1104
NECROTIZING
Table 1. Neurological Causes of Palatal and Pharyngeal Dysfunction (Cont’d) Myasthenia gravis Myasthenic-myopathic Muscle Dystrophy Oculopharyngeal Myotonic lnflammatory Poly/dermatomyositis
syndrome (Lambert-Easton)
jury is not mentioned in texts as a complication of general anesthesia.‘,12 Superficial injury from packs and large, cuffed endotracheal tubes has been cited as the major cause of post-oral surgery sore throat, but neurologic dysfunction has not been reported.13 References 1. DeJong RN: The Neurologic Examination York, Harper & Row. 1970
(3rd ed). New
2. Weiss K, Kramar R, Fit? P: Cranial and cervical nerve in-
J Oral Marillofac
SOFT-TISSUE
INFECTIONS
Local complications of carotid artery_ surgery. J I_ Cardiovasc Surg 28: 171, 1987 3. Sataloff RT, Myers DL, Kremer FB: Management of cranial nerve injury following surgery of the skull base. Otolaryngot Clin North Am 17577, 1984 4. Broomhead IW: The nerve supply to the nerves of the soft palate. Br .I Plastic Sure 4:l. 1951 5. Kerr AG, Groves J: Sco&Brown’s Otolaryngology, Basic Sciences, vol 1 (5th ed). London, Butterworths, 1987 6. English GM: Otolaryngology, vol 3. Philadelphia, PA, Lippincott, 1984 7. Hedden M, Eroz CJ, Donnelly WH, et al: Laryngotrachael damage after prolonged use of ortracheal tubes in adults. JAMA 207:203, 1969 8. Orkin FK, Cooperman LH: Complications in anesthesiology. Philadelphia, PA, Lippincott, 1983 9. Burke RH. Adams JL: Immediate cranial nerve uaralvsis during removal of a mandibular third molar. &al !&u-g Oral Med Oral Path01 63: 172, 1987 10. Stankiewicz JA. Pazevic JP: Hvoonlossal nerve nalsv after tooth extraction. J Oral Maxiliofic Surg 46: 148, 1988 11. Robinson PP: Observation on the recovery of sensation following inferior alveolar nerve injuries. Br J Oral Maxillofat Surg 26: 177, 1988 12. Allen GD: Dental Anesthesia & Analgesia (Local & General) (3rd ed). Baltimore, MD, Williams & Wilkins, 1984 13. Fine J, Kaltman S, Bianco M: Prevention of sore throat after nasotracheal intubation. J Oral Maxillofac Surg 46946, 1988 14. Sexton J, Dohlman L: Benefits of the pharyngeal pack. J Oral Maxillofac Surg 47:891, 1989 juries:
Surg
48:1104-1108,1990
Necrotizing
Soft-Tissue Infections Dental Origin
of
DAN M. FLISS, MD,* FERIT TOVI, MD,t AND HOWARD J. ZIRKIN, MD$.
Complications of dental infections are usually confined to the adjacent soft tissues. Sometimes when fascial spaces are involved, however, deep cervical abscesses may develop that can lead to mediastinitis. Septic thrombophlebitis originating from
Received from Soroka University Hospital, Faculty of Health Sciences, Ben-Gurion University of the Negev, Beer-Sheva, Israel. * Lecturer, Department of Otolaryngology. t Associate Professor, Department of Otolaryngology. $ Senior Lecturer, Pathological Institute. Address correspondence and reprint requests to Dr Fliss: Department of Otolaryngology, Soroka Medical Center, PO Box 151, Beer-Sheva 84101, Israel. 0 1990 American
Association
geons 0278-21931901481 O-001 7$3.00/O
of Oral and Maxillofacial
Sur-
a primary dental infection occasionally results in orbital or intracranial complications. Another uncommon, but life-threatening complication of dental infection is necrotizing soft-tissue infection (NSTI). This fulminant and devastating entity has been reported to develop initially in the cervical fascia, but as the infectious necrotizing process spreads, soft-tissue components below and above the affected fascia also may become involved. Late diagnosis has been associated with increased morbidity and high mortality rates. Among the 15 cases of NSTI treated in the Otolaryngology, Head and Neck Department of the Soroka Medical Center during the last 10 years, 3 cases were of dental origin. This article reports our experience with this unusual and aggressive condition.
