Intrmu~ronal
Journul of Pediatric
OrorhlnolurynRoloR.
20 (1990) 73- 79
Elsevier
PEDOT
00665
Peritonsillar Robert
abscess in Kawasaki
E. Rothfield,
disease
Moises A. Arriaga and Herman
*
Felder
Deprrrtmenr of Oiolaryngologv, L~moemty of Pittsburgh School of Medmne. Eve and Ear Instrture of Plttvhurgh, Plrtshurgh. PA 15-713 (U.S.A.) (Received 6 February 1990) (Revised version received 25 April 1990) (Accepted 18 May 1990)
Kq words: Kawasaki
disease;
Peritonsillar
abscess
Abstract
Mucocutaneous lymph node syndrome, Kawasaki disease, is a potentially fatal pediatric disease characterized by prolonged high fever, conjunctivitis. stomatitis, myocarditis, aseptic meningitis and coronary artery vasculitis. We present peritonsillar abscess as a previously unreported otolaryngologic symptom and presentation of Kawasaki disease. A previously healthy 7-year-old boy required hospitalization for a peritonsillar abscess. Despite adequate surgical drainage and appropriate intravenous antibiotics, the patients’ systemic symptoms persisted. After the week of hospitalization, the child was transferred to the intensive care unit with acute myocarditis, heart failure and severe arthritis. The diagnosis of Kawasaki disease was confirmed with echocardiographic evidence of coronary artery aneurysms and the development of the characteristic hand and foot desquamation. The patient’s symptoms resolved with salicylates and intravenous gamma globulin therapy. He was discharged in good condition after 3 weeks of hospitalization. This is the first report of Kawasaki syndrome presenting with peritonsillar abscess. Although we discuss a unique presentation of this disease, Kawasaki syndrome often exhibits other otolaryngologic findings early in its course. A literature review of the clinical characteristics, pathogenesis and therapy of this disease is presented.
* Presented at the Annual Meeting of the Society for Ear, Nose. and Throat Advances in Children. Santa Momca, CA, November 30, 1989. Corre.7pondenc.e: R.E. Rothfield, Department of Otolaryngology, University of Pittsburgh School of Medicine. The Eye and Ear Institute of Pittsburgh, Suite 500, 203 Lothrop Street. Pittsburgh. PA 15213, U.S.A.
0165-5X76/90/$03.50
fi~j1990 Elsevier Science
Publishers
B.V. (Biomedical
Division)
74
Introduction Mucocutaneous lymph node syndrome, an acute self-limited but potentially fatal illness in children, was initially described by Kawasaki in 1967 and is being recognized with increased frequency in the United States [6]. The disease is characterized by prolonged high fever, conjunctivitis, stomatitis, cervical adenitis, periungual desquamation, arthritis and coronary artery vasculitis. We present a case of peritonsillar abscess as a previously unreported symptom and mode of presentation for Kawasaki disease.
