Clinical Vignette
Brandy, a 10-year-old female spayed boxer cross, is presented for exercise-induced weakness, panting, decreased appetite, edema in the pelvic limbs, and an enlarged abdomen. On physical examination, weak pulses, muffled heart sounds, and a distended abdomen were identified.
What tests would you select next? How could the muffled heart sounds, edema, and abdominal distention be linked? We will come back to Brandy at the end of the chapter after a discussion of the pathophysiology of abdominal distention.
Definition and Problem Recognition
Abdominal distention may be defined as a sudden or gradual increase in the size of the abdomen. Abdominal distention may be due to either fluid accumulation or organomegaly (Fig. 8-1 ). Ascites generally refers to an abnormal accumulation of a transudate or modified transudate fluid in the peritoneal cavity. These two types of fluid are rarely associated with infection or severe inflammation, but exudates are, and therefore exudates in the abdomen almost always result in a very ill patient. In addition, the resultant clinical signs associated with exudates are commonly acute in nature. The finding of an exudative fluid should alert the clinician to pursue an aggressive and rapid diagnostic course of action since many causes of exudates require emergency management and/or surgery. Other associated signs, such as vomiting, diarrhea, abdominal pain, polydipsia, polyuria, polyphagia, and edema, may be clues to the etiology of abdominal distention and/or ascites and will be discussed later.
Pathophysiology
Pathophysiologic mechanisms of ascites are similar to those of expansion of extracellular fluid elsewhere in the body (edema). There are two general categories: (1) those in which the primary event is escape of plasma into tissue spaces with resultant hypovolemia with secondary renal retention of electrolytes and water and (2) a primary disturbance, which results in excessive retention of electrolytes and water, leading to extracellular fluid expansion and transudation of fluid from plasma into tissue spaces. General mechanisms of ascites formation include (1) decreased colloid osmotic pressure (hypoalbuminemia), (2) increased capillary hydrostatic pressure, (3) increased capillary permeability, (4) obstruction of lymph flow, and (5) excessive renal retention of sodium and water. Many times more than one of these mechanisms will simultaneously contribute to the fluid accumulation.
FIGURE 8-1. Initial plan for determining the cause for abdominal distention.
Hypoalbuminemia (see Chapter 55), in the absence of other mechanisms of ascites, must be severe (usually less than 1.0 g/dL) in order to lower plasma oncotic pressure sufficiently to result in ascites; however, lesser magnitudes of hypoalbuminemia may facilitate the formation of ascitic fluid whenever other causes exist, such as increased capillary permeability. For example, ascites in a patient which has a serum albumin concentration of 1.4 g/dL is unlikely to develop secondary to the hypoalbuminemia alone, and therefore, the clinician should consider that other mechanisms of ascites formation could exist the patient. The animal should be evaluated for another coexisting disorder, such as one of the other general causes listed above.
Thoracic and abdominal venous obstruction result in increased capillary hydrostatic pressure and may cause ascites. Protein content of ascitic fluid varies depending on the anatomic site of venous obstruction, and this fact may be helpful in localizing and determining the causes of ascites listed in Table 8-1 (Greene 1979).
Experimentally produced transient (duration of a few minutes) portal venous obstruction alone does not cause ascites. Lymph flow from the bowel markedly increases, and it probably compensates for the obstructed portal venous drainage. Sustained portal hypertension does cause ascites and is referred to as presinusoidal obstruction. Persistently increased intestinal capillary hydrostatic pressure causes dilation of lacteals and increased fluid transudation into the bowel lumen, and from the serosal surfaces into the peritoneal cavity. Intestinal lymph is lower in protein than hepatic lymph; therefore, ascites caused by chronic portal stasis is generally low in protein (less than 2.5 g/dL). The most common cause of chronic portal stasis in dogs and cats is liver disease characterized by inflammation or fibrosis diffusely affecting the portal tracts and triad area (see Table 8-1).
