A modified two-step technique for the retrieval of a chemoport catheter fragment with inaccesible ends.

BACKGROUND: Migration of central venous catheters is a rare but serious complication. The endovascular approach has been widely used for the retrieval of such fragment, with the two-step technique used for removal of catheter fragments with inaccessible ends. In this case report, we describe a modification of this technique that was used after first attempting the two-step technique unsuccessfully. CASE PRESENTATION: A 42-year-old female with breast cancer had a chemoport inserted for chemotherapy. After 6 cycles of chemotherapy the port could not be flushed and a chest radiograph demonstrated a migrated catheter fragment. CT scan demonstrated that one end of the fragment was in the liver in the middle hepatic vein and the other in the right atrial appendage. A modified 2 step technique, using a pigtail catheter, hydrophilic wire and snare was used to remove this fragment. CONCLUSION: In this case report we highlight a new modification of the 2-step technique that can be employed when the conventional 2 step technique does not work.

Endovascular management of a congenital hepatic arterioportal malformation in a low resource setting.

BACKGROUND: Arterioportal malformations, a rare type of vascular malformation, have significant associated morbidity and mortality. Management requires a carefully thought out approach by a multidisciplinary team. Low resource settings have an added challenge of limited treatment options and consumables. CASE PRESENTATION: We report a case of a 14-month-old male with failure to thrive due to a congenital hepatic arterioportal fistula. He was successfully treated via an endovascular approach with metallic coil embolization. CONCLUSION: Hepatoportal fistula, a rare hepatic vascular malformation, has limited treatment options which can further be restricted by overall patient wellness. Minimally invasive endovascular treatment options can offer a high rate of success and reverse the morbidity associated with the disease as was seen with our case.

Point-of-care measurements reveal release of purines into venous blood of stroke patients.

Stroke is a leading cause of death and disability. Here, we examine whether point-of-care measurement of the purines, adenosine, inosine and hypoxanthine, which are downstream metabolites of ATP, has potential to assist the diagnosis of stroke. In a prospective observational study, patients who were suspected of having had a stroke, within 4.5 h of symptom onset and still displaying focal neurological symptoms at admission, were recruited. Clinical research staff in the Emergency Departments of two hospitals used a prototype biosensor array, SMARTCap, to measure the purines in the venous blood of stroke patients and healthy controls. In controls, the baseline purines were 7.1 ± (SD) 4.2 µM (n = 52), while in stroke patients, they were 11.6 ± 8.9 µM (n = 76). Using the National Institutes for Stoke Scale (NIHSS) to band the severity of stroke, we found that minor, moderate and severe strokes all gave significant elevation of blood purines above the controls. The purine levels fall over 24 h. This was most marked for patients with haemorrhagic strokes (5.1 ± 3.6 µM, n = 9 after 24 h). The purine levels measured on admission show a significant correlation with the volume of affected brain tissue determined by medical imaging in patients who had not received thrombolysis or mechanical thrombectomy. ClinicalTrials.gov Identifier: NCT02308605.

Magnetic Resonance investigation into the mechanisms involved in the development of high-altitude cerebral edema.

Rapid ascent to high altitude commonly results in acute mountain sickness, and on occasion potentially fatal high-altitude cerebral edema. The exact pathophysiological mechanisms behind these syndromes remain to be determined. We report a study in which 12 subjects were exposed to a FiO2 = 0.12 for 22 h and underwent serial magnetic resonance imaging sequences to enable measurement of middle cerebral artery velocity, flow and diameter, and brain parenchymal, cerebrospinal fluid and cerebral venous volumes. Ten subjects completed 22 h and most developed symptoms of acute mountain sickness (mean Lake Louise Score 5.4; p < 0.001 vs. baseline). Cerebral oxygen delivery was maintained by an increase in middle cerebral artery velocity and diameter (first 6 h). There appeared to be venocompression at the level of the small, deep cerebral veins (116 cm3 at 2 h to 97 cm3 at 22 h; p < 0.05). Brain white matter volume increased over the 22-h period (574 ml to 587 ml; p < 0.001) and correlated with cumulative Lake Louise scores at 22 h (p < 0.05). We conclude that cerebral oxygen delivery was maintained by increased arterial inflow and this preceded the development of cerebral edema. Venous outflow restriction appeared to play a contributory role in the formation of cerebral edema, a novel feature that has not been observed previously.