CHAPTER 15 Jennifer Klaus Blue Pearl Veterinary Partners, Phoenix, Arizona The gastrointestinal (GI) tract is a series of hollow organs, responsible for the assimilation, digestion, and absorption of ingested nutrients and expulsion of waste material. The components of the GI tract are the mouth, pharynx, esophagus, stomach, small intestines, cecum, large intestines, and anus. Effective GI motility and an intact functioning GI mucosal barrier are essential for normal digestive activity and protection from luminal pathogens. The GI tract and liver are considered the “shock organs” of dogs [1] and suffer major changes in their motility, ultrastructure, and function during low blood flow and hypoxemic conditions [2]. The splanchnic circulation supplies the GI tract and is particularly vulnerable to hypoxia. A reservoir of pathogens is present in the GI lumen, ready to translocate to the systemic circulation should local immunological and other defensive mechanisms fail [2]. The presence of cytokines may cause the loss of epithelial tight junction barrier function. Tumor necrosis factor has been shown to have a central role in diseases associated with intestinal barrier dysfunction, such as inflammatory bowel disease or intestinal ischemia [3]. Dogs subjected to severe GI hypoxia for one hour prior to fluid resuscitation developed gut barrier failure and bacterial translocation. Gastrointestinal bacteria and endotoxin were found in the portal and systemic circulation of these dogs and resulted in sepsis and multiple organ dysfunction syndrome (MODS) [4]. Clinical signs of GI dysfunction can run the spectrum from mild changes in appetite to severe changes with sloughing intestinal mucosa. Life‐threatening complications such as third body fluid spacing, loss of proteins, fluids and electrolytes, enteric bacterial translocation, sepsis, and eventually death can be a consequence of significant GI dysfunction [2]. The GI tract can complicate any disease process and impact recovery in any ICU patient. A careful assessment of diagnostic and monitoring data can assist in early recognition of potential GI tract contributions to disease. Treatment for shock and GI hypoxia should always be aggressive, replacing lost fluids and electrolytes and providing nutrition early to aid intestinal barrier cells during their healing process. The initial history and physical examination provide a baseline of information for finding the cause of GI clinical signs and for monitoring for trends of change in the patient. Point of care (POC) testing provides important data to guide the therapy at the cage side. Many of the consequences of GI disorders are diagnosed and the response to treatment monitored with the results of the minimum database. However, making a definitive diagnosis of the GI component of the disease can require more advanced testing, to include clinicopathological testing, radiographs, contrast studies, ultrasound, or computed tomography (CT). Treatment with intravenous fluids, oxygen, analgesics, electrolyte replacement, and possibly broad‐spectrum antibiotics should not be withheld in critical patients as diagnostic testing is pursued. The signalment (age, sex, breed) is important since certain dog breeds can have a predisposition to GI disorders such as gastric dilation volvulus syndrome (GDV), mesenteric volvulus, and pancreatitis. While vomiting and diarrhea are the more common presenting complaints, it is important to ask about ptyalism, prehension of food, decreased ability or discomfort with opening the mouth or swallowing, facial asymmetry, and interest in food or appetite. Pharyngeal dysphagia is suspected when there is impaired initiation of the involuntary passage of food through the oropharynx. Clients might report that the pet is gagging or coughing during or after swallowing. The actual mechanics of vomiting as well as the described color and contents of the vomitus can assist in localizing the problem within the GI tract (Figure 15.1, Table 15.1). It is important to differentiate between vomiting and regurgitation from the history [5]. Regurgitation is the passive expulsion of food or fluid from the stomach or esophagus without abdominal contractions. Most commonly, it occurs immediately after eating but can occur several hours later. The regurgitated material often includes a clear or frothy white liquid (saliva) with or without undigested or partially digested food. Regurgitation directs diagnostic efforts to problems of the esophagus or significant gastric motility disorders (passive vomiting) (see Table 15.1). Figure 15.1 Algorithm for the general approach to a patient with vomiting. The four main mechanisms for stimulating the vomiting center with their receptor types are in light blue boxes. Some of the primary causes of stimulation of the receptors are listed surrounding each box. The final pathway for the stimulation of vomiting