Salivary Gland Pathology. Группа авторов

Figure 3.6. Lacrimal probes are utilized to probe the salivary ducts. The four shown in this figure incrementally increase in size. Cannulation of salivary ducts begins with the smallest probe and proceeds sequentially to the largest to properly dilate the duct. It is recommended that patients initiate a course of antibiotics prior to probing salivary ducts to not exacerbate the sialadenitis by introducing oral bacteria proximally into the gland.

      Radiographs of the salivary glands may be obtained after performing the history and physical examination. Since radiographic analysis of the salivary glands is the subject of Chapter 2, this discipline will not be discussed in detail in this chapter. Nonetheless, plain films and specialized imaging studies may be of value in evaluating patients with a clinical diagnosis of sialadenitis. Obtaining screening plain radiographs such as a panoramic radiograph and/or an occlusal radiograph is important data to obtain when a history exists that suggests an obstructive phenomenon. The presence of a sialolith on plain films, for example, represents very important diagnostic information to direct therapy. It permits the clinician to identify the etiology of the sialadenitis and to remove the stone at an expedient time frame. Such expedience may permit the avoidance of chronicity such that gland function can be maintained.

Bacterial Salivary Gland Infections

      ACUTE BACTERIAL PAROTITIS

      World history indicates that acute bacterial parotitis (ABP) played a significant role in its chronicles, particularly in the United States. We are told that the first case of acute bacterial parotitis occurred in Paris in 1829 in a 71‐year‐old man where the parotitis progressed to gangrene (McQuone 1999; Miloro and Goldberg 2002). As mumps plays a role in the differential diagnosis of infectious parotitis, Brodie's distinction between acute bacterial parotitis and viral mumps in 1834 represents a major inroad into the understanding of this pathologic process (Brodie 1834; Goldberg and Bevilacqua 1995). Prior to the modern surgical era, ABP was not uncommonly observed, and indeed represented a dreaded complication of major surgery, with a mortality rate as high as 50% (Goldberg and Bevilacqua 1995). Ineffective postoperative intravascular volume repletion with resultant diminished salivary flow and dry mouth were the norm rather than the exception. President Garfield sustained a gunshot wound to the abdomen in July 1881 and developed chronic peritonitis and ultimately died several weeks later. The terminal event was described as suppurative parotitis that led to sepsis (Goldberg and Bevilacqua 1995; Carlson 2009).

      It has been pointed out that upper and lower aerodigestive tract surgeries require patients to be without oral nutritional intake or with limited oral intake postoperatively (McQuone 1999). The reduction of salivary stimulation predisposes these patients to acute bacterial parotitis, with an estimated incidence of 1 in 1000 postoperative patients (Andrews et al. 1989). Other statistics showed 3.68 cases per 10,000 operations in the preantibiotic era compared with 0.173 in 10,000 operations in the antibiotic era (Robinson 1955). The prophylactic use of antibiotics has probably contributed to the reduction of cases of acute bacterial parotitis. In addition, intraoperative and postoperative intravenous hydration became well accepted in the 1930s, particularly during World War II, therefore also contributing to the reduction in the incidence of ABP. In 1958, Petersdorf reported seven cases of staphylococcal parotitis and the 1960s ushered in several reports of ABP as a disease making a comeback (Petersdorf et al. 1958; Goldberg and Bevilacqua 1995). Of Petersdorf's seven cases, five of the patients had undergone surgery, and two of the patients died in the hospital. Oral and maxillofacial surgeons began to report cases of ABP in the literature in the 1960s (Goldberg and Harrigan 1965; Guralnick et al. 1968). These cases were most likely due to the emergence of penicillin‐resistant bacteria (Lewis 1995), like contemporary reports of methicillin‐resistant Staphylococcus aureus parotitis (Nicolasora 2009).

      The parotid gland's relative propensity for infection results from physiologic and anatomic factors. Parotid saliva differs from that of the submandibular and sublingual glands. Parotid saliva is predominantly serous compared to the mucinous saliva from the submandibular and sublingual glands. Mucoid saliva contains lysosomes and IgA antibodies, which protect against bacterial infection. Mucins also contain sialic acid, which agglutinates bacteria, thereby preventing its adherence to host tissues. Glycoproteins found in mucins bind epithelial cells, thereby inhibiting bacterial attachment to the epithelial cells of the salivary duct.

Variants of ABP and Their Etiology

      Over the past several decades, changes have occurred in the bacterial flora of the oral cavity that directly reflect the identification of organisms in ABP. In part, this change is evident due to the increased incidence of nosocomial and opportunistic infections in patients who are immunocompromised as well as those critically ill patients in hospital intensive care units whose mouths became colonized with microorganisms that were previously only rarely found in the oral cavity (Figure 3.4). Moreover, improved culturing techniques have permitted the identification of anaerobes that were previously difficult to recover in the microbiology laboratory. Finally, the occasionally indiscriminate use of antibiotics has allowed for the occupation of other organisms in the oral cavity such as Gram negative enteric organisms. Bacterial Darwinism has also occurred such that iatrogenically and genetically altered staphylococcal organisms have developed penicillin resistance.

      Acute bacterial parotitis has two well‐defined presentations, hospital acquired (Figure 3.4) and community acquired (Figure 3.5) variants. Numerous factors predispose the parotid gland to sialadenitis. Retrograde infection is recognized as the major cause of ABP. Resulting from acute illness, sepsis, trauma, or surgery, depleted intravascular volume may result in diminished salivary flow that in turn diminishes the normal flushing action of saliva as it passes through Stensen duct. Patients with salivary secretions of modest flow rates show bacteria at the duct papillae and in cannulated ducts, while patients with salivary secretions of high rates show bacteria at the duct papillae but not within the duct (Katz et al. 1990). In a healthy state, fibronectin exists in high concentrations within parotid saliva, which promotes the adherence of Streptococcus species and Staphylococcus aureus around the ductal orifice of the Stensen duct (Katz et al. 1990). Low levels of fibronectin such as those occuring in the unhealthy host are known to promote the adherence of Pseudomonas and Escherichia coli. This observation explains the clinical situation whereby colonization resulting from dehydration leads to a Gram positive sialadenitis in ABP compared to the development of Gram negative sialadenitis of the parotid gland in immunocompromised patients (Miloro and Goldberg 2002). Depending on the health of the host, therefore, specific colonized bacteria can infect the parotid gland in a retrograde fashion. Hospital acquired ABP still shows cultures of Staphylococcus aureus in over 50% of cases (Goldberg and Bevilacqua 1995). Methicillin‐resistant Staphylococcus aureus should be ruled out in this population of inpatients. Critically ill and immunocompromised inpatients may also show Pseudomonas, Klebsiella, Escherichia coli, Proteus, Eikenella corrodens, Haemophilus influenzae, Prevotella and Fusobacterium species. Postoperative parotitis has been reported from 1 to 15 weeks following surgery, but most commonly occurs within 2 weeks after surgery (McQuone 1999). The peak incidence of this disease seems to be between postoperative days 5 and 7.

      Community acquired