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Abdominal Compartment Syndrome A case base approach to Intra-Abdominal Hypertension & Abdominal Compartment Syndrome

Brandon Braddock, MPAS, PA-C

Pulmonary/Critical Care

Objectives

S Identify etiologies of Intra-abdominal hypertension and Abdominal compartment syndrome

S Identify clinical signs and symptoms of Intra-abdominal hypertension and Abdominal compartment syndrome

S Recognize and implement the use of bladder pressures for the diagnosis of Intra-abdominal hypertension and Abdominal compartment syndrome

S Recognize and understand treatment modalities for Intra-abdominal hypertension and Abdominal compartment syndrome

Patient History

S Patient S: 35 year old obese Caucasian female

S PMHx

S Chronic anemia

S Poly-substance abuse w/ IVDA

S Alcohol abuse

S Alcohol induced Cirrhosis

S R hip abscess

S Chronic pancreatitis

Surgical Hx

S Bilateral total hip arthroplasty – 2009

S Recurrent R hip infections and chronic dislocations

ED Presentation

S Chief Complaint:

S Altered mental status

S Last seen in her usual state of health by patient’s significant other one night prior when she went to bed.

S HPI:

S Reportedly, upon waking, the patient was confused and was repeatedly saying “I’m scared.” Patient’s significant other denied patient’s active IVDA however did report patient takes morphine & dilaudid which she obtained “on the streets”

ED Presentation cont.

S Vital Signs

S Temperature: 95.9° F

S Heart rate: 120bpm

S Respiration rate: 26 breaths/min

S SpO2: 95%

S Blood pressure: 79/48mmHg

S Relevant physical Exam:

S Pale, jaundiced appearing – moderate distress

S Lungs clear

S Normal BS, soft, non-tender, non-distended abdomen

S + Edema/erythema of R hip w/ blanching & purulent drainage

S Awake, alert – not following commands

ED Presentation cont.

S Relevant Lab Results

S WBC 3.1

S Hgb 5.8

S Platelets: 127

S aPTT 68.4

S PT 34.1/INR 3.44

S Glucose 149

S BUN 10/Cr 2.9

S Sodium 126

S Potassium 2.7

S Arterial lactate 4.55

S Relevant Imaging Studies

S CT brain – neg

S CT abdomen/pelvis - pancolitis, chronic pancreatitis, bibasilar consolidation

S CT R. lower extremity – Chronic hip dislocation, surrounding edema

Assessment

S Severe sepsis with septic shock and multi-organ failure secondary to:

S Pancolitis

S PNA

S UTI

S Cx (+) MSSA Bacteremia

S Acute hypoxemic respiratory failure defined as hypoxemia w/ PaO2 < 60 on ABG

S Required intubation & full MVS

S Septic shock induced hypotension defined as: a systolic BP less than 90mmHg for a period greater than 15 minutes despite adequate fluid resuscitation or Lactate > 4 (previous guidelines)

S Refractory to IVF (30ml/kg) & required vasopressor support

Assessment cont.

S Acute stage 3 renal failure defined as a rise in sCr 3x baseline or UO < 0.3ml/kg/hr for > 24 hours or anuria for > 12 hours despite adequate fluid resuscitation secondary to septic shock

S Metabolic acidosis secondary to renal failure, type A hyper-lactatemia & decreased strong ion difference

S Electrolyte abnormalities secondary to renal failure & septic shock

S Disseminated Intravascular Coagulopathy (DIC) secondary to septic shock:

S Thrombocytopenia

S Coagulopathy

S Acute encephalopathy secondary to septic shock

S Altered mental status & no intracranial abnormality identified on CT brain

Clinical Course

S Large volume fluid resuscitation: 25L +

S IVF – isotonic solution (NS 0.9%) re: hypotension

S PRBC & FFP re: anemia & coagulopathy

S IV Abx re: infectious etiologies

S IV sedation (Fentanyl/Propofol) re: vent management targeting a RASS -1

S Significant third-spacing (interstitial edema)

S Mechanical ventilatory support

S Multi-disciplinary team

S Intensivist, Ortho, Nephro, ID, PCP, Heme/Onc, General Surgery, PT/OT/ST, RN, Respiratory, Dietary, Social Services

Repeat Physical Exam

S Hypoactive bowel sounds

S Misleading – majority of

critically ill patients develop

hypoactive bowel sounds

S Distended abdomen

S Firm/rigid abdomen

S Generalized anasarca – third

spacing

S Decreasing urinary output

S Increasing vasopressor requirement

S Worsening hypoxemia

S Increased peak pressures –

indicative of poor chest wall

compliance or increased

abdominal pressures

S Increased FiO2 requirement

S Resultant atelectasis

Diagnostics Intra-vesicular pressure

(bladder pressure): greater

than 25

Repeat CT abdomen/pelvis:

Diffuse severe colonic wall

thickening (Colitis)

Assessment 2.0

S Severe sepsis with septic shock and multi-

organ failure – refractory to aggressive

treatment

S Required multiple vasopressors

S Acute hypoxemic respiratory failure –

declining status with increased V/Q

mismatch + hypervolemia induced

pulmonary edema requiring - increased

PEEP & FiO2

S Acute stage 3 renal failure – progressive to

anuria despite optimal fluid resuscitation

& improved sCr

S DIC – refractory w/ worsening

coagulopathy – INR rising

Assessment 2.0 cont.

