Widespread Ischemia Research Articles

A299 ACUTE TUMOUR RUPTURE POST-TRANSARTERIAL CHEMOEMBOLIZATION IN A PATIENT WITH HEPATOCELLULAR CARCINOMA

Abstract Background Hepatocellular carcinoma (HCC) is the most common primary liver malignancy, with increasing worldwide incidence. Transarterial chemoembolization (TACE) is an interventional radiological (IR) therapy used largely in intermediate stage HCC, which can provide successful bridge or downstaging to liver transplantation and increased survival rates. Tumour rupture is a very rare complication of TACE, with an estimated incidence of 0.68%. Potential risk factors include tumour size ampersand:003E 10 cm, and location of lesions in the right lobe or near the liver capsule. However, the pathophysiology of post-TACE tumour rupture is still not fully understood. Aims We aim to describe a case of HCC tumour rupture that occurred in the first 30 hours post-TACE. We also aim to highlight the extent of multiorgan ischemia associated with this tumour-related arterial bleed. Methods A PubMed literature review was done to ensure that post-TACE tumour rupture was a rare and sparsely reported event. Subsequently, inpatient notes, laboratory and imaging data were obtained from the patient's medical record in an anonymized manner. Results A 66-year-old male with alcohol-related liver cirrhosis (MELDNa 7; Child-Pugh Class A) was diagnosed with a 3.3 cm HCC, spanning segments 5 and 8. Six months later, after multidisciplinary discussion, he underwent successful elective TACE of a segment 8 artery that was supplying the HCC, as a bridge to liver transplantation. The next day, he developed diffuse abdominal pain, emesis, tachycardia, and abdominal firmness and tenderness. Labs showed a 45 g/L drop in hemoglobin (121 g/L to 76 g/L), leukocytosis (27.0 x109/L), and an elevated lactate (4.4 mmol/L). Computed tomography (CT) scan confirmed tumour rupture, with moderate-to-large hemoperitoneum with active bleeding from the embolized region of the HCC, and associated gas. Emergent IR-guided embolization was performed to the bleeding segment 8 artery. CT scan two days later revealed interval ischemic infarction of the spleen, pancreatic tail, and stomach. This widespread ischemia was suspected to be due to hypovolemic hypoperfusion vs. post-TACE embolic phenomena. Aggressive supportive measures, antibiotics, and anticoagulation were implemented. Due to tumour rupture, the patient was deemed no longer a suitable candidate for liver transplantation. Futility of definitive management was discussed, and the patient opted for medical care without resuscitation. After optimization of nutritional and physical functioning parameters, he was discharged home with medical management for pain and ascites. Conclusions Post-TACE tumour rupture is a rare occurrence for which the pathophysiology is not fully understood. This case provides an important reminder of this potential adverse event. Early detection and management are imperative to facilitating a favourable outcome in this life-threatening condition. Funding Agencies None

Clinical and cultural conflicts.

By some accident of genealogy, I recently found myself flying to an Arabian Gulf state to act as the next-of-kin and surrogate advocate for a relative who had suffered a catastrophic brain stem infarction. My uncle, a 71-year-old lifelong bachelor still in active employment, had been admitted to a private hospital with massive bilateral vertebrobasilar artery thrombosis. CT scans showed widespread infarction of the cerebellum, brain stem, and occipital cortex. He developed coning, at which time my sister, who lived in the region, was contacted to give consent for surgery. Having already discussed the details with me, she attempted to refuse but was told that this was not an option and that surgery had to be performed. The operation notes, which in part read like a Gothic horror novel, confirmed visible, widespread ischaemia with marked tissue oedema. The surgery report detailed debridement of visibly necrotic areas of the brain stem. I attended to find a body totally unresponsive to any stimuli, immobile, externally ventilated, parenteral nutrition in place, bladder catheterised. The neurosurgeon greeted us amicably but did become slightly confused when …

Was it a fatal whiplash injury or not? Clinical forensic anatomy: a key to shed light on a case

