Management of Abdominal Compartment Syndrome

1. Dr. Fiifi Brakatu

2. Outline
Case Presentation
Definitions of ACS and IAH
Grading of IAH
Epidemiology, Etiopathogenesis and
Pathophysiology
Diagnosis of ACS
Management of ACS and its therapeutic
complications

3. OBJECTIVES
By the end of this talk you will
be able to:
1. Outline the common causes and
pathophysiology underlying IAH
and ACS
2. Know how to diagnose them
3. Discuss medical and surgical
therapies

4. Case Presentations

5. Case Report 1

6. Case Report 1
55yo F - Ingested bleach
Presented with lethargy, diffuse abdominal
pain and tenderness
SBP - 80 mmHg
CXR - Pneumoperitoneum
Rx - Intubated + massive resus with 14L IV
Crystalloids
Exploratory Lap - multiple perforations
along the greater curvature and fundus of
the stomach. The entire small and large
intestines oedematous and dilated.
Intraop EGD - denuded gastric mucosa
and hyperaemic oesophageal mucosa.
The duodenal mucosa appeared normal.
Surgery - Total gastrectomy with stapled
closure of the distal oesophagus and
duodenal stump.
The abdominal wall fascia was closed
primarily. During the 104-minute
operation, she received five additional
litres of crystalloid and one unit of blood.

7. Post-Op
SBP was consistently below 90 mmHg for 10 hours, in spite of inotropes + persistent
severe metabolic acidosis.
Abdomen palpably tight and initial IAP (intravesical) - 21 cmH2O.
10hrs postop - IAP increased to 37 cmH2O, peak inspiratory pressure (PIP) had risen
from 34 to 60 cmH2O and CVP from 12 to 21 mmHg.
Urine output was decreasing.
IV Cisatracurium - Immediate decrease IAP to 24 cmH2O, CVP to 11 mmHg and PIP to
30 cmH2O
NMB was maintained by continuous intravenous infusion and train-of-fours were
monitored to titrate the effect.
SBP remained above 100 mmHg
Metabolic acidosis, however, persisted for another 48 hours.

8. The initial plan to re-open her abdominal incision was indefinitely delayed
because the IAP, blood and airway pressures, and urine output all improved
following NMB.
During the subsequent 48 hours while she was under NMB, her IAP ranged from
24 to 26 cmH2O, her CVP was ≤ 14 mmHg, and her PIP was ≤ 30 cmH2O.
When the NMB was discontinued at 48 hours, IAH did not recur.
POD7 - patient required abdominal re-exploration for multiple intra-abdominal
abscesses. She developed worsening acute respiratory distress syndrome and
septic shock.
She died of multiorgan failure 16 days after the initial operation.

9. Case Report 2

10. Definitions

11. Abdominal Compartment Syndrome (ACS)
Abdominal Compartment Syndrome (ACS) is organ dysfunction resulting from
intra-abdominal hypertension (IAH).
Under-recognized because:
● It primarily affects patients who are already quite ill
● Organ dysfunction may be ascribed to progression of primary disease
Multisystemic effects on the body

12. IAH vs ACS
IAH and ACS are distinct clinical entities and
should not be used interchangeably
Intra-abdominal Pressure (IAP) is the steady
state pressure concealed within the abdominal
cavity.
Normal IAP: <5 in adults and children
Critically ill patients, an IAP of 5 to 7 is
considered normal

13. Abdominal Perfusion Pressure (APP)
n=144
APP superior to MAP and
intravesical pressure in predicting
survival from IAH and ACS
APP superior to other resuscitation
endpoints - arterial pH, base deficit,
lactate and hourly urine rate
Target APP of 60 linked with
improved survival in IAH and ACS
NB: Increasing MAP in order to
improve APP paradoxically worsens
IAH

14. ● IAH = sustained IAP > 12
● ACS = sustained IAP >20
(irrespective of APP) + new
organ dysfunction or failure

15. Grading of IAH

16. Grades of IAH
IAH is less frequent in children due to
better compliance of abdominal wall in
children
Children have lower baseline MAP than
adults and so organ dysfunction occurs
at lower IAP than adults

17. Clinical Grades of IAH
● Hyperacute - elevation of IAH lasting only seconds
○ Eg. Valsalva maneuvres eg, laughing, sneezing, defecating
○ Gastric distention following endoscopy can result in ACS
● Acute - Develops over hours
○ Results from trauma/intra-abdominal haemorrhage
● Subacute - Develops over days
○ Usually medical cases
● Chronic - develops over months (pregnancy) or years (morbid
obesity)
○ Does not result in ACS but predisposes patient to ACS if they develop hyperacute
or acute IAH

18. Epidemiology, Etiopathogenesis and
Pathophysiology

19. Epidemiology
Incidence is less well characterized
Incidence highest among critically ill patients
Incidence varies considerably among trauma patients

20. Etiopathogenesis
ACS can be classified as:
● Primary ACS - due to injury or disease in the
abdominopelvic region
○ Abdominal trauma, hemoperitoneum, pancreatitis
○ Intervention of the primary condition is often needed
● Secondary ACS - refers to conditions that do not
originate from the abdomen or pelvis
○ Aggressive fluid resuscitation, sepsis, burns (TBSA>30%),
pelvic fractures
● Tertiary (Recurrent) ACS - ACS develops again
following previous treatment of primary or
secondary ACS
● Pathogenesis is
multifactorial
○ Capillary leak
○ Shock with
ischemia-reperfusion
injury
○ Release of vasoactive
substances
○ Oxygen free radicals
○ Massive increase in
extracellular volume

