1. Abdominal Compartment Syndrome in Trauma
David Chow
Supervisors: Dr KC Chan, Dr KW Chan

2. Important message
Abdominal compartment syndrome (ACS) is a clinical condition in which elevated intraabdominal pressure (IAP) leads to impaired end-organ perfusion of the viscera and kidneys causing gut ischaemia and renal insufficiency. (Not limited to traumatic injury)
Ultimate result is multiple system organ dysfunction and death if not appropriately diagnosed and treated.

4. What is IAP? Intra-abdominal pressure (IAP)
- the steady-state pressure concealed within the abdominal cavity
- include: abdominal organs volume; space occupying lesions (blood, fluid, tumor); abdominal wall compliance
Abdomen as a closed box
Elasticity and its contents determine the pressure within the abdomen (content: solid organs, hollow viscera, ascites, blood, SOL)
IAP varies with respiration: increases with inspiration when the diaphragm goes downwards; decreases with expiration

5. What is APP? Abdominal perfusion pressure (APP)
- analogous to cerebral perfusion pressure
- APP = MAP – IAP
- a target APP of at least 60mmHg for improved survival from ACS
Think of cerebral perfusion pressure;
The abdominal wall as a rigid box which contains the solid organs and blood
APP, by considering both arterial inflow (MAP) and restrictions to venous outflow (IAP), has been demonstrated to be statistically superior to either parameter alone in predicting patient survival from IAH and ACS.
A target APP of at least 60mmHg has been demonstrated to correlate with improved survival from ACS.
When there is increase in IAP (i.e. intra-abdominal pressure), there is decrease in abdominal perfusion pressure (APP). When there is much increase in IAP, the APP will decrease to such a level leading to the detrimental effect of abdominal compartment syndrome.
MAP = DBP + 1/3 (SBP – DBP)

6. Filtration gradient (FG)
= glomerular filtration pressure (GFP) – proximal tubular pressure (PTP)
FG=GFP-PTP=MAP-2xIAP (at IAH)
Inadequate renal perfusion pressure and renal FG as key cause of IAP induced renal failure
Oliguria is one of the first visible signs of elevated IAP
FG is the mechanical force across the glomerulus and equals the difference between glomerular filtration pressure and the proximal tubular pressure.
In IAH, PTP = IAP and therefore, GFP can be estimated as MAP – IAP

7. IAP measurement Various methods have been proposed for IAP measurement
the most widely accepted one was by intra-vesicular pressure.
An objective IAP measurement is important: (NOT by physical exam nor clinical judgement); so as to prevent development of abdominal compartment syndrome.
A variety of techniques may be used to measure IAP:
e.g. needle puncture of abdomen during peritoneal dialysis or laparoscopy
transduction of intravesicular/bladder, gastric, colonic or uterine pressure via balloon catheter)
IVC pressure
“The bladder technique” is most widely used because of its simplicity, safety and minimal cost.
Pitfalls:
gastric distension, neurogenic bladder, compression from pelvic haematoma or packing and preexisting intraabdominal hypertension secondary to obesity, ascites and pregnancy
contraidications: bladder trauma

8. Bladder pressure measurement
A closed, needle free system
Does not increase the risk of UTI
1mmHg = 1.36mmH2O
A closed, needle-free system for measurement of intravesicular
pressure. Normal saline (1,000 mL), a 60-mL Luer lock
syringe, and a segment of pressure tubing are attached to a disposable
pressure transducer connected to two stopcocks. An 18-gauge
angiocatheter is inserted into the culture aspiration port of the
urinary drainage tubing and the needle removed leaving the plastic
infusion catheter in place. The infusion catheter is connected to the
pressure tubing and the system flushed with normal saline. The
infusion catheter may be taped to the urinary drainage tubing for added security
The reference standard for intermittent IAP measurement is via the bladder with a maximal instillation volume of 25ml sterile saline

9. IAP Measurement standard
In mmHg
Supine
End-expiration
Transducer zeroed at mid-axillary line
Instillation volume of no greater than 25ml NS
30-60 seconds after instillation of priming fluid (to allow bladder detrussor muscle relaxation)
Absence of abdominal muscle contraction
Just to highlight that there is a global reference standard in measurement of IAP by intravesicular pressure measurement method so as to ensure consistent IAP result

