Volume 70 July 1977
483
United Services Section President Howard Hanley CBE FRCS
Meeting 7 October 1976
Papers Benign Parotid Swellings: a Review by Surgeon Vice Admiral Sir James Watt FRCS FRCP (Ministry of Dejence, Empress State Building, London SW6 I TR) Parotid swelling may disguise a diverse and obscure etiology. A classification is proposed in Table 1, based upon analysis of 70 naval cases for the years 1959-1975. Table I Benign parotid enlargement
(1) Congenital anomalies (2) Trauma (3) Duct Obstruction (4) Infection (a) Acute: (i) Pyogenic (ii) Viral (b) Chronic: (i) Postobstructive (ii) Specific
(5) Allergic and auto-allergic reactions (6) Disorders of nutrition (7) Miscellaneous (a) 'Sialectasis'
(b) Cysts
(c) Masseteric hypertrophy (d) Pneumoparotitis
Congenital Anomalies Jones (1953) described congenital ectodermal dysplasia associated with dry mouth and ascending parotid infection in 2 orphan brothers. Smith (1953) found three generations of a family with radiological evidence of duct dilatation, and Pearson (1961) had two pairs of siblings with parotid swelling and terminal duct dilatation. Rose (1954) considered the duct dilatation congenital and the cause of recent secondary infection in 10 children, but Nicholson (1923) attributed duct obstruction
to pressure by congenital excess of lymphoid tissue in the gland parenchyma. Congenital dermoid inclusions and cysts have been described and May et al. (1973) reported an arteriovenous malformation with associated facial palsy.
Trauma Parotid swelling may result from extra- or intraoral trauma. Joffe's 17 South African cases were caused by knife wounds, road traffic accidents and blunt trauma, occasionally followed by cysts and fistulk (Joffe 1967). One naval case resulted from a direct blow; another, following intensive rifle practice, was associated with tinnitus, deafness and temporal headache. Sialadenopathy may result from cedema of the duct orifice caused by ill-fitting dentures in adults (Furstenberg & Blatt 1968). In children, when the third molar tooth erupts, the parotid papilla is traumatized as it is sucked between the teeth when food is chewed on the opposite side (Rose 1954). Parotid swelling in 2 naval cases followed dental treatment which presumably caused papillary cedema. Duct Obstruction Apart from trauma, duct obstruction may be caused by calculus, stricture, food (Cone 1966), and mucus secretion (Patey 1965). Swelling of the duct epithelium also occurs as an allergic response and in the 'sicca' or Sj0gren syndrome, Patey & Thackray (1955) have described lymphoid tissue in and around intralobar ducts which breaches the walls and allows radiopaque dye to escape during sialography, causing 'punctate sialectasis'. Mucous plugs obstructing the terminal duct may be discharged explosively into the mouth with a stream of clear or turbid saliva. Calculus is rare in the parotid and occurred in only 3 of Rose's 75 cases (Rose 1954) and 4 of 70 naval cases. Rose believes aggregates of cellular debris and coagulated mucin with or without microorganisms form the essential organic nidus.
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Proc. roy. Soc. Med. Volume 70 July 1977
Calcium deposition depends upon infection by ammoniacal organisms which raise the pH. Calculi occur at the sigmoid bend where the duct enters the mouth or at the anterior border of the masseter. Obstruction and consequent diminished secretion lead to infection, multiple strictures and cysts. Parotid massage produces a sluggish salivary flow and a cord-like Stenson's duct may be palpable. Sialography reveals dilated segments alternating with strictures and metaplastic duct epithelium with stricture formation seen in biopsy material (Furstenberg & Blatt 1968). Pyogenic Infection In children, males predominate and infection ascends from mouth or postnasal space (Jones 1953). Females predominate in recurrent pyogenic infections of adults (Payne 1933). The duct orifice is inflamed and drips pus, infecting organisms being Strep. viridans, pneumococcus, Staph. aureus, haemolytic streptococcus a'nd Staph. albus (Pearson 1961). Sialograms may be normal or show terminal duct obstruction. The length and shape of the duct and rate of salivary flow normally prevent infection and xerostomia predisposes (Blatt 1964). Acute septic parotitis is apparently on the increase. Spiers & Mason (1972) believe antihistamines, anticholinergics, hypotensive'drugs, certain tranquillizers and sedatives are more important in causing xerostomia than the dehydration formerly responsible. Yonkers et al. (1972) blamed poor oral hygiene. Duff (1972) reported facial palsy associated with a parotid abscess and Harris (1971) discussed 41 cases of unilateral acute suppurative parotitis secondary to virus infections in Uganda, of which 10 were due to Coxsackie virus B.
