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Oliguria in Intensive Care |
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In this patient’s case, it turns out that her blood pressure at the preoperative screening clinic was 165/95 (MAP = 115mmHg). Intra-operatively her pressure was, on average 80/60mmHg (MAP 66mmHg) (she was given multiple boluses of phenylephrine), and her systolic pressure never rose above 90mmHg. Her MAP has been between 65 and 70mmHg. This patient developed acute renal failure and required dialysis.
She is treated with 1 litre of hextend (6% hydroxyethyl starch buffered in Ringer’s lactate) , her CVP rises to 14cmH2O, she puts out little urine, and her blood pressure remains 90/50 mmHg (MAP 63). The resident starts a norepinephrine infusion, targeted at a MAP of >80mmHg, and the patient’s urinary output increases to 70 to 100ml/hour. Over the next 48 hours, each time the vasopressor was weaned and the MAP fell below 75mmHg, so too did the urinary output. Eventually, the patients blood pressure recovers, and she is weaned from ventilation and vasopressors without further difficulty. The cause of the vasoplegia was considered to be release of inflammatory mediators (particularly inducible nitric oxide synthetase) due to fecal soiling. PATHOLOGICAL VASODILATION. Explain why these patients became oliguric
The kidney is a urine producing and concentrating factory, it works most efficiently with a continuous flow of blood, at the same perfusing pressure. The volume of renal filtrate closely matches the renal plasma flow, so that the kidney does not have to do too much work at high blood pressures, and if pressures are low, it does very little work at all. There are three physiological principles that belie this concept: renal autoregulation, renal medullary hypoxia, and tubuloglomerular feedback. The first relates to the volume of material flowing along the production line of the factory, the second relates to the workers, the third a self control mechanism. We know that the kidney likes a certain rate of blood flow, and so, over a range of mean arterial pressures, renal plasma flow is kept constant by a variety of reflex mediators.
Figure 1: Renal Medullary Hypoxia This process, autoregulation, also takes place in the brain. Similarly, the workers in the factory, the tubular cells, are fed by oxygen and nutrients derived from blood in the vasa-recta, which have the same origin as the tubular filtrate. If the renal perfusion pressure falls, the amount of oxygen and nutrients supplied to these cells also falls. They are in a precarious position in the first place – the renal medulla, due to the active countercurrent pumping of sodium and chloride, is one of the most energy hungry tissues in the body, while, the blood in the vasa recta is deoxygenated and slushy (high hematocrit). This makes tubular cells particularly vulnerable to ischemic injury. Thus, below a certain mean arterial pressure, the kidney switches off a considerable amount of its filtration activities, and the patient becomes oliguric. As this represents a self-protection reflex, the term “Acute Renal Success” has been used, and it is nicely described in scenario 2 above. Tubuloglomerular feedback is a kind of quality control mechanism. The macula densa, which lies in the distal tubule (and this is located at the junction of afferent and efferent arterioles), monitors the concentration of sodium delivered to the distal part of the nephron. The macula densa forms a complex with cells located in the afferent and efferent arterioles, known as the juxta-glomerular apparatus. If the concentration of sodium chloride delivered to the distal tubule falls (meaning that more is being reabsorbed proximally, and GFR has also fallen), then renin is released which stimulates production of angiotensin II, which in turn increases efferent arteriolar resistance, and reduces afferent arteriolar resistance. Aldosterone is produced which increases sodium reabsorption in the distal tubule. Likewise, and more importantly with regard to this topic, if the amount of sodium reaching the distal tubule increases, the macula densa recognizes that this represents an increase in the metabolic load for the relatively ischemic medulla, and afferent arteriolar vasoconstriction takes place, with a resultant decrease in GFR: acute renal success.
Figure 2: Renal Autoregulation and Urinary Output The patient in scenario 1 is different, she has gone into acute renal failure. Acute renal failure is often called “acute tubular necrosis”, as, in most cases, the kidney is damaged by ischemic insult. It is believed that if medullary blood flow falls below 20% of normal, then the cells therein have inadequate supplies of oxygen for basal function, and die. Sloughing off of cells damaged by ischemia causes the collection of casts in the tubular space, obstructing urinary flow, creating a back-pressure to Bowman’s capsule, and reducing filtration by increasing hydrostatic pressure on the renal side. Acute renal success and acute renal failure can be distinguished by the capacity of the renal tubules to perform their primary function – reabsorb sodium and concentrate the urine. If the urinary sodium is high (>80mEq), and the urinary osmolality is low (equal to that of the plasma), then the patient is in acute renal failure.
Figure 3: the Juxtaglomerular Apparatus |
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Please note: these tutorials are for personal study purposes only. They are not currently peer reviewed, and no responsibility will be taken for mistakes or inaccuracies. Reproduction of information is forbidden. All material is copyrighted by the GasWorks Group. |
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