DANGEROUS DILEMMAS
Educational Objectives
| The goal of this program is to improve diagnosis and treatment of potentially deadly conditions and diseases encountered
in the emergency department. After hearing and assimilating this program, the clinician will be better able to:
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 | 1. Manage dialysis patients who present with chest pain, dyspnea, heart failure, and other cardiovascular complications.
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| 2. Address vascular access complications common among dialysis patients.
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| 3. Explain the potential causes of altered mental status and dysequilibrium among dialysis patients.
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| 4. Describe various treatment options for burns from chemical solvents such as hydrofluoric acid.
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| 5. Diagnose and treat Kawasaki disease, intussception, and elapid envenomation.
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Faculty Disclosure
In adherence to ACCME Standards for Commercial Support, Audio-Digest requires all faculty and members of the planning
committee to disclose relevant financial relationships within the past 12 months that might create any personal conflicts of interest.
Any identified conflicts were resolved to ensure that this educational activity promotes quality in health care and not a
proprietary business or commercial interest. For this program, the faculty and planning committee reported nothing to disclose.
Acknowledgments
Dr. Lim was recorded at 37th Annual Scientific Assembly, held May 29-31, 2008, in San Diego, CA, and sponsored
by the American College of Emergency Physicians (ACEP), State Chapter of California, Inc. Dr. Schrading was recorded
at PA ACEP Scientific Assembly 2008, Advances, Controversies and Technology, held April 6ץ, 2008, in
Harrisburg, PA, and sponsored by ACEP and the Pennsylvania Chapter of ACEP. The Audio-Digest Foundation
thanks the speakers and the sponsors for their cooperation in the production of this program.
| DIALYSIS DILEMMAS —Ingrid Lim, MD, Staff Physician, Permanente Medical Group, Department of Emergency Medicine,
San Francisco Kaiser Medical Center, San Francisco, CA
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| Chest pain: investigate cardiovascular, pulmonary, musculoskeletal, and gastrointestinal (GI) causes first; in dialysis
patients—renal osteodystrophy weakens bones, making rib fractures more likely; consider anaphylactoid reaction in
patients taking angiotensin-converting enzyme (ACE) inhibitors who develop chest pain during dialysis; tunneled
catheter malposition causes chest pain as dialysis begins
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| Acute coronary syndrome (ACS): 50% of all end-stage renal disease (ESRD) deaths due to ischemia; 25% to 40% of dialysis
patients have left ventricular dysfunction at baseline; many have concomitant risk factors for coronary artery disease
(CAD); both CAD and silent ischemia more common among dialysis patients, and they become ischemic at lesser degrees
of coronary artery occlusion; chest pain during dialysis most likely ischemic; delay dialysis for 24 hr in patients
with suspected ACS or unstable angina
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| Troponin elevation: among asymptomatic ESRD patients, baseline higher for cardiac troponin T (cTnT) than for cardiac
troponin I (cTnI; (20% vs 0.4%); creatine kinase MB (CK-MB)—baseline affected by renal function; normal CK-
MB fraction <5 ng/mL; in 30% to 50% of asymptomatic ESRD patients, baseline elevated but usually <8 ng/mL; values
of 20 or 30 ng/mL pathologic
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| Interventions: same as for non-ESRD patients; in addition to CAD, pay special attention to correctable factors, such as
anemia, volume overload, and hypertension
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| Pericarditis: 2 types specific to renal patients
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| Uremic pericarditis: occurs in 6% to 10% of patients with advanced renal failure; usually occurs before or shortly after
initial dialysis; correlates with serum urea nitrogen (BUN) >60 mg/dL; typical pericarditis changes often absent; if
electrocardiography (ECG) reveals typical pericarditis changes, investigate possibility of infectious or other pericardial
etiology
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| Dialysis-associated pericarditis (DAP): occurs in 13% of patients already on dialysis; usually due to insufficient dialysis
or increased catabolic states, eg, sepsis
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| Treatment: initiate or intensify dialysis; most patients respond in 7 to 14 days, ie, chest pain resolves and effusion decreases;
if no improvement, drain required
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| Pericardial effusions: accompany pericarditis in 50% of renal patients; complicated, sometimes bloody; 20% risk for
progression to tamponade; diagnosis—compare current to previous chest radiographs; ultrasonography (US) useful
and easy; effusion chronic in 30% of dialysis patients; distinguishing effusion from tamponade—along with chest
pain, fluid, and hypotension, look for right ventricle (RV) collapse