Viral Infections Howlett et al. (1957) have also implicated the Coxsackie virus, Sandford & Sulkin (1959) the ECHO virus, 'and Anderson (1972) has suggested mycoplasma. Riley (1956) claims recurrent mumps infection is rare and the parotid swelling a hypersensitivity reaction to the mumps virus, and Dishon et al. (1974) have reported acute parotitis in sensitized rats following a single intraductal challenge with the sensitizing antigen, but nonreactivity when multiple intraductal challenges were given. Lewis & Utz (1961) ascribed parotid swelling in an American naval patient to lymphocytic-choriomeningitis virus, and it is seen in glandular fever. Banks (1968) suggests that the common result of virus infections, sensitivity and autoimmune reactions is diminished secretion leading to retrograde infection, mucous metaplasia in duct walls, recurrent duct obstruction, infection and swelling. The condition is reversible until main duct changes occur with secondary stricture and calculus.
Chronic Infections Chronic infections may follow obstruction, sialography revealing beading and dilatation of the ducts, globular or cavitary collections of opaque medium or generalized destruction of duct and gland structure. Specific infections are rare and include tuberculosis, actinomycosis, rhinosporidiosis (Chandra et al. 1971), brucellosis and bacillary dysentery (Borsanyi & Blanchard 1961). Greenberg et al. (1964) found parotitis in 23 (6 %) of 388 patients suffering from sarcoid. Thirteen were women. Kveim test was positive in 770 and Mantoux negative in 81 %. The condition is usually bilateral and there may be palsy of the facial nerve. Allergic and Auto-allergic Reactions Swelling appeared after intravenous pyelography, exposure to paint and eating cabbage in 1 naval case. A patient of Pearson (1969), a life-long asthmatic, developed parotitis and flushing of the face after eating cheese or milk. It was accompanied by migraine in another and followed the eating of eggs (Pearson 1961). Such patients were almost exclusively women of middle age or beyond. Pressure over the gland expelled a plug of mucus containing numerous eosinophils and clear saliva. The main parotid duct was markedly dilated. Three of Jones' (1953) patients had a family history of allergy and 2 mothers had suffered recurrent parotid swelling during adolescence. In 1933, Sj0gren described parotid enlargement associated with dry eyes and mouth and rheumatoid arthritis. Its etiology is obscure and may be associated with other connective tissue disorders: scleroderma, polyarteritis nodosa and polymyositis. Rheumatoid factor is present in most cases and antinuclear factor in about two-thirds, thyroid and gastroparietal autoantibodies are also encountered and gammaglobulins are increased (Grahame & Lessof 1975). On long-term follow up, Bark & Perzik (1968) have found a significant number of patients with disabling and fatal autoimmune diseases such as systemic lupus erythematosus. Of the 41 patients in Blatt's (1964) series, 20 had rheumatoid arthritis or polyarthralgia and 13 keratoconjunctivitis. The swelling of duct epithelium reported by Maynard (1965) appears part of the same immune response. Any hypersensitivity reaction causing xerostomia invites sialadenopathy, which has occurred after eating oysters and shrimps, poisoning by lead and mercury (Beck 1942), following excretory pyelography (Imbur & Bourne 1972) and general anesthesia. Reilly (1970) concluded that belladonna, depolarizing neuromuscular-blocking drugs, succinylcholine, straining, coughing and the Valsalva manceuvre contributed, and found that Negroes were specially susceptible.
