ENT ATLAS PDF

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Fig. a–c “High” ear piercing (Fig. , arrow) complicated by infection ( frequently pseudomonas) may lead to abscess formula- tion. The puncture with high. The organizational structure of this atlas including numbers of pages is: Download the PDF to view the article, as well as its associated figures and tables. GLOBAL ATLAS OF ALLERGIC RHINITIS AND CHRONIC RHINOSINUSITIS. VIII. Finland. Elina Toskala, MD, PhD. Dept of Otolaryngology-Head and.


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PDF download for A Color Atlas of Otolaryngology, Article Information This atlas, written by four prominent otolaryngologists, includes color photographs. PDF download for A Color Atlas of Otolaryngology, Article Information . Otolaryngology–Head and Neck Surgery. ISSN: Online ISSN: OPEN ACCESS ATLAS OF OTOLARYNGOLOGY, HEAD &. NECK OPERATIVE SURGERY. PAROTIDECTOMY. Johan Fagan. The facial nerve is central to.

Some hazardous specimens and growing microorganisms are processed in biological safety cabinets 2. Bacteria and fungi have characteristic appearance on a variety of culture medium 2. The final identification is based on biochemical tests by recognition of metabolic end-products or enzymes.

In the microbiology laboratory, differentiating normal from pathogenic flora depends on information provided about clinical presentation, findings, and also on local epidemiological knowledge. This consists of cabinets with receiving wells for blood culture bottles. As microorganisms grow, liberated carbon dioxide is detected by a colour changing sensor that sets off an alarm alert.

Gram stain and culture of the blood is performed on the positive culture bottles. A higher biosafety level is applied for stringent conditions depending on the degree of biohazard of the suspected microorganism.

Blood agar; B: These are 1—2 mm round pale colonies surrounded by a zone of haemolysis halo. Blood is heated hence chocolate colour before pouring in culture plates to release essential nutrients for bacterial growth from lysed red blood cells. Processing of specimens for viral or tuberculosis microscopy and culture may be limited to specialist laboratories 2. Serological tests for direct detection of antigen as well as antibodies formed in response to infection is useful in certain cases 2.

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It can be helpful in culturenegative cases e. Mycoplasma pneumoniae , or in cases where routine culture is not possible, as with viruses, e. Molecular-based techniques like DNA probes bacterial 16SrRNA or polymerase chain reaction PCR for genetic analysis are being constantly improved, but in most places these are not yet widely available for clinical diagnostic purposes.

Various species of Candida can be identified by the colour of their colonies. Table 2. Pharyngeal exudates seen in this condition can also be present in infections caused by adenovirus, herpes simplex virus HSV and infectious mononucleosis. There has been an epidemic increase in Corynebacterium diphtheriae infection which is also known to produce a characteristic grey membrane across the posterior pharynx more recently in the former Soviet Union. Group C and G streptococci can also cause pharyngitis but not rheumatic fever as is sometimes the case in GAS infection.

HSV and coxsackie viruses often cause ulcers in the mouth and pharynx. Enteroviral upper respiratory infections are more common in summer months.

In adults with epiglottitis, blood culture taken prior to starting antibiotics can yield H. The microbiological aetiology of sinusitis reflects upper respiratory commensals. Fungal sinusitis with moulds Table 2. In its simple form it responds to topical antibiotics but treatment of aggressive infection with Group A streptococci and Staphylococcus aureus or the malignant form with Pseudomonas aeruginosa will require systemic antibiotics 2.

The use of 7-valent pneumococcal conjugate polysaccharide vaccine and HiB has reduced the incidence of otitis media caused by S.

Nontypable strains of H. Viruses, mostly RSV and adenovirus, cause the majority of acute otitis media. Nosocomial infection of the sinuses or postoperative wound infections of the ear, nose, throat, head, and neck is usually due to resistant gram-negative bacilli coliforms and Pseudomonas species and MRSA methicillin-resistant Staphylococcus aureus depending on local prevalence in hospitals 2.

Resistance demonstrated by no zones, or smaller zones around the antibiotic disc, to clockwise, from top right ciprofloxacin Cip , erythromycin E , metronidazole MZ , and cefoxitin Fox. Susceptibility, demonstrated by a clear zone around the antibiotic disc, to clockwise from top linezolid LZD , tetracycline TE , and fucidic acid FD. The suggested treatment regimes are not exhaustive and prescribing antibiotics should always take into consideration the local sensitivity profiles for the infecting organisms.

The choice of an antibacterial compound for a particular patient and a specific infection is based on several factors: The local sensitivity profile, where available, is useful when empiric treatment is being considered.

Minimum inhibitory concentration MIC is the lowest concentration of an antimicrobial that will inhibit the visible growth of a microorganism after overnight incubation. However, when the infection is located in a site where penetration is poor, such as an abscess cavity in the neck or in complicated sinusitis, drainage of pus collection is paramount.

Sometimes, despite adequate MIC at the site of infection, activity may be reduced due to the local environment, such as an unfavourable pH. Antibiotics inhibit or abolish the growth of microorganisms bacteria and fungi through a number of mechanisms, as shown in Table 3. Antibacterials are broadly classified into bactericidals, that kill bacteria directly, and bacteriostatics, which prevent them from dividing. However, these classifications are based on laboratory behaviour and, in practice, both classes are capable of ending a bacterial infection.

In the treatment of most ENT infections acquired in the community, the choice of either a bacteriostatic or bactericidal antibiotic is of limited importance. However, in patients with severe infection, especially in immunocompromised states, a bactericidal agent must be used. Resistance Acquired resistance commonly occurs through one of the following mechanisms: Resistance can be passed on horizontally e. Knowledge of resistance patterns in the local environment is important and multi-disciplinary working with microbiologists is important in planning the treatment regime for serious infections.

