Acute cholecystitis

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* Etiology, incidence, and risk factors

* Classification according to etiology

* Rating anatomoclinical

* Clinical Picture

* Scan Clinic

* Complementary Tests

* Complications of acute cholecystitis

* Treatment

* Classes rare acute cholecystitis

* Bibliography

Acute cholecystitis is the condition most spectacular feature of the pathology of the bile ducts is an inflammatory process that develops in the gallbladder wall, being the most common complication of chronic cholecystitis. It is one of the original paintings emergency abdominal frequently surpassed only by acute appendicitis.

Etiology, incidence, and risk factors:

The main cause of acute cholecystitis cholelithiasis whose calculations obstruct the cystic generating 95% of cases. In 5% of acute cholecystitis due other causes such as edema of the mucosa of the cystic duct, and this percentage includes acute acalculous cholecystitis which attend to other factors such as sepsis, trauma, alcohol, collagen disorders, syndrome Acquired immunodeficiency, and diabetes.

Nothing should be mentioned as promoters of acute cholecystitis, less frequently, volvulus of the gallbladder, the angulation of vesicular trap, benign tumors, cysts, gallbladder cancer, and even exceptionally vascular anomalies. Acute cholecystitis occur more often in women than in men and become more common with age in both sexes.

Classification according to etiology:

Mechanical 1.Colecistopata

2.Colecistopata septic

Chemical 3.Colecistopata

4.Colecistopata ischemia (vascular injury)

Gallbladder mechanics

It is the most frequent acute cholecystitis.

o Organic causes:

Cholelithiasis

Scarring of the cystic lesions

Primary neoplasm vesicular

Hepatocoledoco primary neoplasm

Metastatic adenopathy

Volvulus of the gallbladder.

Parasitic

o Causes spasmodic:

Spasm of the sphincter of Liitkens-Oddis

Septic gallbladder disease:

* By continuity canalicular

* By hematogenous (metastatic)

* By contiguity

Most common germs

: Anaerobic Gram negative

Proteus, E. col., Klebsiella, Enterobacter and Bacteroides fragilis

The frequency of anaerobic infections in the elderly increases.

Gallbladder chemistry:

Is one in which penetration occurs inside pancreatic juice by biliopancreatic circulatory disturbance.

 

Gallbladder disease (very rare variety):

Etiology:

Volvulus of gallbladder with cystic artery compression

Thrombosis or embolism capable of causing infarction of the gallbladder wall.

Extrinsic compression of the feeding vessels by adenopathy or embedded stones

in the cystic duct.

Syndrome (ptosis) stroke-Couvelaire gregoine visceral

Cholecystitis exfoliatrices dissecans.

CLASSIFICATION anatomoclinical

Edematos gallbladder: – Where the wall has a varying degree of vascular congestion and edema

Gallbladder suppurative: – There is significant inflammatory cell infiltration of the mucosa with obstruction this in relation to vascular disorders.

Gangrenous gallbladder: – Where there is acute hemorrhagic infarction with necrosis and perforation is the successive stage.

Perforated Gallbladder: The gallbladder is presented-swollen, edematous, with hyperemic serosa, with areas of necrosis and pseudo membrane.

Higher stage ignition occurs and infiltration of neighboring organs leading to Plastron Vesicular which involved the transverse colon, right colon and its mesentery, omentum, stomach and duodenum and anterior parietal peritoneum.

Physiopathogenesis

A consequence of cystic obstruction, bladder, it is affected gallstone or stepwise acalculous biophysical, biochemical and bacteriological hypertensive, which follows one of two clinical types: one is the pathophysiological regression in a 72 hour period that occurs on average 90 to 95% of cases, the other progressive behavior is persistent and worsening of disease complications.

