IgM-enriched solution BT086 improves host defense capacity and energy store preservation in a rabbit model of endotoxemia.

INTRODUCTION: The therapeutic value of intravenous immunoglobulin (IVIG) as an adjuvant therapy in sepsis remains debatable. We hypothesized that intravenous administration of BT086, a predominantly IgM IVIG solution, would improve host defense in an established rabbit model of endotoxemia and systemic sepsis. METHODS: New Zealand white rabbits were randomized into the following four groups: (1) the negative control group without lipopolysaccharide (LPS, control), (2) the positive control group with LPS infusion (LPS group), (3) the albumin-treated LPS group (ALB+LPS group), and (4) the BT086-treated LPS group (BT086 + LPS group). A standardized amount of E. coli was intravenously injected into all of the animals. The vital parameters, the concentration of E. coli in the blood and other organs, the residual granulocyte phagocytosis activity, and the levels of the inflammatory mediators were measured. Histological changes in the lung and liver tissue were examined following autopsy. RESULTS: The elimination of E. coli from the bloodstream was expedited in the BT086-treated group compared with the LPS- and albumin-treated groups. The BT086 + LPS group exhibited higher phagocytic activity of polymorphonuclear neutrophils (PMNs) than the control and ALB+LPS groups. The liver energy stores were higher in the BT086 + LPS group than in the other groups. CONCLUSION: Our data suggest that the IgM-enriched IVIG has the potential to improve host defense in a rabbit model of endotoxemia. Studies using different animal models and dosages are necessary to further explore the potential benefits of IgM-enriched IVIG solutions.

[Distributive shock]. / Distributiver Schock.

In shock there is a significant mismatch between oxygen supply and consumption. In recent years the classification of forms of shock has been established based on pathophysiological and clinical aspects. The term distributive shock includes septic, anaphylactic and neurogenic shock. All these forms share a distinct vasoplegia with a relative volume deficiency. The adequate treatment of patients with distributive shock includes a rapid diagnosis and a consistent emergency treatment consisting of volume and catecholamine administration as well as additional specific emergency procedures when necessary.

[Perioperative visual loss after nonocular surgery]. / Erblindung nach nichtophthalmologischen Eingriffen.

Perioperative visual loss (POVL) after nonocular surgery is a rare but unexpected event and represents a devastating complication. It is most often associated with cardiac, spinal as well as head and neck surgery. The etiology of POVL remains incompletely understood. Any portion of the visual system may be involved, from the cornea to the occipital lobe. The most common site of permanent injury is, however, the optic nerve itself and ischemia is the most often presumed mechanism. Multiple factors have been proposed as risk factors for POVL, including long duration in the prone position, decreased ocular perfusion pressure, excessive blood loss and anemia, hypotension, hypoxia, excessive fluid replacement, elevated venous pressure, head positioning and a patient-specific vascular susceptibility which may be anatomic or physiologic. However, the risk factors for any given patient or procedure may vary. The underlying specific pathogenesis of these neuro-ophthalmic complications remains unknown and physicians should be alert to the potential for loss of vision in the postoperative period. This review updates readers on the incidence, suspected risk factors, diagnosis and treatment of POVL in the setting of nonocular surgery.

[Perioperative visual loss after nonocular surgery]. / Erblindung nach nichtophthalmologischen Eingriffen.

Perioperative visual loss (POVL) after nonocular surgery is a rare but unexpected event and represents a devastating complication. It is most often associated with cardiac, spinal as well as head and neck surgery. The etiology of POVL remains incompletely understood. Any portion of the visual system may be involved, from the cornea to the occipital lobe. The most common site of permanent injury is, however, the optic nerve itself and ischemia is the most often presumed mechanism. Multiple factors have been proposed as risk factors for POVL, including long duration in the prone position, decreased ocular perfusion pressure, excessive blood loss and anemia, hypotension, hypoxia, excessive fluid replacement, elevated venous pressure, head positioning and a patient-specific vascular susceptibility which may be anatomic or physiologic. However, the risk factors for any given patient or procedure may vary. The underlying specific pathogenesis of these neuro-ophthalmic complications remains unknown and physicians should be alert to the potential for loss of vision in the postoperative period. This review updates readers on the incidence, suspected risk factors, diagnosis and treatment of POVL in the setting of nonocular surgery.