volume 27 • number 10 in this issue · dialysis disequilibrium syndrome. 6. list the admission...

Volume 27 • Number 10

October

2013

In This IssueLesson 19 Dialysis Emergencies Page 2

Patients with end-stage renal disease (ESRD) who are on dialysis can present with a multitude of emergent conditions caused by or complicated by their dialysis. Emergency physicians must understand the pathophysiology of ESRD and the potential complications of dialysis in order to provide optimal care for these patients.

Lesson 20 Noninvasive Hemodynamic Monitoring 4Given the dangers of both volume over-resuscitation and under-resuscitation of a critically ill patient, accurately monitoring hemodynamics to guide this resuscitation is critical. There are several invasive techniques to help guide resuscitation (eg, central venous pressure monitoring); however, newer noninvasive and minimally invasive methods offer useful alternatives.

ContributorsJonathan M Glauser, MD, FACEP, and Candace Leigh, MD, wrote “Dialysis Emergencies ” Dr. Glauser is a senior faculty member at the MetroHealth Medical Center Residency Training Program in Emergency Medicine and an associate professor of emergency medicine at Case Western Reserve University, in Cleveland, Ohio. Dr. Leigh is a resident at Case Western Reserve University, in Cleveland, Ohio.

Sharon E Mace, MD, FACEP, reviewed “Dialysis Emergencies.” Dr. Mace is professor of medicine at the Cleveland Clinic Lerner College of Medicine, Case Western Reserve University, director of the Observation Unit and director of Pediatric Education and Quality Improvement at the Cleveland Clinic Foundation, and faculty for the MetroHealth Medical Center Emergency Medicine Residency Program in Cleveland, Ohio.

Haney Mallemat, MD, and Michael Scott, MD, wrote “Noninvasive Hemodynamic Monitoring ” Dr. Mallemat is an assistant professor in the Department of Emergency Medicine at the University of Maryland School of Medicine in Baltimore, Maryland. Dr. Scott is a physician in the Departments of Emergency Medicine and Internal Medicine at the University of Maryland Medical Center in Baltimore.

Amal Mattu, MD, FACEP, reviewed “Noninvasive Hemodynamic Monitoring.” Dr. Mattu is professor and vice chair, Department of Emergency Medicine, and director of faculty development and emergency cardiology fellowships at the University of Maryland School of Medicine in Baltimore.

Frank LoVecchio, DO, MPH, FACEP, reviewed the questions for these lessons. Dr. LoVecchio is research director at the Maricopa Medical Center Emergency Medicine Program and medical director of the Banner Poison Control Center, Phoenix, Arizona, and a professor at Midwestern University/Arizona College of Osteopathic Medicine in Glendale, Arizona.

Louis G Graff IV, MD, FACEP, is Editor-in-Chief of Critical Decisions. Dr. Graff is professor of traumatology and emergency medicine at the University of Connecticut School of Medicine in Farmington, Connecticut.Contributor Disclosures In accordance with the ACCME Standards for Commercial Support and policy of the American College of Emergency Physicians, all individuals with control over CME content (including but not limited to staff, planners, reviewers, and authors) must disclose whether or not they have any relevant financial relationship(s) to learners prior to the start of the activity. These individuals have indicated that they have a relationship which, in the context of their involvement in the CME activity, could be perceived by some as a real or apparent conflict of interest (eg, ownership of stock, grants, honoraria, or consulting fees), but these individuals do not consider that it will influence the CME activity. Sharon E. Mace, MD, FACEP; Masimo, consulting fees; Gebauer, contracted research, non-CME services; Baxter, contracted research; Luitpold, contracted research. Joshua S. Broder, MD, FACEP; GlaxoSmithKline; his wife is employed by GlaxoSmithKline as a research organic chemist. All remaining individuals with control over CME content have no significant financial interests or relationships to disclose.Method of Participation This educational activity consists of two lessons with a posttest, evaluation questions, and a pretest; it should take approximately 5 hours to complete. To complete this educational activity as designed, the participant should, in order, take the pretest (posted online following the previous month’s posttest), review the learning objectives, read the lessons as published in the print or online version, and then complete the online posttest and evaluation questions. Release date October 1, 2013. Expiration date September 30, 2016.Accreditation Statement The American College of Emergency Physicians is accredited by the Accreditation Council for Continuing Medical Education to provide continuing medical education for physicians. The American College of Emergency Physicians designates this enduring material for a maximum of 5 AMA PRA Category 1 Credits™. Physicians should claim only the credit commensurate with the extent of their participation in the activity. Each issue of Critical Decisions in Emergency Medicine is approved by ACEP for a maximum of 5 ACEP Category I credits. Approved by the AOA for 5 Category 2-B credits. A minimum score of 75% is required.Commercial Support There was no commercial support for this CME activity.Target Audience This educational activity has been developed for emergency physicians.

■ Also in This Issue ∙ The LLSA Literature

Review / Page 13 ∙ The Critical ECG

/ Page 23 ∙ The Critical Image

/ Page 25 ∙ CME Questions

/ Page 26 ∙ The Drug Box / Page 28

■ Next Month ∙ Highly Sensitive

Troponin Assays ∙ Confusion in the Elderly

Critical Decisions in Emergency Medicine

2

■ ObjectivesOn completion of this lesson, you should be able to:

1. Describe the key elements in the history and physical examination that directly influence management of patients with end-stage renal disease (ESRD).

2. Demonstrate the diagnostic and therapeutic evaluation of the hypotensive dialysis patient.

3. Describe the evaluation of a febrile patient with ESRD on hemodialysis.

4. Describe the most common vascular access emergencies.

5. List symptoms suggestive of acute dialysis disequilibrium syndrome.

6. List the admission criteria for patients undergoing renal replacement therapy.

7. Discuss the evaluation and treatment of infections directly related to peritoneal dialysis.

■ From the EM Model15.0 Renal and Urogenital Disorders 15.2 Complications of Renal Dialysis

Jonathan M. Glauser, MD, FACEP, and Candace Leigh, MD

Dialysis Emergencies

Lesson 19

Problems associated with end-stage renal disease (ESRD) and dialysis are ubiquitous in emergency medicine. During 2004, there were approximately 309,000 people treated for ESRD by hemodialysis. This was nearly double the number from one decade before.1 The overall cost of ESRD in the United States rose to $29 billion in 2009, an increase of 3.7% from the year before.2 In 2008 alone, the Centers for Disease Control and Prevention (CDC) estimated that there were 37,000 bloodstream infections among hemodialysis patients with central lines, one-fourth of which may have proved lethal.3 The burdens of dialysis, in both financial and human terms, will continue to affect the practice of emergency medicine.

Case Presentations

■ Case OneA 48-year-old woman presents via

ambulance after a generalized tonic-clonic seizure witnessed at home by a family member. The patient had completed her first dialysis session without any difficulty 1 hour prior to the event and has no prior history of seizure or malignancy. Paramedics administered intravenous lorazepam at the scene. She arrives drowsy and confused but answering some questions appropriately. A cardiac monitor shows a regular, narrow complex rhythm. Vital signs are blood pressure 105/72, pulse rate 82, respiratory rate 14, temperature 36.4ºC (97.5°F), and pulse oximetry 98% on 2 L oxygen via nasal cannula.

She is moving all extremities to command, with intact strength and sensation. Pupils are equal and reactive. The remainder of her neurologic examination is nonfocal. She appears well hydrated. Heart and lung examinations are unremarkable. A fistula in her right upper extremity is clean, dry, and nonerythematous.

■ Case Two

A 55-year-old man presents by private vehicle with his wife. Over the past 6 hours, the patient has noticed increasing pain and pallor in the hand distal to the right upper extremity fistula used for his hemodialysis. His last session, yesterday, was uncomplicated. The patient admits he has experienced these symptoms multiple times before, but they had previously lasted less than an hour and had been much less severe. Vital signs are blood pressure 142/92, pulse rate 80, respiratory rate 18, temperature 36.2°C (97.2°F), and pulse oximetry 97% on room air. His right hand is notably pale compared with the opposite hand, and the right radial pulse is present but significantly reduced compared with the left. The patient notes decreased sensation in a similar distribution compared with the left, but motor function is intact and equal. A fistula is present in right upper arm, and a palpable thrill is noted. The remainder of the examination is unremarkable.

■ Case ThreeA 59-year-old man was found with

severe shortness of breath outside

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October 2013 • Volume 27 • Number 10

• What are the key questions in the history and essential elements of the physical examination of a patient with ESRD?

• What details are most important in evaluating a hypotensive patient with ESRD?

• What electrolyte abnormalities should emergency physicians consider in dialysis patients?

• How is cardiac arrest managed in an ESRD patient?

• What signs and symptoms are indicative of dialysis disequilibrium syndrome, and how should it be managed?

• What therapeutic options are available for ESRD patients in the setting of acute pulmonary edema or possible cardiac tamponade?

• What are the diagnostic and therapeutic approaches to the febrile dialysis patient?

• What emergency considerations are directly related to the vascular access site itself?

• When should the ESRD patient be admitted to the hospital?

Critical Decisions

his home by a neighbor. He became unresponsive shortly after arrival of EMS and was intubated at the scene. On arrival at the hospital, the patient is recognized by emergency department staff as a frequent patient, mainly because of nonadherence to his dialysis regimen. Vital signs are blood pressure 72/48, pulse rate 115, respiratory rate 16 on a ventilator, temperature 36.6°C (97.9°F), and pulse oximetry 98% on 100% oxygen. He is immediately placed on a monitor, which shows a regular narrow complex tachycardia. His heart sounds are distant and muffled, and there are diffuse crackles in all lung fields. Jugular venous distention, 3+, is present as well as 2+ bilateral equal lower extremity edema. There is no evidence of traumatic injury or rash. A 12-lead ECG shows decreased voltage and electrical alternans.

End-Stage Renal DiseaseCauses of ESRD parallel those

of acute renal failure, with diabetes mellitus and hypertension being the most prominent (Table 1). Factors causing problems in patients with renal insufficiency and ESRD generally are related to one of a handful of broad considerations: inability to excrete excess water, inability to excrete toxic metabolites, inability to control electrolyte levels, failure of hematopoiesis, or failure of vitamin D activation. Because 85% of erythropoietin is produced in the kidneys, anemia occurs

without erythropoietin replacement. Vitamin D deficiency contributes to secondary hyperparathyroidism and development of renal bone disease. The most common emergency department complaints of ESRD patients generally reflect these principles (Table 2).

Both acute and chronic renal failure may lead to uremia, the advanced form of azotemia in which multiorgan system derangements become evident. These include

electrolyte disturbances, volume disturbances, bleeding, metabolic acidosis, and anemia. Hyperkalemia may be life-threatening, as pericarditis and pericardial effusion can be. Persistent nausea and vomiting can lead to dehydration and shock.

There are numerous common causes for death in ESRD. Myocardial infarction is frequent, and can result from the same underlying disorders, such as hypertension and diabetes mellitus, that caused renal failure in the first place. Other cardiac causes for death include arrhythmia, cardiac tamponade, medication toxicity (digitalis and others), ischemic or hypertrophic cardiomyopathy, conduction system disease, and acetate cardiotoxicity. Cardiac causes account for approximately 50% of ESRD deaths.5 Troponin levels may be elevated in patients with elevated creatinine levels (false positives). Caregivers should know the limits of normal for their laboratories.

Infection, especially Staphylococcus aureus sepsis, may be related to impaired neutrophil, T, and B lymphocyte function. Pulmonary infections are common. Withdrawal-from-dialysis suicide has been implicated in approximately 20% of deaths, with a slightly higher rate of withdrawal from therapy in patients older than 65 years. Cerebrovascular disease, including intracranial hemorrhage, occurs frequently, as does malignancy. Electrolyte

Table 1 Causes of ESRD

Collagen vascular disease, vasculitis; systemic lupus erythematosus, scleroderma, Wegener granulomatosis, polyarteritis nodosa

Diabetes mellitus (35% overall)

Glomerulonephritis

Hereditary diseases: polycystic kidney disease, Alport syndrome, medullary cystic disease

HIV

Hypertension (30% overall, 40% in black patients)

Nephrotoxins: radionuclide dyes, heroin, amphotericin B, aminoglycosides

Obstructive uropathy: prostatic obstruction, retroperitoneal fibrosis or tumor, nephrolithiasis

Reflux nephropathy in children and adolescents


4

disturbances, including hyperkalemia and hypercalcemia, may be life threatening.6 Gastrointestinal bleeding may be from peptic ulcer disease, colonic diverticula, or arteriovenous malformations. Other potentially lethal gastrointestinal events include bowel infarction and ischemia. Dementia frequently contributes to morbidity and mortality.

CRITICAL DECISIONWhat are the key questions in the history and essential elements of the physical examination of a patient with ESRD?

It is important to determine the underlying cause for the patient’s ESRD, as an underlying disease such as diabetes mellitus can affect the presenting complaint. It is important to know the patient’s dry weight as a means of assessing volume status, as well as whether it was achieved at last dialysis. It is critical to know the schedule of the patient’s dialysis (M-W-F, T-Th-S), as well as whether any sessions were missed and why. Recall that 20% of dialysis patients withdraw from therapy before death. It is important to know whether there has been retention of the patient’s native kidneys, as a source

for hypertension, nephrolithiasis, or infection. Since intra-dialysis hypotension is a common presenting complaint, knowledge of baseline vital signs can be critical. Bone pain can indicate fractures as a sign of renal osteodystrophy. Coughing can suggest heart failure. Clues to inadequate dialysis include anorexia, nausea, vomiting, diarrhea, weakness, and impaired alertness.

