SYNOPSIS: Intra-abdominal Hypertension and the Abdominal Compartment Syndrome

Could your ICU patient have raised intra-abdominal pressure? If they do, how do you detect it? What pressure should trigger some action...and what options do you have for managing this problem if it arises? We'll look at these questions and tease out some answers in this SYNOPSIS.

Intra-abdominal hypertension (IAH) is a much more common phenomenon in the ICU patient that you might think. Many clinicians still regard this almost entirely a problem of the surgical patient population, perhaps after trauma or laparotomy. However, this is NOT the case. There are some common factors in all ICU patients that put them at risk for developing this phenomenon. In very simple terms you can think of the abdominal cavity as a box with 3 distensible sides (the lateral abdominal walls and the diaphragm) and a distensible lid (the anterior abdominal wall). For the purposes of discusion we'll assume that the bottom of the box (the posterior wall, spine etc.) is fixed, as is the fourth side (the pelvic floor). The rules for this scenario include the facts that there are limits to the distensibility of this box, and the box cannot burst outwards.

You can think of the box as containing:

• normal contents (such as the bowel and other organs, blood inside blood vessels)
  
• abnormal contents such as free intraperitoneal fluid or blood, overdistended bowel (with air or fluid), abnormal tissue masses (tumour, haematoma within organs or muscle) and abnormal retroperitoneal content (blood/haematoma/tumour)

The distensible box can accommodate some of these extra contents with little change in internal pressure as long as the walls and lid are distending easily, but as their compliance falls and they get stiffer the pressure inside the box starts to climb dramatically. At that point we're going to get problems. This is a situation analogous in many ways to that of intracranial hypertension. As pressure rises within the abdominal cavity, inflow of blood, especially venous return from the lower limbs, is reduced. Organs are "squeezed" and initially their microvascular flow is perturbed. Beyond this, their venous outflow and perfusion pressure are reduced, the diaphragm is domed up into the thorax compressing the bases of the lungs and pushing against the heart. At some point organ perfusion reaches a critically low level and organ failure ensues. At this stage the train is a runaway...organ ischaemia produces fluid extravasation which further increases the pressure and a vicious downward spiral ensues. The development of organ failure secondary to raised intra-abdominal pressure is ABDOMINAL COMPARTMENT SYNDROME. This is SERIOUSLY BAD NEWS!! You need to detect patients at risk for IAH, diagnose IAH an early stage, and take some steps to manage it before it reaches these critical levels, so how do you do that?

Who is at risk? 

Classically, the patients considered at risk for IAH and ACS were post-laparotomy or abdominal trauma/inflammation, e.g ruptured abdominal aortic aneurysm, severe acute pancreatitis. This is PRIMARY IAH/ACS. Medical patients were considered low risk. This view has been challenged as IAH has received more attention, and experts contend that if you actually look for IAH in your ICU patients you will find it in all groups. This is not a huge surprise as medical ICU patients with severe sepsis and septic shock for example have many reasons for abdominal contents to change for the worse:

• reduced oncotic pressure secondary to hypoalbuminaemia adding to capillary leak
• Inflammation with global capillary leak allowing fluid to gather in peritoneum, pleural cavities and bowel wall
  
• high crystalloid resuscitation rates exacerbating tissue and bowel wall oedema
• electrolyte abnormalities and potentially drug therapy altering bowel motility and contributing to ileus

The end result is abnormal bowel lumen and wall size as well as free fluid in the abdominal cavity in a surprising number of non-surgical patients.  This gives rise to SECONDARY IAH/ACS. If your patient has 2 or more of the following you should screen them for IAH: 

• Large volume resuscitation > 3.5 L in 24 hours
• Acidosis
• Hypothermia
  
• Coagulopathy or polytransfusion
• Abdominal Surgery/Primary Fascial Closure
  
• Ileus
• Pulmonary, renal or hepatic dysfunction
  

Madigan et al (J Trauma. 2008; 64: 280-285) studied extremity trauma patients and found that the group who developed ACS had similar injury scores to the non-ACS group, but had  significantly higher crystalloid infusion volumes (9.9L v 2.7L) [Read the article here].

What clinical signs should you be watching for? 

This is where it gets a little more difficult! One thing we can say with certainty is that manual abdominal palpation is not a reliable way to assess intra-abdominal pressure. What you really need to look for are signs of organ dysfunction that may be related to increased intra-abdominal pressure. This organ dysfunction is common in ICU so you are going to have to start with the presence of dysfunction then remember to ask yourself is this a case where abdominal pressure might be driving the organ failure? Your patient might have:

• systemic acidosis with potentially raised lactate
• splinting of the diaphragm with worsening respiratory failure
• oliguria despite volume resuscitation, often with renal impairment
• high gastric residuals
• swinging arterial trace, elevated CVP/PAWP, right ventricular dysfunction
• high intracranial pressure

How do you detect and monitor IAH?