Clinical vigilance is necessary to reduce the emergence of resistant strains Table 3. Thus, parenteral administration should be reserved for patients who are severely ill e. Oral treatment can be commenced once the patient shows clinical improvement. They act by binding to penicillinbinding proteins and inhibit the final step in the synthesis of the peptidoglycan layer of the cell wall.

Table 3. Resistance to penicillin is widespread in staphylococci and in pneumococci in some geographic areas. Ampicillin and amoxycillin extend the activity of penicillin among gram-negative organisms such as H. Penicillinase-resistant penicillins e. Carboxypenicillins and ureidopenicillins are especially active against pseudomonas infections. Cephalosporins are categorized into four generations based on their activity profile. As a rule of the thumb, the activity of cephalosporins against gram-negative bacteria is greater with the newer generations.

The fourth generation cephalosporins, however, have true broad spectrum activity. First generation cephalosporins act well against grampositive bacteria, including penicillinase-producing staphylococci. Second and third generation cephalosporins are active against the bacterial agents causing sinusitis and otitis media and against resistant H. Third generation cephalosporins are primarily used against multi-drug-resistant gram-negative agents such as Pseudomonas spp. Carbapenems are primarily used against gramnegative bacteria resistant to third generation cephalosporins.

Aminoglycosides This class of antibiotics is not used as frequently in ENT infections. They are bactericidal and prevent protein synthesis by binding irreversibly to the 30S subunit of the bacterial ribosome.

Their primary indication is in managing gram-negative infections, especially of nosocomial origin, but they are active against staphylococci and Pseudomonas spp.

They exhibit poor penetration into abscess cavities and renal and otic toxicity is one of the major reasons for reduced use. However, topical aminoglycosides are very effective in controlling bacterial otitis media. Macrolides Erythromycin, clarithromycin, and azithromycin are very commonly used for community acquired ENT infections.

These are bacteriostatic antibiotics, and act by interfering with protein biosynthesis and binding to the 50S subunit of the ribosome. The spectrum includes gram-positive bacteria with limited activity against gram-negative organisms. It must be noted that bacteria that are resistant to erythromycin are also resistant to clarithromycin and azithromycin, owing to a similar mechanism of action.

The latter two have fewer gastrointestinal side-effects compared to erythromycin. These are primarily used in streptococcal pharyngotonsillitis, acute sinusitis, and in patients allergic to penicillin. Unlike penicillin, it must be recognized that Streptococcus pyogenes resistance to macrolides exists. Clarithromycin and azithromycin are also used in treating nontuberculous mycobacterial infection.

Lincosamides Clindamycin is the only lincosamide that is widely used. This class of agents is bacteriostatic with a mechanism of action similar to the macrolides. It is active against grampositive aerobes streptococci and staphylococci and all strict anaerobes. Antibiotic associated diarrhoea and pseudomembranous colitis is a well-documented complication that is also associated with most of the other antibiotics. Fluoroquinolones This group of antibiotics is bactericidal, acting by inhibiting DNA replication and transcription.

These antibiotics have excellent activity against gram-negative organisms, including Pseudomonas spp. The newer quinolones are also active against gram-positive bacteria. Major indications in ENT practice include second-line therapy for sinusitis after treatment failure and pseudomonal skull base osteomyelitis malignant external otitis. Ophthalmic preparations can be used topically in chronic otitis media to eradicate Pseudomonas spp.

Tetracyclines These are bacteriostatic drugs that act by binding reversibly to the 30S ribosomal subunit and blocking translation. They have a wide spectrum of gram-positive and gram-negative activity, but resistance is common of late. MRSA is susceptible to tetracylines but treatment should be advised based on susceptibility tests. It disrupts the DNA structure after being actively transported into anaerobic bacteria to be converted into its active form.

It penetrates into abscess cavities very well, but has no activity against aerobic organisms. Topical metronidazole is used on malodorous wounds to reduce anaerobic growth. For this reason, sensitivity reports have no clinical implication.

Thus, topical therapy has very high success rates in controlling the infection and resistance is not an issue. Topical antibiotic preparations include aminoglycosides gentamicin and framycetin , fluoroquinolones, gramicidin, and polymixin, often in combination. Choice of antibacterial therapy Pharyngotonsillitis Acute otitis media and acute sinusitis The organisms causing acute otitis media and acute sinusitis have a similar distribution in children and adults. Apart from viruses, Streptococcus pneum oniae, Haemophilus influe nzae , Mo raxe lla c atarrhalis, and Stre pto c o c c us pyogenes are implicated.

Cultures are difficult to obtain in both scenarios without invasive means and therapy is generally empirical. Given the above spectrum, amoxicillin is recommended as the first-line agent and success with this agent is well documented. Resistance to penicillin and amoxicillin is seen in S. In these instances, a change in antibiotic is needed. The choice is best made taking into account local sensitivities and directed by culture results if appropriate.

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Therapy is typically administered for 5—7 days for uncomplicated acute otitis media and 10—14 days for acute sinusitis. Treatment failures can occur with acute sinusitis with inadequate doses or resistant organisms. In such instances, longer courses of culture directed antibiotics for 4—6 weeks may be required to eradicate the infection. Chronic otitis media and topical antibiotics Pseudomonas aeruginosa and Staphylococcus aureus are the common pathogens seen in this setting.

However, a 0. Moreover, this concentration greatly exceeds the laboratory reported MIC GAS pharyngitis must be treated with a full day course of oral penicillin, with erythromycin being used in penicillinallergic individuals. Penicillin resistance has not been reported so far and newer antibiotics do not offer any advantage. No treatment is required for pharyngitis caused by viruses, Mycoplasma or Chlamydia as these are self limiting. Epiglottitis Antibiotic therapy should target H.

