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Immediate treatment is the most important factor in a favorable prognosis. A delay in treatment greater than six hours or the presence of peritonitis, sepsis, hypotension, or disseminated intravascular coagulation are negative prognostic indicators.
Historically, GDV has held a guarded prognosis. Although "early studies showed mortality rates between 33% and 68% for dogs with GDV," studies from 2007 to 2012 "reported mortality rates between 10% and 26.8%". Mortality rates approach 10% to 40% even with treatment. A study determined that with prompt treatment and good preoperative stabilization of the patient, mortality is significantly lessened to 10% overall (in a referral setting). Negative prognostic indicators following surgical intervention include postoperative cardiac arrhythmia, splenectomy, or splenectomy with partial gastric resection. Interestingly, a longer time from presentation to surgery was associated with a lower mortality, presumably because these dogs had received more complete preoperative fluid resuscitation and were thus better cardiovascularly stabilized prior to the procedure.
As a general rule, GDV is of greatest risk to deep-chested dogs. The five breeds at greatest risk are Great Danes, Weimaraners, St. Bernards, Gordon Setters, and Irish Setters. In fact, the lifetime risk for a Great Dane to develop GDV has been estimated to be close to 37 percent. Standard Poodles are also at risk for this health problem, as are Irish Wolfhound, Doberman Pinschers, Rottweilers, German Shorthaired Pointer, German Shepherds, Rhodesian Ridgebacks. Basset Hounds and Dachshunds have the greatest risk for dogs less than .
The prognosis for non-ischemic cases of SBO is good with mortality rates of 3–5%, while prognosis for SBO with ischemia is fair with mortality rates as high as 30%.
Cases of SBO related to cancer are more complicated and require additional intervention to address the malignancy, recurrence, and metastasis, and thus are associated with poorer prognosis.
All cases of abdominal surgical intervention are associated with increased risk of future small-bowel obstructions. Statistics from U.S. healthcare report 18.1% re-admittance rate within 30 days for patients who undergo SBO surgery. More than 90% of patients also form adhesions after major abdominal surgery.
Common consequences of these adhesions include small-bowel obstruction, chronic abdominal pain, pelvic pain, and infertility.
Colitis is inflammation of the colon. Acute cases are medical emergencies as the horse rapidly loses fluid, protein, and electrolytes into the gut, leading to severe dehydration which can result in hypovolemic shock and death. Horses generally present with signs of colic before developing profuse, watery, fetid diarrhea.
Both infectious and non-infectious causes for colitis exist. In the adult horse, "Salmonella", "Clostridium difficile", and "Neorickettsia risticii" (the causative agent of Potomac Horse Fever) are common causes of colitis. Antibiotics, which may lead to an altered and unhealthy microbiota, sand, grain overload, and toxins such as arsenic and cantharidin can also lead to colitis. Unfortunately, only 20–30% of acute colitis cases are able to be definitively diagnosed. NSAIDs can cause slower-onset of colitis, usually in the right dorsal colon (see Right dorsal colitis).
Treatment involves administration of large volumes of intravenous fluids, which can become very costly. Antibiotics are often given if deemed appropriate based on the presumed underlying cause and the horse's CBC results. Therapy to help prevent endotoxemia and improve blood protein levels (plasma or synthetic colloid administration) may also be used if budgetary constraints allow. Other therapies include probiotics and anti-inflammatory medication. Horses that are not eating well may also require parenteral nutrition. Horses usually require 3–6 days of treatment before clinical signs improve.
Due to the risk of endotoxemia, laminitis is a potential complication for horses suffering from colitis, and may become the primary cause for euthanasia. Horses are also at increased risk of thrombophlebitis.
Laparotomy for other forms of volvulus, especially anal volvulus.
Specific causes of colic are best managed with certain drugs. These include:
- Spasmolytic agents, most commonly Buscopan, especially in the case of gas colic.
- Pro-motility agents: metoclopramide, lidocaine, bethanechol, and erythromycin are used in cases of ileus.
- Anti-inflammatories are often used in the case of enteritis or colitis.
- Anti-microbials may be administered if an infectious agent is suspected to be the underlying cause of colic.
- Phenylephrine: used in cases of nephrosplenic entrapment to contract the spleen, and is followed by light exercise to try to shift the displaced colon back into its normal position.
- Psyllium may be given via nasogastric tube to treat sand colic.
