. If a nose is broken and deformed it may be possible to straighten it soon after the injury, although the casualty may be reluctant to permit this. Apply cool compresses and pressure to areas of bruising. Pressure over the soft tissues of the nose will control almost all nose bleeds, although rarely it may be necessary to pack a nostril using either a nasal tampon or ribbon gauze lubricated with paraffin ointment or a suitable antibiotic ointment.
Detailed diagnosis of facial bone fractures is impossible and irrelevant in a remote environment. Fractures to both the mandible and maxilla will cause pain and swelling, limit diet, and may threaten the airway. The best advice is to arrange early evacuation to the nearest specialist care. However, this may take time and in the interim the following can help, assuming there are no other life-threatening injuries:
• Reduce and stabilize the fracture.
• Apply comfortable and supportive bandaging.
• Arrange for a soft food or liquid diet if the upper and lower teeth have been splinted together.
• Provide details of the circumstances of the accident, treatment to date, and medication.
• Arrange for a carer to accompany the patient to specialist care.
There are two common fracture sites. Both are seen following a fall or blow to the chin.
• Condylar fracture: a horizontal fracture through the base of the condyle about 2 cm below the temporomandibular joint (TMJ).
• Vertical fracture: in the premolar region, often associated with the mental foramen, which is positioned between the root apices of the lower premolar teeth. The nerve exiting this hole provides sensation to the lower lip.
Treatment of a condylar fracture
A condylar fracture is beyond your ability to reduce in the field. It will typically present as an inability to open and close the mouth, and pain in and below the TMJ. The upper face may be very swollen. Treat as follows:
• Make casualty comfortable with padded vertical bandaging to immobilize the mandible.
• If there are no contraindications, give NSAIDs (ibuprofen or diclofenac) to reduce swelling. If swallowing tablets proves difficult, persuade the casualty that suppositories are a good idea.
• Arrange soft food diet.
Treatment of a vertical fracture
In a very remote area, you may be able to reduce and splint a vertical fracture through the mental region of the mandible using figure-of-eight wiring (Fig. 10.2) around the teeth. The location of the fracture will often be obvious, as there may be a step between the fractured segments. The muscles of the neck will have the effect of pulling the most mobile fractured element downwards. The objective is to identify teeth that are not mobile on either side of the fracture line and reduce the fracture by splinting using wire in lengths of about 20 cm. Once the fracture is reduced, it can be located by applying a figure-of-eight wire to the opposing upper teeth and then connecting the two sets of wires. That is the theory. This is a fussy procedure that is possible in the field if you have good light, an accurately placed mandibular local anaesthetic block, wire, strong tweezers, and wire-cutting thin-nosed pliers. The patient will need to be stoical.
• Decide whether to attempt wire splinting.
• Apply padded vertical bandaging.
• If no contraindication, give NSAIDs (ibuprofen or diclofenac) to reduce swelling. If swallowing is difficult, persuade the casualty that suppositories are a good idea.
• Arrange soft food diet.
There are many categories. Fractures will most commonly occur to the zygomatic arch where the chewing muscles attach. Difficulty in opening and closing the jaw will be typical, with pain in the region of the temporalis muscle. Fractures of the middle third of the face may be suspected if there is evidence of periorbital bruising and swelling. This can look quite dramatic. Make the casualty as comfortable as possible with vertical padded bandaging (Fig. 9.3) and evacuate immediately.
• Examine for signs of significant head injury in patients with nasal injuries.
• The diagnosis of a nasal fracture is a clinical one. X-rays are not routinely required. Swelling, tenderness, and possibly deformity of the bridge of the nose are visible.
• It is essential to look for and exclude a septal haematoma—a smooth swelling of the midline of the nose that can develop into septal necrosis. In the wilderness a septal haematoma should be incised under local anaesthetic, and then the nostrils packed to prevent recurrence.
• Swelling often prevents an early assessment of the degree of nasal deformity. Between 5 and 7 days after injury, the nose should be re-examined; if there is evidence of deformity or septal deviation, the patient requires evacuation for specialist ENT assessment and management. Deformities should be corrected operatively within 10 days of injury.
• Open fractures of the nose require prophylactic antibiotics such as co-amoxiclav or erythromycin.
Blow-out fracture of orbit following blunt trauma
Blunt trauma to the globe of the eye, perhaps from a fall or a punch, can cause the bony orbit to fracture (Fig. 9.4). The weakest point is the orbital floor and a blow-out fracture inferiorly often causes prolapse of orbital fat into the maxillary sinus below. There can also be tethering of the inferior rectus eye muscle, causing double vision, particularly when the patient looks up.
Diagnosis is made of the basis of:
• Pain on eye movement
• Double vision (diplopia)
• Sunken eye (enophthalmos).
If you suspect this injury:
• Check visual acuity
• Assess globe integrity
• If the double vision is intolerable, cover the damaged eye with a patch (see Fig. 9.6).
Injuries of this type may also lead to:
• Corneal abrasion
• Hyphaema (blood in the anterior chamber of the eye)
• Subluxed lens
• Vitreous haemorrhage
• Retinal detachment
• Posterior globe rupture.
If visual acuity is reduced following blunt trauma, evacuation is imperative.
Neck injuries occurring in remote areas are challenging as they are accompanied by a fear of missing an unstable injury that could lead to neurological impairment. In an urban environment it is relatively straightforward to immobilize patients with neck injuries for short periods en route to hospital where significant injuries can be excluded by an experienced emergency physician or radiological imaging. Such practice in remote areas may not be as appropriate, as prolonged immobilization during evacuation is potentially harmful to the patient and to rescuers. Therefore thorough examination techniques and appropriate experience are required in assessing and managing cervical spine injuries in the expedition environment.
Anyone who has had a significant force applied to their head or neck, especially if they are now unconscious, should be considered to have a neck injury and should have their neck initially immobilized until it can be fully assessed. The history taken should include the mechanism of injury, location of pain, and the presence of any neurological symptoms. Examination should identify areas of localized tenderness, swelling, or bruising. Sensation, tone, and power should also be examined and documented for all four limbs. Active range of cervical spine movement should only be assessed if the medic is sure that the presence of any significant underlying injury is unlikely.
When initially assessing a patient with a potential neck injury, the patient's head should be gently supported on either side. Avoid covering the patient's ears as this makes communication difficult. The head and spine should be held in a neutral position. Careful manual in-line stabilization is a satisfactory method of preventing further injury.
If a neck injury cannot be excluded in the field then the patient will require immobilization for transfer. Complete spinal immobilization is only possible if a properly fitted cervical collar is used, together with sandbags on each side of the head, and tapes to fix position relative to the two sides of the stretcher. Cervical collars used without bags or tape provide insufficient immobilization. Cervical collars come in a variety of sizes. In the expedition setting it is appropriate to carry one adult multi-size collar such as the Stifnek select™. This cuts down on weight and cost.