Antibiotic therapy should be continued for 7—10 days and should be tailored, if necessary, to the organism recovered in culture. Unvaccinated children exposed to patients should receive prophylaxis with rifampicin. Neck space abscesses These are life-threatening infections and empirical therapy should be started soon after a clinical diagnosis is made. This should cover streptococci, oral anaerobes, and S. Once cultures are obtained, the antibiotics can be changed to reflect sensitivity.

Drainage of abscess is essential, as antibiotics do not reach bacteria in the presence of pus. A good history, coupled with examination of the ear under magnification after cleaning out the ear canal, is necessary to achieve the diagnosis.

Significant vital structures crowded in a small area, proximity to the intracranial compartment and the variety of infectious syndromes makes this a challenging aspect of ENT practice. Infections of the pinna Pre-auricular sinuses are commonly asymptomatic and require no treatment.

They appear as small pits or dimples anterior to the root of the antihelix. More extensive sinuses will collect squamous debris and can become infected.

Incision and drainage will be needed if an acute abscess develops but formal excision of the tract is necessary to prevent recurrence 4. Sebaceous cysts occur in the lobule of the ear and can become infected, but most infections in this area are secondary to ear piercing.

Abscesses will require incision and drainage 4. Infection of the perichondrium of the pinna can be secondary to an infected wound on the pinna or an otitis externa. The pinna becomes thickened, erythematous, and tender 4. Treatment should be prompt with broadspectrum intravenous antibiotics initially. If untreated, the infection leads to a loss of cartilage and a cauliflower ear appearance.

Infections of the external ear canal The squamous epithelium of the tympanic membrane and ear canal is migratory in nature. The squamous epithelium over the drum is very thin and is only one cell thick. The skin 4. The confined space of the ear canal means that it is not possible to have a desquamating stratified squamous epithelium on the drum or the ear canal. If this were the case the desquamated cells would collect in the ear canal and lead to a build up of debris.

The migratory nature of the epithelium avoids this problem. The squamous epithelium grows out radially across the surface of the drum until it reaches the annulus and then grows out laterally along the ear canal.

The ceruminous glands, which produce the wax, are only located in the outer third of the ear canal. As a result, in a normal ear, the skin gradually migrates out towards the meatus taking excess wax with it. The normal ear is selfcleansing and the antiseptic, hydrophobic nature of wax keeps the medial end of the external ear canal relatively clean with only scanty growths of commensals present. Typically these are Staphylococcus epidermidis, Corynebacterium spp.

It gives rise to a very tender localized swelling. Oedema in a confined area gives rise to severe pain. There may be little in the way of pus present. Infections are usually caused by Staphylo coccus aureus. The principle of treatment is to reduce the swelling in the ear canal using impregnated wicks.

These are strips of ribbon gauze that can be soaked in topical agents. They need to be replaced or removed after 24—48 hours. For furunculosis, a wick soaked in ichthammol glycerin is the treatment of choice 4. Wicks soaked with creams containing steroid and antibiotic may also be effective. Additional oral antistaphylococcal antibiotics are of value if there is erythema visible on the pinna.

The swelling is caused by local oedema and very little pus and so surgical drainage is rarely effective. In mild cases the ear canal will appear red and in more severe cases there will be acute oedema of the ear canal with narrowing of the meatus and a variable amount of debris in the canal. The aetiology of acute otitis externa may be idiopathic, traumatic due to scratching of the ear canal or injudicious use of cotton buds or related to water with an accompanying history of water getting into the ear as a result of swimming or syringing.

Treatment will vary depending on the degree of oedema. If the canal is inflamed and there is no evidence of debris, topical antibiotic drops or sprays containing broad-spectrum antibiotics and steroids may be all that is required 4. Cases where there is significant oedema will be very tender and will require gentle microsuction of any debris 4. This is followed by the introduction of wicks to remove the oedema of the ear canal.

These can be ribbon gauze wicks impregnated with ichthammol glycerin or steroid and antibiotic creams 4. Inserting a dessicated expandable ear wick followed by addition of a topical antibiotic drop preparation can also be effective 4. If the patient is toxic or there is associated erythema of the pinna or face then additional systemic antibiotics are required.

In early acute otitis externa the infecting organisms are likely to be staphylococcal or streptococcal in nature, but with time the organisms soon change to those seen in chronic otitis externa. As the ear responds to treatment, further suction clearance to clear the build up of any further debris may be necessary. Frequency of microsuction is highly variable. Wicks tend to dry out in 24—48 hours and therefore need to be changed every 24—48 hours.

The common reasons for persistence of the condition are: Pse udo m o nas spp. Hearing aid moulds and antiseptic dressing used after ear surgery can also cause allergic reactions 4. Although it may simply be a result of an acute otitis externa that is slow to resolve, in the majority of cases the failure of resolution is due to direct or indirect trauma 4.

This condition is common in patients who have a tendency to eczema. The patient complains of an itching in the ear accompanied by variable amounts of discomfort and pain.

The ear will tend to discharge and there will be a blocked feeling in the ear. In mild cases, the eczematous inflammation of the ear canal may be the only disease process 4. The inflamed skin loses its natural migratory ability and there is decreased wax production. There is a tendency for dry desquamated cells to collect in the ear canal. Treatment at this stage is gentle microsuction of any debris and use of steroid drops to settle the eczema and stop the itching.

Itching of the ear canal tempts the patient to use cotton buds, hair grips, pen tops, finger nails, and so on to rub or scratch the ear canal.

A scratch inside the ear canal breaks the integumental layer of the skin and allows for infection to spread subcutaneously, giving rise to the classic appearance of a chronic infective otitis externa 4. The ear 4. This is likely to be required to be done repeatedly depending on the response to treatment. Milder cases will respond to simple drops and sprays, more severe cases benefit from insertion of steroid and antibiotic cream or ointment in the ear canal.

