Pleural Fluid

Lining the entire thoracic cavity (see Chapter 69) of the body is a serous membrane called the parietal pleura. Covering the outer surface of the lung is another membrane called the visceral pleura (Figure 77-1). Within the pleural space between the lung and chest wall is a small amount of fluid called pleural fluid that lubricates the surfaces of the pleura (the membranes surrounding the lungs and lining the chest cavity). Normally, equilibrium exists among the pleural membranes, but in certain disease states, such as cardiac, hepatic, or renal disease, excess amounts of this fluid can be produced and accumulates in the pleural space; this is known as a pleural effusion. Pleural effusions can either be exudative or transudative. Exudative pleural effusions are caused by inflammation, infection, and cancer, whereas transudative effusions are due to systemic changes, such as congestive heart failure.

Normal pleural fluid contains few or no cells and has a consistency similar to serum, but with a lower protein count. Pleural fluid containing numerous white blood cells is indicative of infections. Pleural fluid specimens are collected by thoracentesis, a procedure in which a needle is inserted through the chest wall into the pleural space and the excess fluid aspirated. This fluid is then submitted to the laboratory as thoracentesis fluid, pleural fluid, or empyema fluid. The fluid, or effusion, can then be analyzed for cell count, total protein, glucose, lactate dehydrogenase, amylase, cytology, and culture. The total protein and glucose results determine if the effusion is transudate or exudate. The patient’s serum or plasma glucose level is needed to compare with the results indicated in the body fluid. Several characteristics can be used to determine whether a fluid is a transudate or exudate (Table 77-2). When effusions are extremely purulent or full of pus, the effusion is referred to as an empyema. Empyema often arises as a complication of pneumonia, but other infections near the lung (e.g., subdiaphragmatic infection) may seed microorganisms into the pleural cavity. It has been estimated that 50% to 60% of patients develop empyema as a complication of pneumonia.

Peritoneal Fluid

The peritoneum is a large, moist, continuous sheet of serous membrane lining the walls of the abdominal-pelvic cavity and the outer coat of the organs contained within the cavity (Figure 77-2). In the abdomen, these two membrane linings are separated by a space called the peritoneal cavity, which contains or abuts the liver, pancreas, spleen, stomach and intestinal tract, bladder, and fallopian tubes and ovaries. The kidneys occupy a retroperitoneal (behind the peritoneum) position. Within the healthy human peritoneal cavity is a small amount of fluid that maintains the surface moisture of the peritoneum. Normal peritoneal fluid may contain as many as 300 white blood cells per milliliter, but the protein content and specific gravity of the fluid are low. During an infectious or inflammatory process, increased amounts of fluid accumulate in the peritoneal cavity, a condition called ascites. Most cases of ascites are due to liver disease, and in severe cases, the abdomen is often distended. The fluid can be collected for testing by paracentesis (the insertion of a needle into the abdomen and removal of fluid). The peritoneal or ascites fluid can then be analyzed for amylase, protein, albumin, cell count, culture, and cytology. Often ascitic fluid contains an increased number of inflammatory cells and an elevated protein level.

Agents of infection gain access to the peritoneum through a perforation of the bowel, through infection within abdominal viscera, by way of the bloodstream, or by external inoculation (as in surgery or trauma). On occasion, as in pelvic inflammatory disease (PID), organisms travel through the natural channels of the fallopian tubes into the peritoneal cavity.

Peritoneal Dialysis Fluid

More than 900,000 patients with end-stage renal disease are maintained on continuous ambulatory peritoneal dialysis (CAPD). One in every 10 American adults, totaling more than 20 million, suffer from some type of chronic kidney disease. In this treatment, fluid is injected into the peritoneal cavity and subsequently removed, which allows exchange of salts and water and removal of various wastes in the absence of kidney function. Because the dialysate fluid is injected into the peritoneal cavity via a catheter, the break in the skin barrier places the dialysis patient at significant risk for infection. The average incidence of peritonitis in these patients is up to two episodes per year per patient. Peritonitis is diagnosed by the presence of two of the following: cloudy dialysate, abdominal pain, or a positive culture from dialysate. Although white blood cells are usually plentiful (a value of leukocytes >100/mL is usually indicative of infection), the number of organisms is usually too low for detection on Gram stain of the peritoneal fluid sediment unless a concentrating technique is used; fungi are more readily detected. Many recent studies show that improved sensitivity can be achieved by using automated blood culture systems in which 10 mL of fluid is inoculated into culture bottles.