Patients transferred on stretchers are prone to pressure area necrosis; this is more common in the presence of a sensory deficit. For this reason, spinal boards, whether commercially manufactured or improvised, should be used for extrication only, and should not be used for evacuation. Best practice for prolonged transfer of spinally-injured patients is a vacuum mattress, but only very large expeditions would be likely to take such a piece of equipment. It would be advisable to place a Thermarest™ or Karrimat™ type sleeping mattress under the patient if carried on a hard surface during evacuation.
Most but not all spinal injuries will result from one of the following three causes:
• A fall from a height
• Being struck by a falling object
• A high speed road traffic collision (RTC).
The neck should always be fully immobilized if there has been a dangerous mechanism of injury, such as:
• Fall >1 m or five stairs
• After diving
• A high speed road traffic collision (>65 mph), a rollover, or ejection from a vehicle.
• If the patient is over 65 years of age, the risk of injury increases and immobilization is recommended.
• The casualty is fully alert (GCS score 15)
• The casualty is not under the influence of drugs or alcohol
• There is no distracting painful injury such as a chest, abdominal, or thigh fracture
• There are no neurological signs or symptoms such as tingling
• There is no midline bony tenderness of the neck bones
and if any of the following apply:
• The neck pain has a delayed onset
• The patient is sitting or has walked since the injury
• The neck injury followed a rear-end vehicle collision.
then it should be safe to let the patient move their head 45° to the left and right slowly. If this is possible then the neck collar can be removed and investigations are not required. Stop and reapply the collar if tingling develops in the extremities. These rules follow the principles of NICE guidelines and the Canadian rules for radiography of cervical spines following injury2.
Acute neck sprains
These most commonly result from low velocity rear-end road traffic collisions. The trapezius and sternomastoid muscles may be injured. Neck sprains are managed with analgesia and encouragement to mobilize. Immobilization with neck collars causes stiffness and should be avoided.
Fractures and dislocations of the neck
These are indicated by the mechanism of injury, usually severe pain, and localized midline tenderness of the cervical spine. Assessment and exclusion without the aid of X-rays is difficult, especially for the inexperienced. If in doubt, immobilize and evacuate for specialist assessment.
A person should be considered to have a head injury if they have suffered any trauma to the head, apart from superficial lacerations to the face. Head injuries can be:
• Direct or indirect
• Closed or open
and may result in:
• Primary or secondary brain damage.
It is best to avoid a head injury! About 60% of adults with moderate head injuries and 85% with severe head injuries remain disabled 1 year after their accident. Even a minor head injury can ruin a trip: 3 months later 80% have persistent headaches and 60% have memory problems.
• Direct head injuries are caused by a blow to the head of some form; this can result in a closed injury, without penetration of the skull, or an open injury, where the skull is penetrated.
• Indirect injury is caused by a ‘whiplash’ effect of the brain moving within the skull, though without a direct blow to the head; this can result in brief concussion, but in a young adult is unlikely to cause significant damage.
History and examination
• Ask about amnesia for events before or after the injury. Brief amnesia, of less than 1 min, is common with even mild concussion, but any significant amnesia should be a cause for concern. Significant head injuries are usually associated with amnesia of 30 min or more.
• Care is particularly needed for high energy injuries, for example a pedestrian struck by a vehicle, any high speed road traffic collision or any accident involving motorized off-road vehicles such as snowmobiles, jet skis, or quad bikes. High-energy injuries also include any significant fall from a height, or any rock fall.
• Assess level of consciousness, using the Glasgow Coma Scale ( [link]). This is easily and reliably administered with minimal experience and is particularly useful to monitor progress. Failure of the GCS to improve and, in particular, a fall in GCS is of significant concern. The scale has a range of 3–15. A score of 8 or less indicates a very severe head injury, one that, if it were available, would prompt immediate critical care. A score of 12 or less at any point after a closed head injury indicates possible significant injury, but secondary intracranial bleeding can develop even in someone fully conscious initially.
• Carry out careful inspection of the head, looking particularly for signs of any skull fracture. Classically basal skull fracture may be associated with:
• Carry out and document a simple neurological examination. As a minimum this should include:
• Examination of pupil size and reaction.
• Check of visual acuity.
• Eye movements.
• Examine tympanic membranes if possible.
• Always assess hearing.
• Gag reflex if not fully conscious.
• Examine for any focal motor deficit, including plantar responses.
• Check for any sensory loss.
• Ask about paraesthesia.
• Check for ataxia.
• Look out for irritability and/or altered behaviour, persistent headaches, or vomiting. An apparent convulsion at the moment of impact is a well recognized feature of concussion, often seen in contact sports, and need not be of great significance. Any subsequent seizure is of great concern.
• Do not attribute a depressed conscious level and/or altered behaviour to intoxication with alcohol or drugs unless you are sure that there has been no significant brain injury. Any intoxicated person with a suspected head injury needs close observation.
• Always carefully examine the spine, especially the cervical spine in any significant head injury, particularly those with a dangerous mechanism of injury. Around 10–15% of those knocked out with a head injury have an associated neck injury ( [link]).
• Document any findings and repeat examination; judgement is needed to determine the frequency and extent of repeat examination, but if you are concerned about a possible significant head injury it would be reasonable to repeat GCS every 15 min for 2 h; by then the GCS should be 13 or better. Continue to repeat regularly until the GCS is normal, and do not leave the person alone for 24 h.
Avoiding head injury
Wear a helmet! Even a minor head injury from a falling stone, or standing up too quickly in a confined space such as a cave, can result in persistent dizziness, headaches, and poor concentration.
Closed head injury:
• Results from falls, RTCs, etc.
• Typically high energy injury.
• No penetration of the skull.
• Primary damage tends to be diffuse:
• Diffuse axonal injury.
• Some focal damage, particularly to vulnerable areas such as frontal lobes, anterior temporal, and posterior occipital poles.
• Results from bullet wounds, etc. with penetration of the skull.
• Primary damage is largely focal but the effects can be just as serious.
Secondary deterioration is usually due to:
• Oedema (swelling) of damaged tissue, resulting in increased intracranial pressure and possible brain herniation.
• Intracranial haemorrhage (bleeding) from torn vessels, which can be:
• Subdural: between the dura and the brain.
• Extradural: outside the dura, beneath the skull vault.
Swelling inside the closed cranium interferes with blood flow into the brain. Cerebral perfusion pressure (CPP) is the balance of mean arterial pressure (MAP) less intracranial pressure (ICP):
CPP = MAP − ICP
It is therefore important to maintain blood pressure, with fluid replacement, and minimize ICP. Factors that increase ICP that can be correctable in the wilderness include pain and hypoxia due to altitude.
Management options for a significant head injury in a remote environment are limited.
• Maintain airway and breathing, and replace fluids when possible.
• Assess and manage cervical spine.
• Give adequate analgesia to control pain, and try to be calm and provide reassurance. Opiates, if available, may be needed to control severe pain, but can mask signs of deteriorating cerebral function. Tramadol is best avoided unless nothing else is available as it can increase the risk of seizures and can cause confusion.
• Elevation of the head to 20° improves venous outflow from the brain and may reduce ICP, therefore increasing CPP. This should only be attempted after any hypovolaemia has been corrected. If a patient is hypovolaemic, elevating the head will reduce MAP.
