Diverticulosis is generally discovered through one of the following examinations for appropriate treatment
Barium enema: This x-ray test involves injection of liquid material into the colon through a tube inserted in the rectum. The x-ray image shows the anatomy of the colon, and can identify if diverticula, large polyps or growths are present.
Colonoscopy: This test uses a thin, flexible tube with a light and camera to view the inside of the colon. Diverticula as well as polyps and other growths can be seen with this instrument.
CT scan: This x-ray test takes multiple cross section pictures of the body. It is not generally performed to make a diagnosis of diverticulosis, but this type of exam may identify diverticula.
Patients with diverticular disease should be counselled on the benefits of a high fibre diet. Bulking agents and laxatives could also be added until stools are soft and defaecation is painless.
Patients with acute diverticulitis are admitted to hospital for bed rest, nil by mouth (with iv fluids), analgesics, and IV antibiotics (e.g. cefuroxime and metronidazole). Patients presenting with PR bleeding are resuscitated and given blood transfusion.
Complicated disease (perforation, abscess, multiple attacks, uncontrollable bleeding) usually requires surgery to remove the diseased segment of colon. There are various surgical techniques available depending on the site of the disease, and a temporary stoma is usually needed (a "stoma bag"), although this is reversed after around 6 weeks.
CONSERVATIVE MANAGEMENT
Patients with acute diverticulitis are admitted to hospital for bed rest, nil by mouth (with iv fluids), analgesics, and IV antibiotics (e.g. cefuroxime and metronidazole). Patients presenting with PR bleeding are resuscitated and given blood transfusion.
Complicated disease (perforation, abscess, multiple attacks, uncontrollable bleeding) usually requires surgery to remove the diseased segment of colon.
There are various surgical techniques available depending on the site of the disease, and a temporary stoma is usually needed (a "stoma bag"), although this is reversed after around 6 weeks.
SURGICAL TREATMENT
INDICATIONS :Recurrent attacks -and Complications
OPERATIVE PROCEDURES
IDEAL OPERATION
This is a one stage resection ,which involves removal of affected segment 10 - 20 cm long and restoration of continuity by end-to-end anastomosis .
IN CASES OF OBSTRUCTION & INFLAMMATORY EDEMA AND ADHESIONS a preliminary transverse colostomy can be done as a first stage. In second stage of resecion is performed after 3 weeks or later when inflammation has subsided.Colostomy is closed after a further 2 weeks. IN ACUTE PERFORATION proximal colostomy can be done ,Exteriorization , Primary resection.
HARTMANN'S OPERATION colostomy after excision with closure of defunctioned distal bowel .
Restoration of bowel continuity can be done at a later stage by means of stapling guns .
IN FISTULA resection of diseased bowel. ,closure of fistula .
WHERE REFINED DIETS ARE MORE COMMON THAN RICH IN FIBRE
DIVERTICULAR DISEASES OF COLON
Diverticula of colon are acquired rupture of colonic mucosa ,protruding through broadside muscle at points where murder vessels understand colonic surround .They consist of mucosa and submucosa that have cut the muscular coats . They are pulsion diverticula being pushed out by increased intraluminal push .Although they haw involve the whole of the colon .They are most ordinary in the colon
Diverticular disease is most ordinary in Western society ,where civilised diets are more ordinary than diets rich in fibre and hence the stool is inferior bulky . Patients with diverticular disease have shortened ,thickened colonic muscle which reflects work hypertrophy from years of a baritone fibre diet and resulting small hard stools .High intra-luminal pressure occur ,pushing the diverticulae out through the surround .The inclination of divertculae to form in the colon colon is explained by Laplace's law which states that the push within a tube is
inversely proportional to the radius.
PATHOGENESIS
DIVERTICULOSIS two factors are essential 1.exaggerated peristaltic contractions with abnormal elevation of intraluminal push ,and foci of muscle imperfectness in colonic surround.
DIVERTICULITIS it is the secondary land and is cod to rousing of one or more diverticula.