is through the vomiting or emetic center located in the brainstem. The character and color of the vomitus can provide an initial impression of the location within the gastrointestinal tract that is primarily affected. While many potential causes for vomiting are possible, those listed should be considered and ruled out when there is potential for life‐threatening complications. General treatment guidelines are listed in the orange box, with common complications to be anticipated listed in the pink box. 5HT3, serotonergic receptor; α2, adrenergic receptor; A‐B, acid–base; D2, dopaminergic receptor; GI, gastrointestinal; H1, histaminergic receptor; M1, cholinergic receptor; NK1, neurokinin receptor; R/O, rule out. Table 15.1 Common changes in force or timing of vomiting and potential pathology. Vomiting is a centrally coordinated oral expulsion of gastric or upper duodenal contents. There are prodromal signs including lip smacking and ptyalism as well as coordinated contraction of the upper GI organs. The abdominal wall muscles are observed to forcefully contract. Bilious (yellow‐green) material in the vomitus originates from the duodenum and helps to differentiate vomiting from regurgitation when the physical action has not been observed. Nonproductive vomiting can be an early sign of GDV and warrants immediate therapeutic and diagnostic investigation. The presence of diarrhea directs diagnostic efforts toward the small and large intestines. The reported character and consistency of the diarrhea can help differentiate between these two anatomical locations (Table 15.2). Small bowel disease typically has more significant clinical consequences, with substantial fluid, electrolyte and protein loss, than does large bowel disease. Therefore, where the GI problem is located could influence the intensity of diagnostic, therapeutic, and monitoring efforts. Table 15.2 Typical characteristics of small bowel versus large bowel diarrhea. A report of restlessness, reluctance to lie down or any evidence of pain upon touching the abdominal region can direct diagnostic efforts to rule out potentially life‐threatening problems such as GDV, mesenteric volvulus, septic peritonitis, or necrotizing pancreatitis. Exposure to medications (i.e., antibiotics, anticholinergics) or toxins (i.e., numerous plant toxins, cleaning agents, and chemicals) with GI side effects or medications that have potential GI toxicity (i.e., nonsteroidal‐antiinflammatory medication and steroids) is important historical information. A review of current prescription and over‐the‐counter medications might reveal recent treatment with protein pump inhibitors or gastroprotectants, as well as oral medications that can be seen on radiographs (bisthmus subsalicylate, Pepto‐Bismol®). Feeding habits should be explored, with focus on the degree of appetite and when the pet last ate normally. Information regarding the type and consistency of the food, any prescription diets, a recent change in content, brand or bags/cans, or treats and access to table scraps (human food) or trash can provide important information to guide diagnostics. Rarely, contamination of pet foods occurs in commercial diets, followed by a recall of the food. If the history warrants further investigation, there are internet resources available to alert the clinician to current and common pet food recalls (Table 15.3). Table 15.3 Websites that list major pet food recalls. Physical examination findings attributable to the GI tract typically start with assessment of temperature, pulse, and respiration. Fever combined with GI signs will direct efforts toward treating infectious, inflammatory or septic conditions. Hypothermia can be a consequence of shock, with poor perfusion due to GI fluid loss. Heart and pulse rate, combined with mucous membrane color, pulse intensity and capillary refill time, provide a reflection of peripheral perfusion, often affected by substantial acute fluid and electrolyte loss into the GI tract. Chronic fluid losses can cause dehydration without impacting perfusion, resulting in tacky or dry mucous membranes with mild dehydration and prolonged skin tent or sunken eyes with more severe dehydration. Increased respiratory rate and effort can be a consequence of aspiration of vomitus, pain or acute respiratory distress syndrome secondary to sepsis associated with GI disorders. Direct examination of the GI tract begins with the oral cavity, pharynx, and teeth [5]. Hypersalivation, discharge or malodor from the oral cavity can suggest gingivitis or systemic metabolic disease. Tooth health is evaluated as a source of infection or anorexia. Abnormalities in the integrity of the jaw and bite could reflect traumatic injury or renal secondary hyperparathyroidism, or neuromuscular disorders, such as tetanus or (masseter) muscle myositis. Oral mucous membrane, tongue or gingival discoloration, ulcers or masses are