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Ludwig's angina
Ludwig’s Angina Case Report, with Review of Bacteriology
BURT R
MEYERS,
WILLIAM
LAWSON,
SHALOM
Z
M.D M D., D.D S
HIRSCHMAN,
M D
New York, New York
From The Divrsron of Infectious Drseases, Departments of Medrcrne and Otolaryngology, Mt Sinar School of Medicine of the City Universrty of New York, New York, New York 10029. Requests for reprints should be addressed to Dr Burt Meyers, The Mount Sinal Hosprtal, 100th Street and Fifth Avenue, New York, New York 10029 Manuscrrpt received July 15, 1970
and Current Therapy
A fifty-two year old man in whom Ludwig’s angina developed following tooth extraction is described, and the literature describing the bacteriology, pathogenesis and treatment of this syndrome is reviewed. Gram-negative organisms are isolated infrequently from these cases, but in the case cited Escherichia coli and Pseudomonas aeruginosa were recovered. Present emphasis in the management of patients with Ludwig’s angina is on antimicrobial therapy for control of infection rather than surgical drainage procedures. Maintenance of an adequate airway is the most important therapeutic procedure. Since gramnegative and anaerobic organisms may be the infecting agents, initial antimicrobial therapy should be broad enough to inhibit these organisms. The hazard of sudden airway obstruction in this syndrome is demonstrated in the case presented. In 1836 von Ludwig [l] described five cases of infections involving the floor of the mouth. Through the years this clinical condition was known as Morbus strangulatorius, angina maligne and garotillo (Spanish, after the hangman’s loop), all names alluding to the respiratory obstruction so prominent in the morbidity of this disease. This entity has subsequently come to be known as Ludwig’s angina. The syndrome was extensively reviewed in the early 1940’s at which time ninety-six cases had been reported [2-41, and the pathogenesis, diagnostic criteria and bacteriology were discussed. Emphasis in these reports was placed on the need for surgical drainage as soon as the diagnosis was made. A more recent report [5] suggests that surgical drainage may not be necessary and that emphasis be placed on antimicrobial therapy. All investigators have concurred that maintenance of an adequate airway is imperative in the management of this condition. We recently treated a patient with this syndrome from whom two gram-negative organisms were isolated. We report this case and review the syndrome, emphasizing the bacteriology and current status of therapy. CASE REPORT A fifty-eight Outpatient
year
old
Department
August 1972
Negro
man
because
came of
pam
to The and
Mount
Sinai
swelling
of
The American Journal of Medicine
Hosprtal the
Volume 53
right
257
LUDWIG’S
ANGINA-MEYERS
ET AL.
Figure 1. Appearance of patient after tracheostomy, showing submandibular space involvement with cervicofacial swelling and protrusion of the tongue. side of the face and neck. Five days previously a right mandibular second molar had been extracted, and progressive right facial and cervical enlargement and tenderness, with difficulty in swallowing, had subsequently developed. Past medical history included hospitalization at another institution eight months previously for pulmonary tuberculosis (the patient was currently being treated with isoniazid). There was also a history of alcoholic cirrhosis and penicillin allergy. On admission the patient’s blood pressure was 140/80 mm Hg, pulse rate 88/minute and regular, respirations 24/minute and rectal temperature 101°F. He was a well developed, slightly obese elderly man in acute distress because of extensive cervical and orofacial swelling. Examination of the head and neck revealed protrusion of the tongue from the oral cavity, with bilateral elevation of the floor of the mouth to the occlusal surfaces of the mandibular teeth. A recent extraction wound was present in the right mandibular molar area. The tongue was markedly edematous and elevated, precluding direct visualization of the posterior oropharynx and larynx. There was massive swelling and marked induration of the right submaxillary and submental spaces, and moderate involvement of the left submaxillary space (Figure 1). The trachea was midline, respiration was unimpaired, ana the chest was clear on auscultation. The remainder of the physical examination was within normal limits. 258
