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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_1611_Библиотеки_им_академика_М_И_Перельмана.pdf
41
Primary IAH/ACS (formerly termed surgical or abdominal IAH/ACS) is “a condi-
tion associated with injury or disease in the abdominopelvic region that may require
surgical or radiological intervention or stabilization.” Common examples of condi-
tions leading to primary ACS include severe acute pancreatitis, abdominal trauma
(with spleen or liver rupture), or ruptured abdominal aortic aneurysms.
Secondary IAH/ACS (formerly termed medical or extra-abdominal IAH/ACS)
refers to “a condition that does not originate in the abdominopelvic region.” Cases
with secondary ACS typically develop as a result of a capillary leak syndrome (sec-
ondary to sepsis, infection or inammation, major burns, or other causes) and other
conditions requiring massive uid resuscitation (e.g., vascular extremity injury).
Recurrent IAH/ACS (previously termed tertiary IAH/ACS) is characterized by
redevelopment of IAH/ACS following surgical (e.g., decompressive laparotomy) or
medical minimally invasive (e.g., percutaneous catheter drainage) treatment of
IAH/ACS.
3.4 Risk Factors Related toAbdominal Hypertension
The C
ab
is one of the most neglected parameters in critically ill patients; however, it
plays a very important role in understanding the deleterious effects of unadapted
IAV on IAP and end-organ perfusion [17]. Measurement of C
ab
is difcult at the
bedside and can only be done in case of a known change (removal or addition) in
IAV. Nevertheless, some indirect measures of C
ab
are available in critically ill
patients that are mechanically ventilated: the ∆IAP (= IAP at the end of inspiration
minus the IAP at the end of expiration) and the abdominal pressure variation (APV
= ∆IAP divided by mean IAP) are such parameters, and they are inversely corre-
lated with C
ab
, i.e., the higher ∆IAP or APV, the lower C
ab
. As stated, true C
ab
can
only be measured in case of addition or removal of a known abdominal volume
(e.g., during laparoscopic insufation, paracentesis, gastric aspiration, etc.) with
simultaneous measurement of the change in IAP. Therefore, if we could identify
patients with a low C
ab
, we could anticipate and select the most appropriate surgical
treatment in order to avoid possible complications related to IAH/ACS.Theoretically
C
ab
not only allows prediction of complications during laparoscopy or mechanical
ventilation, but it also allows identication of patients that would benet from leav-
ing their abdomen open, those in whom to monitor IAP, or those at risk during prone
ventilation, etc. The risk factors for IAH and ACS can be classied into those
decreasing abdominal compliance, those increasing intra-abdominal or intraluminal
contents, and those related to capillary leak and uid overload [22]. Table3.2 lists
some common conditions related to increased IAP.Aside from risk factors for IAH,
patients should also be screened for risk factors for decreased C
ab
(Table3.3).
3 Anatomy andPhysiology oftheAbdominal Compartment
42
3.5 Epidemiology
The reported incidence of IAH ranges between 21 and 58%, while for ACS it ranges
between 1 and 12% among general ICU patients [4–6]. Potential explanations for
heterogeneity in reported incidence and prevalence estimates across studies include
differences in recruited patient samples, differences in IAH grading and classica-
tion, and differences in IAP measurement techniques. A recent individual patient
data meta-analysis of 1669 adult general ICU patients reported that 27.7% had IAH
and 2.7% had ACS (as dened by the WSACS) at ICU admission [6]. When com-
pared to mixed populations of adult ICU patients, trauma and emergency general
surgery patients and those with ruptured AAAs, severe acute pancreatitis, and burns
appear to have a substantially higher incidence and prevalence of IAH and ACS [25,
26]. In a study by Vidal and colleagues, 53% of trauma and emergency surgery
Table 3.2 Risk factors associated with increased IAP (adapted from Malbrain etal. [11] with
permission)
A.Related to increased intra-abdominal contents
– Gastroparesis
– Gastric distention
– Ileus
– Volvulus
– Colonic pseudo-obstruction
– Abdominal tumor
– Retroperitoneal/ abdominal wall hematoma
– Enteral feeding
– Intra-abdominal or retroperitoneal tumor
– Damage control laparotomy
B.Related to abdominal collections of uid, air, or blood
– Liver dysfunction with ascites
– Abdominal infection (pancreatitis, peritonitis, abscess, etc.)
