The Obstructed Kidney (a story in medical education)

hi and welcome to the bowling animation studio my name is Professor Wilfred Duncan mieux and I'm a seasoned urologist this is a course about renal tract obstruction I will adopt a textbook approach and cover the basic physiology and pathophysiology that is relevant to understanding how the kidney responds to the obstructive insult however my goal is to keep a clinical orientation to this lecture and show how basic scientific principles can be used to direct clinical management but first of all I'd like you to meet my friend and colleague dr. Louise Murray hello professor and thanks for inviting me to join you Louise is currently doing her fellowship exams and is revising hard she will be presenting a case history for us and we will discuss the course material together my plan is to divide this course into five sections in part one I will summarize the common ways in which renal tract obstruction may present and highlight some of the specific clinical problems that may arise following this I will cover the basics of renal physiology in part 3 I will discuss some more advanced physiological concepts that will be revisited in part 4 the physiology of obstruction in part 5 we will turn our attention to the practicalities of patient management it will be a rollercoaster of a ride through a huge subject each section will build on the previous one but for revision the individual sections can be watched in isolation let's start with an overview of how renal tract obstruction may present renal tract obstruction may be partial or complete the onset may be acute or it may present in a chronic more insidious way it may involve one side alone or both kidneys may be obstructed together finally the obstructive pathology may involve the upper tracts alone or the upper and lower urinary tracts together clearly there are a myriad of pathologies that may block the kidneys in different ways similarly the consequences of such an obstruction will vary widely Louise let me illustrate this with some examples the commonest course for an acute unilateral upper tract obstruction is renal colic you will be familiar with the patient who presents with acute loin pain now most stones will pass spontaneously but situations can arise where a small stone is retained and the patient may become asymptomatic such an obstruction may then become chronic however there are many other causes of chronic unilateral upper tract obstruction for example congenital pale the ureter it Junction or puj obstructions are not uncommon similarly any neoplastic where inflammatory pathology can cause extrinsic compression to the renal tract in each case a hydrant of Rochas may develop and eventually atrophy of the kidney may occur of course pathologies that cause extrinsic compression can just as readily obstruct both sides pelvic malignancies are the most common culprits and will include cancers of the bladder prostate and cervix however for chronic bilateral upper tract obstructions the key difference is that renal failure may also occur a specific problem to which all obstructed kidneys are more susceptible is infection a hydronephrosis that becomes infected it's called a pioneer process and an obstructed infected system or obstructed pyelonephritis is a surgical emergency the ultrasound-guided placement of Anna Frost me tube is the best management option in the acute situation the commonest cause for an acute bilateral upper and lower tract obstruction is acute retention of urine this occurs in older men and is usually a consequence of benign prostatic disease however I do believe that you have a case to present to us Louise yes indeed prof. I dealt with such a case earlier this week it was late afternoon and an elderly gentleman was brought to the accident and emergency department in acute retention of urine at first his case seemed fairly straightforward but as the night progressed some unfortunate complications developed yes Louise I remember this case well please present the relevant points in this man's history ok prof. Joe Bloggs is a 72 year old man who had previously had little in the way of lower urinary tract symptoms however on Monday morning he woke to find that he had a little difficulty in passing his urine along with some urinary discomfort mmm by Wednesday his voiding difficulty was getting progressively worse and he had started to develop some lower abdominal discomfort on Thursday although he was still voiding in triples he was aware of a marked distension in his lower abdomen on Friday he was feeling febrile and gradually he became unable to pass any urine at all on arrival a diagnosis of acute urinary retention was made and he was easily catheterized a 1.5 liter volume of urine was drained and he was admitted to the urology ward his past medical history was fairly unremarkable he was not constipated and had had no previous lower urinary tract surgery he had taken no additional medication such as an anticholinergic that might have helped to precipitate an episode of urinary retention however he was taking non-steroidal anti-inflammatories for rheumatoid arthritis and an ACE inhibitor for well controlled hypertension but other than that he really was in reasonably good health he'd been settled on the ward and seemed to be quite comfortable however at midnight he suddenly had a cardiac arrest fortunately we were able to resuscitate him quite quickly transient cardiac arrhythmias did continue through the night and we did need to correct a marked hypokalemia that had been identified along with some other mild electrolyte disturbances eventually his condition stabilized and I'm pleased to report that he's now doing well on the ward thanks Louise that summary illustrates the main theme that we will be exploring further in this program but before I tell the viewers what that is please will you