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Overview

Fungal meningitis results from the infection of the meninges by fungi, most commonly cryptococcus. While cryptococcal meningitis occurs worldwide, other fungal meningitis are endemic to specific regions of the world.[1] Fungal meningitis usually affects immunocompromised patients like HIV patients and transplant recipients on chronic immunosuppression medications. The course of the disease is progressive and may lead to complications if a high dose long term treatment with antifungals are not initiated.[2]

Historical perspective

The first report of human cryptococcosis was published by Busse and Busckhe more than 100 years ago; 10 years later, it was identified as the cause of human meningitis. Cryptococcus neoformans, an encapsulated basidiomycetous yeast, represents one of the most common CNS pathogens encountered in clinical practice today. In 1661, Thomas Willis first described the inflammation of meninges and an epidemic of meningitis. In 1891, Heinrich Quincke provided an early analysis of CSF by introducing a new technique of lumbar puncture. Some specific historical feature usually surround the outbreak of rare causes of fungal meningitis. For example, outbreaks of fungal meningitis in 2002 with Exophiala dermatitidis and more recently in 2012 with Exserohilum rostratum were associated with contamination of compounded corticosteroids with resultant severe complications.[3][4][5] The 1980s witnessed an increase in the number of cases of cryptococcus meningitis in the United States and certain African countries largely due to HIV infection

Classification

Fungal meningitis is usually classified according to the causative organism if identified. It may also be additionally classified according to the severity and duration of the disease as mild, moderate, severe, acute, subacute, chronic and recurrent fungal meningitis.[6][7][8][9][10][11][12][13][14]

Pathophysiology

The pathophysiology of fungal meningitis is not very well studied however, it is known to have a lot of similarities with bacterial meningitis. Fungal meningitis usually occurs in immunocompromised patients. The initial step in fungal meningitis is the pulmonary exposure to the fungi by the inhalation of airborne fungal spores. The pulmonary infection is usually self limited and maybe asymptomatic. Fungal infections are not contagious so they do not spread from one person to another.With an associated impaired immune response the fungus may disseminate. For instance in cryptococcal infection, the fungus may remain dormant in the lungs until the immune system weakens and then can reactivate and disseminate to the CNS. Cryptococcus has predilection for CNS dessimination. Although this remains unclear, the presence of a receptor on glial cells for a ligand on the organism has been suggested to enhance its invasion.[15] Cryptococcal meningitis is most common due to the virulence factors of the organism that enhancing invasion of the blood brain barrier. These factors include: polysaccharide capsule which makes the organism withstand phagocytosis and host immune system, melanin production, ability to thrive at mammalian body temperatures, urease production and phospholipase production.[16][17][18][19][20][21][22][23][24] Once the fungi cross the blood brain barrier they cause an inflammation of the meninges and arachnoid space. The inflammation promotes cytokine release mainly tumor necrosis factor (TNF), interleukin 1, interleukin 2 , interleukin 6, interleukin 12, colony-stimulating factors, and interferon-λ.[25][26][27] The cytokines lead to modulation of host system resuting in fever, increase in the permeability of the blood brain barrier and subsequent cerebral edema and increase in the intracranial pressure. The increase in the permeability of the blood brain barrier is the cause of the observed elevation of the protein level in the cerebral spinal fluid.[28]

Causes

Fungal meningitis is initially caused by the inhalation of airborne fungal spores. The pulmonary infection is usually self limiting and can be asymptomatic. The most common cause of fungal infection is cryptococcus neoformans which is usually found in soil and bird excreta.[29] Other common causes of fungal meningitis include; Aspergillus spp., Blastomyces dermatitidis, Coccidioides immitis, Candida spp., Histoplasma capsulatum and Sporothrix schenckii.[30][31][32][2][33] Rarely, fungal meningitis may be caused by Xylohypha (formerly Cladosporium) trichoides, Curvularia, Mucor, Arthrographis kalrae, Pneumocystis jirovecii,[34][35] Cryptococcus albidus,[36], Alternaria spp,[37], Rhodotorula spp, [38] Acremonium spp,[39] Dreschlera spp,[40] Malassezia spp,[41] Scedosporium spp,[42] Arthrographis spp,[43] Blastoschizomyces,[44][45] Paecilomyces,[46][47] Aureobasidium,[48] Clavispora,[49] Ustilago,[50] Exophiala (Wangiella)[51] and Exserohilum[5]

Differentiating fungak meningitis from other Conditions

The differential diagnosis of fungal meningitis includes a range of medical conditions that can be broadly classified into infectious and non infectious. The cerebrospinal fluid analysis and radiological findings help distinguishing fungal meningitis from other causes of meningitis example bacterial meningeal infection, protozoal meningeal infection, viral meningeal infection, and non infectious causes.

