IAH and ACS - Interventional therapies
Introduction:
Intra-abdominal hypertension and the abdominal compartment syndrome cause significant morbidity and mortality, and are present a large variety of patients – both medical and surgical.[1-4] In fact, medical patients – specifically those suffering from severe sepsis, have the highest incidence of IAH reported in the literature.[1, 5-7] Despite the high prevalence of disease in medical patients and extensive literature to the contrary, many physicians and nurses continue to believe that the only treatment for IAH/ACS is surgical decompression – an option they choose not to pursue, therefor ignoring the syndrome all together. In fact, non-operative medical management is the cornerstone to therapy for this syndrome, playing a vital role in both the prevention and the treatment of IAP-induced organ dysfunction.[1, 8] Numerous studies now show that medical management not only improves survival, it prevents progression to full-blown ACS, reduces ICU and hospital length of stay, and results in reduced resource utilization.[9-13] Careful frequent IAP monitoring combined with implementation of medical management for elevated IAP should be implemented in all high-risk patients.
ACS
management:
Given the past focus on the end stage process - the abdominal
compartment syndrome - most treatment discussions have emphasized
emergent surgical decompression.
Based on other commonly treated full blown compartment
syndromes – intracranial (epidural or subdural hematoma), thoracic
(tension pneumothorax), pericardial (cardiac tamponade), and
extremity – all true compartment syndromes are surgical diseases
requiring emergent surgical interventions as soon as possible to
prevent permanent tissue damage or death. True abdominal compartment
syndrome is no different. Failure to provide emergent surgical
decompression leads to prolonged severe mesenteric ischemia as well
as multiple organ hypoperfusion with its attendant high morbidity
and mortality.
IAH management - intervention BEFORE the
patient decompensates:
On the other hand, intra-abdominal hypertension detected early is amenable to non-surgical interventions. By implementing these options early, abdominal compartment syndrome can be prevented in many patients. To accomplish this, intra-abdominal hypertension must be detected before clinical signs of the abdominal compartment syndrome develop. Newer evidence suggests that intra-abdominal pressure measurements done every one to two hours are necessary to establish a trend and avoid missing a rapid increase in pressure.[14, 15] ICU’s should implement effective, reproducible methods for accomplishing this task. Several companies now manufacture devices that allow noninvasive, rapid and reliable IAP monitoring to occur with little nursing effort. All these devices use either bladder pressure or intra-gastric pressure as surrogates for intra-abdominal pressure. These commercially available systems are the AbViser (www.wolfetory.com), the Foley Manometer (www.holtech-medical.com), the IAP-Monitor (www.spiegelberg.de), and the CiMON (www.pulsion.com).
Properly managing the critically ill patient with IAH requires
careful assessment of cardiovascular status with and understanding
of the errors that IAP can introduce to hemodynamic data. It
requires insight into ventilator management to overcome the reduced
chest wall compliance and smaller intrathoracic volumes caused by
higher IAP. Careful fluid and vasopressor management are also key
since to little fluid will increase intestinal ischemia and cytokine
production, while too much will exacerbate the cytokine induced
capillary permeability syndrome that occurs in these patients.
To assist clinicians with the complexities of these patients
and provide some recommendations for management, the World Society
of Abdominal Compartment Syndrome (WSACS) has created both and
assessment algorithm and a medical management algorithm that can be
downloaded from their web site
(http://www.wsacs.org/algorithms.php).
The remainder of this discussion will focus on this
management strategy.
Medical Management:
Download the treatment algorithms now and follow along with this
discussion
http://www.wsacs.org/algorithms.php
or - click here - and here - for the PDF files
Download Dr. Cheatham’s 2009 review on the topic from the World
Journal of Surgery (free)
http://www.springerlink.com/content/72v415n264grv36q/
or -
click here
- for the article
___________________________________________________
Free teaching posters showing the 1. Pathophysiology of IAH/ACS and 2. Clinical signs and interventional approaches to these patients
Click here to obtain information on how to obtain this poster (seen below) to put in your ICU
(click on the posters to see them in higher resolution)
The non-operative management of IAH consists of 5
therapeutic interventions:[1]
1.
Evacuation of contents with the bowel (intraluminal)
2.
Evacuation of extraluminal contents within the abdominal or
retroperitoneal space
3.
Improvement of abdominal wall compliance
4.
Optimization of fluid administration (enough but not too
much)
5.
Optimization of tissue perfusion
Evacuation of intraluminal contents:
Large volumes of air within the GI tract and ileus are both
common occurrences in critically ill patients on ventilators and
numerous drug combinations. These intraluminal fluid and gas
collections increase the volume within the confines of the abdominal
cavity and result in rises in the IAP that can lead to
hypoperfusion.
