Do''s and don''t''s of percutaneous nephrostomy

Percutaneous nephrostomy procedures generally are safe. The associated mortality rate is approximately 0.04%, and the incidence of important complications is 5% (2-4). To minimize complications, certain precautions always should be followed. First, radiologists should perform a preprocedural evaluation of the patient, with correction of marked coagulopathy or thrombocytopenia before all but the most emergent procedures. Second, antibiotics should be administered routinely before nephrostomy drainage; the choice of antibiotics can be based on the specific patient's risk factors for bacteriuria. To minimize the risk of clinically important renal vascular damage, radiologists should do the following: 1. Always achieve adequate visualization of the calices. 2. Identify a posterior calix for puncture that will give access to the appropriate segment of the kidney for anticipated procedures and allow safe creation of a tract. 3. Puncture below the 11th rib (and preferably below the 12th rib when feasible). 4. Puncture the tip of a posterior calix from a 20 degrees-30 degrees, posterolateral oblique approach to avoid major blood vessels. 5. Make a single-wall puncture of the calix. 6. Perform exchange transfusion for opacification of the renal pelvis and calices during percutaneous nephrostomy procedures to minimize the risk of sepsis. Overdistention can increase the likelihood of sepsis or retroperitoneal contamination. 7. Inject contrast material via a catheter placed over a wire to confirm the intracollecting system location of the entry. 8. Avoid unnecessary (complicated, prolonged) procedures in an infected, obstructed system. 9. Use only self-retaining drainage catheters to minimize the risk of inadvertent catheter dislodgment. 10. Create large-bore tracts with a balloon dilation system. By contrast, radiologists should not do the following: 1. Puncture above the 11th rib (unless all other avenues of approach have been exhausted). 2. Lose access to an obstructed kidney once the kidney has been punctured. Placement of a "safety" wire for all complex manipulations is recommended. 3. Panic if excessive bleeding or evidence of adjacent organ injury is seen. Excessive bleeding usually can be stopped with tract tamponade by using a balloon catheter advanced through the tract or with placement of an appropriate-sized nephrostomy tube to occlude the tract. If active bleeding continues or recurs, arteriography should be considered. The quantity of bleeding can be monitored with sequential hematocrit measurements. Almost all renal artery injuries can be treated with minimally invasive procedures, such as selective embolization of the branch artery involved, and this will lead to infarction of only a small segment of kidney, with preservation of functioning renal parenchyma. Injury to an adjacent organ usually can be treated nonsurgically (21,23). The most commonly injured extrarenal abdominal organ is the colon (Fig 6). On occasion, a percutaneous nephrostomy needle may traverse the retroperitoneal segment of the colon, and this type of injury generally can be treated nonsurgically, as well (23). If the colon has been traversed, adequate urinary drainage should be ensured before the transcolonic nephrostomy catheter is removed (so that a nephrocolonic fistula is not maintained). This can be done by placing a ureteral stent and a bladder catheter (18). Once adequate urinary drainage is provided, the nephrostomy catheter can be withdrawn into the colon and used as a percutaneous colostomy drain. The percutaneous colostomy tract should be allowed to mature for several days before this catheter is removed. In addition, appropriate antibiotics should be administered from the time a transcolonic tract is identified until the percutaneous tract has healed completely. Transthoracic entry can cause pneumothorax and pleural effusions. These should be treated only if they are large or cause symptoms (21). (ABSTRACT TRUNCATED)     

Axonal cytoskeleton changes in experimental optic neuritis

Axonal loss and degeneration in multiple sclerosis (MS) and experimental allergic encephalomyelitis (EAE) have been suggested by brain imaging, pathological and axonal transport studies. Further elucidation of the processes and mechanisms of axonal degeneration in demyelinating diseases is therefore of potential importance in order to alleviate the permanent disabilities of MS patients. However, detailed studies in this area are impeded by the small number of reliable models in which the onset and location of demyelination can be well-controlled. In this study, microinjection of polyclonal rabbit anti-galactocerebroside (anti-Gal C) antibody and guinea pig complement was used to induce local demyelination in the rat optic nerve. We found that treatment with appropriate volumes of the antibody and complement could induce local demyelination with minimal pressure- or trauma-induced damage. Local changes in neurofilaments (NFs) and microtubules (MTs) were examined with both immunohistochemistry (IHC) and electron microscopy (EM). On day 1 after microinjection, we observed moderate NF and MT disassembly in the local demyelinated area, although in most cases, no apparent inflammatory cell infiltration was seen. The NF and MT changes became more apparent on days 3, 5, 7 after microinjection, along with gradually increased inflammatory cell infiltration. These results suggested that acute demyelination itself may induce local cytoskeleton changes in the demyelinated axons, and that the ensuing local inflammation may further enhance the axonal damage. When the lesions were stained with specific antibodies for T lymphocytes, macrophages, and astrocytes, we found that most of the cells were macrophages, suggesting that macrophages may play a greater role in inflammation-related axonal degeneration and axonal loss. These results were confirmed and further characterized on the ultrastructural level.