Intra Abdominal hypertension&Abdominal Compartment Syndrome

1. INTRAABDOMINAL HYPERTENSION, AND ABDOMINAL COMPARTMENT SYNDROME Dr.Abdulgafoor.MT ICU – ALKhor hospital , HMC,Doha,Qatar

2. 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

3. 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

4. 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 Hg Intensive care med 2006;32(11)1722-1732

5. 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

6. 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

7. 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

8. 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

9. 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%

10. Incidence of IAH&ACS Population 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%

11. 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

12. 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

13. WSACS IAH/ACS assessment algorithm

14. 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

15. 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, SVO 2 Misleading elevations of PAWP and CVP Cardiac insufficiency Cardiac arrest www.abdominal-compartment-syndrome.org

16. 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

17. 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

18. 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/anuria www.abdominal-compartment-syndrome.org

19. 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

20. Circling the Drain Intra-abdominal Pressure Mucosal Breakdown (Multi-System Organ Failure ) Bacterial translocation Acidosis Decreased O2 delivery Anaerobic metabolism Capillary leak Free radical formation MSOF www.abdominal-compartment-syndrome.org

21. 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

22. Folley manometer

23. 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

24. Abviser Autovalve

25. 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

26. Decompressive Laparotomy Delay in abdominal decompression may lead to intestinal ischemia Decompress Early!

27. Temporary closure techniques (laprostomies ) Bogota bag closure Towel clip closure Polypropylene mesh, Polygelatine mesh, Granulated vicryl mesh Zippers Vacuum assisted wound closure

28. 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.

29. 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

30. 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

31. 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

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

33. 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

34. 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

35. Thank You