United Services Section Disorders of Nutrition Parotid swelling has occurred in emaciated prisoners of war returning to a normal diet. McCance et al. (1951) reported associated gynaecomastia, possibly from temporarily impaired liver function. Parotid swelling in kwashiorkor is regarded as a sign of recovery (Davies 1948). Silverman & Perkins (1966) found bilateral enlargement in obstetric cases, eating corn starch and white or red clay, of whom 880% were Negroes; Jastak (1967) reported parotitis in a 51-year-old diabetic woman who had eaten 12-16 ounces (340-453 g) of starch daily for ten years. Biopsies in other cases showed either increased zymogen storage or increase in granules and he postulated initial stimulation leading to later depletion. Fontoynont (1911) mentions parotid swelling in Madagascan farmers who subsisted on a diet of potatoes and rice, and it is tempting to believe that the very high carbohydrate intake amoung young sailors entering the Navy may be responsible for some of the 18 cases of unknown ttiology in our series. Confectionery consumption by nuclear submarine crews is twice to four times the national average of 6.5 ounces (184 g) per week (Watt 1972). The Pima American Indians have a high prevalence of diabetes mellitus and Levine et al. (1970) found 61 % of cases with asymptomatic parotid enlargement, but no greater frequency among diabetics than nondiabetics matched for age, sex and obesity. Silverman (1975) found asymptomatic bilateral parotid swellings sometimes preceding clinical diabetes and often accompanied by dental caries. Sudden parotid enlargement occurred as part of the 'aedema syndrome' in 3-5 O of Ugandan diabetics on insulin therapy in whom 'irregular dietary patterns and consequent insulin overdosage' was present (Shaper 1966). Alcoholism is a frequent cause of parotid swelling, particularly when associated with hepatic and pancreatic dysfunction. Mandell & Baurmash (1971) reported 3 cases. Fatty infiltration of the parotid was seen in biopsy material from one which they attributed to disturbed lipid metabolism. Parotitis associated with recurrent pancreatitis in a United States marine with a high alcohol intake was described by Isenberg & Boyle (1968). Before the ending of the spirit ration in the Royal Navy, pancreatitis was considerably more common than it is today. Parotid enlargement occurred in 30 % of Borsanyi & Blanchard's (1961) alcoholic cirrhotics but not in nonalcoholic cirrhotics. Since pancreatic disease is often associated, they attributed the parotid response to a common embryological development.
Miscellaneous 'Sialectasis' is no longer regarded as an entity, 'merely a stage in the evolution of parotid struc-
485
tural damage' (Maynard 1965), but masseteric hypertrophy, found in 1 naval case, is a diagnostic pitfall. Cysts may be congenital, obstructive or parasitic. Work & Hecht (1968) and Shaheen et al. (1975) separately described dermoid inclusions which form cholesteatoma-like masses and branchial cysts derived from the first branchial pouch, having a thin capsule lined by squamous epithelium filled with clear fluid. Salivary collections are the feature of traumatic cysts which may be associated with fistulae. One naval case was in this category. Inflammatory cysts are due either to inflammation in preexisting cysts or breakdown of lymphoid tissue within the substance of the gland; Hooper et al. (1975) described a cyst secondary to a root abscess. There were 4 naval cases of pneumoparotitis. One could perform the trick at will. His initial sialogram revealed a dilated right main duct with only the anteroinferior portion of the duct system outlined. He persisted in inflating his parotid until infection supervened. He finally developed gross surgical emphysema of the right side of his face and parotidectomy was performed. Although cured he subsequently developed abnormal behaviour patterns requiring psychiatric treatment. A diver developed swelling following decompression and a sailor reported recurrent unilateral swelling after watchkeeping in a compartment where the atmospheric pressure was 2.5 to 7 lbf/in2 (17.2548.3 kPa) above ambient. The fourth was a bugler. Pneumoparotitis is a rare condition. Rysenaer et al. (1963) reported it in glassblowers and Saunders (1973) described 4 cases in players of wind instruments. A number of patients with recurrent parotid swellings have demonstrated excessive anxiety, a state also associated with xerostomia. The first naval case was self-induced, there was a strong psychological overlay and he first presented following a period of xerostomia induced by antiseasickness tablets.
Conclusion The one common factor associated with the innumerable causes of benign parotid enlargement is xerostomia which influences the quantity and quality of parotid secretion and thus paves the way for duct obstruction and pyogenic infection.
