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Intra-abdominal Hypertension

Intra-abdominal Hypertension. Leanna R. Miller RN, MN, CCRN-CMC, PCCN-CSC, CEN, CNRN, NP. Definitions WCACS, Antwerp Belgium 2007. Intra-abdominal Pressure (IAP): Intrinsic pressure within the abdominal cavity

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Intra-abdominal Hypertension

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  1. Intra-abdominal Hypertension Leanna R. Miller RN, MN, CCRN-CMC, PCCN-CSC, CEN, CNRN, NP

  2. DefinitionsWCACS, Antwerp Belgium 2007 • Intra-abdominal Pressure (IAP): Intrinsic pressure within the abdominal cavity • Intra-abdominal Hypertension (IAH): An IAP > 12 mm Hg (often causing occult ischemia) without obvious organ failure • Abdominal Compartment Syndrome (ACS): IAH with at least one overt organ failing

  3. Types of IAH /ACSWCACS, Antwerp Belgium 2007 • Primary – Injury/disease of abdomino-pelvic region, “surgical” • Secondary – Sepsis, capillary leak, burns, “medical” • Recurrent – ACS develops despite surgical intervention

  4. Physiologic Insult/Critical Illness Inflammatory response Ischemia Fluid resuscitation Capillary leak Tissue Edema (Including bowel wall and mesentery) Intra-abdominal hypertension

  5. Intra-abdominal Hypertension Compartment syndrome occurs when the pressure within a closed anatomic space increases to the point where vascular tissue is compromised with subsequent loss of tissue viability and function. This can occur within any closed body cavity.

  6. Intra-abdominal Hypertension Increased IAP leads to decreased mesenteric blood flow (MBF) and to bacterial translocation (BT), which may contribute to later septic complications and organ failure.

  7. Intra-abdominal Hypertension • IAH provokes the release of pro-inflammatory cytokines which may serve as a second insult for the induction of MOF. • production of interleukin-1 (IL-1 beta), interleukin-6 (IL-6), tumor necrosis factor (TNF-)

  8. Intra-abdominal Hypertension • Symptomatic organ dysfunction that results from increased intra-abdominal pressure (IAP) • Increased IAP is an under-recognized source of morbidity and mortality. • 1-day point-prevalence observational trial conducted in 13 medical ICUs of six countries with 97 patients, 8% had IAP > 20mmHg.1 • The incidence of ACS in trauma patients is estimated to be between 2 and 9 percent.2 1Crit Care Med 2005; 33:315. 2Am J Surg 2002; 184:538.

  9. Intra-abdominal Hypertension Etiology • massive volume resuscitation is the leading cause of ACS. • inflammatory states with capillary leak, fluid sequestration, inadequate tissue perfusion, and lactic acidosis can develop ACS. • gastric overdistention following endoscopy has resulted in ACS.

  10. Intra-abdominal Hypertension • trauma (blunt or open), as a result of the accumulation of blood, fluid or edema.  • gastrointestinal hemorrhage can also lead to increased pressure in the abdominal compartment as ischemic cells swell or fluids collect.  • pancreatitis • pneumoperitoneum

  11. Intra-abdominal Hypertension • syndrome may follow a ruptured abdominal aortic aneurysm • intra-abdominal infection • coagulopathies with abdominal bleeding • cirrhosis • profound hypothermia

  12. Intra-abdominal Hypertension • massive intra-abdominal retroperitoneal hemorrhage • severe gut edema • intestinal obstruction • ascites under pressure • neoplasm

  13. Intra-abdominal Hypertension • Patients who have undergone long surgical procedures with intraoperative hypotension and large fluid requirements are at significant risk, particularly if the abdomen has been closed under pressure in the OR. • External pressure from circumferential burns about the abdomen, application of military anti-shock trousers (MAST), or even tight abdominal restraint devices can cause tension within the abdomen due to external forces and result in ACS

  14. Intra-abdominal Hypertension Recently, awareness of the ACS has increased for 2 primary reasons. • First, the increased use of laparoscopy among general surgeons has brought with it an appreciation of IAP as a readily quantifiable entity. • Second, the more frequent use of planned repeat laparotomy for trauma has allowed both surgeon and intensivist to appreciate the beneficial effects of abdominal decompression upon removal of packing or evacuation of hematoma.