Case report
A previously healthy 7-year-old white male presented with persistent sore throat and fever of 39 o C. Four days prior to admission, the patient had finished a lo-day course of amoxicillin/clavulanate for culture-positive streptococcal tonsillitis. The patient had been diagnosed and successfully treated for streptococcal tonsillitis 4 times over the preceding year, most recently one month prior to the present episode. On admission, the patient appeared ill but not toxic. Physical examination revealed a right peritonsillar abscess with pharyngeal erythema and bilateral cervical adenopathy. A marked leukocytosis with a left shift and thrombocytosis were noted. Incision and drainage of the peritonsillar abscess was performed with aspiration of 5 ml of purulent material and the patient was started on high dose intravenous penicillin. Subsequent cultures of the purulent aspirate were negative and no organisms were seen on gram stain. Postoperatively, the patient did not defervesce and was spiking fevers as high as 39S”C. Over the next 48 h, the patient was noted to develop increased cervical adenopathy and bilateral conjunctivitis. Ticarcillin/clavulanate was added to the antibiotic regimen without apparent effect. By the third postoperative day, the patient appeared toxic, was spiking temperatures to 40.6 o C and had marked increase in his bilateral jugulodigastric and posterior cervical adenopathy. A CT scan was obtained confirming the above clinical findings and showed several of the nodes to contain hypodense centers (Fig. I). On the fourth postoperative day, the patient continued to spike temperatures as high as 40” C with the development of torticollis, trismus and increased cervical adenopathy. Resolution of the conjunctivitis was noted at this time. The penicillin and timentin were discontinued and replaced with IV clindamycin. On the seventh postoperative day (day 21 of the illness), with progression of the above symptoms and fever, the patient was taken to the operating room for a right tonsillectomy and neck exploration. A large phlegmon, but no gross pus, was encountered. The patient continued to spike high fevers and, several hours postoperatively, developed respiratory distress, Chest radiograph revealed bilateral pleural effusions as well as a large pericardial effusion (Fig. 2). In addition, the patient began to complain of generalized arthralgias. Echocardiogram and cardiac catheterization were performed and demonstrated the noted pericardial effusion as well as mild
Fig. 1. CT showing
lymphadenopathy
and several lymph nodes with hypodense
centers
ventricular dysfunction. No abnormalities of the coronary vessels were noted at this time. Pericardiocentesis yielded 144 ml’s of a sterile transudate. Streptozyme was positive at 100 units and the AS0 was positive at 340 units. Rheumatoid factor was negative. The sedimentation rate was 72. On the second and third postoperative days (days 23-24 of the illness), the patient continued to spike high temperatures to 40°C with marked increase in his generalized arthralgias. On the third postoperative day, the patient was also noted to develop a fine macular erythematous rash diffusely along his lower extremities. By postoperative day 4, there were still no positive cultures and it was evident that the etiology of this illness was collagen vascular/immunologic or viral in nature. High-dose aspirin therapy was begun with good resolution of the arthralgias. A 4-day course of gamma globulin therapy was also instituted at this time. The patient continued to spike fevers to 39” C. On postoperative day 5 (day 26 of the illness), periungual desquamation of the patient’s hands was noted, which increased
Fig. 2. Chest radiograph
showing
bilateral
pleural
effusions
and large pericardial
effusion.
over the ensuing days, eventually involving the feet as well (Fig. 3). With this development, the diagnosis of Kawasaki disease was confirmed. A repeat echocardiogram showed complete resolution of the pericardial effusion, but the development of a fusiform aneurysm of the right main coronary artery and a saccular aneurysm of the left anterior descending coronary artery. High-dose aspirin therapy was continued (100 mg/kg/day) for the ensuing two weeks. Over this period of time, the patient defervesced and his other symptoms resolved. He was discharged to his home 40 days after the onset of his illness. Repeat echocardiogram and cardiac catheterization one year later showed complete resolution of the coronary artery aneurysms and good ventricular function.
17
Fig. 3. Periungual
desquamation
of hands
Comment
