Intestinal obstruction symptoms and bowel obstruction treatment

LISTEN YOUR ABDOMEN......

MALFUNCTIONING OF THE BODY THEREBY BLOCKING THE INTESTINE

Undergo HOW to prevent and Treat ?

INTESTINAL OBSTRUCTION

The mall-functioning of the body thereby blocking the gut and preventing the movement of product of digestion. Its a mechanical or  useful impediment  of the gut ,veto the normal transit of the products of digestion. it can become at some level distal to the duodenum of the small gut an is a medical emergency. Although many cases are not treated surgically , is  a surgical problem.

CLASSIFICATION

• ACUTE OBSTRUCTION : Occurs in small intestine.
• CHRONIC OBSTRUCTION :  Occur in large intestine.
• ACUTE-ON-CHRONIC OBSTRUCTION : Spreads from large gut to involved small intestine.

ETIOLOGY

DYNAMIC OBSTRUCTION

  Here an obstructive agent is present.

     LUMINAL OBSTRUCTIONFecal impaction

• Gall stone ileus
• worms eg ascariasis.

     INTRINSIC LESION OF BOWL WALL

•  Inflammatory stricture
• Malignant stricture
• Intussusception

     EXTRINSIC COMPRESSION

•  Adhesions
• Hernias
• Volvulus

ADYNAMIC OBSTRUCTION

Here's no obstructive agent is present.

PARALYTIC ILEUS

• Postoperative
• Peritonitis
• Reflex
• Uremia
• Hpokalemia

 MESENTRIC VASCULAR OCCLUSION

• Embolism
• Thrombosis

SIGNS AND SYMPTOMS

Based on the extent of impediment involved, viscus impediment can result into abdominal pain, abdominal distension, vomiting and regurgitation. (This a information where half-digested concern is remove from the gut into the stomach by contraction and muscle movement, forcefully expelled through the oesophagus and finally outside from the mouth. This is not actually faecal concern that is vomited, but it smells similar). The information of viscus impediment haw be worsen by extraction and electrolyte abnormalities (acid-base imbalance) cod to vomiting. In diminutive gut obstruction, the discompose are cramping and consistent in nature. The discompose is more central and mid-abdominal. Constipation comes after vomiting. In case of large viscus impediment , the discompose is felt in the lower conception of the abdomen. Constipation occurs first and regurgitation haw be irregular.

INVESTIGATIONS

Test that shows obstruction

• Barium enema
• Abdominal CT scan
• Upper GI and small bowl series
• Abdominal film

The field diagnostic tools are blood test, X-rays of the abdomen, CT scanning (computer tomography) and or ultra-sound. In a case of identifying mass, biopsy haw be employed to determine the nature of the mass. Radio logically viscus impediment shows viscus distension and the presence of multiple gas-fluid levels. Contrast enema, diminutive gut series or CT construe can be used to define the level of obstruction, as in either partial or complete and helping to know the cause of the obstruction. In colonoscopy,small gut are diagonalised using ingested camera,while endoscopy is an instrument used to get medical information from inside the embody and laparoscopy is a form of new technique aimed at carrying out abdominal activeness through diminutive incision.unlike the usual large surgical procedure.

TREATMENT

GASTRODUODENAL OR GASROINTESTINAL SUCTION DRAINAGE

REPLACEMENT OF FLUID AND ELECTROLYTES

RELIEF OF OBSTRUCYION BY OPERATION

ANTIBIOTICS 

The treatment for diminutive viscus impediment is both non-surgical called conservative and surgical. Non-surgical treatment involves a nasogastric tub, correction of extraction and electrolyte abnormalities. For patients with cut pain, Opioid discompose reliever haw be used. Antiemetics haw be administered to regurgitation patient. Intestinal Obstruction in Children Intestinal atresia is the main causes of fetal and neonatal viscus obstruction. This is characterised by narrowing or absence of a conception of the intestine. The atresia are usually discovered before birth via Sonagram and treated with using laporotomy after if the area infected is small, surgeon haw be able to remove the damaged conception and the gut is joined back together. In a information where the narrowing is longer and the area is damaged, a temporary stoma haw be placed.

SURGERY

The surgery is performed while you are under general anaesthesia. This means you are unconscious and pain-free .A cut is prefabricated  in your abdomen. The disease conception of the super bowl is distant and the digit healthy ends of bowl are seamed back together ( resected ).The cut is winking , if the entire colon and rectum is distant , it is titled a proctocolectomy. A bowl resection haw be performed as a traditional 'open' machine or as a minimally invasive laproscopic procedure.

