Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_1134_Библиотеки_им_академика_М_И_Перельмана.pdf
Abdominal Compartment Hypertension and Abdominal Compartment Syndrome
Patrick Maluso and Babak Sarani
1 9
Introduction
Intra-abdominal hypertension (IAH) and its most severe
manifestation, abdominal compartment syndrome (ACS),
represent different endpoints on a spectrum of illness. At the
most basic level, cellular dysfunction due to IAH and ACS
results from the same underlying physiology as compartment syndromes in general, namely, derangement in perfusion arising from an increase in pressure within the fi xed
volume of an anatomic compartment. The abdomen and pelvis form one such compartment, bounded by the abdominal
wall, the diaphragm, the back, and the peritoneal refl ection at
the bony pelvis. As with other forms of compartment syndrome, if the pressure within the fi xed abdominal compartment is elevated, physiologic derangements will occur as a
result of impaired capillary and venous blood fl ow. The
resultant metabolic acidosis can be accentuated as a result of
impaired respiratory function from upward pressure on the
diaphragm preventing adequate expansion of the lungs and
therefore ventilation. Common impairments seen in ACS
include decreased venous outfl ow from the splanchnic circulation with resultant malperfusion of the intestines, decreased
glomerular blood fl ow resulting in acute kidney injury, and
decreased cardiac return as a result of compression of the
inferior vena cava.
The exact incidence of ACS is poorly defi ned. Reports
following major operation or severe injury range between 10
and 35 % [
cally ill patients is also poorly described, but the few reports
that exist demonstrate the same incidence as trauma and surgical patients [ 3 , 4 ]. As might be expected, the incidence of
IAH is signifi cantly higher and ranges between 30 and 70 %
P. Maluso , MD • B. Sarani , MD, FACS, FCCM (*)
Department of Surgery , George Washington University ,
2150 Pennsylvania Ave, NW, Suite 6B ,
Washington , DC 20037 , USA
e-mail:
1 – 3 ]. The incidence of ACS in non-injured, criti-
Patrick.maluso@gmail.com; bsarani@mfa.gwu.edu
in either group. The presence of either IAH or ACS is associated with a signifi cant increase in mortality in either group.
D e fi nition and Causes of IAH/ACS
In 2013, the World Society of the Abdominal Compartment
Syndrome (WSACS) published an updated consensus statement on IAH and ACS [ 5 ]. In this statement, they provide
clinical defi nitions and pressure measurement guidelines to
assist clinicians in the diagnosis and treatment of IAH/
ACS. Intra-abdominal pressure (IAP) is defi ned as the
abdominal pressure measured at end expiration in the supine
position without contraction of the abdominal wall musculature. Measurement of the IAP allows for calculation of the
abdominal perfusion pressure (APP), which is derived by
subtracting IAP from the systemic mean arterial pressure
(MAP). Whereas normal IAP ranges between 2 and 7 mmHg,
the WSACS statement defi nes IAH as a sustained IAP
greater than 12 mmHg. IAH is further subdivided into grades
I–IV, as described in Table 19.1 .
ACS is the primary pathological endpoint in IAH and is
associated with end-organ dysfunction or failure in the setting of a sustained IAP >20 mmHg (IAH grades III and IV)
with or without an APP <60 mmHg. It is important to note
Table 19.1 Grading and treatment of intra-abdominal hypertension
Intra-abdominal
Grade
I 12–15 mmHg Sedate patient, diurese,
II 16–20 mmHg Sedate patient, diurese,
III 21–25 mmHg Pharmacologically paralyzed
IV >25 mmHg Decompressive laparotomy
pressure Treatment(s)
paracentesis, loosen abdominal
closure device
paracentesis, loosen abdominal
closure device
patient, loosen abdominal
closure device, decompressive
laparotomy
© Springer International Publishing Switzerland 2016
N.D. Martin, L.J. Kaplan (eds.), Principles of Adult Surgical Critical Care, DOI 10.1007/978-3-319-33341-0_19
233
234
P. Maluso and B. Sarani
Table 19.2 Risk factors for intra-abdominal hypertension
Decreased abdominal wall compliance
Large torso burn
Large ventral hernia repair
Prone positioning
High-volume fl uid resuscitation
Septic shock
Hemorrhagic shock, particularly when resuscitated using
crystalloid solutions
Large surface area burn
Pancreatitis
Increase abdominal content
Tense ascites or hemoperitoneum
Large neoplasm
Severe ileus
Pancreatitis
that factors such as obesity can affect patients’ baseline IAP;
a 2001 prospective study of IAP in hospitalized patients
found a strong correlation between increased IAP and
increased BMI [ 6 ]. Wilson et al. similarly found that anes-
thetized bariatric surgical patient’s baseline IAP increased
by 0.14 mmHg per every unit of BMI but that none of the
patient’s baseline fell within the range of IAH. The average
baseline IAP in the study was 9 ± 6 mmHg and the average
BMI was 48 kg/m 2 .
Although it is diffi cult to predict which patients will develop
IAH, certain broad categories of illness and therapy put patients
at higher risk. Clearly, conditions that decrease abdominal wall
compliance such as burns, abdominal wall operations (especially ventral herniorrhaphy), and prone positioning can predispose patients to IAH [ 7 , 8 ]. Conditions that require large-volume
fl uid resuscitation such as sepsis, burns, and trauma have also
been implicated in IAH [ 1 , 9 , 10 ]. Finally, conditions in which
intra-abdominal contents are increased such as tense ascites,
large tumors, hemoperitoneum, severe ileus, and pancreatitis
can also lead to IAH (Table 19.2 ) [ 5 , 11 , 12 ]. While this list is
by no means comprehensive, it illustrates the broad categories
of illness and treatment that may predispose patients to IAH or
ACS. Moreover, an understanding of the pathophysiology that
can predispose to IAH is important in recognizing at- risk
patients, especially since it can affect patients without primarily abdominal pathologies.
Aggressive, crystalloid-based resuscitation is highly associated with development of both IAH and ACS and subsequent mortality [ 13 ]. In hemorrhaging patients, the incidence
of ACS and mortality decreases as the volume of biologically active colloid, including red blood cell and plasma
transfusion, increases and the volume of crystalloid fl uid
decreases [
14 ]. Similarly, in non-injured, critically ill
patients, although mortality is not changed, resuscitation
with crystalloid is associated with a greater risk of developing IAH and ACS than resuscitation with colloid [ 15 ].
