STUDY - Technical - New Dacian's Medicine
Infections
of the oral cavity and pharynx
Translation Draft
I'm going to start with oral infections.
I'm going to start with oral infections.
The oral cavity extends
from the lips to the circumvalence papillae of the tongue and is
massively colonized with viridans and anaerobic streptococci.
These microorganisms can cause a number of infections at this
level. Gingivitis is a condition of the gums, the incipient form
of periodontal disease.
Anaerobics in the oral cavity, especially gram-negative anaerobic strains of the type Prevotella intermedia, are the most common pathogens. Patients with Vincent angina, also called acute necrotizing ulcerative gingivitis or mouth with grooves, have halitosis and ulceration of the interdental papillae. The cause is oral anaerobics, and treatment with oral penicillin plus metronizadol or just clindamicin is effective for both this condition and gingivitis.
Angina Ludwig is a rapidly progressive, life-threatening cellulite of sublingual and submandibular space, which usually begins at the level of an infected lower molar. Patients are feverish and may experience secretion leaks, which they cannot swallow. Hard edema with woody consistency from the sublingual region pushes the upper and posterior tongue, sometimes causing obstruction of the airways.
Treatment with intravenous antibiotics, active against streptococcus and oral anaerobics (e.g. ampicillin/ sulbactam or penicillin in high dose plus metronizadol) and airway monitoring are essential. Intubation or tracheostomy may be required. It is usually necessary to surgically open the compartments of infected tissue.
Noma or cancrum oris is a fulminant gangrenous infection of oral and facial tissues that occurs in debilitated patients and is extremely common in children. Debuting as a necrotic ulcer in the mandibular gingival tissue, noma is produced by anaerobics in the oral cavity, especially by fusospiral organisms (e.g. Fusobacterium nuclearatum).
Treatment is done with high doses of penicillin, debridement and correction of malnutrition. Herpes simplex frequently causes afebrile inflammation in the lips, but can also produce painful blisters on the tongue and mouth lining. The primary infection may require intravenous hydration and should be treated with acyclovir. Aphthases, caused by excessive development of fungi (usually Candida species) occur in immunodepressed patients and will be treated with topical antifungal solutions (e.g. nistatin) or oral fluconazole.
Pharyngitis, in most cases (supposedly), has viral cause. Many occur as a result of common colds caused by rhinovirus, coronavirus or paraflu virus. Patients have irritated or painful throat, as well as chorysis or cough. The pharynx is inflamed and edematos, but there is no exudation. Influenza virus and adenovirus can cause extremely severe neck pain with fever and myalgia.
In infections with these latter two viruses, there is erythema and pharyngeal edema (however, adenovirus infection usually causes an exudate, thus mimicing streptococcal pharyngitis). Infectious mononucleosis due to Epstein-Barr virus often causes severe neck pain. In half of cases of mononucleosis, exudative pharyngitis or tonsillitis is found, which can also mimic streptococcal infection.
Herpangina, produced by the coxsackie virus, is characterized by fever, sore throat, myalgia and the presence of vesicular enanthema in the soft palate, between the uvula and the tonsils. There are usually two to six lesions, which begin as small papules, which turn into blisters and subsequently ulcerate. Fever and pharyngitis without exudation are common symptoms of acute retroviral syndrome, which occurs a few weeks after HIV infection. The most important bacterial agent of pharyngitis is Streptococcus group A (Streptococcus pyrogenes).
This microorganism is responsible for about 15% of all cases of pharyngitis and can cause significant complications, both suppurative (periamigdalian and retropharyngeal abscess) and non-suppurative (scarlatine, streptococcal toxic shock syndrome, rheumatic fever and acute poststreptococcal glomerulonephritis). Fever, severe sore throat, cervical adenopathy and inflammation of the tonsils and pharynx (which are covered by exudate) are classic symptoms.
However, many cases of streptococcal pharyngitis are moderate, with minimal erythema and without exudation and mineta pharyngitis from the usual cold. Although some patients may actually have viral pharyngitis and are only colonized with group A streptococci, they should still be treated for the alleged streptococcal pharyngitis.