Epidemiology and Demographics

While cryptococcus and candida infections occur worldwide, other fungal infections tend to cluster in specific geographical regions.[52][2] There is an increasing trend of fungal meningitis. This has been attributed to enlarging population of high-risk immunosuppressed patients, more successful pharmacological immunosuppression and chemotherapies, increase in numbers of patients living with human immunodeficiency virus (HIV) infection and the acquired immunodeficiency syndrome (AIDS), migration of susceptible persons into hyperendemic areas and aging of the population.[2][53] Cryptococcal meningitis occurs worldwide but it is highly prevalent in southeast Asia and southern and east Africa where the prevalence of HIV is high.[28] The incidence of cryptococcal meningitis is almost the same as in meningococcal meningitis[54] with an incidence of one case per 100,000 persons.[54] Prior to the introduction of highly active antiretroviral therapy (HAART) in the United States, yearly incidence rate of cryptococcal meningitis was on ascendancy with incidence of 6600 cases per 100,000 persons with AIDS[55] The incidence has decreased with the advent of HAART [56] although cases are still reported.[57] The worldwide incidence of cryptococcal meningitis is pegged at 1,000,000 annually according to an estimate by Centers for Disease Control and Prevention CDC in 2009[58] with approximately half of these resulting in death.[58] The prevalence of fungal meningitis does not vary with gender.[59] Non-Caucasian race have a higher prediclection to developing fungal meningitis especially coccidioidal meningitis[60] The prevalence of fungal meningitis does not vary with age.[59] The major factor accounting for age predilection has to do with the clinical state of the patient and the immune response. For example candida meningitis may occur in older children[61][62] and in adults with neutropenia, often presenting with brain abscesses rather than meningitis.[63] Children with certain conditions have higher incidence of fungal meningitis example myeloperoxidase deficiency,[64][65] chronic granulomatous disease of childhood[66][67] and chronic mucocutaneous candidiasis.[68]

Screening

It is recommended that patients with CD4 counts ≤ 100 cells/μl, should have routine cryptococcal antigen screening. Patients with positive result are offered preemptive anti-fungal therapy.[69][70]

Risk Factors

Fungal meningitis rarely occurs in otherwise healthy individuals. Co-existing medical conditions, immunosuppression and travel history to areas where specific fungi are endemic are risk factors for fungal meningitis. [30][31][32][2][53][71][72][73]

Natural History, Complications and Prognosis

If left untreated, neurological complications might occur. Fungal meningitis may be complicated by abscesses, bone invasion, fluid collections, neurological deficits, ocular invasion, papilledema, neurodevelopmental delays in children, and seizures[74][75][76][77][78] The mortality associated with fungal meningitis is high. Better prognosis is associated with early diagnosis, early initiation of the treatment and compliance of patients with medications.

Diagnosis

History and Symptoms

Fungal meningitis can occur in two main clinical pictures: subacute meningitis and chronic meningitis. Chronic meningitis is characterized by the presence of symptoms for more than four weeks. Commonly, patients with fungal meningitis have a history of one or more of the following chronic sinusitis, Granulocytopenia, chronic renal failure, Diabetes, Pregnancy, persons with diabetes, IV drug abuse, prolonged intravenous therapy, exposure history example travel to or residence inendemic regions of the pathogen, immune suppression examples systemic neoplasia, organ transplantation, Human immunodeficiency virus (HIV) / acquired immunodeficiency syndrome (AIDS), water aspiration as in a case of Pseudoallescheria boydii and traumatic inoculation as in a case of Sporothrix schenckii.[13][52][30][31][32][2][53][71][72][73][79]On presentation patients may have the following symptoms, Headache, Neck stiffness, fever, Fatigue, Night sweats, cranial nerves involvement,[28] Hydrocephalus, cranial neuropathy, Radiculopathy and cognitive and personality changes.[28]

Physical Examination

As in the case of any disease, a complete physical exam must be done on the patient looking for positive and negative symptoms. The clinical presentation of fungal meningitis is usually obscure as are the findings on physical exam. The pertinent findings are low grade fever and possible neurological signs like focal weakness, loss of sensation and cranial nerves involvement. Physical exam findings, including presence of rashes, lymphadenopathy, hepatomegaly, pulmonary disease, ocular pathology (eg, endophthalmitis, vitritis, chorioretinitis, uveitis, optic nerve involvement), and cranial nerve (CN) palsies, may narrow the differential. Papilledema and abducens nerve palsy suggest the presence of increased intracranial pressure (ICP). Kernig's sign and brudzinski's sign are not typically present in fungal meningitis.

