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