INTRAABDOMINAL HYPERTENSION, AND
ABDOMINAL COMPARTMENT SYNDROME
Dr.Abdulgafoor.MTICU –ALKhor hospital ,HMC,Doha,Qatar
In 1863, Marie & Burt described IAP in association with
respiratory function
In 1865 Braune measured IAP through the rectum .
In 1911, Emerson demonstrated mortality in animals In 1947 Bradley published the effect of elevated IAP on
human renal function
In 1989, Kron & Iberty developed a simple method of
measuring IAP
In 1989,Fietsam coined the term Abdominal Compartment
Syndrome
In 2003,Cheetham introduced Abdominal perfusion pressure
WSACS Consensus Definitions &Recommendations
Intra abdominal pressure: Steady state pressure
concealed within abdominal cavity
Abdominal perfusion pressure:
Mean arterial pressure – Intra abdominal pressure
[MAP-IAP]Intensive care med 2006;32(11)1722-1732
Filtration gradient:
Glomerular filtration pressure proximal tubular pressure
FG = GFP-PTP = (MAP-IAP)-PTP = (MAP-IAP)-
IAP
= MAP – 2 X IAP
IAH (Intra Abdominal Hypertension)
= sustained repeated pathologic elevation of IAP > 12mmHg
NOTE: Normal IAP in critical adult patients = 5 7mm HgIntensive care med 2006;32(11)1722-1732
IAP
- Should be expressed in mm Hg
- Measured at end expiration in complete supine position
- After ensuring abdominal contractions are absent
- Transducer zeroed at mid-axillary line
- Reference standard for IAP is via urinary-bladder with
maximum instillation of 25 ml saline
- In Pediatric patients recommended volume is < 1ml/kg
Intensive care med 2006;32(11)1722-1732
Expected IAP
Normal Adult 0-5 mmHg
Typical ICU patient 5-7 mmHg
Post-laparotomy patient 10-15 mmHg
Patient with septic shock 15-25 mmHg
Patient with acute abdomen 25-40 mmHg
Intensive care med 2006;32(11)1722-1732
Grading of IAH/ACS
Abdominal Compartment
syndrome (ACS)
A sustained IAP more
than 20mmHg with or
without APP < 60mmHg
associated with one new
organ dysfunction or
failure
GRADE IAP
Grade 1 12-15 mmHg
Grade 2 16-20 mm Hg
Grade 3 21-25 mm Hg
Grade 4 > 25mmHg
Intensive care med 2006;32(11)1722-1732
CLASSIFICATION
Primary ACS = ACS associated with injury or disease in the
abdomino-pelvic region ( Trauma, Ascitis,Tumor etc )
Secondary ACS = ACS due to conditions not originated
from abdomino-pelvic regions ( Burns, sepsis, massive fluid
resuscitation etc )
Recurrent ACS = ACS developed following previous
surgical or medical treatment of primary or secondary ACS
(following damage control laprotomy & temporary abdominal
closure)Intensive care med 2006;32(11)1722-1732
Prevalence
A multicentre prospective study by Malbrain et al on 21 Dec
2000, in 13 ICU in 6 countries, with IAP cutoff >12mmHg
BMI significantly associated with IAH (P 0.001),In patients
with IAP>12 BMI 27.3+/-6.2 vs 23.8+/-3.3 in IAP<12mmhg
[Intensive care med 2004 30:822-
829]Abdominal pressure:
Total Prevalence MICU prevalence SICU prevalence
IAP > 12 58.8% 54.4% 65%
IAP > 15 28.9% 29.8% 27.5%
IAP > 20 + organ failure
8.2% 10.5% 5.0%
Incidence of IAH&ACSPopulation IAH ACS
MICU 18-78% 4-36%
SICU 32-43% 4-8%
TICU 2-50% 0.5-36%
BURNS 37-70% 1-20%
Liver Transplant 32%
PICU 0.6-0.9%
Incidence
A multicentre prospective study by Malbrain etal in
2005, in 14 ICU in 6 countries
Incidence in general critical patients 10-40%
Incidence in surgical patients 30-80%
Nonsurvivors had a higher mean IAP on admission than
survivors (11.4+/-4.8Vs9.5+/-4.8 mmHg)
Independent predictors of mortality: Age, APACHE II score,
type of admissions, presence of liver dysfunction, occurrence
of IAH during ICU stay
Critical care med 2005, 33:No;2
Causes of IAH/ACS
Spontaneous - Peritonitis, intra abdominal abscess,
Intestinal obstructions, Ruptured abdominal aortic
aneurysm, Tension pneumoperitoneum, Acute
pancreatitis, Acute mesenteric ischemia, bowel