Laboratory Findings

A lumbar puncture is essential for the diagnosis of fungal meningitis and initiation of the appropriate treatment. The cerebrospinal fluid (CSF) of a patient having fungal meningitis is distinguished by the presence of lymphocytosis, low glucose level and high proteins level. Specific CSF stains and cultures as well as serologies help in determining the specific nature of the causative fungi. Biopsy of skin lesions, chest radiography, ophthalmologic examination, computed tomography or MRI of the brain, in addition to cultures of CSF, blood, and sputum, may provide essential diagnostic clues.

CT

The diagnosis of fungal meningitis mainly relies on the results of the cerebrospinal fluid (CSF) analysis, stain and culture. The role of imaging is to rule out other differential diagnosis of the initial presentation. In addition, brain imaging must be done when the patient has signs of increased intracranial pressure to prevent brain herniation.

MRI

The diagnosis of fungal meningitis mainly relies on the results of the cerebrospinal fluid (CSF) analysis, stain and culture. The role of imaging is to rule out other differential diagnosis of the initial presentation. In addition, brain imaging must be done when the patient has signs of increased intracranial pressure to prevent brain herniation. Also, MRI can detect meningeal enhancement, tumors and para-meningeal infections (brain abscess).[28]


Treatment

Fungal meningitis, such as cryptococcal meningitis, is treated with long courses of high dose antifungals. In addition, frequent lumbar punctures are recommended in order to relieve the increased intracranial pressure[80].

References

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  2. 2.0 2.1 2.2 2.3 2.4 2.5 Gottfredsson M, Perfect JR (2000). "Fungal meningitis". Semin Neurol. 20 (3): 307–22. doi:10.1055/s-2000-9394. PMID 11051295.
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  28. Villanueva JL, Cordero E, Caballero-Granado FJ, Regordan C, Becerril B, Pachón J (1997). "Pneumocystis carinii meningoradiculitis in a patient with AIDS". Eur J Clin Microbiol Infect Dis. 16 (12): 940–2. PMID 9495679.
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  35. Rosales CM, Jackson MA, Zwick D (2004). "Malassezia furfur meningitis associated with total parenteral nutrition subdural effusion". Pediatr Dev Pathol. 7 (1): 86–90. doi:10.1007/s10024-003-4030-5. PMID 15255040.
  36. Symoens F, Knoop C, Schrooyen M, Denis O, Estenne M, Nolard N; et al. (2006). "Disseminated Scedosporium apiospermum infection in a cystic fibrosis patient after double-lung transplantation". J Heart Lung Transplant. 25 (5): 603–7. doi:10.1016/j.healun.2005.12.011. PMID 16678041.
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Peritonsillar abscess
ICD-10 J36
ICD-9 475
DiseasesDB 11141
eMedicine emerg/417 


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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Kiran Singh, M.D. [2] Prince Tano Djan, BSc, MBChB [3]

Synonyms and Keywords: PTA, tonsillar abscess, intratonsillar abscess

Overview

Peritonsillar abscess (PTA), also commonly referred to as quinsy, is defined as a collection of pus located between the tonsillar capsule and the pharyngeal constrictor muscles. It is the most common deep tissue infection of the neck.[1] Historically, it has been thought of as a complication of acute tonsillitis. However, recent studies have proposed additional hypothesis surrounding its pathogenesis making the understanding of the disease a medical dilemma.[2]

Historical perspective

The outline below shows the historical perspective of peritonsillar abscess.[3]

  • In second and third century BC, Celcius was the first to document in literature the treatment and pathogenesis of tonsillar pathology.
  • In 1700s peritonsillar abscess was first described.
  • In the 1930s and 1940s prior to the advent of antibiotics, surgical management was the most common treatment option for peritonsillar abscess. Interval tonsillectomy was mostly done after symptom resolution.
  • By 1947, Chaud tonsillectomy or immediate surgical tonsillectomy became the treatment option.

Classification

On the basis of computed tomographical findings, peritonsillar abscess may be classified into 3 broad categories based on the following:

1. Shape of the abscess

On the basis of shape it may be classified as:[4]

  • Oval type or
  • Cap type

2. Location of the abscess

On the basis of abscess location it may be differentiated into the following:[4]

3. Shape and location

On the basis of shaped and location it may be classified as:[4]

Pathophysiology

Anatomy

A good understanding of the tonsil and its surrounding space is important in the pathogenesis of peritonsillar abscess. The palatine tonsils are found in an anatomical structure called tonsillar fossa. This fossa is bounded anteriorly by palatoglossal muscle, posteriorly by palatopharyngeal muscle, laterally by a fibrous capsule and tonsillar crypts medially. Contents of the tonsillar crypts are expelled by contraction of the tonsillopharyngeus muscle.[5] The tonsils form during the last months of pregnancy and becomes fully formed by 6 to 7 years of age. It then undergoes involution until small size remains in older population. Located within the soft palate is the supratonsillar space occupied by series of 20 to 25 salivary glands described as Weber's glands. The ducts of these glands form a common duct which opens onto the posterior surface of the tonsil after passing through the tonsillar capsule. It is proposed that the secretions from these glands play a rule in food digestion. Peritonsillar abscesses form in the area between the palatine tonsil and its capsule.

