STUDY - Technical - New Dacian's Medicine
Ear and
mastoid infections
Translation Draft
I'll start with the auricular cellulite and pericondritis.
I'll start with the auricular cellulite and pericondritis.
In the ear cellulitis the
ear is usually swelled, erythematous, warm and moderately
painful. The earlobe is extremely swollen and hyperemic. In the
patient's history there may be a minor ear injury (e.g. due to
earrings, cotton wool sticks or scratching in the ear).
Treatment consists in the application of warm compresses and intravenous administration of active antibiotics against S. aureus and other streptococci. Pericondritis, an infection of the ear pericondr, is commonly accompanied by infection of the cartilage of the outer ear (condritis). Disruption associated with blood supply to cartilage may cause ear deformity. The ear pavilion is swollen, warm, hyperemic and extremely sensitive, the earlobe is usually spared.
The most common history is burns, frostbite or major ear trauma (e.g. after boxing). Pseudomonas aeruginosa and S. aureus are the most common pathogens. Pericondritis should be treated with antibiotics such as ticarcillin/ clavulanic acid intravenously with ciprofloxacin orally for at least 4 weeks. Incision and drainage can be useful for crop production and for infection resolution, which is often slow. This infection should be distinguished from recurrent pericondritis which is a rheumatological condition.
Let's move on to external otitis. The external auditory duct is approximately 2.5 cm long and is lined with skin. Underlying the skin, in the lateral half of the conduction there is cartilage, and in the medial half, temporal bone. The skin in the bone portion of the duct has no subcutaneous layer and is attached directly to the periosteum, which is an important feature for the pathogenicity of invasive external otitis.
Cerumen secreted by glands acidifies the conduction and suppresses the multiplication of bacteria. However, the uncut skin and moisture in the duct make it extremely sensitive to P. aeruginosa, a hydrofilal organism. Acute external otitis or swimmer's ear occurs most frequently in the summer and may be due to decreased acidity of the auditory conduction, with consecutive bacterial overdevelopment. The ear is itchy and painful, and the auditory conduction is swollen and hyperemic. The most common pathogens are P. aeruginosa, S. aureus or other streptococci.
Treatment consists in cleaning the ear with mixtures of acetic acid alcohol and in topical administration of antibiotics in the form of ear drops with polymixin-neomycin. Herpes zoster in the auditory conduction produces severe otalgia and is often accompanied by ipsilateral facial paralysis due to damage to the genicular ganglion of the cranial nerve VII (Ramsay Hunt syndrome).
Recent data suggest that intravenous acyclovir treatment reduces the incidence of permanent facial paralysis, but no results of relevant clinical studies have been published. Conical external otitis causes pruritus to a greater extent than otalgia and is often due to irritation by repeated minor trauma to the duct (e.g. scratching the ear or the use of cotton wool sticks) or by draining a chronic infection from the middle ear.
In the latter case, treating chronic otitis media with antibiotics will also solve the problem of external otitis. Invasive external otitis ("malignant") is a potentially life-threatening infection, usually caused by P. aeruginosa which, starting from the external auditory duct, slowly invades adjacent soft tissues, mastoid, temporal bone and eventually spreads to the base of the skull. It occurs mainly in diabetic patients whose diabetes, unlike that of patients with mucormycosis, is usually well controlled.
Often there is a history of otalgia and otorrhea lasting several months. The physical examination reveals an edematized conduction, with granulation tissue in the posterior wall (at the cartilage-bone junction). In some cases patients have trimus or partial facial paresis (cranial nerve VII). Also, sometimes the cranial nerves IX, X and XI are affected. Signs of intradural damage, such as meningitis, temporal lobe infection or cerebral abscess are rarely encountered. Fever is rarely found in malignant external otitis. and when it does, it usually has low values.
Laboratory tests usually show a normal number of leukocytes, but a high value of VSH. TC and MRI examinations are essential for determining the extent of bone and soft tissue extension, helping the otorinolaringologist surgeon (ORL) to decide on optimal biopsy localization.
Cultures in the secretion of the external auditory duct are not always eloquent and in almost all cases, antibiotic therapy should not be started before histopathological examination and through cultures of a specimen of deep tissue. After this specimen has been taken, empirical intraoperative intravenous antibiotic therapy with active antibiotics against Pseudomonas may be initiated. P. aeruginosa is the pathogen involved in over 95% of cases, and the rest of the pathogens include Staphylococcus epidermitis, Aspergillus, Fusobacterium and Actinomyces.