Obstruction of blood flow draining hepatic sinusoids, termed postsinusoidal obstruction, causes production of a high-protein (greater than 2.5 g/dL) ascites derived from the hepatic lymph. Protein content is high because hepatic sinusoidal capillaries are more porous and “leaky” than capillaries elsewhere in the body. With increased hydrostatic pressure in the hepatic sinusoids, relatively large albumin molecules can readily extravasate into formed lymph. Extrahepatic portal venous pressure is generally normal or only slightly increased with postsinusoidal obstruction. Some examples of postsinusoidal obstruction include right-sided heart failure (multiple causes), obstructed caudal vena cava, pericardial effusion, constrictive pericarditis, and lesions of major hepatic veins or thoracic caudal vena cava, such as thrombosis (see Table 8-1). Therefore, when a modified transudate is present in the abdomen this usually signals that the problem causing the abdominal effusion exists in the thoracic cavity (Neer 1997).
Table 8-1. Causes of abdominal effusion
Abdominal masses (e.g., neoplasms, granulomas, and “walled-off” abscesses) may cause intra-abdominal vascular damage and leakage of blood or plasma, resulting in high-protein ascites (see Table 8-1) but this is less common than the thoracic causes listed above. On the other hand, if a mass restricts portal blood flow (presinusoidal), resulting in sustained portal hypertension, low-protein intestinal lymph contributes to the formation of the ascitic fluid. Low-protein ascites (with normal serum albumin) in the presence of an abdominal mass signifies that portal venous obstruction is present and that portal hypertension exists (Greene 1979).
The pathophysiologic events of intra-abdominal exudate formation vary with the particular etiology of the exudate. Rapid accumulation of blood in the abdomen, such as may occur following trauma or rupture of a splenic hemangiosarcoma, may be associated with signs of hypovolemic shock. A rent in the urinary system with accumulation of urine in the peritoneal or retroperitoneal spaces will result in signs identical to acute renal failure or uremia. Leakage of bile into the peritoneal cavity results in a chemical peritonitis and icterus. A ruptured bowel usually leads to septic peritonitis with signs of endotoxemia and septic shock.
The pathophysiological mechanisms of nonfluid causes of abdominal distention vary depending on the cause. For example, ileus may be secondary to peritonitis or an obstructed bowel. Lack of normal bowel motility may allow proliferation of pathogenic intestinal bacteria and subsequent absorption of endotoxins. Intra-abdominal masses may impinge on normal abdominal organs and cause disruption of function, resulting in signs such as anorexia, vomiting, diarrhea, and/or icterus. With gastric volvulus, abdominal venous return is severely restricted and signs of hypovolemic shock may occur. Lastly, enlargement of any abdominal organ (organomegaly) should be considered as a potential cause of abdominal distention. The enlargement in this situation may be the only historical or physical examination finding, or there could be secondary clinical manifestations if the enlargement affects the function of a particular organ or adjacent organs such as those events described above.
Diagnostic Plan
History and Physical Examination
The history may be helpful in narrowing the potential causes of abdominal distention. An example would be a history of polydipsia, polyuria, and polyphagia in a dog with a distended, pendulous abdomen suggesting hyperadrenocorticism. A history of collapse, with subsequent recovery, and the associated finding of an abdominal mass could signify hemangiosarcoma of the spleen, which has resulted in periodic intra-abdominal bleeding episodes. The physical examination should be complete. Associated findings such as respiratory distress, tachycardia, heart murmurs, and peripheral edema may point to right-sided heart failure or pericardial disease as the etiology of abdominal distention. An appropriate diagnostic plan would be instituted to evaluate for these differentials. Ballottement of the abdomen should be done carefully to determine if a fluid wave is present; with experience, false-positive results are infrequent, but small amounts of abdominal fluid cannot always be detected by this method alone. The physical examination should focus on determining if the distention is due to fluid or organomegaly. If this cannot be determined from the physical examination, then additional diagnostics will be needed (see below).
Other Diagnostic Procedures
If it is difficult to determine whether the abdominal distention is fluid or organomegaly, then plain abdominal radiographs or abdominal ultrasonography should be done first. This will direct further test selection. Occasionally, both fluid and organomegaly will coexist, and in this instance fluid analysis is usually the next test to perform. As a clinical pearl, if neoplasia is suspected, then thoracic radiographs should be performed next. There is no need to expend energy, finances, and perform an eloquent workup on a patient, just to find out at a later time that thoracic metastatic disease exists.