tell us about his urine output prior to his cardiac arrest well reviewing his fluid charts is really quite interesting it does seem that he was experiencing a fairly marked urinary diuresis actually in excess of 200 mils per hour yes and this is always a worry when we relieve an obstructed urinary tract it is likely that this man suffered from a complicated post obstructive diuresis I will be discussing this in depth but first we need to make sure that we truly understand the inner workings of the kidney you see when the kidney is in distress she responds in a predictable way but before we discover what that is let's make sure that we have a sound understanding of basic renal physiology climb on board and let the ride begin the kidney comprises three anatomically distinct regions the cortex which can be divided into outer and inner regions the medulla which forms discrete pyramidal zones and the collecting system and a high magnification the cortex can be seen to house thousands of thread-like tubules called nephrons the nephron is the basic functioning unit of the kidney the Bowman's capsule is at the head of this filtration unit the glomerulus is the leash of capillaries within the Bowman's capsule that receives blood from an afferent arteriole the efferent arteriole takes blood away from the nephron the Vaser rector arises from the efferent arteriole and selectively reabsorbs the filtrate along the nephron the Vaser rector merges with the venous circulation each region of the nephron is functionally distinct the proximal tubule reabsorbs 80% of all the salts and water filtered likewise most amino acids and glucose are handled by this segment of the nephron the loop of Henle is a very specialized portion of the nephron that descends from the renal cortex into the renal medulla it uses an active metabolic process to create a localized region of hypertonicity this facilitates the reabsorption of water by the collecting ducts as they pass through this space the main function of the collecting ducts is to fine tune the reabsorption of water this process is regulated by a hormone produced in the hypothalamus and released from the posterior pituitary gland this hormone is known as the antidiuretic hormone or ADH the more specific term for this hormone is arginine vasopressin AVP or simply vasopressin this is also the region of the nephron that controls the coupled interchange of potassium and hydrogen ions as such the collecting ducts are the prime regulatory sites for both potassium and acid-base balance the distal convoluted tubule continues the reabsorption of salt and water and is important in the handling of certain ions such as calcium however the most important function relates the role it plays in what is referred to as glimmer yellow tubular balance specialized cells in the distal convoluted tubule the macula densa cells communicate with the afferent and efferent glomerular arterioles the association between these structures is subtle and collectively they make up what is known as the juxtaglomerular apparatus on closer inspection we can see that the component parts of this apparatus the distal convoluted tubule and the afferent and efferent vessels are really quite tightly associated is this a concept with which you are familiar Louise yes prof. the concept of a discreet juxtaglomerular thing is well described in the text books but please tell me do you regard the juxtaglomerular apparatus as being an anatomical or a physiological concept well it's both really but to understand why they should be we need to study the ultra structure of these elements if you reduce this apparatus to its individual parts we can start by building from the Bowman's capsule the outer or parietal epithelial layer houses the glomerular tuft of capillaries an inner or visceral epithelial layer specializes to form cells known as pata sites that in sheath the capillaries this interface forms a three layered filtration surface the small clementa capillaries have a fenestrated endothelium this endothelium is covered with the basement membrane this membrane separates the capillary surface from the interdigitating pata sites the filtrate from the capillaries crosses these three barriers sequentially xx the Bowman's space from here the filtrate enters the proximal tubules the glomerulus is a highly specialized vascular structure it receives blood from the afferent arteriole at a relatively high pressure usually about thirty five millimeters of mercury the capillary path is long and provides a huge surface area for the filtration of plasma however resistance in these vessels is very low so the blood pressure drop in the afferent arteriole is minimal changes in afferent or efferent arteriole resistance will profoundly affect glomerular function for example increasing afferent arteriole resistance will reduce lamellar pressure and filtration will diminish in contrast increasing efferent arteriole resistance will result in a rise in climber Euler pressure and the filtration fraction will increase these events are mediated by a complex interplay of chemical and neurovascular reflexes now I used to with me Louise yes prof. what you've described is a simple filtering system varying the in-and-out pressures regulates the amount of fluid filtered absolutely but hold on tight so I'm going to take this puppy up a gear and the confluence of the glomerular arterioles a part of the endothelium has become highly specialized to form one unknown as the juxtaglomerular cells now these respond to a number of different stimuli including direct innovation from the sympathetic nervous system however the feedback mechanism based on the nature of the filtrate entering the distal tubules perhaps the most important within the district convoluted tubules and macula densa cells will respond to varying concentrations of solute within the filtrate in turn they