Diagnosis: Physiologic Markers of ACS
Regardless of the method used for measurement of IAH or
ACS, a protocol for initiation of IAP measurements or appropriate clinical suspicion is a key fi rst step. An understanding
of the physiologic derangements resultant from IAH and
their subsequent clinical effects is critical in the early recognition of the organ system dysfunction that heralds IAH and
impending ACS. This understanding should necessarily
inform decisions to measure IAP and ultimately to treat ACS
before more permanent damage or death has occurred. At the
least, intra-abdominal pressure should be measured in
patients with two or more of the risk factors noted in
Table 19.2 [ 16 ].
Cephalad pressure on the diaphragm due to IAH has a
direct effect on pulmonary compliance [ 17 ]. This decreased
compliance affects pulmonary function by a progressive
decrease in tidal volume, residual volume, and functional
residual capacity. These effects are accentuated with increasing IAP [ 18 ]. Patients with ACS will not be able to breathe
spontaneously and will require mechanical ventilation. In
mechanically ventilated patients, the effects of IAH can be
recognized by the resultant increase in peak inspiratory and
mean airway pressures [ 19 ]. The changes in compliance and
subsequent hypoventilation manifest initially as hypercapnic
respiratory failure but can progress to hypoxemia as well.
The blood gas derangements usually correct promptly with
treatment (namely, abdominal decompression) [ 20 , 21 ].
The hemodynamic effects of IAH/ACS center on
decreased venous return to the heart due to compression of
the inferior vena cava from the IAH itself as well as transmitted intrathoracic pressures (ITP). Increasing IAP has the
additional effect of increasing systemic vascular resistance
by compression of the aorta and splanchnic circulation,
thereby increasing afterload and decreasing stroke volume.
Moreover, transmitted increases in IAP increase enddiastolic pressures, thereby decreasing cardiac fi lling, an
effect that is exacerbated by hypovolemia [
together, these hemodynamic derangements cause a net
decrease in cardiac output with resultant hypotension [
Renal function is also commonly adversely affected in
ACS and is manifest by oliguria with IAP above 15 mmHg
and anuria with IAP above 30 mmHg. The mechanism of
acute kidney injury is multifactorial, resulting both from prerenal and intrarenal processes. IAP of 20 mmHg or more has
been shown to increase renal vascular resistance by 555 % in
a canine model [ 23 ]. The decreased cardiac output described
above certainly has effects on renal blood fl ow, contributing
to prerenal failure; however, IAH has also been shown to be
an independent cause of renal impairment [
ciated with a decrease in renal plasma fl ow and glomerular
fi ltration rate, attributable to renal arterial, venous, and
parenchymal compression [ 25 ]. These derangements lead to
20 , 21 ]. Taken
22 ].
24 ]. IAH is asso-
19 Abdominal Compartment Hypertension and Abdominal Compartment Syndrome
235
increased activation of the renin-angiotensin-aldosterone
hormone signaling cascade with resultant increase in systemic vascular resistance which, in turn, feedbacks into the
already-described imbalance in cardiac output [ 26 ].
The hepatobiliary system is especially sensitive to
increased IAP, even after controlling for cardiac output. An
increase of only 10 mmHg in abdominal pressure can cause
a signifi cant decrease in hepatic venous, arterial, and microcirculatory blood fl ow [
fests as an increased plasma lactate level which is not
attributable solely to cardiac output derangements, suggesting reduced hepatic clearance [ 28 ]. This functional decrease
in serum lactate clearance confounds the use of lactate levels
as a resuscitative endpoint in patients with IAH. In addition,
the rising lactate levels lower the serum pH, which can result
in further myocardial depression as well as arteriole dilation
thereby leading to additional lowering of the systemic blood
pressure and worsening cellular respiration.
As discussed above, serum lactate elevations in IAH are
multifactorial and are also partly attributable to the effects of
increased IAP on bowel perfusion. In a porcine model, IAP
of 20 mmHg caused signifi cant impairment of mesenteric
blood fl ow with a concomitant decrease in mucosal blood
fl ow and drop in mucosal pH, indicating signifi cant bowel
ischemia [ 29 ]. Other studies have also shown decrease in
bowel mucosal oxygen levels in the setting of IAH [ 30 ]. The
bowel ischemia seen in IAH not only results in interstitial
edema thereby contributing to development of ACS but is
also a key pathologic feature that leads to further physiologic
decompensation. By impairing mucosal blood fl ow even in
the setting of normal mean arterial pressures, IAH has been
shown to cause translocation of intraluminal bacteria after as
little as 60 min of IAP over 25 mmHg [ 31 ]. This bacterial
translocation may contribute to septic shock if ACS is not
treated quickly.
27 ]. Impaired hepatic function mani-
Diagnosis: Measurement of Abdominal Pressure
In a series of 110 consecutive ICU patients who had undergone abdominal surgery, clinical estimation of IAP by an
intensivist was compared with direct measurement of IAP
and was found to have only 60.9 % sensitivity for detecting
IAP >18 mmHg [ 3 , 32 ]. Because of the unreliability of clini-
cal examination alone in diagnosing IAH, objective measurement of IAP is key in the management of critically ill
patients in whom IAH or ACS are suspected. Multiple methods of measurement of IAP, both direct and indirect, have
been described.
Direct measurement of IAP, while theoretically most
accurate, is necessarily invasive and therefore not broadly
useful as a screening apparatus for identifying patients with
IAH. Means of direct measurement include the use of intraperitoneal pressure transducers and measurement of pressures through peritoneal dialysis catheters or ascites drainage
catheters.
Indirect measurement techniques include measurement of
peak ventilator pressures (although this is complicated by
concerns of lung and chest wall compliance), central venous,
intravesical, rectal, and intrauterine pressures. Among indirect measurement techniques, measurement of bladder pressures is generally considered the gold standard for diagnosis
of IAH due to its ease and minimally invasive nature [ 5 , 16 ].
This technique should be performed while patients are fully
supine, as patient position can affect pressure readings. IAP
should be measured at end expiration with the abdominal
wall musculature fully relaxed, conditions which are hard to
replicate consistently without the use of chemical sedation
and mechanical ventilation. In order to measure intravesical
pressures, 20 ml of sterile water or saline is instilled into the
bladder, and a manometer zeroed at the level of the midaxillary line is used to record the pressure transmitted from the
abdomen, through the bladder wall, and into the column of
fl uid. The procedure must be done under sterile conditions
and with sterile fl uids in order to prevent contamination of
the catheter system and therefore iatrogenic urinary tract
infections. In one prospective trial of serial IAP measurements via intravesical pressures, instillation of volumes
greater than 50 cc was shown to artifi cially increase the measured IAP [ 33 ]. There is a commercially available product
which connects to the urinary catheter and may decrease the
probability of technical error in measuring abdominal pressure, but the procedure can also be carried out by inserting a
needle connected to a pressure transducer into the sampling
port of a urinary catheter.
