what every critical care nurse needs to know: abdominal

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What every Critical Care Nurse Needs to Know:

Abdominal Compartment Syndrome 101

Amanda Di Florio RN. BN. CNCC (c)

Sandra Cook RN. BN. CNCC (c).

Montreal General Hospital Intensive Care Unit

Potential Conflict of Interest

• I Amanda Di Florio have no Conflict of Interest to declare

• I Sandra Cook have no Conflict of Interest to declare

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MGH – MUHCLevel 1 trauma

center

• 25-35 cases a year of ACS with a required “open abdomen”

• MVC’s, stabbings, crush injuries, gunshot injuries, sepsis, pancreatitis, falls with pelvic fractures,

Why should we worry?

• Melbrain et al. (2004)– A multicentre ( 13 ICU’s) epidemiological study found a prevalence of IAH (

IAP>12mm/ hg) 58.8%

• Vidal et al. (2008)– In a single site study of 83 critically ill patients found 31% had IAH at time of

admission and another 33% developed the condition after admission.

– ACS developed in 12% (10) of the pt.’s and 80% ( 8/10) of them died.

• Reintam et al ( 2008) – Studied IAP in 257 patients receiving mechanical ventilation. They found 97

patients (37% ) developed IAH . The patients with IAH had a significantly higher mortality than those without.

– Concluded that development of IAH is an independent risk factor for death.

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IAH/ACS a long history….

• Heinricius• Demonstrates

I IAP leads respiratory dysfunction then death in animal models

1890

• Emerson • Describes the

Cardiovascular derangements in animal models secondary to I IAP

1911• Wendt• First

described the association of IAH and renal dysfunction

1913

• Kron• Use the term

ACS to describe the pathophysiology resulting from IAH

1980’s

World Society of the Abdominal Compartment Syndrome (WSACS)

2006

• The WSACS created consensus definitions and recommendations for treatment of those with IAH and ACS.

2013

• The WSACS updated the consensus guidelines definitions and clinical practice guidelines

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The Sequence of Events

• Intra‐Abdominal Pressure

• Normal Healthy Person 0 to 5 mmHg

IAP

• Trauma

Burns

Massive Transfusion

Pancreatitis

• Severe Sepsis

Insult • Intra‐AbdominalHypertension

• IAP > 12 mmHg

IAH

• Abdominal Perfusion Pressure

• APP = MAP ‐ IAP

• Goal: Keep > 60 mmHg

APP• Abdominal Compartment Syndrome

• IAP > 20 mmHg

• APP < 60 mmHg

• New Onset Organ Failure

ACS

Four Types of IAHHyperacute

AcuteSubacuteChronic

Three Types of ACS

PrimarySecondaryRecurrent

Intra-Abdominal Pressure (IAP)

• A Steady state pressure within the abdominal cavity

• In healthy person IAP is 0 to 5 mmHg.

• Varies with intra-thoracic pressure during normal breathing

• Average IAP of critically ill pt. can range from 5 to 7mmHg.

• Pt. with increased abdominal girth that developed slowly may have a higher baseline IAP;

• Morbidly obese or pregnant person can have an IAP of 10 to 15 mmHg without sequelae.

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Abdominal Perfusion Pressure (APP)

• Elevated Intra-abdominal pressure reduces blood flow to the abdominal viscera

• Is calculated by Mean Arterial Pressure (MAP) minus the IAP

• A target APP of at least 60 mmHg correlated with improved survival from IAH and ACS

• APP a better resuscitative endpoint than;

• Arterial pH, • Base deficit• Arterial lactate and• Hourly urine output for

predicting outcomes

APP = MAP – IAP

Intra-Abdominal Hypertension (IAH)

• Is Defined as a sustained intra-abdominal pressure > 12 mmHg.

• Determined arbitrarily but used in many studies and identifies an inappropriately elevated pressure.

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Grades of IAP

• Grade 1 – IAP 12 to 15 mmHg



• Grade 4 – IAP > 25 mmHg

Hyper-acute:

- Elevation of the intra- abdominal pressure lasting only seconds.

