Metastatic staphylococcal lung abscess due to a cutaneous furuncle

The Netherlands

JOURNAL OF MEDICINE ELSEVIER

Netherlands Journal of Medicine 47 (1995) 291-295

Brief report

Metastatic staphylococcal lung abscess due to a cutaneous furuncle Mattijn Buwalda

*'1, B e n S p e e l b e r g

2

Department of Intensive Care, St Radboud University Hospital, Nijmegen, Netherlands Received 7 June 1994; revised 12 April 1995; accepted 13 April 1995

Abstract A seemingly trivial infection of the skin can lead to fulminant staphylococcal pneumonia and death. This case history describes the evolution of a fatal Staphylococcus aureus sepsis complicated by the development of multiple lung abscesses in a 17-year-old patient. A pre-existing cutaneous furuncle was the only identifiable cause. Early bacteraemic symptoms are described. Multiple cavitory lesions could be seen on a CAT-scan. The authors would like

to stress the importance of early and adequate antibiotic treatment. Keywords: Staphylococcus aureus; Furuncle; Sepsis; Lung abscess

1. Introduction Pneumonia is one of the most serious infections that Staphylococcus aureus may cause [1,2]. Community-acquired S. aureus pneumonia is usually preceded by an influenza A virus infection (air-borne) or right-sided endocarditis in drug addicts (blood-borne) [2,3]. H a e m a t o g e n o u s staphylococcal pneumonia secondary to soft tissue infection has been described in a study of a group of 10 patients one of whom died [3].

* Corresponding author, van Ostadestraat 384"', 1074 XA Amsterdam, Netherlands. 1Present address: Intensive Care, Department of Surgery, University Hospital Utrecht, Utrecht, Netherlands. 2 Present address: Department of Intensive Care, St Elisabeth Hospital, Hilvarenbeekseweg 60, 5000 LC Tilbnrg, Netherlands.

Different percentages for pneumonia due to staphyloccal sepsis are reported in the literature. It is important to look for the identifiable cause of staphylococcal sepsis. Patients with a staphylococcal sepsis preceded by an apparent primary staphylococcal infection, such as a soft tissue infection, tend to develop fewer metastatic foci than patients presenting without a known primary source [4]. The following is a case report of a young patient (17 years) in whom a furuncle was the only identifiable cause of his fatal pneumonia. We would like to stress the importance of early detection and treatment.

2. Case report A 17-year-old boy, without a previous medical history, was referred to a local hospital, by his GP. The patient complained of a painful swollen

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left ankle and right knee, fever, anorexia and general discomfort over the past 5 days. Approximately 2 months earlier, he had suffered from a furuncle (diameter 6 cm) on his right thigh, which had spontaneously ruptured after 7 days. On admission, the patient's temperature was 38.5°C. His blood pressure measured 135/80 mmHg with a regular supraventricular tachycardia of 128 beats/min. Auscultation of the heart and lungs appeared to be normal. Examination of the throat revealed pharyngitis. Normal bowel sounds could be heard in the abdomen although the right flank was painful on percussion. On the right thigh, a fresh furuncle was found near the remnants of the previously healed one. Laboratory tests showed; ESR 48 mm in 1 h (normal value 0-10 mm), haemoglobin 8.6 mmol/1 (normal value 8.1-10.7), leukocytes 4.4 x 109/1 (3.511.0), thrombocytes 117 x 109/1 (120-350), sodium 130 mmol/1 (137-144), potassium 3.5 mmol/l (3.4-4.6), urea 14.3 mmol/1 (3.0-7.0), serum crea-

tinine 81 /zmol/1 (60-110), bilirubin 76 /zmol/l (< 10), alkaline phosphatase 98 IU/1 (< 120), alanine transaminase 42 IU/1 (< 30), aspartate transaminase 131 IU/1 (< 25), lactate dehydrogenase 522 IU/1 (< 330), 7-glutaminate transaminase 23 IU/1 ( < 45). A chest radiograph and electrocardiogram showed no abnormalities. S. a u r e u s was cultured from blood and the remnants of the furuncle. Staphylococcal sepsis was clinically diagnosed and treatment started with flucloxacillin 4 x 1 g intravenously. On day 2 of admission, the patient became taehypnoeic. Further examination revealed a rightsided pleural friction rub and a systolic heart murmur. A chest X-ray indicated signs of moderate infiltration in the right upper lobe. A blood gas analysis showed normal values. Because of the established clinical deterioration, the flucloxacillin dose was increased to 6 x 1 g intravenously. An echocardiogram made on day 4 of

Fig. 1. Mid-thoracicCAT scan showingmultiplecavitorylesions(and a pleural fluidaccumulation).