Diagnosis is made with the help of cultures, and lately rapid antigenic tests have become available (these tests are specific but not very sensitive, a positive test can be considered equivalent of a positive culture, whereas a negative test requires confirmation through cultures).
10 days oral treatment with penicillin (or erythromycin) is required in patients with penicillin allergy, with shorter duration treatment not resulting in the eradication of the micro-organism. An alternative with the same efficacy is a single intramuscular dose of benzatin penicillin.
Other active antibiotics against streptococcus (e.g. cephalexin, amoxicillin, cefuroxime or cerfprozil) may also be used, although studies on the prophylaxis of acute articular rheumatism are only available for penicillin. Other bacterial causes of pharyngitis include Streptococcus group C and G, Neisseria gonorrhoeae, Arcanobacterium haemolyticum, Yersinia enterocolica and, very rarely, Corynebacterium diphtheriae.
Mycoplasma pneumoniae and C. pneumoniae can also produce pharyngitis. Untreated streptococcal pharyngitis may be followed by periamigdalian abscess (amygdalitis. Anaerobics in the oral cavity also play a role in tonsillitis. Patients experience severe neck pain and have a "hot potato" voice.
Physical examination reveals pronounced unilateral periamigdalswelling swelling and erythema with uvula deflection. Immediate aspiration by an otorinolaringologist is required in combination with antibiotic treatment with penicillin plus metronidazole, clindamicin or ampicillin/ sulbactam.
Now let's move on to laryngitis, croup and epiglotitis.
Laringitis is characterized by hoarseness. Most cases of acute laryngitis are caused by viruses (rinoviruses, influenza viruses, paraflu viruses, coxsackie virus, adenoviruses or respiratory sincithvirus). Acute laryngitis may also be associated with Streptococcus group A and M. catarrhalis.
Laryngitis should be differentiated from epiglotitis. The purpose of treatment is only to improve symptoms, except in cases where the cultures in the throat are positive for Streptococcus group A (in which case penicillin should be used) or possibly for M. catarrhalis (where erythromycin should be used).
Chronic laryngitis of infectious etiology is rare and should be differentiated from hoarseness from neoplastic etiology. Tuberculosis laryngitis can be confused with laryngeal cancer when examined by direct laryngoscopy. Laryngeal and supraglotic lesions include hyperemia and thickening of the mucosa, nodules and ulcerations.
In a recent study, a history of fever and night sweats was rare, and lung radiological examinations most commonly revealed apical thickening and fibrosis. Biopsy highlights granulomas with acid-resistant bacilli. Cultures should be carried out to confirm the diagnosis and assess the sensitivity of the pathogenic germ.
Laryngeal tuberculosis is highly contagious and should be treated with the same precautions and therapeutic measures as active lung disease. Fungal infections that cause laryngitis include histoplasmosis, blastomycosis and candidiasis. Histoplasma and Blastomyces can produce laryngeal nodules, with or without ulceration. In addition to aphtha, Candida may cause laryngitis in immunodepressed patients or in patients with chronic mucocutaneous candidiasis.
Acute crup or laryngotraheobronchitis is an infection of the upper and lower respiratory tract that produces an important subglotic edema. It mainly affects children between 2 and 3 years of age and usually occurs 1 to 2 days after the onset of upper respiratory tract infection. Symptomatology includes fever, hoarseness, barking cough and respiratory strichor.
The most common etiological agent is the paraflu virus, although the crust can also be produced by other respiratory viruses (e.g. influenza virus or respiratory sincithial virus) and M. pneumoniae. The crust must be particularly epiglotted. Epiglotitis usually evolves faster and produces a toxic state. Neck X-rays can be very helpful, but they don't definitely rule out epiglottitis.
In croup, antero-posterior x-rays of the neck highlight subglotic edema (the sign of "clepsy"), in epiglotitis the lateral incidence X-rays highlighting a thickened epiglottis. Patients with severe forms of croup should be hospitalized, monitored by pulse-oxymetry for hypoxemia and closely monitored if airway obstruction would require intubation. Humidification is commonly indicated, but few controlled clinical trials have assessed its benefits. Nebulized adrenaline gives patients with marked stidor a temporary improvement (2 hours), but these patients should be observed for the detection of recurrent edema. Glucocorticoid therapy is controversial.