You need to measure the intra-abdominal pressure. This is most commonly done using the intravesical or bladder pressure technique. Measurement MUST be standardised or you will get a different reading every time it is checked...this is tedious and clinically harmful!! There are several KEY points to bladder pressure measurement. The World Society for Abdominal Compartment Syndrome has issued standardised guidance on how to do this right. Intra-abdominal pressure is measured in mmHg and NOT cm H₂0.

 

What does the intra-abdominal pressure value tell us, and when should you worry?

The WSACS defines intra-abdominal hypertension as an IAP value > 12 mmHg when measured correctly. IAP is then graded as follows:

• Grade I intra-abdominal hypertension 12-15 mmHg
• Grade II intra-abdominal hypertension 16-20 mmHg
• Grade III intra-abdominal hypertension 21-25 mmHg
• Grade IV intra-abdominal hypertension > 25 mmHg

"Normal" IAP in the critically ill is 5-7 mmHg. It may be 10-15 mmHg in a patient post-laparotomy and has been recorded at up to 25 mmHg in septic shock. An IAP > 15mmHg can cause significant end-organ dysfunction and death...you do NOT need IAP > 25 to diagnose abdominal compartment syndrome! Generally speaking ACS is uncommon (but not impossible) below IAP 20 mmHg.

The WSACS has defined abdominal compartment syndrome as "a sustained IAP > 20 mmHg (with or without abdominal perfusion pressure < 60 mmHg) that is associated with new organ dysfunction/failure"

How do you manage intra-abdominal hypertension/acs?

There are some key points that need to be attended to. You need to:

• Ensure adequate abdominal perfusion pressure. Analogous to cerebral perfusion pressure, the APP = MAP - IAP. It should be kept > 60 mmHg so if your patient has IAP 20 mmHg you should be thinking about raising their mean arterial pressure to at least 80 mmHg.\
• Take steps to reduce intra-abdominal pressure
• • is your patient adequately sedated and not fighting the ventilator?
  • if they are adequately sedated, is there a need for neuromuscular blockade to improve abdominal wall compliance?
  • do you need to reduce head of the bed elevation? HOB > 20 degrees is used for VAP reduction but increases IAP. It is not yet known whether this increase is simply gravitational and without effect, or if it aggravates the problems of high pressure, so consider lowering the head of the bed if IAP is very high
  • Can you drain fluid or air from the GI lumen? Insert NG tube, consider rectal decompression, enemas, prokinetics etc.
  • Can you reduce extravascular water (oedema) and enhance colloid pressure? Consider diuretics and colloids to achieve negative extravascular balance while maintaining adequate intravascular volume. Continuous haemofiltration might have a role here.
  • Can you drain free intra-abdominal fluid e.g. ascites or blood. Consider ultrasound guided paracentesis.
  • If all of these fail and IAP is critical (i.e. you have established ACS) consider surgical decompressive laparotomy

 

Visit the World Society of the Abdominal Compartment Syndrome website 

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SYNOPSIS: Sedation Vacations in the ICU

Walk into an ICU even as recently as a few years ago and you’d have noticed that many patients remained sedated virtually 24/7 through their illness. This was done with the best of intentions - critical illness can be uncomfortable, disorienting and distressing and staff wanted to avoid that for their patients. Of course, as we all know, the law of unintended consequences has a habit of turning seemingly logical practices on their heads. We now understand that our good intentions contributed to prolonged ICU and hospital stay, increased costs, psychological difficulties for the patients and increased rates of ventilator associated pneumonia. Let’s look at the paper that initially informed our current knowledge and changed our practice by encouraging us to wake our patients daily using “sedation vacations” where we can.

In the New England Journal of Medicine in 2000 Kress and colleagues studied 128 mechanically ventilated patients receiving continuous sedative infusions, and randomised them to either daily interruption until the patient awakened, or interruption at the discretion of the treating physician. They were concerned that continuous uninterrupted infusions prevented assessment of patient neurology and exposed the patients to high cumulative doses of drug leading to tissue saturation and very slow elimination which prolonged recovery. Within each patient group there was further randomisation to midazolam infusion or propofol. End points of the study were the duration of mechanical ventilation, the length of stay in the intensive care unit, and the length of stay in the hospital. In the control group, the percentage of days during which sedation was stopped varied from 0 to 54%, demonstrating that left to their own devices, many clinicians failed to recognise or anticipate a need to reduce the dose of sedation. The results of this study started the ball rolling on the incorporation of this simple practice into our daily ICU rounds. The results were impressive:

1. The median duration of mechanical ventilation in the intervention group was 2.4 days shorter than it was in the control group (relative risk of extubation, 1.9; 95 percent confidence interval, 1.3 to 2.7; P<0.001).
   
2. Although hospital length of stay did not differ between groups, the median ICU length of stay in the intervention group was 3.5 days shorter (P=0.02).
3. Fewer tests were performed to assess changes in mental status in the intervention group (6 CT scans of the brain) than in the control group (13 CT scans of the brain, 2 MRI scans of the brain, and 1 lumbar puncture; P=0.02).
4. There was no significant difference in the rate of adverse events including accidental extubation or line removal, reintubation, or in the need for tracheostomy.

