Mesenteric Ischemia
Mesenteric Ischemia

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Mesenteric Ischemia

This 74 year-old male presents in our office with a vague abdominal pain and no additional complaints pain is described as diffuse located primarily in the lower abdomen.
The whtte cell count was 24.500 with 90% neutrofils.

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mesenteric ischemia

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Patients with mesenteric ischemia have a rare, potentially life-threatening disease and may present to the primary care or emergency medicine physician. Acute and chronic forms of mesenteric ischemia share many similarities and have many differences.

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mesenteric ischemia

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While acute mesenteric ischemia is a surgical emergency, patients with chronic mesenteric ischemia typically present with a more benign process.

The specific causes of mesenteric ischemia include the following:

  • Acute thrombotic and acute embolic mesenteric artery ischemia
  • Visceral venous thrombosis
  • Chronic mesenteric ischemia
  • Nonocclusive mesenteric ischemia.

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mesenteric ischemia

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Acute mesenteric ischemia is interruption of intestinal blood flow by embolism, thrombosis, or a low-flow state. It leads to mediator release, inflammation, and ultimately infarction. Abdominal pain is out of proportion to physical findings. Early diagnosis is difficult, but angiography and exploratory laparotomy have the most sensitivity; other imaging modalities often become positive only late in the disease.

Treatment is by embolectomy, revascularization of viable segments, or resection; sometimes vasodilator therapy is successful. Mortality is high.

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mesenteric ischemia

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Etiology and Pathophysiology

The intestinal mucosa has a high metabolic rate and, accordingly, a high blood flow requirement (normally receiving 20 to 25% of cardiac output), making it very sensitive to the effects of decreased perfusion.

Ischemia disrupts the mucosal barrier, allowing release of bacteria, toxins, and vasoactive mediators, which in turn leads to myocardial depression, systemic inflammatory response syndrome (see Sepsis and Septic Shock), multisystem organ failure, and death.

Mediator release may occur even before complete infarction. Necrosis can occur as soon as 10 to 12 h after the onset of symptoms.

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mesenteric ischemia

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Three major vessels serve the abdominal contents: the celiac trunk, the superior mesenteric artery (SMA), and the inferior mesenteric artery (IMA). The celiac trunk supplies the esophagus, stomach, proximal duodenum, liver, gallbladder, pancreas, and spleen.

The SMA supplies the distal duodenum, jejunum, ileum, and colon to the splenic flexure. The IMA supplies the descending colon and sigmoid colon and the rectum.

Collateral vessels are abundant in the stomach, duodenum, and rectum; these areas rarely develop ischemia. The splenic flexure is a watershed between the SMA and IMA and is at particular risk of ischemia.

mesenteric ischemia

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Causes of Acute Mesenteric Ischemia
Occlusion Type

Risk Factors

Arterial embolus (> 50%) Coronary artery disease, heart failure, valvular heart disease, atrial fibrillation, history of arterial emboli
Arterial thrombosis (10%) Generalized atherosclerosis
Venous thrombosis (5–15%) Hypercoagulable state, inflammatory conditions (eg, pancreatitis, diverticulitis), trauma, heart failure, renal failure, portal hypertension, decompression sickness
Nonocclusive ischemia (25%) Low flow states (eg, heart failure, shock, cardiopulmonary bypass) and splanchnic vasoconstriction (eg, vasopressors, cocaine)
mesenteric ischemia

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Symptoms and Signs

The early hallmark of mesenteric ischemia is severe pain but minimal physical findings. The abdomen remains soft, with little or no tenderness.

Mild tachycardia may be present. Later, as necrosis develops, signs of peritonitis appear, with marked abdominal tenderness, guarding, rigidity, and no bowel sounds. The stool may be heme-positive (increasingly likely as ischemia progresses).

The usual signs of shock develop and are frequently followed by death.

Sudden onset of pain suggests but is not diagnostic of an arterial embolism, whereas a more gradual onset is typical of venous thrombosis. Patients with a history of postprandial abdominal discomfort (which suggests intestinal angina) may have arterial thrombosis.

 

 

 

mesenteric ischemia

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Diagnosis

Clinical diagnosis more important than diagnostic tests Mesenteric angiography if diagnosis unclear.