• If the casualty is at altitude sufficient to cause hypoxia then, if possible, bring them down, and give oxygen when available.
• Steroids should not be given; they have been shown to increase mortality rates.
• Secondary deterioration owing to cerebral oedema may respond to diuretics. Mannitol is preferred because it causes less electrolyte disturbance than loop diuretics, but it is unlikely to be available. Furosemide and other diuretics should be used with care; give sufficient to induce diuresis, but ensure that blood pressure is maintained.
• Deterioration caused by intracranial bleeding is usually untreatable in the wilderness, though a doctor familiar with the technique might in desperation attempt a burr hole to relieve a developing extradural haematoma.
• The major issue is whether to arrange evacuation. This decision depends on the situation and the severity of the injury. Most head injuries do not require neurosurgery, but there are many factors following any significant injury that are better managed in hospital, and secondary deterioration because of intracranial bleeding is potentially correctable. If evacuation is realistically possible, following anything other than a minor head injury it should be arranged.
• Infection: meningitis is a recognized complication of any skull fracture where the integrity of the blood–brain barrier may be breached. If transfer to hospital may be delayed it is appropriate to give a broad spectrum antibiotic. There is particular risk if there is a CSF leak, a common presentation of which is the loss of clear, slightly salty, watery fluid coming from the nose or ear.
• Seizures: epileptic seizures can occur early or late. Early seizures, within 24 h, may not require long-term treatment, but in the wilderness any seizure is best treated until definitive care is available. A seizure should be considered a sign of possible intracranial deterioration. Medication available is likely to be limited to a benzodiazepine such as lorazepam or diazepam. The risk of sedation is outweighed by the need to control seizures.
• Neurological symptoms: these can be divided into minor symptoms that can follow any concussion, and more significant deficits. Headaches, disequilibrium, and poor concentration are common after minor head injury; they are likely to last for up to 3 months and possibly longer. Benign positional vertigo can follow any blow to the head; it results in intense vertigo with a sensation of spinning precipitated by movement of the head. Give prochlorperazine or cyclizine and arrange an ENT assessment.
Severe head injuries have protean consequences, and may require long-term rehabilitation.
An episode of transient loss of consciousness is often referred to as a ‘blackout’. This is a useful colloquialism, because it makes no inference as to the mechanism of transient loss of consciousness, or the underlying pathophysiology.
Blackouts commonly result from:-
• A disorder of the circulation—e.g. syncope (fainting).
• A disorder of the brain—e.g. epilepsy.
• A disorder of the psyche—e.g. psychogenic blackouts.
It may prove difficult, if not impossible, to determine the cause of some blackouts in the wilderness. Misdiagnosis is common, with rates exceeding 25% even if diagnostic facilities exist. Any previous diagnosis in an expedition member should be treated with caution, particularly if there are unusual features about the new attack.
Blackouts are universal, although the possible causes vary between populations owing to various factors, including endemic diseases and cultural factors. Various neurological infections such as neurocysticercosis may present with seizures; many conditions associated with HIV, particularly toxoplasmosis, may cause epilepsy, and there are a number of well recognized culturally determined causes of psychogenic attacks, such as Latah in Malaysia. Latah occurs in certain cultural groups, where a minor fright leads to a prolonged and vigorous physical display of fear or anger over which the victim has little or no control. These factors may influence the likely causes of blackouts seen in local populations.
Doctors often assume that a blackout is neurological, due to epilepsy. In fact, cardiac syncope accounts for most blackouts, and of these the majority are cases of reflex syncope, with up to 30% of people suffering reflex syncope during their lives. In contrast, epilepsy only affects about 0.5% of the population at any one time, with a lifetime incidence of 2%, although many of these will develop at one or other extreme of age. Blackouts are also often seen in the absence of organic physical disease; these attacks may be accompanied by apparent convulsive movements, and the possibility that an episode may be psychological should be considered, particularly in the context of stressful situations.
Syncope is a cardiovascular disorder. Causes can therefore be divided into cardiac and vascular:
• Cardiac causes are either underlying structural heart disease or an arrhythmia. Sudden death in young people is occasionally associated with a structural cardiomyopathy. An arrhythmia in the wilderness is likely to be a marker of myocardial infarction. Syncope during (as opposed to after) exercise is potentially serious and may presage sudden cardiac death owing to a familial arrhythmia syndrome such as long QT.
• Vascular causes are more likely, and include:
• Reflex causes, such as vasovagal syncope.
• Situational causes, such as cough and micturition syncope.
• Postural causes, such as orthostatic hypotension which may reflect dehydration.
• In hot environments, consider heatstroke.
• Pulmonary embolism.
Diagnosis is made from the history, particularly the circumstances around the blackout. Syncope results in transient self-limited loss of consciousness owing to transient global cerebral hypoperfusion, typically leading to collapse; most attacks, particularly those with vascular causes, therefore occur when patient is upright, although fainting can occur while sitting.
• The patient may recall a brief prodrome of lightheadedness, when voices sounded distant, and vision faded.
• Onset is rapid; recovery is spontaneous, complete, and usually prompt.
• During the episode the pulse may be slow and blood pressure low, but often the episode is too brief and the bystanders too panicked for either to be reliably measured.
• The patient characteristically appears limp and white.
• Myoclonic limb jerks commonly occur. These are usually brief, but complex movements resembling epilepsy can be seen. This ‘convulsive syncope’ often results in panic in bystanders and may be reported as an ‘epileptic fit’ by even medically trained observers unfamiliar with the phenomenon.
• The profound pallor of syncope often results in witnesses saying afterwards that they thought that the person had died.
• During recovery there may be brief bewilderment, but prolonged confusion is rare.
• If the person gets up too quickly they may collapse again.
• Victim may be sweaty, and complain of thirst.
Broadly, epilepsy, as a disorder, can be classified as idiopathic, a condition in isolation, or symptomatic, resulting from some underlying disease. The resulting seizures are either generalized, involving the whole brain from onset, or focal, starting in one area but then maybe generalizing.
• Idiopathic epilepsy usually starts in childhood, and is therefore unlikely to be a diagnostic issue in the wilderness; however, there are some syndromes that may first appear during adolescence, and may therefore affect youth groups (see below). Idiopathic epilepsies usually cause generalized seizures, tonic–clonic convulsions, myoclonus, and absences.
• Symptomatic epilepsy, particularly in the context of wilderness medicine, is more likely to result in focal or secondarily generalized seizures. The fit may indicate an underlying localized brain disorder, and in these circumstances concern should be raised about infection, including cerebral malaria.
A separate classification describes the resultant seizures: these are partial or generalized.
• More likely to be caused by a symptomatic epilepsy; that is, where pathology has developed in part of the brain, causing the seizures—this is potentially of more concern in the wilderness.
• Start in one area, and spread; this is reflected in the associated symptoms and behaviour, which may or may not result in loss of awareness, and which may or may not result in collapse.
• An essential component of any witness's account, to determine that the episode is a partial seizure, is therefore a detailed description of the onset of the attack, which may include automatic behaviour, asymmetrical limb jerking, or a forced turn of the head.
