JCAHO B.IT.C.H.E.S. – QA measures and Community Acquired PNA (CAP)
THE QUESTION - A lot of “too-doo” has been made recently by the powers that be in our departmetn regarding antibiotics given within a 4 hour window for patients suspected of having community acquired pneumonia (CAP), with an expected 90% compliance rate. Being individuals inherently opposed to rigid guidelines, Stack and I wondered where and why these guidelines came from, and whether there will be any adverse outcomes from a seemingly arbitrary standard such as this (i.e., increasing drug resistance). Granted, as residents, armed with any such data, we are unlikely to take down the monolith of JCAHO and the rest of the bureaucracy, but, will the data give us a way to BITCH, EBM style?
THE ANSWER (in parts):
I. THE BACKGROUND : Community acquired pneumonia (CAP) is currently one of four diagnoses identified by the federal Centers for Medicare and Medicaid Services (CMS) to be used as measures of quality improvement (the others being ACS, heart failure and surgical wound infections). In case you don’t know, CMS is a big agency – they gave out over $480 billion (that’s $480,000,000,000) in funding related to medicare and medicaid in 2004. When our wonderful president, GW Bush signed the Medicare Prescription Drug Benefit in 2004, the bill also provided $400-450 million annually to help incentivize quality improvement indicators in these diagnoses. In order to get their share of the funding, hospitals that accept medicare must submit their performance data for 10 quality measures, 6 of which fall under the realm of CAP (see below, data available at hospitalcompare.hhs.gov):
Quality Indicator BIDMC Average (USA) Average (MA)
1. Assessed/Given Influenza Vaccine 21% 70% 75%
2. Assessed/Given Pneumococcal Vaccine 93% 67% 71%
3. Given Abx w/in 4hrs of arrival 91% 79% 80%
4. Oxygenation measured 100% 99% 100%
5. Given smoking cessation advice/counselling 94% 79% 80%
6. Given most appropriate initial Abx 86% 83% 85%
7. Blood Cx given prior to Abx 94% 90% 90%
As you can see, BIDMC performs fairly well compared to other hospitals. So why the emphasis on full compliance? Color me cynical, but it appears that the possibility of future “pay per performance” is a likely reason. Currently, this is being piloted in the “Premier’s Hospital Quiality Incentive Demonstration Project,” a program started among 268 Medicare recipient hospitals in 2003. In this pilot, hospitals in the top 10% of quality performance measures recieve a 2% bonus, and hospitals in the second decile receive a 1% bonus. And coming soon, the bottom 20% will also be penalized 1-2% per annum as well. Many commentators see this as a future direction of all Medicare-recipient hospitals.
II. THE DATA.
So… to the point of this discussion – quality indicator number 3 above – Antibiotic administration within 4 hours of arrival for patient admitted with a diagnosis of CAP. Where did this data come from? It is, in fact, based entirely on two retrospective studies.
The first, Meehan et al (JAMA 1997) looked at 14,069 medicare patients > 65 yo who were admitted for CAP. Excluded from this study were pts < 65 yo, HIV+, transplant recipients, recently hospitalized, chemotherapy within 2 months, transferred from other hospitals, and patients who either did not recieve antibiotics, or recieved them > 100 hrs after admission. The primary outcome was 30d mortality rates. This study showed a marginal, but statistically significant improvement in 30 day mortality when patients recieved antibiotics within 8 hours of arrival (OR 0.85; 95% CI 0.75-0.96). Interestingly, they also showed that patients who recieved antibiotics within 1 hour had a 20% increase in mortality rate at 30days. Hmmmm. Note, the analysis all tried to control for “how sick the patient was” by adjusting based on the Pneumonia Severity Index (PSI; a prospectively studied and validated severity scoring system),
The second study, Houck et. al. Arch Intern Med 2004 is very similar. They retroepectively studied the medical records of a random sample of 18, 204 medicare patients again > 65yo with community acquired pneumonia. The primary outcomes were severity adjusted mortality (both in hospital and within 30 days), readmission rates within 30 days, and lenght of stay. Unlike Meehan et al, who used 8 hrs as a cutoff, these used the now-institutionalized 4 hour window. They found (and please note again, mortality rates are severity adjusted by the PSI):
Abx < 4 hrs Abx > 4 hrs OR (95% CI)
In hospital mortality 6.8% 7.4% 0.85 (0.74-0.96)
30d mortality 11.6% 12.7% 0.85 (0.76-0.95)
Length of stay > 5d 42.1% 45.1% 0.90 (0.83-0.96)
Yeah… not too impressive, I know. An absolute decrease of 0.6 %(in house) or 1.1% (30d) mortality rate. Interestingly, they also found a “trend” that patietns who had recieved antibiotics within 24hrs prior to admission (super-duper early!!!) had a increased mortality rate (OR 1.18 (CI 0.97-1.45), p=0.10).
What to make of this data? Well, first of all, from a methodological standpoint, all of these are retrospective, medical review studies, with all of the inherent problems (unmeasured confounders). For example – maybe patients who have a delay in diagnosis of CAP, and therefore delayed antibiotic administration, are inherently sicker – eg, maybe patients with pneumonia diagnosed by CT scan (and therefore, presumably later in the course) had a negative CXR because they were hypovolemic, or they were too sick to go for an PA and lateral (and had a crappy, false negative single view AP), or the provider was worried enough to get a CT scan for another reason.
Secondly, other very similar studies with very similar methodologies show absolutely no influence of timing to antibioitcs on mortality or length of stay measures! (See for example, Dedier J et al, Arch Intern Med 2001). There are no prospective studies that have confirmed the importance of early antibiotics in CAP.
Finally, it is also noteworthy that the current JCAHO reccomendations (that we are held to) for early antibiotics are not only for patients > 65yo (the population that the, albeit limited, data has been studied in), but for all patients > 18 yo – patients who would have been excluded from these same studies.
III. Conclusions
Conclude whatever you want from the above. It seems to me that the present requirements for 4 hour antibiotics are, at best based on very sketchy, non-prospectively validated data for a specific patient population of Medicare patients (older than 65). At worst, they are artificial constructs being implemented more for the financial benefit of the hospitals than for the medical benefit of the patient. In fact, it is not too hard to imagine situations in which this could actually lead to a net harm to our patients – will the increased/less discriminant use of antibiotics lead to more antimicrobial drug resistance, or more adverse reactions to antibiotics? Will patients with possible pneumonia be triaged faster from the waiting room to meet these requirements than patients who are sicker but aren’t “lucky enough” to have diseases that are tied into the hospital reimbursement system? I don’t know… but these seem to be real risks, all the worse if “pay for performance” takes hold, or god forbid, expands.
