Infections and Immunity Flashcards
What age range is peri-orbital cellulitis most common in?
0-15 years with a peak incidence in children younger than 10 years.
It is twice as common in males compared to females.
What time of year is peri-orbital cellulitis most common?
There is bi-modal seasonal variation, with peak occurrence in late winter/early spring, attributed to the increased incidence of upper respiratory tract infection and paranasal sinusitis in the same seasons of the year.
Most common cause of peri-orbital cellulitis?
Sinus related infections (35% will go on to develop peri-orbital cellulitis). Most commonly ethmoidal.
What are the two forms of peri-orbital cellulitis and pathophysiology?
Infection anterior to the septum is pre-septal and posterior is post-septal. The orbital septum is the only barrier impeding spread of infection from the eyelid into the orbit.
Commonly peri-orbital cellulitis occurs as a result of contiguous spread from surrounding periorbital structures such as the paranasal sinuses. Ethmoidal sinusitis is the most common cause of orbital cellulitis, especially in neonates who have not yet formed their frontal sinuses.
Up to 38% of children may have multiple sinus involvement.
Other causes of peri-orbital cellulitis
Other causes include:
- dacrocystitis
- dental infection
- endophthalmitis
- trauma
- foreign bodies
- insect bites
- skin infections (impetigo)
- eyelid lesions (chalazia, hordeola)
- iatrogenic causes such as eyelid and oral procedures.
Most common organism causing PO cellulitis:
Staphylococcus aureus is usually the most common pathogen.
Organisms are those generally responsible for acute rhinosinusitis, such as Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis, Staphylococcus aureus, group A streptococcus, and upper respiratory tract anaerobes.
Clinical features of PO cellulitis:
- Acute onset of swelling, redness, warmth and tenderness of the eyelid.
- Eyelid oedema in the absence of orbital signs such as gaze restriction and proptosis.
- Fever, malaise, irritability in children.
- Ptosis.
Important: normal vision, no proptosis and full ocular mobility
Clinical features of orbital cellulitis
Orbital features:
- Proptosis
- Ophthalmoplegia
- Decreased visual acuity
- Loss of red colour vision – first sign of optic neuropathy
- Chemosis
- Painful diplopia
What kind of classification can be used in PO cellulitis?
Chandler Classification
Investigations in PO cellulitis
- Full neuro, ENT and eye exam
- Bloods and sepsis screen if necessary
- VBG if systemically unwell
- Swab of purulent nose discharge
CT of head can determine if there is orbital involvement if unsure.
Treatment of PO celullitis
Mild pre-septal cellulitis in children older than 1 year of age, treatment is typically rendered on an outpatient basis with empiric broad spectrum oral antibiotics,
Children can be initially admitted to hospital, as they should be considered to have orbital cellulitis until proven otherwise (ie repeated examinations normal, good response to antibiotics in the first 24 hours and normal CT scan).
Oral co-amoxiclav may be used both for adults and for children as long as there is no allergy to penicillin. Clinical improvement should occur over 24-48 hours.
Hospital management may involve intravenous therapy (eg, intravenous ceftriaxone until response is seen) and further investigation to confirm preseptal cellulitis (only) and that there are no unusual organisms involved.
The ENT team is generally consulted if sinusitis is present.
Treatment of orbital cellulitis:
However, treatment of orbital cellulitis consists of hospital admission (ENT surgeons and optical) IV abx, nasal decongestants, steroid nasal drops and nasal douching.
Intravenous antibiotics are used (eg, cefotaxime and flucloxacillin) with addition of metronidazole in patients over 10 years of age with chronic sinonasal disease . Treatment lasts for 7-10 days.
Optic nerve function is monitored four-hourly (pupillary reactions, visual acuity, colour vision and light brightness appreciation).
Surgery is indicated where there is CT evidence of an orbital collection, where there is no response to antibiotic treatment and where visual acuity decreases.
Complications of PO cellulitis
-Progression of infection to orbital cellulitis, especially in young children.
-Unusual complications include:
Lagophthalmos (inability to close the eyelids completely over the globe).
Lid abscess.
Cicatricial ectropion.
Lid necrosis.
Complications of orbital cellulitis:
- Exposure keratopathy (which can lead to visual loss through permanent damage to the cornea).
- Raised intraocular pressure.
- Central retinal artery or vein occlusion.
- Endophthalmitis.
- Optic neuropathy.
-Orbital abscess: More often associated with post-traumatic orbital cellulitis.
Total loss of vision can occur through direct extension of the infection to the optic nerve.
Intracranial (rare):
Meningitis.
Brain abscess.
Cavernous sinus thrombosis.
Most common ages of glandular fever:
1-6 and 18-22.
Most adults are antibody positive by the age of 30 (90%). In 50% of these they won’t have had symptoms.
Infectious organism of glandular fever:
EBV in most cases (a human herpes simplex virus)
-10% are cytomegalovirus
What is the transmission mechanism of glandular fever?
Droplet transmission. 4-6 week incubation period.
Glandular fever symptoms:
- Low-grade fever, fatigue and prolonged malaise. Fatigue and malaise may persist for several months after the acute infection has resolved.
- Sore throat; tonsillar enlargement is common, classically exudative and may be massive; palatal petechiae and uvular oedema.
- Fine macular non-pruritic rash, which rapidly disappears.