Autopsy is the oldest method of medical investigation. Many studies underscore the need for autopsies also in the era of technical progress emphasizing the continuing discrepancies between ante-mortem and post-mortem diagnoses. The forensic pathologist (and anatomist, too) has to know in depth the anatomy and how to study it using the dissection techniques with the help of new pre and post autoptical technologies. Forensic radiology must integrate the expertise of forensic pathologist, the challenge is to unite all disciplines by direct and intense communication. Furthermore, histology plays a fundamental role in the final diagnosis and the collection of the samples requires the correct visualization and isolation of all the supposed organ lesions. We present a case report with a multidisciplinary method to the cadaver, about a presumed “road murder”, in which the forensic clinical anatomical approach was directed to the cause and means of death. A case of a 79 years old man victim of a frontal crash is presented. At the scene, the driver was found comatose (GCS 3) and carried to the Emergency Department. At the ED, the patient was subjected to CT scan of brain and angio CT scan, directed, in particular, to epiaortic vessels. CT scan showed a widespread ischemia of cortical and subcortical areas of pariar, occipital and cerebellar lobes; angio CT scan revealed the complete occlusion of the lumen of both vertebral arteries, at the level of the third cervical vertebra. The man died about 4 days after his admittance to the hospital. Was it a death after a whiplash injury or not? Before performing autopsy, a head and neck CT scan was carried out. Autopsy was performed 6 days later, and was carried according to a protocol for the examination of the V3 – V4 segments of the vertebral artery. Imaging first, and then autopsy, revealed completely different findings from those shown in ante mortem CT scan, that revealed the true cause of death.

Acute aortic dissection flap prolapsing into the left ventricle on transthoracic echocardiography.

A 62-year-old man with a history only of untreated hypertension presented with acute onset right buttock pain and leg weakness. He had neither significant chest pain nor initial hemodynamic disturbance (BP 106/28, pulse 55). Examination revealed marked weakness of the right leg with absence of palpable pulses. An ECG unexpectedly showed widespread ischemia. A transthoracic echocardiogram (TTE) was performed. There was no parasternal window, but in the apical four-, five-chamber and subcostal five-chamber views a large flap of aortic intima, with a hinge point immediately distal to the aortic valve (AV), was seen prolapsing through the AV during diastole (Fig. 1a) associated with severe aortic regurgitation (Fig. 1b). The flap prolapsed into the left ventricle in diastole (Fig. 1c) and returned to its original position during systole, partially closing the dissection orifice (Fig. 1d and supplementary video). Aside from mild anterior hypokinesis, left ventricular size and systolic function appeared normal. There was no significant pericardial effusion. The diagnosis of type A aortic dissection (AD), extending from the aortic root to iliac vessels and involving most major branches, was confirmed on contrast computed tomogram. The patient unfortunately died in the intensive care unit shortly afterward before surgery could be undertaken. Isolated leg pain and weakness as the presenting features of AD occur in less than 4 % of cases [1]. TTE is a portable, easily accessible tool that can be used in the initial investigation of suspected AD but is often overlooked. The sensitivity for detecting AD is reported as being between 59 and 83 % (highest in type A dissection) and specificity between 63 and 93 % with reverberation artifacts from either the walls of the left atrium or the pulmonary artery accounting for much of the potential for false-positive TTE studies [2]. In addition to the ability to identify a dissection flap, and thus provide a definitive diagnosis, TTE is also useful to identify complications such as aortic regurgitation, aortic root dilatation and pericardial effusion. TTE can also differentiate AD from myocardial infarction in the acutely unwell patient with chest pain where the presence or absence of left ventricular regional wall motion abnormalities is invaluable [3]. Prolapse of an aortic dissection flap into the ventricle is rare, although one report using TEE suggested a prevalence as high as 15 % in ADs involving the ascending aorta. Previous reports in the literature are scant [4–6]. Mechanistically a large flap of aortic intima, anchored proximally, moves to and fro with pulsatile blood flow. Complications may occur because of the extent and propagation of the false lumen, the acute left ventricular hemodynamic changes due to severe acute aortic regurgitation or direct coronary ostial obstruction during diastole by the dissection flap. The appearance of the prolapsing intimal flap on TTE is highly unusual and infrequently reported, and accurate identification may be difficult, particularly if imaging windows are suboptimal. In this case, despite the absence of a parasternal window, a modified subcostal Electronic supplementary material The online version of this article (doi:10.1007/s12574-012-0143-z) contains supplementary material, which is available to authorized users.