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| Air embolism: symptoms vary; syncope or seizures if embolism occurs while seated; dyspnea and chest pain if while recumbent;
examination—“mill-wheel” murmur classic sign; “snowstorm” appearance on US (due to air bubbles)
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| Treatment: clamp line closed; position patient in left lateral decubitus position in Trendelenburg to isolate air in apex of RV;
administer 100% oxygen; air may be aspirated from RV if central line in place; perform chest compressions if cardiac arrest
occurs to help break up air lock blocking RV outflow
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| Dyspnea: usually due to volume overload; infection, inflammatory origins, or air embolism also possible; examination
may not reveal signs of volume overload or congestive heart failure (CHF); chest radiograph may appear normal; detect
volume overload by comparing patient’s known “dry weight” with current weight
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| Congestive heart failure: 10 to 30 times higher prevalence among renal patients; CHF plus ESRD independent predictor
for mortality (83% in 3 yr)
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| Brain natriuretic peptide (BNP): not correlative with volume status; BNP >500 pg/mL in dialysis patients may indicate
CHF
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| Aminoterminal pro-BNP (NT-proBNP): NT-proBNP >1200 pg/mL in dialysis patients may indicate CHF; some studies
lower cutoff to NT-proBNP >500 pg/mL; nonelevated levels of either BNP can help rule out CHF
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| Management of CHF: hemodialysis fastest method; diuretics, eg, furosemide, effective even in anuric patients; nesiritide
also useful; phlebotomy—balance potential usefulness against risk of increasing patient’s anemia; can return autotransfused
blood to patient during dialysis; sorbitol-induced diarrhea—advocated by some clinicians
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| High-output cardiac failure: high-volume fistulas (20%-30% of cardiac output per minute) increase blood flow and workload
on heart; subsequent cardiac remodeling, or ventricular enlargement, can result in CHF; distinguishing from
other CHF—warm extremities, wide pulse pressure (bounding pulses), hyperkinetic heart, or systolic flow murmur;
Branham sign—drop in heart rate after temporary occlusion of access; treatment—surgical banding to reduce flow
through access; sometimes access removed entirely
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| Altered mental status: characterized by weakness, confusion, and drowsiness; etiology—uremia; drug effects, dysequilibrium
syndrome, and dialysis dementia; increased risk in dialysis patients for—stroke, cerebral hemorrhage,
and subarachnoid bleeding; have low threshold for ordering computed tomography (CT); treatment—add intravenous
(IV) desmopressin (DDAVP) to other options for cerebral hemorrhage and subarachnoid bleeding
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| Dysequilibrium syndrome: symptoms occur during or within 12 hr of dialysis; severe headache and vision changes reported;
severe symptoms include seizures, coma, and death; cause may be cerebral edema brought on by osmotic
shifts; occurs most frequently in patients new to dialysis or those with high BUN brought down too rapidly
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| Treatment: usually self-limiting; provide supportive care; can use mannitol or hypertonic saline in patients with seizures
and in more severe cases; usual antiseizure drugs not removed by dialysis, so no need to supplement them if
administered
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| Dialysis dementia: usually appears in patients after 2 yr of dialysis; thought to be due to aluminum accumulation; symptoms
include cognitive dysfunction, memory loss, myoclonic jerks, and seizures; deferoxamine binds aluminum and
improves symptoms
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| Uremic encephalopathy: diagnosis of exclusion; malaise, confusion, and memory loss improve with dialysis; objective
findings available through electroencephalography (EEG) and magnetic resonance imaging (MRI); allow nephrologists
to make diagnosis
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| Hyperkalemia: uncommon in well-dialyzed patients; usually due to dietary indiscretion or missed dialysis; dialysis patients
can often tolerate elevated potassium levels, but such levels remain potentially life-threatening
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| ECG changes: renal patients may not show changes characteristic of hyperkalemia; do not assume absence of hyperkalemia
if ECG normal
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| Treatments: calcium gluconate and calcium chloride—to stabilize cardiac membrane; do not administer to patients on
digoxin until digoxin level determined; chloride can irritate peripheral veins; sodium bicarbonate—administer only
to acidotic patients; insulin—use regular insulin; glucose—administer only to euglycemic patients; sodium polystyrene
sulfonate (Kayexalate)—nephrologists recommend administering 10 g for every 0.1 mEq/L over normal level