Wednesday, December 5, 2007
ACS- Calibrating your Dispo-Meter
ACS- CALIBRATING YOUR DISPO-METER
1) What is the risk of ACS in young patients presenting to the ED with Chest Pain?
Marsan R et al. “Evaluation of a clinical decision rule for young adults pts w/CP” Acad Emerg Med. Jan 2005.
Prospective, observational study of 1023 pts age 24-39 with CP (Excl cocaine CP)
Outcome – ACS (AMI/Unstable angina) at 30d
- Overall risk = 5.4%
- No cardiac Hx + No RFs (HTN, hyperchol, Tobacco, FHx) = 1.8%
- No cardiac Hx + No RFs + nl ECG = 1.0%
- No cardiac Hx + No RFs + nl ECG + 1 set normal enzymes = 0.14%
- No cardiac Hx + nl ECG + pos Rfs (ie smoker) = 1.3%
- (note = “normal EKG” is true normal; ie, no t-wave inversions etc. )
2) What % of pts with negative inpt evaluation for CP have ACS w/in 1 year?
Prina L et al. “Outcome of pts with a final dx of CP of undetermined origin admitted under the suspicion of ACS” Annals of EM. Jan 2004.
Retrospective chart review of 230 pts with DC dx of CP unknown origin
- 79% had ETT, Stress ECHO, MIBI or cath
- Overall 1 year rate of ACS = 4.4% (10 pts)
o Those with testing = 3.3%
o Those without testing = 8.2%
- Risk greatest in those with pre-existing CAD
- CONCLUSION - Pts with preexisting CAD/RFs should be considered at risk for adverse coronary events, even after a recently negative study
3) Do conventional cardiac RFs (DM, HTN, smoking, hypercholesterolemia, family hx of CAD) help identify those pts with ACS who present to the ED?
Han J et al. “The Role of Cardiac RF Burden in diagnosing ACS in the Emergency Department Setting” Annals of EM. Feb 2007.
Post-hoc analysis of itrACS registry (10,806 ED visits for suspected ACS)
Excludes + cocaine/amphetamine, left AMA, incomplete records.
- LIKELIHOOD RATIOS (by age group):
- CONCLUSIONS: Cardiac RFs have little role in diagnosing ACS in ED setting, especially in older patients (may have some limited utility in patients < 40)
4) How much does a clearcut alternative non-cardiac cause of chest pain lessen the probability of ACS?
Hollander J, Chase M et al. “Relaionship between a clear-cut alternative noncardiac diagnosis and 30-day outcome in ED pts with chest pain” Acad Emerg Med. March 2007.
Prospective cohort study of 1995 pts >30 with CP in urban, tertiary ED
Collected demographic/clinical data and whether MD (residents) thought clear cut alternative Dx after ED evaluation
Outcomes: Death, MI, revascularization within 30days
- Those with clear-cut alternative still had 4% event rate at 30d (LR(-) 0.45)
- CONCLUSIONS – Clear-cut alternative Dx reduces likelihood of ACS, but not to level safe enough to allow discharge from ED.
5) What are the presenting symptoms of pts diagnose with ACS who didn’t complain of chest pain?
Breiger D L et al. “ACS without chest pain, an underdiagnoses and undertreated high-risk group; insights from the global registry of acute coronary events. Chest. Aug 2004.
Multinational prospective observational study of 1763 pts w/o ACS, >18, admitted for ACS
- Most common presentations w/o chest pain:
o Dyspnea = 49.3%
o Diaphoresis = 25.2%
o Nausea/vomitting = 24.3%
o Syncope = 19.1%
- These pts generally older, women, or had hx HTN, DM or heart failure.
6) Which pts with new onset Afib should have further evaluation for ACS?
Zimetbaum P et al. “Incidence and predictors of MI among pts w/Afib” JACC. Oct 2000..
Prospective cohort study of 255 pts presenting to ED w/ primary Dx of AF
- 190 admitted, 109 (57%) had a standard r/o MI protocol
- Incidence of MI = 5.5% (6 pts)
- Predictors of MI
(Major ST segement change = >2mm depression or any ST elevation
- Note – small #MIs lead to large confidence intervals
C-spine Clearance in The Obtunded Trauma Patient
This one offered by our excellent chief resident, trauma extraordinaire, and world liberator, Dave Callaway.
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CT Based Protocols for C Spine Clearance in the Obtunded Blunt Trauma Patient
1. Hogan GJ, Mirvis SE, Shanmuganathan K, Scalea TM. Exclusion of unstable cervical spine injury in obtunded patients with blunt trauma: is MR imaging needed when multi-detector row CT findings are normal? Radiology. 2005 Oct;237(1):106-13.
a. 1400 trauma patients received helical CT (HCT) with 4-16 slice scanner AND MRI
b. 366 obtunded blunt trauma patients with negative HCT got MRI
c. MRI stats
i. Negative 354/366
ii. Positive 12/366
1. Cord contusion 7/12 (no intervention)
2. Ligamentous injury 4/12 (single column, no interv)
3. Interveterbral disk edema 3/12 (no intervent)
4. Combination 1/12 (no intervention)
d. Conclusions:
i. CT Sensitivity for ligamentous injury 98.9%
ii. CT Sensitivity for unstable cervical injury 100%
iii. MRI very sensitive for injuries, however helical CT reliable excludes clinically significant injury
2. Brohi K, Healy M, Fotheringham T, Chan O, Aylwin C, Whitley S, Walsh M. Helical computed tomographic scanning for the evaluation of the cervical spine in the unconscious, intubated trauma patient. J Trauma. 2005 May;58(5):897-901.
a. Four hundred thirty-seven unconscious, intubated, blunt trauma patients underwent CT scanning of the cervical spine.
b. 61 pt w/ cervical spine injury- 31 (7.0%) were unstable.
c. CT scanning had a sensitivity of 98.1%, a specificity of 98.8%, and a negative predictive value of 99.7%.
d. Conclusion: Significant ligamentous injury results in malalignment or malrotation detectable by HCT. Therefore, Helical CT is sensitive enough to clear cervical spine in obtunded blunt trauma patient.