will produce a variety of chemical mediators these are likely to include prostaglandin and prostacyclin type molecules furthermore this chemical crosstalk is also moderated by the intervening mesangial cells the net result is the production of renin by the juxtaglomerular cells renin activates the renin-angiotensin system angiotensinogen is converted to angiotensin one angiotensin converting enzyme or ACE then converts this to the powerfully vasoactive substance angiotensin ii angiotensin ii can alter the resistance in both the afferent and efferent limbs of the glomerulus which action predominates will depend very much on the circumstances and also the differing local nephron let me just pause you there prof i understand that the macula densa cells crosstalk with the juxtaglomerular cells which in turn produce Renan Renan is part of the renin-angiotensin system which results in the production of progressively more vasoactive compounds and ultimately angiotensin ii controls the filtering system by tweaking the afferent and efferent arterioles that's correct luiz well summarized but professor what is this about differing local nephron groups well this is the real key to understanding renal function listen carefully and all will become clear what you need to appreciate Luiz is that there are functional distinctions between regional nephron groups within the cortex on closer inspection we can identify peripheral short loop nephrons in the outer zones these loops descend to the outer parameter regions of the medulla they perform most of the day-to-day filtration operations and their ability to concentrate urine is modest the inner or juxta medullary nephrons have long loops of Henle that dip deep into the medullary apical regions these nephrons are distinguished for their ability to produce a markedly concentrated urine the outer renal cortex receives a rich flow of well oxygenated blood in this region an arterial flow rate of 5 liters per minute would be normal the afferent arterioles will have an oxygen partial pressure of about 50 millimeters of mercury these parameters are optimal for outer cortical nephrons function within the inner cortical region the flow rate drops to about 3 liters per minute this is diminish further within the apical medullary zones here flow rates are sluggish at about 0.2 of a liter per minute similarly the partial pressure of oxygen may be as low as 15 millimeters of mercury however the juxta medullary nephrons are well adapted to function in these more ischemic conditions indeed they are the nephrons that the kidney turns to in times of stress as a general rule whenever the kidney is in trouble she will usually respond by shunting blood to these inner zones am i still making sense Louise indeed prof. I can see how important these blood shunts are but how are they controlled and how may they very well this blood shunting is mediated through two main mechanisms first there are the sympathetic nervous reflexes that innervate and act directly on the juxtaglomerular cells gradually the process of glomerular tubular balance has mediated through the juxtaglomerular apparatus will fine-tune these shunts the sympathetic reflexes act promptly at the time of acute obstruction if this obstruction is bilateral then afferent constriction in the outer cortical nephrons will reduce filtration and blood flow will be shunted inwards for the gesture medullary or deep nephrons Ephrem constriction will predominate and glamourlou filtration will be maintained if the obstruction is unilateral then these protective mechanisms will cause afferent arteriole or constriction at both levels and the kidney on that side will markedly reduce or function as the clinical situation changes that juxtaglomerular apparatus will constantly adjust regional blood flow as appropriate it is this fine tuning of afferent and efferent lamellar resistance that is central to understanding both intra regional shunting and have the kidney responds to obstructive pathology I can see now how important it is to understand this concept of regional shunting great stuff Louise but let's both pause and see we can take stock yes let me see if I can summarize what we have learnt so far so from the beginning first the Bowman's capsule receives an ultra filtrate of plasma from the glomerular target at the proximal tubule then reabsorbs 80% of all salt and water and nearly all of the amino acids and glucose filtered the loop of Henle creates a highly osmotic concentration gradient in the surrounding tissues the collecting ducts pass through these zones of high salt concentration which given their very osmotic nature facilitate the fine-tuning of water reabsorption however this reabsorption process does require the presence of the posterior pituitary hormone ADH otherwise known as vasopressin the collecting ducts are also responsible for controlling both zoom and acid-base balance the distal convoluted tubule continues the process of salt and water reabsorption in addition this region is pivotal for controlling the mechanism of gloom hollow tubular balance the highly specialized macula densa cells respond to changes in the concentration of passing solute this information is relayed to the juxtaglomerular cells which along with autonomic nervous inputs Auto regulate the flow of blood through each nephron collectively these structures make up the juxtaglomerular apparatus it is this specialized Association of cell types that controls Granero filtration by regulating the arterial flow both into and out of the nephron if afferent arteriole ur constriction predominates filtration will be reduced and blood shunts away from that nephron if efferent constriction predominates the Mariella filtration is maintained throughout the kidney they can be subtle differences in regional blood flow at times this will allow for the recruitment of specialist