Surgery Notes

The radiology of the abdomen can detect 90% of radiopaque urinary calculi. You can perform an ultrasound, but its sensitivity is 80 to 85%. These tests do not always confirm the obstruction because the system does not always appear dilated collector, especially if it is an acute injury, the ureter is enclosed (in retroperitoneal fibrosis or tumor) or the patient hypovolemia. If you suspect an obstruction, antegrade or retrograde studies with contrast can set the location of the blockage and indicate the treatment. A postvoid catheterization can assess blockages urinary incontinence.
Ultrasound and CT are useful because the presence of a normal or large kidneys indicates reversibility of the process, unlike a small kidney, which suggests chronic renal failure. Arteriography may be indicated or renal venography if the clinic suggests a vascular process. Has not been established although the importance of MRI, although it may be useful when you think that contrast can be dangerous. Scintigraphic studies can only exclude renal artery occlusion because it is difficult to interpret the images when it is very impaired renal function.
You can perform a kidney biopsy if you do not reach a diagnosis.

Prognosis
The IRA and its immediate complications (fluid overload, metabolic acidosis, hyperkalaemia, bleeding) are treatable, but the survival remains approximately 60% despite dietary and dialysis treatments strongest. It seems unlikely that these results will improve by the frequent association with sepsis, respiratory failure, severe injury, burns, surgical complications or consumptive coagulopathy.

Prophylaxis and treatment
The IRA can be prevented by maintaining a proper fluid balance, blood volume and BP during major surgery and thereafter, by isotonic NaCl infusion in patients with severe burns and rapid transfusion in case of hypotension due to hemorrhage. When you need a vasopressor drug, intravenous administration 1 to 3 mg / kg / min of dopamine may increase renal blood flow and excretion of urine, although there is no clinical evidence to avoid the IRA. In cases of incipient IRA, the administration of furosemide with mannitol or dopamine is able to regain normal excretion of urine or convert an oliguric to non-oliguric ARF, although there are few data demonstrating a decrease in mortality.

Avoid dehydration and depletion of the ECF in patients undergoing cholecystography or renal failure patients undergoing urography, especially when the cause is multiple myeloma. Avoid urography and angiography in patients with renal failure, given the high incidence of renal impairment. The higher incidence observed in the elderly is associated with a decrease in GFR associated with aging. Before starting treatment in patients killer with certain malignancies (lymphoma, leukemia) should be assessed treatment with allopurinol and urine alkalinization (sodium bicarbonate or oral acetazolamide) and try to increase the urinary excretion by increasing the oral intake of fluids or iv administration of them to reduce urate crystalluria.

Dialysis improves electrolyte disturbances and allows for adequate nutrition. There is no consensus on when dialysis should be initiated, how often you should be and even if this technique improves the survival or recovery. However, hemodialysis with biocompatible membranes (polysulfone, polyacrylonitrile, polymethylmethacrylate) instead of cuprofano membranes improves the recovery of renal function and reduces the incidence of mortality.

The IRA must be treated without dialysis only when this technique is available or if the course of the IRA is not complicated and has <>

When relieving the obstruction, polyuria may occur with excretion of large amounts of Na, K, Mg and other solutes, which can be determined self-limited hypokalaemia, hyponatraemia, hypernatraemia, hypomagnesemia or contraction of the ECF with peripheral vascular collapse. In many patients, a diuresis occurs abruptly after removal of the obstruction as a physiological response to the expansion of the LEC during the obstruction, which does not compromise the volume status. An overly careful management of water and salt after relieving the obstruction may prolong diuresis.

Postrenal. The most common cause of sudden cessation, with total frequency of urinary excretion among adults is obstruction of bladder outflow. This process may be related to benign prostatic hyperplasia with carcinoma of the prostate or cervix and retroperitoneal processes. To produce an azotemia, we need to clog the two urinary tract or one where the patient has only one functioning kidney. Other less common causes intraluminal the existence of bilateral renal calculi, papillary necrosis, coagulated blood and bladder carcinomas and between extraluminal causes include retroperitoneal fibrosis, tumors, colorectal and other malignancies. In children, obstructive congenital defects collector or excretory urinary system are other possible causes.
Renal. The mechanisms that are considered responsible for the hipofiltración highlight the marked reduction in renal blood flow, decreased glomerular permeability, tubular obstruction by cell swelling and interstitial or cellular debris and blocking the spread of glomerular filtrate through the tubular epithelium injured. These factors are interdependent, though not all are so necessary in each individual patient, in addition, there are large variations in these factors from one patient to another and sometimes in the same patient. The importance of these factors reflects the lack of correction of acute tubular necrosis famous term that was used to define the basic alteration.
The renal vasculature is very sensitive to endothelin, a potent vasoconstrictor that reduces renal blood flow and GFR. Antiendothelin antibodies or endothelin receptor antagonists can protect the kidney against ischemic ARF.

The tubular structural changes depend on the lesion and its seriousness, but always observed edema and inflammation in the interstitium. In cases of ischemic bullae often occur in the apical membranes of proximal tubule epithelial cells with brush border loss of polarity and disruption of tight junctions between them. Although the overall structural integrity of the vessels seems preserved glomerular epithelial cells often show swelling with scanning electron microscopy.

The IRA of any etiology is usually associated with hypocalcemia, hyperphosphatemia and secondary hyperparathyroidism. The pathophysiology of these effects is a temporary loss of production in the injured kidney calcitriol and phosphate retention. You can see a significant hypocalcemia in patients with ARF mioglobinú America, which seems due to the combined effects of the deposit of Ca in the necrotic muscle, decreased production of calcitriol and bone resistance to parathyroid hormone (PTH). During the recovery phase of an FRS, hypercalcemia may occur when increased production of calcitriol, bone begins to respond to PTH and when mobilized Ca deposits of injured tissues.