By Abd El-Monem M. Kozea, Mohamed M. E. Abd El-Monsef, Soaad Abd El-Badie Attia El-Afify
Foundations Abd and limb CS
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Compartment Syndromes Dr Mark Wheatcroft Vascular Surgeon St Michael’s Hospital, Toronto Associate Professor University of Toronto
Transcript of Foundations Abd and limb CS
Compartment Syndromes
Dr Mark Wheatcroft Vascular Surgeon St Michael’s Hospital, Toronto Associate Professor University of Toronto
Disclosures: None
Learning Objectives
l Describe the pathophysiology of compartment
syndrome
l List the common causes
l Apply methods of assessment to reach a diagnosis
l Describe the treatment of compartment syndrome
l Definitions l History l Classification l Pathogenesis l Measurement l Pathophysiology l (ACS in AAA patients) l Clinical management
Introduction: Abdominal Compartment Syndrome
Compartment Syndrome
l “ a condition in which increased tissue pressure in a confined anatomic space, causes decreased blood flow leading to ischaemia and dysfunction”
l “may lead to permanent impairment of function”
Compartment Syndrome -
What is it & what happens?l Blood flow requires a pressure gradient
Blood flow / Perfusion
Arterial pressure (MAP) HIGH
Venous capillary pressure LOW
Pressure gradient
Flow
Blood flow / Perfusion
Arterial pressure (MAP) HIGH
Venous capillary pressure INCREASED
Pressure gradient
Flow
Blood flow / Perfusion
Arterial pressure (MAP) HIGH
Venous capillary pressure HIGH
NO gradient
NO Flow
No Flow = No perfusion = ISCHEMIA
Intra-abdominal pressure & hypertension
l “Normal” in critically ill: IAP = 5 – 7 mmHg
Consensus definitions: l IAH: Sustained or repeated pathologic elevation in
IAP >12mmHg •ACS:
Sustained IAP>20mmHg with new onset end-organ dysfunction
Abdominal Compartment Syndrome
Abdominal pressure >20mmHg with new organ dysfunction
l Clinical syndrome of increased IAP, increased airway pressure, hypoxia & oliguria
Definition
Abdominal Perfusion Pressure
l Same concept as cerebral perf. press.
l APP = MAP – IAP
l APP is possibly a better resus. end point than pH, base deficit, lactate & even UO.
l APP > 60mmHg improves survival from IAH & ACS
History
l 1890: IAP death due respiratory function l 1911: IAP VR cardiac failure l 1947: IAP UO due to GFR
l 1940: Ogilvie advised against abdo closure under tension, advocating impregnated canvas.
l 1984: Kron coins the term ACS following observation of AAA patients
l Early IAP renal impairment independent of BP or CO
l Described use of urinary catheter as a method of measuring IAP
ACS
l Increasingly recognized cause of:
l Decreased C.O. l Decreased U.O. l Increased airway pressure l Metabolic acidosis
Frequency of ACS
l Trauma: 0.5 – 36% l Burns: 1 – 20% l Surgery: 4 – 8% l Pancreatitis: 36%
l Mortality: 25 – 75%
Classification & Pathogenesis
ACS
Chronic Ascites Obesity
Acute
Secondary (extra -abdominal)
Extrinsic pressure – tight closure Burns Shock suits Sepsis Capillary leak
Intraperitoneal - Common Trauma Post op bleeding Bowel Obstruction Peritonitis Visceral oedema Large incisional hernia closure AAA
Retroperitoneal -less common Pancreatitis Trauma Pelvic bleeding Sepsis AAA
Multifactorial Ischaemia-reperfusion injury Fluid resus & ECF volume Capillary leak Oxygen free radicals
Primary
RecurrentACS redevelops after management of primary or secondary ACS
Risk Factors for ACS
1. Reduced Abdo wall compliance
2. Increased intra- luminal contents
3. Abdominal collections
4. Cap. leak & Fluid resus
Many ICU patients
1. Reduced Abdo wall compliance
Obesity Abdominal surgery Prone positioning Rectus sheath hematoma Burns with abdominal eschars Mechanical ventilation with high positive end-expiratory pressure Ventilator dyssynchrony
2. Increased intra-luminal contents
Gastric distention Gastroparesis Colonic pseudo-obstruction Volvulus Abdominal tumor Intra-abdominal or retroperitoneal tumor Damage control laparotomy Enteral feeding
2. Increased intra-luminal contents
