Advice on Infusion System Management
Strict attention to detail can combat hypotony
Steve Charles, MD, FACS, FICS
Since the inception of pars plana vitrectomy, surgeons have occasionally experienced excessively low intraocular pressures during vitreoretinal surgery. New techniques and technologies have greatly improved surgical outcomes but have created special challenges with respect to the infusion system.
Gravity-fed infusion systems were simplistic and could only cause low IOP if the bottle was too low or if the infusion fluid was depleted. Sutured 20-gauge vitrectomy resulted in low intraoperative IOP if the cannula was initially placed or displaced intraoperatively into the suprachoroidal space and not detected. Ventedgas forcedinfusion (VGFI) created the false impression that IOP was controlled, when in fact, as much as 25 mm Hg of difference existed between infusion pressure and IOP, with typical flow rates during vitreous removal and especially fragmenter use.
The fragmenter lumen, unlike the vitreous cutter, is not obstructed by an inner needle or port opening and closing. Low intraoperative IOP has been wrongly blamed on the machine, when in fact, surgeons were using infusion pressures that were too low (15-20 mm Hg) to compensate for infusion line and cannula resistance. It is useful to recall Ohm's law of fluidic resistance: Pressure = Flow x Resistance.
There are many causes of excessively low IOP during vitrectomy; each of these will be discussed.
Inadvertent suprachoroidal infusion is a relatively common cause of low pressure and other, more serious complications during vitrectomy with 23-g and 25-g surgery, as well as the 20-g sutured systems used for over three decades. Sut ureless 25-g vitrectomy initially used straight-in trocar cannula trajectories to produce sclerotomies perpendicular to the sclera (Figure 1).
Figure 1. Improper insertion of the cannula can lead to suprachoroidal infusion, resulting in hypotony.
When 23-g, sutureless surgery was introduced subsequently, oblique trocar-cannula entry was used in order to construct a scleral tunnel to reduce wound leakage. Initially, surgeons used a two-plane approach: The initial trocar-cannula insertion segment was approximately 30° relative to the sclera and the second segment trajectory perpendicular to the sclera. Some surgeons even incorrectly believed that a biplanar incision was constructed, although this belief was not true because the scleral tunnel was created before changing the trajectory.
More recently, most surgeons using both 23- and 25-g systems have switched to oblique entry in order to create a long scleral tunnel, often with excessively steep angles (5-10°). This method is often incorrectly referred to as beveled wound construction. Although near tangential entry creates a long scleral tunnel, it increases the chances of infusing into the suprachoroidal or subretinal space. If the cannula is in the suprachoroidal space, early in the case the choroid elastically expands, allowing infusion without hypotony; later, the choroid can no long er expand, and infusion becomes limited, alerting the surgeon to the problem.
Unfortunately, some surgeons incorrectly conclude that the hypotony was the primary problem that subsequently caused a choroidal effusion. A single-plane 15° trajectory produces a scleral tunnel with the highest resistance to leakage.
The author has always advised inspecting the infusion cannula with the operating microscope or indirect ophthalmoscope after insertion and before initiating infusion. Unfortunately, many surgeons have discontinued this practice since 23-/25-g sutureless vitrectomy began; clearly, we must not omit the crucial step of observing the tip of the infusion cannula, although it is best practice inserting the infusion port in the cannula with the infusion pressurized to prevent bubbles. The naked eye and endoilluminator provide insufficient magnification to make the determination that the cannula has penetrated the choroid and nonpigmented pars plana epithelium; microscope visualization is essential.
Adhesively fastening the infusion cannula tubing and associated stopcock(s) and connectors to the drape is imperative to prevent traction on the infusion cannula and the eye. Inadvertent and unrecognized pulling on the tubing by the assistant or surgeon can easily cause the cannula to pull partially out, causing a suprachoroidal infusion later in the case. Adhesively fastening the infusion cannula tubing to the drape with the eye in the primary position and with a short tubing loop can result in a suprachoroidal infusion when the eye is rotated to view the periphery creating tension on the cannula.
