What are the manifestations of tuberculous peritonitis?
There are two types of peritonitis, acute and chronic, the latter being the most common.
Acute tuberculous peritonitis is mostly due to the hematogenous spread of cornified tuberculosis, but can also be due to the sudden rupture of intra-abdominal tuberculous lesions and mesenteric lymph nodes. Patients often present with acute abdominal pain that spreads to the whole abdomen, accompanied by low-grade fever and abdominal distension. On physical examination, there is more widespread mild abdominal pressure pain, rebound pain and abdominal muscle tension. Systemic signs of toxicity are not as severe as those of bacterial peritonitis. The white blood cell count is not high.
Chronic tuberculous peritonitis usually has a slow onset. It presents with chronic tuberculosis toxicity symptoms, such as wasting, weakness, poor appetite, anemia, night sweats, and irregular low-grade fever. According to the main clinical manifestations, it can be divided into three types: ascites type, mucocele type, and cheese ulcer type.
The ascites type has a slow onset, with gradual distention of the abdomen until a large amount of ascites may appear, accompanied by vague abdominal pain, abdominal distention and diarrhea. On physical examination, there is mild abdominal pressure pain and mobile turbid sounds on percussion. The peritoneal puncture is a straw-yellow exudate, a few of which may be bloody, sometimes coffee-colored and mixed, containing small yellow flaky crystals (cholesterol). The exudative form of tuberculous peritonitis may be isolated or may be part of a multiple pluritis with combined tuberculous pleurisy, pericarditis, or meningitis.
The adherent form is characterized by recurrent incomplete small bowel obstruction. There is often paroxysmal abdominal pain and distention with nausea and vomiting. On physical examination, the abdominal wall is often tender. Sometimes, intestinal patterns and peristaltic waves of different sizes can be detected, and the abdomen is distended and distended, with hyperactive bowel sounds. Diarrhea can occur again after the obstruction is released. The disease is often chronic in appearance due to malnutrition, and the body is thin.
The clinical symptoms of the cheese ulcer type are severe. Due to caseous necrosis and liquefaction of the tuberculosis lesion, sometimes secondary to purulent bacterial infection, the patient may develop flaccid fever, progressive wasting, anemia, weakness, and even cachexia. There is often abdominal pain, diarrhea, or symptoms of intestinal obstruction such as abdominal distention and lack of defecation and exhaustion. Abdominal masses of varying sizes can be found with pressure pain. The abdominal wall is tender or plate-like. When the caseous liquefied lesion ulcerates into the abdominal cavity, a limited purulent peritonitis appears. When the lesion penetrates into the abdominal wall, there may be redness and swelling of the abdominal wall and even ulceration to form an abdominal wall fistula or umbilical fistula.
How to diagnose tuberculous peritonitis?
(1) Medical history.
Children and young adults with a history of tuberculosis or with evidence of extraperitoneal tuberculosis. Fever of unknown origin for more than two weeks, weakness, poor appetite, wasting with abdominal distension, abdominal pain, diarrhea, etc., while leukocytes and classification are normal or mildly increased, and increased blood sedimentation should be highly suspected. In addition, patients should be asked whether they have a recent history of exposure to tuberculosis, and whether they have taken hormones or have low resistance due to other factors.
(2) Physical examination.
The fever is mainly low in the afternoon, and some of them may show moderate or high fever. It may be accompanied by night sweats, weight loss, and in severe cases, swelling, anemia, linguitis, stomatitis, and vitamin A deficiency. The abdomen is tender to palpation, and there may be pressure pain, mostly without rebound pain. Some patients may have palpable abdominal masses, and about 1/3 of patients have positive ascites signs. In combination with intestinal or mesenteric lymphatic tuberculosis, intestinal obstruction may be present. Routine gynecologic examination should also be performed in married female patients to exclude pelvic tuberculosis.
(3) Laboratory tests.