Wicks can be used if there is significant oedema, but when the ear canal is reasonably open, insertion of cream or ointment into the ear canal using a 2 ml syringe with a plastic intravenous cannula attached is often easier 4. These treatments will often require to be repeated. Appearance of a normal ear canal with normal wax usually indicates that the problem has been solved.

Oral antibiotics are rarely needed or helpful. Patients will often complain of recurrent problems over many years. This is usually due to incomplete eradication of the initial infection. In chronic low-grade otitis externa it may be possible to gain control by using topical antiseptic solutions such as aluminium acetate or alcohol and acetic acid mixtures. These work by inhibiting bacterial growth by acidifying the ear canal. Clinically, the appearance may be the same as that of chronic bacterial otitis externa and the diagnosis is only made by fungal growth on aural swabs.

Alternatively, the clinical appearance may be that of an obvious fungal growth with visible hyphi and on otoscopy a dry or wet mould can be seen. Aspergillus species are most commonly isolated. The treatment is similar to that of the triple therapy of the chronic otitis externa with: As the topical antibiotic and steroid creams often contain nystatin, these agents may be suitable but specific treatment with antifungal creams and drops such as econazole or clotrimazole may be required.

Fungal infections have a reputation for reoccurring which is due to reactivation of persisting spores. Therefore, antifungal topical agents are recommended for 4—6 weeks. This can be quite thick so that the canal appears shorter than normal.

The infective process has resolved but a conductive hearing loss results 4. Bony exostosis: They are thought to be secondary to periosteal inflammation induced by the cold water or otitis externa. Treatment is usually unnecessary 4. On otoscopy there is blistering of the ear canal or drum. It is usually a single blister and has a characteristic appearance.

It may be accompanied by a middle ear effusion. The condition is self-limiting but is painful and topical steroid drops can be used to try to ease the discomfort 4.

It presents with a painful ear often accompanied ZOSTER A herpes zoster infection based on the geniculate ganglion of the facial nerve is given the eponym Ramsey—Hunt syndrome 4.

The patient presents with pain ENT Final. There may be an associated sensorineural hearing loss and tinnitus. On examination, as well as a facial palsy, there will be vesicles evident in the external ear.

The commonest site is the conchal bowl but the canal wall or drum can also be involved. If there is a discomfort from the vesicles and crusting in the ear canal this may be alleviated by using topical steroid and antibiotic drops. It is usually selflimiting and any treatment required is analgesia. The tympanic membrane will be hyperaemic but otherwise normal. It is most common in childhood, particularly in the first 2 years of life.

The first phase of an infection will start with a viral upper respiratory tract infection. At this stage there would be slight hyperaemia of the tympanic membrane with no middle ear effusion. Over the next 24—48 hours blockage of the eustachian tube is followed by a bacterial infection of the middle ear cleft.

The bacteria migrate up the eustachian tube from the nasopharynx. By the time the bacterial pyogenic infection has become established the drum will appear red with a middle ear effusion and the yellowish appearance of pus visible through the drum.

The pus will fill the middle ear and mastoid air cell system. The classical presentation is therefore initially with the symptoms of a coryza which is followed by otalgia and a conductive hearing loss. There is an accompanying pyrexia, but no otorrhoea.

The otalgia may persist for a further 24—48 hours. If the infection resolves by bursting through the drum, there will be a sudden discharge of pus which is usually mixed with fresh blood and a decrease in the otalgia and the accompanying pyrexia.

In young children, particularly those under 2, it can be easy to miss a diagnosis of acute otitis media. At this age children may not localize pain to the ear and just complain of ill defined ache or falsely localize the pain to the abdomen. It is therefore necessary to examine the ears of all pyrexial children to exclude the diagnosis. Once a pyogenic infection of the middle ear space is established there are several possible outcomes: It is usually the posterior part of the tympanic membrane that thins and then bulges laterally before perforating.

There is then a discharge of pus which is associated with bleeding from vessels on the surface of the drum. The bleeding can be more obvious than the pus. The commonest outcome is resolution of the infection with drying of the otorrhoea and healing of the tympanic membrane. The majority of acute perforations will heal spontaneously as above, but a persisting perforation may persist particularly if the acute otitis media becomes a recurrent problem. The infection may resolve spontaneously, but if the eustachian tube remains blocked a sterile effusion will persist in the middle ear cleft.

The inter-relationship between glue ear and acute otitis media is two-fold. Glue ear can occur as a result of an episode of acute otitis media and equally the presence of glue ear makes some children more prone to recurrent episodes of acute otitis media. Recurrent episodes of acute otitis media. Treatment of acute otitis media in the primary care setting remains contentious. There are several large studies which indicate that the use of antibiotics is unwarranted and that the outcome of acute otitis media is not affected by prescribing oral antibiotics.

The consensus view in primary care is that there is no need for antibiotics in the first 48 hours and children with a putative diagnosis of acute otitis media can be treated with analgesia alone. However, in order to include large numbers of subjects, these studies have had relatively lax entry criteria and may have inadvertently included a significant number of patients with viral acute otitis media rather than those ENT Final. This would tend to mask any benefit achieved by using antibiotics in bacterial cases.

There therefore remains a case for use of oral antibiotics in acute otitis media of more than 48 hours duration, particularly if the patient is pyrexial. See below. ACUTE 4. The advent of antibiotics has greatly reduced the instance of this disease and it is now uncommon, but cases still occur and the condition has the risk of serious ENT Final. In acute mastoiditis there is an osteitis, i. In acute otitis media the middle ear cleft will contain pus but the surrounding bone is not infected.

In acute mastoiditis the bone of the mastoid and middle ear is infected. Classically the osteitis will only develop 7—10 days after the onset of an acute pyogenic otitis media. The symptoms and signs of acute otitis media will be compounded by increasing pain and a swinging pyrexia. Young children become increasingly lethargic and systemically unwell.