of 5.5 mEq/L for maximum of 100 g; alternatively, administer as retention enema; dialysis—fastest way to lower potassium
level; can remove 40 mEq in first hour; nebulized albuterol—give 4 to 8 times normal dose (10 mg) to renal
patients; combining insulin and nebulized albuterol decreases potassium levels faster than either treatment alone; protects
from insulin-induced hypoglycemia
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| Complications of vascular access: arteriovenous (AV) fistula—access of choice; anastomosis joins native artery to
native vein; least prone to complications; synthetic grafts—looped or diagonal conduit between artery and vein; more
prone to complications than fistulas; tunneled catheters—ideal for emergent dialysis until more permanent access
achieved; less prone to infection, but more prone to other complications; can cause central venous stenosis
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| Examination: document presence of thrill or bruit; thrill—palpation by hand may prove difficult with older calcified fistulas;
use stethoscope to listen for bruit; should hear low pitched sound during systole and diastole; high-pitched or discontinuous
sound signifies stenosis; use bedside Doppler if bruit still not audible; blood pressure cuffs—do not place
on access arm; may induce thrombosis; blood draws—allowable on access arm; tourniquet allowable if distal to access
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| Emergency access: place 1 to 2 cm below anastomosis; avoid central lines due to risk for stenosis; if imperative, use groin
area; avoid subclavian lines; avoid sites where compression to stop bleeding may prove difficult
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| Thrombosis: absence of thrill or bruit indicates obstructive clot; stenosis (narrowing of lumen) most common cause; most
likely to occur in grafts; not true emergency
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| Treatment: consult nephrologist; removal by local intra-arterial thrombolysis with tissue plasminogen activator (TPA);
or mechanical thrombectomy with Trerotola device; do not flush fistula; may rupture vessel or cause venous embolism
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| Infection: manage access infections aggressively; at minimum, administer vancomycin to cover methicillin-resistant Staphylococcus
aureus (MRSA); provide coverage for other staphylococci and gram-negative bacteria; ensure reliable
follow-up to initial IV antibiotic dose; treat source if known; if not known, presume line and treat with antibiotics; septic
patients—hospitalize and remove infected portion of catheter or access; fistula infections usually treated with IV antibiotics
alone; respiratory infections—cough or fever absent in some renal patients with pneumonia, who may exhibit
only dyspnea or malaise; urinary tract infections—may develop even in anuric patients (symptom suprapubic tenderness)
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| Bleeding: potential causes include heparin use, thrombocytopenia, nonadhering platelets, or malfunction of graft; aneurysms
may develop at repeated puncture sites; treatment—apply firm but gentle pressure for 10 to 15 min to avoid
causing thrombosis; if ineffective, use topical Gelfoam with soaked-in reconstituted thrombin powder; if necessary, consider
one-time dose of IV DDAVP, or FFP; extreme bleeding may require tourniquet and vascular consultation; once
bleeding ceases, observe in emergency department for 1 to 2 hr for early thrombosis or other complications
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| DON’T SEND THIS HOME: DEADLY DISCHARGED CASES —Walter A. Schrading, MD, Assistant Clinical Professor
of Emergency Medicine, PA, State University Medical College, University Park, PA, and Attending Physician, Department
of Emergency Medicine, York Hospital, York, PA
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| Hydrofluoric acid exposure: hands usual site of exposure; symptoms possibly delayed by 1 to 8 hr after exposure to
diluted (20%-50%) solutions found in household products; presentation—severe burning pain, erythema, and blistering;
can eventually resemble third-degree burn; systemic symptoms may include hypocalcemia, with nausea, vomiting,
and abdominal pain; severe cases with wider skin exposure may result in hypotension and death; diagnosis—ECG to
reveal any QT prolongation associated with hypocalcemia; electrolyte studies, especially calcium and magnesium
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| Treatment: for limited exposures, use topical calcium gluconate solution; for burns to fingertips, mix 10% calcium gluconate
gel and apply to inside of glove; if not on fingers, infiltrate area with 5% calcium gluconate subcutaneously; for extensive
involvement of hand, intra-arterial injection of calcium gluconate, mixing 10 mL of 10% calcium gluconate into 40 mL of
dextrose in water (D5W), injected slowly into radial artery; hospitalize patients with burns 50 to 100 cm2 or larger
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| Kawasaki disease: autoimmune vasculitis; inflammatory disease of medium-sized vessels; leading cause of acquired heart
disease in children ≤5 yr of age; highest incidence in children 18 to 24 mo of age; 95% of cases in children ≤10 yr of age;
20% to 25% of untreated patients develop cardiovascular sequelae, including coronary artery aneurysms; <10% of patients