While measurement of intravesical pressures remains the
gold standard for objective measurement of IAP, this technique may not be feasible in a certain subset of patients, such
as those with a history of cystectomy and those with traumatic bladder injury or pelvic hematoma/intra-abdominal
packing that would make measurement either unreliable or
contraindicated. For situations such as these, a variety of
other measurement strategies have been described. Several
authors have suggested the use of inferior vena cava pressure
monitoring via a standard central venous catheter. Studies
evaluating this technique have demonstrated good correlation between IVC pressures and other validated methods
[ 34 ]. Another method involves measurement of gastric pres-
sures via a naso- or orogastric tube but is complicated by
contractions of the migrating motor complex, which may
confound results of intermittent readings. A related technique involving the use of a continuously monitored gastric
manometry balloon has been validated in vivo by comparison with insuffl ation pressures during laparoscopic cholecystectomy [
35 ]. The continuous method of measurement
236
P. Maluso and B. Sarani
negates the confounding effects of the migrating motor
complex contractions; however, it is unclear whether enteral
feeding may confound the measurements. Other novel
techniques involving the use of specialized catheters
(for intravesical, rectal, intrauterine use) with embedded
microchips have been described but are less cost-effective
than the simpler techniques described above [
Whereas the majority of studies on the topic use absolute
IAP as an endpoint for analysis, some retrospective studies
have found that APP may be a more clinically useful endpoint in the diagnosis and treatment of IAH. In their review
of 144 patients treated for IAH, Cheatham et al. found that
APP was superior to other commonly used endpoints such as
serum lactate or urine output in predicting patient survival
[ 37 ]. According to their data, an APP of less than 60 mmHg
is predictive of the need for urgent intervention and is useful
as both a resuscitative endpoint and a predictor of need for
surgical decompression. Another study of cirrhotic patients
with septic shock found that APP less than 55 was associated
with mortality and also found that this value was more predictive of survival than other traditional measures of endorgan perfusion, such as central venous oxygen saturation,
serum lactate level, and MAP [ 38 ].
36 ].
Treatment
Once the diagnosis of ACS has been made, appropriate treatment strategies are based on rapid relief of the intraabdominal pressure in order to restore perfusion to the
abdominal viscera and resolve the derangements in cardiopulmonary function. Although the defi nitive management of
ACS is surgical decompression of the abdomen, lower-grade
IAH may be amenable to nonsurgical measures (Table 19.1 ).
Lower-grade IAH that is exacerbated by abdominal wall tension (e.g., third-spacing of fl uids or a tight abdominal wall
repair following ventral herniorrhaphy) may be improved by
neuromuscular blockade (NMB). In one prospective study,
patients with IAH were given a short trial of NMB using
cisatracurium and experienced an average 4 mmHg decrease
in IAP; however, the response was short-lived and showed no
effect on the patients’ urinary output. Similarly, the patient’s
APP did not increase, suggesting the limited clinical utility
of NMB for IAH and further suggesting that it is ineffective
for true ACS [ 39 ].
For selected patients in whom IAH is due to acutely
increased intraperitoneal fl uid volumes, such as patients with
tense ascites, paracentesis has been shown to be effective in
avoiding decompressive laparotomy. In a case series of burn
patients, paracentesis using a peritoneal dialysis catheter
avoided laparotomy and effectively relieved IAH [ 40 ]. Other
studies have shown the effi cacy of paracentesis for relief of
IAH due to massive ascites in cirrhotic patients. With
drainage of ascites, Savino et al. showed a decrease of
10 mmHg IAP with concomitant improvement in cardiac
index, urinary output, and creatinine clearance [
patients for whom IAH is largely due to free fl uid within the
peritoneal cavity, percutaneous drainage may have at least a
temporizing role, if not a defi nitive one, in the management
of IAH.
While other therapies discussed have limited roles in the
temporization and management of IAH and should be
attempted where appropriate, ACS with its inherent organ
system dysfunction merits urgent defi nitive management
with decompressive laparotomy in most cases [ 16 , 42 ].
However, laparotomy carries many risks which should be
carefully weighed against the patient’s clinical situation
before the decision is made to proceed. Consideration of
patients’ fi tness for travel to an operating room, especially
with regard to their need for high-level positive-pressure
ventilation not amenable to transport without a ventilator,
should inform decisions as to the setting for operation. While
the intensive care unit is capable of managing pulmonary and
physiologic changes after decompression, it is often diffi cult
to control surgical bleeding, and maintenance of a sterile
environment is more diffi cult. Post-decompression physiological changes must also be anticipated when attempting
laparotomy. A sudden rapid increase in pulmonary compliance can lead to respiratory alkalosis if ventilator settings are
not adjusted post-decompression. Ideally, vasopressor doses
can be rapidly titrated down following decompression,
because venous return to the heart and cardiac output should
improve almost instantly.
41 ]. In
Management of the Open Abdomen
After decompressive laparotomy, there are numerous strategies for management of the subsequent open abdomen.
Leaving the abdomen open, while critical to management of
ACS, exposes patients to new risks. The risk of complications resulting from the open abdomen rises with duration of
therapy, with a signifi cant increase in patients left open for
more than 8 days [ 43 ]. Exposure of the abdominal viscera to
the environment may lead to formation of entero- atmospheric
fi stulae and also leads to signifi cant fl uid and heat losses.
Frequent manipulation of the bowel also exposes patients to
an up to 20 % risk of entero-atmospheric fi stula formation.
Additionally, an open abdomen poses a signifi cant nutritive
risk to already-catabolic patients: roughly 2 g of protein are
lost for every liter of fl uid removed from the peritoneal cavity [ 44 ]. For these reasons, multiple methods for temporary
abdominal closure or coverage of the viscera have been
described. With temporary coverage, fl uid and protein losses
are decreased and more easily quantifi ed, and septic complications are reduced [
45 , 46 ].
19 Abdominal Compartment Hypertension and Abdominal Compartment Syndrome
237
Even with temporary closure, patients with an open
abdomen are at signifi cant risk for loss of abdominal domain,
wherein the abdominal musculature retracts the fascia laterally. With loss of domain, attempts at primary closure of the
fascia or skin when ACS has resolved may fail, resulting in
large ventral hernia defects in up to a third of patients.
Finally, even though temporary closure can decrease risks
associated with an open abdomen, it can nevertheless leave
patients susceptible to increases in IAP and recurrence of
ACS [
47 ]. In these instances, the temporary closure device
needs to be upsized to allow for further expansion of abdominal domain.