M. Buwalda, B. Speelberg/ Netherlands Journal of Medicine 47 (1995) 291-295

admission showed no signs of endocarditis. On the same day the PaO 2 decreased to 57 mmHg (PaCO~ 33 mmHg) and oxygen was supplemented. The abnormal chest X-ray progressed to a confluating infiltrative pattern of all lung fields together with bilateral pleural fluid. The flucloxacillin dose was increased to 6 x 2 g intravenously and the patient was transferred to the University Hospital Nijmegen where he was admitted to the ICU with respiratory insufficiency. On arrival the patient was still able to communicate. He complained of a sore throat and pain in all his joints. His parents stated that he had not suffered from a recent upper respiratory tract infection or skin lacerations (other than the furuncle). There had been no previous immunological disturbances, infections or drug abuse. Until the symptoms described above appeared, the patient had always been a healthy, physically active person. We saw an icteric dyspnoeic patient with generalized red, swollen, painful joints. There were no meningeal signs. Generalized crepitations could be heard. No cardiac murmur could be detected. There was normal peristalsis and neither liver nor spleen appeared to be enlarged. Laboratory tests revealed a further increase in bilirubin (186 t~mol/l) and alkaline phosphatase (153 IU/I). A blood gas analysis with nasal oxygen (5 l / m i n ) showed the following results: PaO 2 13.9 (normal 10.6-13.3) kPa, PaCO 2 5.2 (normal 4.5-6.0) kPa. Serology excluded the possibility of a recent respiratory virus infection. The chest radiograph showed bilateral infiltrative changes. An ultrasound of the abdomen showed a normal liver and a splenomegaly; no abscesses were found. An echocardiograph did not show any signs of endocarditis. His treatment regimen was changed to flucloxacillin 500 m g / h i.v. continuously. The next day (day 12 after the start of symptoms) the patient developed a respiratory insuffiency with PaCO 2 up to 11.2 kPa. He was intubated and ventilated with SIMV 20 × 750 ml, P E E P 5 cm H 2 0 , FIO 2 70%. A whole body CAT-scan showed consolidated lungs, ascites, hepatosplenomegaly and a small abscess in the left psoas muscle (diameter 1 cm) (see Fig. 1).

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Fig. 2. The first chest radiograph on which the cavitorylesions could be seen.

On day 15 the chest X-ray showed cavitory lesions in the right upper, right middle and left upper lobe (see Fig. 2). The temperature increased and the patient required inotropic support (dopamine 10 m i c r o g r a m s / k g / m i n and norepinepherine 5 /.~g/kg/min) for 5 days. At that time the blood cultures also tested positive for Klebsiella oxytosa for which gentamycin (2 × 120 mg i.v. for 5 days) and ciprofloxacin (2 X 200 mg i.v. for 12 days) was added to the antibiotic regimen. The patient was given a tracheal stoma. On day 22 the patient's fever was gone, the liver function tests were normalized and he was haemodynamicaly stable without inotropic support. By that time he was ventilated with pressure control 27 cm above PEEP, P E E P 14 c m H 2 0 , respiratory frequency 20/rain, FIO 2 65%. After 10 days of artificial ventilation, a tension pneumothorax in the right upper lobe appeared for which 2 pleural drains were inserted. During the rest of the admission period bilateral pneumothoraces required 3 more drains to be inserted (3 on the right and 2 on the left) (see Fig. 3). Gradually higher inspiratory pressure and FiO 2 were called for. Finally, even ventilation with PRVC 20 × 480 ml and FiO 2 100% with 5 c m H 2 0 PEEP, re-

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Fig. 3. Chest radiograph with 5 pleural drains in situ.

sulted in high inspiratory pressures up to 60 c m H 2 0 and a persisting hypoxaemia and hypercapnia. The respiratory acidoses did not react to bicarbonate (8.4% 30 m l / h i.v.) and TRIS buffer (50 m l / h r i.v.) therapy. Thirty-six days after the first symptoms occurred and 24 days after initiating mechanical ventilation, the patient died of progressive hypoxaemia. Autopsy was not performed.