This case demonstrates many of the characteristic features of Kawasaki disease, a number of which may lead to presentation to an otolaryngologist. Diagnostic criteria for Kawasaki disease as set forth by the Centers for Disease Control are as follows [ 11: (1) fever > 5 days duration; and (2) presence of 4 of the 5 following conditions: (a) bilateral conjunctival injection (b) changes in the mucous membranes of the respiratory tract including erythema (c) changes in the peripheral extremities including erythema, edema. and periungual desquamation (d) rash (e) cervical lymphadenopathy. Although cervical lymphadenopathy is seen in 50-75% of patients, it is typically non-suppurative and peritonsillar abscess has not been reported as a presenting manifestation or sequelae of this disease. In addition to the above criteria, other common manifestations of the disease include arthralgia, diarrhea, pneumonia, meatal inflammation and cardiac disease [9]. Although only 20% of patients will manifest cardiac abnormalities, it is in this subgroup of patients in whom the potential mortality is greatest. Less common manifestations of the disease include seizures, jaundice, encephalopathy, uveitis, pleural effusions, hydrops of the gall bladder and pancreatitis [5]. Kawasaki disease has been characterized by 3 distinct phases. The acute phase, lasting 7-10 days, is associated with fever, conjunctival injection, stomatitis, rash,
changes in the extremities and perivasculitis of the coronary arteries. The subacute phase, lasting lo-25 days, is associated with resolution of the fever and rash but development of periungual desquamation, arthralgias and coronary artery aneurysms and myocardial dysfunction. The last stage, the convalescent phase, begins with the resolution of all signs and symptoms of illness and ends approximately two months after the onset of illness with the normalization of the sedimentation rate. The mortality of Kawasaki disease, up to 2% of patients, is a result of the cardiac pathology, which has been reported in up to 20% of patients. Pathologically, the acute phase is characterized by perivasculitis of the coronary arteries, pericarditis and inflammation of the conductive system. The subacute phase is associated with coronary artery aneurysms, obstruction and thrombosis, and myocardial inflammation and fibrosis. The convalescent phase may demonstrate scarring, calcification, stenosis, recanalization or, in up to 50% of patients, spontaneous resolution of coronary artery aneurysms [2]. Laboratory findings in Kawasaki disease are non-specific and non-diagnostic. However, 3 of the most consistent findings include thrombocytosis, leukocytosis and an elevated sedimentation rate, all of which were noted in the present case. Until the etiology of Kawasaki disease is understood, definitive therapy is not possible. Nevertheless, efforts are directed at diminishing the cardiac insult by reducing myocardial and coronary artery wall inflammation and by lessening the incidence of thrombosis by limiting platelet aggregation [3,4]. High dose aspirin therapy (100 mg/kg) has been employed with apparent good success in lessening the acute manifestations of the disease and in decreasing the morbidity of coronary artery disease. Intravenous gamma globulin has also been reported as effective in reducing coronary disease, the mechanism by which it effects this is, however, unknown [7,8]. These two drugs have become the mainstay of treatment and appear to reduce coronary artery involvement, decrease the duration of fevers and lessen arthralgias.
Conclusion The incidence and recognition of Kawasaki disease in the United States is With this increased incidence there will be increasing numbers of increasing. patients presenting with this disease to otolaryngologists. When faced with a patient with the standard stigmata of a viral illness (fever, rash, conjunctivitis, pharyngeal erythema and cervical adenopathy) but with prolonged and unexplained fever, the diagnosis of Kawasaki disease should be entertained. Recognition of this disease entity, with the attendant appropriate medical treatment, will help to lessen both its morbidity and mortality.
References 1 Centers for Disease Control, Kawasaki disease, New York, Morbid. Mort. Wkly Rep., 29 (1980) 61-63.
79
2 Kato, H., Ichinose, E., Yoshioka, F., et al.. Fate of coronary aneurysms in Kawasaki disease: serial coronary angiography and long-term follow-up study, Am. J. Cardiol.. 49 (1982) 1758-1766. 3 Kato. H.. Koike. S. and Yokoyama, T., Kawasaki disease: effect of treatment on coronary artery involvement, Pediatrics, 63 (1979) 175-179. 4 Koren, G., Rose. V., Lavi. S., et al., Probable efficacy of high dose salicylates in reducing coronary artery involvement in Kawasaki disease, J. Am. Med. Assoc., 254 (1985) 7677769. 5 Lewis, M.J. and Neal, W.A., Kawasaki disease: an update. W. Virginia Med. J.. 84 (1988) 657-660. 6 Morens, D.M.. Anderson, L.J. and Hurwitz, E.S.. National surveillance of Kawasaki disease. Pediatrics. 65 (1980) 21-25. 7 Nagashima, M.. Matsushima. M.. et al., High dose gamma globulin therapy for Kawasaki disease. J. Pediatr., 110 (1987) 71-74. 8 Newberger, J.E., Takahashi, M.. Burns, J.C.. et al.. The treatment of Kawasaki syndrome with intravenous gamma globulin, N. Engl. J. Med.. 63 (1979) 1755179. 9 Rowley, A.H.. Gonzalez-Crussi. F. and Shulman, ST.. Kawasaki syndrome, Rev. Infect. Dis.. 10 (1988) l-15.