The significance of vital signs is self-explanatory. Vascular access should be evaluated for a bruit or thrill. Shunt thrombosis usually is from outflow stenoses in the venous circulation. The site should be examined for erythema, warmth, swelling, tenderness, and discharge. Infection, if present, can be subtle. The cardiac examination should focus on murmurs, distant heart sounds possibly indicative of pericardial effusion, and evidence for fluid retention indicative of heart failure.

The neurologic examination may reveal neuropathy, asterixis, lethargy, somnolence, hiccups, myoclonic twitching, or altered mental status. As bleeding always is a consideration in uremic patients with suboptimal platelet function, subdural hematoma should be suspected with focal deficits or depressed level of consciousness, especially in instances of concurrent anticoagulant use, hypertension, or excessive ultrafiltration. A rectal examination may be performed to diagnose gastrointestinal bleeding.

Clinical features of chronic renal failure can manifest in a variety of systems. Possible central nervous system abnormalities include neuropathy (peripheral and autonomic), lethargy, fatigue, seizures, singultus, coma, and dementia. Uremic encephalopathy typically shows memory loss, decreased attentiveness, slurred speech, or asterixis. Dialysis dementia can occur after 2 years of dialysis, possibly related to oral or dialysate aluminum. Possible cardiopulmonary presentations of ESRD include heart failure, pulmonary edema, pericarditis, hypertension, and

pericardial effusions. High-output heart failure can be related to anemia or the presence of an arteriovenous fistula. Gastrointestinal features of uremia include nausea, vomiting (mandating a check for hypercalcemia or hyponatremia), anorexia, symptoms of peptic ulcer disease, uremic gastroparesis, and constipation. Dermatologic manifestations of uremia include pallor (anemia), pruritus, and crystallized urea from sweat (uremic frost).

Historically, patients are sent to emergency departments from dialysis centers with specific problems such as bleeding or hypotension. In the future, many more patients may be presenting who are on home hemodialysis, and more patients are managed on home peritoneal dialysis (PD).7 The blood and the dialysate are separated by a semipermeable membrane. The hemodialysis process can be divided into two parts—the blood circuit and the dialysate circuit. There are alarms for blood leaks, air detection, blood pump torque, and others, which should shut off the blood pump, clamp the venous return line, and isolate the patient. While it is not reasonable for emergency physicians to deal with kinks in the lines, clots, or venous access, they should be aware of problems caused by the process itself. Specifically, polyvinyl chloride (PVC) is a constituent of blood tubing, and leaching of phthalate from the PVC can cause anaphylaxis. Nitrates, chloramines, or overheated dialysate (>46°C) can cause hemolysis. Air embolus, a complication of approximately 1 in 2,000 treatments, can result from a leak of 60 to 125 mL of air. Electrolyte abnormalities due to proportioning problems can cause abnormal sodium, potassium, calcium, magnesium, and osmolality.8

The most common intermittent and continuous renal replacement therapies in clinical practice are, respectively, intermittent hemodialysis, continuous venovenous hemofiltration/hemodiafiltration, and peritoneal dialysis. Continuous

Table 2 Most common emergency department presenting complaints for patients on dialysis4

Abdominal pain

Access-related morbidity from thrombosis or infection

Bleeding shunt/contaminated shunt

Chest pain

Electrolyte abnormalities

Hypertension (30% overall, 40% in black patients)

Shortness of breath/congestive heart failure

Syncope

Vomiting, nausea

Weakness, dizziness

5


venovenous hemofiltration/hemodiafiltration is able to remove larger volumes, as it continues around the clock. Peritoneal dialysis tends not to induce hypotension.

Access to the patient’s bloodstream became practical with the development of the Quinton and Scribner external arteriovenous (AV) shunt in 1960.9 The internal radiocephalic AV fistula in 1966 was developed by Brescia and Cimino.10 This created an anastomosis of the radial artery and cephalic vein at the wrist. An alternative is a brachiobasilic fistula between the brachial artery and cephalic vein above the elbow. Dacron and polytetrafluoroethylene grafts for subcutaneous AV conduits now constitute most of the permanent access in the United States.11 Alternative dialysis accesses that the emergency physician may encounter include percutaneous venous catheters typically placed in the internal jugular or subclavian veins (Hickman).12 These are tunnel-cuffed catheters, and should not be removed by pulling.

Of all access systems, the external AV fistula has the highest survival rate, with a two-year survival rate of more than 75%. Graft occlusion is very common. Access salvage may be possible via embolectomy balloon, mechanical thrombolysis, or pulsed urokinase. Monitoring techniques prospectively prior to graft occlusion include measurements of dynamic and static venous pressure and direct intra-access measures of blood flow via ultrasound dilution and duplex color flow Doppler.11 Currently the mean length of hemodialysis treatment is 3.5 hours, three times per week. In the future, patients may undergo daily nocturnal home hemodialysis—two hours of daily treatment at a blood flow rate of 200 mL/min. This requires the availability of a dialysis machine with a second person at home to assist with vascular access.

Care of the patient with a dialysis line includes several general precepts.

Do not draw blood from a central dialysis line or fistula if possible; in general, try to avoid venipuncture in the nondominant arm and in the upper part of the dominant arm of patients with ESRD; and do not use the involved arm for blood pressure determination. If the patient is in extremis, and the fistula or graft must be used, cleanse the site scrupulously; after the puncture, apply firm but nonocclusive pressure for at least 10 minutes, and document a thrill both before and after the puncture.13 In general avoid the use of meperidine for analgesia because its metabolites accumulate in patients with renal failure and can induce seizures. Avoid magnesium-containing cathartics or phosphate-containing enemas (because of a danger of hypermagnesemia or hyperphosphatemia). Maturation of most shunts takes about 6 weeks, although polytetrafluoroethylene grafts mature in 3 to 4 weeks.11 This has implications for pseudoaneurysm formation following puncture. Autogenous AV fistulas usually mature in 8 to 16 weeks but can take longer (3 to 6 months, possibly up to 1 year), necessitating nephrology referral when serum creatinine reaches 3 to 4 mg/dL to allow for a long lead time pre-dialysis. Ultrafiltration affords fast and efficient fluid removal. A widespread numerical index of dialysis adequacy is the concept of Kt/V, where dialyzer clearance = K; duration of dialysis = t; volume of distribution of urea in the body = V. The Kt/V should be greater than 1.2 per session.14 Most patients require 9 to 12 hours of dialysis per week broken into several sessions (M-W-F, T-Th-S).

CRITICAL DECISIONWhat details are most important in evaluating a hypotensive patient with ESRD?

Intradialysis hypotension is the most frequent complication of dialysis, affecting 10% to 30% of patients. The most common cause is excessive rate or amount of

ultrafiltration with hypovolemia. Other causes for volume loss such as bleeding or gastrointestinal fluid losses should be sought. Treatment generally starts with a 250- to 500-mL normal saline challenge intravenously in 100-mL to 200-mL increments. Dry weight is traditionally a critical parameter in assessing volume status, set at the weight below which symptoms such as nausea, cramping, vomiting, and hypotension occur. Bioimpedance measurements can provide a more accurate assessment of total body water and of intracellular and extracellular volume.15 It has been reported that inferior vena cava dimensions (IVC) by hand-carried ultrasound may give a much more accurate gauge of volume status. The maximal IVC diameter was measured within 2.5 cm of the junction with the right atrium, and could be assessed in 89% of patients, noting that 39% of patients in their study who were at or above dry weight were, in fact, hypovolemic. How this translates into the future emergency assessment of the potentially hypovolemic patient remains to be ascertained.16

Serious causes of hypotension should be ruled out in ESRD patients. Common causes are sepsis, bleeding, hyperkalemia, and pericardial tamponade. Hyperlactatemia (vasodilation, headache, cardiac toxicity) has been minimized now with use of bicarbonate dialysate, which allows the elimination of acetate as the alkali source.12 When the cause of the hypotension cannot be identified, consideration should be given to other serious causes, as follows17:

• Cardiac causes: left ventricular dysfunction, hypoxia, coronary ischemia, arrhythmias, pericardial tamponade;

• Electrolyte disorders: magnesium, potassium, calcium;

• Air embolism, which is rare with current technology;

• Hypoxemia;• Drugs (narcotics,

antihypertensives/beta-blockers,


6

anxiolytics);• Excess heat retention (prevented

with reduced-temperature dialysis bath (35°C);

• Hypersensitivity reaction to ethylene oxide (sterilizes the dialyzer) or polyacrylonitrile (membrane material), especially if the patient is taking ACE inhibitors (these block breakdown of kinins);

• Autonomic neuropathy; and• Acetate-based dialysate.There is increasing evidence that

subclinical myocardial ischemia occurs during dialysis. This may be evidenced by elevated troponin and creatine kinase MB levels, by silent ST depression during dialysis, or by left ventricular wall motion abnormalities. It has been proposed that ischemia during dialysis might contribute to the development of uremic cardiac failure, especially if the ischemia occurs 3 times per week.18

CRITICAL DECISIONWhat electrolyte abnormalities should emergency physicians consider in a dialysis patient?

Symptoms referable to hyperkalemic cardiac toxicity can include weakness from bradyarrhythmia or tachyarrhythmias, with possible hypotension or cerebral hypoperfusion. Patients can present with paralysis or intestinal ileus. Suicidal thoughts may suggest missed dialysis. Progressive ECG changes include increase (tenting) in amplitude of T waves in the precordial leads V2, V3, II, and III, with lengthening of the PR interval. Later findings that are more ominous include widening of the QRS complex, disappearance of P waves, and the presence of a sine wave pattern preterminally. In general, serious hyperkalemia should be uncommon unless one of the following is involved: dietary indiscretion, inadequate dialysis, red cell lysis associated with a large hematoma or gastrointestinal bleeding, or rhabdomyolysis (from seizure or severe exercise). Medications that

can exacerbate hyperkalemia include digitalis, propranolol and other beta-blockers, succinylcholine, potassium salts including potassium penicillin, and ACE inhibitors.

The management of hyperkalemia entails the use of intravenous calcium for cardiac protection. Intravenous calcium works immediately to normalize the ECG, but its effects are brief. Bicarbonate, insulin, and glucose work within approximately 20 minutes and redistribute potassium from the extracellular to the intracellular space for up to 2 hours.19 Sodium polystyrene sulfonate orally or via retention enema will work within 90 to 240 minutes to lower potassium by enhanced excretion. There is some recently presented evidence that ion-exchange resins for the treatment of hyperkalemia may be neither as safe nor as effective as traditionally thought. Sodium polystyrene sulfonate in fact has not been demonstrated to increase fecal potassium losses in experimental animals.20 The concomitant use of sorbitol to decrease the incidence of fecal impaction and to speed delivery of resin to the colon has been implicated in cases of colonic necrosis, bleeding, ischemic colitis, and perforation, prompting safety labeling changes by the US Food and Drug Administration.21 Others argue that, so long as sodium polystyrene sulfonate is given with 33% sorbitol (and not 70%), colonic necrosis is not a significant risk. As of now, the only alternatives for actually excreting potassium from the body involve loop diuretics, which require adequate kidney function, and hemodialysis, which may not be quickly available22 As with insulin-glucose combinations, beta-agonist therapy serves to redistribute potassium to the intracellular space and may be used even in patients without reactive airway disease (Table 3). Patients ultimately may need dialysis, making these measures temporizing ones until the patient can be dialyzed.

Hypocalcemia, hyperphosphatemia, and secondary hyperparathyroidism are common

in chronic renal failure. Secondary hyperparathyroidism may develop into tertiary hyperparathyroidism or an autonomously hyperfunctioning parathyroid gland. Many ESRD

Table 3 Management of hyperkalemia

Antagonize cardiac effects on the heart

Calcium chloride (1.4 mEq/mL), 5 mL IV bolus, or calcium gluconate (0.4 mEq/mL), 10 to 20 mL slow IV. May repeat every 5 minutes if ECG appearance does not improve. Lasts less than 1 hour. Watch for digitalis toxicity. If the patient is on digitalis, mix calcium gluconate in 100 mL of 5% dextrose and infuse over 10 to 20 minutes.23

Drive potassium into cells

Sodium bicarbonate, 50 to 100 mEq IV. Downside: volume overload.Insulin (10 units regular) followed by D50, 50 to 100 mL, may drop potassium by 0.6 to 1 mEq/L after 1 hour. 24 May need to infuse 10% dextrose at 50 mL/hr to prevent hypoglycemia.23 Forty units of regular insulin may be added to 1,000 mL of 10% dextrose and infused at 25 mL/hour

Albuterol by nebulization 5 mg in saline inhaled, may repeat 2 to 3 times (20 mg total).24,25 Intravenous albuterol, 0.5 mg IV in 100 mL of 5% glucose over 15 minutes, has decreased serum potassium by 1.1 mEq/L and may have effects up to 6 hours.26

If intubated, hyperventilate.