Bile trapped concentrated chemical and causes inflammation of the mucosa vesicular release phosphokinase which splits phospholipids and cause pressure buildup in the bladder, which can lead to bacterial infection and drilling with increased virulence. Mucus production increases pressure and generates intra vesicular pain affecting the venous and arterial wall ischemia, infarction areas, drilling and even gangrene of the gallbladder. The systemic impact will result in bacteremia, fever, leukocytosis and increased transaminases.

Clinical picture:

Symptoms

Acute cholecystitis is a symptom complex characterized by local events in the right upper quadrant and systemic manifestations involving the rest of the body.

Local signs and symptoms:

1. Pain: Located on the Murphy point below the costal margin in the midclavicular line and radiates to the shoulder and scapular region homo side. It occurs usually after fatty foods or foods that are not tolerated by the liver, is extremely painful and kept for several hours, usually seventy-two, is a good indicator of the process, because if the condition refers resolved or increases intensity when a complication occurs.

2. Painful Palpable Mass: location subcostal midclavicular line. Corresponds to full inflamed gall bladder. It is painful on palpation. It occurs from 20 to 33%.

Systemic signs and symptoms:

1. Nausea and Vomiting: In 60% of cases.

2. Mild fever: 38 to 39 , often 50 to 60%, possibly with chills.

3. Jaundice: appears in 20% of patients, is of slight intensity. Be explained by understanding the common bile duct by the swollen gallbladder.

4. Leukocytosis Moderate: From 12,000 to 15,000 leukocytes caused by the proliferation and virulence of bacteria and the eventual content vesicular bacteremia.

Clinical examination:

1.Hipersensibilidad in the upper right quadrant, the epigastrium or both sites.

2.Signo Murphy: Interruption of inspiration during deep palpation of the right upper quadrant, is not constant but pathognomonic when present.

3.Se palpable swelling in vesicular region.

4.Ictericia in 10% of cases.

The clinical course of acute cholecystitis is almost periodic. Symptoms are maintained for a period of 72 hours in 90% of patients and spontaneously transmitting the patient to normalize the eight to ten days. In contrast, if the picture is not unlike forwards and intensifies the pain, local signs, fever, leukocytosis and worsens the condition of the patient must be admitted imminent or has already been installed as a complication likely empyema , drilling or other.

Complementary Tests

Plain abdominal radiography:

Although it is necessary in the study of abdominal pain, rarely provides specific evidence of acute cholecystitis. In 20% can be calculations, if they are radiopaque. In emphysematous cholecystitis will outline the silhouette of the gallbladder.

Abdominal ultrasound:

Is the diagnostic procedure of choice. It is a safe, fast and accurate for diagnosis of acute cholecystitis, with a sensitivity ranging between 90 and 95%, and specificity between 70 and 90%. This depends on a number of criteria to be classified as major or minor.

Older UTS criteria:

* Lithiasis impacted in the neck of the gallbladder or in the cystic duct.

* Edema of the gallbladder wall greater than 3 mm.

* Band and continuous intermediate focal hyperechoic.

* Gas intraluminal with posterior shadowing.

* Murphy ultrasound, consisting of low focal vesicular hypersensitivity transducer. Although operator dependent, has a positive predicative value of 92%.

* Marked irregularity and gallbladder wall thickening dela asymmetric present in gangrenous cholecystitis.

UTS Minor criteria:

* Presence of gallstones.

* Liquid vesicular peri absence of ascites, which may involve a localized perforation and abscess.

* Bile ecstasy.

* Expansion of the gallbladder and spherical shape.

Scintigraphy:

Use iminodiacetic acid derivatives labeled with 99m Tc. The sensitivity ranges from 95 to 97% and specificity between 90 and 97%. The absence of evidence vesicular filling cystic obstruction and is the hallmark of acute cholecystitis, while viewing a normal gallbladder discarded. You need to take pictures later, since in many situations, such as liver disease and choledocholithiasis, gallbladder can be filled after several hours.