3. Schuster R, Waxman K, Sanchez B, Becerra S, Chung R, Conner S, Jones T. Magnetic resonance imaging is not needed to clear cervical spines in blunt trauma patients with normal computed tomographic results and no motor deficits. Arch Surg. 2005 Aug;140(8):762-6.
a. 2603 blunt trauma patients, 100 c- spine or SC injuries
b. HCT detected 85/100
c. All 15 missed had neurologic deficits on exam
d. Withdrawal/localization adeqaute in assessing motor fx in comatose patient
e. 12 comatose patients, moving all 4 extrem on arrival w/ nml CT of cervical spine were examined with MRI. All MRI results were negative for injury. No patients experienced neurologic deterioration. No patient required operative management of spinal injury.
f. MRI added no clinical information
g. Conclusion: Obtunded blunt trauma patients w/ normal motor examination results and normal CT results of the c- spine do not require further radiologic examination before clearing the cervical spine.
************************
CT Based Protocols for C Spine Clearance in the Obtunded Blunt Trauma Patient
1. Hogan GJ, Mirvis SE, Shanmuganathan K, Scalea TM. Exclusion of unstable cervical spine injury in obtunded patients with blunt trauma: is MR imaging needed when multi-detector row CT findings are normal? Radiology. 2005 Oct;237(1):106-13.
a. 1400 trauma patients received helical CT (HCT) with 4-16 slice scanner AND MRI
b. 366 obtunded blunt trauma patients with negative HCT got MRI
c. MRI stats
i. Negative 354/366
ii. Positive 12/366
1. Cord contusion 7/12 (no intervention)
2. Ligamentous injury 4/12 (single column, no interv)
3. Interveterbral disk edema 3/12 (no intervent)
4. Combination 1/12 (no intervention)
d. Conclusions:
i. CT Sensitivity for ligamentous injury 98.9%
ii. CT Sensitivity for unstable cervical injury 100%
iii. MRI very sensitive for injuries, however helical CT reliable excludes clinically significant injury
2. Brohi K, Healy M, Fotheringham T, Chan O, Aylwin C, Whitley S, Walsh M. Helical computed tomographic scanning for the evaluation of the cervical spine in the unconscious, intubated trauma patient. J Trauma. 2005 May;58(5):897-901.
a. Four hundred thirty-seven unconscious, intubated, blunt trauma patients underwent CT scanning of the cervical spine.
b. 61 pt w/ cervical spine injury- 31 (7.0%) were unstable.
c. CT scanning had a sensitivity of 98.1%, a specificity of 98.8%, and a negative predictive value of 99.7%.
d. Conclusion: Significant ligamentous injury results in malalignment or malrotation detectable by HCT. Therefore, Helical CT is sensitive enough to clear cervical spine in obtunded blunt trauma patient.
3. Schuster R, Waxman K, Sanchez B, Becerra S, Chung R, Conner S, Jones T. Magnetic resonance imaging is not needed to clear cervical spines in blunt trauma patients with normal computed tomographic results and no motor deficits. Arch Surg. 2005 Aug;140(8):762-6.
a. 2603 blunt trauma patients, 100 c- spine or SC injuries
b. HCT detected 85/100
c. All 15 missed had neurologic deficits on exam
d. Withdrawal/localization adeqaute in assessing motor fx in comatose patient
e. 12 comatose patients, moving all 4 extrem on arrival w/ nml CT of cervical spine were examined with MRI. All MRI results were negative for injury. No patients experienced neurologic deterioration. No patient required operative management of spinal injury.
f. MRI added no clinical information
g. Conclusion: Obtunded blunt trauma patients w/ normal motor examination results and normal CT results of the c- spine do not require further radiologic examination before clearing the cervical spine.
Q/A with Tony Friedman Volume 3.0 - RSICP
Rapid Sequence intubation and elevation of ICP
THE QUESTION:
I've noticed that we go to great lengths to premedicate brain bleed/trauma patients before intubation, with the goal of preventing increased intracranial pressure and potential herniation. On the other hand, I've seen intubation delayed up to 10 minutes to get all those medications lined up and administered, and it frequently seems to disrupt the flow of the resuscitation. Are we really doing more good than harm with this?
THE ANSWER:
The elevated ICP with intubation phenomenon has been noted predominantly in patients undergoing intubation for elective neurosurgical procedures who already have ICP monitors in place [1,2]. Obviously, it would be impossible to achieve a similar level of monitoring before RSI in acutely brain-injured patients. The head injury cocktail we're trained to use here consists of lidocaine 1.5 mg/kg, vecuronium 1 mg, fentanyl 3-5 mcg/kg, etomidate .03 mg/kg, and succinylcholine 1.5-2 mg/kg. The first three agents are included to blunt the presumed increase in ICP. I'll present the supporting data for each agent individually.
Lidocaine
Lidocaine is commonly used as a premedicating agent in academic emergency departments in the USA [3] and is used infrequently in the UK [4]. The literature was nicely reviewed in 2001 by an English group and only 6 studies were found, none of which addressed the central issue of whether pretreatment with lidocaine improved the outcome of brain-injured patients undergoing RSI [5]. The strongest supporting evidence for lidocaine comes from a 1980 study by Bedford et al. in which 10 patients undergoing elective resection of cerebral neoplasm received lidocaine prior to intubation, and 10 did not [6]. Other premedications such as morphine, atropine, and diazepam were used in all cases. The authors found that pretreatment with 1.5 mg/kg lidocaine reduced the average rise in ICP with intubation by 12 mmHg. The study's applicability is limited by the small numbers and non-RSI protocol.
Three small studies examined the effect of lidocaine on the ICP response to endotracheal suctioning in intubated patients [7,8,9]. All found that lidocaine reduced either the baseline ICP or the ICP increase with suctioning, but each study was limited by factors such as lack of blinding or small size. Due to the fact that these were non-paralyzed intubated patients undergoing suction rather than laryngoscopy and intubation, the application of these studies to brain-injured patients undergoing RSI is dubious. The other two studies described in the English review provided minimal applicable evidence for lidocaine.
The conclusion of the English reviewers was that the evidence does not support the use of lidocaine for RSI in patients with head injury. However, Ron Walls reviewed essentially the same data in 1993 and found the evidence for using lidocaine "compelling" [10]. I was unable to find more recent literature that addressed the usefulness of lidocaine in RSI. However, it should be noted that the standardized emergency airway course in the United States recommends use of lidocaine in RSI of brain-injured patients. Despite the weakness of supportive evidence, an American physician choosing not to use lidocaine could be vulnerable to accusations of not adhering to the established standard of care.
Vecuronium
The concept of administering a low "defasciculating" dose of a nondepolarizing paralytic agent arises from the observation that succinylcholine itself may contribute to elevation in ICP [1,11]. It should be noted that the evidence of this effect is far from conclusive, and several studies have also been published which reach the opposite conclusion. The mechanism of this purported succinylcholine effect has not been clearly established, but may involve afferent input to the brain from muscle spindle receptors [12].
