INTRAABDOMINAL HYPERTENTION

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INTRAABDOMINAL HYPERTENTION ABDOMINAL
COMPARTMENT SYNDROME
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important values

• Normal intra-abdominal pressure is 0 - 5 mmHg. 
• Pressures gt 13 mmHg may be sufficient to restrict
  perfusion to the organs of the gut. 
• If the abdominal compartment pressures is between
  16-25 mmHg, hypervolemic volume expansion therapy
  can be used to maintain the perfusion pressure
  gradient for the abdominal organs. 
• When compartment pressures exceed  25 mmHg,
  decompression surgery should be considered to
  prevent organ damage.  Pressure may rise rapidly
  with active bleeding. Edema (which occurs with
  any ischemic insult) will generally result in a
  later rise in the pressure (27 hours or more post
  insult). 

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Classify IAH into 4 groups

• Hyperacute(sec,min)laughing,strain,coug-hing,snee
  z,physical activities)
• Acute?(couple H)trauma,hge
• Subacute ?(couple days) most medical cases.
• Chronic morbid obesity,intraabdominal
  tumor,pregnancy.

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Patients at risk for ACS include

• 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
• neoplasm

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• syndrome may follow a ruptured abdominal aortic
  aneurysm
• intra-abdominal infection
• Coagulopathies with abdominal bleeding
• cirrhosis, or
• profound hypothermia

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• massive intra-abdominal retroperitoneal
  hemorrhage,
• severe gut edema
• intestinal obstruction
• ascites under pressure.

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• 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.2

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• 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.

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The Pathophysiology of IAH
?IAP
VASCULAR COMPRESSION
DIRECT ORGAN COMPRESSION
DIAPHRAGMATIC ELEVATION
?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
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• 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.

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• Increased IAP leads to decreased MBF and to
  Bacterial translocation (BT), which may
  contribute to later septic complications and
  organ failure.

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

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Anaesthetic Implications of ACS
Pulmonary Implications

Renal implications
Porto-systemic visceral Implications
Cardiovascular Implications  
Central nervous system Implications
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Effects on CVS

• As intraabdominal pressure increases above 10
  mmHg, cardiac output declines, despite normal
  arterial pressures.
• Additionally, whole body oxygen consumption, pH,
  and PO2 decrease.
• Intraabdominal hypertension affects cardiac
  function by pushing the hemidiaphragms 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.1,4

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On the pulmonary system

• The most commonly noted effects of IAH on the
  pulmonary system are elevated peak inspiratory
  pressures, decreases in Pao2 and increases in
  Paco2 requiring the use of complete ventilatory
  support to maintain adequate oxygenation and
  ventilation.
• Hypercarbia, hypoxemia, and acidosis are evident
  when arterial blood gases are measured.6
• Positive end-expiratory pressure has been shown
  to exacerbate the cardiac and respiratory
  consequences of IAH.

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Pulmonary effects of increased intra-abdominal
pressure (2)

• mechanical ventilation often necessary
• high peak airway pressures ?barotrauma
• high PEEP often required further compromising CO

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Pulmonary effects of increased intra-abdominal
pressure (3)

• Pressure on the IVC predisposes to venous stasis
  and increased risk of thromboembolism

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Renal effects

• include decreased renal plasma flow, glomerular
  filtration rate, and glucose reabsorption.
  Oliguria also occurs, with anuria noted in animal
  models when IAP reaches 30 mmHg.1 These effects
  occur without significant decreases in blood
  pressure(mechanical,? RVR,compression of R
  vein?outflow obstuction?? intraparenchymal
  pressure?shunting of blood from R cortex) .
• 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.7

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• 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.1

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Experimental
Control
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Aldosterone level (ng/dl)
15
10
5
0
0
5
10
15
20
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Fluids
IAP (mmHg above baseline)
Effect of increased intra-abdominal pressure on
plasma aldosterone. The increased levels are
reduced by volume expansion (J Trauma
199742997-1003)
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Plasma renin activity (ng/ml/hr)
Experimental
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Control
25
20
15
10
5
0
0
5
10
15
20
25
Fluids
IAP (mmHg above baseline)
Effect of increased intra-abdominal pressure on
plasma renin activity. The increased levels are
reduced by volume expansion (J Trauma
199742997-1003)
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IAH and Splanchnic Flow

• Increases in IAP have adverse effect on
  splanchnic flow
• gt15mmHg??SMA blood flow
• marked reduction in hepatic artery and portal
  venous blood flow
• leads to mucosal acidosis and oedema

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Cycle of events created by IAH on splanchnic
circulation
Splanchnic hypoperfusion
Hepatic ischaemia
Gut mucosal acidosis Bowel oedema
IAH
Coagulopathy hypothermia acidosis
Unrelieved
?Free oxygen radicals Distant organ damage
Intra-abdominal bleeding
ACS
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• They 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.
• The 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.