- Example: laughing, coughing, straining, sneezing, physical activity.

Acute:

- Elevation of IAP that develop over hours.

- Results from trauma or intra-abdominal hemorrhage

- Can lead to rapid development of ACS.

Subacute:

- Refers to the elevation of the intra-abdominal pressure that

develops over days.

- Most common in medical patients

- Can lead to ACS.

Chronic:

Refers to elevation of the intra-abdominal pressure that develops over months (pregnancy) or years (morbid

obesity)

Doesn’t cause ACS

Does place pt. at higher risk for developing ACS

Types of Intra-abdominal

Hypertension

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Abdominal Compartment Syndrome (ACS)

• The Abdominal Cavity bound by; Peritoneum, Diaphragm, Abdominal Wall ( Muscle, Fascia, and Skin) , Ribs & Bony Pelvis.

• Increased pressure within the abdomen directly impacts systemic pathophysiology

• Unlike the compartments in the extremities

Abdominal Compartment Syndrome (ACS)

• Organ dysfunction caused by IAH can result in; respiratory insufficiency, renal, cardiac and neurologic impairment

• If not recognized and treated promptly

• Results in irreversible organ failure

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Abdominal Compartments Syndrome (ACS)

• Is defined as a sustained intra-abdominal pressure > 20 mmHg with or without APP < 60 mmHg.

• Associated with new organ dysfunction

Primary Abdominal Compartment Syndrome

• Occurs with injury in the abdominopelvic region

• Including etiology such as;

• Ruptured Abdominal Aortic Aneurysms

• Abdominal trauma• Retroperitoneal

Hemorrhage from pelvic fractures

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Secondary Abdominal Compartment Syndrome

• Results from Critical Illness;

• Originating outside the abdominopelvic region requiring large-volume resuscitation.

Etiology’s such as;

• Mangled Extremities

• Burns

• SIRS & Septic Shock

• Severe Pancreatitis,

Recurrent Abdominal Compartment Syndrome

• Redevelopment of ACS after previous medical or surgical therapy for primary or secondary ACS.

• Continue to monitor (IAP) bladder pressures even after surgical decompression with open abdomen

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Risk Factors for IAH and ACS

• Major Trauma• Burns• Acidosis• Hypothermia• Poly-Transfusion; >10

Units of blood/ 24 hours• Massive Fluid

Resuscitation; > 5L/24 hours

• Damage Control Laparotomy (DCL)

WSACS 2013

Pathophysiology of IAH/ACS

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Cardiovascular System

• Compression of vena cava with reduced venous return

• Elevated intra-thoracic pressure with multiple negative cardiac effects

• Result:• ↓cardiac output• Increased SVR• Increased cardiac

workload• Decreased tissue

perfusion• Misleading elevations

of CVP and PAOP• Cardiac insufficiency;

cardiac arrest

Respiratory System

• Elevated diaphragm,• ↓ lung volumes• Alveolar inflation• Stiff thoracic cage• ↑ interstitial fluid

• Result:

• ↑ Intrathoracic pressure

• ↓venous return to heart -worsening cardiac problems

• ↑ peak pressures

• ↓tidal volumes

• Barotrauma

• Atelectasis

• Hypoxia & Hypercarbia

• ARDS

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Renal System

• 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!

Central Nervous System

• 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

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Gastrointestinal System

• Compression and 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

Hepatic System

• Livers ability to remove lactic acid is impaired by the increased IAP

• Even at IAP of 10 mmHg.

• Even if CO and MAP are both normal

• Lactic acidosis may clear more slowly despite adequate fluid resuscitation.

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Clinical Presentation

• Recognize IAH early so it can be treated before progressing to ACS

• Challenge to communicate with intubated patient

• If they can convey symptoms they may complain of;

• Malaise & weakness

• Light-headedness

• Dyspnea

• Abdominal bloating

• Abdominal pain

Physical Exam of Abdomen

• Most pt.’s have a tense and distended abdomen

• Physical examination of the abdomen is a poor predictor of ACS.