• The patient may afterwards recall a strong unpleasant smell, or a brief but intense sense of déjà-vu.
• Involve the whole of the brain.
• Best recognized form is a tonic–clonic convulsion.
• Onset is sudden with an initial tonic phase; all muscles stiffen, the limbs are rigid, and there may be a strangled cry; the person falls to the ground. Victim may become cyanosed.
• The subsequent clonic phase involves rhythmic jerking of the limbs; initially this may be vigorous, but the movements slow and become irregular.
• Victim is then usually unconscious for a period.
• When they come round they may be confused, which can be prolonged, muscles may ache, and they will usually complain of headache.
• They may have bitten the tongue (usually the side).
• The tonic–clonic seizure itself rarely lasts more than 1–2 min, but post-ictal drowsiness and confusion can be prolonged, with general malaise occasionally lasting 24 h or more.
• A generalized tonic–clonic convulsion can also develop from an initial partial seizure, the seizure activity starting focally and then spreading to the whole brain; these are secondarily generalized convulsions.
The other types of generalized seizures are unlikely to be an issue in the wilderness. These include collapse, rigid (tonic seizure) or without loss of muscle tone (atonic seizure); these usually only occur in the context of a complex epilepsy associated with learning disability. Generalized seizures also include absences, with preserved posture, and daytime myoclonus, both of which may be seen in idiopathic childhood and juvenile epilepsies which will usually have been previously diagnosed.
These range from simple panic attacks with hyperventilation, which rarely cause blackout and are usually readily recognized, to a wide spectrum of non-epileptic seizures. Patients are usually adolescents or young adult women3 and may have very frequent episodes, sometimes occurring many times a day. Attacks are non-stereotypical and unresponsive to medication, without obvious cause for apparent intractable epilepsy. The assessment of psychogenic blackouts is likely to be very difficult in the wilderness, requires specialist advice, and, although the circumstances of an expedition may well predispose to such attacks, the diagnosis should only be made with extreme caution.
Differential diagnosis of blackouts and seizures
If you consider that the blackout is due to syncope, then check for any systemic illness, which may have predisposed to this:
• Anaemia is a common factor, particularly in young women who faint; check for blood loss—acute or chronic.
• Dehydration or heat exhaustion.
• Salt deficiency.
• Excess alcohol can predispose to fainting, possibly due to dehydration, and excess alcohol can also be a factor in epileptic seizures.
• Hypoxia and high altitude cerebral oedema (HACE [link]) may cause fitting.
• An initial epileptic seizure may be an indication of an underlying neurological disease presenting for the first time. This is especially likely if the seizures are focal in onset. There are several possible causes:
• Neurocysticercosis is the most common cause of new adult onset epilepsy in rural, developing countries with poor hygiene, where pigs are allowed to roam freely. It results from human ingestion of the eggs from the pork tape worm. Visitors are vulnerable, the condition usually presenting some months after exposure. Other parasitic diseases, including schistosomiasis, may also present with epilepsy.
• Bacterial meningitis can cause seizures, but the individual is likely to be unwell with fever, photophobia, and a stiff neck at this stage. Likewise, cerebral malaria can present with seizures, and should always be considered in malarial zones.
• There is a specific epilepsy syndrome, juvenile myoclonic epilepsy (JME), which commonly starts in adolescence, and in which seizures typically occur in the morning, precipitated by sleep deprivation with or without excess alcohol. JME presents with generalized convulsions and is often accompanied by myoclonic jerks. It may be a consideration in youth groups; there is often but not always a family history.
Few investigations are possible in the wilderness. Check pulse and temperature to check for systemic illness, and check blood glucose if possible. If you consider syncope and have access to ECG then this is worthwhile. Measure oxygen saturation if a pulse oximeter is available.
• Assess whether the diagnosis is likely to be epilepsy, or if the episode might be convulsive syncope.
• Question the patient carefully for any prior history that they may have concealed to secure a place on the trip. If they are confused, or you doubt their medical history, consider contacting their family or GP if communications are available.
• Carry out as comprehensive a neurological examination as you are able to, looking carefully for papilloedema if possible, and checking for any persisting focal neurological deficit.
• If you assess this to be a first seizure, particularly if the patient is unwell, if there are any focal features to the seizure, or focal neurological deficit, then evacuate if at all possible.
• Consider cerebral malaria ( [link]) and give therapeutic doses of antimalarials if in doubt.
• Seizures can rarely complicate HACE ( [link]); if this is the case then intensify treatment for the HACE and hasten descent.
• If you believe that a team member has developed epilepsy for the first time in a wilderness environment, particularly in the tropics, then seek expert advice or evacuate if possible.
• During the seizure, move the patient only if essential to protect from injury. Take the pulse; it is quicker and easier to compare the patient's pulse to your own, rather than to try and count it. If the pulse is weak, thready, and particularly if slow then consider convulsive syncope.
• Turn patient on their side into the recovery position.
• Give oxygen if available, particularly if the seizure is prolonged.
• Do not attempt to force anything into their mouth.
• Your choice of available anti-epileptic drugs is likely to be limited. Most seizures are self-limiting, and a single seizure does not require treatment unless the situation is such that a further seizure could be catastrophic.
• If the seizure is prolonged, with a convulsion lasting more than 2 min, then give any available benzodiazepine intravenously, intramuscularly or rectally at a dose equivalent to 20 mg of diazepam (30 mg if rectal).
• If you wish to give continuing preventive treatment, either following repeated seizures or if any further seizures might be particularly hazardous, then give the equivalent of oral diazepam dose 10 mg twice daily, and increase to 20 mg twice daily if seizures occur despite this. There may be a compromise between anti-epileptic treatment and sedation; individual circumstances must be considered, but if possible avoid sedation following any significant head injury. In many parts of the developing world the locally available anti-epileptic is likely to be phenobarbitone, or maybe phenytoin. If either is available then, to prevent further seizures, give 60 mg of phenobarbitone initially, then 30 mg daily thereafter, or 1000 mg phenytoin initially, then 300 mg daily thereafter.
• An alcoholic binge-induced seizure may be complicated by hypoglycaemia; in chronic alcoholics there may well be thiamine deficiency, and correcting the hypoglycaemia without supplementing thiamine can precipitate Wernicke's encephalopathy. Therefore, if alcohol may be a factor, glucose should be accompanied by thiamine.
Migraine is a disorder characterized by recurrent, usually unilateral, moderate to severe headaches that may be accompanied by dizziness, nausea, vomiting, or extreme sensitivity to light and sound. Migraine is common in young adults. Most migraine sufferers will be aware of their liability to headache, so a first attack would be unusual but could be precipitated by, for instance, altitude. The cause of migraine is unknown; the two main hypotheses focus on either a primary vascular instability, or on an imbalance of central neurotransmitters.
Women may be more prone to migraine if on the oral contraceptive pill.
Focal migraine is a contraindication to the use of the oral contraceptive pill—it may increase risk of stroke, so the Pill should be stopped if focal migraines develop. Stress, tiredness, exertion, and menstruation may precipitate migraine in susceptible individuals. There are a number of well recognized dietary precipitants:
• Alcohol, especially red wine.
