Myths in Emergency Medicine
July 10, 2005
Authors: Lisa Freeman Grossheim, MD, FACEP, Assistant Professor, Emergency Medicine, University of Texas Medical School at Houston; Ranessa Crawford, MD, Department of Emergency Medicine, University of Texas Medical School at Houston.
Peer Reviewers: Sandra Schneider, MD, FACEP, Professor and Chair, Department of Emergency Medicine, University of Rochester, NY; and J. Stephen Stapczynski, MD, FACEP, Chair, Emergency Medicine Department, Maricopa Medical Center, Phoenix, AZ.
What is a medical myth? It can be defined as something that we are taught that is just plain wrong. There are many ways that these myths develop. Dr. Robert Flaherty sums it quite well with several theories. The Plausible Theory model dictates that if it makes physiologic sense, then it must be true. The Lazy I model is based upon the premise that it ought to work, and it sure is easy. The Dogma model states that if the experts say so, then it must be true. The Bad Research model is based upon poor early research that suggested the myth, or initial research to refute the myth was poorly done. And last, but not least, the Bad Researcher model describes things such as researchers’ enthusiasm for a positive result, the tendency to overestimate the benefits and underestimate the risks of a therapy, or the subconscious tendency for reviewers and editorial committees to ‘back a winner’.1
Physicians tend to assume that just because something was shown by a research study and published in a journal, it is correct and can be used in practice.2 Evidence-based medicine, as defined in the 1990s when the term was coined is the “conscientious, explicit and judicious use of current best evidence in making decisions about the care of individual patients. The practice of evidence-based medicine means integrating individual clinical experience with the best available external clinical evidence from systematic research.”3 One of the greatest achievements of evidence-based medicine is the development of meta-analyses and systematic reviews, which summarize the best available evidence on a topic.2
This article will review and dispute some commonly held beliefs about dogma in the practice of emergency medicine.— The Editor
Fact or fiction? Droperidol is unsafe to use in the emergency department (ED).
Droperidol (Inapsine) is a high-potency, rapid-acting butyrophenone similar to haldoperidol that has been used widely in the United States since its approval by the Food and Drug Administration (FDA) in 1970. It is an antagonist of dopamine2 receptors in the limbic system. It also produces a mild alpha-adrenergic blockade with resultant peripheral vascular dilatation.4
The maximum recommended initial dose is 2.5 mg intramuscular (IM) or slow intravenous (IV) bolus. Droperidol has FDA approval for the prevention of post-operative nausea and vomiting. However, it also was used widely for off-label indications (e.g., rapid tranquilization of the violent or psychotic patient and treatment of acute migraine headache).4 Many physicians in the emergency medicine and anesthesiology communities who have used droperidol for years believed the action taken by the FDA was inappropriate because of its basis on limited and scientifically suspect data.5
On December 5, 2001, the FDA added a black box warning for droperidol that stated, “recent research has shown QT prolongation within minutes after injection of a dose of droperiodol at the upper end of the labeled dose range. Prolonged QT is dangerous because it can cause a potentially fatal heart arrythymia known as Torsades de pointes (TdP). In the last year, there have been reports of TdP within or below the currently labeled dose range, as well as reports of sudden death or other serious cardiac adverse events.”6
QT Prolongation. QT prolongation, whether familial or acquired, is considered to be a risk factor for the development of TdP and sudden death. Sudden death caused by TdP is uncommon and difficult to prove. There is no consensus regarding the precise degree of QT prolongation that is clinically significant, although most clinicians would consider a QTc interval of more than 500 msec or a change in QT interval of more than 60 msec to represent at least some risk.4 A consistent relationship between the length of the QT interval and the risk of torsades has not been established. The risk also varies from patient to patient.4
Drug-induced QT prolongation is related to blockade of potassium efflux from the myocardial cells. This syndrome has been reported with hundreds of medications, either alone (e.g., quinidine, procainamide, or thioridazine) or in combination (e.g., terfenadine and erythromycin). (See Table 1.)