Whenever abdominal fluid is present, paracentesis and fluid analysis prior to other diagnostic procedures should be performed. This is accomplished by using a 20- to 22-gauge, 1 in. needle and a 6 mL syringe. If the animal is fractious, it is safer to use a butterfly needle unit. Although the risks of this procedure are minimal, it is probably better to tap the right cranial quadrant to avoid the spleen. Appropriate clipping and skin preparation should be done. Fluid analysis, including protein content (determined using a refractometer), cell count and differential, sediment examination, and culture/sensitivity, if indicated, should be performed. Only a small amount of fluid (less than 1–3 mL) is required. The type of fluid present will then dictate the next diagnostic procedures. For example, most causes of exudate (high protein and cellularity) formation will result in a surgical approach; a low-protein ascites (transudate) would point to hepatic disease, protein-losing diseases (GI, renal), or causes of portal hypertension; a high-protein ascites with low cellularity (modified transudate) should point to a thoracic cause or possibly an abdominal mass with associated venous compression. The removal of large amount of ascitic fluid may worsen hypoalbuminemia and should be avoided unless fluid distention is resulting in serious respiratory distress.
Edema
Problem Definition
Edema, accumulation of body fluid in tissues, results from expansion of the interstitial fluid volume. This increase in the extravascular compartment of the extracellular fluid can occur in a localized or generalized distribution, depending on the underlying cause. Determining the etiology for the edema formation is usually necessary before a definitive resolution to the edema can be achieved. Simply treating the symptom (edema) is usually not adequate. In many patients though, treatment for edema may need to be instituted prior to a definitive diagnosis since increased tissue fluid pressure may directly interfere with physiologic functions such as proper tissue nutrition.
Pathophysiology
The interstitial fluid space is highly structured; it consists of collagen fibers embedded in a gel matrix. Fluid within this network, although relatively mobile, is in dynamic equilibrium with the blood capillary network and enters as a result of hydrostatic pressure on the arteriolar network. Narrow pores in the capillary endothelium normally restrict the migration of large plasma proteins into the interstitial space, while allowing free passage of water and small solute molecules. Since the interstitial fluid protein concentration is normally much lower than that of plasma, the colloidal osmotic pressure of intravascular protein facilitates fluid retention in the vascular space. Under normal circumstances, excess fluid filtered into the interstitial spaces does not accumulate but is reabsorbed into the venous blood via local lymphatic circulation so that only a minimal amount of extracellular tissue fluid normally exists. The return of fluid via lymphatic circulation is also somewhat influenced by interstitial compartment compliance. Normally, entry of fluid into the interstitial space causes a marked increase in tissue pressure, which further restricts the movement of fluid out of the vascular space.
Disease processes cause edematous fluid formation by disrupting the normal fluid dynamics in the interstitial space. Increased capillary permeability from endothelial damage can result in vascular leakage and interstitial fluid accumulation. Hypoproteinemia will also result in expansion of the interstitial compartment, as will reduced blood flow or an obstruction of lymphatic or venous circulation.
Albumin, the smallest plasma protein, is the primary source of plasma colloidal oncotic pressure and attracts fluid to remain within the vascular space. Edema usually does not become evident until the serum albumin concentration falls below 1.0 g/dL.
Extensive generalized edema is associated with a reduction of plasma volume and a simultaneous increase of extracellular fluid space. This results in decreased renal excretion of sodium by presumed hormonal mechanisms. This solute retention promotes extracellular fluid accumulation and exacerbates edema formation. Generalized edema is usually secondary to low albumin levels or severe right-sided congestive heart failure.
Focal, limb, or regional edema is usually associated with disease of the local lymph nodes or lymphatics, resulting in poor lymphatic drainage, infection/inflammation of the local tissues, or obstruction of local venous drainage. The diagnostics selected should allow one to assess these three mechanisms of edema formation. For example, edema of the head should signal the possibility of a mediastinal mass, obstructing venous return from the head.