• Citrus fruits.
History and examination
Migraine usually produces a fairly stereotypical progression of symptoms.
• Prodromal: many notice a change in mood, or other biological functions that may predate the headache by more than a day. These symptoms include negative or positive features; for instance, depression or restlessness, tiredness or listlessness.
• Aura: the aura is characterized by visual abnormalities, including flashes, shimmering, and other hallucinations.
• Headache phase. The headache itself is typically one-sided but may affect both sides of the head. It is usually gradual in onset, moderate to severe in pain intensity, throbbing, and worse with physical exertion, and it can last anywhere from 2 h to 2 days in children and 4 h to 3 days in adults. The headache stage is often accompanied by loss of appetite, nausea, vomiting, sensitivity to light and sound, blurred vision, tenderness of the scalp or neck, lightheadedness, sweating, and pallor. In severe cases there may be visual field defects and lateralizing limb weakness; these are very frightening symptoms which should be treated seriously unless the patient knows that they are regularly associated with their migraines.
Diagnosis of migraine at low altitude is usually straightforward, particularly if the individual has a prior history.
The main issue at high altitude is distinguishing migrainous headache from acute mountain sickness (AMS). AMS commonly produces a throbbing headache with nausea, and may be indistinguishable from migraine. Any headache developing at altitude should be assumed to be AMS and treated as such, including adequate hydration and descent if severe.
• Rest, hydration, and adequate analgesia.
• If the individual is known to have migraine they may have brought their medication with them. Otherwise, give 900 mg soluble aspirin with available antiemetic, which should be given with a glass of milk, if available, to protect the stomach. Metoclopramide or domperidone are particularly useful as they promote gastric emptying, but avoid metoclopramide in adolescents and young adults, as it can precipitate an extrapyramidal reaction. Prochlorperazine is a suitable alternative.
Complications are unlikely. Migraine can occasionally result in stroke. If migraine develops for first time in women on oral contraception then this should be stopped, particularly if migraine has focal features.
If features suggestive of stroke develop at altitude, assume AMS with likely high altitude cerebral oedema (HACE [link]).
On an expedition, many factors may disturb sleep, including time zone shifts, unfamiliar harsh living conditions, physical discomfort, environmental extremes, sport-specific disturbances (night watches sailing/dawn starts climbing), and psychological factors such as anxiety about the venture ahead or homesickness. Few things erode team morale and daytime performance as much as disturbed sleep; however, forward planning and simple measures can improve things considerably.
General measures to improve sleep
• Comfortable bed—careful choice of tent site, padded sleeping mat, under-tent lumps shifted before night fall.
• Temperature control—fan, hot water bottle (e.g. tomorrow's boiled drinking water wrapped in a fleece), appropriate sleeping bag and mat.
• Mosquito deterrents—nets and repellents.
• Ear plugs.
• Safe environment—away from rock fall, avalanche run out zones, flood pathways, or marauding animals.
• Secure valuables if necessary.
Many body functions are under circadian control, including hormone secretion, body temperature, cellular and enzymatic function, and sleep. The natural circadian rhythm approximates 24 h. Rapid travel across time zones is associated with desynchronization between the body's circadian clock and the actual local time, resulting in jet lag. This is experienced as difficulty getting to sleep following an eastward flight, wakening early following a westward flight, disturbed sleep, daytime sleepiness, difficulty concentrating, irritability, depressed mood, anorexia, and nocturia. These symptoms usually only pose a minor inconvenience for travelers; however, performance, including decision-making, may be impaired in the first few days following arrival in a new time zone, and this should be allowed for in the travel schedule.
Decreasing jet lag
• Obtain adequate sleep. Use daytime flights in preference or sleep as much as possible during overnight flights. Use short naps terminated by an alarm clock to improve daytime alertness and concentration. Avoid napping late in the day as this will decrease the drive to sleep at night.
• Adopt the new time frame in the country you are leaving and in transit, including bed and get up times and meal times. Adhere strictly to the new time zone on arrival.
• Optimize light exposure. The light–dark cycle is the principle time cue for resetting human circadian rhythms. Bright light exposure during the daytime for the new time zone and avoidance of bright light at other times of day may have a beneficial effect on the circadian clock and jet lag. This usually means maximizing the exposure to light early in the day after flying eastwards and late in the day after flying westwards.
• Take exercise. Exercise both improves sleep quality and has a minor effect on entraining circadian rhythms, with night-time exercise delaying the circadian clock.
• Avoid excess caffeine and alcohol as these can have a deleterious effect on sleep quality.
• Short-acting hypnotic drugs used on overnight flights and for a few nights after arrival may help. Drug-induced sleepiness carrying over into the next day must be taken into account, particularly after short flights followed by driving.
• Melatonin is a hormone that is secreted by the pineal gland and linked to the circadian rhythm; it has soporific and temperature lowering effects. However, there is no consistent evidence that it has a beneficial effect upon jet lag.
• The high altitude environment is often associated with harsh living conditions and cold that may disrupt sleep. In addition, hypoxia directly disturbs sleep by leading to waxing and waning of breathing, known as periodic breathing.
• Pathophysiology of sleep disordered breathing at altitude:
• Reduced oxygen tension or hypoxia stimulates breathing at high altitude. This lowers carbon dioxide below the critical level required to stimulate breathing, known as the apnoeic threshold. During wakefulness, cortical drives to breathe are maintained; however, during sleep the relative importance of chemical drives to breathe increase, and an apnoea, or pause in breathing, may ensue. Central apnoeas are frequently followed by arousals consisting of increases in heart rate, respiratory rate, and awakening or lightening of sleep, which lower carbon dioxide again, thereby helping to sustain periodic breathing. A brisk hypoxic ventilatory response (HVR) produces a greater overshoot in ventilation, so leading the cycle to repeat itself. Periodic breathing results. Recurrent awakenings or lightening of sleep impair sleep quality, and if the sleep duration period cannot be extended may lead to fatigue the next day.
Periodic breathing and central apnoeas are nearly universal in native lowlanders at high altitude. This is in contrast to Sherpa natives who are longstanding high altitude dwellers, and is attributed to their blunted HVR. With increasing altitudes, the proportion of the night spent in periodic breathing increases, and periodic breathing hyperpnoea/hypopnoea cycle time decreases.
Implications of sleep-disordered breathing at altitude
• It is likely that poor sleep and sleep disruption reported by climbers act synergistically with hypoxaemia to impair judgement, vigilance, and safety at extreme altitude.
• Sleep disturbance at altitude is a feature of AMS and high altitude pulmonary oedema (HAPE) ( [link]). Vigilance amongst group members must be maintained to recognize these conditions, and to take rapid action in the event of severe AMS or onset of HAPE.
• Periodic breathing is increased by a brisk HVR. It may be argued that this is a ‘good’ thing (the brisker HVR is associated with reduced oxygen desaturations during exercise at altitude), or a ‘bad’ thing (at extreme altitudes ventilation is greater during exercise, and therefore the trekker has less ventilatory reserve between their actual ventilation and maximum voluntary ventilation).
