Introduction with a clinical conundrum
A 66-year-old man is transferred from an outside hospital due to inability to be liberated from the ventilator. He presented a week earlier with pneumonia and sepsis. He received six liters of fluid initially, and has been running net positive 1-2 liters daily since then (for a total of about 15 liters net positive). Despite receiving this volume he has developed a mild acute kidney injury with a creatinine of 1.7 mg/dL.
On examination he is grossly edematous. He is maintaining a MAP of 60 mm off vasopressors. His urine output is poor at about 20 ml/hr. His intraabdominal pressure is 18 mm. His plateau pressures on the ventilator are elevated. How should this patient be managed?
Abdominal compartment syndrome & intraabdominal hypertension
Very high pressures within the abdomen may cause a compartment syndrome with organ failure. Compression of the inferior vena cava causes reduced venous return and hypotension. Lung compression causes atelectasis and impaired ventilation. Compression of renal veins impairs renal perfusion. Gut hypoperfusion also occurs, causing translocation of bacteria into circulation leading to vasodilatory shock. Untreated, this creates a spiral of multiorgan failure and death.
Intraabdominal hypertension is defined as elevated pressure without overt organ failure (table below). Among critically ill patients, intraabdominal hypertension is much more common than abdominal compartment syndrome. Although moderate intraabdominal hypertension doesn't cause obvious multiorgan failure, it may cause organ injury particularly to the kidneys.
Elevated intraabdominal pressures are common in sepsis
Abdominal hypertension classically occurs in patients with surgical abdominal disease. However, it can also occur in any patient with systemic inflammation undergoing large-volume fluid resuscitation. For example, it is common among medical ICU patients undergoing large-volume fluid resuscitation for sepsis (Ortiz-Diaz 2014). Daugherty 2007 prospectively studied 40 septic medical ICU patients who received >5 liters over 24 hours. 85% had an intraabdominal pressure >12 mm and 33% had a pressure >20 mm.
More recently, Anvari 2015 analyzed abdominal pressures among 53 patients admitted to a medical ICU with at least two risk factors for intraabdominal hypertension (table below). Among these patients, a majority had pressures >12 mm, while 16% had pressures above 20 mm.
Diagnosing abdominal compartment syndrome in sepsis is difficult
Differentiating between abdominal hypertension and abdominal compartment syndrome is generally tricky. Technically the diagnosis of compartment syndrome is made on the basis of higher pressures (at least 20 mm) and new organ failure. However, these two entities exist as a continuum, rather than being fundamentally distinct:
This differentiation becomes nearly impossible in the context of septic shock. The primary defining feature of compartment syndrome is new organ failure. However, patients in septic shock already have organ failure. It's often impossible to know how much of this failure may be caused by elevated intraabdominal pressure.
Consequently, it's hard to make an irrefutable diagnosis of compartment syndrome in septic patients. This may lead to under-recognition and under-treatment of this condition. For example, in the Daugherty study above, 10 patients met diagnostic criteria for abdominal compartment syndrome. However, none underwent laparotomy (one patient was scheduled for surgery but arrested beforehand).
Management: Lowering intraabdominal pressure
Although common, the management of sepsis-associated intraabdominal hypertension is unclear. The following interventions seem sensible:
- Avoid additional fluid resuscitation.
- Once the acute phase of illness has passed, remove fluid with diuresis or dialysis. Numerous studies have demonstrated that fluid removal reduces intraabdominal pressure (Regli 2015).
- Drainage of ascites if significant volumes are present. Placing an indwelling peritoneal catheter may be more effective than paracentesis.
- Management of ileus or constipation.
- Avoidance of bucking the ventilator (with use of comfortable ventilator settings and treatment of pain/agitation).
- Reverse Trendelenberg position? (Might limit transmission of pressure to thorax and avoid abdominal compression that results from elevating the head of the bed).
- Orogastric tube suction is generally reserved as a last resort, as this will impair nutrition.
Surgical consultation for possible laparotomy is reasonable in patients with abdominal pressures >20 mm and overt compartment syndrome refractory to medical intervention. However, most patients don't have a sufficiently clear-cut compartment syndrome to merit laparotomy.
