https://aasldpubs.onlinelibrary.wiley.com/doi/epdf/10.1053/jhep.2000.16597

Recent portal or mesenteric venous thrombosis: increased recognition and frequent recanalization on anticoagulant therapy.

In preparing this Position Statement, all relevant scientific literature was identified and reviewed critically by acknowledged experts using agreed criteria. Well-conducted clinical and experimental studies were given precedence over anecdotal case reports and abstracts were not usually considered. A draft Position Statement was then produced and subjected to detailed peer review by an international group of clinical toxicologists chosen by the American Academy of Clinical Toxicology and the European Association of Poisons Centres and Clinical Toxicologists. The Position Statement went through multiple drafts before being approved by the boards of the two societies and being endorsed by other societies. The Position Statement includes a summary statement for ease of use and is supported by detailed documentation which describes the scientific evidence on which the Statement is based. Gastric lavage should not be employed routinely in the management of poisoned patients. In experimental studies, the amount of marker removed by gastric lavage was highly variable and diminished with time. There is no certain evidence that its use improves clinical outcome and it may cause significant morbidity. Gastric lavage should not be considered unless a patient has ingested a potentially life-threatening amount of a poison and the procedure can be undertaken within 60 minutes of ingestion. Even then, clinical benefit has not been confirmed in controlled studies. Unless a patient is intubated, gastric lavage is contraindicated if airway protective reflexes are lost. It is also contraindicated if a hydrocarbon with high aspiration potential or corrosive substance has been ingested.

Position statement: gastric lavage. American Academy of Clinical Toxicology; European Association of Poisons Centres and Clinical Toxicologists.

Context. The first update of the 1997 gastric lavage position paper was published by the American Academy of Clinical Toxicology and the European Association of Poisons Centres and Clinical Toxicol...

/pdf/position-paper-update-gastric-lavage-for-gastrointestinal-202eiwa0a8.pdf

Position paper update: gastric lavage for gastrointestinal decontamination

Mesenteric venous thrombosis.

Ischemia has been traditionally defined as an insufficiency of oxygen delivery by the blood. Lately it has become clear that such a view is too restrictive. Hypoperfusion may be caused by both anatomic and functional impediments to either inflow to or outflow from an organ. Furthermore, the pathophysiologic consequences are likely to involve not only cellular hypoxia, but also a restricted supply of nutrients and other important molecules, and an abnormal elimination of physiologic wastes such as carbon dioxide. Acute mesenteric ischemia (AMI) is, therefore, a severe anatomic or functional limitation of the splanchnic circulation, resulting in a dual defect of intestinal hypoxia and cellular hypercarbia. It is a complex syndrome that includes three related processes: occlusive mesenteric ischemia, nonocclusive ischemia, and sepsis-induced splanchnic ischemia. Acute occlusive mesenteric ischemia is caused by a local impairment of splanchnic blood flow. Arterial occlusion is usually caused by embolism rather than thrombosis. Mesenteric vein thrombosis is responsible for 20% of acute occlusive mesenteric ischemia. This condition is termed primary when no predisposing factors can be identified. Secondary mesenteric vein thrombosis may occur in portal hypertension, intraabdominal infection, and carcinomatosis (particularly gastrointestinal and pancreatic). Nonocclusive mesenteric ischemia is caused by the nonobstructive reduction in oxygen delivery below the critical level where oxygen consumption becomes supply dependent and tissues resort to anaerobic metabolism. Nonocclusive mesenteric ischemia has been observed in shock syndromes, low-flow states, drug-induced vasoconstriction, hypotension complicating vasodilator therapy, and other conditions. Preexisting vascular disease such as diabetes with small vessel disease or arteriosclerosis will predispose to nonocclusive ischemia. Visceral hypoxia is characterized by a reduction in synthesis and an acceleration of the catabolism of adenosine triphosphate. Ischemia finally occurs because either oxygen consumption is reduced or oxygen demand is excessive, or a combination of both. Depressed mesenteric oxygen consumption generally develops because of diminished oxygen delivery. It may also be the consequence of severely reduced cellular oxygen uptake, or an abnormal oxygen utilization apparatus. Excessive acid is produced and buffered, thereby generating CO2 anaerobically. The increase in CO2 production, coupled with a reduction in CO2 removal due to a reduced or absent blood flow, forms the basis for cellular, tissue, and venous hypercarbia. Splanchnic flow is sensitive to numerous factors including the autonomic nervous system, hormones, endogenous mediators, and various drugs. Reperfusion injury is the secondary damage that occurs to ischemic tissues after the reestablishment of blood flow. It is characterized by intense vasospasm and ischemic injury of the intestinal mucosa. This may be due to oxygen-derived free-radical-mediated cellular damage. This secondary nonocclusive transformation of an occlusive ischemia provides a rationale for vasodilatory therapy of occlusive splanchnic ischemia. Sepsis is intricately associated with mesenteric ischemia. The evolution of primary AMI is almost always complicated by sepsis due to enteric organisms. Sepsis-induced gastrointestinal tract dysfunction appears due to visceral ischemia, probably caused by uncontrolled inflammation. When sepsis occurs in AMI, it usually marks the point at which the local disease process acquires a multisystemic dimension, heralding the syndrome of multisystem organ failure with its dismal prognosis. The difficulty of an early diagnosis is probably the most important cause of the high mortality, which varies from 60% to 90%. The diagnosis is particularly difficult in the elderly because of the lack of specificity and the paucity of symptoms. The diagnosis of AMI must be made on the basis of a high index of suspicion. Clinical clues include nausea, vomiting, and diffuse abdominal pain that is out of proportion to symptoms. The difficult diagnosis is compounded by the paucity of revealing laboratory data, which are often nonspecific and consist of a moderate leukocytosis, hyperamylasemia, and lactic acidosis. Rarely, a plain film of the abdomen may suggest the diagnosis. Angiography may demonstrate vasospasm, arterial occlusion, and venous obstruction. Other diagnostic modalities under investigation include mucosal tonometry, ultrasonic duplex scanning, flexible endoscopy, laparoscopy, surface oximetry, infrared photoplethysmography, and 31P magnetic resonance spectroscopy. Most cases of AMI are diagnosed long after the episode has started. The treatment of mesenteric ischemia has two major goals: the prevention of mesenteric infarction and the forestallment of sepsis and sepsis-induced multisystem organ failure. Management of established AMI involves treating the local intestinal injury as well as the systemic consequences, including sepsis. There are three types of care: resuscitative, operative, and nonoperative.