recorded. Evaluation of the sublingual area may reveal ulceration, injury, ranulas or string foreign bodies. The pharynx is then examined externally by palpation or visualized orally following sedation if disease is suspected in this area, such as pharyngeal dysphagia. Abdominal examination should focus on the presence of discomfort, distension, organ abnormalities, and GI sounds. Abnormalities can be detected on abdominal palpation in both dogs and cats, and include cranial organomegaly (liver or spleen enlargement), a distended urinary bladder, masses, intestinal impaction with feces, GI foreign material, increased intestinal thickness, and a gravid uterus. In cats, large or small kidneys and an enlarged spleen may also be differentiated. If the abdomen is generally distended, the clinician should palpate and ballot to differentiate between fat, free abdominal fluid, abdominal muscle weakness or organ enlargement. A positive fluid wave requires a large volume of fluid (40 mL/kg) to be present [6]. Abdominal pain is a significant finding and should be differentiated from spinal pain or generalized pain or anxiety. The pain is then localized as cranial, midabdominal, caudal or generalized abdominal pain. A review of the organs located in that abdominal region can direct diagnostic efforts. This physical finding could indicate severe problems and warrants timely testing, including radiographs, ultrasound, and laboratory analysis, including abdominal fluid analysis [7]. Auscultation of the abdomen should be done at least twice daily for patients with potential GI disorders. Listening with a stethoscope directly under the abdomen is preferred in smaller patients, and a four‐quadrant approach is used when listening to larger dogs. If no GI sounds are heard within two minutes, ileus is present and warrants concern for mechanical or functional obstruction. Increased GI sounds can signify hypermotility. The rectal examination completes the examination of the caudal abdomen. The prostate in males, cervix or caudal uterus in females, urethra and aortic pulse should be palpated ventrally. Anal sacs are examined at the 4 and 8 o’clock positions and should be easily expressed. Sublumbar lymph nodes should be palpated dorsally. Masses, strictures or other pelvic canal abnormalities such as perineal hernias should be identified as well as anal tone noted. The character of the rectal mucosa and pelvic and sacral bone structure are also noted. Fecal character is evaluated to determine if constipation, obstipation or diarrhea is present. Melena and hematochezia can be indicative of significant increases in intestinal permeability or the first sign of a coagulation disorder [1,2]. Point of care testing in the ICU can guide initial stabilization and diagnostic testing. Point of care diagnostics can not only provide invaluable information on the cause of GI disturbance, but may also help determine the severity of disease and direct urgent care. The minimum database will provide the initial POC testing and consists of a packed cell volume (PCV), total protein (TP), blood urea nitrogen (BUN), blood glucose, electrolytes, blood gas, and coagulation profile. Hemoconcentration due to severe dehydration or third body fluid spacing can elevate the PCV and TP. A PCV ≥60% with little to no increase in protein concentration and acute onset of raspberry jam‐like bloody diarrhea should prompt consideration of hemorrhagic gastroenteritis (HGE) in dogs [8]. Blood in the stool or vomitus necessitates assessment of coagulation, to include platelet estimate, prothrombin time, and activated partial thromboplastin time. Severe inflammation of the GI tract can cause albumin loss and lower the TP. Blood glucose can be decreased with sepsis, neonatal malnutrition, hypoadrenocorticism, xylitol toxicity or severe liver dysfunction [7]. Elevations in BUN with concentrated urine suggests dehydration and renal hypoperfusion, digested blood in the GI tract, a high‐protein diet, or postrenal obstruction [9]. Anorexic animals with diarrhea often present with significant electrolyte changes, including sodium (Na+), chloride (Cl‐), potassium (K+), and magnesium (Mg++) loss. Hyperkalemia with hyponatremia should prompt consideration of adrenocortical insufficiency or whipworm (Trichuris vulpis) infection, both of which can present with diarrhea [7]. Hypokalemia is the most common electrolyte abnormality in the vomiting patient [5]. Acid–base status trends towards metabolic acidosis due to intravascular volume deficits associated with vomiting, diarrhea or third body fluid spacing. However, metabolic alkalosis in concert with hypochloremia with or without hyponatremia and hypokalemia points to gastric outflow or high duodenum obstruction. Rarely, patients with gastrinomas or with frequent unrelenting vomiting without obstruction will also develop metabolic alkalosis [5]. A fecal examination is