MICROSCOPIC FEATURES
DIVERTICULOSIS
Muscular hypertrophy in colonic segments affected by diverticular changes.saccule are found penetrating between the mesentric and lateral teniae at points where entering arterioles branch out into submucosa .Diverticulae are small ,flask like or spherical outpouchings usually 0.5 to 1 cm in diameyer .Walls of diverticula are usually thin ,made up of mucosa and submucosa enclosed within fat or an intact peritoneal covering .
DIVERTCULITIS
Inflammatory changes are present ,to produce both diverticulitis and periverticulitis and sometimes localized peritonitis .
SIGN AND SYMPTOMS OF DIVERTICULOSIS AND DIVERTICULITIS
Most patients with diverticulosis have no symptoms. Many will never know they have the condition until it is discovered during an endoscopic or radiographic (Xray) examination. While most people have no symptoms, some individuals may experience pain or discomfort in the left lower abdomen, bloating, and/or a change in bowel habits.
Other conditions such as irritable bowel syndrome and stomach ulcers cause similar problems, so the symptoms do not always mean a person has diverticulosis. People with chronic symptoms should visit their doctor or health care provider.
The most common symptom of diverticulitis is abdominal pain. The most common sign on examination is tenderness in the lower left side of the abdomen. Usually, the pain is severe and comes on suddenly, but it can also be mild and become worse over several days. The intensity of the pain can fluctuate. A person may experience cramping, nausea, vomiting, fever, chills, or a change in bowel habits...... read more
Scientist theorize that appendix is a remnant of an ancient digestive tract .They believe that it might have been used by early man to digest tough leaves and bark.But it can create lot of trouble by causing Acute appendicitis.
The appendix is a worm like extension of the cecum and for this reason,has been called the Vermiform appendix.The average length of the appendix is 8-10 cm ( ranging from 2-20 cm ).The appendix appears during the fifth month of gestation and several lymphoid follicles are scattered in its mucosa.Such follicle increase in number when individuals are aged 8-20 years.
LOCATION
1.Base of appendix:
it is found attached to posteromedial surface of cecum about 2.5 cm below the ileicecal junction.
2.Body and tip of appendix:
a. Retrocecal (74 %)
b. Pelvic (21 %)
c. Paracecal (2 % )
d .Subcecal ( 1.5 % )
e. Periileal (1 %)
f. Postileal (0.5 % )
Vermiform appendix has a complete peritoneal covering, which is attached to lower layer of mesentry of small intestine to form a short mesentry of its own.the mesoappendix,but there is some variations.distal 1/3 of its may be bereft of mesoappendix.
ETIOLOGY
SEX: Males are more commen than female.
SOCIAL STATUS: Upper and middle class
DIET: One relatively rich in meat,& devoid of simple diet rich in cellulose
Familial susceptibility.
OBSTRUCTION OF LUMEN OF APPENDIX:Fecoliyh ,a stricture,a foriegn body,a rond worm.or thread worms.
DISTAL OBSTRUCTION OF COLON: Carcinoma of right colon.
Abuse of purgatives.
BACTERIA: a mixture of E coli,enterococci,non hemolytic streptococci,anaerobic streptococci,Cl welchi,& bacteroids.
PATHOLOGY
NON OBSTRUCTIVE ACUTE APPENDICITIS
Inflammation usually begins in mucosa,& less often in ymph follicles,but on reaching the loose submucosa it progresses rapidly.Organ becomes turgid and dusky red with mucosal hemmorrhages.Vascular supply of distal part of appendix is at risk.because here is the artery is inframural & liable to occlusion by in inflammation or thrombosis,this may lead to gangrene of tip.
Inflammation may progress sufficiently slowly for protective barriers to form ,& the resulting peritonitis is localized .It can terminate in one of the following ways:
Resoluton
Ulceration
Suppuration
Fibrosis
Gangrene
OBSTRUCTIVE ACUTE APPENDICITIS
Products of inflammation becomes pent up,so that it proceeds more rapidly & more certainly to gangrene or perforation.Often within 12-18 hrs,appendix distal to obstruction become gangrenous.Perforation occurs most often at the site of an impacted fecolith before protective adhesions have had time to form-Escaping purulent & gaseous contents are under high pressure ,& early widespread peritonitis is liable to ensue -Subphrenic & pelvic abcesses are a later sequel if patient survives the initial peritonitis.