Pathogenesis

The pathogenesis of peritonsillar abscess is still not well-understood.[2] There are two proposed theories believed to be involved in the pathogensis of peritonsillar abscess formation.[5][3][6][7]

Some authorities believe that blockage of drainage from tonsillar crypt in acute tonsillitis results in spread of infection into the peritonsillar space.

  • 2. Involvement of Weber's gland account for the abscess formation. Some believe that peritonsillar abscess arises from infectious process involving group of salivary glands called Weber's glands located in the supratonsillar space.

Antigenic response following any disturbance arising from within the tonsillar crypt mucosa allows for lymphocytic interaction. This disruption in the crypt epithelium may be preceded by infectious process. Invasion and proliferation of the tonsillar crypt by infectious pathogens results in localized edema and influx of neutrophils. This is clinically seen as inflamed tonsil with or without exudation.[5] Pus accumulation within tissue behind the supratonsillar space leads to tonsillar bulging, uvula and palate deviation.

Causes

Peritonsillar abscess (PTA) usually arises as a complication of an untreated or partially treated episode of acute tonsillitis. The infection, in these cases, spreads to the peritonsillar area (peritonsillitis). This region comprises of loose connective tissue and is hence susceptible to formation of abscess. Peritonsilar abscess can also occur de novo. Both aerobic and anaerobic bacteria can be causative.[8][8]

Life-threatening causes

Life-threatening conditions may result in death or permanent disability within 24 hours if left untreated. Peritonsillar abscess may become a life-threatening condition and must be treated as such irrespective of the cause.[9][8]

Most common cause

The most frequent pathogen of peritonsillar abscess is Streptococcus pyogenes.[9][8][10][11]

Common causes

Some common causes of peritonsillar abscess include:[9][8]

Less common causes

Less common causes of peritonsillar abscess include:[9][8]

Differentiating Peritonsillar abscess from Other Diseases

Disease/Variable Presentation Causes Physical exams findings Age commonly affected Imaging finding Treatment
Peritonsillar abscess Severe sore throat, otalgia fever, a "hot potato" or muffled voice, drooling, and trismus[1] Aerobic and anaerobic

bacteria most common is

Streptococcus

pyogenes.[9][8][10][11]

Contralateral deflection of the uvula,

the tonsil is displaced inferiorly and medially, tender submandibular and anterior cervical lymph nodes, tonsillar hypertrophy with likely peritonsillar edema.

The highest occurrence is in adults between 20 to 40 years of age.[1] On ultrasound peritonsillar abscess appears as focal irregularly marginated hypoechoic area.[12][13][14][15][12][13] Ampicillin-sulbactam, Clindamycin, Vancomycin or Linezolid
Croup Has cough and stridor but no drooling. Others are Hoarseness, Difficulty breathing, symptoms of the common cold, Runny nose, Fever Parainfluenza virus Suprasternal and intercostal indrawing,[16] Inspiratory stridor[17], expiratory wheezing,[17] Sternal wall retractions[18] Mainly 6 months and 3 years old

rarely, adolescents and adults[19]

Steeple sign on neck X-ray Dexamethasone and nebulised epinephrine
Epiglottitis Has stridor and drooling but no cough. Other symptoms include difficulty breathing, fever, chills, difficulty swallowing, hoarseness of voice H. influenza type b,

beta-hemolytic streptococci, Staphylococcus aureus,

fungi and viruses.

Cyanosis, Cervical lymphadenopathy, Inflammed epiglottis Used to be mostly found in

pediatric age group between 3 to 5 years,

however, recent trend favors adults

as most commonly affected individuals[20]

with a mean age of 44.94 years

Thumbprint sign on neck x-ray Airway maintenance, parenteral Cefotaxime or Ceftriaxone in combination with Vancomycin. Adjuvant therapy includes corticosteroids and racemic Epinephrine.[21][22]
Pharyngitis Sore throat, pain on swallowing, fever, headache, abdominal pain, nausea and vomiting Group A beta-hemolytic

streptococcus.

Inflammed pharynx with or without exudate Mostly in children and young adults,

with 50% of cases identified

between the ages of 5 to 24 years.[23]

_ Antimicrobial therapy mainly penicillin-based and analgesics.
Tonsilitis Sore throat, pain on swallowing, fever, headache, cough Most common cause is

viral including adenovirus,

rhinovirus, influenza,

coronavirus, and

respiratory syncytial virus.

