The Acute Abdomen

Symposium on Gastroenterology

The Acute Abdomen

A . R. Dillon, D .V.M ., M.S. ,* and]. S. Spano, D.V.M., Ph.D.t

This article will address a diagnostic approach to syndromes that induce or mimic the signs of acute abdominal pain. The traumatized abdomen is unique and will not receive special attention. Broadly defined, the acute abdomen is a common and potentially frustrating clinical presentation; it may be a guarded abdomen and stilted gait in one dog and vomiting and shock in another. The wide diversity of syndromes, clinical signs, and objective findings is apparent. Add the client variable, and the assessment of a dog with abdominal pain offers the blending of science and art. The corresponding incidence of recurrent abdominal pain in human beings is staggering and just as frustrating, even though the patients can talk. The incidence of recurrent abdominal pain is reportedly 9 to 15 per cent of the general pediatric population. Organic disease has generally been demonstrated in only 4 to 20 per cent of clinical cases . In a review of 1000 consecutive emergency room cases of abdominal pain in adults, no diagnosis was determined in 41 per cent of the cases. The most common diagnoses were gastroenteritis, pelvic inflammatory disease, urinary tract infection, ureteral stones, appendicitis, cholecystitis, intestinal obstruction, constipation, ulcer, dysmenorrhea, pregnancy, pyelonephritis, and gastritis. An exaggerated stress reaction has been described as the most common cause by some and a "catch-all diagnosis" by others. BASIC CONCEPTS AND PAIN PERCEPTION

If we consider the organ systems contained wholly m; in part in the abdomen, we can appreciate the diversity of signs and diseases when *Diplomate, American College of Veterinary Internal Medicine; Associate Professor, Department of Small Animal Surgery and Medicine, Scott-Ritchey Research Program, Auburn University School of Veterinary Medicine, Auburn , Alabama tDiplomate, American College of Veterinary Pathologists; Associate Professor, Department of Pathology, Auburn University School of Vete rinary Medicine, Auburn , Alabama

Veterinary Clinics of North America: Small Animal Practice-Vol. 13, No. 3, August 1983

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becomes overwhelming if we consider that the liver, gallbladder, spleen, adrenal glands, kidneys, ureters, stomach, pancreas, bowel, bladder, urethra, reproductive organs, vessels, and lymph nodes are all encased in a cavity bounded by diaphragm, ribs, spine, skeletal muscles, and pelvis. Perception of Pain Noxious stimuli are perceived as pain, owing to nonspecific stimulation of free nerve endings. There are no specific pain receptors. The classic Adelta nerve fibers, which transmit sharp or localized pain in the peripheral nervous system, are present primarily in muscle and skin. The C nerve fibers, which transmit dull, poorly localized, chronic pain, are found in periosteum, muscle, peritoneum, and viscera. The abdominal viscera receive innervation via the autonomic nervous system, with contributions from the parasympathetic and sympathetic nerves. Although 90 per cent of vagal fibers are sensory, the vagus nerves do not transmit pain from the gastrointestinal tract and the ability to feel abdominal pain is unaltered after vagotomy. Abdominal visceral pain is transmitted via splanchnic nerves. The visceral afferent fibers in the splanchnic nerves course through the splanchnic ganglion, join the sympathetic chain, reach the site of the cell body in the dorsal root ganglion via the white rami communicantes, and then synapse in the spinal cord. Thus visceral pain can be modulated at the spinal cord level by more dominant fibers (myelinated A-alpha) which mediate touch and proprioception and by higher centers. At other locations in the spinal cord and reticular formation of the brain, the impulses can be further altered before visceral pain is consciously perceived. Since most abdominal viscera receive afferents from both sides of the spinal cord and from overlapping multisegmental innervation, visceral pain is poorly localized. Thus, even though our patients cannot talk, most abdominal visceral pain is poorly localized as a dull midline burning sensation. Despite experimental evidence, the concept of referred pain in an area, with similar central afferent innervation as the affected viscus, lacks clinical application in animals. Thus with visceral pain, C fibers transmit the sensation of protopathic pain. Cells at the spinal cord level may be excited, facilitated, or inhibited by other peripheral nerves. Higher centers can further modulate the signals. Although the original "gate theory" may be incorrect, the concept seems valid. The pain threshold varies among people and varies in the same person based on conditions. Evidence indicates that this may also be true in animals. Pain inhibitory mechanisms in animals were demonstrated by stimulating periventricular and periaqueductal gray matter and medullary raphe nuclei. Pathophysiology of Abdominal Pain Abdominal viscera are insensitive to many stimuli that evoke pain to the skin. Cutting or crushing of viscera does not result in perceptible sensation. There is no evidence for specific visceral pain receptors, pain being from mucosal and epithelial receptors, tension· receptors, and serosal receptors. The factors initiating visceral pain are ones that affect free nerve

