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Intra-Abdominal Hypertension Trina Banerjee Outline Definitions/Categories/Stages Incidence Causes Diagnosis Pathophysiology Treatment Definitions I Intra-abdominal pressure (IAP): – Pressure within the abdominal cavity – <5-7 mm Hg, with upper limit 12 mm Hg Abdominal Perfusion Pressure (APP): – MAP (mean arterial pressure) – IAP – Normal is 60 mm Hg and above Definitions II Intra-abdominal Hypertension (IAH): – IAP >10-12 on three different measurements or – APP<60mmHg on two separate occassions Abdominal CompArtment Syndrome (ACS): – Subcategory of IAH – Sustained IAP>20 with organ dysfunction Categories Primary : – Either Hyperacute (second to minutes) or Acute (Hours) – Results from abdominal trauma Secondary: – Either Subacute (days) or Chronic (Months ) – Results from extrabdominal causes Stages Stage I : 12-15 Stage II : 16-20 Stage III : 21-24 Stage IV : >25 Incidence In mixed ICU population the incidence of IAH can be 30-50% In mixed ICU populations the incidence of ACS can be 4-8% Causes Conditions that Decrease abdominal wall compliance Conditions that increase intraluminal contents Conditions related to abdominal collections of fluid, air, or blood Conditions related to capillary leak and fluid resucitation Decreased abdominal wall compliance Mechanical ventilation PEEP Basal pneumonia High BMI Pneumoperitoneum Abdominal surgery with tight closure Anti-shock garments Prone positioning Abdominal wall bleeding or rectus sheath hematomas Correction of large hernias, gastroschisis, or omphocele Burns with abdominal eschars Increased Intraluminal Contents Gastroparesis Gastric distension Ileus Volvulus Colonic pseudo-obstruction Abdominal tumor Retroperitoneal/Abdominal wall hematoma Enteral feeding Abdominal wall tumor Damage control laparotomy Collections of fluid, air, or blood Ascites Abdominal infection Hemoperitoneum Pneumoperitoneum Laparoscopy with excesive inflation pressures Major trauma PD Capillary leak and fluid resucitation pH<7.2 Hypothermia Coagulopathy Polytransfusion Sepsis Transfusions with capillary leak Major burns Diagnosis Physical Exam: – Highly inaccurate Direct: – Intraperitoneal catheter attached to a pressure transducer Indirect: – Transduction of a bladder, colonic, gastric, or uterine pressure from a balloon – Measure at end expiration in the supine position with absent abdominal wall contractions, at the level of the midaxillary line at the iliac crest after the instillation of a volume of 20-25 cc Pathophysiology General Pathophysiology I The Pressure in ACS decreases venous return: – Increased IAP compromises venous return, by compressing the portal vein and IVC. – There is also increased afterload because of the increased abdominal pressure and thoracic pressure. – Cardiac output then goes down (this occurs at a IAP of 10), and therefore oxygen delivery This leads to decreased arterial pressure, resulting in deceased MAP General Pathophysiology II Decreased MAP causes Ischemic Organs: – Organs become ischemic and then swell. Local release of lactate and adenosine. – Abdominal viscera swelling limits diaphragmatic movement, which limits alveolar recruitment. There is hypoxia and hypercapnia. Increased intrathoracic pressure which further limits venous return. It also increases central venous pressure. It also compresses the heart – The venous return sits in the liver and kidneys Intest. Pathophysiology The rise in pressure causes decreased blood flow to the gut, resulting in bacterial translocation Can result in abdominal wall ischemia Liver Pathophysiology There is decreased blood flow to the liver causing impaired hepatocellular function Liver dysfunction starts at a IAP of 10 – Decreased hepatic artery flow, decreased venous portal flow, increase in the portacollateral circulation – Reduced lactate clearance, altered glucose metabolism, altered mitochondrial function Brain Pathophysiology Cerebral