Treatment of periodic breathing
• Periodic breathing and nocturnal hypoxaemia diminish with acclimatization. Graduated, slow ascent, allowing time for acclimatization ( [link]), will improve sleep quality. When severe, descent should be considered.
• Increased sleep duration may compensate in part for reduced sleep quality. This is often impractical during climbing expeditions!
• At extreme altitudes, oxygen supplementation during sleep improves sleep quality.
• Acetazolamide significantly reduces periodic breathing at altitude. It also helps to prevent and treat altitude-related illness ( [link]).
• Temazepam has been shown to reduce periodic breathing at altitude without any impairment of next day vigilance, reaction time, or cognition.
Ophthalmology is viewed by the general physician with anything from mild boredom to abject fear. Unfortunately, these fears may have to be faced in the wilderness and this section is designed to equip you with the tools you need to assess and treat an eye problem in the field.
It is important to have a basic understanding of ocular anatomy to assess the severity of an injury. Figure 9.5 shows an external and internal view of the eye; note that the cornea is continuous with the sclera and also that the conjunctiva lines the inside of the eyelids and covers the sclera up to the cornea.
Pre-expedition ocular history
• Do you wear contact lenses?
• If yes, what type are they? (e.g. hard/soft, monthlies/dailies)
• Have you ever been treated by a doctor for an eye problem?
• Have you ever had laser eye surgery or any other operation on your eyes?
• If yes, what kind and when?
• Does anyone in your family suffer from glaucoma or any other eye disease?
• Are you diabetic?
• Visual acuity is the single most important sign when examining the eye and you do not need a Snellen chart to test it; either compare it with the other eye or simply ask the patient if their vision has changed.
• Do not be afraid to dilate the pupil to obtain a reasonable view of the retina. If tropicamide alone is used, it can be easily reversed with pilocarpine in the extremely unlikely event of an acute rise in intraocular pressure owing to angle closure.
• Measurement of intraocular pressure does not require specialist equipment. Ask the patient to close their eyes and, with your thumbs, simply press gently on the globe, comparing one eye with the other. This will easily reveal the ‘marble’ of high pressure from the ‘avocado’ of normal pressure.
• Fluorescein is useful to assess the integrity of the corneal epithelium and the globe. It should only be administered after topical anaesthetic (e.g. amethocaine). It is best viewed with a blue light in the dark.
Drops or ointment?
• Drops are easy to administer but are shortlived. Ointment has a soothing, lubricating effect but blurs the vision. It is therefore worth having antibiotics in both preparations depending on the patient's needs.
• Acute eye problems are often very painful, and the patient may require systemic analgesia.
Refractive surgery and high altitude
Refractive surgery is becoming increasingly popular amongst outdoor enthusiasts. However, high altitude can affect the surgical results, causing blurred vision which resolves upon descent. During this type of surgery, the refractive power of the cornea is changed either through surgical incisions or laser ablation. Radial keratotomy (RK) has now been superseded by laser in situ keratomilieusis (LASIK), laser epithelial keratomilieusis (LASEK), and photorefractive keratectomy (PRK).
RK tends to cause long-sightedness (hypermetropia) at altitude whereas LASIK, LASEK, and PRK may cause short-sightedness (myopia) at altitude. This phenomenon is not predictable and can severely affect vision.
Any decreased vision, redness or pain in the eyes of someone who has had refractive surgery should be taken seriously, as they are more vulnerable to infection. If necessary, consider descent and evacuation.
Patients should be advised not to have refractive surgery within 3 months of an expedition as refraction can be unstable and the eye is at risk of infection.
Contact lens users are vulnerable to dry eyes and serious corneal infection in the wilderness setting, so they should be advised on sensible contact lens use (no more than 8 h a day) and strict hygiene when handling lenses. They should also be reminded to take their spectacles as well as plenty of spare contact lenses.
Any potential infection, even what appears to be a simple conjunctivitis, should be taken very seriously. Contact lens wear should be stopped and intensive broad spectrum antibiotic drops should be started (e.g. ofloxacin hourly). If there is no improvement within 5 days, the patient should be evacuated.
A 29 year old short-sighted man took daily disposable soft contact lenses for his attempt on Mount Everest (8848 m) from the north side. However during his summit bid he forgot to remove or change his lenses for four days. As the sun rose on summit day he removed his goggles and put on his designer sunglasses. After the ‘Second Step’ his vision started to become blurred so that as he reached the summit he was unable to appreciate the view and more importantly navigate. He was helped back down the mountain by two Sherpas on what was luckily a fine day. He was diagnosed with snow blindness and bacterial keratitis; a doctor was able to peel the contact lenses from his eyes with difficulty but the subsequent corneal scarring has left his visual acuity permanently reduced.
• Dry eyes can be exacerbated by the dry, windy, bright conditions found at high altitude or in polar regions. Contact lens wearers are particularly vulnerable.
• Eyes are red, painful, and gritty. Symptoms are relieved by topical anaesthetic; subsequent fluorescein reveals punctuate staining.
• Use an ocular lubricant frequently.
• Minimize contact lens wear.
• Goggles can decrease tear evaporation.
• Although usually just a nuisance, severely dry eyes are very painful, can significantly blur vision, and leave the eyes open to infection.
Conjunctivitis is the most common eye problem that is likely to be encountered in the wilderness setting.
Symptoms and signs
Unilateral or bilateral red, painful eyes with pus (bacterial), profuse watering (viral), or itch (allergic) depending on aetiology. Usually there is no decrease in visual acuity and, while the conjunctiva is red and inflamed, the cornea is clear.
Bacterial conjunctivitis should respond rapidly to topical antibiotics, whereas viral conjunctivitis can persist for many days but is eventually self-limiting. If the patient is a contact lens wearer then follow the specific advice earlier in the chapter. Allergic conjunctivitis may respond to sodium cromoglicate.
Bacterial and especially viral conjunctivitis are extremely contagious so strict hygiene measures should be enforced.
A corneal abrasion is a tear in the corneal epithelium, usually through mild trauma such as removing a contact lens or perhaps even whilst asleep.
Symptoms and signs
An acute and exquisitely painful eye. Topical anaesthetic will provide immediate relief, but should not be used as a treatment. Fluorescein will confirm the diagnosis.
Snow blindness is caused by unprotected exposure of the cornea and conjunctiva to ultraviolet light (UV-B). Like sunburn, by the time you realize there is a problem, it is too late, and it can be extremely painful.
Prevention and treatment are discussed on [link].
Corneal foreign body
Occasionally the protective blink reflex fails and allows a foreign body to embed itself into the cornea. This can be metallic or organic; a metallic foreign body will often leave a rust ring.
Symptoms and signs
Red, painful, gritty eye, and foreign body sensation. The foreign body is usually very small, but fluorescein and a magnifying loupe can assist identification and removal.
• Don't forget to evert the eyelid to exclude a subtarsal foreign body.
• The foreign body should be removed either with a cotton bud or a 25 G needle. Irrigation with sterile saline may also assist removal.
• Antibiotic ointment.
