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Cholecystitis : Overview

Author
Alan A Bloom, MD Associate Clinical Professor of Medicine, Albert Einstein College of Medicine; Attending Physician, Department of Gastroenterology, Veterans Affairs Hospital, Bronx

Alan A Bloom, MD is a member of the following medical societies: American College of Physicians, American Gastroenterological Association, American Medical Association, American Society for Gastrointestinal Endoscopy, New York Academy of Medicine, and New York Academy of Sciences


Coauthor(s)
Zahir Amin, MD, MBBS, MRCP, FRCR Consulting Staff, Department of Imaging, University College Hospital, UK

Zahir Amin, MD, MBBS, MRCP, FRCR is a member of the following medical societies: British Institute of Radiology, British Medical Association, and Royal College of Radiologists

BS Anand, MD Professor, Department of Internal Medicine, Division of Gastroenterology, Baylor College of Medicine

BS Anand, MD is a member of the following medical societies: American Association for the Study of Liver Diseases, American College of Gastroenterology, American Gastroenterological Association, and American Society for Gastrointestinal Endoscopy




Cholecystitis is defined as inflammation of the gallbladder that occurs most commonly because of an obstruction of the cystic duct from cholelithiasis. Ninety percent of cases involve stones in the cystic duct (ie, calculous cholecystitis), with the other 10% of cases representing acalculous cholecystitis.[1]

Risk factors for cholecystitis mirror those for cholelithiasis and include increasing age, female sex, certain ethnic groups, obesity or rapid weight loss, drugs, and pregnancy. Although bile cultures are positive for bacteria in 50-75% of cases, bacterial proliferation may be a result of cholecystitis and not the precipitating factor.




Acalculous cholecystitis is related to conditions associated with biliary stasis, including debilitation, major surgery, severe trauma, sepsis, long-term total parenteral nutrition (TPN), and prolonged fasting. Other causes of acalculous cholecystitis include cardiac events; sickle cell disease; Salmonella infections; diabetes mellitus; and cytomegalovirus, cryptosporidiosis, or microsporidiosis infections in patients with AIDS. For more information, see the Medscape Reference article Acalculous Cholecystopathy.

Uncomplicated cholecystitis has an excellent prognosis, with a very low mortality rate. Once complications such as perforation/gangrene develop, the prognosis becomes less favorable. Some 25-30% of patients either require surgery or develop some complication.

The most common presenting symptom of acute cholecystitis is upper abdominal pain. The physical examination may reveal fever, tachycardia, and tenderness in the RUQ or epigastric region, often with guarding or rebound. However, the absence of physical findings does not rule out the diagnosis of cholecystitis.

Delays in making the diagnosis of acute cholecystitis result in a higher incidence of morbidity and mortality. This is especially true for ICU patients who develop acalculous cholecystitis. The diagnosis should be considered and investigated promptly in order to prevent poor outcomes.

Initial treatment of acute cholecystitis includes bowel rest, intravenous hydration, correction of electrolyte abnormalities, analgesia, and intravenous antibiotics. For mild cases of acute cholecystitis, antibiotic therapy with a single broad-spectrum antibiotic is adequate. Outpatient treatment may be appropriate for cases of uncomplicated cholecystitis. If surgical treatment is indicated, laparoscopic cholecystectomy represents the standard of care.

Patients diagnosed with cholecystitis must be educated regarding causes of their disease, complications if left untreated, and medical/surgical options to treat cholecystitis. For patient education information, see the Liver, Gallbladder, and Pancreas Center, as well as Gallstones and Pancreatitis.

Ninety percent of cases of cholecystitis involve stones in the cystic duct (ie, calculous cholecystitis), with the other 10% of cases representing acalculous cholecystitis.[1]

Acute calculous cholecystitis is caused by obstruction of the cystic duct, leading to distention of the gallbladder. As the gallbladder becomes distended, blood flow and lymphatic drainage are compromised, leading to mucosal ischemia and necrosis.