Frequency:

Mesenteric ischemia accounts for 0.1% of all hospital admissions. Risk factors for this disease include atherosclerosis, arrhythmias, hypovolemia, congestive heart failure, recent myocardial infarction (MI), valvular disease, advanced age, and intra-abdominal malignancy.
Mesenteric artery stenosis is found in 17.5% of independent elderly adults.

mesenteric ischemia

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Patients with mesenteric ischemia have a very typical presentation. However, the diagnosis may be overlooked because of the vague nature of the patients' symptoms.

Depending on the type of mesenteric ischemia, patients may present with a variety of signs and symptoms.

Patients may present with a history of postprandial pain, typically starting 20-30 minutes after their last meal, that may last up to 60-90 minutes. Because of this, they develop food fear and experience subsequent weight loss.
Patients may be severely malnourished upon presentation.

Diagnostic Tests:

  • No reliable test
  • Helpful adjuncts include
  • ABG – acidosis indicates ischemia but only develops in 50%
  • Lactic acid
    • Amylase
    • Creatine phosphokinase
    • D-Dimer (100% sensitivity in one study with 38% specificity)
    • Leukocytosis - greater than 15K supports diagnosis.

 

 

 

mesenteric ischemia

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Prognosis

If diagnosis and treatment take place before infarction occurs, mortality is low; after intestinal infarction, mortality approaches 70 to 90%.

For this reason, clinical diagnosis of mesenteric ischemia should supersede diagnostic tests, which may delay treatment.

mesenteric ischemia

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Appendiceal Carcinoid Tumor

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Appendiceal Carcinoid Tumor

The prognosis of appendiceal carcinoids is best predicted by the size of the tumor. Tumors less than 2 cm in size (found in approximately 95 percent of patients) are unlikely to have metastasized when diagnosed. In contrast, up to 30 percent of larger tumors have already metastasized at diagnosis.

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Appendiceal Carcinoid Tumor

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Carcinoid tumor of the appendix

Appendix - Carcinoid tumors are the most common neoplasms in the appendix. Approximately 1 in 300 appendixes contain a carcinoid tumor, almost always as a incidental finding. Appendiceal carcinoids are felt to arise from endocrine cells in the lamina propria and submucosa

Metastatic Carcinoid Tumors and the Carcinoid Syndrome — As noted previously, 90 percent of patients with the carcinoid syndrome have metastatic disease, typically to the liver. Exceptions are bronchial and ovarian tumors that can produce symptoms without metastasis. Patients with the carcinoid syndrome may benefit from therapies for the different components of the syndrome.

Appendiceal Carcinoid Tumor

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Carcinoid Tumor of the Appendix

Most patients with appendiceal carcinoids are asymptomatic. Symptoms are more likely with large tumors, those located at the base of the appendix, and with metastatic disease.

The majority of tumors are located in the distal one-third of the appendix where they are unlikely to cause obstruction. In approximately 10 percent of patients, tumors are located at the base, where they can cause obstruction, leading to appendicitis. Features of the carcinoid syndrome may be present in patients with tumors that have metastasized to the liver.

The prognosis of appendiceal carcinoids is best predicted by the size of the tumor, and the presence or absence of nodal or distant metastases. Tumors less than 2 cm in size (found in approximately 95 percent of patients) are unlikely to have metastasized when diagnosed. In contrast, up to 30 percent of larger tumors have already metastasized at diagnosis.

 

 

 

Lung Adenocarcinoma.

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Lung Adenocarcinoma.

This 72 year-old male with a long standing history of heavy smoking underwent a screening due to a dysphagia. The upper endoscopy was unremarkable.

Lung Adenocarcinoma.

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Computer Axial Tomography.

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Lung Adenocarcinoma.

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Large cell adenocarcinoma of the lung.
(Microscopic detail).

Lung Adenocarcinoma.

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Pleural retraction due to lung adenocarcinoma.

Lung Adenocarcinoma.

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Pleural retraction due to lung adenocarcinoma.

Gallbladder Adenocarcinoma and litiasis.

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Gallbladder Adenocarcinoma and litiasis.

Gallbladder adenocarcinoma is an aggressive tumor and is one of the digestive tract malignancies with the poorest prognosis. Because of loco-regional extension and delayed diagnosis, curative resection is often impossible.

Gallbladder Adenocarcinoma litiasis.

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Gallbladder Adenocarcinoma and litiasis.

Gross appearance of gallblader carcinoma filling all the cavity and invading the wall.

Although uncommon, carcinoma of the gallbladder (GB) is the most common primary hepatobiliary carcinoma, is the fifth most common malignancy of the GI tract, and predominantly affects older persons with long-standing cholecystolithiasis.