August 1972
The American Journal of Medicine
Two hours after admission an intra-oral diagnostic incision was made under local anesthesia in the floor of the mouth, adjacent to the tooth socket, to obtain material for bacteriologic culture. Treatment was begun with intravenous erythromycin; however, this was changed to cephalothin and streptomycin when gram-negative organisms were isolated. Progressive respiratory distress developed, leading to sudden respiratory arrest sixteen hours after admission, for which the patient required emergency tracheostomy and resuscitation. The hemoglobin level was 13.7 gm/lOO ml and the white blood cell count 11,9OO/cu mm, with 33 polymorphonuclear leukocytes, 50 band forms, 15 lymphocytes and 2 atypical lymphocytes. Urinalysis showed a pH of 5, specific gravity 1.022, no glucose or albumin and an occasional white cell per high power field. The blood urea nitrogen was 10 mg/ 100 ml, fasting blood sugar 100 mg/lOO ml, uric acid 7.4 mg/lOO ml, total protein 7.3 gm/lOO ml with an albumin to globulin ratio of 2.9:4.4, bilirubin 1.3 mg/ 100 ml, serum glutamic oxaloacetic transaminase @GOT) 150 international microunits, alkaline phosphatase 55 international microunits and lactic acid dehydrogenase (LDH) 200 international microunits. Aerobic and anaerobic cultures were made of the drainage fluid obtained from the intra-oral incision before antibiotic therapy was instituted. Escherichia coli and Pseudomonas aeruginosa were isolated initially and for several days thereafter while the patient was receiving antibiotic treatment. Cultures of the tracheal aspirate yielded Esch. coli and Serratia marcescens. Initially the patient required frequent tracheal suctioning, productive of frank pus. A chest roentgenogram revealed hazy pulmonary infiltrates consistent with aspiration pneumonia. He remained febrile (101°F) and continued to have cervico-facial swelling for four or five days on the antibiotic regimen, after which fever and swelling gradually subsided. The tracheostomy was decannulated on the seventh day, and he was discharged from the hospital after sixteen days. COMMENTS Ludwig’s changed although mortality
angina as a clinical entity remains unsince its original description in 1836 [l], the modes of therapy and the resultant have been greatly modified in the last
twenty-five years [2-41. Ludwig’s description [I] of the syndrome as a rapidly spreading gangrenous cellulitis or phlegmon, brawny in character without abscess formation, originating in the area of the submaxillary gland and extending by continuity without involving the salivary glands or lymph nodes, has been repeatedly shown to be accurate by subsequent investigators, with only minor modifications [6,7]. Whether the infection initially involves the sublingual [8] or submaxillary spaces [6,7], in order to meet the criteria of Ludwig’s angina it must eventually involve both [9] and spread along the fascial planes of the head
Volume 53
LUDWIG’S
and neck. Tschiassny [6] labelled other primary or secondary suppurative submaxillary infections pseudo-Ludwig’s angina because they did not fulfill the anatomic requirement of involving the two spaces. The lack of suppuration became evident when incision and drainage were the only therapeutic modalities available in the preantibiotic era [2,4]. Fewer cases have been reported in recent years because many fail to meet the diagnostic criteria outlined and because of the widespread use of early antibiotic therapy for oral infections. However, the occasional cases that do arise are a therapeutic emergency because of the rapid progression of symptoms and early airway obstruction. The pathogenesis of the condition is usually related to precipitating factors within the oral cavity such as dental infections, foreign bodies and lacerations of the floor of the mouth, compound mandibular fractures and other maxillofacial injuries; however, in a number of cases no antecedent local factors were found [2,3,5,10]. In the series of thirty-one cases reported by Williams [2], there