10. Normal IAP
> 15mmHg can cause significant end- organ dysfunction, failure and patient death
Normal adult
0-5mmHg
Typical ICU patient
5-7mmHg
Post-laparotomy patient
10-15mmHg
Patient with septic shock
15-25mmHg
Patient with acute abdomen
25-40mmHg

11. Intra-abdominal hypertension (IAH)
Sustained or repeated pathological elevation in IAP >=12mmHg
Most clinicians concerned only when IAP exceeds 20-25mmHg
Grade I
IAP mmHg
Grade II
IAP mmHg
Grade III
IAP mmHg
Grade IV
IAP > 25 mmHg
The more severe the degree of IAH the more urgent is the need for decompression of the abdomen (by either medical or surgical methods) with resolution of the damaging pressure

12. Abdominal Compartment Syndrome (ACS)
Sustained IAP > 20mmHg (with or without an APP <60mmHg) that is associated with new organ dysfunction/failure
i.e. ACS = IAH + organ dysfunction
ACS as the natural progression of these pressure-induced end-organ changes and develops if IAH is not recognized and treated in a timely manner

14. Signs of ACS Abdominal distension
Oliguria refractory to volume administration
Elevated ICP
Hypercarbia
Hypoxemia refractory to increasing FiO2 and PEEP
Refractory metabolic acidosis

15. Pathophysiology
ACS has detrimental effect to whole body, involving all body systems
CVS – cephalad deviation of diaphragm; reduce venous return and reduce cardiac output
RS – increase intrathoracic pressure resulting in extrinsic compression of lung and leads to pulmonary dysfunction
Renal – renal artery blood flow has been demonstrated to be preferentially diminished in comparison to both celiac and superior mesenteric artery blood flow in elevated IAP
GI – reduction of mesenteric blood flow leading to bowel ischaemia, metabolic acidosis, in turn causing edematous bowel and further aggravate the IAP
CNS – can increase ICP and therefore decrease CPP
Adapted from “ Abdominal Compartment Syndrome: pathophysiology and definitions” by Michael L Cheatham 2009.

16. Primary ACS
Primary ACS is a condition associated with injury or disease in the abdominopelvic region that frequently requires early surgical or interventional radiological intervention.
E.g. traumatic injury, ascites/fluid, abdominal tumor

17. Secondary ACS
Secondary ACS refers to condition that do not originate from the abdominopelvic region.
E.g. sepsis/capillary leak, burns, massive resuscitation

18. Recurrent ACS
Recurrent ACS refers to the condition in which ACS redevelops following previous surgical or medical treatment of primary or secondary ACS

19. How often does ACS/IAH occur?
IAH is quite common but under-diagnosed in ICU.
Incidence and prognosis of intraabdominal hypertension in a mixed population of critically ill patients: A multiple-center epidemiological study*
Critical Care Medicine 2005
Incidence and prognosis of intraabdominal hypertension in a mixed population of critically ill patients: A multiple-center epidemiological study*
Manu L. N. G. Malbrain, MD; Davide Chiumello, MD; Paolo Pelosi, MD, PhD; David Bihari, MD; Richard Innes, MD;
V. Marco Ranieri, MD, PhD; Monica Del Turco, MD; Alexander Wilmer, MD, PhD; Nicola Brienza, MD; Vincenzo Malcangi, MD;
Jonathan Cohen, MD; Andre Japiassu, MD; Bart L. De Keulenaer, MD; Ronny Daelemans, MD; Luc Jacquet, MD, PhD;
Pierre-François Laterre, MD, PhD; Günther Frank, MD; Paulo de Souza, MD; Bruno Cesana, MD;
Luciano Gattinoni, MD, PhD
Critical Care Medicine 2005 Vol. 33 No.2
A total number of 265 consecutive patients were included in the study involving 14 ICU in 6 countries within 4 weeks study period.
Within these patients, 140 patients had a normal IAP (<12mmHg) [67.9%], 85 patients had IAH >12mmHg [32.1%] and 11 patients had ACS [4.2%]

20. Risk factors for IAH/ACS
Diminished abdominal wall compliance
e.g. trauma/burn, high BMI, central obesity, tight closure after abdominal surgery
Increased intra-abdominal contents
e.g. gastroparesis, ileus, IO
Increased abdominal contents
e.g. hemo/pnuemoperitoneum, ascites
Capillary leak / Fluid resuscitation
e.g. acidosis, coagulopathy, pancreatitis, sepsis, etc. I

21. If two or more risk factors for IAH/ACS are present, a baseline IAP measurement should be obtained.
If IAH is present (i.e. sustained IAP > 12mmHg), serial IAP measurement should be performed throughout the patient’s critical illness.