Third‐Degree Atrioventricular Block in a Horse Secondary to Rattlesnake Envenomation

Third‐Degree Atrioventricular Block in a Horse Secondary to Rattlesnake Envenomation

Reversible widespread ischemia after early reperfusion detected by initial diffusion-weighted magnetic resonance imaging

We herein report the time-related dynamic changes according to the diffusion-weighted image (DWI) findings after a cerebral ischemic attack in a 63-year-old woman. At 2 weeks after undergoing a lower limb amputation due to diabetic atherosclerosis, she experienced a sudden loss of consciousness and right hemiparesis. Magnetic resonance image revealed left frontal and parietal areas with an increased signal on the DWI, and magnetic resonance angiography (MRA) showed the left middle cerebral artery to be occluded at the superior M2 branch. However, on the next day the lesion on DWI, except for the gray matter, was observed to have almost completely resolved, and MRA showed complete recanalization of the left superior M2 branch with diminished clinical symptoms. Although a few cases of reversible DWI-identified lesions have been described in the literature, the occurrence of large, reversed DWI lesions in the middle cerebral artery territory with severe apparent diffusion coefficient decreases, as seen in our case, are exceedingly rare.

Investigation of Estrogen Status and Increased Stroke Sensitivity on Cerebral Blood Flow after a Focal Ischemic Insult

Recently the authors have shown that female stroke-prone spontaneously hypertensive rats (SHRSPs) in proestrus (high endogenous estrogen), sustain more than 20% smaller infarcts after middle cerebral artery occlusion (MCAO) compared with SHRSPs in metestrus (low endogenous estrogen). Because estrogen has vasodilator properties, the authors investigated whether the estrous state influences cerebral blood flow (CBF) after MCAO. CBF was measured 2.5 hours after a distal MCAO by [14C]iodo-antipyrine autoradiography in conscious SHRSPs either in metestrus or in proestrus. There were no significant differences in CBF when analyzed either at predetermined anatomic regions or by cumulative distribution analysis of areas with flow <25 mL/100 g/min. As a positive internal control, the authors compared results in SHRSPs with those in their normotensive reference strain, Wistar Kyoto rat. SHRSPs displayed more severe and widespread ischemia than Wistar Kyoto rats. Thus, the absence of demonstrable CBF differences between estrous states appears to be unrelated to the CBF measurement paradigm. In conclusion, the smaller infarct size afforded in proestrus in SHRSPs is unlikely to be due to an influence on CBF.

Diffusion-Weighted Magnetic Resonance Imaging in Brain Death

To the Editor: The case report on diffusion-weighted imaging (DWI) in brain death by Lovblad and Bassetti1 in the February issue of Stroke may be appealing but deserves elaboration. The DWI studies in the case report shows widespread ischemia, and the MR angiography shows absence of flow in the intracranial portion of the carotid arteries. However, it is not stated in the report whether there was flow void in the extracranial carotid arteries. Its presence may have suggested a diagnosis of bilateral carotid artery occlusion (eg, due to dissection) resulting in bilateral hemispheric infarction as the cause for the patient’s coma. Additionally, the authors did not comment on whether there was flow in the basilar artery. This information may have been available to the authors but was not commented on in the text. However, much more disturbing is that this communication wrongly suggests that an imaging modality can diagnose brain death even when the clinical examination shows some remnant of brain stem reflexes. We are not certain what the authors meant by “The neurological examination after the MRI showed an intubated comatose patient who had deteriorated neurologically.”1 It is possible that the patient had met the criteria for brain death, but the authors did not provide details on clinical testing. Brain death is the irreversible loss of function of the brain and brain stem.2 3 The diagnosis of brain death in adults in the United States is not, as the authors stated, “usually supported by confirmatory tests.” The article quoted here did not propose that view.2 The guidelines proposed by the American Academy of Neurology stated that “… confirmatory test is not mandatory but desirable when specific components of the clinical testing cannot be reliably performed. …”3 Differences in recommendations for confirmatory tests after a …

Abstracts of Literature

Abstracts of Literature

Crossed cerebellar diaschisis after middle cerebral artery infarction

It is unclear whether crossed cerebellar diaschisis (CCD) is merely an epiphenomenon, as its clinical significance remains uncertain. We retrospectively analysed the positron emission tomographic (PET) findings in 28 patients with a chronic, stable middle cerebral artery (MCA) infarct and in 22 controls, using the steady state technique and 15O. Also, the Orgogozo scores on admission and at the time of the PET examination were compared in the patients with MCA infarction. Based on the asymmetry index and the 95% confidence limits for regional cerebellar blood flow (rCBF) and oxygen consumption (rCMRO 2) in the control group, the stroke patients were subdivided in a group with ( n = 8) and a group without ( n = 20) CCD. The CCD group had lower values of rCMRO 2 in the infarct and border areas compared to those of the non-CCD patients. The infarct location within the MCA territory was similar but the size was somewhat larger in the CCC group. The degree of neurological improvement was better in the non-CCD group. Although persistence of CCD has no real clinical significance it appears to be correlated to more severe and widespread ischaemia in the affected MCA territory and to the lack of significant clinical improvement.

