Emergencies in the Dialysis Patient
Emergencies in the Dialysis Patient
Authors:
Larissa I. Velez, MD, FACEP, Program Director, Emergency Medicine, University of Texas Southwestern, Dallas; Staff Toxicologist, North Texas Poison Center, Dallas.
Fernando L. Benitez, MD, FACEP, Associate Professor, Emergency Medicine, University of Texas Southwestern, Dallas.
Walter Green, MD, Assistant Professor, Emergency Medicine, University of Texas Southwestern, Dallas.
Ann Czarnik, MD, FACEP, Assistant Program Director, Emergency Medicine Residency, University of TexasAustin.
Robert A. Weston, MD, Emergency Medicine, University of Texas Southwestern, Austin.
Peer Reviewer:
Jonathan Glauser, MD, Department of Emergency Medicine, MetroHealth Medical Center, Cleveland, OH.
As a group, I find most emergency physicians skeptical of many of the "advanced" technologies used to treat chronic diseases. I attribute this to our biased experience with these patients; those who do well are not likely to come to the ED very often. We typically see those with problems and complications, which unduly influences our opinion about the benefits of such treatments. So it is with patients receiving dialysis therapy. This issue of EM Reports will review the myriad of problems related to renal failure and its treatment.
J. Stephan Stapczynski, MD, Editor
Definitions
Kidney disease is classified based on glomerular filtration rate (GFR), according to the Kidney Disease Outcomes Quality Initiative Guidelines of the National Kidney Foundation. Chronic kidney disease (CKD) involves kidney damage (by pathology, imaging, or clinical tests) or GFR < 60 mL/min/1.73 m2 for 3 months or longer. A GFR of 60 is chosen, as it defines loss of at least 50% of the normal adult kidney function. This article discusses the end stage renal disease (ESRD) or kidney failure patient (stage 5), as defined by a GFR of less than 15 mL/min/1.73 m2 or treatment with dialysis.
There are two modalities for dialysis: hemodialysis (HD) and peritoneal dialysis (PD). The decision to do one instead the other is based on kidney function, overall health, personal preferences, home situation, and the presence of gastrointestinal conditions such as inflammatory bowel disease and diverticular disease. PD has two modalities: automated PD (APD) and continuous ambulatory PD (CAPD).
Epidemiology
The number of patients with ESRD and on dialysis has been steadily increasing. In 2009, there were 370,274 patients on HD and 27,522 patients on PD in the United States.
More than half of the ESRD cases are attributed to diabetes mellitus (DM), with hypertension (HTN) being the second most common cause.1 African Americans, Native Americans, and Hispanics are at greater risk of developing ESRD.1
The costs for ESRD are staggering. This population constitutes 1.9% of Medicare patients but accounts for 8.1% of the Medicare budget spending (2009 data).2 The cost per patient is estimated at $82,000 per year when on HD and $61,000 per patient per year when on PD. This is significantly higher than the estimated annual cost of $30,000 for a kidney transplant patient.
ED Evaluation
The ED evaluation of the dialysis patient should follow the same steps as with every acutely ill patient. However, with these patients, other important items to address include:
1. The HD/PD access site must be located and evaluated. Access points can become both clotted (HD) and infected (HD and PD). The HD access points can also bleed. Rarely, the shunts cause high-output cardiac failure. In general, vital signs in the arm with a HD access point are to be avoided.
2. The last HD session: This can provide a gauge of the chances for hyperkalemia and other major electrolyte changes. Longer intervals also make the patient more prone to volume overload.
3. If known, and if the patient is not in extremis, the dry versus actual weight can help further define volume status.
4. In PD patients, any changes to the color or transparency of the dialysate fluid is an indication of infection.
5. Ask the patient if he or she still makes urine. Patients with some residual urine output are partially protected from the fluid overload and electrolyte complications described below.
6. Ask the patient about the precipitating cause of his or her renal failure. These conditions likely still exist and may contribute to the symptoms the patient is experiencing and may also influence treatment in the ED.
Electrolyte Emergencies
Hyperkalemia. Hyperkalemia is common in the dialysis patient, and is also one of the few lethal electrolyte disorders.
First, the physician should make sure the sample is not hemolyzed. Hemolysis is a common cause for falsely elevated potassium levels.
Potassium levels are of concern at a level of 6 mEq/L or above; however, the urgency of treatment is based on the absolute potassium level, the rapidity of the rise, and a multitude of other factors such as the presence of acidosis and other electrolyte disturbances.3 In general, ECG changes mandate treatment, but a normal ECG is never reassuring, especially with potassium levels greater than 6 mEq/L.3
The usual teaching for the progression of the ECG in hyperkalemia is: peaked T waves, widened QRS, the P wave disappears, and, finally, a sine wave.4 Ventricular fibrillation in some cases may be the first electrocardiographic manifestation.3 Heart blocks can also be seen in profound hyperkalemia. It is critical to remember that the typical ECG progression is not always stepwise and is very patient-dependent.3
The emergency management of hyperkalemia should follow a chronological sequence: (see Table 1)
Table 1: Management of Hyperkalemia
|
Drug |
Dose |
Onset of Action |
Duration of Action |
Mechanism of Action (MOA) |
|
Adapted from: Weisberg LS. Crit Care Med 2008;36:3246-3251. |
||||
|
Calcium chloride |
10 mL of 10% solution IV (use only central line or in code situation) over 10 minutes Can repeat in 5 min |
Immediate |
30-60 min |
Antagonizes cell excitation |
|
Calcium gluconate |
10 mL of 10% solution IV over 10 min; can repeat in 5 min |
Immediate |
30-60 min |
Antagonizes cell excitation |
|
Insulin |
10 units regular insulin IV, with 25 g of D50W IV; should use D5W or D10W infusions thereafter |
20 min |
4-6 hours |
Intracellular K redistribution |
|
Albuterol |
10-20 mg by nebulizer |
30 min |
2 hours |
Intracellular K redistribution |
|
Terbutaline |
7 mcg/kg body weight, SQ |
< 60 min |
Intracellular K redistribution |
|
|
Sodium bicarbonate |
150 mEq/L at 1-2 cc/kg/hr |
Hours |
While infused |
Intracellular K redistribution |
|
Furosemide |
40-80 mg IV |
15 min |
2-3 hours |
Urinary K excretion |
|
Bumetanide |
2-4 mg IV |
15 min |
2-3 hours |
Urinary K excretion |
|
Sodium polystyrene sulfonate |
30-60 g PO or enema |
At least 12 hours (probably longer) |
At least 24 hours |
Fecal K excretion |
1. Antagonism of the effects on excitable cells, especially the myocardium;
2. Redistribution of potassium to the intracellular compartments;
3. Increasing the elimination of potassium from the body.3
Management of Hyperkalemia. Calcium salts work by membrane stabilization of the myocytes without altering the total potassium concentration. This should be the first intervention in a patient who has myocardial irritation from hyperkalemia.3 The salts of calcium are available in two formulations: calcium chloride and calcium gluconate.
