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CASE 87: A PAIN IN THE EAR
A 55-year-old woman presents with a painful left ear, having returned from France 1 week
ago, where she swam in the local river on a daily basis. Since returning, she has noticed an
itch in her left ear and has regularly tried to relieve it using cotton ear buds and later eardrops
from the pharmacy. This itch turned into an ache, and she noticed the cotton ear bud looked
a ‘dirty brown’. The ache worsened, and she now also has what feels to her like a ‘blocked
ear’. She has no history of headache, facial weakness, diculty swallowing or fever.
The patient has no significant medical history.
Examination
General examination was unremarkable. She was apyrexial and had no cervical
lymphadenopathy.
Examination of the left ear reveals a red and swollen external auditory canal with a yellowish
crusting discharge. The auditory canal is narrowed, but the tympanic membrane is visible
and looks normal. The pain is made worse by pulling on the pinna (earlobe) and pushing on
the tragus of the left ear. There is no redness, swelling or tenderness on any other area of the
ear or surrounding tissues.
Her voice is normal, and she has no abnormalities of her cranial nerves.
INVESTIGATIONS
Microbiology
Swabs of the external auditory canal were sent for MC&S and fungal culture. Culture grew
a mixed growth of Pseudomonas aeruginosa and Staphylococcus epidermidis. Fungal
culture was negative.
QUESTIONS
1. What is the clinical diagnosis?
2. What are the predisposing factors and most common cause of this condition?
3. What is the treatment?
DOI: 10.1201/9781003242697-91
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ANSWERS
The diagnosis is acute otitis externa (AOE), also known as ‘swimmer’s ear’. AOE is distin-
guished from chronic otitis externa by the pathogenesis and duration of symptoms, with the
former of <3 weeks duration and the latter >3 months. Otitis externa is defined as inflamma-
tion of the external auditory canal. It is similar to cellulitis of skin and soft tissue elsewhere.
It is a common condition and is responsible for up to 20% of referrals to ear/nose/throat
(ENT) clinics.
Most cases of acute and chronic otitis externa are caused by bacterial infection, the most
common pathogen being P. aeruginosa. Another common bacterium is Staphylococcus aureus.
Fungal infection such as Candida species and Aspergillus niger may be found in the chronically
infected external ear canal.
This patient has a number of predisposing factors which put her at risk of developing AOE,
namely regular exposure to water (swimming), trauma to the external auditory canal from
foreign bodies in the ear, cotton ear buds and eardrops (especially if used after being previ-
ously opened). Eczema or other inflammatory skin conditions can predispose to chronic or
recurrent infection.
Earwax protects against water and keeps the pH slightly acidic in order to inhibit bacterial
growth. Removal of the wax by cleaning reduces this protective mechanism. Earphones and
hearing aids can also cause trauma, increasing the risk of infection. Water exposure, alkaline
eardrops and soap also act to reduce the protective acidity.
Treatment of the acute episode is with a combination of aural toilet (most commonly by using
microsuction) and topical antibiotics. Systemic antibiotics are indicated only if the infection
extends beyond the ear canal to surrounding structures. Topical steroids reduce inflamma-
tion and can be combined with topical antibiotics.
A severe complication of AOE is necrotising otitis externa, which is an extension of infection
into the surrounding tissue and bones (osteomyelitis) at the base of the brain, with possible
further extension to the cranial nerves and brain. This complication is more common in the
elderly, diabetics, immunocompromised and those who have received radiotherapy to the
head and neck. Treatment of this complication requires long-term systemic antibiotics and
close follow-up with measurement of inflammatory markers and imaging of the skull base.
KEY POINTS
•
AOE (‘swimmer’s ear’) is characterised by localised itching, reduced hearing and
pain, especially on moving the pinna and tragus (with or without a discharge).
•
The most common pathogen causing AOE is P. aeruginosa.