Table 1. Risk Factors for Torsades de Pointes
High doses of droperidol have been shown to cause QT prolongation in healthy patients.7,8 Lischke and colleagues demonstrated that fact in doses ranging from 0.1 mg to 0.2 mg/kg. The increase in the QT interval was dose-related.8 Another study had similar results in both healthy patients and those with cardiovascular disease. The dose used was 0.25 mg/kg, which equals 17.5 mg in a 70-kg adult. No cases of Torsades occurred in any study patient.8 Smith and colleagues reported a similar incidence of QT prolongation in patients who received droperidol (3.1%) as in the general population (4%).7
The Evidence. A review of the Medwatch fatality reports related to droperidol revealed that 83% of the cases were received from countries outside the United States. Of these foreign cases, 49% were fatalities from droperidol at doses of 50 mg or greater, 20 times the accepted dose. Even acetaminophen becomes dangerous at 20 times the recommended dose.9 The FDA cited two studies in the justification for the black box warning; both are European studies that involved doses much larger than those used in the United States.10
In a review of 120 cases describing adverse cardiac or respiratory events associated with droperidol, 19 involved doses less than 10 mg. Of those 19 cases, all had at least one confounding issue that made it difficult to attribute the adverse event to droperidol alone.6
Manufacturer Issues. The behavior of a major manufacturer of droperidol, Janssen-Cilag, has been cause for concern and played a role in the FDA initiating an investigation into droperidol. In March 2001, Janssen-Cilag stopped selling droperidol in Europe as an antipsychotic agent. Three months later, the company reported a large backlog of old adverse events to the FDA, including the reporting of eight deaths on one day. FDA regulations require drug companies to report adverse events within 15 days of becoming aware of them.11 The warning was intended to apply only to the oral preparation, but the company eventually decided to withdraw all formulations. The decision may have been based partially on economic projections for decreasing use of droperidol.4,12,13 Jansen currently markets risperdal (Risperdone), which is one of the most frequently prescribed antipsychotic agents in the United States.9 The largest U.S. supplier of droperidol, Akron Pharmaceuticals, sold 5 million vials of Inapsine in the year before the black box warning.11 The frequency at which this drug has been administered almost guarantees that some association with adverse events will occur.5
Clinicians have varying degrees of experience with droperidol as well as a widely variable tolerance for risk. The use of droperidol is a decision of the risks versus benefits and depends upon the individual clinical circumstance. If a clinician wants to continue to use droperidol, it is prudent to avoid using it in patients who are at risk for prolonged QTc as discussed previously. Unfortunately, strict avoidance of the risk factors would exclude many of the patients in whom droperidol might be useful.4 Alternatives to droperidol exist. Older, less expensive alternatives for nausea can be used (e.g., promethiazine [Phenergan] or prochloroperazine [Compazine]). A more expensive alternative is ondansetron (Zofran), which costs approximately $140 per IV dose. An alternative for rapid tranquilization is ziprasidone (Geodon), an agent unrelated to droperidol or the butyrophenones. However, Geodon costs almost $500 per 20-mg IM injection, compared with droperidol, which costs fewer than $20 per 2.5-mg dose.14 Geodon should be used with caution for treatment of behavioral disorders in the elderly; it has been associated with a slightly increased risk of death in elderly patients with dementia.15
Coincidentally, in March 2001, GlaxoSmithKline (GSK) cited a shortage of raw materials as the cause of a shortage of another widely used drug, Compazine. Following that development, supplies of other antiemetics, such as metoclopramide (Reglan) and Phenergan have been more limited, while GSK continues to produce the much more expensive drug Zofran without difficulty.11,16
FACT: Droperidol has a long record of safe use, but with the black box warning issued by the FDA, physicians are unlikely to take the medicolegal risk by using the drug.
Fact or Fiction? Cephalosporins cannot be used safely in penicillin-allergic patients.
How often are patients who claim to be allergic to penicillin truly allergic? Is it okay to use a cephalosporin in a patient who reports being allergic to penicillin? Penicillin allergy frequently is reported to the physician because the patient was told when he or she was a child that they are allergic to it. Rashes, wheezing, or even arthralgias may be attributed erroneously to an allergy to penicillin when they were actually a manifestation of the disease for which penicillin was prescribed. Since its introduction in the 1940s, penicillin has been associated with allergic reactions, including those that have been fatal. Early studies reported that one-fourth to one-third of deaths from anaphylaxis to penicillin administration occurred in patients with a history of a penicillin allergy.17-19 However, the data in those retrospective studies are incomplete. Because of the concern for potential anaphylaxis, a physician may avoid the use of penicillin and other beta-lactam antibiotics in a patient in whom a beta lactam might be the drug of choice.17
Cross-reactivity between the two families of antibiotics was feared when the first cephalosporins were created because of the similarities in their structure to penicillin, which is a shared beta-lactam ring.20 Clinical studies addressing this issue are far from conclusive. Issues concerning the reliability of a history of penicillin allergy, as well as the significance of skin testing and levels of antibodies to antibiotics, make interpreting the results somewhat difficult.20
Penicillin Allergy. Oral penicillins and cephalosporins often are avoided unnecessarily when they may be the most appropriate treatment for an outpatient infection. Diseases in which a penicillin or cephalosporin is the firstline drug include pharyngitis, otitis media, sinusitis, and cellulitis. The subsequent use of a broader spectrum agent from a different class often adds to the cost of therapy and the worsening of bacterial resistance.21 Of those patients with a history of penicillin allergy who are skin tested for penicillin allergy, 40-90% have negative immediate skin tests.22 Recent experience data suggest that less than 10% of patients with a history of penicillin allergy have a positive skin test.23 Additionally, penicillin allergy decays over time.21 The greatest fear of giving penicillin to a potentially allergic patient is the development of anaphylaxis. Some patients are extremely sensitive to penicillin; systemic reactions and death can occur with very small amounts of penicillin in these rare patients.17 However, most antibiotic-related anaphylaxis occurs with parenteral exposures. Anaphylaxis from oral antibiotics is rare.24-26
Cephalosporin Cross-Reactivity. The incidence of allergic reactions to cephalosporins in penicillin-allergic (by history) patients has been reported to vary from 8-15%.17,27,22,28 The incidence of allergic reactions to cephalosporins in nonpenicillin-allergic patients is approximately 2%.22,28 Most of these reactions are skin manifestations. Anaphylaxis due to cephalosporin exposure is very rare — 0.4% in penicillin-allergic patients and 0.02% in nonpenicillin allergic patients.20 In a study by Goodman and colleagues, 2431 orthopedic patients received a parenteral intra-operative cephalosporin. In a record review, there was only one case of an allergic reaction noted, and it was a rash in a nonpenicillin-allergic (by history) patient.20 Cephalosporins vary considerably in their cross-reactivity with penicillin. For example, cephalexin does not cross-react at all with the penicillin nucleus.20 The first-generation cephalosporins have more chance of cross-reactivity with penicillin than do the advanced generation (third or fourth) cephalosporins, as the advanced generation cephalo-sporins’ structure is less like penicillin. The cross-reactivity between penicillins and second- or third-generation cephalo-sporins is probably no higher than the cross-reactivity between cepahlosporins and other classes of antibiotics.29 The results of penicillin skin-testing do not predict cephalosporin allergy, which again suggests that there is limited cross-reactivity between the antibiotic classes.29 The most common adverse reactions to cephalosporins include skin eruptions (e.g., maculopapular or morbilliform) and drug fever.30 Urticaria also is seen. Overall, skin manifestations are seen in 1-3% of patients.31
Assessing Risk. Patients with a history allergy to penicillin have a three-fold greater risk of a subsequent reaction to any medication, not only cephalosporins.32 If a physician is contemplating giving a cephalosporin to a patient with a penicillin allergy, the nature of the allergy should be obtained. If there is a history of severe penicillin sensitivity, a cephalosporin should not be used. The practice parameter published jointly by the American College of Allergy, Asthma and Immunology, the American Academy of Allergy, Asthma and Immunology, and the Joint Council of Allergy, Asthma and Immunology states, “Only 15% of patients with a history of an allergy to penicillin will have a positive skin test, and, of those, 98% will tolerate a cephalo-sporin. However, those patients who react (less than 1%) may have fatal anaphylaxis.”33 In patients without a history of severe penicillin sensitivity who require a cephalosporin, a small test dose, either oral or parenteral, is reasonable.