was a pre- or postextraction dental etiology in 51 per cent; in the series of twenty cases reported by Williams and Guralnick [4], in 90 per cent; and in the series of fifty-four cases reported by Taffel and Harvey [3], in 57 per cent. Tschiassny [6], in an anatomic study of the dental factors in the etiology of Ludwig’s angina, implicated the molar teeth, especially the second and third molars, because of the position of their root apices beneath the mylohyoid ridge and the relative thinness of the mandibular alveolar bone lingually, giving dental infections ready access into the submaxillary space (Figure 2). The mandibular premolar teeth are only rarely involved [6, lO,ll]. Systemic disease may play a role in the etiology, as Ludwig’s angina has been reported in patients with acute glomerulonephritis [12], chronic glomerulonephritis [ll], systemic lupus erythematosus [3] and hypersensitivity states [5]. Males are affected two to three times as often as females, and although it occurs most frequently in middle aged subjects, it has been reported in the neonate [ 131. In the case described Esch. coli and Ps. aeruginosa were isolated from the draining tooth socket prior to the administration of antimicrobial agents. The occurrence of mixed isolates is not uncommon in these cases. Taffel and Harvey [3] reported that the majority of the cultures in their forty-five cases revealed the presence of more than one organism. Williams [2] isolated “hemolytic” streptococci in 72 per cent of his thirty-one
ANGINA-MEYERS
ET AL
cases, although the type of hemolysis was not described. Streptococci were recovered in all of the sixteen bacterial isolates in the twenty cases of Ludwig’s angina reported in another review [4]. In eight of these cases fusiform bacilli and spirillalike forms were seen on smear [4]. Reference was made to the possibility that anaerobes may have played a pathogenetic role in some of the cases described, but no anaerobic cultures were obtained in any of them [4]. Staph. aureus and Staph. albus isolated by Taffel and Harvey [3] were considered the pathogens in three cases. Williams et al. [4] cultured these organisms not infrequently, Staph. albus in four isolates, Staph. aureus in three isolates and in two instances uncategorized staphylococci. These were single isolates in four of the cases, but the investigators considered them contaminants and not of primary importance [4]. Steinhauser [13], however, recently described a twelve day old infant with Ludwig’s angina in whom Staph. aureus was the only isolate, and he considered it to be the nwthnonn
August 1972
Figure 2. Transverse section of mandible through second molar, showing thinness of lingual cortex below mylohyoid muscle attachment. Hematoxylin and eosin stain, original magnification X 3.5.
The American Journal of Medicine
Volume 53
259
LUDWIG’S
ANGINA-MEYERS
ET AL
Gram-negative aerobic organisms have been described in these cases, including Hemophilus influenzae, Esch. coli, Pseudomonas species and Neisseria catarrhalis [3]. The site of isolation and the frequency of their occurrence were not further detailed. It is our impression that the isolation of gram-negative organisms in cases of Ludwig’s angina is not a frequent occurrence. In the case described in this report Ps. aeruginosa and Esch. coli were isolated from the infected tooth socket. Foul smelling pus found in some of the cases described suggests that anaerobic organisms such as Vincent’s spirilliform and fusiform bacilli and anaerobic streptococci were present [4]. We did not isolate anaerobic organisms in our case, although cultures were taken in thioglycollate broth. In many hospitals this medium is present only in blood culture bottles but is not used for culturing exudates. The glucose broth which is used may not support anaerobic growth, especially if a delay occurs in transferring the specimen from the bedside to the microbiological laboratory. With the increasing use of appropriate media we expect that in the future more anaerobic organisms will be isolated in cases of Ludwig’s angina. In the preantibiotic era, Ludwig’s angina was considered to be a surgical emergency and was treated with various drainage procedures, utilizing submandibular [2-4,101 and intra-oral incisions [14]. Some investigators even advocated removal of the submaxillary gland [15]. Suppuration was an infrequent finding, noted in only one of fifty-one cases [2,4], and the rationale for the procedure was decompression of the submandibular space. The real danger of the condition was recognized, then as it is now, to be mechanical airway obstruction rather than fulminant sepsis. Early tracheostomy under local anesthesia is acknowledged by all as the primary surgical procedure in the management of this condition As the sublingual space becomes progressively