CLINICAL FEATURES
Age incidence : Increasingly common during childhood & adolescence ,maximum incidence is between 20 & 30 years.
NON-OBSTRUCTIVE ACUTE APPENDICITIS
SYMPTOMS
Abdominal pain which shift : Initially there is constant, vague pain around umblicus,in epigastrium,or it may be generalized.After a few hours pain become intense .& shift to the point where inflammed appendix irritates partial peritoneum ( usually in right iliac fossa ).
Gastric function Upset : Anorexia, nausea, infrequent vomiting & stops as soon as stomach is empty.Usually constipation is present ,but occasionally diarrhea occur.
SIGNS
GENERAL SIGNS : Pyrexia ( 99 - 100 F )
Tachycardia ( 80 - 90 per min )
Tongue ( white & furred )
A special fetor oris
LOCAL SIGNS
Localized tenderness after the pain shifts, either at McBurney's point or elsewhere ( determined by the site of appendix ).
Muscle guarding & rigidity in right iliac fossa .
Rebound tenderness at McBurney's point in right iliac fossa.
Pressure on left iliac fossa may cause pain in right iliac fossa.
Release of pressure on left iliac fossa may cause pain in right iliac fossa.
Last three manoeuvres cause pain because they move the inflamed appendix.
OBSTRUCTIVE ACUTE APPENDICITIS
Sequence of clinical events occurs much more quickly:
Onset is abrupt .& there may be severe generalized abdominal colic from start.However ,the pain shifts in the usuall way.
Vomiting is common
Temperature can be normal
Local signs are as mentioned above.
INVESTIGATIONS
Appendicitis is essentially a clinical diagnosis.
The following may be useful.
Urine analysis may exclude urinary tract infection.
Pregnancy test to exclude ectopic pregnancy.
Abdominal x-ray is of little value.
A normal white cell count does not exclude appendicitis.
Ultrasound may be helpful in the assesment of an appendix mass or abcess.
Ultrasound adds little to the clinical diagnosis of acute appendicitis.
Scoring system and computer-aided diagnosis may be helpful.
Meta analysis suggest the following to be useful predictor of appendicitis in patients with abdominal pain.
THE APPENDIX DOES NOT APPEAR TO HAVE ANY FUNCTION IN THE HUMAN BODY ...SO HOW CAN WE PANIC THROUGH NON FUNCTION ORGAN ???
TREATMENT
INDICATION FOR SURGICAL CONSULTATION AND SURGERY A surgeon should evaluate any patient with classic migrating abdominal tenderness. Because only a little more than half of patients with appendicitis present with a classic history and physical findings, acute appendicitis should be on the list of possible diagnoses for any patient with abdominal pain. Thus, a surgeon should also evaluate patients with focal RLQ tenderness or progressively worsening abdominal pain. To minimize the time between show and appendectomy, obtain surgical conference prior to performing additional diagnostic studies, such as CT scan, ultrasound, and technetium (Tc)-labeled WBC scan.3
Indications for operation Any patient with suspected appendicitis who has (1) persistent discompose and becomes febrile, (2) an increasing WBC count, or (3) worsening clinical examination findings should undergo extirpation or at least diagnostic laparoscopy. In patients with an atypical presentation, the most important determination for extirpation is serial physical examinations. The WBC count often does not process after the patient is admitted and hydrated; therefore, any patient sent home from the emergency department should undergo a follow-up evaluation the incoming day.3
APPENDICECTOMY Open by giving INCISION
Grid-iron incision.
Paramedian incision.
Rutherford Morison's incision.
