Sudden respiratory distress with cyanosis and aphonia. Airway obstruction can occur at any level within the airway. Partial airway obstruction leads to noisy breathing, with stridor, gurgling, or snoring. Complete airway obstruction is associated with distress and marked respiratory effort, with paradoxical chest and abdominal movement (‘seesaw breathing’) and use of accessory muscles of respiration. This may be followed by collapse with loss of consciousness and progress to cardiorespiratory arrest. Look for chest and abdominal movements, and listen and feel for airflow at the nose and mouth.
• Pharyngeal occlusion by tongue and other upper airway muscles, 2° to loss of muscle tone. This may be 2° to drugs, alcohol, a neurological event, or cardiorespiratory arrest
• Vomit or blood
• Inhaled foreign body, which may also cause laryngeal spasm
• Laryngeal obstruction due to oedema from burns, inflammation, or anaphylaxis
• Excessive bronchial secretions, mucosal oedema, bronchospasm: may cause airway obstruction below the larynx
• Infection such as epiglottitis
• Any cause of chronic airway obstruction, such as an airway tumour or extrinsic compression due to tumour or lymphadenopathy, may deteriorate precipitously.
Call for senior anaesthetic help early
• Open the airway with backwards head tilt, chin lift, and forward jaw thrust. In cases of trauma, do not tilt the head in case of cervical spine injury, but perform a jaw thrust only
• If unsuccessful at restoring normal respiration, visually inspect the mouth for obvious obstruction, and remove it with a finger sweep. Leave well-fitting dentures in place
• If there is a witnessed history of choking, consider performing the Heimlich manoeuvre to dislodge the particle (firm and rapid pressure applied beneath the diaphragm in an upwards movement), or directly visualize the airway with a laryngoscope, and use McGill’s forceps to remove the particle or with bronchoscope and the use of biopsy forceps
• If the patient is breathing, consider inserting an airway to maintain patency: oropharyngeal (Guedel) or nasopharyngeal. Maintain oxygenation, using mask with reservoir bag, delivering 10–15L/min. If there is no spontaneous respiratory effort, insert a laryngeal mask or endotracheal tube, and deliver O2 via self-inflating bag with supplemental O2 10 L/min and reservoir bag. If not breathing and cannot be ventilated, a cricothyroidotomy may be necessary (see pp. [link]–[link])
• Suction out secretions
• Maintain circulation with cardiac compression, if necessary
• Seek definitive treatment for the cause of airway obstruction, as appropriate.
Helium–O2 mixtures can be used for patients with airway obstruction, often due to tumour compression or invasion. Helium has a lower density than nitrogen and can improve airflow, and, when used with O2, ventilation rapidly improves and work of breathing is decreased. It can be used as an interim measure until more definitive management is available, such as radiotherapy, or to allow time for radiotherapy to take effect. The evidence relating to its use is mainly case studies, with no RCTs. Doses used = 80:20 or 70:30 helium to O2 ratio; optimum dose unclear. Use the highest helium ratio which keeps O2 saturations >90%. If it works, it will be effective within minutes.
IgE-mediated type I hypersensitivity reaction to allergen. Histamine release causes the clinical syndrome. Typical allergens include bee or wasp sting, peanuts, fish, drugs, foods, latex, contrast media, muscle relaxants, anaesthetic agents. Incidence of anaphylaxis is increasing.
Typically a rapid onset of symptoms of varying severity:
• Also rhinitis, abdominal pain, vomiting, diarrhoea, sense of impending doom.
Symptoms typically resolve within minutes to hours. It is not clear what determines severity of anaphylaxis in individuals. Asthma and cardiovascular disease are important comorbidities that carry a worse prognosis in anaphylaxis. Patient may have had previous episodes of severe allergic-type reactions. May need in-hospital observation for 6–12h.
• Biphasic anaphylaxis is a further episode, typically within 10h, after the initial anaphylaxis seems to have resolved, without further allergen exposure
• Protracted anaphylaxis lasts for hours or days.
Management of anaphylaxis
• Remove likely allergen
• Cardiopulmonary resuscitation if necessary
• Airway and breathing Administer high-flow O2 through non-rebreathe mask. If airway obstruction present, consider tracheal intubation. Airway swelling may make this difficult, and cricothyroidotomy may need to be performed (see pp. [link]–[link])
• Circulation Give adrenaline (epinephrine) IM 1:1, 000 solution 0.5mL (500 micrograms). Repeat after 5min if no improvement or deterioration
• In those with profound shock and immediately life-threatening anaphylaxis, such as during anaesthesia, or those with no pulse, IV adrenaline can be given slowly, 100 micrograms/min or 1mL of 1:10, 000 solution/min. Stop as soon as there is a response. This can be hazardous and needs cardiac monitoring
• IV fluids if hypotension persists: 1–2L rapidly infused
• Antihistamines, such as chlorphenamine 10mg slow IV or IM, for itch and urticaria
• Consider steroids: 100mg hydrocortisone slow IV or IM
• Consider nebulized salbutamol or adrenaline if bronchospasm
• On discharge, provide IM self-administered adrenaline and advise on future episodes, medicalert bracelet, and card
• Offer allergy service/immunology referral
• Consider C1 esterase inhibitor deficiency, especially if repeated episodes.