Second most common

causes are bacterial;

Group A streptococcal

bacteria,[24]

Fever, especially 100°F or higher.[25][26]Erythema, edema and Exudate of the tonsils.[27] cervical lymphadenopathy, Dysphonia.[28] Primarily affects children

between 5 and 15 years old.[29]

Intraoral or transcutaneous USG may show an abscess making CT scan unnecessary.[4][30][31] Antimicrobial therapy mainly penicillin-based and analgesics with tonsilectomy in selected cases.
Retropharyngeal abscess Neck pain, stiff neck, torticollis

fever, malaise, stridor, and barking cough

Polymicrobial infection.

Mostly; Streptococcus

pyogenes, Staphylococcus aureus and respiratory anaerobes (example; Fusobacteria, Prevotella,

and Veillonella species)[32][33][34][9][35][36]

Child may be unable to open the mouth widely. May have enlarged

cervical lymph nodes and neck mass.

Mostly between 2-4 years, but can occur in other age groups.[37][38] On CT scan, a mass impinging on the posterior pharyngeal wall with rim enhancement is seen[39][40] Immediate surgical drainage and antimicrobial therapy. emperic therapy involves; ampicillin-sulbactam or clindamycin.

Epidemiology and Demographics

Prevalence and incidence

The incidence of peritonsillar abscess is highest between November to December and April to May in the northern hemisphere. This has been associated with the highest rates of streptococcal pharyngitis and exudative tonsillitis around that these times.[41][42]

Age

Peritonsillar abscess occur in all age groups. The highest occurrence is in adults between 20 to 40 years of age.[1][43][44]

Race

There is no racial predilection to developing peritonsillar abscess.

Gender

Males are more commonly affected with peritonsillar abscess than female with male to female ratio of approximately 1.4:1. However, equal male to female ratios have been reported in some studies as well.[45][46][47][48][49][50][51]

Developed and developing countries

Peritonsillar abscess has not been found to vary significantly among countries.

Risk Factors

Common risk factors in the development of peritonsillar abscess include:[52][53]

  • Smoking
  • Previous peritonsillar abscess episodes
  • History of recurrent pharyngotonsillitis
  • Poor oral hygiene

Screening

There are no screening recommendations for peritonsillar abscess.

Natural History, Complications, and Prognosis

Natural history

Peritonsillar abscess if left untreated may result in extraperitonsillar extension.[54][55]

Complications

The following are some complications that may follow peritonsillar abscess:[1][56][57][58][59]

Peritonsillar abscess may spread through the deep fascia of the neck with associated rapid progression to a more serious infection.

Prognosis

The prognosis of peritonsillar abscess is good with early and appropriate treatment.[60][61][62][63]

Diagnosis

History and Symptoms

  • Unlike tonsillitis, which is more common in the pediatric age group, peritonsillar abscess has a more even age spread — from children to adults.
  • Symptoms start appearing 2-8 days before the formation of abscess. Common symptoms are:[1]

Physical Examination

Physical examination findings suggestive of peritonsillar abscess include the following:[1][65][3][66]

Appearance of the Patient

  • They are usually acutely-ill looking.

Vital Signs

HEENT


Image below shows edematous and inflamed tonsillar with contralacteral uvula deviation:[67]


200PX

Neck

Lungs

  • May be in obvious respiratory distress with flaring of ala nasi, subcostal and intercostal recessions.
  • Increased respiratory rate in both children and adults
  • Decreased air-entry depending of degree of airway obstruction

Extremities

Laboratory Findings

Although the diagnosis of peritonsillar abscess may be made without the use of laboratory findings, the following nonspecific laboratory findings may be seen:[2][5][3][6][7]

  • This usually shows leukocytosis with neutrophilic predominance
  • This is useful too in patients presenting with dehydration
  • Gram stain, culture and sensitivity for sample after abscess drainage.
  • Emperic therapy should be initiated and modified accordingly when results are ready.

Imaging Findings

The diagnosis of peritonsillar abscess may be made without the use of imaging however, imaging options may help in differentiating peritonsillar abscess from other simialr conditions example, peritonsillar cellulitis, retropharyngeal abscess and epiglottitis.

Ultrasound

This is helpful in differentiating peritonsillar abscess from peritonsillar cellulitis as well as a guide during abscess drainage. The approach may be intraoral or submandibular.[68][14][69][70][71]

On ultrasound the following may be found:[12][13][14][15][12][13]

  • Peritonsillar abscess appears as focal irregularly marginated hypoechoic area.
  • Irregular hypoechoic areas within the tonsil may represent pockets of developing purulence or necrosis called intratonsillar abscesses.
  • Peritonsillar cellulitis appears as enlarged tonsil (arrows) with ill-defined margins and markedly increased echogenicity of surrounding soft tissues that suggests significant inflammatory change/cellulitis.