perforation Postoperative - Peritonitis, abscess, ileus, Intra peritoneal
haemorrhage Post- traumatic - Intra-, retro-peritoneal bleeding, Post-
resuscitation visceral oedema Iatrogenic - Laparoscopic procedure, abdominal packing,
Abdominal closure under tension, endoscopic procedures
WSACS IAH/ACS assessment algorithm
Physiologic Insult
Ischemia Inflammatory response
Capillary leak
Tissue Edema (Including bowel wall and mesentery)
Intra-abdominal hypertension
Fluid resuscitation
ACS overview:www.abdominal-compartment-syndrome.org
Physiologic Sequelae
Cardiac: • Increased intra-abdominal pressures causes:
• Compression of the vena cava with reduction in venous return to the heart
• Elevated ITP with multiple negative cardiac effects• The result:
• Decreased cardiac output increased SVR• Increased cardiac workload• Decreased tissue perfusion, SVO2
• Misleading elevations of PAWP and CVP• Cardiac insufficiency Cardiac arrest
www.abdominal-compartment-syndrome.org
Physiologic Sequelae
Pulmonary: • Increased intra-abdominal pressures causes:
• Elevation of the diaphragms with reduction in lung volumes
• Cytokines release, immune hyper-responsiveness
The result:• Elevated intrathoracic pressure (which further
reduces venous return to heart, exacerbating cardiac problems)
• Increased peak pressures, Reduced tidal volumes• Barotrauma, atelectasis, hypoxia, hypercarbia• ARDS (indirect - extrapulmonary)
www.abdominal-compartment-syndrome.org
Physiologic Sequelae
Gastrointestinal:
Compression / Congestion of mesenteric veins
and capillaries
Reduced cardiac output to the gut
The result:
• Decreased gut perfusion, increased gut edema and leak
• Ischemia, necrosis, cytokine release, neutrophil priming
• Bacterial translocation
• Development and perpetuation of SIRS
• Further increases in intra-abdominal pressure
www.abdominal-compartment-syndrome.org
Physiologic Sequelae
Renal: • Elevated intra-abdominal pressure causes:
• Compression of renal veins and arteries
• Reduced cardiac output to kidneys
• Corticomedullary shunting of plasma flow
• Elevated Rennin, Aldosterone & ADH
The Result:• Decreased renal artery and vein flow
• Renal congestion and edema
• Decreased glomerular filtration rate (GFR)
• Acute tubular necrosis (ATN)
• Renal failure, oliguria/anuriawww.abdominal-compartment-syndrome.org
Physiologic Sequelae
Neuro: • Elevated intra-abdominal pressure causes:
• Increases in intrathoracic pressure
• Increases in superior vena cava (SVC) pressure with
reduction in drainage of SVC into the thorax
The Result:
• Increased central venous pressure and IJ pressure
• Increased intracranial pressure
• Decreased cerebral perfusion pressure
• Cerebral edema, brain anoxia, brain injury
www.abdominal-compartment-syndrome.org
Circling the Drain
Intra-abdominal Pressure
MucosalBreakdown
(Multi-System Organ Failure)
Bacterial translocation
Acidosis
Decreased O2 delivery
Anaerobic metabolism
Capillary leak
Free radical formation
•www.abdominal-compartment-syndrome.org
Intra-Abdominal Pressure Monitoring
• Physical examination: Inaccurate;sensitivity40-61%,positive predictive value 45-76(Can J Surg2000;43:207)
• Intraluminal bladder pressure (Indirect gold standard)
• Intragastric pressure• Rectal pressure• Uterine pressure• Inferior venacaval pressure
Folley manometer
Closed system for intravesical pressure
• Originally described by Kron& coworkers in 1984• Modified by Iberti & coworkers in 1987,Cheetham in 1998• Modified by Malbrain in 2004 as a complete closed system
Abviser Autovalve
Surgical treatment options
Decompressive laparotomy followed by
Laprostomies
On-demand relaprotomy
STAR : STaged Abdominal Repair
A rule of Thumb: When looking at the abdomen
horizontally,the gut can be seen above the level of
wound , leave the abdomen open and close temporarily.