PREVENTION


It depends on the cause,treatment of conditions ( such as tumor and hernias ) that are attendant to obstruction,may reduce the risk.some causes of obstruction are not preventable.

EXPECTATION

The outcome varies with the cause of obstruction.

How to listen your body in crisis with Volvulus ?

VOLVULUS  ( Twisting of intestine )

VOLVULUS  refers to the winding of a assets of the intestine around itself or a stalk of mesentery tissue to cause an obstruction. Volvulus occurs most ofttimes in the colon, although the breadbasket and small bowel crapper also twist. The conception of the digestive grouping above the volvulus continues to function and haw swell as it fills with digested food, fluid, and gas. A condition called strangulation develops if the mesentry of the bowel is twisted so tightly that murder line is cut off and the tissue dies. This condition is called gangrene.

VOLVULUS IS A SURGICAL EMERGENCY because gangrene crapper amend quickly, cause a mess in the wall of the bowel (perforation), and become life-threatening.

ITS AXIAL ROTATION HAS DIFFERENT TYPES

Volvulus Neonatorum

Volvulus of Small Intestine

Volvulus of Cecum

Volvulus of Sigmoid Colon

VOLVULUS NEONATORUM an intestinal obstruction in a new born resulting from a twisting of the bowl caused by malrotation or nonfixation of the colon .Floating of cecum , together with whole of small intestine which has a narrow attachment ,revolves.

Arrested rotation  , in which cecum remains in left hypochondrium ,and a peritoneal band is found running from cecum to right side of abdomen and then across the 2nd part of duodenum ( transduodenal band of Ladd )

In the clinical fearures ,there is some symptoms of Repeated vomiting , which will be bile stained .can also cause abdominal distension .

It can cause some signs of Dehydration and abdominal distension.
Few diagnostic test ,that shows or revealed a diseased portion.For this reason we can do PLAIN ABDOMINAL X-RAY it reveal stomach and upper part of duodenum are greatly distended ith air ,so called 'double stomach.

This condition needs immediate surgery included :

Early Laprotomy
Whole of the midgut is delivered on to the surface .
Untwisting is done in opposite direction .
Transduodenal band of Ladd is divided .
Abdomen is closed in layers .

VOLVULUS OF CECUM  nearly always occur in a clockwise direction. First twist obstructs the ascending colon  ,if a 2nd twist occurs ,it obstructs the ileum also .Axial torsion, the most common form of volvulus, occurs with the development of a twist of 180-360^o; along the longitudinal axis of the ascending colon. This form has a high mortality rate because the obstructive process is associated with vascular compromise, which can lead to gangrene and perforation, often on the antimesenteric border, where the ischemic changes may be most pronounced.

Nonspecific abdominal symptoms occasionally occur with abnormalities of fixation. Traction on the superior mesenteric artery with partial compression of the duodenum, gallbladder, pylorus, or kidneys has been implicated. The most important complication of the abnormalities of fixation is a volvulus of the right side of the colon and/or cecum.

The common presentation of a cecal volvulus is an acute abdomen, with colicky abdominal pain of sudden onset. Most cases of cecal volvulus reportedly occur in patients with a mobile, defectively fixed right colon while they are asleep. Normal movement of the patient from side to side during sleep may result in displacement of the right colon to an ectopic or abnormal location. When gaseous distention occurs, the displaced right colon is trapped, resulting in symptomatic acute volvulus.

The diagnosis is mostly based on plain abdominal radiographic findings aided by those of single-contrast barium enema examination. CT is useful in identifying signs of ischemia, which include mural thickening, infiltration of the mesenteric fat, and pneumatosis intestinalis. Treatment is surgical, but reduction of the volvulus has been reported after barium enema examination.colonoscopy may be considered for the purpose of decompression. Simple abdominal radiographs had a low diagnostic accuracy but revealed bowel obstruction. 

TREATMENT 

Laprotomy should be done ,Deflate the ballooned cecum by insertion of a needle .Untwisting is accomplished in opposite direction ,ie anticlockwise . Cecostomy is performed  , which relieves the distension  , and fixes the organ to abdominal wall ( preventing recurrence ) ,If cecum is gangrenous ,right hemicolectomy is performed .Abdominal wound is closed .