3. Discussion S t a p h y l o c o c c u s a u r e u s is still the most common bacterial pathogen encountered in the community [5]. Mortality due to S. a u r e u s sepsis has remained high and is related to age ( > 60 years 62% versus < 60 years 25.3%), acquisition of bacteraemia (community 29.3% versus hospital 59.4%), leukocytosis, creatinine level and hyperbilirubinaemia [6,7]. S. a u r e u s accounts for 11% of all community-acquired bacteraemias and 40% of all S. a u r e u s bacteraemias are acquired in the community [5]. In a recent survey, pertaining to 2746 cases of bacteraemia, S. a u r e u s was isolated in 373 cases (13.6%) [8]. S. a u r e u s bacteraemia is found in all age-groups and in both sexes equally.[8] Cardiac diseases, malignancy and dia-

betes are the most common underlying diseases [6]. The heart can also be involved in staphyloccocal sepsis. It is often difficult to prove pre-existing cardiac disease in patients hospitalized for staphylococcal sepsis. In hospital, the respiratory tract and the intravenous catheter line are the most common portals of entry. In contrast, skin laceration (including soft tissue infection) and intravenous drug abuse form the most frequent portal of entry in community-acquired cases of S. a u r e u s bacteraemia [7,9]. When at hospital admission blood and sputum cultures test positive for S. a u r e u s , and there is roentgenographic evidence of pulmonary infiltration, normally bacteraemic S. a u r e u s pneumonia will be diagnosed. In such a case one assumes the pneumonia to be the portal of entry for the following bacteraemia. In the present patient the situation had been reversed. Much has been published concerning haematogenously derived staphylococcal pneumonia related to I.V. drug abuse and endocarditis. Naraqui et al. [3] described 10 patients with a haematogenous S. a u reus pneumonia secondary to soft tissue infection. Interestingly, their ages ranged from 12-45 years (average 22), which is significantly lower than the average age of patients admitted to hospital with a staphylococcal pneumonia (82% > 60 years of age) [10]. In the Naraqui series, all 10 patients were admitted with a diagnosis of pneumonia while initially in only 7 of them the co-existing tissue infection was thought to be relevant. Early detection of a staphylococcal sepsis whether accompanied by pneumonia or not is important in view of the high mortality rate. Unfortunately a seemingly trivial soft tissue infection in a young and healthy individual is not always recognized as a potential portal of entry. In the present case valuable days were lost before adequate treatment could be instituted. A persistent fever and malaise, arthralgia, purulent sputum, pleuritic chest pain and shortness of breath are symptoms which may indicate subsequent haematogenous spread. The presence of a source of staphylococcal bacteraemia, the scattered nature of the rales on auscultation of the chest and cavitory lesions seen on the chest roentgenogram,

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should l e a d to a p r o v i s i o n a l diagnosis o f S. aureus p n e u m o n i a w h e n c u l t u r e results a r e n o t y e t available [3]. I n t h e p r e s e n t case t h e f u r u n c l e was t h e m o s t likely s o u r c e f r o m which t h e S. aureus sepsis evolved. F o r an u n c o m p l i c a t e d furuncle, the usual t r e a t m e n t is incision a n d d r a i n a g e once the lesion b e c o m e s fluctuant. In severe, n o n - h e a l i n g o r rec u r r e n t furuncles a n d in abscesses o c c u r r i n g in i m m u n o d e f i c i e n t p a t i e n t s , systemic antibiotics a r e r e c o m m e n d e d . T h e p a t i e n t s h o w e d signs of a r t h r a l g i a a n d / o r arthritis. U n f o r t u n a t e l y , an asp i r a t i o n o f o n e o f the j o i n t s was not p e r f o r m e d . Positive g r a m stain results w o u l d have c o n f i r m e d t h e diagnosis o f m e t a s t a t i c S t a p h y l o c o c c u s aureus sepsis b e f o r e c u l t u r e results w e r e available. In r e t r o s p e c t , t h e p r e s e n t p a t i e n t h a d initially b e e n t r e a t e d with an i n a d e q u a t e d o s e o f flucloxacillin (4 x 1 g) which could have c o n t r i b u t e d to t h e fatal o u t c o m e . T h e a d d i t i o n o f g e n t a m y c i n a n d / o r r i f a m p i c i n to s t a n d a r d t h e r a p y with flucloxacillin is n o t g e n e r a l l y a c c e p t e d . B l o o d cult u r e s a r e r e q u i r e d w h e n the p a t i e n t has a fever o r o t h e r signs of systemic infection [11]. W h e n t h e r e is clinical suspicion o f a S. aureus b a c t e r a e m i a , early a n d a d e q u a t e i n t r a v e n o u s a n t i b i o t i c t h e r a p y is i n d i c a t e d even b e f o r e t h e c u l t u r e results a r e known.

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