– Hemoperitoneum
– Pneumoperitoneum
– Laparoscopy with excessive ination pressures
– Major trauma
– Peritoneal dialysis
C.Related to capillary leak and uid resuscitation
– Acidosis
a
(pH below 7.2)
– Hypothermia
a
(core temperature below 33°C)
– Coagulopathy
a
(platelet count below 50,000/mm
3
OR an activated partial thromboplastin time
(APTT) more than two times normal OR a prothrombin time (PTT) below 50% OR an
international standardized ratio (INR) more than 1.5)
– Polytransfusion/trauma (>10 units of packed red cells/24 h)
– Sepsis (as dened by the American–European Consensus Conference denitions)
– Severe sepsis or bacteremia
– Septic shock
– Massive uid resuscitation (>5L of colloid or >10L of crystalloid/24 h with capillary leak
and positive uid balance)
– Major burns
a
The combination of acidosis, hypothermia, and coagulopathy has been forwarded in the literature
as the deadly triad [23, 24]
M.L.N.G. Malbrain et al.
43
patients developed IAH, while more than 12% developed ACS during their ICU stay
[27]. Another study of patients with major torso trauma-related hemorrhagic shock
requiring massive uid resuscitation reported a 13% incidence of ACS [28]. The
Table 3.3 Factors associated
with decreased abdominal
compliance (adapted from
Malbrain etal. [11] with
permission)
A. Related to anthropomorphy and
demographics
• Male gender
• Youngage (goodelastic recoil)
• Obesity (weight, BMI)
• Android composition (sphere, apple shape)
• Increased visceral fat
• Waist-to-hip ratio > 1
• Short stature
B. Related to comorbidities and/or increased
noncompressible IAV
• Fluid overload
• Bowels lled with uid
• Stomach lled with uid
• Tense ascites
• Hepatomegaly
• Splenomegaly
• Abdominal uid collections, pseudocyst,
abscess
• Sepsis, burns, trauma, and bleeding
(coagulopathy)
C. Related to abdominal wall and diaphragm
• Umbilical hernia repair
• Muscle contractions (pain)
• Body builders (six pack)
• Interstitial and anasarca edema (skin,
abdominal wall)
• Abdominal burn eschars (circular)
• Thoracic burn eschars (circular)
• Tight closure after abdominal surgery
• Abdominal Velcro belt or adhesive drapes
• Prone positioningand prone ventilation
• HOB > 45°
• Pneumoperitoneum
• Pneumatic anti-shock garments
• Abdominal wall bleeding
• Rectus sheath hematoma
• Correction of large hernias
• Gastroschisis
• Omphalocele
• Mechanical ventilation (positive pressure)
• Fighting with the ventilator
• Use of accessory muscles
• Use of positive end-expiratory pressure
(PEEP)
• Presence of auto-PEEP (tension
pneumothorax)
• COPD emphysema (diaphragm attening)
• Basal pleuropneumonia
3 Anatomy andPhysiology oftheAbdominal Compartment
44
incidence of IAH/ACS among patients with burns is correlated with the volume of
crystalloids infused during resuscitation and the total percentage of burned surface
area (TBSA) [29, 30]. Even in severe burn patients without abdominal injury or
surgery or even in those without abdominal wall burn eschars, IAH and ACS can
still develop during the course of the disease [29, 30]. Patients with very extensive
burns above 50% TBSA or higher are most likely to develop IAH/ACS, particularly
if they have concurrent inhalational injury [26].
3.6 Abdominal Pressure Measurement
The WSACS recommends measuring IAP “when any known risk factor for IAH/
ACS is present in a critically ill or injured patient” [3]. Because of the uidlike
nature of the abdomen following Pascal’s law, the IAP can be measured in nearly
every body part: rectal, uterine, inferior vena cava, femoral vein, bladder, and gas-
tric pressure measurements have all been described and suggested as IAP surrogates
or estimates, one even better than the other [31]. As stated before, the use of direct
intraperitoneal pressure measurement cannot be advocated in patients because of
the complication risks (bleeding, infection) and should only be used in an experi-
mental setting or when combined with uid drainage (paracentesis). A recent study
concluded that femoral vein pressure (FVP) cannot be recommended as a surrogate
measure for IAP even at IAP values above 20 mmHg. However, an elevated FVP
was a good predictor of IAH.Over the years, bladder pressure measurements have
been forwarded as the gold standard technique [3]. Figure3.1 shows a homemade
device for repeated IAP measurements via the bladder. As shown in Fig.3.2, inter-
mittent screening for IAH can be performed by measuring the height of the urine
column as a cost-effective estimate for IAP (with the FoleyManometer, Holtech
Medical, Charlottenlund, Denmark or the UnoMeter AbdoPressure, Convatec,
Greensboro, North Carolina, USA) [33].
