1)positive tuberclin test

2)chest radiograph

3)CT scan

4)cytology/biopsy (FNAC)

5)AFB staining

6)mycobacterial culture

Adenitis is a general term for an inflammation of a gland. Often it is used to refer to lymphadenitis which is the inflammation of a lymph node.

"Lymph adenitis" or "lymph node adenitis" is caused by infection in lymph nodes. The infected lymph nodes typically become enlarged, warm and tender. A swelling of lymph nodes due to growth of lymph cells is called lymphadenopathy. Types include:

- Neck

- Cervical adenitis is an inflammation of a lymph node in the neck.

- Tuberculous adenitis (scrofula) is a tuberculous infection of the skin of the neck caused by "Mycobacterium tuberculosis". Non-tuberculous adenitis can also be caused by "Mycobacterium scrofulaceum" or "Mycobacterium avium".

- Abdomen

- Mesenteric adenitis is an inflammation of the mesenteric lymph nodes in the abdomen. It can be caused by the bacterium "Yersinia enterocolitica". If it occurs in the right lower quadrant, it can be mistaken for acute appendicitis, often preceded by a sore throat.

Incision drainage with proper evacuation of the fluid followed by anti-tubercular medication.

According to present research, PFAPA does not lead to other diseases and spontaneously resolves as the child gets older, with no long term physical effects.

However, PFAPA has been found in adults and may not spontaneously resolve.

Acute prostatitis is relatively easy to diagnose due to its symptoms that suggest infection. The organism may be found in blood or urine, and sometimes in both. Common bacteria are "Escherichia coli, Klebsiella, Proteus, Pseudomonas, Enterobacter, Enterococcus, Serratia," and "Staphylococcus aureus." This can be a medical emergency in some patients and hospitalization with intravenous antibiotics may be required. A complete blood count reveals increased white blood cells. Sepsis from prostatitis is very rare, but may occur in immunocompromised patients; high fever and malaise generally prompt blood cultures, which are often positive in sepsis. A prostate massage should never be done in a patient with suspected acute prostatitis, since it may induce sepsis. Since bacteria causing the prostatitis is easily recoverable from the urine, prostate massage is not required to make the diagnosis. Rectal palpation usually reveals an enlarged, exquisitely tender, swollen prostate gland, which is firm, warm, and, occasionally, irregular to the touch. C-reactive protein is elevated in most cases.

Prostate biopsies are not indicated as the (clinical) features (described above) are diagnostic. The histologic correlate of acute prostatitis is a neutrophilic infiltration of the prostate gland.

Acute prostatitis is associated with a transiently elevated PSA, i.e., the PSA is increased during an episode of acute prostatitis and then decreases again after it has resolved. PSA testing is not indicated in the context of uncomplicated acute prostatitis.

The differential diagnosis of Rosai–Dorfman disease includes both malignant and nonmalignant diseases, such as granulomatosis with polyangiitis, Langerhans cell histiocytosis, Langerhans cell sarcoma, lymphoma, sarcoidosis, and tuberculosis. The disease is diagnosed by biopsy of affected tissues. Microscopic examination of stained specimens will show histiocytes with lymphocytes and possibly other types of cells trapped within them, a phenomenon known as emperipolesis. Upon immunohistochemical staining, the histiocytes will be positive for S100, CD68, and CD163 but negative for CD1a.

Some signs and symptoms indicate the need for early referral. These include

- Difficulty swallowing

- Vocal stridor

- Ear pain

- Recent weight loss

- History of smoking

- Current or recent radiotherapy treatment (in the neck region)

- Recent neck surgery or surgery involving endotracheal tubing

- Person is a professional voice user (teacher, singer, actor, call center worker, and so on)

Long-term antibiotics, while they decrease rates of infection during treatment, have an unknown effect on long-term outcomes such as hearing loss. This method of prevention has been associated with emergence of antibiotic-resistant otitic bacteria. They are thus not recommended.

Pneumococcal conjugate vaccines (PCV) in early infancy, decreases the risk of acute otitis media in healthy infants. PCV is recommended for all children, and, if implemented broadly, PCV would have a significant public health benefit. Influenza vaccine is recommended annually for all children. PCV does not appear to decrease the risk of otitis media when given to high-risk infants or for older children who have previously experienced otitis media.

Risk factors such as season, allergy predisposition and presence of older siblings are known to be determinants of recurrent otitis media and persistent middle-ear effusions (MEE). History of recurrence, environmental exposure to tobacco smoke, use of daycare, and lack of breastfeeding have all been associated with increased risk of development, recurrence, and persistent MEE. Thus, cessation of smoking in the home should be encouraged, daycare attendance should be avoided or daycare facilities with the fewest attendees should be recommended, and breastfeeding should be promoted.