•
Pathogenesis is multi-factorial and includes removal of protective earwax, trauma,
and excessive moisture in the ear canal.
•
Treatment of AOE is topical antibiotics, and patients should be counselled on how
to prevent further episodes.
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CASE 88: A RED EYE
A 27-year-old man presents with a red and painful left eye. He complains that when he wakes
in the morning the eyelid of his left eye is stuck together, and he has noticed his eyelid looks a
bit swollen. He says a few days ago he felt an irritation and thought he might have something
in his eye, but couldn’t see anything. He doesn’t remember any specific trauma to the eye. He
hasn’t been swimming and hasn’t used any eye drops recently. He has noticed a few people
at work with ‘pink eye’ but hasn’t had intimate contact with any of them. He says his vision is
normal, although bright light is uncomfortable, and he hasn’t noticed any redness or rash on
his face other than inside his eye. He has had no urethral discharge and is in a monogamous
sexual relationship. He has no significant medical history.
Examination
General examination was unremarkable. He is apyrexial, and his vital signs are normal.
As shown in Figure 88.1, his left eye is noted to be sensitive to light on examination. There is
a watery discharge present. The conjunctiva is erythematous and mildly oedematous with a
few small subconjunctival haemorrhages in the periphery. There is no membrane present on
the conjunctiva. He has pre-auricular lymphadenopathy, but no submandibular or cervical
lymph nodes are palpable.
Figure 88.1 Conjuctival erythema. No ciliary injection or corenal involvement noted.
QUESTIONS
1. What is the differential and most likely diagnosis?
2. What are the common organisms causing this condition?
3. What investigations should be done?
4. What is the most appropriate treatment?
DOI: 10.1201/9781003242697-92
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ANSWERS
An acute red eye can be caused by many conditions, and a history and examination should
guide the dierential diagnosis. The following are common causes to consider:
1. Acute conjunctivitis, which can be viral, bacterial, fungal, parasitic, mycobacterial
or chlamydial
2. Other eye conditions
a. Anterior uveitis
*
—inflammation of the anterior structures of the uvea (the pig-
mented vascular inner layer of the eye comprising the iris, ciliary body and
choroid)
b. Keratitis,
*
i.e., corneal inflammation, which may be bacterial or viral
c. Corneal abrasion,
*
foreign body,
*
or corneal ulcer
*
d. Acute closed-angle glaucoma
*
e. Trauma with subconjunctival haemorrhage
f. Chemical injury
*
3. Systemic conditions presenting with red eyes:
a. Allergic conjunctivitis—Other signs of atopy should be present
b. Measles—Commonly presenting with rash, coryza, conjunctivitis and cough
c. Episcleritis and scleritis
*
associated with inflammatory bowel disease and con-
nective tissue diseases
*
These require urgent ophthalmology evaluation.
The most likely diagnosis is acute viral conjunctivitis, commonly known as ‘pink eye’. It is
unilateral on presentation but often spreads to infect the other eye. In its mildest form it is
associated with a watery discharge, redness of the eye and eye irritation but not significant
pain. If severe pain is present, other diagnoses should be sought.
The most common cause of conjunctivitis is viral, which is often associated with pre-auric-
ular lymphadenopathy. Adenoviruses, coxsackieviruses and herpes viruses (herpes simplex
virus [HSV], varicella zoster virus [VZV]) are the commonly associated viruses.
Photophobia, as in this case, suggests involvement of the cornea. A more specific diagnosis to
consider is acute epidemic kerato-conjunctivitis, caused by specific strains of adenovirus. It
spreads by contact or respiratory fomites and occurs most notably in schools, places of work,
and institutions, where it can lead to significant outbreaks. It is more severe than other forms
of adenoviral conjunctivitis and can cause marked eye pain and damage to both the conjunc-
tiva and cornea that can lead to permanent scarring.
Bacterial conjunctivitis diers clinically in that there is usually a muco-purulent discharge
and matting of the eyelids; lymphadenopathy is uncommon, and there is often an associated
traumatic process predisposing to infection.