• An eye pad is not usually necessary and can encourage infection.
• Remember to ask about the mechanism of injury, as a high velocity foreign body, such as a shard of metal from an ice-axe, is more likely to penetrate the globe.
Immediately irrigate a chemical injury before any further assessment.
A chemical splash can be sight-threatening. It is important to identify the chemical because alkali penetrates the ocular tissues much faster than acid and therefore has a worse prognosis.
Symptoms and signs
• A red irritable eye following chemical splash.
• Visual acuity may be impaired.
• If severe, there may be blepharospasm.
• Immediate profuse irrigation, preferably with sterile normal saline and a giving set. If unavailable, use the cleanest water at hand.
• Check the pH with litmus paper and continue irrigation until pH is 7.
• If unsure of pH, irrigate for a minimum of 30 min.
• Antibiotic ointment (e.g. chloramphenicol tds).
• Ocular lubrication (e.g. artificial tears hourly).
• Cycloplegic drops for pain relief (e.g. cyclopentolate tds).
• If there is any concern regarding a chemical injury, especially if visual acuity is impaired or if there was any delay initiating irrigation, evacuation for specialist treatment is indicated.
• Remember that a white eye following chemical injury could indicate severe ischaemia.
The eyelids play an important role in protecting the eye and preventing corneal desiccation. If they are damaged, the eye can be rendered vulnerable.
• Firm pressure to stop bleeding.
• Check visual acuity.
• Assess globe integrity.
• Examine the eyelid carefully for any embedded foreign body.
• Decide whether the eyelid margin is interrupted.
• Remove any foreign body from the eyelid.
• Clean the wound thoroughly.
• Consider primary repair using a 6/0 non-absorbable suture if the eyelid margin is interrupted and the ends are not opposed. This is especially important with the upper eyelid.
• Antibiotic ointment.
• Broad spectrum oral antibiotics to prevent orbital cellulitis.
• Patch the eye if there is concern about corneal exposure.
• Corneal exposure is a problem, especially after upper eyelid laceration. This can affect visual acuity and encourage infection.
• Lacerations near the medial canthus may involve the tear duct and, if left unrepaired, may cause a permanent watery eye (epiphora).
• A patient with an eyelid laceration with the eyelid margin severed should be evacuated—a primary repair needs to be done properly by an ophthalmic surgeon under magnification. A poor repair performed in the field is likely to result in a permanent defect in the lid margin, which will require revision at a later date.
• Always check that there is no underlying penetrating injury to the globe, especially if the mechanism of eyelid injury was high velocity.
Penetrating eye injury
A penetrating eye injury involves disruption of the globe integrity and is a serious, sight-threatening problem. The mechanism of injury is important in determining whether there could be an intraocular foreign body or a perforating injury (entry and exit).
Symptoms and signs
• Decreased vision.
• Soft watery eye.
• Peaked pupil.
• Expulsion of ocular contents.
• A casualty with a suspected penetrating eye injury should be evacuated as soon as practical.
• Do not touch any expulsed ocular contents.
• If available, use a topical antibiotic eye ointment.
• Start broad spectrum systemic antibiotics.
• Both eyes should move as little as possible.
• Protect the injured eye using a double pad and eye shield (Fig. 9.6).
• An increased suspicion of penetrating injury should be maintained in any high velocity eye injury, such as those involving firearms or hammering.
Orbital cellulitis is a sight-threatening condition that can also be life-threatening if it spreads to form a brain abscess. The infection often arises from an adjacent ethmoid sinus or from mild trauma to the orbital region.
Symptoms and signs
• Reduced and painful eye movements.
• Conjunctival redness.
• Possible visual loss.
• General malaise.
• Broad spectrum antibiotics, preferably intravenous.
• Optic nerve function should be closely monitored (see below).
• Immediate evacuation for hospitalization.
Preseptal cellulitis involves only the eyelid. There is periorbital inflammation and swelling but none of the other features mentioned above. However, preseptal cellulitis can progress to orbital cellulitis so should be treated with broad spectrum oral antibiotics and closely watched.
Painful loss of vision
Painful loss of vision should be of great concern to the expedition doctor, especially if no obvious cause can be found, such as snow blindness. Always consider evacuation for specialist evaluation.
Tests of optic nerve function in the wild
• Visual acuity: compare with the other eye.
• Colour vision: ‘How red is my hat compared with the other eye?’
• Visual fields: simple confrontational fields.
• Pupils: check for a relative afferent pupillary defect.
• Ophthalmoscopy: look for optic disc pallor compared to the other eye.
Painless loss of vision
Painless loss of vision in one or both eyes, even transiently, should be taken very seriously. Follow the list of investigations as above, especially the tests of optic nerve function. If there is any doubt the patient should be evacuated for specialist assessment.
• Amaurosis fugax (transient ischaemic loss of vision).
• Cerebral hypoxia.
• High altitude retinopathy (HAR).
• Hypertensive retinopathy.
• Ischaemic optic neuropathy.
• Retinal artery occlusion.
• Retinal vein occlusion.
• Vitreous haemorrhage.
• Retinal detachment.
HAR is defined as ‘one or more haemorrhages in either eye of a person ascending above 2500 m’. It is normally asymptomatic but affects around 30% of lowlanders ascending to 5000 m.
• Retinal haemorrhages (flame, pre-retinal, dot and blot).
• Cotton wool spots.
• Optic disc hyperaemia.
• Decreased visual acuity (only if the macula is affected).
Retinal vascular tortuosity and engorgement are part of the normal physiological retinal response to the hypoxia of high altitude. However, a combination of factors, including exertion and speed of ascent, cause HAR. It is confusing to include papilloedema in the definition of HAR as this implies raised intracranial pressure; the relationship between HAR and the potentially fatal high altitude cerebral oedema (HACE) is not yet known.
Any visual disturbance at altitude is an indication for descent.
Ocular first aid kit
The first aid kit listed below is lightweight and will fit into a small pouch. However, as an expedition doctor you should have some experience of using a magnifying loupe and ophthalmoscope as well as administering eye drops and applying a double eye pad.
A 36-year-old man was diagnosed with hypertension several months before a trekking expedition to climb Mera Peak (6476 m) in Nepal. He was prescribed a beta-blocker which had controlled his blood pressure, but he regularly forgot to take his medication during the trek into base camp. At 4200 m a doctor was summoned as he had gone suddenly blind in both eyes and was feeling unwell. Dilated fundoscopy revealed multiple haemorrhages and cotton wool spots consistent with HAR. However, his blood pressure was 220/110 and a diagnosis of hypertensive retinopathy was made. He was re-started on his medication and evacuated by helicopter whereupon he made a full recovery.
• Pentorch ± blue filter.
• Pocket ophthalmoscope.
• Magnifying loupe.
• Eye pads.
• Eye shield.
• Surgical tape.
• pH paper.
• Minor operations kit.
• Single use drops (‘Minims’™):
• Tetracaine (amethocaine)/Benoxinate (topical anaesthetic).
• Fluorescein 1% (use only after topical anaesthetic for corneal staining).
• Cyclopentolate 1% (pupil dilation and pain relief).