It's the turn of the epiglotitis. Acute epiglotitis (superglotitis) is a life-threatening, rapidly progressive cellulite of the epiglottis, which can cause complete obstruction of the airways. Debuts with cellulite of the space between the base of the tongue and the epiglottis, pushing the posterior epiglottis. Subsequently, the epiglottis also becomes snowed, threatening the airways. Epiglotitis is a condition very common in children 2 to 4 years of age, but it can also affect older children or adults. With the advent of the vaccine against H. influenzae (1985), the total incidence of epiglotitis in children decreased.
Classically, the small child with epiglottitis presents fever, irritability, dysphonia and dysphagia, which started a few hours ago, is bent forward and has abundant oral secretions. Some adolescents and adults may experience less fulminant clinical manifestations, with symptoms (especially sore throat) beginning one or two days ago. Adults may experience dyspnoea (25%), abundant oral secretions (15%) and stidor (10%).
Epiglotitis is a medical emergency because obstruction, because airway obstruction can occur suddenly. X-rays in the lateral incidence of the neck that highlight an increased volume epiglottis (the "thumb" sign), are useful if they are positive, but can also be false negatives. The value of obtaining these X-rays has also been called into question, as X-rays may critically delay measures to ensure airway permeability.
Direct viewing of the pharynx with a tongue presser is not indicated, as it can immediately cause laryngospasm and airway obstruction. On the other hand, the child suspected of epiglotitis should be transported (in an orthostatic position) to the operating room for the purpose of examining the epiglottis with the fibre optic laryngoscope, taking all necessary measures for immediate control of the airways. If the epiglottis appears from a cherry-red, an endotracheal probe without a sleeve will be inserted.
Diagnosis in adults is also made by directly viewing the epiglottis with a flexible fiber optic laryngoscope, also only after the necessary measures have been taken to ensure the permeability of the airways.
All patients should be carefully monitored in an intensive care unit and treated with active antibiotics against H. influenzae. This microorganism is responsible for almost all pediatric cases and is isolated from the blood in about 100% of cases. In adults, blood cultures are positive in about 25% of cases, all of which are due to H. influenzae.
Other pathogenic germs isolated from the pharynx of adults with epiglotitis include Haemophilus parainfluenzae, S. pneumoniae, Streptococcus group A and (rarely) S. aureus, however, the correlation between pharyngeal and epiglottic courts is not clear. In children, cefuroxin, ceftriaxone, ampicillin/ sulbactam or trimetoprim-sulfamethoxazole may be administered intravenously. If the patient with Epiglotitis with H. influenzae had family contacts including an unvaccinated child under the age of 4, all family members including the patient should be treated prophylactically with rifampicin for the purpose of eradicating the h. influenzae carrier status.
Deep throat infections can threaten life by compromising the airways, affecting the advent of carotid or by disseminating in the mediastinum. Submandibular space infections have been previously treated (angina Ludwig from oral tract infections). I'll still only treat infections of the pharyngeal lateral space.
The lateral pharyngeal space, also called the parapharyngeal or pharyngomaxillary space, is located in the super-lateral portion of the neck and extends from the hyoid bone to the base of the skull. It is deeply arranged towards the lateral wall of the pharynx, lateral lymthal and the adventiness of the carotid and medial to the parotid gland. Infection of this space may be a consequence of tonsillitis, pharyngitis with adenoid alverida, parotiditis, mastoiditis or periodontal infections.
At presentation, most patients have toxic status, fever, sore throat, odinophagia and leukocytosis. The limited infection saddle the posterior (retrostiloid) portion of the lateral pharyngeal space causes swelling of the lateral wall of the pharynx, which may go unnoticed because it is behind the palatopharyngeal arch. The damage to the anterior portion of the lateral pharyngeal space causes the medial displacement of the tonsil, swelling of the parotid and trismus glands. Neck stiffness or torcolis on the contralateral side may occur.
The diagnosis is confirmed by contrast CT. Treatment includes ensuring airway permeability, surgical drainage in the operating room and intravenous administration of active antibiotics against streptococcus and oral anaerobics (e.g. ampicillin/ sulbactam).
