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Acute suppurative parotitis: A forgotten cause of upper airway obstruction
Acute suppurative parotitis: A forgotten cause of upper airway obstruction Peter R. Saunders, FFARCS, DRCOG,a and David W. Macpherson, FDSRCS, FRCS(Edin),b London, England THE
ROYAL
LONDON
HOSPITAL
AND
ST. GEORGE’S
HOSPITAL
A patient had threatened upper airway obstruction as a result of bilateral acute suppurative parotitis. Because of the rarity of this condition in recent times, accurate diagnosis was delayed and fiber-optic intubation in the intensive care unit was required to safeguard the airway. Management is described with reference to the surgical anatomy and previously reported cases.
(ORAL SURC ORAL MED ORAL PATHOL 1991;72:412-4)
T
he incidence and associated morbidity and mortality of suppurative parotitis have been dramatically reduced in recent years. This is the result of improved control of fluid and electrolyte balance, the advent of antibiotics, and especially the evolution of the semisynthetic penicillins effective against Staphylococcus aureus, the most common causal organism. The decreasedincidence of this condition may have led to an increased failure to recognize it when it does occur, so that it may still be allowed to take its clinical course without specific treatment. This can then lead to potentially lethal complications such as severe edema of the face and neck with glottic obstruction.’ In this case such a sequenceof events was likely and it became necessary to safeguard the airway by nasotracheal intubation with a fiber-optic bronchoscope. CASE REPORT
A 42-year-old, 77 kg woman was admitted to the hospital for elective total abdominal hysterectomy. She had a history of menorrhagia with secondary iron deficiency anemia, which had been treated successfully with iron tablets, and her preoperative hemoglobin level was 11.7 gm/dl. Her blood pressure was 130/90 mm Hg, and her heart rate was 86 beatslmin. Anesthesia and surgery were %eniorRegistrar,Departmentof Anaesthetics,TheRoyalLondon Hospital, Whitechapel. bSeniorRegistrar,Departmentof Oral andMaxillofacial Surgery, St. George’sHospital. 7/12/26894
412
uneventful, blood loss was minimal, and the blood pressure and heart rate remained stable. However, 2 hours postoperatively she had an episode of hypotension, with a blood pressure of 80/50 mm Hg and a heart rate of 120 beats/min, which respondedtemporarily to polygeline (Haemaccel). Six hours postoperatively she had a further hypotensive episode,and on this occasionpulsatile bleeding was observed through the abdominal incision. Exploratory laparotomy showed brisk hemorrhage from the right uterine artery. Successful hemostasis was achieved, but her perioperative hemoglobin level was now found to be 5.2 gm/dl, and 6 units of blood were transfused in addition to colloid and crystalloid solutions. On the third postoperative day she becamefebrile with a temperature of 39.5” C. Firm, tender, bilateral preauricular swellings were noted, which 12 hours later had progressedto involve the submandibular region and the neck in addition to the face. The patient was anxious and had difficulty in breathing, which was improved by sitting up. Clinically, she was dyspneic but acyanotic and well hydrated. Examination revealed normal vesicular breathe sounds and no inspiratory stridor. Acute angioneurotic edema and hereditary angioedema were considered as potential diagnoses. Parotitis was also considered, but was thought unlikely because of the bilateral nature of the swelling. Edema of the glottis can be associatedwith all three conditions, and becauseof the rapidly spreading edema of the face and neck, it was decided to transfer the patient to the intensive care unit for elective tracheal intubation to safeguard the airway. A fiber-optic bronchoscope and an anesthetic machine were prepared. The patient was monitored with an electrocardiograph, a blood pressure monitor, and a pulse oxime-
Acute suppurative parotitis
Volume72 Number 4 ter; a 16-gaugecannula was already in situ. A surgeon with a tracheostomy set was at hand. The patient was given 0.25 mg glycopyrrolate and 8 mg dexamethasoneintravenously. She then inhaled 2 ml of 4% lidocaine through a nebulizer, and 2 ml of 2% lidocaine was instilled into each nostril. After preoxygenation with 100% oxygen for 3 minutes, 2.5 mg midazolam was given intravenously. The patient was then successfully intubated through the right nostril with a 6.5 mm cuffed nasal endotracheal tube with a fiber-optic bronchoscope. During the next 72 hours steroid treatment was continued in reducing doses,and the swellings diminished in size such that only bilateral parotid swellings remained. During this time blood was examined for paramyxovirus and coxsackievirus titers, bacterial culture, and complement fixation tests. Hemoglobin level was 13 gm/dl, and leukocyte count was 13.5 X 109/L, with 95% granulocytes. On the postoperative day 6, blood cultures were positive for S. aureus, and floxacillin, 500 mg 4 times daily intravenously, was introduced. At this time pus was expressed from both parotid ducts, which also grew S. aureus(Fig. 1). During the next 4 days the parotid swellings gradually subsided, and although her general condition continued to improve, pus could still be expressedfrom the parotid ducts. She was discharged 12 days postoperatively. DISCUSSION