3.7 Pathophysiologic Implications ofIncreased IAP
Being linked and bound by the diaphragm, the thoracic and abdominal compartment
cannot be seen in isolation. As stated above, Haven Emerson conducted numerous
experiments in dogs showing that the contraction of the diaphragm is the main fac-
tor causing the rise in IAP during inspiration [9]. Changes in IAP are paralleled by
changes in pleural pressures. Changes in thoracic compliance are reected by
changes in abdominal compliance and vice versa; as a consequence, increased IAP
will result in reduced chest wall compliance. The interactions between different
body compartments have been referred to as the polycompartment model and syn-
drome [7, 34]. For instance, transmission of airway pressures to the abdomen results
from interactions between the thoracic and abdominal compartment, and the per-
centage of pressure transmission is called the thoracoabdominal index (TAI) of
transmission. This occurs in patients under positive pressure ventilation, application
M.L.N.G. Malbrain et al.
45
of positive end-expiratory pressure (PEEP), presence of intrinsic or auto-PEEP, or a
tension pneumothorax. Conversely transmission of pressure from the abdomen to
the thorax is called abdomino-thoracic index of transmission (ATI), and this occurs
in any physiologic (pregnancy) or pathologic condition associated with increased
IAP.The ATI ranges from 20 to 80% and is on average 50% [35]. The knowledge of
these interactions help us to understand the cardiorespiratory dynamics of patients
with IAH/ACS.As a rule of thumb, transmural CVP (CVP
tm
) can be calculated as
follows based on the end-expiratory value (CVP
ee
): CVP
tm
= CVP
ee
− (IAP × ATI).
The interactions between compartments are not only dependent on the specic elas-
tance of the different components but also on baseline pressures within the different
compartments. Increased IAP has a two-sided effect: the abdominal wall is moved
outward (abdominal extension), and the gaseous contents of hollow organs within
the abdominal cavity are compressed inward since gas is compressible, while uid
Fig. 3.1 Modied method for intrabladder pressure monitoring (adapted from Desie etal. [32]
with permission)
- Wash hands and follow universal antiseptic precautions
Set-Up:
Method of measurement:
A Foley catheter is placed under sterile conditions and the urinary drainage system connected.
Using a sterile field and gloves, the drainage tubing is cut (with sterile scissors) 40cm after the culture
aspiration port after desinfection.
A ramp with 3 stopcocks is connected to a conical connection piece at each side with a male/male
adaptor.
The ramp is then inserted in the drainage tubing.
A standard intravenous (IV) infusion set is connected to a bag of 500mL of normal saline or D5W and
attached to the first stopcock.
A 60-mL syringe is connected to the second stopcock and the third stopcock is connected to a pressure
transducer via rigid pressure tubing.
The system is flushed with normal saline
The pressure transducer is fixed at the symphysis or the thigh.
Connect the transducer to the monitor via the special pressure module and ensure a normal waveform
on the scope.
Select a scale from 0 to 20 or 40 mmHg
If the patient is awake, explain the procedure.
If the patient is sedated, ensure good sedation.
Place the patient in a complete supine position.
Zero the pressure module at the midaxillary line of the patient at the level of the iliac crest (mark for
future reference) by turning the proximal stopcock on to the air and the transducer
At rest the 3 stopcocks are turned “off” to the IV bag, the syringe and transducer giving an open way for
urine to flow into the urometer or drainage bag, said otherwise the 3 stopcocks are turned “on” to the
patient.
To measure IBP, the urinary drainage tubing is clamped distal to the ramp-device and the third stopcoc
k
is turned “on” to the transducer and the patient and “off” to the drainage system.
The third stopcock also acts as a clamp.
The first stopcock is turned “off” to the patient and “on” to the IV infusion bag, the second stopcock is
turned “on” to the IV bag and the 60-mL syringe.
Aspirate 20-25ml of normal saline from the IV bag into the syringe.
The first stopcock is turned “on” to the patient and “off” to the IV bag and the 20-25ml of normal saline
is instilled in the bladder through the urinary catheter.
The first and second stopcock are then turned “on” to the patient, and thus turned “off” to IV tubing and
the syringe.
The third stopcock already being turned “on” to the transducer and patient allows then immediate IBP
reading on the monitor.