The common bacterial causes include Staphylococcus aureus, Haemophilus influenzae and
Streptococcus pneumoniae, the latter two being more common in children than in adults. Neisseria
gonorrhoeae causes a severe conjunctivitis and is associated with conjunctivitis in neonates born
to infected mothers and sexually active adults. There is copious discharge, swelling of the
conjunctiva, marked pain, and (atypically for bacterial conjunctivitis) pre-auricular lymph-
adenopathy. Chlamydia trachomatis is also associated with neonatal and sexually transmitted
conjunctivitis. This causes a milder infection with less discharge and pain in the eye, but can
lead to severe complications and corneal scarring with associated visual defects. In neonates
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Case 88: A Red Eye
273
it is associated with chlamydial pneumonia and therefore will require systemic as well as
topical treatment.
Most cases of conjunctivitis are viral, and investigation is not necessary unless there are symp-
toms to suggest a more serious cause or the infection is non-resolving. If the infection is non-
resolving or if a bacterial (or other non-viral) cause is suspected, appropriate swabs should
be sent to the laboratory for microscopy, culture and sensitivity (MC&S) and/or molecular
testing (polymerase chain reaction [PCR]) for viruses and Chlamydia sp., as these symptoms
suggest a more serious or sight-threatening aetiology. Investigation is always indicated in neo-
natal conjunctivitis, as distinguishing between C. trachomatis, N. gonorrhoeae and more common
bacterial causes determines treatment of the neonate and the mother and partner(s).
Most cases of viral conjunctivitis resolve spontaneously without any treatment. In more
severe disease such as acute epidemic kerato-conjunctivitis, treatment is aimed at relieving
symptoms and preventing spread. Patients are infectious for approximately 10–14 days after
onset. If vision is aected, topical steroids may be helpful, but steroids should be prescribed
only after consultation with a specialist, as these can worsen the infection. If a membrane is
present, removal of this prior to the steroids may improve vision, but may lead to superficial
bleeding on removal.
Bacterial and chlamydial conjunctivitis should always be treated with appropriate antibiot-
ics. In most cases topical treatment is sucient. The exceptions are that of neonatal C. tra-
chomatis, as mentioned above, and less common causes such as chronic bacterial, fungal and
parasitic infections.
Prophylaxis against neonatal conjunctivitis with topical agents is common practice, as the
sequelae of untreated infection can be severe. In the UK, this has been replaced by antenatal
screening, but is still commonly used in countries with a high prevalence or no resource for
antenatal screening.
KEY POINTS
•
Acute viral conjunctivitis is the most common cause of inflammation of the eye.
The most common organisms are adenovirus, coxsackievirus and herpes viruses.
•
Red eye in patients with reduced visual acuity, photophobia, ciliary injection, cor-
neal involvement, contact lens use or moderate pain should prompt same-day
ophthalmological assessment.
•
Symptoms include localised itching and irritation, redness and eye discharge.
•
Treatment other than symptomatic relief is often not required, as most viral con-
junctivitis resolves spontaneously. Bacterial and chlamydial conjunctivitis should
always be treated with appropriate antibiotics. Corneal involvement should
prompt urgent ophthalmology assessment.
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CASE 89: CHILD WITH A RASH
A 3-year-old child is brought into the GP with a rash on her face, arms, legs, and body. The
mother said it started on the face 4 days ago and spread to the limbs and then trunk over a
few days. The child has a fever and is very irritable with poor feeding. She is up to date with
her scheduled vaccinations and has been healthy since birth, which involved an uncompli-
cated, full-term vaginal delivery.
Examination
As shown in Figure 89.1, there is a maculopapular rash on the face, trunk, buttocks and limbs
with a more extensive, symmetrical papular rash on the cheeks in a butterfly distribution.