Interventions as simple as nasogastric suction and rectal tube
drainage are often very effective in treating these problems and
lowering IAH.[8] Administration of prokinetic motility agents can
further assist in expelling intraluminal material (erythromycin 200
mg IV q 8 hours, metoclopramide 10 mg IV q 6 hours). If IAP
continues to rise and enteral nutrition is running – it may need to
be slowed and on rare occasion stopped altogether. On very rare
occasions the only intervention for massively distended bowel is
colonoscopic decompression or even abdominal surgery.
Evacuation of extraluminal space occupying masses:
Free fluid in the abdomen, retroperitoneal abscess or hematomas – all can increase IAP. Assessment with physical exam, ultrasound and CT can reveal these problems and if IAH develops percutaneous drainage of these fluid collections – whether free fluid in the peritoneum or confined abscesses - is often very effective in reducing IAP, improving organ perfusion and preventing the need for surgical intervention.[11, 16-20, 61] In fact, even in the absence of visible ascites, IAP can be reduced in high risk patients with percutaneous catheter placement. In one small study in 8 patients, Reed et al were able to reduce IAP by 6 mm and increased abdominal perfusion pressure by 16 mm Hg and MAP by 10 mm Hg within 30 minutes of catheter placement in patients whose IAP crossed the 20 mm Hg threshold.[21] Six of these patients did not require decompressive laparotomy, avoiding the need to manage and open abdomen. Survival was 75% (3 of 4) in whom intervention was done early. Paracentesis and drainage of any free fluid visible on ultrasound can be very effective in the burn population as well as liver failure patients and some pediatric cases.[16, 22, 23] It results in an immediate reduction in abdominal contents with a corresponding drop in intra-abdominal pressure as well as an improvement in physiologic parameters such as urine output. Paracentesis often needs to be repeated to maintain a low pressure or the catheter can be left in place for a few days – making IAP monitoring all that much more important to assist in predicting when the procedure needs to be repeated or the indwelling catheter removed. The most recent clinical data which will be published in Chest in late 2011 notes that in cases where patients are advancing to ACS and are being considered for decompressive surgery, if they have free fluid on ultrasound that can be drained, surgical intervention can be avoided in as many as 80% of cases.[69] Given the high costs and morbidity associated with decompressive surgery, this intervention can result in a huge reduction in resource consumption. Following these impressive results these authors have instituted mandatory ultrasound to assess for free fluid in every case of IAH where the IAP exceeds 15 mm Hg. If free fluid is sited the ultrasound is used to guide percutaneous drainage and the catheter is left in place for a few days to continue removing the inflammatory liquid.
Very recent data also suggests that drainage of this
fluid reduces inflammatory cytokine levels both in the
intra-abdominal space as well as in the serum – a therapeutic
intervention that may further enhance recovery from the illness.[24]
First slide shows photos of intraluminal and extraluminal fluid collections to be drained and reduce intraabdominal pressure. Second slide shows photos of actually draining fluid (and leaving catheter in place) in cases with IAH. Third slide shows lung and histologic look at lung tissue in pigs that underwent septic abdomen with ACS followed by sham therapy versus intraperitoneal resuscitation.
Improve Abdominal Wall Compliance:
As the abdominal wall becomes progressively more distended it can
no longer stretch – eventually reaching a compliance threshold past
which the pressure within the abdomen increases dramatically.
Muscular tone often lowers this threshold – especially if the
patient is in pain or is working against the ventilator.[2, 25]
In fact, IAP fluctuations during mechanical ventilation can
be a useful indicator of reduced abdominal wall compliance/tighter
abdomen – if there is a large difference between end inspiratory IAP
and end-expiratory IAP that patient is developing more serious
problems with IAH.[26] Sometimes very simple interventions such as
administration of additional pain medication or sedation is all that
is needed to reduce IAP.[27] Because body position affects IAP,
another easy bedside intervention is to “unfold” the abdomen –
straightening out the body (from the 30 degree head of bed
elevation) and placing the patient supine with reverse
Trendelenburg.[28, 29, 74] Prone positioning also increases IAP and care
must be taken on positioning the abdomen during prone positioning to
avoid significant bowel ischemia.[30] If medical interventions fail
and the patients IAP exceeds 20 mm Hg, a trial of neuromuscular
blockade (NMB) is warranted as there is some published evidence and
extensive clinical experience demonstrating the effectiveness of
this intervention at higher levels of IAP.[1, 31-34, 60, 72]
It works by giving total relaxation to the abdominal and
thoracic wall musculature and may buy time for the patient to begin
mobilizing fluid. In many situations, dramatic reductions in IAP
with substantial increases in urine output and reduction in total
body edema.[35] Reduction of
peak inspiratory pressure and improvements in ventilation parameters
are also witnessed with NMB.[72]
However, if capillary leak continues this treatment effect
may only have transient effects.
