Supportive measures may be instituted prior to surgery. These measures include fluid resuscitation. Intravenous opioids can be used for pain control.

Antibiotics are often not needed. If used they should target enteric organisms (e.g. Enterobacteriaceae), such as "E. coli" and "Bacteroides". This may consist of a broad spectrum antibiotic; such as piperacillin-tazobactam, ampicillin-sulbactam, ticarcillin-clavulanate (Timentin), a third generation cephalosporin (e.g.ceftriaxone) or a quinolone antibiotic (such as ciprofloxacin) and anaerobic bacteria coverage, such as metronidazole. For penicillin allergic people, aztreonam or a quinolone with metronidazole may be used.

In cases of severe inflammation, shock, or if the person has higher risk for general anesthesia (required for cholecystectomy), an interventional radiologist may insert a percutaneous drainage catheter into the gallbladder ('percutaneous cholecystostomy tube') and treat the person with antibiotics until the acute inflammation resolves. A cholecystectomy may then be warranted if the person's condition improves.

Homeopathic approaches to treating cholecystitis have not been validated by evidence and should not be used in place of surgery.

Abdominal pain is often the predominant symptom in patients with acute pancreatitis and should be treated with analgesics.

Opioids are safe and effective at providing pain control in patients with acute pancreatitis. Adequate pain control requires the use of intravenous opiates, usually in the form of a patient-controlled analgesia pump. Hydromorphone or fentanyl (intravenous) may be used for pain relief in acute pancreatitis. Fentanyl is being increasingly used due to its better safety profile, especially in renal impairment. As with other opiates, fentanyl can depress respiratory function. It can be given both as a bolus as well as constant infusion.

Meperidine has been historically favored over morphine because of the belief that morphine caused an increase in sphincter of Oddi pressure. However, no clinical studies suggest that morphine can aggravate or cause pancreatitis or cholecystitis. In addition, meperidine has a short half-life and repeated doses can lead to accumulation of the metabolite normeperidine, which causes neuromuscular side effects and, rarely, seizures.

Treatment is focused on preventing deposition of uric acid within the urinary system by increasing urine volume with potent diuretics such as furosemide. Raising the urinary pH to a level higher than 7 (alkalinization) is often difficult to attain, although sodium bicarbonate and/or acetazolamide are sometimes used in an attempt to increase uric acid solubility.

Dialysis (preferably hemodialysis) is started if the above measures fail.

In the management of acute pancreatitis, the treatment is to stop feeding the patient, giving them nothing by mouth, giving intravenous fluids to prevent dehydration, and sufficient pain control. As the pancreas is stimulated to secrete enzymes by the presence of food in the stomach, having no food pass through the system allows the pancreas to rest. Approximately 20% of patients have a relapse of pain during acute pancreatitis. Approximately 75% of relapses occur within 48 hours of oral refeeding.

The incidence of relapse after oral refeeding may be reduced by post-pyloric enteral rather than parenteral feeding prior to oral refeeding. IMRIE scoring is also useful.

For most people with acute cholecystitis, the treatment of choice is surgical removal of the gallbladder, laparoscopic cholecystectomy. Laparoscopic cholecystectomy is performed using several small incisions located at various points across the abdomen. Several studies have demonstrated the superiority of laparoscopic cholecystectomy when compared to open cholecystectomy (using a large incision in the right upper abdomen under the rib cage). People undergoing laparoscopic surgery report less incisional pain postoperatively as well as having fewer long term complications and less disability following the surgery. Additionally, laparoscopic surgery is associated with a lower rate of surgical site infection.

During the days prior to laparoscopic surgery, studies showed that outcomes were better following early removal of the gallbladder, preferably within the first week. Early laparoscopic cholecystectomy (within 7 days of visiting a doctor with symptoms) as compared to delayed treatment (more than 6 weeks) may result in shorter hospital stays and a decreased risk of requiring an emergency procedure. There is no difference in terms of negative outcomes including bile duct injury or conversion to open cholecystectomy. For early cholecystectomy, the most common reason for conversion to open surgery is inflammation that hides Calot's triangle. For delayed surgery, the most common reason was fibrotic adhesions.

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).

Treatment of acute proliferative glomerulonephritis consists of blood pressure (BP) control:also a renal biopsy may be needed to be performed at some point. A low-sodium diet may be needed when hypertension is present. In individuals with oliguric acute kidney injury, the amount of potassium should be controlled.