• Progressive oliguria & increased ventillatory and hemodynamic instability requirements is more predictive of ACS

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Chest X-ray

• Shows decreased lung volumes

• Atelectasis

• Elevated hemi-diaphragms

Computed Tomography

• Tense infiltrates of retro-peritoneum that is out of proportion to peritoneal diseases

• Extrinsic compression of IVC

• Massive abdominal distention

• Direct rectal compression or displacement

• Bowel wall thickening• Bilateral inguinal hernia

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Abdominal Ultrasound

• To identify lesions and guide insertion of a percutaneous catheter drain

Diagnostic Evaluation

• Definitive diagnosis of ACS requires measurement of the Intra-abdominal pressure

• Should be measure at a low threshold

• Especially for those with:

• Trauma

• Liver transplantation

• Bowel obstruction

• Pancreatitis

• Peritonitis

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Measuring Intra-abdominal Pressure

• Many Indirect methods to measure IAP;

• Intra-gastric

• Intra-colonic

• Intra-vesicular (Bladder)

• Inferior Vena Cava

• Hollow wall of bladder acts as a membrane to transduce pressure

• Intra-vesicular (bladder) is the standard method to screen for IAH and ACS.

Measuring Bladder Pressure

• Simple

• Accurate

• Minimally Invasive

• Additional pressure isn’t imparted from the musculature

• Commercial products are available

• Can be performed with routine supplies available in ICU

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Indication for Measuring Bladder Pressure

• Early diagnosis is essential!!!

• ONE of the following criteria is met:

1. New ICU admission OR

2. Evidence of clinical deterioration

• And Pt. has TWO or MORE risk factors

WSACS 2013

Bladder Pressure Equipment

• Transducer• Transducer cable,• Foley• Foley drainage bag• Clamps• Luer lock syringe 60ml• 18 G needle• Normal saline• 3-way stopcock• Newer Foley bags have

needleless connection

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Preparation of Equipment

• Prime transducer set and monitoring lines with 0.9% NS

• Connect 3 way tap to the end monitoring cable

• Attach 60 ml LuerLock syringe to side port of 3 way tap.

Preparation of Equipment

• Insert an 18 G needle into the aspiration port

• Or Connect needless Luer Lock.

• Connect needle to the transducer set up.

• Secure Connections• Keep cables air and

bubble free.

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Bladder Pressure Setup

Bladder Pressure Measurement Method

• Measure in supine Position.

• If not possible - Elevation of the HOB will result in a Higher IAP.

• Always measure in the same position.

• Level the transducer at the mid-axillary line

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• Zero the transducer to atmospheric pressure.

• Clamp the drainage tube to the urine bag

• Fill the bladder with 1ml/kg (maximum 25mls) of NS 0.9%

• Use the same volume of NSfor each measurement.

• Avoid abdominal muscle wall contraction.


• Minimizes the effects of pulmonary pressures

• Abdominal blood flow produces fluctuations in the waveform.

• Air or kinking in the system lines may dampen the waveform.

• Allow 30-60seconds for equilibrium to occur.

• Obtain the mean pressure reading upon end expiration

Ventilator Breath End‐Expiration

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Management of ACS

• Consists of Supportive Care to reduce IAP

• If needed abdominal decompression

• Surgical Decompression of the abdomen is considered definitive management

WSACS 2013

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Goals of Supportive Care

• Evacuate Intra-Luminal Contents

• Evacuate Intra-Abdominal Space occupying Lesions

• Improve abdominal wall compliance;

• Correct positive fluid balance

• Organ Support

WSACS 2013

Evacuate Intra-Luminal Contents

• Insert NGT or OGT• Use Gastro-/Colonic Prokinetic agents

before constipation occurs• Assess tolerance of Nutrition• If residuals are high – feedings should

be decreased or discontinued.• Monitor bowel movements and

fecaloma • Administration of Enemas• Insert Rectal Tube • Consider Coloniscopic Decompression