Although muscular weakness is a concern when prolonged
neuromuscular blockade is used, this is still worth trying when
compared to the morbidity of an open abdomen – an exception might be
in the patient on aminoglycoside in whom neuropathy from NMB is more
common. Another similar option for reducing IAP is via epidural
analgesia. Hakobyan and colleagues performed a small study on
critically ill postoperative patients where epidural analgesia was
began when IAP exceeded 15 mm Hg.[25] They found a reduction in IAP
from 15.7 mm Hg to 5.9 mm Hg one hour after institution of epidural
analgesia. There was no associated drop in MAP that is often seen
with epidural analgesia. They hypothesized that the absence of
hypotension and further hemodynamic compromise was due to a decrease
of IAP, which in turn compensated for decreased preload secondary to
medication-induced sympathectomy.
Improving abdominal wall compliance reduces IAP by shifting the pressure-volume compliance curve to the right
Place patient supine or in reverse Trendelenburg to improve abdominal wall compliance and reduce IAP very easily at the bedside
If IAP rises above 20 mm Hg, a trial of chemical paralysis is warranted as this may reduce IAP, improve renal perfusion and lead to diuresis and persistent IAP reductions.
Optimize fluid resuscitation:
Optimal fluid resuscitation may be the most difficult task in any
critically ill patients, and it is made more complicated in the
presence of elevated IAP.
In the presence of IAH, many of the hemodynamic parameters
are difficult to interpret (see hemodynamic monitoring section)
while simultaneously over-resuscitation leads to excessive fluid
sequestration in the gut, higher IAP and worse outcomes. The complex
interactions of intra-abdominal, intrathoracic and intravascular
pressures make accurate volume assessment using CVP and PAOP
somewhat difficult. Functional hemodynamic parameters such as SVV
and PPV are also effected and less predictive of fluid
responsiveness.[36-38] End-diastolic volumetric indices and/or
echocardiographic indices will improve clinician’s ability to
interpret vascular filling.[37-39] If these are not available, IAP
values can be used to correct standard CVP and PAOP measurements to
obtain a more accurate reflection of volume status (see correction
formula in IAH and hemodynamic monitoring errors section).[39]
Initial adequate
resuscitation using standard guidelines should be implemented, but
modified as the IAP rises – at which point very careful assessment
of further fluid administration using passive leg raising
(or small fluid boluses) while observing pulse pressure
variation or beat to beat stroke volume or volumetric data is
essential – and difficult.[38, 39] Despite the ongoing controversy
of colloid vs crystalloid, patients with IAH probably should be
considered for colloid or hypertonic saline fluids boluses rather
than isotonic fluids.[1, 40, 41] Never the less, often these
patients are fluid overloaded – and judicious removal of this excess
fluid will often reduce IAP, improving renal perfusion and function
and lead to fluid mobilization and diuresis.[12, 17] One option is
to combine diuretics with colloids in an effort to mobilize fluid
from the bowel wall and diurese that fluid before the colloids leak
into the extravascular space.[42, 43] O’Mara et al found that
colloid resuscitation of patients at very high risk of
intra-abdominal hypertension (major burn patients) resulted in
dramatic reductions in IAP and a trend towards improved
outcomes.[40] Du also confirmed the efficacy of colloid
resuscitation using HES rather than lactated ringers in a randomized
group of severe pancreatitis patients. The HES group had lower IAP
values, faster return to negative fluid balance and less
requirements for mechanical ventilation - saving precious ICU
resources.[73] Another effective method is to institute
hemofiltration and remove excess fluid as the IAP is rising but
before overt organ failure occurs.[12, 17, 44] Oda et al, after
substantial investigation into the effects of cytokines on
intra-abdominal hypertension, determined that continuous
hemofiltration was able to reduce cytokine blood levels as well as
interstitial fluid. They predicted that this in combination with
colloid infusion to maintain adequate intravascular volume could
reduce progression of intra-abdominal hypertension to abdominal
compartment syndrome and improve outcome in severe pancreatitis. In
a prospective study, they began continuous hemofiltration on all
severe pancreatitis patients with IAP of 15 mm Hg or higher.[12]
Using this protocol on 17 patients, they successfully reduced
cytokine levels and IAP levels
(from 15 mm Hg to less than 10) in all their severe acute
pancreatitis cases – reducing their historical mortality from 40%
down to 6%. Mullens found that reducing IAP by fluid removal with
hemofiltration and or paracentesis was more effective in treating
renal insufficiency than hemodynamic optimization in patients
suffering congestive heart failure.[17, 45] Other authors confirm
that decompensated CHF with preserved ejection fraction is highly
likely to be due to IAH.[62] Other recently presented abstracts
confirm the survival benefits seen with hemofiltration in both
pancreatitis cases as well as in patients suffering from severe
sepsis.[46-48]
Hernandez, et al, who demonstrated a 51% incidence of IAH/ACS in
septic shock patients[49] also found that implementation of
hemofiltration in hemodynamically unstable sepsis patients failing
all other therapy resulted in a dramatic reduction in mortality in
those that responded (mortality 21% in responders versus 83% in
non-responders).[47] Picinni et al, also found a survival advantage
to early hemofiltration in septic shock patients, demonstrating a
survival improvement and reduced ICU length of stay in those who
underwent hemofiltration compared to those who did not (55% survival
versus 27.5% survival, LOS 9 days versus 16 days).[48]
Optimize tissue perfusion:
Following appropriate volume resuscitation, abdominal blood flow
show be optimized.[50] This is reflected in the concept of abdominal
perfusion pressure (APP). The concept is essentially identical to
that related to cerebral perfusion pressure. Tissue blood flow is
directly related to the mean arterial pressure delivered to the
tissue (MAP) minus the pressure within the abdominal compartment
(IAP): APP = MAP-IAP.