Remove potassium from the body

Sodium polystyrene sulfonate, 25 to 50 g PO or by enema (less effective). Give with 50 mL of 70% sorbitol to prevent constipation

Hemodialysis or peritoneal dialysis

Loop diuretic if urine is produced

7


patients for this reason have had parathyroid gland removal. Hypermagnesemia can present early with hyporeflexia, vasodilation, flaccidity, and profound muscle weakness. More severe elevations of serum magnesium (Mg >10 mEq/dL) present with bradyarrhythmias, flaccidity, vasodilation, hypotension, respiratory failure, or asystole. Treatment includes calcium chloride or calcium gluconate as temporizing measures until dialysis, with later dietary modification. Hypercalcemia may present with nausea, vomiting, constipation, generalized weakness, hypertension, decline in level of consciousness, or seizures. Treatment options include hemodialysis (with a low calcium bath), synthetic salmon calcitonin, or hydration with normal saline if the patient is volume depleted. Severe acidosis may necessitate dialysis.27

CRITICAL DECISIONHow is cardiac arrest managed in an ESRD patient?

Cardiac arrest may be handled in standard fashion. However, strong consideration should be given to the possibility of life-threatening hyperkalemia. Consider empiric treatment with calcium chloride, bicarbonate, or glucose/insulin infusions. The possibility of uremic pericardial effusions or cardiac tamponade should be considered.28

CRITICAL DECISIONWhat signs and symptoms are indicative of dialysis disequilibrium syndrome, and how should it be managed?

Dialysis disequilibrium syndrome (DDS) occurs during or within 12 hours of dialysis. Symptoms include headache, malaise, nausea, vomiting, muscle cramps, hypertension, restlessness/confusion, altered mental status, seizures, and death.29 It is thought to be related to elevated intracranial pressure and rapid lowering of serum osmolarity during dialysis. In patients with chronic kidney disease with a high urea concentration, it has been proposed

that decreasing initial dialysis time and dialysis blood flow rate on beginning dialysis may prevent DDS.30 Treatment may include anticonvulsants as needed, mannitol, possibly hypertonic saline, and hyperventilation. It is primarily a clinical syndrome, although an electroencephalogram can show diffuse metabolic encephalopathy, and diffusion-weighted magnetic resonance imaging can show osmotic demyelination of pontine and extrapontine areas.30,31 Other pathology should be ruled out, including malignancy, complex ventricular arrhythmias, subdural hematoma, intracerebral abscess, electrolyte and glucose abnormality, meningitis, sepsis, and hypertensive encephalopathy.

CRITICAL DECISIONWhat therapeutic options are available for ESRD patients in the setting of acute pulmonary edema or possible cardiac tamponade?

Fluid overload and pulmonary edema occur frequently in chronic renal failure patients. Diagnosis is facilitated when the patient knows his/her dry weight and is suggested by the following: excess weight over dry weight of more than 5 pounds, chest radiograph, physical examination, missed dialysis, or dietary indiscretion. B-type natriuretic peptide is elevated at baseline in the ESRD patient. Treatment may entail a variety of modalities, not all of which depend on urine output or diuresis (Table 4). Note that in one report, an intravenous line was established in only 29 of 46 patients presenting with acute heart failure from fluid overload, and only 6 of these received any parenteral medications. It is possible to manage heart failure in the dialysis patient without an intravenous line.37 Endotracheal intubation, positive end-expiratory pressure, mask noninvasive pressure support ventilation, or continuous positive airway pressure may be performed as needed. AV fistulas causing high-output heart failure may

require surgical binding of the fistula to reduce blood flow.

Symptoms of uremic pericarditis and/or tamponade can include dyspnea, cough, positional chest pain, and possibly malaise or fever. Physical examination can demonstrate jugular venous distention, pulsus paradoxus greater than 10 mm Hg, tachycardia, hypotension, tachypnea, narrow pulse pressure, or friction rub. The ECG may show electrical alternans or low voltage. Diagnosis is made by echocardiography or by

Table 4 Treatment for pulmonary edema in the ESRD patient

60 to 100 mg furosemide for pulmonary vasodilation. There is evidence that an intravenous bolus of furosemide at no more than 5 mg/min to minimize ototoxicity may decrease central blood volume by approximately 13%.32

ACE inhibitors (Captopril sublingual, others)

Intravenous nesiritide rapidly lowers capillary wedge pressure and is not metabolized by the kidney.33,34

The standard dose is 2 mcg/kg bolus, followed by an infusion at a rate of 0.01 mcg/kg/minute. Its major side effect is hypotension.

Nitrates: sublingual nitroglycerin (NTG), transdermal NTG, intravenous NTG, or nitroprusside

Oxygen

Possibly intravenous morphine

Possibly: phlebotomy of 250 to 500 mL of blood prior to dialysis35

Sitting position

Sorbitol 70% in 50 to 100 mL doses every 20-60 minutes will usually cause an osmotic shift of fluid into the bowel, resulting in fluid loss and reduction in pulmonary capillary wedge pressure.36

Ultrafiltration/hemodialysis for fluid overload


8

invasive demonstration of equal left and right atrial pressures, although invasive means are not practical in the emergency department setting. Treatment entails aggressive volume support, intensive hemodialysis, and possibly pericardiocentesis. If the patient is unstable, a pericardial window or partial pericardiectomy may be required. Other causes of pericarditis such as AIDS or systemic lupus erythematosus may need to be considered.

CRITICAL DECISIONWhat are the diagnostic and therapeutic approaches to the febrile dialysis patient?

In 2008, the CDC estimated that 37,000 bloodstream infections occurred among hemodialysis patients with central lines, and that one in four died as a result. Dialysis infections are second only to vascular disease as a cause of death among hemodialysis patients.38 If infection is suspected, blood should be drawn for cultures as above. Urine culture should be obtained, if the patient produces urine. It may be desirable to get one culture from a percutaneous dialysis catheter with involvement of a nephrologist. Antibiotics such as vancomycin and an aminoglycoside (2 to 5 mg/kg) pending culture results should be administered. Vancomycin is preferred because it covers methicillin-resistant organisms. Alternative antibiotics for sepsis include piperacillin/tazobactam, ticarcillin/clavulanate, imipenem, meropenem, and a third-generation cephalosporin with anti-Pseudomonas activity such as ceftazidime. Sites of infection to consider include blood access sites, both new and old (Staphylococcus aureus and epidermidis); endocarditis; septic pulmonary emboli; osteomyelitis; septic arthritis; and urinary tract infections (especially in patients with polycystic kidney disease). Pneumonia can present as dyspnea or malaise. Consider odontogenic, extremity cellulitis, and perirectal abscess as possible sites of infection.

CRITICAL DECISIONWhat emergent considerations are directly related to the vascular access site itself?

When considering infection, vancomycin should be administered with or without gram-negative coverage (gentamicin). Findings of infection can be subtle and may include malaise, intermittent fever, relative hypotension, and an elevated WBC count. This may be a source for sepsis. Complications such as epidural abscess, pulmonary emboli, empyema, bacterial meningitis, osteomyelitis, septic arthritis (wrist, knee, shoulder), and endocarditis, especially of the aortic valve, should be considered.

Thrombosis and stenosis (intimal hyperplasia) are the commonest causes for inadequate flow. The physician should document presence or absence of a thrill or bruit over the access site, and whether the patient needs emergent or urgent (within 24 hours) dialysis.

Followup should be coordinated with the patient’s nephrologist. If hyperkalemia or fluid overload is not present, patients may not have an untoward event from missing a single hemodialysis session. Stenosis can be treated within 24 hours by a vascular surgeon with angioplasty, injection of a thrombolytic agent into the access, or by angiographic clot removal.

If a double lumen catheter is used in subclavian vein aneurysms, pseudoaneurysms may cause pain, impingement on surrounding nerves, or marked thinning or erosion of overlying skin. Hemodialysis requires a flow rate of 300 mL/minute. Ischemia of the arm from a “steal” syndrome can result in pain, with a pale cool distal extremity. Symptoms can include decreased or absent pulse, sensory or motor impairment, and ischemic ulceration of digits. Surgical treatments have traditionally included access ligation and banding which should increase flow in the artery distal to the fistula by increasing resistance to fistula outflow. More recently, coil embolization of

collateral veins of hemodialysis has proved effective in improving distal pulses, coolness, and pain from symptomatic steal syndrome.39

Prolonged bleeding times should be expected in patients with ESRD. These can result from uremia-induced platelet dysfunction or from heparin anticoagulation. A normocytic normochromic anemia frequently complicates renal failure and is multifactorial. Decreased erythropoietin production, blood loss, and hemolysis are major considerations.19

Transfusion generally is not necessary for asymptomatic patients whose hematocrit is greater than 18%. Prolonged bleeding times may be treated with desmopressin (desamino-8-D-arginine vasopressin), 0.3 mcg/kg IV or SQ, 82 or 83 mcg/kg intranasally. Onset of effect is 1 to 2 hours. It lasts 4 to 8 hours and works by stimulating the release of stored factor VIII and von Willebrand factor. It may be repeated in 8 to 12 hours. Alternatively, cryoprecipitate, 10 units over 10 to 15 minutes, may be administered every 12 to 24 hours. This corrects bleeding time for approximately 4 hours. Conjugated estrogens 25 mg/day (or 0.6 mg/kg acutely) for 7 days have effects lasting 21 days.

Vascular access hemorrhage should be managed in general with direct pressure at the puncture site for 5 to 10 minutes. In the unusual event that pressure alone does not suffice and over-anticoagulation is suspected, protamine 10 to 20 mg (0.01 mg/IU of heparin, assuming 1,000 to 2,000 units of heparin used on the average) may be given. Application of topical sponges impregnated with thrombin or other chemical thrombotics have been used. Cryoprecipitate, 10 units every 12 to 24 hours, may be effective, as it is rich in von Willebrand factor. It is mandatory to check for a bruit after pressure or protamine administration, and it is advisable to observe for 1 to 2 hours for evidence of rebleeding.

Air embolism is an acute

9


cardiorespiratory or neurologic complication of dialysis. Patients may present with dyspnea, tachypnea, chest pain, hypotension, confusion, or cardiac arrest. A “millwheel” cardiac murmur may be audible. Treatment includes clamping the access/venous bloodline and placing the patient supine or left lateral decubitus in Trendelenburg. Hyperbaric oxygen therapy may be considered. If the patient is in cardiac arrest, the physician may aspirate the right ventricular outflow tract, followed possibly by hyperbaric therapy.

CRITICAL DECISIONWhen should ESRD patients be admitted to the hospital?

ESRD patients should be hospitalized for any indication for emergency hemodialysis, generally related to fluid overload or to hyperkalemia (Table 5). If pericardial tamponade or air embolism is suspected, or if the patient developed chest pain during dialysis, the patient should be observed in the hospital pending further testing. Neurologic presentations precluding discharge include altered mental status and uremic encephalopathy as manifested by asterixis, myoclonic twitching, lethargy, or new onset seizure. Hyperkalemia may be managed as above; however, if the serum potassium is more than 7 or there are electrocardiographic changes from baseline, the patient should be admitted to a monitored bed. Patients with lower potassium may be discharged if treated with sodium polystyrene sulfonate, dialysis is planned within 8 hours, and the patient is reliable. Any patient requiring emergency treatment with a modality that redistributes potassium, including calcium, albuterol, insulin-glucose, or bicarbonate, should be admitted. It is advisable to admit patients with hemodynamically significant gastrointestinal bleeding, including bright red blood from stool and melena.

Febrile ESRD patients with the following presentations should be

considered for hospitalization: ill-appearance, dyspnea, hypotension, unreliable home environment, or specific infection (pneumonia, urosepsis, obvious shunt site infection). If a shunt infection is merely suspected, it may be acceptable to discharge after culture of the blood and access site, with intravenous antibiotics and followup with the patient’s nephrologist within 24 hours.40 Central venous catheter-related blood stream infections pose a thorny clinical problem. Most cases of bacteremia result from S. aureus or S. epidermidis, with risk for endocarditis, osteomyelitis, or other septic sequelae such as epidural abscess, septic arthritis, and death. Diagnosis can be definitively made when blood cultures

drawn from the central venous catheter and from venous blood grow the same organism. Treatment options have historically included leaving the catheter in place, with antibiotic administration; catheter exchange over a guidewire (with antibiotic therapy); and removal of the catheter followed by replacement later.41 Clearly, these options should be discussed with the patient’s nephrologist, especially given the difficulty many patients have with alternative intravenous access. See Table 5 for additional admission criteria.

