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This chapter will:
Discuss the technical and clinical complications of hemodialysis in the intensive care unit.
Explain how to recognize and treat clinical and technical complications of this treatment.
Acute kidney injury (AKI) requiring renal replacement therapy (RRT) in the intensive care unit (ICU) is a serious condition with a reported mortality rate as high as 50% to 80%. The choice of RRT depends on logistics and the patient's clinical condition. Although intermittent hemodialysis (IHD) may be used to manage AKI in the ICU, sustained low-efficiency dialysis (SLED) is also a popular therapy for critically ill patients. This latter modality has evolved as a conceptual and technical hybrid of continuous and intermittent therapies, with therapeutic aims that combine the desirable properties of each of the following component modalities :
A lower rate of ultrafiltration for optimized hemodynamic stability
Low-efficiency removal of solutes to minimize solute dysequilibrium
Intermittent treatments allowing patients to leave the unit for diagnostic and therapeutic procedures during scheduled down time.
This chapter reviews the various hazards complicating the course of IHD/SLED in patients with AKI receiving treatment in the ICU. Complications may be classified generally into two broad categories, clinical and technical. The clinical complications are vascular access problems, air embolism, hemolysis, and electrolyte and acid-base disorders. The clinical complications are bleeding, thrombosis, hypotension, hypoxemia, bioincompatibility, and allergic reactions, arrhythmias, febrile reactions, and dialysis dysequilibrium syndrome. The chapter also discusses other miscellaneous issues related to dialysis in AKI, including recovery of renal function, nutrition, and dialysis dosing.
Table 154.1 lists the vascular access problems associated with hemodialysis performed to treat AKI in patients receiving intensive care.
FEMORAL CATHETER | INTERNAL JUGULAR CATHETER | SUBCLAVIAN CATHETER | |
---|---|---|---|
Complications of insertion | Puncture of the femoral artery Groin hematoma Retroperitoneal hematoma Increased risk of infection |
Puncture of the carotid artery Local hematoma Risk of pneumothorax, hemothorax Rupture of the superior vena cava Pericardial tamponade |
Puncture of subclavian artery Risk of pneumothorax, hemothorax Rupture of the superior vena cava Pericardial tamponade Lesions of the brachial plexus |
Advantages | Technically easy procedure; used by inexperienced operators Used when the cardiovascular condition of patient (pulmonary edema) does not allow thoracic catheterization |
Low recirculation rate Low venous stenosis rate Ambulation possible |
Low recirculation rate Low infection rate Ambulation possible |
Disadvantages | Highest infection rate Highest recirculation rate (longer catheters [>19 cm] required) Used only in bed-bound patients Should not be left in place longer than 5 days |
Technically difficult More prone to infectious complications, particularly in patient with tracheotomy Trendelenburg position required for placement |
Technically difficult High rate of central venous stenosis Trendelenburg position required for placement |
At present, double-lumen, noncuffed dialysis catheters are the preferred means of obtaining acute dialysis vascular access. If it is anticipated that a catheter will be needed for more than a week, a tunneled cuffed catheter should be inserted to take advantage of the lower infection rates and higher blood flow rates associated with such catheters. Noncuffed, double-lumen catheters are inserted percutaneously, by means of the Seldinger insertion method, at any of three different deep venous sites: femoral, internal jugular, or subclavian. The anatomic venous site usually is chosen according to the clinical context and the physician's experience. Ideally, such dialysis catheters should be placed in the internal jugular or femoral position, the right internal jugular being the preferred site. Insertion into the right jugular vein is associated with a lower probability of major complications, because there is an almost straight venous path from the insertion site to the right atrium. The subclavian route should be avoided whenever possible, because insertion of subclavian catheters is associated with an unacceptable rate of central venous thrombosis and stenosis, leading to loss of potential sites for future arteriovenous fistulas and grafts. This issue is of particular importance, because it is frequently difficult to determine which patients with AKI need continuous renal replacement therapy either at the time of discharge or in the future. The stenosis that forms in association with a subclavian catheter may be silent until an arteriovenous fistula or graft is created on the ipsilateral arm; the most common clinical presentation in this situation is ipsilateral arm swelling with subclavian vein stenosis. In patients with preexisting cardiovascular implantable electronic devices placed via the subclavian approach, it is easier as well as simpler to place the dialysis catheter on the contralateral side.