Most infections originate from the patient’s own skin flora; Staphylococcus epidermidis and S. aureus are the most common etiologic agents, followed by streptococci, aerobic or facultative gram-negative bacilli, Candida spp., Corynebacterium spp., and others. The oxygen content of peritoneal dialysate is usually too high for the development of anaerobic infection. Among the gram-negative bacilli isolated, Pseudomonas spp., Acinetobacter spp., and the Enterobacteriaceae are frequently observed.

Pericardial Fluid

The heart and contiguous major blood vessels are surrounded by the pericardium, a protective tissue. The area between the epicardium, which is the membrane surrounding the heart muscle, and the pericardium is called the pericardial space and normally contains 15 to 20 mL of clear fluid. If an infectious agent is present within the fluid, the pericardium may become distended and tight, and eventually tamponade (interference with cardiac function and circulation) can ensue. Up to 500 mL of fluid can accumulate during infection, which may seriously complicate cardiac function.

Agents of pericarditis (inflammation of the pericardium) are usually viruses, especially Coxsackie virus. Parasites, bacteria, certain fungi, and noninfectious causes are also associated with this disease.

Myocarditis (inflammation of the heart muscle itself) may accompany or follow pericarditis. The pathogenesis of disease involves the host inflammatory response contributing to fluid buildup as well as cell and tissue damage. Common causes of myocarditis include viral infections with Coxsackie virus, echoviruses, or adenovirus. The most common etiologic agents of pericarditis and myocarditis are listed in Box 77-1. Other bacteria, fungi, and parasitic agents have been recovered from pericardial effusions.

Patients who develop pericarditis resulting from agents other than viruses are often immunocompromised or suffering from a chronic disease. An example is infective endocarditis, in which a myocardial abscess develops and then ruptures into the pericardial space.

Joint Fluid

Arthritis is an inflammation in a joint space. Infectious arthritis may involve any joint in the body. Infection of the joint usually occurs secondary to hematogenous spread of bacteria or, less often, fungi, as a direct extension of infection of the bone. It may also occur after injection of material, especially corticosteroids, into joints or after insertion of prosthetic material (e.g., total hip replacement). Although infectious arthritis usually occurs at a single site (monoarticular), a preexisting bacteremia or fungemia may seed more than one joint to establish polyarticular infection, particularly when multiple joints are diseased, such as in rheumatoid arthritis. In bacterial arthritis, the knees and hips are the most commonly affected joints in all age groups.

In addition to active infections associated with viable microorganisms within the joint, sterile, self-limited arthritis caused by antigen-antibody interactions may follow an episode of infection, such as meningococcal meningitis. When an etiologic agent cannot be isolated from an inflamed joint fluid specimen, either the absence of viable agents or inadequate transport or culturing procedures may be the cause. For example, even under the best circumstances, Borrelia burgdorferi is isolated from the joints of fewer than 20% of patients with Lyme disease. Nonspecific test results, such as increased white blood cell count, decreased glucose, or elevated protein, may indicate that an infectious agent is present but inconclusive.

Overall, Staphylococcus aureus is the most common etiologic agent of septic arthritis, accounting for approximately 70% of infections. In adults younger than 30 years of age, however, Neisseria gonorrhoeae is isolated most frequently. Haemophilus influenzae has been the most common agent of bacteremia in children younger than 2 years of age, and consequently it has been the most frequent cause of infectious arthritis in these patients, followed by S. aureus. The widespread use of H. influenzae type B vaccine should contribute to a change in this pattern. Streptococci, including groups A (Streptococcus pyogenes) and B (Streptococcus agalactiae), pneumococci, and viridans streptococci, are prominent among bacterial agents associated with infectious arthritis in patients of all ages. Among anaerobic bacteria, Bacteroides, including B. fragilis, may be recovered and Fusobacterium necrophorum, which usually involves more than one joint in the course of sepsis. Among people living in certain endemic areas of the United States and Europe, infectious arthritis is a prominent feature associated with Lyme disease. Chronic monoarticular arthritis is frequently due to mycobacteria, Nocardia asteroides, and fungi. Some of the more frequently encountered etiologic agents of infectious arthritis are listed in Box 77-2.