VOLVULUS OF SIGMOID COLON  

This  is the terminal section of the colon. Two body differences can increase the risk of colon volvulus. One is an elongated or movable colon colon that is unengaged to the left sidewall of the abdomen. Another is a narrow mesentery that allows winding at its base. Sigmoid volvulus, however, can occur modify without an body abnormality.

This type of twisting in the sigmoid can occur due to Band or Adhesions ( peridiverticulitis ) ,Overloaded pelvic colon ,Long pelvic mesocolon .Narrow attachment of pelvic mesocolon.

Loop  may rotate  half a turn , in which event spontaneous rectification sometimes occur .After the loop has rotated 1 1/2 turns ,veins involved in torsion are compressed  ,and loop becomes greatly congested .if it rotates more than 1 1/2 turns ,blood supply is cut off entirely and loop becomes gangrenous .Rotation nearly always occur in anticlockwise direction .

In clinical fearures ,it can shows the sumptoms of  sudden severe abdominal pain ,often coming on while the patient is straining at stool .Abdominal distension  ,hiccough and retching occur early ,Vomiting occur late ,absolute constipation .

some sgns of abdominal distension ,abdominal guarding and tenderness

DIAGNOSTIC INVESTIGATION

PLAIN ABDOMINAL X-RAY 
A connatural stark abdominal x-ray will demonstrate a huge air filled distended bowel like the appearance of an inverted U, with the convexity of the U covering the right upper abdominal quadrant. This appearance has been described as the kidney noodle shape, coffee noodle shape, bent inner plaything shape, ace of spades or ‘Omega loop Sign’. You can wager an example down in the inventiveness section.
  

BARIUM ENEMA 

With a water solvable metal enema, the distention in the sigmoid colon can be demonstrated to be cod to a twist, as it will show an Atlantic of rank obstruction with some twisting in the so called shuttle beak or shuttle of beast sign. 

TREATMENT

DEFLATION AT SIGMOIDOSCOPY 

Sigmoidoscopy is carried out and when obstruction is reached an attempt  is made to coax a soft rectal tube into twisted gut .This will immediately deflate the gut and operation can be delayed for a few days until the patient is more fit.

OPERATION 

Laparotomy is performed ( immediately if dilation is not successful ) .Untwist the gas filled viscus in aclockwise direction .Simultaneously ,a rectal tube is passed to deflate the colon .Resection and end-to-end anastomosis is carried out .Abdominal wound is closed.

70% adult cases of chronic pancreatitis are caused by chronic alcohol use

Main culprits are heavy alcohol consumption and gallstones for chronic pancreatitis

CHRONIC PANCREATITIS 

is a relapsing disorder which may arise  insidiously or following repeated attacks of acute pancreatitis .The most commonest cause is chronic alcohol consumption and accompanied by a protien and fat rich diet .Other causes include cystic fibrosis ,hypercalcemia ,hyperlipidemiaand a rare familial pancreatitis .Pathological changes include parenchymal destruction ,fibrosis ,loss of acini ,calculi and duct stenosis with dilatation behind the stenosis.At operation the gland feels hard and irregular and may be mistaken for carcinoma .Calcification is often seen on plain abdominal X-ray.This is thought to be due to calcification of protien precipitates in ducts .

 Pancreatic duct obstruction : due to Stricture e.g.after trauma or acute pancreatitis.Occlusion by pancreatic cancer.

 Hyperparathyroidism ,cystic fibrosis ,Hereditory pancreatitis ,Infantile malnutrition ,Idiopathic ,Stenosis of ampulla of vater . In 12 % of adults ,etiology is unknown.

 Initially pancreas may appear normal.Later pancreas enlarges and becomes hard due to sclerosis ,while the ducts become distorted and dilated with areas of ectasia .Calcified stones ,weighing from a few mg 200 g ,may form within ducts .Ducts become occluded with gelatinous protein-rich fluid and debris ,to form cysts.

Lesions affect a particular lobule producing ,Ductular metaplasia and hyperplasia ,Atrophy of acini ,Interlobular fibrosis .

In clinical features there is symptom of discompose in epigastrium ,which alter to left and correct hypochondrium and finished to back .boring discompose to biliary colic in character .duration about 3-4 days ,and exacerbated by beverage consumption.Vomiting ,anorexia ,Steatorrhea ,and Weight loss ( results from anorexia ,malabsorption steatorrhea and vomiting .It can cause some symptoms of diabetes mellitus ,these are late feature and includes polyuria ,polydipsia ,weight loss and imperfectness.