REFERENCES Anderson K A
(1972) British Medical Journal ii, 766 Banks P (1968) Oral Surgery, Oral Medicine, Oral Pathology 25, 732-745 Bark C J & Perzik S L (1968) American Journal of Clinical Pathology 49, 683-689 Beck A (1942) Surgery, Gynecology and Obstetrics 74, 604-675
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Proc. roy. Soc. Med. Volume 70 July 1977
Blatt I M (1964) Laryngoscope 74, 1684-1746 Borsanyi S J & Blanchard C L (1961) Southern Medical Journal 54, 678-682 Chandra K, Ratnakar C, Ramachandran P C & Parkash S (1971) Journal of Laryngology & Otology 85, 1083-1085 Cone R B (1966) Laryngoscope 76, 561-562 Davies J N P (1948) Lancet i, 317-320 Dishon T, Rosemann J, Sela J, Ulmansky M & Boss J H (1974) Immunology 26, 145-153 Duff T B (1972) Journal of Laryngology & Otology 86, 161-165 Fontoynont M (1911) Presse Medicale 19, 455-459 Furstenberg A C & Blatt I M (1968) Laryngoscope 78, 1165-1181 Grahame R & Lessof M H (1975) In: Conybeare's Textbook of Medicine, 16th edition. Ed. W N Mann. Churchill Livingstone, Edinburgh & London; p 792 Greenberg G, Anderson R, Sharpstone P & James D G (1964) British Medical Journal ii, 861-862 Harris D L (1971) British Journal of Surgery 58, 861 Hooper R, Saxon R & Tropp A (1975) Journal of Laryngology & Otology 89, 427-433 Howlett J G, Somlo F & Katz F (1957) Canadian Medical Association Journal 77, 5-7 Imbur D J & Bourne R B (1972) Journal of Urology 108, 629-630 Isenberg J & Boyle J D (1968) Gastroenterology 55, 277-281 Jastak R (1967) Henry Ford Hospital Medical Journal 15, 259-261 Joffe N (1967) American Journal oJ Roentgenology, Radium Therapy and Nuclear Medicine 100, 656-663 Jones H E (1953) Archives of Disease in Childhood 28, 182-186 Levine S B, Sampliner R E, Bennett P H, Rushforth N B, Burch T A & Miller M (1970) Annals of Internal Medicine 73, 571-573 Lewis J M & Utz J P (1961) New England Journal of Medicine 265, 776-780 McCance R A, Dean R F A & Barrett A M (1951) Medical Research Council Special Report Series No. 275 Mandell L & Baurmash H (1971) Journal of the American Dental Association 82, 369-373 May M, Lucente F E & Farrell F W (1973) Laryngoscope 83, 2020-2023 Maynard J D (1965) British Journal of Surgery 52, 784-789 Nicholson G W (1923) Guy's Hospital Reports 73, 43-46 Patey D H (1965) Annals of the Royal College of Surgeons 36, 26-44 Patey D H & Thackray A C (1955) British Journal of Surgery 43, 43-50 Payne R T (1933) Lancet i, 348-353 Pearson R S B (1961) Gut 2, 210-217 (1969) Practitioner 203, 41-48 Reilly D J (1970) Anarsthesia and Analgesia Current Researches 49, 560-563 Riley H D (1956) Southern Medical Journal 49, 523-528 Rose S S (1954) Annals of the Royal College of Surgeons 15, 374-401 Rysenaer L, Van Deinse J B E & Stuyt L B J (1963) Practica oto-rhino-laryngologica 25, 128 Sandford J P & Sulkin S E (1959) New England Journal of Medicine 261, 1113-1122 Saunders H F (1973) New England Journal of Medicine 289, 698
Shaheen N A, Harboyan G T & Nassif R I (1975) Journal of Laryngology & Otology 89, 435-444 Shaper A G (1966) British Medical Journal i, 803 Silverman D E (1975) Journal oJ the American Medical Association 232, 20 Silverman M & Perkins R L (1966) Annals oJ lnternal Medicine 64, 842-846
Sjogren H
(1933) Acta ophthalmologica Suppl. 2, 1-151 Smith M (1953) British Medical Journal ii, 1359 Spiers C F & Mason D K (1972) Scottish Medical Journal 17, 62-66 Watt J
(1972) Journal of the Royal Naval Medical Service 58, 12-34 Work W P & Hecht D W (1968) Annals oJ Otology, Rhinology & Laryngology, 77, 462-467 Yonkers A J, Krous H F & Yarington C T (1972) Laryngoscope 82, 1239-1247
Early Diagnosis and Pitfalls in Diagnosis of Aseptic Bone Necrosis in Divers by Surg. Rear Admiral J A B Harrison QHP FRCR (Institute of Naval Medicine, Alverstoke, Gosport, Hampshire, P012 2DL) The purpose of this presentation is to define the criteria by which it is possible to make an early definitive radiological diagnosis of the bone lesions of dysbaric osteonecrosis in divers, and to define the common pitfalls in making such a diagnosis. The main difficulty in the accurate early diagnosis of the lesions is twofold: is the radiological appearance a variant of normal bone structure - or perhaps a minor dysplasia of bone; or is it aseptic bone necrosis caused by something other than a dysbaric environment? In divers working under controlled decompression the lesions we have found are early and diagnosis is based on changes in trabecular structure with areas of increased, or more rarely decreased, density which in the juxta-articular lesions occur close to the articular surface which may collapse. In divers shaft lesions predominate and in these the changes occur in medullary bone. The lesions are usually symptomless when first detected and are often multiple. In view of the complexity of the tissue structure of bone it is not surprising that its macroscopic appearances as displayed by radiology shows considerable variation. It is the differentation of early pathological densities and lucencies from the normal variants in both trabecular bone structure and in cortical bone which presents the major problem of radiological diagnosis. It is a greater problem than the differentiation of the pathological
