HD in humans was first made possible by the invention of the rotating-drum artificial kidney by Kolff et al in 1943. Access to the patient's bloodstream was not practical until the development of the external AV shunt by Scribner in 1960. Brescia and Cimino in 1966 developed the subcutaneous AV fistula, which made HD safer and more acceptable. RRT became universally available after Congress passed the Medicare entitlement for the treatment of ESRD in 1973.

TECHNICAL ASPECTS The nephron removes toxins and maintains internal homeostasis through an elegant combination of glomerular filtration followed by selective reabsorption and secretion of water and solutes. HD uses the brute force techniques of ultrafiltration and clearance to replace the functions of the nephron. HD substitutes a hemodialyzer filter for the glomerulus to produce a ultrafiltrate of plasma. Adjustment of the pressure gradient across the hemodialyzer filter during HD controls the amount of fluid removal (ultrafiltration). Solute removal (clearance) during HD is dependent on the filter pore size, the amount of ultrafiltration (solute drag), and the concentration gradient across the filter (diffusion). Solute diffusion down chemical gradients from the blood to the dialysis fluid (dialysate) determines their final blood concentration. Since hemodialyzer pore size prevents the filtration of proteins, dialysate consists only of electrolytes (Na +, K+, Cl-, HCO3-, Ca++, and Mg++) and glucose, whose concentrations are varied to control their clearance.11 During HD, blood is removed from the vascular access site by large-bore needles (typically 15 g), circulated through the dialysis machine at rates of 300 to 500 mL/min, and returned to the patient. The dialysate usually flows at a rate of 500 to 800 mL/min through the dialysis filter in the direction opposite to blood flow. Small amounts of heparin, 1000 to 2000 IU, are typically used to prevent thrombosis at the vascular access site. hD sessions typically take 3 to 4 h.

Ultrafiltration and clearance usually occur simultaneously during dialysis but can be separated by adjusting the HD settings. In fluid-overloaded patients, adding suction to the dialysate side of the hemodialyzer filter augments ultrafiltration. Dialysate flow can be lowered, minimizing clearance to prevent hypotension during dialysis. When fluid loss is not desired during dialysis (for patients below their dry weight) balancing dialysate and blood pressures across the filter limits fluid removal. Decreasing the dialysate concentration of the desired solute can augment clearance of specific electrolytes (e.g., potassium).

Long-term successful hemodialysis is dependent on reliable access to the patient's circulation. 12 The external Scribner AV shunt provided adequate vascular access but only lasted on average 1 year. The Brescia-Cimino AV fistula formed by the anastomosis of a native artery and vein in the forearm has a much greater longevity. In cases where a native artery or vein are not suitable for fistula creation, an interposing vascular graft made of an autologous vein, polytetrafluorethylene, or bovine carotid artery must be used for vascular access. These grafts generally have a higher complication rate and shorter functional life expectancies than do natural AV fistulas.

COMPLICATIONS OF THE VASCULAR ACCESS Vascular access is the Achilles heel of HD, and complications of the vascular access account for more inpatient hospital days than any other complication of HD.

Vascular Access Stenosis and Thrombosis Thrombosis and stenosis of the vascular access are the most common complications. Grafts generally have a higher rate of stenosis, secondary to endothelial hyperplasia, than do fistulas. Stenosis or thrombosis presents with loss of bruit and thrill over the access. Stenosis and even thrombosis are not emergencies and can be treated within 24 h by either angiographic clot removal or angioplasty.

Vascular Access Infection The vascular access provides the most common portal of entry for infection in dialysis patients. Vascular grafts have a higher incidence of infection than do AV fistulas. Patients with an infected access often present with only signs of systemic sepsis, such as fever, hypotension, or an elevated white blood cell count. Classic signs of pain, erythema, swelling, and discharge from an infected vascular access are often missing. The most common organism is Staphylococcus aureus, followed by gram-negative bacteria.13 Patients with access infections usually require hospital admission. Vancomycin is the drug of choice (1 g intravenously) because of its effectiveness in methicillin-resistant organisms and long half-life (5 to 7 days) in dialysis patients. An aminoglycoside (gentamicin 100 mg intravenously initially and after each dialysis) is usually added empirically to cover gram-negative organisms.

