1 Vascular Surgery Klinikum rechts der Isar Technische Universität München, Munich, Germany. Email: anovotny{at}lycos.de
Sir,
A haemodynamic subclavian steal phenomenon is usually found in patients with an occlusion of the subclavian artery in its proximal segment. Motion of the ipsilateral arm and the consecutively increased demand of blood hereby lead to a retrograde blood-flow in the ipsilateral vertebral artery, which in turn may result in ischaemia of brain areas supplied by the vertebrobasilar circulation. Hitherto, two cases have been reported in the literature, where subclavian steal was caused solely by the presence of a high-flow brachiocephalic shunt [1,2]. We describe a case in which subclavian steal was caused by an arterio-venous (AV) shunt in the absence of a relevant subclavian stenosis, leading to an extensive infarction of the posterior cortex in the setting of cardiopulmonary resuscitation (CPR).
Case
A 62-year-old man with end-stage renal disease (ESRD) was admitted with a repeated attack of diverticulosis. His access for haemodialysis was established by an above-elbow arteriovenous interposition of a brachiocephalic prosthetic polytetrafluoroethylene graft. He subsequently underwent a sigmoidectomy. Ten days after the operation the patient developed lower left quadrant abdominal pain, became febrile and showed the clinical (tachypnea, tachycardia, hypotension) and laboratory signs (leukocytosis, hyperbilirubinaemia, rising levels of aminotransferases) of sepsis. A computed tomography (CT) scan revealed a retroperitoneal haematoma in the lower left abdomen. The patient was immediately transferred to the operating room for emergency laparotomy. After evacuation of the haematoma, a Hartmann's pouch and a terminal colostomy were created. The patient was taken to the Surgical Intensive Care Unit for post-operative care. On post-operative day (POD) 1, he developed ventricular fibrillation. CPR was started immediately. The patient was hypotensive during resuscitation with a systolic pressure of 70 mmHg. After successful resuscitation, the patient remained comatose with the pupils showing no response to light. A cranial CT scan showed bilateral hypodense lesions of the occipital cortex, consistent with ischaemic infarction. On POD 3, Doppler-ultrasonographic examination of the supraaortal branches showed a minor stenosis of the right Internal Carotid Artery (ICA), with a maximum velocity (Vmax) of 1.2 m/s. On the left side a 50% stenosis of the ICA with a Vmax of 2.0 m/s was found. The intervertebral segment of the left vertebral artery showed retrograde blood-flow.
Manual compression of the haemodialysis shunt on the left upper arm led to a reversal of flow from retrograde to antegrade in the left vertebral artery. Taken together, all these findings were highly suspicious of a haemodynamically induced cerebral infarction during CPR in combination with a subclavian steal syndrome induced by the low resistance of the arteriovenous shunt. Since only partial compression of the shunt did not restore antegrade perfusion of the vertebral artery, the decision to sacrifice the angioaccess was made. The shunt was ligated under local anaesthesia the same day. Further neurological examinations revealed global hypoxic brain damage, which was most profound in the posterior circulation, including the middle brain and brain stem. During the following days the patient developed generalized seizures and blood pressure instability. On POD 8 he died of sepsis and multiple organ failure.
Discussion
In haemodialysis, angioaccess is usually achieved by radialcephalic or brachialcephalic AV shunts whose haemodynamic conditions are characterized by high blood volumes and low vascular resistance. In high-flow shunts, shunt perfusion alone may even be in the scale of normal cardiac output (CO; 56 l/min) [1]. In the setting of CPR, where the maximum achievable CO is limited for mechanical reasons, the redistribution of blood volume in favour of shunt perfusion may become deleterious.
Usually, reversal of flow in the vertebral artery alone rarely, if ever, results in permanent neurological damage [3,4]. Remarkably, our patient had no history of vertebrobasilar insufficiency or any other neurological symptoms. Different to our case, the patients in the few similar cases described in literature [1,2] showed symptomatic subclavian steal and were bearing shunts with an extremely high volume throughput (>1.2 and 5.8 l/min, respectively). Furthermore, the course of their illness was rather benign.
Also remarkable is the fact that it was obviously just the presence of the shunt that caused the steal. Since a relevant stenosis of the subclavian artery could not be detected in the Doppler examination, a magnetic resonance angiography performed on the patient the year before for other reasons was reviewed. Assuming that there was no relevant change in findings since that examination, we were at the most dealing with a minor stenosis of the subclavian artery. This haemodynamically irrelevant stenosis together with the high shunt volume led to subclavian steal.
The pre-existence of two unfavourable conditions, atherosclerosis of the supra-aortal branches and subclavian steal caused by a brachiocephalic AV shunt, in combination with a decreased CO during CPR induced an ischaemia that was apparantly so profound that it led to an extensive posterior circulation stroke.
ESRD patients are particularly prone to having the spectrum of comorbid conditions seen in our case. Atherosclerosis is a very common problem in this population, predisposing patients to subclavian steal [4,5]. Furthermore, Doppler examinations of vertebral artery flow suggest that asymptomatic subclavian steal in patients with AV shunts may even be present without proximal subclavian stenosis [2].
The coincidence of all those factors seen in our case remains unusual, but we nevertheless feel that doctors involved in the care of ESRD patients should be aware of this rare complication when having to perform CPR on a patient on haemodialysis.
Conclusions
It may be concluded from our case that measures should be taken in order to prevent an eventual steal phenomenon during CPR on a patient with a brachial AV shunt. An easy solution would be to compress the shunt with a tourniquet or blood pressure cuff. This measure may also increase blood supply to the brain by decreasing the share of cardiac output lost through the shunt, even in cases where no steal phenomenon is present. In order to get a better idea of the actual incidence of asymptomatic subclavian steal in patients with a haemodialysis shunt, vertebral blood flow has to be examined in a representative number of patients. Without this data, we would suggest compression of the AV shunt whenever a haemodialysis patient does not respond quickly to resuscitative efforts, even with the risk of consecutive shunt thrombosis.
References