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endings which ultimately reach the conscious level. Compared with skin, there is a paucity of nerve endings in the viscera. Tension and inflammation are the keys to the understanding of abdominal pain. The nerve endings of pain fibers in a hollow viscus (bowel, gallbladder, urinary bladder) are in the submucosa and muscle layers; therefore, distention (intestinal obstruction), forceful contraction (hypersegmentation), or traction (adhesions) will produce pain. In the solid organs (kidney, liver, prostate), the capsule is the site of nerve endings; therefore, stretching of the capsule from acute parenchymal disease will cause pain. In contrast, the ovary is relatively insensitive to most stimuli because it does not have a distinct capsule. The parietal peritoneum and mesentery have an abundance of pain fibers, but the omentum and visceral peritoneum are relatively insensitive. The rapid rate of onset of tension is important in the production of conscious visceral pain. Inflammation, regardless of the etiology, and ischemia may induce visceral pain by releasing tissue proteinases and vasoactive substances that stimulate nerve endings. The inflammation usually must be acute and at the site of numerous nerve endings to cause severe abdominal pain. In addition to pain from ischemia, involvement of the blood vessels can cause pain associated with the adventitia because of pain fibers. In contrast to visceral and referred pain, parietal pain is more easily localized because of defined dermatomes. The nerve impulses of parietal pain travel via C nerve fibers in the somatic sensory nerves and reach the thoracolumbar spinal cord at the level corresponding to the cutaneous dermatomes. This innervation is lateralized and has specific dermatomes. Thus, somatic pain of the rib cage, abdominal muscles, adnexal muscles, or parietal peritoneum (connective tissue) would tend to be exaggerated by movement and to be more point-sensitive and localized than visceral pain.

CLINICAL CONSIDERATIONS Given the potential list of systems involved and the type of stimulant for corresponding pain fibers (preceding section), a list of differential diagnoses can be developed (Table 1). Owing to the wide diversity of causes, abdominal pain can be divided into acute and recurrent presentations. The history, physical examination, and initial data base will suggest a conservative approach (hide and watch), a diagnostic plan (further testing), empirical therapy (shotgun plan), or surgical procedure (a chance to cut is a chance to cure). Determining the correct plan is often frustrating and difficult. The acuteness of the illness and the condition o£ the patient usually determine the clinical plan. Recurrent abdominal pain often requires a careful deliberate diagnostic plan. In acute disease, prompt supportive care based on a tentative diagnosis and a decision to perform exploratory surgery may be the most important considerations. History Although the importance of history is self-evide~t, the nonspecific signs and acuteness of the syndrome often reveal little and frustrate both

Table I.

Causes of Abdominal Pain

LIVER

Acute liver diseases that distend the hepatic capsule Cholangiohepatitis, gallbladder distention from obstruction or infection SPLEEN

Torsion Subcapsular hemorrhage or tumor Rupture Infarction

PERITONEUM

Peritonitis Adhesions Adjacent inflammatory disease Abscesses REPRODUCTIVE TRACT

Acute metritis Ovarian cysts Vaginal trauma Prostatitis Torsion of testicles (retained or intrascrotal)

STOMACH

Gastritis Ulcers Dilatation or volvulus KIDNEYS

Acute nephritis or nephrosis Acute pyelonephritis Infarction Acute hydronephrosis Retroperitoneal disease or neoplasia

DIAPHRAGM, RIBS, AND CHEST

Pleuritis Trauma Thoracic inflammatory diseases Fractured ribs Inflammatory esophageal diseases ABDOMINAL MUSCLES

Infections or abscesses Trauma, blunt or penetrating Rupture or hematoma of muscle

PANCREAS

Inflammation Neoplasia BOWEL

Obstruction Acute intussusception Enteritis (focal or diffuse) or colitis Hypersegmentation Adhesions Infarction Torsion of mesentery Perforation Ileus Parasites, if invasive Subserosa! hemorrhage Mesenteric lymphadenitis URETERS

Calculi Obstruction BLADDER

Acute distention Rupture (trauma) Cystitis Calculi URETHRA

Stone Infection Obstruction Trauma BLOOD VESSELS

Emboli Traction from mass adhesions or surgery Venous hypertension

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SPINE AND ADNEXAL MUSCLES

Disc herniation Discospondylitis Sublumbar abscesses Neoplasia of spine or cord Trauma Spinal arthritis PELVIS