1105
FLISS ET AL
Report of Three Cases Case I A 43-year-old man was referred to our outpatient clinic with submandibular swelling and mild trismus. On physical examination he was febrile (lOOSoF) and the involved skin was edematous and erythematous. The oral examination showed a peridental infection of the left mandibular second molar. Subcutaneous emphysema was palpated along the medial border of the sternocleidomastoid muscle. Results of the routine laboratory examinations included hemoglobin 9 g/dL white blood cell count of 18,OOO/pL with a marked shift to the left, and an erythrocyte sedimentation rate of 45 mm/h. Blood chemistry values showed hypoalbuminemia of 2.7 g/dL. Radiographs of the neck showed a soft-tissue swelling and the presence of air in the upper neck. The chest radiograph showed a widening of the upper mediastinum. Intravenous crystalline penicillin, 12,000,OOO units. and gentamycin, 240 mg daily, were initiated. The carious tooth was extracted and the upper neck was explored. Necrosis of the subcutaneous tissues and superficial fascia was detected. A grey, foul-smelling, watery discharge was evident in the involved region. Wide debridement of the fascia, subcutaneous tissues, and adjacent muscle was performed. In addition, the anterior mediastinum was explored through the pretracheal fascial space using blunt finger dissection. Purulent material was evacuated from this region and polyethylene tubes were inserted for drainage and irrigation. Bacteriologic cultures yielded Enterobacter coalastea, Streptococcus liridans, and Pseudomonas aeruginosa. The histologic findings consisted of a severe infectiousinflammatory process of the soft tissue, including dermis, fascia, and muscles. There was extensive thrombosis and vasculitis of small arteries and veins. Regions of necrosis of the dermal fat and muscle were present, but the epidermis was well preserved. Bedside wound care included the change of dressing twice daily and local debridement of necrotic tissues. In addition, copious irrigations with povidone iodine and hydrogen peroxide were performed. The patient improved gradually. Healthy granulation tissue covered the debrided region. Secondary epithelization occurred by the 3rd postoperative week. The patient was discharged from the hospital by the 5th week of hospitalization in good condition.
a shift to the left, and hypoalbuminemia of 2.1 g/dL. The chemistry screen, coagulation profile, and liver function test results were normal. Intravenous crystalline penicillin was initiated (12,000,OOO units daily). The patient’s condition did not improve and by the end of the 1st week surgery was indicated and the submandibular region was explored. Necrosis of the subcutaneous fat, muscular tissue, and superficial fascia were present (Fig 1). Small amounts of foul-smelling discharge were found. The region was widely debrided. The wound was packed and daily irrigations with povidone iodine and hydrogen peroxide were performed, together with bedside debridement of necrotic tissues. Cultures taken during surgery grew Proteus mirabilis, Enterococcus, and Escherichia coli; accordingly, gentamycin and metronidazole were added to the antibiotic regimen. The histologic features of the excised soft tissues of the neck were compatible with a necrotizing infection with severe inflammatory reaction, large regions of necrosis, vasculitis, and thrombophlebitis. Gram stains detected a mixture of gram-positive cocci and gram-negative rods. The patient’s condition improved gradually and on the 12th day of hospitalization, the mandibular cyst was removed. On the same occasion, the involved tooth was extracted. He was discharged in good condition on the 20th day of hospitalization.
Case 3 A lPyear-old man was transferred to the emergency department in a toxic, febrile condition. Five days before his referral, a periodontal infection of the mandibular left first molar had been diagnosed by the dentist and parenteral penicillin had been prescribed. Despite the antibiotic therapy the patient developed a progressive toxic condition On admission, the patient was acutely ill and disoriented. His temperature was 101.8”F. The blood pressure
Case2 A 44-year-old man was referred to our department because of a painful left submandibular swelling. He was treated by his dentist with oral erythromycin for 4 days before his referral, but pain and swelling progressed. He had a history of multiple sclerosis and had been on steroid therapy during the last 6 months. At the time of admission, the patient was febrile (101°F) and his blood pressure was 90/70 mm Hg. The skin overlaying the upper neck was erythematous, edematous, and diffusely indurated, with no discrete line of demarcation. Examination of the oral cavity was not possible because of severe trismus. Radiographs of the mandible showed the presence of a radicular cyst surrounding the root of the mandibular left second molar. A radiograph of the chest was normal. Routine laboratory data included hemoglobin 8.5 g/dL, hematocrit 23%. white blood cell count of 18,00O/(~L with
FIGURE 1. Necrotizing infection of the upper neck. The involved soft tissue appears pale and avascular. The polyethylene tube is draining the floor of mouth.
1106
was 90/60 mm Hg and there was a pulse rate of 112. A diffuse erythematous and nonfluctuant swelling of the lower left face and neck extending to the clavicle was present. The patient’s mouth had a foul odor. Trismus limited the intraoral examination. Crepitus was elicited on palpation of the neck. Routine laboratory studies showed a white blood cell count of 2O,OOO/p.Lwith a shift to the left, hemoglobin 9.2 g/dL, and hypoalbuminemia of 2.5 g/dL. Plain radiographs of the neck showed gas bubbles in the soft tissues. The chest radiograph showed widening of the anterior mediastinum, pleural effusions, and left lower lobe pneumonia. A computed tomography (CT) scan confirmed the radiographic findings (Fig 2). Suspecting a gas-producing infection, antibiotic therapy with crystalline penicillin, gentamycin, and metronidezole was initiated before surgery. Exploration of the neck was performed under general anesthesia. Massive necrosis of the subcutaneous fat, superficial fascia, and muscular tissues was detected. A foul-smelling exudate was found covering these structures. The involved fascia and surrounding skin and muscles were widely excised (Fig 3). The mediastinum was approached through the paratracheal fascia and purulent discharge was drained. Polyethylene tubes were inserted. The wound was packed. The neck wound and mediastinum were irrigated with povidone iodine and hydrogen peroxide three times daily. Additionally, new developing necrotic foci were debrided. Cultures revealed the presence of Enrerobacter, Klebsiella pneumoniae, and anerobic streptococcus. Histologic study of the debrided cervical soft tissues showed a necrotizing infection, including vasculitis and thrombophlebitis. Despite the aggressive treatment, the clinical condition of the patient deteriorated. He became unconscious and developed seizures. Computerized tomography of the skull revealed no brain pathology; however, bilateral pansinusitis was detected. Additionally, CT of the chest was compatible with persistent mediastinal infection. Accordingly, drainage of the maxillary sinuses was performed and copious amounts of purulent discharge were obtained. The ethmoidal sinuses were drained by sinusoscopy. Subsequently, the patient was taken to the operating room and the mediastinum was explored by a transternal approach. Postsurgically, the patient gradually became afebrile and regained consciousness. By the 3rd month of hospitalization, healthy granulation tissue covered the denuded cervical structures and secondary epithelization took place. He was discharged free of symptoms.
