1. ABDOMINAL COMPARTMENT SYNDROME DR. F MOSAI REGISTRAR: GEN SURGERY MEDUNSA

2. ACS OUTLINE 1.DEFINATIONS: IAH, ACS 2.RISK FACTORS 3.AETIOLGY 4.PATHOPHYSIOLOGY 5.DIAGNOSIS 6.TECHNIQUES OF MASURING IAP 7.PREVENTION OF ACS 8.MANAGEMENT 9.COMPLICATIONS OF ASSOCIATED WITH Mx

3. 1. DEFINATIONS  IAH: sustained or repeated pathological increase in IAP= 12mmHg or more  [PAEDS:] IAH: sustained or repeated pathological increase in IAP=10mmHg or more  ACS: sustained IAP=20mmHg or more(with or without an APP<60mmHg) that is associated with new organ dysfunction/failure  [PEADS] ACS: sustained increased IAP >10mmHg ass with new or worsening organ dysfx that can be attributed to increase in IAP

4. 2. RISK FACTORS  Diminished abdominal wall compliance  Major burns, abd surgery, major trauma, prone position  Increased intraluminal contents  Volvulus, gastric distension, gastroparesis, Ileus, colonic pseudo-obstruction  Increased Intra-abdominal contents  Haemoperitonium/pneumoperitonium or intra-peritoneal fluid collection,tumours

5. 2. RISK FACTORS  Capillary leak/fluid resuscitation  Massive fluid resuscitation or positive fluid balance, damage control laparotomy, hypothermia  Others/miscellaneous  Mechanical ventilation, increase BMI, sepsis, shock,coagulopathy

6. 3. AETIOLOGY  Acute:  Retroperitoneal: pancreatitis, bleed, visceral oedema, aortic aneurism  Intraperitoneal: bleed, bowel obstruction, ileus, oedema, gastric dilatation  Abdominal wall: burn eschar, repair of gastroschisis or omphalocele, reduction of large hernias, laparotomy closure under tension  Chronic:  Obesity,ascitis, intra-abd tumors, preganancy, peritoneal dialysis

7. 4. PATHOPHYSIOLOGY  CNS: ↓ venous outflow  ↑ ICP ->cerebral oedema-> ↓ CPP  CVS: ↑ systemic vascular resistance due to compression at the level of the capillary bed : ↓ venous return :diaphram displacement →↑ intrathoracic pressure →↓ ventricular compliance →↓ CO + SV

8. 4. PATHOPHYSIOLOGY  Resp: ↑ diaphram →↓ pulmonary compliance : ↓ TLC, ↓ FRC, ↓ RV : V/Q abnormal and hypoventilation → hypoxia and hypercarbia  ABD: ↓ flow in mesenteric, intestinal, hepatic and portal venous flow → ischaemia and ↑ risk of translocation

9. 4. PATHOPHYSIOLOGY  Renal: ↑ IAP → obstruct renal outflow +renal arteries : ↑ ADH, renin and aldosterone → ↑ vascular resistance, Na + H2O

10. 5. DAIGNOSIS  Hx:  ↓ urine output with ↑ CVP  ↑ Peak airway pressure  Massive volume resuscitation  Damage control laparotomy  shock

11. 5. DAIGNOSIS CRITERIA FOR Dx 1.IAP >25mmHg (30cmH ₂ O) AND 2. One or more of the following  Oligouria (0.5ml/kg/h)  ↑ pulmonary pressure (>45cmH ₂ O)  Hypoxia  ↓ CO  Hypotension  Acidosis AND(to comfirm Dx)

12. 5. DAIGNOSIS 3. Abdominal decompression lead to clinical improvement

13. 6. TECHNIQUE TO MEASURE IAP  Sterile procedure  Supine position, Θ abd muscle contraction  Transducer, zero at the level of midaxillary line  Place a special catheter and empty bladder  Clamp catheter and instill ≤25ml sterile saline into bladder and wait 30sec for detrusor muscle relaxation before measuring pressure  Measure at end expiration at the phlebostatic axis  [Peads: instill 1ml/kg, min:3ml-max:25ml)

14. 7. PREVENTION OF ACS  Prophylactic use of open abdomen after trauma damage control laparotomy  Damage control resuscitation  Limitation of crystalloid fluids  ↑ ratio of plasma/packed red blood cell for resuscitation of massive haemorrhage  Keep fluid balance neutral or even negative  Body positioning(trendelenberg)

15. 8. MANAGEMENT 1.Non-operative(MEDICAL)  Indications:  IAH  Secondary or recurrent ACS with no progressive organ failure 2. Operative  Indications:  Primary ACS/ overt ACS  Secondary or recurrent ACS with progressive organ failure  IAH( failed non-operative Rx)

16. 8. MANAGEMENT 1.Non-operative Mx  Improve abdominal wall compliance  Sedation and analgesia  Paralysis(neuromascular blockade)  Trendelenberg position( avoid head of bed >30°)  Evacuate intraluminal contents  NG-decompresion  Rectal/colonic decompression  Gastro/colo-prokinetics(e.g. Neostigmine)

17. 8. MANAGEMENT  Evacuate abdominal fluid collection  PCD(abscess, haematoma)  Paracentesis(not recommended)  Correct positive fluid balance  Avoid excessive fluid resuscitation  Diuretics(NOT RECOMMENDED)  Colloid or hypertonic fluids  Albumin (NOT RECOMMENDED)  Hemodialysis/ultrafiltration(NOT RECOMMENDED)

18. 8. MANAGEMENT  Damage control resuscitation  Limit crystalloid iv fluid  ↑ plasma/packed red blood cell ratio for massive hemorrhage

19. 8. MANAGEMENT 2. Operative  Acute decompresive laparotomy  Wound cover after laparotomy  Silo Bag closure  3l Bogota bag (with closed suction to control fluid exudate)  Sandwish and vacuum pack technique  NPWT(negative pressure wound therapy)  Bioprosthetic mesh closure(NOT RECOMMENDED FOR ROUTINE USE)

20. 9. COMPLICATIONS  Intraoperative  Surgical related  Sudden release of IAP lead to reperfusion injury, SIRS, Acidosis, hyperkalemia and ↑ myglobin  Rx: consider: 1l 0.45% saline with 50g Mannitol and 50mmol sodiun bicarbonate  Anaesthetic related  Aspiration ( ↑ IAP)

21. 9. COMPLICATIONS  Post-operative  Short term(due to prolong open abdomen)  Visceral adhessions  Loss of soft tissue coverage  Lateralization of the abdominal musculature and its fascia  Malnutrion  Enteric fistulae  Long term  Incisional hernia  Adhessive bowel obstruction