Dislocation of joints Fractures Muscular diseases MASSES

Rapidly growing masses that distend bowel or capsules, stretch vasculature, or cause adhesions Direct involvement of nerves SYSTEMIC

Infections Bleeding dyscrasias H yperviscosity Polycythemia Drugs (lead poison1ng, certain antibiotics, etc.) Uremia Abdominal epilepsy?? Hemolytic crisis Bacterial endocarditis Embolization Systemic lupus erythematosus TRAUMA

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client and clinician. To determine the correct diagnostic plan, the following questions should be asked. l. What is the nature of the pain? Is the animal presented because it cries when handled? How was it handled? Or does the dog just pace and act anxious? Has it ever happened before? Often the abdominal pain is not noted by the owner, who just senses something is not right. Is the pain of consistent intensity or are there periods of normality? Therefore the determination of duration and chronology of the signs needs no explanation. The frequency and severity of pain have to be correlated historically with the dog's attitude if depression or lethargy were also noted. Periods of decreased painfulness may reflect systemic illness. 2. A diagnostic pearl is often gleaned from correlation of signs with eating, drinking, time of day, exercise, defecations, sexual activity, medication, or exposure to environmental toxins or other animals. What are the aggravating or alleviating factors? Owners are often reluctant to provide information that may reflect on their role (for example, "He might have been kicked. " "Well, he could have gotten some antifreeze. " "I guess he could have gotten a pork chop bone."). 3. The diagnostic approach is greatly simplified if other signs correlate with abdominal pain. The key is to identify affected organ systems. The gastric function (vomiting), bowel habits (diarrhea, constipation), urinary habits (bloody urine, polyuria), abdominal contour, last estrus or sexual contact, attitude, and gait should all be explored for correlation. Are there associated signs? Physical Diagnosis In addition to a complete systematic examination, careful attention to the animal's responses may provide a clue to the location and intensity of the pain. The position the animal chooses to assume, manner of gait, biting or licking habits, position at defecation or urination, and responses to being handled will aid in the identification of the organ systems involved. As stated previously, the dog with nonspecific visceral pain may pace, stretch, lie on cool surfaces, and be restless. Parietal pain is of a more intense and localized nature; the dog may be reluctant to move and is generally more resistant to being handled. Shock in an animal with an acute abdomen generally indicates blood loss, sepsis, or trauma. The evaluation of the abdomen includes inspection, palpation, auscultation, and rectal examination. Abdominal distention (bowel or ascites), masses, symmetry, angle of ribs, and so forth, can be :missed if the dog is not viewed from afar. Initial palpation should be gentle, with the objective of determining whether distention or large masses are present: If a specific focus for pain can be found on palpation, the rest of the abdomen should be carefully examined first, to avoid muscle guarding from painful palpation. A significant portion of the abdominal contents are encased in the rib cage. Review of anatomy via abdominal radiographs will reinforce the fact that the examiner must palpate anterior to the last rib to find many structures. By palpating from behind the standing patient, gentle persistent digital pressure from both sides along the edge of the ribs in an anterior direction will allow the anterior abdomen to be explored. This may be facilitated by

