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

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

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

Definition APP (Abdominal perfusion pressure): MAP - IAP 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 Surg 1989; 55:396–402 Paeds ACS reported at IAP>17mmHg or >10 if associated with OD APP (Abdominal perfusion pressure): MAP - IAP

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

ACS Definition Primary Secondary Recurrent 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

Incidence De Waele JJ, et al. Am J Kidney Dis Incidence De Waele JJ, et al. Am J Kidney Dis. 2011;57: 159-69 Thabet FC, et al. J Intensive Care Med. 2015: 1-6 IAH % ACS % Major abdominal surgery NA 33-41 Liver Transplant 31 Major Trauma 50 13-36 ICU 30-54 5-12 Septic shock 51-76 33 Severe acute pancreatitis 59-84 25-56 Paediatric patients 13%* 1-10% *Increased abdominal wall compliance?

Pathogenesis Monro-Kellie doctrine Extrapolate to the abdomen… Pressure volume relationship of structures within rigid cranial vault Extrapolate to the abdomen… Cranium Abdomen Organ(s) Brain Liver, Spleen, Gut Fluid CSF Ascites Enclosing structure Skull Abdominal cage Lesion Tumor, Blood Blood, Air, Oedema, Tumor, Ascites Pressure ICP IAP Perfusion CPP (60-70) APP (>60)* Rigid - kind of Rigid *APP >50 predicts survival better than MAP and IAP Cheatham ML, et al. J Trauma 2000;49: 621–626

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

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 Complicated intra-abdominal infection

Liver trauma – intra-abdominal haemorrhage, Packing

SNP abdominal decompression

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

Polycompartmental hypertension Air (tension) Air Retroperitoneal bleed

There is rarely just one cause

Cont intragastric monitoring 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 Cont intragastric 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

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

Pathophysiology Abviser™

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 hypovolaemic states or sepsis

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

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

Treatment of IAH/ACS

Treatment

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

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