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Acute Cholecystitis

Acute cholecystitis is an acute inflammatory process of the gallbladder accompanied with right upper abdominal pain, tenderness, and fever and is usually triggered by obstruction of the cystic duct.  The most common cause of acute cholecystitis is a continuous obstruction of the cystic duct by gall stones causing acute inflammation of the gallbladder.

The prevalence of cholecystitis is similar to the prevalence of gallstones.  Cholecystitis commonly found in women with 2-3 times greater frequency than in males.  Pregnancy can also increase the risk of cholecystitis, because progesterone in pregnant women can cause gall bladder emptying and common bile litogenesis estrogen increases in pregnancy.  In addition, cholecystitis also influenced by age.  Get older  the greater the risk of gallstones which can cause cholecystitis, because estrogen androgen inhibits enzimatik conversion of cholesterol to bile acids that increase cholesterol saturation of bile.  The groups of different ethnicities, one of them. Indians and Scandinavians have an increased risk of gallstones that can cause cholecystitis.  The risk is lower in sub-Saharan Africa and Asia, in the United States tend to whites than blacks.  Lifestyle factors such as diet, obesity, and medecines separately by hormonal especially in women.
Many patients with cholecystitis to complete recovery for 1-4 days, although it needs to be done surgery or cause complications.  Patients with cholecystitis have a mortality rate of around 10-50%, with 4% of patients suffering from cholecystitis calculous, 15% and 10-15% empysematous cholecystitis caused by perforation.

Physiology bile production and flow
Bile produced by the liver as much as 500-600 mL per day which then flowed into the gallbladder and stored there.  Hepatic bile is an isotonic and contain electrolyte which has a composition similar to plasma electrolyte composition.  But the electrolyte composition of bile in the gallbladder that are different from the hepatic bile because many inorganic anions (chloride and bicarbonate) and water reabsorbed through gallbladder epithelium, so that the bile concentration increased from 3-4 g / dL to 10-15 g / dL  in the gallbladder.
The main ingredient contained in the bile are bile acids (80%), phospholipids and non esterified cholesterol (4%).  Lecithin is a major phospholipid found in bile, although it also found lisolesitin and phosphatidil etanolamin in a small percentage.  Phospholipids would be hydrolyzed in the intestine and did not participate in the enterohepatic cycle.
Instead of bile acids into the enterohepatic cycle except litokolat acid.  Some of the major bile acids are cholic acid (cholic acid) and (chenodeoxycholic acid).
These acids conjugated with glycine and taurine, and in the lumen of the colon converted by bacteria into secondary bile acids (amino acids deoxycholate and litokolat).  Acid litokolat almost not found in bile, because this acid is not included in the enterohepatic cycle.  Bile acids are detergent-like molecules, can dissolve substances that are basically insoluble millimolar, bile acid molecules will aggregate to form aggregates called micelles (micelle).  Solubility of cholesterol in bile depends on the concentration of cholesterol itself and comparison between bile acids and lecithin.  Comparison of normal will dissolve cholesterol, whereas the ratio of abnormal causes precipitation of crystals of cholesterol in bile.  This is one of the factors the initial formation of cholesterol stones.  The human body efficiently conserve bile acids through the enterohepatic circulation.
Bile acids, either not conjugated or conjugated, are passively absorbed along the intestinal lumen, but active transport as important role in the conservation of bile acids.  Transport activism is particularly the case in the distal ileum.  Bile acids are absorbed into the portal flow and taken back by the hepatocytes, then reconjugated and secreted.  Under normal circumstances, bile acid enterohepatic circulation experience as much as five to ten times a day.  Bile acid absorption through the intestinal lumen is very efficient, so that bile acids are wasted in faeces only about 0.3 to 0.6 g per day, and the amount will be replaced by de novo synthesis of bile acids in the liver.  Bile acids returning to the liver via enterohepatic circulation will inhibit the de novo synthesis and enterohepatic circulation interruption in return will increase bile acid synthesis.
In the fasting state, Oddi sphincter pressure increased so that impede the flow of bile from the duct into the duodenum choledochus.  This prevents the reflux of duodenal contents into the duct choledochus and also facilitate gallbladder filling.  Cholecystokinin released by the duodenal mucosa in response to amino acid intake of fat and otherwise facilitate the emptying of the gallbladder.
Cholecystokinin cause gall bladder contraction and relaxation of sphincter of Oddi, so that bile can flow from the gallbladder into the duodenum.

  Etiology and Pathogenesis
In nearly 90% of cases accompanied by Cholelitiasis.  Inflammatory response caused by three factors, namely, mechanical, chemical, and bacterial.  Mechanical inflammation due to increased intra-luminal pressure and stretch the lead to depressed blood vessels and ischemia of the mucosal wall infarction and gangrene can occur.  Chemical inflammation caused by the release lisolesitin (due to the action of phospholipase on lecithin in bile), reabsorption of bile salts, prostaglandins and other inflammatory mediators are also involved.  Lisolesitin toxic gallbladder mucosa.  Bacterial inflammation that play a role in 50-85% of cases of acute cholangitis.  Germs are often isolated from the culture fluid gall bladder, among others, E.  Coli, Klebsiella spp, Streptococcus spp and Clostridium spp.
Generally cholecystitis is associated with colelithiasis.  Cholecystitis