FIGURE 2. CT scan showing widening of the media&mm secondary to necrotizing infection of dental origin.
NECROTIZING
SOFT-TISSUE
INFECTIONS
FIGURE 3. Necrotizing soft-tissue infection of dental origin. Note the necrotic appearance, with the whitish appearance of the sternocleidomastoid muscle and the other soft tissues.
Discussion Necrotizing soft-tissue infection, although rare, presents a serious threat to the patient’s life.‘-‘4 It is characterized by widespread necrosis of the superficial fascia with extensive undermining of the sur-
rounding tissues. This entity was first described by Joseph Jones, an American Civil War surgeon who cited 2,642 cases, of which 1,142 (46%) proved fatal. I5 Meleney’6-i8 added three important observations to the understanding of the disease: subcutaneous necrosis as an essential feature of the disease, the dominant role of Streptococcus hemofyticus as an etiologic factor, and the synergistic nature of the causative bacterial flora. Because of their usual occurrence in the abdominal wall, perineum, and lower extremities, NSTls are well recognized by general surgeons.’ They have been reported to occur after surgery, trauma, and even spontaneously. Spankus13 reviewed the literature describing necrotizing infections involving the craniocervical area. Dental infections were the single most common source, followed by blunt trauma, minor trauma, peritonsillar abscesses, and osteoradionecrosis. Diabetes mellitus is a frequent predisposing factor, as are immunosuppressive conditions, atherosclerosis, malignancy, and cirrhosis.” One of our patients presented in an immunosuppressed state. The disease most commonly occurs in middle-aged adults; however, no sexual or racial predilection has been found. ‘6.2’-22 Various organisms have been reported as responsible for NSTIs. P-hemolytic streptococcus was first considered by Meleney” and then by Wilson2’
1107
FLISS ET AL
as the primary causative agent of the disease. Stone and Martin” found gram-negative rods in the majority of their cases. Menda and colleaguesZ3 cultured facultative and obligate anaerobic microorganisms in their series. Guiliano et a12’ were able to demonstrate the synergistic behavior of the involved organisms. Both anerobes and facultative organisms have been found responsible for the development of NSTIs. In only one of our cases was anaerobic organisms cultured (Case 3). In the other two cases, anaerobic cultures were negative, but the presence of cocci in gram stains was suggestive of the anaerobic nature of these organisms. The characteristic pathologic features of the disease include progressive spreading gangrene of the subcutaneous fat and deep fascia, which tends to undermine the skin, usually leaving it intact until late in the course of the infection. The histologic picture is one of necrosis and dense polymorphonuclear infiltration in the deep dermis and fascial planes, with vasculitis and venous thrombosis (Fig 4). The latter is the cause of direct or metastatic spread of the disease. The epidermis is spared at the initial stage, but as the disease progresses, the infectious inflammatory process extends to all softtissue layers and involves both the superficial dermis (Fig 5) and muscles (Fig 6). Although Wilson” and other authors described this entity as developing initially in the fascia, our
FIGURE 4. Vasculitis tissue (hematoxylin-eosin.
involving veins in subcutaneous adipose original magnification x200).
histologic findings indicate that even in the early clinical stages of the disease, tissue above and below the fascia is involved by the pathologic process. The apparently normal tissue at the periphery of the initial lesion also was found to exhibit histologic changes characteristic of a necrotizing infection. Hence, the disease at any given stage appears to be more widespread than its gross appearance would indicate. Necrotizing soft-tissue infections may remain quiescent in their early stages and the local findings are subtle and nonspecific. The overlying skin is hot, red, edematous, and often painful. Despite this noncharacteristic clinical picture, severe constitutional symptoms appear. The local signs often change within short periods of time; the involved area becomes numb and a dusky discoloration becomes evident. Electrolyte deficit, acid-base imbalance, leukocytosis, hypoalbuminemia, and high fever were found in our patients. Radiologic studies of the involved region have been suggested as a useful method for the early diagnosis of the disease because they may demonstrate the presence of soft-tissue gas even in the absence of crepitation. All authors agree that the prognosis depends on early diagnosis and appropriate treatment. The differential diagnosis includes erysipelis, clostridial gas gangrene, echthyma gan-
FIGURE 5. Severe inflammation of dermis and subcutaneous adipose tissue, with sparing of the epidermis (hematoxylin-eosin, original magnification X75).