Most complications result from damage to the carotid fascia and the vessels containing them. These complications are frequently fatal and include tromoboflebitis of the jugular vein, erosion of the carotid artery and mediastinitis. The thrombophlebitis of the jugular vein is characterized by high fever, chills and painful sensitivity of the neck at the angle of the mandible. Erosion of the carotid artery is usually reported by small repeated hemorrhages in the oral cavity. Adiacent cranial nerve damage causes ipsilateral Horner syndrome, hoarseness or unilateral tongue paralysis. Dissemination of infection along the carotid fascia to the posterior mediastinum produces mediastinitis with a mortality of 50%. MRI is useful in differentiating carotid and jugular damage.
Let me introduce you to a few things about retropharyngeal space infection. The retropharyngeal space lies between the pharynx and the paravertebral fascia and extends from the base of the skull to the mediastinum. Infection of this space may result from the dissemination of an infection of the lateral pharyngeal space or by the lymphatic dissemination of an infection with a more cranial localization (posterior sinuses, adenoid formations, nasopharynx) to the retropharyngeal lymph nodes.
Retropharyngeal abscess is most common in infants and young children, probably because later retropharyngeal ganglia evolve. Retropharyngeal abscess may also occur as a result of trauma to the posterior pharynx (e.g. endoscopy in adults, perforations due to falls in children, etc.) or through the anterior dissemination of infection in cervical osteomyelitis.
Symptoms include fever, dysphagia and marked odinophagia and "potato-hot" voice. Physical examination may reveal abundant oral secretion, oral stiffness and swelling of the posterior pharyngeal wall. Advanced forms show dyspnea and stidor.
The diagnosis can be confirmed by X-ray or CT of the lateral soft tissues of the neck. Treatment requires ensuring airway permeability and emergency surgical drainage. Antibiotics should be given intravenously, the antibiotics chosen being necessary to be active against streptococcus, oral anaerobics, S. aureus and H. influenzae (e.g. only ampicillin/ sulbactam or clindamicin with ceftriaxone). Potential complications include airway obstruction, intraoral rupture of the abscess with consecutive aspiration pneumonia and mediastinitis.
Anaerobics in the oral cavity, especially gram-negative anaerobic strains of the type Prevotella intermedia, are the most common pathogens. Patients with Vincent angina, also called acute necrotizing ulcerative gingivitis or mouth with grooves, have halitosis and ulceration of the interdental papillae. The cause is oral anaerobics, and treatment with oral penicillin plus metronizadol or just clindamicin is effective for both this condition and gingivitis.
Angina Ludwig is a rapidly progressive, life-threatening cellulite of sublingual and submandibular space, which usually begins at the level of an infected lower molar. Patients are feverish and may experience secretion leaks, which they cannot swallow. Hard edema with woody consistency from the sublingual region pushes the upper and posterior tongue, sometimes causing obstruction of the airways.
Treatment with intravenous antibiotics, active against streptococcus and oral anaerobics (e.g. ampicillin/ sulbactam or penicillin in high dose plus metronizadol) and airway monitoring are essential. Intubation or tracheostomy may be required. It is usually necessary to surgically open the compartments of infected tissue.
Noma or cancrum oris is a fulminant gangrenous infection of oral and facial tissues that occurs in debilitated patients and is extremely common in children. Debuting as a necrotic ulcer in the mandibular gingival tissue, noma is produced by anaerobics in the oral cavity, especially by fusospiral organisms (e.g. Fusobacterium nuclearatum).
Treatment is done with high doses of penicillin, debridement and correction of malnutrition. Herpes simplex frequently causes afebrile inflammation in the lips, but can also produce painful blisters on the tongue and mouth lining. The primary infection may require intravenous hydration and should be treated with acyclovir. Aphthases, caused by excessive development of fungi (usually Candida species) occur in immunodepressed patients and will be treated with topical antifungal solutions (e.g. nistatin) or oral fluconazole.