Acute suppurative parotitis has probably been known since the time of Hippocrates? but it was not differentiated from mumps until 1834, by Brodie.3 Yonkers et a1.4cite that Cruveilhier in 1836 gave the first clinically accurate description and proposedthat it was caused by infection that ascended from the mouth after suppression of salivary flow. In 1881 US. President JamesA. Garfield sustained an abdominal gunshot wound in an assassination attempt and, after abdominal surgery, died 10 weeks later from the complications of suppurative parotitis.5 By the late 1930s better understanding of fluid therapy, electrolyte balance, and general surgical care resulted in a marked decreasein the incidence of this disease,and the advent of the sulfonamides and penicillin in the 1940s led to its virtual eradication. This led Robinson6 in 1955 to describe surgical parotitis as a vanishing disease. Unfortunately, the indiscriminate use of antibiotics resulted in the resurgence of acute suppurative parotitis caused by antibiotic-resistant S. aureus with a mortality rate of 30%~~This may have coincided with an increase in the number of older surgical patients. Byars* reintroduced the original technique of incision and drainage described in 1923 by Blair and Padgett9 and modified it to preserve the facial nerve. Prompt treatment significantly reduced the associated morbidity and mortality rate. to In the 1960sthe advent of
413
Fig. 1. Pus draining from left parotid duct.
semisynthetic penicillins active against penicillinaseproducing staphylococci once again enabled control of suppurative parotitis. Surgical anatomy
The parotid gland is normally protected from infection by the flushing effect of free-flowing serous secretions and by the spiral configuration of the duct, which hinders the retrograde movement of oral microflora. The parotid is a purely serous gland and secretes no bacteriostatic mucin. It is therefore especially susceptible to retrograde infection from the staphylococci colonizing in the duct when the flow of secretion is diminished. The gland is ensheathedin a strong fibrous capsule formed by the splitting of the superficial layer of the deep cervical fascia. Dense septa separate its lobules, and adequate drainage through the duct may therefore be impossible, especially when multiple abscesses occur deep in the gland. The tense capsule may prevent the development of fluctuation as a sign of suppuration. The only weaknessin this fascial capsule is adjacent to the loose areolar tissue of the lateral pharyngeal wall, which extends superiorly to the base of the skull and inferiorly to the mediastinum. Respiratory obstruction, which may result from edema of the larynx or pharynx, or from rupture of a parotid abscessinto the lateral pharyngeal wall, and septicemia are the most common sequelae.Pneumonia may follow aspiration of pus. Acute suppurative parotitis usually affects older, malnourished, and dehydrated postoperative patients. Drugs with diuretic and/or anticholinergic properties, such as phenothiazines and antidepressants, may contribute to its onset. The condition usually presents
4 14 Saunders and Macpherson
after the second postoperative day, with pain, fever, and swelling, and is bilateral in 20% of cases.5 No preoperative predisposing factors that might have made her more susceptible to acute suppurative parotitis were present in our patient. She was a fit, well-nourished, middle-aged woman undergoing a routine elective procedure. Delay in the recognition of postoperative hypovolemia and the need for her to undergo another laparotomy probably contributed to the onset of the condition. When caused by S. aureus it usually progresses quickly, with rapidly spreading edemaof the face and neck. In our patient the condition was bilateral, which is uncommon, and this may have delayed early diagnosis and the prompt start of appropriate treatment. The differential diagnosis might have been resolved earlier by observation of purulent exudate from the opening of Stensen’sduct, either spontaneously or as the result of catheterization and irrigation’ * and bacteriologic identification of the causal organism. In a situation where the patency of the airway is being progressively threatened and where a definitive diagnosis has yet to be made, the airway must be secured without delay. Although steroid therapy had significantly reduced the swelling, it had disguised the underlying diagnosis, which was made only after the patient had been extubated. Leukocytosis and neutrophilia are commonly seenpostoperatively and were not a basis on which the diagnosis of acute suppurative parotitis could have been made, although the presence of pronounced granulocytosis should have suggestedthat the underlying cause was an infective one. Steroids attenuate the normal responseto infection, and this patient showed only a mild fluctuant pyrexia, thus disguising the potential seriousnessof the condition. Treatment of the infection was given as a result of finding a positive blood culture rather than of making the correct specific diagnosis. This was
ORAL SL’RGORAL MED ORAL PATHCII October 199I
made only subsequently when pus was observed draining bilaterally from Stensen’s duct. Acute suppurative parotitis is an uncommon complication of surgery. Nonetheless, it remains a potentially lethal condition and in this case occurred in a previously healthy, relatively young patient after a routine elective procedure. Fortunately, the introduction of steroids, in the absenceof a definitive diagnosis, helped prevent the rapid progression of edemaand the threatened upper airway obstruction. However, earlier diagnosis of the underlying condition and introduction of appropriate antibiotics might have prevented this life-threatening complication. REFERENCES 1. Spratt JS. The etiology and therapy of acute pyogenic paroti-
tis. Surg Gynecol Obstet 1961;112:391-405. 2. Speirs CF, Mason DK. Acute septic parotitis: incidence, aeti-
ology and management. Scot Med J 1972;17:62-6. 3. Gustafson JR, Acute parotitis. Surgery 1951;29:786-801. 4. Yonkers AJ, Krous HF, Yarington CT. Surgical parotitis.