S Acute cholestasis secondary to septic

shock as evident by rising

aminotransferases & bilirubin

S Critical-illness related adrenal insufficiency

– required stress dose steroids

S Worsening metabolic acidosis w/ pH 7.0

by ABG & worsening hyper-lactatemia

despite initial improvement

S DDx now includes

S Intra-abdominal hypertension &

abdominal compartment syndrome as

a result of

S Diffuse colitis & generalized ileus

S Cholestasis

S Septic shock

S Profound interstitial edema

secondary to large volume

resuscitation and septic shock

induced capillary leak

Defining IAH & ACS

S Intra-Abdominal Hypertension (IAH)

S A steady state pressure of greater than 12mmHg concealed within the abdominal cavity

S Abdominal Perfusion Pressure (APP)

S Defined as Mean Arterial Pressure (MAP) – Intra-Abdominal Pressure (IAP)

S Abdominal Compartment Syndrome (ACS)

S A sustained IAP > 20mmHg (with or without an APP < 60) that is associated with new organ dysfunction/failure – research purposes

Defining IAH & ACS

S Primary Intra-Abdominal Hypertension or ACS

S Condition associated with injury or disease originating from

the abdomino-pelvic cavity

S Secondary Intra-Abdominal Hypertension or ACS

S Condition associated with injury or disease not originating

from the abdomino-pelvic cavity

Intra-abdominal Hypertension

S Grade I- defined as intra-abdominal pressure 12-15 mmHg

S Grade II- defined as intra-abdominal pressure 16-20 mmHg

S Grade III- defined as intra-abdominal pressure 21-25 mmHg

S Grade IV- defined as intra-abdominal pressure > 25 mmHg

IAH Acuity

S Acute

S Elevated IAP developing over the course of several hours i.e trauma, intra-abdominal hemorrhage – concerning for progression to ACS

S Subacute

S Elevated IAP developing over days i.e. critically ill patients

S Critically ill patients generally have an IAP 5-7mmHg

S Chronic

S Elevated IAP developing over months/years i.e pregnancy, obesity – generally not progressive to ACS

Risk Factors

Primary

S Abdominal trauma

S Abdominal surgery

S Cirrhosis w/ascites

S Gastroparesis/ileus

S Ogilvie’s syndrome

S Volvulus

S Pancreatitis

S Abdominal abscess

S Retroperitoneal bleed

Secondary

S Large IVF resuscitation

S Mechanical ventilation

S Sepsis and/or septic shock

S Burns

S Metabolic acidosis

S Third spacing/interstitial

edema

Physiologic Consequence Cardiovascular

S Impaired cardiac function

S Increased IAP leads to reduced ventricular compliance & contractility

S Can occur at IAP as low as 10mmHg

S Exacerbated in underlying heart failure

S Reduced venous return

S Increased IAP leads to compressed IVC and decreased preload & decreased cardiac output – exacerbated by hypovolemia

S Increased systemic vascular resistance & venous hydrostatic pressure

S Increased third spacing & DVT risk

Physiologic Consequence Pulmonary

S Increased risk of alveolar barotrauma

S Increased peak & plateau pressures

S Reduced lung & chest wall compliance

S Increased V/Q mismatch – arterial hypoxemia & hypercapnia

S Accentuated in patient’s requiring large IVF, bronchospasm (COPD exacerbation) & pt’s requiring increased PEEP

S Increased risk of pulmonary infection/ventilator acquired pneumonia

S Increased duration of vent support – poor ventilation

S Increased atelectasis, edema, pleural effusions

S May require NIPPV and/or MVS if not already

Physiologic Consequence Renal

S Renal vein compression

S Increases venous resistance and impaired venous drainage; studies

suggest the primary cause of renal impairment

S Renal artery vasoconstriction & sympathetic response

S Induced by sympathetic nervous system & RAAS system due to decreased cardiac output

S Oliguria typically noted when IAP > 15mmHg

S Anuria occurring when IAP > 30mmHg

Physiologic Consequence Gastrointestinal

S Mesenteric ischemia

S Decreased mesenteric vein flow due to increased intestinal edema

leading to worsening IAP and possibly ACS as well as bowel necrosis

and lactic acidosis – vicious cycle

S Studies suggested mesenteric blood flow is reduced with an IAP as

low as 10mmHg

S Intestinal mucosal perfusion decreased with IAP > 20mmHg

Physiologic Consequence Gastrointestinal

S Bowel hypo-perfusion

S Targeting abdominal profusion pressure – 60mmhg (MAP – IAP)

