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Age changes in the inferior alveolar artery
British Journal of Oral and Maxillofacial Surgery (1989) 27, 83-84 0 1989 The British Association of Oral and Maxillofacial Surgeons
02664356x/89/0027-0083/$10.00
LETTERS AGE CHANGES
IN THE INFERIOR
TO THE EDITOR
ALVEOLAR
ARTERY
I have considered carefully the contents of the letter and I would appreciate the opportunity to publish the following reply: Reply by Mr P. A. Heasman
and Mrs J. Ellis (nee Adamson).
We are grateful to John Bradley for his detailed analysis of our data and findings and for his valuable suggestions and conclusions he has drawn from his comparison of our respective data British Journal of Oral and Maxillofacial Surgery, (1988), 26, 517. Indeed, many of the comments were similar to the valuable points which were raised by one of the papers referees. We do not wish to elaborate on each of the points which Mr Bradley raised but we are delighted that our paper has stimulated such detailed interest and, as Mr Bradley noted, we hope that it will stimulate further research in this area. P. A. HEASMAN Department of Operative Dentistry, University of Newcastle upon Tyne
NEW TREATMENT
FOR LUDWIG’S
ANGINA
Sir, Two distinct treatment methods are in current use for Ludwig’s angina. In both, airway maintenance is regarded as paramount in importance. One group achieve this by early tracheostomy or cricothyroidotomy (Lindner, 1986), reserving surgical drainage for localised abscesses. The other group advocate immediate surgical decompression of the obstructing oedema via submandibular incisions (Allen et al., 1985). Both groups administer high dose parenteral broad spectrum antibiotics to combat infection. However, neither of these treatments are universally successful. Occasionally, the neck and oral cavity swelling progresses unabated despite appropriate antibiotic therapy, or surgical intervention (Schwartz et al., 1974). Aspiration pneumonia may develop following tracheostomy (Selmo et al., 1973) and disfiguring neck scars are a frequent consequence. Death may still ensue despite treatment. (Barkin et al., 1975). It has been proposed that this bizarre cellulitic response to a common source of infection is due to the release of hyaluronidases and fibrinolysins by specific micro-organisms. These enzymes would open fascial planes, facilitating the spread of infection (Chow et al., 1978). However, the micro-organisms listed by Hought et al. (1980) m a review of Ludwig’s angina are remarkably similar to those cultured from Bartlett and O’Keefe’s (1979) series of localised perimandibular abscesses. In addition, several patients who developed Ludwig’s angina have been noted to suffer with pre-existing chronic disorders (Schwartz et al., 1974; Barkin et al., 1975). We considered that Ludwig’s angina might be a manifestation of a deficiency in host defence mechanisms, rather than the result of the activity of specific micro-organisms. We therefore decided to employ a treatment protocol using exogenous glucocorticosteroids to augment one of the body’s natural responses to infection in conjunction with high dose b oad spectrum antibiotics. Surgical decompression usually yields only small volumes of oedema fluid ag d rarely pus. As a result, this surgical treatment would be omitted, and tracheostomy would only be used in emergency. It has been possible to assess this treatment policy in a 46-year-old Caucasian woman who developed Ludwig’s angina from infection around her 67. Her condition had deteriorated over the 24 h prior to admission despite the administration of high doses of penicillin and metronidazole orally, but she improved dramatically following the addition of dexamethasone to this regime. Two days after admission, the Ludwig’s angina had resolved completely and an abscess had localised around the affected tooth. This drained spontaneously when the tooth was extracted under general anaesthesia. No single hospital sees sufficient cases to embark on a prospective treatment trial for Ludwig’s angina. Therefore, in the light of the rapidly successful outcome of this case, with no postoperative morbidity, we invite other surgeons to participate with us in a multicentre prospective trial of this new non-invasive treatment policy.
83
02664356x/89/0027-0083/$10.00
LETTERS AGE CHANGES
IN THE INFERIOR
TO THE EDITOR
ALVEOLAR
ARTERY
I have considered carefully the contents of the letter and I would appreciate the opportunity to publish the following reply: Reply by Mr P. A. Heasman
and Mrs J. Ellis (nee Adamson).
We are grateful to John Bradley for his detailed analysis of our data and findings and for his valuable suggestions and conclusions he has drawn from his comparison of our respective data British Journal of Oral and Maxillofacial Surgery, (1988), 26, 517. Indeed, many of the comments were similar to the valuable points which were raised by one of the papers referees. We do not wish to elaborate on each of the points which Mr Bradley raised but we are delighted that our paper has stimulated such detailed interest and, as Mr Bradley noted, we hope that it will stimulate further research in this area. P. A. HEASMAN Department of Operative Dentistry, University of Newcastle upon Tyne
NEW TREATMENT
FOR LUDWIG’S
ANGINA
Sir, Two distinct treatment methods are in current use for Ludwig’s angina. In both, airway maintenance is regarded as paramount in importance. One group achieve this by early tracheostomy or cricothyroidotomy (Lindner, 1986), reserving surgical drainage for localised abscesses. The other group advocate immediate surgical decompression of the obstructing oedema via submandibular incisions (Allen et al., 1985). Both groups administer high dose parenteral broad spectrum antibiotics to combat infection. However, neither of these treatments are universally successful. Occasionally, the neck and oral cavity swelling progresses unabated despite appropriate antibiotic therapy, or surgical intervention (Schwartz et al., 1974). Aspiration pneumonia may develop following tracheostomy (Selmo et al., 1973) and disfiguring neck scars are a frequent consequence. Death may still ensue despite treatment. (Barkin et al., 1975). It has been proposed that this bizarre cellulitic response to a common source of infection is due to the release of hyaluronidases and fibrinolysins by specific micro-organisms. These enzymes would open fascial planes, facilitating the spread of infection (Chow et al., 1978). However, the micro-organisms listed by Hought et al. (1980) m a review of Ludwig’s angina are remarkably similar to those cultured from Bartlett and O’Keefe’s (1979) series of localised perimandibular abscesses. In addition, several patients who developed Ludwig’s angina have been noted to suffer with pre-existing chronic disorders (Schwartz et al., 1974; Barkin et al., 1975). We considered that Ludwig’s angina might be a manifestation of a deficiency in host defence mechanisms, rather than the result of the activity of specific micro-organisms. We therefore decided to employ a treatment protocol using exogenous glucocorticosteroids to augment one of the body’s natural responses to infection in conjunction with high dose b oad spectrum antibiotics. Surgical decompression usually yields only small volumes of oedema fluid ag d rarely pus. As a result, this surgical treatment would be omitted, and tracheostomy would only be used in emergency. It has been possible to assess this treatment policy in a 46-year-old Caucasian woman who developed Ludwig’s angina from infection around her 67. Her condition had deteriorated over the 24 h prior to admission despite the administration of high doses of penicillin and metronidazole orally, but she improved dramatically following the addition of dexamethasone to this regime. Two days after admission, the Ludwig’s angina had resolved completely and an abscess had localised around the affected tooth. This drained spontaneously when the tooth was extracted under general anaesthesia. No single hospital sees sufficient cases to embark on a prospective treatment trial for Ludwig’s angina. Therefore, in the light of the rapidly successful outcome of this case, with no postoperative morbidity, we invite other surgeons to participate with us in a multicentre prospective trial of this new non-invasive treatment policy.
83