The gluconate is less potent, as it has less calcium per weight. Calcium gluconate cannot be pushed as a bolus in general, as it causes hypotension. It requires intact liver metabolism to release calcium and, therefore, is not the best option for patients with chronic liver disease or those patients in shock or cardiac arrest. One definite benefit of this formulation is that it does not cause vein irritation, so it can be infused via a peripheral vein.3
Calcium chloride is about three times more potent than the gluconate, as it contains more calcium per weight. It can be pushed, but only when using a central line, as it is very irritating to the veins and will cause tissue necrosis if it extravasates. The molecule disassociates when in plasma without any metabolism.3
The effects of the calcium salts are short-lived, estimated at 30-60 minutes. Frequently, re-dosing will be needed.
Albuterol and other beta adrenergics work by redistribution of the potassium into the cell. To reduce the serum potassium by 0.6-1 mEq/L, large doses should be used (10-20 mg). Terbutaline has also been used, causing a decrease of serum potassium by an average of 1.3 mEq/L within 60 minutes of dosing. Both medications will cause tachycardia. The effects of the beta adrenergics are blunted in patients using beta-blockers. Up to 40% of patients can be resistant to the hypokalemic effect of the beta adrenergic agents, even when not using beta adrenergic blockers.5 Therefore, these agents should never be used alone.3
Insulin and glucose work by redistribution of potassium into the cell. The most important consideration when using insulin and glucose is that the combination often results in hypoglycemia. Therefore, use two ampules of 50% dextrose instead of one unless the patient is hyperglycemic, and closely monitor the glucose after dosing.
Since the volume of insulin is so small, dilute 10 units in 10 mL of saline so the dose does not stay in the port. Otherwise, flush the dose with 10 mL of saline. The onset of effects is about 20 minutes, and lasts for 4-6 hours.
Sodium bicarbonate works by potassium redistribution into the cell, but the efficacy of this common intervention is not well supported by the literature. A secondary mechanism of action for bicarbonate is possibly by urinary alkalinization, resulting in increased urinary potassium excretion. It should probably only be used if significant acidemia is present. The limited literature showing some benefit uses infusions rather than boluses or discrete doses.3 The effect of the bicarbonate is very modest, at best, and lasts only while infused.3
Loop diuretics work by increasing potassium elimination by the kidney. Of course, these drugs will not have any effect in the anuric patient, but potassium is eliminated even in severely impaired kidney function.
Sodium polystyrene sulfonate (SPS; Kayexalate®) works by increased elimination from the gut. The cation exchange resin has a preference for binding potassium. In the gut lumen, it exchanges the sodium ion for a potassium ion, which is then fecally excreted. SPS can be administered orally or by an enema. Sorbitol is added to avoid concretions, and the premixed suspension is the only formulation available in many U.S. hospitals.6
Contrary to teaching, SPS will not lower the potassium until about 12-24 hours after administration, making it a poor choice when managing hyperkalemia in the ED. It is also uncomfortable and inconvenient for the patient, as it causes diarrhea.6
Hemodialysis (HD) is the definitive means for removing excess potassium and the preferred treatment for hyperkalemia. The serum potassium falls by about 1 mEq/L by 60 minutes of HD, and plateaus after 180 minutes with an average decrease of 2 mEq/L.3
Hypermagnesemia. Mild to moderate hypermagnesemia is frequently found in the patient with ESRD due to decreased renal excretion, but also from increased intake of magnesium-containing products such as laxatives, enemas, and antacids.7 The results of mild to moderate hypermagnesemia (2.2-5 mEq/L) include progressive flaccid muscle weakness, areflexia, drowsiness, and confusion. Findings with severe hypermagnesemia (> 5 mEq/L) include bradycardia, heart blocks on ECG, decreased level of consciousness, hypotension, and cardiac arrest. Hypermagnesemia is treated with 5-10 mL of intravenous calcium gluconate (10% solution) given over 5 minutes, prior to initiation of emergent HD.
Hypocalcemia. Hypocalcemia is a frequent occurrence in patients with renal failure. It is caused by a decrease in the conversion of 25 hydroxyvitamin D to its active form 1,25 dihydroxyvitamin D in the kidney. Hypocalcemia also results from the aggressive treatment of metabolic acidosis with intravenous sodium bicarbonate.7
Hypocalcemia is defined as a serum calcium level less than 8.5 mg/dL or an ionized calcium less than 4.2 mg/dL. Ionized levels are more accurate in identifying calcium disturbances in patients with ESRD because total serum calcium levels are affected by pH changes, albumin fluctuations, and hyperphosphatemia.8 Symptoms developing when ionized calcium levels fall below 2.5 mg/dL include perioral and fingertip paresthesias, muscle cramps, and muscle weakness. Physical examination findings include hyperreflexia, positive Chvostek and Trousseau signs, and a prolonged QT interval on ECG. At ionized levels below 1.6 mg/dL, tetany, seizures, and heart failure can ensue.
Treatment for severe, symptomatic hypocalcemia begins with 10 mL of 10% calcium chloride IV, given over 10-20 minutes. This is followed by a continuous infusion of 0.02 to 0.08 mL/kg/hr of 10% calcium chloride. Alternatively, 10% calcium gluconate IV may be used. Follow the serum calcium level after the initial IV bolus and then every 4-6 hours while using the infusion. Treatment with IV calcium should be reserved only for treatment of severe or symptomatic hypocalcemia.