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elevating the forelimbs. An attempt should be made to trap all structures in the anterior abdomen and let them slip between the fingers of both hands. (Example: The ileocecal valve is anterior to the edge of the last rib at the level of the second lumbar vertebrae. In the case of ileocolic intussusception, the mass is inaccessible in many dogs unless this or similar techniques are employed.) Palpation of the abdomen should be an attempt to find and locate all normal structures, not to search vainly for the abnormal. The fact that a normal organ seems displaced often may be the diagnostic clue. A combination of rectal examination and abdominal palpation will aid in the identification of structures in the posterior abdomen. Abdominal rigidity or guarding may require that sedation or anesthesia be used . However, the general nature and especially any specific tender points should be recorded first . Usually, visceral pain is generalized without any specific foci unless the adjacent parietal peritoneum is involved. Rarely, visceral pain can be localized to liver or kidney or segment of bowel. However, point-sensitive tenderness can be seen, for example, in prostatitis, focal peritoneal inflammation, and somatic pain associated with lumbar muscles, intervertebral discs, painful pleural disease, and so forth. The degree of pain often belies the severity of diseases. (Example: Often, little acute pain is associated with generalized peritonitis or bowel infarction, but severe pain is associated with sublumbar abscesses or acute bowel enteritis .) Although abdominal auscultation receives little attention in small animals, increased borborygmus may indicate hypersegmentation from acute enteritis, bowel obstruction, toxic reactions, or fluid accumulation in bowel. A decrease in gut sounds may relate to fluid accumulation in abdomen, or hypomotility of bowel from chronic bowel distention, peritonitis, ileus, or chronic enteritis. CAUSES OF ABDOMINAL PAIN A review of the list of potential causes of abdominal pain (see Table 1) will allow more ready recognition of the types of diseases to be ruled out. Based on innervation, the hepatic diseases likely to cause pain would be syndromes causing acute stretching of the hepatic capsule. Therefore, acute parenchymal diseases regardless of cause (infectious hepatitis, toxic hepatocellular disease, severe embolization) will cause swelling, edema, or both, with a resultant nonspecific painful abdomen. Localized subcapsular lesions such as infiltrative tumors, inflammatory disease, trauma, and hemorrhage will occasionally induce pain. Gallbladder diseases are rare, but dogs with gallbladder stones, cholecystitis, or a ruptured gallbladder (probably due to one or both of the preceding) have been presented for acute abdominal pain. The hepatomegaly of congestive heart failure, diffuse infiltrative diseases (tumor, fungi), fatty infiltration, and steroid-induced hepatopathy is usually not painful. Because of the tremendous variation in the size of each dog's spleen at any point in time , it is no surprise that the spleen is rarely the cause of pain. Notable exceptions are splenic torsion, splenic trauma or acute subcapsular hemorrhage, and severe infarction. The vascular component

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e than the capsular pain fibers may be the source of the pain in these

roi~ns. Severe splenomegaly may cause displacement of other organs, and s~:etching of blood vessels may occasionally cause vague signs of abdominal discomfort. Considering abdominal pain from bowel, the only areas of the gastrointestinal tract that routinely reach conscious levels are the proximal esophagus, and rectum and anus. (This concept is reinforced by the loss of pain sensation as human beings swallow something very hot or cold.) Therefore, distention, acute inflammation, and vascular involvement are the key to differential diagnosis. Pyloric stenosis induces postprandial pain through forced contraction against a closed sphincter. Gastric dilation is another classic example of distention causing pain. Bowel obstruction induces distention which reflexively stimulates fluid secretion, causing more distention with increased segmentation and pain. With prolonged obstruction, muscle fatigue and ileus may ensue, leading to a distended nonpainful abdomen. Therefore, an acute intussusception is often characterized by an acutely painful abdomen with scanty and sometimes bloody stools. If edematous and inflamed, the "mass" itself can be painful. Classically, chronic intussusception, in which ischemic intussusception has undergone necrosis, is not a painful disease and signs are associated with a partial obstruction and hypoproteinemia and anemia due to the denuded bowel segment. Cecal inversion may mimic the latter pattern. Because the abdomen is often guarded after surgery, postsurgical intussusception is often overlooked. Acute invasive or denuding diseases of the bowel mucosa (parvovirus, salmonella, heavy metal poisoning, etc.) may cause severe abdominal pain from a combination of direct exposure of nerves to inflammatory agents, (kinin, bowel contents) and reflex hypersegmentation (cramping) caused by direct stimulation of myopathic plexus in the bowel wall. Perforation of bowel may cause localized pain if a focal peritonitis affects the parietal peritoneum, but may cause no pain if walled off in the omentum. Because of the time delay in inflammatory response and white cell chemotaxis, the absence of abdominal pain immediately after a penetrating wound (gunshot) does not mean absence of bowel perforation. Abdominal pain related to maldigestion is rarely observed in animals despite the high incidence of childhood abdominal pain related to lactose intolerance. Bloating, flatulence, and abdominal pain in people has been attributed to disorders of intestinal motility in combination with an abnormal pain response to bowel distention rather than from increased volumes or composition of intestinal gas. (This should not be confused with uncomplicated excessive flatulence.) Infarction of small segments of bowel often do not induce pain. However, early in the course of severe vascular occlusion from surgery, torsion of mesenteric vessels, volvulus, and so forth, nonspecific abdominal guarding is present. The abatement of abdominal pain in many vascular diseases may not reflect improvement but signifY early stages of shock. Abdominal pain from constipation, anal disease, or hypermotile rectal disease (spastic colon) is commonly reported as tenesmus. The causes of the various syndromes are often not easily defined. ·Large bowel diseases