FACT: Many patients who report a history of penicillin allergy are not truly allergic and cephalosporins can be used safely in the vast majority of patients who report a penicillin allergy.
Fact or Fiction? Acute appendicitis in pregnant women presents as right upper quadrant pain.
Appendicitis is the most frequently encountered extrauterine disease requiring surgical treatment during pregnancy.34 The proven incidence of acute appendicitis is similar in pregnant and nonpregnant women. There is an urgency in making the diagnosis of appendicitis because it is a potentially life-threatening process for the mother and may also affect the fetus with preterm labor and delivery.35 The alterations of anatomy and physiology in the pregnant woman make the diagnostic criteria of appendicitis difficult to apply. Signs and symptoms common to both normal pregnancy and appendicitis include anorexia, nausea and vomiting, mild to moderate leukocytosis, and pain.35
Obstetrics teaching for nearly 70 years has been that the pain of appendicitis migrates upward with the growing uterus; thus, pain in the right upper quadrant of the abdomen would be expected in the third trimester.35 This concept was based on an 1932 article by Baer and colleagues,36 which described changes in appendiceal location as pregnancy progresses. Baer, using barium studies performed in 78 women, showed that the growing uterus pushes the appendix upward and with a counterclockwise rotation of the tip. Theoretically, this movement would change the location of perceived pain toward the right upper quadrant or right flank with advancing gestational age.
Attempts to validate Baer’s findings have been attempted unsuccessfully. In a prospective study, the location of the appendix was evaluated in three groups: group A, 165 women between 37 and 40 weeks of pregnancy who underwent elective cesarean delivery; group B, 26 women between 19 and 39 weeks of gestation with acute appendicitis who underwent appendectomy; and group C (the control group), 100 non-pregnant women with acute appendicitis who underwent appendectomy. Appendix location was considered normal within 2 cm of the McBurney point (i.e., one-third of the distance from the anterior superior iliac spine to the umbilicus); otherwise, it was considered to be a position change. No significant differences in appendix location were found between pregnant women who had elective cesarean deliveries and pregnant women who had appendectomies secondary to acute appendicitis compared with the control group of non-pregnant women who had appendectomies.37
In a retrospective review, researchers looked at 66,993 deliveries during the 10-year study period; 67 of the women (0.1%) had a preoperative clinical diagnosis of appendicitis.35 Acute appendicitis was confirmed histologically in 45 (67%) of the 67 women, for a true incidence of 1 in 1493 women. This study was unable to corroborate the hypothesis of Baer’s study36 that suggested a right-upper-quadrant location for the pain of appendicitis in the third trimester. Rather, the data supported the concept that more than 80% of patients with acute appendicitis have pain in the right lower quadrant in all trimesters.35
As a result of the Baer study, many surgeons make their incision above McBurney’s point during the second and third trimester to enhance the probability of easily locating the appendix.38 A small retrospective surgical study was performed to ascertain the optimal incision for removal of the appendix during pregnancy. This limited study found that incisions made over McBurney’s point can effectively locate the appendix in all pregnant women with appendicitis.38
A high clinical suspicion is necessary to make the diagnosis, and because of overlap with normal pregnancy symptoms, a higher false-positive rate (30%) is not only acceptable, but necessary to avoid unacceptable delay, with the possibility of increased morbidity and mortality rates.38 The previous concept about the appendix being located in the right upper quadrant during pregnancy can cause inappropriate delay in making the correct diagnosis and lead to maternal and fetal death (2-43%).36,37 For evaluation of the real location of the appendix during pregnancy, larger studies would need to be conducted.37 Realizing that the Baer study cannot be reproduced owing to health hazards of x-ray exposure, a magnetic resonance imaging or ultrasonography study examining the position of the appendix in gravid patients would be a welcome addition to the literature.38
FACT: The presentation of acute appendicitis in most pregnant patients is the same as in other patients – right lower quadrant pain.