483
United Services Section President Howard Hanley CBE FRCS
Meeting 7 October 1976
Papers Benign Parotid Swellings: a Review by Surgeon Vice Admiral Sir James Watt FRCS FRCP (Ministry of Dejence, Empress State Building, London SW6 I TR) Parotid swelling may disguise a diverse and obscure etiology. A classification is proposed in Table 1, based upon analysis of 70 naval cases for the years 1959-1975. Table I Benign parotid enlargement
(1) Congenital anomalies (2) Trauma (3) Duct Obstruction (4) Infection (a) Acute: (i) Pyogenic (ii) Viral (b) Chronic: (i) Postobstructive (ii) Specific
(5) Allergic and auto-allergic reactions (6) Disorders of nutrition (7) Miscellaneous (a) 'Sialectasis'
(b) Cysts
(c) Masseteric hypertrophy (d) Pneumoparotitis
Congenital Anomalies Jones (1953) described congenital ectodermal dysplasia associated with dry mouth and ascending parotid infection in 2 orphan brothers. Smith (1953) found three generations of a family with radiological evidence of duct dilatation, and Pearson (1961) had two pairs of siblings with parotid swelling and terminal duct dilatation. Rose (1954) considered the duct dilatation congenital and the cause of recent secondary infection in 10 children, but Nicholson (1923) attributed duct obstruction
to pressure by congenital excess of lymphoid tissue in the gland parenchyma. Congenital dermoid inclusions and cysts have been described and May et al. (1973) reported an arteriovenous malformation with associated facial palsy.
Trauma Parotid swelling may result from extra- or intraoral trauma. Joffe's 17 South African cases were caused by knife wounds, road traffic accidents and blunt trauma, occasionally followed by cysts and fistulk (Joffe 1967). One naval case resulted from a direct blow; another, following intensive rifle practice, was associated with tinnitus, deafness and temporal headache. Sialadenopathy may result from cedema of the duct orifice caused by ill-fitting dentures in adults (Furstenberg & Blatt 1968). In children, when the third molar tooth erupts, the parotid papilla is traumatized as it is sucked between the teeth when food is chewed on the opposite side (Rose 1954). Parotid swelling in 2 naval cases followed dental treatment which presumably caused papillary cedema. Duct Obstruction Apart from trauma, duct obstruction may be caused by calculus, stricture, food (Cone 1966), and mucus secretion (Patey 1965). Swelling of the duct epithelium also occurs as an allergic response and in the 'sicca' or Sj0gren syndrome, Patey & Thackray (1955) have described lymphoid tissue in and around intralobar ducts which breaches the walls and allows radiopaque dye to escape during sialography, causing 'punctate sialectasis'. Mucous plugs obstructing the terminal duct may be discharged explosively into the mouth with a stream of clear or turbid saliva. Calculus is rare in the parotid and occurred in only 3 of Rose's 75 cases (Rose 1954) and 4 of 70 naval cases. Rose believes aggregates of cellular debris and coagulated mucin with or without microorganisms form the essential organic nidus.
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Proc. roy. Soc. Med. Volume 70 July 1977
Calcium deposition depends upon infection by ammoniacal organisms which raise the pH. Calculi occur at the sigmoid bend where the duct enters the mouth or at the anterior border of the masseter. Obstruction and consequent diminished secretion lead to infection, multiple strictures and cysts. Parotid massage produces a sluggish salivary flow and a cord-like Stenson's duct may be palpable. Sialography reveals dilated segments alternating with strictures and metaplastic duct epithelium with stricture formation seen in biopsy material (Furstenberg & Blatt 1968). Pyogenic Infection In children, males predominate and infection ascends from mouth or postnasal space (Jones 1953). Females predominate in recurrent pyogenic infections of adults (Payne 1933). The duct orifice is inflamed and drips pus, infecting organisms being Strep. viridans, pneumococcus, Staph. aureus, haemolytic streptococcus a'nd Staph. albus (Pearson 1961). Sialograms may be normal or show terminal duct obstruction. The length and shape of the duct and rate of salivary flow normally prevent infection and xerostomia predisposes (Blatt 1964). Acute septic parotitis is apparently on the increase. Spiers & Mason (1972) believe antihistamines, anticholinergics, hypotensive'drugs, certain tranquillizers and sedatives are more important in causing xerostomia than the dehydration formerly responsible. Yonkers et al. (1972) blamed poor oral hygiene. Duff (1972) reported facial palsy associated with a parotid abscess and Harris (1971) discussed 41 cases of unilateral acute suppurative parotitis secondary to virus infections in Uganda, of which 10 were due to Coxsackie virus B.