Hyperphosphatemia. Hyperphos-phatemia is defined as a serum phosphorus concentration greater than 5 mg/dL. Elevated serum phosphorus levels occur in ESRD when the GFR falls below 30 mL/kg/1.73 m2, and it is due to decreased renal filtration and excretion. Chronically elevated levels are associated with increased cardiovascular mortality risk and altered homeostasis of bone metabolism pathways (see below). This forms the basis for treatment of hyperphosphatemia with phosphate binding agents and dietary phosphate restriction in ESRD.7,9
Hyperphosphatemia is usually mild, but severe elevations (greater than 7 mg/dL) with concomitant life-threatening hypocalcemia can be seen with ingestions of large amounts of sodium phosphate laxatives used for bowel preparation. It can also be caused by the use of phosphate-containing medications such as calcium phosphate. Patients with severe hyperphosphatemia must have a rapid correction with intensive HD.7,9
Cardiovascular Emergencies
Pulmonary Edema/Volume Overload. Fluid overload with resulting pulmonary edema is a frequent cause of emergency presentation in dialysis patients. Contributing factors include excessive salt and fluid intake; missed dialysis sessions; failure to achieve dry weight during dialysis; uncontrolled hypertension; pre-existing congestive heart failure; and new-onset acute coronary syndrome (ACS) or cardiac arrhythmias. Patients with fluid overload present with the complaints of shortness of breath, dyspnea on exertion, fatigue, and increasing edema. Physical examination findings include hypertension, decreased breath sounds, rales, elevated jugular venous pressure, and peripheral edema or anasarca. Estimated dry weight versus actual weight, if known and feasible, may also be used to evaluate the degree of volume overload present.7,10
The chest X-ray will show pulmonary vascular congestion, interstitial edema, and/or pulmonary effusion. An ECG can demonstrate precipitants of volume overload such as arrhythmias or ischemia. Brain natriuretic peptide (BNP) is not a reliable marker of acute volume overload in ESRD.11 The BNP is elevated in most HD patients and its interpretation in this acute setting has not been well established.7 However, chronic elevations of BNP are associated with increased mortality in this patient population.12
Emergent HD is the definitive treatment for volume overload and acute pulmonary edema. However, several initial steps in the ED can temporize these patients while arranging for HD. High-dose intravenous loop diuretics, such as furosemide (maximum dose of 120-240 mg IV), are useful in those with residual urine output. Control of elevated blood pressure and vasodilatation with SL, IV, or cutaneous nitroglycerin is critical. The target should be a 20-25% decrease in MAP.
Noninvasive positive pressure ventilation (NIPPV) using CPAP or BiPAP has been used in patients with respiratory distress. It requires a cooperative patient who can follow instructions and can protect his/her airway. There are no evidence-based guidelines on the use of NIPPV for ESRD patients in pulmonary edema. Intubation may be necessary prior to emergent HD if the patient is unable to tolerate NIPPV and the above interventions are ineffective in reducing the respiratory distress.
Angina/Chest Pain. Cardio-vascular disease accounts for the deaths of about 50% of patients with ESRD.13 The relative risk of coronary artery disease in these patients is 5-30 times greater than that of the general population. The combination of traditional risk factors for coronary artery disease (CAD) (especially DM and HTN) and conditions related to ESRD, including uremia, hyperphosphatemia, and hyperparathyroidism, result in chronic systemic inflammation with endovascular injury and dysfunction.7,10
ESRD can lead to significant baseline ECG abnormalities that can make the ECG interpretation more challenging, such as left ventricular hypertrophy and other changes related to electrolyte disorders.
Serum troponin T levels may be chronically elevated due to decreased renal clearance; however, an elevated value should not be attributed solely to ESRD, and an appropriate evaluation and observation period to rule out ACS is indicated.10,14
Dialysis-dependent patients with ACS should be treated with traditional therapies including aspirin, clopidogrel (Plavix®), and morphine. Thrombolytics and glycoprotein IIb/IIIa inhibitors do not require dose modification. However, if enoxaparin (Lovenox®) is used instead of unfractionated heparin, it is given only once daily, as it is renally cleared.
Hypertensive Emergencies
Approximately 85% of patients undergoing dialysis have hypertension. Contributing factors include volume overload, decreased vascular compliance, increased renin secretion, and increased sympathetic tone. Noncompliance with antihypertensives in this patient population may precipitate a hypertensive emergency.
In the ED, the initial goal of therapy for hypertensive emergency is lowering of the mean arterial pressure (MAP) by 20-25% using parenteral agents. Overly aggressive reduction of blood pressure can result is worsening of cardiac ischemia, worsening renal dysfunction, and cerebral ischemia. Intravenous agents of choice for hypertensive encephalopathy include labetalol and nicardipine. Sodium nitroprusside is best avoided in ESRD patients, as the metabolic by-product of its administration, thiocyanate, may accumulate with toxic effects. Parenteral nitroglycerin can be used to control hypertension if cardiac ischemia exists. Emergent HD may be necessary in cases of volume overload.
Pericarditis/Tamponade. The presentation of a pericardial effusion depends on how rapidly the fluid accumulated. The slower the rate of accumulation, the less dramatic the presentation, as the pericardium has time to stretch. These patients may be ill when first seen but will tolerate delays to management. Between 80-120 cc of pericardial fluid can accumulate without elevating the intrapericardial pressure. Beyond that, 20-40 additional milliliters almost doubles the intrapericardial pressure. This pressure is transmitted directly to the heart, causing increased atrial and central venous pressures. The end result is decreased cardiac output and decreased coronary perfusion.15
Beck described the classic physical findings of tamponade in 1935. However, up to two-thirds of patients will not have the triad of elevated central venous pressure (CVP), low arterial blood pressure, and muffled heart sounds. Jugular venous distention (JVD), in particular, may not be present, especially if the precipitant of tamponade is dehydration.
Pulsus paradoxus is described as another common finding in tamponade. It is an exaggeration of the normal drop in systolic blood pressure that occurs with inspiration. This finding is not reliably present in many patients with tamponade.16
The chest X-ray with a chronic effusion will reveal a "water bottle" shaped heart. However, a normal heart size does not exclude tamponade.