Read the paper: Kress Daily Interruption of Sedative Infusions NEJM 2000_342_1471-1477

The Institute For Healthcare Improvement (IHI) incorporated the practice of daily sedative vacation into their “Ventilator Bundle” aimed at reducing the incidence of ventilator associated pneumonia. The IHI ventilator bundle has 4 key components:

1. Elevation of the head of the bed to between 30 and 45 degrees
2. Daily “sedative interruption” and daily assessment of readiness to extubate
3. Peptic ulcer disease (PUD) prophylaxis
4. Deep venous thrombosis (DVT) prophylaxis (unless contraindicated)

You might want to visit their website to read more on this or read their Getting Started Kit on preventing VAP.
You might also take some time to brush up on the pharmacology of the sedative agents currently in use in the ICU. Many of these agents behave very differently when given as bolus doses or short term infusions compared to infusion over > 48 hours. This may result from accumulation of the parent drug in tissues, saturation or impairment of metabolic pathways, accumulation of active metabolites, or organ-failure related reduction in excretion. To give you some background on this, why not view our overview course on sedation and analgesia in the ICU.

SYNOPSIS: Genomics, Proteomics and Bio-informatics...new tools for Critical Care?

The Human Genome Project captured the imagination and has delivered a wealth of information on the human genetic sequence, but it doesn't end there. In fact it's barely a start! We have known for years that genetic variability results in clinical variability...some people are more at risk for a given disease than others, no surprise right? For a long time this information seemed stuck in the realms of chronic disease states and familial diseases and risk estimates, but that's changing. We now have tantalising information on the influence of genetics on our response to, and outcome from, cetain critical illnesses.

Before we go into that let's get our definitions staright and review some (very!) basic genetics:

GENOMICS is a very broad term referring to the study of genetic material and information.

FUNCTIONAL GENOMICS aims specifically to determine the function, the raison d'etre, for that genetic material...what's it do...why is it there?

PHYSIOLOGICAL GENOMICS is another term used to describe the application of molecular studies to correlate variation in DNA, RNA and protein with the physical state (the phenotype) of the patient. 

PROTEOMICS is the study of all of the proteins expressed in an organism (that expression being under the control of the genes) and how alteration in these proteins might induce, or result from, disease.

When we are thinking about the role of gene variation in disease, within the ICU or elsewhere, we can look at it at 3 broad levels:

• The DNA or the GENOME: variation in genetic material may arise from mutations within a gene. The effect of these mutations will depend on their frequency, the region of the gene in which they occur (i.e effector regions, promoter regions, or non-functional regions), whether nucleotide substitution affects function, and the presence or absence of other mutations that must co-exist in order for disease susceptibility to occur. We KNOW that genomic variation can lead to susceptibility to disease. Single Nucleotide Polymorphisms (SNP) are one element of variation. SNP's are defined as individual mutations involving a change in nucleotide within a gene, the frequency of this nucleotide subsitution being > 1%. There appears to be a complex relationship between SNP's, with a group of separate alterations being potentially necessary for the effect to occur. This explains why the presence of a particular SNP in one population can increase susceptibility to disease but not do so in a separate population. This makes identifying disease-related SNP's a difficult process, and it has been reported that only 5% of SNP-disease associations are durable across multiple studies.

• The RNA or the Transcriptome: While a patient's genome is relatively stable through their life, by functional necessity cells and tissues must be able to adapt to local conditions through alterations in gene expression. This brings us closer to the real functional characteristics that occur in disease states and may be of particular interest to us in critical care. Signal transduction at cell level in response to receptor stimulation can lead to measurable alteration in messenger RNA (mRNA) levels. We might find an increase in mRNA linked to the production of specific proteins (e.g. receptors, effector substances etc.) in response to a septic insult. Unfortunatley this still doesn't get us to the heart of the matter. It is one thing to demonstrate an increase in the messenger (the mRNA), but it is another to demonstare that the transcribed orders so transmitted were carried out (translated). Control and feedback mechanisms mean that increases in mRNA do not always lead to increased protein expression, and inferences drawn from such increases must be viewed with caution. Ideally, we need to take another step closer to the front line to see if and when the orders are carried out.

• The expressed proteins or the Proteome: This is where the rubber hits the road. For a gene variation or upregulation of mRNA to have a meaningful effect their has to be some change in the ultimate product...the proteins expressed. The physiology and functionality of a cell is determined by the proteins it contains. It isn't quite as simple as measuring and identifying these proteins. They are compartmentalized, present within complexes, or even altered after expression (post-translational modification sucg as phosphorylation) and degraded. Despite these limitations, significant progress has been made in proteomics allowing characterisation of subprotein groups e.g. membrane proteins.

It is likely that the rapid progress made so far will continue, and on the basis of alteration in gene expression, mRNA levels in blood (rather than tissue) or specific protein patterns, we will be able to identify patients whose phenotype is more likely to move to severe sepsis and septic shock after a given insult, and to do this at a stage when clinical and demographic parameters do not differ from those in patients who subsequently have a benign course.