Gastric distention Gastroparesis Colonic pseudo-obstruction Volvulus Abdominal tumor Intra-abdominal or retroperitoneal tumor Damage control laparotomy Enteral feeding
3. Intra-abdominal collections
Ascites Hemoperitoneum Pneumoperitoneum Major trauma Laparoscopy with excessive inflation pressures Peritoneal dialysis Abdominal inflammation-peritonitis, pancreatitis Abdominal abscess
3. Intra-abdominal collections
Ascites Hemoperitoneum Pneumoperitoneum Major trauma Laparoscopy with excessive inflation pressures Peritoneal dialysis Abdominal inflammation-peritonitis, pancreatitis Abdominal abscess
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4. Capillary leak & fluid resuscitation
Acidosis Hypothermia Coagulopathy Massive transfusion Trauma Sepsis Large volume fluid resuscitation Major burns
4. Capillary leak & fluid resuscitation
Acidosis Hypothermia Coagulopathy Massive transfusion Trauma Sepsis Large volume fluid resuscitation Major burns
Measurement of IAP
Direct l Catheter placed at laparotomy/
laparoscopy l Highly accurate l Potential for infection l Not all patients need one at time
of surgery
Indirect l Intra-vesical l Intra-gastric l Rectal catheter l Femoral vein catheter l Less invasive l Less infection risk l Can be placed at any time post
op
Intravesical Catheter
l Bladder is a passive diaphragm when volume is 25ml
l Standard urinary catheter l Empty bladder filled with 25ml saline l Catheter clamped l Needle connected to pressure transducer inserted
into aspiration port l Accurate to within 3mmHg (range 5 to 50mmHg) l Dedicated catheter kit now in use in ITU
Standards
l mmHg (1mmHg = 1.36 mmH2O) l End expiration l Supine l Zeroed at MAL l Measured 30 – 60 secs after instillation
Pathophysiology of IAP
l CVS l Renal l Respiratory l GI l (CNS)
Cardiovascular Systeml CO due to pre- & after-load
l Mainly venous return due to increased resistance in IVC / portal circulation
l IAP transmitted to thorax ITP = CVP resistance in SVC and cardiac tamponade
l Caused by pressures as low as 15mmHg
l Exacerbated by hypovolaemia
l Cellular O2 delivery, anaerobic metabolism, ischaemia, endothelial damage and capillary leakage.
Renal Systeml Multifactorial – pre-renal & renal l Pre-renal - CO renal perfusion l Renal:
l Oliguria at 15mmHg, anuria >30mmHg
IAP
Compression of RV
Renal vasc resistance
Renal perfusion
GFRReninAldosterone
ADH
Respiratory Systeml IAP intra-thoracic volume lung capacity
& compliance resp. failure
l Peak airway pressure Alveolar volutrauma
l Compliance V/Q mismatch
l Also Pulm. Vasc. Resistance
l Effects at pressures as low as 15mmHg
GI Systeml IAP blood flow in mesenteric & hepatic
arteries
l blood flow to intestinal mucosa
l Bowel tissue oxygenation drops at 15mmHg
l Effects potentiated by hypovolaemia
l Organ ischaemia & bacterial translocation
CNS
l IAP Lumbar venous plexus & Central venous drainage
l PaCO2 cerebral arterial inflow
l Altered CNS function
Summary of effects
Rajasurya V, Surani S. World J Gastroenterol. 2020 Jan 21; 26(3): 266–278.
Overall
l IAP > 20mmHg can have profound effects on all the above systems
l Up to 93% improvement in organ function following decompression
ACS in AAA Patients
l All ACS studies small l Majority in trauma patients l Few & small studies in AAA surgery l Mostly retrospective l More common in RAAA - Multi-organ failure common cause
of death - ? Due to ACS
Studies to date:
l Fietsam: 4% incidence of ACS in RAAA American Surgeon 1989 (55).
l IAP >18mmHg significant risk factor for renal impairment ANZ J Surgery 1990 (60)
l Rasmussen: improved survival with early mesh closure in at risk patients
J Vascular Surgery 2002 (35)
Prospective Study
l Papavassiliou et al. Eur J Vasc Endovasc Surg 2003
l IAP significantly higher at closure of RAAA than elective AAA
l At risk of ACS if IAP > 15mmHg
Management of ACS - Prevention
l Recognition of at risk patients: Hb < 100g/l Pre-op arrest SBP < 90mmHg for > 18min > 3.5l fluid resus per hour of surgery T < 33ºC Base deficit > 13
• Benefit from open abdomen strategy?