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IAP 25mmHg for 60 min
pp
IAP 15mmHg for 60 min
Baseline
Bowel TPO2
5
3
Axillary TPO2
1
0
20
40
60
80
100
Effects of increasing IAP on bowel mucosal oxygen
(tissue partial pressure, TPO2) compared with
systemic tissue oxygenation in the axilla (J
Trauma 199539519-522)
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• 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 ?

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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 oedema.

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Intracranial Derangements and IAH

• IAH associated with
• ?ICP
• ?CPP
• cerebral ischaemia
• ? Why?
• may be due to impairment of cerebral venous
  outflow

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• increased intrathoracic pressure causing
  increased resistance to cerebral venous return
  associated with IAH( ?pseudotumor cerebri).
• 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

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• 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. 

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• Measurement of I A P

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Measurement of IAP
Indirect
Direct
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Direct Monitoring

• The most direct, accurate way to measure
  intraabdominal pressure is through an
  intraperitoneal catheter attached to a water
  manometer or pressure transducer, the preferred
  method in most experimental studies of IAH.1,6,15
  Its use in the clinical situation is limited by
  the potential complications, specifically the
  risk of peritoneal contamination or bowel
  perforation. Abdominal pressure measured during
  laparoscopy is another example of direct
  measurement

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Indirect Monitoring

• Intraabdominal pressure may be indirectly
  measured by measuring pressure within certain
  abdominal organs.
• The first indirect method described involves
  placement of transfemoral catheters into the
  inferior vena cava. The associated risks of this
  procedure include infection and thrombus
  formation.
• measurement of gastric pressure through
  gastrostomy or nasogastric tubes
• esophageal stethoscope catheter
• urinary bladder pressure measurement.

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Bladder Pressure Monitoring

• At intravesical volumes less than 100 mL, the
  bladder acts as a passive reservoir, accurately
  reflecting intraabdominal pressure within a range
  of 5 to 70 mmHg.1,16 When bladder volumes exceed
  100 mL, the intrinsic contraction of the bladder
  wall causes bladder pressure to increase.

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• The basic technique of bladder pressure
  measurement is not complicated. Fifty to 100 mL
  of sterile saline is injected into the bladder
  through a Foley catheter while the tubing to the
  drainage bag is clamped distal to the aspiration
  port.
• The clamp is then opened to allow fluid to fill
  the tubing proximal to the clamp and the tubing
  is then reclamped.
• A 16-gauge needle attached to a water manometer
  or a pressure transducer is then inserted into
  the aspiration port of the catheter, zeroed to
  the level of the symphysis pubis, and the
  intraabdominal pressure recorded.
• Use of the pressure transducer attached to the
  bedside monitor allows a pressure waveform to be
  printed. Slight variation will be seen with the
  respiratory cycle.
• Measurements should always be taken at end
  expiration because the diaphragm is elevated at
  this point, and thoracic pressure is less likely
  to influence the pressure reading

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• Patient positioning affects the accuracy of
  bladder pressure measurements. Monitoring should
  occur with the patient supine so that the weight
  of the abdominal contents pressing on the bladder
  does not falsely elevate the reading. Should the
  patient be unable to remain supine, the position
  at which the first measurement is taken should be
  noted and subsequent measurements taken with the
  patient in that position.2 Although the
  individual reading may be inaccurate, trends in
  abdominal pressure can still be assessed.

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• Others describe the use of a three-way Foley
  catheter, with the saline injected into one of
  the ports. Because three-way Foley catheters are
  not routinely used, their use requires either
  identification of the patient at risk before the
  catheter is inserted, or replacement with a
  three-way catheter when the need to measure IAP
  is identified. This increases costs and the
  potential for infection. Burch et al.7 described
  a technique in which the drainage tubing is
  clamped distal to the aspiration port and 50 mL
  of saline is injected through the aspiration port
  of the Foley catheter

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• Unfortunately, this procedure requires that the
  closed urinary drainage system be opened each
  time pressure is measured, placing the patient at
  increased risk of infection.
• Strict aseptic technique is essential. A sterile
  towel should be placed under the Foley catheter
  to maintain sterility.

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• In patients having a neurogenic bladder or in
  those having a small contracted bladder (e.g.,
  after radiotherapy), measurements may be
  inaccurate.