Although the exact mechanism of acalculous cholecystitis is unclear, several theories exist. Injury may be the result of retained concentrated bile, an extremely noxious substance. In the presence of prolonged fasting, the gallbladder never receives a cholecystokinin (CCK) stimulus to empty; thus, the concentrated bile remains stagnant in the lumen.[2, 3]

A study by Cullen et al demonstrated the ability of endotoxin to cause necrosis, hemorrhage, areas of fibrin deposition, and extensive mucosal loss, consistent with an acute ischemic insult.[4] Endotoxin also abolished the contractile response to CCK, leading to gallbladder stasis.

Etiology

Risk factors for calculous cholecystitis mirror those for cholelithiasis and include the following :

  • Female sex
  • Certain ethnic groups
  • Obesity or rapid weight loss
  • Drugs (especially hormonal therapy in women)
  • Pregnancy
  • Increasing age

Acalculous Cholecystitis is related to conditions associated with biliary stasis, to include the following :


  • Critical illness
  • Major surgery or severe trauma/burns
  • Sepsis
  • Long-term total parenteral nutrition (TPN)
  • Prolonged fasting


Other causes of acalculous cholecystitis include the following :

  • Cardiac events, including myocardial infarction
  • Sickle cell disease
  • Salmonella infections
  • Diabetes mellitus[5]
  • Patients with AIDS who have cytomegalovirus, cryptosporidiosis, or microsporidiosis
  • Patients who are immunocompromised are at increased risk of developing cholecystitis from a number of different infectious sources. Idiopathic cases exist.

Epidemiology




An estimated 10-20% of Americans have gallstones, and as many as one third of these people develop acute cholecystitis. Cholecystectomy for either recurrent biliary colic or acute cholecystitis is the most common major surgical procedure performed by general surgeons, resulting in approximately 500,000 operations annually.

Age distribution for cholecystitis



The incidence of cholecystitis increases with age. The physiologic explanation for the increasing incidence of gallstone disease in the elderly population is unclear. The increased incidence in elderly men has been linked to changing androgen-to-estrogen ratios.


Sex distribution for cholecystitis




Gallstones are 2-3 times more frequent in females than in males, resulting in a higher incidence of calculous cholecystitis in females. Elevated progesterone levels during pregnancy may cause biliary stasis, resulting in higher rates of gallbladder disease in pregnant females. Acalculous cholecystitis is observed more often in elderly men.

Prevalence of cholecystitis by race and ethnicity




Cholelithiasis, the major risk factor for cholecystitis, has an increased prevalence among people of Scandinavian descent, Pima Indians, and Hispanic populations, whereas cholelithiasis is less common among individuals from sub-Saharan Africa and Asia.[6, 7] In the United States, white people have a higher prevalence than black people.

Prognosis



Uncomplicated cholecystitis has an excellent prognosis, with very low mortality. Most patients with acute cholecystitis have a complete remission within 1-4 days. However, 25-30% of patients either require surgery or develop some complication.


Once complications such as perforation/gangrene develop, the prognosis becomes less favorable. Perforation occurs in 10-15% of cases. Patients with acalculous cholecystitis have a mortality ranging from 10-50%, which far exceeds the expected 4% mortality observed in patients with calculous cholecystitis. In patients who are critically ill with acalculous cholecystitis and perforation or gangrene, mortality can be as high as 50-60%.




Refferences :


1. Huffman JL, Schenker S. Acute acalculous cholecystitis - a review. Clin Gastroenterol Hepatol. Sep 9 2009;[Medline]. 




2. Donovan JM. Physical and metabolic factors in gallstone pathogenesis. Gastroenterol Clin North Am. Mar 1999;28(1):75-97. [Medline].

3. Sitzmann JV, Pitt HA, Steinborn PA, et al. Cholecystokinin prevents parenteral nutrition induced biliary sludge in humans. Surg Gynecol Obstet. Jan 1990;170(1):25-31. [Medline].

4. Cullen JJ, Maes EB, Aggrawal S, et al. Effect of endotoxin on opossum gallbladder motility: a model of acalculous cholecystitis. Ann Surg. Aug 2000;232(2):202-7. [Medline]

5. Forbes LE, Bajaj M, McGinn T, et al. Perihepatic abscess formation in diabetes: a complication of silent gallstones. Am J Gastroenterol. Apr 1996;91(4):786-8. [Medline].