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(mucosal or transmural) classically do not cause a guarded abdomen on palpation. "Renal pain" unfortunately is an abused and misused term . Only kidney diseases causing acute swelling of renal parenchyma and stretching of the renal capsule will cause pain . The general absence of palpable pain after kidney biopsy is evidence of the relative insensitivity of the renal tissue itself. Subcapsular hemorrhage or retroperitoneal complications associated with any kidney diseases or procedures may invoke pain that may be point-sensitive. It is unknown if dogs develop the chronic low back pain of pyelonephritis, reported in people. The severe pain of the passage of a ureteral stone probably does not exist or is rare in the dog. However, experimentally induced hydroureter with acute hydronephrosis does cause abdominal pain in dogs. The acute pain of urethral obstruction with severe bladder distention and vigorous muscle contractions may give way to a less guarded abdomen as the bladder becomes atonic and systemic complications induce depression. Stranguria, dysuria, and cystitis may be interpreted as abdominal pain by clients. The canine peritoneum is more resistant to inflammatory and infectious agents than is the human peritoneum. The various presentations of acute pancreatitis, from simple abdominal guarding to severe pain, underscore the wide latitude of clinical signs from focal peritonitis. We have induced diffuse bile peritonitis, hemoperitoneum, and diffuse bacterial peritonitis without causing abdominal pain even though the appropriate gross lesions were present. However, clinical cases with localized peritonitis or severe inflammation of bowel or an organ adjacent to the parietal peritoneum have been presented for acute abdominal pain. This type of pain may be more easily localized and like other somatic pain may cause a shortened gait in hindlimbs or a reluctance to move. Intervertebral disc herniation, sublumbar abscesses, discospondylitis, and other musculoskeletal problems can easily be confused with visceral pain on the basis of clinical presentation. Unfortunately, in the zeal to find the cause of abdominal pain, musculoskeletal causes (see Table 1) are often overlooked. Sublumbar abscesses are often overlooked even at exploratory laparotomy unless specifically ruled out. (How often does the average surgeon carefully examine the crura of the diaphram and the area dorsal to the aorta!) Except for acute metritis and the occasional pyometra, the nongravid dog or cat rarely has abdominal pain attributable to the uterus. This is in contrast with the high incidence of pelvic pain in women. However, male dogs are frequently presented for abdominal pain that can be linked to acute prostatitis. In addition, intrascrotal testicular torsion (uncommon), orchitis, and testicular trauma or hemorrhage can all produce initial clinical signs of abdominal pain. Torsion of a retained intra-abdominal testicle has caused severe acute abdominal pain and should be considered in the dog with only one testicle in the scrotum. The torsed testicle is usually small, hemorrhagic, edematous, and positioned at the posterior pole of the kidney. Masses within the abdomen such as neoplasia or large granulomas may cause pain in several ways: by acutely distending a hollow viscus, stretching an organ capsule, or stretching vessels or peritoneum. Masses may second-

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Table 2.

Laboratory Evaluation of Acute Abdominal Pain

PHASE I

Complete blood count Urinalysis Blood urea nitrogen Total serum protein Abdominal radiograph Four-quadrant paracentesis Fecal examination: ova, smears, occult blood Careful monitoring of vital signs PHASE 2

SGPT (ALT) Alkaline phosphatase BSP retention, bilirubin, blood ammonia, albumin, globulin Blood glucose Serum lipase Serum calcium phosphate, sodium, potassium, chloride, bicarbonate Peritoneal lavage Blood and fluid cultures Contrast radiography (depending on sign) Thoracic radiography Parvovirus titers Platelet count, prothrombin time Repeat Phase 1 PHASE 3

Laparoscopy Exploratory laparotomy

arily induce pain in other organs. However, masses can directly involve nerves or blood vessel innervation and cause a more chronic persistent pain sensation. Pain is not related to the size of the mass. A wide scope of systemic diseases has been identified as causing abdominal pain (see Table 1). Many of these secondarily affect other abdominal organs by causing ischemia or infarction, by causing inflammation, or by altering bowel motility. Based on the frequent complaints in people, the association of drug-induced abdominal pain should not be lightly dismissed by veterinarians. DIAGNOSTIC PLAN The approach to diagnosing the cause of abdominal pain is obviously dependent on whether the signs are acute or recurrent, the nature of other associated signs (vomiting, posterior weakness, polyuria, and so forth), and the initial examination. The initial step is to rule out major organ disease that is life-threatening. For example, the finding of abdominal pain, polyuria, and dehydration together dictate that syndromes such as acute renal disease, acute hepatic disease, acute pancreatitis with diabetes, and pyometra have to be ruled out as soon as possible. Depending on laboratory facilities available, a staged approach is preferred (Tai5les 2 and 3). In a seriously ill patient, a blood sample should be collected and set aside before

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Table 3.