  15. Intra-abdominal Hypertension • Interpreting IAP • 0 – 5 mm Hg normal • 6 – 11 mm Hg minimal elevation common finding in ICU • 12 – 15 mm Hg Grade I • 16 – 20 mm Hg Grade II • 21 – 15 mm Hg Grade III – high risk for ACS • > 25 mm Hg Abdominal Compartment Syndrome

  16. Intra-abdominal Hypertension Abdominal Compartment Syndrome “. . . . . . .the end result of a progressive, unchecked increase in intra-abdominal pressure from a myriad of disorders that eventually leads to multiple organ dysfunction”

  17. Intra-abdominal Hypertension

  18. Grading System for ACS

  19. Elevated IAP

  20. Intra-abdominal Hypertension • IAH may develop rapidly • Monitor the trend: rising IAP or sustained IAH poor prognosis • Recommendation: Measure IAP at each Urine Output determination

  21. Physiologic Sequelae

  22. The Pathophysiology of IAH IAP DIAPHRAGMATIC ELEVATION VASCULAR COMPRESSION DIRECT ORGAN COMPRESSION RVP IVC Flow Cardiac compression Intrathoracic pressure Cardiac preload Cardiac contractility Systemic afterload PV pressure CARDIAC OUTPUT Renal Vascular Resistance Splanchnic Vascular Resistance RENAL FAILURE ABDOMINAL WALL ISCHAEMIA/OEDEMA RESPIRATORY FAILURE ICP SPLANCHNIC ISCHAEMIA

  23. Effects on CVS • As intra-abdominal pressure increases above 10 mmHg, cardiac output declines, despite normal arterial pressures. • Additionally, whole body oxygen consumption, pH, and PO2 decrease. • Intra-abdominal hypertension affects cardiac function by pushing the hemi-diaphragms upward, thus transmitting the abdominal pressure to the heart and its vessels. • This decreases preload and increases afterload on the left ventricle and at the same time creates a hemodynamic picture of low cardiac output and high filling pressures

  24. Physiologic Sequelae Cardiac: • Increased intra-abdominal pressures cause: • Compression of vena cava with reduced venous return • Elevated intra-thoracic pressure with multiple negative cardiac effects • Result: • Decreased cardiac output, increased SVR • Increased cardiac workload • Decreased tissue perfusion • Misleading elevations of CVP and PAOP • Cardiac insufficiency; cardiac arrest

  25. Effects on Pulmonary System • most commonly noted effects of IAH on the pulmonary system are: • elevated peak inspiratory pressures • decreases in PaO2 • increases in PaCo2 • requires the use of complete ventilatory support to maintain adequate oxygenation and ventilation. • positive end-expiratory pressure has been shown to exacerbate the cardiac and respiratory consequences of IAH.

  26. Physiologic Sequelae Pulmonary: • Increased intra-abdominal pressures causes: • Elevated diaphragm, reduced lung volumes & alveolar inflation, stiff thoracic cage, increased interstitial fluid • 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)

  27. Pulmonary Effects of IAH • mechanical ventilation often necessary • high peak airway pressures  barotrauma • high PEEP often required  further compromising CO

  28. Pulmonary Effects of IAH Pressure on the IVC predisposes to venous stasis and increased risk of thromboembolism

  29. IAH and Splanchnic Flow • increases in IAP have adverse effect on splanchnic flow • >15mmHg  SM blood flow • marked reduction in hepatic artery and portal venous blood flow • leads to mucosal acidosis and edema

  30. IAH and Splanchnic Flow Splanchnic hypoperfusion Hepatic ischemia Gut mucosal acidosis Bowel edema IAH Coagulopathy hypothermia acidosis Unrelieved Free oxygen radicals Distant organ damage Intra-abdominal bleeding ACS

  31. Intra-abdominal Hypertension • measured mucosal and intestinal blood flow and intramucosal pH (pHi) and found that mesenteric and mucosal blood flow decreased when IAP reached 20 mmHg, with intestinal mucosal flow declining to 61% of baseline • At an IAP of 40 mmHg, intestinal flow decreased to 28% of baseline • Intestinal mucosa showed signs of a severe degree of acidosis, measured by tonometer. These changes in splanchnic blood flow occurred despite maintenance of baseline cardiac output with volume loading

  32. Intra-abdominal Hypertension • blood flow to virtually every abdominal organ decreased significantly. The only exception was the adrenal gland; the reason this organ is not affected is unknown ?

