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Admission to Telemetry Beds, Thrombocytopenia, CO Poisoning

Waxman, Matthew MD

doi: 10.1097/01.EEM.0000360604.58053.57
Living with the LLSA


Author Credentials and Financial Disclosure:

Dr. Waxman is an Assistant Clinical Professor of Medicine at the David Geffen School of Medicine at the University of California at Los Angeles, and an emergency physician and hospitalist at UCLA-Olive View Medical Center.

Dr. Waxman has disclosed that he serves as an editorial consultant to Talecris, Inc. All other faculty and staff in a position to control the content of this CME activity have disclosed that they have no financial relationships with, or financial interests in, any commercial companies pertaining to this educational activity.

Learning Objectives: After reading this article, the physician should be able to:

  1. Summarize emergency department diagnoses that warrant inpatient telemetry monitoring upon hospital admission.
  2. Describe the medications that can cause drug-induced thrombocytopenia.
  3. Discuss key features in the clinical presentation, diagnosis, and management of carbon monoxide intoxication.

Release Date: September 2009

Article from the 2009 Reading List

When Do Patients Need Admission to a Telemetry Bed?

Chen EH, Hollander JE

J Emerg Med


The authors weighed the evidence on many common ED diagnoses for the need for telemetry monitoring on hospital admission. With limited inpatient telemetry bed availability, inappropriate use of these beds can affect ED flow and contribute to ED boarding and crowding. Although the American Heart Association provides comprehensive guidelines for electrocardiographic monitoring for inpatients, the authors focused on many noncardiac conditions, and examined them from the perspective of the emergency physician.

This review concludes that several clinical scenarios mandate cardiac monitoring when these conditions are the reason for admission: automatic implantable defibrillator has fired, second- or third-degree AV block, prolonged QT interval, acute coronary syndrome, acute heart failure, pulmonary edema, and acute cerebral vascular disease. Patients who receive massive blood transfusions, defined by the authors as greater than 10 units in 24 hours, also should be on telemetry because of the arrhythmia risk from citrate-inducing hypomagnesemia and hypocalcemia.

Patients with stable cardiac conditions being admitted for another reason, such as an AICD being admitted for cellulitis, need not necessarily be admitted to a telemetry bed. Syncope patients with underlying cardiac disease or other risk factors such as older age, abnormal ECG, heart failure, or ventricular arrhythmia have a greater risk for arrhythmia-induced syncope, and also require telemetry monitoring. The evidence did not show that patients with a normal ECG on presentation and suspicion for a neurologic etiology of syncope (i.e., vasovagal syncope) benefit from a telemetry bed.

Patients with gastrointestinal hemorrhage after an endoscopy may benefit from a telemetry bed because the medications given during the procedure can cause arrhythmias. Hyperkalemic patients with a potassium level greater than 6.5 mmol/L or with an abnormal ECG on presentation should be admitted to a telemetry bed. Patients with hypokalemia, hypomagnesemia, or hypocalcemia require telemetry on admission only if they present with a prolonged QT interval or if they are taking digitalis.

There is no evidence, according to this review, to admit patients to telemetry for blood transfusion, low-risk chest pain evaluation, acute exacerbations of chronic obstructive pulmonary disease, or hemodynamically stable patients with pulmonary embolus. Receiving a few units of blood does not lead to increased risk of arrhythmias from citrate toxicity nor does telemetry detect nonhemolytic transfusion reactions. Recent studies have shown that patients admitted for risk stratification of chest pain are not likely to develop arrhythmias nor does cardiac monitoring help decide which stress modality is most appropriate. In a large study, patients with DVT and PE treated at home with low molecular weight heparin and no telemetry monitoring had a risk of death less than one percent. Patients with pulmonary embolus admitted for anticoagulation do not need a telemetry bed.

Article from the 2009 Reading List

Drug-Induced Immune Thrombocytopenia

Aster RH, Bougie DW

N Engl J Med


Drug-induced thrombocytopenia (DIT) is an uncommon cause of low platelets in inpatients and outpatients but an important clinical entity to identify. DIT is often misattributed to more common causes of low platelets such as coronary artery bypass grafting, sepsis, or chronic ethanol abuse. This review does not discuss heparin-induced thrombocytopenia because its major sequela is thrombosis, not thrombocytopenia.

Patients with DIT will typically have been taking the sensitizing drug for at least one week or longer before presenting with petechial hemorrhages or ecchymoses from thrombocytopenia. Platelet inhibitors such as abciximab are unique in that they can cause a rapid decrease in platelet counts within only a day or two of exposure. Nausea, malaise, chills, fever, and lightheadedness often precede the bleeding signs of thrombocytopenia. More severe bleeding manifestations such as mucosal hemorrhage from gums and gastrointestinal or urinary tract bleeding are seen with platelet counts less than 20,000. Rarely, patients with drug-induced thrombocytopenia may present with renal failure or disseminated intravascular coagulation indicating overlap with thrombotic thrombocytopenic purpura or hemolytic uremic syndrome.

This paper summarizes multiple drug categories and some representative drugs implicated in five or more reports of DIT. Notable examples of drugs mentioned in the article are included here. New biologic antibody therapies such as infliximab and rituximab have been associated with an acute, severe, self-limiting thrombocytopenia, and are widely used in treating cancer and rheumatologic diseases. The cardiac medication amrinone, the antiepileptic valproate, and the antibiotic linezolid can cause an indolent, chronic thrombocytopenia in up to 30 percent of patients on long-term therapy. Quinine was the first drug associated with DIT, and although rarely used now as an antimalarial, it is often prescribed for muscle cramps.