Vascular Access Hemorrhage Hemorrhage from a vascular access can produce life-threatening blood loss. Hemorrhage can result from aneurysms, anastomosis rupture, or overanticoagulation. Bleeding that requires the patient to come to the emergency department should immediately be controlled with digital pressure at the puncture sites for 5 to 10 min, and the patient should be observed for 1 to 2 h afterward. Continued or life-threatening hemorrhage may require the placement of a tourniquet proximal to the access. A vascular surgeon should be consulted if bleeding cannot quickly be brought under control. If overanticoagulation is a concern, the effects of heparin can be reversed by protamine given at a dose of 0.01 mg/IU heparin dispensed during dialysis. If the dose of heparin is unknown, 10 to 20 mg protamine will be sufficient to reverse 1000 to 2000 IU heparin. If bleeding stops, the patient should be observed for 1 to 2 h for rebleeding or thrombosis. Occasionally a newly inserted vascular access will continue to ooze at the insertion despite pressure. DDAVP can be administered as an adjunct to direct pressure. If the emergency physician is unfamiliar with the use of DDAVP in this situation, the nephrologist should be consulted.

Vascular Access Aneurysm Vascular access aneurysms result from repeated puncturing, leading to bulging of the wall. True aneurysms are very rare, occurring in less than 4 percent of fistulas or grafts. Most aneurysms are asymptomatic, with patients occasionally complaining of pain or an associated peripheral impingement neuropathy. Aneurysms rarely rupture, causing hemorrhage.

Vascular Access Pseudoaneurysm Pseudoaneurysms result from subcutaneous extravasation of blood from puncture sites. Patients commonly present with bleeding and infections at access sites. Bleeding from the puncture site is usually controlled by digital pressure or a subcutaneous suture carefully placed at the puncture site. Vascular surgery may be required for continued bleeding or infection.

Vascular Insufficiency Vascular insufficiency of the extremity distal to the vascular access occurs in approximately 1 percent of all patients. The so-called steal syndrome is the result of preferential shunting of arterial blood away from nutrient arteries to the low-pressure venous side of the access. Patients present with exercise pain, nonhealing ulcers, and cool, pulseless digits. Steal syndrome is diagnosed by Doppler ultrasound or angiography and is repaired surgically.

High-Output Heart Failure High-output heart failure can occur when greater than 20 percent of the cardiac output is diverted through the access. Branham's sign, a drop in heart rate after temporary access occlusion, is useful for detecting this complication. Doppler ultrasound can accurately measure access flow rate and establish the diagnosis. Surgical banding of the access is the treatment of choice to decrease flow and treat heart failure.

COMPLICATIONS DURING HEMODIALYSIS TREATMENT Intradialysis Hypotension Hypotension is the most frequent complication of HD, occurring during 10 to 30 percent of treatments (Table89-2). Excessive ultrafiltration from underestimation of the patient's ideal blood volume (dry weight) is the most common cause of intradialysis hypotension.14 In fact, dry weight is often clinically defined when hypotension prevents further fluid removal. Dry weight is often underestimated because of changes in the ratio of muscle mass to blood volume over time.

TABLE 89-2 Differential Diagnosis of Intradialysis Hypotension

Predialysis volume deficiency is an important contributing factor to intradialysis hypotension. Predialysis losses can be suspected when the patient is below dry weight and are usually due to GI bleeding, vomiting, diarrhea, or decreased intake of salt and water. Intradialysis volume loss can occur from blood tubing or hemodialyzer filter leaks.

Factors other than the patient's predialysis volume may cause intradialysis hypotension. Fluid removal during HD averages 1 to 2 L over a 4-h session but removal of up to 2 L/h hour is possible. Maintenance of normal blood pressure during ultrafiltration is dependent on fluid movement from the interstitial space replenishing the intravascular volume. These fluid shifts are direct consequences of the decrease in intravascular hydrostatic pressure and the increase in serum osmolality caused by ultrafiltration. Blood pressure stability during ultrafiltration is also dependent on increased systemic vascular resistance, heart rate, and contractility caused by increased autonomic tone.

Defenses against intradialysis hypotension can be defeated by a large number of factors. Hypotension often occurs when ultrafiltration and clearance are carried out simultaneously. During clearance, serum osmolality decreases, limiting interstitial fluid refilling of the intravascular space. Autonomic dysfunction, especially common in diabetic patients, may result in failure to increase cardiac output and peripheral resistance during ultrafiltration. Decreased sympathetic tone also increases nitric oxide production, potentiating hypotension. Hypotension is also caused by increased nitric oxide generated in platelets and endothelial cells by an as yet unidentified uremic toxin. Antihypertensive medications and narcotics can both block sympathetic reflexes, resulting in hypotension. Decreases in vascular tone during hemodialysis occur in patients with sepsis, after eating, and when dialysate temperatures are greater than 37°C. Cardiac dysfunction during hemodialysis secondary to dysrhythmias, LV hypertrophy, hypoxia, and myocardial ischemia can prevent reflex increases in heart rate and contractility. Finally, pericardial effusion and tamponade decrease cardiac preload, thus potentiating intradialysis hypotension.