The pus spreads through eroded areas of the cortical bone lateral to the mastoid cell system or through thrombosed mastoid emissary veins and then lies subcutaneously over the mastoid process behind the ear.

Initially this will just cause erythema behind the ear, but progresses to form a red tender swelling behind the ear. The post-aural sulcus disappears and the pinna is pushed forwards 4. In early cases where there is just erythema behind the ear, there will be tenderness over the antrum of the mastoid. This lies deep to the triangular fossa of the pinna and pressure in the fossa will elicit the tenderness. On examination of the ear canal it is often difficult to see the drum as the posterior-superior segment of the ear canal is oedematous and the canal is narrowed.

When the drum is seen it will be erythematous and pus may be visible in the middle ear. Acute mastoiditis has significant associated morbidity and potential mortality. The spreading osteitis leads to bone erosion and further spread of infection. Posterior spread into the sigmoid sinus causes a lateral sinus thrombosis and potential septicaemia. Superior spread through the tegmen or roof of the middle ear cleft into the middle cranial fossa results in meningitis or temporal lobe abscess see 4.

If the infection is advanced to the extent that there is a swelling behind the pinna, pus is present and surgical drainage is necessary. At operation the subcutaneous pus is drained and the mastoid antrum is opened and also drained. Further exploration of the mastoid air cell system and the sigmoid sinus may be necessary 4.

In earlier cases where there is just erythema and tenderness over the mastoid with no clinical or radiological evidence of intracranial infection, then it is reasonable to treat with intravenous antibiotics for the first 24 hours. If there is improvement then antibiotics may be continued and surgery may not be necessary. If there is no clinical improvement after 24 hours, cortical mastoidectomy is required.

The bacteria that cause acute mastoiditis are the same as those that cause acute otitis media, i. Streptococcus pyogenes, S. The infection may come from externally as a result of swimming or showering, or it may spread up the eustachian tube as is seen in acute otitis media. The larger the perforation the more prone it will be to recurrent infections. An infected perforation may be slightly uncomfortable but pain is not usually a significant feature. There is no confined space and the otorrhoea will discharge through the perforation and the patient will complain of an unpleasant odour associated with the discharge.

Hearing may feel slightly reduced 4. Swabs can be taken to identify the bacterial pathogen, but in long-standing cases mixed growth with coliforms and Pseudomonas species are common. More acute infections are caused by the usual upper respiratory tract commensals but are seen less frequently. Prompt resolution is usually achieved by use of topical broad-spectrum antibiotic drops or sprays. Additional use of oral antibiotics may be helpful in refractory cases.

Recurrent infections can be treated by careful avoidance of the precipitating causes, i.

The best long-term solution to a recurrent infection is surgical repair of the perforation tympanoplasty or myringoplasty. A patient with grommets in situ will present with slightly smelly discharge from the affected ear. Pain is not usually a significant feature but the hearing is usually reduced.

The source of the infection may be external from dirty water or via the eustachian tube when it is associated with an upper respiratory tract infection. However, contrary to popular belief, there is no evidence that children that swim with grommets in situ are any more prone to infections that those who do not. On examination the otorrhoea may make visualization of the grommet difficult. In an older child suction clearance will help, but most children tolerate this poorly.

Swabs can ENT Final. The mainstay of treatment is topical antibiotic drops and sprays with a broad spectrum of activity. The addition of broad-spectrum oral antibiotics with antianaerobic activity may be necessary in refractory cases.

Long-term grommets are more prone to infections than short-term grommets. When infections become recurrent or persistent removing the grommet usually solves the problem 4.

The squamous epithelium of the outer surface of the tympanic membrane would normally migrate away from the drum. However, when a retraction pocket has been formed usually in the pars flaccida or postero-superior segment of the pars tensa , the migratory nature of the squamous epithelium is not able to function.

The epithelium then desquamates dead ENT Final. This pocket of dead skin constitutes a cholesteatoma. More dead epithelial cells are continually added and so the cholesteatoma enlarges. Proteolytic and osteolytic enzymes are released by the dying epithelial cells and this adds to the slow local destructive nature of the condition. As the lesion enlarges it causes further damage by local erosion, but this process accelerates when the lesion becomes secondarily infected. On examination it may be possible to see the classical appearances of cholesteatoma with white keratin collecting in a retraction pocket in the attic region or in the posterosuperior part of the tympanic membrane 4.

Uninfected, dry keratin oxidises slowly forming a firm brown crust 4. Once infection is present the view is often obscured by otorrhoea and granulation or polyp formation 4. Infected cholesteatomas are also associated with acute damage to the facial nerve causing a facial nerve palsy. Erosion of the roof of the middle ear allows intracranial complications such as temporal lobe ENT Final. B The same ear immediately following surgical removal of the granulations revealing the underlying cholesteatoma.

In a discharging ear when cholesteatoma is suspected, initial treatment is with topical broad-spectrum antibiotic and steroid containing drops. These agents may dry up the otorrhoea and decrease the size of any granulations or polyps and make the cholesteatoma more evident.

If an aural polyp persists or the attic region does not become clearly visible, then a formal examination under anaesthesia ENT Final. The definitive treatment for a cholesteatoma is surgical excision. Once cholesteatoma has become infected there is a risk of developing a secondary mastoiditis with osteitis, which gives a clinical appearance very similar to that of acute mastoiditis. In this situation the patient will present a history of slow progressive hearing loss which is now accompanied by an offensive otorrhoea, pain, and post-aural swelling.

The result is a variably sized cavity which is in continuity with the external ear canal. In a well designed and maintained cavity there may be the occasional collection of wax but the cavity remains infection free. However, infections in a mastoid cavity are relatively common and common aetiologies include: These all cause infections that are analogous to an otitis externa, i.