The causes of dialysis catheter malfunction depend on the time of introduction. In general, immediate catheter malfunctions are related to catheter position, whereas late malfunctions (more than 2 weeks after insertion) are related more often to thrombus or fibrin sheath formation.
Thrombosed, noncuffed catheters can be exchanged over a guidewire or treated with thrombolytics as long as the exit site and tunnel are not infected. Exit site, tunnel tract, or systemic infections should prompt the removal of noncuffed catheters. The thrombolytic agent used to treat thrombosis of a catheter varies with local practice. In the United States, for example, tissue plasminogen activator (tPA) is used commonly for catheter thrombolysis. This agent may be effective even in low doses of 1 mg per lumen. Thrombosis of cannulated veins is another complication of indwelling catheters. The incidence of venous thrombosis ranges from 20% to 70%, depending on the site and diagnostic modalities used. Deep vein thrombosis develops after activation of the coagulation cascade by an inflammatory process, which is triggered by the presence of the intraluminal foreign body and venous endothelial lesions. The patient has edema of the ipsilateral limb, which may be tender and painful. The presence of venous thrombosis is confirmed by ultrasonography. Treatment consists of catheter removal and anticoagulation.
Infection is a common complication in dialysis-dependent patients in whom a catheter is used. Bacteremia usually results either from migration of microorganisms from the skin through the exit site and down the catheter into the bloodstream or from contamination of the catheter lumen. The cuff represents a significant barrier for periluminal bacterial penetration, and infection rates with cuffed catheters are markedly lower than those with uncuffed catheters. Reported bacteremia rates vary from 3.8 to 6.5 per 1000 catheter-days for uncuffed catheters and 1.6 to 5.5 for tunneled cuffed catheters. In one study, the risk of bacteremia was higher after 1 week at the femoral site and after 3 weeks at the internal jugular site, and increased three-fold with the use of the femoral rather than the internal jugular site. In another study, this risk was increased sixfold by the use of the internal jugular rather than the subclavian site (no femoral catheters were used in this study), likely because of a difference in the density of skin flora between the insertion sites. A third study that compared the outcomes of uncuffed and cuffed catheters found an infection rate of 2.9 per 1000 catheter-days for tunneled cuffed catheters, 15.6 for uncuffed jugular catheters, and 20.2 for uncuffed femoral catheters.
Prevention of infection requires strict aseptic care at the time of catheter insertion as well as optimal exit site care with regular review of the exit site and aseptic dressing change. The use of either povidone-iodine ointment or mupirocin ointment has been shown in randomized controlled trials to significantly reduce the risk of bacteremia from tunneled cuffed catheters. For temporary catheters, povidone-iodine and mupirocin ointments with dry gauze exit site dressings are reported to be similarly useful. Use of a chlorhexidine-impregnated sponge (Biopatch) over the site of short-term arterial and central venous catheters (CVCs) has been shown to decrease the risk of catheter-related bloodstream infections (CRBSI) in a multicenter study.
Access recirculation has not been as well defined for temporary cuffed catheters as for tunneled cuffed catheters. Access recirculation depends on the design and site of the catheter. Access recirculation is higher in femoral catheters than in those located elsewhere, especially if the catheter is shorter than 20 cm. Recirculation rates of 4%, 5%, and 10% (depending on whether the site was internal jugular, subclavian, or femoral) have been reported with temporary venous catheters and a fixed blood flow of 250 mL/min. Interestingly, these recirculation rates did not significantly change at higher blood flow rates (up to 400 mL/min). On the other hand, short femoral catheters (15 cm) exhibit higher recirculation rates, which rise further with higher blood flow rates. Finally, it is worth remembering that in up to half of the treatments, catheters will have to be used with inflow and outflow lines in reversed configuration—using the arterial line for venous return and the venous line for blood aspiration. In this context, recirculation rates of about 20% to 30% have been measured. The impact of access recirculation on dialysis dose has been shown by the study of Leblanc et al., who reported that the urea reduction ratio (URR) was significantly higher with subclavian catheters (62.5%) than with femoral catheters (54.5%) despite identical IHD operating parameters for both sites.