S Increased bacterial translocation

S Can occur at IAP of only 10mmHg – more prominent in cases of hemorrhage

S Hepatic dysfunction

S Impaired toxin clearance i.e Lactate

S Impaired production of coagulation factors

S Impaired protein production i.e Albumin

S Leads to decreased hydrostatic pressure & development of ascites & increased IAP

S Exacerbated in patients with underlying liver disease; our patient has a hx of EtOH

cirrhosis

Physiologic Consequence Central Nervous System

Cerebral Ischemia

S Increased intracranial pressure

leading to decreased cerebral

perfusion & ultimately cerebral

ischemia

S Secondary to decreased

venous return/decreased

cardiac output

Symptoms

S Generalized complaints

S Malaise/fatigue

S Weakness

S Dyspnea

S Abdominal bloating

S Abdominal pain

S Limitations in patient

assessment/symptoms

S Patient’s unable to

communicate

S Encephalopathic

S Mechanical ventilatory

support

Physical Signs

S Distended/firm abdomen

S Decreased bowel sounds - misleading

S Significant third spacing

S + Fluid wave (ascites)

S Increased JVD

S Worsening obtundation

S Cool/diaphoretic skin

S Progressive organ dysfunction despite

treatment

S Progressive oliguria/anuria

S Increased vent support

S Increased FiO2

S Increased PEEP

S Decreased tidal volumes

S Refractory hypotension

Physical Signs

S Limitation in physical exam

S Poor predictor of ACS; prospective cohort study (N=42) of

blunt abdominal trauma demonstrated:

S Sensitivity 56%

S Specificity 87%

S PPV 35%

S NPV 94%

Diagnostics

S Imaging: not helpful in the diagnosis of ACS

S Chest radiograph may show:

S Low lung volumes, raised hemi-diaphragm, atelectasis

S CT abdomen/pelvis may show:

S Extrinsic compression of IVC

S Abdominal distention

S Renal compression

S Bowel thickening

S Inguinal herniation

Diagnostics

S Definite dx requires intra-abdominal pressure monitoring

S Can be measured via multiple modalities including:

S Intragastric

S Intracolonic

S Intravesicular (bladder)

S IVC catheters

S Gold standard as defined by the WSACS for IAH/ACS screening:

S Intravesicular (bladder) pressure

Bladder Pressure Technique

S Patient must be in supine position

S Clamp Foley catheter drainage tube

S Instill a maximum of 25ml sterile saline into the bladder via the aspiration port of the Foley

S 18g needle attached to a pressure transducer is inserted into the aspiration port (needle-less systems available)

S Pressure is measured at end-expiration once the transducer is zeroed at the level of the mid-axillary line

Therapeutic Interventions

Noninvasive Bowel Decompression

S Nasogastric or orogastric tube placement

S Placement of bowel management systems. i.e Rectal tube placement

S Maintain supine position or head of bed no greater than 30 degrees of elevation if possible (risk assessment for VAP, aspiration, ICP)

Invasive Decompression

S Procedure dependent upon cause

S Ascites paracentesis

S Abdominal

abscess/hematoma/hemoperi

toneum percutaneous

needle aspiration

S Burns escharotomy

Therapeutic Interventions

S Definitive therapy: treat underlying cause

followed by:

S Abdominal decompression

S Controversial in regards to timing of

surgical decompression

S All pt’s w/ IAP > 25mmHg

S Some clinicians suggest

decompression w/ IAP 15-

25mmHg – felt there is improved

APP & pt outcome

S Some clinicians recommend

following the APP

S Retrospective study

demonstrated APP

<50mmHg more predictive

of mortality w/ increased

specificity/sensitivity than

MAP or IAP alone

S Open abdomen with temporary closure

Therapeutic Intervention

Patient S

S Due to patient’s refractory and progressive multi-organ failure in conjunction with elevated intra-vesicular pressures she underwent abdominal decompression and was noted intra-operatively to have IAP in excess of 20mmHg

S She was transferred back to SICU post-operatively in critical condition however tolerated the procedure adequately

S Vasopressor requirement had improved

S 24hrs post-op she underwent closure of

her open abdomen after resolution of

the acute phase of her abdominal

compartment syndrome

Outcome

S Unfortunately, due to patient S’s severe and refractory multi-

organ failure triggered by severe sepsis and septic shock

further treatment was deemed futile.

S At the discretion of her significant other, as well as input

from a multifaceted team, a terminal wean was requested.

S Ultimately, the patient succumbed to her illness following

withdrawal of life support.

Summary

S Intra-abdominal Hypertension & Abdominal Compartment Syndrome can be caused by numerous etiologies both primary and secondary

S Early recognition of developing signs/symptoms prompts urgent treatment

S Although IAH alone is not a predictor of MOF, mortality for patients who progress to ACS ranges from 40-100 percent

S Bladder pressures remain the gold standard for IAP monitoring

S Definitive treatment is by surgical abdominal decompression

References

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