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Group C streptococcal endocarditis associated with intubation-induced tracheal stenosis
376
IJC 0109E
Group C streptococcal endocarditis associated with intubation-induced tracheal stenosis C.M. Jack, M.M. Khan and A.A.J. Adgey Regional Medical Cardiology Centre, Royal Victorra Hosprtal. Belfast BTIZ 6BA. Northern Ireland (Received
29 September
1983; accepted
17 October
1983)
We describe a 44-year-old woman with Group C haemolytic streptococcal endocarditis who developed tracheal stenosis as a result of endotracheal intuhation. She recovered fully following valve replacement for continuing left ventricular failure due to mitral and aortic incompetence and subsequent resection of the steno& tracheal segment with reanastomosis of the trachea.
Infective endocarditis due to Lancefield Group C streptococci is rare [l]. When it occurs. it pursues an acute and rapidly destructive course, leading to valvular incompetence and early cardiac failure [l-3]. Tracheal stenosis is increasingly detected in patients who have been intubated and in those who have undergone tracheostomy [4,5]. We report a case of infective endocarditis which was associated with tracheal stenosis due to endotracheal intubation. Treatment was by valve replacement for continuing left ventricular failure due to mitral and aortic incompetence, followed by resection of the stenosed tracheal segment and reanastomosis of the trachea.
Case Report A 44-year-old woman was admitted to hospital in March 1980. with a 5-day history of joint pains, rigors and cough. She had previously been in good health and had no prior medical history. On admission she was pyrexial. A loud pansystolic murmur of mitral incompetence was heard at the apex. Blood cultures demonstrated presence of Group C haemolytic streptococci and she was commenced on parenteral antibiotics. A diagnosis of septicaemia had been made with the probability of bacterial endocarditis because of the signs of mitral incompetence. Five days after admission the patient developed pulmonary oedema complicated by an asystolic cardiac arrest. Resuscitation was successful but she required artificial ventilation. Following resuscitation an endotracheal tube was left in situ for 6 days Correspondence and reprint requests to: A.A.J. Adgey. M.D., Royal Victoria Hospital. Belfast BT12 6BA. Northern Ireland.
International Journal of Cardrology, 5 0 Elsevier Science Publishers B.V.
(1984)376-379
Regional
Medical
Cardiology
Centre.
Fig. Cross-sectional echocardiogram in the left parastemal long axis view showing aortic and mitral valves. AML = anterior mitral leaflet; A0 = aorta; LA = left atrium;
vegetations on the LV = left ventricle.
and then a tracheostomy was performed. The patient improved gradually but artificial ventilation was required for 1 month following the tracheostomy for continuing left ventricular failure and respiratory difficulties. She was then weaned off the ventilator. In April 1980 the patient was transferred to this centre. On admission aortic and mitral incompetence were present. An echocardiogram showed vegetations on the aortic and mitral valves and a flail mitral leaflet (Fig). Parenteral antibiotics were continued. Over the next few days the patient became increasingly more dyspnoeic in association with pronounced stridor and difficulty in expectorating sputum. Laryngoscopy showed paralysis of the left vocal cord. Bronchoscopy showed a stenosis of the trachea which was dilated. The patient continued to
378
have difficulty in expectoration in association with stridor and repeat bronchoscopy 6 days later again showed tracheal stenosis. Dilatation of the stenosed segment was again carried out. Cardiac catheterisation confirmed severe regurgitation of both mitral and aortic valves with continuing left ventricular failure. At surgery the following day vegetations were confirmed on both valves and there was a flail mitral leaflet. The aortic valve was not bicuspid. During the operation the inhalational agents were given via an endotracheal tube. Aortic and mitral valve replacement was carried out. Sectioning of the removed mitral and aortic valves showed no evidence of prior rheumatic infection or myxomatous degeneration. In the post-operative period the patient again required ventilation using both endotracheal and nasotracheal intubation. The patient was extubated after 5 days. During the convalescent period and following extubation the tracheal stenosis recurred. The patient had difficulty with expectoration and became increasingly dyspnoeic. Emergency bronchoscopy had to be carried out on 2 separate occasions and the stricture dilated on both occasions. At operation in late June 1980 (16 weeks after her initial hospital admission) the stricture was found to be 3 cm in length and 18 cm from the patient’s lower lip. The 3 cm stenosed segment of the trachea was resected using a novel anaesthetic technique. Anaesthesia was induced by the