Journul of Pediatric
OrorhlnolurynRoloR.
20 (1990) 73- 79
Elsevier
PEDOT
00665
Peritonsillar Robert
abscess in Kawasaki
E. Rothfield,
disease
Moises A. Arriaga and Herman
*
Felder
Deprrrtmenr of Oiolaryngologv, L~moemty of Pittsburgh School of Medmne. Eve and Ear Instrture of Plttvhurgh, Plrtshurgh. PA 15-713 (U.S.A.) (Received 6 February 1990) (Revised version received 25 April 1990) (Accepted 18 May 1990)
Kq words: Kawasaki
disease;
Peritonsillar
abscess
Abstract
Mucocutaneous lymph node syndrome, Kawasaki disease, is a potentially fatal pediatric disease characterized by prolonged high fever, conjunctivitis. stomatitis, myocarditis, aseptic meningitis and coronary artery vasculitis. We present peritonsillar abscess as a previously unreported otolaryngologic symptom and presentation of Kawasaki disease. A previously healthy 7-year-old boy required hospitalization for a peritonsillar abscess. Despite adequate surgical drainage and appropriate intravenous antibiotics, the patients’ systemic symptoms persisted. After the week of hospitalization, the child was transferred to the intensive care unit with acute myocarditis, heart failure and severe arthritis. The diagnosis of Kawasaki disease was confirmed with echocardiographic evidence of coronary artery aneurysms and the development of the characteristic hand and foot desquamation. The patient’s symptoms resolved with salicylates and intravenous gamma globulin therapy. He was discharged in good condition after 3 weeks of hospitalization. This is the first report of Kawasaki syndrome presenting with peritonsillar abscess. Although we discuss a unique presentation of this disease, Kawasaki syndrome often exhibits other otolaryngologic findings early in its course. A literature review of the clinical characteristics, pathogenesis and therapy of this disease is presented.
* Presented at the Annual Meeting of the Society for Ear, Nose. and Throat Advances in Children. Santa Momca, CA, November 30, 1989. Corre.7pondenc.e: R.E. Rothfield, Department of Otolaryngology, University of Pittsburgh School of Medicine. The Eye and Ear Institute of Pittsburgh, Suite 500, 203 Lothrop Street. Pittsburgh. PA 15213, U.S.A.
0165-5X76/90/$03.50
fi~j1990 Elsevier Science
Publishers
B.V. (Biomedical
Division)
74
Introduction Mucocutaneous lymph node syndrome, an acute self-limited but potentially fatal illness in children, was initially described by Kawasaki in 1967 and is being recognized with increased frequency in the United States [6]. The disease is characterized by prolonged high fever, conjunctivitis, stomatitis, cervical adenitis, periungual desquamation, arthritis and coronary artery vasculitis. We present a case of peritonsillar abscess as a previously unreported symptom and mode of presentation for Kawasaki disease.