There is some evidence that breastfeeding for the first year of life is associated with a reduction in the number and duration of OM infections. Pacifier use, on the other hand, has been associated with more frequent episodes of AOM.

Evidence does not support zinc supplementation as an effort to reduce otitis rates except maybe in those with severe malnutrition such as marasmus.

The cornerstone of diagnosis is an accurate history, and a good clinical examination of the eye, to eliminate traumatic uveitis. Ultrasonography is a useful tool, as it can detect a thickened iris, but only in the hands of an expert.

Laryngitis that continues for more than three weeks is considered chronic. If laryngeal symptoms last for more than three weeks, a referral should be made for further examination, including direct laryngoscopy. The prognosis for chronic laryngitis varies depending on the cause of the laryngitis.

PFAPA syndrome typically resolves spontaneously. Treatment options are used to lessen the severity of episodes. Treatment is either medical or surgical.

One treatment often used is a dose of a corticosteroid at the beginning of each fever episode. A single dose usually ends the fever within several hours. However, in some children, they can cause the fever episodes to occur more frequently. Interleukin-1 inhibition appears to be effective in treating this condition.

Surgical removal of the tonsils appears to be beneficial compared to no surgery in symptom resolution and number of future episodes. The evidence to support surgery is; however, of moderate quality.

Adhesive otitis media occurs when a thin retracted ear drum becomes sucked into the middle-ear space and stuck (i.e., adherent) to the ossicles and other bones of the middle ear.

Antibiotics are the first line of treatment in acute prostatitis. Antibiotics usually resolve acute prostatitis infections in a very short time, however a minimum of two to four weeks of therapy is recommended to eradicate the offending organism completely. Appropriate antibiotics should be used, based on the microbe causing the infection. Some antibiotics have very poor penetration of the prostatic capsule, others, such as ciprofloxacin, trimethoprim/sulfamethoxazole, and tetracyclines such as doxycycline penetrate prostatic tissue well. In acute prostatitis, penetration of the prostate is not as important as for category II because the intense inflammation disrupts the prostate-blood barrier. It is more important to choose a bactericidal antibiotic (kills bacteria, e.g., a fluoroquinolone antibiotic) rather than a bacteriostatic antibiotic (slows bacterial growth, e.g. tetracycline) for acute potentially life-threatening infections.

Severely ill patients may need hospitalization, while nontoxic patients can be treated at home with bed rest, analgesics, stool softeners, and hydration. Men with acute prostatitis complicated by urinary retention are best managed with a suprapubic catheter or intermittent catheterization. Lack of clinical response to antibiotics should raise the suspicion of an abscess and prompt an imaging study such as a transrectal ultrasound (TRUS).

Some patients have no symptoms, spontaneous remission, or a relapsing/remitting course, making it difficult to decide whether therapy is needed. In 2002, authors from Sapienza University of Rome stated on the basis of a comprehensive literature review that "clinical observation without treatment is advisable when possible."

Therapeutic options include surgery, radiation therapy, and chemotherapy. Surgery is used to remove single lymph nodes, central nervous system lesions, or localized cutaneous disease. In 2014, Dalia and colleagues wrote that for patients with extensive or systemic Rosai–Dorfman disease, "a standard of care has not been established" concerning radiotherapy and chemotherapy.

Horses that suffer from this disease can never be considered cured, although they can be managed by careful use of the therapy described above, and fast detection of new flare-ups. If the disease is not properly treated, it will eventually lead to blindness.

For acute pericarditis to formally be diagnosed, two or more of the following criteria must be present: chest pain consistent with a diagnosis of acute pericarditis (sharp chest pain worsened by breathing in or a cough), a pericardial friction rub, a pericardial effusion, and changes on electrocardiogram (ECG) consistent with acute pericarditis.

A complete blood count may show an elevated white count and a serum C-reactive protein may be elevated. Acute pericarditis is associated with a modest increase in serum creatine kinase MB (CK-MB). and cardiac troponin I (cTnI), both of which are also markers for injury to the muscular layer of the heart. Therefore, it is imperative to also rule out acute myocardial infarction in the face of these biomarkers. The elevation of these substances may occur when inflammation of the heart's muscular layer in addition to acute pericarditis. Also, ST elevation on EKG (see below) is more common in those patients with a cTnI > 1.5 µg/L. Coronary angiography in those patients should indicate normal vascular perfusion. Troponin levels increase in 35-50% of people with pericarditis.