• Artificial tears (dry eyes and snow blindness).
• Tropicamide 1% (for pupil dilation).
• Pilocarpine 2% (for reversal of pupil dilation by tropicamide).
Other topical medication:
• Antibiotic ointment and drops (e.g. chloramphenicol) (conjunctivitis, any minor infection, or snow blindness).
• Ofloxacin (reserve for more serious corneal infection and all contact lens-related infection).
• Sodium cromoglycate (allergic conjunctivitis).
• Fluorometholone (mild steroid; use cautiously in snow blindness).
These drops are given four times daily except ofloxacin, which can be given hourly for serious corneal infection.
• Remember oral analgesia is required for a painful eye.
Ear problems are relatively common, particularly on diving expeditions owing to pressure changes and prolonged exposure to salt water.
This is an infection of the outer ear usually associated with constant moisture due to diving or living in tropical environments. The ear is itchy, painful, and a discharge may occur. In severe cases, hearing loss develops if the external canal is blocked by debris and swelling. Movement of the pinna elicits pain. Severe cases result in systemic upset with lymphadenopathy. The external canal looks swollen and red debris is usually obvious.
Otitis externa should be treated by gentle cleaning of the external canal with saline or clean water. A combination preparation of antibiotic and steroid such as Gentisone HC™ should be used four times a day. Severe cases merit oral antibiotics such as co-amoxiclav. Avoid further exposure to water until the condition has resolved.
This is a viral or bacterial infection of the middle ear. It presents as pain and decreased hearing. The pain is made worse by changes in pressure. It may be associated with an upper respiratory tract infection.
Through an otoscope, the eardrum will usually appear red. If there is pus collected behind the drum it can appear yellow. In some cases the drum will perforate, with hearing loss, relief of pain, and a pus discharge.
Prescribe painkillers such as co-codamol and a non-steroidal drug such as ibuprofen or diclofenac for pain. In the expedition environment you should prescribe a basic antibiotic such as amoxicillin or erythromycin.
A decongestant such as oral pseudoephedrine or nasal drops may help to relieve Eustachian tube obstruction.
Very occasionally, severe cases of otitis media can be complicated by mastoiditis which causes pain, tenderness, and inflammation over the mastoid process, the bony prominence immediately behind and below the pinna. High dose oral or, ideally, intravenous antibiotics should be commenced and the patient must be evacuated for specialist care because there is a small risk that meningitis or cerebral abscess could develop.
Tympanic membrane rupture due to trauma
This may be caused by direct trauma or associated with a base of skull fracture. Most eardrum perforations heal spontaneously and do not require specific management. Avoid swimming until the hole has healed.
This results from changes in pressure during diving, usually due to failure to equalize adequately or in the presence of a blocked Eustachian tube.
Middle ear barotrauma or ‘squeeze’ causes pain, and the tympanic membrane will appear inflamed or blood may be visible behind it. In severe cases the drum may rupture, with bleeding from the ear. In simple cases treatment is symptomatic, with analgesia and decongestants. In the presence of tympanic rupture, amoxicillin or erythromycin should be prescribed. Do not dive until fully resolved.
Inner ear barotrauma is unpleasant. It results from inner ear haemorrhage or a rupture of the oval window. Patients experience vertigo, hearing loss, and tinnitus. Evacuation and examination by an ENT surgeon is advised.
Foreign bodies in the ear
On expeditions, these are most commonly insects that have crawled into the external canal. Insects should be drowned in oil and will usually float out. Other foreign bodies may require removal with suitable hooks.
If difficulty is experienced in foreign body removal, do not persist at the expense of damage to the tympanic membrane or external canal.
Epistaxis (nose bleed)
Nose bleeds are quite common in expedition situations, and may be precipitated by the low humidity found at altitude, in cold climates, or aircraft cabin atmospheres. Other associations include direct trauma to the nose and upper respiratory tract infections. Ninety per cent are anterior and 10% are posterior.
First aid measures are usually effective in controlling haemorrhage. Press on the soft part of the nose with a finger for 15 min. If simple pressure is unsuccessful, try cauterizing off any identified anterior bleeding points with a silver nitrate stick. Before cauterizing the vessel you should apply a topical local anaesthetic such as lidocaine and adrenaline. Look up the nose using a head torch and apply the cauterization stick to the bleeding point for no longer than 5 s.
If cautery is not possible or is unsuccessful, then insert a commercially available nasal tampon. Such tampons should be lubricated before insertion. Once correctly positioned, expand the device by dropping saline from a syringe. Often both nostrils have to be packed. They are uncomfortable so prescribe painkillers. If nasal tampons are unavailable, then the nose can be packed with lubricated gauze or a small vaginal tampon.
Nasal packs can precipitate sinusitis and in the expedition setting amoxicillin should be prescribed. Leave the packs in place for 48 h and then remove them.
If bleeding continues despite insertion of a nasal tampon, it is probable that the bleeding point is in the posterior part of the nose. Remove the tampon and insert a deflated urinary catheter along the floor of the nose. Gently inflate the balloon with air and pull the catheter forward until resistance is felt. The pack or tampon should then be re-inserted.
A patient with a persistent nose bleed that does not respond to the measures described will have to be evacuated for further treatment and investigation which must include a blood count and clotting studies. Rarely, transfusion is required.
Coryza (common cold)
Upper respiratory tract infections are very common and infection has often originated before departure. The condition is usually self-limiting and requires only symptomatic treatment. Catarrh may block sinus openings and Eustachian tubes. Pressure differences may cause ear or sinus pain, which may be severe. Nasal decongestants such as phenylephrine taken before travel can help. Antibiotics are worthwhile if persistent sinus pain and tenderness suggests secondary bacterial infection.
Sore throats with painful swallowing are common in travellers, especially following air travel. The throat infection may be associated with fever and systemic upset. Most are viral in origin. Pus around the tonsils suggests bacterial infection but it is not usually possible to differentiate the two clinically.
Most cases of tonsillitis settle with time and analgesia. In the remote setting, if symptoms fail to improve after a few days then antibiotics should be prescribed. The antibiotic of choice for the most common bacterial pathogen, beta haemolytic streptococcus, is penicillin V 500 mg for 7 days. Erythromycin is an alternative in penicillin-allergic patients.
Peritonsillar abscess (quinsy)
Quinsy causes severe unilateral throat pain and dysphagia, with associated pyrexia and systemic upset. Trismus (an inability to open the mouth due to pain) and drooling occur. The tonsil is swollen, inflamed, and deviated medially; the uvula is usually displaced away from the affected side. Intravenous antibiotics are required. In the remote setting the abscess should be drained by needle aspiration rather than incision and drainage.
Throat foreign bodies
These are most commonly fish or chicken bones. The patient complains of pain, especially on swallowing. Foreign bodies stuck in the tonsil or base of the tongue can usually be seen and removed with forceps. If no foreign body is visible it is possible that it may simply have scratched the pharyngeal mucosa on passing. A foreign body stuck out-of-sight in the pharynx may become infected and abscesses can develop, so if symptoms persist the patient must be evacuated for further treatment.