nephron groups and the protection of others how this is executed will depend very much on differing physiological and clinical circumstances well that was a first-class summary Louise and provides us with an excellent overview of the basics of kidney function we are now ready to move on to part three of this course the more advanced aspects of renal physiology at the tail end of your summary you spoke of the auto regulation of afferent and efferent arterial blood flow and how this is important to understanding blood shunting we've also established that angiotensin ii is central to this process you reminded us that the macula densa cells signal changes in the concentration of passing solute the juxtaglomerular cells respond by producing renin which sparks the renin-angiotensin system this is a cascade of enzymatic activity resulting in the production of angiotensin ii angiotensin ii also mediates the second important response notably the production of a steroid or hormone aldosterone from the outer cortex of the adrenal gland all DOS theorem facilitates the reabsorption of salt and water from the collecting ducts sodium is reabsorbed at the expense of potassium and water is retained this retention of water results in an increase in total body fluid volume and a rise in blood pressure the expansion of total body fluid volume results in an increase in the venous return to the right side of the heart in response to this volume receptors in the right atrium produce a hormone known as atrial natriuretic peptide or ANP this tends to offset the physiological processes described so far notably ANP seeks to offload body fluid volume and to reduce blood pressure it achieves this in three main ways first ANP facilitates the loss of salt and water from the collecting ducts in doing so sodium is actively secreted into the collecting ducts in exchange for potassium therefore plasma concentrations of potassium will rise the second action is to inhibit the production of auto-steer own from the adrenal cortex and third iamp will inhibit the production of renin from the juxtaglomerular cells but in doing so it also mediates his own unique action the glomerular arteriole specifically EMP stimulates afferent arteriole or dilatation along with warrent constriction the net effect of this is to markedly increase the blood flow in the vase erector in doing so the vase erector tends to wash out solute from the medullary regions this concept of medullary washout is important clearly it will reduce the concentrating ability of the nephron during the obstructive phase not only is the urine production reduced but the urine that is formed is usually of a weaker concentration however the washout of solute from the renal medulla is dramatically worsened with the relief of obstruction I will be building on this idea in part four of the course but for now let us simply accept that the accumulation of ANP may be priming the kidney for a more significant washout that may follow indeed to conclude the third part of this course let us appreciate that under normal physiological conditions all of these adjustments are subtle there are several interacting Auto regulatory systems that work to normalize body fluid volume and blood pressure however in the context of bilateral renal obstruction these consequences can become markedly more profound last night Joe Bloggs suffered from one of the more severe consequences of renal tract obstruction it is by understanding the physiological events that had taken place prior to his catheterization and then following the relief of his obstruction that we might have been able to have made some predictions about the possible outcomes in doing so we could perhaps have minimized his risk and that brings us on to part 4 of this course distel obstruction puts bank pressure on the nephron both the collecting ducts and the thin a sending limb of the loop of Henle are particularly susceptible to the insult of distal obstruction predictably damage to these structures can lead to the inability of the kidney to concentrate urine so the reduced volume of urine that is accumulating in the obstructed system will become diluted now how relevant this degree of dilution is in clinical terms is very much one of degree put simply the kidney is a concentrating organ and so normally the urine is hypertonic relative to plasma if the kidney is struggling to perform then the concentrating ability may diminish and at the barest minimum it may break even with an isotonic urine however if the kidney is really in trouble the urine she makes will be hypotonic to plasma I pause Louise to stress that this distinction is of central importance to the story I tell following the relief of obstruction the detection of a hypotonic urine usually indicates greater problems but more of that in a moment if we just dwell on these nephron regions that are particularly susceptible to the obstructive insult then it should be clear that in addition to the problem of producing a concentrated urine certain electrolyte disturbances are also common as we have established the collecting ducts are the principal sites for potassium and hydrogen ion regulation it is not unusual to detect a wide range of perturbations specific for these ions and problems with acid-base balance may also follow in the case of post obstructive problems hypokalemia is one of the more common presentations I'm getting the picture here prof. but let us have a short pause to summarize obstruction to the collecting system increases back pressure on the nephron this is transmitted first to the most distal part of the nephron and then to the most fragile part of this structure understandably the collecting ducts and the loops of Henle are the regions that take the biggest hit it follows that electrolyte disturbances are common in particular obligations of potassium and hydrogen ion function