Definition
“Intestinal stroke”, also known as intestinal vascular accident, is caused by blood vessel disorders in the intestine, resulting in acute and chronic ischemic damage to the corresponding intestinal tract, which may lead to bruising, edema or ulceration of the intestinal wall. In severe cases, it can lead to intestinal perforation, intestinal necrosis, secondary peritonitis and infectious shock. The incidence of this disease is increasing in the middle-aged and elderly population in recent years, and it is worth to be alert and pay more attention if it is combined with cardiovascular disease and diabetes.
Typology
Currently, the disease is classified into arterial ischemic stroke and venous stasis stroke according to the cause of the disease.
Etiology and clinical manifestations
Arterial intestinal stroke mainly occurs due to embolism of the superior mesenteric artery, which is easy to enter because of the large diameter of the main trunk of the mesenteric artery and the inclined angle with the abdominal aorta, and the embolus usually comes from the wall thrombus of the heart. In addition, emboli can also come from atherosclerotic plaques and occasionally bacterial emboli. Therefore, these diseases are more frequent in the elderly, especially with a history of rheumatic heart disease, atrial fibrillation, endocarditis, myocardial infarction, atherosclerosis, valvular disease and valve replacement.
In contrast, venous intestinal strokes mostly occur in the superior mesenteric vein and are most commonly caused by hypercoagulable states resulting from inherited or acquired diseases such as myeloproliferative disorders, tumors, abdominal inflammation, post-surgery, liver cirrhosis and portal hypertension. Those using oral contraceptives account for 9% to 18% of young women with superior mesenteric vein embolism.
Regardless of the cause of intestinal stroke, the clinical manifestations are similar, and although most signs and symptoms are not specific, they still have characteristics that are of some value for diagnosis.
There are mostly prodromal symptoms such as abdominal pain, abdominal discomfort, and change in bowel pattern (diarrhea or constipation). Patients at this stage have atypical symptoms and no clear signs on physical examination, only indeterminate deep abdominal pressure pain, and no specific changes in various laboratory tests and ancillary examinations, so it is difficult to diagnose intestinal stroke at this time. As the disease enters the progressive stage, the development of the disease is significantly accelerated, and the patient’s symptoms are suddenly aggravated, the abdominal pain is severe and persistent, but the localization is not exact. General pain medications are ineffective, and strong analgesics such as prednisolone or dulcolax are often required for temporary relief, which may be accompanied by abdominal distension, nausea and vomiting. In the early stage of progression, the patient’s symptoms are obviously aggravated but the signs are few, and there are no obvious signs of peritoneal irritation such as muscle tension, pressure pain and rebound pain. Subsequently, the ischemia of the intestinal canal gradually worsens, with edema and exudation of the intestinal wall and secondary peritonitis, then the corresponding signs appear. At this stage, abnormalities in blood routine and blood and urine amylase may occur due to ischemia of abdominal organs and secondary infection.
Examination
Laboratory tests show a marked increase in white blood cell count, even up to 20×109/L or more. Metabolic acidosis and elevated serum lactate levels can be used to determine the presence of intestinal necrosis, but are often a sign of advanced disease.
1. Abdominal plain film examination
Specific signs of intestinal ischemia and intestinal obstruction can be demonstrated: finger pressure signs in the intestinal lumen suggest intestinal mucosa ischemia, and intestinal wall emphysema or free gas in the portal vein are characteristic signs of intestinal infarction caused by mesenteric vein thrombosis.
2. Abdominal color Doppler ultrasonography
Mesenteric vein thrombosis can be detected, but CT examination should be used for cases suspected of mesenteric artery and vein thrombosis.
3.CT examination can make the diagnosis in 90% of patients
In cases of superior mesenteric vein thrombosis, CT angiography is the better test, not only to show the mesenteric vessels and determine the extent of the involved intestinal vessels, but also to exclude other diseases that cause abdominal pain. CT can also observe the severity of ischemic necrosis in the small intestine.
4. Selective mesenteric artery angiography
It can show stenosis or occlusion at the exit of the celiac artery and superior mesenteric artery. It may show thrombosis in large veins or delayed visualization of the superior mesenteric veins.
5. MRI examination
It also has a high sensitivity and specificity for diagnosis, but is gradually being replaced by CT angiography due to the long operation time.
6.Other
Patients with mesenteric vein thrombosis can have plasma hemoperitoneum, when diagnostic laparotomy may be useful for diagnosis. Pneumoperitoneal manipulation during laparoscopy may increase intra-abdominal pressure and decrease mesenteric blood flow and should be avoided. Colonoscopy 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 intestinal canal caused during the examination.
Diagnosis
The diagnosis of this disease relies on imaging in addition to symptoms and signs.
Treatment
Arterial intestinal strokes are classified as acute and chronic.
1. Acute superior mesenteric artery occlusion
Treatment includes surgery and thrombolytic and anticoagulant therapy. Surgery can clarify the diagnosis, restore the patency of the superior mesenteric artery, and determine the viability of the small intestine. Early surgery can prevent and reduce small intestine necrosis. Thrombolytic and anticoagulant therapy is not only applied to elderly patients in critical condition, but also applied to the perioperative process to promote the dissolution of small thrombus and prevent the extension of thrombus, which can help the recovery of ischemic intestine.
(1) Non-surgical treatment actively treats the primary disease and observes the presence of intestinal necrosis.