Scleral depression, while valuable to examining peripheral vitreoretinal traction, is another opportunity to cause inadvertent suprachoroidal infusion by causing torque on the cannula, as the eye is rotated by the depressor. In addition, scleral depression can force blood clots, dense scar tissue, peripheral vitreous or silicone oil into the infusion cannula and tubing, effectively plugging it and giving the false impression of machine failure.
Placing the infusion cannula too close to the lower lid, rather than just inferior to the horizontal meridian, is a common cause of suprachoroidal infusion created when the eye is rotated down to visualize the inferior periphery, and the cannula is rotated into the suprachoroidal space.
Kinking of the more flexible silicone tubing terminal segment of the infusion cannula can be caused by the surgeon or assistant accidentally pulling on the tubing. This problem is exacerbated by using excessively low infusion pressure settings (10-25 mm Hg), insufficient to straighten out the tubing kink. The author has always used 45 mm Hg, except when operating on small children or patients with very low systemic blood pressure, typically under general anesthesia.
Frictional losses in the infusion line are often underestimated by the surgeon. There are significant frictional losses in the infusion system with typical flow rates; typically a 10-20 mm Hg gradient. Although the Alcon Constellation Vision System has an IOP Compensation System, this technology cannot always overcome frictional losses in the line when excessively low-pressure settings (10-25 mm Hg) are combined with high outflow rates.
The Alcon IOP Compensation System uses push prime to determine the precise fluidic resistance in the actual infusion system. This is accomplished by infusing at a precise pressure monitored by redundant pressure sensors and measuring the flow with an ultrasonic flow sensor. Ohm's law for fluidics is calculated and the resistance value used to increase infusion pressure during surgery, based on realtime flow sensing, to compensate for frictional losses in the infusion circuit.
Kinking as well as multiple bubbles in the infusion line increase resistance to flow and cause pressure to drop, ultimately resulting in excessively low IOP. The IOP Compensation System is most effective when used to slow the rate of IOP drop when using 23-g or especially 25-g infusion and a 20-g fragmenter to remove dense lens fragments after the vitreous has been removed. Occlusion break will result in ocular collapse if the surgeon does not respond quickly enough; the IOP Compensation System gives the surgeon more time to reduce vacuum when an occlusion break is recognized.
Surgeon remediation of intraoperative low IOP should be systematic; the first step is to inspect the cannula with the microscope to make sure that it extends all the way through the choroid and non-pigmented ciliary epithelium. If not, a 25-g MVR blade can be used to incise the tissue covering the cannula, while pressing the cannula into the eye with smooth forceps.
Another option is to move the infusion system port to the supranasal cannula. The infusion tubing should be examined for kinking or inadvertent disconnection. Kinking is most common when excessively low infusion pressure settings are used, and the tubing angulates at the fluid-air stop-cock/valve.
If a suprachoroidal infusion occurs, infusion can be performed through a cannula with a 25-g needle (if 25-g surgery) into the center of the eye, while recompressing the choroid against the sclera, and typically the suprachoroidal fluid will disappear or egress around the cannulas; cut-down drainage is never necessary. If choroidals are present, a 6 mm cannula, instead of a 4 mm cannula, can be used and infusion initiated with a 25-g needle, as described above.
Although some surgeons believe that occult ischemia occurs with infusion settings of 25-45 mm Hg, there is zero evidence for this theory. Using infusion settings of 10-20 mm Hg causes miosis, bleeding and corneal astigmatism from contact lens pressure on the cornea, and instrument forces on the sclerotomies, as well as scleral infolding, are often mistakenly thought to be choroidals.
In summary, careful and continuous attention to details can prevent infusion system problems, and a systematic approach to remediation can address intraoperative hypotony without compromising outcomes. RP
|Steve Charles, MD, FACS, FICS, is clinical professor of ophthalmology at the University of Tennessee College of Medicine in Memphis. Dr. Charles reports significant financial interest in Alcon. He can be reached via e-mail at firstname.lastname@example.org.|