damage to the loops diminishes the kidneys ability to create that zone of high solute concentration in the renal medulla with collecting ducts that may well already be impaired passing through the zone of reduced tissue tonicity the result is quite understandably a reduction in the ability of the kidney to produce a concentrated urine that's correct Louise and when the obstruction is relieved this is likely to get worse for a number of reasons first there is usually a sudden and dramatic restoration of blood flow to the kidney indeed for a short period of time the kidney may even become somewhat hyperemic this huge gush of blood may further drive the washout of solid from the renal medulla so the specter of medullary washout that have begun with the accumulation of atrial natriuretic peptide is now compounded with a hyperemic restoration of blood flow and given the possible impairment of the components of the nephron that are central to concentrating urine any urine produced at this time will be diluted and watery that's correct Louise but still the kidney needs to offload that excess body fluid volume a diaeresis of some sort is really inevitable now you just remarked that there will also have been an accumulation of atrial natriuretic peptide of course this isn't likely to drive further salt and water loss as well as facilitating the medullary washout in addition there may also have been a buildup of osmotically active compounds such as urea which may further contribute an osmotic component to the diaeresis but Louise realize that all this is essentially a normal physiological response as long as the kidney is producing a urine that is more concentrated than plasma then she's doing her job the barest minimum that will be acceptable in health would be a urine that is isotonic with plasma the problem comes if the tubular impairment leads to a can't cope situation if this happens then salt and water floods through the kidneys and the normal regulation of electrolytes fails there may be problems with acid-base balance and untoward potassium shifts by and large although the loss of body salts is great the relative loss of water is greater that is why the urine is hypotonic relative to plasma and that Louise is why a hypotonic urine is a sinister development so in essence we have two distinct forms of post obstructive diuresis one that is physiological and unlikely to lead to problems and one that is pathological and should cause us concern yes this latter situation is essentially one of a salt and water losing the property and can lead to electrolyte and therefore cardiac problems but prof. is there a simple way to distinguish between the two of them indeed Louise they can in fact be distinguished by the definition so I will conclude this session by defining the to clinical subtypes of post obstructed diuresis in part 5 of the course I will tighten this definition as you will then see how this shapes my clinical management prof. I have a feeling that a crucial number is stealthily gliding towards us from the deep a number that identifies the Sinister and a number that is key to guiding clinical management so I feel that we should pay very close attention to the building of this definition quite simply the offloading of the excess fluid accumulation comprises a normal physiological diuresis and the volumes of urine produced will vary in degree in health most kidneys can comfortably handler loss of up to 200 mils per hour by and large losses of greater than 200 mils per hour that are sustained for more than a few hours tend to be more worrisome so I like to define a post obstructive diuresis as being a urine output of more than 200 mils per hour over any four-hour period as long as the chemi can maintain a concentration of urine that is at least isotonic with plasma then the diaeresis remains physiological however if it can't and the urine becomes hypotonic relative to plasma then the diaeresis has become both salt and water losing and is pathological determining whether the urine is hypertonic isotonic or hypotonic relative to plasma is really quite simple the normal serum osmolality is about 300 milliosmoles per liter urine that is isotonic with plasma has a specific gravity of 1.0 one urine is normally concentrated to between three and eight hundred millions more per liter which equates to a specific gravity of about 1.0 – very concentrated urine say greater than 800 million small per litre has a specific gravity in excess of one point zero three urine that is hypotonic relative to plasma has a specific gravity of less than one point zero one so prof. the bottom line seems to be that one point zero one is a pivotal number and one that we should remember that's correct and that would be a good point at which to end this session in part five of the course I will be turning to patient management you will see how we use this simple number to shape our clinical when we return I will be asking you how we can simply determine the specific gravity of urine well prof. we can easily measure the concentration of the urine with a dipstick most urine lab sticks allow us to measure the specific gravity of urine absolutely and that is central to the management of a post obstructive diuresis if the specific gravity is less than one point zero one the urine is hypertonic to plasma so Louise we can now be really clear on our clinical definition again a post obstructive diuresis is defined as a urine output of greater than 200 mils per hour sustained over any four-hour period if the kidney is concentrating the urine relative to plasma in as a physiological diuresis and the specific gravity is greater than one point zero one if the kidney fails to concentrate urine we have a pathological diuresis and the specific gravity is less than one point zero one now Louise we also need to be mindful of the risk factors that might predispose