Numerous techniques exist for temporary closure of the
open abdomen and will be discussed subsequently. These
techniques can be broadly classifi ed based on their use of a
“silo,” negative pressure device, or a patch closure, and some
may be used in conjunction with others. Each technique carries unique drawbacks and benefi ts with regard to their cost
and to their ability to manage and quantify fl uid losses, minimize dressing changes, and minimize loss of domain.
The simplest temporary closure method is the silo, in
which a sterile translucent plastic sheet or bag is sutured to
the skin at the margins of the laparotomy. Commercial solutions, such as the Bogota Bag ™ , may be used, or, alternatively, bags for intravenous fl uids or dialysate may be
substituted as a cost-saving measure [ 48 ]. This method of
closure is inexpensive, relatively simple, and allows for
visual inspection of the viscera, but it hinders removal of
fl uid from the peritoneal cavity. Fluid buildup can lead to
recurrent ACS or may result in deposition of fi brinous debris
on the intestines, although the clinical ramifi cations of the
latter are uncertain. Furthermore, these devices have to be
sutured in place, thereby making their placement both time
and labor intensive. Of the techniques described, the use of a
silo is associated with the highest rate of failure for attempted
primary fascial closure, with up to 70 % of attempts failing in
one meta-analysis [ 49 ].
Patch-based techniques of closure are similar to silos, but
involve suturing a synthetic material as an interposition
between the fascial edges rather than the skin edges. While
these techniques do decrease the lateral retraction of the fascia and minimize loss of abdominal domain, they are suboptimal for control of fl uid losses. Two main, commercially
available techniques exist for patch closure: the Wittmann
Patch and the polytetrafl uoroethylene (PTFE, Gore-Tex ™ )
patch. In the Wittmann Patch, two sheets are sewn to the lateral edges of the fascial defect and connected at the midline
with the use of a Velcro-like closure. This technique allows
for expansion or contraction of the abdominal wall defect in
response to changes in IAP. Furthermore, signifi cantly higher
rates of fascial closure are possible due to decreased fascial
retraction supplemented by staged approximation of the
abdominal wall [
50 ]. Meta-analysis has shown the Wittmann
Patch to be superior to all other methods of temporary closure
in terms of rate of primary fascial closure with up to 90 % of
patients successfully closed [
49 ]. Similar to the Wittmann
Patch, PTFE patches also allow for dynamic closure of the
abdominal wall by serial plication of the midline of the patch
to increase tension on the fascia. In one series, this technique
allowed for similar primary closure rates to the Wittmann
Patch, with 89 % of patients successfully closed [ 51 ]. Aside
from their diffi culty in management of fl uid losses, both
patch techniques share a common major drawback in their
effects on the health of the fascial edges. Repeated fascial
suturing from changing patches and the increased traction on
the fascia can lead to necrosis of the edges of the fascia,
which often necessitates debridement prior to fi nal closure.
This may make fi nal fascial apposition challenging.
Negative pressure wound therapy (NPWT) systems, also
known as vacuum-assisted closure (VAC) devices, are the
most commonly used form of temporary closure device.
Both commercially available sponge-based varieties
(AbThera VAC therapy) and improvised towel-based lowercost alternatives (Barker’s VAC) have been described. In
each system, an inert layer is inserted into the abdomen to
protect the viscera and is then covered with a self-adhesive
plastic sheet to which suction is applied. NWPT systems are
superior in their ability to manage and quantify fl uid/protein
losses and may be used in conjunction with patch techniques.
Additionally, the application of negative pressure to the
wound opposes the lateral forces on the fascia without
directly manipulating it, thereby improving primary closure
rates without compromising the edges of the fascia.
Towel-based systems (Barker’s VAC) are easy to apply
and are lower cost than their commercially available alternatives. In these, a surgical towel is adhered to an inert polyethylene sheet, such as Ioban ™ , and is inserted between the
viscera and the underside of the abdominal wall. Small slits
are cut in the polyethylene sheet to allow drainage of fl uids,
and drain tubing is placed over the towel before placement of
a self-adhesive elastic sheet over the abdominal wall defect.
The drain tubing is then attached to a closed-suction system
to provide negative pressure and drainage of excess fl uid [ 52 ,
53 ]. Although this technique is simple, low cost, and allows
for expansion of the abdominal wall under increased pressure, it does not provide effective suction to all portions of
the abdominal cavity, allowing fl uid to accumulate in the pelvis and paracolic gutters. Placement of additional drain tubing in dependent portions of the abdomen may mitigate these
effects but increases the complexity of the system and has
not been studied.
Commercial systems work by a similar mechanism to
towel-based systems but use a perforated Silastic sheet
inserted into the abdomen between the viscera and abdominal wall and are covered with a sterile sponge cut to fi ll the
abdominal wall defect. The wound is then covered with a
238
P. Maluso and B. Sarani
self-adherent elastic sheet, and a proprietary closed-suction
system is applied [
54 ]. Because the perforated Silastic sheet
can be inserted into dependent portions of the abdomen, this
closure technique allows for application of more uniform
suction to all parts of the abdomen, offering improved fl uid
management.
Meta-analysis has shown NWPT to be intermediate
between patch- and silo-based systems in its ability to
achieve primary fascial closure, with rates of 52 % for improvised towel-based systems and 60 % for sponge-based commercial systems [ 49 ]. A prospective, multicenter study of
towel-based and sponge-based systems found similar rates of
primary abdominal closure in patients requiring an open
abdomen for more than 48 h, with a 51 % closure rate in
towel-based and a 69 % closure rate in sponge-based systems. More importantly, the study was the fi rst to show a
difference in other outcomes between systems. All-cause
30-day mortality was signifi cantly higher in the towel-based
cohort than in the sponge-based cohort (30 versus 14 %,
p < 0.05) despite their similar disease severity [ 55 ]. The
authors speculate that this difference may be attributable to
the systems’ relative effectiveness in removing fl uid rich in
infl ammatory cytokines from the abdomen. The use of additional dependent drains in towel-based systems, as described
above, may mitigate some of this survival benefi t, but further
study is required.
Closure of the Open Abdomen
Regardless of the method chosen for management of the
open abdomen, once therapeutic objectives have been
achieved and an open abdomen is no longer necessary, defi nitive abdominal closure should be attempted as quickly as
possible to minimize the deleterious effects of an open abdomen described above. Generally speaking, the length of time
the abdomen is left open correlates with the incidence of
complications, and a longer duration of open abdomen correlates with decreased rates of closure [ 43 ]. With every
return to the operating room for washout or inspection of the
abdomen, the patient should be assessed for potential closure. If repeated attempts at fascial closure are unsuccessful,
functional closure using an inlay mesh or intentional creation of a ventral hernia with skin-only closure and planned
future ventral herniorrhaphy may be attempted.