In a small study of patients administered succinylcholine before and after vecuronium 0.14 mg/kg, significant elevation in ICP was frequently observed with the succinylcholine dose given before vecuronium but not with the dose given after vecuronium [13]. In a small control group receiving two doses of succinylcholine without vecuronium, a small average elevation in ICP was seen with both doses. It should be noted that the groups are very small, the data presentation is significantly flawed, and a full paralyzing dose of vecuronium was used. Interestingly, despite the use of the term "defasciculating dose", patients that were observed to fasciculate with the initial dose of succinylcholine did not sustain significant increase in ICP. Therefore, prevention of fasciculation is unlikely to be a factor in the effect of vecuronium on ICP.
A subsequent study evaluated the effect of pretreatment with a small, non-paralyzing dose of metocurine on the ICP increase with succinylcholine administration [14]. They found an average increase in ICP of 12 mmHg without pretreatment, compared to no significant change in ICP with pretreatment. Only 6 patients were included in each group although they reported that their results achieved significance. They did not offer a pharmacologic explanation of why this particular low dose of a nondepolarizing paralytic would attentuate the ICP response without inducing paralysis. The groups were too small to determine a significant difference in the incidence of fasciculations.
Based primarily on this data, Ron Walls advocates administration of vecuronium or pancuronium at 0.01 mg/kg 2-3 minutes before administration of succinylcholine [10]. Interestingly, an English group reviewed essentially the same data and concluded that there was no significant evidence either that succinylcholine caused elevated ICP in patients with acute brain injury, or that treatment with a low dose nondepolarizing paralytic would attenuate that effect [15]. Ron Walls is listed as a coauthor on that study so he appears to be covering his bases fairly well (note to would-be department chairmen). An alternative would be to use a full dose of nondepolarizing agent as an alternative to succinylcholine, but vecuronium and pancuronium are impractical for RSI due to their delayed onset (approximately 100 seconds) and prolonged effect (approximately two hours). Rocuronium has been advocated but represents a significant additional expense and may not provide optimal conditions for RSI [16].
Fentanyl
The advocacy for use of fentanyl as a premedication in RSI is based on its well-described effects on hemodynamic parameters during intubation. I did not find any studies that addressed the direct effect of fentanyl on ICP. RSI is well described to result in elevations in heart rate, blood pressure, and plasma catecholamine concentrations [17], and this is hypothesized to contribute indirectly to elevated ICP. Fentanyl effectively attenuates these hemodynamic responses [18,19] without inducing significant hypotension [20]. In his review, Ron Walls advocates that it be administered at 3-5 mcg/kg 1-3 minutes before laryngoscopy [10]. This seems to be purely based on the avoidance of tachycardia and hypertension with intubation, and not on any evidence of a direct effect on ICP.
Other agents
There is evidence that thiopental, propofol, and beta blockers attenuate the hemodynamic and intracerebral response to laryngoscopy and intubation, but their hypotensive qualities have made their use unpopular in brain-injured patients. In very hypertensive patients (e.g spontaneous ICH) thiopental especially may be considered as an induction agent at 3-5 mg/kg [21].
It is important to remember that virtually all data supporting the use of premedication in brain injury is based on ICP measurements in elective neurosurgical patients who underwent conventional induction of anesthesia rather than RSI. Therefore, it is difficult to advocate their use prior to RSI in acutely brain-injured patients. However, none of these medications has been demonstrated to have any harmful effects when used during RSI. I think that the decision to use these medications can be made by the individual on a case by case basis, keeping in mind that the top priority should always be securing the airway and maintaining adequate oxygenation. I don't think the evidence justifies delaying intubation in a hypoxic patient, as hypoxia has been definitively associated with increased mortality in traumatic brain injury [22].
Considering the controversy that has existed for 10-15 years regarding premedication, it is rather surprising that no randomized prospective trial of these agents has been published that addresses neurologic outcome and mortality. It seems that such a study would be relatively simple to design and implement, considering the fairly high frequency of brain-injured patients requiring intubation, and could result in a significant paradigm shift in emergency medicine practice either here or on the other side of the Atlantic.
References:
1. Burney et al. 1975 Anaesth Analg 54:687
2. Rudy et al. 1986 Heart Lung 15:488
3. Silber et al. 1997 Am J Emerg Med 15:263
4. Butler et al. 2001 Emerg Med J 18:343
5. Robinson et al. 2001 Emerg Med J 18:453
6. Bedford et al. in Shulman et al. 1980 Intracranial Pressure IV, Springer: 595
7. Donegan et al. 1980 Anesthesiology 52:516
8. White et al. 1982 Anesthesiology 57:242
9. Yano et al. 1986 Anesthesiology 69:651
10. Walls. 1993 Ann Emerg Med 22:1008
11. Thompson et al. 1982 Ann Emerg Med 10:526
12. Mori et al. 1973 Br J Anaesth 45:605
13. Minton et al. 1986 Anesthesiology 65:165
14. Stirt et al. 1987 Anesthesiology 67:50
15. Clancy et al. 2001 Emerg Med J 18:373
16. Perry et al. 2003 Cochrane Database Syst Rev Issue 1
17. Takeshima et al. (1964) Anaesth Analg 43:201
18. Ebert et al. (1989) Can J Anaesth 36:301
19. Helfman et al. (1991) Anesth Analg 72:482
20. Miller et al. (1988) Can J Anaesth 35:219
21. Shapiro et al. (1973) Br J Anaesth 45:1057
22. Stocchetti et al. 1996 J Trauma 40:764
THE QUESTION:
I've noticed that we go to great lengths to premedicate brain bleed/trauma patients before intubation, with the goal of preventing increased intracranial pressure and potential herniation. On the other hand, I've seen intubation delayed up to 10 minutes to get all those medications lined up and administered, and it frequently seems to disrupt the flow of the resuscitation. Are we really doing more good than harm with this?
THE ANSWER:
The elevated ICP with intubation phenomenon has been noted predominantly in patients undergoing intubation for elective neurosurgical procedures who already have ICP monitors in place [1,2]. Obviously, it would be impossible to achieve a similar level of monitoring before RSI in acutely brain-injured patients. The head injury cocktail we're trained to use here consists of lidocaine 1.5 mg/kg, vecuronium 1 mg, fentanyl 3-5 mcg/kg, etomidate .03 mg/kg, and succinylcholine 1.5-2 mg/kg. The first three agents are included to blunt the presumed increase in ICP. I'll present the supporting data for each agent individually.