our patient to the pathological state notably anything that might contribute to tubular damage so a prolonged acute obstruction will be of greater risk than one that is rapidly relieved yes and pre-existing renal problems or heart failure may also be relevant I guess coexisting infection must be of huge importance indeed and certain drugs can be of concern you will recall have the chatter between the macula densa cells and the juxtaglomerular apparatus relies on prostaglandins well if the patient has been taking a non-steroidal anti-inflammatory then this can be problematic likewise the renin-angiotensin response can be compromised by ACE inhibitors used to treat hypertension well clearly prof. all these potential problems can be rapidly identified at the time of presentation absolutely as soon as the catheter is placed the volume of urine is measured and an empty drainage bag attached so that an accurate measure of the subsequent urine output can be recorded the urine is dipstick test to establish the baseline specific gravity and for the possibility of infection we always send the urine for formal microscopy and culture and if there is any likelihood of infection a broad-spectrum antibiotic is commenced blood tests are sent to establish both the electrolyte status and renal function but most important Louise we must realize that our job is only half done we now need to monitor our patient and check on the urine output every four hours if the output is in excess of 200 miles per hour we must monitor the specific gravity of the urine at all times the patient should be encouraged to eat and drink any potential fluid and electrolyte problems can best be offset by the normal ingestion of solute and of course profit that is what food and drink is that's right whatever you do don't starve your patient and if he does develop a significant post obstructive diuresis well as long as he's concentrating his urine and the specific gravity remains one point zero one or above just make sure that he is eating and drinking and if he has a significant diuresis and the specific gravity falls below one point zero one then he has a pathological salt and water losing diuresis and he would need to have intravenous fluids once you begin with normal saline although potassium may need to be added if subsequent blood electrolytes detect any evidence of hyperkalemia I normally recommend that 80% of the previous hourly urinary loss is given back as intravenous fluid but again do make sure that he is eating and drinking normally and finally prof. at what point do we stop or tail back on our intravenous fluids that's easy Louise once the specific gravity of the urine is one point zero one or greater then you know that the kidneys are able to adequately concentrate again and you can stop chasing your tail Joe Bloggs was an unfortunate but lucky man the cute retention of urine is a common presentation of benign prostatic disease in older men if we use our definition we can determine that 50% of those men will display a post obstructive diuresis that is 50% of men who require urgent catheterization to relieve their inability to void will produce a urine output of greater than 200 mils per hour sustained over any four hour period in 85% of those the diaeresis will be physiological that is the urine will be concentrated relative to plasma and the specific gravity will be greater than 1.0 one in 15 percent of men the diaeresis will be pathological the kidney will fail to concentrate urine and both salt and water will be lost as water is lost in relatively greater amounts the urine is hypotonic and the specific gravity is less than 1.0 one of this letter group 3% will suffer with the clinical problem as a consequence of these fluid and electrolyte disturbances Joe Bloggs was one such man I do believe that he may have had several of the risk factors that may have contributed to his problem from his history it would seem that he had been going into attention for several days he had had a prolonged acute obstruction and who one might infer that the bank pressure on his kidneys was more than just an acute event there was a significant time period during which damage to the susceptible nephron parts could have occurred furthermore the fact that he was taking both non-steroidal anti-inflammatory medication as well as an ACE inhibitor could have blunted his recovery response finally his case history does suggest that there may have been an Associated urinary tract infection so it may be that his management could have been a little tighter post obstructive diuresis is a phenomenon that we should always seek to identify as you have seen the management really is quite simple indeed professor Muir the take-home message is clear whenever an obstruction to the renal tract is relieved there is a high likelihood that a diaeresis will follow if the urine output is greater than 200 mils per hour over any four hour period then we should be wary of systemic problems if the specific gravity of urine falls below one point zero 1 then intravenous fluid and electrolyte management is needed the patient must also be encouraged to even drink normally and you're right that really is quite simple you


  1. i had a uworld step2ck question on this, man who has only 1 kidney comes in with flank pain has low urine output with intermittent high output episodes, his K+ is 3.4. answer: urinary outflow obstruction, they explained how it was post obstructive diuresis. i didn't think it was so important to really read up on till i saw this video..

    thanks, i think it was definitively important to highlight the obstruction causing the whole loss of gradient due to washout thus leading to inability of Na+ and K+ reabsortion and thus high urine outflow… and thus arrythmia. and the hypotonic fluid aka 1.01 was good to see

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