Thursday, June 22, 2006

Pharyngitis Phacts

I'm looking to hit a couple "hot-button" topics coming up. As well I'm trying to set up a LLSA review forum. I'd like to do a little review of pharyngitis. I feel that this is one topic where I see a huge variation in work-ups and evaluation. I think we probably over-test and over-treat this diagnosis. So let's review this, shall we?
  • Let me start off by saying this is a chief complaint that enables us to perform a lot of patient education. I think you'll find that sitting down with a patient or parent for five minutes will save them time (waiting for lab tests), you time (quicker dispositions) and money (paying for said lab tests and the antibiotics they probably don't need). Also the antibiotic choices I see are varied and too aggressive for a pharyngitis that is a) probably a virus b) self-limiting and likely will get better on its own and c) too broad spectrum when treating one specific, easily treated bacteria. These are important points to consider the next time you're tempted to test and treat.
  • MOST CASES OF PHARYNGITIS ARE DUE TO VIRUSES. This should probably be the first and last sentence out of your mouth to the patients.
  • The majority of cases of acute pharyngitis are self-limiting and only need supportive care (again an important discussion point).
  • Seven million cases of pharyngitis visits annually in the US.
  • Common viruses behind acute pharyngitis: Coxsackievirus, echovirus, adenovirus, HSV, and EBV (usually associated with LAD, splenomegaly). Consider mono as well (especially in patients with posterior cervical LAD).
  • Group A Beta-Hemolytic Strep (GABHS) is the bacterial infection that we end up over-treating for.
  • GABHS is the cause of only 15-30% of acute pharyngitis in pediatrics. It causes only 10% of adult acute pharyngitis cases. These are nice facts to present to patients/parents during your educational talk with them.
  • Other bacterial causes are Group C, Group G Beta-hemolytic strep, Corynebacterium diphtheriae, Mycoplasma, Chlamydia and Neisseria gonorrhoeae (if you have to ask how it got there, I'm not going to be the one telling you).
  • Pharyngeal diphtheria typically has the grayish brown pseudomembrane. They can have significant soft tissue edema and cervical LAD resulting in the "bull-neck" appearance.
  • Most cases of pharyngitis occur in winter and early spring.
  • Group C hemolytic strep can cause outbreaks (especially in teenagers and adults).
  • I'm not going to go over the typical clinical features of acute GABHS. I think we're all well versed on this.
  • Scarlet Fever: A URI due to GABHS with a classic "sandpaper" rash. This occurs because of a pyrogenic exotoxin released by GABHS. The occurence of Scarlet fever has significantly decreased in frequency and virulence over the years.
  • The rash associated with Scarlet Fever blanches and is typically more pronounced in the flexor surfaces of elbows, axilla and groin.
  • Scarlet Fever rash typically has its onset 24-48 hours after the first signs of the pharyngitis. It'll typically last 3-4 days and results commonly in desquamation.
  • The tongue can commonly give a "strawberry" appearance due to desquamation and promient papillae.
  • So since we know that viruses cause the majority of acute pharyngitis, are there clinical signs that suggest a viral etiology? I'm glad you asked...
  • The Centor criteria: No longer should these be pimp questions, but educational tools for your patients. The four Centor criteria are a) history of fever b) tonsillar exudates c) no cough, and d) tender anterior cervical lymphadenopathy (lymphadenitis). If the patient meets all four criteria, it's more likely bacterial. Other symptoms consistent with viral pharyngitis are headaches, coryza, cough, rhinorrhea, myalgias, conjunctivitis, exanthem, and odynophagia.
  • Some have taken the position that you should not test or treat patients with none or only one of these criteria, since these patients are unlikely to have GABHS infection. Again, if they have met ZERO OR ONE criteria, do not bother testing or treating with antibiotics. Supportive care only.
  • For patients with two or more criteria the following three options are recommended by Internal Medicine docs: OPTION #1) Test patients with two, three, or four criteria by using a rapid antigen test, and limit antibiotic therapy to patients with positive test results. OPTION #2) Test patients with two or three criteria by using a rapid antigen test, and limit antibiotic therapy to patients with positive test results or patients with four criteria (don't test, just treat); or OPTION #3) Do not use any diagnostic tests, and limit antibiotic therapy to patients with three or four criteria.
  • My personal feeling is that these are a little conservative even for the simple fact that individuals that meet ALL FOUR Centor criteria still only 50% of the time have GABHS. Thus why not simply avoid testing all patients and simply treat the ones who have only met ALL FOUR Centor criteria? Some docs (including myself) take this approach.
  • Testing: Sensitivity of RSA is 90-95% when done correctly (big caveat). Specificity of most RSA's are 60-95%. Also no test can distinguish those infected with acute GABHS and those that are carriers.
  • Throat cultures: why bother getting them? They typically need 48 hours to be accurate. Also since RSA's are typically 95% sensitive, what's the benefit. By the time you get the results back, they'll probably confirm what you already know. Also only 50% of positive throat cultures are acutely infected (people can also be carriers).
  • Treatment: So if symptoms typically resolve in 3-4 days after treatment, why bother? Antibiotics have been shown to shorten the course in 13% by a whopping one day. So again, why bother treating? The one reason to treat is due to the possibility of acute rheumatic fever secondary to GABHS (as a quick aside antibiotics DOES NOT change the incidence of glomerulonephritis secondary to GABHS). With regards to the treatment to prevent rheumatic fever, antibiotics can be delayed up to nine days after the onset of symptoms and still be effective. Other reasons are because GABHS can progress to a PTA, retropharyngeal abscess, sinusitis, OM, or mastoiditis. Again, rare sequelae to GABHS.
  • Acute rheumatic fever typically doesn't occur for 2-4 weeks after onset of the acute pharyngitis. Post-streptococcal glomerulonephritis doesn't occur for 3 weeks until onset of original symptoms. The incidence of rheumatic fever is typically 0.3% (up to 3% in epidemic outbreaks). Still very small when you consider that only 10-15% of the cases will be due to GABHS AND only 0.3% of those patients could develop rheumatic fever. Your patients probably will have a greater chance of having an anaphylatic reaction to the antibiotics you give them.
  • IF despite this blog, you're still determined to treat you have only two accetable choices of antibiotics. You should give everyone PCN unless they're allergic. IF they're allergic to PCN then the only reasonable option is Erythromycin. Do not use amoxicillin, cephalosporins, maxipime, etc. GABHS has never become resistant to PCN in cultures. Therefore why use a more broad-spectrum, expensive antibiotic when PCN works perfectly fine?
  • If you're going to treat you have a choice of either PCN V (oral) or G (IM). I'm a personal fan of IM (I know, I'm sadistic). To me, it's easier to do a one time shot, versus qid oral dosing for ten days. If you ever look at studies that show how compliant patients are when taking 40 doses of a medicine, you'd not even bother writing the Rx. Also if the patient is going to be better in 3-4 days, do you really forsee them continuining a ten day course?
  • Doses: PCN G 1.2 million units (greater than 27 kg) IM or 0.6 MU if less than 27 kg) one time IM.
  • PCN V 250 mg PO bid/tid x 10 days in children; In adults 250 mg PO tid/qid x 10 days or 500 mg PO bid x 10 days. (Again is it really worth it?)
  • Again, if they're PCN allergic, erythromycin is the best alternative.
  • Thus, if you take away some key points from this, review the Centor criteria with the patient/parents, explain the disease epidemiology, the logic behind not testing and whether antibiotics are warrented. You probably can significantly shorten LOS in the ED, increase patient satisfaction and decrease patient cost.
  • Hope this was helpful. I'm out.