DILLON AND

J. S.

SPANO

Laboratory Evaluation of Recurrent Abdominal Pain

PHASE I

Complete blood count Urinalysis Blood urea nitrogen Total protein Abdominal radiography Fecal examination Four-quadrant paracentesis PHASE 2

SGPT (ALT) Alkaline phosphatase BSP retention, blood ammonia Albumin, globulin Blood glucose Serum lipase Serum calcium, phosphate, sodium, potassium, chloride, bicarbonate Blood cultures Careful neurologic examinations Gastrointestinal series, intravenous urography Thoracic radiography Platelet count, prothrombin time Blood lead assay Brucella titers Aspirations of lymph node for cytology LE cell preparation, antinuclear antibody titer PHASE 3

Peritoneal lavage Endoscopy Arteriography Radioactive isotope scan Exploratory laparotomy

any therapy is instituted. If the initial evaluation is negative or inconclusive, then the next appropriate steps are taken (see Tables 2 and 3). Concomitant diseases (heartworms) and secondary problems (prerenal uremia) must be considered. The severity of signs and the client's concern usually dictate the aggressiveness of the clinical approach. Laboratory results or physical findings referable to an organ system (hematuria, vomiting, bloody diarrhea, penile discharge, icterus, anemia, stranguria, gas-filled bowel, fractured ribs, and so forth) will help form a more direct diagnostic plan and a more specific route to the correct diagnosis. However, the frequent presentation of animals with only nonspecific recurrent or persistent abdominal pain to referral hospitals indicates the potential frustration enc6untered by clinicians and clients.

SIGNIFICANCE OF LABORATORY TESTS Hematology Of the common laboratory tests available, ·several deserve special attention. The initial complete blood count must be correlated with body

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temperature and repeated if abnormal to attempt to establish a trend. Any markedly elevated white cell count with a left shift is indicative of a localized infection, septicemia, inflammation, or area of necrosis. However, many animals with an acute abdomen have an elevated white count associated with a stress leukogram. The markedly elevated white blood cell count often observed in acute leukemia may be associated with abdominal pain because of secondary involvement of the liver. The finding of leukopenia in the dog has become synonymous with parvovirus infections of late; however, overwhelming septicemia, salmonella infections, and hypoplastic disease of bone marrow can cause low white blood cell counts and be associated with acute abdomen syndromes. Furthermore, parvovirus cannot be ruled out on the basis of a normal or elevated white cell count. Anemia associated with abdominal pain presents an interesting situation. The anemia associated with acute hemorrhage into a body cavity or bowel will be nonregenerative until bone marrow stimulation has occurred. Sufficient hemorrhage can occur in these situations for shock to occur before body fluid shifts begin to decrease the hematocrit. In addition, considerable hemorrhage into a bowel can occur and, because of transit time or disease, blood may not be immediately apparent in the stool. Abdominal pain can be seen with vascular tumors such as hemangiosarcomas, where a regenerative anemia can be associated with nucleated red blood cells and red cell fragments observed on the peripheral smear. Splenic torsion results in occlusion of the splenic veins but rarely the splenic arteries, and therefore an anemia with splenomegaly. A decreasing hematocrit in a patient with an acute abdomen is an indication for paracentesis . A microcytic hypochromic anemia and hypoproteinemia may be observed in animals with chronic blood loss in the bowel. Intermittent bleeding into the abdomen with occasional periods of collapse is noted in abdominal tumors. Bleeding defects (disseminated intravascular coagulation, thrombocytopenia, thrombocytopathies, coagulopathies) with subcapsular hemorrhage in liver and kidney or bowel wall may cause pain with or without anemia and other systemic signs . Feces The examination of feces should include fecal flotation for ova, direct smears for protozoa, bacteria, foreign material, and ova, and testing for occult blood. False-positive occult blood tests due to blood products in the diet dictate that the animal's ration also be tested. Some parasitic diseases (amebiasis, protothecosis, etc.) are demonstrated only after bowel biopsy. Renal Function

Diseases of the urinary tract can be the cause of or secondary to acute abdomen syndromes. Pain from the lower urinary tract usually has accompanying clinical signs of anuria, stranguria, or abnormal discharge. Acute nephrosis will cause an elevated blood urea nitrogen, and fixed specific gravity but changes in urinary electrolytes (sodium, phosphate) and the presence of cellular or granular casts in urine may precede this elevation • and be a more sensitive indicator.