REMOVAL OF APPENDIX A retractor is placed under the medial side of peritoneum & abdominal wall is lifted up.Any pus or serous exudate is removed with a sucker & a pack is inserted into wound on medial side.Using a a swab,cecum is withdrawn.A finger may be inserted into wound to aid delivery of appendix.Cecum is grasped by an assistant. Atissue -holding forceps is applied around the appendix in such a way as to encircle the organ & yet not damage it .Base of mesoappendix is clamped in a hemostat,tied & severed.when mesoappendix is broad,procedure must be repeated with a 2nd or a 3rd hemostat.Appendix ,now completely freed,is crushed near its junction with cecum in a hemostat,which is removed & reapplied just distal to crushed portion.A catgut ligature is tied around crushed portion close to cecum,& an atraumatic catgut purse-string suture is inserted into cecum about 1.25 cm frombase & is left untied until appendix has been amputated with a scalpal below hemostat.Stump is invaginated while purse -string suture is tied,thus burying the appendix stump. PERITONEAL LAVAGE Peritoneum is washed out with antibiotic laden irrigating fluids.
ANTIBIOTICS Prophylactic antibiotics active against aerobic & an aerobics organism are given in 2 doses ( one at the time of surgery & next 8-12 hours later ) DRAINAGE OF PERITONEAL CAVITY Unnecessary, provided adequate peritoneal lavage has been done.However ,performed if there is considerable purulent fluid in retrocecal space or pelvis, or if there is persistent oozing. DRAINAGE OF PARIETES Indicated if there is any soiling of wound ,especially in obese & in children. COMPLICATIONS OF APPENDICECTOMY EARLY
ILeus
Wound sepsis
Residual abscess
Intestinal obstruction from adhesins
Fecal fistula
Pyelophlebitis
Postoperative thrombosis & embolism
Actinomycosis
Pulmonary complications (pulmonary collapse or pneumonia )
LATE
Intestinal obstruction from adhesions
Incisional hernia
Right inguinal hernia following grid iron incision
INTESTINAL TUBERCULOSIS Is a Major Health Problem in Many Underdeveloped Countries
BUT
A Recent Significantly Increase In Developed Countries In Association With HIV Infection
TUBERCULOSIS OF INTESTINE
Some bacterial infections are surgically important include INTESTINAL TUBERCULOSIS usually seen in the uk as ileocecal tuberculosis and present with thickening and narrowing of the terminal ileum.It may be indistinguishable from crohn's disease on naked eye examinaton.although pale tubercle may be seen on the serosa in tuberculosis.Complications include adhesive obstruction ,perforation and malabsorption due to widespread mucosal involvement or lymphatic blockage.
INTESTINAL TUBERCULOSIS is a field health problem in some underdeveloped countries. A recent momentous increase has occurred in matured countries, especially in connexion with HIV infection. Autopsies of patients with pulmonary TB before the epoch of effective treatment demonstrated viscus involvement in 55-90% of mortal cases. The previously noted regular connexion between pulmonary TB and viscus TB no longer prevails, and only a minority of patients (<50%) with abdominal TB now hit deviant dresser radiographic findings. However, approximately 20-25% of patients with GI TB hit pulmonary TB. Any conception of the GI system haw be infected, although the ileum and colon are common sites.
Pathologically GI TB is characterized by inflammation and fibrosis of the bowel surround and the regional lymph nodes. Mucosal ulceration results from necrosis of Peyer patches, lymph follicles, and vascular thrombosis. At this initiate of the disease, the changes are reversible and healing without scarring is possible. As the disease progresses, the ulceration becomes confluent, and comprehensive fibrosis leads to bowel surround thickening, fibrosis, and pseudotumoral mass lesions. Strictures and fistulae formation may occur.
We can categarize Intesinal Tuberculosis into Three TYPES on gross pathologic examination
ULCERATIVE modify of TB is seen in approximately 60% of patients. Multiple ostensible ulcers are largely confined to the epithelial surface. This is considered a highly active modify of the disease, with the daylong axis of the ulcers rectangular to the daylong axis of the bowel.