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Evacuate Intra- abdominal Fluid Collections

• Percutaneous Catheter Drainage (PCD) to Drain;

• Hemoperitoneum

• Ascities (Paracentesis)

• Intra-Abdominal Abscess

• Retroperitoneal Hematoma

• Can occupy space in abdomen and increase IAP

• Avoids the need for subsequent open abdomen decompression

Improve Abdominal Wall Compliance

• Sedation and pain control• Avoid agitation contracts abdominal muscle

–↑ IAP• Debridement of Abdominal eschar if Burn

pt.• Remove constrictive abdominal dressings• Avoid elevating HOB > 30⁰ - Conflicts with

VAP bundle• Compromise by placing pt. in reverse

Trendelenburg (except when measuring IAP)

• Paralysis ↓ abdominal muscle contraction• ↓CO2 production & permits better

ventilation

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Fluid Balance

• Large-Volume Crystalloids Resuscitation for shock can lead to ACS

• Goal Directed Fluid Therapy• Avoid excessive fluid resuscitation• Aim for Zero to negative fluid balance by

the 3rd day• Hypertonic NS or Colloids to help reduce

bowel edema.• Diuretics • Use of CRRT

Hemofiltration

• WSACS made no recommendation regarding the use of Renal replacement therapy

• Used to mobilize fluid in Hemodynamically stable pt. with IAH

• After the acute resuscitation has been completed

• And inciting issues/source control has been addressed.

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Diuretics

• WSACS made no recommendation regarding the use of Diuretics

• To aid mobilize fluids in Hemodynamically stable pt. with IAH

• After Acute resuscitation has been completed and inciting issues/sources have been controlled.

Albumin

• WSACS made no recommendation regarding the administration of albumin versus not

• To help mobilize fluids in Hemodynamically stable pt. with IAH after the acute resuscitation has been done.

• And inciting issues and sources have been controlled.

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Organ Support

• Keep APP> 60 mmHg or greater with fluids

• Inotropes & Vasopressors can be used

• IAH can falsely elevated CVP and PAWP

• WSACS recommends using formula to correct for this

CVP corrected = CVP measured ‐ IAP/2PCOP corrected = PCOP measured ‐ IAP/2

Ventilation & Oxygenation

• High Peak Pressure and Higher Mean Airway Pressures can be problematic

• Decrease Tidal Volumes

• Pressure –limited Mode

• Permissive Hypercapnia may be necessary

• PEEP – may reduce ventilation perfusion mismatch and Improve Hypoxia

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The Open Abdomen

• Abdominal incision which opens abdomen because of concern of abdominal compartment syndrome

• Abdominal wall and fascia are surgically opened

Indications for the Open Abdomen

• Abdominal trauma

• Ruptured abdominal aortic aneurysm

• Retroperitoneal hemorrhage

• Pancreatitis

• Extensive burns

• Sepsis

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Pathophysiology of the Abdomen

• Intestine is highly vascularized• Rich network of arteries, veins,

capillaries and lymphatic vessels

• In pathologic states there is a decrease in clearance of fluid from extracellular space.

• Resulting in swelling of the intestinal wall, interfering with perfusion of bowel

Pathophysiology of the Abdomen

• Peritoneal surface is highly vascularized

• Colonized with inflammatory cells

• Trauma results in excretion of pro-inflammatory substances

• That increase the local inflammatory response

• Leading to SIRS and potentially MODS.