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• It is also possible that bladder pressure may not
  capture an elevation of the abdominal compartment
  pressure if there is a loculated area. 
• While abdominal compartment pressure monitoring
  via the bladder may provide valuable information
  regarding patients with abdominal hypertension,
  abdominal compartment syndrome should not be
  ruled out in the presence of a normal pressures
  if persistent clinical findings exist

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Grading system for ACS
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CT findings

• CT findings common included tense infiltration
  of the retroperitoneum out of proportion to
  peritoneal disease,
• extrinsic compression of the inferior vena cava
  by retroperitoneal hemorrhage or exudate, and
  massive abdominal distention with an increased
  ratio of anteroposterior-to-transverse abdominal
  diameter (positive round belly sign ratio gt .80
  p lt .001).
• Direct renal compression or displacement, bowel
  wall thickening with enhancement, and bilateral
  inguinal herniation were each present in two of
  the four patients.
• Radiologists should be aware of this
  life-threatening syndrome.
• In the appropriate clinical setting, CT findings
  of increased intraabdominal pressure should be
  swiftly communicated to other physicians involved
  in treating the patient because the abdominal
  compartment syndrome requires emergent surgical
  decompression.

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Central nervous system Implications
?ICP ?CPP
retinal capillaries rupture Valsalva retinopathy
Sudden decrease of central vision
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Management of ACS
Prevention vs. Formal Closure?
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     Management 

• Prevention
• Identification
• of patients at risk
• Monitoring

Adequate resuscitation Adequate ventilation
Non-surgical interventions Paracentesis
Neuromuscular blockade CNAP Gut emptying
Octreotide
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Prevention of ACS (2)Open abdomen technique

• Most commonly used open abdomen techniques
  include
• Bogota bag (25)
• absorbable mesh (17)
• Prolene mesh (14)
• silastic mesh (7)
• miscellaneous (28)

• Current opinion does not support liberal use of
  an open abdomen technique to prevent ACS

The Journal of Trauma, Infection and Critical
Care 199947 509-511
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• An alternative technique is the 'vacuum-pack'
  technique. Here the 3 litre bag is opened and
  placed into the abdomen to protect the gut
  contents, under the sheath. This has been
  referred to as the Bogota bag, after the city in
  Colombia, South America, of its inception.9
• Two large calibre suction drains are placed over
  this, and a large adherent steridrape placed over
  the whole abdomen. The suction catheters are
  connected to high-displacement suction to provide
  control of fluid losses and create the
  'vacuum-pack' effect

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• The easiest method to control the open abdomen is
  to use a silo-bag closure. A 3 litre plastic
  irrigation bag is emptied and cut open so it lies
  flat. The edges are trimmed and sutured to the
  skin, away from the skin edges, using a
  continuous 1 silk suture. It is useful to place a
  sterile absorbent drape inside the abdomen to
  soak up some of the fluid and ease control of the
  laparostomy.

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Adverse Effects of Surgical Decompression

• Sudden release of the abdominal compartment
  syndrome may lead to an ischaemia-reperfusion
  injury The mechanism was postulated to be related
  to washout of anaerobic metabolic products by
  reperfusion of the previously underperfused
  splanchnic bed causing acidosis, vasodilatation,
  cardiac dysfunction and arrest. Prior to release
  the patient should be pre-loaded with crystalloid
  solution. Mannitol and vasodilators such as
  dobutamine or the phosphodiesterase inhibitors
  may have a place here.

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MEDICAL DECOMPRESSION

• The adverse cardiovascular and pulmonary effects
  of intra-abdominal hypertension IAH were
  reversed with pharmacological neuromuscular
  blockade (NMB(

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     Management 

• Prevention
• Identification
• of patients at risk
• Monitoring

Adequate resuscitation Adequate ventilation
Non-surgical interventions Paracentesis
Neuromuscular blockade CNAP Gut emptying
Octreotide
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Prognosis

• The death rate in patients with ACS is extremely
  high.
• Several small series have reported death rates
  ranging from 42 to 71.These high rates must be
  considered in the context of the patients'
  underlying disease.
• The majority of these patients are critically
  ill and are admitted to the intensive care unit
  with severe intra-abdominal sepsis,
  intra-abdominal injuries or after repair of a
  ruptured abdominal aortic aneurysm.
• Even with prompt recognition and abdominal
  decompression, the frequency of multiple organ
  dysfunction and death is high because of the
  severity of the initial physiologic insult.

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• However, in the face of elevated IAP and a
  clinical picture consistent with ACS, the chance
  of survival is extremely low without urgent
  abdominal decompression.1

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