Case report
A previously healthy 7-year-old white male presented with persistent sore throat and fever of 39 o C. Four days prior to admission, the patient had finished a lo-day course of amoxicillin/clavulanate for culture-positive streptococcal tonsillitis. The patient had been diagnosed and successfully treated for streptococcal tonsillitis 4 times over the preceding year, most recently one month prior to the present episode. On admission, the patient appeared ill but not toxic. Physical examination revealed a right peritonsillar abscess with pharyngeal erythema and bilateral cervical adenopathy. A marked leukocytosis with a left shift and thrombocytosis were noted. Incision and drainage of the peritonsillar abscess was performed with aspiration of 5 ml of purulent material and the patient was started on high dose intravenous penicillin. Subsequent cultures of the purulent aspirate were negative and no organisms were seen on gram stain. Postoperatively, the patient did not defervesce and was spiking fevers as high as 39S”C. Over the next 48 h, the patient was noted to develop increased cervical adenopathy and bilateral conjunctivitis. Ticarcillin/clavulanate was added to the antibiotic regimen without apparent effect. By the third postoperative day, the patient appeared toxic, was spiking temperatures to 40.6 o C and had marked increase in his bilateral jugulodigastric and posterior cervical adenopathy. A CT scan was obtained confirming the above clinical findings and showed several of the nodes to contain hypodense centers (Fig. I). On the fourth postoperative day, the patient continued to spike temperatures as high as 40” C with the development of torticollis, trismus and increased cervical adenopathy. Resolution of the conjunctivitis was noted at this time. The penicillin and timentin were discontinued and replaced with IV clindamycin. On the seventh postoperative day (day 21 of the illness), with progression of the above symptoms and fever, the patient was taken to the operating room for a right tonsillectomy and neck exploration. A large phlegmon, but no gross pus, was encountered. The patient continued to spike high fevers and, several hours postoperatively, developed respiratory distress, Chest radiograph revealed bilateral pleural effusions as well as a large pericardial effusion (Fig. 2). In addition, the patient began to complain of generalized arthralgias. Echocardiogram and cardiac catheterization were performed and demonstrated the noted pericardial effusion as well as mild
Fig. 1. CT showing
lymphadenopathy
and several lymph nodes with hypodense
centers
ventricular dysfunction. No abnormalities of the coronary vessels were noted at this time. Pericardiocentesis yielded 144 ml’s of a sterile transudate. Streptozyme was positive at 100 units and the AS0 was positive at 340 units. Rheumatoid factor was negative. The sedimentation rate was 72. On the second and third postoperative days (days 23-24 of the illness), the patient continued to spike high temperatures to 40°C with marked increase in his generalized arthralgias. On the third postoperative day, the patient was also noted to develop a fine macular erythematous rash diffusely along his lower extremities. By postoperative day 4, there were still no positive cultures and it was evident that the etiology of this illness was collagen vascular/immunologic or viral in nature. High-dose aspirin therapy was begun with good resolution of the arthralgias. A 4-day course of gamma globulin therapy was also instituted at this time. The patient continued to spike fevers to 39” C. On postoperative day 5 (day 26 of the illness), periungual desquamation of the patient’s hands was noted, which increased
Fig. 2. Chest radiograph
showing
bilateral
pleural
effusions
and large pericardial
effusion.
over the ensuing days, eventually involving the feet as well (Fig. 3). With this development, the diagnosis of Kawasaki disease was confirmed. A repeat echocardiogram showed complete resolution of the pericardial effusion, but the development of a fusiform aneurysm of the right main coronary artery and a saccular aneurysm of the left anterior descending coronary artery. High-dose aspirin therapy was continued (100 mg/kg/day) for the ensuing two weeks. Over this period of time, the patient defervesced and his other symptoms resolved. He was discharged to his home 40 days after the onset of his illness. Repeat echocardiogram and cardiac catheterization one year later showed complete resolution of the coronary artery aneurysms and good ventricular function.
17
Fig. 3. Periungual
desquamation
of hands
Comment