CT scan

Coronal contrast-enhanced CT scan of the neck may identify the peritonsillar abscess.[14]

Treatment

Medical Therapy

Parenteral therapy is the preferred first line route of administration until the temperature of the patient has settled and clinically improved and then switched to oral therapy to complete a 14-day course.[61]

Antimicrobial Regimen

Below are the antimicrobial regimen available in treating peritonsillar abscess.[67]

  • Preferred regimen in children: Ampicillin-sulbactam 50 mg/kg per dose [maximum single dose 3 g] IV 6h
  • Alternative regimen in adults: Clindamycin 600mg IV 6-8h
  • Alternative regimen in children: Clindamycin 13 mg/kg per dose [maximum single dose 900 mg] IV 8h

The above alternative therapy are employed in the following situations:

Pathogen-directed antimicrobial therapy

  • Resistant Gram-positive cocci

For resistant Gram-positive cocci infections IV Vancomycin or Linezolid is added to the above emperic therapy.

Surgery

Surgical modalities in the management of peritonsillar abscess involve the use of the following:

Indications for tonsillectomy in peritonsillar abscess

  • Severe upper respirtaory obstruction
  • Previous episodes of severe recurrent pharyngitis or peritonsillar abscess
  • Unresolving peritonsillar abscess after antibiotics incision and drainage

Prevention

There are no definite preventive measures for peritonsillar abscess, however, immunization against certain organisms in chikdhood may decrease the burden of peritonsillar abscess resulting from such infections.

  • Immunization with the Hib vaccine protects children.[72]
  • In the United states, vaccination against Hib in children was initiated in the 1980s. Immunity against Hib has been adequate with an increasing level of immunization among children.
  • Post-splenectomy patients are also recommended to be immunized.[72]

References

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External links

ka:პერიტონზილური აბსცესი nl:Peritonsillair abces fi:Kurkkupaise











Physical Examination

Physical examination findings suggestive of peritonsillar abscess include the following:[1][2][3][4]

Appearance of the Patient

  • They are usually acutely-ill looking.

Vital Signs

HEENT

Neck

Lungs

  • May be in obvious respiratory distress with flaring of ala nasi, subcostal and intercostal recessions.
  • Increased respiratory rate in both children and adults
  • Decreased air-entry depending of degree of airway obstruction

Extremities

  • Cyanosis












Variable Croup Epiglottitis Pharyngitis Tonsilitis Retropharyngeal abscess
Presentation Cough Sore throat, pain on swallowing, fever, headache, abdominal pain, nausea and vomiting Sore throat, pain on swallowing, fever, headache, cough Neck pain, stiff neck, torticollis

fever, malaise, stridor, and barking cough

Stridor
Drooling
Others are Hoarseness, Difficulty breathing, symptoms of the common cold, Runny nose, Fever Other symptoms include difficulty breathing, fever, chills, difficulty swallowing, hoarseness of voice
Causes Parainfluenza virus H. influenza type b, beta-hemolytic streptococci, Staphylococcus aureus, fungi and viruses. Group A beta-hemolytic streptococcus. Most common cause is viral including adenovirus, rhinovirus, influenza, coronavirus, and respiratory syncytial virus. Second most common causes are bacterial; Group A streptococcal bacteria,[5]  Polymicrobial infection. Mostly; Streptococcus pyogenes, Staphylococcus aureus and respiratory anaerobes (example; Fusobacteria, Prevotella, and Veillonella species)[6][7][8][9][10][11]
Physical exams findings Suprasternal and intercostal indrawing,[12] Inspiratory stridor[13], expiratory wheezing,[13] Sternal wall retractions[14] Cyanosis, Cervical lymphadenopathy, Inflammed epiglottis Inflammed pharynx with or without exudate Fever, especially 100°F or higher.[15][16]Erythema, edema and Exudate of the tonsils.[17] cervical lymphadenopathy, Dysphonia.[18] Child may be unable to open the mouth widely. May have enlarged

cervical lymph nodes and neck mass.

Age commonly affected Mainly 6 months and 3 years old

rarely, adolescents and adults[19]

Used to be mostly found in

pediatric age group between 3 to 5 years,

however, recent trend favors adults

as most commonly affected individuals[20]

with a mean age of 44.94 years.