GB epithelial tumors tend to behave similarly to other GI adenocarcinomas. When the diagnosis is made incidentally at the time of cholecystectomy, surgical resection can be curative; however, more commonly, the tumor is unresectable and rarely diagnosed preoperatively despite patients' symptoms. Early diagnosis can improve the clinical outcome and cure rate of GB carcinoma.

 

 

 

Gallbladder Adenocarcinoma litiasis.

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Gross appearance of gallblader carcinoma filling all the cavity and invading the wall.

The exact etiology of GB carcinoma is unknown; however, several associated factors have been identified. One hypothesis suggests that irritation of the GB mucosa by stones causes chronic inflammation and, followed by repetitive epithelial repair, may cause malignant transformation. Approximately 15 years is required for dysplasia to progress to invasive carcinoma.

Gallbladder Adenocarcinoma litiasis.

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Gross appearance of gallblader carcinoma filling all the cavity and invading the wall.

Patients with GB carcinoma have an overall mean survival rate of 6 months, and the 5-year survival rate is 5%.

Gallbladder Adenocarcinoma litiasis

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Associated findings and risk factors for GB carcinoma are as follows:

Several risk factors have been identified for GBC, many of which share a common characteristic of chronic gallbladder inflammationlamina propria and submucosa

  • Cholecystolithiasis, which is present in 70-90% of patients (duration may be a key factor in development of cancer). Composition of the bile with cholesterol stones (most commonly implicated).

    Genetic factors.
  • Calcification of the GB wall (carcinoma in 25% of patients with "porcelain" GB).
  • Infections by Salmonella typhi.
  • Environmental carcinogens.
  • Gallbladder polyps
  • Helicobacter - Helicobacter colonization of the biliary epithelium (particularly H. bilis) has been implicated in the pathogenesis of gallbladder disease including gallbladder cancer based upon detection of Helicobacter-derived cytotoxins and surface proteins using sensitive molecular and immunohistochemical techniques. The strength of this association requires further clarification.

 

 

 

Gallbladder Adenocarcinoma litiasis

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Gallbladder cancer (GBC) is an uncommon but highly fatal malignancy; fewer than 5000 new cases are diagnosed each year in the United States.

The majority are found incidentally in patients undergoing exploration for cholelithiasis; a tumor will be found in 1 to 2 percent of such cases.

The poor prognosis associated with GBC is thought to be related to advanced stage at diagnosis, which is due both to the anatomic position of the gallbladder, and the vagueness and nonspecificity of symptoms.

Gallbladder Adenocarcinoma litiasis.

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Microscopic pattern of gallblader carcinoma

Gallbladder Adenocarcinoma litiasis.

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Microscopic detail of lymphatic and gallblader wall invasion.

Gallbladder Adenocarcinoma litiasis.

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Microscopic detail of lymphatic and gallblader wall invasion.

Gallbladder Adenocarcinoma litiasis.

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Gallbladder Adenocarcinoma litiasis.

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Giant Ovarian Serous Cystadenoma.

Giant Ovarian Serous Cystadenoma.

This 35 year-old female, presented with voluminous serous cystadenoma of the ovary. She was treated surgically with good results.

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Macronodular Cirrhosis

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Macronodular Cirrhosis

Larger nodules separated by wider scars and irregularly distributed throughout the liver usually due to an infectious agent such as viral hepatitis which does not diffuse uniformly throughout the liver.

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Known causes of cirrhosis account for about 90-95% of the cases. Most common etiologies include alcoholism, autoimmune chronic hepatitis and chronic viral hepatitis.

Less common causes include hemochromatosis, primary biliary cirrhosis, sclerosing cholangitis, drug-induced liver disease and chronic biliary obstruction. Other causes include a1-antitrypsin deficiency, severe steatohepatitis in the morbidly obese and Wilson's disease.

The remaining 5-10% of patients with cirrhosis of the liver have no known cause, a condition termed cryptogenic cirrhosis. Over the last 10 years, the rate of cryptogenic cirrhosis has fallen from 30% to current levels. The most likely cause for this fall has been the availability of testing for hepatitis C.

The etiology of the cirrhosis usually cannot be determined by the pathologic appearance of the liver (with some notable exceptions, including hemochromatosis and a1-antitrypsin deficiency).

Terms previously used such as portal cirrhosis or postnecrotic cirrhosis have been replaced by classifications that include three anatomic categories.