The ECG in a pericardial effusion shows low voltages and other non-specific changes. Electrical alternans is also nonspecific, with the exception of total electrical alternans, which involves both the P and QRS waves.16
The management of a symptomatic pericardial effusion involves several steps. First, intravascular pressure should be restored, as low CVP due to low intravascular volume results in further decreases of cardiac output. Emergent HD should be arranged. Pericardial effusions in stable HD patients can often be treated with intensive HD alone, while a minority require pericardiocentesis.15 However, for the unstable or crashing patient, the definitive management is with a pericardiocentesis. This procedure should be done with ultrasound guidance to minimize complications and improve success rates.17
Bedside transthoracic echocardiography is the fastest and most reliable diagnostic study. For the diagnosis of a pericardial effusion, two views are best: the subxiphoid and the parasternal long axis.18,19
Tamponade physiology is identified by the presence of right atrial early diastolic collapse. This is the most sensitive sonographic finding, especially when this collapse persists throughout diastole.18 Less sensitive findings include increased right ventricular size with diastolic collapse and late expansion; minimal to no change to the IVC diameter with respiration; and paradoxical septal wall motion.18
Hematologic and Gastrointestinal Emergencies
Anemia and Bleeding. Most patients with CKD will develop a normocytic and normochromic anemia secondary to the diminished renal production of erythropoietin and decreased red blood cell survival. Erythropoietin or darbepoetin alfa is often given to these patients to maintain a hemoglobin level between 10-11 g/dL. Without intervention, most patients with CKD would eventually have their hematocrit stabilize between 15% and 25%.20,21
Platelet dysfunction frequently manifests as easy bruising or mucosal bleeding, but may present as abnormal bleeding after procedures, intracranial hemorrhage, or spontaneous retroperitoneal bleeding. The underlying pathology is not fully understood but seems to be a combination of both intrinsically abnormal platelet function and the effects of uremic toxins and anemia.
Patients on dialysis appear to have a moderately increased risk of esophagitis, gastritis, and angiodysplasia, creating an additional risk for GI bleeding.22,23 The use of anticoagulation during HD is an added risk for more severe bleeding.
As the pathogenesis of uremic bleeding is multifactorial, emergent bleeding in the patient with CKD may respond best to a combination of treatments. Administration of dDAVP is effective in patients with uremic bleeding through stimulation of factor VIII and von Willebrand factor release. The preferred route is IV, with a single dose of 0.3 mcg/kg given over 15-30 minutes. It may also be given subcutaneously with the same dosing. The intranasal dose is 3 mcg/kg. The onset of action is within one hour and the half-life between 3 and 9 hours.24-26
If patients are unresponsive to dDAVP, cryoprecipitate in a dose of 10 bags over 30 minutes may be administered. Conjugated estrogen infusions can be very helpful. Although the duration of action is long (approximately 1 week), the onset of effects is about 6 hours, limiting its use in the critically ill. Finally, dialysis may be employed to improve bleeding time.25 If bleeding patients are found to be anemic, they should be transfused with packed red blood cells to a hematocrit of 25-30%.
Metabolic Bone Disease. CKD-MBD is a syndrome that encompasses abnormalities in calcium, phosphorus, parathyroid hormone (PTH), or vitamin D metabolism; changes in bone mineralization, volume, and turnover; and extra-skeletal calcification, including vascular or other soft-tissue calcification.27 The disorder leads to notable morbidity and mortality. These patients have significantly increased relative risk of hip and lumbar fractures.28,29
In CKD, the measured serum concentrations of phosphate and calcium generally remain normal until estimated GFR drops to approximately 20 mL/min/1.73 m2. Gradually, the proximal tubules' ability to produce 1,25-dihydroxyvitamin D3 (calcitriol) is significantly reduced, and calcium levels fall. This stimulates PTH release. PTH acts to increase renal phosphate excretion, but the damaged kidneys have impaired phosphate excretion. This, in combination with the promotion of bone resorption caused by PTH, results in elevated serum phosphate concentrations.30
The increased bone turnover in response to PTH results in weak bones that are prone to fracture. Osteitis fibrosa cystica occurs in this setting as bone is replaced with fibrous tissue. Rarely, there may be a localized occurrence called a Brown tumor or an osteoclastoma. This generally presents as a painful cystic area in the bone that appears as a lytic lesion on X-ray. As treatment of secondary hyperparathyroidism has improved, the prevalence of this disorder has decreased.31
Osteomalacia, a disorder wherein bones have defective mineralization, has also become less common. It was seen in patients in whom aluminum-containing antacids were used to help bind phosphate in the intestines. Aluminum interferes with the bone mineralization process, causing increased relative volumes of the soft, organic portion of the bone matrix, called the osteoid. Other trace metals may also result in osteomalacia.32
Adynamic bone disease is currently the most common presentation of renal osteodystrophy. This results from the exogenous suppression of the parathyroid gland through treatments such as calcium-containing phosphate binders and vitamin D analogues. The low activity of the osteoclasts and osteoblasts results in structurally weak bone, increasing fracture risk. Additionally, this form of renal bone disease is associated with increased extra-skeletal calcification, as patients often are hypercalcemic.33,34
Metastatic calcification is the final entity in CKD-MBD. While extra-skeletal calcification can occur anywhere, an important manifestation of this is calciphylaxis or calcific uremic arteriolopathy.35 As the latter name implies, there is calcium deposition and hardening of small vessels, which can lead to ischemia. Calciphylaxis presents as very painful, violaceous lesions that may progress to necrosis. The risk factors include: female gender, obesity, chronic dialysis, and the use of certain drugs, such as corticosteroids and warfarin.
Treatment standards are not well established but may include discontinuation of vitamin D analogues and using non-calcium-containing phosphate binders such as sevelamer (RenaGel®, Renvela®). In cases of severe, secondary hyperparathyroidism, cinacalcet (Sensipar®) may be helpful. The most promising recent development in calciphylaxis treatment is the use of sodium thiosulfate, which acts as an antioxidant and increases calcium solubility.36 Its use, however, is off-label, dosing varies, and administration is during or after dialysis.
For the emergency physician, it is important to recognize that CKD patients are at risk for fractures and vascular disease, both calciphylaxis and possibly also coronary artery disease.