Laryngoscope 1972;82:1239-47. 5. Goldberg MH. Infections of the salivary glands. In: Topazian
RG, Goldberg MH, eds. Oral and maxillofacial infections. Philadelphia: WB Saunders, 1987:239-53. 6. Robinson JR. Surgical parotitis, a vanishing disease.Surgery 1955;38:703-7. 7. Carlson RG, Glas WW. Acute suppurative parotitis. Arch Surg 1963;86:163-7. 8. Byars LT. Preservation of the facial nerve in operations for benign conditions of the parotid area. Ann Surg 1952;136:41221. 9. Blair VP, Padgett EC. Pyogenic infection of the parotid glands
and ducts. Arch Surg 1923;7:1-36. 10. Krippaehne WW, Hunt TK, Dunphy JE. Acute suppurative parotitis, a study of 161 cases. Ann Surg 1962;156:251-7. 11. Goldberg MH, Harrigan WF. Acute suppurative parotitis. ORAL SURGORAL MED ORAL PATHOL1965;20:28l-6. Reprint requests:
D. W. Macpherson, FDSRCS, FRCS(Edin) 43 Tavistock Terr. London N19 4BZ, U.K.
ROYAL
LONDON
HOSPITAL
AND
ST. GEORGE’S
HOSPITAL
A patient had threatened upper airway obstruction as a result of bilateral acute suppurative parotitis. Because of the rarity of this condition in recent times, accurate diagnosis was delayed and fiber-optic intubation in the intensive care unit was required to safeguard the airway. Management is described with reference to the surgical anatomy and previously reported cases.
(ORAL SURC ORAL MED ORAL PATHOL 1991;72:412-4)
T
he incidence and associated morbidity and mortality of suppurative parotitis have been dramatically reduced in recent years. This is the result of improved control of fluid and electrolyte balance, the advent of antibiotics, and especially the evolution of the semisynthetic penicillins effective against Staphylococcus aureus, the most common causal organism. The decreasedincidence of this condition may have led to an increased failure to recognize it when it does occur, so that it may still be allowed to take its clinical course without specific treatment. This can then lead to potentially lethal complications such as severe edema of the face and neck with glottic obstruction.’ In this case such a sequenceof events was likely and it became necessary to safeguard the airway by nasotracheal intubation with a fiber-optic bronchoscope. CASE REPORT
A 42-year-old, 77 kg woman was admitted to the hospital for elective total abdominal hysterectomy. She had a history of menorrhagia with secondary iron deficiency anemia, which had been treated successfully with iron tablets, and her preoperative hemoglobin level was 11.7 gm/dl. Her blood pressure was 130/90 mm Hg, and her heart rate was 86 beatslmin. Anesthesia and surgery were %eniorRegistrar,Departmentof Anaesthetics,TheRoyalLondon Hospital, Whitechapel. bSeniorRegistrar,Departmentof Oral andMaxillofacial Surgery, St. George’sHospital. 7/12/26894
412
uneventful, blood loss was minimal, and the blood pressure and heart rate remained stable. However, 2 hours postoperatively she had an episode of hypotension, with a blood pressure of 80/50 mm Hg and a heart rate of 120 beats/min, which respondedtemporarily to polygeline (Haemaccel). Six hours postoperatively she had a further hypotensive episode,and on this occasionpulsatile bleeding was observed through the abdominal incision. Exploratory laparotomy showed brisk hemorrhage from the right uterine artery. Successful hemostasis was achieved, but her perioperative hemoglobin level was now found to be 5.2 gm/dl, and 6 units of blood were transfused in addition to colloid and crystalloid solutions. On the third postoperative day she becamefebrile with a temperature of 39.5” C. Firm, tender, bilateral preauricular swellings were noted, which 12 hours later had progressedto involve the submandibular region and the neck in addition to the face. The patient