 

 

 

Cirrhosis of the Liver

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Classification of Cirrhosis

Morphologic: Macronodular Micronodular Mixed

Histologic: Portal, Post-necrotic, Post Hepatitic, Biliary, CongestiveETIOLOGIC AGENTS: Genetic, Toxic, Infectious, Biliary, Vascular, Cryptogenic This peculiar transformation of the liver was identified by the first anatomic pathologist, Gianbattista Morgagni in his 500 autopsies published in 1761 but the name of "cirrhosis" (greek=orange color) was given by Laennec in 1826 because of the yellowish-tan color of the cirrhotic liver .

Only in 1930, one hundred years later, however, the first theory as to the pathogenesis of this disorder was advanced by Roessle: parenchymal degeneration, regeneration and scarring which is now understood according to the following sequence:

  • Injury
  • Degeneration
  • Fibrosis
  • Formation of fibro-vascular membranes
  • Parenchymal dissection into nodules
  • Rearrangement of blood
  • Cirrhosis

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Laparoscopy of Cirrhosis and Liver Biopsies

Laparoscopy of Cirrhosis and Liver Biopsies

 

 

 

hepatic infiltration of malignant melanoma

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Image and Video of Laparoscopy of extensive hepatic infiltration of malignant melanoma


hepatic  malignant melanoma

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Image and Video of Laparoscopy of extensive hepatic infiltration of malignant melanoma.

With the harmonic scalpel, some fragments for their respective histopathology are extracted.

 










Elephantiasis nostras verrucosa

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Elephantiasis nostras verrucosa on the legs with morbid obesity.

This 42 year-old male with morbid obesity more than 500 libs. Came to our office to ask for help for weigh lost.

Elephantiasis nostras verrucosa (ENV), is an unusual progressive cutaneous hypertrophy due to chronic lymphedema, and repeated inflammatory episodes.

It usually manifests over the lower extremities as non-pitting edema with lichenification, hyperkeratotic papules, nodules, and verrucous, cobblestone-like plaques.

Elephantiasis nostras verrucosa

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The condition has also been reported rarely on the upper extremities, ears, face, scrotum, chest, genitalia, buttocks, and periorbital region.

Histolopathology shows acanthosis and hyperkeratosis of the epidermis and dilated lymphatic spaces in the dermis.

Elephantiasis nostras verrucosa

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Elephantiasis nostras verrucosa represents longstanding obstruction of the lymphatic drainage, leading eventually to grotesque enlargement of the chronically dependent and immobile part(s) of the body.

Chronic persistent lymphedema may lead to recurrent streptococcal lymphangitis, which can also be the predisposing factor.

The microorganisms may gain entry into the lymphatics through minor injuries, interdigital fissures, or tinea pedis.

Elephantiasis nostras verrucosa

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Recurrence is common due to the protein rich edema. In the previous reports of abdominal ENV, it was hypothesized that the massiveness of the panniculus caused increased interstitial and intravascular pressure predisposing the patients to chronic low-grade cellulitis and lymphangitis.

Elephantiasis nostras verrucosa

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The condition may also occur secondary to trauma, surgery, tumor-obstruction, radiation, portal hypertension, congestive heart failure and Kaposi sarcoma.

The differential diagnosis includes filariasis, pretibial myxedema, and stasis dermatitis. Obesity is a significant predisposing factor.

Enterocutaneous Fistula

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Postoperative enterocutaneous fistulas

This is a 49 year-old lady, because of complications of bullet wound and multiple abdominal surgery, develops enterocutaneous fistula.

In the video clip is shown output of liquid emerging from one of the fistulas.



Enterocutaneous Fistula

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In the video clip is shown output of liquid emerging from one of the fistulas

Enterocutaneous fistulas may result from a wide variety of conditions and circumstances. Care of these patients can be quite challenging, frustrating, and, ultimately, rewarding. The patient with an enterocutaneous fistula presents the surgeon with a plethora of challenges, and a command of related anatomy, physiology, and metabolism is necessary to successfully meet these challenges.

Postoperative enterocutaneous fistulas, the focus of this brief review, account for approximately 80% of enterocutaneous fistulas. The remainder of enterocutaneous fistulas may occur spontaneously, as a result of tumor, irradiation, or inflammation.

Enterocutaneous Fistula

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In the video clip is shown output of liquid emerging from one of the fistulas

Treatment of patients with postoperative enterocutaneous fistulas requires an understanding of the metabolic and anatomic derangements. In order for mortality of patients with postoperative fistulas to be minimized, nutrition, volume, and electrolyte derangements must be corrected. This must be done in addition to replacing ongoing losses in these areas. Malnutrition is easier to prevent than correct. Once established, malnutrition may be difficult to correct, especially with concomitant sepsis, but malnutrition and sepsis remain principal causes of death in patients with fistulas.