It is unclear whether or not acute proliferative glomerulonephritis (i.e., poststreptococcal glomerulonephritis) can be prevented with early prophylactic antibiotic therapy, with some authorities arguing that antibiotics can prevent development of acute proliferative glomerulonephritis, while others reject that antibiotics can prevent acute proliferative glomerulonephritis.

Mucous membrane pemphigoid may be managed with medication (cyclophosphamide and prednisolone).

Laryngopharyngeal reflux treatment primarily involves behavioural management and medication. Behavioural management involves aspects such as

- Wearing loose clothing

- Eating smaller, more frequent meals

- Avoiding certain foods (e.g. caffeine, alcohol, spicy foods)

Anti-reflux medications may be prescribed for patients with signs of chronic laryngitis and hoarse voice. If anti-reflux treatment does not result in a decrease of symptoms, other possible causes should be examined. Over-the-counter medications for neutralizing acids (antacids) and acid suppressants (H-2 blockers) may be used. Antacids are often short-acting and may not be sufficient for treatment. Proton pump inhibitors are an effective type of medication. These should only be prescribed for a set period of time, after which the symptoms should be reviewed. Proton pump inhibitors do not work for everyone. A physical reflux barrier (e.g. Gaviscon Liquid) may be more appropriate for some. Antisecretory medications can have several side-effects.

When appropriate, anti-reflux surgery may benefit some individuals.

The treatment of pancreatitis is supportive and depends on severity. Morphine generally is suitable for pain control. There are no clinical studies to suggest that morphine can aggravate or cause pancreatitis or cholecystitis.

The treatment that is received for acute pancreatitis will depend on whether the diagnosis is for the mild form of the condition, which causes no complications, or the severe form, which can cause serious complications.

Acute care is the early and specialist management of adult patients suffering from a wide range of medical conditions requiring urgent or emergency care usually within 48 hoursof admission or referral from other specialties.

Acute hospitals are those intended for short-term medical and/or surgical treatment and care. The related medical speciality is acute medicine.

Acute GPP typically requires inpatient management including both topical and systemic therapy, and supportive measures. Systemic glucocorticoid withdrawal is a common causative agent. Withdrawal or administration of certain drugs in the patient's previous medication regimen may be required. Oral retinoids are the most effective treatment, and are considered first line. Cyclosporine or infliximab may be required for particularly acute cases.

The treatment of mild acute pancreatitis is successfully carried out by admission to a general hospital ward. Traditionally, people were not allowed to eat until the inflammation resolved but more recent evidence suggests early feeding is safe and improves outcomes. Because pancreatitis can cause lung damage and affect normal lung function, oxygen is occasionally delivered through breathing tubes that are connected via the nose. The tubes can then be removed after a few days once it is clear that the condition is improving. Dehydration may result during an episode of acute pancreatitis, so fluids will be provided intravenously. Opioids may be used for the pain. Early feeding does not appear to cause problems and may result in an ability to leave hospital sooner.

Currently, there is no direct treatment for AEN. Only treatment is for the underlying main diseases or conditions. Appropriate hydration is set. Antacids are also added for further recovery support. Common support drugs of antacids are either H receptor antagonists, and/or a proton pump inhibitor. Sucralfate was used as an option. Parenteral nutrition greatly increased chance of recovery. An esophagectomy can be issued if the disorder is severe enough.

It is important to weigh the benefits and harms before using antibiotics for acute otitis media. As over 82% of acute episodes settle without treatment, about 20 children must be treated to prevent one case of ear pain, 33 children to prevent one perforation, and 11 children to prevent one opposite-side ear infection. For every 14 children treated with antibiotics, one child has an episode of either vomiting, diarrhea or a rash. If pain is present, treatment to reduce it should be initiated.

- Antibiotics should be prescribed for severe bilateral or unilateral disease in all infants and children with severe signs and symptoms, such as moderate to severe ear pain and high fever.

- For bilateral acute otitis media in infants younger than 24 months of age, without severe signs and symptoms, antibiotics should be prescribed.

- When non-severe unilateral acute otitis media is diagnosed in young children either antibiotic therapy is given or observation with close follow-up based on joint decision making between parent(s)/caregiver in infants 6 to 23 months of age. If the child worsens or fails to improve in 2 to 3 days antibiotics should be administered.

- Children 24 months or older with non-severe disease can have either antibiotics or observation.