22. IAH/ACS management Four principles: - serial monitoring of IAP
- optimization of systemic perfusion and organ function
- institution of specific medical interventions to reduce IAP
- prompt surgical decompression for refractory IAH

23. IAH/ACS Management
While surgical decompression is commonly considered the only treatment, non-operative medical management strategies play a vital role in the prevention and treatment of IAH-induced organ dysfunction and failure.

24. Medical treatment options
Improve abdominal wall compliance
- Neuromuscular blockade
- sedation and analgesia
- avoid head of bed > 30 degrees
Evacuate intra-abdominal contents
Evacuate abdominal fluid collections
Correct positive fluid balance
- avoid excess fluid resuscitation
Organ support
A brief trial of NMB may be considered in selected patients with mild to moderate IAH while other interventions are performed to reduce IAP
NMB is unlikely to be an effective therapy for patients with severe IAH or the patient who has already progressed to ACS
No prospective trials have been performed evaluating the benefits and risks of sedation and analgesia in IAH/ACS
(pain/agitation can increase abdominal muscle tone)
Organ support:
Maintain APP >= 60mmHg with vasopressors
Optimize ventilation, avelolar recruitment

26. Surgical abdominal decompression
Immediate decompressive laparotomy reduces IAP and restores systemic perfusion
Appropriate for patients with ACS refractory to less invasive treatments
Should not be delayed until organ failure is irreversible

27. Surgical decompression should be performed in patients with ACS that is refractory to other treatment options
Presumptive decompression should be considered at the time of laparotomy in patients who demonstrate multiple risk factors for IAH/ACS

30. ACS in trauma
Although there can be different reasons leading to the development of ACS, the most common scenario of ACS is after major abdominal trauma.

31. Incidence Study conducted in Zurich in 2000:
17 patients out of 311 patients with severe abdominal and/or pelvic trauma developed ACS
Incidence and clinical pattern of the abdominal compartment syndrome after “damage-control” laparotomy in 311 patients with severe abdominal and/or pelvic trauma
Wolfgang Ertel, MD; Andreas Oberholzer, MD; Andreas Platz, MD; Reto Stocker, MD; Otmar Trentz, MD
Critical Care Medicine 2000
Incidence and clinical pattern of the abdominal compartment
syndrome after “damage-control” laparotomy in 311 patients with
severe abdominal and/or pelvic trauma
(retrospective analysis)
Wolfgang Ertel, MD; Andreas Oberholzer, MD; Andreas Platz, MD; Reto Stocker, MD; Otmar Trentz, MD(retrospective analysis)
Critical Care Medicine 2000 Vol 28 No.6
A total of 311 patients with severe abdominal and/or pelvic trauma and “damage-control” laparotomy on day of admission:
17 of them (5.5%) developed ACS because of persistent intra-abdominal/retroperitoneal bleeding or visceral edema.

32. Damage control surgery in trauma
Deadly Triad of trauma patient: Coagulopathy, hypothermia and metabloic acidosis
Basic principles
Control haemorrhage
Prevent contamination
Avoid further injury
The deadly triad: hypothermia, coagulopathy and metabolic acidosis.
Once established, it will form a viscous cycle and is difficult to overcome.
The central tenet of damage control surgery is that patients die from a triad of coagulopathy, hypothermia and metabolic acidosis. Once this metabolic failure has become established it is extremely difficult to control haemorrhage and correct the derangements. If the patient is to survive the operation must be foreshortened so that they can be transferred to a critical care facility where they can be warmed and the hypothermia and acidosis is corrected. Once this is achieved the definitive surgical procedure can be carried out as necessary - the 'staged procedure'

33. Peritoneal packing

34. After damage control surgery in trauma patient
Massive intestinal edema
Intra-abdominal packing
Retroperitoneal haematoma
Leading to increasing IAP
If tight closure of abdominal wound made, may lead to ACS!!
Massive intestinal oedema often follows laparotomy for major tra uma where there has been prolonged shock. Crystalloid resuscitation, capillary leakage due to activated inflammatory mediators and reperfusion injury all contribute to this tissue swelling. Combined with intra-abdominal packing or retroperitoneal haematomas this may render the abdomen difficult or impossible to close. If the abdomen is closed, intra-abdominal pressure may rise to a level (>25 cmH2O) where it leads to significant cardiovascular, respiratory, renal and cerebral dysfunction.