Lidocaine
Lidocaine is commonly used as a premedicating agent in academic emergency departments in the USA [3] and is used infrequently in the UK [4]. The literature was nicely reviewed in 2001 by an English group and only 6 studies were found, none of which addressed the central issue of whether pretreatment with lidocaine improved the outcome of brain-injured patients undergoing RSI [5]. The strongest supporting evidence for lidocaine comes from a 1980 study by Bedford et al. in which 10 patients undergoing elective resection of cerebral neoplasm received lidocaine prior to intubation, and 10 did not [6]. Other premedications such as morphine, atropine, and diazepam were used in all cases. The authors found that pretreatment with 1.5 mg/kg lidocaine reduced the average rise in ICP with intubation by 12 mmHg. The study's applicability is limited by the small numbers and non-RSI protocol.
Three small studies examined the effect of lidocaine on the ICP response to endotracheal suctioning in intubated patients [7,8,9]. All found that lidocaine reduced either the baseline ICP or the ICP increase with suctioning, but each study was limited by factors such as lack of blinding or small size. Due to the fact that these were non-paralyzed intubated patients undergoing suction rather than laryngoscopy and intubation, the application of these studies to brain-injured patients undergoing RSI is dubious. The other two studies described in the English review provided minimal applicable evidence for lidocaine.
The conclusion of the English reviewers was that the evidence does not support the use of lidocaine for RSI in patients with head injury. However, Ron Walls reviewed essentially the same data in 1993 and found the evidence for using lidocaine "compelling" [10]. I was unable to find more recent literature that addressed the usefulness of lidocaine in RSI. However, it should be noted that the standardized emergency airway course in the United States recommends use of lidocaine in RSI of brain-injured patients. Despite the weakness of supportive evidence, an American physician choosing not to use lidocaine could be vulnerable to accusations of not adhering to the established standard of care.
Vecuronium
The concept of administering a low "defasciculating" dose of a nondepolarizing paralytic agent arises from the observation that succinylcholine itself may contribute to elevation in ICP [1,11]. It should be noted that the evidence of this effect is far from conclusive, and several studies have also been published which reach the opposite conclusion. The mechanism of this purported succinylcholine effect has not been clearly established, but may involve afferent input to the brain from muscle spindle receptors [12].
In a small study of patients administered succinylcholine before and after vecuronium 0.14 mg/kg, significant elevation in ICP was frequently observed with the succinylcholine dose given before vecuronium but not with the dose given after vecuronium [13]. In a small control group receiving two doses of succinylcholine without vecuronium, a small average elevation in ICP was seen with both doses. It should be noted that the groups are very small, the data presentation is significantly flawed, and a full paralyzing dose of vecuronium was used. Interestingly, despite the use of the term "defasciculating dose", patients that were observed to fasciculate with the initial dose of succinylcholine did not sustain significant increase in ICP. Therefore, prevention of fasciculation is unlikely to be a factor in the effect of vecuronium on ICP.
A subsequent study evaluated the effect of pretreatment with a small, non-paralyzing dose of metocurine on the ICP increase with succinylcholine administration [14]. They found an average increase in ICP of 12 mmHg without pretreatment, compared to no significant change in ICP with pretreatment. Only 6 patients were included in each group although they reported that their results achieved significance. They did not offer a pharmacologic explanation of why this particular low dose of a nondepolarizing paralytic would attentuate the ICP response without inducing paralysis. The groups were too small to determine a significant difference in the incidence of fasciculations.
Based primarily on this data, Ron Walls advocates administration of vecuronium or pancuronium at 0.01 mg/kg 2-3 minutes before administration of succinylcholine [10]. Interestingly, an English group reviewed essentially the same data and concluded that there was no significant evidence either that succinylcholine caused elevated ICP in patients with acute brain injury, or that treatment with a low dose nondepolarizing paralytic would attenuate that effect [15]. Ron Walls is listed as a coauthor on that study so he appears to be covering his bases fairly well (note to would-be department chairmen). An alternative would be to use a full dose of nondepolarizing agent as an alternative to succinylcholine, but vecuronium and pancuronium are impractical for RSI due to their delayed onset (approximately 100 seconds) and prolonged effect (approximately two hours). Rocuronium has been advocated but represents a significant additional expense and may not provide optimal conditions for RSI [16].
Fentanyl
The advocacy for use of fentanyl as a premedication in RSI is based on its well-described effects on hemodynamic parameters during intubation. I did not find any studies that addressed the direct effect of fentanyl on ICP. RSI is well described to result in elevations in heart rate, blood pressure, and plasma catecholamine concentrations [17], and this is hypothesized to contribute indirectly to elevated ICP. Fentanyl effectively attenuates these hemodynamic responses [18,19] without inducing significant hypotension [20]. In his review, Ron Walls advocates that it be administered at 3-5 mcg/kg 1-3 minutes before laryngoscopy [10]. This seems to be purely based on the avoidance of tachycardia and hypertension with intubation, and not on any evidence of a direct effect on ICP.
Other agents
There is evidence that thiopental, propofol, and beta blockers attenuate the hemodynamic and intracerebral response to laryngoscopy and intubation, but their hypotensive qualities have made their use unpopular in brain-injured patients. In very hypertensive patients (e.g spontaneous ICH) thiopental especially may be considered as an induction agent at 3-5 mg/kg [21].
It is important to remember that virtually all data supporting the use of premedication in brain injury is based on ICP measurements in elective neurosurgical patients who underwent conventional induction of anesthesia rather than RSI. Therefore, it is difficult to advocate their use prior to RSI in acutely brain-injured patients. However, none of these medications has been demonstrated to have any harmful effects when used during RSI. I think that the decision to use these medications can be made by the individual on a case by case basis, keeping in mind that the top priority should always be securing the airway and maintaining adequate oxygenation. I don't think the evidence justifies delaying intubation in a hypoxic patient, as hypoxia has been definitively associated with increased mortality in traumatic brain injury [22].
Considering the controversy that has existed for 10-15 years regarding premedication, it is rather surprising that no randomized prospective trial of these agents has been published that addresses neurologic outcome and mortality. It seems that such a study would be relatively simple to design and implement, considering the fairly high frequency of brain-injured patients requiring intubation, and could result in a significant paradigm shift in emergency medicine practice either here or on the other side of the Atlantic.