done as a POC test for patients with diarrhea (especially in younger animals). A direct fecal exam in addition to zinc sulfate centrifugation should be performed. In dogs with diarrhea within the United Sates, 29.6% of those less than six months of age had intestinal parasites, while those greater than one year of age had a 6.1% prevalence of parasites. Whipworms, however, seem to be the only parasite detected with increased frequency in dogs over six months of age, attributable to the long prepatent period and lack of direct transmission from dams to pups [10]. Similar to dogs, the prevalence for the majority of parasites is highest in cats less than six months of age. Hookworms and tapeworms, however, are more commonly found in cats between one and five years of age [11]. Giardia and Trichuris can be difficult to identify, requiring multiple fecal examinations or other modalities to make the diagnosis. Enzyme‐linked immunosorbent assays can be used as POC snap tests to detect canine parvovirus, Giardia spp., and Cryptosporidium parvum antigens. Repeat fecal examination is also important, since as many as 41.5% of all treated cats and dogs with a history of parasites are positive for at least one parasite on repeat fecal examination following treatment [11]. A complete blood cell count (CBC), serum biochemistry, and urinalysis are evaluated. Ideally, blood and urine are collected prior to intravenous fluid administration. Neutropenia prompts testing for parvoviral enteritis, but can also be associated with other causes of viral enteritis, sepsis or infection with Salmonella spp. Leukocytosis with immature neutrophils (bands) is a common finding with systemic infection or inflammation. A stress leukogram featuring leukocytosis with lymphopenia and eosinopenia is a nonspecific finding, common with gastroenteritis in any debilitated animal. A normal leukogram in a systemically ill patient should prompt an adrenal corticotropin stimulation test for adrenocortical insufficiency [7]. A complete serum biochemical profile will evaluate concurrent organ dysfunction. The BUN, creatinine, and urinalysis can indicate renal dysfunction as a cause of uremic GI ulceration. Hyperphosphatemia, when renal function is normal, can occur with massive cell necrosis, such as GI thrombosis, torsions or entrapment. Amylase and lipase blood tests provide very little insight into the etiology of GI distress. SNAP canine (or feline) pancreatic lipase testing is more sensitive and specific for pancreatitis, but false negatives and positives are common. Positive canine pancreatic lipase levels have been detected in dogs with heart disease, hyperadrenocorticism, renal disease, ehrlichiosis and obesity [12–16]. Levels of amylase, lipase, and canine‐specific pancreatic lipase on abdominal fluid tests may provide additional insight in dogs suspected of having pancreatitis [17]. Elevated blood ammonia (NH3) levels may indicate severe liver dysfunction or portosytemic shunting, which can lead to signs of hepatic encephalopathy, vomiting or diarrhea. Portovascular anomalies may lead to severe GI distress, GI ulcerations, and sepsis. Blood ammonia levels should be run immediately (or stored on ice, separated from red blood cells (RBCs)) to avoid false elevation due to production by aging RBCs, or false decrease in samples exposed to air [18–20]. Elevation of NH3 levels should prompt additional diagnostics of liver function. Inflammatory changes on a fecal smear can provide indication for fecal culture or bacterial PCR testing. Fecal culture, however, can be insensitive, with only 10.8% of dogs with diarrhea having positive cultures for pathogens, some of which are potentially false positives [21]. Acid‐fast staining can also be used to confirm Campylobacter jejuni on a fecal smear [7]. Real‐time fecal PCR testing is also available in dogs and cats and detects toxin genes or organisms associated with disease with increased sensitivity over fecal culture. The results can be confounding, however, as virtually all of the tested bacteria, including Campylobacter spp., E. coli, Salmonella spp. and Clostridium spp. have been isolated from clinically healthy dogs and cats [22]. Of concern, however, is the potential impact of zoonotic bacterial infections on human health. Zoonotic bacteria include Salmonella spp., Campylobacter spp., Clostridium difficile, Shigella spp., and Yersinia enterocolitica [7,22]. Abdominal effusion occurs in patients as a consequence of increased capillary hydrostatic pressure, decreased capillary oncotic pressure, vascular permeability, obstruction of lymphatic drainage or a combination of these factors. When the effusion is of a large quantity, fluid can be collected by the four‐quadrant abdominocentesis technique. Ultrasound‐guided centesis or a diagnostic peritoneal lavage (Box 15.1) are necessary to collect fluid from specific abdominal locations or when