6. Huang J, Chang CH, Wang JL, Kuo HK, Lin JW, Shau WY, et al. Nationwide epidemiological study of severe gallstone disease in Taiwan. BMC Gastroenterol. Aug 22 2009;9:63. [Medline].

7. Lee SW, Yang SS, Chang CS, Yeh HJ. Impact of the Tokyo guidelines on the management of patients with acute calculous cholecystitis. J Gastroenterol Hepatol. Aug 3 2009; [Medline]


Source : http://emedicine.medscape.com
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An Update on Emerging Therapies for the Practical Management of Diabetes

Eleuterio Ferrannini, MD; Dr. Diamant; Dr. Barnett; Dr. Davies, PhD; Dr. Hanefeld, PhD
CME Released: 10/24/2011; Valid for credit through 10/24/2012




Despite the availability of multiple pharmacologic agents, the treatment of patients with type 2 diabetes mellitus remains suboptimal. Given the disease's high and increasing prevalence, the morbidity, mortality, and economic consequences of type 2 diabetes are a great burden to patients, healthcare systems, and society.


Newer incretin-based agents for the treatment of type 2 diabetes include the glucagon-like peptide-1 (GLP-1) agonists, such as exenatide (now also available as a once-weekly injection) and liraglutide, as well as the dipeptidyl peptidase-4 (DPP-4) inhibitors, such as sitagliptin, saxagliptin, and the recently approved linagliptin, which can be used as a single dose even in patients with moderate to severe renal impairment.

Both classes have important clinical advantages in terms of weight control, reduced risk for hypoglycemias, and their effects on the insulin-secreting beta cells.

The latest emerging class is the SGLT2 inhibitors, which suppress glucose reabsorption in the kidney, thereby leading to the excretion of glucose in the urine. Once approved, they will be the only orally available antidiabetic drugs to trigger body weight reduction. They are also unique in that their glucose-lowering mechanism is completely insulin independent.

Together, these new classes have greatly expanded the choices for clinicians to help patients with type 2 diabetes achieve tighter glycemic control and better outcomes today and in the future.


Source : http://www.medscape.org/viewarticle/751705




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New Frontiers in Diabetes Management: The Next Generation of Insulins

Bernard Zinman, MD; Stephen Colagiuri, MD; Stephen Gough, MD, FRCP; Chantal Mathieu, MD, PhD
CME Released: 12/22/2011; Valid for credit through 12/22/2012


A wealth of clinical evidence indicates that tight glycemic control can prevent or delay complications in both type 1 and type 2 diabetes, but achieving this goal is a continuing challenge.

Clinicians often do not initiate or intensify therapy appropriately in their patients with diabetes. More aggressive treatment is necessary and should include earlier introduction and appropriate intensification of insulin therapy in patients with type 2 diabetes. Unfortunately, earlier initiation of insulin is hindered by fear of hypoglycemia, weight gain, and injections. Fear of hypoglycemia remains a major challenge for both physicians and patients and is a significant barrier to achieving optimal glycemic control.


Physicians treating patients with diabetes need to be comfortable with the use of insulin, as well as confident about integrating new formulations of insulin into their diabetes treatment plans.


Neutral protein Hagedorn (NPH) insulin is associated with a distinct peak at 6 hours, which may cause hypoglycemia, does not provide 24-hour control, and is associated with high inter- and intra-individual variability.

The advent of the long-acting insulin analogues in the past decade has revolutionized insulin therapy by offering flexibility in dosing and more options for tailoring therapy.

Next-generation basal insulin analogues are being studied, addressing the major challenges in diabetes care. The furthest along in development is degludec, with an elimination half-life longer than 24 hours. It is associated with significantly less pharmacodynamic variability which may be directly related to the drug's lower rate of hypoglycemic episodes.

Another basal insulin analogue designed to deliver improved clinical features is LY2605541, which has just moved into phase 3 clinical development.


Source : http://www.medscape.org/viewarticle/755996



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