(2) Anticoagulation and thrombolytic therapy: At present, commonly used thrombolytic agents include urokinase, streptokinase, t-PA, etc. Among them, t-PA can specifically bind to thrombus and dissolve fibrin into monomer, with good thrombolytic effect and low incidence of bleeding complications. Commonly used anticoagulants include heparin and low-molecular heparin. The routes of thrombolysis and anticoagulant use are systemic intravenous administration and direct catheter administration. The clinical efficacy of catheter administration via superior mesenteric artery is significantly higher than that of peripheral venous administration. In addition to thrombolytic and anticoagulant agents, the application of vasodilators is also important. The commonly used vasodilator drugs include poppersine, which can dilate the blood vessels, improve blood circulation, lateralize the formation of collateral vessels and help the recovery of the ischemic intestine before and after transseptal artery catheterization. Different modalities such as mechanical embolization, balloon dilation and stent implantation can be performed in combination to resolve the stenosis or occlusion of blood vessels.
(3) Surgical treatment ① embolism is located in one branch, involving local intestinal necrosis, intestinal resection and small bowel anastomosis are performed. If the embolism is located in the main trunk of superior mesenteric artery and all small intestine and right hemicolectomy are necrotic, then total small intestine and right hemicolectomy will be performed, and postoperative parenteral nutrition support will be provided. If the embolism is located in the main trunk of the superior mesenteric artery and the intestinal canal is not necrotic, the embolism will be removed by veinotomy or balloon retrieval. ④If there is no blood or less blood outflow from the superior superior mesenteric artery after embolization, then an autologous saphenous vein or artificial vessel should be performed to bypass and anastomose between the abdominal aorta or common skeletal artery and superior mesenteric artery. When intraoperative intestinal vascularity cannot be determined, the method of small intestinal stoma and secondary dissection can avoid resection of unnecessary resections and prevent the occurrence of short bowel syndrome; at the same time, it effectively prevents anastomotic fistula and stenosis of the anastomosis.
2. Chronic mesenteric vascular occlusion
(1) Non-surgical therapy with small amount and many meals, oral vitamin C, E and vasodilator drugs, and static dextran.
(2) Minimally invasive interventional therapy After action arteriography, intra-arterial stent implantation is feasible to improve vascular occlusion.
(3) Surgical therapy ①Thrombus endothelial debridement. (2) Autologous vein bypass surgery across the stenotic segment. (③Superior mesenteric artery stenosis segment is removed, and then this artery is reimplanted into the aorta. (iv) Stenosis of the abdominal artery and autologous vein bypass surgery between the abdominal aorta and the splenic artery; or end-to-end anastomosis of the splenic artery and the abdominal aorta. ⑤ stenosis at the outlet of the superior mesenteric artery, autologous vein bypass surgery between the middle colonic artery below the opening and the abdominal aorta below the level of the renal artery.
Venous intestinal stroke
1. Surgical treatment
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 superior mesenteric vein thrombosis require surgical exploration; currently, for patients who have not yet developed peritonitis, placement of a thrombolytic tube under minimally invasive conditions is preferred. Thrombolytic drugs include streptokinase, urokinase, and rt-PA, and treatment options include thrombolysis via SMA cannulation, percutaneous hepatic puncture portal vein cannulation, and TIPS route thrombolysis. Intraluminal catheter aspiration, embolization, balloon dilation and stent implantation can be performed. Transcatheter aspiration, thrombus mashing and local thrombolysis are safe and effective methods for the treatment of symptomatic PV-SMV thrombosis. The efficacy is better for patients with early disease and without definite peritonitis.
However, urgent surgery is required for patients with definite signs of peritonitis, transmural bowel necrosis, and abdominal puncture showing bloody fluid. Intraoperatively, if the diagnosis of mesenteric vein thrombosis is established, anticoagulation should be initiated. Due to the lack of a clear boundary between the ischemic and normal intestinal vessels, the emphasis on obtaining normal intestinal segments for bowel resection may result in the removal of too many viable intestinal vessels, leading to short bowel syndrome. Therefore, we should be more cautious in performing intestinal resection for this disease, with the principle of preserving the viable intestinal canal as much as possible.
To avoid removing too much potentially viable bowel, a damage control surgical philosophy is best: emergency removal of the necrotic bowel, no attempt to restore bowel continuity, open abdominal cavity, and planned reoperative exploration. Stage 1: rapid resection of necrotic small bowel, parallel intraoperative bolus removal, preservation of suspiciously viable bowel, stoma at both ends of the bowel using the stoma as a window to observe the viability of the bowel can save some patients with poor conditions from secondary exploration and laparotomy if necessary. Stage 2: ICU resuscitation, observation of intestinal tube viability, and continuation of anticoagulation therapy to prevent recurrence of thrombosis. Observe intestinal blood supply through stoma and open abdominal cavity, and actively intestinal rehabilitation treatment. Stage 3: Definitive restoration of intestinal continuity and intestinal stoma reduction with intestinal anastomosis.
2. Drug treatment
If there is no intestinal necrosis, mesenteric vein thrombosis can be treated with medication instead of 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 administration of heparin anticoagulation 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 by giving heparin 5000 U intravenously, followed by a continuous infusion to maintain the activated partial thromboplastin time at more than twice the 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.
3. Other treatments
Other supportive treatments include gastrointestinal decompression, fluid resuscitation, and fasting. Oral anticoagulants may be given after it is clear that there is no further ischemia in the intestinal canal. Although esophageal varices and bleeding may occur, the benefits of long-term anticoagulation therapy still outweigh the risk of bleeding. In patients without new thrombosis, anticoagulation should be maintained for a period of 6 months to 1 year.