Descending necrotizing mediastinitis: a case report

Descending necrotizing mediastinitis: a case report

European Journal of Radiology Extra 49 (2004) 53–56 Descending necrotizing mediastinitis: a case report Canan Akman a,∗ , Yasemin Ayarcan a , Kursat ...

207KB Sizes 1 Downloads 118 Views

European Journal of Radiology Extra 49 (2004) 53–56

Descending necrotizing mediastinitis: a case report Canan Akman a,∗ , Yasemin Ayarcan a , Kursat Bozkurt b , Bulent Tutluoglu c , Mustafa Yaman c b

a Department of Radiology, Cerrahpasa Medicine School, Istanbul University, Cerrahpasa Istanbul 34300, Turkey Department of Cardiothoracic Surgury, Cerrahpasa Medicine School, Istanbul University, Cerrahpasa Istanbul 34300, Turkey c Department of Chest Diseases, Cerrahpasa Medicine School, Istanbul University, Cerrahpasa Istanbul 34300, Turkey

Received 17 June 2003; received in revised form 22 October 2003; accepted 24 October 2003

Abstract Descending necrotizing mediastinitis (DNM) is a relatively rare inflammatory pathology with high mortality rates unless an appropriate surgical treatment is undertaken. Early evaluation by means of thoracic computed tomography (CT) scanning is extremely useful for diagnosis and surgical treatment planning. We present a case of DNM in a 38-year-old man. He was admitted to hospital with a history of cough, fever and shortness of breath persisting for 15 days. Physical examination revealed orthopnoea, tachypnoea, and edema of the head and neck. Tonsils and the walls of the hypo- and oropharynx were hyperemic and hypertrophic, and tonsils were covered with an exudative membrane. Plain chest X-ray showed widening of the superior mediastinum. On CT examination there were air and air–fluid levels within mediastinal dense fatty planes that extended from the thoracic inlet to the subcarinal region along the retrotracheal–paraesophageal area. No contrast leakage into the mediastinum was detected with esophagography. Because of suspicion of mediastinitis and worsening of the patient’s symptoms, he underwent right thoracotomy. Widespread purulent material was observed in the middle and posterior mediastinal compartments. Mediastinal drainage, followed by extensive debridement of the necrotic tissue were carried out. Bacteriologic result from materials obtained through the mediastinal drainage yielded methicillin-resistant Staphylococcus aureus. Intravenous antibiotic (glycopeptides) therapy was performed. After the cultures of drained fluid became negative and control CT scan revealed complete regression of the pathologic findings, the patient was discharged from hospital. © 2003 Elsevier Ireland Ltd. All rights reserved. Keywords: Mediastinitis; Mediastinum; Abnormalities; CT

1. Introduction

2. Case report

Descending necrotizing mediastinitis (DNM) is a relatively rare inflammatory pathology with high mortality rates unless an appropriate surgical treatment is undertaken. Early evaluation by means of thoracic computed tomography (CT) scanning is extremely useful for diagnosis and surgical treatment planning [1,2]. Recently we diagnosed and successfully treated a patient with DNM. The treatment consisted of both surgery and medical therapy. By means of surgery mediastinal drainage through right thoracotomy was done. Continuous mediastinal irrigation was performed post-operatively, and the patient recovered well. Immediate drainage of the primary lesion and the mediastinum is important once the diagnosis of DNM is established.

A 38-year-old man was admitted to hospital with a history of cough, fever and shortness of breath persisting for 15 days. He was a heavy smoker and his past medical history included chronic cough that worsened in winter. Physical examination revealed orthopnoea, tachypnoea, and edema of the head and neck. On physical examination tonsils and the walls of the hypo- and oropharynx were hyperemic and hypertrophic, and tonsils were covered with an exudative membrane. On laboratory examination white blood cell count was 17,200 with 88% neutrophils, and 12% lymphocytes. Erythrocyte sedimentation rate (ESR) was elevated (85 mm/h). Serum biochemistry was normal except for an increased fasting blood glucose level (155 mg/dl). Blood gas analysis indicated hypoxemia (pO2 , 65 mmHg; pCO2 , 45 mmHg). Plain chest X-ray showed widening of the superior mediastinum (Fig. 1). On CT examination there were air images, fluid attenuation and air–fluid levels within mediastinal dense fatty planes that extended from the thoracic inlet to the



Tel.: +90-212-588-4800x218. E-mail address: [email protected] (C. Akman).