Management: Defending the abdominal perfusion pressure
In the context of elevated intraabdominal pressure, the perfusion pressure for organs in the abdomen (e.g. the kidneys) may be calculated as follows:
Abdominal Perfusion Pressure = MAP – (Abdominal compartment pressure)
This is analogous to the cerebral perfusion pressure:
Cerebral Perfusion Pressure = MAP – (Intracranial pressure)
The abdominal perfusion pressure may be more important than the abdominal compartment pressure. Observational studies have found that an abdominal perfusion pressure below 60 mm may predict death better than either lactate or urine output (Cheatham 2000). A logical approach may be to increase the MAP goal, in order to defend the abdominal perfusion pressure:
Target MAP > (Abdominal compartment pressure) + 60 mm
In patients with a normal intraabdominal pressure (~5 mm), this yields the usual MAP target of above 65 mm. However, for patients with intraabdominal hypertension (e.g., pressure of 15-20 mm), it would suggest a slightly higher MAP target (>75-80 mm). The SENSIPAM trial proved that targeting higher MAPs is reasonably safe and potentially effective. It’s possible that patients with intraabdominal hypertension may represent a subset of patients who could benefit from a slightly higher MAP goal.
The practice of adjusting a MAP goal based in abdominal compartment pressure is often advocated, but remains untested. Pending investigation, this seems like a reasonable intervention based on general physiologic principles (similar to increasing MAP targets for patients with elevated intracranial pressure).
Dangers of unrecognized intraabdominal hypertension
Early recognition of abdominal hypertension may facilitate effective management based on simple interventions. Alternatively, unrecognized intraabdominal hypertension may lead to a misguided and ineffective resuscitative strategy. For example, undiagnosed intraabdominal hypertension might cause clinicians to accept an inadequate MAP.
Unrecognized intraabdominal hypertension may also lead to over-resuscitation. For example:
- Intraabdominal hypertension may compress the inferior vena cava, producing an ultrasound image suggesting hypovolemia.
- Abdominal compartment syndrome is associated with lactic acidosis.
- Intraabdominal hypertension increases pulse-pressure variation, probably due to poor thoracic compliance with exaggerated swings in intrathoracic pressure during ventilation (Regli 2015).
A small inferior vena cava, persistently elevated lactate, and high pulse-pressure variation could prompt the clinician to administer more fluid. However, this would only worsen the situation by causing more tissue edema and higher abdominal pressures.
Over-resuscitation and intraabdominal hypertension
A growing body of literature suggests that volume overload in critically illness is harmful. For example, Paul Marik just published a study relating the volume of fluid received by septic patients during the first hospital day to mortality (Marik 2017). Receipt of >5 liters of fluid correlated with increased mortality:
Intraabdominal hypertension may be an important mechanism whereby over-resuscitation causes harm:
- Large-volume resuscitation is the most important cause of intraabdominal hypertension among patients without primary abdominal pathology. For example, investigators have found linear relationships between fluid volume and intraabdominal pressure among CABG and burn patients (figure below). Conversely, fluid removal reduces intraabdominal pressure.
- Animal and human data show that intraabdominal hypertension causes organ injury. Several studies have found intraabdominal pressures to be an independent risk factor for mortality (Ortiz-Diaz 2014).
- Numerous studies prove that intraabdominal hypertension is common in critically ill patients who receive large-volume resuscitation.
If intraabdominal hypertension is an important mediator of harm from volume overload, this would have important clinical implications. For example, serial measurement of intraabdominal pressure could detect that the patient is developing intraabdominal hypertension (an indication to stop giving fluid).
One common misconception is that if a patient doesn't have pulmonary edema, then it is safe to give additional fluid. Unfortunately, life isn't this simple. Even in the absence of pulmonary congestion, dangerous abdominal congestion may be occurring. Pulmonary congestion relates to left ventricle function (elevation of pulmonary capillary wedge pressure), whereas intraabdominal congestion relates to right ventricle function (elevation of central venous pressure). Therefore, it is possible for a patient with impaired right ventricular function to develop severe intraabdominal congestion despite having dry lungs.
Intraabdominal hypertension and chronic sepsis
Following initial recovery from sepsis, many patients develop a persistent state of renal failure, volume overload, and endothelial failure (“chronic sepsis“). This may be a common cause of chronic critical illness following septic shock, an intractable and morbid condition.
It is likely that abdominal hypertension is a significant player in chronic sepsis. As discussed earlier, volume overload increases intraabdominal pressure. One of the earliest consequences of intraabdominal hypertension is oliguric renal failure (Patel 2016). This may create a vicious cycle leading to intractable volume overload and worsening renal failure:
Renoresuscitation refers to sepsis resuscitation with an emphasis on preserving renal function and fluid balance, in efforts to avoid chronic sepsis. It is possible that early recognition and management of abdominal hypertension could play a useful role in this resuscitative strategy.