Rotavirus‐Induced Changes in the Microcirculation of Intestinal Villi of Neonatal Mice in Relation to the Induction and Persistence of Diarrhea

SummaryUsing a histochemical peroxidase technique, under conditions that preferentially stain erythrocytes, we have shown changes in the microcirculation of villi of neonatal mice infected with murine rotavirus. Between 18 and 48 h postinfection (PI), throughout all areas of the small intestine there occurred, sequentially, a marked ischemia and atrophy of villi. By 72 h PI, villi had recovered their normal height and showed incipient hyperemic microcirculation. At 96 h PI, hyperemic microcirculation was most marked. Between 120 and 144 h PI, a second phase of villus atrophy occurred, which was more attenuated and confined to the upper and middle regions of the intestine. This phase was not accompanied by a widespread ischemia of villi: a minority of villi were short and ischemic but many appeared hyperemic. Recovery of villus microcirculation occurred at 168 h PI, which coincided with recovery from diarrhea. These changes in villus microcirculation are discussed in relation to the pathology and pathophysiology of rotavirus infection. We make two novel suggestions. First, the reduction in red cells flowing through villi in the early stages of the infection instigates hypoxia and hence atrophy of villi. The ensuing but ephemeral increase in rate of cell division, necessary for the reconstitution of villi, induces hypersecretion. Second, the increase in numbers of erythrocytes found in villi during their regrowth phase and throughout the remaining time course of the infection perturbs the countercurrent system, lowering the osmolality of the hyperosmotic zone located at villus tips, thereby impairing water absorption and prolonging diarrhea.

Rotavirus-Induced Changes in the Microcirculation of Intestinal Villi of Neonatal Mice in Relation to the Induction and Persistence of Diarrhea

Using a histochemical peroxidase technique, under conditions that preferentially stain erythrocytes, we have shown changes in the microcirculation of villi of neonatal mice infected with murine rotavirus. Between 18 and 48 h postinfection (PI), throughout all areas of the small intestine there occurred, sequentially, a marked ischemia and atrophy of villi. By 72 h PI, villi had recovered their normal height and showed incipient hyperemic microcirculation. At 96 h PI, hyperemic microcirculation was most marked. Between 120 and 144 h PI, a second phase of villus atrophy occurred, which was more attenuated and confined to the upper and middle regions of the intestine. This phase was not accompanied by a wide-spread ischemia of villi: a minority of villi were short and ischemic but many appeared hyperemic. Recovery of villus microcirculation occurred at 168 h PI, which coincided with recovery from diarrhea. These changes in villus microcirculation are discussed in relation to the pathology and pathophysiology of rotavirus infection. We make two novel suggestions. First, the reduction in red cells flowing through villi in the early stages of the infection instigates hypoxia and hence atrophy of villi. The ensuing but ephemeral increase in rate of cell division, necessary for the reconstitution of villi, induces hypersecretion. Second, the increase in numbers of erythrocytes found in villi during their regrowth phase and throughout the remaining time course of the infection perturbs the countercurrent system, lowering the osmolality of the hyperosmotic zone located at villus tips, thereby impairing water absorption and prolonging diarrhea.

Coronary artery spasm induced by intravenous epinephrine overdose

A 27-year-old man was accidentally given 2 mg intravenous epinephrine instead of 2 mg naloxone. He immediately developed chest pain, nausea, and diaphoresis. An ECG taken shortly after the epinephrine administration showed widespread ischemia. Forty-five minutes later the tracing still showed an early repolarization pattern, but ST elevation was less marked and the patient was asymptomatic. Serum potassium was 3.2 mEq/L and serum catecholamines, drawn approximately 20 minutes after the epinephrine administration, were 10 times normal (dopamine, 173 ng/L; epinephrine, 1,628 ng/L; norepinephrine, 1,972 ng/L). There are seven other reports of intravenous epinephrine overdose in the English literature. Two of the previously reported cases had 12-lead ECGs within the first hour. In both there was evidence of transient ischemia similar to that observed in this case. Most of the patients has symptoms consistent with angina, and several developed pulmonary edema. These findings suggest that, in humans, large intravenous doses of epinephrine are likely to produce coronary artery spasm and may decrease coronary artery perfusion.