aims to desensitize a person to an allergen to which they are sensitive, thus minimizing their allergic reaction. Suitable for people with allergic asthma and/or allergic rhinitis, with specific IgE to the allergen identified as causing symptoms. Useful in those who cannot avoid allergen exposure. Small amounts of a single or multiple allergens are injected once or twice weekly, with slowly increasing dose strengths until the maximum dose of the allergen is administered, which can take up to 12 months. Mechanism unknown but probably related to increased IgG binding to the allergen, falling allergen-specific IgE levels, and decreased amount of circulating inflammatory cytokines. Can protect against anaphylaxis for 3–5y, but ‘top-up’ doses necessary. Effective for dust, grass, tree and weed pollen, mould spores, latex, and insect venom, as well as some animal allergens. Side effects of administration: anaphylaxis, bronchoconstriction, local reaction. Some centres may not perform in people with severe or unstable asthma because of the risk of death.
A diagnostic test to accurately identify anaphylaxis will be useful, as current tests involving measurement of serum or plasma tryptase or plasma histamine are not perfect. Tryptase levels need to be checked as soon as possible after emergency treatment has started, with a second sample 1–2h later but within 4h of the anaphylactic episode. They may not be raised. Histamine levels have usually returned to baseline within 60min, and therefore measurement may not be helpful.
Further study of biphasic reactions is needed, along with work on the ideal duration of observation post-anaphylaxis and the effect of specialist allergy services on health care-related QoL.
Abramson M et al. Allergen immunotherapy for asthma. Cochrane Database Syst Rev 2003;4:CD001186.Find this resource:
Resuscitation Council (UK). Emergency treatment of anaphylactic reactions. Guidelines for healthcare providers. http://www.resus.org.uk.
NICE CG134. Initial assessment and referral following emergency treatment for anaphylactic episode, 2011.Find this resource:
Kannan JA, Epstein TG. Immunotherapy safety: what have we learned from surveillance surveys? Curr Allergy Asthma Rep 2013;13:381–8.Find this resource:
Acute URTIs include rhinitis, pharyngitis, tonsillitis, and sinusitis.
URTIs are the commonest cause of time off work in the UK. The majority are managed by GPs and will not reach a respiratory specialist. They are usually self-limiting and often do not require specific treatment.
Nasal congestion with rhinorrhoea, mild malaise, and sneezing. Most commonly due to viral infection (the common cold). Topical decongestants may be useful. There is no evidence for the use of antibiotics or antihistamines.
Oral Candida infection is common in those who have received antibiotics, are immunosuppressed, or are on oral or inhaled steroids. Seen as white plaque-like lesions on the tongue and pharyngeal mucosa. Treat with oral nystatin or amphotericin lozenges, and with oral hygiene. Severe infection can be debilitating, leading to difficulties with eating, especially in the elderly. Exclude underlying immunocompromise (e.g. HIV, leukaemia) in those with persisting infection despite treatment.
Acute epiglottitis (supraglottitis)
is infection mainly localized to the epiglottis and surrounding supraglottic structures. It is commoner in children than adults, but a mortality of up to 7% is reported in adults. This is due to upper airways obstruction from grossly oedematous upper airway tissue and can be life-threatening.
• Haemophilus influenzae, streptococci, and staphylococci are causative organisms
• Acute epiglottitis typically presents with a sore throat, fever, drooling, hoarseness. Inspiratory stridor is less common, but it can also present with acute upper airway obstruction and CXR infiltrates consistent with pulmonary oedema (due to high negative intrathoracic pressure)
• Diagnosis is made by visualizing epiglottis (direct or indirect laryngoscopy), but this may not be possible
• May need airway protection with an endotracheal tube or tracheostomy: liaise with ENT/anaesthetic colleagues early
• In severe infection, epiglottic swabs may be of diagnostic use, but beware of precipitating airway obstruction. Treat with third-generation cephalosporin for 2 weeks (to cover β-lactam-producing H. influenzae). Change to amoxicillin if sensitive.