Peritoneal Dialysis Overview

In the United States, 16% to 17% of those who need dialysis undergo

Table 5 Admission criteria for ESRD patients

Any indication for emergency hemodialysis, generally related to fluid overload or to hyperkalemia

Pericardial tamponade or air embolism is suspected

Patient developed chest pain during dialysis (observation rather than admission is an option)

Neurologic presentations precluding discharge include altered mental status

Serum potassium is above 7 or there are electrocardiographic changes from baseline

Patient requires emergency treatment with a modality that redistributes potassium

Hemodynamically significant gastrointestinal bleeding

Febrile ESRD patients with ill appearance, dyspnea, hypotension, unreliable home environment, or specific infection (pneumonia, urosepsis, obvious shunt site infection)

Central venous catheter–related blood stream infections (observation vs admission)

Suspected disequilibrium syndrome, as this can proceed to seizures, coma, and death

Persistent vomiting from any cause (inability to take oral fluids)

Refractory severe hypertension (diastolic >130 despite treatment), scleroderma renal crisis

Malignant hypertension, especially with hypertensive encephalopathy or cardiovascular decompensation

Arrhythmia related to electrolyte abnormality, or which would otherwise warrant hospitalization

Symptomatic pulmonary edema after treatment; if dialysis or hemofiltration is available in the emergency department, hospitalization may not be indicated

Symptomatic hypermagnesemia with or without cardiotoxicity

Hypercalcemia with cardiovascular dysfunction or acute neurologic symptoms

Inability to control bleeding from dialysis site


10

peritoneal dialysis (PD). Although the relative incidence of PD is higher in some countries, the mortality from renal failure does not seem to favor either hemodialysis or PD.42 PD uses a slow rate of solute and volume removal and is therefore useful in hemodynamically unstable patients. The amount of ultrafiltration is determined by osmotic pressure differences between the patient’s blood and the dialysate, which is a function of the concentration of glucose in the dialysate.

Continuous ambulatory peritoneal dialysis (CAPD) generally is repeated four times per day, infusing 2 liters of dialysate with dwell times of 4 to

6 hours. Typically, approximately 8 liters of fluid is infused and 10 liters drained, for a net daily removal of approximately 2 liters of fluid. Intermittent peritoneal dialysis (IPD) is characterized by rapid cycling of dialysis fluid at intervals of 60 minutes or less. Continuous cycling peritoneal dialysis (CCPD) consists of rapid fluid exchanges during the night using an automated cycler. There is a greater incidence of peritonitis with CAPD relative to IPD or CCPD.40 PD obviates the need for anticoagulation, although the peritoneal access is a potential source of complications such as catheter leaks and peritonitis.43 Dialysis can

be performed with varying glucose formulations to control fluid volume via ultrafiltration. The focused physical examination in the PD patient should especially include an examination of the abdomen for hernia, bowel sounds, and rebound. Since continuous renal replacement therapies appear superior to PD in solute and volume removal and in correction of acid-base disturbances, it has been proposed that PD is best utilized in hemodynamically unstable patients in whom vascular access has been exhausted and in those with limited disease severity.43

Peritonitis is always a major concern and the most common complication of PD. It may present with abdominal pain, cloudy dialysate (over 100 WBCs in dialysate, with more than 50% polymorphonuclear leukocytes), fever, rebound tenderness, nausea, and vomiting. The incidence is approximately once per 15 patient-months of dialysis.44

Commonly isolated organisms include bacteria such as S. epidermidis, S. aureus, Streptococcus, and gram-negative bacteria (Acinetobacter, Pseudomonas, Enterobacteriaceae), although fungal (Candida), anaerobic, and mycobacterial infections occur as well. Treatment may include several rapid exchanges of fluid, followed by antibiotics in the dialysate: cephalothin 200 to 500 mg/L of dialysate, or vancomycin (1 g IV loading, then 30 to 50 mg/kg intraperitoneal [IP] dose per 2 L exchange if methicillin-resistant S. aureus [MRSA] is present). Some try to avoid these agents due to vancomycin-resistant enterococcus emergence. Gentamicin IM/IV then IP (8 mg/L first exchange, followed by 4 mg/L subsequently) has been employed successfully. Treatment lasts for 7 to 14 days. Heparin 500 to 2,500 units/liter prevents fibrin formation. Ceftazidime, 1 g IP or IV, is an acceptable alternative, with aztreonam, 3 g IP or IV, if gram-negative organisms are suspected. Patients may be treated on an outpatient basis, depending on their

Pearls• Subclinical myocardial ischemia occurs during dialysis in some patients

and can be evidenced by elevated troponins and creatine kinase MB, by silent ST depression during dialysis, or by left ventricular wall motion abnormalities. This can lead to development of cardiac failure.

• Do not underestimate the value of cardiac ultrasonography in the evaluation of a hypotensive patient with ESRD.

• Proper examination of the site of vascular access is absolutely necessary in the thorough physical evaluation of patients with ESRD.

• Avoid venipuncture in the nondominant arm and in the upper part of the dominant arm of patients with ESRD in order to preserve future fistula sites.

• Neurologic findings, both focal and nonfocal, in the patient undergoing dialysis may be due to dialysis disequilibrium syndrome (DDS).

• Many of the currently accepted emergency-department-administered therapies for the treatment of hyperkalemia are short acting and may be of little use. Actions to ensure timely dialysis can be key.

• Pain in the arm should raise suspicion for vascular steal or carpal tunnel syndrome as complications of fistulas.

• Focused physical examination of patients with peritoneal dialysis catheters and abdominal pain should concentrate on the detection of bacterial peritonitis and hernias.

Pitfalls• Failing to consider that uremia can present in many

ways, including cardiovascular collapse.

• Failing to dose renally excreted medications appropriately for the patient’s amount of renal function, and not considering alternative therapies if available.

• Not considering sepsis, bleeding, and other causes for hypotension and other vital sign derangements.

11


appearance. Treatment typically requires a 7- to 10-day course of antibiotics.

Catheter infections (exit site and tunnel infections) present with localized pain, erythema, swelling, or discharge around the catheter exit site. Frequent causative bacteria include S. aureus and Pseudomonas aeruginosa on culture around the catheter. The diagnosis may require ultrasound. Treatment may require incision and drainage and oral antibiotics (first-generation cephalosporin, ciprofloxacin, or dicloxacillin). Catheter leaks present with abdominal wall edema and clear fluid from the catheter ostium. Treatment entails stopping peritoneal dialysis, necessitating short-term hemodialysis. Dialysate fluid should be cultured, and a nephrologist should be consulted for consideration of empiric therapy for peritonitis. Besides antibiotic therapy, surgical correction may be required.

Abdominal or inguinal hernias are risks due to increased intraperitoneal pressure. They should be referred for surgical repair, as incarceration poses a potential risk. Hydrothorax is a rare complication of PD and is generally right-sided. Diagnosis may be made by methylene blue injection into the peritoneal fluid. Therapy includes temporary discontinuance of PD, necessitating hemodialysis, at least temporarily.

CRITICAL DECISIONWhich patients undergoing PD should be admitted?

Patients with leaks as a mechanical complication of their PD should be admitted. PD patients with peritonitis should be admitted if the following are present: severe pain, vomiting, hypotension, ileus, hemodynamic instability, high fever, inability to administer antibiotics at home, or unreliable followup within 24 to 48 hours. Patients should be admitted if there is suspected visceral perforation such as fecal material in peritoneal drainage. Other considerations for admission in the PD patient include

incarcerated, incisional or inguinal hernia; pain or vomiting from suspected bowel obstruction; and severe hyperglycemia in diabetic patients from a hyperosmolar dialysate.

Case Resolutions

■ Case OneThe woman presenting after

seizure-like activity was monitored closely. After 4 hours in the emergency department, her mental status returned to baseline, at which time she had no complaints. Laboratory evaluation demonstrated no electrolyte abnormality. A CT scan of her head was unremarkable. She was admitted and observed overnight. DDS was considered as a possible cause for her new-onset seizure activity as the events occurred after her first dialysis session. The patient’s nephrologist was contacted, and subsequent dialysis sessions were implemented with slower blood flow rates with a gradual increase in dialysis clearance. For completeness, the patient underwent an outpatient MRI and EEG, which were both unremarkable. The patient had no further seizure activity. ■ Case Two

The man with the hand and arm pain presented with vascular steal syndrome. The management of this condition is aimed at reestablishing vascular flow and preserving function of the fistula for future vascular access. His digital/brachial index was measured at 0.5, further suggesting steal syndrome as the diagnosis. A vascular surgeon was consulted and recommended admission for surgical management due to moderate to severe symptoms and risk for further ischemia. The next morning, the patient underwent an MR angiography to confirm vascular steal syndrome and a procedure to decrease the vascular resistance distally to allow for adequate distal blood flow.

■ Case ThreeThe patient who arrived intubated

and unresponsive became pulseless approximately 5 minutes after arrival. Cardiopulmonary resuscitation was initiated for pulseless electrical activity (PEA) arrest. Bedside cardiac ultrasonography was performed and showed a large fluid collection in the pericardial space and significant right ventricular collapse. An urgent pericardiocentesis was performed under ultrasound guidance through a subxiphoid approach with return of approximately 250 mL of clear yellow fluid. A catheter was maintained in the pericardial space. The patient immediately regained a weak pulse but blood pressures remained tenuous with mean arterial pressures in the low 60s. He was started on an infusion of epinephrine via right internal jugular central venous catheter at 2 mcg/min, and 2 liters of normal saline were infused. Chest radiograph showed an enlarged cardiac silhouette, blunting of bilateral costophrenic angles, and vascular congestion. Laboratory results were remarkable for a BNP of more than 5,500 and a lactate of 9.4. A repeat ECG showed no ischemic ST changes but continued to demonstrate low voltage and tachycardia. The patient was transferred to a cardiac ICU for acute pericardial tamponade, with concurrent uremia and volume overload. One hour after the patient arrived in the emergency department, while waiting for the dialysis team and nephrologist to arrive, the patient again became pulseless. The rhythm again was PEA. Despite aggressive resuscitation measures and a readjustment of the pericardial catheter, the patient died.

SummaryRenal failure continues to cause a

high rate of morbidity and mortality in the United States. With the aging population and survival from medical problems such as sepsis, diabetes, and hypertension, it is expected that the prevalence of renal failure will increase in the United States over


12

time. Emergency physicians should recognize various techniques for renal replacement therapy and be prepared to manage a variety of metabolic and structural disorders that occur in this population.

References1. Klevens RM, Edwards JR, Andrus ML, et al. Dialysis

Surveillance Report: National Healthcare Safety Network (NHSN)- data summary for 2006. Semin Dial. 2008;21(1):24-28.

2. United States Renal Data System. USRDS annual data report: CKD in the general population. 2012. Available at: http://www.usrds.org/atlas.aspx. Accessed January 5, 2012.

3. Centers for Disease Control and Prevention. National Healthcare Safety Network (NHSN) tracking infections in outpatient dialysis facilities. Last updated July 22, 2013. Available at: http://www.cdc.gov/nhsn/dialysis/. Accessed August 8, 2013.

4. Sacchetti A, Harris R, Patel K, Attewell R. Emergency department transportation of renal dialysis patients: indications for EMS transport directly to dialysis centers. J Emerg Med. 1991;9(3):141-144.

5. Levey AS, Eknoyan G. Cardiovascular disease in chronic renal disease. Nephrol Dial Transplant. 1999;14(4):828-833.

6. USRDS 1997 annual data report. The USRDS dialysis morbidity and mortality study (Wave 2). Available online at: http://www.usrds.org/download/1997/ch04.pdf. Accessed August 8, 2013.

7. Thodis ED, Oreopoulos DG. Home dialysis first: a new paradigm for new ESRD patients. J Nephrol. 2011;24(4):398-404.

8. Misra M. The basics of hemodialysis equipment. Hemodial Int. 2005;9:30-36.

9. Quinton W, Dillard D, Scribner BH. Cannulation of blood vessels for prolonged hemodialysis. Trans Am Soc Artif Intern Organs. 1960;6:104-113.

10. Brescia MJ, Cimino JE, Appel K, Hurwich BJ. Chronic hemodialysis using venipuncture and a surgically created arteriovenous fistula. N Engl J Med. 1996;275(20):1089-1092.

11. Schwab SJ, Harrington JT, Singh A, et al. Vascular access for hemodialysis. Kidney Int. 1999;55(5):2078-2090.

12. Uribarri J. Past, present, and future of end-stage renal disease therapy in the United States. Mt Sinai J Med. 1999;66(1):14-19.

13. Wolfson AB. Chronic renal failure and dialysis. In: Rosen, Barkin, eds. Emergency Medicine: Concepts and Clinical Practice. 4th Ed. Mosby; St. Louis:1998; 2278-2292.

14. Luyckx VA, Bonventre JV. Dose of dialysis in acute renal failure. Semin Dial. 2004;17(1):30-36.

15. Palmer BF, Henrich WL. Recent advances in the prevention and management of intradialytic hypotension. J Am Soc Nephrol. 2008;19(1):8-11.

16. Brennan JM, Ronan A, Goonewardena S, et al. Handcarried ultrasound measurement of the inferior vena cava for assessment of intravascular volume status in the outpatient hemodialysis clinic. Clin J Am Soc Nephrol. 2006;1(4):749-753.

17. Pastan S, Bailey J. Dialysis therapy. N Engl J Med. 1998;338(20):1428-1437.

18. Selby NM, McIntyre CW. The acute cardiac effects of dialysis. Semin Dialysis. 2007;20(3):220-228.

19. Costa J, Crausman RS, Weinberg MS. Acute and chronic renal failure. J Am Podiatr Med Assoc. 2004;94(2):168-176.

20. Sterns RH, Rojas M, Bernstein P, Chennupati S. Ion-exchange resins for the treatment of hyperkalemia: are they safe and effective? J Am Soc Nephrol. 2010;21(5):733-735.

21. US Food and Drug Administration: Kayexalate (sodium polystyrene sulfonate) powder. Available at: http://www.fda.gov/Safety/MedWatch/SafetyInformation/ucm186845.htm. Accessed on August 8, 2013.