Pharyngitis, in most cases (supposedly), has viral cause. Many occur as a result of common colds caused by rhinovirus, coronavirus or paraflu virus. Patients have irritated or painful throat, as well as chorysis or cough. The pharynx is inflamed and edematos, but there is no exudation. Influenza virus and adenovirus can cause extremely severe neck pain with fever and myalgia.
In infections with these latter two viruses, there is erythema and pharyngeal edema (however, adenovirus infection usually causes an exudate, thus mimicing streptococcal pharyngitis). Infectious mononucleosis due to Epstein-Barr virus often causes severe neck pain. In half of cases of mononucleosis, exudative pharyngitis or tonsillitis is found, which can also mimic streptococcal infection.
Herpangina, produced by the coxsackie virus, is characterized by fever, sore throat, myalgia and the presence of vesicular enanthema in the soft palate, between the uvula and the tonsils. There are usually two to six lesions, which begin as small papules, which turn into blisters and subsequently ulcerate. Fever and pharyngitis without exudation are common symptoms of acute retroviral syndrome, which occurs a few weeks after HIV infection. The most important bacterial agent of pharyngitis is Streptococcus group A (Streptococcus pyrogenes).
This microorganism is responsible for about 15% of all cases of pharyngitis and can cause significant complications, both suppurative (periamigdalian and retropharyngeal abscess) and non-suppurative (scarlatine, streptococcal toxic shock syndrome, rheumatic fever and acute poststreptococcal glomerulonephritis). Fever, severe sore throat, cervical adenopathy and inflammation of the tonsils and pharynx (which are covered by exudate) are classic symptoms.
However, many cases of streptococcal pharyngitis are moderate, with minimal erythema and without exudation and mineta pharyngitis from the usual cold. Although some patients may actually have viral pharyngitis and are only colonized with group A streptococci, they should still be treated for the alleged streptococcal pharyngitis.
Diagnosis is made with the help of cultures, and lately rapid antigenic tests have become available (these tests are specific but not very sensitive, a positive test can be considered equivalent of a positive culture, whereas a negative test requires confirmation through cultures).
10 days oral treatment with penicillin (or erythromycin) is required in patients with penicillin allergy, with shorter duration treatment not resulting in the eradication of the micro-organism. An alternative with the same efficacy is a single intramuscular dose of benzatin penicillin.
Other active antibiotics against streptococcus (e.g. cephalexin, amoxicillin, cefuroxime or cerfprozil) may also be used, although studies on the prophylaxis of acute articular rheumatism are only available for penicillin. Other bacterial causes of pharyngitis include Streptococcus group C and G, Neisseria gonorrhoeae, Arcanobacterium haemolyticum, Yersinia enterocolica and, very rarely, Corynebacterium diphtheriae.
Mycoplasma pneumoniae and C. pneumoniae can also produce pharyngitis. Untreated streptococcal pharyngitis may be followed by periamigdalian abscess (amygdalitis. Anaerobics in the oral cavity also play a role in tonsillitis. Patients experience severe neck pain and have a "hot potato" voice.
Physical examination reveals pronounced unilateral periamigdalswelling swelling and erythema with uvula deflection. Immediate aspiration by an otorinolaringologist is required in combination with antibiotic treatment with penicillin plus metronidazole, clindamicin or ampicillin/ sulbactam.
Now let's move on to laryngitis, croup and epiglotitis.
Laringitis is characterized by hoarseness. Most cases of acute laryngitis are caused by viruses (rinoviruses, influenza viruses, paraflu viruses, coxsackie virus, adenoviruses or respiratory sincithvirus). Acute laryngitis may also be associated with Streptococcus group A and M. catarrhalis.
Laryngitis should be differentiated from epiglotitis. The purpose of treatment is only to improve symptoms, except in cases where the cultures in the throat are positive for Streptococcus group A (in which case penicillin should be used) or possibly for M. catarrhalis (where erythromycin should be used).
Chronic laryngitis of infectious etiology is rare and should be differentiated from hoarseness from neoplastic etiology. Tuberculosis laryngitis can be confused with laryngeal cancer when examined by direct laryngoscopy. Laryngeal and supraglotic lesions include hyperemia and thickening of the mucosa, nodules and ulcerations.