more involved, the tongue is further elevated and displaced, and the supraglottic larynx becomes edematous and distorted, compromising the airway. Respiratory obstruction occurs rapidly, and at times abruptly, with dyspnea and stridor as signs of advanced respiratory embarrassment. Cyanosis should be regarded as a premorbid sign. Sepsis, with mediastinal involvement and metastatic abscesses, is a late occurrence in the untreated case, and is not an immediate threat to life. Because of the distortion of the upper airway, direct laryngoscopy and intubation are considered extremely dangerous procedures and may result in laryngospasm and sudden death [2,10,16]. If a general anesthetic is required for surgery it should be administered through a tracheostomy. Incision and drainage should be reserved for the presence of fluctuation, which generally occurs late in this condition, although aspiration may be attempted to obtain fluid for bacteriologic analysis. After the airway is secure, a regimen of intensive antibiotic therapy is instituted for the control of infection. Because of impaired deglutition and the frequent complication of bronchopneumonia, we suggest the use of a cuffed tracheostomy tube to help prevent aspiration. When the bacterial offenders are unknown, administration of antimicrobial agents can be instituted promptly after cultures are taken and smears performed of any drainage obtained. In view of the isolates described in the discussion of the bacteriology, we would recommend that initial coverage be broad-based, to include agents directed against penicillinase-producing staphylococci, gram-negative organisms and fusospiroforms. chetal Cephalosporin derivatives, a semisynthetic penicillin, erythromycin or lincomytin and an aminoglycoside may be considered. This regimen may be altered when culture and sensitivity reports become available. With proper primary antibiotic therapy, incision and drainage may not be required.
REFERENCES
5
6
7 8
260
Von Ludwig FW MedrcmischesCorrespondenz. Blatt Des Wurttembergrschen Arztlrchen Vereins 6 21, 1836. Wrllrams AC Ludwig’s angina Surg Obstet Gynec 70 140,194o Taffel M, Harvey SC Ludwig’s angina. an analysis of 45 cases Surgery 11 841, 1942 Williams AC, Guralnick WC The diagnosis and treatment of Ludwig’s angina. New Eng J Med 288 443, 1943. Johnson WS, Devme KD, Wellman WE, Fischbach JE Ludwig’s angina concepts of therapy with report of a case Oral Surg 16. 1023, 1963 Tschrassny K. Ludwig’s angina an anatomic study of the role of the lower molar teeth in Its pathogenesis Arch Otolaryng (Chicago) 38. 485, 1943. Thomas TT Ludwig’s angina. an anatomrc, cknical, and statistical study Ann Surg 48 161, 1908. Grodmsky M Ludwig’s angina an anatomical and chniCal study with review of the literature. Surgery 25.
August 1972
The American Journal of Medicine
9 10 11. 12
13 14.
15 16
Volume 53
678.1936. Ashhurst APC Ludwig’s angma Arch Surg 18 2047, 1929. Kelly JJ, Hodge GE, Grossman A Ludwrg’s angina. Canad Med Ass J 77: 1089.1957 Gutman D, Laufer D, Neder A. Ludwig’s angrna report of two cases J Oral Surg 23: 277, 1965 Davis DG, Burrell RB. Ludwig’s angina with associated acute glomerulonephrrhs a discussion with report of a case. J Michigan Med Sot 59 1223,196O Steinhauser PR Ludwig’s angina. report of a case in a 12 day old boy J Oral Surg 25. 251, 1967 Houser K. Ludwrg’s angina intra-oral incisions In infectrons of the floor of the mouth Arch Otolaryng (Chicage) 16 317,1932 Colp R: Treatment of deep mfectrons of submaxillary triangle. Surg Clin N Amer 13 315, 1933 Campbell MB. A hazardous anesthetic J Roy Army Med Corps 105 135, 1959.