intravenous administration of althesin and maintained with nitrous oxide in oxygen with halothane delivered by a face mask. After intubation anaesthesia was continued with an infusion of althesin. The patient continued to breathe spontaneously. During the operation, a short tracheal tube was passed to lie proximal to the stenosed tracheal segment. During the tracheal resection and reanastomosis, 100% oxygen was allowed to flow through the tracheal tube and flood the surgical field. The distal tracheal segment was not intubated and in effect the patient continued to breathe spontaneously through the distal tracheal segment below the resection. Special care was taken by the surgical team to keep the trachea free from blood. The respiratory pattern was closely observed during the operation and frequent arterial blood samples were taken for gas analysis throughout. The upper and lower parts of the remaining trachea were joined in an end-to-end anastomosis, after freeing from connective tissue. The patient made good progress and was discharged from hospital 2 weeks later without complications. She remains very well at review 3 years later and has returned to full working capacity. Discussion
As far as we know, this is the only case of bacterial endocarditis complicated by tracheal stenosis that has been reported during the past decade. Serious systemic infections such as septicaemia or endocarditis caused by Lancefield Group C streptococci are extremely rare. Mohr et al. [l] reported the results of 150,000 blood cultures over 9 years and found that Group C streptococci were isolated in only 8 patients. There are 11 previously reported cases of Lancefield Group C endocarditis [l-3]. Five of these patients died. With the acute and rapidly destructive course of Group C endocarditis leading to early cardiac decompensation [l], it is not surprising that our patient despite early antibiotic therapy had an acute fulminant illness with rapid haemodynamic deterioration, left ventricular failure and an asystolic arrest. This patient came to valvular replacement because of continuing left ventricular failure due to aortic and mitral incompetence. All 3 of the previous patients who underwent urgent heart surgery have survived [1,2]. In 7 of the 11 previously reported cases the infection became established on normal heart valves [1,2]. Our patient was in good health before admission and had no history of rheumatic infection. Histology of the valves did not show any evidence of rheumatic valvular disease or myxomatous degeneration.
379
Tracheal stenosis consequent on endotracheal intubation has been reported with increasing frequency over the past 12 years [4,5]. As an iatrogenic disease it is becoming more frequently recognized. Tracheal stricture has occurred after as short a time period as 72 hours intubation [6]. Of all the causative factors, prolonged intubation is probably the most significant. Our patient was initially intubated for 6 days. The anaesthetic technique employed during the tracheal resection and anastomosis in this case is also of interest. The patient was allowed to breathe spontaneously through the distal tracheal segment during the resection. The distal segment was kept free of blood and 100% oxygen was delivered to the surgical field via the proximal tracheal segment. Anaesthesia was maintained by an intravenous infusion of althesin. Unrestricted access to the 2 ends of the trachea improved the speed and ease of the operation. Acknowledgements We are grateful to J. Cleland, and anaesthesia in this patient.
H.M. Stevenson
and M. Lyons who carried out the surgery
References Mohr DN, Feist, DJ, Washington JA II, Hermans PE. Infections due to Group C streptococci in man. Am J Med 1979;66:450-456. Davies MK, Ireland MA, Clarke DB. Infective endocarditis from Group C streptococci causing stenosis of both the aortic and mitral valves. Thorax 1981;36:69-71. Ghoneim ATM, Cooke EM. Serious infection caused by Group C streptococci. J Clin Pathol 1980;33:188-190. Gott VL. Cardiothoracic surgery. Surg Gynecol and Obstet 1972;134:259-263. Gamsu G, Borson DB. Webb WR, Cunningham JH. Structure and function in tracheal stenosis. Am Rev Resp Dis 1980;121:519-531. Rubio PA, Farrell EM, Bautista EM. Severe tracheal stenosis after brief endotracheal intubation. South Med J 1979;72:1628-1629.
IJC 0109F
Postural hypotension and labile blood pressure associated with severe hypophosphatemia Amin A. Nanji 1 and Hugh J. Freeman
’
’ Division of Clinical Chemistry
Vancouoer General Hospital and Department of Pathology; 2 Department of Medicine, Health Sciences Center, University of British Columbia, Vancouver, Canada
(Received
27 June 1983; revision received 14 October
1983; accepted
19 October
Correspondence and reprint requests to: Dr. Amin A. Nanji, Division of Clinical General Hospital, 855 West 12th Avenue, Vancouver. B.C., Canada V5Z lM9.
International Journal of Cardiology. 5 (1984) 379-381 0 Elsevier Science Publishers B.V.