  33. Physiologic Sequelae Gastrointestinal: • Increased intra-abdominal pressures causes: • Compression/Congestion of mesenteric veins and capillaries • Reduced cardiac output to the gut • Result: • Decreased gut perfusion, increased gut edema and leak • Ischemia, necrosis • Bacterial translocation • Development and perpetuation of SIRS • Further increases in intra-abdominal pressure

  34. Effects on Renal System • decreased renal plasma flow, glomerular filtration rate, and glucose reabsorption. • oliguria also occurs, with anuria noted in animal models when IAP reaches 30 mmHg • effects occur without significant decreases in blood pressure (mechanical, ↑ PVR, compression of renal vein→ outflow obstruction→ ↑ intraparenchymal pressure → shunting of blood from renal cortex)

  35. Effects on Renal System • improvement of cardiac output does not improve renal function, nor do renal blood flow and glomerular filtration rate improve. • the placement of ureteral stents failed to improve renal function. • improvement in renal function occurred only after abdominal decompression

  36. Intra-abdominal Hypertension • These findings suggest that the effects of IAH on renal function are related to compression of the renal parenchyma itself and to compression of renal vasculature and are not related to decreased cardiac output. • other mechanisms proposed include shunting of blood away from the renal cortex into the medulla, decreased renal arterial flow with a concomitant increase in renal vascular resistance, and the presence of high levels of renin, aldosterone, and antidiuretic hormones.

  37. Physiologic Sequelae Renal: • Elevated intra-abdominal pressure causes: • Compression of renal veins, parenchyma • Reduced cardiac output to kidneys • Result: • Reduced blood flow to kidney • Renal congestion and edema • Decreased glomerular filtration rate (GFR) • Renal failure, oliguria/anuria • Mortality of renal failure in ICU is over 50% - DO NOT WAIT for this to occur!

  38. Effects on CNS • The rise in intra-abdominal pressure, intrathoracic pressure leads to a rise in central venous pressure which prevents adequate venous drainage from the brain, leading to a rise in intracranial pressure and worsening of intracerebral edema.

  39. Intracranial Derangements • IAH associated with • ICP • CPP • cerebral ischemia • ?Why? • may be due to impairment of cerebral venous outflow

  40. Central Nervous System Implications retinal capillariesrupture Valsalva retinopathy ICP CPP Sudden decrease of central vision

  41. Intra-abdominal Hypertension • increased intrathoracic pressure causing increased resistance to cerebral venous return associated with IAH( ?pseudotumorcerebri). • Volume expansion further increased ICP. Cerebral perfusion pressure declined as ICP increased and cardiac output declined. • Only abdominal decompression reversed effects of IAH. • The exact level of IAH that results in elevated ICP and decreased CPP in the brain injured patient is unknown

  42. 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 • Result: • Increased central venous pressure and IJ pressure • Increased intracranial pressure • Decreased cerebral perfusion pressure • Cerebral edema, brain anoxia, brain injury

  43. Multisystem Organ Failure Intra-abdominal Pressure Mucosal Breakdown (Multi-System Organ Failure) Bacterial translocation Acidosis Decreased O2 delivery Anaerobic metabolism Capillary leak Free radical formation MSOF

  44. IAH / ACS Affects Outcome Points: • IAH and ACS are common entities in the critical care environment (including your own). • IAH and ACS increase morbidity, mortality and ICU length of stay………… However: • Clinical signs of IAH are unreliable and only show up late in the clinical course …..SO • Early monitoring (TRENDING) & detection of IAH with early intervention is needed to reduce these complications.

  45. Measurement of IAP

  46. Diagnosis of ACS • Intra – abdominal pressure  25 mmHg or 30 cmH20/ urine • One or more of the following signs of clinical deterioration • ↑ pulmonary pressures • ↓ cardiac output • ↓ urinary output • acidosis • hypoxia • hypotension • abdominal decompression results in clinical improvement

  47. Indications for IAP Monitoring • postoperative (abdominal surgery) • ventilated pts with other organ failure • patients with signs of ACS: • oliguria, hypoxia, hypotension, acidosis, mesenteric ischemia, ileus, elevated ICP. • high cumulative fluid balance • abdominal packing

  48. Intra-abdominal Hypertension Abdominal compartment pressure monitoring is done to help recognize life threatening elevations in pressure before ischemia or infarction of the abdominal organs occurs.  When a patient exhibits a distended and taut abdomen, the measurement of abdominal compartment pressure can provide direction regarding the need for decompressive surgery

  49. Measurement of IAP Indirect Direct

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