Implications for sepsis guidelines
The 2016 Surviving Sepsis Guidelines recommend that all patients receive 30 cc/kg fluid within three hours. Although this seems reasonable in most patients, it may not apply to all patients because it ignores individual patients' physiology.
Another problem with these guidelines is that they focus on avoiding under-resuscitation, while ignoring over-resuscitation. It's possible that over-resuscitation is even more dangerous than under-resuscitation. Traditionally, it was believed that application of vasopressors before adequate volume resuscitation (“pressors with an empty tank”) would cause unopposed vasoconstriction and poor cardiac output. However, we now appreciate that vasopressors actually cause venoconstriction which increases preload. Thus, the concept that patients must receive large-volume fluid resuscitation before vasopressors is wrong.
If the guidelines are going to specify a mandatory minimum fluid volume (30 cc/kg), they should attempt to achieve balance by also suggesting a maximum fluid balance. For example, it could be recommended that clinicians should pay close attention to the patient's inputs and outputs, with avoidance of running the patient severely volume positive (e.g. >80 cc/kg net positive).
Polycompartment syndrome
This post has focused on the renal implications of intraabdominal hypertension, but some other consequences bear mention. Intraabdominal hypertension is closely linked with elevated intrathoracic pressures (Rastogi 2014). In severe cases, elevated intraabdominal and intrathoracic pressures may lead to increased intracranial pressure, a phenomenon termed polycompartment syndrome.
To illustrate the relevance of this physiology, below is a mind-blowing lecture by Thomas Scalea exploring this from the perspective of intracranial pressure (spoiler alert: he treated a young woman with refractory ICP elevation by using ECMO to decompress her thorax):
Resolution of the case
How should we manage our patient with massive volume overload, intraabdominal hypertension, and soft blood pressure? This is a bit of a paradox:
- In order to recover from intraabdominal hypertension, he requires fluid removal.
- Intraabdominal hypertension and elevated intrathoracic pressure both impair preload, making it doubtful whether he could tolerate diuresis. His blood pressure is already tenuous.
To manage this physiology, the following interventions were used simultaneously (a “squeeze and diurese” strategy).
- Vasopressin was initiated, titrated to achieve an abdominal perfusion pressure >60 mm. In his case, this involved targeting MAP >78 mm.
- He was aggressively diuresed with a combination of indapamide and furosemide.
Over the next few days he diuresed about 10 liters. Meanwhile, his kidney injury resolved. His pulmonary function improved and he was liberated from the ventilator.
- Intraabdominal hypertension is common among septic patients receiving large-volume resuscitation, but usually overlooked.
- Intraabdominal hypertension may cause occult organ injury (especially kidney injury), even in the absence of frank abdominal compartment syndrome.
- Diagnosing intraabdominal hypertension may identify patients at risk from further fluid administration. Such patients may benefit instead from volume removal.
- Abdominal perfusion pressure is equal to the abdominal pressure subtracted from the MAP, analogous to cerebral perfusion pressure. Maintaining an abdominal perfusion pressure >60 mm might be beneficial.
- The best approach to intraabdominal hypertension is prevention, by using a conservative fluid resuscitation strategy.
Related
- Renoresuscitation for septic shock (PulmCrit)
- Marik on fluids in sepsis & Weingart's response (EMCrit)
- Marik & Bellomo: A rational approach to fluid therapy in sepsis, Br J Anaesthesia 2015
- Thomas Scalea on cutting-edge ICP management (EMCrit)
Addendum: After posting this, Dr. Manu Malbrain (@Manu_Malbrain) made some suggestions regarding additional references to add. Here they are, with his comments:
- Consensus definitions paper: Intensive Care Medicine 2013.
- Review paper on polycompartment syndrome: Anesthesiol Intensive Ther 2014.
- Abdominal compliance is the key factor in predicting organ failure: Critical Care 2016.
- Meta-analysis and systematic review showing fluid balance as etiology for intraabdominal hypertension: Minerva Anesthesiol 2014.
- Systematic review on risk factors for intraabdominal hypertension: Critical Care 2013.
Image credit: Kidney
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I support this concept and agree that volume overload kills, but good luck trying to sell diuresis for patients with an AKI on pressors. It’s probably the right thing to do, but will be a difficult cultural shift. A few developments will be helpful though. Evidence supporting early RRT w UF for volume overload, and a replacement for sCr as a measurement of renal function should help. Both are on the horizon.