Viral Infections Howlett et al. (1957) have also implicated the Coxsackie virus, Sandford & Sulkin (1959) the ECHO virus, 'and Anderson (1972) has suggested mycoplasma. Riley (1956) claims recurrent mumps infection is rare and the parotid swelling a hypersensitivity reaction to the mumps virus, and Dishon et al. (1974) have reported acute parotitis in sensitized rats following a single intraductal challenge with the sensitizing antigen, but nonreactivity when multiple intraductal challenges were given. Lewis & Utz (1961) ascribed parotid swelling in an American naval patient to lymphocytic-choriomeningitis virus, and it is seen in glandular fever. Banks (1968) suggests that the common result of virus infections, sensitivity and autoimmune reactions is diminished secretion leading to retrograde infection, mucous metaplasia in duct walls, recurrent duct obstruction, infection and swelling. The condition is reversible until main duct changes occur with secondary stricture and calculus.
Chronic Infections Chronic infections may follow obstruction, sialography revealing beading and dilatation of the ducts, globular or cavitary collections of opaque medium or generalized destruction of duct and gland structure. Specific infections are rare and include tuberculosis, actinomycosis, rhinosporidiosis (Chandra et al. 1971), brucellosis and bacillary dysentery (Borsanyi & Blanchard 1961). Greenberg et al. (1964) found parotitis in 23 (6 %) of 388 patients suffering from sarcoid. Thirteen were women. Kveim test was positive in 770 and Mantoux negative in 81 %. The condition is usually bilateral and there may be palsy of the facial nerve. Allergic and Auto-allergic Reactions Swelling appeared after intravenous pyelography, exposure to paint and eating cabbage in 1 naval case. A patient of Pearson (1969), a life-long asthmatic, developed parotitis and flushing of the face after eating cheese or milk. It was accompanied by migraine in another and followed the eating of eggs (Pearson 1961). Such patients were almost exclusively women of middle age or beyond. Pressure over the gland expelled a plug of mucus containing numerous eosinophils and clear saliva. The main parotid duct was markedly dilated. Three of Jones' (1953) patients had a family history of allergy and 2 mothers had suffered recurrent parotid swelling during adolescence. In 1933, Sj0gren described parotid enlargement associated with dry eyes and mouth and rheumatoid arthritis. Its etiology is obscure and may be associated with other connective tissue disorders: scleroderma, polyarteritis nodosa and polymyositis. Rheumatoid factor is present in most cases and antinuclear factor in about two-thirds, thyroid and gastroparietal autoantibodies are also encountered and gammaglobulins are increased (Grahame & Lessof 1975). On long-term follow up, Bark & Perzik (1968) have found a significant number of patients with disabling and fatal autoimmune diseases such as systemic lupus erythematosus. Of the 41 patients in Blatt's (1964) series, 20 had rheumatoid arthritis or polyarthralgia and 13 keratoconjunctivitis. The swelling of duct epithelium reported by Maynard (1965) appears part of the same immune response. Any hypersensitivity reaction causing xerostomia invites sialadenopathy, which has occurred after eating oysters and shrimps, poisoning by lead and mercury (Beck 1942), following excretory pyelography (Imbur & Bourne 1972) and general anesthesia. Reilly (1970) concluded that belladonna, depolarizing neuromuscular-blocking drugs, succinylcholine, straining, coughing and the Valsalva manceuvre contributed, and found that Negroes were specially susceptible.