To avoid this delay can be used iv morphine sulfate in patients without filling in 30-60 minutes. This increases the pressure of the sphincter of Oddi and favors the reflux of bile into the gall bladder. There can be false-positive chronic cholecystitis, liver disease, prolonged fasting, total parenteral nutrition and critical patients.

Other techniques:

Oral cholecystography is not useful in acute cholecystitis.

ERCP is only appropriate in patients who have also impacted stones

in the common bile duct.

Tomography and magnetic resonance imaging are indicated only in the

differential diagnosis of selected cases.

Complications of acute cholecystitis

a. Drilling 1. With localized action

2. With generalized peritonitis

b. Abscess pericholecystic

c. Empyema

d. Rupture

e. Gangrene

f. Fistulization 1. Colecistointestinal

a) cholecystoduodenal

b) Colecistoyeyunal

2. Cholecystocolonic

3. Colecistoduodenocolnica

g. Gallstone ileus

h. Subphrenic abscess

a.Perforacin

The drill has two modes: with action localized and generalized peritonitis.

1.

Drilling invasion is locating localized loss around the vesicle. Occurs when peritoneal reaction with concurrence of omentum to confine the pus and cause an abscess or localized peritonitis pericholecystic.

Signs local and systemic effects are exacerbated, the pain intensifies with reaction-parietal peritoneum contracture. General symptoms also increase: fever, chills, and leukocytosis of 20,000 or more. For diagnostic ultrasonography is useful.

Treatment: Cholecystectomy evacuation and drainage of abscesses, based on antibiotics and bactericides.

2. Perforation with generalized peritonitis is spreading the biliopus, the rest of the peritoneal cavity, is when there is no reaction and polluted peritoneoepiploica tabicante entire peritoneal cavity causing generalized peritonitis. Signs and symptoms are related to the latter condition.

The diagnosis is clinical and imaging with diagnostic puncture led to propitiate culture and sensitivity of the content.

Treatment is the policy of generalized peritonitis with effusion and peritoneal washing, and cholecystectomy if the general permit, but evacuation of operational risk is high. If the patient’s general complications permit shall be cholecystectomy. . Mortality reaches 15-20%.

b. Abscess pericholecystic

It is the most frequent complications. It consists of the collection of pus around the gallbladder from a perforation of the same or even without perforation or rupture vesicular contaminants diapedesis through vesicularEl Wall-imaging diagnosis is clinical. The treatment consists in evacuating, flushing and cholecystectomy.

c. Empyema (Piocolecisto)

It is the transformation of the contents of the vesicle in pus. It’s invasion, proliferation and increased virulence of bacteria that contaminate the contents of the vesicle, transforming it into a pocket of pus under tension.

The symptoms of empyema corresponds to the infection of the gallbladder and abdominal sepsis with the complex local and systemic pain, fever, tachycardia, chills and leukocytosis of about 20,000. It is the most common complication, about 50% of them, with a mortality rate of 15%.

The diagnosis is clinical, and hematic ecosonographic. Treatment consists of urgent cholecystectomy or cholecystostomy if Local phlogosis and poor patient require less operative time and less traumatic action.

d. Vesicle breakdown

It has been described as one of the most serious complications. Converge pathologically increased vesicular content and its action on the walls thereof experiencing venous circulatory collapse of arterial ischemia and myocardial presence multiple; increased intra vesicular tension acting on a weakened wall of the break itself.

The violent outcome of highly contaminating vesicular content produces a localized peritoneal reaction initially but quickly spread. The diagnosis is ecosonographic. Treatment is cholecystectomy with drainage. Mortality is high, around 20%.

e. Vesicular Gangrene

It is the most advanced state of damage of the gallbladder wall and clinically the most severe. It is caused by ischemia and necrosis of the localized wall or full distention of the bladder with a content empiematoso; may contribute twisting of the vesicle. It often occurs in diabetics and immunocompromised.

In the presence of anaerobic bacteria and clostridia predominate.