HYPERTROPHIC modify is seen in approximately 10% of patients and consists of thickening of the bowel wall with scarring; fibrosis; and a rigid, masslike appearance that mimics that of a carcinoma.
ULCEROHYPERTROPHIC modify is a subtype seen in 30% of patients. These patients hit a compounding of features of the ulcerative and hypertrophic forms.
Clinical features of viscus TB include abdominal pain, weight loss, anemia, and feverishness with night sweats. Patients may present with symptoms of obstruction, correct iliac fossa pain, or a palpable mass in the correct iliac fossa. Hemorrhage and perforation are constituted complications of viscus TB, although free perforation is less frequent than in doc disease. The diagnosis of purging tuberculosis requires a broad index of suspicion. In cases where the information available does not reveal a definite differentiation between colonic tuberculosis and Crohn's disease.
Intestinal tuberculosis is a thin disease in western countries, affecting mainly immigrants and immunocompromised patients. Intestinal tuberculosis is a diagnostic challenge, especially when active pulmonary infection is absent. It may mimic many other abdominal diseases.
The most common place of GI TB is the ileocecal region, if the area can be reached with a flexible endoscope. A rapid diagnosis can be achieved if smudge or culture results are positive or if caseating granulomas are seen in biopsy samples. In countries where GI TB is endemic, a therapeutic trial of antituberculosis treatment haw be justified if the clinical picture is compatible with TB.
TREARMENT OF INTESTINAL TUBERCULOSIS
A course of chemotherapy
Surgery is required in cases of complicated obstruction in HYPERPLASTIC TUBERCULOSIS - Right hemicolectomy with removal of diseased segment of ileum or defunctioning ileocolostomy .
Surgery is required in cases of Stricture causing intestinal obstruction or in perforation in ULCERATIVE TUBERCULOSIS
Its an acute inflammatory process caused by the effects of enzymes released from the pancreatic acini . There are numerous aetiological factors .
The pancreas is a super gland behind the breadbasket and close to the duodenum—the first part of the diminutive intestine. The pancreas secretes digestive juices, or enzymes, into the duodenum through a tube titled the pancreatic duct. Pancreatic enzymes join with bile—a liquefied produced in the liver and stored in the gallbladder—to digest food. The pancreas also releases the hormones insulin and glucagon into the bloodstream. These hormones help the body regulate the glucose it takes from food for energy.
PATHOGENESIS of acute pancreatitis is obscureb,but two main mechanism may be involved
1.DUCT OBSTRUCTION __ this may lead to reflux of bile into the pancreatic ducts causing injury .Alternatively increased intraductal pressure may damage the pancreatic acini ,leading to leakage of pancreatic enzymes which may further damage the pancrease .
2.DIRECT ACINAR DAMAGE __ this may be caused by viruses ,bateria ,drugs or trauma .
The appearance of the pancrease in acute pancreatitis may be explained by release of pancreatic enzymes. Protease release causes widespread destruction of the pancrease and increases further enzyme release ,with consequent further damage.Release of lipase causing fat necrosis resulting in characteristic yellowish-white flecks on the pancrease ,mesentry and omentum .Often with calcium deposition.Other enzymes ,e.g. elastase ,destroy blood vessels ,leading to haemmorrhage within the pancrease and haemmorrhagic exudate into the peritoneum .Haemmorrhage may be extensive ,leading to acute haemmorrhagic pancreatitis.
BIOCHEMICAL CHANGES increased serum amylase. Amylase is released from the damaged acini and enters the blood stream .The serum amylase is released in the acute phase ( 24 - 48 h) but later falls to normal .Occasionally with acute haemmorrhagic pancreatitis the destruction of pancreatic acini is so swift and complete that the serum amylase may not be raised by th time the patient reaches hospital. Hypocalcaemia ,this arises become of deposition of calcium in areas of fat necrosis .Hyperglycemia ,this occurs because of associated damage to the pancreatic islets .Abnomal liver function tests may occur , especially raised bilirubin and alkaline phosphatase due to mild obstruction of the bile ducts by oedema .