- Anthelminthics for parasitic causes of colic.
Fetal and neonatal bowel obstructions are often caused by an intestinal atresia, where there is a narrowing or absence of a part of the intestine. These atresias are often discovered before birth via an ultrasound, and treated with using laparotomy after birth. If the area affected is small, then the surgeon may be able to remove the damaged portion and join the intestine back together. In instances where the narrowing is longer, or the area is damaged and cannot be used for a period of time, a temporary stoma may be placed.
Gastric volvulus of unknown cause comprises two thirds of cases and is presumably due to abnormal laxity of the gastrosplenic, gastroduodenal, gastrophrenic, and gastrohepatic ligaments. Type 1 gastric volvulus is more common in adults but has been reported in children.
In a cecal volvulus, the cecum may be returned to a normal position and sutured in place, a procedure known as cecopexy. If identified early, before presumed intestinal wall ischemia has resulted in tissue breakdown and necrosis, the cecal volvulus can be detorsed laparoscopically.
The combined type of gastric volvulus is a rare form in which the stomach twists mesentericoaxially and organoaxially. This type of gastric volvulus makes up the remainder of cases and is usually observed in patients with chronic volvulus.
With early intervention, morbidity and mortality of cases of intestinal obstruction is low. The outcome is in part dependent upon congenital comorbidities and delays in diagnosis and management.
The causes are divided into benign or malignant.
- Benign
- Peptic ulcer disease
- Infections, such as tuberculosis; and infiltrative diseases, such as amyloidosis.
- A rare cause of gastric outlet obstruction is blockage with a gallstone, also termed "Bouveret's syndrome".
- In children congenital pyloric stenosis / congenital hypertrophic pyloric stenosis may be a cause.
- A pancreatic pseudocyst can cause gastric compression.
- Pyloric mucosal diaphragm could be a rare cause.
- Malignant
- Tumours of the stomach, including adenocarcinoma (and its linitis plastica variant), lymphoma, and gastrointestinal stromal tumours
In a peptic ulcer it is believed to be a result of edema and scarring of the ulcer, followed by healing and fibrosis, which leads to obstruction of the gastroduodenal junction (usually an ulcer in the first part of the duodenum).
Horses may develop pharyngitis, laryngitis, or esophagitis secondary to indwelling nasogastric tube. Other complications include thrombophlebitis, laminitis (which subsequently reduces survival rate), and weight loss. Horses are also at increased risk of hepatic injury.
Survival rates for DPJ are 25–94%. Horses that survive the incident rarely have reoccurrence.
Meckel's diverticulum occurs in about 2% of the population. Prevalence in males is 3–5 times higher than in females. Only 2% of cases are symptomatic, which usually presents among children at the age of 2.
Most cases of Meckel's diverticulum are diagnosed when complications manifest or incidentally in unrelated conditions such as laparotomy, laparoscopy or contrast study of the small intestine. Classic presentation in adults includes intestinal obstruction and inflammation of the diverticulum (diverticulitis). Painless rectal bleeding most commonly occurs in toddlers.
Inflammation in the ileal diverticulum has symptoms that mimic appendicitis, therefore its diagnosis is of clinical importance. Detailed knowledge of the pathophysiological properties is essential in dealing with the life-threatening complications of Meckel's diverticulum.
The lifetime risk for a person with Meckel's diverticulum to develop certain complications is about 4–6%. Gastrointestinal bleeding, peritonitis or intestinal obstruction may occur in 15–30% of symptomatic patients (Table 1). Only 6.4% of all complications requires surgical treatment; and untreated Meckel's diverticulum has a mortality rate of 2.5–15%.
Table 1 – Complications of Meckel's Diverticulum:
The exact causes are not known. It is not associated with a particular gene, but there is some evidence of recurrence in families.
Gastrointestinal perforation, also known as ruptured bowel, is a hole in the wall of part of the gastrointestinal tract. The gastrointestinal tract includes the esophagus, stomach, small intestine, and large intestine. Symptoms include severe abdominal pain and tenderness. When the hole is in the stomach or early part of the small intestine the onset of pain is typically sudden while with a hole in the large intestine onset may be more gradual. The pain is usually constant in nature. Sepsis, with an increased heart rate, increased breathing rate, fever, and confusion may occur.