Patients may have mild to moderate anemia with normal or slightly high white blood cells and classification. Tuberculin reaction is strongly positive, and most patients have increased sedimentation. Abdominal puncture may draw straw-yellow fluid, which naturally coagulates after resting, and a few are light blood-colored, occasionally celiac-like. Most of the ascites tests are exudate, but some severe patients with hypoproteinemia or combined with cirrhosis and other diseases may show leaky fluid. The positive rate of ascites etiology is resistant, and it is more difficult to concentrate the antacid bacilli. Ultrasound and CT examination can suggest signs of intestinal adhesions, and X-ray examination can reveal signs of multiple calcified foci, intestinal obstruction, colonic fistula and extracolonic masses, and barium meal examination of the stomach and intestines can show signs of intestinal tuberculosis. Laparoscopy has a confirmatory value but is limited to patients with free ascites.
What are the treatment measures for tuberculous peritonitis?
Tuberculous peritonitis is a chronic disease and the principle of treatment is to strive for early, adequate and long course treatment to achieve cure and prevent recurrence or complications. At the same time, attention should be paid to strengthening nutrition and preventing overwork.
Anti-tuberculosis treatment is commonly used: isoniazid 0.3, rifampicin 0.45 morning dose, streptomycin 0.75 intramuscular injection once a day, streptomycin medication 1 to 2 months after the change to twice a week, to not cause toxic reactions as appropriate to extend its course.
After the disease is controlled, it is changed to isoniazid and rifampicin oral maintenance therapy, and liver function is monitored regularly. If liver function damage occurs, rifampicin can be changed to oral aminobutanol. The course of treatment should be 1 to 1.5 years, 2 years if necessary. In patients with hematogenous dissemination or severe toxemia, adrenocorticotropic hormone can be added to effective anti-tuberculosis drug therapy to reduce toxemia. The addition of other antimicrobials is appropriate in the presence of coexisting septic peritonitis.
Surgical intervention is required in cases of acute complete intestinal obstruction with adherent abdominal tuberculosis, intestinal perforation with caseous type, or encapsulated pus due to limited peritonitis, or abdominal wall fistula or vaginal fistula. If the adhesions are loose and limited, release is feasible. If the adhesions are limited but very tight, it is not advisable to forcibly separate them, and the segment of the intestine can be removed or the upper and lower ends of the obstruction can be laterally anastomosed. Primary tuberculous lesions in the abdominal cavity, such as tuberculosis of the fallopian tubes and intestine, should be resected if possible. Caseous lesions that cannot be resected can be excised or scraped, and anti-tuberculosis drugs can be put in. For chronic incomplete intestinal obstruction, non-surgical treatments such as fasting, fluid replacement, gastrointestinal decompression and Chinese and Western medicines should be adopted as far as possible, which are mostly effective.
What is mesenteric lymphatic tuberculosis? What are the manifestations? How to diagnose and treat mesenteric lymphatic tuberculosis?
Mesenteric lymphatic tuberculosis is often secondary to tuberculosis of other organs, such as intestinal tuberculosis and tubal tuberculosis. Primary mesenteric lymphatic tuberculosis occurs when Mycobacterium tuberculosis swallowed into the gastrointestinal tract enters the corresponding lymphatic vessels directly through the intestinal mucosa. The latter is mostly seen in children and adolescents.
Mesenteric lymphatic tuberculosis is often secondary to tuberculosis of other organs, such as intestinal tuberculosis and tuberculosis of the fallopian tubes. For example, mesenteric lymphatic tuberculosis occurs when Mycobacterium tuberculosis entering the gastrointestinal tract is swallowed and enters the corresponding lymphatic vessels directly through the intestinal mucosa.
Its clinical symptoms may include abdominal pain, diarrhea and abdominal distension, in addition to general TB symptoms such as fever and lethargy. On palpation of the abdomen, enlarged lymph nodes of 2-3 cm in diameter can be found in the right lower or middle abdomen, sometimes multiple lymph nodes coexist, with immovable and uneven margins and pressure pain.