Primary fascial closure refers to the direct approximation
of the fascial edges and is the ideal method for closing the
abdomen given that it has the lowest incidence of complications following an open abdomen. Care must be taken when
attempting primary fascial closure as it may precipitate
return of abdominal compartment syndrome if the patient
still requires large-volume fl uid resuscitation or there is
excessive tension on the abdominal wall [
56 ]. Despite its
superiority in properly selected patients, primary closure
nevertheless has a high incidence of hernia formation, with
up to 30 % of open abdomen patients developing a ventral
hernia at some point after closure [ 57 ]. Because of this high
incidence of hernia formation, primary fascial closure can be
augmented with mesh reinforcement. Permanent, synthetic
meshes are relatively contraindicated in patients with risk
factors for mesh infection such as wound soilage, and many
authors recommend the use of biologic mesh in these
instances. More advanced techniques of fascial closure such
as a separation of abdominal wall components laterally to
allow for direct apposition of the fascia at the midline may be
used, but a detailed discussion of these methods is beyond
the scope of this chapter [
58 ].
If primary fascial closure is not possible, an alternative is
functional closure by approximating the superior and inferior aspects of the fascial defect as much as possible then
placing a mesh inlay as a bridge between the edges of the
remainder of the fascial defect. The biologic mesh inlay acts
as scaffolding for ingrowth of native fascial tissue [ 59 ]. Once
the mesh is placed, the skin is closed over the repair, and
drains can be placed over the mesh to close the space and
prevent seroma accumulation as needed. However, most
studies fi nd that the mesh will stretch over time resulting in a
bulge and “neo-hernia” due to excessive abdominal wall laxity. If skin closure is not possible, functional closure should
be avoided as exposed mesh will undergo accelerated
degradation until a granulation tissue bed forms over the viscera. This process usually occurs over several weeks. The
resultant granulation tissue will require skin grafting and
will ultimately lead to a ventral hernia. While the late incidence of ventral hernia formation after functional closure is
not well established, one study using acellular dermal matrix
for repair of ventral hernias has shown an 80 % incidence of
hernia formation over a mean follow-up of 21.4 months
despite skin closure over the mesh [ 60 ].
Because of the dismal outcomes associated with functional closure of the abdominal wall, many surgeons prefer
to create a ventral hernia with plans for subsequent defi nitive
ventral herniorrhaphy (and possible component separation)
once the patient has fully recovered and the volume of the
abdominal contents has returned to normal. Skin-only closure is one option for tissue coverage of the abdominal viscera based on this strategy.
If the skin edges are similarly too retracted to allow for
closure without undue tension or increased abdominal pressure, the abdomen can be left open until the viscera have
become self-adherent and adherent to the abdominal wall,
creating a “block” of tissue within the abdominal wall defect.
This process is allowed to continue until a granulation tissue
bed has grown over the viscera. An absorbable mesh
(e.g., Vicryl ™ ) can be sutured to the skin edges to cover the
viscera and prevent evisceration until a granulation bed has
19 Abdominal Compartment Hypertension and Abdominal Compartment Syndrome
239
formed. After the defect is adequately covered with a granulation tissue bed, a split-thickness skin graft can be placed.
Finally, these patients can return for elective ventral hernia
repair after a 6–12-month interval. This interval allows maturation and ultimately dissolution of intra-abdominal adhesions and yields a lower incidence of enterotomy at the time
of defi nitive hernia repair [
61 ]. However, the granulation
phase, prior to skin grafting, is associated with up to 20 %
risk of developing an entero-atmospheric fi stula formation.
This risk is highest in patients with an exposed
anastomosis [ 62 ].
Conclusion
Intra-abdominal hypertension and abdominal compartment syndrome are common following resuscitation in
critically ill or injured patients. Failure to recognize the
disorders in a timely fashion is associated with signifi cant
morbidity as well as mortality. Because physical exam
does not offer a sensitive means to diagnose either disorder, patients at risk for IAH or ACS should routinely have
their intra-abdominal pressure measured and undergo
interventions to lower the IAP when signifi cantly elevated
pressures are noted.
References
1. Balogh Z, McKinley BA, Cocanour CS, et al. Secondary abdominal
compartment syndrome is an elusive early complication of traumatic shock resuscitation. Am J Surg. 2002;184:538–43; discussion 43–4.
2. Balogh Z, McKinley BA, Holcomb JB, et al. Both primary and sec-
ondary abdominal compartment syndrome can be predicted early
and are harbingers of multiple organ failure. J Trauma. 2003;54:848–
59; discussion 59–61.
3. Department of Surgical Education. Intraabdominal pressure moni-
toring. In: Orlando; 2008. Available at:
care.net/Guidelines/intraabdominal_pressure_monitoring.pdf.
Accessed 11/20/2015
4. Vidal MG, Ruiz Weisser J, Gonzalez F, et al. Incidence and clinical
effects of intra-abdominal hypertension in critically ill patients. Crit
Care Med. 2008;36:1823–31.
5. Kirkpatrick AW, Roberts DJ, De Waele J, et al. Intra-abdominal
hypertension and the abdominal compartment syndrome: updated
consensus defi nitions and clinical practice guidelines from the
World Society of the Abdominal Compartment Syndrome. Intensive
Care Med. 2013;39:1190–206.
6. Sanchez NC, Tenofsky PL, Dort JM, Shen LY, Helmer SD, Smith RS.
What is normal intra-abdominal pressure? Am Surg. 2001;67:243–8.
7. Hering R, Wrigge H, Vorwerk R, et al. The effects of prone position-
ing on intra-abdominal pressure and cardiovascular and renal function
in patients with acute lung injury. Anesth Analg. 2001;92:1226–31.
8. Wilson A, Longhi J, Goldman C, McNatt S. Intra-abdominal pres-
sure and the morbidly obese patients: the effect of body mass index.
J Trauma. 2010;69:78–83.
9. Madigan MC, Kemp CD, Johnson JC, Cotton BA. Secondary
abdominal compartment syndrome after severe extremity injury:
are early, aggressive fl uid resuscitation strategies to blame?
J Trauma. 2008;64:280–5.
.
http://www.surgicalcritical-
10. Regueira T, Bruhn A, Hasbun P, et al. Intra-abdominal hypertension: incidence and association with organ dysfunction during early
septic shock. J Crit Care. 2008;23:461–7.