BURT R
MEYERS,
WILLIAM
LAWSON,
SHALOM
Z
M.D M D., D.D S
HIRSCHMAN,
M D
New York, New York
From The Divrsron of Infectious Drseases, Departments of Medrcrne and Otolaryngology, Mt Sinar School of Medicine of the City Universrty of New York, New York, New York 10029. Requests for reprints should be addressed to Dr Burt Meyers, The Mount Sinal Hosprtal, 100th Street and Fifth Avenue, New York, New York 10029 Manuscrrpt received July 15, 1970
and Current Therapy
A fifty-two year old man in whom Ludwig’s angina developed following tooth extraction is described, and the literature describing the bacteriology, pathogenesis and treatment of this syndrome is reviewed. Gram-negative organisms are isolated infrequently from these cases, but in the case cited Escherichia coli and Pseudomonas aeruginosa were recovered. Present emphasis in the management of patients with Ludwig’s angina is on antimicrobial therapy for control of infection rather than surgical drainage procedures. Maintenance of an adequate airway is the most important therapeutic procedure. Since gramnegative and anaerobic organisms may be the infecting agents, initial antimicrobial therapy should be broad enough to inhibit these organisms. The hazard of sudden airway obstruction in this syndrome is demonstrated in the case presented. In 1836 von Ludwig [l] described five cases of infections involving the floor of the mouth. Through the years this clinical condition was known as Morbus strangulatorius, angina maligne and garotillo (Spanish, after the hangman’s loop), all names alluding to the respiratory obstruction so prominent in the morbidity of this disease. This entity has subsequently come to be known as Ludwig’s angina. The syndrome was extensively reviewed in the early 1940’s at which time ninety-six cases had been reported [2-41, and the pathogenesis, diagnostic criteria and bacteriology were discussed. Emphasis in these reports was placed on the need for surgical drainage as soon as the diagnosis was made. A more recent report [5] suggests that surgical drainage may not be necessary and that emphasis be placed on antimicrobial therapy. All investigators have concurred that maintenance of an adequate airway is imperative in the management of this condition. We recently treated a patient with this syndrome from whom two gram-negative organisms were isolated. We report this case and review the syndrome, emphasizing the bacteriology and current status of therapy. CASE REPORT A fifty-eight Outpatient
year
old
Department
August 1972
Negro
man
because
came of
pam
to The and
Mount
Sinai
swelling
of
The American Journal of Medicine
Hosprtal the
Volume 53
right
257
LUDWIG’S
ANGINA-MEYERS
ET AL.
Figure 1. Appearance of patient after tracheostomy, showing submandibular space involvement with cervicofacial swelling and protrusion of the tongue. side of the face and neck. Five days previously a right mandibular second molar had been extracted, and progressive right facial and cervical enlargement and tenderness, with difficulty in swallowing, had subsequently developed. Past medical history included hospitalization at another institution eight months previously for pulmonary tuberculosis (the patient was currently being treated with isoniazid). There was also a history of alcoholic cirrhosis and penicillin allergy. On admission the patient’s blood pressure was 140/80 mm Hg, pulse rate 88/minute and regular, respirations 24/minute and rectal temperature 101°F. He was a well developed, slightly obese elderly man in acute distress because of extensive cervical and orofacial swelling. Examination of the head and neck revealed protrusion of the tongue from the oral cavity, with bilateral elevation of the floor of the mouth to the occlusal surfaces of the mandibular teeth. A recent extraction wound was present in the right mandibular molar area. The tongue was markedly edematous and elevated, precluding direct visualization of the posterior oropharynx and larynx. There was massive swelling and marked induration of the right submaxillary and submental spaces, and moderate involvement of the left submaxillary space (Figure 1). The trachea was midline, respiration was unimpaired, ana the chest was clear on auscultation. The remainder of the physical examination was within normal limits. 258
