Intraabdominal Pressure

Chapter 206 Intraabdominal Pressure





INTRODUCTION


Intraabdominal pressure (IAP) and intraabdominal hypertension (IAH) have been recognized in animals and humans for over 150 years.1,2 A discussion of IAP in pregnancy was published in 1913, and the effects of IAH on renal function in people was described in 1947.3,4 One of the first published studies was undertaken simply to prove whether IAP was positive or negative and involved a series of very different procedures in different species.1 Original research into the physiologic effects of IAH was performed in several species once the normal IAP was established.2 These studies were quite variable, not often repeated, and used techniques that we would find unacceptable for technical and humane reasons today. Scientists believed it was important to establish the parameters at that time, though, as surgery and interventional medicine was evolving.


IAP refers simply to the pressure within the abdominal cavity, regardless of the actual reading. IAH refers to increased IAP (>5 cm H2O) in a general way, with or without abdominal compartment syndrome (ACS). ACS occurs when the IAH is causing adverse effects on physiologic function, usually at or near 35 cm H2O. It is considered primary ACS if the trauma or disease occurs within the abdominal cavity (fractured liver or spleen, penetrating foreign body, peritonitis, neoplasia, hepatic abscess, pancreatitis) or secondary if the inciting disease is extraperitoneal (burns or thoracic trauma, usually followed by massive fluid resuscitation or high-pressure mechanical ventilation).


Both primary and secondary ACS are associated with multiple organ dysfunction and a worsened prognosis.5 This is an important distinction because it is highly recommended to monitor IAP in patients who do not have intraperitoneal disease. Resolution of the ACS can significantly improve outcome in patients without primary abdominal disease who develop multiple organ dysfunction.6,7


The effects of rising IAP on organ function are well documented.8-11 Visceral perfusion, abdominal blood flow, central venous pressure, pulmonary pressures, cardiac output, and renal function are all adversely affected by an increasing IAP, and early changes can be seen when levels exceed 10 cm H2O. Much of the research documenting systemic effects of ACS has been performed in dogs.11-17 Little clinical work in veterinary medicine has documented the effects of ACS in hospitalized patients, however the disease processes in which it is recognized in humans exist in our small animal patients and the technology for monitoring and responding to changes are the same. Several comprehensive reviews of the subject have been published in the human medical literature.18-21


IAH has been documented in human patients with ruptured abdominal aortic aneurysm, abdominal hemorrhage from trauma, occluded mesenteric artery, ruptured or necrotic bowel, bile peritonitis,10 blunt trauma to any of the abdominal organs, gastric perforations, bladder ruptures,18 and large abdominal masses.22 In many of these cases, there was a previous surgical procedure and the IAH mandated a reexploration of the abdomen. Fluid infusions and effusions in dogs,11 morbid obesity,23 antishock trousers,24 and pregnancy in humans3 are also conditions that have been documented to increase IAP.



METHODS OF INTRAABDOMINAL PRESSURE MEASUREMENT


IAP has been measured via catheters placed in the inferior vena cava, stomach,25,26 urinary bladder, and the peritoneal cavity.27 The urinary bladder method is the easiest to use in small animal patients and provides consistent, accurate measurements.27 A urethral catheter is inserted aseptically so that the tip is just inside the trigone of the urinary bladder. A Foley catheter is preferred to ensure that the fenestrations lie just inside the bladder. A sterile urine collection system is attached in the usual way, but two three-way stopcocks are placed in the system. A water manometer is attached to the upright stopcock port. A 35-cc to 60-cc syringe of 0.9% sodium chloride or a bag of 0.9% sodium chloride and an intravenous administration set are attached to the distal stopcock port for filling the manometer and infusing the bladder. The bladder is emptied and 0.5 to 1 ml/kg of 0.9% sodium chloride is instilled to distend it slightly. This lessens the likelihood that the bladder wall will obstruct the catheter fenestrations.


The bladder is essentially a passive conduit of the pressure within the abdomen, although infusion of too much saline into it will falsely elevate the IAP. The system is zeroed to the patient’s midline at the symphysis pubis and the manometer filled with isotonic saline. The stopcock is closed to the fluid source, so that the meniscus in the manometer can drop and equilibrate with the pressure in the urinary bladder. The difference between the reading at the meniscus and the zero point is the IAP. The patient should be laterally recumbent when obtaining measurements. Patient position affects measurement28 and should therefore be the same at each measurement. Appropriate aseptic technique for placement and handling of the urethral catheter and the measurement system prevents a urinary tract infection in an otherwise healthy dog.29


Normal IAP in dogs is 0 to 5 cm H2O. Healthy dogs undergoing elective abdominal surgery (ovariohysterectomy) had a postoperative IAP ranging from 0 to 15 cm H2O. No problems associated with IAH were observed.29 Normal IAP has not been documented in cats. Clinically, the author has used the parameters noted for dogs when caring for cats, with good results.

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Sep 10, 2016 | Posted by in SMALL ANIMAL | Comments Off on Intraabdominal Pressure

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