Indian J Crit Care Med 2004;8:26-32
Decompressive Laparotomy
Delay in abdominal
decompression may
lead to intestinal
ischemia
Decompress Early!
Temporary closure techniques
(laprostomies)
• Bogota bag closure
• Towel clip closure
• Polypropylene mesh,
• Polygelatine mesh,
• Granulated vicryl mesh
• Zippers
• Vacuum assisted wound closure
Bogota bag closure• A 3 litre plastic
irrigation bag is emptied and cut open so it lies flat. The edges are trimmed and sutured to the skin, away from the skin edges, using a continuous 1 silk suture. It is useful to place a sterile absorbent drape inside the abdomen to soak up some of the fluid.
Vacuum assisted dressing(vacuum pack)
A 3L bag is placed to protect
the gut.
2 suction drains placed over
this and a large adherent
steridrape placed over
whole abdomen and
suction catheter connected
to high suction
Reperfusion syndrome
Sudden release of ACS may cause ischemia reperfusion
injury causing acidosis, vasodilatation, cardiac
dysfunction and arrest
Decompression of mesenteric vascular bed
Release of lactate, potassium
Increased production of free radicals
Exhaustion of antioxidant defense system
Translocation of bacteria sepsis MODS
Abrupt fall in SVR and filling pressures:
Hypotension, asystole
Precautions: preloading with crystalloids
Decompression cocktail
I L Normal saline :Augments preload
100 mmol Sodabicarb: Neutralizes acidosis
50 gm mannitol :Diuresis
Indian J Crit Care Med 2004;8:26-32
Does IAH / ACS affect patient outcome?
Pupelis, 2002: Clinical significance of increased intra-
abdominal pressure in severe acute pancreatitis.
37 cases of severe pancreatitis
26 cases with IAP < 25 mm Hg:
19% SIRS & MODS 0 % mortality
Mean ICU stay 9 days
11 cases with IAP > 25 mm Hg:
64% SIRS & MODS 36 % mortality
Mean ICU stay 21 days Acta Chir Belg 2002;102:72-74
Does IAH / ACS affect patient outcome?Biancofiore 2004: Intra-abdominal pressure in liver
transplant recipients: incidence and clinical significance.
Prospective observational study in 108 liver transplants• 32% developed IAP > 25 mm Hg:
• Renal failure in 32%; permanent dialysis 9%, higher mortality • 68% with IAP < 25 mm Hg:
• Renal failure 8%; permanent dialysis 0%
“The critical IAP values… with the best sensitivity specificity, were 23 mm Hg for postoperative ventilatory delayed weaning (P <.05), 24 mm Hg for renal dysfunction (P <.05), and 25 mm Hg for death (P <.01).”
ANZ surgery 2005;75(4):A1-A23
Take home message
Abdominal compartment syndrome is not just an abdominal problem,but rather,a systemic condition!
Always look for the risk factors and monitor IAP in high risk group.
Focus on the APP as the therapeutic endpoint
This is a field of ongoing research
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