August 1972
The American Journal of Medicine
Two hours after admission an intra-oral diagnostic incision was made under local anesthesia in the floor of the mouth, adjacent to the tooth socket, to obtain material for bacteriologic culture. Treatment was begun with intravenous erythromycin; however, this was changed to cephalothin and streptomycin when gram-negative organisms were isolated. Progressive respiratory distress developed, leading to sudden respiratory arrest sixteen hours after admission, for which the patient required emergency tracheostomy and resuscitation. The hemoglobin level was 13.7 gm/lOO ml and the white blood cell count 11,9OO/cu mm, with 33 polymorphonuclear leukocytes, 50 band forms, 15 lymphocytes and 2 atypical lymphocytes. Urinalysis showed a pH of 5, specific gravity 1.022, no glucose or albumin and an occasional white cell per high power field. The blood urea nitrogen was 10 mg/ 100 ml, fasting blood sugar 100 mg/lOO ml, uric acid 7.4 mg/lOO ml, total protein 7.3 gm/lOO ml with an albumin to globulin ratio of 2.9:4.4, bilirubin 1.3 mg/ 100 ml, serum glutamic oxaloacetic transaminase @GOT) 150 international microunits, alkaline phosphatase 55 international microunits and lactic acid dehydrogenase (LDH) 200 international microunits. Aerobic and anaerobic cultures were made of the drainage fluid obtained from the intra-oral incision before antibiotic therapy was instituted. Escherichia coli and Pseudomonas aeruginosa were isolated initially and for several days thereafter while the patient was receiving antibiotic treatment. Cultures of the tracheal aspirate yielded Esch. coli and Serratia marcescens. Initially the patient required frequent tracheal suctioning, productive of frank pus. A chest roentgenogram revealed hazy pulmonary infiltrates consistent with aspiration pneumonia. He remained febrile (101°F) and continued to have cervico-facial swelling for four or five days on the antibiotic regimen, after which fever and swelling gradually subsided. The tracheostomy was decannulated on the seventh day, and he was discharged from the hospital after sixteen days. COMMENTS Ludwig’s changed although mortality
angina as a clinical entity remains unsince its original description in 1836 [l], the modes of therapy and the resultant have been greatly modified in the last
twenty-five years [2-41. Ludwig’s description [I] of the syndrome as a rapidly spreading gangrenous cellulitis or phlegmon, brawny in character without abscess formation, originating in the area of the submaxillary gland and extending by continuity without involving the salivary glands or lymph nodes, has been repeatedly shown to be accurate by subsequent investigators, with only minor modifications [6,7]. Whether the infection initially involves the sublingual [8] or submaxillary spaces [6,7], in order to meet the criteria of Ludwig’s angina it must eventually involve both [9] and spread along the fascial planes of the head
Volume 53
LUDWIG’S
and neck. Tschiassny [6] labelled other primary or secondary suppurative submaxillary infections pseudo-Ludwig’s angina because they did not fulfill the anatomic requirement of involving the two spaces. The lack of suppuration became evident when incision and drainage were the only therapeutic modalities available in the preantibiotic era [2,4]. Fewer cases have been reported in recent years because many fail to meet the diagnostic criteria outlined and because of the widespread use of early antibiotic therapy for oral infections. However, the occasional cases that do arise are a therapeutic emergency because of the rapid progression of symptoms and early airway obstruction. The pathogenesis of the condition is usually related to precipitating factors within the oral cavity such as dental infections, foreign bodies and lacerations of the floor of the mouth, compound mandibular fractures and other maxillofacial injuries; however, in a number of cases no antecedent local factors were found [2,3,5,10]. In the series of thirty-one cases reported by Williams [2], there was a pre- or postextraction dental etiology in 51 per