The first line antibiotic treatment, if warranted, is amoxicillin. If there is resistance or use of amoxicillin in the last 30 days then amoxicillin-clavulanate or another penicillin derivative plus beta lactamase inhibitor is recommended. Taking amoxicillin once a day may be as effective as twice or three times a day. While less than 7 days of antibiotics have less side effects, more than seven days appear to be more effective. If there is no improvement after 2–3 days of treatment a change in therapy may be considered.

A treatment option for chronic suppurative otitis media with discharge is topical antibiotics. A Cochrane review found that topical quinolone antibiotics can improve discharge better than oral antibiotics. Safety is not really clear.

Oral and topical pain killers are effective to treat the pain caused by otitis media. Oral agents include ibuprofen, paracetamol (acetaminophen), and opiates. Topical agents shown to be effective include antipyrine and benzocaine ear drops. Decongestants and antihistamines, either nasal or oral, are not recommended due to the lack of benefit and concerns regarding side effects. Half of cases of ear pain in children resolve without treatment in three days and 90% resolve in seven or eight days. The use of steroids is not supported by the evidence for acute otitis media.

If the cause is obstruction of the urinary tract, relief of the obstruction (with a nephrostomy or urinary catheter) may be necessary.

The myriad causes of intrinsic AKI require specific therapies. For example, intrinsic AKI due to vasculitis or glomerulonephritis may respond to steroid medication, cyclophosphamide, and (in some cases) plasma exchange. Toxin-induced prerenal AKI often responds to discontinuation of the offending agent, such as ACE inhibitors, ARB antagonists, aminoglycosides, penicillins, NSAIDs, or paracetamol.

The use of diuretics such as furosemide, is widespread and sometimes convenient in improving fluid overload. It is not associated with higher mortality (risk of death), nor with any reduced mortality or length of intensive care unit or hospital stay.

A low fat diet is indicated. The use of drugs which are known to have an association with pancreatitis should be avoided. Some patients benefit from the use of pancreatic enzymes on a supplemental basis. One study indicated that 57 percent of dogs, who were followed for six months after an acute pancreatitis attack, either continued to exhibit inflammation of the organ or had decreased acinar cell function, even though they had no pancreatitis symptoms.

During an acute flare-up, therapy is targeted at reducing the inflammation present, and dilating the pupil. Mydriasis is important, as pupillary constriction is the primary reason for pain. Anti-inflammatory therapy is usually given both systemically, often in the form of flunixin meglumine, and topically, as prednisolone acetate. The mydriatic of choice is atropine. In the periods between acute attacks, no therapy has been shown to be beneficial.

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.

There are no approved treatments for canine pancreatitis. Treatment for this disease is supportive, and may require hospitialization to attend to the dog's nutritional and fluid needs, pain management, and addressing any other disease processes (infection, diabetes, etc.) while letting the pancreas heal on its own. Treatment often involves "resting" the pancreas for a short period of time by nil per os/nothing per os (NPO)/nil by mouth (NBM), in which the patient receives no food or fluids by mouth, but is fed and hydrated by intravenous fluids and a feeding tube. Dehydration is also managed by the use of fluid therapy. However, a specialist from Texas A&M University has stated "There is no evidence whatsoever that withholding food has any beneficial effect." Other specialists have agreed with his opinion.

Canine pancreatitis is complex, often limiting the ability to approach the disease.

If neither hyperuricemia nor gout is present, then the risk of uric acid nephrolithiasis can be reduced by the use of antiuricosuric drugs. One should also consider eating a low purine diet. Additionally, making the urine pH more alkaline is protective.

The treatment of mesenteric ischemia depends on the cause, and can be medical or surgical. However, if bowel has become necrotic, the only treatment is surgical removal of the dead segments of bowel.

In non-occlusive mesenteric ischemia, where there is no blockage of the arteries supplying the bowel, the treatment is medical rather than surgical. People are admitted to the hospital for resuscitation with intravenous fluids, careful monitoring of laboratory tests, and optimization of their cardiovascular function. NG tube decompression and heparin anticoagulation may also be used to limit stress on the bowel and optimize perfusion, respectively.

Surgical revascularisation remains the treatment of choice for mesenteric ischaemia related to an occlusion of the vessels supplying the bowel, but thrombolytic medical treatment and vascular interventional radiological techniques have a growing role.

If the ischemia has progressed to the point that the affected intestinal segments are gangrenous, a bowel resection of those segments is called for. Often, obviously dead segments are removed at the first operation, and a second-look operation is planned to assess segments that are borderline that may be savable after revascularization.