Wednesday, June 07, 2006

Bob's Bits

So I received a request from a partner whose identity will remain anonymous. Let's just call this person "Rob Rarrali"... Well "Rob" requested some info on a couple of topics and since I aim to please, let's try to enlighten the group. In this discussion we'll discuss peritonsillar abscesses (PTA)'s:
  • To drain or not to drain?
  • To CT or not to CT?
  • To Admit or 'vaya con dios'?
  • What Abx?
  • When to involve ENT?

To begin with let's review some background information on the subject. Fun useless fact of the day: The other name for PTA is "Quinsy". The diagnosis of PTA is not always easy. Obviously your landmarks can be distorted, trismus may limit visualization and most importantly the hallitosis may prevent close inspection. One case series showed that the clinical diagnosis of PTA is only 78% sensitive (not great). The most common actual diagnosis (if it's not a PTA) is peritonsillar cellulitis. This can as well give you tonsillar erythema and edema.

Why do we care so much about PTA's. Won't they just eventually burst, drain and resolve? Well silly, of course if you want to wait for that to happen, you'll need to hope they avoid airway obstruction. Also, PTA's untreated can resolve in caudad spread with mediastinitis, sepsis and pericardial tamponade. Other than that, they're not such a big deal. All of the literature I reviewed felt that needle aspiration or I&D were required. Not one mentioned observation and IV Abx as being adequate treatment for a true PTA.

Also if you do perform a needle aspiration, the false negative rate for experienced physicians is still 10-12% (likely higher in the inexperienced or those using the patented "Mattison Blind Repeated Stabbing Technique")... Ergo, we want to make sure that there's actually an abscess to drain if we're going to go through this much trouble.