Abdominal perfusion pressure, which more accurately reflects
actual tissue oxygen delivery may be more predicative of patient
outcome that the IAP measurement alone.[50, 51] Once patients are
adequately fluid resuscitated, inotropic support to improve tissue
blood delivery should be considered if abdominal perfusion pressure
is less than 60 mm Hg.[50, 52]
Miscellanous ideas
Above are brief discussions relating to removal of inflammatory cytokines via percutaneous drainage or dialysis which results in improved outcomes in animals and in small human studies. Others are investigating drug infusions that modify inflammatory responses. One interesting concept brought forth in a single study is the use of theophylline infusions to block adenosine receptors.[70] Using this therapy in a non-randomized trial on patients with IAH < 20 mm Hg these authors noted a dramatic improvement in survival. This increased survival relating to theophylline infusion correlated with improving serum concentrations of IL-10, urea, and creatinine, as well as 24-h urine output, fluid balance, mean arterial pressure, and O(2)Sat. Obviously this is very preliminary data requiring further confirmation. Other studies using doxycycline to reduce inflammatory mediators and improve cellular outcome are also being conducted.[71]
Surgical options:
Decompressive laparotomy
When
all else fails and patients progress from intra-abdominal
hypertension to the abdominal compartment syndrome, the patient has
progressed from an urgent medical process to a surgical
emergency.[53] These patients are suffering from end stage tissue
ischemia that has progressed to severe cellular dysfunction with
impending cell death. The most appropriate treatment is emergent
surgical decompression either via open abdominal technique or
perhaps initially with subcutaneous fasciotomy and if that fails
conversion to an open abdomen.[53, 61] Waiting just a few hours will lead to
higher incidence of dead bowel and higher mortality. The exact
pressure at which abdominal decompression should occur is dependent
on a number of host factors including age, underlying co-morbidities
and physiologic evidence of developing ACS. With the exception of
very high intra-abdominal pressures there are no established
guidelines where a definite intervention is necessary.
Many experts recommend that the entire clinical picture must
be taken into account and one specific pressure cutoff cannot be
used.[54, 55] However, since several experts note improved outcomes
with decompression at lower pressures (25 mm Hg or more), if there is any question it
is probably best to err on the side of early decompression.[55-57]
In the case of trauma laparotomies – especially after damage control surgery where the patient has had substantial fluid resuscitation, the surgeon should probably just leave the abdomen open. While this results in a reduced risk of ACS, it is not a guarantee. Gracias et al found 25% of surgical patients with their abdomens left open after trauma laparotomies still developed ACS within a relatively short time period.[58] Ordonez et al confirmed this issue in a large study – citing 33% recurrent ACS with Bogata bag closure and 13% with KCI vacuum packs all of which required emergent intervention in patients with “open abdomens.”[59, 66] They point out that this complication occurs because no abdomen is truly “open” since all have some type of a dressing. Those patients who developed ACS despite an “open abdomen” did poorly: 60% mortality with ACS versus 7% mortality if ACS did not occur. The authors use this data to emphasize the importance of continued intra-abdominal pressure monitoring in all at risk patients, including “open abdomens” because fluid can re-accumulate in the space beneath the dressing and ACS can develop (this can still occur even with modern negative pressure dressings). See no such thing as an open abdomen section of this web site for further discussion on the topic.
This photos is from a patients with abdominal compartment syndrome who was not making urine, difficult to ventilate and had low abdominal perfusion pressure - medical therapy was too little or ineffective, but surgical therapy was life saving with immediate improvement in urine output, ventilation and perfusion. Clearly it would be bad for his physiology to try to "stuff" these guts back into the abdomen and suture it closed.
-
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