Fact or Fiction? Epinephrine is unsafe for use in digital anesthesia.
One of the strongest admonitions given to medical students and residents is not to inject local anesthetics with epinephrine into the digits. This prohibition is promulgated by essentially all surgical, hand, plastic, and dermatological texts.39 This belief has been taught based on the rationale that epinephrine causes vasoconstriction via alpha-receptors in the digital (i.e., end-type, terminal) arteries leading to ischemia and gangrene.40
Recent reviews of the literature by Denkler39 in 2001 and Krunic41 in 2004 evaluated all reported cases of digital necrosis after local anesthesia. Denkler’s review of the world’s literature from the past 120 years documented 48 cases of digital necrosis from local anesthetics. None of those cases involved the use of lidocaine (Xylocaine), and only 21 entailed the use of epinephrine. The majority occurred more than 50 years ago when epinephrine was diluted by hand.39 Krunic’s literature review revealed 50 cases of digital gangrene after local anesthesia; 21 of these cases involved the use of epinephrine, and the concentration was reported in only four. Careful analysis of these 21 reports failed to show that epinephrine by itself was the cause of the necrosis. Other factors also were present and included the use of older compounds (e.g., cocaine, eukain, and procaine), infiltration of excessive volumes producing increases of the extravascular pressure and resultant vessel occlusion, postoperative burns, infection, and inappropriate tourniquet application.41
There are data from recent randomized trials that support the safety of epinephrine in digital anesthesia. In 1998, Sylaidis and Logan did a prospective study on digital arterial perfusion after performing digital blocks with 2% lidocaine with 1:80,000 concentration of epinephrine.44 Although transient reduction in digital blood flow was recorded, finger perfusion was maintained without the development of digital ischemia or gangrene in any of 100 consecutive cases.41 In 2001, Wilhelmi and colleagues performed a prospective randomized double-blinded study to evaluate the role for epinephrine augmentation of digital block anesthesia by safely prolonging its duration of action and providing a temporary hemostatic effect.43 They compared 1% lidocaine with 1:200,000 epinephrine vs lidocaine alone in 31 and 29 patients, respectively. Digital blocks were performed using the dorsal approach with one patient (3.2%) requiring additional injections to maintain anesthesia in the epinephrine group vs five patients (17.2%) in the lidocaine-alone group. Hemostasis with a tourniquet was applied in 69% of cases in the lidocaine group vs only nine patients (29%) in the epinephrine group. No complications were reported in the epinephrine group, and the authors now routinely use lidocaine with epinephrine for digital blocks at their institution. They also reported an additional 121 cases treated in this fashion with no episodes of digital gangrene.43 In 2003, another study reported on 43 consecutive patients divided in two groups with 25 digital lacerations requiring suturing, nail removal, or drainage of a suppurative process in each group.44 A total of 50 digital blocks were performed in a consistent fashion with plain 2% lidocaine or 2% lidocaine mixed with 1:100,000 epinephrine. The procedures performed were simple suturing (72%), nail removal (14%), and drainage of a suppurative process (10%). Within 10 minutes after injection, only 48% of patients from the plain-lidocaine group had complete analgesia vs 84% in the lidocaine-with-epinephrine group. The plain-lidocaine group required one or two additional injections to obtain satisfactory anesthesia in 24% of patients compared with only 4% of individuals in the lidocaine-with-epinephrine group. Additional hemostasis was not necessary in the lidocaine-with-epinephrine group compared with 20% of patients in the plain-lidocaine group, who required the application of a tourniquet or other maneuver for bleeding control. The group of lidocaine-with-epinephrine patients experienced on average 25% less pain and durations of anesthesia lasting twice as long as patients in the plain-lidocaine group. During the follow-up period of 11 days, no incidents of finger ischemia or necrosis were detected in any of the patients in either group.44 In 2004, researchers reported having used digital blocks and infiltrative anesthesia lidocaine 2% with epinephrine 1:100,000 without complications in 73 cases (i.e., 46 fingers and 27 toes).41
However, reports of complications continue to appear. In Denkler’s 2001 review, 15 recent cases of digital ischemia resulting from anesthetics with epinephrine, epinephrine solutions, or EpiPen injections were reported.39 All were reversed, including those involving concentrated epinephrine (1:1000), if treated up to 13 hours after injury.39 In 2002, De Monaco and colleagues reported two cases of fingertip necrosis after plain lidocaine use.45 The first patient was a 31-year-old healthy male who underwent CO2 laser ablation of multiple warts on the right index finger and developed severe infection, swelling, and pain after the procedure. The necrosis actually occurred following surgical debridement, complicated by severe edema. The authors considered postoperative infection and carbonization produced by the continuous wave laser technique as the cause. The second case was a 61-year-old female with progressive panaritium (i.e., onychocryptosis) of the right middle finger who underwent surgical revision and drainage. The patient was then found to have scleroderma and Raynaud’s phenomenon with severe microvascular disease of the fingers.45
Recent literature concludes that the use of lidocaine with adequately diluted epinephrine (1:100,000 to 1:200,000) in digital blocks appears to be safe and has not been demonstrated to cause digital gangrene or systemic complications in properly selected patients. The advantages of epinephrine use include more rapid onset of analgesia, longer duration of postoperative pain control, reduced use of tourniquet and other maneuvers to control bleeding, lower systemic absorption, and a smaller amount of anesthetic required to achieve optimal pain control resulting in less risk of toxicity.41 All procedures inherently have potential complications and risk verses benefit must be weighed in each case.