Emergencies Related to Access
The hemodialysis patient must have vascular access. For urgent treatment, this is often accomplished using a double-lumen central venous catheter. A tunneled catheter with internal jugular access on the right, with the tip of the catheter ending at the caval-right atrial junction, has the lowest complication rate. Several companies manufacture double-lumen catheters to allow dialysis.
A common practice is to initiate HD with a central venous dialysis catheter with the ultimate goal to establish an arteriovenous (AV) fistula in the nondominant forearm.37 An AV fistula uses no prosthetic material, but is a surgically created direct anastomosis of an artery and a vein. Dialysis via a forearm AV fistula using a radial artery anastomosis to the cephalic vein is preferable, although brachial artery anastomosis with the basilic or cephalic vein is also common. Other, less common sites used to create AV fistulas include the proximal thigh. AV fistulas are advantageous due to their lower infection rates when compared to either central venous catheter access or AV grafts.37
AV fistulas typically will fail after prolonged use due to aneurysm or thrombosis. In other cases, adequate veins may not exist. These conditions will require the creation of an AV graft using a synthetic material such as polyurethane or polytetrafluoroethylene. The graft constructed is commonly in a U-shaped tunnel in the subcutaneous tissue of the forearm, although many configurations are possible when sites become exhausted or are no longer usable. Unfortunately, AV grafts have higher complication rates than AV fistulas, including thrombosis, infection, pseudoaneurysm, and limb loss.37
Infection is a common complication of central venous access in the dialysis patient and may require removal of the device. The patient may have signs of infection with local erythema, swelling, and purulent discharge at the catheter site. They may also have fever and chills and an elevated white blood cell count. The findings may also be more subtle, with only malaise and a history of fever being described.
These infections often require removal of the tunneled catheter if the patient appears ill or septic. When the catheter is removed, the tip should be sent for culture.38 The traditional approach requires removing a catheter if infection is considered likely, while some authors do not think removal is necessary in all cases.37,39
Some infected AV fistulas can be salvaged with antibiotic therapy alone, while an infected AV graft will require surgical excision similar to any other prosthetic device that becomes infected. The most common bacterial pathogens in the renal patient are Staphylococcus aureus, including MRSA, as well as coagulase-negative Staphylococcus and Streptococcus. Initial antibiotic choices must include coverage for MRSA, and gram-negative and gram-positive organisms.37
Bleeding from a central venous catheter is initially treated with direct pressure at the site where the catheter enters the vessel. Unfortunately, pressure applied to where a tunneled catheter penetrates the dermis will not be adequate and should be directed to where the catheter penetrates the central vessel. Unfortunately, one of the disadvantages of a subclavian line is the inability to apply direct pressure at the catheter's entrance into the subclavian vein.
An AV fistula or graft with persistent bleeding should initially be treated with elevation and direct pressure. However, over-aggressive or prolonged pressure can cause thrombosis of the access site and should be avoided. Several methods of direct pressure can be attempted, including digital pressure, gauze and elastic wraps, or plastic vascular clamps supplied by a dialysis unit. Topical agents may be used as well, such as Surgicel®, or chemical cautery using a silver nitrate applicator.40 A small figure-of-eight suture may be employed if persistent bleeding is noted at the hemodialysis puncture site. Nylon suture is less inflammatory, although absorbable suture material is becoming more common in the emergency setting due to patient compliance issues. Care must be taken to prevent injury to the actual AV fistula or graft, and the suture technique should be as superficial as possible.
A clotting disorder can be the reason for persistent bleeding. In those cases, PT/INR/PTT should be obtained. If the heparin used during dialysis causes a prolonged PTT, it can be reversed with IV protamine.
Bleeding must be controlled in the ED and the pressure device removed prior to discharge. AV fistula or graft patency, adequate flow and bruit, and hemorrhage control should be verified. Strict warnings must be given to the patient.
Clotted catheters, fistulas, and grafts are also common problems. Thrombosed catheters can be treated with tPA or urokinase. Dosing protocols vary widely between institutions, and consultation is recommended before treatment.37,41
If an AV fistula or graft becomes thrombosed, the cause should be investigated. Venous stenosis is a likely etiology. If stenosis is the cause, it will have to be treated or reoccurrence is likely. The thrombosis can be treated with pharmacologic intervention to dissolve the clot, or surgical removal may be undertaken. Immediate consultation with a vascular surgeon is needed to determine the treatment plan. Interventional radiology, when available, can also help with methods such as thrombolysis and angioplasty.42
Aneurysms, which are full-thickness dilatations of a vessel wall, develop over time with AV fistulas. Current recommendations are to repair an aneurysm in a fistula only if it occurs at the arterial anastomosis site, but other areas do not necessitate surgical intervention, as they are considered benign.37
Pseudoaneurysms occur in an AV graft after venipuncture when a leak develops and a hematoma forms outside of the graft. Increased swelling at a graft site, especially large enough to threaten the viability of overlying skin, should raise suspicion of a pseudoaneurysm. This will need surgical correction. If a pseudoaneurysm is inadvertently punctured during dialysis or otherwise, hemorrhage control can be very difficult.37
A steal syndrome may develop in which the required arterial blood for the distal limb is diverted through the fistula. That extremity develops ischemia. An arterial stenosis or thrombosis can also occur, limiting the supply of oxygenated blood to the distal tissue. The patient complains of a cold extremity, pallor, numbness, weakness, or severe pain. The resultant ischemia can cause permanent nerve and tissue damage in hours, and emergency surgical intervention is needed.43
High-output congestive heart failure (CHF) can also occur after placement of an AV fistula for hemodialysis.44 AV fistulas have high flow rates. In such patients, the AV fistula flow rate exceeds 2000 mL/min.45,46 In these cases, a flow reduction surgery or closure of the fistula is indicated.47,48 The effect of an AV fistula on preload and high-volume flow on the heart can be demonstrated at the bedside. Branham's sign, also known as Nicoladoni-Israel-Branham sign, is the development of bradycardia when an AV fistula is manually compressed. When the compression of the AV fistula is released, the bradycardia resolves.49
Problems During and After Hemodialysis
Hypotension. Hypotension after dialysis may result in the patient being sent to the ED for evaluation. Several factors may be causative, including excessive ultrafiltration during dialysis, which is treated with cautious isotonic crystalloid infusion. Other factors related to HD can contribute to hypotension, including using dialysate fluid warmed to 37° C, acetate-containing dialysate, and recent food ingestion.37
Hypotension before or after dialysis may also imply a more serious disease. Sepsis is an obvious concern due to both an impaired immune system and venous access devices such as central catheters. Vasopressors, such as dopamine or norepinephrine, may be required if the hypotension persists after rational fluid administration.50
Bedside ultrasonography is helpful to exclude pericardial tamponade, although many renal patients will have pericardial effusions that are not the cause of hypotension (see above).51 Ultrasonography can also be used to identify volume status, and serial measurements of the IVC can guide fluid administration.