- Transient bilateral upper lid oedema.
- Lymphadenopathy, especially neck glands.
- Nausea and anorexia.
- Also fatigue, photophobia, arthralgia and myalgia can occur
Older adults and elderly patients often have few throat symptoms or signs and have little or no lymphadenopathy.
Later signs include:
- Mild hepatomegaly and splenomegaly with tenderness over the spleen.
- Jaundice occurs in fewer than 10% of young adults but in as many as 30% of infected elderly patients.
What would find on examination of a glandular fever patient?
- Enlarged inflamed tonsils, often meeting in the middle and referred to as “kissing tonsils”
- Significant cervical lymphadenopathy (both anterior and posterior cervical chains)
- Abdominal tenderness & splenomegaly (in as many as 50%)
- Hepatomegaly (in as many as 25%)
- Palatal petechiae
What tests might you do to confirm your diagnosis of glandular fever and what might you see?
FBC- lymphocytosis
LFTs- 75% will have elevation of liver enzymes
The monospot test is the primary technique for identifying infection with Epstein-Barr virus. However it relies on the generation of non-specific heterophile IgM autoantibodies, which are not produced immediately following viral infection of B lymphocytes and may take a week to appear.
When might abx be prescribed in glandular fever?
When there is bacterial superinfection (can occur in up to 30% of cases). In this case penicillin based abx will be prescribed.
DO NOT give amoxicillin
Possible complications of glandular fever?
- Post viral fatigue
- Epstein-Barr virus has shown to be associated with the development of a number of different lymphomas (Burkitts, Hodgkins, T Cell) as well as nasopharyngeal carcinoma.
- Guillan Barre
- Encephalitis can occur, resulting in fever, seizures, unusual behavior or gait disturbance. It is sometimes preceded by symptoms of glandular fever, but may also occur without preceding symptoms.
- Splenic rupture: avoid contact sports for 4-6 weeks post symptoms
General glandular fever advice for parents:
- Stay hydrated
- No need to be excluded from school unless for own wellbeing
- Advice paracetamol/ibuprofen for fever control
- Let them know there is no specific therapy
Typical age range of kids and type of kid affected by Kawasaki infection:
- 6 months to 5 years. Peak incidence 18-24 months.
- East Asian children more likely to be affected
- Boys more than girls.
Typical features of Kawasaki disease:
- Fever lasting 5 or more days (abrupt onset)
Along with 4/5 of:
- Erythema, desquamation and swelling of skin of the extremities
- Bilateral conjunctivitis
- Inflammation of the lips, tongue “strawberry” and mouth
- Cervical lymphadenopathy (usually unilateral and non-tender)
- Polymorphous rash
Often have marked irritability!
What is incomplete Kawasaki?
Incomplete Kawasaki disease is the term given to those with fever but without enough other features to fit the diagnostic criteria.
Features of a Kawasaki rash
- Rash (widespread non-vesicular within 3-5 days of fever)
- It usually begins with nonspecific erythema of the soles, palms and perineum, spreading to involve the trunk and the rest of the extremities.
- It is often itchy and variable in appearance but is never vesiculo-bullous.
- It is usually markedly red and may appear macular, morbilliform, papular, scarlatiniform, urticarial, akin to erythema multiforme or be made up of very many tiny micropustules.
Not contagious
Cardiac signs in Kawasakis (not always)
Cardiovascular signs are usually nonspecific. Tachycardia, a hyperdynamic precordium, a gallop rhythm or a flow murmur may be present; however, these signs are not unusual in febrile patients without Kawasaki disease. There are occasionally signs of valvular incompetence.
Describe the acute phase of Kawasakis:
Highly febrile. Very irritable. Toxic-appearing. Oral changes rapidly following. Oedema and erythema of feet. Rash especially common in the perineal area.
1-2 weeks
Describe the subacute phase of Kawasaki:
Gradual improvement. The fever settles. Desquamation of the perineum, palms, soles. Arthritis, arthralgia. Thrombocytosis. Coronary artery aneurysms. Myocardial infarction
2-8 weeks
Describe the convalescent phase of Kawasaki:
Resolution of remaining symptoms. Laboratory values return to normal. Aneurysms may resolve or persist. Beau's lines. Cardiac dysfunction and myocardial infarction may still occur.
Months to years
What is Kawasaki disease?
Self-limited acute vasculitic syndrome of unknown aetiology
How do you diagnose Kawasaki’s?
- Clinical diagnosis
- May be deranged bloods e.g. thrombocythaemia, leukocytosis, neutrophilic, elevation of transaminases and bilirubin, raised ESR, CRP.
What is essential to do in Kawasaki’s?
ECHO! It can reveal dilatation and aneurysms of the coronary arteries, as well as allowing assessment of the pericardium and left ventricular/valvular function. Serial echocardiography is often needed to detect occult coronary artery disease as the illness evolves.
How do you manage Kawasaki’s?
- Usually cared for on an inpatient basis with cardiology input
- Aspirin for it’s antiplatelet and antipyretic effect.
- IV immunoglobulin (antibodies from healthy donor to fight disease). This is specifically gamma globulin. Symptoms should improve in 36 hours, if not a second dose is given
- Corticosteroids if IG is not working/ at high risk of heart problems
-Need follow up appointment after resolution of symptoms for ECHO. If normal, stop aspirin.