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
3 Anatomy andPhysiology oftheAbdominal Compartment
46
is not. The effects of increased IAP on end-organ function are numerous: neuro-
logic, respiratory, cardiovascular, hepatic, and renal adverse effects have all been
described in patients with IAH and ACS [7, 36–39]. Increased IAP leads to organ
dysfunction of all abdominal organs due to arterial blood ow limitation, venous
outow obstruction (diminished venous return to the heart), and impaired microcir-
culatory ow, necessitating more uid loading, causing mesenteric vein compres-
sion and venous hypertension, and nally triggering a vicious cycle. Kidney failure
is the most often and consistently described organ failure associated with IAH, but
hepatic, adrenal, and gastrointestinal dysfunctions have also been reported repeat-
edly. It is especially important to note that IAH can lead to increased bacterial trans-
location lending truth to the statement “the gut is the motor of sepsis.” Figure3.3
illustrates the different deleterious effects of increased IAP on end-organ function.
IV infusion bag
to
monitor
Pressure
transducer
Pressure
tubing
Urine
drainage
Ramp with 3 stopcocks
123
Normal
tubing
Foley
catheter
60 mL
syringe
Fig. 3.1 (continued)
M.L.N.G. Malbrain et al.
47
Fig. 3.2 Intrabladder pressure monitoring with the FoleyManometerLV (adapted from Desie etal.
[32] with permission)
This technique that uses the patient’s own urine as pressure transmitting medium is a surprisingly simple, reliable,
and cost-effective clinical tool. Based on a modified version of the IAP monitoring technique described by Kron et
al. (40), the disposable FoleyManometer (or UnoMeter AbdoPressure) provides a closed sterile circuit which
connects between the patient´s Foley catheter and the urine collection device. Each IAP determination takes about
10 seconds, and no subsequent correction of urine output is required. The technique uses a low bladder infusion
volume, has a needle-free sampling port and can measure IAP in a range from 0 - 40 mmHg. Therefore, it is an
ideal technique to screen critically ill patients for IAH.
- Open the FoleyManometer LV (Holtech Medical, Charlottenlund, Denmark, www.holtech-medical.com) or
UnoMeter AbdoPressure (Convatec, Greensboro, North Carolina, USA) pouch and close the tube clamp
- Place the urine collection device under the patient's bladder and tape the drainage tube to the bed sheet.
- Insert the FoleyManometer between catheter and drainage device.
- Prime the FoleyManometer with 20ml of sterile saline through its needle-free injection/sampling port.
- Prime only once i.e. at initial set-up, or subsequently to remove any air in the manometer tube.
PANEL A, Initial set-up:
3 Anatomy andPhysiology oftheAbdominal Compartment
48
- Let the urine drain in between IBP measurements
- Urine sampling from the needle-free port is facilitated by temporarily opening the red clamp. Remember
to close clamp afterwards.
- Avoid a U-bend of the large urimeter drainage tube (which will impede urine drainage).
- Replace the FoleyManometer whenever the Foley catheter or the urine collection device is replaced, or at
least every 7 days.
- Place the "0 mmHg" mark of the manometer tube at the midaxillary line at the level of the iliac crest
(mark for future reference) and elevate the filter vertically above the patient.
- Open the bio-filter clamp, and read IBP (end-expiration value) when the meniscus has stabilized after
about 10 seconds.
- Close clamp after IBP measurement and place the FoleyManometer in its drainage position.
PANEL B, Urine drainage
PANEL C, Intravesical pressure Monitoring
:
40 mmHg
IVP
zero
reference
Fig. 3.2 (continued)
M.L.N.G. Malbrain et al.