1108
NECROTIZING
SOFT-TISSUE
INFECTIONS
and changing of dressing (at least twice daily), is an important part of the treatment. Attention also should be paid to the recognition and debridement of the newly developing foci of infection. References
FIGURE 6. Necrotic muscle fibers widely separated by an extensive, acute, inflammatory infiltrate (hematoxylin-eosin. original magnification X 125).
grenosum, and pyoderma gangrenosum.25-27 Once the diagnosis is suspected on clinical grounds or established by histologic findings, therapy should be initiated without delay. Antimicrobial agents should be effective against gram-positive, gramnegative, and anaerobic organisms. Because the infection often exhibits a fulminating course, there is no time to wait for culture results.28 Later, the antibiotic regimen can be varied according to the culture and sensitivity results. Mediastinitis complicated the course of NSTIs in two of our cases. Treatment consisted of decompression of the mediastinum through a pretracheal approach using blunt finger dissection. Following drainage of this space, polyethylene suction tubes were placed through the thoracic inlet and the region was irrigated with povidone iodine and hydrogen peroxide. Antibiotic treatment, although important in preventing septicemia and metastatic abscesses, is always adjunctive to surgery. Excision of the involved fascia together with the adjacent soft tissues is the keystone of the surgical treatment. The use of frozen section examinations during surgery, as was performed in the presented cases, will contribute to the maximal erradication of the pathologic process. Daily wound care, including bedside debridement
I. Levine TM, Wurster CF. Krespi UP: Medianstinitis occurring as a complication of odontogenic infections. Laryngoscope 96:747, 1986 2. McCurdy JA, MacInnis EL, Hays LL: Fatal mediastinitis after a dental infection. J Oral Surg 35:726, 1977 3. Moncada R, Warpeka R, Pickleman J, et al: Mediastinitis from odontogenic and deep cervical infections. Chest 73:497, 1978 4. Hendler BH, Quinn PD: Fatal mediastinitis secondary to odontogenic infection. J Oral Surg 36:308, 1978 5. Cogan IC: Necrotizing mediastinitis, secondary to descending cervical cellulitis. Oral Surg 36:307, 1973 6. Roser SM, Chow AW, Brady FA: Necrotizing fascitis. J Oral Surg 35730. 1977 7. Crowson WN: Fatal necrotizine fascitis develonina after tooth extraction. Am J Surg 3%525, 1973 ’ 8. Krespi TP, Lawson W, Blaugrund SM, et al: Massive necrotizing infections of the neck. Head Neck Surg 3:473, 1981 9. Gallin JL, Johnson JT: Cervical necrotizing fascitis. Otolaryngol Head Neck Surg 89:935, 1981 10. Wills PI, Vernon RP: Complications of space infections of the head and neck. Laryngoscope 91:1125, 1981 I 1. Richardson JO, Fox GL, Groves FL, et al: Necrotizing fascitis of the neck: A complication of dental extraction. Tex Med 71:69, 1975 12. Mruthyunjaya B: Necrotizing fascitis. Report of case. J Oral Surg 3960, 1981 13. Spankus ME, Flint PW, Smith RJH: Craniocervical necrotizing fascitis. Otolaryngol Head Neck Surg 92:261, 1984 14. Dierks EJ, Meyerhoff WL, Schultz B, et al: Fulminant infections of odontogenic origin. Laryngoscope 97:271, 1987 15. Jones J: Investigation upon the nature, causes and treatment of hospital gangrene as it prevailed in the confederate armies-1861-1865, in: Surgical Memoirs of the War of Rebellion. New York. U.S. Sanitv Commission. 1871. DD __ 317-365 16. Meleney FL: Hemolytic streptococcus gangrene. Arch Surg 9:317:365. 1924 17. Meleney FL: Bacterial synergism in disease processes. Ann Surg 14:961, 1939 18. Meleney FL: A differential diagnosis between certain types of infectious gangrene of the skin. Surg Gynecol Obstet 56:847, 1939 19. Meade DW, Mueller B: Necrotizing infections of subcutaneous tissue and fascia. Ann Surg 168:274, 1968 20. Wilson B: Necrotizing fascitis. Am Surg 1818:416, 1952 21. Rea WJ, Wyric WJ Jr: Necrotizing fascitis. Am Surg 172: 957, 1970 22. Stone HH, Martin JD: Synergistic necrotizing cellulitis. Am Surg 175:702, 1972 23. Menda KB: Necrotizing fascitis. Bacteriology and clinical features, in Program and Abstracts of the 14th Interscience Conference on Antimicrobial Agents. San Francisco, September 11-B, 1974 (abstr 275) 24. Giuliano A, Lewis F, Hadley K, et al: Bacteriology of necrotizing fascitis. Am J Surg 134:52, 1977 25. Beck HJ, Salassa JR, McCaffrey TV, et al: Life threatening soft tissue infections of the neck. Laryngoscope 94:354,1984 26. Salassa JR, Winkelman RK, McDonald JT: Malignant pyoderma. Otolaryngol Head Neck Surg 89:917, 1981 27. Wolfman DE, Fenton W, Donald PJ: Typhus induced facial necrosis. Otolaryngol Head Neck Surg 94:390, 1983 28. Tovi F: Diagnosis and treatment of extensive odontogenic infections. J Oral Maxillofac Surg 41:141, 1983 (letter to the editor)