FACT: Judicious use of epinephrine in digital anesthesia can prolong the length of anesthesia, decreases bleeding, and has not been shown to result in significant complications.
Fact or Fiction? Digital rectal exams are necessary on all patients presenting with trauma or abdominal pain.
Every year millions of patients present to EDs for the evaluation and treatment of blunt trauma.46 As part of this evaluation, many surgical and emergency medicine texts have stressed the importance of performing a digital rectal examination (DRE) in every trauma patient.47-50 The DRE is accepted widely as an essential component in the initial assessment of trauma. The American College of Surgeons Committee on Trauma course in Advanced Trauma Life Support (ATLS) teaches that the evaluating physician must “place tubes and fingers in every orifice” of the patient during the secondary survey evaluation.50 Even the informal vernacular of surgical residency education makes reference to this issue with the often-quoted adage that the digital rectal examination should be omitted only ‘when the patient has no rectum or the doctor has no fingers’ (source unknown). However, no data have been published that justify its routine use in all seriously injured patients.51 The DRE may assist in the detection of spinal cord injury, pelvic fractures, distal bowel injuries, or urethral disruptions.52
In 2001, Porter and Ursic conducted a prospective observational study of all (423) injured patients arriving at a Level II trauma center during a six-month period.51 The objective of this study was to determine what, if any, affect on subsequent treatment and management decisions the initial DRE had on injured patients arriving in the ED. A DRE was performed on all patients during the secondary survey phase of their initial evaluation shortly after arrival to the ED. The results of the rectal examination were noted for each patient, with particular attention placed on the presence or absence of gross blood, occult blood result, prostatic examination, rectal vault integrity, and rectal sphincter tone. In addition, the patient’s hemodynamic parameters while in the ED and the injuries that were sustained were noted, as was his final disposition. Overall, the rectal examination influenced therapeutic decision-making in five cases (1.2%). The DRE is unlikely to affect initial management when applied indiscriminately to all seriously injured patients during the secondary survey. Patients in whom the rectal examination may have a higher probability of influencing management are those with penetrating injuries in proximity to the lower gastrointestinal tract, questionable spinal cord damage, and severe pelvic fractures with potential urethral disruption, or open fractures in continuity with the rectal vault. The occult blood test results do not add useful information, and the test should be discontinued as part of the secondary survey of injured patients.52
Researchers in 2004 attempted to develop a clinical decision rule that would allow for safe deferral of DRE in blunt trauma patients in a retrospective case series that reviewed specific trauma evaluation forms for consecutive blunt trauma patients requiring trauma team activation.52 The authors reviewed the medical records of all adult blunt trauma patients meeting trauma team activation criteria during a 14-month period. The results of the DRE and six predictor variables—abnormal neurologic examination, abdominal tenderness, pelvic stability, blood at the urethral meatus, blood pressure less than 90 mm Hg, and age younger than 65 years—were recorded. Patients with abnormal DREs had their discharge summaries reviewed for specific criteria to determine if the abnormal DRE was a true- or false-positive examination. Of the 579 patients, 53 had abnormal DREs, 34 of which were true positives. Classification and regression tree (CART) analysis retained three predictors: abnormal neurologic examination, blood at the urethral meatus, and age older than 65 years, and accurately classified all patients with a true-positive abnormal DRE. The probability of a true-positive abnormal DRE in a patient with a normal neurologic examination, no blood at the urethral meatus, and age younger than 65 years was between 0% and 0.8%. Adult patients with blunt trauma and a normal neurologic examination, with no blood at the urethral meatus, and who are younger than 65 years have an exceedingly low likelihood of a true-positive abnormal DRE. If validated, patients who meet these three criteria may have the DRE safely deferred.
There is no doubt that every trauma patient requires a thorough evaluation, which should include an appropriate physical examination and all indicated tests and procedures. However, the DRE most likely should be applied selectively rather routinely in the traumatized patient.51 Porter and Ursic suggested four situations in which rectal examination should be performed: 1) penetrating trauma in proximity to the rectum, 2) pelvic fractures, 3) in anticipation of rapid-sequence intubation, and 4) when neurogenic shock from a spinal cord injury cannot be excluded entirely or confirmed by the general physical examination.51 The DRE is administered easily and quickly and is associated with virtually no complications. When applied to selected patient groups, a correctly performed and timely rectal examination can yield useful information that potentially may alter management and therapeutic decisions.51
DRE is considered by many to be an essential component in the evaluation of patients with abdominal pain, although multiple studies have reported that it rarely contributes to patient management.53 Routine DRE in children with abdominal pain has fallen slowly out of favor, but it still is preformed regularly in adults. In 2004, researchers carried out a prospective observational study to assess the significance of DRE in 100 consecutive adults with acute abdominal pain.53 In that study, routine DREs did not alter clinical diagnosis or initial management of any patient nor did it detect any unrelated pathology.