cent; in the series of twenty cases reported by Williams and Guralnick [4], in 90 per cent; and in the series of fifty-four cases reported by Taffel and Harvey [3], in 57 per cent. Tschiassny [6], in an anatomic study of the dental factors in the etiology of Ludwig’s angina, implicated the molar teeth, especially the second and third molars, because of the position of their root apices beneath the mylohyoid ridge and the relative thinness of the mandibular alveolar bone lingually, giving dental infections ready access into the submaxillary space (Figure 2). The mandibular premolar teeth are only rarely involved [6, lO,ll]. Systemic disease may play a role in the etiology, as Ludwig’s angina has been reported in patients with acute glomerulonephritis [12], chronic glomerulonephritis [ll], systemic lupus erythematosus [3] and hypersensitivity states [5]. Males are affected two to three times as often as females, and although it occurs most frequently in middle aged subjects, it has been reported in the neonate [ 131. In the case described Esch. coli and Ps. aeruginosa were isolated from the draining tooth socket prior to the administration of antimicrobial agents. The occurrence of mixed isolates is not uncommon in these cases. Taffel and Harvey [3] reported that the majority of the cultures in their forty-five cases revealed the presence of more than one organism. Williams [2] isolated “hemolytic” streptococci in 72 per cent of his thirty-one
ANGINA-MEYERS
ET AL
cases, although the type of hemolysis was not described. Streptococci were recovered in all of the sixteen bacterial isolates in the twenty cases of Ludwig’s angina reported in another review [4]. In eight of these cases fusiform bacilli and spirillalike forms were seen on smear [4]. Reference was made to the possibility that anaerobes may have played a pathogenetic role in some of the cases described, but no anaerobic cultures were obtained in any of them [4]. Staph. aureus and Staph. albus isolated by Taffel and Harvey [3] were considered the pathogens in three cases. Williams et al. [4] cultured these organisms not infrequently, Staph. albus in four isolates, Staph. aureus in three isolates and in two instances uncategorized staphylococci. These were single isolates in four of the cases, but the investigators considered them contaminants and not of primary importance [4]. Steinhauser [13], however, recently described a twelve day old infant with Ludwig’s angina in whom Staph. aureus was the only isolate, and he considered it to be the nwthnonn
August 1972
Figure 2. Transverse section of mandible through second molar, showing thinness of lingual cortex below mylohyoid muscle attachment. Hematoxylin and eosin stain, original magnification X 3.5.
The American Journal of Medicine
Volume 53
259
LUDWIG’S
ANGINA-MEYERS
ET AL
Gram-negative aerobic organisms have been described in these cases, including Hemophilus influenzae, Esch. coli, Pseudomonas species and Neisseria catarrhalis [3]. The site of isolation and the frequency of their occurrence were not further detailed. It is our impression that the isolation of gram-negative organisms in cases of Ludwig’s angina is not a frequent occurrence. In the case described in this report Ps. aeruginosa and Esch. coli were isolated from the infected tooth socket. Foul smelling pus found in some of the cases described suggests that anaerobic organisms such as Vincent’s spirilliform and fusiform bacilli and anaerobic streptococci were present [4]. We did not isolate anaerobic organisms in our case, although cultures were taken in thioglycollate broth. In many hospitals this medium is present only in blood culture bottles but is not used for culturing exudates. The glucose broth which is used may not support anaerobic growth, especially if a delay occurs in transferring the specimen from the bedside to the microbiological laboratory. With the increasing use of appropriate media we expect that in the future more anaerobic organisms will be isolated in cases of Ludwig’s angina. In the preantibiotic era, Ludwig’s angina was considered to be a surgical emergency and was treated with various drainage procedures, utilizing submandibular [2-4,101 and intra-oral incisions [14]. Some investigators even advocated removal of the submaxillary gland [15]. Suppuration was an infrequent finding, noted in only one of fifty-one cases [2,4], and the rationale for the procedure was decompression of the submandibular space. The real danger of the condition was recognized, then as it is now, to be mechanical airway obstruction rather than fulminant sepsis. Early tracheostomy under local anesthesia is acknowledged by all as the primary surgical procedure in the management of this condition As the sublingual space becomes progressively