Intravenous antibiotic treatment should be continued for 6 to 8 weeks in advanced cases (in early cases, if cultures show a strain of cypradrloxacine-sensitive Pseudomonas, the 2 weeks of antibiotic treatment in combination intravenously may be followed by oral monotherapy with ciprofloxacin).
It's the turn of the average otitis, and I'm going to start with acute otitis media. The middle ear communicates with the nasopharynx through Eustachio's tube. When the trunk gets stuck, in the middle ear and mastoid cavities, fluid accumulates, which constitutes a culture medium conducive to any bacteria present.
Acute otitis media (OMA) or middle ear infection may result. Viral infections of the upper respiratory tract, which can produce edema of the mucosa of Eustachio's tube, often precede or accompany episodes of OMA. Otitis media, similar to respiratory tract infections, is more common during autumn, winter and spring, and the incidence decreases with age (more than two-thirds of children under 3 years of age had at least one episode of OMA and the prevalence among adults is only 0.25%).
Symptomatology includes otalgia, fever and hearing-so-called. On otoscopic examination, the tympanic membrane shows decreased movements at instillation and usually appears red, opaque, bulging or retracted. Occasionally spontaneous perforations of the tympanic membrane and otorea are observed. For paediatric cases, OMA bacteriology was defined: S. pneumoniae (35%), H. influenzae (25%) and M. catarrhalis (15%) are the microorganisms most commonly found in newborns (group B streptococcus and gram-negative bacilli are important for OMA etiology in newborns). In a quarter of pediatric cases, viruses are found, either isolated or in combination with bacteria.
Small-scale studies in IMA adults have shown S. pneumoniae (21%) and H. influenzae (26%) as the most commonly encountered pathogens. Approximately 90% of H. influenzae infections are due to unclassified strains, those due to type B may be associated with bacteremia or meningitis.
Treatment of otitis media is empirical, diagnostic timpanocentesis being indicated only for patients with toxic status, immunodepressed patients or those with infections refractory to the initial treatment. Although about one-third of H. influenzae strains and at least three-quarters of M. catarrhalis strains produce b-lactamase, most specialists believe that amoxicillin treatment is effective in routine cases.
Other active medicines against most b-lactamase-producing strains are amoxicillin/ clavulanate, trimetoprim-sulfamethoxazole, erythromycin-sulfixazole, clarithromycin and 2nd generation cephalosporins. Penicillin resistance of pneumococcus, an increasingly important problem, is not mediated by b-lactamase.
Resistant strains may respond to treatment with erythromycin or sulfamides but serious infections require intravenous treatment with vancomycin or cephalosporin 3rd generation. Adjuvant treatment of OMA with antihistamines does not bring any benefit. Recurrent episodes of OMA in children are due to the same pathogenic germs that cause the primary episode of OMA (S. pneumoniae, H. influenzae and M. catarrhalis). Most early recurrences (75%) are not, however, relapses, but are due to different microorganisms or different strains of the same microorganism that produced the original episode.
The aspects of OMA recurrences in adults are probably similar, but have not yet been well studied. Recurrent OMA treatment should include active medicines against b-lactamase-producing strains. Patients with frequent recurrences (e.g. 3 episodes within 6 months) may benefit from antibiotic prophylaxis with amoxicillin or sulfisoxazole one dose per day during the winter months, although the risk benefit ratio should be weighed in selecting new resistant strains.
Medium otitis with fluid overflow or mean severe otitis is characterized by the persistence of fluid in the middle ear for several months, with no other signs of infection. This condition is associated with a hearing leave of 25 dB in the affected ear. Fluid cultures in the middle ear are frequently negative, although fluid overflows have been remitted more quickly in children treated with antibiotics than in control groups in some clinical trials. Adenoidectomy, myringotomy or timpanostomy tubes have been shown to reduce the duration of fluid persistence in some children.
I'll complete the otitis with a few elements about chronic suppurated otitis media. Patients with chronic suppurated otitis media experience chronic purulent secretions that leak through the perforated tympanic membrane. Patients with chronic suppurated otitis media fall into two categories: those with cholestatoms and those without. In both children and adults, aerobic cultures in the aurical secretion show a high percentage of S. aureus, P. aeruginosa and enteric gram negative bacilli (Klebsiella, Escherichia Coli, Proteus).
In 50% of cases anaerobics, Prevotella, Fusobacterium, Porphyromonas and some species of Bacteroides are highlighted, usually in mixed crops with aerobics. The CT examination should be used to exclude a surgically treated outbreak, such as an infected cholestatom or mastoid seizure.