United Services Section Disorders of Nutrition Parotid swelling has occurred in emaciated prisoners of war returning to a normal diet. McCance et al. (1951) reported associated gynaecomastia, possibly from temporarily impaired liver function. Parotid swelling in kwashiorkor is regarded as a sign of recovery (Davies 1948). Silverman & Perkins (1966) found bilateral enlargement in obstetric cases, eating corn starch and white or red clay, of whom 880% were Negroes; Jastak (1967) reported parotitis in a 51-year-old diabetic woman who had eaten 12-16 ounces (340-453 g) of starch daily for ten years. Biopsies in other cases showed either increased zymogen storage or increase in granules and he postulated initial stimulation leading to later depletion. Fontoynont (1911) mentions parotid swelling in Madagascan farmers who subsisted on a diet of potatoes and rice, and it is tempting to believe that the very high carbohydrate intake amoung young sailors entering the Navy may be responsible for some of the 18 cases of unknown ttiology in our series. Confectionery consumption by nuclear submarine crews is twice to four times the national average of 6.5 ounces (184 g) per week (Watt 1972). The Pima American Indians have a high prevalence of diabetes mellitus and Levine et al. (1970) found 61 % of cases with asymptomatic parotid enlargement, but no greater frequency among diabetics than nondiabetics matched for age, sex and obesity. Silverman (1975) found asymptomatic bilateral parotid swellings sometimes preceding clinical diabetes and often accompanied by dental caries. Sudden parotid enlargement occurred as part of the 'aedema syndrome' in 3-5 O of Ugandan diabetics on insulin therapy in whom 'irregular dietary patterns and consequent insulin overdosage' was present (Shaper 1966). Alcoholism is a frequent cause of parotid swelling, particularly when associated with hepatic and pancreatic dysfunction. Mandell & Baurmash (1971) reported 3 cases. Fatty infiltration of the parotid was seen in biopsy material from one which they attributed to disturbed lipid metabolism. Parotitis associated with recurrent pancreatitis in a United States marine with a high alcohol intake was described by Isenberg & Boyle (1968). Before the ending of the spirit ration in the Royal Navy, pancreatitis was considerably more common than it is today. Parotid enlargement occurred in 30 % of Borsanyi & Blanchard's (1961) alcoholic cirrhotics but not in nonalcoholic cirrhotics. Since pancreatic disease is often associated, they attributed the parotid response to a common embryological development.
Miscellaneous 'Sialectasis' is no longer regarded as an entity, 'merely a stage in the evolution of parotid struc-
485
tural damage' (Maynard 1965), but masseteric hypertrophy, found in 1 naval case, is a diagnostic pitfall. Cysts may be congenital, obstructive or parasitic. Work & Hecht (1968) and Shaheen et al. (1975) separately described dermoid inclusions which form cholesteatoma-like masses and branchial cysts derived from the first branchial pouch, having a thin capsule lined by squamous epithelium filled with clear fluid. Salivary collections are the feature of traumatic cysts which may be associated with fistulae. One naval case was in this category. Inflammatory cysts are due either to inflammation in preexisting cysts or breakdown of lymphoid tissue within the substance of the gland; Hooper et al. (1975) described a cyst secondary to a root abscess. There were 4 naval cases of pneumoparotitis. One could perform the trick at will. His initial sialogram revealed a dilated right main duct with only the anteroinferior portion of the duct system outlined. He persisted in inflating his parotid until infection supervened. He finally developed gross surgical emphysema of the right side of his face and parotidectomy was performed. Although cured he subsequently developed abnormal behaviour patterns requiring psychiatric treatment. A diver developed swelling following decompression and a sailor reported recurrent unilateral swelling after watchkeeping in a compartment where the atmospheric pressure was 2.5 to 7 lbf/in2 (17.2548.3 kPa) above ambient. The fourth was a bugler. Pneumoparotitis is a rare condition. Rysenaer et al. (1963) reported it in glassblowers and Saunders (1973) described 4 cases in players of wind instruments. A number of patients with recurrent parotid swellings have demonstrated excessive anxiety, a state also associated with xerostomia. The first naval case was self-induced, there was a strong psychological overlay and he first presented following a period of xerostomia induced by antiseasickness tablets.
Conclusion The one common factor associated with the innumerable causes of benign parotid enlargement is xerostomia which influences the quantity and quality of parotid secretion and thus paves the way for duct obstruction and pyogenic infection.