This case demonstrates many of the characteristic features of Kawasaki disease, a number of which may lead to presentation to an otolaryngologist. Diagnostic criteria for Kawasaki disease as set forth by the Centers for Disease Control are as follows [ 11: (1) fever > 5 days duration; and (2) presence of 4 of the 5 following conditions: (a) bilateral conjunctival injection (b) changes in the mucous membranes of the respiratory tract including erythema (c) changes in the peripheral extremities including erythema, edema. and periungual desquamation (d) rash (e) cervical lymphadenopathy. Although cervical lymphadenopathy is seen in 50-75% of patients, it is typically non-suppurative and peritonsillar abscess has not been reported as a presenting manifestation or sequelae of this disease. In addition to the above criteria, other common manifestations of the disease include arthralgia, diarrhea, pneumonia, meatal inflammation and cardiac disease [9]. Although only 20% of patients will manifest cardiac abnormalities, it is in this subgroup of patients in whom the potential mortality is greatest. Less common manifestations of the disease include seizures, jaundice, encephalopathy, uveitis, pleural effusions, hydrops of the gall bladder and pancreatitis [5]. Kawasaki disease has been characterized by 3 distinct phases. The acute phase, lasting 7-10 days, is associated with fever, conjunctival injection, stomatitis, rash,
changes in the extremities and perivasculitis of the coronary arteries. The subacute phase, lasting lo-25 days, is associated with resolution of the fever and rash but development of periungual desquamation, arthralgias and coronary artery aneurysms and myocardial dysfunction. The last stage, the convalescent phase, begins with the resolution of all signs and symptoms of illness and ends approximately two months after the onset of illness with the normalization of the sedimentation rate. The mortality of Kawasaki disease, up to 2% of patients, is a result of the cardiac pathology, which has been reported in up to 20% of patients. Pathologically, the acute phase is characterized by perivasculitis of the coronary arteries, pericarditis and inflammation of the conductive system. The subacute phase is associated with coronary artery aneurysms, obstruction and thrombosis, and myocardial inflammation and fibrosis. The convalescent phase may demonstrate scarring, calcification, stenosis, recanalization or, in up to 50% of patients, spontaneous resolution of coronary artery aneurysms [2]. Laboratory findings in Kawasaki disease are non-specific and non-diagnostic. However, 3 of the most consistent findings include thrombocytosis, leukocytosis and an elevated sedimentation rate, all of which were noted in the present case. Until the etiology of Kawasaki disease is understood, definitive therapy is not possible. Nevertheless, efforts are directed at diminishing the cardiac insult by reducing myocardial and coronary artery wall inflammation and by lessening the incidence of thrombosis by limiting platelet aggregation [3,4]. High dose aspirin therapy (100 mg/kg) has been employed with apparent good success in lessening the acute manifestations of the disease and in decreasing the morbidity of coronary artery disease. Intravenous gamma globulin has also been reported as effective in reducing coronary disease, the mechanism by which it effects this is, however, unknown [7,8]. These two drugs have become the mainstay of treatment and appear to reduce coronary artery involvement, decrease the duration of fevers and lessen arthralgias.
Conclusion The incidence and recognition of Kawasaki disease in the United States is With this increased incidence there will be increasing numbers of increasing. patients presenting with this disease to otolaryngologists. When faced with a patient with the standard stigmata of a viral illness (fever, rash, conjunctivitis, pharyngeal erythema and cervical adenopathy) but with prolonged and unexplained fever, the diagnosis of Kawasaki disease should be entertained. Recognition of this disease entity, with the attendant appropriate medical treatment, will help to lessen both its morbidity and mortality.
References 1 Centers for Disease Control, Kawasaki disease, New York, Morbid. Mort. Wkly Rep., 29 (1980) 61-63.
79
2 Kato, H., Ichinose, E., Yoshioka, F., et al.. Fate of coronary aneurysms in Kawasaki disease: serial coronary angiography and long-term follow-up study, Am. J. Cardiol.. 49 (1982) 1758-1766. 3 Kato. H.. Koike. S. and Yokoyama, T., Kawasaki disease: effect of treatment on coronary artery involvement, Pediatrics, 63 (1979) 175-179. 4 Koren, G., Rose. V., Lavi. S., et al., Probable efficacy of high dose salicylates in reducing coronary artery involvement in Kawasaki disease, J. Am. Med. Assoc., 254 (1985) 7677769. 5 Lewis, M.J. and Neal, W.A., Kawasaki disease: an update. W. Virginia Med. J.. 84 (1988) 657-660. 6 Morens, D.M.. Anderson, L.J. and Hurwitz, E.S.. National surveillance of Kawasaki disease. Pediatrics. 65 (1980) 21-25. 7 Nagashima, M.. Matsushima. M.. et al., High dose gamma globulin therapy for Kawasaki disease. J. Pediatr., 110 (1987) 71-74. 8 Newberger, J.E., Takahashi, M.. Burns, J.C.. et al.. The treatment of Kawasaki syndrome with intravenous gamma globulin, N. Engl. J. Med.. 63 (1979) 1755179. 9 Rowley, A.H.. Gonzalez-Crussi. F. and Shulman, ST.. Kawasaki syndrome, Rev. Infect. Dis.. 10 (1988) l-15.