Acute mesenteric ischemia: pathophysiology, diagnosis, and treatment.

We report a case of isolated superior mesenteric vein thrombosis with acute ischemic bowel disease, diagnosed early by a screening ultrasound scan of the upper abdomen and definitively assessed by computed tomography and angiography. This report stresses the contribution of cross-sectional techniques in the early diagnosis and management of venous occlusive disease of the small bowel.

Mesenteric vein thrombosis: early CT and US diagnosis and conservative management.

https://www.annemergmed.com/article/S0196-0644(84)80594-6/pdf

Esophageal perforation: An unusual complication of gastric lavage

A number of techniques of surgical endoscopy have been used in the management of a post-traumatic biliary fistula. The endoscopic sphincterotomy with placement of a perfused nasobiliary catheter, followed by the insertion of a biliary stent allowed the fistula to dry out. A secondary stricture of the left hepatic duct was treated by endoscopic internal drainage after the insertion of a transhepatic guidewire by an epigastric route. This kind of combined transhepatic and endoscopic procedure is useful in some difficult cases.

Endoscopic management of a post-traumatic biliary fistula.

The value of colonoscopy in the diagnosis and management of severe hematochezia

On 1 250 patients admitted to our hospital for gastrointestinal hemorrhage from 1979 to 1987, 4% (50) had severe hematochezia with a bleeding point distal to the ligament of Treitz. Fourty-four patients needed a transfusion of the least 2 red cell units and 6 patients had hypovolemia and anemia. All the patients underwent colonoscopy with a total of 68 examinations. Precise diagnosis of the bleeding lesion by colonoscopy was made in 41 (82%). Bleeding diverticula and ulcers were the most frequent lesions. Seventeen patients were examined by angiography, which was diagnostic in 6 patients. Fourteen patients were treated endoscopically by electro coagulation. One perforation occurred and two patients had persistent bleeding. Nine patients were managed surgically; two complications occurred. No rebleeding occurred in any patient. We conclude that colonoscopy is a safe method of diagnosing the source of lower intestinal hemorrhage. Moreover, half of the 50 patients ceased to bleed spontaneously with a supportive medical therapy.

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Mesenteric vein thrombosis: early CT and US diagnosis and conservative management.

Esophageal perforation: An unusual complication of gastric lavage

Endoscopic management of a post-traumatic biliary fistula.

The value of colonoscopy in the diagnosis and management of severe hematochezia

The value of colonoscopy in the diagnosis and management of severe hematochezia