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W Schummer

Publications and source records attributed to W Schummer.

29 records · Page 2Linked to original sources
PubMed2002

[Differential diagnosis of left-sided thoracic venous catheters: case report of a persistent left superior vena cava].

The differential diagnosis of left-sided thoracic central venous catheters is discussed in context with the cannulation of a persistent left superior vena cava. In this case the catheter tip was seen lying to the left of the spine on frontal chest X-ray. In addition to the descending aorta, differential diagnoses are a persistent left-sided superior vena cava as well as other smaller veins such as the left internal thoracic vein, the left superior intercostal vein, or the pericardiophrenic vein. The misplacement of a venous catheter in a pericardiophrenic vein may result in a fatal pericardial tamponade.

Adult↗
PubMed2002

Loss of the guide wire: mishap or blunder?

We describe four cases of lost guide wires during central venous catheterization. Although percutaneous catheterization of central veins is a routine technique, it is a procedure requiring advanced operating skills, expert supervision, and attention to detail in order to prevent adverse effects.

Adult↗
PubMed2001

[Perforation of the superior vena cava due to unrecognized stenosis. Case report of a lethal complication of central venous catheterization].

We report on a case of fatal perforation of the superior vena cava. The perforation occurred after catheterization of the left internal jugular vein with a hemodialysis catheter, due to an unrecognised stenosis of the superior vena cava. Vascular trauma induced by a previous, also left-sided, subclavian vein-hemodialysis catheter (in place for 14 days), seemed to be the most likely pathomechanism of the stenotic lesion. It should be emphasised that this is a frequent complication especially of left-sided dialysis catheters. In the case described a stenosis was complicated by a misdirected second hemodialysis catheter. Although being repositioned under fluoroscopic control via a guide wire, an extravasal placement occurred but was unrecognised. In order to rule out catheter misplacement, the position of every central venous catheter has to be controlled. Standard methods are either chest X-ray or right atrial electrocardiography. Additionally, confirmation of correct intravenous placement requires a combination of free venous backflow of all lumen and/or blood gas analysis or venous pressure monitoring. Only a combination of tests gives ample certainty as each test for itself has its pitfalls. After placement of hemodialysis catheters, in particular left-sided catheters, we demand chest X-ray in order to verify that the catheter runs parallel with the long axis of the superior vena cava. In doubtful cases the threshold for contrast-enhanced angiographic control of the catheter should be low. If a perforation by the catheter is suspected it should be ruled out by computed tomographic scanning or transesophageal echocardiography.

Aged↗
PubMed2001

Dysfunction of vasomotor reactivity in severe sepsis and septic shock.

OBJECTIVE: Perfusion abnormalities are an overall phenomenon in severe sepsis and septic shock, leading to organ dysfunction. We investigated whether carbon dioxide (CO2)-induced vasomotor reactivity (VMR) is impaired in septic patients, compared with values obtained outside sepsis. DESIGN: Prospective, clinical study. SETTING: Six-bed neurologic critical care unit of a university hospital. PATIENTS AND PARTICIPANTS: Eight consecutive patients with severe sepsis and septic shock. MEASUREMENTS AND RESULTS: CO2-reactivity was measured during and outside a period of severe sepsis or septic shock according to ACCP/SCCM criteria by means of transcranial Doppler sonography and near-infrared spectroscopy (NIRS). VMR was calculated as the percentage change of cerebral blood flow velocity (normalized CO2-reactivity, NCR) and absolute changes in concentration of oxygenated hemoglobin, deoxygenated hemoglobin, total hemoglobin (HbO2, Hb, HbT) and Hbdiff (difference between HbO2 and Hb) in micromol/l per 1% increase in end-tidal CO2 (CR-HbO2, CR-Hb, CR-HbT, CR-Hbdiff). NCR and NIRS-reactivities were significantly reduced during severe sepsis and septic shock compared with values outside sepsis (mean, SD, Wilcoxon): NCR 11.0 (7.1) versus 30.7 (13.0), p < 0.02; CR-HbO2 0.70 (0.61) versus 2.33 (1.11), p < 0.02; CR-Hb -0.17 (0.74) versus -1.42 (1.28), p < 0.04; CR-HbT 0.53 (0.48) versus 1.05 (0.40), p < 0.03; CR-Hbdiff 0.91 (1.33) versus 3.75 (2.33), p < 0.02. This indicates a severely disturbed VMR. CONCLUSIONS: In the advent of a disturbed cerebral autoregulation, critical drops in blood pressure during sepsis are transferred directly into the vascular bed, leading to cerebral hypoperfusion. This mechanism might contribute to the pathogenesis of septic encephalopathy.

Aged↗