The exposure of the hemodialysis patient to heparin, as well as other clotting disorders, predisposes them to hemorrhage from several sites. Common sites of hemorrhage resulting in hypotension are the gastrointestinal tract, retroperitoneal space, and soft tissues. Complaints of abdominal pain or musculoskeletal pain in the setting of hypotension will require an investigation for occult hemorrhage.
Finally, cardiogenic shock, myocardial infarction, dysrhythmias, and hyper- or hypokalemia may also be the etiology for hypotension. Anaphylactic reactions due to dialysis have also been reported.52
Disequilibrium. Disequilibrium syndrome usually occurs after the first episode of hemodialysis in patients newly diagnosed with renal failure, when uremia is pronounced. The rapid removal of urea and other ions produces an osmolar gradient between the brain and plasma, with resultant cerebral edema. Patients present with nausea, vomiting, muscle cramps, altered consciousness, seizures, and focal neurologic signs that mimic ischemic stroke.53,54 The required evaluation, therefore, can be quite extensive. Cerebral edema may be identified on CT scan or MRI. These patients may require admission to the intensive care unit.
Peritoneal Dialysis (PD) Emergencies
Insertion (exit) site infection is identified by the presence of purulent drainage at the site of the PD catheter. Redness may be a sign of infection, but also could be a localized skin reaction to recent instrumentation or trauma.55 These infections often spread to the tunnel and into the peritoneum, resulting in peritonitis. Staph. aureus and P. aeruginosa are often the culprits. The infections can spread quickly and, therefore, must be aggressively treated.55 Oral antibiotics for a minimum of two weeks, after site cultures, are indicated.55
Peritonitis remains a leading cause for mortality in PD patients. It is also a major reason for patients switching to HD. A cloudy effluent is presumed peritonitis, with or without the presence of abdominal pain.55 Upon examination of the effluent, a WBC count greater than 100/μL, and at least 50% PMNs is the cutoff used to diagnose peritonitis. Make sure that the dialysate has at least an hour, but ideally two hours, of dwell time. In cases of shorter dwell times, the percentage of PMNs, regardless of the total WBC count, is a better indicator of peritonitis.55 The gram stain is often negative, and cultures of the effluent, along with blood cultures, should also be sent.
Start empiric antibiotics in the ED.55 Current guidelines recommend intraperitoneal (IP) antibiotics over IV antibiotics. Coverage should include both gram-positive and gram-negative organisms.
Pain Management in the ESRD/Dialysis Patient
About one-third of the dialysis patients receive pain medications, some of them chronically, and many of them in the ED. Pain is a common and multi-factorial complaint in ESRD patients.
Initial analgesia in those with mild to moderate pain should start with acetaminophen.56 Nonsteroidal anti-inflammatory drugs (NSAIDs) can be used concomitantly. Due to the potential gastrointestinal and renal effects of the NSAIDs, make sure the dosing is restricted in time and amount.57
Opioid analgesics are generally recommended for moderate to severe pain.57 Care must be taken when choosing and dosing opioid analgesics. Impaired clearance can lead to accumulation of the parent compound and active metabolites. (See Table 2.)
Table 2: Opioid Use in ESRD Patients57-59
|
Opioid |
Metabolism and Excretion |
Dosing Recommendations |
|
Morphine |
The 6-glucuronide metabolite, which is very potent, can accumulate and cause respiratory depression. The 3-glucuronide also accumulates, and is thought to mediate CNS excitation. |
Reduce the dose and the frequency of dosing. Beware of many different available formulations. |
|
Hydromorphone and hydrocodone |
Hydrocodone is metabolized by the liver into hydromorphone, which in turn is metabolized to the 3-glucuronide. This molecule has no analgesic activity, but is neuro-excitatory. Hydromorphone and its metabolites are renally excreted and easily dialyzable. |
Use lower doses and less frequent dosing as a starting point. Beware of the acetaminophen component of the hydrocodone preparations. |
|
Oxycodone |
It is metabolized by the liver to several inactive and one active compound (oxymorphone), all of which are renally excreted. |
The data on ESRD patients is scant, and it should be used with caution. It has higher abuse potential. Beware of the acetaminophen component in some preparations. |
|
Codeine |
It is mainly metabolized to the 6-glucuronide, and both compounds are renally excreted. Cases of excessive sedation due to drug accumulation have been reported. Codeine is not dialyzable. |
Codeine should be avoided in ESRD patients. |
|
Methadone |
It is eliminated by both the kidneys and the feces. There are no reported cases of adverse effects in ESRD patients. |
There is limited information on safety and dosing in ESRD. |
|
Fentanyl |
Fentanyl is metabolized by the liver to norfentanyl. Cases of respiratory depression due to accumulation of drug have been reported. |
Use with caution. |
|
Meperidine |
Meperidine and its metabolites are renally excreted. The most toxic metabolite is normeperidine. Its accumulation results in CNS excitation and seizures. |
Do not use in the ESRD patient. |
Drugs to Avoid in ESRD
Although it is widely taught that succinylcholine should be avoided as it increases serum potassium, it appears that this elevation only occurs in patients who have up-regulated receptors, such as those with neuromuscular diseases. In a retrospective search of hyperkalemic patients undergoing anesthesia, there were no adverse events. This study was small, locating only 38 patients with elevated serum potassium.60 Given the lack of a large study, it is best to avoid succinylcholine when a known hyperkalemic patient needs to have rapid sequence induction.