NECROTIZING
Table 1. Neurological Causes of Palatal and Pharyngeal Dysfunction (Cont’d) Myasthenia gravis Myasthenic-myopathic Muscle Dystrophy Oculopharyngeal Myotonic lnflammatory Poly/dermatomyositis
syndrome (Lambert-Easton)
jury is not mentioned in texts as a complication of general anesthesia.‘,12 Superficial injury from packs and large, cuffed endotracheal tubes has been cited as the major cause of post-oral surgery sore throat, but neurologic dysfunction has not been reported.13 References 1. DeJong RN: The Neurologic Examination York, Harper & Row. 1970
(3rd ed). New
2. Weiss K, Kramar R, Fit? P: Cranial and cervical nerve in-
J Oral Marillofac
SOFT-TISSUE
INFECTIONS
Local complications of carotid artery_ surgery. J I_ Cardiovasc Surg 28: 171, 1987 3. Sataloff RT, Myers DL, Kremer FB: Management of cranial nerve injury following surgery of the skull base. Otolaryngot Clin North Am 17577, 1984 4. Broomhead IW: The nerve supply to the nerves of the soft palate. Br .I Plastic Sure 4:l. 1951 5. Kerr AG, Groves J: Sco&Brown’s Otolaryngology, Basic Sciences, vol 1 (5th ed). London, Butterworths, 1987 6. English GM: Otolaryngology, vol 3. Philadelphia, PA, Lippincott, 1984 7. Hedden M, Eroz CJ, Donnelly WH, et al: Laryngotrachael damage after prolonged use of ortracheal tubes in adults. JAMA 207:203, 1969 8. Orkin FK, Cooperman LH: Complications in anesthesiology. Philadelphia, PA, Lippincott, 1983 9. Burke RH. Adams JL: Immediate cranial nerve uaralvsis during removal of a mandibular third molar. &al !&u-g Oral Med Oral Path01 63: 172, 1987 10. Stankiewicz JA. Pazevic JP: Hvoonlossal nerve nalsv after tooth extraction. J Oral Maxiliofic Surg 46: 148, 1988 11. Robinson PP: Observation on the recovery of sensation following inferior alveolar nerve injuries. Br J Oral Maxillofat Surg 26: 177, 1988 12. Allen GD: Dental Anesthesia & Analgesia (Local & General) (3rd ed). Baltimore, MD, Williams & Wilkins, 1984 13. Fine J, Kaltman S, Bianco M: Prevention of sore throat after nasotracheal intubation. J Oral Maxillofac Surg 46946, 1988 14. Sexton J, Dohlman L: Benefits of the pharyngeal pack. J Oral Maxillofac Surg 47:891, 1989 juries:
Surg
48:1104-1108,1990
Necrotizing
Soft-Tissue Infections Dental Origin
of
DAN M. FLISS, MD,* FERIT TOVI, MD,t AND HOWARD J. ZIRKIN, MD$.
Complications of dental infections are usually confined to the adjacent soft tissues. Sometimes when fascial spaces are involved, however, deep cervical abscesses may develop that can lead to mediastinitis. Septic thrombophlebitis originating from
Received from Soroka University Hospital, Faculty of Health Sciences, Ben-Gurion University of the Negev, Beer-Sheva, Israel. * Lecturer, Department of Otolaryngology. t Associate Professor, Department of Otolaryngology. $ Senior Lecturer, Pathological Institute. Address correspondence and reprint requests to Dr Fliss: Department of Otolaryngology, Soroka Medical Center, PO Box 151, Beer-Sheva 84101, Israel. 0 1990 American
Association
geons 0278-21931901481 O-001 7$3.00/O
of Oral and Maxillofacial
Sur-
a primary dental infection occasionally results in orbital or intracranial complications. Another uncommon, but life-threatening complication of dental infection is necrotizing soft-tissue infection (NSTI). This fulminant and devastating entity has been reported to develop initially in the cervical fascia, but as the infectious necrotizing process spreads, soft-tissue components below and above the affected fascia also may become involved. Late diagnosis has been associated with increased morbidity and high mortality rates. Among the 15 cases of NSTI treated in the Otolaryngology, Head and Neck Department of the Soroka Medical Center during the last 10 years, 3 cases were of dental origin. This article reports our experience with this unusual and aggressive condition.
