These alternative diagnoses include but are not limited to:
Perforated peptic ulcer
Acute pancreatitis
Liver abscess
Pneumonia
Myocardial ischemia
Hiatal hernia
Biliary colic
Choledocholithiasis
Cholangitis
Appendicitis
Colitis
Acute peptic ulcer exacerbation
Amoebic liver abscess
Acute intestinal obstruction
Kidney stone
Biliary ascariasis

Treatment
Surgery
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 Calots triangle. For delayed surgery, the most common reason was fibrotic adhesions. Other
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.
As a rough guide, a non-infected ulcer can be expected to heal at approximately 0.6mm/day. Complications
In cases where the ulcer is not healing:

Is there a persistent source of irritation? Foreign body
Self traumatisation
Iatrogenic. Is it infected? Review antibiotic therapy
C+S if not already performed. Immunosuppression? Cushings
Steroid therapy. Compliance? Is what youve prescribed getting onto the eye? None of the above? Abnormal epithelium may have formed, keratectomy may be appropriate.Melting ulcers reflect inappropriate collagenolysis of the corneal stroma, by matrix-metalloproteinases (MMPs). Bacterial pathogens (especially Pseudomonas and β-haemolytic Streptococcus) induce the corneal epithelial cells and resident leucocytes to upregulate pro-inflammatory, and MMP-activating cytokines (IL-1,-6 and -8). These bacteria can also produce their own proteinases. The combination of exogenous, and upregulated endogenous, proteinases leads to a rapid breakdown of collagen, with the characteristic melting appearance. Untreated this can lead to perforation within 12 hours (so act hard and fast!). There are several therapeutic options for inhibiting MMPs:

Autogenous serum – administer topically as often as possible. Keep refrigerated and change every 8 days. EDTA  - 0.05% q1h
Acetylcysteine – 5-10% q1h
Tetracyclines – Doxycycline especially has been shown to have anti-MMP effects
Tetanus antitoxin – can be delivered sub-conjunctivally. Contains macroglobulins with anti-collagenase effects.A combination of the above may be necessary early in the disease course. Effective antibiosis is also paramount, and gentamicin is a good empirical choice (although there are some reports of gentamicin-resistant Pseudomonas species). Obviously, treating an eye this frequently in practice will be difficult, so referral is probably the best option. See also
Corneal abrasion
Keratitis


== References ==