References:
1. Burney et al. 1975 Anaesth Analg 54:687
2. Rudy et al. 1986 Heart Lung 15:488
3. Silber et al. 1997 Am J Emerg Med 15:263
4. Butler et al. 2001 Emerg Med J 18:343
5. Robinson et al. 2001 Emerg Med J 18:453
6. Bedford et al. in Shulman et al. 1980 Intracranial Pressure IV, Springer: 595
7. Donegan et al. 1980 Anesthesiology 52:516
8. White et al. 1982 Anesthesiology 57:242
9. Yano et al. 1986 Anesthesiology 69:651
10. Walls. 1993 Ann Emerg Med 22:1008
11. Thompson et al. 1982 Ann Emerg Med 10:526
12. Mori et al. 1973 Br J Anaesth 45:605
13. Minton et al. 1986 Anesthesiology 65:165
14. Stirt et al. 1987 Anesthesiology 67:50
15. Clancy et al. 2001 Emerg Med J 18:373
16. Perry et al. 2003 Cochrane Database Syst Rev Issue 1
17. Takeshima et al. (1964) Anaesth Analg 43:201
18. Ebert et al. (1989) Can J Anaesth 36:301
19. Helfman et al. (1991) Anesth Analg 72:482
20. Miller et al. (1988) Can J Anaesth 35:219
21. Shapiro et al. (1973) Br J Anaesth 45:1057
22. Stocchetti et al. 1996 J Trauma 40:764
Q/A with Tony Friedman Volume 2.0 - Treatment of Cellulits in the ED
2. Treatment of cellulitis in the ED.
THE QUESTION:
There seems to be a lot of variation in the way we manage cellulitis in the department. Is there any evidence that a single dose of IV antibiotics before discharge is superior to immediate discharge on PO antibiotics? What are the options for outpatient IV antibiotics? And what about patients with chronic bilateral leg edema who come in with redness of both legs? Should I be treating that as cellulitis or is a different pathology present?
THE ANSWER:
While many reviews acknowledge the practice of administering a single dose of IV antibiotic before discharge, none of them cited any supporting data and I was unable to find any studies specifically addressing this question in a Medline search. Therefore, this practice cannot be assumed to have an advantage over immediate discharge with a prescription for oral antibiotics.
If you are not comfortable with discharge of the patient on oral antibiotics and ongoing observation of the patient in the ED is not an option, one alternative to admission is outpatient intravenous antibiotic therapy. As PICC line placement and home visits for antibiotic administration can rarely be arranged rapidly, the best option is likely for the patient to return to the ED or primary physician's office at intervals for administration of antibiotics. Practical considerations favor a once daily antibiotic over one that must be administered more frequently, such as cefazolin or oxacillin.
Ceftriaxone has been used for outpatient IV therapy of cellulitis for at least 20 years. Several studies indicate clinical cure rates of 75-80% and improvement rates of 15-20%, with only 5% treatment failure rates [1]. Daily dosage of ceftriaxone has also been shown to have equivalent clinical efficacy to cefazolin [2] and gentamicin/clindamycin [3] in clinical trials. However, a failure rate of 4/8 was reported in the subgroup of diabetic patients with foot infections in a small study [4].
An alternative to ceftriaxone is once daily dosage with IV cefazolin with a daily PO dose of 2g probenecid. Probenecid reduces renal excretion of cefazolin, maintaining bactericidal concentrations in the blood for 24 hours. In one study, probenecid was administered with daily doses of ceftriaxione or cefazolin with similar treamtent failure rates of 7% and 8% respectively [5]. Another study found no significant difference in clinical cure rate between cefazolin/probenecid and ceftriaxone (86% and 96% respectively, p = 0.11). Despite the apparent trend towards an increased cure rate with ceftriaxone, the authors state that the study was sufficiently powered to exclude a significant difference between the two therapies. Adverse reactions such as nausea were more common with cefazolin/probenecid [6]. Also keep in mind that probenecid may potentially alter levels of other renally excreted medications.
There appears to be no solid evidence basis for oral versus intravenous antibiotic therapy regimens for cellulitis. Perhaps for this reason, wide practice variation has been noted in the treatment of cellulitis in urban emergency departments [7]. A large randomized prospective trial comparing pure oral therapy, single-dose IV therapy followed by oral, and outpatient IV therapy for efficacy, cost and patient satisfaction would go a long way towards resolving the issue.
It is important to remember that cellulitis is not the only condition that causes leg erythema. DVT is an obvious consideration with unilateral erythema and asymmetric swelling. It is well known to dermatologists that simple lower extremity edema may result in erythema in certain individuals [8], although this does not appear to have been formally studied. Nifedipine has been asssociated with erythematous edema of the lower extremities [9]. Another condition to keep in mind is varicose eczema, which is characterized by erythema along with crusting and/or scaling in one or both legs [10]. Small vesicles may frequently occur as well. While it can be difficult to distinguish erythematous edema or varicose eczema from cellulitis based on appearance, the diagnose of cellulitis should be reconsidered in a well-appearing patient without fever or leukocytosis. In addition, the simultaneous appearance of erythema on both legs should suggest a non-infectious etiology, although bilateral lower extremity cellulitis has been reported in large series [11].
One final point for cellulitis is that blood cultures are generally low yield and should not be routinely obtained. One study showed that only 2% of 553 patients with community-acquired cellulitis had positive blood cultures [12]. However, 3/10 patients with cellulitis superimposed on chronic lymphedema did have positive blood cultures [13], so this subgroup might require a different approach.
References
1. Gainer. (1991) Hosp Pract 26 Suppl 5:24
2. Bradsher et al. (1984) Am J Med 77:62
3. Gordin et al. (1985) Antimicrob Agents Chemother 27:648
4. Eron et al. (1983) Antimicrob Agents Chemother 23:731
5. Brown et al. [1996] J Emerg Med 14:547
6. Grayson et al. [2002] Clin Infect Dis 2002 34:440
7. Dong et al. (2001) Am J Emerg Med 19:535
8. Cox. (2002) Clin Med 2:23
9. Bridgman. (1978) Br Med J 1:578
10. Quartey-Papafio. (199) Br Med J 318:1672
11. Dupuy et al. (1999) Br Med J 318:1591
12. Perl et al. (199) Clin Infect Dis 29:1483
13. Woo et al. (2000) J Clin Microbiol Inf Dis 19:294
THE QUESTION:
There seems to be a lot of variation in the way we manage cellulitis in the department. Is there any evidence that a single dose of IV antibiotics before discharge is superior to immediate discharge on PO antibiotics? What are the options for outpatient IV antibiotics? And what about patients with chronic bilateral leg edema who come in with redness of both legs? Should I be treating that as cellulitis or is a different pathology present?