With regards to CT, yes, it's an excellent test in the diagnosis of PTA (nearly 100% sensitive). However, in the acute patient who doesn't want to stay supine or has impending airway issues, I don't feel comfortable waiting for the BMP to be drawn so they can get their CT w/ IV contrast to evaluate and confirm what I already suspect is there (thus delaying definitive treatment by at least 2 hours usually).

So why don't we just stick a needle in suspected PTA's? Well of course, the concern is about tapping into "big red" (aka carotid artery).

An interesting study done by Blaivas et al (Am J Emerg Med 2003;21:155-158) evaluated the ue of bed-side U/S by ED docs to confirm the presence and assist in aspiration of PTA's. Prior studies evaluated intraoral (IO) placement of an U/S probe (which to me is the most difficult part of this study to stomach. I gag brushing my teeth, much less tolerating an U/S probe in my mouth while I already have a PTA - and let's keep the jokes about gagging and probes in mouth to a minimum people)...

Earlier studies showed sensitivities of detecting PTA's with IO probes to be 89-92% while specificity was 80-100%. This particular study evaluated the use of IO probes by ED physicians in 6 probable PTA cases. Three of the cases ended up being confirmed as peritonsillar cellulitis on U/S, while the other three were confirmed PTA and they utilized real-time guidance to perform the aspiration (two of the three originally had multiple blind attempts resulting in failure aspiration was successful w/ an IO probe). Now obviously this is a small N, however it's the only study looking at ED docs using these probes.

Now seeing that we still need a portable U/S probe and the fact that our ENT coverage is improving, I think realistically we won't be doing IO-guided aspirations in the next year. However, if we have the portable SonoSite with an IO probe, it'd be an excellent way to quickly confirm the diagnosis. Plus, if ENT is not readily available, we could perform real-time IO-guided aspiration. Also, the odds of tapping into "big red" are significantly reduced by the IO technique. Finally, there are IO probes that have guide needles already attached so it's point and shoot (no hand-eye coordination required for those video-game challenged).

What about antibiotics? Well obviously in peritonsillar cellulitis IV abx are required (and no I&D). Preferred Abx are PCN + Flagyl. Other choices are cefoxitin, augmentin, and clindamycin. You'll need the same spectrum of Abx for abscesses.

As for ENT consultation, once I have a PTA diagnosed, I try to get a hold of them. It sounds like we'll have some difficulty at MGMC for awhile. The question is whether IV Abx and close observation is adequate. From my experience and point of view, all PTA's need to be seen by ENT that day. If that means having to transfer to another ED and then having them be d/c'd home fine. If that means IV Abx in the ED and the patient being seen in less than six hours, that's acceptable.

Hope this has been helpful. More questions to be answered soon.