was anxious and had difficulty in breathing, which was improved by sitting up. Clinically, she was dyspneic but acyanotic and well hydrated. Examination revealed normal vesicular breathe sounds and no inspiratory stridor. Acute angioneurotic edema and hereditary angioedema were considered as potential diagnoses. Parotitis was also considered, but was thought unlikely because of the bilateral nature of the swelling. Edema of the glottis can be associatedwith all three conditions, and becauseof the rapidly spreading edema of the face and neck, it was decided to transfer the patient to the intensive care unit for elective tracheal intubation to safeguard the airway. A fiber-optic bronchoscope and an anesthetic machine were prepared. The patient was monitored with an electrocardiograph, a blood pressure monitor, and a pulse oxime-
Acute suppurative parotitis
Volume72 Number 4 ter; a 16-gaugecannula was already in situ. A surgeon with a tracheostomy set was at hand. The patient was given 0.25 mg glycopyrrolate and 8 mg dexamethasoneintravenously. She then inhaled 2 ml of 4% lidocaine through a nebulizer, and 2 ml of 2% lidocaine was instilled into each nostril. After preoxygenation with 100% oxygen for 3 minutes, 2.5 mg midazolam was given intravenously. The patient was then successfully intubated through the right nostril with a 6.5 mm cuffed nasal endotracheal tube with a fiber-optic bronchoscope. During the next 72 hours steroid treatment was continued in reducing doses,and the swellings diminished in size such that only bilateral parotid swellings remained. During this time blood was examined for paramyxovirus and coxsackievirus titers, bacterial culture, and complement fixation tests. Hemoglobin level was 13 gm/dl, and leukocyte count was 13.5 X 109/L, with 95% granulocytes. On the postoperative day 6, blood cultures were positive for S. aureus, and floxacillin, 500 mg 4 times daily intravenously, was introduced. At this time pus was expressed from both parotid ducts, which also grew S. aureus(Fig. 1). During the next 4 days the parotid swellings gradually subsided, and although her general condition continued to improve, pus could still be expressedfrom the parotid ducts. She was discharged 12 days postoperatively. DISCUSSION
Acute suppurative parotitis has probably been known since the time of Hippocrates? but it was not differentiated from mumps until 1834, by Brodie.3 Yonkers et a1.4cite that Cruveilhier in 1836 gave the first clinically accurate description and proposedthat it was caused by infection that ascended from the mouth after suppression of salivary flow. In 1881 US. President JamesA. Garfield sustained an abdominal gunshot wound in an assassination attempt and, after abdominal surgery, died 10 weeks later from the complications of suppurative parotitis.5 By the late 1930s better understanding of fluid therapy, electrolyte balance, and general surgical care resulted in a marked decreasein the incidence of this disease,and the advent of the sulfonamides and penicillin in the 1940s led to its virtual eradication. This led Robinson6 in 1955 to describe surgical parotitis as a vanishing disease. Unfortunately, the indiscriminate use of antibiotics resulted in the resurgence of acute suppurative parotitis caused by antibiotic-resistant S. aureus with a mortality rate of 30%~~This may have coincided with an increase in the number of older surgical patients. Byars* reintroduced the original technique of incision and drainage described in 1923 by Blair and Padgett9 and modified it to preserve the facial nerve. Prompt treatment significantly reduced the associated morbidity and mortality rate. to In the 1960sthe advent of
413
Fig. 1. Pus draining from left parotid duct.