Sudden, unceasing discompose in the upper part of the abdomen is a hallmark of acute pancreatitis, though other medical conditions crapper also cause this type of pain. The discompose may wrap around your upper body and involve the back in a band-like pattern. The discompose typically lasts days and is ofttimes relieved by leaning forward. Some grouping hit only slight abdominal tenderness and in 5 to 10 percent of people, there is no discompose at all.
In grouping with gallstone pancreatitis, gallbladder discompose may become before pancreatic pain. Gallbladder discompose (referred to as biliary colic) occurs in the right upper abdomen, extending to the back and right shoulder. The discompose gradually increases in intensity, is constant, and may be attended by sickness and vomiting. Gallbladder discompose ofttimes follows a meal.
In grouping with alcoholic pancreatitis, the symptoms of acute pancreatitis ofttimes become digit to three days after an alcohol binge or after stopping drinking. Pain is attended by sickness and regurgitation in most people. In severe cases, the initial symptom may be shock or coma.
Other conditions that have been linked to pancreatitis are:
Damage to the ducts or pancreas during surgery
High murder levels of a fat titled triglycerides (hypertriglyceridemia)
Injury to the pancreas from an accident
Blockage of the pancreatic duct or common bile duct, the tubes that pipage enzymes from the pancreas
Diagnosing accent pancreatitis is often difficult because of the deep location of the pancreas. The student will likely visit one or more of the mass tests:
•Abdominal ultrasound. Sound waves are dispatched toward the pancreas finished a handheld device that a technician glides over the abdomen. The good waves bounce soured the pancreas, gallbladder, liver, and other organs, and their echoes make electrical impulses that create a picture—called a sonogram—on a recording monitor. If gallstones are causing inflammation, the good waves will also bounce soured them, showing their location.
•Computerized picturing (CT) scan. The CT construe is a noninvasive x ray that produces three-dimensional pictures of parts of the body. The person lies on a table that slides into a donut-shaped machine. The effort may exhibit gallstones and the extent of alteration to the pancreas.
•Endoscopic ultrasound (EUS). After spraying a solution to numb the patient’s throat, the student inserts an endoscope—a thin, flexible, aflame tube—down the throat, finished the stomach, and into the small intestine. The student turns on an ultrasound adhesion to the scope that produces good waves to create seeable images of the pancreas and bile ducts.
•Magnetic kinship cholangiopancreatography (MRCP). MRCP uses attractable kinship imaging, a noninvasive effort that produces cross-section images of parts of the body. After being lightly sedated, the patient lies in a cylinder-like plaything for the test. The technician injects dye into the patient’s veins that helps exhibit the pancreas, gallbladder, and pancreatic and bile ducts.
IT OCCURS SUDDENLY AND SUBSIDE IN FEW DAYS IF TREATS PROPERLY.
EACH YEAR ABOUT 210,000 PEOPLE IN THE US ARE ADMITTED TO THE HOSPITAL WITH ACUTE PANCREATITIS.
TREATMENT
The goals of communication of accent pancreatitis are to alleviate pancreatic inflammation and to correct the inexplicit cause. Treatment commonly requires hospitalisation for at small a few days."Treatment of accent pancreatitis" BED REST SUPPORTIVE INTRAVENOUS THERAPY restore adequate blood volume as soon as possible e.g by physiological saline .A careful fluid balance chart should be kept ,with appropiate allowance made for insensible loss .Daily serum electrolyte estimations are made ,together with acid-base studies.Full water replacement is given by intravenous route .Calories are given as glucose .Na ,K ,and Cl are given in appropriate amounts .ca deficiency, if develops , is treated by Ca gluconate IV
NASOGASTRIC ASPIRATION continuous suction removes gastric HCl from entering duodenum,that suppressing hormonal stimulation of exocrine secretions of pancrease .It also brings relief from persistent nausea and vomiting.
