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netherlands journal of critical care Copyright ©2006, Nederlandse Vereniging voor Intensive Care. All Rights Reserved. Received August 2006; accepted in revised form September 2006 c l i n i c a l i m a g e Incomplete circle of Willis H.R.H. de Geus, J. Bakker Department of Intensive Care, Erasmus University Medical Centre Rotterdam, The <strong>Netherlands</strong> Abstract. A 60-year-old woman presented with acute headache and loss of consciousness. On admission her Glasgow coma scale score was 6. She was intubated in order to secure the airway. The computer tomography scan (CT-scan) showed a huge amount of subarachnoidal blood probably due to an aneurysmal haemorrhage. Further CT-angiography and image reconstruction identified the aneurysm as being situated in the anterior communicating artery (Figure 1). Furthermore there was an incomplete circulus arteriosus cerebri (circle of Willis) with an absent posterior communicating artery on both sides and the right anterior cerebral artery originating in the left carotid artery with absence of communication between the right anterior cerebral artery and the right middle cerebral artery. There were no neurosurgical or endovascular treatment options. Despite optimal management by preventing vasospasm with excessive fluid infusion, calcium channel blockers and dobutamine she developed frontal lobe ischaemia (Figure 2) and cardiac failure with acute pulmonary oedema. After a fulminant re-bleed our patient was brain-dead and further medical treatment was discontinued. Merkkola et al studied 87 post-mortem patients identifying missing posterior communicating arteries in 46% and missing or incomplete anterior communicating arteries in 22%. (1) The developmental absence of both communicating systems is rare and proved fatal in this case of subarachnoidal haemorrhage. Because of the high risk of ischaemia during neurosurgical or endovascular intervention the treatment of the aneurysm in these cases is suboptimal, thus increasing the risk of a fatal re-bleed. Figure 1b. Normal circle of Willis; 1=anterior communicating artery, 2=anterior cerebral artery, 3=middle cerebral artery, 4=carotid artery, 5=posterior communicating artery, 6=posterior cerebral artery, 7=basilar artery. Figure 1a. Reconstruction image showing the anterior communicating artery aneurysm. The right anterior cerebral artery originates in the left carotid artery. There is no connection between the right anterior cerebral artery and the right middle cerebral artery. Both posterior communicating arteries are absent, there is no communication between the basilar blood flow and the blood flow of the carotid arteries. Figure 2. Left and right frontal lobe ischaemia due to vasospasm of the anterior cerebral arteries and inadequate blood supply due to the incomplete circulus arteriosus cerebri. Visible blood in posterior horn of the left lateral ventricle. Correspondence: H.R.H. de Geus E-mail: geushrhde@yahoo.com References 1. Merkkola P, Tulla H, Ronkainen A, Soppi V, Oksala A, Koivisto T et al. Incomplete circle of Willis and right axillary artery perfusion. Ann Thorac Surg 2006; 82(1):74-79. 530 neth j crit care • volume 10 • no 5 • october 2006
netherlands journal of critical care Copyright ©2006, Nederlandse Vereniging voor Intensive Care. All Rights Reserved. Received January 2006; accepted in revised form July 2006 c a s e r e p o r t Ventricular septal rupture as an early and fatal complication of acute myocardial infarction: case-report E.J. Lust 1 * , W.K. Lagrand 1 , M. van der Ent 1 , A.P.W.M. Maat 2 , M.L. Simoons 1 1 Departments of Cardiology and 2 Cardiothoracic Surgery Intensive Care Thorax Centre, University Medical Centre Rotterdam, The <strong>Netherlands</strong> Key words: acute myocardial infarction, ventricular septal rupture Abstract. This article presents the history of a patient who developed ventricular septal rupture (VSR) after acute myocardial infarction (AMI). Clinical presentation, diagnostic work-up and treatment are described. The literature on this subject is also discussed. Introduction Ventricular septal rupture is a feared and potentially lethal complication of AMI. Occurrence of VSR has declined over the years due to improved coronary reperfusion treatment (1). For this reason, clinicians are nowadays less often confronted with VSR and experience of this