In a recent study, a history of fever and night sweats was rare, and lung radiological examinations most commonly revealed apical thickening and fibrosis. Biopsy highlights granulomas with acid-resistant bacilli. Cultures should be carried out to confirm the diagnosis and assess the sensitivity of the pathogenic germ.
Laryngeal tuberculosis is highly contagious and should be treated with the same precautions and therapeutic measures as active lung disease. Fungal infections that cause laryngitis include histoplasmosis, blastomycosis and candidiasis. Histoplasma and Blastomyces can produce laryngeal nodules, with or without ulceration. In addition to aphtha, Candida may cause laryngitis in immunodepressed patients or in patients with chronic mucocutaneous candidiasis.
Acute crup or laryngotraheobronchitis is an infection of the upper and lower respiratory tract that produces an important subglotic edema. It mainly affects children between 2 and 3 years of age and usually occurs 1 to 2 days after the onset of upper respiratory tract infection. Symptomatology includes fever, hoarseness, barking cough and respiratory strichor.
The most common etiological agent is the paraflu virus, although the crust can also be produced by other respiratory viruses (e.g. influenza virus or respiratory sincithial virus) and M. pneumoniae. The crust must be particularly epiglotted. Epiglotitis usually evolves faster and produces a toxic state. Neck X-rays can be very helpful, but they don't definitely rule out epiglottitis.
In croup, antero-posterior x-rays of the neck highlight subglotic edema (the sign of "clepsy"), in epiglotitis the lateral incidence X-rays highlighting a thickened epiglottis. Patients with severe forms of croup should be hospitalized, monitored by pulse-oxymetry for hypoxemia and closely monitored if airway obstruction would require intubation. Humidification is commonly indicated, but few controlled clinical trials have assessed its benefits. Nebulized adrenaline gives patients with marked stidor a temporary improvement (2 hours), but these patients should be observed for the detection of recurrent edema. Glucocorticoid therapy is controversial.
It's the turn of the epiglotitis. Acute epiglotitis (superglotitis) is a life-threatening, rapidly progressive cellulite of the epiglottis, which can cause complete obstruction of the airways. Debuts with cellulite of the space between the base of the tongue and the epiglottis, pushing the posterior epiglottis. Subsequently, the epiglottis also becomes snowed, threatening the airways. Epiglotitis is a condition very common in children 2 to 4 years of age, but it can also affect older children or adults. With the advent of the vaccine against H. influenzae (1985), the total incidence of epiglotitis in children decreased.
Classically, the small child with epiglottitis presents fever, irritability, dysphonia and dysphagia, which started a few hours ago, is bent forward and has abundant oral secretions. Some adolescents and adults may experience less fulminant clinical manifestations, with symptoms (especially sore throat) beginning one or two days ago. Adults may experience dyspnoea (25%), abundant oral secretions (15%) and stidor (10%).
Epiglotitis is a medical emergency because obstruction, because airway obstruction can occur suddenly. X-rays in the lateral incidence of the neck that highlight an increased volume epiglottis (the "thumb" sign), are useful if they are positive, but can also be false negatives. The value of obtaining these X-rays has also been called into question, as X-rays may critically delay measures to ensure airway permeability.
Direct viewing of the pharynx with a tongue presser is not indicated, as it can immediately cause laryngospasm and airway obstruction. On the other hand, the child suspected of epiglotitis should be transported (in an orthostatic position) to the operating room for the purpose of examining the epiglottis with the fibre optic laryngoscope, taking all necessary measures for immediate control of the airways. If the epiglottis appears from a cherry-red, an endotracheal probe without a sleeve will be inserted.
Diagnosis in adults is also made by directly viewing the epiglottis with a flexible fiber optic laryngoscope, also only after the necessary measures have been taken to ensure the permeability of the airways.
All patients should be carefully monitored in an intensive care unit and treated with active antibiotics against H. influenzae. This microorganism is responsible for almost all pediatric cases and is isolated from the blood in about 100% of cases. In adults, blood cultures are positive in about 25% of cases, all of which are due to H. influenzae.