This tends to lead to mastoid cavity infections when the patient develops an upper respiratory tract infection. The bacteria gain access to the mastoid cavity via the eustachian tube 4.

Treatment is the same as that used to combat chronic otitis externa. The principles are: A variety of techniques may be needed. Both features contribute to a tendency to recurrent infection. Polyps are essentially localized areas of granulation tissue 4. They maybe small or fill the ear canal 4. The most common cause of an aural polyp is an underlying cholesteatoma, but they are also seen protruding through central tympanic membrane perforations and occasionally with chronic otitis externa.

Small polyps may respond to topical treatment with antibiotic and steroid creams or drops or sprays. These are used for 7—14 days; on review of the patient it is then necessary to establish whether there is an underlying perforation or cholesteatoma.

If the polyps persist and the drum is not fully visible or if the polyp is large on presentation, an aural polypectomy and examination of the underlying tympanic membrane under general anaesthesia will be necessary. However, the common antibiotics used, such as gentamicin and neomycin, have the potential to be ototoxic. Ototoxicity can take the form of sensorineural hearing loss or vestibular toxicity.

There is no perceived risk to patients with an intact tympanic membrane, but when the middle ear is open, i. Once in the middle ear, it is possible that they could soak through the oval or round windows and into the labyrinth and hence cause sensorineural hearing loss or vestibular loss. In practice there are case reports of sensorineural hearing loss associated with gentamicin. The risk appears to be greater with long-term use of these agents and particularly if they are being used when there is no evidence of infection being present.

The thickened middle ear mucosa that is found in infected ears is probably protective and less permeable to the ototoxic agents than normal thin middle ear mucosa. Gentamicin-based drops are very effective, particularly against the commonly found Pseudomonas infections.

Most of the alternative preparations are less effective against Pseudomonas except for ciprofloxacin-based drops, but as yet these are not licensed for otological use in the UK.

Persisting middle ear infections are ototoxic in their own right and long-standing infections will release toxins which have a significant risk of sensorineural hearing loss. The risk of ototoxicity from an infective otitis is thought to be higher than the risk of ototoxicity from the judicious use of gentamicin-containing antibiotic drops.

It is for this reason the British Association of Otolaryngologists, Head and Neck Surgeons in the UK gives the following advice on the use of topical agents in the presence of an open middle ear: This is a reflection of the relentless destructive nature of this infection but it is an infective rather than a neoplastic process.

It is caused by a Pseudomonas aeruginosa infection of the skull base. This may start in the ear canal, mastoid, or middle ear. Once the osteitis is established the infection spreads across the skull base 4. Clinically, the patient is usually elderly, diabetic, or otherwise immunocompromised. In the early stages the symptoms will be of discomfort or pain and possible otorrhoea.

On examination, granulations maybe evident in the ear canal or in the middle ear segment.

As the infection spreads into the temporal bone, facial nerve palsies 4. Infections spreading through into the labyrinth will be associated with sensorineural hearing loss and vertigo. Infection then spreads medially towards the petrous apex and jugular bulb where it can cause ninth, tenth, and eleventh nerve palsies, or more posteriorly where it causes twelfth nerve palsy.

Diagnosis can be difficult as it is sometimes difficult to distinguish between the infective process and a malignant destruction of the skull base.

Biopsies of the granulations will show an inflammatory process. There will be systemic markers of an infective process and Pseudomonas is usually grown from culture of the otorrhoea. MR scanning will show a destructive enhancing lesion and CT will show demineralization of the skull base.

Open Access Atlas of Otolaryngology, Head & Neck Operative Surgery

Prompt aggressive treatment is required as this condition is associated with a high mortality as well as morbidity. Long-term antibiotic treatment with antipseudomonal agents such as ciprofloxacin is required. The otic capsule of the inner ear is made of very dense bone and is resistant to erosion, but once erosion has occurred usually in the region of the lateral semicircular canal or oval window , an acute inflammatory reaction takes place within the inner ear.

This is associated with sensorineural hearing loss accompanied by acute vertigo, nausea, and vomiting. Viral infections, particularly those caused by herpes simplex, have been implicated most frequently.

A classic history is of a slight discomfort in the region of the ear followed by an acute onset of a complete facial palsy which usually comes on overnight 4. Treatment with the use of high-dose steroids to reduce the oedema in the canal has long been advocated and recent studies have demonstrated benefit, but there is no good evidence to prove that the use of antiherpetic medication improves the outcome. The classic history is of a patient who develops an acute rotatory vertigo that is associated with severe nausea and vomiting that persists for up to 1 week.

A history of preceding upper respiratory tract infection is usually present.

There is then usually a steady resolution of symptoms, although more minor recurrent attacks may occur which become gradually less severe and less frequent. This condition is self-limiting and apart from symptomatic support with labyrinthine sedatives no treatment is necessary. A comprehensive history and examination, including nasendoscopy, is necessary to arrive at a differential diagnosis.

Viral infections are ubiquitous. Despite a similar spectrum of bacterial infective organisms, there is geographical variation to antibiotic sensitivity and some infections rhinoscleroma, fungal rhinosinusitis are endemic. Infections of the external nose 5. There is an erythematous area of skin with well demarcated edges 5.

It is caused by a streptococcal group A infection, which usually starts in a small laceration of the skin. The laceration may not be visible but often starts in the nasal vestibule or outer ear canal, i.

The disease is associated with pain and high temperature. In rare cases blisters and necrotic areas can appear. The first-line treatment is intravenous penicillin. Following a primary infection, recurrent infections can occur after activation of the dormant virus.