In the case of enterocutaneous fistulas, the diagnosis is usually obvious, with external drainage of enteric contents. Most postoperative enterocutaneous fistulas are identified in the immediate postoperative period and follow a predictable scenario. The typical patient is 5 or 6 days postoperative, with a fever and persistent ileus. A wound abscess becomes apparent, is drained, and the patient's fever resolves. Within 24 hours, the fistula becomes obvious and enteric contents appear on the wound dressing. Once the diagnosis is made, therapy should be initiated as described below.

 

 

Enterocutaneous Fistula

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In the video clip is shown output of food emerging from one of the fistulas.

Table II Treatment phases

Phase Time Course Primary goals
1. Recognition and stabilization 24–48 hours Correct fluid and electrolyte imbalances
Drainage of intra-abdominal abscesses
Control of sepsis
Control of fistula drainage
Ensure adequate skin care
Aggressive nutritional support
2. Investigation after 7–10 days Determine anatomy and fistula characteristics
3. Decision up to 4–6 weeks Determine likelihood of spontaneous closure
Plan course of therapy
4. Definitive therapy after 4–6 weeks or if closure is unlikely Closure of fistula
Reestablish gastrointestinal continuity
Secure closure of abdomen
5. Healing 5–10 days after closure onward Ensure adequate nutritional support
Transition to oral intake

 

Enterocutaneous Fistula

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The two fistulas which are delimited by cotton swabs are observed .

Phase 4: Definitive therapy

If the anatomic features of the fistula preclude spontaneous closure or an anatomically favorable fistula has not closed in the expected time frame (4–5 weeks of sepsis free adequate parenteral nutrition), the patient should be prepared for operative closure. Ideally, with meticulous skin care and control of fistula drainage, the abdominal wall will be healthy, enhancing the opportunity for secure abdominal closure. The patient is prepared for operation in the standard fashion, with intraluminal antibiotics and mechanical bowel preparation. Discontinuation of enteral nutrition prior to operation may decrease abdominal distension and aid in abdominal closure.

Entering the abdomen through a new incision is preferred if possible. Dissection to free the bowel from the ligament of Treitz to the rectum is then carried out. The bowel should be freed from all adhesions to ensure that there is no obstruction. This usually requires extensive dissection, meticulous technique, and, not infrequently, a great deal of time. The highest closure and lowest complication rates may be obtained by resection of the involved section of bowel with end-to-end anastomosis. Other procedures should be performed only if this is not possible. Enteral access for the postoperative period should be established, either through a gastrostomy, which can also be used for gastric decompression, a feeding jejunostomy, or preferably both.

One circumstance in which resection and end-to-end anastomosis should not be performed is the patient with a duodenal fistula. Satisfactory closure of these fistulas can be achieved with a bypass procedure, such as gastrojejunuostomy.

At the end of the operation, secure abdominal wall closure should be obtained. If the abdominal wall has been compromised, such as with partial destruction by sepsis, a plastic surgeon should be consulted to assist closure, and flaps may be necessary.


Enterocutaneous Fistula

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An endoscopy is performed via fistula, path is observed from jejunum-duodenum to stomach.

Phase 5: Healing

In the postoperative period, it is necessary to ensure that the patient continues to receive full nutritional support. Adequate protein and calories must be provided to maximize healing and minimize complications. Although enteral nutrition may be attempted early in the post-operative course, it is nearly impossible to meet the patient's entire nutritional demand by this route. Thus, postoperative care will most likely include parenteral and enteral supplementation in an overlapping manner.

After fistula closure, whether by spontaneous or surgical means, the patient will need to resume oral intake. This my be especially difficult in an individual who has had little or no oral intake for 4 to 6 weeks or more, and enlisting the assistance of a dietician and the patient's family is often helpful. Weaning enteral and parenteral nutritional supplementation and switching to nocturnal tube feeds may help to increase appetite.

 

Enterocutaneous Fistula

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Pylorus is seen from the duodenal bulb, seen from the way of the enterocutaneous fistula endoscopy: jejunum-duodenum--stomach.

 

 

 

Enterocutaneous Fistula

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Stomach is observed in the way of endoscopy from enterocutaneous fistula jejunum-duodenum to -stomach. At the right gastric cardia is observed.

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