REFERENCES Anderson K A
(1972) British Medical Journal ii, 766 Banks P (1968) Oral Surgery, Oral Medicine, Oral Pathology 25, 732-745 Bark C J & Perzik S L (1968) American Journal of Clinical Pathology 49, 683-689 Beck A (1942) Surgery, Gynecology and Obstetrics 74, 604-675
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Blatt I M (1964) Laryngoscope 74, 1684-1746 Borsanyi S J & Blanchard C L (1961) Southern Medical Journal 54, 678-682 Chandra K, Ratnakar C, Ramachandran P C & Parkash S (1971) Journal of Laryngology & Otology 85, 1083-1085 Cone R B (1966) Laryngoscope 76, 561-562 Davies J N P (1948) Lancet i, 317-320 Dishon T, Rosemann J, Sela J, Ulmansky M & Boss J H (1974) Immunology 26, 145-153 Duff T B (1972) Journal of Laryngology & Otology 86, 161-165 Fontoynont M (1911) Presse Medicale 19, 455-459 Furstenberg A C & Blatt I M (1968) Laryngoscope 78, 1165-1181 Grahame R & Lessof M H (1975) In: Conybeare's Textbook of Medicine, 16th edition. Ed. W N Mann. Churchill Livingstone, Edinburgh & London; p 792 Greenberg G, Anderson R, Sharpstone P & James D G (1964) British Medical Journal ii, 861-862 Harris D L (1971) British Journal of Surgery 58, 861 Hooper R, Saxon R & Tropp A (1975) Journal of Laryngology & Otology 89, 427-433 Howlett J G, Somlo F & Katz F (1957) Canadian Medical Association Journal 77, 5-7 Imbur D J & Bourne R B (1972) Journal of Urology 108, 629-630 Isenberg J & Boyle J D (1968) Gastroenterology 55, 277-281 Jastak R (1967) Henry Ford Hospital Medical Journal 15, 259-261 Joffe N (1967) American Journal oJ Roentgenology, Radium Therapy and Nuclear Medicine 100, 656-663 Jones H E (1953) Archives of Disease in Childhood 28, 182-186 Levine S B, Sampliner R E, Bennett P H, Rushforth N B, Burch T A & Miller M (1970) Annals of Internal Medicine 73, 571-573 Lewis J M & Utz J P (1961) New England Journal of Medicine 265, 776-780 McCance R A, Dean R F A & Barrett A M (1951) Medical Research Council Special Report Series No. 275 Mandell L & Baurmash H (1971) Journal of the American Dental Association 82, 369-373 May M, Lucente F E & Farrell F W (1973) Laryngoscope 83, 2020-2023 Maynard J D (1965) British Journal of Surgery 52, 784-789 Nicholson G W (1923) Guy's Hospital Reports 73, 43-46 Patey D H (1965) Annals of the Royal College of Surgeons 36, 26-44 Patey D H & Thackray A C (1955) British Journal of Surgery 43, 43-50 Payne R T (1933) Lancet i, 348-353 Pearson R S B (1961) Gut 2, 210-217 (1969) Practitioner 203, 41-48 Reilly D J (1970) Anarsthesia and Analgesia Current Researches 49, 560-563 Riley H D (1956) Southern Medical Journal 49, 523-528 Rose S S (1954) Annals of the Royal College of Surgeons 15, 374-401 Rysenaer L, Van Deinse J B E & Stuyt L B J (1963) Practica oto-rhino-laryngologica 25, 128 Sandford J P & Sulkin S E (1959) New England Journal of Medicine 261, 1113-1122 Saunders H F (1973) New England Journal of Medicine 289, 698
Shaheen N A, Harboyan G T & Nassif R I (1975) Journal of Laryngology & Otology 89, 435-444 Shaper A G (1966) British Medical Journal i, 803 Silverman D E (1975) Journal oJ the American Medical Association 232, 20 Silverman M & Perkins R L (1966) Annals oJ lnternal Medicine 64, 842-846
Sjogren H
(1933) Acta ophthalmologica Suppl. 2, 1-151 Smith M (1953) British Medical Journal ii, 1359 Spiers C F & Mason D K (1972) Scottish Medical Journal 17, 62-66 Watt J
(1972) Journal of the Royal Naval Medical Service 58, 12-34 Work W P & Hecht D W (1968) Annals oJ Otology, Rhinology & Laryngology, 77, 462-467 Yonkers A J, Krous H F & Yarington C T (1972) Laryngoscope 82, 1239-1247
Early Diagnosis and Pitfalls in Diagnosis of Aseptic Bone Necrosis in Divers by Surg. Rear Admiral J A B Harrison QHP FRCR (Institute of Naval Medicine, Alverstoke, Gosport, Hampshire, P012 2DL) The purpose of this presentation is to define the criteria by which it is possible to make an early definitive radiological diagnosis of the bone lesions of dysbaric osteonecrosis in divers, and to define the common pitfalls in making such a diagnosis. The main difficulty in the accurate early diagnosis of the lesions is twofold: is the radiological appearance a variant of normal bone structure - or perhaps a minor dysplasia of bone; or is it aseptic bone necrosis caused by something other than a dysbaric environment? In divers working under controlled decompression the lesions we have found are early and diagnosis is based on changes in trabecular structure with areas of increased, or more rarely decreased, density which in the juxta-articular lesions occur close to the articular surface which may collapse. In divers shaft lesions predominate and in these the changes occur in medullary bone. The lesions are usually symptomless when first detected and are often multiple. In view of the complexity of the tissue structure of bone it is not surprising that its macroscopic appearances as displayed by radiology shows considerable variation. It is the differentation of early pathological densities and lucencies from the normal variants in both trabecular bone structure and in cortical bone which presents the major problem of radiological diagnosis. It is a greater problem than the differentiation of the pathological