Sun exposure and stress are common triggers. The typical lesions are found around the lips and the nose. The first symptoms are paraesthesia and a burning sensation. Later, small blisters develop which burst and leave the typical crusted, herpetic lesion 5. The herpes simplex infection disappears without scarring after a couple of days. There is no evidence to support the use of topical antiviral agents, but in severe cases, especially in immunocompromised patients, systemic antivirals acyclovir and famciclovir may reduce the duration of symptoms if taken early in an attack.

Prevention is possible in the presence of clear-cut triggers. The fistula comprises a duct of squamous cell epithelium and can extend from the glabella to the tip of the nose. In rare cases there can be an extension intracranially.

Intermittent secretions from the opening of the fistula can occur and secondary infections are common. A complete excision of the fistula and the duct is the therapy of choice in order to avoid recurrence 5. Treatment is the complete removal of the foreign body. Piercings and studs around the nasal vestibule can be the focus of a Staphylococcus aureus infection or a localized cellulitis streptococcal.

Removal of the foreign body and appropriate antibiotic therapy is required. In children, digital trauma leads to a chronic inflammation of the vestibule which becomes secondarily infected. Recurrent epistaxis is common and topical antiseptic creams will often eradicate the bacterial overgrowth and allow resolution of the vestibulitis and the recurrent epistaxis.

In adults, infection in the hair follicles of the nasal vestibule causes a folliculitis 5. Inside the nose the proliferations are much more filliform and treatment is surgical removal as topical agents and cryotherapy are difficult to administer in this region 5. A direct blow on the nasal tip is the commonest mechanism of injury, and there may or may not be an associated nasal fracture.

The haematoma detaches septal perichondrium from the septal cartilage. If this occurs bilaterally the septal cartilage becomes detached from its blood supply, which comes via the perichondrium, and undergoes necrosis. Septal haematoma is a less common result of nasal trauma than a fractured nose. It can occur with relatively minor injuries, particularly in children, where an associated fracture is unusual.

In adults an associated nasal fracture is more common and it can also occur as an early complication following septal surgery. Haematomas will therefore present with a history of nasal obstruction following on from an episode of trauma. Anterior rhinoscopy reveals obliteration of the nasal cavity bilaterally by a soft swelling arising from the septum. They need early surgical drainage as left untreated the haematoma becomes secondarily infected and by 7 days the haematoma has become a septal abscess.

A septal abscess will present 5 or more days after the trauma and the patient will have developed toxaemia, pyrexia, and increasing pain 5.

Acutely, this condition has a significant associated morbidity with cavernous sinus thrombosis, orbital cellulitis, and meningitis all described as possible complications. Prompt surgical drainage is required but by this stage there is always a loss of septal cartilage, leading to a septal perforation 5.

If this is excessive, or if it occurs in a child, this will often lead to a saddle nose deformity in the long term 5. Infection is not normally thought to be part of the aetiology in the majority of cases, but patients with nasal polyps are more prone to problems with chronic infective rhino-sinusitis see below.

In addition, some patients with chronic sinusitis can develop an inflammatory hyperplasia of the nasal mucosa. This leads to the development of localized nasal polyps, which will originate in the area of the uncinate process and the middle meatus 5. Simple inflammatory nasal polyps present with nasal obstruction and hyposmia as the main symptoms, with little accompanying pain. Treatment is predominantly surgical although steroids used both topically or systemically may have a role.

Polyps associated with underlying infected chronic sinusitis are more likely to have associated sinus pain. Round objects such as plastic beads are common and tend to become stuck just anterior to the inferior turbinate, where they are visible and cause nasal obstruction.

Foreign bodies such as sponge, 5. The foreign body may not be visible, so all children presenting with a unilateral foul smelling nasal discharge need an examination under anaesthesia to exclude the presence of a foreign body. This will be initially viral but there may be a secondary bacterial infection see below. Adenoiditis will often coexist with tonsillitis. Adenoid tissue is at its most prominent between the ages of 3 and 7 years 5. Hyperplasia of the tissue will lead to increased nasal obstruction, hyponasal voice, rhinorrhoea 5.

Treatment is essentially that of an upper respiratory tract infection in the acute phase and adenoidectomy with or without grommet insertion or tonsillectomy in recurrent cases. The term rhinitis implies an infection predominantly in the nasal mucosa.

Sinusitis predominantly affects the sinus mucosa but in reality most infective conditions affect both areas and are best described as rhinosinusitis. A distinction is made between acute and chronic sinusitis. The acute form can last up to 2 weeks but is frequently recurrent in nature.

Chronic rhinosinusitis implies persistence of the inflammation and symptoms for 12 weeks or longer. Spread is by aerosol droplets and contact. There are four stages of infection: Mild toxaemia. Rhinorrhoea become thicker, secondarily infected and discoloured 5. Treatment is supportive.

Anti-inflammatory and decongestant medication may ameliorate symptoms. Antibiotics are not indicated. The sinuses are normally kept infection free by continuous movement of a mucus blanket over the respiratory epithelium of the sinuses, through the sinus ostia, and into the nasal cavity.

ENT Infections: An Atlas of Investigation and Management

Therefore, any factor that interrupts this process increases the chances of infection. The following anatomical features have all been implicated in sinus disease, but their relative importance is the subject of debate: Nasal polyps and other nasal disease processes may also block the sinus ostia.

Failure of the mucociliary clearance from the sinuses through the ostia leads to stasis and the formation of pus in the sinus. The rest are caused by Streptococcus group A, Streptococcus milleri, Staphlococcus aureus, Neisseria spp.

Anaerobic pathogens such as Peptostreptococcus, Bacteroides spp. In principle, a bacterial sinusitis is a secondary infection of a primary viral sinusitis. The symptoms will, therefore, initially be those of a coryza but the patient will then develop facial pain.