The following tests can be performed for diagnosis.
(a) Blood picture and sedimentation: total white blood cell count is usually normal, red blood cells and hemoglobin are often low, and mild to moderate anemia is present, with ulcerated patients being the most common. In patients with active lesions, the blood sedimentation is often increased.
(ii) Stool examination.
(iii)X-ray examination: abdominal X-ray plain film, which shows several round or oval uneven density spots or speckled masses of calcified shadow at the attachment of mesenteric roots, and the shadow is in front of the spine in lateral film.
(d) Fiber colonoscopy: direct observation of lesions in the whole colon, cecum and ileocecal region is possible, and biopsy or sampling for bacterial culture is also feasible.
As with pulmonary tuberculosis, treatment should emphasize early, combined, appropriate dosage and full course of medication.
(a) Rest and nutrition: reasonable rest and nutrition should be the basis for the treatment of tuberculosis.
(ii) Anti-tuberculosis drug therapy: The selection and usage of anti-tuberculosis drugs are the same as those for pulmonary tuberculosis.
(C) Symptomatic treatment: Belladonna, atropine or other anticholinergic drugs can be used for abdominal pain.
Since mesenteric lymphatic tuberculosis is often secondary to pulmonary tuberculosis, the primary disease should be diagnosed and treated actively, public health publicity should be strengthened, patients should be educated to avoid swallowing sputum and not spitting, and milk should be sufficiently sterilized before drinking.
What is acute superior mesenteric artery embolism? What are the manifestations?
Superior mesenteric artery embolism (SMAE) refers to acute complete vascular occlusion caused by an embolus entering the superior mesenteric artery. Embolism of the superior mesenteric artery can cause a sudden decrease or loss of blood supply to the superior mesenteric artery, resulting in muscle dysfunction of the intestinal wall and acute ischemia and necrosis of the intestine. Clinically, superior mesenteric artery embolism is a rare disease, with an annual incidence of about 816/100,000, but once it occurs, the condition is extremely dangerous and the mortality rate is extremely high, reaching 70% to 100%.
The emboli of superior mesenteric artery embolism mainly originate from the heart, such as the wall embolus after myocardial infarction, the valve redundancy of subacute bacterial endocarditis, the redundancy of rheumatic heart valve lesions and the dislodgement of the left ear and left atrial appendage thrombus, as well as the dislodgement of the thrombus formed after prosthetic valve replacement; there are also the dislodgement of the appendage thrombus or atheromatous plaque of atherosclerosis of large arteries and the bacterial emboli of abscess or sepsis. emboli, etc.
The occurrence of superior mesenteric artery embolism is also related to the anatomy of the superior mesenteric artery. The superior mesenteric artery divides from the abdominal aorta at a small angle. The branch travels almost parallel to the abdominal aorta and in the same direction as the mainstream of blood flow, which, together with the thick lumen, makes it easy for dislodged emboli to enter and cause embolism at the narrowing or bifurcation of the vessel. The embolism is usually found in the middle colonic artery or within 3-10 cm below it.
The disease is more common in men than in women, and is more frequent between the ages of 40 and 60. Most patients have a history of heart disease that can form arterial emboli, such as myocardial ventricular aneurysm after myocardial infarction, atrial arrhythmia, rheumatic valve disease, aortic atherosclerosis, etc. More than 1/3 of patients have a history of limb or cerebrovascular embolism.
The onset of the disease is rapid, with sudden onset of severe abdominal pain, accompanied by frequent vomiting. In the initial stage, the symptoms of abdominal pain and signs do not match each other, and the abdominal pain is severe while the abdominal signs are mild. When the patient vomits bloody watery material or passes dark red blood stool, the abdominal pain symptoms are reduced, but abdominal pressure pain, rebound pain, abdominal muscle tension and other signs of peritoneal irritation appear, and weak bowel sounds disappear. When there is mobile turbid sound on percussion examination, bloody exudate can be extracted by laparotomy, which indicates that intestinal canal infarction has occurred. As the disease progresses, the patient may show signs of peripheral circulation failure such as abdominal distension, weak pulse, cyanosis of lips, cyanosis of fingertips and cool skin.
