Jul 142016

low tidal volume ventilation for abdominal surgeryJon-Emile S. Kenny [@heart_lung]

"An' it ain't no use in turnin' on your light, babe, I'm on the dark side of the road ..."

-Bob Dylan

A 44 year old man with cryptogenic cirrhosis is admitted with large ascites and acute kidney injury.  A 50 mL, diagnostic paracentesis reveals 12 PMNs and he is admitted from the emergency department for further evaluation of his renal dysfunction.  On the medical floor, initial urine sodium is < 10 mEq/L and urine osmolality is 1100 mOsm/kg.  He is labeled as ‘pre-renal’ and given 3 litres of lactated ringers overnight.  The following morning, his urine output is minimal and his creatinine has quintupled.

Cirrhosis and the Kidneys

The pathophysiology of renal dysfunction in cirrhosis is complex, rendering facile explanation illusory; however, this brief review seeks to shed light on the - sometimes forgotten - 'venous side of the road.'  Traditionally, the often-invoked mechanism of renal dysfunction in cirrhosis is the physiologically nebulous construct of ‘arterial under-filling’ - induced by splanchnic endotoxemia.  Like cirrhosis, ‘ineffective arterial perfusion’ has been raised to explain the pathophysiology of kidney injury in acute decompensated heart failure.  Yet a provocative, retrospective, analysis revealed no correlation between cardiac output, cardiac index, arterial blood pressure and the likelihood of worsening renal function.  Importantly, there was a strong, direct correlation between central venous pressure and the likelihood of worsening renal function.  While this study does not prove, mechanistically, that renal venous pressure is the underlying cause of impaired glomerular filtration, it certainly raises surprising questions; especially given that hepatic vein wedge pressure is directly related to sodium avidity in patients with cirrhosis.

Renal Venous Pressure

Intra-abdominal pressure [IAP] has been noted to be an underappreciated enemy of the kidneys.  Indeed, large volume paracentesis improves glomerular filtration and creatinine in both cirrhosis and heart failure.  But how might removal of abdominal fluid improve GFR?  It has been known for well-over a century that increasing renal venous pressure results in salt-avid renal physiology.  That is, raising the pressure within the renal vein leads to low urine sodium, high urine osmolality and augmented renin release.  The mechanism by which this occurs is not entirely clear but may be a consequence of elevated renal interstitial pressure and nephron and/or afferent arterial collapse within the encapsulated kidney.  Notably, development of intra-abdominal hypertension in healthy volunteers reduces GFR and renal plasma flow which is completely reversed with attenuation of the intra-abdominal hypertension.  Interestingly, in a porcine model, compression of the renal vein, but not the kidney itself reduced GFR.

Portal Blood Flow

In a terrific review detailing abdominal-renal interactions in heart failure, the importance of portal blood flow is described.  When portal blood flow is diminished, there is accumulation of adenosine within the liver and this triggers renal vasoconstriction via a hepatorenal reflex.  From a teleological perspective, this is an appropriate response as falling hepatic blood flow may indicate a true hypovolemic state.  However, if external compression from ascites and rising intra-abdominal pressure is the etiology, a vicious cycle may result.  The diminution of portal blood flow would be compounded by splanchnic venodilation in response to spontaneous bacterial peritonitis [SBP] which may partially explain why SBP and large ascites are particularly potent perpetrators of kidney injury, profound renal vasocontriction and salt-avidity.

Cardiac Loading

Raised IAP to as low as 10 mmHg is known to embarrass venous return and thereby hinder cardiac output.  In hypovolemic patients, even lesser levels of IAP may impair cardiovascular function.  One may postulate that in the venodilated, cirrhotic state, that increased intra-abdominal pressure retards venous return by causing vascular waterfall physiology.  Therefore, diminished venous return to the heart may ultimately play some role in renal underperfusion.  What may be less appreciated is the role that intra-abdominal hypertension plays in determining left ventricular afterload.  Presumably, compression of the arterial tree raises the impedance against which the left ventricle ejects which actually antagonizes the underlying vasodilated physiology of cirrhosis.  Interestingly, it is hypothesized that the rapidity at which IAP is reduced may drive the negative aftereffects of large volume paracentesis.  If there is a rapid drop in IAP, venous return to the heart will increase – and promote cardiac output – but there may can be a comparatively greater fall in LV afterload.  The ultimate consequence being attenuation of the mean arterial pressure and, therefore, renal perfusion.  Thus, when a large volume paracentesis [> 5 litres removed] is performed, slow extraction should be sought.  As well, biventricular function and albumin replacement should be carefully considered.

Abdominal Compliance

Finally, the genesis of IAP requires mention.  The degree to which IAP rises is determined both by the increase in abdominal volume [IAV] and the abdominal compliance [Cab].  The compliance curve of the abdomen is an exponential relationship - a nearly ubiquitous relationship in vivo.  In other words, the change in IAP for a certain change in IAV tends to be minimal at a small abdominal volume.  However as abdominal volume rises, the curve bends upwards such that for the same change in IAV, a much greater rise in IAP ensues.  The reason for this relationship depends upon the abdomen’s change in geometry in the supine position from somewhat ellipsoid, to spherical as its volume rises.  Normal IAP is roughly 5 mmHg and a normal compliance dictates an increase in IAP of 1 mmHg for every 250-450 mL of IAV rise.  As the abdomen stretches and becomes pressurized at higher volume, this compliance value can change to an increase in IAP of 1 mmHg for every 60-90 mL IAV rise.  Importantly, this dictates that only a small decrement in IAV can have very profound reduction in IAP when the clinician aims to correct IAH.  Conditions associated with lower abdominal compliance are: tissue/subcutaneous edema, high mesenteric fat/androgynous fat distribution, young age, short stature, hepatosplenomegaly, head-of-bed > 45 degrees, among others.  Importantly, differences in abdominal compliance between patients may make direct comparison of IAV removed [e.g. ascites drainage] difficult because a given volume removed may have drastically different effects on the reduction in IAP; and, accordingly, the hemodynamic effects described herein.  Figure 1 describes a summary of the renal consequences of increased IAP.


Figure 1: IAV is intra-abdominal volume, Cab is abdominal compliance, which both affect intra-abdominal pressure [IAP]. Mechanical compression of the cardiovascular system results in diminished renal perfusion, renal vasoconstriction and a neuro-humoural response which favours salt and water avidity. In cirrhosis, slow removal of IAV [i.e. ascites] may reverse this pathophysiology.  While the kidneys will behave 'hypovolemic,' the provision of fluids will worsen this vicious cycle.


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Intra-abdominal Pressure and Renal Function: The Venous Side of the Road