22. Pathophysiology

23. Diagnosis of ACS

24. Clinical Presentation
Early recognition is key
Most patients with ACS are critically ill and unable to
communicate
Symptoms - Malaise, lethargy, lightheadedness, dyspnea,
abdominal pain, and abdominal pain
Tense abdominal distension
Progressive oliguria and increased ventilatory requirements
Hypotension, elevated JVP, tachycardia, peripheral edema,
acute pulmonary decompensation
Evidence of hypoperfusion - cool skin, obtundation, restlessness,
lactic acidosis

26. Imaging
Imaging is not helpful in the diagnosis of ACS
CXR - may show decreased lung volumes,
atelectasis and elevated hemidiaphragm
Abd CT scan - tense infiltration of retroperitoneum
out of proportion to peritoneal disease, extrinsic IVC
and renal compression or displacement,bowel wall
thickening or bilateral inguinal herniation

27. Diagnostic Evaluation
Requires measurement of IAP (done
indirectly)
● Intravesical - standard - simple,
minimally invasive and accurate
● Intragastric
● Intracolonic
IVC catheters Bladder pressure may not
be accurate in patients with abdominal
packs, fractures, intraperitoneal
adhesions, hematomas, neurogenic
bladder, obesity, and pregnancy.

28. Indications for IAP monitoring
● Post-op abdominal surgery patients
● Patients with abdominal trauma
● Ventilated patients with other organ failure
● Patients with signs of ACS - oliguria, hypoxia,
hypotension, acidosis, mesenteric ischemia,
ileus, elevated ICP
● Patients with high cumulative fluid balance
● Patients with abdominal packing

31. Management of ACS

32. Management of ACS
● Surveillance - serial IAP measurements for those at high risk
● Conservative measures
○ Nasogastric and Colonic Decompression
○ Body Positioning - head elevation >20deg
○ Prokinetics - neostigmine
○ Judicious Fluid Management
○ Sedation and Optimal Analgesia - improves abdominal wall compliance
○ Neuromuscular Paralysis and ventilatory support
○ Percutaneous Catheter Drainage
NB: No role for diuresis - it may worsen AKI!
● Surgical Decompression - definitive treatment when end organ function is
threatened

33. Surgical Decompression - Escharotomy

34. Surgical Decompression - Decompressive Laparotomy

35. Passive Temporary Abdominal Closure - Bogota Bag (Silo)
Traditionally an x-ray cassette cover, 3 L sterile fluid bag, or other such large sterile
plastic covering is used.

36. Passive Temporary Abdominal Closure

37. SSG applied after absorbable mesh
TAC. It results in incisional hernia.
Absorbable Mesh TAC is often
associated with extrusion of parts
of the mesh

38. Negative Pressure Therapy Techniques
● Passive methods
● Active - Negative Pressure Therapy

39. Negative Pressure Therapy Techniques - VAC
Never apply the VAC directly over the intestine.

40. Negative Pressure Therapy Techniques - AbThera System

41. Complications of Decompressive Laparotomy
● Fluid loss
● Infection
● Loss of the abdominal wall domain
● Enteroatmospheric fistulae
● n=649
● Entero-atmospheric fistulas are influenced by
the duration of open abdomen treatment and
by the nutritional status of the patient.
Peritonitis, intestinal anastomosis, negative
pressure and oral or enteral nutrition were not
risk factors for EAF during OA treatment.

42. Enteroatmospheric Fistula (EAF)
Early fascial closure within 5 to 7 days helps mitigate the risk of EAF

43. Management of EAFs
EAFs almost never close spontaneously
Definitive repair usually requires major surgical intervention and abdominal wall reconstruction 6 to 12 months after the
original insult
● Immediate treatment of sepsis if present
● Nutrition
● Fluid and electrolyte support in the form of
parenteral nutrition (PN)
● Wound/effluent control
● Protection of surrounding tissues and
exposed bowel

44. Take Home Message
● Clinical examination is often unreliable in the diagnosis of IAH or ACS
● A high index of suspicion is necessary for early diagnosis, before IAH
progresses to ACS
● Delayed decompressive laparotomy is a serious error which may result in
organ failure and death.
● In adults, 25 mL should be instilled and in children, 1 mL/kg (minimum, 3
mL; maximum 25 mL) should be instilled to avoid bladder overdistension
and falsely elevated IAP measurements
● Wait 30 to 60 seconds before pressure measurement for detrusor muscle
relaxation, to avoid a falsely elevated pressure.
● IAP should be measured at end-expiration with the patient supine
● Close the fascia within 5 to 7 days to prevent EAF

45. References
Cheatham, M et al. Abdominal Perfusion Pressure: A Superior Parameter in the
Assessment of Intra-abdominal Hypertension, The Journal of Trauma: Injury,
Infection, and Critical Care: October 2000 - Volume 49 - Issue 4 - p 621-627
Demetrios Demetriades, Ali Salim, Management of the Open Abdomen,Surgical
Clinics of North America,Volume 94, Issue 1,2014,
Federico C, et al. Open abdomen and entero-atmospheric fistulae: An interim
analysis from the International Register of Open Abdomen (IROA), Injury, Volume
50, Issue 1,2019,Pages 160-166,