1571-4675/$ – see front matter © 2003 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/S1571-4675(03)00120-2

54

C. Akman et al. / European Journal of Radiology Extra 49 (2004) 53–56

Fig. 1. Postero-anterior chest radiography demonstrates widening of the superior mediastinum.

subcarinal region along the retrotracheal–paraesophageal area (Fig. 2a and b). Esophagography was performed with a water-soluble contrast agent and no contrast leakage into the mediastinum was detected. Because of suspicion of mediastinitis and worsening of the patient’s symptoms, he underwent right thoracotomy. Widespread purulent mate-

rial was observed in the middle and posterior mediastinal compartments. Mediastinal drainage, followed by extensive debridement of the necrotic tissue were carried out. He had an uneventful post-operative recovery. The patient was given antibiotherapy for 4 weeks as the culture of the surgical material yielded methicillin-resistant Staphylococcus

Fig. 2. Contrast-enhanced CT scans through the level of the thoracic inlet (a) and the subcarinal region (b) demonstrate the presence of air and air–fluid levels within the superior and posterior mediastinum that extended along the retrotracheal–paraesophageal area, obliteration of normal mediastinal fatty planes and thickening of esophageal wall (arrows).

C. Akman et al. / European Journal of Radiology Extra 49 (2004) 53–56

55

Fig. 3. Control CT scan through the level of the subcarinal region shows complete regression of the pathologic findings following extensive surgical debridement, excision of necrotic tissues and intravenous broad-spectrum antibiotic therapy (arrow).

aureus. The glycopeptide antibiotic vancomycin was used. Control CT scan revealed almost complete regression of the pathologic findings (Fig. 3).

3. Discussion Mediastinitis is the inflammation of the tissue around trachea–bronchial system, vascular structures and esophagus. Acute infections of the mediastinum are relatively uncommon. They are often associated with characteristic signs and symptoms such as retrosternal pain and fever, and many are fulminating and lethal. Most cases are associated with esophageal perforation and/or esophageal-cardiac surgery. Less common causes include direct extension of infection from adjacent tissues and tracheal or bronchial perforation following intubation, bronchoscopy or penetrating trauma. Rarely, mediastinitis is secondary to hematogenous spread of infection from an extrathoracic source, such as septic arthritis [3–6]. Chronic disease is most often the result of a tuberculous or fungal infection. Although chronic infections are characteristically insidious in at onset and unassociated with clinical manifestations, some patients may have symptoms or signs related to obstruction or compression of one or more mediastinal structures [7,8]. In addition to cases of chronic mediastinitis of infectious origin, there is a group of mediastinopathies of unknown cause characterized by the accumulation of dense fibrous tissue [9]. Descending necrotizing mediastinitis is an acute, polymicrobial infection of the mediastinum. Mostly originating from an odontogenic, pharyngeal or cervical infection, this necrotizing process descends into the mediastinum, pleural spaces, pericardium using the existing contiguous deep anatomic spaces of the neck. Propagation of pharyngeal infections into the mediastinum occurs predominantly via the parapharyngeal and carotid space and via the retropharyngeal, prevertebral spaces. The middle layer of deep cervical fascia fuses with the parietal pericardium at the level of the tracheal bifurcation and also closely adheres laterally to the mediastinal pleura. This anatomic relationship may explain not only the extension of necrotizing mediastinitis but also involvement of the pericardial and pleural cavity [1,2]. The

diagnostic criteria proposed by Estrera et al. [10] included clinical manifestations of severe oropharyngeal infection, demonstration of characteristic roentgenographic features of mediastinitis, documentation of necrotizing mediastinal infection at operation and/or post-mortem examination and establishment of the relationship of the oropharyngeal infection with mediastinal process. The main radiographic manifestation of DNM is widening of the mediastinum that is usually more evident superiorly. Air may be visible within the mediastinum as well as in the soft tissue planes of the neck. Pneumothorax and/or hydropneumothorax may also be evident. CT findings include esophageal wall thickening, obliteration of normal mediastinal fatty planes, air or air–fluid levels within the mediastinum or in the soft tissues of the neck [11,12]. CT examination of the chest is crucial both for diagnosis and treatment, preoperative CT scanning provides valuable information about the involvement of the mediastinal compartments by the inflammatory and necrotizing process. Dissemination of the disease determines the prognosis and surgical approach [1]. DNM is classified by CT as local and diffuse forms, according to the degree of dissemination. The diffuse type has the worst prognosis. Localized DNM (Type I) is localized to the upper mediastinum above the carina. Infection may extend to the lower anterior mediastinum (diffuse DNM-Type IIA), or to both anterior and posterior mediastinum (diffuse DNM-Type IIB). Type I may not always necessitate aggressive drainage, although transcervical approach may sometimes be necessary. Type IIA may require subxiphoid drainage and thoracotomy is the preferred operation for IIB lesions [1,13]. In our case, the presence of oropharyngeal infection with characteristic CT findings of mediastinitis suggests the diagnosis. As the majority of acute mediastinal infections results from esophageal perforation, esophagography was performed, but there was no contrast leakage into the mediastinum or pleural space. The patient had no history of recent thoracic surgery or penetrating trauma leading to mediastinal infection. Distinction from tuberculous mediastinitis was done with acute onset of the disease, increased white blood cell count and absence of typical radiographic findings such as pulmonary parenchymal infiltration and/or