PAIN RELIEF Originally it was thought that analgesia should not be provided by morphine because it haw drive symptom of the musculus of Oddi and exacerbate the pain, so the drug of choice was meperidine. However, due to lack of effectualness and risk of toxicity of meperidine, more recent studies hit institute morphine the analgesic of choice. Meperidine haw ease be utilised by some practitioners in more secondary cases, or where morphine is contraindicated.
PROPHYLACTIC ANTIBIOTICS given as a prophylactic against infection of necrotic retroperitoneal tissue ,and also against bronchopneumonia .A broad spectrum antibiotic ,e.g. cefoperazone should be given for 3-5 days.
EDOSCOPIC SPHINCTEROTOMY gallstone pancreatitis will be improved ,if a stone is obstructing the ampulla of vater . Surgical options for pussy necrosis include:
Minimally intrusive management - necrosectomy through small incision in wound (left flank) or breadbasket
Conventional management - necrosectomy with ultimate drainage
Closed management - necrosectomy with closed continuous postoperative lavage
Open management - necrosectomy with planned staged reoperations at definite intervals (up to 20+ reoperations in some cases)
COMPLICATIONS include : Pancreatic Pseudocyst __ this is a localized collection of fluid in the lesser sac of peritoneum. Pancreatic Abscess , Stress induced gastric erosion with haemate mesis or melena .Acute renal failure ,Toxic psychosis ,Multiple organ failure ,chronic pancreatitis . PROGNOSIS the overall mortality is between 10 % and 20 % .With severe haemmorrhagic pancreatitis the mortality rate reaches 50 % .The usual cause of mortality is multiple organ failure .
5 TO !0 % MORTALITY OCCURS IN PATIENTS OLDER THAN 60 YEARS.
ACUTE CHOLECYSTITIS : is an inflammation of the gall bladder ,and is usually associated with stones. Occasionally it occurs without stones,i.e. acalculous cholecystitis.The later may be due to infection with E coli .Clostridia,or rarely Salmonella typhi. Acalculous cholecystitis may occur after prolonged starvation or total parenteral nutrition. Stasis is probably a contributing factor in the latter conditions .
The gall bladder becomes oedematous ,with mucosal ulceration ,and a fibrinopurulent exudate .Acute inflammatory cells infiltrate the wall . Even in the presence of thrombosis of the cystic artery ,gangrene is rare ,as the gall bladder gains a blood supply directly from the liver via the gall bladder bed .However ,gangrene does occasionally occur with perforation of the gall bladder ,resulting in generalised bile peritonitis or a localised abscess depending on whether the gall bladder has been walled off by adhesions or not .An empyema of the gall bladder may also result, suppuration occuring within the gall bladder and the gall bladder becoming distended with pus. Occasionally the gall bladder may fistulate into the duodenum.
Factors that haw initiate the inflammatory process include the manufacture of inflammatory mediators (eg, lysolecithin and prostaglandins); an increase in intraluminal pressure in association with compromise of the murder supply; and chemical botheration by bile acids.
90 % calculous and 10 % acalculous, Acalculous cholecystitis associated with higher complication rate and associated with acute illness ( i.e. burns ,trauma, major surgery ) ,fasting ,hyperalimentation leading to gall bladder stasis ,vasculitis ,carcinoma of gall bladder or common bile duct ,some gall bladder infections ( Leptospira ,Streptococcus,Parasitic ,etc.) but in >50% of cases an underlying explanation is not found.
In patients who hit emphysematous cholecystitis, ischemia of the gall bladder surround is followed by infection with gas-forming organisms that display pedal in the bladder lumen, in the gall bladder wall, or both. In 30-50% of patients, preexisting diabetes mellitus is present; the male-to-female ratio is 5:1.1 Gas haw be confined to the gall bladder; however, in 20% of cases, pedal is also seen in the rest of biliary tree. Gallstones are not inform in 30-50% of cases, and the mortality rate is 15%.1 There is a predisposition for gangrene formation and perforation, but clinical symptoms are mild; much symptoms can be deceptive. Emphysematous cholecystitis haw occur after chemoembolization performed as palliation for hepatocellular carcinoma; after fat embolism during aortography; and after gall bladder hypoperfusion during viscus resuscitation.