1105
FLISS ET AL
Report of Three Cases Case I A 43-year-old man was referred to our outpatient clinic with submandibular swelling and mild trismus. On physical examination he was febrile (lOOSoF) and the involved skin was edematous and erythematous. The oral examination showed a peridental infection of the left mandibular second molar. Subcutaneous emphysema was palpated along the medial border of the sternocleidomastoid muscle. Results of the routine laboratory examinations included hemoglobin 9 g/dL white blood cell count of 18,OOO/pL with a marked shift to the left, and an erythrocyte sedimentation rate of 45 mm/h. Blood chemistry values showed hypoalbuminemia of 2.7 g/dL. Radiographs of the neck showed a soft-tissue swelling and the presence of air in the upper neck. The chest radiograph showed a widening of the upper mediastinum. Intravenous crystalline penicillin, 12,000,OOO units. and gentamycin, 240 mg daily, were initiated. The carious tooth was extracted and the upper neck was explored. Necrosis of the subcutaneous tissues and superficial fascia was detected. A grey, foul-smelling, watery discharge was evident in the involved region. Wide debridement of the fascia, subcutaneous tissues, and adjacent muscle was performed. In addition, the anterior mediastinum was explored through the pretracheal fascial space using blunt finger dissection. Purulent material was evacuated from this region and polyethylene tubes were inserted for drainage and irrigation. Bacteriologic cultures yielded Enterobacter coalastea, Streptococcus liridans, and Pseudomonas aeruginosa. The histologic findings consisted of a severe infectiousinflammatory process of the soft tissue, including dermis, fascia, and muscles. There was extensive thrombosis and vasculitis of small arteries and veins. Regions of necrosis of the dermal fat and muscle were present, but the epidermis was well preserved. Bedside wound care included the change of dressing twice daily and local debridement of necrotic tissues. In addition, copious irrigations with povidone iodine and hydrogen peroxide were performed. The patient improved gradually. Healthy granulation tissue covered the debrided region. Secondary epithelization occurred by the 3rd postoperative week. The patient was discharged from the hospital by the 5th week of hospitalization in good condition.
a shift to the left, and hypoalbuminemia of 2.1 g/dL. The chemistry screen, coagulation profile, and liver function test results were normal. Intravenous crystalline penicillin was initiated (12,000,OOO units daily). The patient’s condition did not improve and by the end of the 1st week surgery was indicated and the submandibular region was explored. Necrosis of the subcutaneous fat, muscular tissue, and superficial fascia were present (Fig 1). Small amounts of foul-smelling discharge were found. The region was widely debrided. The wound was packed and daily irrigations with povidone iodine and hydrogen peroxide were performed, together with bedside debridement of necrotic tissues. Cultures taken during surgery grew Proteus mirabilis, Enterococcus, and Escherichia coli; accordingly, gentamycin and metronidazole were added to the antibiotic regimen. The histologic features of the excised soft tissues of the neck were compatible with a necrotizing infection with severe inflammatory reaction, large regions of necrosis, vasculitis, and thrombophlebitis. Gram stains detected a mixture of gram-positive cocci and gram-negative rods. The patient’s condition improved gradually and on the 12th day of hospitalization, the mandibular cyst was removed. On the same occasion, the involved tooth was extracted. He was discharged in good condition on the 20th day of hospitalization.
Case 3 A lPyear-old man was transferred to the emergency department in a toxic, febrile condition. Five days before his referral, a periodontal infection of the mandibular left first molar had been diagnosed by the dentist and parenteral penicillin had been prescribed. Despite the antibiotic therapy the patient developed a progressive toxic condition On admission, the patient was acutely ill and disoriented. His temperature was 101.8”F. The blood pressure
Case2 A 44-year-old man was referred to our department because of a painful left submandibular swelling. He was treated by his dentist with oral erythromycin for 4 days before his referral, but pain and swelling progressed. He had a history of multiple sclerosis and had been on steroid therapy during the last 6 months. At the time of admission, the patient was febrile (101°F) and his blood pressure was 90/70 mm Hg. The skin overlaying the upper neck was erythematous, edematous, and diffusely indurated, with no discrete line of demarcation. Examination of the oral cavity was not possible because of severe trismus. Radiographs of the mandible showed the presence of a radicular cyst surrounding the root of the mandibular left second molar. A radiograph of the chest was normal. Routine laboratory data included hemoglobin 8.5 g/dL, hematocrit 23%. white blood cell count of 18,00O/(~L with
FIGURE 1. Necrotizing infection of the upper neck. The involved soft tissue appears pale and avascular. The polyethylene tube is draining the floor of mouth.
1106
was 90/60 mm Hg and there was a pulse rate of 112. A diffuse erythematous and nonfluctuant swelling of the lower left face and neck extending to the clavicle was present. The patient’s mouth had a foul odor. Trismus limited the intraoral examination. Crepitus was elicited on palpation of the neck. Routine laboratory studies showed a white blood cell count of 2O,OOO/p.Lwith a shift to the left, hemoglobin 9.2 g/dL, and hypoalbuminemia of 2.5 g/dL. Plain radiographs of the neck showed gas bubbles in the soft tissues. The chest radiograph showed widening of the anterior mediastinum, pleural effusions, and left lower lobe pneumonia. A computed tomography (CT) scan confirmed the radiographic findings (Fig 2). Suspecting a gas-producing infection, antibiotic therapy with crystalline penicillin, gentamycin, and metronidezole was initiated before surgery. Exploration of the neck was performed under general anesthesia. Massive necrosis of the subcutaneous fat, superficial fascia, and muscular tissues was detected. A foul-smelling exudate was found covering these structures. The involved fascia and surrounding skin and muscles were widely excised (Fig 3). The mediastinum was approached through the paratracheal fascia and purulent discharge was drained. Polyethylene tubes were inserted. The wound was packed. The neck wound and mediastinum were irrigated with povidone iodine and hydrogen peroxide three times daily. Additionally, new developing necrotic foci were debrided. Cultures revealed the presence of Enrerobacter, Klebsiella pneumoniae, and anerobic streptococcus. Histologic study of the debrided cervical soft tissues showed a necrotizing infection, including vasculitis and thrombophlebitis. Despite the aggressive treatment, the clinical condition of the patient deteriorated. He became unconscious and developed seizures. Computerized tomography of the skull revealed no brain pathology; however, bilateral pansinusitis was detected. Additionally, CT of the chest was compatible with persistent mediastinal infection. Accordingly, drainage of the maxillary sinuses was performed and copious amounts of purulent discharge were obtained. The ethmoidal sinuses were drained by sinusoscopy. Subsequently, the patient was taken to the operating room and the mediastinum was explored by a transternal approach. Postsurgically, the patient gradually became afebrile and regained consciousness. By the 3rd month of hospitalization, healthy granulation tissue covered the denuded cervical structures and secondary epithelization took place. He was discharged free of symptoms.