Mostly in children and young adults,

with 50% of cases identified

between the ages of 5 to 24 years.[21]

Primarily affects children

between 5 and 15 years old.[22]

Mostly between 2-4 years, but can occur in other age groups.[23][24]
Imaging finding Steeple sign on neck X-ray Thumbprint sign on neck x-ray Intraoral or transcutaneous USG may show an abscess making CT scan unnecessary.[25][26][27] On CT scan, a mass impinging on the posterior pharyngeal wall with rim enhancement is seen[28][29]
Treatment Dexamethasone and nebulised epinephrine Airway maintenance, parenteral Cefotaxime or Ceftriaxone in combination with Vancomycin. Adjuvant therapy includes corticosteroids and racemic Epinephrine.[30][31] Antimicrobial therapy mainly penicillin-based and analgesics. Antimicrobial therapy mainly penicillin-based and analgesics with tonsilectomy in selected cases. Immediate surgical drainage and antimicrobial therapy. emperic therapy involves; ampicillin-sulbactam or clindamycin.












Treatment

Treatment is, as for all abscesses, through surgical incision and drainage of the pus, thereby relieving the pain of the stretched tissues. The drainage can often be achieved in the Outpatient Department using a guarded No. 11 blade in an awake and co-operative patient. Sometimes, a needle aspiration can suffice. Antibiotics are also given to treat the infection.

Peritonsillar abscesses are widely considered one of the most painful complications, primarily the surgical draining of the abscess itself. The patient is operated on awake, surgically slicing open the tonsil and draining the abscess.

Complications

  • Parapharyngeal abscess
  • Extension of abscess in other deep neck spaces leading to airway compromise
  • Septicaemia





Alternaria spp[32]

Rhodotorula spp [33]

Acremonium spp.[34]

Dreschlera spp[35]
Malassezia spp[36]
Scedosporium spp[37]
Arthrographis spp[38]
Blastoschizomyces (11, 12),
Paecilomyces (13, 14), 

Aureobasidium (15),

Clavispora (16), Ustilago (17),

Exophiala (Wangiella) (18),
and Exserohilum (19, 20).
On the other hand, most cases of fungal CNS infections are caused by only a few important species, 

The common causes of fungal meningistis may be classified into two subgroups. This inlcudes:


Primary fungal pathogens of humans

All of these may cause CNS infections. This group includes: C. neoformans (22, 23),

Coccidioides immitis (24, 25, 26),

Blastomyces dermatitidis (27, 28),

Paracoccidioides brasiliensis (29, 30),

Sporothrix schenckii (31, 32),

H. capsulatum (33, 34), 

Pseudallescheria boydii (Scedosporium apiospermum) (35, 36),

dematiaceous fungi (37, 38, 39).

The second group is considered opportunists, which take advantage of significant immune defects in the host. This group includes

Candida species (40, 41, 42),

Aspergillus species (43, 44, 45),

mucormycosis (46, 47), and

Trichosporon species (48, 49).



Title:Fungal Meningitis Author / Creator:Horan ; Perfect, Jennifer, John L. R. Language: English Is Part Of: Infections of the Central Nervous System Identifier: ISBN: 978-1-4698-8366-3 Source: Gale Virtual Reference Library (GVRL)


According to severity of the disease
Mild
  • Early diagnosis and treatment
  • Responds to medical treatment
  • Typical clinical presentation
  • Good prognosis
Moderate
  • May present late with typical or atypical symptoms
  • May present with complications
  • Variable response to treatment
Severe
  • Presents with complications or prolonged illness
  • Immunocompromised
  • Common in extremes of age
  • Delayed diagnosis and treatment
  • Surgical treatment may be required in addition to medical treatment
  • Increased morbidity and mortality
According to the duration of disease[39]
Acute
  • Lasts few weeks
  • Patient acutely ill
  • Mostly in HIV-associated patients
  • Impaired consciousness
  • Seeks medical treatment early due to sudden deterioration
Subacute
  • Lasts less than 4 weeks
  • Patient acutely ill
  • Mostly in HIV-associated patients
  • Impaired consciousness
  • Seeks medical treatment early due to sudden deterioration
Chronic
  • Lasts more than 4 weeks
  • Gradual deterioration of patient
  • Prolonged history of atypical symptoms
  • Common in older patients
Recurrent
  • Multiple episodes which lasts less than 4 weeks
  • History of incompliance to medication
  • immunosuppression may be the underlying cause










Variable Empyema Thoracis Lung abscess Pleural effusion Pneumonia Lung cancer
Presentation Variable presentation

but may follow long standing pneumonia

Usually has history of aspiration pneumonia, alcoholics, drug abusers, seizure disorder, have undergone recent general anesthesia, or have a nasogastric or endotracheal tube. Usually follows pneumonia as a complication presents with fever, pleuritc chest pain, cough mostly asymptomatic but may

have cough productive with

hemoptysis and

chronic history of smoking

Causes In general any bacteria

can cause an empyema, however different bacteria are associated

with different rates of empyema formation.[1]  Common causes include bacteroidesfusobacterium

haemophilus influenzaepneumococcal infections,

staphylococcus aureus,

streptococcusTB

Lung abscess is commonly caused by bacterial infections and these include bacteroides, peptostreptococcus and prevotella mostly after aspiration Common causes of transudative pleural effusion include;[1][2][3][4][5] left ventricular failureNephrotic syndrome, and cirrhosis, while common causes of exudative pleural effusions[6] are bacterial pneumonia and malignancy Pneumonia can result from a variety of causes, including infection with bacteriavirusesfungiparasites, and chemical injury to the lungs Direct cause of lung cancers

is DNA mutations that often

result in either activation

of proto-oncogenes

(e.g. K-RAS) or the inactivation of tumors suppressor genes

(e.g. TP53) or both. The risk of these genetic mutations may be increased following exposure to environmental components example smoking