11. Reintam Blaser A, Parm P, Kitus R, Starkopf J. Risk factors for
intra-abdominal hypertension in mechanically ventilated patients.
Acta Anaesthesiol Scand. 2011;55:607–14.
12. Reintam Blaser A, Parm P, Kitus R, Starkopf J. Intra-abdominal
hypertension and gastrointestinal symptoms in mechanically ventilated patients. Crit Care Res Pract. 2011;2011:982507.
13. Kasotakis G, Duggan M, Li Y, et al. Optimal pressure of abdominal
gas insuffl ation for bleeding control in a severe swine splenic injury
model. J Surg Res. 2013;184:931–6.
14. Neal MD, Hoffman MK, Cuschieri J, et al. Crystalloid to packed
red blood cell transfusion ratio in the massively transfused patient:
when a little goes a long way. J Trauma Acute Care Surg.
2012;72:892–8.
15. Holodinsky JK, Roberts DJ, Ball CG, et al. Risk factors for intraabdominal hypertension and abdominal compartment syndrome
among adult intensive care unit patients: a systematic review and
meta-analysis. Crit Care. 2013;17:R249.
16. Cheatham ML, Malbrain ML, Kirkpatrick A, et al. Results from the
international conference of experts on intra-abdominal hypertension and abdominal compartment syndrome. II. Recommendations.
Intensive Care Med. 2007;33:951–62.
17. Obeid F, Saba A, Fath J, et al. Increases in intra-abdominal pressure
affect pulmonary compliance. Arch Surg. 1995;130:544–7; discussion 7–8.
18. Pelosi P, Quintel M, Malbrain ML. Effect of intra-abdominal pressure on respiratory mechanics. Acta Clin Belg. 2007;62 Suppl
1:78–88.
19. Gattinoni L, Pelosi P, Suter PM, Pedoto A, Vercesi P, Lissoni
A. Acute respiratory distress syndrome caused by pulmonary and
extrapulmonary disease. Different syndromes? Am J Respir Crit
Care Med. 1998;158:3–11.
20. Cullen DJ, Coyle JP, Teplick R, Long MC. Cardiovascular, pulmonary, and renal effects of massively increased intra-abdominal pressure in critically ill patients. Crit Care Med. 1989;17:118–21.
21. Ridings PC, Bloomfi eld GL, Blocher CR, Sugerman HJ.
Cardiopulmonary effects of raised intra-abdominal pressure before
and after intravascular volume expansion. J Trauma. 1995;39:
1071–5.
22. Barnes GE, Laine GA, Giam PY, Smith EE, Granger HJ.
Cardiovascular responses to elevation of intra-abdominal hydrostatic pressure. Am J Physiol. 1985;248:R208–13.
23. Harman PK, Kron IL, McLachlan HD, Freedlender AE, Nolan SP.
Elevated intra-abdominal pressure and renal function. Ann Surg.
1982;196:594–7.
24. Sugrue M, Jones F, Deane SA, Bishop G, Bauman A, Hillman
K. Intra-abdominal hypertension is an independent cause of postoperative renal impairment. Arch Surg. 1999;134:1082–5.
25. Bradley SE, Bradley GP. The effect of increased intra-abdominal
pressure on renal function in man. J Clin Invest. 1947;26:1010–22.
26. Bloomfi eld GL, Blocher CR, Fakhry IF, Sica DA, Sugerman
HJ. Elevated intra-abdominal pressure increases plasma renin activity and aldosterone levels. J Trauma. 1997;42:997–1004; discussion –5.
27. Diebel LN, Wilson RF, Dulchavsky SA, Saxe J. Effect of increased
intra-abdominal pressure on hepatic arterial, portal venous, and
hepatic microcirculatory blood fl ow. J Trauma. 1992;33:279–82;
discussion 82–3.
28. Burchard KW, Ciombor DM, McLeod MK, Slothman GJ, Gann
DS. Positive end expiratory pressure with increased intra- abdominal
pressure. Surg Gynecol Obstet. 1985;161:313–8.
29. Diebel LN, Dulchavsky SA, Wilson RF. Effect of increased intraabdominal pressure on mesenteric arterial and intestinal mucosal
blood fl ow. J Trauma. 1992;33:45–8; discussion 8–9.
240
P. Maluso and B. Sarani
30. Bongard F, Pianim N, Dubecz S, Klein SR. Adverse consequences
of increased intra-abdominal pressure on bowel tissue oxygen.
J Trauma. 1995;39:519–24; discussion 24–5.
31. Diebel LN, Dulchavsky SA, Brown WJ. Splanchnic ischemia and
bacterial translocation in the abdominal compartment syndrome.
J Trauma. 1997;43:852–5.
32. Sugrue M, Bauman A, Jones F, et al. Clinical examination is an
inaccurate predictor of intra-abdominal pressure. World J Surg.
2002;26:1428–31.
33. Malbrain ML, Deeren DH. Effect of bladder volume on measured intravesical pressure: a prospective cohort study. Crit Care. 2006;10:R98.
34. Lee SL, Anderson JT, Kraut EJ, Wisner DH, Wolfe BM. A simplifi ed approach to the diagnosis of elevated intra-abdominal pressure.
J Trauma. 2002;52:1169–72.
35. Sugrue M, Buist MD, Lee A, Sanchez DJ, Hillman KM. Intraabdominal pressure measurement using a modifi ed nasogastric
tube: description and validation of a new technique. Intensive Care
Med. 1994;20:588–90.
36. Malbrain ML. Different techniques to measure intra-abdominal
pressure (IAP): time for a critical re-appraisal. Intensive Care Med.
2004;30:357–71.
37. Cheatham ML, White MW, Sagraves SG, Johnson JL, Block EF.
Abdominal perfusion pressure: a superior parameter in the assessment of intra-abdominal hypertension. J Trauma. 2000;49:621–6;
discussion 6–7.
38. Al-Dorzi HM, Tamim HM, Rishu AH, Aljumah A, Arabi YM. Intraabdominal pressure and abdominal perfusion pressure in cirrhotic
patients with septic shock. Ann Intensiv Care. 2012;2 Suppl 1:S4.
39. De Laet I, Hoste E, Verholen E, De Waele JJ. The effect of neuromuscular blockers in patients with intra-abdominal hypertension.
Intensive Care Med. 2007;33:1811–4.
40. Corcos AC, Sherman HF. Percutaneous treatment of secondary
abdominal compartment syndrome. J Trauma. 2001;51:1062–4.
41. Savino JA, Cerabona T, Agarwal N, Byrne D. Manipulation of
ascitic fl uid pressure in cirrhotics to optimize hemodynamic and
renal function. Ann Surg. 1988;208:504–11.