35. To tackle the problem
Let the abdominal wound open!! (The need for temporary closure and staged re-operation)
Absorbable mesh closure
Plastic IV bag closure
Vacuum pack dressing
Wittmann patch
KCI VAC dressing
Only perform temporary abdominal closure!

36. Absorbable mesh closure
• Absorbable mesh is used to create a temporary
abdominal wall preventing evisceration
• Mesh may be removed after 7-10 days and
primary abdominal wall closure performed
• May also be left in place long-term with split
thickness skin grafting following sufficient
granulation
• Graft can be excised and ventral hernia repaired
9-12 months later

37. Plastic IV (BOGOTA) Bag closure
• Uses plastic sheeting to create a temporary
abdominal wall
– 3 liter IV bag split on three sides
– plastic X-ray cassette cover
– Silastic sheeting
• Sewn to skin or fascia; covered by occlusive drape
to prevent fluid loss
• Abdominal contents can be viewed
–Useful in patients with ischemic bowel

38. Vacuum Pack closure A common method for managing the open abdomen
• Allows the abdominal contents
to expand without increasing IAP
• Allows third-space fluid to be
suctioned off
• Inexpensive
• Necessary materials available in
any hospital
• Easily changed at the bedside

39. KCI VAC dressing A commercially available device
which uses continuous suction
to effect a “vacuum-assisted
closure” of the abdominal wall

40. The need for re-operation
For removal of clots and abdominal packs
Complete inspection of any missed injuries
Restoration of intestinal integrity
Proper abdominal wound closure
The principles of reoperation are removal of clots and abdominal packs, complete inspection of the abdomen to detect missed injuries, haemostasis and restoration of intestinal integrity and abdominal wound closure.
Timing of reoperation is critical. There is usually a window of opportunity between correction of metabolic failure and the onset of the systemic inflammatory response syndrome and multiple organ failure. This window usually occurs at hours after the first procedure. There is a tradeoff between earlier re-operation, when the patient may be less stable and bowel-well oedema marked, and delaying the procedure to a point where cardiovascular, respiratory and renal failure make the procedure hazardous. Vascular shunts should be removed and grafts inserted at the earliest opportunity as these may dislodge or clot once coagulopathy is corrected. If packs are left in the abdomen it is generally recommended that these are removed at hours, although there is little evidence to suggest that leaving them longer is detrimental.\
Trauma.org

41. Postinjury Primary Abdominal Compartment Syndrome

42. What is the role of intensive care?
Prevent the occurrence of the deadly triad: metabolic acidosis, hypothermia and coagulopathy
Prevention of abdominal compartment syndrome
Serial monitoring of IAP
Early detection of risk factors and signs of ACS/IAH
Consult surgeon for consideration of abdominal decompression if persistent IAP with impending organ failure

43. Independent predictors for mortality in IAH
IAH during ICU admission
Age
APACHE II score
Type of intensive care admission
Presence of liver dysfunction
Malbrain ML, Chiumello D, Pelosi P, Bihari D, Innes R, Ranieri M, Del Turco M, Wilmer A, Brienza N, Malcangi V, Cohen J, Japiassu A, De Keulenaer BL, Daelemans R, Jacquet L, Laterre PF, Frank G, Souza P, Cesana B, Gattinoni L. Incidence and prognosis of intraabdominal hypertension in a mixed population of critically ill patients: A multiple-center epidemiological study. Crit Care Med 2005;33:315-22

44. References
Results from the International Conference of Experts on Intra- abdominal Hypertension and Abdominal Compartment Syndrome. I. Definitions.Malbrain ML et al. Intensive Care Med. (2006)
Results from the International Conference of Experts on Intra- abdominal Hypertension and Abdominal Compartment Syndrome. II. Recommendations.Cheatham ML et al. Intensive Care Med. (2007)
Incidence and prognosis of intraabdominal hypertension in a mixed population of critically ill patients: a multiple-center epidemiological study.Malbrain ML et al. Crit Care Med. (2005)
Incidence and clinical pattern of the abdominal compartment syndrome after "damage-control" laparotomy in 311 patients with severe abdominal and/or pelvic trauma.Ertel W et al. Crit Care Med. (2000)