Signs of jaundice haw be present ( due to narrowing of retropancreatic bile duct ) A protective ,hard epigastric mass haw indicate formation of a sac . ( best way to palpate pancreas is to invoke the enduring to correct and hips and knees are flexed .Left costal margin is deeply palpated.This will evoke tendrness in accent and habitual pancreatitis ( Mallet-Guy's sign ).

DIAGNOSTIC INVESTIGATIONS

The identification of habitual pancreatitis is typically based on tests on pancreatic structure and function, as direct biopsy of the pancreas is thoughtful excessively risky. Serum amylase and lipase may well not be elevated in cases of advanced habitual pancreatitis, but are often utilised as markers for sleuthing pancreatic inflammation in acute pancreatitis. A secretin stimulation effort is thoughtful the gold standard functional effort for identification of habitual pancreatitis but not often utilised clinically. The observation that bi-carbonate production is impaired early in habitual pancreatitis has led to the rationale of ingest of this effort in early stages of disease (sensitivity of 95%). Other ordinary tests utilised to determine habitual pancreatitis are faecal elastase measurement in stool, serum trypsinogen, Computed tomography (CT) scans, ultrasounds, EUS, MRI's, ERCP and MRCP's. Pancreatic calcification crapper often be seen on plain abdominal X-rays, as well as CT scans.

There are other non-specific laboratory studies useful in identification of habitual pancreatitis. Serum bilirubin and alkaline phosphatase crapper be elevated, indicating stricturing of the ordinary bile funiculus cod to edema, fibrosis or cancer. When the habitual pancreatitis is cod to an autoimmune process, elevations in ESR, IgG4, rheumatoid factor, ANA and antismooth hooligan antibody may be seen. The ordinary symptom of habitual pancreatits, steatorrhea, crapper be diagnosed by two assorted studies: Sudden staining of feces or soiled fruitful organic over 24hr on a 100g fruitful diet. To check for pancreatic exocrine dysfunction, the most sensitive and specific effort is the measurement of soiled elastase, which crapper be done with a azygos crap sample, and a value of inferior than 200 ug/g indicates pancreatic insufficiency.

TREATMENT

MEDICAL TREATMENT  

Aimed at controlling discompose and malabsorption .Intermittent attacks treated like accent pancreatitis.Alcohol and super fatty meals must be avoided .Narcotics for severe discompose ,but subsequent addiction is common ,Patients unable to maintain adequate hydration should be hospitalized ,while those with milder symptoms crapper be managed on an ambulatory basis. Surgery haw curb discompose if there is a ductal stricture .Subtotal pancreatectomy haw also curb discompose but at the outlay of exocrine insufficiency and diabetes .Malabsorption is managed with a low fat diet and pancreatic enzymes equal ( 8 customary tablets or 3 viscus glazed tablets with meals ).Because pancreatic enzymes are inactivated by Elvis ,agents that turn Elvis creation ( e.g . omeperazole or sodium bicarbonate ) haw improve their efficacy ( but should not be presented with viscus glazed preparation ) Insulin haw be needed to curb serum glucose .

SURGICAL TREATMENT

Traditional Surgery for Chronic Pancreatitis tends to be divided into two areas - resectional and drainage procedures.New and proven transplantation options preclude the patient from decent diabetic following the surgical removal (resection) of their pancreas. This is achieved by transplanting backwards in the patients own insulin-producing beta cells.

DISTAL PANCREATOMY it consist of distal pancreatic resection up to portal vein ,and it is performed if head of pancreas is relatively normal .

PANCREATODUDENECTOMY it is performed if head of pancreas is mainly involved .

LONGITUDINAL  PANCREATOJEJUNOSTOMY  it is performed if pancreatic duct is grossly dilated .

COMPLICATIONS  

Vitamin B6 malabsorption in 40 % of alcohol induced and all cystic fibrosis cases.Impaired glucose tolerance .Nondiabetic retinopathy due to vitamin A and/ or zinc deficiency,Gastrointestinal bleeding ,icterus ,effusion ,subcutaneous fat necrosis and bone pain occasionally occur .Increased risk for pancreatic carcinoma .Narcotic addiction common.

Here's some information when your intestine is inactive or Paralytic ileus

PARALYTIC ILEUS 

 

It is  a state in which intestine fails to transmit peristaltic waves and is due to failure in neuromuscular mechanism and Obstruction of the gut cod to paralysis of the viscus muscles. The paralysis does not need to be complete to cause ileus, but the viscus muscles must be so inactive that it prevents the passage of food and leads to a useful closure of the intestine.

