Introduction

Large pleural effusion in a critically ill patient may prevent successful weaning from ventilation. Mortality associated with thoracentesis is rare and should be viewed as a critical incident. We report a case of sudden death which clinically seemed to be associated with thoracentesis, but autopsy proved otherwise.

Case Report

A 64-year-old male underwent a partial gastrectomy for bleeding ulcer. He had a past history of hypertension, chronic obstructive airways disease and perforated duodenal ulcer. The post-operative stay in the intensive ace unit (ICU) was prolonged due to slow weaning from mechanical ventilation, inadequate absorption of enteral feed and abdominal distension. After 26 days in the ICU he was transferred to a surgical ward and was regularly reviewed by the critical care outreach team.

On the surgical ward his unresolved issues were abdominal distension and a persistent, productive cough. Several days later he developed septic shock and was readmitted to ICU. Sputum culture confirmed the presence of methicillin resistant Staphylococcus aureus (MRSA) and Streptococcus pneumoniae and a blood culture was positive for MRSA. Treatment with intravenous cefuroxime, vancomycin and rifampicin was commenced.

In the ICU he had recurrent episodes of tachypnoea, bronchospasm, hypoxia and paroxysmal atrial fibrillation. Chest radiograph (CXR) showed bilateral pleural effusions. A right thoracentesis was successfully performed under local anaesthesia with aseptic technique. A large-bore intravenous cannula was advanced over the 6th rib in mid axillary line whilst aspirating on a small syringe attached to the cannula, until fluid returned into the syringe. The needle was removed and a three-way tap and 50ml syringe were attached to the plastic cannula. Aliquots of pleural fluid were aspirated and disposed of via the three-way tap until fluid could no longer be aspirated. We believed weaning was delayed due to a combination of bronchopneumonia, congestive cardiac failure and ascites. A transthoracic echocardiogram revealed a mobile mass attached to the mitral valve. Patient had no peripheral stigmata of infective endocarditis. A long term central venous catheter was unlikely as our unit practice is to change such catheters between 7 to 10 days. Thus the exact nature of mitral valve mass was unclear. Following consultation with the cardiologist and the microbiologist low molocular weight heparin and intravenous gentamicin was added to the treatment. Consultant cardiologist considered mitral valve replacement was a very high risk strategy.

A left thoracentesis was now attempted; using the same technique described above, but was unsuccessful. It is difficult to determine why the procedure failed, the possibilities include: the patient was not positioned optimally, the cannula kinked or became blocked with a blood clot or other material or the cannula was not long enough. Soon after this procedure, the patient became dyspnoeic and hypoxic. He developed haemoptysis (up to 250 to 300 mls) tachycardia, hypotension and hepatomegaly. Haemoptysis was controlled and haemodynamics improved marginally with fluid boluses, packed red cells, fresh plasma and adrenaline. However, he remained hypoxic, requiring high airway pressures to provide adequate tidal volumes. CXR revealed bilateral pleural effusion. A 24Ch (8mm diameter, 40 cm long) Kendall Argyle intercostal chest drain was inserted with blunt dissection into left hemithorax through the same space where previous pleural tap was unsuccessful. Up to 1.5 litres of lightly blood-stained fluid was drained. The patient continued to deteriorate and then had an asystolic cardiac arrest. Since the relationship between pleural aspiration and death was uncertain, autopsy was requested following full discussion with the family.

The post-mortem examination confirmed endocarditis with a mitral valve vegetation measuring 2.5 cm in diameter, which had partly destroyed the valve but was also large enough to obstruct it. Other important findings were bilateral lung consolidation, pleural effusion, ascites, peripheral oedema and congested hepatomegaly. There did not appear to be any evidence that the death was related to the thoracentesis; there was no evidence of acute haemorrhage either into the pleural, pericardial or mediastinal spaces or into the lungs or abdomen.

Discussion

Pleural effusion in critically ill patients is common. The incidence of pleural effusions in the ICU varies depending on the screening methods, from approximately 8% for physical examination to more than 60% for routine ultrasonography.1 Heart failure is the most frequent cause of bilateral effusions seen in medical ICU patients2. Large pleural effusions can be one of the factors preventing successful weaning from ventilator. During thoracentesis, iatrogenic pneumothorax, haemothorax or haemopneumothorax are all possible, with associated morbidity and mortality.

In our patient therapeutic thoracentesis was performed to facilitate weaning. Post procedure life threatening deterioration was believed to be due to haemothorax, pneumothorax or both. Following fluid resuscitation and chest drain insertion, the patient still had signs of cardiogenic shock, hypoxia, high airway pressures and massive hepatomegaly. At this stage we hypothesize that progressive deterioration and inadequate response to resuscitation was due to the large vegetation obstructing the mitral valve.

Bacterial endocarditis rarely leads to functional mitral stenosis or obstruction; indeed it typically leads to mitral regurgitation. A MEDLINE search found 24 reported cases mitral valve endocarditis causing obstruction. This condition often goes unrecognised until late in the course of the disease.3 The organisms that have been reported to cause types of obstructive vegetations are fungi4 producing “fungus balls”, Streptococcus (viridans group or group B)5 , Vancomycin Reistant Enterococcus (VRE)6 and Staphylococcus aureus or MRSA.6 We believe the probable causative organism in this case was MRSA. Whilst the majority of cases of endocarditis leading to mitral valve obstruction occur in patients with pre-existing mitral valve disease or mitral prostheses, this patient was unusual in that he had native valve endocarditis with obstruction. Interestingly, the transthoracic echocardiogram did not demonstrate obstruction. This may have been due to relatively poor views or it may be that the vegetation grew significantly after echocardiogram. Indeed it has been reported that this type of vegetation can rapidly expand and lead to sudden death.6

Outcome following mitral valve endocarditis with obstruction is poor and to our knowledge no patient has survived without surgery3 while sudden death occurs in almost a third of cases.6

Correspondence to

Dr. N S Parekh MD,MRCP,FRCA Department of Anaesthesia and Critical Care New Cross Hospital Wolverhampton WV10 0QP UK Fax: +44 1902 695644 E mail: Nilesh.Parekh@rwh-tr.nhs.uk