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Decompressive Laparotomy

• Used in cases of ACS (only definitive treatment)

• Should be performed when IAP>20 with new or progressive organ failure

• Recommended for the trauma or acute general surgical patient under physiologic stress: acidosis, hypothermia, hypocoagulable state, prolonged hypotension

Decompressive Laparotomy

• Ischemic or embolic events (Ischemic bowel)

• Intra-abdominal infections (ie: necrotizing pancreatitis)

• Goal is for formal abdominal fascial closure within 48-72 hrs of the initial laparotomy

• Daily trips to the O.R. are often required for incremental closure of the abdominal fascia

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Benefits of Decompressive Laparotomy

• Decrease in intrathoracic pressure

• Improved oxygenation/ventilation

• Increased cardiac output

• Increased urine output

• Ease of re-exploration (2nd look)

• Control of abdominal contents

• Decrease in risk of IAH and ACS

• Fascial preservation for closure of the abdominal wall

Complications: Fluid Loss

• Significant amount of fluid can be lost through an open abdomen

• Requires close monitoring of negative pressure wound system suction output/overall pt. Intake and output

• Risk of hypovolemia

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Complications: Fluid Loss

• Loss of hypotonic fluid from the wound and peritoneal cavity can result in hypovolemic hypernatremia

• Serum Na+ levels need to be closely monitored

• In these cases, isotonic fluids should be used in the hypovolemic pt.

Complications: Protein Loss

• Fluid secreted by the peritoneum is rich in protein

• Should be replaced by enteral nutrition

• Serum Albumin IV may be used • Large amounts of protein loss

from the wound can result in changes in oncotic pressure at the capillary bed level

• Resulting in further loss of circulating volume into the interstitial space

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Complications: Fistula Formation• Enteroatmospheric-fistulas

• Caused by breakdown of exposed intestines

• Allows for abnormal communications to form between intestines and the outside

• Extremely difficult to manage- pt will require many OR’s in attempt to reconstruct

Complications: Fistula Formation

• Longer time lapse until fascial closure or wound coverage with skin grafting results in higher rates of fistula formation

• Fistula repair can typically occur 6-12 months after initial laparotomy

• Prevention:

• Protect exposed viscera

• Suction dressing (negative pressure wound system or VAC therapy)

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• Minimization of fistula output: nasogastric drainage diverts gastric secretions from entering the proximal small bowel

• PPI’s or H2 – receptor antagonists will decrease the volume and acidity of gastric secretions resulting in decreased fistula output


• Subcutaneous Octreotide : somatostatin analogue

• Octreotide inhibits the secretion of many GI hormones; gastrin, glucagon, cholecystokinin, secretin, insulin, and vasoactive intestinal peptide.

• Inhibits gastric acid secretion, pancreatic exocrine secretion, intestinal and gallbladder contractility

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Complications: Loss of Domain

• Musculature of abdominal wall retracts the fascia laterally.

• Unopposed forces of the oblique muscles pull the abdominal wall in a lateral direction

• Soft tissue shrinks making re-approximation difficult over time

Complications: Loss of Domain

• Sometimes fascia is not able to be brought back to the midline

• Resulting in a ventral hernia

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Complications: Hernia

• Damage to the abdominal fascia results in hernia formation

• Closure of the abdominal wall with skin, muscle, and peritoneum will result in hernia formation over time

Complications: Hernia

• Little risk of strangulation of the bowel

• But cause deformity and discomfort to the pt.

• Can be caused by;• Abdominal distension,• Abdominal wall tension• Fistula formation • Pt. underlying medical status• Closure of hernia is very

complex

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Complications: Infection

• Large open surface area provides a venue for bacterial colonization

• Abdominal cavity infections

• Large potential for abscess formation

• Use of prophylactic antibiotics

• Post open abdomen there is tissue destruction, contamination, hematoma and inflamed tissue that may require aggressive debridement

• Leading to an intense inflammatory response

Complications: Bleeding/hemorrhage

• Bowels and splanchnic organs have a rich blood supply.