Surgical drainage of infected areas of the middle ear followed by prolonged local administration of antibiotic drops was the main method of treatment for suppurated chronic otitis media. Recent reports on nonsurgical treatment of suppurated otitis media in children without cholestatom, with intravenous antibiotics chosen on the basis of crop results, are however encouraging. Tuberculosis otitis media, a rare but commonly misdiagnosed cause of suppurated chronic otitis media, is characterized by multiple perforations of the tympanic membrane, extensive granulation tissue and severe hearing loss. Anti-tuberculosis treatment will be given.
Let's talk a little bit about mastoiditis now. Mastoid is the portion of the temporal bone located behind the ear, which contains a system of pneumatic cells in the form of honeycomb, wallpapered with respiratory epithelium. These pneumatic cells communicate with the middle ear. The existence of a fluid in the middle ear, a prelude to otitis media, is almost always accompanied by the existence of a fluid in the mastoid. True mastoiditis, however, has become a rarity in the antibiotic era, probably due to the prompt treatment of otitis media.
Mastoiditis is characterized by the erosion of bone septums between mastoid pneumatic cells. Patients with acute mastoiditis experience pain, tenderness and swelling in the mastoid. In the case of subperiostal abscess or cellulite, the ear flag is pushed outwards and forward. CT can highlight bone destruction or a drainable mastoid abscess. Data on mastoid bacteriology varied.
Some cases involve microorganisms similar to those involved in OMA (S. pneumoniae, H. influenzae), others can be attributed to S. aureus and gram negative bacilli, including Pseudomonas. Ideally, treatment should be guided by the results of cultures in the middle ear fluid obtained by timpanocentesis. Initial treatment with broad-spectrum antibiotics, such as ticarcillin/ clavulanate plus gentamicin intravenously, may subsequently be restricted.
At the end of this post I will present something about the complications of otitis media and mastoiditis. Extracranial complications include hearing leave, labyrinthitis with consecutive vertigo and facial nerve paralysis. Other complications of mastoiditis occur when the infection spreads under the period of the temporal bone, producing a subperiostal abscess or when it exceeds the tip of the mastoid, generating a deep neck abscess in the sternocleidomastoid muscle (Bezold's abscess). Intracranial complications include epidural abscess, thrombophlebitis of the dural veins (usually of the sigmoid sinus), meningitis and cerebral abscess.
Tomorrow we'll talk about oral tract and pharynx infections.
Treatment consists in the application of warm compresses and intravenous administration of active antibiotics against S. aureus and other streptococci. Pericondritis, an infection of the ear pericondr, is commonly accompanied by infection of the cartilage of the outer ear (condritis). Disruption associated with blood supply to cartilage may cause ear deformity. The ear pavilion is swollen, warm, hyperemic and extremely sensitive, the earlobe is usually spared.
The most common history is burns, frostbite or major ear trauma (e.g. after boxing). Pseudomonas aeruginosa and S. aureus are the most common pathogens. Pericondritis should be treated with antibiotics such as ticarcillin/ clavulanic acid intravenously with ciprofloxacin orally for at least 4 weeks. Incision and drainage can be useful for crop production and for infection resolution, which is often slow. This infection should be distinguished from recurrent pericondritis which is a rheumatological condition.
Let's move on to external otitis. The external auditory duct is approximately 2.5 cm long and is lined with skin. Underlying the skin, in the lateral half of the conduction there is cartilage, and in the medial half, temporal bone. The skin in the bone portion of the duct has no subcutaneous layer and is attached directly to the periosteum, which is an important feature for the pathogenicity of invasive external otitis.
Cerumen secreted by glands acidifies the conduction and suppresses the multiplication of bacteria. However, the uncut skin and moisture in the duct make it extremely sensitive to P. aeruginosa, a hydrofilal organism. Acute external otitis or swimmer's ear occurs most frequently in the summer and may be due to decreased acidity of the auditory conduction, with consecutive bacterial overdevelopment. The ear is itchy and painful, and the auditory conduction is swollen and hyperemic. The most common pathogens are P. aeruginosa, S. aureus or other streptococci.
Treatment consists in cleaning the ear with mixtures of acetic acid alcohol and in topical administration of antibiotics in the form of ear drops with polymixin-neomycin. Herpes zoster in the auditory conduction produces severe otalgia and is often accompanied by ipsilateral facial paralysis due to damage to the genicular ganglion of the cranial nerve VII (Ramsay Hunt syndrome).