THE ANSWER:
While many reviews acknowledge the practice of administering a single dose of IV antibiotic before discharge, none of them cited any supporting data and I was unable to find any studies specifically addressing this question in a Medline search. Therefore, this practice cannot be assumed to have an advantage over immediate discharge with a prescription for oral antibiotics.
If you are not comfortable with discharge of the patient on oral antibiotics and ongoing observation of the patient in the ED is not an option, one alternative to admission is outpatient intravenous antibiotic therapy. As PICC line placement and home visits for antibiotic administration can rarely be arranged rapidly, the best option is likely for the patient to return to the ED or primary physician's office at intervals for administration of antibiotics. Practical considerations favor a once daily antibiotic over one that must be administered more frequently, such as cefazolin or oxacillin.
Ceftriaxone has been used for outpatient IV therapy of cellulitis for at least 20 years. Several studies indicate clinical cure rates of 75-80% and improvement rates of 15-20%, with only 5% treatment failure rates [1]. Daily dosage of ceftriaxone has also been shown to have equivalent clinical efficacy to cefazolin [2] and gentamicin/clindamycin [3] in clinical trials. However, a failure rate of 4/8 was reported in the subgroup of diabetic patients with foot infections in a small study [4].
An alternative to ceftriaxone is once daily dosage with IV cefazolin with a daily PO dose of 2g probenecid. Probenecid reduces renal excretion of cefazolin, maintaining bactericidal concentrations in the blood for 24 hours. In one study, probenecid was administered with daily doses of ceftriaxione or cefazolin with similar treamtent failure rates of 7% and 8% respectively [5]. Another study found no significant difference in clinical cure rate between cefazolin/probenecid and ceftriaxone (86% and 96% respectively, p = 0.11). Despite the apparent trend towards an increased cure rate with ceftriaxone, the authors state that the study was sufficiently powered to exclude a significant difference between the two therapies. Adverse reactions such as nausea were more common with cefazolin/probenecid [6]. Also keep in mind that probenecid may potentially alter levels of other renally excreted medications.
There appears to be no solid evidence basis for oral versus intravenous antibiotic therapy regimens for cellulitis. Perhaps for this reason, wide practice variation has been noted in the treatment of cellulitis in urban emergency departments [7]. A large randomized prospective trial comparing pure oral therapy, single-dose IV therapy followed by oral, and outpatient IV therapy for efficacy, cost and patient satisfaction would go a long way towards resolving the issue.
It is important to remember that cellulitis is not the only condition that causes leg erythema. DVT is an obvious consideration with unilateral erythema and asymmetric swelling. It is well known to dermatologists that simple lower extremity edema may result in erythema in certain individuals [8], although this does not appear to have been formally studied. Nifedipine has been asssociated with erythematous edema of the lower extremities [9]. Another condition to keep in mind is varicose eczema, which is characterized by erythema along with crusting and/or scaling in one or both legs [10]. Small vesicles may frequently occur as well. While it can be difficult to distinguish erythematous edema or varicose eczema from cellulitis based on appearance, the diagnose of cellulitis should be reconsidered in a well-appearing patient without fever or leukocytosis. In addition, the simultaneous appearance of erythema on both legs should suggest a non-infectious etiology, although bilateral lower extremity cellulitis has been reported in large series [11].
One final point for cellulitis is that blood cultures are generally low yield and should not be routinely obtained. One study showed that only 2% of 553 patients with community-acquired cellulitis had positive blood cultures [12]. However, 3/10 patients with cellulitis superimposed on chronic lymphedema did have positive blood cultures [13], so this subgroup might require a different approach.
References
1. Gainer. (1991) Hosp Pract 26 Suppl 5:24
2. Bradsher et al. (1984) Am J Med 77:62
3. Gordin et al. (1985) Antimicrob Agents Chemother 27:648
4. Eron et al. (1983) Antimicrob Agents Chemother 23:731
5. Brown et al. [1996] J Emerg Med 14:547
6. Grayson et al. [2002] Clin Infect Dis 2002 34:440
7. Dong et al. (2001) Am J Emerg Med 19:535
8. Cox. (2002) Clin Med 2:23
9. Bridgman. (1978) Br Med J 1:578
10. Quartey-Papafio. (199) Br Med J 318:1672
11. Dupuy et al. (1999) Br Med J 318:1591
12. Perl et al. (199) Clin Infect Dis 29:1483
13. Woo et al. (2000) J Clin Microbiol Inf Dis 19:294
Q/A with Tony Friedman (BIDMC HAEMR 2004)
The first entry (actually, the first three entries) will be taken from an earlier iteration of "B.I.T.C.H.E.S" - a previous graduate of the program, Tony Friedman, used to do a similar thing, which he (more politically correctly) named " Question Box". Some of the older residents in the program had saved a couple of these, which were all useful and interesting.
The first is on a topic that all ED residents know and love....(NOTE that these are copied directly from Tony's excellent work.
Total Resident Irradiation
THE QUESTION:
I've noticed that in a trauma, as soon as I hear someone yell "X-RAY!" I see a similar effect as if they had yelled "GRENADE!". Suddenly a huge flux of residents, nurses, and techs rushes for the door save for the unlucky few crushed underneath the horde. Foleys are left half inserted, laryngoscopes dangle from mouths, and syringes implanted in the femoral artery wiggle suggestively. After the danger has passed, everyone surges back into the room and tries to recall what was going on before the thermonuclear assault. Is all this really necessary? How dangerous are x-rays in a trauma?
THE ANSWER: This question has indeed been addressed in several studies. The most relevant, from 1994, assessed radiation exposure in surgical residents, ER attendings, and ER nurses according to dosimeters clipped outside of protective garments [1]. In one year, surgical residents were exposed to an average of 780 radiographs while ER attendings and nurses were exposed to 347 and 86 radiographs respectively. The average yearly exposure for surgical residents was 20 mrem, while ED attendings and nurses had average yearly exposures of about 3.5 mrem. Exposure per radiograph appeared to be approximately .03 mrem (lower for ER attendings, who presumably were watching safely from the corner of the room).
Much higher levels of exposure were found in a study from 1990 [2]. Residents were exposed to 481 radiographs over 3 months and sustained average monthly whole body exposure of 120 mrem, which extrapolates to a yearly exposure of approximately 1500 mrem. Average whole body exposure per radiograph was about 1.3 mrem, more than 40 times the average exposure seen in the first study described. I think this level is much less reflective of our exposure at BIDMC because their residents removed the cervical collar and manually stabilized the cervical spine during C-spine radiographs (duh!). Furthermore, at BIDMC plain radiographs of the cervical spine are rarely performed in trauma resuscitation. However, it would be useful to repeat the study due to the large discrepancy in average exposure per radiograph.