22. 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(10):1723-1726.

23. Perazella MA. Approach to hyperkalemic end-stage renal disease patients in the emergency department. Conn Med. 1999;63(3):131-136.

24. Allon M, Copkney C. Albuterol and insulin for treatment of hyperkalemia in hemodialysis patients. Kidney Int. 1990;38(5):869-872.

25. Kemper MJ, Harps E, Müller-Wiefel DE. Hyperkalemia: therapeutic options in acute and chronic renal failure. Clin Nephrol. 1996;46(1):67-69.

26. Montoliu J, Lens XM, Revert L. Potassium-lowering effect of albuterol for hyperkalemia in renal failure. Arch Intern Med. 1987;147(4):713-717.

27. Alpern RJ, Sakhaee K. The clinical spectrum of chronic metabolic acidosis: homeostatic mechanisms produce significant morbidity. Am J Kidney Dis. 1997;29(2):291-302.

28. Causes of death. United States Renal Data System. Am J Kidney Dis. 1998;32(2 Suppl 1):S81-S88.

29. Shaikh N, Louon A, Hanssens Y. Fatal dialysis disequilibrium syndrome: A tale of two patients. J Emerg Trauma Shock. 2010;3(3):300.

30. Patel N, Dalal P, Panesar M. Dialysis disequilibrium syndrome: a narrative review. Semin Dial. 2008;21(5):493-498.

31. Agildere AM, Benli S, Erten Y, et al. Osmotic demyelination syndrome with a disequilibrium syndrome: reversible MRI findings. Neuroradiology. 1998;40(4):228-232.

32. Schmieder RE, Messerli FH, deCarvalho JG, Husserl FE. Immediate hemodynamic response to furosemide in patients undergoing chronic hemodialysis. Am J Kidney Dis. 1987;9(1):55-59.

33. Colucci WS, Elkayam U, Horton DP, et al. Intravenous nesiritide, a natriuretic peptide, in the treatment of decompensated congestive heart failure. N Engl J Med. 2000;343(4):246-253.

34. McCullough PA, Nowak RM, McCord J, et al. B-type natriuretic peptide and clinical judgment in emergency diagnosis of heart failure: analysis from Breathing Not Properly (BNP) Multinational Study. Circulation. 2002;106(4):416-422.

35. Eiser AR, Lieber JJ, Neff MS. Phlebotomy for pulmonary edema in dialysis patients. Clin Nephrol. 1997;47(1):47-49.

36. Anderson CC, Shahvari MB, Zimmerman JE. The treatment of pulmonary edema in the absence of renal function. A role for sorbitol and furosemide. JAMA. 1979;241(10):1008-1010.

37. Sacchetti A, McCabe J, Torres M, Harris RL. ED management of acute congestive heart failure in renal dialysis patients. Am J Emerg Med. 1993;11(6):644-647.

38. Centers for Disease Control and Prevention. Dialysis event surveillance. Available at: http://www.cdc.gov/nhsn/dialysis/dialysis-event.html. Accessed on August 8, 2013.

39. Kariya S, Tanigawa N, Kojima H, et al. Transcatheter coil embolization for steal syndrome in patients with hemodialysis access. Acta Radiol. 2009;50(1):28-33.

40. Hodde LA, Sandroni S. Emergency department evaluation and management of dialysis patient complications. J Emerg Med. 1992;10(3):317-334.

41. Katneni R, Hedayati SS. Central venous catheter-related bacteremia in chronic hemodialysis patients: epidemiology and evidence-based management. Nat Clin Pract Nephrol. 2007;3(5):256-266.

42. Maier A, Stocks F, Pommer W, et al. Hemodialysis versus peritoneal dialysis: a case control study of survival in patients with chronic kidney disease stage 5. Ther Apher Dial. 2009;13(3):199-204.

43. Teehan GS, Liangos O, Jaber BL. Update on dialytic management of acute renal failure. J Intensive Care Med. 2003;18(3):130-138.

44. Bloembergen WE, Port FK. Epidemiological perspective on infections in chronic dialysis patients. Adv Ren Replace Ther. 1996;3(3):201-207.

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The LLSA Literature Review“The LLSA Literature Review” summarizes articles from ABEM’s “2014 Lifelong Learning and Self-Assessment Reading List.” These articles are available online in the ACEP LLSA Resource Center (www.acep.org/llsa) and on the ABEM Web site.

Article 6

Post Cardiac Arrest Syndrome: A Review of Therapeutic StrategiesReviewed by J. Stephen Bohan, MD, MS, FACEP; Harvard Affiliated Emergency Medicine Residency; Brigham and Women’s Hospital

Stub D, Bernard S, Duffy SJ, Kaye DM. Post cardiac arrest syndrome: a review of therapeutic strategies. Circulation. 2011;123(13):1428-1435.

Out-of-hospital cardiac arrest (OHCA) occurs in 325,000 people a year in the United States. For those in whom spontaneous circulation is restored, much of the subsequent disability can be attributed to cerebral and cardiac dysfunction resulting from prolonged whole body ischemia.

There is some evidence that such patients do better if directed to regional centers that have facilities and programs such as therapeutic hypothermia and circulatory support. The American Heart Association recommends that patients be taken to such centers. It appears that patients with ventricular fibrillation or ventricular tachycardia do better than patients with asystole or pulseless electrical activity.

Hyperoxia may be as detrimental as hypoxia. The goal of treatment should be normal oxygenation, and a target mean arterial pressure of 65 to 100 mm Hg is probably reasonable. Circulatory support with balloon pumps or extracorporeal membrane oxygenation may be associated with improved outcomes.

Neuroprotection with hypothermia has been shown to improve neurologic outcomes in two international studies and now constitutes a guideline recommendation from authoritative international committees in patients with ventricular fibrillation and ventricular tachycardia. It may provide benefit to both the brain and the heart. Although it seems intuitive that therapeutic hypothermia should be started as early as possible, a study of prehospital-induced hypothermia found no difference in outcome between the intervention group and those who did not receive therapeutic hypothermia until arriving at the hospital.

OHCA patients with ST-segment elevation myocardial infarction (STEMI) who survive to hospital arrival should receive diagnostic and therapeutic coronary interventions, although the timing of these interventions related to

therapeutic hypothermia is uncertain as is their use in those with non-STEMI events.

Highlights ∙ OHCA patients with return of spontaneous circulation

should receive structured care, preferably at centers with the facilities and experience relevant to this syndrome.

∙ Goal-directed therapy is important.

∙ Therapeutic hypothermia has a solid evidence base and should be implemented in all OHCA patients who arrive at the hospital with spontaneous circulation.

∙ OHCA patients with STEMI benefit from coronary interventions.


14

■ ObjectivesOn completion of this lesson, you should be able to:

1. Discuss the role of lactate as a marker of hemodynamically effective resuscitation.

2. Describe the ways that bedside ultrasonography can be used to estimate central venous pressure and to predict volume responsiveness.

3. Describe the available minimally invasive methods of hemodynamic monitoring and the conditions required for them to be accurate.

4. Describe the currently available noninvasive monitors of cardiac output.

5. Discuss the role of the passive leg raise test in predicting volume responsiveness.

■ From the EM Model19.0 Procedures and Skills Integral to the Practice of Emergency Medicine 19.2 Resuscitation

Haney Mallemat, MD, and Michael Scott, MD

Noninvasive Hemodynamic Monitoring

Lesson 20

Critically ill patients presenting to an emergency department require urgent resuscitation. As a deeper understanding has developed of the dangers of both under- and over-resuscitation,1-3 this process has become significantly more challenging. There is evidence that noninvasive blood pressure cuffs are sometimes inaccurate in critically ill patients and that traditional end points of resuscitation such as blood pressure, heart rate, and shock index can be within normal limits despite ongoing shock.4,5 Tools were needed to monitor hemodynamics; of particular interest was a way to predict which patients would respond favorably to fluid administration and other resuscitative parameters. The pulmonary artery catheter was the first continuous hemodynamic monitoring device to gain widespread use and, although it has remained the gold standard for hemodynamic monitoring in research trials, its efficacy has been questioned at the bedside because it is a highly invasive catheter and has been associated with several complications (eg, pulmonary artery rupture, catheter-related blood stream infections, etc.).6 This article will focus on several noninvasive hemodynamic monitoring methods and devices available to emergency physicians to better delineate hemodynamic end points of resuscitation (Table 1).

Case Presentations

■ Case OneA 57-year-old man with a history of

heart failure and renal transplant on immunosuppressive agents presents with 1 day of fever and an admission blood pressure of 80/55. His initial serum lactate is 6. After receiving 2 liters of normal saline intravenously, his pressure improves slightly to 88/60. A repeat lactate is 4.5. He is tachypneic to 26, and continues to be tachycardic with a regular rate of 110. The emergency physician thinks that the patient may still be intravascularly volume-depleted but is concerned that giving more intravenous fluids could worsen his respiratory status.

■ Case TwoA 22-year-old woman arrives

from a nearby hotel because she had “passed out.” Her friends, who accompanied her, report that they are in town to run a marathon but that the patient is not able to run as planned because of an injury to her left calf that has required her to wear an orthopedic boot on that leg for the past 3 weeks, interfering with her training. Her initial vital signs are blood pressure 80/50, pulse rate 140, respiratory rate 25, temperature 37°C (98.6°F), and oxygen saturation 97% on room air. She and her friends deny any infectious signs or symptoms, and she denies any past medical history.

■ Case ThreeA 45-year-old woman

with a history of nonischemic cardiomyopathy and atrial fibrillation,

15


• Can lactate clearance be used as an end point of resuscitation in place of central venous oxygen saturation?

• In what ways can bedside ultrasonography be used to more completely determine a patient’s hemodynamic status?

• What are the truly noninvasive hemodynamic monitoring systems available today?

• What are the limitations of the more common, minimally invasive continuous hemodynamic monitoring systems?

• What is the most direct way to predict a patient’s volume responsiveness without giving fluids?

Critical Decisions

for which she takes warfarin, comes in because she has been short of breath for the past 3 days. Her chest radiograph is read by radiology as consistent with infiltrates versus edema bilaterally and recommends clinical correlation. She is afebrile, with blood pressure 85/50, pulse rate 110, respiratory rate 23, and oxygen saturation 94% on room air. The physician is considering placing a central line to transduce a central venous pressure (CVP) because he is concerned that this could be either sepsis due to pneumonia or acute heart failure, when the patient’s INR comes back at 10.

CRITICAL DECISION Can lactate clearance be used as an end point of resuscitation in place of central venous oxygen saturation?

It has been more than 10 years since Dr. Emanuel Rivers and his colleagues published their landmark trial describing an early goal-directed protocol for resuscitating patients in sepsis.1 The early goal-directed therapy (EGDT) protocol studied an algorithm that targeted specific physiologic end points: CVP, mean arterial pressure (MAP), and central venous oxygen saturation (Scvo2) continuously monitored through a central line. Rivers demonstrated a 16% reduction in mortality in the patients who received resuscitation according to this protocol within the first 6 hours of emergency department presentation.

Despite the demonstrated mortality reduction of EGDT, surveys conducted post-publication have demonstrated resistance to placing central lines and therefore acquiring Scvo2 samples in US emergency departments.7 Dr. Alan Jones recognized this limitation and sought to determine if resuscitation could be assessed using serum lactate levels in place of the Scvo2, therefore potentially eliminating the need for a central line.8 Serum lactate has long been used by clinicians to guide resuscitation and as a marker of tissue perfusion; reductions in lactate levels during resuscitation suggest that patients are clinically responding to therapy. Lactate is an attractive clinical marker because it can be easily sampled from a peripheral vein without the need for a central line. Jones hypothesized that serial reductions in lactate could be used as a surrogate for the measurement of Scvo2 during resuscitation of septic patients.

Jones performed a multicenter prospective-randomized non-inferiority trial to compare two EGDT protocols for patients with sepsis. The control group received the original EGDT protocol (as originally described by Rivers) with an Scvo2 of 70% as one of the end points, while the experimental group received the EGDT protocol with one revision; the Scvo2 end point was replaced with lactate clearance. Lactate clearance was defined as a 10% reduction in serum lactate level over 2 hours.

The investigators did not find a significant mortality difference between groups and concluded that lactate clearance was non-inferior to Scvo2 when used as part of an EGDT protocol in septic patients. The authors therefore concluded that lactate clearance allows for resuscitation without the need for a central line and Scvo2 monitoring.

There have been several critics of Jones’s study including the original EGDT author, Dr. Rivers.9 Critics claim that although serum lactate is an important parameter to measure, it cannot substitute for Scvo2 because Scvo2 provides unique hemodynamic information that should be used in conjunction with lactate. Rivers also claimed that the population in Jones’ study is different than the population in Rivers’ original EGDT study and the results should not be extrapolated to all septic patients. Another major criticism is that, while a central line is not needed to measure lactate, certain septic patients require vasopressors and inotropes (both of which require a central line), so substituting lactate for Scvo2 does not necessarily

Table 1 Noninvasive hemodynamic monitoring methods

Lactate clearance

Bedside ultrasonography

Respirophasic variation in the IVC

Distensibility index

RUSH examination

Passive leg raise maneuver

Monitoring devices

Bioreactance monitoring of electrical phase shifts (reflecting stroke volume and cardiac output)

Doppler ultrasonography (intermittently measuring stroke volume and cardiac output


16

eliminate the need for a central line in these patients. In spite of these criticisms, it appears that lactate clearance is a valuable tool, allowing clinicians to noninvasively monitor a patient’s hemodynamic status and response to resuscitation.