Nitroprusside is a very potent antihypertensive agent. Its metabolites are renally excreted and will accumulate in renal failure. If using nitroprusside, monitor the patient closely for signs of toxicity and try to wean the medication as soon as feasible.
Conclusions and Take Home Points
HD and PD patients have many complications that require ED visits and management.
Among the electrolyte derangements, hyperkalemia is a major cause for morbidity and mortality.
Infectious complications are many. Specifically, peritonitis must be a consideration in PD patients with either a change in effluent color or abdominal pain. Line infection is also a common source of infection in those with tunneled catheters.
Metabolic bone disease has been decreasing in incidence and prevalence, but is still a common cause for fractures and a source for pain in ESRD patients. In managing moderate to severe pain, remember that most opioid analgesics require dosing modifications to prevent adverse drug effects.
References
1. Chapter one: Incidence, prevalence, patient characteristics, and treatment modalities. United Sates Renal Data System 2009; http://www.usrds.org/2011/pdf/v2_ch01_11.pdf. Accessed April 6, 2012.
2. United States Renal data System: 2011 USRDS Annual Data Report. Volume two: Atlas of End-Stage Renal Disease in the United States 2011; http://www.usrds.org/2011/pdf/v2_00_intro_11.pdf. Accessed April 6, 2012.
3. Weisberg LS. Management of severe hyperkalemia. Crit Care Med 2008;36(12):3246-3251.
4. Surawicz B. Electrolytes and the electrocardiogram. Postgrad Med 1974;55(6):123-129.
5. Allon M, Dunlay R, Copkney C. Nebulized albuterol for acute hyperkalemia in patients on hemodialysis. Ann Intern Med 1989;110(6):426-429.
6. Sterns RH, Rojas M, Bernstein P, et al. Ion-exchange resins for the treatment of hyperkalemia: Are they safe and effective? J Am Soc Nephrol 2010;21(5):733-735.
7. Venkat A, Kaufmann KR, Venkat K. Care of the end-stage renal disease patient on dialysis in the ED. Am J Emerg Med 2006;24(7):847-858.
8. Calvi LM, Bushinsky DA. When is it appropriate to order an ionized calcium? J Am Soc Nephrol 2008;19(7):1257-1260.
9. Molony DA, Stephens BW. Derangements in phosphate metabolism in chronic kidney diseases/endstage renal disease: Therapeutic considerations. Adv Chronic Kidney Dis 2011;18(2):120-131.
10. Power A, Duncan N, Goodlad C. Management of the dialysis patient for the hospital physician. Postgrad Med J 2009;85(1005):376-381.
11. Mueller C, Laule-Kilian K, Scholer A, et al. B-type natriuretic peptide for acute dyspnea in patients with kidney disease: Insights from a randomized comparison. Kidney Int 2005;67(1):278-284.
12. Sommerer C, Beimler J, Schwenger V, et al. Cardiac biomarkers and survival in haemodialysis patients. European J Clin Invest 2007;37(5):350-356.
13. Arulkumaran N, Montero RM, Singer M. Management of the dialysis patient in general intensive care. Br J Anaesth 2012;108(2):183-192.
14. Kanwar M, Hashem M, Rosman H, et al. Usefulness of clinical evaluation, troponins, and C-reactive protein in predicting mortality among stable hemodialysis patients. Am J Cardiol 2006;98: 1283-1287.
15. Han JH, Chandra A, Mulgund J, et al. Chronic kidney disease in patients with non-ST-segment elevation acute coronary syndromes. Am J Med 2006;119: 248-254.
19. Callaham M. Pericardiocentesis in traumatic and nontraumatic cardiac tamponade. Ann Emerg Med 1984;13:924-945.
16. Kwasnik EM, Koster K, Lazarus JM, et al. Conservative management of uremic pericardial effusions. J Thorac Cardiovasc Surg 1978;76:629-632.
17. Maggiolini S, Bozzano A, Russo P, et al. Echocardiography-guided pericardiocentesis with probe-mounted needle: Report of 53 cases. J Am Society Echocardiography 2001;14:821-824.
18. Weekes AJ, Quirke DP. Emergency echocardiography. Emerg Med Clin North Am 2011;29:759-787, vi-vii.
19. Nagdev A, Stone MB. Point-of-care ultrasound evaluation of pericardial effusions: Does this patient have cardiac tamponade? Resuscitation 2011;82:671-673.
20. Singh AK, Szczech L, Tang KL, et al. Correction of anemia with epoetin alfa in chronic kidney disease. N Engl J Med 2006;355:2085-2098.
21. KDOQI Clinical Practice Guidelines and Clinical Practice Recommendations for Anemia in Chronic Kidney Disease. Am J Kidney Dis 2006;47(5 Suppl 3):S11-145.
22. Alvarez L, Puleo J, Balint JA. Investigation of gastrointestinal bleeding in patients with end stage renal disease. Am J Gastroenterol 1993;88:30-33.
23. Chalasani N, Cotsonis G, Wilcox CM. Upper gastrointestinal bleeding in patients with chronic renal failure: role of vascular ectasia. Am J Gastroenterol 1996;91:2329-2332.
24. Boccardo P, Remuzzi G, Galbusera M. Platelet dysfunction in renal failure. Semin Thrombosis Hemostasis 2004;30:579-589.
25. Noris M, Remuzzi G. Uremic bleeding: Closing the circle after 30 years of controversies? Blood 1999;94:2569-2574.
26. Sohal AS, Gangji AS, Crowther MA, et al. Uremic bleeding: Pathophysiology and clinical risk factors. Thrombosis Research 2006;118:417-422.
27. Moe S, Drueke T, Cunningham J, et al. Definition, evaluation, and classification of renal osteodystrophy: A position statement from Kidney Disease: Improving Global Outcomes (KDIGO). Kidney Int 2006;69:1945-1953.
28. Block GA, Klassen PS, Lazarus JM, et al. Mineral metabolism, mortality, and morbidity in maintenance hemodialysis. J Am Soc Nephrol 2004;15:2208-2218.
29. Moe SM, Chertow GM. The case against calcium-based phosphate binders. Clin J Am Soc Nephrol 2006;1:697-703.
30. Levin A, Bakris GL, Molitch M, et al. Prevalence of abnormal serum vitamin D, PTH, calcium, and phosphorus in patients with chronic kidney disease: Results of the study to evaluate early kidney disease. Kidney Int 2007;71:31-38.