 

IN POSTOPERATIVE ETIOLOGY  

Ileus commonly follows some types of surgery, especially abdominal surgery  ,Normal lyintestinal motility and absorption returns in about 16 hours ,However ,postoperative ileus may br prolonged , if there is  Hypoproteinemia ,Latent renal failure , If gastrointestinal suction is continued beyond the point at which effective bowl sounds have returned .PERITONITIS initially as a normal response to prevent dissemination .Later bacterial toxins  prevent normal activity of nerve plexuses.

It also crapper result from certain DRUGS  like Uremia ( in renal failure ,following prostatectomy ) , HYPOKALEMIA, IN REFLEX ETIOLOGY Spinal injuries or ribs injuries, ,sometime Retroperitoneal haemorrhage , inflammation anywhere within the abdomen that touches the intestines, and diseases of the viscus muscles themselves  and Application of the plaster jacket.

Irrespective of the cause, closure causes constipation ( no passage of flatus ,for upto 48 hours after laparotomy ), abdominal distention, ( more marked and drum like tympanitic ) and sickness and vomiting ( effortless ,large volume and with dirty fluid ) Respiratory distress. On listening to the abdomen with a stethoscope, some or no bowel sounds are heard (because the bowel is inactive) after laparotomy. Also titled disfunction ileus. Also simply titled ileus.with sign of Tachycardia ,there may be wound dehiscence .

Ileus may increase bond formation, because intestinal segments have more prolonged contact, allowing fibrous adhesions to form, and intestinal distention causes serosal injury and ischemia. Intestinal distention has been shown to drive adhesions in foals . Repeat celiotomy to decompress chronically distended small gut and vanish fibrinous adhesions is also a multipurpose method of treating ileus and reducting adhesions, and it has been related with a good outcome  

DIAGNOSTIC TEST FORPARALYTIC ILEUS: 

The list of diagnostic tests mentioned in various sources as used in the diagnosis of Paralytic ileus includes:

Stethoscope Examination of the abdomen : when a doctor ty o listen with a stethoscope to the abdomen there will be few or no bowel sounds ,indicating that the intestine has stopped functioning .ileus can be confirmed by X-ray of abdomen .computed tomography scans (CT  scan ) or ultrasound .it may be necessary to do more invasive test msuch as barium enema or upper GI series if the obstruction is mechanical.Blood test also are useful in diagnosing paralytic ileus .barium enema used in some obstruction cases but it can cause few problems by increasing pressure or intestinal contents if used in ileus Also in doubtful cases with mechanical obsruction involving the gastrointestinal tract .

So its use is contraindicated in these typs of cases .but in some caes it should be used first . 

TREATMENT OF PARALYTIC ILEUS 

Always seek professional medical advice about any treatment or change in treatment plans, patients may be treated with supervised bed rest in a infirmary , and bowel rest ,where nothing is taken by representative ,and patients are feed intravaneously or finished the ingest of a nasogastric

tube .A nasogastric plaything is a plaything inserted finished the nose down to the throat and into the breadbasket.A kindred plaything can be inserted in the gut .The contents are then suctioned out .In some cases ,especially where there is a machine like obstruction ,surgery may be needed . Drug therapies that encourage intestinal motility ( ability of the gut to more spontaneously ) such as morphine or pethidine , in repeated small doses .Fluid and electrolytes balance ,especially serum K and blood urea.

PROPHYLACTIC TREATMENT 

Routine nasogastric suction and withholding fluids by representative after laparotomy until normal bowel sounds returns ,and /or passage of flatus occurs .in most of the cases ileus are not preventable  ,surgery to remove a tumr or other intestinal obstruction will help prevent a repetition .

Intestinal tuberculosis is significantly increasing in developed countries with HIV

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

Acute pancreatitis

ACUTE PACREATITIS 

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.

 

Treatment of pancreatitis

Treating pancreatitis

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 .

Acute pancreatitis
Sign and symptoms
Causes
Patophysiology
Diagnosis

Cholecystitis acute

INCIDENCE RATE APPROXIMATELY SAME IN WORLDWIDE

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.

Gall stones(cholelithiasis)-Gall bladder problems common in women eat high fibre diet for prevention

PATHOLOGICAL CONDITIONS OF THE GALL BLADDER ARE COMMON SURGICAL PROBLEMS....