1983)
Chemistry.
Vancouver
IJC 0109E
Group C streptococcal endocarditis associated with intubation-induced tracheal stenosis C.M. Jack, M.M. Khan and A.A.J. Adgey Regional Medical Cardiology Centre, Royal Victorra Hosprtal. Belfast BTIZ 6BA. Northern Ireland (Received
29 September
1983; accepted
17 October
1983)
We describe a 44-year-old woman with Group C haemolytic streptococcal endocarditis who developed tracheal stenosis as a result of endotracheal intuhation. She recovered fully following valve replacement for continuing left ventricular failure due to mitral and aortic incompetence and subsequent resection of the steno& tracheal segment with reanastomosis of the trachea.
Infective endocarditis due to Lancefield Group C streptococci is rare [l]. When it occurs. it pursues an acute and rapidly destructive course, leading to valvular incompetence and early cardiac failure [l-3]. Tracheal stenosis is increasingly detected in patients who have been intubated and in those who have undergone tracheostomy [4,5]. We report a case of infective endocarditis which was associated with tracheal stenosis due to endotracheal intubation. Treatment was by valve replacement for continuing left ventricular failure due to mitral and aortic incompetence, followed by resection of the stenosed tracheal segment and reanastomosis of the trachea.
Case Report A 44-year-old woman was admitted to hospital in March 1980. with a 5-day history of joint pains, rigors and cough. She had previously been in good health and had no prior medical history. On admission she was pyrexial. A loud pansystolic murmur of mitral incompetence was heard at the apex. Blood cultures demonstrated presence of Group C haemolytic streptococci and she was commenced on parenteral antibiotics. A diagnosis of septicaemia had been made with the probability of bacterial endocarditis because of the signs of mitral incompetence. Five days after admission the patient developed pulmonary oedema complicated by an asystolic cardiac arrest. Resuscitation was successful but she required artificial ventilation. Following resuscitation an endotracheal tube was left in situ for 6 days Correspondence and reprint requests to: A.A.J. Adgey. M.D., Royal Victoria Hospital. Belfast BT12 6BA. Northern Ireland.
International Journal of Cardrology, 5 0 Elsevier Science Publishers B.V.
(1984)376-379
Regional
Medical
Cardiology
Centre.
Fig. Cross-sectional echocardiogram in the left parastemal long axis view showing aortic and mitral valves. AML = anterior mitral leaflet; A0 = aorta; LA = left atrium;
vegetations on the LV = left ventricle.
and then a tracheostomy was performed. The patient improved gradually but artificial ventilation was required for 1 month following the tracheostomy for continuing left ventricular failure and respiratory difficulties. She was then weaned off the ventilator. In April 1980 the patient was transferred to this centre. On admission aortic and mitral incompetence were present. An echocardiogram showed vegetations on the aortic and mitral valves and a flail mitral leaflet (Fig). Parenteral antibiotics were continued. Over the next few days the patient became increasingly more dyspnoeic in association with pronounced stridor and difficulty in expectorating sputum. Laryngoscopy showed paralysis of the left vocal cord. Bronchoscopy showed a stenosis of the trachea which was dilated. The patient continued to
378
have difficulty in expectoration in association with stridor and repeat bronchoscopy 6 days later again showed tracheal stenosis. Dilatation of the stenosed segment was again carried out. Cardiac catheterisation confirmed severe regurgitation of both mitral and aortic valves with continuing left ventricular failure. At surgery the following day vegetations were confirmed on both valves and there was a flail mitral leaflet. The aortic valve was not bicuspid. During the operation the inhalational agents were given via an endotracheal tube. Aortic and mitral valve replacement was carried out. Sectioning of the removed mitral and aortic valves showed no evidence of prior rheumatic infection or myxomatous degeneration. In the post-operative period the patient again required ventilation using both endotracheal and nasotracheal intubation. The patient was extubated after 5 days. During the convalescent period and following extubation the tracheal stenosis recurred. The patient had difficulty with expectoration and became increasingly dyspnoeic. Emergency bronchoscopy had to be carried out on 2 separate occasions and the stricture dilated on both occasions. At operation in late June 1980 (16 weeks after her initial hospital admission) the stricture was found to be 3 cm in length and 18 cm from the patient’s lower lip. The 3 cm stenosed segment of the trachea was resected using a novel anaesthetic technique. Anaesthesia was induced by the intravenous administration of althesin and maintained with nitrous oxide