CRITICAL DECISIONIn what ways can bedside ultrasonography be used to more completely determine a patient’s hemodynamic status?

Bedside ultrasonography has become an essential tool for the modern emergency physician. It allows for the rapid diagnosis of disease (eg, cholecystitis, pneumothorax, etc.) at the patient’s bedside, without ionizing radiation. The utility of ultrasonography can also be expanded to include the noninvasive assessment and monitoring of hemodynamic status in critically ill patients. Three ultrasound techniques will be described here: 1) respirophasic variation of the inferior vena cava (IVC), 2) the IVC distensibility index, and 3) the RUSH protocol.

Respirophasic Variation of the Inferior Vena Cava

The IVC is relatively easy to visualize on ultrasonography and undergoes a respirophasic variation in spontaneously breathing patients. The initial size of the IVC and the degree of variation can be used to approximate CVP (Figure 1), which is an important end point during resuscitation as recommended by the Surviving Sepsis guidelines.10 Although the accuracy of CVP, and hence IVC variation, as a resuscitative end point has been called into question,11 until a new goal-directed protocol is validated that does not monitor CVP, IVC variation can be used as a useful adjunct during resuscitation.

The Distensibility IndexThe IVC can also be visualized and

measured in mechanically ventilated patients. In these cases, however, IVC variation does not estimate

CVP; instead, IVC variation in the mechanically ventilated patient (called the distensibility index [DI]) helps predict which hypotensive patients will hemodynamically improve when given a fluid bolus (called volume responsiveness) and which patients will not.12 The distensibility index is an accurate and well-validated marker for volume responsiveness.

The positive pressure delivered from the mechanical ventilator causes the IVC to distend (ie, positive intrathoracic pressure reduces venous return to the heart) and when the positive pressure breath is released, the IVC returns to its size at baseline. The degree of IVC variation that occurs throughout a respiratory cycle can be measured and entered into the formula to determine the DI (Figure 2).

A DI greater than 18% indicates that a patient is volume responsive and that hemodynamics will likely improve with administration of a fluid bolus. A DI less than 18% indicates that a patient is not volume responsive and would likely not benefit from a fluid bolus. In order for the DI to serve as an accurate predictor of volume responsiveness, patients must 1) not be breathing

spontaneously during mechanical ventilation, 2) receive a tidal volume of at least 7 mL/kg of ideal body weight (based on sex and height), 3) be in normal sinus rhythm, and 4) not have right ventricular dysfunction. Although there are several criteria to fulfill in order to use the DI, it is a useful noninvasive tool for assessing the need for fluid boluses in hemodynamically unstable and mechanically ventilated patients.

The RUSH Examination Ultrasound has been incorporated

into several protocols for the rapid hemodynamic assessment of the critically ill patient (FATE, FREE, etc.).13,14 One of the more popular protocols in emergency medicine is the Rapid Ultrasound in SHock (RUSH) protocol described by Perera, et al.15 The RUSH protocol takes a physiologic approach to the hypotensive patient, using a three-step process to evaluate 1) the pump (ie, the heart); 2) the tank (ie, intravascular volume status); and 3) the pipes (ie, integrity of large arteries and veins). In addition to noninvasively assessing a patient’s hemodynamic status, the RUSH examination can also be used to detect the potential underlying

Figure 1 Ultrasound image of the inferior vena cava with M-mode demonstrating the amount of collapsibility over a respiratory cycle

17


etiologies for hemodynamic compromise making the examination a powerful tool at the bedside.

The Pump: HeartThe pump or cardiac portion of

the RUSH examination has three components. The first component is to determine the presence or absence of a pericardial effusion and, if present, the potential for tamponade. Pericardial effusions are relatively easy to see with ultrasound (Figure 3). Ultrasound also has the added benefit of assisting the clinician in performing a pericardiocentesis if tamponade is present.

The second component of the cardiac assessment is to determine the size and function of the left ventricle in order to assess whether the left heart is the underlying cause for shock and if that cause is reversible. For example, a large and poorly contracting left ventricle can indicate acute ventricular dysfunction (eg, an acute myocardial infarction), and a small and hyperdynamic heart may indicate other causes of hemodynamic instability (eg, hypovolemia).

The final component of the cardiac portion of the RUSH examination is assessment of the right ventricle. A normally sized and functioning right ventricle is reassuring; however, acute pathology may give clues to the

underlying reasons for hemodynamic instability. For example, detection of right ventricular enlargement with poor contractility can indicate a massive pulmonary embolism causing a secondary obstructive shock. Rapid detection of this can lead to thrombolytics and reversal of hemodynamic compromise.

The Tank: Intravascular Volume Status

The second goal of the RUSH examination is to evaluate the effective intravascular volume status in order to distinguish patients in need of volume resuscitation due to volume depletion from those patients who do not require fluid repletion secondary to volume overload. Evidence of intravascular depletion can be demonstrated by visualizing the IVC for significant respirophasic variations in the spontaneously breathing patient or using the distensibility index in mechanically ventilated patients. If the clinician determines that the patient is intravascularly depleted, the focus should shift to looking for potential sources of volume loss such as hemorrhage. The thorax and abdomen can be easily visualized to detect evidence of volume loss such as hemothorax (eg, secondary to penetrating chest trauma) or free intraperitoneal fluid

(eg, from ruptured aortic aneurysm), respectively (Figure 4).

Besides loss of intravascular volume, hypotensive patients can have a relative reduction in intravascular volume secondary to external compression of great veins and a reduction in blood return to the heart. The classic example is a tension pneumothorax, which can be easily and rapidly detected by ultrasound and is included in the protocol.

At the other end of the intravascular spectrum is a patient who has too much intravascular volume and whose tank is “too full.” It is important to identify critically ill patients in volume overload because the resuscitative strategy may shift from hemodynamic support with rapid volume administration to support with vasopressors or inotropes. Ultrasound can be used to assess for volume overload in a variety of ways: 1) as discussed previously, it can show a dilated IVC with little respirophasic variation; 2) it can show evidence of third-spaced fluids such as pleural effusions or ascites; and 3) it can reveal B-lines (the sonographic representation of extravascular lung water), indicating pulmonary edema.

The Pipes: Assessment of Aorta and Lower Extremity Veins

The third and final portion of the RUSH protocol is the evaluation of the aorta and the lower extremity veins. Specifically, the thoracic and abdominal aorta are evaluated for signs suggestive of aneurysm or dissection, which could lead to hemorrhagic or obstructive shock (if the dissection extends into the pericardial sac), respectively.

Following assessment of the aorta, the lower extremity veins are evaluated for obstruction secondary to thromboembolism. Demonstrating venous thromboembolism in the setting of hypotension may suggest an acute and massive pulmonary embolism as the cause of hemodynamic compromise and the need for emergent thrombolysis.

Figure 2 Distensibility index (Maximum=maximum IVC diameter; Minimum=minimum IVC diameter)


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CRITICAL DECISIONWhat are the truly noninvasive hemodynamic monitoring systems available today?

Advances in technology have led to the creation of a number of commercially available hemodynamic monitors. These monitors range from completely noninvasive to minimally invasive requiring only an arterial line and/or a central line. These devices provide clinicians with hemodynamic measurements such as stroke volume, cardiac output, and volume responsiveness (as a function of stroke volume or pulse pressure variation) that allow a focused and goal-directed resuscitation. Each device differs in its method of deriving and monitoring cardiac output, and therefore each has certain limitations depending on the patient and clinical scenario.

One type of monitor uses a small Doppler ultrasound probe intermittently applied to the patient’s chest to acquire hemodynamic measurements such as stroke volume and cardiac output. Doppler is a more direct and potentially more accurate measurement of cardiac output than some of the methods used in other devices. Some studies, however, have suggested that it can be inaccurate in clinical conditions with high cardiac output (eg, hyperthyroid

storm).16-18 Other studies of this type of device have demonstrated an inability to obtain adequate signal in up to 24% of patients.17 Another limitation is that the monitor does not provide continuous data because it must be intermittently applied, reducing its utility in patients with rapidly fluctuating hemodynamics. Despite these limitations, in certain clinical scenarios these devices can provide important hemodynamic data noninvasively.

The second type of noninvasive monitor is a bioreactance system that uses electrodes that adhere to the anterior chest wall to analyze and interpret electrical phase shifts created by movement of fluids within the chest to report meaningful hemodynamic information to the clinician (stroke volume and cardiac output).19

These bioreactance monitors have been shown to correlate well with traditional hemodynamic assessments20 and several studies suggest they might be superior to the Doppler-based monitors because they provide continuous measurements.21 Although further clinical trials are needed to determine whether this technology can improve patient outcomes, its benefits are that 1) there is little to no dependence on

the skill of the operator, 2) it provides continuous measurement of cardiac output, 3) it can be used in patients with arrhythmias, and 4) it can more rapidly recognize changes in cardiac output compared to traditional continuous cardiac output monitors.

CRITICAL DECISIONWhat are the limitations of the more common, minimally invasive continuous hemodynamic monitoring systems?

The second class of monitors we will discuss are minimally invasive, using an arterial line to provide continuous hemodynamic monitoring. These monitors work on the assumption that stroke volume (and therefore cardiac output) is related to blood pressure, arterial compliance, and systemic vascular resistance (SVR); therefore all of these measurements can be derived from an analysis of the arterial waveform obtained from an arterial line. These devices require an arterial catheter (and in some instances a central venous catheter); however, they can be helpful in managing patients who already require an arterial line for careful hemodynamic monitoring.

One such device integrates arterial waveform analysis into a software algorithm to determine stroke volume, cardiac output, and SVR. The benefit of this device is that only an arterial catheter is required for continuous hemodynamic monitoring. Despite its perceived benefits, however, there is some evidence that it is inaccurate in certain clinical conditions such as high output states, low SVR, and during rapid alterations in cardiac output.22

Other systems also provide continuous hemodynamic measurements by arterial waveform analysis, but these systems intermittently undergo calibration to provide more precise hemodynamic measurements. Unfortunately, calibration requires a central line, making these devices a little more than minimally invasive. Another disadvantage to these systems is that

Figure 3 Subcostal ultrasonographic view demonstrating pericardial tamponade causing shock. Right atrial collapse in the setting of pericardial effusion is concerning for tamponade.

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measurements can be inaccurate during certain clinical states (eg, low-flow states and tricuspid or pulmonary regurgitation). Additionally, one device uses lithium for calibration, which renders it unsuitable for use in certain populations (ie, patients taking lithium therapeutically, patients weighing <40 kg, pregnant patients, and, possibly, patients who have recently received neuromuscular blocking agents).23

In addition to continuously monitoring cardiac output, all of these systems are able to predict volume responsiveness in some patients through the measurement of stroke volume or pulse pressure variation, allowing clinicians to determine the point at which further fluid administration will no longer be hemodynamically favorable. It is important to note that there are several criteria that must be met before stroke volume variation and pulse pressure variation can be trusted to accurately predict volume responsiveness, as follows: 1) patients must be mechanically ventilated with ideal tidal volumes of at least 8 mL/kg of ideal body weight; 2) patients cannot be making spontaneous respirations; and 3) they must be in a normal sinus rhythm.24

CRITICAL DECISIONWhat is the most direct way to predict a patient’s volume responsiveness without giving fluid?

The passive leg raise (PLR) maneuver is being used with good results to predict volume responsiveness. The idea behind PLR is simple; the lower extremity veins contain a certain volume of blood (approximately 150-200 mL in each leg) and, therefore, elevating a patient’s legs above the heart should provide an autologous and “retractable” fluid bolus to the central circulation. The response to this autologous bolus can be measured to predict if the patient will have positive hemodynamic response to exogenous fluid administration. If the PLR does not improve hemodynamics,

returning the patient to the normal position will cause the blood volume to return to the lower extremities with few ill effects.

During a PLR, the patient is placed in a semirecumbent position (head of bed 45°, legs flat) for several minutes while hemodynamic parameters are measured with ultrasound or the devices described above; these measurements represent the hemodynamic baseline. The patient’s head and thorax are then lowered to 0° while the legs are raised into a 45° position. The same hemodynamic parameters are measured again over the next 5 minutes.

Increased cardiac output in response to PLR is a very accurate predictor of volume responsiveness across multiple studies using different types of cardiac output monitoring. One of the most exciting aspects of PLR is that it has few limitations; it is valid for ventilated or nonventilated patients, patients with or without spontaneous respirations, and for patients with or without arrhythmias.25 For all these reasons, the PLR seems to be a powerful and well-validated tool to predict volume responsiveness.

Case Resolutions

■ Case OneBecause the middle-aged

hypotensive patient with an initial serum lactate of 6 responded to fluid administration with an initial lactate clearance of more than 10%, the emergency physician thought that resuscitative efforts were going in the right direction, so he gave only one more liter of normal saline. Two hours later the patient’s lactate was 3, and his respiratory status had improved. He was transferred to the medical ICU in stable condition.