31. Cunningham J, Locatelli F, Rodriguez M. Secondary hyperparathyroidism: Pathogenesis, disease progression, and therapeutic options. Clin J Am Soc Nephrol 2011;6:913-921.
32. Malluche HH. Aluminium and bone disease in chronic renal failure. Nephrol Dial Transplant 2002;17 Suppl 2:21-24.
33. Monier-Faugere MC, Malluche HH. Trends in renal osteodystrophy: A survey from 1983 to 1995 in a total of 2248 patients. Nephrol Dial Transplant 1996;11 Suppl 3:111-120.
34. Moe SM, Drueke T. Improving global outcomes in mineral and bone disorders. Clin J Am Soc Nephrol 2008;3 Suppl 3:S127-130.
35. Brandenburg VM, Cozzolino M, Ketteler M. Calciphylaxis: A still unmet challenge. J Nephrol 2011;24:142-148.
36. Watson M, Abbott KC, Yuan CM. Damned if you do, damned if you don't: Potassium binding resins in hyperkalemia. Clin J Am Soc Nephrol 2010;5: 1723-1726.
37. National Kidney Foundation. NKF-KDOQI Clinical Practice Guidelines. 2001; http://www.kidney.org/professionals/kdoqi/guidelines_updates/doqi_uptoc.html - va. Accessed March 30, 2012.
38. Blot F, Nitenberg G, Chachaty E, et al. Diagnosis of catheter-related bacteraemia: A prospective comparison of the time to positivity of hub-blood versus peripheral-blood cultures. Lancet 1999;354:1071-1077.
39. Deliberato RO, Marra AR, Correa TD, et al. Catheter related bloodstream infection (CR-BSI) in ICU patients: Making the decision to remove or not to remove the central venous catheter. PloS One 2012;7:e32687.
40. Krywko DM SC. Indwelling vascular devices: Emergency access and management. In: Roberts JR HJ, ed. Clinical Procedures in Emergency Medicine. Philadelphia: Saunders; 2004:418-430.
41. Donati G, Coli L, Cianciolo G, et al. Thrombosis of tunneled-cuffed hemodialysis catheters: Treatment with high-dose urokinase lock therapy. Artificial Organs 2012;36:21-28.
42. Haage P, Gunther RW. Radiological intervention to maintain vascular access. European J Vascular Endovascular Surgery 2006;32:84-89.
43. Reifsnyder T, Arnaoutakis GJ. Arterial pressure gradient of upper extremity arteriovenous access steal syndrome: Treatment implications. Vascular Endovascular Surgery 2010;44:650-653.
44. Anderson CB, Codd JR, Graff RA, et al. Cardiac failure and upper extremity arteriovenous dialysis fistulas. Case reports and a review of the literature. Arch Intern Med 1976;136:292-297.
45. Di Lullo L, Floccari F, Polito P. Right ventricular diastolic function in dialysis patients could be affected by vascular access. Nephron Clin Pract 2011;118:c257-261.
46. Malik J, Tuka V, Mokrejsova M, et al. Mechanisms of chronic heart failure development in end-stage renal disease patients on chronic hemodialysis. Physiological Research/Academia Scientiarum Bohemoslovaca 2009;58: 613-621.
47. Santoro D, Savica V, Bellinghieri G. Vascular access for hemodialysis and cardiovascular complications. Minerva Urol Nefrol 2010;62:81-85.
48. Wasse H, Speckman RA, McClellan WM. Arteriovenous fistula use is associated with lower cardiovascular mortality compared with catheter use among ESRD patients. Semin Dial 2008;21:483-489.
49. Sharma A, Swan KG. Branham's bradycardic reaction. Ann Vasc Surg 2010;24:295-298.
50. Havel C, Arrich J, Losert H, et al. Vasopressors for hypotensive shock. Cochrane Database Syst Rev 2011(5):CD003709.
51. Frommer JP, Young JB, Ayus JC. Asymptomatic pericardial effusion in uremic patients: Effect of long-term dialysis. Nephron 1985;39:296-301.
52. Acute allergic-type reactions among patients undergoing hemodialysismultiple states, 2007-2008. MMWR Morbid Mortal Wkly Rep 2008;57:124-125.
53. Attur RP, Kandavar R, Kadavigere R, et al. Dialysis disequilibrium syndrome presenting as a focal neurological deficit. Hemodial Int 2008;12:313-315.
54. Patel N, Dalal P, Panesar M. Dialysis disequilibrium syndrome: A narrative review. Semin Dial 2008;21:493-498.
55. Li PK, Szeto CC, Piraino B, et al. Peritoneal dialysis-related infections recommendations: 2010 update. Perit Dial Int 2010;30:393-423.
56. Henrich WL, Agodoa LE, Barrett B, et al. Analgesics and the kidney: Summary and recommendations to the Scientific Advisory Board of the National Kidney Foundation from an Ad Hoc Committee of the National Kidney Foundation. Am J Kidney Dis 1996;27:162-165.
57. Kurella M, Bennett WM, Chertow GM. Analgesia in patients with ESRD: A review of available evidence. Am J Kidney Dis 2003;42:217-228.
58. Dean M. Opioids in renal failure and dialysis patients. J Pain Symptom Management 2004;28:497-504.
59. Gasche Y, Daali Y, Fathi M, et al. Codeine intoxication associated with ultrarapid CYP2D6 metabolism. N Engl J Med 2004;351:2827-2831.
60. Schow AJ, Lubarsky DA, Olson RP, et al. Can succinylcholine be used safely in hyperkalemic patients? Anesth Analg 2002;95:119-122.
As a group, I find most emergency physicians skeptical of many of the "advanced" technologies used to treat chronic diseases. I attribute this to our biased experience with these patients; those who do well are not likely to come to the ED very often.Subscribe Now for Access
You have reached your article limit for the month. We hope you found our articles both enjoyable and insightful. For information on new subscriptions, product trials, alternative billing arrangements or group and site discounts please call 800-688-2421. We look forward to having you as a long-term member of the Relias Media community.