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Correspondence

Another neurological complication of central venous cannulation

Schummer, W.; Schummer, C.

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European Journal of Anaesthesiology: January 2002 - Volume 19 - Issue 1 - p 73-75

EDITOR:

We report a case of cerebral infarction with secondary haemorrhage caused by internal jugular venepuncture in a patient with renal failure. According to definition and author, the rate of complications during central venous cannulation is as high as 12%, and fatal complications still occur [1]. A 74-yr-old male attended his General Practitioner with complaints of acute epistaxis, coughing up blood-stained sputum and a 14-day history of nausea and loss of appetite. Blood analysis revealed elevated values for potassium (6.4 mmol L−1) and creatinine (9.4 mg dL−1). Noteworthy in his past medical history was long-standing coronary artery disease with two previous myocardial infarctions, a compensated renal impairment and a large supra- and infrarenal aortic aneurysm. He was admitted to hospital for treatment of acute renal failure. Laboratory evaluation before venepuncture showed: prothrombin time 58% (normal: 80-130%); partial thromboplastin time 36.5 s (normal: 25-38 s); prothrombin international normalized ratio 1.45; platelet count 105 × 109 L−1; blood urea nitrogen 104 mg dL−1. With the aid of ultrasound a haemodialysis catheter was inserted into the right internal jugular vein by the Seldinger technique. The procedure was reported as uncomplicated. After cannulation the patient developed a large haematoma at the puncture site, most likely due to a coagulation defect. It was not reported whether manual compression had been applied. Before haemodialysis, 40 mg enoxaparin was injected (pre-filter) into the extracorporeal circulation. No problems occurred during the dialysis. After dialysis, a left hemiparesis with anisocoria, followed by stupor occurred. Computerized tomography showed infarction in the territory of the right middle cerebral (MCA) and anterior cerebral artery (ACA) with secondary haemorrhage (Fig. 1). The patient was transferred to our university clinic where surgical evacuation of the clot was performed through a hemicraniectomy. Unfortunately the patient's condition failed to improve after operation and he died 10 days later in multiple organ failure.

Figure 1
Figure 1:
Infarction in the right anterior and middle cerebral artery territories with secondary haemorrhage and consecutive midline shift.

Why did cerebral infarction take place? The most compliant explanation would be an unrecognized puncture of the carotid artery. Punctures of the carotid artery have been observed in 0.5-4.4% of internal jugular vein cannulations and consecutive cerebral damage has been reported [2,3]. In our case, we cannot exclude carotid artery puncture for certain, despite the fact that the cannulation was performed using ultrasound guidance and had been reported as uneventful.

Furthermore, one should consider the possibility of cardiac emboli or a carotid artery dissection. The first has been ruled out by a postoperative transoesophageal echocardiography, the latter by Duplex sonography. After resolution of the neck haematoma Duplex ultrasonography showed atheromatous plaques within the carotid artery. Furthermore, a 60% stenosis of the carotid artery was demonstrated (Fig. 2). In such circumstances it seems reasonable to suggest that the haematoma caused a partial obstruction of the carotid artery with the devastating consequences of infarction.

Figure 2
Figure 2:
Duplex scanning of the right internal carotid artery just above the carotid bulb: cardiac index was 2.2 L min−1 m−2 under high dose inotropic support at the time of investigation. (a) Flow-velocities showing a stenosis of 60%, (b) colour-coded Duplex sonography showing stenosis with aliasing phenomena (high velocity flow areas).

Neck haematoma need not to be of arterial origin to cause cerebral infarction in the presence of arteriosclerotic plaques in the carotid artery [4]. Ipsilateral carotid stenosis greater than 50% is strongly associated with territorial cerebral infarcts and haemodynamic impairment may also contribute to infarct size. Independent of source, an important argument against the diagnosis of embolism is the extent of the infarction, i.e. the whole territory of the ipsilateral ACA and MCA. We regard this as proof for a temporary complete obstruction of the right carotid artery at least, due to neck compartment syndrome.

Neurological complications of central venous cannulation were first reviewed in 1988 [5]. Cerebral damage after carotid or jugular vein obstruction due to carotid puncture, development of large haematomas and/or manual compression were reported as the most serious neurological complications of jugular venepuncture [2,3]. These authors advised that the internal jugular route should not be used in anticoagulated patients or in patients with diseases of the carotid or vertebral arteries. Nevertheless, there are other articles reporting on cannulation in coagulopathies [6], which state that skilled physicians can perform central venous access procedures safely in patients with disorders of haemostasis. Patients most likely to experience bleeding from these procedures are patients with severe thrombocytopenia [6]. A prolonged bleeding time is a common finding in chronic renal failure even in a well-dialysed patient [7]. It is also well known that patients with bleeding disorders are at a higher risk of developing haematomas, even after minor trauma to blood vessels [7]. Furthermore, in patients with acute renal failure bleeding is a common and potentially fatal complication arising from multiple acquired defects of normal haemostasis [7]. Finally, blood urea nitrogen greater than 60 mg dL−1 may be considered a risk factor because of uraemic thrombocytopathia [8]. This is usually manifested by spontaneous mucosal bleeding (epistaxis, gingival bleeding), prolonged bleeding from skin puncture sites, and excessive postoperative bleeding [7]. The clinical impact of this bleeding diathesis is substantial, with up to 44% of patients who require acute haemodialysis having severe haemorrhage, and with haemorrhagerelated mortality reported to be as high as 10% [7]. Ironically, there is even some recent concern that haemodialysis itself transiently impairs the bleeding time immediately after the procedure [8].

In our patient we believe that the haematoma - no matter whether venous or arterial in origin - caused a neck compartment syndrome due to a coagulation defect. This resulted in a temporary obstruction of the carotid artery with consecutive infarction. Due to haemodialysis-induced derangement of the bleeding diathesis secondary bleeding into the infarcted areas took place.

We would like to emphasize that cannulation of neck vessels in patients with bleeding diathesis must be performed with utmost caution, especially in the presence of stenotic disease of the carotid and/or vertebral arteries. Perhaps more 'old fashioned' approaches such as use of the external jugular or the femoral veins are more prudent in these circumstances.

W. Schummer

Klinik für Neurologie, Universitätsklinikum Eppendorf; Hamburg, Germany; Klinik für Anästhesiolgie und Intensivtherapie; Friedrich-Schiller Universität; Jena, Germany

C. Schummer

Klinik für Anästhesiologie und Intensivtherapie; Friedrich-Schiller Universität; Jena, Germany

References

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© 2002 European Academy of Anaesthesiology