For the purposes of comparison, annual background radiation that we are all exposed to averages 100 mrem per year. In the 1994 study, even the most heavily exposed personnel received only an additional 20% exposure on top of background radiation. The National Council of Radiation Protection (NCRP) permits an annual occupational exposure of 5000 mrem, which further emphasizes the negligible exposure received during trauma resuscitations. Even assuming the exposure levels of the 1990 study, a worker would have to be exposed to several thousand films annually to exceed the NCRP recommendations.
Even for pregnant personnel, radiation exposure is not clinically significant. The NCRP permits occupational exposure of 500 mrem over the course of the pregnancy, which dwarfs the 20 mrem maximal annual exposure from trauma resuscitations.
This data suggests that it is not appropriate to interrupt a resuscitation, especially in the middle of procedures, in order to avoid radiation exposure. In addition, it is important to remember that these exposures were derived from dosimeters placed outside of protective aprons. Therefore, even the practice of wearing lead aprons in resuscitations owes more to superstition than it does to actual science.
References _1. Ciraulo et al. (1994) J Trauma 36:703 _2. Weiss et al. (199) Ann Emerg Med 19:134
(Reply from One of our attendings)
Tony
As usual great discussion but a few quick things. Your underlying premise is absolutely correct: We need not worry so much about incidental radiation exposure when in the room for X-rays, etc. However, you made a couple of mistakes with units. An "exposure" is not measured in Rem, it is measured as below:
Exposure:Roentgens (Common Units), Coulomb/Kg (SI units)
Radioactivity: Curie (CU), Becquerel (SI)
Absorbed dose: Rad (CU), Gray (SI)
Dose Equivalent: Rem (CU), Sievert (SI)
There are easy conversions between Common Units and SI units
Also, The Biologic Effects of Ionizing Radiation (BIER V) Committee of the National Research Council found if 100,000 people were exposed to a one-time absorbed dose of 10 rem (10,000 mrem) and were followed over their lifetime, about 790 more would die of cancer. A one-time dose of 10 rem is substantially more deleterious than a chronic exposure of much smaller units over time equaling 10 rem. As per your discussion this makes our exposure in routine radiography close to negligible.
Greg
The first is on a topic that all ED residents know and love....(NOTE that these are copied directly from Tony's excellent work.
Total Resident Irradiation
THE QUESTION:
I've noticed that in a trauma, as soon as I hear someone yell "X-RAY!" I see a similar effect as if they had yelled "GRENADE!". Suddenly a huge flux of residents, nurses, and techs rushes for the door save for the unlucky few crushed underneath the horde. Foleys are left half inserted, laryngoscopes dangle from mouths, and syringes implanted in the femoral artery wiggle suggestively. After the danger has passed, everyone surges back into the room and tries to recall what was going on before the thermonuclear assault. Is all this really necessary? How dangerous are x-rays in a trauma?
THE ANSWER: This question has indeed been addressed in several studies. The most relevant, from 1994, assessed radiation exposure in surgical residents, ER attendings, and ER nurses according to dosimeters clipped outside of protective garments [1]. In one year, surgical residents were exposed to an average of 780 radiographs while ER attendings and nurses were exposed to 347 and 86 radiographs respectively. The average yearly exposure for surgical residents was 20 mrem, while ED attendings and nurses had average yearly exposures of about 3.5 mrem. Exposure per radiograph appeared to be approximately .03 mrem (lower for ER attendings, who presumably were watching safely from the corner of the room).
Much higher levels of exposure were found in a study from 1990 [2]. Residents were exposed to 481 radiographs over 3 months and sustained average monthly whole body exposure of 120 mrem, which extrapolates to a yearly exposure of approximately 1500 mrem. Average whole body exposure per radiograph was about 1.3 mrem, more than 40 times the average exposure seen in the first study described. I think this level is much less reflective of our exposure at BIDMC because their residents removed the cervical collar and manually stabilized the cervical spine during C-spine radiographs (duh!). Furthermore, at BIDMC plain radiographs of the cervical spine are rarely performed in trauma resuscitation. However, it would be useful to repeat the study due to the large discrepancy in average exposure per radiograph.
For the purposes of comparison, annual background radiation that we are all exposed to averages 100 mrem per year. In the 1994 study, even the most heavily exposed personnel received only an additional 20% exposure on top of background radiation. The National Council of Radiation Protection (NCRP) permits an annual occupational exposure of 5000 mrem, which further emphasizes the negligible exposure received during trauma resuscitations. Even assuming the exposure levels of the 1990 study, a worker would have to be exposed to several thousand films annually to exceed the NCRP recommendations.
Even for pregnant personnel, radiation exposure is not clinically significant. The NCRP permits occupational exposure of 500 mrem over the course of the pregnancy, which dwarfs the 20 mrem maximal annual exposure from trauma resuscitations.
This data suggests that it is not appropriate to interrupt a resuscitation, especially in the middle of procedures, in order to avoid radiation exposure. In addition, it is important to remember that these exposures were derived from dosimeters placed outside of protective aprons. Therefore, even the practice of wearing lead aprons in resuscitations owes more to superstition than it does to actual science.
References _1. Ciraulo et al. (1994) J Trauma 36:703 _2. Weiss et al. (199) Ann Emerg Med 19:134
(Reply from One of our attendings)
Tony
As usual great discussion but a few quick things. Your underlying premise is absolutely correct: We need not worry so much about incidental radiation exposure when in the room for X-rays, etc. However, you made a couple of mistakes with units. An "exposure" is not measured in Rem, it is measured as below:
Exposure:Roentgens (Common Units), Coulomb/Kg (SI units)
Radioactivity: Curie (CU), Becquerel (SI)
Absorbed dose: Rad (CU), Gray (SI)
Dose Equivalent: Rem (CU), Sievert (SI)
There are easy conversions between Common Units and SI units
Also, The Biologic Effects of Ionizing Radiation (BIER V) Committee of the National Research Council found if 100,000 people were exposed to a one-time absorbed dose of 10 rem (10,000 mrem) and were followed over their lifetime, about 790 more would die of cancer. A one-time dose of 10 rem is substantially more deleterious than a chronic exposure of much smaller units over time equaling 10 rem. As per your discussion this makes our exposure in routine radiography close to negligible.
Greg
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