Diagnosis / Work up
l Measure IAP l U&Es, FBC, Coag, Amylase, lactate, ABG. l ECG l CXR - ?perf l CT abdo: “Round belly sign” IVC collapse Thickened bowel wall Bilat. ing. Hernias AAA
Management
l 1. Serial monitoring of IAP
l 2. Optimize systemic perfusion & organ function
l 3. Specific medical Rx to reduce IAP
l 4. Surgical decompression
2. Optimize perfusion
l Adequate but judicious fluid resus. (avoid overload)
l Vasopressors / inotropes
3. Medical Rx to reduce IAPl Improve abdo wall compliance Sedation & analgesia NMB Positioning
l Evac. Intra-luminal contents NGT/Rectal tube
l Evac. Abdo fluid collections Percutaneous
l Correct +ve fluid balance Early CVVH/diuretics
4. Surgical decompression
l Refractory ACS l Life-saving l “presumptive decompression” in at risk
cases l Bogota bag l VAC dressing
“there is often a delicate balance between effective tamponade of bleeding and the untoward physiological effects of ACS”
“ACS without expedient decompression is uniformly fatal”
Finally
From a vascular surgeon’s perspective:
An aortic graft in an open abdomen is very risky
Limb Compartment Syndrome
Why does it matter?
l Muscle and nerve ischemia l Untreated progresses to necrosis l Permanent disability l Limb loss
Compartment Syndrome -
What is it & what happens?l Blood flow requires a pressure gradient
Blood flow / Perfusion
Arterial pressure (MAP) HIGH
Venous capillary pressure LOW
Pressure gradient
Flow
Blood flow / Perfusion
Arterial pressure (MAP) HIGH
Venous capillary pressure INCREASED
Pressure gradient
Flow
Blood flow / Perfusion
Arterial pressure (MAP) HIGH
Venous capillary pressure HIGH
NO gradient
NO Flow
No Flow = No perfusion = ISCHEMIA
Lower leg compartments
l Deep fascia - l enveloping entire leg l separating the 4 compartments
l Fixed volume l Little capacity for expansion
Image courtesy of “fastbleep.com"
Increased compartment volumecell swelling, interstitial fluid,
blood, venous occlusion
Increased compartment pressure
Increased venous capillary pressure
Decreased gradient
Decreased flow / perfusion
ISCHEMIA
Compartment Syndrome - What causes it?
l Ischemia / reperfusion injury - ALI l Trauma - crush, fracture l Severe DVT - Phlegmasia l Intra-compartment hemorrhage
Assessment & Diagnosis - History
l At risk patient - relevant injury l High index of suspicion
l Pain l Out of proportion l Unresponsive to immobilization l Increased with passive movement l Little response to opiates
l Neurological dysfunction - paraesthesia
l Swollen, tender & tense compartments l Neurological dysfunction l Pulselessness - LATE sign l Compartment pressures
Assessment & Diagnosis - Examination
CLINICAL DIAGNOSIS!
l From a vascular surgeon’s perspective:
“if you think it, do it!”
“no-one should regret doing a fasciotomy. Plenty have regretted not doing one”
Compartment Pressures - Measurement
l Stryker compartment monitor (emerg / ward)
l Arterial line + needle (OR / ICU)
l Normal < 10 - 12mmHg
Compartment Pressures - Interpretation
l MAP - ICP < 40mmHg
l DP - ICP < 10mmHg= Compartment Syndrome
Treatment
l Fasciotomy - emergency
l Medical interim management l Keep BP up l Keep Hgb up l Oxygenate l Loosen dressings / split cast etc
Wound care
l Non-adherent absorbent dressings l Transfuse as required l Delayed primary closure l VAC l Split skin graft
Image courtesy of: biomedcentral.com & healioswoundsolutions.com
Fasciotomy - long term complications
l Neurological dysfunction l Chronic swelling / CVI l Scars
Other compartments…….l Thigh l Buttock l Forearm l Abdomen
l All managed with the same basic principles
Summary - compartment syndrome
l SURGICAL EMERGENCY! l Limb threatening condition l Clinical diagnosis l High index of suspicion l Requires 4 compartment fasciotomy