How to diagnose and treat acute superior mesenteric artery embolism?
Risk factors for this disease have been suggested to include age > 50 years, valvular heart disease, arrhythmias, and recent myocardial infarction. Based on the patient’s history of heart disease or arterial embolism, sudden onset of severe abdominal pain with mild signs, accompanied by vomiting and dark red bloody stools, combined with laboratory tests [elevated white blood cell count, elevated serum enzymes lactate dehydrogenase (LDH), alkaline phosphatase (AKP), creatine myokinase (CK), etc.], acute superior mesenteric artery embolism should be considered as a possibility.
(1) Laboratory tests: white blood cell count can be significantly elevated, mostly in the range of 25-40 × 109 /L, and there may be signs of hemoconcentration and metabolic acidosis. Serum enzymatic examination may show elevated serum LDH, AKP, CK. Recently, the level of D2 dimer, a marker of fibrinogen, has been found to be useful in the diagnosis of superior mesenteric artery embolism. The results of laboratory tests are not specific for the diagnosis of superior mesenteric artery embolism, but can reflect the criticality of the disease and help to make the suspected diagnosis and exclude the diagnosis.
(2) abdominal plain film: X-ray examination is difficult to clarify the phenomenon of intestinal ischemia, there is no special performance in the early stage, and it is only used to exclude other diseases, it can be seen that the large and small intestines are mildly or moderately dilated and inflated, and in the late stage, due to the large amount of fluid in the intestinal cavity and abdominal cavity, the abdomen generally has increased density.
(3) Color ultrasound: Doppler color ultrasound can determine the presence or absence of embolism and the site of embolism according to the direction and speed of blood flow, but in the case of intestinal obstruction, the dilatation of the intestinal canal can interfere with the correctness of diagnosis.
(4) CT examination: general CT examination is not specific for the diagnosis of acute superior mesenteric artery embolism. In recent years, the specificity and sensitivity of two-stage CT (Biphasic CT) angiography for the diagnosis of mesenteric vascular embolism reached 100% and 73%, which can not only observe the mesenteric vascular condition, but also reflect the changes of intestinal canal, abdominal organs and surrounding tissues. In addition to the filling defect of the main trunk of the superior mesenteric artery (SMA) due to embolism, the imaging also shows weakening of the intestinal wall, thickening of the intestinal wall, diffuse pneumatization of the intestinal canal, mesenteric edema and ascites.
(5) Angiography: Selective superior mesenteric arteriography is considered the gold standard for the diagnosis of acute superior mesenteric artery embolism, and can be used to make a definitive diagnosis before intestinal infarction and dissection. It has been suggested that mesenteric angiography should be performed in all patients with combined risk factors and unspecified abdominal pain. By understanding the abdominal trunk, mesenteric artery and its branches, the site of embolism can be determined according to the sudden interruption of the contrast medium. Embolic obstruction of the superior mesenteric artery is usually located within 3 to 10 cm from the beginning of the superior mesenteric artery and at the beginning of large branches. Selective superior mesenteric artery angiography can clearly show the location of the embolus and the presence or absence of collateral circulation. After the angiogram is completed, a contrast tube is left in the superior mesenteric artery for the application of medications such as antispasmodics or thrombolytics, and the tube can be infused with medications after the procedure for adjunctive therapy, and the effect of treatment can be observed by repeat imaging. The main imaging manifestations are sudden disruption of the superior mesenteric artery or branches, hemimelia, filling defect, and weakening of the intestinal wall, and the diagnostic sensitivity is 96%. Although color ultrasound and CT examination are helpful for the early diagnosis of acute superior mesenteric artery embolism, they are not as intuitive and accurate as arteriography. Therefore, when mesenteric artery occlusion is suspected, hospitals with conditions should not hesitate to perform superior mesenteric artery angiography. The clinical manifestation of acute superior mesenteric artery embolism varies depending on the specific location, extent, urgency and time of onset of the embolism, which makes the diagnosis very difficult and the misdiagnosis rate is as high as 90%-95%.