56

C. Akman et al. / European Journal of Radiology Extra 49 (2004) 53–56

peripherally enhanced bulky necrotic lymphadenopathies. The only possible source of mediastinal infection was acute tonsillo-pharyngitis that spread to the posterior mediastinum through the fascial planes. CT scan of the chest revealed Type IIB DNM as classified by Endo et al. [13], and thoracotomy was performed for mediastinal drainage and debridement. Bacteriologic results from materials obtained through the mediastinal drainage at thoracotomy yielded methicillin-resistant S. aureus. In the present case, the outcome was favorable following surgical mediastinal drainage, extensive debridement and excision of necrotic tissues, wide mediastinal irrigation and intravenous antibiotic therapy. After the cultures of drained fluid became negative, the patient was discharged from hospital. Radiologic work-up is necessary and crucial both in the diagnosis and post-treatment follow-ups. Routine use of the CT scan is highly recommended in patients with deep cervical infection for early detection of mediastinitis when mediastinal widening is observed on chest roentgenograms. An algorithm including CT imaging for diagnosis and surveillance, and serial transcervical and transthoracic operative drainage may reduce mortality from DNM. Delayed diagnosis and inadequate drainage are the main causes of the high mortality rate in this life threatening condition.

References [1] Marty-Ane CH, Berthet JP, Alric P, Pegis JD, Rouviere P, Mary H. Management of descending necrotizing mediastinitis: an aggressive treatment for an aggressive disease. Ann Thorac Surg 1999;68(1):212–7.

[2] Freeman RK, Vallieres E, Verrier ED, Karmy-Jones R, Wood DE. Descending necrotizing mediastinitis: an analysis of the effects of serial surgical debridement on patient mortality. J Thorac Cardiovasc Surg 2000;119(2):260–7. [3] Jolles H, Henry DA, Roberson JP, Cole TJ, Spratt JA. Mediastinitis following median sternotomy: CT findings. Radiology 1996;201(2):463–6. [4] Goodman LR, Kay HR, Teplick SK, Mundth ED. Complications of median sternotomy: computed tomographic evaluation. AJR Am J Roentgenol 1983;141(2):225–30. [5] Carrol CL, Jeffrey Jr RB, Federle MP, Vernacchia FS. CT evaluation of mediastinal infections. J Comput Assist Tomogr 1987;11(3):449– 54. [6] Curtis JJ, Clark NC, McKenney CA, et al. Tracheostomy: a risk factor for mediastinitis after cardiac operation. Ann Thorac Surg 2001;72(3):731–4. [7] Weinstein JB, Aronberg DJ, Sagel SS. CT of fibrosing mediastinitis: findings and their utility. AJR Am J Roentgenol 1983;141(2):247– 51. [8] Ramakantan R, Shah P. Dysphagia due to mediastinal fibrosis in advanced pulmonary tuberculosis. AJR Am J Roentgenol 1990;154(1):61–3. [9] Mole TM, Glover J, Sheppard MN. Sclerosing mediastinitis: a report on 18 cases. Thorax 1995;50(3):280–3. [10] Estrera AS, Landay MJ, Grisham JM, Sinn DP, Platt MR. Descending necrotizing mediastinitis. Surg Gynecol Obstret 1983;157(6):545– 52. [11] Christoforidis A, Nelson SW. Spontaneous rupture of the esophagus with emphasis on the roentgenologic diagnosis. AJR Am J Roentgenol 1957;78:574. [12] Fraser RS, Colman N, Müller NL, Pare PD. Mediastinal disease. In: Fraser and Paré’s diagnosis of diseases of the chest. 4th ed. Philadelphia: WB Saunders; 1999. p. 2851–74. [13] Endo S, Murayama F, Hasegawa T, et al. Guideline of surgical management based on diffusion of descending necrotizing mediastinitis. Jpn J Thorac Cardiovasc Surg 1999;47(1):14–91.