42. De Waele JJ, Hoste EA, Malbrain ML. Decompressive laparotomy
for abdominal compartment syndrome – a critical analysis. Crit
Care. 2006;10:R51.
43. Miller RS, Morris Jr JA, Diaz Jr JJ, Herring MB, May AK.
Complications after 344 damage-control open celiotomies.
J Trauma. 2005;59:1365–71; discussion 71–4.
44. Cheatham ML, Safcsak K, Brzezinski SJ, Lube MW. Nitrogen balance, protein loss, and the open abdomen. Crit Care Med.
2007;35:127–31.
45. Agalar F, Eroglu E, Bulbul M, Agalar C, Tarhan OR, Sari M. Staged
abdominal repair for treatment of moderate to severe secondary
peritonitis. World J Surg. 2005;29:240–4.
46. Holzheimer RG, Gathof B. Re-operation for complicated secondary peritonitis – how to identify patients at risk for persistent sepsis.
Eur J Med Res. 2003;8:125–34.
47. Gracias VH, Braslow B, Johnson J, et al. Abdominal compartment
syndrome in the open abdomen. Arch Surg. 2002;137:1298–300.
48. Fernandez L, Norwood S, Roettger R, Wilkins 3rd HE. Temporary
intravenous bag silo closure in severe abdominal trauma. J Trauma.
1996;40:258–60.
49. Boele van Hensbroek P, Wind J, Dijkgraaf MG, Busch OR,
Goslings JC. Temporary closure of the open abdomen: a systematic
review on delayed primary fascial closure in patients with an open
abdomen. World J Surg. 2009;33:199–207.
50. Weinberg JA, George RL, Griffi n RL, et al. Closing the open abdomen: improved success with Wittmann Patch staged abdominal closure. J Trauma. 2008;65:345–8.
51. Vertrees A, Kellicut D, Ottman S, Peoples G, Shriver C. Early
defi nitive abdominal closure using serial closure technique on
injured soldiers returning from Afghanistan and Iraq. J Am Coll
Surg. 2006;202:762–72.
52. Barker DE, Kaufman HJ, Smith LA, Ciraulo DL, Richart CL,
Burns RP. Vacuum pack technique of temporary abdominal closure:
a 7-year experience with 112 patients. J Trauma. 2000;48:201–6;
discussion 6–7.
53. Brock WB, Barker DE, Burns RP. Temporary closure of open
abdominal wounds: the vacuum pack. Am Surg. 1995;61:30–5.
54. Miller PR, Meredith JW, Johnson JC, Chang MC. Prospective evaluation of vacuum-assisted fascial closure after open abdomen:
planned ventral hernia rate is substantially reduced. Ann Surg.
2004;239:608–14; discussion 14–6.
55. Cheatham ML, Demetriades D, Fabian TC, et al. Prospective study
examining clinical outcomes associated with a negative pressure
wound therapy system and Barker’s vacuum packing technique.
World J Surg. 2013;37:2018–30.
56. Biffl WL, Moore EE, Burch JM, Offner PJ, Franciose RJ, Johnson
JL. Secondary abdominal compartment syndrome is a highly lethal
event. Am J Surg. 2001;182:645–8.
57. Patel NY, Cogbill TH, Kallies KJ, Mathiason MA. Temporary
abdominal closure: long-term outcomes. J Trauma. 2011;70:
769–74.
58. Sailes FC, Walls J, Guelig D, et al. Synthetic and biological mesh in
component separation: a 10-year single institution review. Ann
Plast Surg. 2010;64:696–8.
59. Diaz Jr JJ, Guy J, Berkes MB, Guillamondegui O, Miller RS.
Acellular dermal allograft for ventral hernia repair in the compromised surgical fi eld. Am Surg. 2006;72:1181–7; discussion 7–8.
60. Jin J, Rosen MJ, Blatnik J, et al. Use of acellular dermal matrix for
complicated ventral hernia repair: does technique affect outcomes?
J Am Coll Surg. 2007;205:654–60.
61. Jernigan TW, Fabian TC, Croce MA, et al. Staged management of
giant abdominal wall defects: acute and long-term results. Ann
Surg. 2003;238:349–55; discussion 55–7.
62. Rao M, Burke D, Finan PJ, Sagar PM. The use of vacuum-assisted
closure of abdominal wounds: a word of caution. Colorectal Dis.
2007;9:266–8.
Nutrition in the Surgical ICU Patient
Beth E. Taylor and Craig M. Coopersmith
2 0
Introduction
Nutrition holds a pivotal role in the care of surgical and trauma
patients admitted to the surgical intensive care unit (ICU).
Critically ill surgical ICU patients are in a catabolic state driven
by a systemic infl ammatory response to insult or injury coupled
with complications from infections, multiple organ dysfunction
syndrome (MODS), and prolonged hospitalization [
Superimposed upon the host response to critical illness, the metabolic response to surgery or trauma also leads to an altered hormonal milieu that shifts from sparing of lean body mass to
increased utilization as a gluconeogenic substrate and support of
immune function and repair of tissue [ 5 ]. This use of lean body
mass for energy combined with the physical unloading of muscle
with bedrest, inactivity, and immobility leads to a progressive
loss of skeletal mass [ 6 ]. A major goal of nutrition therapy is to
help attenuate the metabolic response to stress, prevent oxidative
cellular injury, favorably modulate immune responses, and slow
the loss of lean body mass. Improvement in the clinical course of
the surgical ICU patient may be achieved by early and adequate
nutrition therapy (primarily by the enteral route), appropriate
macro- and micronutrient delivery, and meticulous glycemic
control. Unfortunately, early and consistent delivery of enteral
nutrition (EN) is often challenging in this patient population.
1 – 4 ].
Nutrition Assessment
Determination of which critically ill patients will benefi t the
most from nutritional intervention has been diffi cult to defi ne.
Recently, the American Society for Parenteral and Enteral
B. E. Taylor , DCN, RD, CNSC, FCCM (*)
Food and Nutrition , Barnes-Jewish Hospital ,
St. Louis , MO 63110 , USA
bet1217@bjc.org
e-mail:
C. M. Coopersmith , MD
Department of Surgery , Emory University Hospital ,
Atlanta , GA 30322 , USA
Nutrition (ASPEN) and the Academy of Nutrition and
Dietetics (Academy) have published defi nitions that take into
account the deleterious impact of infl ammation on nutritional
status and distinguish between acute and chronic malnutrition
(Table 20.1 ) [ 7 , 8 ]. ASPEN and the Academy suggest those
patients defi ned as “severely malnourished” will obtain the
greatest benefi t from early nutrition intervention. The key
components of the current ASPEN/Academy defi nition of
“severe malnutrition” include energy intake, degree of recent
weight loss or gain, body fat, muscle mass, presence or
absence of fl uid accumulation, and grip strength [ 7 , 8 ].