■ Case TwoIn the case of the young woman

who had passed out in her hotel room, the RUSH examination showed a small, hyperdynamic left ventricle and a large right ventricle, with no evidence of pericardial effusion, pneumothorax, enlarged aorta, or abdominal free fluid. Venous examination, however, showed a noncompressible left femoral vein. Her presentation was suspected to be caused by a large pulmonary embolism. Given her instability, she was taken for emergent thrombectomy by interventional radiology. She was discharged from the hospital, ambulatory and to her home, 5 days later.

Figure 4 Thoracic ultrasound image of a patient following penetrating thoracic trauma. The patient here experienced hemorrhagic shock.


20

■ Case ThreeBecause the woman who had

presented with shortness of breath had an INR of 10, more traditional (and invasive) forms of hemodynamic monitoring were contraindicated, so the emergency physician decided to measure her cardiac output in response to the PLR maneuver using a noninvasive monitor. When this maneuver was performed, there was no change in the patient’s cardiac output, suggesting that her condition was more likely an exacerbation of her heart failure than sepsis due to pneumonia. The emergency physician started the patient on furosemide, bilevel positive airway pressure, and dobutamine, and she was transferred to the cardiac care unit in stable condition.

SummaryThere are a variety of modalities

to help emergency physicians guide and monitor the resuscitation of the critically ill patient. Lactate clearance is a relatively simple and powerful tool to determine the

Pearls• A decrease in lactate of 10% over 2 hours may be as good a

marker of adequate resuscitative efforts as Scvo2, negating the need for invasive central venous catheterization.

• In the right clinical setting, the distensibility index of the IVC and arterial-waveform derived hemodynamic monitoring can predict volume responsiveness in hemodynamically unstable patients with good accuracy.

• A bioreactance system using electrodes attached to the chest to detect movement of fluid within the chest may represent an accurate, truly noninvasive method of continuous cardiac output monitoring across a wide range of clinical situations, although larger outcome-based trials are needed.

• The PLR maneuver has been shown to predict volume responsiveness in critically ill patients across a number of different monitoring modalities.

Pitfalls• Using lactate level as a predictor of volume responsiveness.

• Relying on IVC distensibility index to predict volume responsiveness in patients with right heart dysfunction.

• Relying on arterial-waveform–derived hemodynamic monitoring or IVC distensibility in spontaneously breathing patients, patients with arrhythmias, or patients on low tidal volume ventilation.

adequacy of resuscitation. Bedside ultrasonography can also be used both to noninvasively diagnose the cause of hemodynamic instability and to monitor the adequacy of resuscitation.

There are also a number of commercially available hemodynamic monitors. Newer modalities are perhaps still somewhat lacking in clinical trials but represent truly noninvasive methods of cardiac output monitoring. Some older systems, while requiring an arterial catheter and therefore not qualifying as truly noninvasive, have been extensively validated as reliable methods to measure cardiac output and to predict volume responsiveness in mechanically ventilated patients without arrhythmias.

Finally, no matter what method of hemodynamic monitoring is used, the PLR test appears to be a powerful predictor of volume responsiveness across a wide range of patient characteristics.

References1. Rivers E, Nguyen B, Havstad S, et al. Early goal-

directed therapy in the treatment of severe sepsis and septic shock. N Engl J Med. 2001;345(19):1368-1377.

2. Marchick MR, Kline JA, Jones AE. The significance of non-sustained hypotension in emergency department patients with sepsis. Intensive Care Med. 2009:35(7):1261-1264.

3. Boyd JH, Forbes J, Nakada TA, et al. Fluid resuscitation in septic shock: a positive fluid balance and elevated central venous pressure are associated with increased mortality. Crit Care Med. 2011;39(2):259-265.

4. Rady MY, Rivers EP, Martin GB, et al. Continuous central venous oximetry and shock index in the emergency department: use in the evaluation of clinical shock. Am J Emerg Med. 1992;10(6):538-541.

5. Rady MY, Rivers EP, Nowak RM. Resuscitation of the critically ill in the ED: responses of blood pressure, heart rate, shock index, central venous oxygen saturation, and lactate. Am J Emerg Med. 1996;14(2):218-225.

6. Wiener RS, Welch HG. Trends in the use of the pulmonary artery catheter in the United States, 1993-2004. JAMA. 2007;298(4):423-129.

7. Carlbom DJ, Rubenfeld GD. Barriers to implementing protocol-based sepsis resuscitation in the emergency department—results of a national survey. Crit Care Med. 2007;35(11):2525–2532.

8. Jones AE, Shapiro NI, Trzeciak S, et al. Lactate clearance vs central venous oxygen saturation as goals of early sepsis therapy: a randomized clinical trial. JAMA. 2010;303(8):739-746.

9. Rivers EP, Elkin R, Cannon CM. Counterpoint: should lactate clearance be substituted for central venous oxygen saturation as goals of early severe sepsis and septic shock therapy? No. Chest. 2011;140(6):1408-1413; discussion 1413-1419.

10. Dellinger RP, Levy MM, Carlet JM, et al. Surviving Sepsis Campaign: international guidelines for management of severe sepsis and septic shock: 2008. Crit Care Med. 2008;36(1):296-327.

11. Marik P, Baram M, Vahid B. Does central venous pressure predict fluid responsiveness? A systematic review of the literature and the tale of seven mares. Chest. 2008;134(1):172-178.

12. Barbier C, Loubières Y, Schmit C, et al. Respiratory changes in inferior vena cava diameter are helpful in predicting fluid responsiveness in ventilated septic patients. Intensive Care Med. 2004;30(9):1740-1746.

13. Jensen MB, Sloth E, Larsen KM, Schmidt MB. Transthoracic echocardiography for cardiopulmonary monitoring in intensive care. Eur J Anaesthesiol. 2004;21(9):700-707.

14. Murthi SB, Hess JR, Hess A, et al. Focused rapid echocardiographic evaluation versus vascular catheter-based assessment of cardiac output and function in critically ill trauma patients. J Trauma Acute Care Surg. 2012;72(5):1158-1164.

15. Perera P, Mailhot T, Riley D, Mandavia D. The RUSH exam: Rapid Ultrasound in SHock in the evaluation of the critically lll. Emerg Med Clin North Am. 2010;28(1):29-56, vii.

16. Boyle M, Steel L, Flynn GM, et al. Assessment of the clinical utility of an ultrasonic monitor of cardiac output (the USCOM) and agreement with thermodilution measurement. Crit Care Resusc. 2009;11(3):198-203.

17. Chong SW, Peyton PJ. A meta-analysis of the accuracy and precision of the ultrasonic cardiac output monitor (USCOM). Anaesthesia. 2012;67(11):1266-1271.

18. Tan HL, Pinder M, Parsons R, et al. Clinical evaluation of USCOM ultrasonic cardiac output monitor in cardiac surgical patients in intensive care unit. Br J Anaesth. 2005;94(3):287-291.

19. Keren H, Burkhoff D, Squara P. Evaluation of a noninvasive continuous cardiac output monitoring system based on thoracic bioreactance. Am J Physiol Heart Circ Physiol. 2007;293(1):H583-H589.

20. Raval NY, Squara P, Cleman M, et al. Multicenter evaluation of noninvasive cardiac output measurement by bioreactance technique. J Clin Monit Comput. 2008;22(2):113-119.

21. Squara P, Denjean D, Estagnasie P, et al. Noninvasive cardiac output monitoring (NICOM): a clinical validation. Intensive Care Med. 2007;33(7):1191-1194.

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22. Mayer J, Boldt J, Poland R, et al. Continuous arterial pressure waveform-based cardiac output using the Flo Trac/Vigileo: a review and meta-analysis. J Cardiothorac Vasc Anesth. 2009;23(3):401-406.

23. Reuter DA, Huang C, Edrich T, et al. Cardiac output monitoring using indicator-dilution techniques: basics, limits, and perspectives. Anesth Analg. 2010;110(3):799-811.

24. Marik PE, Cavallazzi R, Vasu T, Hirani A. Dynamic changes in arterial waveform derived variables and fluid responsiveness in mechanically ventilated patients: a systematic review of the literature. Crit Care Med. 2009;37(9):2642-2647.

25. Cavallaro F, Sandroni C, Marano C, et al. Diagnostic accuracy of passive leg raising for prediction of fluid responsiveness in adults: systematic review and meta-analysis of clinical studies. Intensive Care Med. 2010;36(9):1475-1483.


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23

October 2013 • Volume 27 • Number ?

The Critical ECGA 39-year-old man with end-stage acquired immunodeficiency syndrome (AIDS) presents with fever, dyspnea, and chest pressure; blood pressure is 90/35.

Sinus tachycardia, rate 105, low voltage. Low voltage is defined by QRS amplitudes in all of the limb leads smaller than 5 mm or in all of the precordial leads smaller than 10 mm. The differential diagnosis of low voltage includes myxedema, large pericardial effusion, large pleural effusion, end-stage cardiomyopathy, severe chronic obstructive pulmonary disease, severe obesity, infiltrative myocardial diseases, constrictive pericarditis, and prior massive MI. The combination of low voltage plus tachycardia should prompt early consideration of a large pericardial effusion. The patient in this case had an urgent echocardiogram, which demonstrated a large pericardial effusion and tamponade. Bacteria were cultured from the pericardial fluid and blood. Despite pericardiotomy and treatment with intravenous antibiotics, he died of sepsis.

Feature Editor: Amal Mattu, MD, FACEP

From: Mattu A, Brady W. ECGs for the Emergency Physician. London: BMJ Publishing; 2003:126,150. Available at www.acep.org/bookstore. Reprinted with permission.


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25

October 2013 • Volume 27 • Number ?

The Critical ImageA 91-year-old man presenting with ataxia, tremor, and difficulty with activities of daily living over the past 6 months He is concerned that he may require nursing home placement. He reports falling approximately 2 months ago. Vital signs are blood pressure 119/68, heart rate 88, respiratory rate 18, temperature 36.7°C, and oxygen saturation 97% on room air. The physical examination results are normal, with the exception of an intention tremor and ataxic gait.

A noncontrast head CT scan (A) performed at the time of the patient’s initial emergency department visit shows large bilateral subdural hematomas (SDH), each more than 1.5 cm in thickness. Despite this, the patient has no midline shift, presumably because the bilateral locations result in counteracting forces. Mass effect is present; this 91-year-old patient would be expected to have age-appropriate brain atrophy, with prominent sulci, but in this case most sulci have been effaced by mass effect of hemorrhage.

The hemorrhage is of variable age, indicated by varying density. Here, some areas of older hemorrhage are identical in density (isodense) to normal brain parenchyma, making recognition more difficult despite their large size. Other areas are more acute, with a brighter (hyperdense) appearance.

A noncontrast CT 1 week later (B), without intervention, shows that the subdural collections are evolving. Some regions are now hypodense (darker than) compared to adjacent brain parenchyma. Other hyperdense regions have expanded, suggesting acute rebleeding. Note the continued effacement of sulci.

A noncontrast CT image obtained 5 months later (C), without neurosurgical intervention, shows that the subdural collections have resolved and sulci are again evident.

Subdural hematomas classically assume a concave shape, cupping the surface of the brain. Acute hemorrhage can be obvious because of its hyperdense appearance. Subacute hemorrhage can be more subtle; look for effacement of sulci as a clue to the presence of isodense SDH.

The normal symmetry of the brain is often disturbed by pathology, drawing our attention. However, bilateral pathology can escape notice by preserving symmetry.

In general, acute hemorrhage is denser than normal brain parenchyma and becomes less dense with the passage of time, becoming hypodense within three weeks. Delayed increase in density is sometimes observed, attributed to rebleeding.1

The patient was treated without surgery and had complete resolution of his hematomas on repeat head CT within 5 months. His neurologic examination remained stable.1. Lee KS, Bae WK, Bae HG, et al. The computed tomographic attenuation and the age of subdural hematomas. J Korean Med Sci. 1997;12:353-359.

Feature Editor: Joshua S. Broder, MD, FACEP. See also Diagnostic Imaging for the Emergency Physician (winner of the 2011 Prose Award in Clinical Medicine, the American Publishers Award for Professional and Scholarly Excellence) by Dr. Broder, available from the ACEP Bookstore, www.acep.org/bookstore.

A Isodense

SDH

B

Hypodense

SDH

Sulci effaced

SDH

Hyperdense

SDHSulci

C


26

Qualified, paid subscribers to Critical Decisions in Emergency Medicine may receive CME certificates for up to 5 ACEP Category I credits, 5 AMA PRA Category 1 Credits™, and 5 AOA Category 2-B credits for answering the following questions. To receive your certificate, go to www.acep.org/newcriticaldecisionstesting and submit your answers online. On achieving a score of 75% or better, you will receive a printable CME certificate. You may submit the answers to these questions at any time within 3 years of the publication date. You will be given appropriate credit for all tests you complete and submit within this time. Answers to this month’s questions will be published in next month’s issue.