Often, the timing of hypotension is helpful in the differential diagnosis. Hypotension early in the dialysis session usually occurs with patients who are below dry weight from preexisting hypovolemia. Hypotension near the end of dialysis is usually the result of excessive ultrafiltration, but pericardial or cardiac disease is still a possibility.

Intradialysis hypotension produces nausea, vomiting, and anxiety. Orthostatic hypotension, tachycardia, dizziness, and even syncope may occur.

Treatment of intradialysis hypotension includes placing the patient in the Trendelenburg position and stopping HD. If hypotension persists, the patient is given salt by mouth (broth) or normal saline solution 100 to 200 mL intravenously. If these conservative measures fail, excessive ultrafiltration is very unlikely, and a more extensive evaluation is justified. These patients are commonly transferred to the emergency department for further evaluation.

The emergency physician should conduct a detailed investigation of volume status, cardiac function, pericardial disease, infection, and GI bleeding that may be producing or contributing to hypotension. Remember that estimation of this patient's blood volume by clinical criteria has already failed in the dialysis unit. The decision to undertake further volume expansion or administer vasopressors to support blood pressure may require invasive hemodynamic monitoring in an intensive care setting.

Dialysis Disequilibrium Dialysis disequilibrium is a clinical syndrome occurring at the end of dialysis characterized by nausea, vomiting, and hypertension, which can progress to seizure, coma, and death. This syndrome should be distinguished from other neurologic disorders, such as subdural hematoma, stroke, hypertensive crisis, hypoxia, and seizures. Dialysis disequilibrium is produced when large solute clearances occur during HD, as during the patient's first dialysis session or in hypercatabolic patients. The cause of dialysis disequilibrium is believed to be cerebral edema from an osmolar imbalance between the brain and the blood. During high solute removal, the blood has a transiently lower osmolality than the brain, favoring water movement into the brain and causing cerebral edema. This condition can be prevented by limiting solute clearance when initiating HD. Treatment consists of stopping dialysis and administering mannitol intravenously to increase serum osmolality.

Air Embolism Air embolism is always a risk when blood is pumped through an extracorporeal circuit. The clinical presentation depends on the patient's body habitus at the time of the air embolism. If the patient was sitting, air will pass retrograde through the internal jugular vein to the cerebral circulation, causing symptoms of increased intracranial pressure. In a recumbent position, air will go into the right ventricle and pulmonary circulation, causing pulmonary hypertension and systemic hypotension. The passage of air through a right-to-left (e.g., patent foramen ovale) creates an arterial air embolism, which can lodge in the coronary or cerebral circulation, causing myocardial infarction or stoke.

Patients with an air embolism typically present with symptoms of acute dyspnea, chest tightness, and unconsciousness, sometimes progressing to full cardiac arrest. Physical examination may show cyanosis and a churning sound in the heart from air bubbles in the blood.

Treatment consists of clamping the venous bloodline and placing the patient supine. Traditional recommendations have often included the Trendelenburg position with the left side down, presumably to favor air trapping in the right ventricle. However, experimental and anecdotal clinical evidence does not indicate any special benefit of this position. Other suggested therapies for vascular air embolism include percutaneous aspiration of air from the right ventricle, intravenous steroids, full heparinization, and a hyperbaric chamber to reduce bubble size and promote resorption.

Hemolysis and Electrolyte Shifts In the United States, dialysate is prepared by proportionally mixing a dialysate concentrate with water. Errors in proportional mixing can produce severe electrolyte abnormalities, resulting in rapid osmolar shifts and hemolysis.

Hypercalcemia and Hypermagnesemia In some communities, water contains high concentrations of calcium and magnesium and produces a final dialysate high in these minerals. This dialysate can result in the "hard water syndrome," characterized by clinically significant hypercalcemia and hypermagnesemia in HD patients. These patients present with nausea, vomiting, headaches, burning skin, muscle weakness, lethargy, and hypertension. Treatment consists of properly filtering the dialysis water to lower calcium and magnesium concentrations.

EVALUATION OF HEMODIALYSIS PATIENTS Patients on HD may present to the emergency department for complications related to their ESRD or HD, or these conditions may be incidental to the reason for the visit. The past medical history is very important in HD patients, since many of the same diseases that caused ESRD (e.g., hypertension, diabetes, etc.) persist after the patient's kidneys have failed. Questions should be asked about the patient's ESRD and HD ( Iable 89:3). Repeated episodes of intradialysis hypotension may provide important early clues to pericardial tamponade or myocardial ischemia. Repeated access infections may represent a worsening immunologic status.

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