Treatment of acute superior mesenteric artery embolism.
The treatment principle of superior mesenteric artery embolism is to quickly remove the embolus in the blood vessel and restore the blood perfusion of superior mesenteric artery, including systemic treatment, interventional treatment and surgical treatment.
(1) Systemic treatment: The initial treatment principle for all patients with superior mesenteric artery embolism is to resuscitate and stabilize the circulation, and broad-spectrum antibiotics should be given to those who are suspected of further ischemic manifestations. For patients whose intestinal canal is not yet necrotic, arteriography confirms the embolization of the superior mesenteric artery branches, and the distal blood flow can still be filled, the mesenteric vessels can be dilated and released from spasm by intramuscular injection of poppy bases, and conservative treatment by systemic anticoagulation and expectoration of heparin; at the same time, the predisposing diseases, such as treatment of arrhythmia, can be removed to prevent the dislodgement of emboli in other parts, and the relatively ischemic intestinal canal will recover blood supply with the establishment of collateral circulation. Close observation of changes in the condition during treatment and repeat angiography if necessary.
(2) Interventional treatment.
(1) Infusion of poppy bases via superior mesenteric artery: If the diagnosis of acute superior mesenteric artery embolism is confirmed by imaging, a catheter is left in the superior mesenteric artery and poppy bases are injected at a rate of 30-60 mg/h. After 24-48 hours of continuous infusion, imaging is performed again to confirm that the mesenteric vessels are dilated and filled, and the thrombus is released before the catheter is removed. If the intubation of poppyine is ineffective or if peritonitis is present, surgery should be performed immediately.
Urokinase thrombolysis via superior mesenteric artery: Patients with mesenteric artery embolism without intestinal necrosis confirmed by mesenteric angiography can be treated with urokinase thrombolysis, but it must be controlled within 8h of abdominal pain without signs of peritoneal irritation. This can avoid resection of the intestinal canal or reduce the scope of necrosis, and reduce the mortality rate to a certain extent.
(3) Transfemoral artery puncture of superior mesenteric artery aspiration therapy: In recent years, some scholars have used long sheaths of arteries with large caliber and dilating tubes as a tool for aspiration of embolus by negative pressure, and at the same time, poppy bases can be given for antispasmodic and urokinase thrombolysis with satisfactory results.
(3) Surgery: For patients with pre-existing heart valve disease or atrial fibrillation who present with acute abdominal pain, nausea, vomiting, elevated leukocytes and metabolic acidosis, dissection should be actively performed. Acute superior mesenteric artery embolization surgery procedure:
If the blood flow of the superior mesenteric artery can be restored, the viability of the involved intestinal segment should be re-evaluated, and the non-viable intestinal segment should be removed and decided whether to be anastomosed or externalized. Even if the patient has intestinal infarction, embolization should be performed first to improve the blood supply to the ischemic intestine and to reduce the extent of bowel resection to avoid short bowel syndrome. The main surgical method is to remove the embolus via superior mesenteric artery incision with Fogarty balloon catheter.
② Superior mesenteric artery diversion: If the embolized segment is long and there is no blood flow or poor blood flow even after the embolus is removed, it indicates that the proximal artery has obstructive lesions, and diversion can be performed. Clinically, we mostly use the autologous saphenous vein (also can be used artificial blood vessel) to do bypass surgery between the abdominal aorta or iliac artery and the open superior mesenteric artery below the embolism.
(3) Intestinal resection: If the embolism is found to be located at the distal end of a branch or trunk, and the intestinal canal is ischemic and necrotic but the scope is not large, early necrotic intestinal canal resection should be performed. For those who are not completely sure whether the intestinal tube is still viable, the suspected intestinal tube can be placed externally to avoid disturbing the high-risk patients as much as possible, and then secondary treatment can be performed after the patient has passed the acute phase, or the rejuvenated intestinal tube can be placed into the abdominal cavity, or the inactive intestinal tube can be safely removed.