Clinical Overview
Complaints are typical for the attack is acute cholecystitis biliary colic and tenderness as well as an increase in body temperature.  Nearly 60-70% of patients reported ever have previous abdominal colic pain that healed spontaneously.  The pain often occur late at night or dawn, usually on the upper right quadrant of the abdomen or epigastrium and radiating down the right corner of the scapula, the right shoulder.  Pain feels like in the drill or the like is pressed and no comfortable body position.  Pain usually increases to a plateau and can last for 30-60 minutes without abating, his trademark for more than three hours and after that the pain shifted from the epigastrium to the right quadrant of the abdomen, not like a short spasm of biliary colic.
Attacks can be triggered by eating fatty foods or heavy meals at night.  The patient was sweating, lying when moving and curved body position.  Often accompanied by nausea, vomiting and fever.  The spectrum of symptoms in acute cholecystitis wide, in some patients into severe and acute pain in a short time.
On physical examination of patients obtained pain in the right upper quadrant which often extends to the epigastrium.  Classic signs of Murphy showed significant pain and limited inspiration on palpation (that in) below the right costal arch.  In most cases (30-40%) can be touched a gallbladder mass.
Jaundice observed in 20% of cases, mostly mild (bilirubin <4.0 mg / dl).  If the bilirubin concentration is high, should be considered a stone in the bile duct extrahepatic.
Laboratory tests found leukocytosis and counts that showed a shift to the left.  Disruption of liver function tests such as the increase of serum bilirubin, alkaline phosphatase / gamma-GT and serum transaminase suspicious biliary tract obstruction (stone choledochus).  The increase in levels of serum amylase and lipase striking or suspicious of acute pancreatitis.
Ultrasound examination will show gallstones in 90-95% of cases, gallbladder wall thickening (edema), Murphy sign and  pericholestitic cholesyntigraphy (eg HIDA) will confirm the diagnosis when biliary tract showed no visualization of the gallbladder which was evidence of duct obstruction  cystic.

Diagnosis of acute cholecystitis is established on the basis of disease history typical physical examination.  The existence of the triad of right upper quadrant pain, fever and acute cholecystitis leukocytosis very suspicious.  Abdominal ultrasound examination showed edema and the presence of gallbladder stones in it in most cases.

Complications of Acute cholecystitis
a.  Empyema and gallbladder hydrops
gallbladder empyema usually occurs as a result of progression from acute cholecystitis with persistent cystic duct obstruction, and superinfection with stagnant bile which is accompanied by the formation of pus.
The clinical manifestations  resembling cholangitis with high fever, severe pain in the right upper quadrant and leukocytosis  real.  Empyema at high risk for gram-negative sepsis or perforation.  When the diagnosis suspicious circumstances, immediate surgical intervention with an appropriate antibiotic protection.  Or mucocele from gallbladder hydrops may also arise as a result of prolonged obstruction cystic duct, usually by a large solitary stone.  In these circumstances, a clogged gallbladder lumen widened with progressive by mucus (mucocele) or by a clear transudate (hydrops).  On physical examination found the mass of visible, easily palpable, not pain that sometimes extends from the upper right quadrant to the right iliac fossa in.  Usually asymptomatic although may arise chronic pain in the right upper quadrant.  In these patients needs to be done cholecystectomy.
b.  Gangrene and gallbladder perforation
gangrenous gallbladder caused by ischemia and necrosis of the wall and predispose to the occurrence of perforation.  Gallstones may erode the wall of a necrotic.  Another situation that can be reason including severe distension gallbladder, vasculitis, diabetes mellitus, empyema resulting torque of artery occlusion.  Perforation usually occurs in the fundus, which is part of at least vasculary perforation into the omentum will cause pericholesistic abscess, perforation into adjacent organs will cause internal  fistula biliary into the duodenum, jejunum, hepatic flexure of the colon or the stomach.  More rarely happen again 1-2% free perforation into the peritoneal cavity, the prognosis is poor with mortality rates around 30%.  Handling of adequate antibiotics and surgical measures as soon as possible.
c.  Gallstone ileus
when a large gallstone (> 3.5 cm) into the fistula and into the intestine, gallstone ileus can occur.  Location valvulus ileocaecal obstruction is common.  In these patients there were complaints of symptoms and radiological examination of intestinal obstruction.
Diagnosis is confirmed by radiological examination.  Plain abdomen showed small bowel obstruction in the presence of the bile duct and an ectopic gallstone.  Action choice is laparotomy with stone extraction (or push the stone into the colon)
d.  Abscess pericholesistic
pericholecystic abscess is a form of perforation most often occurs with localized content and tightly restricted by the omentum and adjacent viscera.  This situation need to be suspected when a slow recovery of acute cholecystitis, specially there is  second episode of fever, right upper abdominal pain or mass arising in the upper right abdomen.  By ultrasonography and CT scan of this abscess will appear.  This situation occurs mainly in older patients or patients receiving long-term steroid with a fever and a minimal inflammatory response.
e.  Cholecystitis emphysematus
This term is used to indicate gallbladder infection with gas forming organisms, E coli, Clostridium welchii or Streptocoocus anaerobic.  Patients in a state of severe pain, a palpable mass in the abdomen.  On radiological examination of the gallbladder appears as a shadow of a pear limited gas formed is very clear.  Sometimes it appears air infiltrating the wall and surrounding tissue.  In the upright position the liquid surface appears in the gallbladder.  CT scan can also reveal the gas.  The form of adequate antibiotic therapy and surgery.

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