semisynthetic penicillins active against penicillinaseproducing staphylococci once again enabled control of suppurative parotitis. Surgical anatomy
The parotid gland is normally protected from infection by the flushing effect of free-flowing serous secretions and by the spiral configuration of the duct, which hinders the retrograde movement of oral microflora. The parotid is a purely serous gland and secretes no bacteriostatic mucin. It is therefore especially susceptible to retrograde infection from the staphylococci colonizing in the duct when the flow of secretion is diminished. The gland is ensheathedin a strong fibrous capsule formed by the splitting of the superficial layer of the deep cervical fascia. Dense septa separate its lobules, and adequate drainage through the duct may therefore be impossible, especially when multiple abscesses occur deep in the gland. The tense capsule may prevent the development of fluctuation as a sign of suppuration. The only weaknessin this fascial capsule is adjacent to the loose areolar tissue of the lateral pharyngeal wall, which extends superiorly to the base of the skull and inferiorly to the mediastinum. Respiratory obstruction, which may result from edema of the larynx or pharynx, or from rupture of a parotid abscessinto the lateral pharyngeal wall, and septicemia are the most common sequelae.Pneumonia may follow aspiration of pus. Acute suppurative parotitis usually affects older, malnourished, and dehydrated postoperative patients. Drugs with diuretic and/or anticholinergic properties, such as phenothiazines and antidepressants, may contribute to its onset. The condition usually presents
4 14 Saunders and Macpherson
after the second postoperative day, with pain, fever, and swelling, and is bilateral in 20% of cases.5 No preoperative predisposing factors that might have made her more susceptible to acute suppurative parotitis were present in our patient. She was a fit, well-nourished, middle-aged woman undergoing a routine elective procedure. Delay in the recognition of postoperative hypovolemia and the need for her to undergo another laparotomy probably contributed to the onset of the condition. When caused by S. aureus it usually progresses quickly, with rapidly spreading edemaof the face and neck. In our patient the condition was bilateral, which is uncommon, and this may have delayed early diagnosis and the prompt start of appropriate treatment. The differential diagnosis might have been resolved earlier by observation of purulent exudate from the opening of Stensen’sduct, either spontaneously or as the result of catheterization and irrigation’ * and bacteriologic identification of the causal organism. In a situation where the patency of the airway is being progressively threatened and where a definitive diagnosis has yet to be made, the airway must be secured without delay. Although steroid therapy had significantly reduced the swelling, it had disguised the underlying diagnosis, which was made only after the patient had been extubated. Leukocytosis and neutrophilia are commonly seenpostoperatively and were not a basis on which the diagnosis of acute suppurative parotitis could have been made, although the presence of pronounced granulocytosis should have suggestedthat the underlying cause was an infective one. Steroids attenuate the normal responseto infection, and this patient showed only a mild fluctuant pyrexia, thus disguising the potential seriousnessof the condition. Treatment of the infection was given as a result of finding a positive blood culture rather than of making the correct specific diagnosis. This was
ORAL SL’RGORAL MED ORAL PATHCII October 199I
made only subsequently when pus was observed draining bilaterally from Stensen’s duct. Acute suppurative parotitis is an uncommon complication of surgery. Nonetheless, it remains a potentially lethal condition and in this case occurred in a previously healthy, relatively young patient after a routine elective procedure. Fortunately, the introduction of steroids, in the absenceof a definitive diagnosis, helped prevent the rapid progression of edemaand the threatened upper airway obstruction. However, earlier diagnosis of the underlying condition and introduction of appropriate antibiotics might have prevented this life-threatening complication. REFERENCES 1. Spratt JS. The etiology and therapy of acute pyogenic paroti-
tis. Surg Gynecol Obstet 1961;112:391-405. 2. Speirs CF, Mason DK. Acute septic parotitis: incidence, aeti-
ology and management. Scot Med J 1972;17:62-6. 3. Gustafson JR, Acute parotitis. Surgery 1951;29:786-801. 4. Yonkers AJ, Krous HF, Yarington CT. Surgical parotitis.
Laryngoscope 1972;82:1239-47. 5. Goldberg MH. Infections of the salivary glands. In: Topazian
RG, Goldberg MH, eds. Oral and maxillofacial infections. Philadelphia: WB Saunders, 1987:239-53. 6. Robinson JR. Surgical parotitis, a vanishing disease.Surgery 1955;38:703-7. 7. Carlson RG, Glas WW. Acute suppurative parotitis. Arch Surg 1963;86:163-7. 8. Byars LT. Preservation of the facial nerve in operations for benign conditions of the parotid area. Ann Surg 1952;136:41221. 9. Blair VP, Padgett EC. Pyogenic infection of the parotid glands
and ducts. Arch Surg 1923;7:1-36. 10. Krippaehne WW, Hunt TK, Dunphy JE. Acute suppurative parotitis, a study of 161 cases. Ann Surg 1962;156:251-7. 11. Goldberg MH, Harrigan WF. Acute suppurative parotitis. ORAL SURGORAL MED ORAL PATHOL1965;20:28l-6. Reprint requests:
D. W. Macpherson, FDSRCS, FRCS(Edin) 43 Tavistock Terr. London N19 4BZ, U.K.