GALL STONES ( CHOLELITHIASIS )

In medicine, gallstones (choleliths) are crystalline bodies formed within the embody by increment or concretion of normal or deviant bile components.In 80% of patients gall stones are composed predominantly of cholesterol with smaller amounts of calcium salts and bile pigments . They are referred to as mixed stones , are usually multiple with a faceted surface , and have a characteristic laminated surface on cross section. Only about 10 % of them contain sufficient calcium to be visible on a plain X-ray .Pure cholestrol stones form less than 10% of stones .They are usually solitary ( the cholestrol " solitaire " ) up to 5 cm in diameter ,and have a characteristic radial arrangement of crystals on cross section . Cholestrol stones usually form in bile which is supersaturated with cholestrol. When bile contains more cholestrol than can be solublised in the bile- acid -lecithin micelles ,crystals of cholestrol form in the bile .

The greater the concentration of bile acids and lecithin in bile ,the greater is the amount of cholestrol that can be contained in the mixed micelles .Lecithin is important because lecithin - cholestrol mixed micelles can solubilise more cholestrol than can micelles of bile acids alone .Following Crohn's disease of the terminal ileum or ileal resection thebile salt pool is reduced because of lack of absorption of bile salts ,and the liver can not make good the losses .

Such patients are prone to cholestrol stones. Oestrogen increases the hepatic synthesis of cholestrol ,and this may explain why females of child - bearing age have a higher incidence of cholestrol stones . A high animal fat ,low fibre diet is also associated with cholestrol stones because of excretion in bile of the excess cholestrol absobed from the gut.Clofibrate , a cholestrol-lowering agent ,has been implicated in cholestrol stone formation ,because it increases excretion of cholestrol in the bile . Decreased gall bladder motility probably plays a rle in aetiology of gall stones .

Cholestrol and other substances which form the nuclei for gall stone formation must remain in the gall bladder long enough for crystal growth to occur .Stasis occurs during pregnancy due to the smooth muscle relaxing effect of progesterone.Motility of the gall bladder is also decreased during starvation and total parenteral nutrition , due to decreased stimulation of the gall bladder by CCK.Stones may also form after vagotomy ,because of lack of vagal potentiation of CCK.Bile pigment stones account for about 10 % of stones in the UK.The major constituent is the calcium salt of unconjugated bilirubin.

They are associated with chronic haemolytic disease where there is breakdown of red cells with release of excessive bilirubin.Pure pigment stones occur in sickle cell disease , thalassaemia and hereditary spherocytosis .Pigment stones are found in the Far East ,where they are associated with biliary tract infection with E.coli and Bacteroides fragilis ,These organism produce beta-glucuronidase which splits bilirubin diglucuronide and releses free bilirubin.The latter combines with calcium to form the relatively insoluble calcium bilirubinate.

PATHOLOGICAL CONSEQUENCES OF GALL STONES ARE :

• Inflammation of the gall bladder ,acute cholecystitis ,chronic cholecystitis ,acute on chronic cholecystitis
• obstructive jaundice due to impaction of a stone at the lower end of the common bile duct : secondary biliary cirrhosis may result .
• ascending cholengitis
• empyema of the gall bladder.
• mucocele
• gall stone ileus __ a fistula occurs between the gall bladder and duodenum ,and a large stone enters the small bowel ,causing obstruction .usually at the terminal ileum .
• pancreatitis ,usually associated with multiple small stones .
• carcinoma of gall bladder .
• perforation of the gall bladder .
  

Medicines titled chenodeoxycholic acids (CDCA) or ursodeoxycholic acid (UDCA, ursodiol) may be given in preventive form to dissolve cholesterin gallstones. However, they may take 2 eld or longer to work, and the stones may return after communication ends.

Rarely, chemicals are passed into the gallbladder finished a catheter. The chemical apace dissolves cholesterin stones. This communication is not used rattling often, because it is difficult to perform, the chemicals can be toxic, and the gallstones may return.

Cholecystectomy (gallbladder removal) has a 99% chance of eliminating the recurrence of cholelithiasis. Only symptomatic patients staleness be indicated to surgery. The lack of a gall bladder does not seem to have any perverse consequences in some people. However, there is a momentous assets of the population — between 5 and 40% — who amend a information called postcholecystectomy syndrome which haw drive gastrointestinal painfulness and persistent discompose in the upper right abdomen. In addition, as some as 20% of patients amend chronic diarrhea.

Electrohydraulic damper wave lithotripsy (ESWL) of the gallbladder has also been utilised for selected patients who cannot have surgery. Because gallstones often become backwards in many patients, this treatment is not utilised very often any more.