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Glycosuria can be seen in hereditary tubular disease, diabetes mellitus, acute nephrosis, and occasionally in severe stress where hyperglycemia exceeds the renal tubular maximum for reabsorption. Prerenal uremia with elevated BUN (<150 mg per dl) and a concentrated specific gravity may underscore the volume depletion or renal hypotension. The presence of hematuria (red blood cells in urine sediment) in the dog with an acute abdomen could be associated with renal infarction, pyelonephritis, bleeding abnormalities, prostatic disease, or neoplasia of the urinary tract. Hemoglobinuria is indicated by red-colored urine but absence of red blood cells in the urine sediment. It must be kept in mind that myoglobin will give a false-positive test for blood using Dipstick tests. The ability to void urine does not rule out a ruptured bladder, torn ureter, or ruptured kidney . Experimentally, a blood urea nitrogen level is elevated earlier and is more diagnostic than serum creatinine level after urine is injected into the canine abdomen. Further, given the retroperitoneal position of the kidneys and ureters, fluid accumulation is often not free in the abdomen, and contrast radiology is required to demonstrate renal or urethral rupture. Abdominal pain from ureteral stones is rarely reported but acute hydronephrosis or hydrometers is a possible cause. Citing the kidneys as the origin of abdominal pain seems to be a convenient yet often inaccurate supposition. Biochemical Tests

Owing to the innervation of the liver, abdominal pain of hepatic origin is acute parenchymal or subcapsular in origin. Therefore leakage enzymes (ALT) are useful as a screening test. In severe acute hepatotoxic diseases, the elevation of ALT will precede the increased production of alkaline phosphatase. The degree of elevation of ALT correlates with the degree of hepatocellular damage, but does not indicate the prognosis or reversibility. When acute liver disease is noted, blood ammonia concentrations and Bromsulphalein (BSP) retention (in the absence of icterus) are indicated to determine the functional capacity of the liver. Chronic infiltrative diseases (tumors, systemic fungi, and so forth) may cause pain, and the appropriate tests for hepatic disease are indicated. Since acute and chronic hepatic diseases may affect the clotting system, hepatic screening tests are always indicated when abnormal coagulograms are found . As a general rule, icteric dogs presented with minimal clinical signs have obstructive or periportal disease. Icteric dogs presented depressed often have diffuse severe hepatocellular disease. Serum lipase reportedly is the most consistently elevated pancreatic enzyme in acute pancreatitis. However, false-positive r'esults in the absence of pancreatic disease have been associated with corticosteroid therapy and renal failure. Focal pancreatitis may cause clinical signs without significant elevation in serum lipase. Serum lipase is always indicated in diabetic dogs with evidence of vomiting or acute abdominal pain. A discussion of electrolytes is beyond the scope of this article. They contribute to the differential diagnosis of organic disease and aid in a plan for supportive therapy. The only parameter'" with potential diagnostic significance in bowel disease (other than those associated with fluid loss) is

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erum inorganic phosphate levels. Based on clinical studies in humans and