Recent data suggest that intravenous acyclovir treatment reduces the incidence of permanent facial paralysis, but no results of relevant clinical studies have been published. Conical external otitis causes pruritus to a greater extent than otalgia and is often due to irritation by repeated minor trauma to the duct (e.g. scratching the ear or the use of cotton wool sticks) or by draining a chronic infection from the middle ear.
In the latter case, treating chronic otitis media with antibiotics will also solve the problem of external otitis. Invasive external otitis ("malignant") is a potentially life-threatening infection, usually caused by P. aeruginosa which, starting from the external auditory duct, slowly invades adjacent soft tissues, mastoid, temporal bone and eventually spreads to the base of the skull. It occurs mainly in diabetic patients whose diabetes, unlike that of patients with mucormycosis, is usually well controlled.
Often there is a history of otalgia and otorrhea lasting several months. The physical examination reveals an edematized conduction, with granulation tissue in the posterior wall (at the cartilage-bone junction). In some cases patients have trimus or partial facial paresis (cranial nerve VII). Also, sometimes the cranial nerves IX, X and XI are affected. Signs of intradural damage, such as meningitis, temporal lobe infection or cerebral abscess are rarely encountered. Fever is rarely found in malignant external otitis. and when it does, it usually has low values.
Laboratory tests usually show a normal number of leukocytes, but a high value of VSH. TC and MRI examinations are essential for determining the extent of bone and soft tissue extension, helping the otorinolaringologist surgeon (ORL) to decide on optimal biopsy localization.
Cultures in the secretion of the external auditory duct are not always eloquent and in almost all cases, antibiotic therapy should not be started before histopathological examination and through cultures of a specimen of deep tissue. After this specimen has been taken, empirical intraoperative intravenous antibiotic therapy with active antibiotics against Pseudomonas may be initiated. P. aeruginosa is the pathogen involved in over 95% of cases, and the rest of the pathogens include Staphylococcus epidermitis, Aspergillus, Fusobacterium and Actinomyces.
Intravenous antibiotic treatment should be continued for 6 to 8 weeks in advanced cases (in early cases, if cultures show a strain of cypradrloxacine-sensitive Pseudomonas, the 2 weeks of antibiotic treatment in combination intravenously may be followed by oral monotherapy with ciprofloxacin).
It's the turn of the average otitis, and I'm going to start with acute otitis media. The middle ear communicates with the nasopharynx through Eustachio's tube. When the trunk gets stuck, in the middle ear and mastoid cavities, fluid accumulates, which constitutes a culture medium conducive to any bacteria present.
Acute otitis media (OMA) or middle ear infection may result. Viral infections of the upper respiratory tract, which can produce edema of the mucosa of Eustachio's tube, often precede or accompany episodes of OMA. Otitis media, similar to respiratory tract infections, is more common during autumn, winter and spring, and the incidence decreases with age (more than two-thirds of children under 3 years of age had at least one episode of OMA and the prevalence among adults is only 0.25%).
Symptomatology includes otalgia, fever and hearing-so-called. On otoscopic examination, the tympanic membrane shows decreased movements at instillation and usually appears red, opaque, bulging or retracted. Occasionally spontaneous perforations of the tympanic membrane and otorea are observed. For paediatric cases, OMA bacteriology was defined: S. pneumoniae (35%), H. influenzae (25%) and M. catarrhalis (15%) are the microorganisms most commonly found in newborns (group B streptococcus and gram-negative bacilli are important for OMA etiology in newborns). In a quarter of pediatric cases, viruses are found, either isolated or in combination with bacteria.
Small-scale studies in IMA adults have shown S. pneumoniae (21%) and H. influenzae (26%) as the most commonly encountered pathogens. Approximately 90% of H. influenzae infections are due to unclassified strains, those due to type B may be associated with bacteremia or meningitis.
Treatment of otitis media is empirical, diagnostic timpanocentesis being indicated only for patients with toxic status, immunodepressed patients or those with infections refractory to the initial treatment. Although about one-third of H. influenzae strains and at least three-quarters of M. catarrhalis strains produce b-lactamase, most specialists believe that amoxicillin treatment is effective in routine cases.
Other active medicines against most b-lactamase-producing strains are amoxicillin/ clavulanate, trimetoprim-sulfamethoxazole, erythromycin-sulfixazole, clarithromycin and 2nd generation cephalosporins. Penicillin resistance of pneumococcus, an increasingly important problem, is not mediated by b-lactamase.