The rash on the body is coalesced in a ‘lacy’ pattern. There are no petechiae present. There
is a mild coryza and pharyngeal erythema, but no lesions, rash or petechiae on the palate or
buccal mucosa. There is no conjunctivitis present. Temperature is 37.7°C, and heart rate is
110 beats/min.
There is no lymphadenopathy or signs of meningeal irritation. The chest is clear and the
abdomen soft and non-tender.
Figure 89.1 A child with a rash.
DOI: 10.1201/9781003242697-93
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Case 89: Child with a Rash
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INVESTIGATIONS
Bloods
Haemoglobin 9.5 g/dL
Red blood cell count
2.5 × 10
6
/mm
3
White cell count
9.6 × 10
9
/L
Neutrophils 52%
Lymphocytes 45%
Platelets
340 × 10
9
/L
C-reactive protein 46 mg/L
QUESTIONS
1.
What is the differential diagnosis?
2. What are the pathogenesis and complications caused by the anaemia associ-
ated with infection?
3. How is the infection diagnosed?
4. What is the recommended treatment?
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ANSWERS
There are a number of possible causes of childhood rashes occurring at this age. The nature
of the rash and the accompanying signs and symptoms should help narrow the dierential
diagnosis. Historically, common childhood rashes were classified according to ‘numbers’, as
in the table below.
Common Childhood Causes of a Maculopapular Rash with No Vesicles and No Petechiae
or Purpura
Disease Common features
Measles (first disease) Prodrome—Coryza, cough, conjunctivitis. Rash on
face, neck and shoulders. Koplik’s spots on mucous
membranes. Vaccine-preventable
Scarlet fever—Group A streptococcus Sore throat, generalised rash with perioral sparing,
(second disease) strawberry tongue, skin peeling following rash
Rubella (third disease) Rapidly fading lacy rash begins on face and spreads
to trunk and limbs. Suboccipital lymphadenopathy.
Vaccine-preventable
Dukes’ disease (fourth disease) Unknown cause
Erythema infectiosum (fifth disease) Slapped cheek rash, lacy rash, anaemia
Roseola infantum/exanthem subitum Pink rash beginning on trunk and spreading out to
(sixth disease) face, neck and limbs. Sore throat and red eyes
Kawasaki’s disease Need to exclude this non-infectious cause
The most likely diagnosis in this case is erythema infectiosum caused by parvovirus B19.
The age of the child, typical rash and anaemia fit with this aetiology. The child is fully vac-
cinated, and therefore measles and rubella are unlikely causes, although there is always the
slim chance of vaccine failure.
Parvovirus B19 infection results in varying manifestations depending on the presence of cer-
tain underlying conditions. Infection may be totally asymptomatic. The most common pre-
sentation is erythema infectiosum, a mild febrile illness with a rash which is more common in
children aged 5–15 years old than in adults. It is commonly seen in spring months. The rash
usually appears later when the viraemia has resolved and the patient is no longer infectious
and can last 7–10 days. It is also known as ‘slapped cheek’ disease, as the facial rash appears
red as if both cheeks have been slapped.
Infection is associated with an arthropathy in adults more commonly than in children, where
it causes a syndrome similar to rubella with fever, rash and marked joint pain. The arthropa-
thy is more prominent in small joints and lasts 1–3 weeks.
Parvovirus B19 is an erythrovirus, infecting red cell progenitor cells in the bone marrow, result-
ing in blockage of red blood cell synthesis. In healthy adults and children, this is only of minor
clinical significance, and recovery of production occurs when the virus clears. This anaemia is
more significant in certain groups of patients where it can lead to significant outcomes.
Complications are due mainly to the anaemia in vulnerable patient groups:
•
In pregnant women, infection in the first trimester can lead to anaemia and cardiac
failure in the fetus. If not treated (fetal blood transfusion), this can lead to hydrops
fetalis (abnormal fluid distribution from intravascular to extravascular compart-
ments) and death of the fetus.
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