The largest study of the use of rectal examinations in patients with possible appendicitis was performed by Dixon and colleagues in 1991.54 Of 1204 patients ranging in age from 7 to 87 years with a chief complaint of right lower quadrant pain, 85% (1024/1204) underwent a rectal examination. The treating physicians were asked to render their diagnosis and disposition plan after taking a history and conducting a physical examination, but before they did a rectal examination. The same physicians were asked to give their diagnosis and disposition after the rectal examination. The rectal examination made no difference in the management plan for any of the patients. The data suggested that physical signs—most importantly abdominal rigidity— were better predictors of appendicitis. The finding of right-sided rectal tenderness was ultimately neither sensitive nor specific for the disease. The authors concluded that a rectal examination is not necessary in patients with right lower-quadrant abdominal pain and physical signs.54
The results of the studies just described suggest that routine DRE is of limited usefulness in patients presenting with abdominal pain. The rectal examination may be deemed necessary when alternative diagnoses are likely. Then, the examination should be used judiciously to rule out specific conditions, including gastrointestinal bleeding, prostatitis, a mass, or perirectal abscess.55
FACT: Digital rectal exams do not add useful information to the clinical presentation of most patients with trauma or abdominal pain.
Fact or Fiction? Lying flat after a lumbar puncture and drinking plenty of fluids can prevent post-lumbar puncture headaches.
Since its introduction more than100 years ago,56 lumbar puncture (LP) has become routine practice for physicians of many medical specialties. Headache is a common sequela of LP, and much research has dealt with possible ways to reduce or prevent the occurrence of post-dural puncture headaches. Puncture of the dura has the potential to allow the development of excessive leakage of cerebrospinal fluid (CSF). Excess loss of CSF leads to intracranial hypotension and a demonstrable reduction in CSF volume.57 Although the loss of CSF and lowering of CSF pressure is not disputed, the actual mechanism producing the headache is unclear. There are two possible explanations. First, the lowering of CSF pressure causes traction on the intracranial structures in the upright position. These structures are pain sensitive, leading to the characteristic headache. Secondly, the loss of CSF produces a compensatory venodilatation vis-à-vis the Monro–Kellie doctrine.57 The Monro–Kellie doctrine, or hypothesis, states that the sum of volumes of the brain, CSF, and intracranial blood is constant. The consequence of a decrease in CSF volume is a compensatory increase in blood volume. Therefore, venodilatation is responsible for the headache.57
There is a large variability in reported frequencies of post-lumbar puncture headache (PLPHA) that should be considered from the outset. A recent review reports the average frequency of PLPHA occurring in patients after diagnostic LP to be 32%.58 PLPHA has been defined in different ways. Definitions range from any headache after LP to HA after LP with definite characteristics—in particular, a constant headache appearing or worsening significantly upon assuming the upright position and resolving or improving significantly upon lying down.58 PLPHA usually occurs within 48 hours of the procedure and resolves spontaneously within a few days, but it can last for a week or more.59
Because the occurrence of PLPHA using any definition is believed to be in the 20-30% range,58 much research has gone into mechanisms by which the incidence of PLPHA can be reduced. Spinal needles have undergone numerous modifications in recent years, the aim being to reduce the incidence of dural puncture headache. The principal factor responsible for the development of a dural puncture headache is the size of the dural perforation. Other factors (e.g., the shape of the dural perforation and the orientation of the spinal needle) have a less significant role.60 Convincing evidence indicates that smaller needle size is associated with lesser risk of heacache.60 For diagnostic LP, use of needles with a diameter smaller than the 20-gauge size may not be practical unless only a small volume of fluid is needed; the time for transducing the opening pressure may be too long, and the flow rate too slow.61 The issue of needle bevel orientation still remains unsolved. A recent review article claims there is enough evidence to support the perpendicular needle bevel orientation,60 while another review article cites five studies demonstrating the benefits of inserting the bevel parallel to the dural fibers.58 Numerous needle designs have been introduced since LP became a routine procedure; however, the Quincke type is the standard needle with a medium cutting bevel and the orifice at the needle tip. The pencil point, noncutting, or atraumatic needles (e.g., the Whitacre or Sprotte) have a duller tip and an oval opening just proximal to the tip. Although atraumatic needles commonly are used by anesthesiologists, most neurologists have never heard of these needles, and only 2% use them.62 In summary, there is convincing evidence in the anesthesia literature that PLPHA is reduced by using noncutting (atraumatic) needles. The data are conflicting in the diagnostic LP literature, but the studies generally have been inadequate to assess the question.60
Another technical issue to consider is the replacement of the needle stylet. In a study, replacement of the stylet before withdrawing the needle resulted in less incidence of PLPHA when using a noncutting needle.63 The authors’ explanation was that a strand of arachnoid may enter the needle with the CSF and, when the needle is removed, the strand may be threaded back through the dural defect and produce prolonged CSF leakage. Whether reinserting the stylet following an LP with a cutting needle would reduce the incidence of PLPHA is not known.58
Other mechanisms (e.g., limiting the amount of CSF removed, bed rest, and increased hydration) for preventing PLPHA have been investigated. The amount of spinal fluid removed is not a risk factor for PLPHA.64 Multiple review articles have shown that bed rest has been of no benefit in preventing PLPHA.58-60 Bed rest still is advised by many physicians today; however, evidence shows no benefit for prevention of PLPHA by bed rest for up to 24 hours in the supine, prone, or head-down position.58 There is no evidence for the use of increased fluids in the prevention of PLPHA.58 Some physicians recommend fluid intake post-LP, although the single prospective study of this practice found that increased intake of oral fluids after the LP had no affect on the occurrence of PLPHA.65
There are many proposed treatments for PLPHA— ranging from the typical pain medications to intravenous caffeine and epidural blood patching to surgery for persistent CSF leaks— that are discussed in the literature. However, where prevention is the main concern, equipment modification continues and new developments must be used. Further revision of technical skills is necessary with changing equipment, and future research with more uniform randomized trials would add to the strength of current recommendations.