CLINICAL FINDINGS
Acute cholecystitis usually occurs with correct upper quadrant discompose and tenderness. The abdominal discompose increases with time. The place of discompose is usually the correct subcostal region, though the discompose haw begin in the epigastrium or the mitt upper quadrant and then shift to the correct subcostal region to the area of the gallbladder inflammation. Referred discompose to the correct shoulder or the interscapular region haw be experienced. Approximately greater than half of patients hit had preceding attacks of similar discompose that spontaneously resolved. Anorexia, nausea, and vomiting haw occur, but vomiting is seldom severe. Most patients are symptom and hit no leukocytosis.
When feverishness occurs, the patient's temperature is seldom higher than 38°C. Chills are unusual; their proximity suggests a case of complicated cholecystitis (abscess or associated cholangitis).
In some patients with acute cholecystitis hit mild jaundice, which haw be related to ordinary hepatic edema, bile duct edema, or both, or to the proximity of calculi within the common bile duct.1 In most patients, improvement occurs within 24 hours after hospitalization, and signs and symptoms gradually subside. Persistent pain, feverishness and leukocytosis, chills, and more nonindulgent localized or generalized compassionateness haw indicate complicated disease, much as abscess manufacture or GB perforation. The utilization of empyema of the GB haw display systemic toxicity, and it haw be predictive of GB perforation.
Acute acalculous cholecystitis is difficult to diagnose clinically. It often occurs in children and in patients who are critically ill or who hit fresh undergone pronounce from nonindulgent trauma, burns, or surgery. Predisposing factors allow prolonged fasting, immobility, and hemodynamic instability. Often, these patients cannot impart pain; however, fever, jaundice, vomiting, abdominal tenderness, leukocytosis, and hyperbilirubinemia are highly suggestive findings.
In approximately 1/3rd of patients, a distended, tender gall bladder haw be palpable as a distinct mass. This is an important clinical finding and haw confirm the diagnosis.
LABORATORY TEST Shows mild leukocytosis ,serum bilirubin alkaline phosphatase and AST may be mildly elevated.
DIAGNOSTIC INVESTIGATIONS
CHEST AND PLAIN ABDOMINAL X-RAYS it can help to exclude other causes ,and show radio-opaque stones .
ORAL CHOLECYSTOGRAPHY it is unreliable during acute attack , and is postponed until patients has recovered.
ULTRASONOGRAPHY confirm the diagnosis.
RADIOISOTOPE SCANNING confirm the diagnosis .
TREATMENT
CONSERVATIVE TREATMENR FOLLOWED BY CHOLECYSTECTOMY
No oral intake ,nasogastric suction .IV fluids and electrolytes ,analgesia ( mepridine or NSAIDS ). and antibiotics ( ureidopenicillins ,ampicillin sulbactam ,third generation cephalosporins ,anaerobic coverage should be added if gangerous or emphysematous cholecystitis is suspected , consider combination with aminoglycosides in diabetic patient or others with signs of gram-negative sepsis.Acute symptoms will resolve in 70% of patients.
SURGERY Optimal timing of surgery depends on patients stabilization and should be performed as soon as feasible. Urgent cholecystectomy is appropriate in most patients with a suspected or confirmed complication. Delayed surgery is reserved for patients with high risk of emergent surgery and where the diagnosis is in doubt.
Recurrent symptoms are common in patients with acute cholecystitis who are treated expectantly; most patients need elective cholecystectomy.
Percutaneous cholecystostomy is a minimally invasive procedure that can goodness patients with serious comorbidity who are at broad venture from major surgery. Percutaneous cholecystostomy can be performed at the bedside low local drug and is suitable for patients in qualifier care units and those with burns. It is the expressed treatment in patients with acalculous cholecystitis , or it may be used as a temporising measure—to pipage pussy bile and retard the requirement for expressed treatment.