Electrocardiogram (ECG) changes in acute pericarditis mainly indicates inflammation of the epicardium (the layer directly surrounding the heart), since the fibrous pericardium is electrically inert. For example, in uremia, there is no inflammation in the epicardium, only fibrin deposition, and therefore the EKG in uremic pericarditis will be normal. Typical EKG changes in acute pericarditis includes

- stage 1 -- diffuse, positive, ST elevations with reciprocal ST depression in aVR and V1. Elevation of PR segment in aVR and depression of PR in other leads especially left heart V5, V6 leads indicates atrial injury.

- stage 2 -- normalization of ST and PR deviations

- stage 3 -- diffuse T wave inversions (may not be present in all patients)

- stage 4 -- EKG becomes normal OR T waves may be indefinitely inverted

The two most common clinical conditions where ECG findings may mimic pericarditis are acute myocardial infarction (AMI) and generalized early repolarization. As opposed to pericarditis, AMI usually causes localized convex ST-elevation usually associated with reciprocal ST-depression which may also be frequently accompanied by Q-waves, T-wave inversions (while ST is still elevated unlike pericarditis), arrhythmias and conduction abnormalities. In AMI, PR-depressions are rarely present. Early repolarization usually occurs in young males (age <40 years) and ECG changes are characterized by terminal R-S slurring, temporal stability of ST-deviations and J-height/ T-amplitude ratio in V5 and V6 of <25% as opposed to pericarditis where terminal R-S slurring is very uncommon and J-height/ T-amplitude ratio is ≥ 25%. Very rarely, ECG changes in hypothermia may mimic pericarditis, however differentiation can be helpful by a detailed history and presence of an Osborne wave in hypothermia.

Another important diagnostic electrocardiographic sign in acute pericarditis is the Spodick sign. It signifies to the PR-depressions in a usual (but not always) association with downsloping TP segment in patients with acute pericarditis and is present in up to 80% of the patients affected with acute pericarditis. The sign is often best visualized in lead II and lateral precordial leads. In addition, Spodick’s sign may also serve as an important distinguishing electrocardiographic tool between the acute pericarditis and acute coronary syndrome. The presence of a classical Spodick’s sign is often a giveaway to the diagnosis.

Rarely, electrical alternans may be seen, depending on the size of the effusion.

A chest x-ray is usually normal in acute pericarditis, but can reveal the presence of an enlarged heart if a pericardial effusion is present and is greater than 200 mL in volume. Conversely, patients with unexplained new onset cardiomegaly should always be worked up for acute pericarditis.

An echocardiogram is typically normal in acute pericarditis but can reveal pericardial effusion, the presence of which supports the diagnosis, although its absence does not exclude the diagnosis.

In predicting the prognosis, there are several scoring indices that have been used as predictors of survival. Two such scoring systems are the Ranson criteria and APACHE II (Acute Physiology and Chronic Health Evaluation) indices. Most, but not all studies report that the Apache score may be more accurate. In the negative study of the APACHE-II, the APACHE-II 24-hour score was used rather than the 48-hour score. In addition, all patients in the study received an ultrasound twice which may have influenced allocation of co-interventions. Regardless, only the APACHE-II can be fully calculated upon admission. As the APACHE-II is more cumbersome to calculate, presumably patients whose only laboratory abnormality is an elevated lipase or amylase do not need assessment with the APACHE-II; however, this approach is not studied. The APACHE-II score can be calculated at www.sfar.org.

Practice guidelines state:

Predicts mortality risk in pancreatitis with fewer variables than Ranson's criteria. Data should be taken from the first 24 hours of the patient's evaluation.

- BUN >25 mg/dL (8.9 mmol/L)

- Abnormal mental status with a Glasgow coma score <15

- Evidence of SIRS (systemic inflammatory response syndrome)

- Patient age >60 years old

- Imaging study reveals pleural effusion

Patients with a score of zero had a mortality of less than one percent, whereas patients with a score of five had a mortality rate of 22 percent. In the validation cohort, the BISAP score had similar test performance characteristics for predicting mortality as the APACHE II score. As is a problem with many of the other scoring systems, the BISAP has not been validated for predicting outcomes such as length of hospital stay, need for ICU care, or need for intervention.

An oral whole cell nontypeable Haemophilus influenzae vaccine may protect against the disease, but "the evidence is mixed".