Tips: The mortality rate of acute superior mesenteric artery embolism is extremely high, and early and correct diagnosis and timely treatment are the keys to reduce the mortality rate. Therefore, when the clinician explains to the patient’s family that the patient has the possibility of this disease, the patient’s family should first be prepared for the worst outcome, and at the same time cooperate with the doctor’s various requirements such as the signature of informed consent for surgery as much as possible, so as not to delay the rescue time in these aspects. It is important to know that when there is intestinal obstruction or even signs of peritonitis, the resuscitation time is calculated in minutes, and the doctor needs to decisively carry out surgical investigation to clarify the diagnosis and treatment, so the patient’s family should not emphasize the accuracy of preoperative diagnosis and delay the treatment time. To restore intestinal blood supply and remove necrotic intestinal tubes and embolized mesentery. In this way, the success rate of patients with acute superior mesenteric artery embolism can be improved to a certain extent.
What is mesenteric vein thrombosis? What are the signs and symptoms?
Mesenteric vein thrombosis accounts for 5% to 15% of all mesenteric vascular ischemic disorders, usually involving the superior mesenteric vein, but rarely the inferior mesenteric vein. The disease is clinically insidious, and the diagnosis is often delayed, with the definitive diagnosis being made in most cases only during open abdominal exploration.
Mesenteric vein thrombosis can be classified as primary or secondary. Those with a definite cause are called secondary, while those with an unknown cause are called primary or idiopathic. As the diagnosis of hereditary coagulation disorders and the ability to identify hypercoagulable states have increased, the proportion of idiopathic cases in this disease has gradually decreased, and now about 75% of mesenteric vein thrombosis can be diagnosed. The most common causes are hypercoagulable states due to genetic or acquired diseases such as tumors, abdominal inflammation, post-surgery, liver cirrhosis and portal hypertension. The use of oral contraceptives accounts for 9-18% of patients with superior mesenteric vein embolism in young women.
The clinical manifestations of mesenteric vein thrombosis can be divided into three types: acute, subacute and chronic. Acute cases have a sudden onset with rapid onset of peritonitis and intestinal necrosis. The subacute cases are those in which the abdominal pain lasts for days or weeks without intestinal necrosis. Chronic mesenteric vein thrombosis is actually a form of prehepatic portal hypertension, and its treatment focuses on the management of portal hypertensive complications such as bleeding from ruptured varices and ascites, and intestinal ischemia is not the key to treatment. Most patients present with a subacute course without intestinal necrosis or variceal bleeding. However, there are patients who develop intestinal necrosis after prolonged abdominal pain, so the so-called acute and subacute manifestations cannot be clearly separated.
The clinical manifestation of mesenteric vascular ischemia, regardless of arterial or venous thrombosis, is abdominal pain that does not coincide with the physical examination. In mesenteric vein thrombosis, the pain is mostly located in the mid-abdomen and is colicky in nature, suggesting that the lesion originates in the small intestine. The duration of symptoms varies widely, with more than 75% of patients having symptoms for more than 2 days at the time of presentation. The symptoms are often accompanied by nausea, loss of appetite, and vomiting. 15% of patients have vomiting blood, blood in the stool, or black stools, and nearly 1/2 of patients have positive fecal occult blood tests. Because of the relatively low incidence and lack of specificity of symptoms, the diagnosis is often delayed. The initial physical examination may be completely normal. Later in the course of the disease, fever, abdominal muscle tension and rebound pain may be present, suggesting intestinal necrosis. Signs of peritonitis are present in approximately 1 /3 to 2 /3 of patients. Intra-intestinal or intra-abdominal exudate may lead to decreased blood volume and circulatory instability, with a systolic blood pressure < 90 mmHg (1 mmHg = 01133 kPa) suggesting a poor prognosis.