the quantity of fluid is small [23]. Abdominal imaging should be performed prior to abdominal fluid collection techniques to avoid the iatrogenic introduction of peritoneal air during the procedure. Fluid collected should be placed in an EDTA tube for cytology, a serum tube for chemistry analysis, and a sterile tube for culture. If the sample is hemorrhagic, it should not clot. Clotting is often seen with inadvertent parenchymal organ puncture and, less commonly, peracute hemoabdomen [23]. A focused abdominal sonogram for trauma (AFAST) scan is sensitive for the diagnosis of abdominal fluid accumulations after trauma (Figure 15.2) [24]. Figure 15.2 Focused abdominal sonogram for trauma (AFAST) scan. The areas outlined by the red circles provide a high yield for demonstrating free abdominal fluid. This may be performed in lateral or dorsal recumbency. Diagnostic peritoneal lavage (see Box 15.1) can prove helpful when diagnosing focal abdominal disease, such as septic peritonitis, which has been compartmentalized by omentum. Biochemical test results of the fluid must be interpreted in light of the dilution of the sample [23]. Fluids obtained by direct paracentesis can be classified as a transudate, modified transudate or exudate based on cell count and total protein analysis [23]. A transudate is extravascular fluid with low protein content and low cell counts. It typically results from increased capillary hydrostatic pressure or diminished capillary colloidal osmotic pressure. The few cells present are typically mononuclear cells. An exudate is an extravascular fluid with high protein content and/or high cell counts; it implies vascular damage, inflammation, infection or hemorrhage. A portion of the recovered fluid is centrifuged and a cytological preparation made of the pellet (exudates with high cell counts may be examined with a direct smear). Romanowsky‐type staining (Diff‐Quik® Stain Kit, Imeb, San Marcos, CA) can be used for cytological evaluation and a gram stain can be performed if bacteria are present to help direct antibiotic therapy. Cytology of the fluid may show evidence of inflammation (white blood cells (WBCs)), infection (bacteria, especially if intracellular), and GI rupture (fibers from plants, meat or other sources). Cytological evaluation alone is up to 87–100% accurate in dogs and cats in making the diagnosis of septic peritonitis [25,26]. Aspiration of bowel loop contents could lead to observation of free bacteria and create a false impression of septic peritonitis. Therefore, the presence of intracellular bacteria or other infectious agent is key to making that diagnosis [23]. Bile peritonitis can also be confirmed when cytology demonstrates phagocytosis of golden‐green‐blue granular pigment by inflammatory cells. However, not all patients with bile peritonitis will have these cytological abnormalities. When the total bilirubin of the abdominal fluid is twice that of serum, the diagnosis of bile peritonitis is likely [27]. However, hemolysis in either sample can elevate the bilirubin result and must be considered when interpreting results [23]. Other biochemical testing of abdominal fluid can include quantification of glucose, lactate, creatinine, and potassium. Abdominal serum amylase and lipase levels have been proposed for the diagnosis of pancreatitis, but have not been validated at this time [23]. The author recommends using the supernatant of the spun abdominal fluid sample on a dry chemistry analyzer for these tests, as POC tests calibrated for whole blood have not been validated for abdominal effusion. A study evaluated abdominal fluid glucose concentration compared to serum concentration in companion animals. It was found that a decrease of 20 mg/dL or greater in abdominal fluid glucose to serum glucose was 100% sensitive and specific for the diagnosis of septic peritonitis in dogs. In cats, the same gradient was 86% sensitive and 100% specific in dogs [28]. In the same study, a small number of dogs had a blood‐to‐fluid lactate difference of −2.0 mmol/L which was also 100% sensitive and specific for a diagnosis of septic peritoneal effusion [28]. Interestingly, degenerate neutrophils and glucose and lactate levels after celiotomy seem to be unreliable predictors of septic peritonitis. A sudden increase in fluid volume, neutrophil quantity, and/or intracellular organisms may be required to diagnose septic peritonitis in postoperative patients [29]. Other patient‐specific parameters of clinical deterioration may be necessary to make the diagnosis. The results from an abdominal fluid sample that provide support for surgical intervention are listed in Table 15.4. Table 15.4 Abdominal fluid sample evaluation.