Patients with uncomplicated acute pericarditis can generally be treated and followed up in an outpatient clinic. However, those with high risk factors for developing complications (see above) will need to be admitted to an inpatient service, most likely an ICU setting. High risk patients include the following:

- subacute onset

- high fever (> 100.4 F/38 C) and leukocytosis

- development of cardiac tamponade

- large pericardial effusion (echo-free space > 20 mm) resistant to NSAID treatment

- immunocompromised

- history of oral anticoagulation therapy

- acute trauma

- failure to respond to seven days of NSAID treatment

Pericardiocentesis is a procedure whereby the fluid in a pericardial effusion is removed through a needle. It is performed under the following conditions:

- presence of moderate or severe cardiac tamponade

- diagnostic purpose for suspected purulent, tuberculosis, or neoplastic pericarditis

- persistent symptomatic pericardial effusion

NSAIDs in "viral" or "idiopathic" pericarditis. In patients with underlying causes other than viral, the specific etiology should be treated. With idiopathic or viral pericarditis, NSAID is the mainstay treatment. Goal of therapy is to reduce pain and inflammation. The course of the disease may not be affected. The preferred NSAID is ibuprofen because of rare side effects, better effect on coronary flow, and larger dose range. Depending on severity, dosing is between 300–800 mg every 6–8 hours for days or weeks as needed. An alternative protocol is aspirin 800 mg every 6–8 hours. Dose tapering of NSAIDs may be needed. In pericarditis following acute myocardial infarction, NSAIDs other than aspirin should be avoided since they can impair scar formation. As with all NSAID use, GI protection should be engaged. Failure to respond to NSAIDs within one week (indicated by persistence of fever, worsening of condition, new pericardial effusion, or continuing chest pain) likely indicates that a cause other than viral or idiopathic is in process.

Colchicine, which has been essential to treat recurrent pericarditis, has been supported for routine use in acute pericarditis by recent prospective studies. Colchicine can be given 0.6 mg twice a day (0.6 mg daily for patients <70 kg) for 3 months following an acute attack. It should be considered in all patients with acute pericarditis, preferably in combination with a short-course of NSAIDs. For patients with a first episode of acute idiopathic or viral pericarditis, they should be treated with an NSAID plus colchicine 1–2 mg on first day followed by 0.5 daily or twice daily for three months. It should be avoided or used with caution in patients with severe renal insufficiency, hepatobiliary dysfunction, blood dyscrasias, and gastrointestinal motility disorders.

Corticosteroids are usually used in those cases that are clearly refractory to NSAIDs and colchicine and a specific cause has not been found. Systemic corticosteroids are usually reserved for those with autoimmune disease.

Before the development of modern cardiovascular surgery, cases of acute mediastinitis usually arose from either perforation of the esophagus or from contiguous spread of odontogenic or retropharyngeal infections. However, in modern practice, most cases of acute mediastinitis result from complications of cardiovascular or endoscopic surgical procedures.

Treatment usually involves aggressive intravenous antibiotic therapy and hydration. If discrete fluid collections or grossly infected tissue have formed (such as abscesses), they may have to be surgically drained or debrided.

Kogoj's spongiform pustules can be observed via histopathology to confirm acute GPP.

Chronic mediastinitis is usually a radiologic diagnosis manifested by diffuse fibrosis of the soft tissues of the mediastinum. This is sometimes the consequence of prior granulomatous disease, most commonly histoplasmosis. Other identifiable causes include tuberculosis, IgG4-related disease and radiation therapy. Fibrosing mediastinitis most frequently causes problems by constricting blood vessels or airways in the mediastinum. This may result in such complications as superior vena cava syndrome or pulmonary edema from compression of pulmonary veins.

Treatment for chronic fibrosing mediastinitis is somewhat controversial, and may include steroids or surgical decompression of affected vessels.

The differential diagnosis for pancreatitis includes but is not limited to cholecystitis, choledocholithiasis, perforated peptic ulcer, bowel infarction, small bowel obstruction, hepatitis and mesenteric ischemia.

Diagnosis requires 2 of the 3 following criteria:

- Characteristic acute onset of epigastric or vague abdominal pain that may radiate to the back (see signs and symptoms above)

- Serum amylase or lipase levels ≥ 3 times the upper limit of normal

- An imaging study with characteristic changes. CT, MRI, abdominal ultrasound or endoscopic ultrasound can be used for diagnosis.

Amylase and lipase are 2 enzymes produced by the pancreas. Elevations in lipase are generally considered a better indicator for pancreatitis as it has greater specificity and has a longer half life.

For imaging, abdominal ultrasound is convenient, simple, non-invasive, and inexpensive. It is more sensitive and specific for pancreatitis from gallstones than other imaging modalities. However, in 25–35% of patients the view of the pancreas can be obstructed by bowel gas making it difficult to evaluate.

A contrast-enhanced CT scan is usually performed more than 48 hours after the onset of pain to evaluate for pancreatic necrosis and extrapancreatic fluid as well as predict the severity of the disease. CT scanning earlier can be falsely reassuring.

ERCP or an endoscopic ultrasound can also be used if a biliary cause for pancreatitis is suspected.