perfusion pressure decreases because of the increase in intrathoracic pressure, resulting in an obstruction of cerebral venous outflow Renal Pathophysiology I IAP Thresholds: – Reduction in renal plasma flow and GFR starting at IAP 15-20 mm Hg – Oliguria starts at 15mmHg – Anuric above 30 mm Hg – Numbers refer to a normovolemic patient. In a septic patient the numbers may be lower Renal Pathophysiology II Pre-renal, Renal, and Postrenal – Pre-renal: Cardiovascular dysfuntion, both from decreased venous return and from compression of the heart, and from increased afterload Increase in ADH response, and can be an Increase in renin/aldosterone/and plasma catecholamines – Renal: Increased pressure on the kidneys and release of inflammatory markers – Post-renal: Direct compression of the ureters A study in the Annals of Surgery in 1982 did not improve with the insertion of ureteral stents Calculations IAP may affect the kidneys more than changes in MAP – RPP=MAP-IAP – FG=GFR-IAP=(MAP-IAP)-IAP=MAP2(IAP) Time Frame Mean time from IAH to ARF is 2.7 days May take between 0-35 days Archives of Surgery 1999 Study Tried to determine if IAH was an independent risk factor for AKI 263 after abdominal surgery Elevated IAP was =/>18mmHg 32.7% of patients with IAH developed AKI Mean time between onset of IAH and AKI 2.7 +/- 6.5 days Intensive Care Medicine 2008 Study Determine at what IAP AKI develops 123 patients admitted > 24 hours in a MICU Bladder Pressure Q24 hours Renal failure associated with IAH if time interval <48 hours 37 patients (30%) developed IAH 16 in the IAH group developed AKI Threshold of IAH 12mmHg Treatment General Principles Serial monitoring of IAP Optimization of systemic perfusion Medical procedures to reduce IAP Prompt surgical decompression for refractory ACS Serial Monitoring of IAP High risk patients every 4-6 hours IAH >12, increase monitoring to hourly or continuous while treatment is being implemented Discontinue when the risk factors of IAH go away or there are no signs of acute organ dysfunctino and IAH measurements have been less than 10-12 for 24-48 hours Optimization of systemic perfusion Fluids increase circulating blood volume Too much fluid may result in IAH To get around this, some practioners have been using hypertonic solutions Journal of Trauma 2006 Study Determine if Hypertonic fluids decrease risk of IAH 48 patients admitted to the burn unit between 2002 and 2004 with burns>40% of their body Patients were given either hypertonic LR (14) or LR (22). IAH was a IAP greater than 30mmHg. Journal of Trauma 2006 Study LR was given at 4mls/kg per percentage of TBSA per 24 hours with a goal of 0.51ml/kg per hour IAH was a IAP greater than 30mmHg Hypertonic LR had 40% less volume infused than the group with the LR Journal of Trauma 2006 Study 14% of patients in the hypertonic LR group developed IAH vs. 50% of the patients in the LR group Serum sodium between 136 and 138meq/L 24 hours after injury in the LR group and 150.7+/-10meq/L in the HLS group, which then decreased to an acceptable level within 2 hours Medical procedures to reduce IAP Bowel Decompression Decrease Intra-abdominal Fluid Increase Abdominal Compliance Correction of Capillary Leak Bowel Decompression Bowel obstruction through either ileus or other causes leads to bowel dialtion and mucosal edema, which will increase the intra-abdominal pressure Correct Electrolytes, stop medications that impair bowel motility, can use gastro-kinetcs (reglan and erythromycin) or colo-kinetics (neostigmine) Decrease Intraabdominal Fluid May be done with lasix/albumin May be done with CRRT Increase abdominal Compliance Muscle relaxants Fentanyl may increase IAH Correction of Capillary Leak Low dose dobutamine corrects intestinal mucosal perfusion Prompt surgical decomporession for refractory ACS 50% mortality rate, but 100% without decompression If the abdominal pressure is dropped too quickly there can be reperfusion injury