FIGURE 2. CT scan showing widening of the media&mm secondary to necrotizing infection of dental origin.
NECROTIZING
SOFT-TISSUE
INFECTIONS
FIGURE 3. Necrotizing soft-tissue infection of dental origin. Note the necrotic appearance, with the whitish appearance of the sternocleidomastoid muscle and the other soft tissues.
Discussion Necrotizing soft-tissue infection, although rare, presents a serious threat to the patient’s life.‘-‘4 It is characterized by widespread necrosis of the superficial fascia with extensive undermining of the sur-
rounding tissues. This entity was first described by Joseph Jones, an American Civil War surgeon who cited 2,642 cases, of which 1,142 (46%) proved fatal. I5 Meleney’6-i8 added three important observations to the understanding of the disease: subcutaneous necrosis as an essential feature of the disease, the dominant role of Streptococcus hemofyticus as an etiologic factor, and the synergistic nature of the causative bacterial flora. Because of their usual occurrence in the abdominal wall, perineum, and lower extremities, NSTls are well recognized by general surgeons.’ They have been reported to occur after surgery, trauma, and even spontaneously. Spankus13 reviewed the literature describing necrotizing infections involving the craniocervical area. Dental infections were the single most common source, followed by blunt trauma, minor trauma, peritonsillar abscesses, and osteoradionecrosis. Diabetes mellitus is a frequent predisposing factor, as are immunosuppressive conditions, atherosclerosis, malignancy, and cirrhosis.” One of our patients presented in an immunosuppressed state. The disease most commonly occurs in middle-aged adults; however, no sexual or racial predilection has been found. ‘6.2’-22 Various organisms have been reported as responsible for NSTIs. P-hemolytic streptococcus was first considered by Meleney” and then by Wilson2’
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as the primary causative agent of the disease. Stone and Martin” found gram-negative rods in the majority of their cases. Menda and colleaguesZ3 cultured facultative and obligate anaerobic microorganisms in their series. Guiliano et a12’ were able to demonstrate the synergistic behavior of the involved organisms. Both anerobes and facultative organisms have been found responsible for the development of NSTIs. In only one of our cases was anaerobic organisms cultured (Case 3). In the other two cases, anaerobic cultures were negative, but the presence of cocci in gram stains was suggestive of the anaerobic nature of these organisms. The characteristic pathologic features of the disease include progressive spreading gangrene of the subcutaneous fat and deep fascia, which tends to undermine the skin, usually leaving it intact until late in the course of the infection. The histologic picture is one of necrosis and dense polymorphonuclear infiltration in the deep dermis and fascial planes, with vasculitis and venous thrombosis (Fig 4). The latter is the cause of direct or metastatic spread of the disease. The epidermis is spared at the initial stage, but as the disease progresses, the infectious inflammatory process extends to all softtissue layers and involves both the superficial dermis (Fig 5) and muscles (Fig 6). Although Wilson” and other authors described this entity as developing initially in the fascia, our
FIGURE 4. Vasculitis tissue (hematoxylin-eosin.
involving veins in subcutaneous adipose original magnification x200).
histologic findings indicate that even in the early clinical stages of the disease, tissue above and below the fascia is involved by the pathologic process. The apparently normal tissue at the periphery of the initial lesion also was found to exhibit histologic changes characteristic of a necrotizing infection. Hence, the disease at any given stage appears to be more widespread than its gross appearance would indicate. Necrotizing soft-tissue infections may remain quiescent in their early stages and the local findings are subtle and nonspecific. The overlying skin is hot, red, edematous, and often painful. Despite this noncharacteristic clinical picture, severe constitutional symptoms appear. The local signs often change within short periods of time; the involved area becomes numb and a dusky discoloration becomes evident. Electrolyte deficit, acid-base imbalance, leukocytosis, hypoalbuminemia, and high fever were found in our patients. Radiologic studies of the involved region have been suggested as a useful method for the early diagnosis of the disease because they may demonstrate the presence of soft-tissue gas even in the absence of crepitation. All authors agree that the prognosis depends on early diagnosis and appropriate treatment. The differential diagnosis includes erysipelis, clostridial gas gangrene, echthyma gan-
FIGURE 5. Severe inflammation of dermis and subcutaneous adipose tissue, with sparing of the epidermis (hematoxylin-eosin, original magnification X75).