With the development of modern hemodialysis machines, the incidence of life-threatening air embolism has diminished. Modern machines contain air bubble detectors, which can stop the pump when air is detected in the system. The two types of air embolism—venous and arterial—are distinguished by the mechanism of air entry and the site where the embolism ultimately lodges.
The two common sites for air entry through the hemodialysis circuit are as follows:
The arterial line, into which air can be sucked because of subatmospheric pressure between the arterial access and the blood pump. Leaks in this segment, which may occur from a loose connector or a crack in the polymeric silicone (Silastic) tubing of the blood pump, may result in air embolism.
Central venous catheters
Occasionally, air in the dialysate fluid may diffuse across the dialysis membrane into the blood, forming bubbles in the venous air trap.
Most causes of air embolism are reported during catheter insertion, incorrect catheter removal, or disconnection of central venous catheters. During dialysis, the air emboli are typically venous. The clinical severity depends on the quantity of the injected air, the rate of air entry, and the site of entry. The patient's body position at the time of embolization determines the clinical manifestations. With the patient in the sitting position, the air first may migrate to the cerebral blood vessels, causing neurologic decompensation and unconsciousness. With the patient in the recumbent position, air reaches the right atrium and right ventricle; foam develops in those chambers and flows into the pulmonary vasculature, which becomes occluded, causing pulmonary hypertension. Symptoms of this complication are dyspnea, chest pain, and cough followed by cardiovascular collapse. In rare cases, air that has entered venous circulation can reach the left heart and then the systemic arterial circulation, where it may provoke coronary and cerebral embolization. Embolization can happen through “paradoxical embolism” via a patent foramen ovale, through passage through physiologic pulmonary arteriovenous shunts, or from incomplete filtering of a large air embolus by the pulmonary capillaries.
Because the majority of affected patients have nonspecific symptoms, air embolism may be difficult to diagnose in the absence of a high level of suspicion for such a possibility. Air embolism should be suspected in dialysis-dependent patients after insertion, manipulation, or removal of a central venous catheter in whom sudden onset of cardiopulmonary or neurologic decompensation develops. Transesophageal echocardiography is a definitive method for detecting intracardiac air. If an air embolism occurs, the venous blood line should be clamped immediately to prevent further entry of air. Management is supportive, with the patient being placed in flat, supine position for arterial air embolism. For venous air embolism, patients may be placed in either a left lateral decubitus position (Durant's maneuver), Trendelenburg position, or left lateral decubitus head down position). Adequate oxygenation is often possible only with an increase in the oxygen concentration of the inspired gas up to 100%. If the patient does not show response within minutes, mechanical ventilation and inotropic support may be needed. If significant foaming has occurred in the right ventricle, causing cardiac arrest, cardiac puncture and aspiration should be performed to remove the foam. Hyperbaric oxygen therapy is an additional aid in treating air embolism. In addition, because chest compressions can force air out of the pulmonary outflow tract and into smaller pulmonary vessels, improving forward blood flow, they can be used as a last-resort maneuver in patients with severe hemodynamic instability.
Clinically significant hemolysis can occur during the dialysis procedure. There are numerous reported causes of acute hemolysis, including oxidant damage (from chloramines, zinc, copper, or nitrate contamination of the dialysate), reduction injury (from formaldehyde used to disinfect reprocessed dialyzers or water treatment system), osmolar injury (from hypotonic or hypertonic dialysate), thermal injury (from overheated dialysate), and mechanical injury (e.g., kinking of blood lines, narrowed aperture of the blood tubing set, pump malocclusion, and the presence of a blood clot at the tip of a subclavian catheter). Clinical manifestations include headache, abdominal pain, nausea, vomiting, chest or back pain, malaise, shortness of breath, and severe hyperkalemia resulting from hemolysis. Immediately after acute hemolysis is suspected or diagnosed, the blood pump should be stopped, the venous blood lines clamped, and the blood discarded. Dialysis should be restarted as soon as the patient is stable, owing to potential fatal hyperkalemia if it is not.
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