Acute pancreatitis is an episode of cellular injury and inflammation of the pancreas parenchyma triggered by autodigestion of pancreatic parenchyma by abnormally activated pancreatic enzymes, its manifestations ranges from mild, moderate-severe and severe pancreatitis. Most episode of acute pancreatitis resolved completely while some develop recurrent acute pancreatitis and in turn progressing to chronic pancreatitis and its sequelae. While many etiologies known may cause acute pancreatitis, current theories propose three mechanism that may be involved in the pathogenesis of acute pancreatitis i.e. duct obstruction, direct acinar injury and defective intracellular transport. Recommendations from current guidelines are very useful to treat acute pancreatitis, few groundbreaking changes from the previously dated guidelines on treating acute pancreatitis are also made,providing us dated evidence-based approach to treat acute pancreatitis. Judicious and aggressive treatment are needed to minimize the damaged area of involved pancreatic parenchyma. Holistic prevention is neededto minimize the incidence of acute pancreatitis, pushing down the numbers of recurrent acute pancreatitis and ultimately may decrease the incidence of chronic pancreatitis and its sequelae.

Acute cholangitis (AC) is a biliary tract emergency which causes significant morbidity and mortality. The direct cause of death in AC is sepsis that leads to irreversible shock and multiple organ failure. The most common predisposition are bile duct stones and previous invasive manipulation of the biliary tree. Biliary infection and biliary obstruction are the two main factors in pathophysiology of AC. Gram-negative bacteria are isolated frequently from bile and blood culture in cholangitis. The most common cause of biliary obstruction is gallstone.The Charcot’s triad which commonly has been used to diagnose AC is severely limited and the clinical presentation of the disease has wide spectrum ranging from mild symptoms to severe life-threatening disease. Thus, the use of the most updated Tokyo Guidelines (TG18) is imperative to diagnose the disease and to assess the severity. The TG18 diagnostic criteria is based on the presence of systemic inflammmation, cholestasis, and evidence on imaging studies of biliary tract. The prompt treatment is tailored according to severity assessed by TG18. Initial treatment includes sufficient fluid replacement, hemodynamic control, electrolyte compensation, intravenous antibiotic administration, and intravenous analgesic administration.  The definitive treatment which related to the pathophysiology of the disease are biliary drainage and antibiotic administration.