Nutritional risk is a combination of nutritional status and
assessment of disease severity. The NRS 2002 and NUTRIC
score have been used to defi ne nutritional risk in randomized
control trials (RCTs) in critically ill patients (Table 20.1 ) [ 9 ,
10 ]. The NUTRIC score has been validated with and without
the use of interleukin-6 [ 10 , 11 ]. Two RCTs in ICU patients
show those at high nutritional risk are more likely to benefi t
from early EN (less infectious complications and mortality)
than their low nutrition risk counterparts [ 10 , 12 ]. For the
surgical patient, current nutritional status, type of surgery,
and potential anatomic alterations should all be considered
when determining potential benefi t from nutrition therapy.
In the ICU setting, traditional protein markers such as
albumin, prealbumin, transferrin, and retinal-binding protein
refl ect the acute-phase response (increase in vascular permeability and decrease in hepatic synthesis) and do not represent nutrition status [ 13 ]. Neither should anthropometrics be
used to determine the adequacy of nutrition therapy given
fl uctuations in fl uid status and sequestration of fl uid into
extracellular spaces. Ultrasound (US), given its ease of use
and availability, is emerging as a bedside tool to measure
muscle mass and determine changes in muscle tissue over
time [ 14 , 15 ]. Computed tomography (CT) scans ordered for
other reasons may also provide a quantifi cation of skeletal
muscle and adipose tissue depots if the lumbar region is
available [ 5 , 6 ]. However, validation and reliability studies
regarding the use of US and CT in the surgical ICU are still
pending.
© Springer International Publishing Switzerland 2016
N.D. Martin, L.J. Kaplan (eds.), Principles of Adult Surgical Critical Care, DOI 10.1007/978-3-319-33341-0_20
241
242
Table 20.1 Scoring systems to determine degree of malnutrition or nutrition risk
ASPEN severe malnutrition NRS 2002 high nutrition risk NUTRIC score high nutrition risk
Meet at least two of the following:
Energy intake: ≤50 % of need for 5 days or
more
Weight loss: >2 % in 1 week, >5 % in 1 month,
>7.5 % in 3 months
Moderate fat loss, muscle wasting, and/or
peripheral edema
BMI body mass index, COPD chronic obstructive pulmonary disease, CHF congestive heart failure, CKD chronic kidney disease, DM diabetes
mellitus, PNA pneumonia, CVA cerebral vascular accident, BMT bone marrow transplant, ICU intensive care unit, APACHE acute physiologic and
chronic health evaluation, SOFA simplifi ed organ failure assessment, Hosp hospital
Total score ≥5 = high risk
Energy intake for 7 days
1 point: <50–75 %
2 points: <25–50 %
3 points: 0–25 %
Weight loss
1 point: >5 % in 3 months
2 points: >5 % in 2 months
BMI 18.5–20.5
3 points: >5 % in 1 month
BMI <18.5
Diagnosis
1 point: chronic condition (e.g. COPD, CHF,
CKD, DM)
2 points: severe PNA, major
Abdominal surgery, CVA
Malignant hematology
3 points: head injury, BMT,
ICU pt (APACHE II >10)
Total score 5–9 = high risk
Age (years)
0 point: <50
1 point: 50–74
2 points: ≥75 years
APACHE II
0 point: <15
1 point: 15–19
2 points: 20–27
3 points: ≥28
SOFA
0 point: <6
1 point: 6–9
2 points: ≥10
# of comorbidities
0 point: 0–1
1 point: ≥2
Days from Hosp to ICU admit
0 point: 0–1
1 point: ≥1
B.E. Taylor and C.M. Coopersmith
Table 20.2 Calculation of nutrition requirements
Energy requirements Protein requirements
Energy
BMI
(Kcal/kg/day) Clinical condition
<15 35–40 Normal (nonstressed) 0.75
15–19 30–35 Critical illness/injury 1.0–1.5
20–25 20–25 ARF (undialyzed) 0.8–1.0
26–29 15–17 ARF (dialyzed) 1.2–1.4
>29 15
Adapted from [
BMI body mass index, Kcal kilocalories, kg kilograms, IBW ideal body
weight, ARF acute renal failure, CVVHD continuous venovenous
hemodialysis
a
Do not exceed 2,000 kcal/day for obese patients – allowing for hypo-
caloric feeding
b
Clinical conditions are not additive: to calculate needs, use highest
value
a
Peritoneal dialysis 1.3–1.5
Burns/sepsis 1.5–2.0
CVVHD 1.7–2.5
89 ], Chap. 5 , Tables 5.5 and 5.15
Protein needs
(grams/kg IBW/day)
b
Energy and Protein Requirements
Energy requirements may be determined using simplistic weight-based formulas (e.g., 25–30 kcal/kg/day),
published predictive equations (e.g., Penn State, Mifflin
St. Jeor) [ 16 , 17 ], or use of indirect calorimetry (IC),
which is considered the gold standard technique to assess
energy requirements [
available, and, in addition, many variables in the ICU
affect the timing and accuracy of IC measurements
18 ]. Unfortunately, IC may not be
including presence of chest tubes, supplemental oxygen,
continuous renal replacement therapy, anesthesia, and
excessive movement. Over 200 predictive equations
exist; however, none has more than approximately 70 %
accuracy in ICU patients [ 19 , 20 ]. Example recommen-
dations using a simplistic weight-based approach are
displayed in Table 20.2 .
Lean body mass utilization for healing of wounds and
supporting immune function is increased in the surgical ICU
patient, thus making protein the most important macronutrient for this patient population. Often protein needs cannot be
met with the use of an enteral formulation alone, and protein
modulars are needed. A weight-based protein requirement
example is presented in Table 20.2 .
Preoperative Period
Patients anticipating major surgery generally undergo procedural planning and stratifi cation of cardiopulmonary risk,
but rarely is the optimization of nutrition management
through the perioperative period addressed. Consideration
for delay of surgery allowing for preop nutrition therapy
would be benefi cial in patients identifi ed as severely malnourished or at high nutrition risk having elective procedures with no time constraints. Unfortunately, the
appropriate duration and measures to determine suffi cient
nutrition therapy remain diffi cult to identify. Current expert
opinion recommends 10–14 days of preoperative nutrition
therapy [ 12 , 24 , 25 ].