An increase in free fluid volume in tissues accounts for the pitting phenomenon that is seen in edematous states. Pressure applied to an edematous area forces the mobile fluid out of the region, resulting in a permanent indentation. The mobility of fluid also explains the continuous weeping of wounds in edematous tissues. The mobility of edema to the lowest portions of the body occurs because of the increased venous volume and back pressure from the gravitational pooling of blood in these areas.
Diagnostic Plan
A thorough history and physical examination can help determine many causes of edema (Table 8-2). Any disease process that produces lymph node enlargement can cause secondary lymph stasis and edema. Fever, warm swelling, and enlarged or painful lymph nodes are associated with inflammatory conditions causing lymphadenomegaly. Regional lymph node enlargement may also occur with lymphoreticular neoplasia. Arteriovenous fistulas may be detected by the presence of a continuous murmur auscultated in the affected extremity. Cardiovascular disorders that result in generalized edema may be detected on physical examination on the basis of pulse character or deficits, respiratory rate, and cardiac auscultation. Suspicious findings can be followed up with electrocardiography, thoracic radiography, and echocardiography. Measurement of central venous pressure is useful in determining the presence of venous obstruction or systemic venous hypertension. Venous or lymphatic occlusion can also be detected by contrast radiography.
The presence of concurrent ascites should be ascertained in any edematous patient, since this finding may help determine the cause of both abnormalities. Ascitic fluid often forms prior to development of subcutaneous edema when it is caused by cardiac disorders and/or portal hypertension. With hypoproteinemia, peripheral edema and ascites may exist concurrently. An analysis of ascitic fluid to determine cell and protein composition (see abdominal distention discussion) often distinguishes the causes of edema.
Laboratory screening should include a complete blood count with a leukocyte differential and, most importantly, the measurement of plasma and urine protein and albumin concentrations (to assess for protein-losing nephropathy/enteropathy). A refractometer can be used for initial screening of plasma protein concentration, but albumin and total protein measurements should always be determined. If hypoproteinemia is found, causes of this problem should be considered (see Chapter 55). Electrolyte concentration in plasma and urine can be examined to determine if the extracellular fluids are being retained in excessive or normal amount in proportion to the electrolytes; this may help determine whether the process is primary or secondary to renal, adrenal, or caudal pituitary dysfunction. Immune or infectious disorders, suspected on the basis of clinical or laboratory findings, have to be confirmed using additional serologic and infectious disease testing. Enlarged lymph nodes should always be subsequently biopsied for histopathologic study. Edema may originate from a variety of disturbances; therefore, multiple abnormalities in laboratory tests may be apparent.
Table 8-2. Pathophysiologic mechanisms and differential diagnoses for edema formation
| I. Decreased capillary integrity (increased permeability) |
| Inflammation |
| Vasculitis |
| Infectious |
| Immune mediated |
| Allergy |
| Trauma |
| Burns |
| Toxins |
| II. Change in tissue gel |
| Myxedema |
| Serous atrophy of subcutaneous fat from cachexia |
| III. Noninflammatory increase in tissue fluid |
| a. Decreased plasma oncotic pressure (hypoalbuminemia) |
| i. Increased albumin loss |
| Renal |
| Gastrointestinal |
| Body cavities |
| Wounds, burns |
| Vasculitis |
| Nephrotic syndrome |
| Protein-losing enteropathy |
| ii. Decreased albumin production |
| Protein malabsorption |
| Hepatic insufficiency from any cause |
| b. Lymphatic hypertension or obstruction |
| Surgical or traumatic injury |
| Neoplasia |
| Lymphatic or lymph node inflammation |
| Congenital lymphedema |
| c. Increased capillary hydrostatic pressure |
| Venous hypertension |
| Venous obstruction |
| Right heart failure or obstruction |
| Arteriovenous fistula |
| Overhydration |
| Arteriolar hypertension |
| Hyperaldosteronism |
| Inappropriate secretion of antidiuretic hormone |
| Acute renal failure |
Clinical Vignette—Conclusion
Stay updated, free articles. Join our Telegram channel
Full access? Get Clinical Tree