Other categories of drugs associated with DIT include histamine receptor antagonists (cimetidine, ranitidine), diuretic agents (hydrochlorothiazide), anticonvulsants (carbamazepine, phenytoin), analgesics (acetaminophen, naproxen, diclofenac), chemotherapeutic agents (fludarabine, oxaliplatin), and antimicrobials (rifampin, sulfonamides, vancomycin).

The mechanism of DIT caused by quinine, sulfonamides, and nonsteroidal anti-inflammatory drugs is a unique antibody that binds to platelets only in the presence of the sensitizing drug. The drug induces antibody production and targets platelets for destruction. Platelet inhibitors tirofiban and eptifibatide are used during angioplasty, and induce DIT by binding antibodies to a change in structural conformation of the glycoprotein IIb/IIIa molecule induced by these agents. Abciximab, also a platelet inhibitor used in angioplasty, causes DIT from a pre-existing antibody, and may cause acute thrombocytopenia on a second exposure to the drug. True autoantibodies induced by a drug without exposure to a sensitizing agent are rare, and this scenario is clinically similar to acute idiopathic thrombocytopenic purpura. Antirheumatic gold salts, procainamide, sulfa drugs, and interferon alpha may directly induce antibodies to platelets.

Drugs should be considered a cause of thrombocytopenia in all patients presenting to the ED with low platelets. A careful medication history including herbal supplements, over-the-counter medications, and recent sulfa or quinine use is key in recognizing DIT. With the exception of heparin, testing for antibodies specific to platelets is costly and not routinely available. If there is a strong suspicion of DIT, the offending medication should be stopped, and the medication regimen changed to compounds of the same class with a different chemical structure. In some cases, a diagnostic challenge has been performed with as little as 1 to 2 mg of the suspected drug causing DIT to see if a further drop in platelets occurs.

Patients with severe bleeding from mucosal, urinary, or gastrointestinal bleeding and low platelet counts should receive platelet transfusions to prevent life-threatening intracranial or pulmonary hemorrhage.

Article from the 2008 Reading List

Carbon Monoxide Poisoning

Kao LW, Nañagas KA

Emerg Med Clin N Am


Carbon monoxide (CO) is a colorless, odorless gas produced from the incomplete combustion of fossil fuels. CO poisoning is the most common toxicological cause of death in the United States with an estimated 5000 fatalities per year. Unintentional causes of death from CO poisoning include indoor heating systems, stoves, charcoal grills, camp stoves, and water heaters. Methylene chloride, found in paint remover and aerosols, is endogenously converted to CO.

CO binds to hemoglobin with an affinity 200 times greater than that of oxygen, and causes a leftward shift in the hemoglobin-oxygen dissociation curve. This binding leads to a relative anemia and tissue hypoxia. Other mechanisms for CO toxicity include direct toxicity at the cellular level, protein binding to other cytochromes, and nitric oxide-mediated cerebral vasodilatation.

The clinical effects of CO poisoning may be easily missed and often mimic nonspecific viral illnesses. Early symptoms include dizziness and benign headache. One-third of patients presenting with symptoms of CO poisoning are missed on initial presentation and discharged home to the CO source. Hypoxia secondary to CO toxicity can unmask underlying cardiovascular disease and present with myocardial infarction, angina, arrhythmias, and hypotension. At high CO levels, poisoning may manifest as seizures, coma, or an acute stroke. CO has a directly toxic effect on skeletal muscle, causing rhabdomyolysis and renal failure. The classic “cherry red” appearance of skin is rare, and not a reliable diagnostic sign.

Diagnosis of CO poisoning requires a high index of suspicion, especially in the winter months. It is important for the clinician to ask about cohabitants with the same symptoms and exposure to indoor heating and cooking appliances. Serum carboxyhemoglobin levels should be checked in patients with suspected CO poisoning. Nonsmokers should have a baseline carboxyhemoglobin level less than 3 percent, and smokers may have a level as high as 10 percent after smoking. Pulse oximetry may be falsely normal in patients with CO exposure because carboxyhemoglobin is difficult to distinguish from oxyhemoglobin by wavelength.

Initial treatment of suspected CO poisoning is 100% supplemental oxygen and supportive care. The indications for hyperbaric oxygen are controversial, but the authors of this review recommend therapy for loss of consciousness, abnormal psychometric testing, neurologic symptoms, cardiovascular dysfunction, metabolic acidosis, pregnancy with an elevated carboxyhemoglobin level, and persistent symptoms despite supplemental oxygen. Some experts recommend hyperbaric therapy in all patients with carboxyhemoglobin levels greater than 25 percent.

Luis M. Lovato, MD, an Associate Clinical Professor at the David Geffen School of Medicine at UCLA, the Director of Critical Care in the Department of Emergency Medicine at Olive View-UCLA Medical Center, and the Medical Editor, serves as the medical editor of this column.

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As part of its continuous certification program, the American Board of Emergency Medicine has developed the Lifelong Learning and Self-Assessment (LLSA) program to promote continuous education of diplomates. Each year, beginning in 2004, 16 to 20 articles are chosen based on the Emergency Medicine Model. A list of these articles can be found on the ABEM web site,

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