The sinuses are normally sterile. The paranasal sinuses communicate with the nose and are therefore susceptible to infection from this route. All the sinuses drain by means of the mucociliary escalator. Blockage of free sinus drainage is a predisposing factor for bacterial infection. Sinusitis is a common cause of persistent cough (see pp. [link]–[link]). Dental sepsis may lead to maxillary sinusitis by direct spread.
complicates 1 in 200 URTIs and usually presents with fever, nasal congestion/purulent discharge, maxillary tooth pain, and sinus pain which is worse on leaning forward. It may be associated with systemic upset. Respiratory viral infection interrupts normal defences of the mucosal lining, producing mucous exudates, with 2° bacterial infection. S. pneumoniae and H. influenzae are the commonest pathogens. S. aureusand S. pyogenes are also causes, with Pseudomonas in CF. Mixed infections with anaerobes are seen in 10%. Specific diagnostic tests are not usually needed. Antibiotic treatment may be indicated if symptoms persist longer than 10 days, or severe symptoms of fever, facial pain, and purulent discharge at onset lasting >3 days.
by definition, if present for >3 months. The ciliated epithelial sinus lining is replaced by thickened stratified squamous lining, with absent cilia, due to repeated infection. Anaerobic infection is more common. Fungal infection is more common in atopic people with nasal polyps. Sinus mycetoma is a rare complication in neutropenic patients, diabetics, and the immunocompromised.
with frontal headache (frontal sinusitis), maxillary pain, pain over bridge of nose (ethmoidal sinusitis), retro-orbital headache (sphenoidal sinusitis), with purulent nasal discharge and blockage. GPA (Wegener’s) may mimic the symptoms of sinusitis.
are not usually warranted, but a sinus radiograph may show an air-fluid level, with thickened mucosal lining, or sinus opacification. CT is more sensitive but not usually warranted unless surgical intervention planned or malignant disease suspected.
Acute pharyngitis and tonsillitis
80–90% are caused by viruses, most commonly adenoviruses, coronaviruses, rhinoviruses, and influenza viruses. Group A streptococci, Streptococcus pneumoniae, and Haemophilus influenzae may cause 2° infection. Mycoplasma and Chlamydia are seen less commonly.
• Pharyngitis and tonsillitis present with a sore throat, which is usually self-limiting. May be associated with fever, malaise, lymphadenopathy, conjunctivitis, headache, nausea, and vomiting
• Infectious mononucleosis (EBV) is associated with pharyngitis in 80% of cases. Diagnose with Paul Bunnell test for heterophil antibodies and atypical mononuclear cells in peripheral blood
• Coxsackie A and herpes simplex cause ‘herpangina syndrome’—ulcerating vesicles on the tonsils and palate
• CMV can also cause pharyngitis associated with lymphadenopathy and splenomegaly
• Lemierre’s syndrome (jugular vein suppurative thrombophlebitis) is a rare anaerobic pharyngeal infection (see p. [link]).
Other causative agents
• Corynebacterium diphtheriae in unvaccinated populations. A pharyngeal membrane may form, with systemic symptoms, and ‘bull neck’ due to cervical lymphadenopathy. Low-grade fever, with a relatively high pulse rate. Treat urgently with diphtheria antitoxin
• Vincent’s angina is anaerobic infection in those with poor mouth hygiene. Caused by Gram-negative Borrelia vincenti and other anaerobic infections. Treat with penicillin
• Group A Streptococcus may cause a more unpleasant illness, with systemic upset and dysphagia, due to pharyngotonsillar oedema.
is usually supportive, but anti-streptococcal antibiotics may be warranted if there is severe infection (fever, tonsillar exudates, tender anterior cervical lymphadenopathy, no cough). There is no evidence that antibiotics reduce the duration of symptoms, but they may reduce complications (e.g. sinusitis, quinsy, and rheumatic fever, which is rare in the Western world). Oral penicillin is the first-line treatment (or a macrolide if penicillin-allergic). Amoxicillin can cause a rash in infectious mononucleosis and so should be avoided. Throat swabs for group A Streptococcus may be helpful in directing treatment.
This is usually part of a generalized URTI. Often viral, but Moraxella catarrhalis, Haemophilus influenzae, and Streptococcus pneumoniae are also causative. It may cause a hoarse voice or aphonia.
include inhaled steroids, occupational exposure to inhaled chemicals, and GORD. If a hoarse voice persists in a smoker, a laryngeal or lung cancer (with recurrent laryngeal nerve involvement) must be excluded. Other causes include tuberculous infection, HSV, CMV, diphtheria, fungal infections, and actinomycoses.
Acute bronchitis, tracheitis, and tracheobronchitis
Inflammation due to infection can occur in any part of the tracheobronchial tree and is termed tracheitis, tracheobronchitis, or bronchitis, depending on the anatomical site. It usually follows viral infection, especially of the common cold type, and is commoner during influenza epidemics. 2° bacterial infection is common, with H. influenzae and S. pneumoniae commonest. There is increased prevalence in the winter months.
with a productive cough, small-volume streaky haemoptysis, and fever. Breathlessness and hypoxia are uncommon, unless there is coexistent cardiorespiratory disease or a concomitant pneumonia. Retrosternal chest pain is common in tracheitis. Examination is often normal.
is usually on the basis of the history. A persisting cough, especially in a smoker, may warrant further investigation.