complication is declining. Symptoms of VSR include chest pain, shortness of breath, and those commonly associated with low cardiac output and shock. At physical examination a harsh, loud holosytolic murmur can be heard along the left sternal border, radiating toward the base, apex and right parasternal area. A palpable parasternal thrill is present in half of the patients. With cardiogenic shock and a low-output state complicating VSR, there is rarely a thrill, and the murmur is difficult to identify because flow across the defect is reduced. Right and left ventricular S 3 are common. Doppler echocardiography is generally diagnostic and can distinguish between VSR, rupture of ventricular free wall and papillary muscle rupture. Pulmonary artery catheterisation may be helpful. In patients with a VSR, an increase in oxygen saturation occurs within the right ventricle. Medical therapy consists of mechanical support with an intra-aortic balloon pump, afterload reduction, diuretics and usually inotropic agents. Most patients, however, need immediate surgical intervention. The aim of this case report is to discuss VSR after AMI and to examine the early recognition, diagnostic features and prompt treatment of the condition. Case history A 65year-old male was admitted to our hospital with a 16 hour history of severe chest pain. The patient’s medical history revealed Buerger’s Disease, resulting in severely diminished arterial perfusion of the limbs. On admission, the chest pain had resolved and he denied shortness of breath. At physical examination he appeared moderately ill, with a blood pressure of 90/60 mmHg and sinus tachycardia of 120/min. Auscultation revealed normal heart sounds with no extra sounds or murmurs. No signs of left- or right-sided Correspondence: E.J. Lust Email: e.lust@erasmusmc.nl heart failure were observed. On electrocardiography a recent anterior wall myocardial infarction was detected, with ST-segment elevation in leads V1 to V5, I and aVL in combination with QS formation in leads V1 to V4. Treatment with aspirin, clopidogrel and a statin was initiated. Because of progressive haemodynamic deterioration, it was decided to perform an immediate coronary angiography, which revealed single vessel disease of the ramus descendens anterior (RDA). Despite several attempts to revascularize the RDA, including stenting, only a greatly reduced flow (TIMI flow 1-2) could be obtained. Considering the no-reflow state at the end of the procedure abciximab was added to the initial medical therapy. Inotropic support was started by means of dobutamine 3 µg/kg/min and noradrenalin 0.012 µg/kg/min. Because of the compromised peripheral arterial vessels it was decided not to insert an intra-aortic balloon pump (IABP). During his stay in the Intensive Care Unit, inotropic support could not be reduced. Repeat echocardiographic examination showed progressive aneurysmal widening of the apex of the left ventricle. Left ventricular function was severely compromised. Other than mitral valve regurgitation grade II/IV, no additional valvular abnormalities were seen. Pericardial effusion was absent. Laboratory examination revealed normal values for haemoglobulin, thrombocytes, leucocytes, and liver- and renal function parameters. Troponin-T and CK-MB increased to maximal values of 16.8 mg/l and 247 U/l, respectively. In the early hours of the next morning,36 hours after onset of chest pain, his clinical condition suddenly deteriorated. The chest pain recurred, accompanied by progressive dyspnoea and nausea. On physical examination blood pressures were lower (70/30 mmHg) with increased heart rates up to 128/min (sinus tachycardia). Central venous pressure (CVP) was elevated. On auscultation a continuous murmur, grade III-IV/VI, was heard with a mid-sternal maximum accompanied by rales at both lung fields. Echocardiographic examination demonstrated a ventricular septal rupture (VSR) (Figure 1) with a maximum velocity over the septum of a minimum of 3 m/s. Mitral valve regurgitation and left ventricular function were unchanged. No tricuspid valve regurgitation was seen. Pulmonary artery catheterisation revealed an oxygen saturation jump from 62 % in the right atrium to 82 % in the pulmonary artery (aortic saturation 99%), resulting in a left to right shunt calculated neth j crit care • volume 10 • no 5 • october 2006 531
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