in oxygen with halothane delivered by a face mask. After intubation anaesthesia was continued with an infusion of althesin. The patient continued to breathe spontaneously. During the operation, a short tracheal tube was passed to lie proximal to the stenosed tracheal segment. During the tracheal resection and reanastomosis, 100% oxygen was allowed to flow through the tracheal tube and flood the surgical field. The distal tracheal segment was not intubated and in effect the patient continued to breathe spontaneously through the distal tracheal segment below the resection. Special care was taken by the surgical team to keep the trachea free from blood. The respiratory pattern was closely observed during the operation and frequent arterial blood samples were taken for gas analysis throughout. The upper and lower parts of the remaining trachea were joined in an end-to-end anastomosis, after freeing from connective tissue. The patient made good progress and was discharged from hospital 2 weeks later without complications. She remains very well at review 3 years later and has returned to full working capacity. Discussion
As far as we know, this is the only case of bacterial endocarditis complicated by tracheal stenosis that has been reported during the past decade. Serious systemic infections such as septicaemia or endocarditis caused by Lancefield Group C streptococci are extremely rare. Mohr et al. [l] reported the results of 150,000 blood cultures over 9 years and found that Group C streptococci were isolated in only 8 patients. There are 11 previously reported cases of Lancefield Group C endocarditis [l-3]. Five of these patients died. With the acute and rapidly destructive course of Group C endocarditis leading to early cardiac decompensation [l], it is not surprising that our patient despite early antibiotic therapy had an acute fulminant illness with rapid haemodynamic deterioration, left ventricular failure and an asystolic arrest. This patient came to valvular replacement because of continuing left ventricular failure due to aortic and mitral incompetence. All 3 of the previous patients who underwent urgent heart surgery have survived [1,2]. In 7 of the 11 previously reported cases the infection became established on normal heart valves [1,2]. Our patient was in good health before admission and had no history of rheumatic infection. Histology of the valves did not show any evidence of rheumatic valvular disease or myxomatous degeneration.
379
Tracheal stenosis consequent on endotracheal intubation has been reported with increasing frequency over the past 12 years [4,5]. As an iatrogenic disease it is becoming more frequently recognized. Tracheal stricture has occurred after as short a time period as 72 hours intubation [6]. Of all the causative factors, prolonged intubation is probably the most significant. Our patient was initially intubated for 6 days. The anaesthetic technique employed during the tracheal resection and anastomosis in this case is also of interest. The patient was allowed to breathe spontaneously through the distal tracheal segment during the resection. The distal segment was kept free of blood and 100% oxygen was delivered to the surgical field via the proximal tracheal segment. Anaesthesia was maintained by an intravenous infusion of althesin. Unrestricted access to the 2 ends of the trachea improved the speed and ease of the operation. Acknowledgements We are grateful to J. Cleland, and anaesthesia in this patient.
H.M. Stevenson
and M. Lyons who carried out the surgery
References Mohr DN, Feist, DJ, Washington JA II, Hermans PE. Infections due to Group C streptococci in man. Am J Med 1979;66:450-456. Davies MK, Ireland MA, Clarke DB. Infective endocarditis from Group C streptococci causing stenosis of both the aortic and mitral valves. Thorax 1981;36:69-71. Ghoneim ATM, Cooke EM. Serious infection caused by Group C streptococci. J Clin Pathol 1980;33:188-190. Gott VL. Cardiothoracic surgery. Surg Gynecol and Obstet 1972;134:259-263. Gamsu G, Borson DB. Webb WR, Cunningham JH. Structure and function in tracheal stenosis. Am Rev Resp Dis 1980;121:519-531. Rubio PA, Farrell EM, Bautista EM. Severe tracheal stenosis after brief endotracheal intubation. South Med J 1979;72:1628-1629.
IJC 0109F
Postural hypotension and labile blood pressure associated with severe hypophosphatemia Amin A. Nanji 1 and Hugh J. Freeman
’
’ Division of Clinical Chemistry
Vancouoer General Hospital and Department of Pathology; 2 Department of Medicine, Health Sciences Center, University of British Columbia, Vancouver, Canada
(Received
27 June 1983; revision received 14 October
1983; accepted
19 October
Correspondence and reprint requests to: Dr. Amin A. Nanji, Division of Clinical General Hospital, 855 West 12th Avenue, Vancouver. B.C., Canada V5Z lM9.
International Journal of Cardiology. 5 (1984) 379-381 0 Elsevier Science Publishers B.V.
1983)
Chemistry.
Vancouver