develop aneurysms if treated ≤10 days after onset
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| Clinical diagnosis: hinges on fever of 5 days’ duration; must have 4 of following signs—bilateral conjunctivitis; oral
mucous membrane changes, especially cracked fissured lips, or inflamed tongue (strawberry tongue); peripheral extremity
changes, including erythema of palms and soles, edema, or desquamation; polymorphous scarlatiniform, maculopapular
rash; cervical lymph node involvement; other signs—include elevated erythrocyte sedimentation rate,
leukocytosis, and elevated liver function tests (LFTs)
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| Treatment: hospital admission; pediatric consultation; aspirin q6h; IV immune globulin (IVIG) at 2 g/kg q2h
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| Coral snake bite: 10% fatality rate without antivenom; early clues to envenomation rare; paucity of local tissue injury,
although may have painful paresthesias; potent neurotoxin causes neuromuscular dysfunction; symptoms possibly delayed
for 10 to 12 hr; toxin leads to bulbar dysfunctions that can end in respiratory failure; other symptoms include
pharyngospasm hypersalivation, generalized weakness, hypotension, tachycardia, and cardiovascular collapse
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| Treatment: admit to hospital; provide local wound care and tetanus injection; definitive identification of coral snake, or
any neurologic symptoms, requires elapid antivenom; skin test (first with 0.02 mL, followed by 4 to 6 vials IV); may
wish to pretreat with diphenhydramine (Benadryl) and methylprednisolone (Solu-Medrol); admit to intensive care unit
if concerned about respiratory failure; observe for symptoms for 24 to 48 hr
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| Intussusception: usually occurs between 3 mo and 5 yr of age; 60% present in first year of life; difficult diagnosis to
make early; characteristic sign of “red-currant jelly” stool not apparent until after condition has worsened; barium enema
both diagnostic and therapeutic; US can reveal telescoping of one section of bowel into another
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| Presentation: classic triad of vomiting, intermittent colic, and bloody or mucus-mixed stool present in only 20% to 40%;
patients frequently draw knees to chest, but otherwise healthy; some lethargy; pallor common; occasional pain on palpation
of abdomen; possible fever in long-standing cases; laboratory findings usually normal
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| Treatment: pediatric surgeon often present during barium enema in event of perforation or other emergency; admit to surgical
service, even if intussusception reduced on barium enema; surgery if necessary
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Suggested Reading
Agarwal R et al: Elapid snakebite as a cause of severe hypertension. J Emerg Med 30:319, 2006; Basile C et al: The
relationship between the flow of arteriovenous fistula and cardiac output in haemodialysis patients. Nephrol Dial Transplant
23:282, 2008; Blanch AJ et al: Pediatric intussusception: epidemiology and outcome. Emerg Med Australas
19:45, 2007; Cavanaugh KL et al: Accuracy of patients’ reports of comorbid disease and their association with mortality
in ESRD. Am J Kidney Dis 52:118, 2008; Chandra A et al: BNP-mediated vasodilation for dialysis-dependent patient
with acute heart failure syndrome in the emergency department. Ren Fail 30:45, 2008; Chang CH et al:
Leukoencephalopathy associated with dialysis disequilibrium syndrome. Ren Fail 29:631, 2007; Dalamaga M et al:
Hypocalcemia, hypomagnesemia, and hypokalemia following hydrofluoric acid chemical injury. J Burn Care Res 29:541,
2008; David S et al: Diagnostic value of N-terminal pro-B-type natriuretic peptide (NT-pro-BNP) for left ventricular
dysfunction in patients with chronic kidney disease stage 5 on haemodialysis. Nephrol Dial Transplan 23:1370, 2008;
Freeman AF, Shulman ST: Kawasaki disease: summary of the American Heart Association guidelines. Am Fam
Physician 74:1141, 2006; Isbister GK, Currie BJ: Suspected snakebite: one year prospective study of emergency department
presentations. Emerg Med (Fremantle) 15:160, 2003; Kaiser AD et al: Current success in the treatment of intussusception
in children. Surgery 142:469, 2007; Liang KV et al: Acute decompensated heart failure and the
cardiorenal syndrome. Crit Care Med 36 (1 Suppl):S75, 2008; Lubich C, Krenzelok EP: Exotic snakes are not always
found in exotic places: how poison centres can assist emergency departments. Emerg Med J 24:796, 2007; Pinna
GS et al: Kawasaki disease: an overview. Curr Opin Infect Dis 21:263, 2008; Schnautz LS, Leggett P: Kawasaki
disease: a ride for little girls too! Crit Care Nurs Clin North Am 20:265, 2008; Sommerer C et al: Cardiac biomarkers
are influenced by dialysis characteristics. Clin Nephrol 68:392, 2007; Thomas D et al: Intra-arterial calcium gluconate
treatment after hydrofluoric acid burn of the hand [published online ahead of print May 28, 2008]. Cardiovasc Intervent
Radiol. doi:10.1007/s00270-008-9361-1; Venkat A et al: Care of the end-stage renal disease patient on dialysis in the
ED. Am J Emerg Med 24:847, 2006.
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