Mechanism of depolarization in the ischaemic dog heart: discrepancy between T-Q potentials and potassium accumulation.

1. To study the origin of ischaemic myocardial depolarization, the diastolic surface potential - T-Q depression-was correlated with subepicardial extracellular K+ accumulation during serial episodes of widespread ischaemia in open-chest dogs, and in isolated, blood-perfused canine hearts. Placement of the reference electrode on a small island of non-ischaemic myocardium simplified the interpretation of the T-Q potentials. 2. In some experiments, changes in resting potential in the ischaemic zone were recorded using a 'contact' monophasic action potential (MAP) electrode. The change in MAP resting potential was linearly related to T-Q depression for a wide range of experimental conditions (R greater than 0.98). T-Q depression is therefore a linear index of depolarization in superficial myocardial cells. 3. The validity of T-Q depression as a 'measure' of local cellular depolarization was further tested by infiltration of isotonic KCl into the superficial myocardium subjacent to the ischaemic zone electrode. Resulting T-Q depression was 2- to 3-fold larger than the maximum values obtained in ischaemia; and the ratio of T-Q depression to the amplitude of the accompanying monophasic potential was consistent with the assumption that KCl had fully depolarized the underlying myocardium (delta Vm = 89 mV). KCl prevented (i.e. occluded) further changes in the T-Q potential during ischaemia. KCl did not have these effects if it was introduced at sites more remote from the electrode (greater than 4 mm). 4. Ischaemic T-Q depression was drastically accelerated by increasing the heart rate from 90 to 180 beats/min and was further accelerated by arterial infusion of CaCl2. These effects were most striking during the first minute of ischaemia. 5. In contrast, the above manoeuvres produced little acceleration of subepicardial K+ accumulation. After CaCl2 infusion, large ischaemic potentials, severe conduction impairment, and arrhythmias could be observed when K+ activity was almost normal (aK = 4.0-4.5 mM). 6. T-Q depression was larger in vivo than in isolated hearts, both absolutely and relative to K+ accumulation. 7. Based on the reproducible amplitude of ischaemic epicardial potential-estimates of cellular depolarization (delta Vm) could be obtained, which were compared with the concurrent change in K+ electrode potential (delta EK) for each experimental condition. 8. Estimated depolarization was nearly identical to delta EK in isolated hearts under basal conditions. However, depolarization significantly exceeded delta EK during rapid pacing, CaCl2 infusion, or during paced occlusions performed in vivo.(ABSTRACT TRUNCATED AT 400 WORDS)

Tributary vein obstruction: pathogenesis and treatment of sequelae.

An acute branch retinal vein obstruction or occlusion is followed by a series of haemodynamic events designed to overcome the obstruction and restore equilibrium within the retinal vasculature. Experimental studies would indicate that the immediate post-obstructive retinal oedema is probably the result of capillary and venular distension due to the sudden increase in intraluminar hydrostatic pressure. The widespread extravasation of blood which occurs some time later is probably the result of degenerative changes in the capillary walls secondary to prolonged stasis and hypoxia. In many tributary vein obstructions, readjustments within the involved retinal microvasculature are effective in overcoming the effects of the obstruction. The involved retinal capillaries gradually return to normal or nearly normal, with preservation of their physiological functions. Good vision is often maintained and no therapy is required. In other cases, often where associated arterial insufficiency exists, significant venous stasis persists and the retinal capillaries remain incompetent with the formation of intraretinal oedema. Evidence available at this time would indicate that selective photocoagulation is of some benefit in preventing the chronic accumulation of macular fluid in certain cases and avoiding the unwanted sequelae of cystic macular degenerative changes and pigmentation abnormalities at the fovea. Photocoagulation appears to be less justified in cases of long-established macular oedema with degenerative changes already in evidence. In certain varieties of tributary vein occlusion characterized by marked arterial insufficiency, the involved capillary bed fails to perfuse fully. Neovascularization is frequently associated with extensive areas of non-perfused retina. Neovascularization, although it may appear 3 – 6 months following the acute obstructive episode, rarely demands treatment within the year. The neovascularization associated with a branch vein occlusion is generally subtle, slow-growing, and responds well to photocoagulation. Papillary neovascularization indicates widespread ischaemia, and often suggests implication of further quadrants of the retina in the ischaemic process. Papillary neovascularization can be indirectly influenced by extensive photocoagulation of the ischaemic retina resulting from the vein occlusion.