Intra-abdominal Hypertension: Emerging concept in AKI

1. Intra-abdominal Hypertension:Emerging concept in AKI Georg Auzinger Honorary Senior Lecturer Liver ICU & ECMO Lead King’s College Hospital London

2. The 4 compartments ICS TCS • Plus a few more: • Ocular • Cardiac • Hepatic • Renal • Pelvic ACS ECS

3. Background • Concept of IAH/ACS known for > a century • Rediscovered only ~30 years ago… despite the obvious! • CCM survey 2006: 25% of paediatric Intensivists never saw a case of IAH/ACS 24% were unaware of measurement methods 33% would never use decompressive laparotomy to treat ACS

4. Definition • IAP: Steady state pressure within abdominal cavity • What is normal – it depends: ICU 5-7mmHg? • IAH: Sustained or repeat elevation of IAP ≥12mmHg • Paeds: IAP>10mmHg • ACS: Sustained IAP>20mmHg associated with new organ dysfunction/failure Fietsam R, et al. Am Surg1989; 55:396–402 • Paeds ACS reported at IAP>17mmHg or >10 if associated with OD • APP (Abdominal perfusion pressure): MAP - IAP

5. IAH Grading • Grade I: IAP 12-15mmHg • Grade II: IAP 16-20mmHg • Grade III: IAP 21-25mmHg • Grade IV: IAP>25mmHg

6. ACS Definition • Primary • Injury or disease of abdomen/pelvis – frequently requires surgery or radiological intervention • Secondary • Conditions not originating from abdomino-pelvic compartment • Recurrent • Syndrome redevelops after initial surgical or medical treatment of primary or secondary ACS

7. IncidenceDe Waele JJ, et al. Am J Kidney Dis. 2011;57: 159-69Thabet FC, et al. J Intensive Care Med. 2015: 1-6 *Increased abdominal wall compliance?

8. Pathogenesis • Monro-Kellie doctrine Pressure volume relationship of structures within rigid cranial vault • Extrapolate to the abdomen… Rigid - kind of Rigid Rigid *APP >50 predicts survival better than MAP and IAP Cheatham ML, et al. J Trauma 2000;49: 621–626

9. But… • Elasticity of abdominal wall and diaphragm • Expressed as ΔP/ΔV

10. Aetiology (not exhaustive) • Increased intra-abdominal volume • Luminal: Gastroparesis, ileus, volvulus, colonic pseudo-obstruction • Solid organ: Hepato- and/or Splenomegaly • Mass lesions • Fluid: Ascites, Haemoperitoneum • Air: Intra and extraluminal • Decreased abdominal wall compliance • Emergency surgery/Damage control – tight closure • Abdominal wall bleeding/oedema/rectus sheath haematoma • Juxta-abdominal process affecting IAP • Surgical correction: Large hernia, gastroschisis, omphalozele • Combination of the above • Fluid shifts/capillary leak – Severe sepsis or septic shock • Massive fluid resuscitation • Burns eschars/sepsis • Severe necrotising pancreatitis • Massive fluid resuscitation • Complicated intra-abdominal infection

11. Liver trauma – intra-abdominal haemorrhage, Packing

12. SNP abdominal decompression

13. ALF - capillary leak, reperfusion injury- intestinal + abdominal wall oedema

14. Polycompartmental hypertension Air (tension) Air Retroperitoneal bleed

15. There is rarely just one cause

16. How do we diagnose • Clinical assessment – physical examination inaccurate: Sensitivity 60% PPV 45-75% • “IAP should be expressed in mmHg and measured at end-expiration in the complete supine position after ensuring that abdominal muscle contractions are absent and with the transducer zeroed at the level of the midaxillary line.” CiMon Contintragastric monitoring Goldstandard • Fluid volume important • Detrusor contraction • <25ml, or 1ml/kg Paeds Bias of -4.9mmHg vs direct measurement IAP≥20 – PPV 0, NPV 0.91

17. Imaging • IVC narrowing • Thickening enhancement of bowel wall • Reduced caliber of abdominal aorta • Displacement/compression of kidney(s) • Relative increase in AP vs transverse abdominal diameter

18. Pathophysiology Abviser™

19. Pathophysiology in relation to AKI • IAH reduces renal arterial blood flow • IAH increases IVC pressure • IAH compresses renal vein – Renal vein pressure (RVP)↑ • ACS increases RAP + reduces gradient for venous return • Oliguria at IAP of 15mmHg • Anuria at IAP of 25mmHg Thresholds lower in hypovolaemicstates or sepsis

20. Pathophysiology • RPP(Renal perfusion pressure): MAP – RVP • RFG(Renal filtration gradient): Glomerular filtration pressure – proximal tubular pressure = RPP – RVP = MAP – 2 x RVP • In case of IAH: RVP = IAP RFG: MAP – 2 x IAP Bradley SE. J Clin Invest 1947;26: 1010–1022 – IAP induced ↑RVP led to sig drop in GFR, RPF and UOP

21. Other factors • Increased intra-capsular/parenchymal pressure • ACS induced reduction in CO: ↑Afterload ↓Preload • ACS induced Catecholamine, Aldosterone, Renin and Angiotensin release • Impaired intestinal perfusion: Bacterial translocation, cytokine release with deleterious effects on renal perfusion

22. Treatmentof IAH/ACS

23. Treatment

24. Summary • IAP, IAH, ACS only fairly recently “re-discovered” • Understanding of its importance under appreciated • Paediatric ICU practice lagging behind? • Syndrome with potentially devastating consequences • ACS in many studies one of the most important outcome predictors • IAH/ACS is frequently a poly-compartmental disease • Warrants a high index of suspicion • Low threshold for monitoring – should be regularly repeated • Early intervention • Whenever possible via least invasive approach PCD > surgery • Less frequently a surgical disease today

25. Summary • Kidneys are a primary target organ during IAH/ACS • AKI occurs very early, initially often subclinical • Prime importance of RVP and RPP • The IVCP and RAP are important and often neglected parameters • As with many other syndromes: Paradigm of early aggressive fluid resuscitation followed by timely restrictive fluid management • Aim to reduce IVCP and RVP • In our hands RRT and UF is an early interventional cornerstone