Yeah, the first time you do this its a bit scary. Obviously I would only do this in an ICU with very close monitoring. If the vasopressor requirements start dramatically rising, then you need to re-think your strategy. Also, I’m generally using low doses of vasopressors to facilitate diuresis (e.g. norepinephrine 5-10 mcg/min or vasopressin 0.02-0.03 U/min). Aside from abdominal hypertension, I do believe that there are some patients who need a low dose vasopressor to balance out the hemodynamic effects of positive pressure ventilation and sedation (especially propofol). So if a patient needs a few mcg/min of norepinephrine, that’s… Read more »
Watch video presentations on deleterious effects of fluid overload on vimeo https://t.co/Y1JgOmzSAe
Hey Josh,
Great post. How do you measure intraabdominal pressure? I find this requires a special type of foley catheter that is not readily available on all floors of the hospital. Are there other ways that I am not aware of?
http://www.surgicalcriticalcare.net/Guidelines/intraabdominal_pressure_monitoring.pdf
I would think the majority of patients in whom this is an active concern should/would be in an ICU.
am doing a wee on this topic. no special foley needed
Hi Scott
You can take me in the loop fior your wee on abdominal hypertension.
Happy to help if needed.
Keep up doing a great job!
Hi Saleem. There are different techniques. Direct intraperitoneally is most invasive one. Indirect methods via stomach or bladder have been described. No need for special Foley. You can use patient’s urine as pressure transmitting medium or you can instill a max of 20ml saline. Patient needs to be supine. Zeroing at level where midaxillary line crosses iliac crest. You can read more on this in my PhD thesis https://t.co/PXbEkQTZlD
Hey Scott, I’m a new ICU RN who previously worked in the ED and I have a question about fluid overload w/ or w/o IAH. Often I take care of patients who are 15+ liters (sometimes 30+) fluid up, who are grossly edematous, on multiple pressors, and who wind up becoming hypotensive despite increasing pressors. When I alert the physician, the order that we get most often is for more isotonic crystalloid. Now I know that of the isotonic crystalloid, half or more winds up in the extravascular spaces, and I also know that my patient already has plenty fluid… Read more »
To Josh and Scott — didn’t realize this was on the PulmCrit side.
Dear Jonathan. You are not missing anything. On the contrary I believe your doctors are missing knowledge on Fluid overload and IAH. Secondary IAH and ACS are indeed often iatrogenic as consequence futile crystalloid resuscitation. I know EVLWI and PVPI monitoring via transpulmonary thermodilution is not common in the USA but it is often used in Europe to guide deresuscitation. This can be done with PAL treatment = PEEP to counteract IAP plus hyperoncotic albumin plus diuretics or CVVH with net UF. Read more via links https://www.ncbi.nlm.nih.gov/m/pubmed/25432556/ and https://www.ncbi.nlm.nih.gov/m/pubmed/22873410/?i=5&from=malbrain%20cordemans and https://www.ncbi.nlm.nih.gov/m/pubmed/22873416/?i=4&from=malbrain%20cordemans Have fun reading I will stop here as I… Read more »
Certainly many of us would use albumin, i.e. hypertonic 25% . (Albumin + Lasix is a time-honored, possibly somewhat time-worn practice for drying out Michelin Man patients.) There is no real evidence it is better than crystalloid, but as you said, it makes sense.
Hey Jonathan – my understanding is that albumin really doesn’t “pull” fluid back into the intravascular space. It may help to keep it from leaving so much by increasing the oncotic pressure in the vasculature and by sustaining/repairing the endothelial glycocalyx where all of that fluid is seeping out. As I understand it, capillary leaking is a one way problem. Fluid returns to the intravascular space through the large lymphatic vessels. This return is impaired by elevated BNP which is often a factor with over-resuscitation. Another clinical conundrum! Open to feedback here as things are never really as simple as… Read more »
Manu and Tabitha — thanks for the information!
Manu, I really wish more providers knew about the findings of those studies. I really enjoyed looking over the IFA website.
You know I was reading another article on this site last week, and there was talk about the glycocalyx and fluid return through the lymph vessels.
Has there been any research on interventions directed toward increasing return through the lymph vessels? How new is this? Do pressors also constrict those as well?
Hey i was just witness to the worst bundle resus to a elderly pt whom was already in fluid overload, speaking with the fam he had a dx heart failure ,a recent fall with subdural hematoma (4wks) asbestos history, and ards. Well idk what the hell went on but I walk by like an hour later to find the patient ipaped unconscious and the poor family devastated. He went up to IIcu and I was visiting overnight discussing with girl I know, he had awefull third spacing , abdomen distended and his poor hands and fingers. What if anyone can… Read more »