FACT: The measure to prevent post-lumbar puncture headaches that is supported by convincing evidence is using a smaller caliber needle.
Fact or Fiction? Patients taking oral contraceptives should be advised to use an additional form of birth control while taking antibiotics.
Millions of women take oral contraceptive pills (OCPs) each year. The first reports of worrisome interactions between antimicrobials and the OCPs appeared in the early 1970s when rifampin was implicated in unwanted pregnancies and in frequent breakthrough bleeding among patients taking OCPs.66 Anecdotal reports of pregnancy coincident with concomitant use of OCPs and antibiotics continue to occur. Many mechanisms have been proposed to explain the possibility of decreased OCP efficacy with antibiotic use. It is commonly believed that drug interactions with OCPS have a pharmacokinetic basis.67 Other hypotheses include decreased enterohepatic circulation, increased liver degradation, antibiotic-induced diarrhea, and displacement of the contraceptive steroid from its bioreceptor site.68 Given the serious consequences of unwanted pregnancy and the frequency at which antibiotics are prescribed, much research has addressed this issue.
In 1999, a review article concluded that the antifungal medication griseofulvin and the broad-spectrum antibiotic rifampin have convincingly shown to induce hepatic enzymes and to have significant interaction with OCPs.66 When either antimicrobial is used by women taking OCPs, additional or alternative contraceptive protection certainly is advisable. Uncertainty persists regarding the other broad-spectrum antibiotics. Good prospective studies of the pharmacokinetics of these drug interactions are few. While failing to find specific evidence for reduced OCP effectiveness on the doses of broad-spectrum antibiotics used in acute infection, they do suggest that variable contraceptive steroid handling could make some women, at some times, more susceptible to OCP failure. The situation with lower-dose, long-term antibiotic administration for dermatologic complaints is less clear. Given that the pharmacokinetic evidence for any interaction between the OCP and higher-dose antibiotics is tenuous, it seems less likely that low maintenance doses of drugs like tetracycline would significantly affect steroid hormone levels in the long-term, especially if resistant gut flora rapidly emerges and reestablishes the enterohepatic circulation of steroid hormones. Given the serious consequences of unwanted pregnancy, the cautious approach of using additional or alternative contraception during short courses of broad-spectrum antibiotics and the initial weeks of long-term antibiotic administration may be justified to safeguard the few unidentifiable women who may be at risk.68
Dickinson and colleagues published a review article in 2001 that proposed that either pharmacodynamic or pharmacokinetic interaction theoretically could inhibit the efficacy of OCPs.67 They found no evidence that any antibiotic directly affects steroid receptor function, or that it serves as a physiologic antagonist of estrogens or progestins. It is commonly believed that drug interactions with OCPs (not involving steroid receptors) have a pharmacokinetic basis.67 Published in Dickinson’s review, the following statements recommended by the Council on Scientific Affairs were adopted as American Medical Association policy in June 2000. 68
1. Women prescribed rifampin concomitantly with OCPs faced significant risk of OCP failure and should be counseled about the additional use of nonhormonal contraceptive methods during the course of rifampin therapy.
2. Women using combined OCPs should be informed about the small risk of interactions with antibiotics and that it is not possible to identify in advance the women who may be at risk of OC failure. Women who are not comfortable with the small risk of interaction should be counseled about the additional use of nonhormonal contraceptive methods. Women who have had previous OCP failures or who develop breakthrough bleeding during concomitant use of antibiotics and OCPs should be counseled about the use of alternate methods of contraception if they engage in intercourse during the period of concomitant use, as they may be part of the subset of women at high risk of contraceptive failure.
A recent article by Archer and Archer reviewed the pharmacokinetic and clinical literature regarding the efficacy of oral contraceptives when used concomitantly with antibiotic therapy.68 They concluded that there were no pharmacokinetic data at that time to support the contention that oral antibiotic use decreases the efficacy of OCPs, except for antituberculosis drugs such as rifampin. There were also no prospective, randomized clinical trials of OCP efficacy and antibiotic use. Lastly, case reports used to support an effect of antibiotics on OCP efficacy are anecdotal and subject to recall bias and lack adequate controls and medication documentation. Thus, there is no firm evidence that supports the contention that OCP potency is reduced by antibiotics (with the exception of rifampin).68
Like all drugs, oral contraceptives are not 100% effective. Thus, it is possible that the case reports of unintended pregnancies during antibiotic therapy simply may represent the normal failure rate of these drugs.69 Current literature supports that—with the exception of rifampin— antibiotics do not significantly reduce the efficacy of OCPs. However, physicians should be aware that there are women who may be at a higher risk of OCP failure due to large interindividual variation in OCP hormone levels.67 A cautious approach is for women on short-term broad-spectrum antibiotic therapy and long term-antibiotic therapy to use an additional nonhormonal method of contraception.67 The period of risk for drug interactions is not known during long-term therapy, but may exist primarily during the first few weeks of therapy or until gut flora become resistant.67 An alternative form of contraception is advised if diarrhea or breakthrough bleeding are noted in women taking OCPs who receive antibiotic therapy, or if the baseline rate of oral contraception failure is unacceptable.67
FACT: The use of concominant oral contraceptives and antimicrobials, with the exception of rifampin or griseofulvin, does not confer significant risk of contraception.
Fact or Fiction? N-acetylcysteine prevents clinically significant contrast-induced nephropathy.