The gangrenous gallbladder perforation and rupture may occur with temporary relief of pain cessation of strife that is reactivated by the irritation caused extravasation content. The imaging diagnosis is made and treatment is cholecystectomy patient with antibiotic saturation.

f. Fistulization

Fistulas are the 2 to 3% of the complications, the most common are colecistocolnicas colecistoduodenales and constituting the first 75% and the latter 15% of the universe of vesicular fistula. Next in colecistoduodenocolnicas often, and colecistoentricas colecistogstricas. Fistulas arise by the apposition of the vesicle to a neighboring viscus whose wall and irritates the gallbladder perforation occur compromises viscus wall that is attached, confined to peritoneal adhesions.

Are difficult to diagnose clinically, and occasionally can be detected by staining of the bile ducts in a radiology gastroduodenal or colonic. Treatment consists of cholecystectomy and raffia defect in the gastrointestinal tract. (Fistulectomy)

g. Gallstone ileus

Is the complication caused by the passage of a gallstone from 2 to 2.5 inches colecistoentrica fistula, either in the duodenum or jejunum and accommodation or “trapping” of calculation in the terminal ileum (usually ileocecal valve) for failing to cross it. The symptomatology corresponds to an intestinal obstruction acute abdomen.

The radiographic image providing gastrointestinal transit known as “white snake head” by the presence of contrast media in the ileum and the image produced by the subtraction calculation ileocecal valve face. Treatment involves removal of calculus and the incision sutured. It is performed in the same operation the colecistoentrica fistula repair.

The diagnosis is made by a clinical triad of neumobilis, radiopacity plate in IDF and intestinal obstruction.

The operation should be explored throughout the small intestine to discover if the lumen calculations, that if they had it would advance to the terminal ileum to use and make another incision enterotomy for removal. The untreated gallstone ileus produces 15% of deaths.

Vesicular i.Plastrn

Is the complication that occurs when an abscess is limited both by the omentum as apposition gut and production of fibrin membranes fibrinoleucocitarias. Treatment consists of analgesia, hydration and antibiotic therapy with weekly monitoring by sedimentation, if surgical tto favorable assessment at 6 months, if complications arise instead tto performed emergency surgery.

Treatment

Treatment of acute cholecystitis is the key point of his study. Being a complex action and unavoidable, there are multiple criteria in their sequence.

The European school was in favor of medical treatment and surgery of spontaneous resolution initial 95% of cases almost always within 72 hours, which allows the operation and differ only in the complications initially undertake it. Meanwhile the American school was always more interventionist and advocated surgical treatment perform input.

At present it is accepted that the goal is to solve the problem by removing the gallbladder, but following a methodological sequence having two stages or phases: initial basic treatment and timely surgical intervention and definitive, ie cholecystectomy. These two stages are consistent and complementary in practice and even overlap.

Basic or Initial Treatment

The goal is to restore the patient to fight the pain, infection, imbalance nutrition hidroelectoltico and attending to patient stabilization and healing of acute cholecystitis. There will therefore be administered analgesics, antibiotics, restore electrolyte balance. These measures require continuous observation and patient care in the emergency area. If during the first 8 hours the symptoms worsen the patient for potential action to avoid any complications.

It consists of:

* Vital Signs every 2h.

* Nasogastric aspiration every 3h and it drained in scoring spreadsheet.

* Parenteral Hydration.

* Antibiotic.

* Analgesic and antispasmodic

* Measure Diuresis

* Supplementary Report.

In conclusion, this initial basic treatment can become final or the first stage of surgery.

Surgical Treatment

It is accepted that the treatment for acute cholecystitis is cholecystectomy, however the conditions of high-risk patients can acquire various techniques such as cholecystostomy. Another technique is laparoscopic cholecystectomy.