The pain is characteristically dull, throbbing, and worse on bending forward. Maxillary sinus pain tends to be felt in the cheek but radiates down into the teeth. Frontoethmoid disease gives pain around, behind, and between the eyes. Isolated sphenoid sinusitis is rare but the pain may be retro-orbital or felt on the vertex. On examination there may be tenderness medially over the maxillary sinus or above the inner canthus of the eye over the fronto-nasal duct region.

Swelling of the face is not seen in uncomplicated sinusitis. Swelling over the cheek is usually indicative of an underlying dental infection.

The maxillary sinus may be clear of infection or may be secondarily infected. The typical endoscopic finding is pus in the middle meatus 5. The diagnosis is made from the history and examination findings but a CT scan of the paranasal sinuses in coronal sequence will show partial or total opacification of the affected sinuses. Treatment of acute sinusitis is the subject of much debate in the primary care setting. Supportive treatments with analgesia and decongestants such as pseudo-ephidrine and xylometazoline are logical.

The role of antibiotics is disputed, and there are understandable concerns about the over-prescription of these agents. Several large studies conducted in the primary care setting suggest that they are of no value, but the entry criteria for some of these studies were lax and it may be that many cases of viral coryza were included, thus diluting any positive benefit for those subjects ENT Final. Studies conducted in the secondary care setting tend to be more supportive of the value of antibiotics.

These studies tend to have the advantage of radiological confirmation of the diagnosis and, therefore, have slightly different entry criteria. Most otolaryngologists would recommend the use of antibiotics in clear cases of bacterial sinusitis with toxaemia. In community acquired sinusitis, a 2 week course of amoxycillin should control the infection. Erythromycin or one of the other macrolide antibiotics is useful in penicillin allergic individuals.

Chronic rhinosinusitis may have an underlying degree of inflammatory rhinitis that is helped by the addition of topical steroid preparations. In addition, recent studies suggest that prolonged courses of low-dose or full-dose clarithromycin which has an anti-inflammatory as well as antimicrobial action may be of benefit. Refractory cases will need endoscopic sinus surgery to enlarge the natural sinus ostia to enhance drainage and restore normal mucociliary clearance.

The classification is still in evolution, but the major categories are identified in Table 5. There is a possible link with the use of air conditioning units which are easily colonized with fungal overgrowths. A high index of suspicion should be maintained to diagnose these infections as, apart from the acute fulminant variant, the others have similar presenting symptoms. The diagnosis is established by meticulous endoscopic examination and characteristic imaging findings.

On the CT scan the fungal ball can appear like a metallic foreign body or have areas of microcalcification 5. The majority of the cases occur in children and the focus of the infection is predominantly in the ethmoid sinuses. Infection spreads through the lamina papyracea into the orbit by passing through bony dehiscences or through thrombosed communicating vessels. Initially there may just be a mild cellulitis with an inflamed upper eyelid, no restriction of eye movement, and no proptosis 5.

It may be difficult to differentiate the diagnosis at this stage from causes of pre-septal infection such as infections of the lacrimal glands 5. Subsequently, a peri-orbital cellulitis may develop in the post-septal part of the orbit. At this point the oedema of the lid is worse, it is difficult to open the eye, and there is proptosis with possible restriction of eye movement and diplopia. If a subperiosteal abscess develops there is a significant risk to the vision. Colour vision tends to be lost before black and white.

Diagnosis is mainly clinical but imaging studies help identify the presence of an abscess or cellulitis and may help differentiate between pre- and septal infections 5. In rare cases an intraorbital abscess can be found. Table 5. Pain, fever, facial swelling, cheek anaesthesia, nasal mucosal necrosis. Rapid progression Control underlying immunosuppression, surgical debridement and antifungal therapy Chronic invasive Immunocompetent Aspergillus spp. Chronic sinusitis symptoms, slower progression with variable course Surgical debridement and antifungal therapy Fungus ball Immunocompetent Aspergillus spp.

Chronic sinusitis-like symptoms, grey clay-like or rubbery mass fungal ball seen on endoscopy 5. Recurrent nasal polyposis, allergic fungal mucin 5. Note opacified ethmoids on the same side. Therapy depends on the state of infection. In early cases in which there is no significant proptosis, restriction of eye movement, or threat to vision systemic intravenous antibiotics and decongestant nasal sprays for the first 24 hours may be effective.

In more advanced cases a surgical approach with external or endoscopic opening of the opacified paranasal sinuses is required. In children and adolescents there is a relatively large cancellous layer in the frontal bone which allows easier spread of infection. An intracranial extension through the posterior wall of the frontal sinus can lead to meningitis or an extradural, subdural, or frontal brain abscess.

The infection is transmitted by the small veins in the diploeic bone which have no valves. The patient will complain of headache and clinical examination shows a soft swelling over the forehead 5. Like this document? Why not share! Embed Size px. Start on. Show related SlideShares at end. WordPress Shortcode.

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Embeds 0 No embeds. No notes for slide. A colour atlas of e n t diagnosis pdf 1. A colour atlas of E. R Bull 2.Features of the fifth edition:Expanded discussion of such topics as facial plastic surgery, care for the pediatric patient, and head and neck disorders More than high-quality full-color photographs and illustrations that demonstrate key concepts Ideal for medical students and residents in otolaryngology-head and neck surgery, this atlas is also a valuable reference for physicians in related specialties.

In rare cases there can be an extension intracranially. If left untreated, this can lead to a discharging fistula.

Treatment involves replacing the valve and prophylaxis against fungal infection. I would recommend this publication to all professionals who are exposed to acute clinical scenarios, from paediatrics to care of the elderly.

Swabs can ENT Final. The first phase of an infection will start with a viral upper respiratory tract infection. In acute otitis media the middle ear cleft will contain pus but the surrounding bone is not infected. The parotid gland is more susceptible compared to the submandibular gland as the salivary secretion is more serous.

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