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INFECTIONS
and changing of dressing (at least twice daily), is an important part of the treatment. Attention also should be paid to the recognition and debridement of the newly developing foci of infection. References
FIGURE 6. Necrotic muscle fibers widely separated by an extensive, acute, inflammatory infiltrate (hematoxylin-eosin. original magnification X 125).
grenosum, and pyoderma gangrenosum.25-27 Once the diagnosis is suspected on clinical grounds or established by histologic findings, therapy should be initiated without delay. Antimicrobial agents should be effective against gram-positive, gramnegative, and anaerobic organisms. Because the infection often exhibits a fulminating course, there is no time to wait for culture results.28 Later, the antibiotic regimen can be varied according to the culture and sensitivity results. Mediastinitis complicated the course of NSTIs in two of our cases. Treatment consisted of decompression of the mediastinum through a pretracheal approach using blunt finger dissection. Following drainage of this space, polyethylene suction tubes were placed through the thoracic inlet and the region was irrigated with povidone iodine and hydrogen peroxide. Antibiotic treatment, although important in preventing septicemia and metastatic abscesses, is always adjunctive to surgery. Excision of the involved fascia together with the adjacent soft tissues is the keystone of the surgical treatment. The use of frozen section examinations during surgery, as was performed in the presented cases, will contribute to the maximal erradication of the pathologic process. Daily wound care, including bedside debridement
I. Levine TM, Wurster CF. Krespi UP: Medianstinitis occurring as a complication of odontogenic infections. Laryngoscope 96:747, 1986 2. McCurdy JA, MacInnis EL, Hays LL: Fatal mediastinitis after a dental infection. J Oral Surg 35:726, 1977 3. Moncada R, Warpeka R, Pickleman J, et al: Mediastinitis from odontogenic and deep cervical infections. Chest 73:497, 1978 4. Hendler BH, Quinn PD: Fatal mediastinitis secondary to odontogenic infection. J Oral Surg 36:308, 1978 5. Cogan IC: Necrotizing mediastinitis, secondary to descending cervical cellulitis. Oral Surg 36:307, 1973 6. Roser SM, Chow AW, Brady FA: Necrotizing fascitis. J Oral Surg 35730. 1977 7. Crowson WN: Fatal necrotizine fascitis develonina after tooth extraction. Am J Surg 3%525, 1973 ’ 8. Krespi TP, Lawson W, Blaugrund SM, et al: Massive necrotizing infections of the neck. Head Neck Surg 3:473, 1981 9. Gallin JL, Johnson JT: Cervical necrotizing fascitis. Otolaryngol Head Neck Surg 89:935, 1981 10. Wills PI, Vernon RP: Complications of space infections of the head and neck. Laryngoscope 91:1125, 1981 I 1. Richardson JO, Fox GL, Groves FL, et al: Necrotizing fascitis of the neck: A complication of dental extraction. Tex Med 71:69, 1975 12. Mruthyunjaya B: Necrotizing fascitis. Report of case. J Oral Surg 3960, 1981 13. Spankus ME, Flint PW, Smith RJH: Craniocervical necrotizing fascitis. Otolaryngol Head Neck Surg 92:261, 1984 14. Dierks EJ, Meyerhoff WL, Schultz B, et al: Fulminant infections of odontogenic origin. Laryngoscope 97:271, 1987 15. Jones J: Investigation upon the nature, causes and treatment of hospital gangrene as it prevailed in the confederate armies-1861-1865, in: Surgical Memoirs of the War of Rebellion. New York. U.S. Sanitv Commission. 1871. DD __ 317-365 16. Meleney FL: Hemolytic streptococcus gangrene. Arch Surg 9:317:365. 1924 17. Meleney FL: Bacterial synergism in disease processes. Ann Surg 14:961, 1939 18. Meleney FL: A differential diagnosis between certain types of infectious gangrene of the skin. Surg Gynecol Obstet 56:847, 1939 19. Meade DW, Mueller B: Necrotizing infections of subcutaneous tissue and fascia. Ann Surg 168:274, 1968 20. Wilson B: Necrotizing fascitis. Am Surg 1818:416, 1952 21. Rea WJ, Wyric WJ Jr: Necrotizing fascitis. Am Surg 172: 957, 1970 22. Stone HH, Martin JD: Synergistic necrotizing cellulitis. Am Surg 175:702, 1972 23. Menda KB: Necrotizing fascitis. Bacteriology and clinical features, in Program and Abstracts of the 14th Interscience Conference on Antimicrobial Agents. San Francisco, September 11-B, 1974 (abstr 275) 24. Giuliano A, Lewis F, Hadley K, et al: Bacteriology of necrotizing fascitis. Am J Surg 134:52, 1977 25. Beck HJ, Salassa JR, McCaffrey TV, et al: Life threatening soft tissue infections of the neck. Laryngoscope 94:354,1984 26. Salassa JR, Winkelman RK, McDonald JT: Malignant pyoderma. Otolaryngol Head Neck Surg 89:917, 1981 27. Wolfman DE, Fenton W, Donald PJ: Typhus induced facial necrosis. Otolaryngol Head Neck Surg 94:390, 1983 28. Tovi F: Diagnosis and treatment of extensive odontogenic infections. J Oral Maxillofac Surg 41:141, 1983 (letter to the editor)