The cause can include trauma such as from a knife wound, eating a sharp object, or a medical procedure such as colonoscopy, bowel obstruction such as from a volvulus, colon cancer, or diverticulitis, stomach ulcers, ischemic bowel, and a number of infections including "C. difficile". A hole allows intestinal contents to enter the abdominal cavity. The entry of bacteria results in a condition known as peritonitis or in the formation of an abscess. A hole in the stomach can also lead to a chemical peritonitis due to gastric acid. A CT scan is typically the preferred method of diagnosis; however, free air from a perforation can often be seen on plain X-ray.
Perforation anywhere along the gastrointestinal tract typically requires emergency surgery in the form of an exploratory laparotomy. This is usually carried out along with intravenous fluids and antibiotics. A number of different antibiotics may be used such as piperacillin/tazobactam or the combination of ciprofloxacin and metronidazole. Occasionally the hole can be sewn closed while other times a bowel resection is required. Even with maximum treatment the risk of death can be as high as 50%. A hole from a stomach ulcer occurs in about 1 per 10,000 people per year, while one from diverticulitis occurs in about 0.4 per 10,000 people per year.
Smoking has been linked to a variety of disorders of the stomach. Tobacco is known to stimulate acid production and impairs production of the protective mucus. This leads to development of ulcers in the majority of smokers.
Chronic stomach problems have also been linked to excess intake of alcohol. It has been shown that alcohol intake can cause stomach ulcer, gastritis and even stomach cancer. Thus, avoidance of smoking and excess alcohol consumption can help prevent the majority of chronic stomach disorders.
One of the most causes of chronic stomach problems is use of medications. Use of aspirin and other non-steroidal anti-inflammatory drugs to treat various pain disorders can damage lining of the stomach and cause ulcers. Other medications like narcotics can interfere with stomach emptying and cause bloating, nausea, or vomiting.
The majority of chronic stomach problems are treated medically. However, there is evidence that a change in life style may help. Even though there is no specific food responsible for causing chronic stomach problems, experts recommend eating a healthy diet which consists of fruits and vegetables. Lean meat should be limited. Moreover, people should keep a diary of foods that cause problems and avoid them.
This can lead to a number of disease manifestations such as:
- Acute midgut volvulus
- Chronic midgut volvulus
- Acute duodenal obstruction
- Chronic duodenal obstruction
- Internal herniation
- Superior mesenteric artery syndrome
Underlying causes include gastric ulcers, duodenal ulcers, appendicitis, gastrointestinal cancer, diverticulitis, inflammatory bowel disease, superior mesenteric artery syndrome, trauma and ascariasis. Typhoid fever, non-steroidal anti-inflammatory drugs, ingestion of corrosives may also be responsible.
Incidence of hiatal hernias increases with age; approximately 60% of individuals aged 50 or older have a hiatal hernia. Of these, 9% are symptomatic, depending on the competence of the lower esophageal sphincter (LES). 95% of these are "sliding" hiatus hernias, in which the LES protrudes above the diaphragm along with the stomach, and only 5% are the "rolling" type (paraesophageal), in which the LES remains stationary, but the stomach protrudes above the diaphragm.
Hiatus hernia are most common in North America and Western Europe and rare in rural African communities. Some have proposed that insufficient dietary fiber and the use of a high sitting position for defecation may increase the risk.
Cancers of the stomach are rare and the incidence has been declining worldwide. Stomach cancers usually occur due to fluctuations in acidity level and may present with vague symptoms of abdominal fullness, weight loss and pain. The actual cause of stomach cancer is not known but has been linked to infection with "Helicobacter pylori", pernicious anemia, Menetriere's disease, and nitrogenous preservatives in food.
Dietary factors such as spice consumption, were hypothesized to cause ulcers until late in the 20th century, but have been shown to be of relatively minor importance. Caffeine and coffee, also commonly thought to cause or exacerbate ulcers, appear to have little effect. Similarly, while studies have found that alcohol consumption increases risk when associated with "H. pylori" infection, it does not seem to independently increase risk. Even when coupled with "H. pylori" infection, the increase is modest in comparison to the primary risk factor.
The diagnosis is suspected based on polyhydramnios in uteru, bilious vomiting, failure to pass meconium in the first day of life, and abdominal distension. The presentations of NBO may vary. It may be subtle and easily overlooked on physical examination or can involve massive abdominal distension, respiratory distress and cardiovascular collapse. Unlike older children, neonates with unrecognized intestinal obstruction deteriorate rapidly.