How is mesenteric vein thrombosis diagnosed and treated?
Blood tests are usually not helpful in the diagnosis of mesenteric vein thrombosis, but metabolic acidosis and elevated serum lactate levels can be used to determine the presence of intestinal necrosis, often in the advanced stages of the disease. 50-75% of patients have a normal abdominal radiograph, and only 5% of patients show specific signs of intestinal ischemia: the presence of acupressure in the intestinal lumen suggests intestinal mucosal ischemia, and pneumatosis of the intestinal wall or free gas in the portal vein is a sign of mesenteric thrombosis. Intestinal wall emphysema or free gas in the portal vein is a characteristic sign of intestinal infarction due to venous thrombosis. CT scan is used in cases where mesenteric vein thrombosis is suspected, but CT can be diagnostic in 90% of patients, but is less accurate for small early portal vein thrombosis. Selective mesenteric angiography can show thrombosis in large veins or delayed mesenteric vein visualization. Magnetic resonance imaging has a high sensitivity and specificity for the diagnosis of mesenteric vein thrombosis, but the procedure is more complicated and less widespread. With the progress of technology, magnetic resonance imaging will have a place in the diagnosis of mesenteric vein thrombosis.
Patients with mesenteric vein thrombosis may have plasma-hemorrhagic ascites, and diagnostic laparotomy may be helpful in this setting. Pneumoperitoneum during laparoscopy may increase intra-abdominal pressure and decrease mesenteric blood flow and should be avoided. Fibrocolonoscopy and gastroduodenoscopy are of limited value because the colon and duodenum are rarely involved. Endoscopic ultrasonography can detect mesenteric vein thrombosis, but is best used in patients without acute symptoms because of the dilatation of the bowel during the examination.
In cases of mesenteric vein thrombosis, CT is the best test, not only to visualize the mesenteric vessels and determine the extent of the involved bowel, but also to exclude other diseases causing abdominal pain. Mesenteric angiography should be used in patients with suspected thrombotic tendencies, in which case the thrombus is often located in smaller vessels of the mesenteric venous system.
Treatment of mesenteric vein thrombosis includes both anticoagulation and anticoagulation combined with surgical treatment. In patients with acute or subacute mesenteric ischemia, heparin therapy should be started as soon as the diagnosis is made. Not all patients with mesenteric vein thrombosis require surgical exploration, but patients with clear signs of peritonitis require urgent surgery. If the diagnosis of mesenteric vein thrombosis is established intraoperatively, anticoagulation therapy should be initiated. Because of the lack of a clear boundary between the ischemic and normal intestine, the emphasis on obtaining a normal intestinal segment for bowel resection may result in the removal of too much viable intestine. Therefore, we should be more cautious in performing intestinal resection in this disease, and the principle is to preserve as much viable intestinal canal as possible. To avoid resection of too many potentially viable intestines, a secondary exploration after 24 hours is preferred. Secondary exploration is particularly useful in patients with extensive involvement of the intestinal canal and some mesenteric flow. In some cases, a conservative bowel resection may be followed by dragging the severed end out of the abdominal wall stoma instead of performing a one-stage intestinal anastomosis, using the stoma as a window to observe the viability of the intestine, which may save some patients with poor conditions from secondary exploration. In rare cases, thrombectomy can be performed if the thrombus is short-lived and confined to the superior mesenteric vein. More extensive thrombosis is not appropriate for tethering. Arterial spasm is a common condition, and removal of potentially revitalized ischemic bowel can be avoided by a combination of intra-arterial poppyine infusion, anticoagulation, and secondary exploration.