Laboratory findings The pleural fluid typically has a low pH (<7.20),

low glucose (<60 mg/dL), and contains infectious organisms.

Therefore, the diagnosis relies on the presence of pus or organisms on gram stain. A positive bacteria culture from pleural fluid is not needed to make diagnosis of empyema.[40][41]

Raised inflammatory markers ( eg high ESRCRP) are usual but not specific The most widely used criteria is to differentiate between exudate and transudate using the light's criteria. Fluid is exudate when:
  • Pleural fluid protein/serum protein ratio >0.5
  • Fluid/serum lactic dehydrogenase (LDH) ratio >0.6
  • Fluid LDH greater than 2/3 the upper limits of normal of the serum LDH
Laboratory findings are non specific example leukocytosis, sputum samples for gram staining and culture. Other tests include urine antigen test, PCR, C-reactive protein and procalcitonin The laboratory findings are 

non specific including:

neutropeniahyponatremia,

hypokalemiahypercalcemia,

respiratory acidosis,

hypercarbiahypoxia, and

tumor cells in sputum and

pleural effusion cytology.

Physical examination On examination, the following

findings may be seen:[42][43][44]

Lateral chest wall swelling

and tenderness, clubbing of the fingernails, dull percussion note, r

educed breath sounds on the affected side of the chest, egophony, coarse crackles, increased tactile fremitus,

mediastinal shift to opposite side with large empyema

Chest examination shows features of consolidation such as localised dullness on percussion, bronchial breath sound etc.

Dental decay is common especially in alcoholics and children. Clubbing is present in one third of patients.

Bulging of the intercostal spaces,

decreased chest expansion

bronchovesicular breath sounds

of decreased intensity, egophony,

dullness to percussion,

decreased or absent fremitus.

Physical examination increased respiratory rate, low oxygen saturation, difficulty breathing, bronchial breathe sounds, increased tactile fremitus crackling sounds, or increased whispered pectoriloquy.  Physical examination findings are non specific and may include decreased/absent breath soundspallor, low-grade fever, tachypnea and cachezia.
CXR Chest X ray of empyema shows air-fluid level continuos homogenous pattern from the mediastinum to the chest wall forming obtuse angle with the lung parenchyma.[45]

Chest xray shows often unilateral cavity containing an air-fluid level and consolidation of lung parenchyema.

A homogenous opacification is noted at the affected side. The costophrenic angle is obliterated with a meniscus. CXR shows areas of diffused opacities. CXR may show lung mass, widening of the mediastinumatelectasis, or pleural effusion.
Chest ultrasound Ultrasound in empyema is positive

for suspended microbubble sign,

air fluid level, curtains sign

and loss of gliding sign.[46]

Ultrasound in lung abscess is negative for suspended microbubble sign, curtains sign and loss of gliding sign but air fluid level may be seen,.[47] Ultrasonography is helpful in making diagnosis of pleural effusion particularly in differentiating effusion from masses.[48] The extended thoracic spine sign on sonography has high sensitivity and specificity for diagnosing pleural effusion.[49] Chest or upper abdominal ultrasound may show subpulmonic effusion as shown below.[50][51][52] Not reqiured unless complicated with empyema USG is helpful in guiding biopsy, staging and estimating prognosis. It may show hypo- and hyperechogenic masses.[53][54][55]
CT scan Seen as a lung mass whose cavity

is regular with smooth

and regular lumen, well-defined

boundary and shape changes

with change in patient's position.[56]

Mass may resolve on antibiotics The split pleura sign is present[57]

(most reliable sign to differentiate

empyema from lung abscess)[58]

Lung mass whose cavity is rregular with undulated lumen, irregular-poorly defined boundary and shape does not change with change in patient's position.[59] Mass may resolve on antibiotics In most cases CT imaging may not provide additional information that would influence the clinical decision-making process.[60][61] [62] CT scan shows heterogeneous opacification of the affected side and cardiomediastinal shift to the opposite site in unilateral effusion.[63]
  • CT findings in pneumonia include:[1]
Seen as a spiculated irregular solid mass that does not resolve on antibiotics
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