• Increased risk of bleeding especially when inflamed or traumatized bowel wall is exposed to air

• Common in trauma pt’s who suffer coagulopathy from hypothermia, acidosis, hypotension, dilution of blood volume, and uncontrolled exhaustion of clotting factors

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Temporary Abdominal ClosureNegative Pressure Wound Systems

• Either surgical towels, fenestrated, non adherent polyethylene sheet is placed over viscera

• Continuous wall suction is applied to the Jackson-Pratt drains

• Sometimes a commercial V.A.C. is used

Temporary Abdominal ClosureNegative Pressure Wound Systems

• Controls abdominal contents, achieves skin closure, achieves fascial closure, removes exudate, quantifies third space losses, promotes granulation and controls infection

• The negative pressure wound system is recommended by the WSACS

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Temporary Abdominal ClosureSkin Only

• Using towel clamps or staples

• Inexpensive, rapid, maintains abdominal domain

• Avoided as it does not control fluid loss from the wound, and increased incidence of ACS reoccurring.

Temporary Abdominal Closure Silo (Bogota Bag)

• Involves suturing a large, sterilized translucent bag to the abdominal fascia or skin

• Low cost• Allows visual inspection of

abdominal viscera• Disadvantages:• More time consuming• Risk of evisceration• Loss of abdominal domain,• Increased risk of ACS

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Temporary Abdominal ClosureZipper (Wittmann Patch)

• Velcro like prosthetic is placed over the abdomen

• Allows for easy entrance into the abdomen for re-exploration

• Facilitates closure of the abdomen with serial narrowing and trimming of the mesh until the abdomen is closed

• Risk of fascial necrosis

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Temporary Abdominal ClosureAbsorbable Mesh

• Polypropylene mesh

• Anchored to the fascia laterally, serial plication of the patch at the midline progressively brings the fascial edges together

Temporary Abdominal ClosureAbsorbable Mesh

• Protects against evisceration

• Disadvantage:

• 50% hernia rate

• Risk of enter cutaneous fistula

• Increased risk of ACS

• WSACS does not recommend routine use of bioprosthetic meshes compared to alternative strategies

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Nutrition Support Considerations

• Early administration of enteral nutrition;

• Improves wound healing

• Reduces hospital and ICU lengths of stay

• Decreases infection rates

• May improve survival after critical illness and injury

• Helps decrease gut edema,

• Helps earlier fascial closure

• Either nasogastric tube or post pyloric tube placement

Nutrition Support Considerations

• Sometimes TPN may need to be used (depending on extent of bowel resection/damage)

• In case of TPN central line or PICC line placement

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Nursing Care

• Monitor the dressing for any signs of leakage

• Notify surgical team if so - dressing will need to be changed

• Abdominal contents should be inspected for; colour, warmth, capillary refill

• Importance of always maintaining a good seal in dressing and drains

• Drains and Jackson-Pratt’s need to be hooked up to suction immediately post-op

Nursing Care

• Sedation and pain control

• Pt. needs to remain sedated due to risk of evisceration if pt too agitated.

• Monitoring CVP’s- negative balance is preferred (aggressive diuresis)

• Pt should remain intubated due to frequent trips to OR for attempts at fascial closure or dressing changes

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Nursing Care

• Enteral feeding-recommended and safe in open abdomen

• Post-op monitoring for bleeding (check the canister, serial Hgb’s, hemodynamics)

• Psychosocial aspects: Body image issues, especially with younger trauma patient population

• Post-op monitoring of bladder pressures for IAH

• Patient positioning: minimal turning, pt cannot be sat up at 90 degrees, risk of evisceration

• Risk of skin breakdown and VAP

• In case of evisceration: cover with moistened sterile dressing and contact stat surgical service

Conclusion

• ACS is extremely common in the critical care patient population

• Unfortunately overlooked or missed

• Increased mortality and morbidity

• ICU nurses play an extremely important role in assessing and caring for these patients

• Should a bladder pressure be considered like a CVP measurement?

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Special Thank You..

• Dr. Andrew Beckett, Trauma staff MGH

• Dr. Kosar Khwaja, Trauma staff MGH

• Ms. Julie Kinnon, Nurse Educator, MGH ICU

• Ms. Cathy Becker, Nurse Educator, MGH ICU

• Ms. Colleen Stone, Head Nurse, MGH ICU

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what every critical care nurse needs to know: abdominal

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