Other pathogenic germs isolated from the pharynx of adults with epiglotitis include Haemophilus parainfluenzae, S. pneumoniae, Streptococcus group A and (rarely) S. aureus, however, the correlation between pharyngeal and epiglottic courts is not clear. In children, cefuroxin, ceftriaxone, ampicillin/ sulbactam or trimetoprim-sulfamethoxazole may be administered intravenously. If the patient with Epiglotitis with H. influenzae had family contacts including an unvaccinated child under the age of 4, all family members including the patient should be treated prophylactically with rifampicin for the purpose of eradicating the h. influenzae carrier status.
Deep throat infections can threaten life by compromising the airways, affecting the advent of carotid or by disseminating in the mediastinum. Submandibular space infections have been previously treated (angina Ludwig from oral tract infections). I'll still only treat infections of the pharyngeal lateral space.
The lateral pharyngeal space, also called the parapharyngeal or pharyngomaxillary space, is located in the super-lateral portion of the neck and extends from the hyoid bone to the base of the skull. It is deeply arranged towards the lateral wall of the pharynx, lateral lymthal and the adventiness of the carotid and medial to the parotid gland. Infection of this space may be a consequence of tonsillitis, pharyngitis with adenoid alverida, parotiditis, mastoiditis or periodontal infections.
At presentation, most patients have toxic status, fever, sore throat, odinophagia and leukocytosis. The limited infection saddle the posterior (retrostiloid) portion of the lateral pharyngeal space causes swelling of the lateral wall of the pharynx, which may go unnoticed because it is behind the palatopharyngeal arch. The damage to the anterior portion of the lateral pharyngeal space causes the medial displacement of the tonsil, swelling of the parotid and trismus glands. Neck stiffness or torcolis on the contralateral side may occur.
The diagnosis is confirmed by contrast CT. Treatment includes ensuring airway permeability, surgical drainage in the operating room and intravenous administration of active antibiotics against streptococcus and oral anaerobics (e.g. ampicillin/ sulbactam).
Most complications result from damage to the carotid fascia and the vessels containing them. These complications are frequently fatal and include tromoboflebitis of the jugular vein, erosion of the carotid artery and mediastinitis. The thrombophlebitis of the jugular vein is characterized by high fever, chills and painful sensitivity of the neck at the angle of the mandible. Erosion of the carotid artery is usually reported by small repeated hemorrhages in the oral cavity. Adiacent cranial nerve damage causes ipsilateral Horner syndrome, hoarseness or unilateral tongue paralysis. Dissemination of infection along the carotid fascia to the posterior mediastinum produces mediastinitis with a mortality of 50%. MRI is useful in differentiating carotid and jugular damage.
Let me introduce you to a few things about retropharyngeal space infection. The retropharyngeal space lies between the pharynx and the paravertebral fascia and extends from the base of the skull to the mediastinum. Infection of this space may result from the dissemination of an infection of the lateral pharyngeal space or by the lymphatic dissemination of an infection with a more cranial localization (posterior sinuses, adenoid formations, nasopharynx) to the retropharyngeal lymph nodes.
Retropharyngeal abscess is most common in infants and young children, probably because later retropharyngeal ganglia evolve. Retropharyngeal abscess may also occur as a result of trauma to the posterior pharynx (e.g. endoscopy in adults, perforations due to falls in children, etc.) or through the anterior dissemination of infection in cervical osteomyelitis.
Symptoms include fever, dysphagia and marked odinophagia and "potato-hot" voice. Physical examination may reveal abundant oral secretion, oral stiffness and swelling of the posterior pharyngeal wall. Advanced forms show dyspnea and stidor.
The diagnosis can be confirmed by X-ray or CT of the lateral soft tissues of the neck. Treatment requires ensuring airway permeability and emergency surgical drainage. Antibiotics should be given intravenously, the antibiotics chosen being necessary to be active against streptococcus, oral anaerobics, S. aureus and H. influenzae (e.g. only ampicillin/ sulbactam or clindamicin with ceftriaxone). Potential complications include airway obstruction, intraoral rupture of the abscess with consecutive aspiration pneumonia and mediastinitis.
A week of the best,
wealthy and pleasant!
Dorin, Merticaru