more involved, the tongue is further elevated and displaced, and the supraglottic larynx becomes edematous and distorted, compromising the airway. Respiratory obstruction occurs rapidly, and at times abruptly, with dyspnea and stridor as signs of advanced respiratory embarrassment. Cyanosis should be regarded as a premorbid sign. Sepsis, with mediastinal involvement and metastatic abscesses, is a late occurrence in the untreated case, and is not an immediate threat to life. Because of the distortion of the upper airway, direct laryngoscopy and intubation are considered extremely dangerous procedures and may result in laryngospasm and sudden death [2,10,16]. If a general anesthetic is required for surgery it should be administered through a tracheostomy. Incision and drainage should be reserved for the presence of fluctuation, which generally occurs late in this condition, although aspiration may be attempted to obtain fluid for bacteriologic analysis. After the airway is secure, a regimen of intensive antibiotic therapy is instituted for the control of infection. Because of impaired deglutition and the frequent complication of bronchopneumonia, we suggest the use of a cuffed tracheostomy tube to help prevent aspiration. When the bacterial offenders are unknown, administration of antimicrobial agents can be instituted promptly after cultures are taken and smears performed of any drainage obtained. In view of the isolates described in the discussion of the bacteriology, we would recommend that initial coverage be broad-based, to include agents directed against penicillinase-producing staphylococci, gram-negative organisms and fusospiroforms. chetal Cephalosporin derivatives, a semisynthetic penicillin, erythromycin or lincomytin and an aminoglycoside may be considered. This regimen may be altered when culture and sensitivity reports become available. With proper primary antibiotic therapy, incision and drainage may not be required.
REFERENCES
5
6
7 8
260
Von Ludwig FW MedrcmischesCorrespondenz. Blatt Des Wurttembergrschen Arztlrchen Vereins 6 21, 1836. Wrllrams AC Ludwig’s angina Surg Obstet Gynec 70 140,194o Taffel M, Harvey SC Ludwig’s angina. an analysis of 45 cases Surgery 11 841, 1942 Williams AC, Guralnick WC The diagnosis and treatment of Ludwig’s angina. New Eng J Med 288 443, 1943. Johnson WS, Devme KD, Wellman WE, Fischbach JE Ludwig’s angina concepts of therapy with report of a case Oral Surg 16. 1023, 1963 Tschrassny K. Ludwig’s angina an anatomic study of the role of the lower molar teeth in Its pathogenesis Arch Otolaryng (Chicago) 38. 485, 1943. Thomas TT Ludwig’s angina. an anatomrc, cknical, and statistical study Ann Surg 48 161, 1908. Grodmsky M Ludwig’s angina an anatomical and chniCal study with review of the literature. Surgery 25.
August 1972
The American Journal of Medicine
9 10 11. 12
13 14.
15 16
Volume 53
678.1936. Ashhurst APC Ludwig’s angma Arch Surg 18 2047, 1929. Kelly JJ, Hodge GE, Grossman A Ludwrg’s angina. Canad Med Ass J 77: 1089.1957 Gutman D, Laufer D, Neder A. Ludwig’s angrna report of two cases J Oral Surg 23: 277, 1965 Davis DG, Burrell RB. Ludwig’s angina with associated acute glomerulonephrrhs a discussion with report of a case. J Michigan Med Sot 59 1223,196O Steinhauser PR Ludwig’s angina. report of a case in a 12 day old boy J Oral Surg 25. 251, 1967 Houser K. Ludwrg’s angina intra-oral incisions In infectrons of the floor of the mouth Arch Otolaryng (Chicage) 16 317,1932 Colp R: Treatment of deep mfectrons of submaxillary triangle. Surg Clin N Amer 13 315, 1933 Campbell MB. A hazardous anesthetic J Roy Army Med Corps 105 135, 1959.