Such tests include:
Computed tomography of the abdomen/pelvis
Abdominal or pelvic ultrasound
Endoscopy and/or colonoscopy

Management
The management of abdominal pain depends on many factors, including the etiology of the pain. In the emergency department, a person presenting with abdominal pain may initially require IV fluids due to decreased intake secondary to abdominal pain and possible emesis or vomiting. Treatment for abdominal pain includes analgesia, such as non-opioid (ketorolac) and opioid medications (morphine, fentanyl). Choice of analgesia is dependent on the cause of the pain, as ketorolac can worsen some intra-abdominal processes. Patients presenting to the emergency department with abdominal pain may receive a "GI cocktail" that includes an antacid (examples include omeprazole, ranitidine, magnesium hydroxide, and calcium chloride) and lidocaine. After addressing pain, there may be a role for antimicrobial treatment in some cases of abdominal pain. Butylscopolamine (Buscopan) is used to treat cramping abdominal pain with some success. Surgical management for causes of abdominal pain includes but is not limited to cholecystectomy, appendectomy, and exploratory laparotomy. Emergencies
Below is a brief overview of abdominal pain emergencies. Epidemiology
Abdominal pain is the reason about 3% of adults see their family physician. Rates of emergency department (ED) visits in the United States for abdominal pain increased 18% from 2006 through to 2011. This was the largest increase out of 20 common conditions seen in the ED. The rate of ED use for nausea and vomiting also increased 18%. References


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Metabolic responses
Most neurons have the ability to use other fuels besides glucose (e.g. lactic acid, ketones). Knowledge of the "switchover" process is incomplete. The most severe neuroglycopenic symptoms occur with hypoglycemia caused by excess insulin because insulin reduces the availability of other fuels by suppressing ketogenesis and gluconeogenesis. A few types of specialized neurons, especially in the hypothalamus, act as glucose sensors, responding to changing levels of glucose by increasing or decreasing their firing rates. They can elicit a variety of hormonal, autonomic, and behavioral responses to neuroglycopenia. The hormonal and autonomic responses include release of counterregulatory hormones. There is some evidence that the autonomic nervous system can alter liver glucose metabolism independently of the counterregulatory hormones. Adjustment of efficiency of transfer of glucose from blood across the blood–brain barrier into the central nervous system represents a third form of compensation which occurs more gradually. Levels of glucose within the central nervous system are normally lower than the blood, regulated by an incompletely understood transfer process. Chronic hypoglycemia or hyperglycemia seems to result in an increase or decrease in efficiency of transfer to maintain CNS levels of glucose within an optimal range. In both young and old individuals, the brain may habituate to low glucose levels with a reduction of noticeable symptoms, sometimes despite neuroglycopenic impairment. In insulin-dependent diabetic patients this phenomenon is termed hypoglycemia unawareness and is a significant clinical problem when improved glycemic control is attempted.