CASE REPORT Arteriovenous shunting and early cortical venous filling in subacute cerebral infarction an old angio- graphic finding revisited Ian C Duncan FFRad(D)SA Unitas Interventional Unit POBox 14031 Lyttelton 0140 Abstract Demonstrated in this report is an example of arteriovenous shunting and early venous filling in an area of cerebral infarction recorded on digital subtraction angiography. This angio- graphic appearance is largely ofhistor- ical interest given the current use of sectional imaging (CT and MR) and altered role of angiography in the imaging of stroke, but should never- theless still be considered amongst the differential causes of cerebral arteriove- nous shunting. Introduction Since the 1970s sectional imaging with computed tomography (CT) and later magnetic resonance imaging (MRl) have replaced cerebral angio- graphyas the methods of choice in the acute and follow-up imaging of cere- bral infarction. Angiography tends to be performed early either to identify any treatable underlying pathology or for direct transarterial treatment by thrombolysis. As a result few cerebral angiograms are done nowadays in the subacute and chronic stages of an infarction and so many of the related angiographic changes during these stages are no longer seen. The case reported here is shown primarily to demonstrate the changes of luxury perfusion and arteriovenous shunting and early cerebral cortical venous fill- ing as captured on digital subtraction angiography. Case report A 39-year-old male patient present- ed to a local academic hospital with clinical evidence of an acute subarach- noid haemorrhage. He was stuporose on admission. An unenhanced CT sean done on the day of admission showed a small clot in the basal sub- arachnoid cisterns and an area of non- haemorrhagic infarction in the right 32 SA JOURNAL OF RADIOLOGY • September 2002 Fig. 1. Unenhanced axial CT scan showing the area of infarction in the right parietal lobe. parietal lobe and posterosuperior aspect of the right temporal lobe. Cerebral angiography was per- formed 6 days after this admission. Selective right internal carotid angio- graphy showed the presence of an elongated saccular aneurysm arising from the communicating segment of the right internal carotid artery (ICA). Vasospasm was seen in the region of the right middle cerebral bifurcation and in the right posterior communi- cating artery. A vascular blush was apparent in the region of the cerebral infarction during the late arterial and capillary phases of the selective right lCA run. Early filling of cortical veins in this region was noted during the late capillary phase prior to the normal venous return phase from the rest of the right cerebral hemisphere. This appearance is in keeping with luxury perfusion and rapid arteriovenous shunting through the infarcted area. Discussion The angiographic pattern of arteri- ovenous shunting with early filling of cortical veins related to an area of cere- bral infarction will be well known to radiologists who performed cerebral angiography in the era prior to cross- CASE REPORT sectional imaging. In 1966, Lassen' introduced the term 'luxury perfu- sion' to describe hyperaemia within damaged brain tissue. Regional loss of autoregulation was thought to be due to lactic acid and carbon dioxide accumulation. This reac- tion could occur within or around an infarcted area. These changes resulted in the shunting of blood, either through dilated capillaries or arteriolo-venular shunts. Angio- graphically this was visible as an enhanced early capillary blush and early venous filling. These angio- graphic changes are particularly evident in the second to third weeks post-ictus, but early venous filling can occasionally be seen very soon after an infarct." In 1973, Leeds and Goldberg' identified a host of pathologies that could exhibit 'luxury perfusion' including cerebral infarction, cerebral trau- ma, inflammatory diseases (includ- ing encephalitis, meningitis and abscess), vasculitis, parenchymal degenerative disease, encephalopa- thy, compression of brain around a space-occupying lesion, vascular spasm (secondary to subarachnoid haemorrhage), and repeated seizures or status epilepticus. Today brain infarcts are diag- nosed and followed up either with CT or MR!. Angiography is usually done early either to exclude an underlying arterial pathology in the neck or brain, or it is done for endovascular treatment with thrombolytic agents. As a result, angiography is not routinely done within days to weeks post-ictus. In our case there was an unknown period of delay before reaching a hospital with scanning and neuro- 33 SA JOURNAL OF RADIOLOGY • September 2002 F/g. 2. Serial dig/tal subtractiOnImages taken dur· Ing a select/ve right Internal carotid arteriogram showing Images at 2.4 sec (A), 3.7 sec (B), 4.5 sec (C). 5.8 sec (D) and 8.8 sec (E). These show the early venous return due to arteriovenous shunting through the infarcted ares (D) prior to the normal venous return from the rest of the brain (E). surgical facilities. Even after admis- sion there was a further 6-day delay before angiography was performed with the result that we saw the cere- brovascular changes at least 1 week post-ictus. Thus we were able to show by means of high-quality dig- ital subtraction angiography this excellent example of luxury perfu- sion with arteriovenous shunting and early venous filling related to cerebral infarction, an angiograph- ic appearance seldom seen nowa- days. References 1. Lassen NA. The luxury-perfusion syndrome and its possible relation to acute metabolic acidosis localised within the brain. Lancet 1966;2: 1113-1115. 2. Huber P. Krayenbuhl H, Yasargil MG. Circulation in cerebrovascular disease and infarcts. In: Huber P, Krayenbuhl H, Yasargil MG, eds. Cerebral Angiography. 2nd ed. New York: Thieme, 1982: 260-263. 3. Burrows EH, Leeds NE. Supratentorial hemispherical lesions. In: Burrows EH, Leeds NE, eds. Neuroradiology. Vol. 1. New York:Churchill Livingstone, 1981:245-294. 4. Leeds NE, Goldberg HI. Abnormal vascular pat- terns in benign intracranial lesions: pseudotu- maul'S of the brain. Am J Roentgenol Radium TIler NI/cl Med 1973; 118: 576-585.