Cholecystectomy

We discuss only the opportunity to run on the specific function of the patients, and can be:

a. Emergency Operation

b. Deferred or Postponed obligatorily Operation

a. Emergency Operation:

The gravity forces of acute cholecystitis, given the imminence of complications or mostly if already filed.

b. Deferred or Postponed obligatorily Operation:

Comprises patients whose characters have moderate acute cholecystitis are similar to those of the previous group but with the aggravation of having chronic diseases that increase the surgical risk and requiring the patient to treat their disease improve it to operate in a timely fashion to avoid ensues another episode of cholecystitis, estimated six weeks before, but today it determines the patient’s recovery. Accessing this chronology 15% of patients.

II. Rare kinds of acute cholecystitis

a. Emphysematous cholecystitis

b. Typhoid Cholecystitis

c. Cholecystitis twist

d. Cholecystitis Neoplasia

Acute cholecystitis emphysematous

Emphysematous acute cholecystitis is characterized by the presence of gas on the walls and inside the vesicle, and this is its most important physical sign. Also commonly found in air ducts. It is one of the most serious causing mortality 10 times greater than the other types of cholecystitis. Affects 75% of men and 25% women. 30% of those affected are diabetic.

Etymologically, over 50% of cases originates Clostridium welchii and grown its contents: Escherichia coli, Bacteroides and anaerobic streptococci fragile. Aergenas bacteria predominate forming gas. Commonly gangrene of the gallbladder wall and gallstones in 70% with cystic duct obstruction.

Fisiopatognicamente hypersecretion occurs wall and gas production by microorganisms aregenos, which distend the bladder, circulation collapse is necrosar wall emphysema summing the gangrene and perforation whose content expelling cause generalized peritonitis.

The symptomatology is that which corresponds to a severe form of acute cholecystitis toxic exacerbated by the contribution of clostridia and immunosuppression of diabetes when present in 40% or immunosuppressive factors.

The imaging diagnosis. Both ultrasound and radiography and CT largely define the gaseous component. Can be made to the imaging contrast to avoid doubt that the gas corresponds to that of surrounding bowel loops. The treatment of cholecystectomy is based on specific antibiotic. The prognosis is affected by a mortality of 40%.

Acute cholecystitis typhoid

Esuna acute cholecystitis as rare but serious usually complicated by perforation. Appears during the third week of typhoid in clinical or subclinical forms of the disease. Characterizes and identifies find B. In Ebertn in gallbladder bile from this acute cholecystitis. Generally alitisicas are vesicles. Also presented cholecystitis in typhoid Salmonella Typhi healthy patient. Treatment is cholecystectomy based on the specific antibiotic.

Acute cholecystitis Twist

It is a rare form of acute cholecystitis because of severe symptoms may develop hemorrhagic infarction of the organ.

Its pathogenesis is due to an anatomical abnormality of the gallbladder with one of these two variables: these are not attached to the liver and hanging the cystic duct and cystic artery or vesicles is having a meso accommodating one to two centimeters .

In both cases the vesicles can give a rotation of 180 degrees or more generating the “blocking” of cystic duct and cystic artery and leading to hemorrhagic infarction twist. Almost always lithiasic vesicles.

The symptoms of these acute cholecystitis is intense and often palpable gallbladder semiologically. The imaging diagnosis and a treatment is to prevent early cholecystectomy necrosis.

Acute cholecystitis Neoplasms

Acute cholecystitis can be caused by the presence and action of benign neoplasms weight (granular cell myoblasts, or polyps) or malignant (carcinoma) who still occupy space elements may obstruct the infundibulum gallbladder or cystic duct creating pathological conditions and etiopathogenic producing acute cholecystitis.

Therefore, we do not mean that the possibility of malignancy in its evolution invade the lumen of the vesicle obstructing it, but the possibility that as foreign and blocks the infundibulum volumetric structure or cystic duct and causing drainage of bile acute cholecystitis. The diagnosis and surgical treatment ecosonographic.

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