History
Henricius, 1890 -- Inc intra-abdominal pressure led to death in animal models
Emerson, 1911 -- respiratory failure if increased intra-abdominal pressure
Thorington, 1923 -- anuria if intra-abdominal pressure > 30
Overholt, 1931 -- measurement
Ogilvie, 1940 -- management of the distended abdomen and late incisional hernia - "if the edges cannot be brought within two inches of eachother... the idea of operation should be discouraged..."
Gross, 1948 -- abdominal compartment syndrome status post diagnosis of omphalocele - "severe crowding of the viscera...is apt to give rise to three seroud and fatal complications... diaphragm pushed upward, impede the return of blood flow, temporary obstruction"
1984 – Kron, et al. Coined term “Abdominal Compartment Syndrome” in post-op ruptured AAA cases - best modern description of ACS
OSWALDO A. BORRAEZ G. resident at National University San Juan de Dios 1982-1985
March, 1984 - " the first patient was a mechanical man (to fix cars) who was working and the car fell on his body. He had broken or explosion hepatic..." " he needed operations several: right hepatectomy, by bleed (two times). in this patient I put the first "bogota bag". "The second patient who needed the bogota bag was a woman with peritonitis gynaecological, a week later. I put the bogota bag, too" " they both left alive"
Pathophysiology
Definition - Abdominal Compartment Syndrome
Sustained IAP > 20 mm Hg
+ New organ dysfunction – most commonly:
1. Impaired Ventilation (PIP > 40)
2. Shock
3. Renal Failure
IAP >20 --> impaired lymph flow --> intestinal edema --> IAP>20
IAP>20 --> dec. capillary perfusion --> tissue ischemia --> cytokine release --> inflammatory response --> 3rd spacing --> IAP>20
IAP>20 --> Cephalad diaphragm displacement --> dec pulmonary compliance --> inc. Pips
IAP>20 --> dec blood flow to abd viscera --> renal failure, liver failure, dec. venous return
Intra-abdominal pressures
APP = MAP – IAP. Target > 60 mm Hg
Normal abdominal pressure 0-7
Abdominal hypertension 12-20
Abdominal compartment syndrome >20
Organ function decreases as intra-abdominal pressure increases
Normal IAP: 5 to 7 in non-obese, increases with increased bmi up to 15 without complications
Intra-abdominal pressure grading:
WSACS Grade I 12-15, II 16-20, III 21-25, IV >25
Burch/Meldrum grade I 10-15, II 16-25, III 26-35, IV >35
Effect of Pt Position on IAP - 30 degrees increases IAP by 4 mmHg, 45 degrees by 9
IAP Monitoring - expressed in mmHg, measured at end-expiration, performed in supine position, zeroed at the iliac crest in the mid-axillary line, performed with an instillation volume of no greater than 25 mL of saline [1mL/kg for kids up to 20kg] (for bladder technique), measured 30-60 seconds after instillation to allow for bladder detrusor muscle relaxation (for bladder technique), measured in the absence of active abdominal muscle contractions
Classification:
Primary – ACS due to injury or disease in abd/pelvis
Secondary – due to non-abd/pelvis etiologies, aggressive resuscitation for other pathology (burns)
Recurrent – redevelopment of 10 or 20 after treatment
Risk Factors
1. Diminished abdominal wall compliance - Acute respiratory fialure, especially with increased intrathoracic pressure; abdominal surgery with primary fascial or tight closure; Major trauma/burns; prone positioning, head of bed > 30 degrees; high body mass index (BMI), central obesity
2. Increased intra-luminal contents - Gastroparesis, ileus, colonic pseudo-obstruction
3. Increased abdominal contents - Hemoperitoneum/pneumoperitoneum; ascites/liver dysfunction
4. Capillary leak/fluid resuscitation - Acidosis (pH < 7.2), Hypotension, polytransfusion (>10 units of blood/24 hrs), hypothermia (<33 C), coagulopathy (PLTS < 55, PT >15, PTT >2xnrml, INR > 1.5), massive fluid resuscitation (>5L/24hrs), Pancreatitis, oliguria, sepsis, major trauma/burns, damage control laparotomy
Treatment/Prevention
Patient has TWO or more risk factors for IAH/ACS upon either ICU admission or in presence of new or progressive organ failure, screen bladder pressures, if elevated, may be developing ACS
Medical treatment options to reduce IAP
1. Improve abdominal wal compliance - sedation and analgesia, neuromuscular blockade, avoid head of bed > 30 degrees
2. Evacuate intra-luminal contents - nasogastric decompression, rectal decompression, gastro-colo-prokinetic agents
3. Evacuate abdominal fluid collections - paracentesis, percutaneous drainage
4. Correct positive fluid balance - avoid excessive fluid resuscitation, diuretics, colloids/hypertonic fluids, hemodialysis/ultrafiltration
5. Organ support - Maintain Abdominal perfusion pressure > 60 mmHg with pressors, optimize ventilation, alveolar recruitment, use transmural airway pressures (Pplat(tm) = Pplat - IAP), consider using volumetric preload indices, If using PAOP/CVP, use transmural pressures: PAOP(tm) = PAOP - 0.5xIAP; CVP(tm) = CVP - 0.5xIAP
Indications for Open Abdomen - damage control, treatment of ACS, prevention of ACS, dehiscence/evisceration, traumatic or infectious abdominal wall loss
Abdominal Decompression with temporary Abdominal Closure: skin closure only, bogota bag, wittman velcro patch, absorbable mesh coverage, vac pac (Control of fluid, speeds edema resolution)
Prevent with temporary closures at initial damage control celiotomy
A word of caution: the open abdomen is not anatomically, physiologically, or in any other way normal & should not be a reflexive treatment modality but one which is utilized very selectively.
Temporary abdominal closure tips
Go cheap - use a IV bag/x-ray cassette
Go soft - can't errode into bowel
Secure well to fascia
Careful with tubes and ostomies
Don't create ACS
Delayed abdominal closure
Bridging alloderm prone to recurrence
Optimal = fascial closure "bolstered with alloderm"
Surgisis = poorly packaged bovine stool
Component separation
Okay if gap 6-8 cm and patient very stable
Extend release from chest wall to near inguinal ligament
Bolster with alloderm