* * Postoperative free abdominal fluid evaluation has not shown a high diagnostic yield in dogs [29]. ** Test results also valid for abdominal lavage fluid samples. PCV, packed cell volume; WBC, white blood cell. An abdominal fluid creatinine to peripheral blood creatinine ratio greater than 2.0 in the dog and cat is a highly sensitive and specific indicator of uroperitoneum. An abdominal fluid potassium to peripheral blood potassium ratio of 1.4 in dogs and 1.9 in cats is also supportive of uroperitoneum [30,31]. Aerobic and anaerobic cultures and susceptibility of abdominal fluid should be submitted based on cytological evidence of an inflammatory process [23,25,26]. The patient must be stabilized prior to performing potentially stressful imaging procedures. Fluid resuscitation with appropriate analgesia and/or sedation in addition to oxygen supplementation are provided as indicated and continued throughout the imaging procedure [23]. Radiography is rapid and readily accessible. Images compatible with pancreatitis, generalized ileus, aerophagia, and free abdominal fluid can direct the need for specific diagnostic or therapeutic procedures. Disorders that require surgical intervention, such as GDV (compartmentalization of stomach gas), linear foreign material (small bowel plication with C‐shaped small intestine gas pockets), uterine distension in nongravid animals, and rupture of hollow viscus or abdominal wall perforation (free abdominal gas) can also be quickly identified [23]. However, radiographic changes may not be diagnostic for other surgical conditions such as nonlinear (particularly textile) foreign body obstruction, intussusception, and mesenteric or other organ volvulus. Assessment of small intestinal diameter width to lumbar vertebra 5 height ratios have also been examined in several studies [32,33] but do not necessarily offer additional information. If an abnormal intestinal pattern is present, contrast studies, repeating the radiographs in 6–12 hours or alternative imaging modalities may provide further information if the patient is stable. Gastrointestinal contrast studies may be appropriate for ruling out small bowel obstruction in selected patients. A negative contrast gastrogram (10–30 mL/kg of air inserted through a nasogastric tube) may outline a gastric foreign object. The air is suctioned out following the study, and the tube may be fixed in place for monitoring and therapeutic purposes. When there is no evidence of GI perforation, 30% barium sulfate suspension (Liquid E‐Z‐Paque®, E‐Z‐EM Canada Inc.) may be administered orally or through a nasogastric or orogastric tube at a dose of 10–12 mL/kg; confirmation of tube placement must be performed prior to administration of barium. The risk of barium aspiration pneumonia exists, and necessitates that contrast be administered cautiously in patients with impaired swallowing reflex, gastric distension or persistent vomiting [23,34]. Lateral and ventrodorsal radiographic views are taken at 0, 15, 30, 60, 90, 120, and 180 minutes after administration or until the contrast agent reaches the colon [24]. When the possibility of GI tract perforation exists, an iodinated contrast agent, such as diatrizoate sodium (Hypaque® Sodium Oral Powder, Nycomed, Princeton, NJ), is chosen instead of barium, and administered as a 30% solution at an oral dose of 2–20 mL/kg. Note, however, that an increased frequency of radiographs may be required since iodinated contrast agents hasten small intestinal transit time (normal time is 3–4 hours in dogs and 1–4 hours in cats) [23]. Ultrasound is an important alternative to consider when a GI perforation is suspected. In patients with a history of trauma, it may be important to determine the integrity of the abdominal compartment. Diaphragmatic tears (without herniation) may not be evident on plain radiographs and a positive contrast peritoneogram may be considered. A peritoneal catheter is placed and 1 mL/lb (2.2 mL/kg) of water‐soluble contrast agent is injected into the peritoneal space. Leakage of the contrast outside the normal abdominal cavity often warrants surgery, to reduce organs to their normal position and to prevent organ entrapment or ischemia. Peritoneal contents which herniate into the thorax causing stomach entrapment or evidence of GI leakage warrant immediate surgical intervention. Thoracic radiographs should be evaluated for evidence of cardiorespiratory disease, esophageal disease or foreign body, and aspiration pneumonia. Thoracic radiographs can also screen for acute lung injury, acute respiratory distress syndrome, metastatic neoplasia, enlarged lymph nodes, and mass lesions [23]. Abdominal ultrasonography has become an invaluable tool to evaluate the GI tract and other abdominal organs. Though operator dependent, ultrasound of the stomach, small intestine, and colon can aid in diagnosing obstructive lesions, inflammation, and neoplastic disease. Gas can preclude complete visualization of portions of the GI tract, so ultrasound can frequently be useful in concert with abdominal radiographs, where gas can help to delineate disease [35].Ultrasound can be used to retrieve peritoneal and retroperitoneal fluid and to aspirate or biopsy various abdominal structures. Doppler ultrasound can assess for blood flow to a particular organ or structure [23]. The abdominal focused abdominal sonogram for trauma (AFAST) is a rapid and efficient way for even inexperienced ultrasonographers to identify free abdominal fluid. The probe is placed in four positions of the abdomen (see Figure 15.2) to identify free fluid (most often black in color on image). If only a scant amount of fluid is noted, rechecking in 6–12 hours is advised as fluid may continue to accumulate and be more accessible. Computed tomography (CT) imaging offers superior tissue contrast. Helical CT provides multiple sections imaged simultaneously, significantly reducing scan and anesthetic time [36]. In companion animals, abdominal CT has been beneficial in defining liver, spleen, pancreatic, adrenal gland and urinary tract anomalies and parenchymal organ perfusion [37]. Acute necrotizing pancreatitis has been differentiated from nonnecrotizing pancreatitis using CT. Endoscopy enables the visualization of the mucosal surface of the pharynx, esophagus, stomach, upper duodenum, rectum, and colon. Biopsies can also be taken during this procedure when indicated. In addition, it becomes an important tool for noninvasive removal of selected esophageal or gastric foreign bodies. Virtual endoscopy of the esophagus and stomach has been simulated using helical CT. Advantages of this included visualization of gastric surfaces from any angle, quantitative lesion measurement with three‐dimensional (3D) software processing, increased speed and the differentiation of intramural and extramural lesions. Limitations of the CT virtual image include retention of fluid or solid food obscuring anatomy, inability to obtain information regarding mucosal color and texture, and an inability to obtain biopsies or retrieve gastrointestinal foreign material [38]. Surgical exploration still has an important role in critical care medicine when other diagnostic methodology has not provided the necessary information or other diagnostic methods are limited or unavailable. The decision to progress to anesthesia in a critical patient must be weighed thoughtfully. Common indications for exploratory laparotomy are listed in Box 15.2. In the event that no definitive cause of the GI disorder is determined, visualization at surgery provides a direct assessment of organ structure with biopsies taken of all appropriate tissues, whether or not they are grossly abnormal. When vomiting or diarrhea is the primary clinical problem, biopsies of the stomach and small intestinal segments (duodenum, jejunum, and ileum) will provide histopathological evidence of the health of the tissues sampled. Large bowel biopsies are indicated only when disease is localized to this section of bowel [23]. Other organs from which samples may be collected include the liver, gallbladder, pancreas, kidneys, lymph nodes, and bladder wall.
Gastrointestinal system motility and integrity
Introduction
Monitoring methods
History
Force or timing of vomiting
Suggested pathology
Following abdominal palpation
Peripheral receptor input to vomiting
Passive effort (no outward sign)
Gastric or esophageal
Undigested food ( > 6 hours post meal)
Gastric atony, pyloric obstruction
Projectile vomiting
Pyloric or upper duodenal ileus or obstruction
Small bowel
Large bowel
Projectile
Liquid
Large volume
Melena, steatorrhea
Signs of systemic illness
Systemic acid–base alterations
Significant loss of
Fluids
Proteins
Electrolytes
“Pudding” consistency
Mucus
Hematochezia
Few systemic alterations
Smaller volume
Tenesmus
Increased frequency
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Physical examination
Point of care diagnostics
Minimum database
Fecal examination
Initial clinicopathological testing
Other fecal diagnostics
Abdominal effusions
Parameter
Significant alteration
Indication of
PCV
>5% increase on repeated sampling
Ongoing hemorrhage
WBC**
>20 000, increasing with repeated sampling
Septic abdomen, severe inflammation or necrosis
Differential**
Predominant cell is neutrophil (>90%)
As above
Cytology**
Intracellular bacteria, hypersegmented and vacuolated WBC, plant or meat fibers
As above
Amylase
>200 IU activity, increasing with repeated lavage
Severe pancreatitis, pancreatic abscess or necrosis
Lipase
Greater than the lipase in the serum, increasing with repeat sampling
As above
Bilirubin
Greater in abdominal fluid than serum
Ruptured biliary tract
Creatinine
Greater in abdominal fluid (2×) than serum
Ruptured urinary tract
Potassium
Greater in abdominal fluid (1.4×) than serum
As above
Glucose
Greater in serum than abdominal fluid*
Septic abdomen
Imaging
Radiography and contrast procedures
Ultrasound
CT scan
Endoscopy
Exploratory laparotomy
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