Resistant strains may respond to treatment with erythromycin or sulfamides but serious infections require intravenous treatment with vancomycin or cephalosporin 3rd generation. Adjuvant treatment of OMA with antihistamines does not bring any benefit. Recurrent episodes of OMA in children are due to the same pathogenic germs that cause the primary episode of OMA (S. pneumoniae, H. influenzae and M. catarrhalis). Most early recurrences (75%) are not, however, relapses, but are due to different microorganisms or different strains of the same microorganism that produced the original episode.
The aspects of OMA recurrences in adults are probably similar, but have not yet been well studied. Recurrent OMA treatment should include active medicines against b-lactamase-producing strains. Patients with frequent recurrences (e.g. 3 episodes within 6 months) may benefit from antibiotic prophylaxis with amoxicillin or sulfisoxazole one dose per day during the winter months, although the risk benefit ratio should be weighed in selecting new resistant strains.
Medium otitis with fluid overflow or mean severe otitis is characterized by the persistence of fluid in the middle ear for several months, with no other signs of infection. This condition is associated with a hearing leave of 25 dB in the affected ear. Fluid cultures in the middle ear are frequently negative, although fluid overflows have been remitted more quickly in children treated with antibiotics than in control groups in some clinical trials. Adenoidectomy, myringotomy or timpanostomy tubes have been shown to reduce the duration of fluid persistence in some children.
I'll complete the otitis with a few elements about chronic suppurated otitis media. Patients with chronic suppurated otitis media experience chronic purulent secretions that leak through the perforated tympanic membrane. Patients with chronic suppurated otitis media fall into two categories: those with cholestatoms and those without. In both children and adults, aerobic cultures in the aurical secretion show a high percentage of S. aureus, P. aeruginosa and enteric gram negative bacilli (Klebsiella, Escherichia Coli, Proteus).
In 50% of cases anaerobics, Prevotella, Fusobacterium, Porphyromonas and some species of Bacteroides are highlighted, usually in mixed crops with aerobics. The CT examination should be used to exclude a surgically treated outbreak, such as an infected cholestatom or mastoid seizure.
Surgical drainage of infected areas of the middle ear followed by prolonged local administration of antibiotic drops was the main method of treatment for suppurated chronic otitis media. Recent reports on nonsurgical treatment of suppurated otitis media in children without cholestatom, with intravenous antibiotics chosen on the basis of crop results, are however encouraging. Tuberculosis otitis media, a rare but commonly misdiagnosed cause of suppurated chronic otitis media, is characterized by multiple perforations of the tympanic membrane, extensive granulation tissue and severe hearing loss. Anti-tuberculosis treatment will be given.
Let's talk a little bit about mastoiditis now. Mastoid is the portion of the temporal bone located behind the ear, which contains a system of pneumatic cells in the form of honeycomb, wallpapered with respiratory epithelium. These pneumatic cells communicate with the middle ear. The existence of a fluid in the middle ear, a prelude to otitis media, is almost always accompanied by the existence of a fluid in the mastoid. True mastoiditis, however, has become a rarity in the antibiotic era, probably due to the prompt treatment of otitis media.
Mastoiditis is characterized by the erosion of bone septums between mastoid pneumatic cells. Patients with acute mastoiditis experience pain, tenderness and swelling in the mastoid. In the case of subperiostal abscess or cellulite, the ear flag is pushed outwards and forward. CT can highlight bone destruction or a drainable mastoid abscess. Data on mastoid bacteriology varied.
Some cases involve microorganisms similar to those involved in OMA (S. pneumoniae, H. influenzae), others can be attributed to S. aureus and gram negative bacilli, including Pseudomonas. Ideally, treatment should be guided by the results of cultures in the middle ear fluid obtained by timpanocentesis. Initial treatment with broad-spectrum antibiotics, such as ticarcillin/ clavulanate plus gentamicin intravenously, may subsequently be restricted.
At the end of this post I will present something about the complications of otitis media and mastoiditis. Extracranial complications include hearing leave, labyrinthitis with consecutive vertigo and facial nerve paralysis. Other complications of mastoiditis occur when the infection spreads under the period of the temporal bone, producing a subperiostal abscess or when it exceeds the tip of the mastoid, generating a deep neck abscess in the sternocleidomastoid muscle (Bezold's abscess). Intracranial complications include epidural abscess, thrombophlebitis of the dural veins (usually of the sigmoid sinus), meningitis and cerebral abscess.
Tomorrow we'll talk about oral tract and pharynx infections.
A restful Sunday, full of
understanding, love and gratitude!
Dorin, Merticaru