CME Questions

1. Which of the following represents the most common causes of renal failure in the United States?A. Acute glomerulonephritisB. Diabetes and hypertensionC. Illegal substance abuse and its complications such as

endocarditisD. Trauma and shock

2. Which is the most acceptable site for blood draws in a patient with end-stage renal disease (ESRD)?A. The dominant arm distal to the elbowB. The nondominant armC. The patient’s fistulaD. The upper part of the dominant arm

3. If a dialysis patient is in extremis and the fistula must be accessed, which of the following is acceptable in the management of the fistula?A. After puncture, an occlusive cuff should be placed for 20

minutes to prevent bleedingB. Firm pressure should be applied to the site for at least 10

minutesC. A simple alcohol wipe should suffice before its useD. Since it is a life-threatening situation, palpation of a thrill and

documentation are unnecessary

4. Which pharmaceutical agents are not traditionally associated with iatrogenic or medication-induced acute renal failure?A. AminoglycosidesB. Angiotensin-converting enzyme (ACE) inhibitorsC. BenzodiazepinesD. Intravenous contrast agents

5. Which of the following medications is preferred in the management of patients with ESRD?A. Calcium gluconate as temporizing measures for

hypermagnesemiaB. Ibuprofen for uremic pericarditisC. Magnesium-containing catharticsD. Phosphate-containing enemas

6. Which of the following is the most common cause for hypotension during dialysis?A. Air embolismB. Excessive rate of ultrafiltration resulting in hypovolemiaC. Gastrointestinal fluid lossesD. Hypercalcemia

7. Which of the following conditions and treatments are correctly paired?A. Bleeding and prolonged bleeding time – cryoprecipitate and

desmopressinB. Ethylene oxide exposure – ACE inhibitors C. Fluid overload associated with hypotension – diuretics, nitrites,

or nesiritide D. Hyperphosphatemia – sodium polystyrene sulfonate

8. Which of the following notes the most common cause/causes for inadequate catheter-related flow?A. Catheter-related septic thrombosisB. Complete central vein thrombosisC. HypotensionD. Thrombosis and stenosis (intimal hyperplasia)

9. Following dialysis a patient develops acute cardiorespiratory compromise. The patient presented with dyspnea, tachypnea, chest pain, hypotension and confusion. A “millwheel” cardiac murmur is audible. No rash is noted. Which of the following accurately describes treatment of this syndrome?A. Clamp the access line and place the patient supine or left lateral

decubitus in TrendelenburgB. Cryoprecipitate, 10 units every 12 to 24 hours, may be effective

treatmentC. Treat patient for an acute allergic reactionD. Vancomycin and gentamycin are appropriate treatment

10. Which of the following medications should be avoided in the emergency management of hyperkalemia?A. Beta-blockersB. Insulin-glucose combinationsC. Intravenous calciumD. Sodium bicarbonate

11. An 88-year-old woman presents from home with 3 days of decreased oral intake, painful urination, and altered mental status. At triage, her vital signs are blood pressure 85/60, heart rate 120, respiratory rate 22, temperature 38.7°C, and Spo2 93% on room air. Her urinalysis is consistent with a urinary tract infection. Her initial lactate is 4. After a normal saline bolus of 2 L, her mental status has returned to baseline and she is breathing comfortably; however, her blood pressure and heart rate are unchanged. The emergency physician wants to place a central line to monitor the patient’s central venous pressure (CVP) to help guide fluid therapy, but the patient and her daughter refuse permission. Bedside ultrasonographic visualization of which of the following allows for estimation of CVP in this patient?A. Carotid arteryB. Femoral arteryC. Inferior vena cavaD. Left ventricular stroke volume

27

Month 2013 • Volume 27 • Number 10

Answer key for September 2013, Volume 27, Number 9

1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20D A D B C B A B D A C B B D A B D C D C

12. In the patient described in question 11, which of the following would be a reasonable option for predicting volume responsiveness?A. Change in cardiac output in response to passive leg raise

maneuverB. IVC distensibility index (DI)C. Pulse pressure variation as measured with pulse contour

waveform deviceD. RUSH examination

13. Which of the following describes the benefit/benefits of a noninvasive bioreactance monitoring system when compared to cardiac output monitoring using a pulmonary artery catheter?A. Ability to be used in the presence of arrhythmiasB. Ability to provide measurement of CVP in addition to cardiac

outputC. Ability to recognize changes in cardiac output in a shorter

amount of time and the noninvasive techniqueD. Accuracy in both ventilated and spontaneously breathing

patients

14. The RUSH protocol involves evaluation of what three general aspects of the patient’s hemodynamic status?A. Bleeding, breathing, and bounce backB. The heart, the kidneys, and the liverC. Preload responsiveness, pulmonary embolism, and pulmonary

edemaD. The pump (ie, the heart), the tank (ie, intravascular volume

status), and the pipes (ie, large arteries and veins)

15. What is generally regarded as the first component of the RUSH examination?A. Evaluating the abdomen for evidence of free fluidB. Evaluating the heart for pericardial effusion and left ventricular

functionC. Evaluating the lower extremity veins for evidence of thrombosisD. Evaluating the lungs for pneumothorax

16. Which of the following is an acceptable starting position from which to measure baseline hemodynamics before performing a passive leg raise (PLR) maneuver?A. Prone positioningB. Reverse Trendelenburg positionC. Semirecumbent positioning (head of bed at 45°, legs flat)D. Supine positioning

17. A 42-year-old man presents in septic shock, presumably because of pneumonia. He is intubated and placed on a tidal volume of 6 mL/kg based on his ideal body weight. He is in normal sinus rhythm with blood pressure 80/40, heart rate 120, and lactate of 6 despite fluid resuscitation with 4 L of normal saline. His stroke volume variation, measured by arterial waveform analysis via an arterial line, is 4%. His IVC distensibility index on bedside ultrasound is 2%. In response to PLR, his cardiac output increases by 20% and his blood pressure remains unchanged. Which of the following is the appropriate next step, and why?A. Continue fluid resuscitation, as his cardiac output increased

significantly in response to PLR, suggesting he is still volume responsive

B. Stop fluid resuscitation and start vasopressors, as his IVC distensibility index suggests he is not volume responsive

C. Stop fluid resuscitation and start vasopressors, as his MAP did not respond to PLR, suggesting he is not volume depleted

D. Stop fluid resuscitation and start vasopressors, as his stroke volume variation suggests he is not volume responsive

18. Which of the following conditions is a contraindication to use of a minimally invasive monitor that uses lithium for calibration?A. Low tidal volume mechanical ventilationB. Pulmonary embolismC. Recent neuromuscular blockadeD. Spontaneous breathing

19. An IVC distensibility index above what value suggests volume responsiveness?A. 6%B. 10%C. 14%D 18%

20. In an IVC measured to be 2 cm in diameter, what value of IVC respirophasic variation would be thought to be equivalent to a CVP of approximately 12?A. 30%B. 60%C. 70%D. 90%

NONPROFITU.S. POSTAGE

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Critical Decisions in Emergency Medicine is the official CME publication of the American College of Emergency Physicians. Additional volumes are available to keep emergency medicine professionals up-to-date on relevant clinical issues.

Editor-in-ChiefLouis G. Graff IV, MD, FACEP Professor of Traumatology and Emergency Medicine, Professor of Clinical Medicine, University of Connecticut School of Medicine; Farmington, Connecticut

Section EditorJ. Stephen Bohan, MS, MD, FACEP Executive Vice Chairman and Clinical Director, Department of Emergency Medicine, Brigham & Women’s Hospital; Instructor, Harvard Medical School, Boston, Massachusetts

Feature EditorsMichael S. Beeson, MD, MBA, FACEP Program Director, Department of Emergency Medicine, Akron General, Akron, Ohio; Professor, Clinical Emergency Medicine, Northeastern Ohio Universities College of Medicine, Rootstown, Ohio

Joshua S. Broder, MD, FACEP Associate Clinical Professor of Surgery, Residency Program Director, Division of Emergency Medicine, Duke University Medical Center, Durham, North Carolina

Amal Mattu, MD, FACEP Professor and Vice Chair, Department of Emergency Medicine, Director, Faculty Development and Emergency Cardiology Fellowships, University of Maryland School of Medicine, Baltimore, Maryland

Robert C. Solomon, MD, FACEP Core faculty, Emergency Medicine Residency, Allegheny General Hospital, Pittsburgh, Pennsylvania; Assistant Professor (adjunct) Emergency Medicine, Temple University School of Medicine, Philadelphia, Pennsylvania

Associate EditorsDaniel A. Handel, MD, MPH, FACEP Vice Chair and Director of Clinical Operations; Associate Professor, Department of Emergency Medicine; Oregon Health & Science University, Portland, Oregon

Frank LoVecchio, DO, MPH, FACEP Research Director, Maricopa Medical Center Emergency Medicine Program; Medical Director, Banner Poison Control Center, Phoenix, Arizona; Professor, Midwestern University/Arizona College of Osteopathic Medicine, Glendale, Arizona

Sharon E. Mace, MD, FACEP Associate Professor, Department of Emergency Medicine, Ohio State University School of Medicine; Faculty, MetroHealth Medical Center/Cleveland Clinic Foundation Emergency Medicine Residency Program; Director, Pediatric Education/Quality Improvement and Observation Unit, Cleveland Clinic Foundation, Cleveland, Ohio

Lynn P. Roppolo, MD, FACEP Associate Emergency Medicine Residency Director, Associate Professor of Emergency Medicine, University of Texas Southwestern Medical Center, Dallas, Texas

Robert A. Rosen, MD, FACEP Medical Director, Culpeper Regional Hospital, Culpeper, Virginia; Associate Professor, Emergency Medicine, University of Virginia School of Medicine, Charlottesville, Virginia

George Sternbach, MD, FACEP Clinical Professor of Surgery (Emergency Medicine), Stanford University Medical Center, Stanford, California

Kathleen Wittels, MD Instructor, Harvard Medical School, Boston, Massachusetts

Editorial StaffMary Anne Mitchell, ELS, Managing EditorMike Goodwin, Creative Services ManagerJessica Hamilton, Educational Products AssistantLexi Schwartz, Subscriptions CoordinatorMarta Foster, Director, Educational Products

Critical Decisions in Emergency Medicine is a trademark owned and published monthly by the American College of Emergency Physicians, PO Box 619911, Dallas, TX 75261-9911. Send address changes and comments to Critical Decisions in Emergency Medicine, PO Box 619911, Dallas, TX 75261-9911, or to [email protected]; call toll free 800-798-1822, or 972-550-0911.Copyright 2013 © by the American College of Emergency Physicians. All rights reserved. No part of this publication may be reproduced, stored, or transmitted in any form or by any means, electronic or mechanical, including storage and retrieval systems, without permission in writing from the Publisher. Printed in the USA.The American College of Emergency Physicians (ACEP) makes every effort to ensure that contributors to its publications are knowledgeable subject matter experts. Readers are nevertheless advised that the statements and opinions expressed in this publication are provided as the contributors’ recommendations at the time of publication and should not be construed as official College policy. ACEP recognizes the complexity of emergency medicine and makes no representation that this publication serves as an authoritative resource for the prevention, diagnosis, treatment, or intervention for any medical condition, nor should it be the basis for the definition of, or standard of care that should be practiced by all health care providers at any particular time or place. Drugs are generally referred to by generic names. In some instances, brand names are added for easier recognition. Device manufacturer information is provided according to style conventions of the American Medical Association. ACEP received no commercial support for this publication. To the fullest extent permitted by law, and without limitation, ACEP expressly disclaims all liability for errors or omissions contained within this publication, and for damages of any kind or nature, arising out of use, reference to, reliance on, or performance of such information.ISSN 2325-0186 (Print) ISSN 2325-8365 (Online)

The Drug BoxNeomycin, Polymyxin B, and HydrocortisoneBy Steven Warrington, MD; Akron General Medical Center

Neomycin, polymyxin B, and hydrocortisone is a combination antibiotic and corticosteroid that is available for ophthalmic, otic, and dermatologic conditions. The medication is used for inflammatory conditions with suspected bacterial infection or with risk of developing bacterial infection. This combination medication should not be used for suspected viral, fungal, or mycobacterial infections

Mechanism of Action Neomycin: Acts on bacterial protein synthesisPolymyxin B: Acts on bacterial cytoplasmic membraneHydrocortisone: Acts on inflammation through suppressing migration of polymorphonuclear leukocytes and capillary permeability changes

Indications Inflammatory conditions warranting a corticosteroid with suspected bacterial infection or risk of bacterial infection

Dosing Otic: 4 drops, 3 to 4 times per dayOcular: 1 or 2 drops, 2 to 4 times per day to start; more frequently if required for severe infectionDermatologic: Topical layer, up to 4 times per day.Pediatric otic >2 years: 3 drops, 3 to 4 times per dayPediatric otic <2 years is an unlabeled use with same dosingAll pediatric ocular and dermatologic uses are unlabeled but use same dosing as adult dose

Side Effects Adverse reactions are secondary to individual medications as well as route delivered. Examples include ototoxicity, corneal thinning, rash, anaphylaxis

Contraindications and Precautions

Hypersensitivity or contraindication to one componentSuspected viral, fungal, or mycobacterial infectionPrecautions: Avoid use of otic preparation in tympanic perforation; limit duration of use to less than 10 daysPregnancy: Category CLactation: Use caution, excretion unknown

Feature Editors: Michael S. Beeson, MD, MBA, FACEP; Steven Warrington, MD

volume 27 • number 10 in this issue · dialysis disequilibrium syndrome. 6. list the admission...

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