A delayed complication after injury in World War II Surov, Alexey; Taege, Christiane; Behrmann, Curd
New England journal of medicine/The New England journal of medicine,
05/2006, Letnik:
354, Številka:
18
Journal Article
In cirrhosis, hepatic arterial vasodilatation occurs in response to reduced portal venous blood flow. However, although the hepatic arterial flow reserve is high in patients with cirrhosis, its ...impact on hepatic function is unknown. This study investigated the effect of adenosine-induced hepatic arterial vasodilatation on different markers of liver function. In 20 patients with cirrhosis (Child-Pugh class A/B/C: n = 2/7/11) adenosine (2-30 μg · min
−1 · kg body wt
−1) was infused into the hepatic artery and hepatic arterial average peak flow velocities (APV), pulsatility indices (PI), and blood flow volumes (HABF) were measured using digital angiography and intravascular Doppler sonography. Indocyanine green (ICG), lidocaine, and galactose were administered intravenously in doses of 0.5, 1.0, and 500 mg/kg body weight in the presence of adenosine-induced hepatic arterial vasodilatation and, on a separate study day, without adenosine. ICG disappearance, galactose elimination capacity (GEC), and formation of the lidocaine metabolite monoethylglycinxylidide (MEGX) were assessed. Adenosine markedly increased APV and HABF and markedly decreased PI. Serum MEGX concentrations were 63.7 ± 18.2 (median, 62; range, 36-107) and 99.0 ± 46.3 (82.5; 49-198) ng/mL in the absence and presence of adenosine infusion, respectively (
P = .001). Adenosine-induced changes in MEGX concentrations were correlated inversely to changes in APV (
r = −0.5,
P = .02) and PI (
r = −0.55,
P = .01) and were more marked in Child-Pugh class C compared with Child-Pugh class A patients (57.4 ± 49.9 44; −14 to 140 vs. 8.4 ± 16.5 13; −11 to 35 ng/mL,
P < .01). In conclusion, hepatic arterial vasodilatation provides substantial functional benefit in patients with cirrhosis. The effect does not depend directly on hepatic arterial macroperfusion and is observed preferentially in patients with decompensated disease. (H
EPATOLOGY 2003;37:385-392.)
Embolization of venous catheter fragments to the pulmonary vasculature is a very rare form of pulmonary embolism which is only sporadically reported in the literature. The incidence and clinical ...picture of this complication are unknown.
In this retrospective analysis between 1999 and 2004, in our clinic, 1,014 port catheters were implanted. In this 5-year period, the patients' files were screened for the incidence of pulmonary embolism of catheter fragments and the accompanying complication rate.
In 11 patients, port catheter dislodgment and embolism into the pulmonary artery occurred. In all the patients' port examination by fluoroscopy, catheter dislocation and embolization were shown. In these 11 patients, no obvious clinical signs indicating dislocation of catheter fragments into the pulmonary circulation were found. None of these patients demonstrated respiratory symptoms. Heart rate, blood pressure, respiration frequency, and even oxygen saturation were normal. In 7 of the 11 patients, malfunction of port catheter was the first indicator of catheter dislocation. In four patients, embolized catheter fragments were an incidental finding. The main cause of catheter embolization was the pinch off syndrome. All embolized catheter fragments were retrieved by a 'goose-neck' snare without complication.
These results suggest that the migration of fractured catheter into the pulmonary artery occurs in 1% of the central port catheter implantation. It is often asymptomatic, and malfunction of the catheter may be the first sign of this complication. The pinch off syndrome might be prevented by using the internal jugular vein or by implantation of the port catheter more laterally in the subclavian vein.
Background & Aims: In cirrhosis, liver blood flow becomes increasingly dependent on the hepatic artery. The aim of this study was to investigate hepatic arterial blood flow volume and resistance and ...hepatic arterial flow reserve in relation to liver function and systemic hemodynamic alterations in patients with cirrhosis.
Methods: In 38 patients with cirrhosis, liver function, cardiac output, and systemic vascular resistance were studied, and hepatic arterial blood flow velocity, flow volume, and pulsatility index at baseline and during intra-arterial administration of adenosine (2–40 μg · min
−1 · kg body wt
−1) were assessed by angiography combined with intravascular Doppler flowmetry.
Results: Hepatic arterial flow velocity was 21 ± 11, 31 ± 17, and 41 ± 27 cm/s; flow volume was 266 ± 246, 342 ± 289, and 417 ± 220 mL/min; and pulsatility index was 2.2 ± 0.7, 1.7 ± 0.6, and 1.5 ± 0.5 in Child–Pugh classes A, B, and C, respectively (differences not statistically significant). Adenosine-induced changes in these parameters were more marked in Child–Pugh class A (68 ± 15 cm/s, 1246 ± 486 mL/min, and −1.14 ± 0.5) than in class C (45 ± 23,
P < 0.05;704 ± 492,
P = 0.02; and −0.58 ± 0.38,
P < 0.05). Using analysis of variance, cardiac index, systemic vascular resistance, and ascites, but not Child–Pugh class, were related to baseline values and adenosine-induced changes.
Conclusions: Adenosine is a potent dilator of the hepatic artery in humans. The data suggest that hepatic arterial blood flow and adenosine-dependent flow reserve in patients with cirrhosis are under systemic hemodynamic or neurohormonal control.
GASTROENTEROLOGY 1999;116:906-914
Intravascular lymphomatosis is characterized by the presence of large lymphoma cells predominantly within small vessels. This report presents two patients with diagnostically misleading neurological ...manifestation of this disease.
Case 1, a 63-year-old man, developed a sensorimotor transverse spinal cord syndrome and encephalopathy. Lumbar puncture revealed albuminocytological dissociation. Magnetic resonance imaging (MRI) showed progression of multifocal infarct-like lesions in the brain, the thoracic cord and the medullary cone. Autoimmune inflammation was suspected, and the patient received immunosuppressive therapy with immunoglobulins, steroids and azathioprine. He died 18 months after the onset of symptoms.
Case 2, a 68-year-old man, showed fluctuating aphasia, disorientation, and fever for several months. Brain MRI-scan, electroencephalography (EEG) and cerebrospinal fluid (CSF) cytology were inconclusive. Premortal biopsy of lesions in liver and right suprarenal gland showed no further characterized malignancy. He died 6 months after the first occurrence of symptoms. Autopsy of both cases revealed an intravascular lymphomatosis. Tumour cells were seen disseminated in extranodal sites including heart, lung, adrenal gland, spleen, thyroid gland and brain.
An intravascular lymphomatosis should be considered when a meningoencephalitic symptomatology is unclear. A biopsy of different organs including the brain and leptomeninges should not be delayed to ensure ante mortem diagnosis and to initiate chemotherapy.
Absolute arrhythmia is the most common cause of cerebral thromboembolism. 1 The intracerebral arteries are usually affected. 2 In contrast, the finding of a large thrombus in the carotid artery as in ...the present case is very rare. 3 Acknowledgement: This article has been adapted from Surov Alexey, Behrmann Curd, Kornhuber Malte.
We report a 62-year-old woman with a locked-in syndrome with bilateral masticatory spasms and persistent trismus, who was still able to yawn. A vascular malformation of the basilar ...artery–megadolichobasilar artery (fusiform aneurysm, vertebrobasilar dolichoectasia) was determined to be the underlying cause of this rare combination of symptoms. A thrombus in the megadolichobasilaris as well as an almost total pontine infarction were demonstrated on CT- and MRI-scans. Thus, trismus may be associated with locked-in syndrome due to megadolichobasilar artery thrombus, although yawning is still possible.
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