In the absence of intestinal necrosis, mesenteric vein thrombosis can be treated medically without surgery. However, there are no indicators that can accurately indicate the risk of intestinal necrosis in patients. In patients without peritonitis or perforation, intravenous antibiotic therapy is not required. However, immediate anticoagulation with heparin early in the course of the disease can significantly improve patient survival and reduce the recurrence rate, even when applied during surgery. Systemic heparin therapy can be started with 5,000 U of heparin given intravenously, followed by a continuous infusion to keep the activated partial thromboplastin time more than twice normal. Anticoagulation may be given even in the presence of gastrointestinal bleeding if the risk of intestinal necrosis is greater than the risk of gastrointestinal bleeding.
Other supportive treatments include gastric suctioning, fluid resuscitation, and fasting. Oral anticoagulants may be given after it is clear that there is no further ischemia in the intestinal tract. Although esophageal varices and bleeding may occur, the benefits of long-term anticoagulation outweigh the risk of bleeding. In patients without new thrombosis, anticoagulation should be maintained for 6 months to 1 year.
Direct thrombolysis by catheter placement into the portal vein with urokinase or tissue fibrinolytic enzyme activator has only been reported in a few trials. The high risk of bleeding, the late presentation of the patient, and the low success rate of thrombolytic therapy have limited the success of this approach to a few cases. If the thrombus is located in a larger vessel, the prognosis is poor, and the expected benefit of performing direct thrombolysis outweighs the risk of bleeding, direct thrombolysis with cannulation may be considered.
What is omentitis?
Omentitis is overwhelmingly caused by various inflammatory conditions in the abdominal cavity. Commonly, tuberculous peritonitis, acute appendicitis, acute cholecystitis, acute pelvic inflammatory disease, diverticulitis, and peritonitis of various natures can cause inflammation of the greater omentum, and in severe cases, adhesions can form later. This acute inflammation usually subsides gradually as the primary lesion is healed. In addition to this, there is also nonspecific necrotizing lipofuscinosis of unknown origin, also known as nonspecific lipofuscinosis.
The greater omentum is a two-layer peritoneum that continues from the greater curvature of the stomach and drapes downward to cover the small intestine and colon, refracting near the upper edge of the pelvis with four mesothelial layers over the transverse colon, but gradually disappearing as the central two mesothelial layers fuse together during development. The size and fat content of the greater omentum are highly variable, its blood circulation is rich, and the cells in the omentum have a strong ability to absorb and resist infection. It has a rapid repair capacity through cell proliferation, fibrous tissue formation and adhesions. The foveal tissue of the omentum is rich in macrophages, and if injected into the peritoneal cavity bacteria or carbon particles can be quickly removed by the omentum and subsequently seen within the phagocytes of the omental mesothelium. The omentum can adhere to sites of inflammation and perforation, and abdominal foreign bodies such as bullets or gauze pellets are often completely encapsulated by the greater omentum. However, the greater omentum is not always beneficial. Due to its physiological and anatomical characteristics, it can also cause a number of diseases, but more rarely, torsion, cysts, infarcts and occasionally tumors. Inflammation is most often a wave of inflammation of the surrounding organs and rarely occurs alone.
What are the manifestations of omentitis? How is it treated?
The manifestations of the various inflammatory diseases that cause omentitis are often significant and distinctive. The main symptom of omentitis is abdominal pain, mostly chronic, persistent or paroxysmal abdominal discomfort, which may be accompanied by abdominal distention, loss of appetite, and other symptoms of digestive disorders. The abdominal pain is mostly in the right side of the abdomen, and adhesions may cause spasmodic abdominal pain, abdominal distension and nausea and other manifestations of incomplete obstruction, and there may also be intra-abdominal pulling sensation. There may be localized pressure pain or palpation of a mass with pressure pain and unclear borders.
The diagnosis is difficult, as the milder cases are mostly masked by the primary lesion. Those with previous history of peritonitis and existing obstructive manifestations such as abdominal distension, abdominal pain, nausea, vomiting and abdominal masses should think of omentitis. Adjunctive radiography may be normal, but may also show intestinal adhesions.
Those with mild symptoms should eat less fibrous food and avoid overeating to relieve symptoms. If there are obstructive symptoms and medical treatment is not effective, surgical treatment should be taken.