Radiocontrast administration is the third leading cause of hospital-acquired renal failure.70 Contrast-induced nephropathy occurs in about 15% of all patients undergoing procedures involving intravenous contrast administration. However, those rates are higher in patients with diabetes or preexisting renal insufficiency.71,72 Contrast agents reduce renal function by altering renal hemodynamics and by exerting direct toxic effects on tubular epithelial cells.73 The cause of contrast-induced nephropathy (CIN) can range from transient elevations in serum creatinine levels to permanent renal failure requiring dialysis.74 ED patients may be at higher risk for CIN because pre-contrast risk is not always considered because the urgency of imaging may preclude other prophylactic measures.70 (See Table 2.)
Table 2. Risk Factors for Contrast-induced Nephropathy
N-acetylcysteine (Mucomyst) has been used for years to treat acute acetaminophen overdose as well as a variety of pulmonary diseases.75N-aceylcysteine (NAC) is a potent vasodilator that enhances renal perfusion and has antioxidant effects.70 Prior to the use of NAC, only saline hydration and low or iso-osmolar contrast agents had shown some benefit in preventing CIN.76,77
In 2000, Tepal and colleagues demonstrated that oral NAC reduced the risk of CIN in 83 stable outpatients with chronic renal insufficiency who were undergoing elective computerized tomography (CT) imaging of the abdomen.73 The patients were given 600 mg orally twice a day on the day before and the day of the study. The control patients’ creatinine levels rose from 2.4 +/- 1.3 m/dL to 2.6 +/- 1.5 mg/dL after 48 hours, while the NAC patients creatinine levels fell from 2.5 +/- 1.3 to 2.1 +/- 1.3 mg/dL. Two percent of the patients in the NAC group and 21% of the patients in the control group had an increase in serum creatinine levels (p = 0.01 95% CI, 0.02-0.09) None of the patients required dialysis. Tepal’s study defined an acute contrast-induced reduction in renal function as an increase in serum creatinine levels of at least 0.5 mg/dL 48 hours after administration of a contrast agent.73 Such an increase may be important because it can increase the duration of hospitalization.78 NAC was adopted widely for use after results of this study were published.
A recent meta-analysis of seven randomized clinical trials including 805 patients of prophylactic oral NAC demonstrated a statistically significant risk reduction in the treatment group.71 Although CIN generally is considered to be an adverse outcome, the clinical importance of CIN as defined in these trials is debatable.71 Most patients had creatinine levels that returned to baseline within days; oliguria and hemodialysis were rare. However, CIN is associated with increased length of hospital stay and increased mortality.72
Studies of NAC prophylaxis for non-urgent contrast procedures have produced conflicting results. Most trials involved patients undergoing elective imaging and studied NAC administration given 12-24 hours before contrast administration.73,79-82
How, if at all, does this apply to the ED setting? Webb and colleagues studied 487 patients with renal dysfunction undergoing cardiac catheterization. The study patients received 500 mg of NAC intravenously immediately before the procedure, and the infusion was continued for 6 hours after the procedure. The patients were high risk with pre-existing impaired renal function (< 50 mL/min glomerular filtration rate). The study was terminated early because of determination of futility. Intravenous NAC was found to be ineffective in preventing CIN.83
The RAPPID study evaluated the use of intravenous NAC in an urgent setting. An acute contrast-induced reduction in renal function was defined as an increase in serum creatinine concentration by 25% at either two or four days after contrast administration. Eighty patients who were to undergo cardiac catheterization were given 150 mg/kg NAC in 500 mL of saline during 30 minutes immediately before the procedure and then 50 mg/kg in 500 mL of saline during 4 hours. The patients in the control group received 1 mL/kg/hr of saline for 12 hours pre-and post-procedure. The NAC group had 5% of patients develop CIN compared with 21% of patients in the hydration group (p=0.045). This fact seems significant until the actual numbers are given closer scrutiny. In the NAC group, the creatinine levels went from 1.85+/-059 to 1.77 +/-0.73 at 48 hours and 1.79 ± 0.73 at 4 days post-contrast. In the hydration group, the creatinine levels went from 1.75 +/-0.41 to 1.81 +/-0.6 at 48 hours and 1.80 +/-0.5 at 4 days. No patient required dialysis.84
The adverse effects seen with oral NAC include mostly gastrointestinal symptoms, including nausea, abdominal pain, and occasionally a headache or chest pain.70 Adverse effects associated with intravenous NAC include itching, flushing and rash, and pulmonary edema (likely due to volume overload).
Current data do not support the use of NAC for urgent radiologic studies requiring intravenous contrast in the ED. Some may argue: Why not use it if it might provide some benefit and it doesn’t appear to have significant risks? One must consider that no therapy is without risks, side effects, and cost. The risk lies in that physicians may overestimate the benefit incurred by the use of NAC and may develop a false sense of security in its ability to prevent CIN, thereby ordering contrast studies and pre-treating with NAC in patients at high risk of renal failure.
FACT: NAC does not prevent clinically significant contrast-induced nephropathy.
Summary
There are many myths in medical practice that are promulgated by well-meaning emergency physicians. As with the issues discussed in this article, some long-standing practices and recent mandates have little basis in the medical literature. Just because you learned it in residency doesn’t make it so. Physicians should actively question and discuss alleged dogmas of medical practice that may not make clinical sense.
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This article will review and dispute some commonly held beliefs about dogma in the practice of emergency medicine.
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