49
CARDIOVASCULAR SYSTEM
1
Difficult preload assessment
Pulmonary artery occlusion pressure
PAOP
Central venous pressure
Transmural filling pressure =
Intra thoracic blood volume index
Global end-diastolic blood volume
index =
=
Extra vascular lung water =
Stroke volume variation
Pulse pressure variation
Right ventricular end-diastolic
volume =
Cardiac output
Venous return
Systemic vascular resistance
Venous thrombosis
Pulmonary embolism
Heart rate =
Mean arterial pressure
=
Pulmonary artery pressure
Left ventricular compliance
Left ventricle regional wall motion
HEPATIC SYSTEM
Hepatic arterial flow
Portal venous blood flow
Porto-collateral flow
Lactate clearance
Glucose metabolism
Mitochondrial function
Cytochrome p450 function
Plasma disappearance rate
Indocyanine green
GASTRO-INTESTINAL SYSTEM
Abdominal perfusion pressure
Celiac blood flow
Superior mesenteric artery blood flow
Blood flow to abdominal organs
Mucosal blood flow
Mesenteric vein compression
Intramucosal pH
Regional CO2
CO2-gap
Success enteral feeding
Intestinal permeability
Bacterial translocation
Multiple organ failure
Intestinal ulcer (re)bleeding
Variceal wall stress
Variceal (re)bleeding
Peritoneal adhesions
1
Cardiovascular effects are exacerbated
in case of hy
povolemia, hemorrhage,
ischemia and high PEEP ventilation
RESPIRATORY SYSTEM
Intrathoracic pressure
Pleural pressure
Functional residual capacity
All lung volumes
(~restrictive disease)
Auto-PEEP
Peak airway pressure
Plateau airway pressure
Dynamic compliance
Static respiratory system
compliance
Static chest wall compliance
Static lung compliance =
Hypercarbia
PaO2 and PaO2/FiO2
Dead-space ventilation
Intrapulmonary shunt
Lower inflection point
Upper inflection point
Extra vascular lung water =
Prolonged ventilation
Difficult weaning
Activated lung neutrophils
Pulmonary inflammatory infiltration
Alveolar edema
Compression atelectasis
RENAL SYSTEM
Renal perfusion pressure
Filtration gradient
Renal blood flow
Diuresis
Tubular dysfunction
Glomerular filtration rate
Renal vascular resistance
Renal vein compression
Ureteral Compression
Anti-diuretic hormone
Adrenal blood flow =
Abdominal wall complications in
CAPD
ABDOMINAL WALL
Compliance
Rectus sheath blood flow
Wound complications
Incisional hernia
ENDOCRINE SYSTEM
Release pro-inflammatory cytokines
(IL-1b, TNF-a, IL-6)
CENTRAL NERVOUS SYSTEM
Intracranial pressure
Cerebral perfusion pressure
Idiopathic intracranial hypertension
in morbid obesity
Fig. 3.3 Pathophysiology of intra-abdominal hypertension
3 Anatomy andPhysiology oftheAbdominal Compartment
50
Conclusions
Although considerable progress relating to IAH and ACS has been made over the
last decades, there is still a general lack of clinical awareness. With our presently
improved understanding of the pathophysiology and epidemiology, future efforts
should be largely focused on dening whether targeted or multifaceted interven-
tions aimed at reducing IAP improve patient-important outcomes. The C
ab
is one
of the most neglected parameters in critically ill patients, although it plays a key
role in understanding the deleterious effects of unadapted IAV on IAP and end-
organ perfusion. If we can identify patients with low C
ab
, we can anticipate and
select the most appropriate medical or surgical treatment option to avoid delete-
rious complications like ACS.
Acknowledgments Dr. MLNG Malbrain is the founding president of WSACS and current trea-
surer; he is a member of the medical advisory board of Pulsion Medical Systems (Maquet Getinge
group), a monitoring company, and consults for KCI, ConvaTec, and Holtech Medical. He is also
a member of the Executive Committee of the International Fluid Academy, an online educational
platform adhering to the FOAM principles (Free Open Access Medical Education, www.uidacad-
emy.org), and part of the not-for-prot organization iMERiT (International Medical Education and
Research Initiative). The other authors have no potential conicts of interest.
Key Messages
1. The diagnosis of IAH/ACS relies on accurate IAP measurement. The cur-
rent gold standard for IAP measurement is intermittently every 4–6 h via
the bladder, using no more than 25 mL of instillation volume, in the com-
plete supine position, using the midaxillary line as a zero reference point
where it crosses the iliac crest.
2. There are many risk factors in relation to IAH, and they can be classied
into those decreasing abdominal compliance, those increasing intra-
abdominal or intraluminal contents, and those related to capillary leak and
uid overload.
3. IAP monitoring should be performed in all critically ill or injured patients
exhibiting one or more risk factors for the development of IAH and contin-
ued until risk factors are resolved and IAP has remained normal for 24–48 h.
4. The incidence of IAH is around 21–58%, and the incidence of ACS is around
1–12% in critically ill patients, depending on the patient population.
5. The abdominal compliance is the most neglected parameter in critically ill
patients although it plays a major role in understanding the deleterious
effects of unadapted IAV on IAP and end-organ perfusion.
6. IAH and ACS cause organ dysfunction through direct compression of the
heart, compression of both arterial and venous perfusion of the abdominal
organs, and abdomino-thoracic pressure transmission. All organ systems
in the human body are affected by IAH.
M.L.N.G. Malbrain et al.