~xperimental and clinical cases in dogs, serum inorganic phosphate levels are significantly elevated in mesenteric vascular occlusion leading to bowel infarction. Experimentally, phosphate levels in peritoneal fluid were higher than in serum when mesenteric arteries or veins were occluded. Other causes of hyperphosphatemia to consider are renal disease and diseases increasing osteoclastic activity in bone. A cursory retrospective review of our clinical cases of mesenteric torsion, volvulus, or severe bowel infarction seems to confirm the tendency to recommend an exploratory laparotomy in acute abdomen patients when hyperphosphatemia is not due to renal failure . Radiographic Findings Radiography plays a significant role in the patient with an acute abdomen. The best use of radiography is not to confirm the location of a palpable mass but to find the more subtle lesions, such as sublumbar abscess (vertebral periosteal reactions), cholangitis (air-filled gallbladder), focal peritonitis (loss of visceral detail), bowel obstruction (distended bowel), linear foreign body (gathering of bowel), ruptured hollow viscera (free air in abdomen), discospondylitis (intervertebral lysis and sclerosis), and subtle disc protrusion (disc narrowing). Contrast radiographic techniques (discussed elsewhere in this issue) such as upper gastrointestinal series, barium enemas, intravenous urograms, double contrast cystograms, myelograms, and arteriograms should be used not as exploratory procedures but rather to confirm a tentative diagnosis. When available, the use of radioactive isotope scans, tomography, and ultrasonography in veterinary medicine are of great diagnostic value. Diagnostic Techniques A diagnostic technique with the capacity to yield a quick answer is paracentesis. All four abdominal quadrants should be initially aspirated with an 18- or 20-gauge needle. The needle should be inserted at an angle (as for venipuncture), with the bevel of the needle toward the abdominal cavity to prevent perforation of viscera. Complications are rare. Negative aspirates should not be equated with the absence of disease. Paracentesis is indicated even when distention or fluid accumulation is not suspected. The aspiration of even the smallest amount of fluid should initiate a cytologic evaluation and culture if bacteria are noted. Experimental and clinical studies in dogs have confirmed the superiority of paracentesis with an indwelling catheter (such flS a peritoneal dialysis catheter) and even more sensitivity with peritoneal lavage techniques. Peritoneal lavage is well described in other texts and is reliable and easy. Briefly, it requires the insertion of an 11-French peritoneal dialysis catheter or a 14-gauge indwelling catheter at a locally anesthetized site just caudal to the umbilicus. After insertion, the catheter is directed dorsally. Fluid is withdrawn if possible. If no fluid is aspirated, an isotonic crystalloid solution (without preservatives) is infused by gravity flow at a rate of 15 to 20 ml per kg of body weight. The abdomen is massaged to mix the contents, then the fluid is collected by gravity flow into an empty

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Table 4.

J.

S . SPANO

Interpretation of Lavage Fluid Laboratory Determinations*

DETERMINATION

Packed cell volume (PCV) Cytologic examination Bilirubin test Amylase activity Leukocyte count Creatinine concentration

INTERPRETATION

When infusing 500 ml of fluid, every 1 per cent PCV means 10 to 20 ml of free blood within the abdominal cavity. Bacteria or vegetable fibers with many neutrophils are indicative of hollow viscus disruption. Many neutrophils are indicative of peritonitis. A positive result (bluish color change) is indicative of biliary or upper intestinal tract disruption. More than 1000 Somogyi units per ml or 200 Karoway units per 100 ml is indicative of intestinal ischemia or pancreatic inflammation and injury. More than 500 per cu mm is indicative of peritonitis. More than 200 cu mm is indeterminate and suggests the need to repeat the test. Volumes greater than that of serum creatinine are indicative of urinary tract injury, with leakage of urine into the abdominal cavity.

*Summary of criteria for interpretation are based on experimental work done with dogs in which blunt trauma to the abdominal wall, peritoneal soilage with fecal contents, blood, bile, urine, or a specific organ injury was accomplished, followed by lavage and analysis of the returned fluid.

intravenous infusion set. Not all fluid need be collected, but only enough for cytology and culture. The fluid can be analyzed for foreign material, leukocyte count, blood, bacteria, amylase, blood urea nitrogen, and bile (Table 4). The inability to read newsprint through the intravenous tubing has been equated with greater than 100,000 red blood cells per j.t.l, and serious abdominal disease, especially after trauma. The hematocrit of fluid obtained via paracentesis will determine if pure blood is present. Blood that does not clot in the syringe is indicative of free blood in the abdomen which has consumed all the clotting factors. Blood aspirated in the procedure will clot. Following contamination of the peritoneal cavity, several hours are needed before leukocytes accumulate. Severe active inflammatory disease of the bowel may cause peritoneal leukocyte accumulation (>500 white blood cells per j.t.l) without peritonitis. However, positive findings via paracentesis or peritoneal lavage usually indicate that an exploratory laparotomy will be rewarding. Endoscopy is usually uninformative in acute abdomen patients unless signs of bowel disease are present. Colonoscopy and a di~ected biopsy often provides tissue for a histologic diagnosis (e.g., ameba, neoplasia, colitis). As a survey procedure, endoscopy can be used to evaluate the esophagus, stomach, duodenum, rectum, colon, and ileocolic valve area. The debate as to the diagnostic value of laparoscopy versus exploratory surgery probably lies in the skills of the clinician. Laparotomy has the practical advantages of allowing surgical correction, if needed, at the time of examination. Thus, the presentation of an animal with abdo~inal pain often provides a painful uncooperative patient and an owner without any supportive

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THE ACUTE ABDOMEN

history. Is it simply dietary indiscretion or is it acute renal failure? A systematic approach through history, physical examination, laboratory test, and diagnostic procedures combined with a high index of suspicion will provide the best chance to determine the right medical or surgical course.

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