Sunday, June 04, 2006

Case Report #1



This will be the first case report. Thanks to Evan for the case. I'll try to provide these in a format that allows you to review the H&P, objective data and then provide some questions with regards to clinical decision making. I'll then provide the diagnosis followed by some learning bullets about the specific case. Ergo, I will withhold some information to allow you to think about the case a bit (ala oral boards). If you have any cases that you think we would be beneficial from a learning standpoint please give me the name and medical record number. These cases can be as simple an interesting x-ray, CT or EKG. The more cases you provide, the more I can put on the site and we all benefit.
I'm still working on some format issues. I don't want the EKG's to be on the top of the blog, but for time being consider the first one to be EKG #1 and the 2nd #2. And now on to case report #1...
CC: "Depressed"
HPI: 76 yo male depressed over a recent diagnosis of dementia. He denies any significant findings on ROS except for depression.
PMHx: Dementia, depression, CAD, HTN, hypercholesterolemia
Meds: Exelon, Triamterene, Digoxin, Lisinopril, Namenda, Pentoxifyline, Zocor
PSHx: CABG x 2
SHx: Denies tobacco or drugs. Rare alcohol use
ROS: Negative for all major systems except depression
V/S: Temp: 98 HR: 78 RR: 18 BP: 167/73 Sats: 98% (RA)
PE: No significant findings except for cardiovascular exam that reveals a bradycardic, irregularly irregular rhythm. Neuro exam non-focal. No other significant findings.
Question #1: Assuming this patient has no history of A-fib, what are some possible etiologies of his new A-fib?
Question #2: If this patient told you he was depressed and took extra medicine, which ones could cause potentially cause the new A-fib?
EKG #1:
An OD panel, cardiac markers and digoxin level were ordered.
Question #3: What are some signs and symptoms of digoxin toxicity?
Question #4: What EKG findings are consistent with digoxin toxicity?
Question #5: What are the criteria for administering Digibind?
The patient was placed on a monitor with a HR of 61. He continued to become more bradycardic. A second EKG was performed.
EKG #2:
Significant lab values included a potassium of 4.8, creatinine of 1.1, ASA, tylenol and EtOH were all negative. The patients digoxin level was 35. The patient admitted to taking #8-10 Exelon 3 mg tablets and #16 Digoxin 0.125 mg tablets two hours PTA. A repeat potassium increased to 5.6. Toxicology was involved early and often. Digibind was appropriately administered and the patient was admitted to the ICU. He later was discharged to a SNF after being cleared by psych.
Learning Points:
  • Digoxin increases the force of myocardial contraction, thereby increasing cardiac output in patients with heart failure. It affects the Na/K+ pump (remember your biochem).
  • In toxic doses, the disruption of the pump prevents transport of K+ into the cells, thus you can get toxic hyperkalemia.
  • Digoxin also increases vagal activity and decreases sympathetic activity. This results in decreased conduction through the AV node.
  • In digoxin toxicity, you can get both tachy- and bradycardias.
  • Common digoxin arrhythmias include EVERYTHING, but pathognomonic are A-fib w/ slow ventricular rate, bidirectional V-tach, and atrial tachycardia w/ associated AV block.
  • Remember as well that digoxin typically gives an ST depression/scooping in the V5-V6 leads "hockey-stick". This is seen even at therapeutic doses. It may help however, in the case of AMS and you don't have a medication list.
  • As a practice, if any patient is on digoxin and they have any complaint that could possibly be due to digoxin toxicity, ALWAYS CHECK A LEVEL. Rarely does this get done in triage and many times I've had to hold a patient while this gets done. So it'd help if we got the word to the triage nurses to be ordering this (my personal opinion).
  • The most common constitutional symptoms are nausea, fatigue, anorexia, and visual disturbances (blue-green halo - "Van Gough effect")
  • The mean peak digoxin level after an oral dose is 2 hours with a range of 0.5-6 hours.
  • In chronic toxicity, the potassium is actually usually low-normal, but high in acute toxicity.
  • Digitalis is found in foxglove, oleander and lily of the valley. (Remember these when you get the altered child who may have been eating plants or people who make home-brewed teas).
  • Patients who are on digoxin are typically also taking diuretics. In these cases they commonly have hypomagnesemia. Try replacing Mg2+ with 1-2 g IV over 2 minutes to help with ventricular dysrhythmias.
  • Indications for Digibind:
  • a) ventricular dysrhythmias
  • b) Progressive and hemodynamically significant bradydysrhythmias unresponsive to atropine
    c) Serum potassium greater than 5 mEq/L
    d) Rapidly progressive rhythm disturbances or rising serum potassium
    e) Coingestion of cardiotoxic drug as β-blockers, calcium channel blockers, or tricyclic antidepressants
    f) Ingestion of plant known to contain cardiac glycosides plus severe dysrhythmias (rare)
    g)Acute ingestion greater than 10 mg plus any one of factors 1 through 6 above
  • h) Steady-state serum digoxin greater than 6 ng/ml plus any one of factors 1 through 6 above
  • There are several formulas for determining how many vials of Digibind you'll administer. My thought is you're not going to remember them (factors include weight, bioavailability -80%, etc). Realistically, you're going to be consulting toxicology anyways AND it's very expensive. Thus, they're going to tell you how much. You also may have to give several doses.

That's it for this first case. Let me know if you thought it was helpful and if you have any cases forward them on.

Thursday, June 01, 2006

June Nubbins

  • I'm looking to get people together in August some time that we can get together and have a group "review" session for the LLSA test for EMCC. Look for dates and times coming up. Before you take the test this year, you may want to wait for the group.
  • I'm going to be posting the first patient case blog in the next couple of days (once I get the home office and scanner up and running). Should be an interesting one so keep an eye out for it. Now on to our journal reviews...
  • Allen, T.L., et al, Am J Emerg Med 23:253, May 2005: PO contrast is not required in CT Abd/pelvis for blunt trauma, especially looking at diaphragmatic injuries. This study is limited by numbers (as you'd expect with a rare injury).
  • Sokolove, P.E., et al, Acad Emerg Med 12(9):808, September 2005: Big surprise, but a seatblet sign in pediatric patients should clue you into the possibility of abdominal trauma and get a CT.
  • Topol, E.J., N Engl J Med 353(2):113, July 14, 2005: Editorial from the former cardiology chair at the Cleveland Clinic- bottom line is that nesiritide is NOT a good drug to use in the ED for CHF exacerbation (same results as NTG gtts with a much higher cost and increase in side effects and mortality).
  • Masip, J., et al, JAMA 294(24):3124, December 28, 2005: Non-invasive ventilation (BiPAP/CPAP) decreases mortality in acute pulmonary edema and should be front-line therapy. These are small, pool studies, but the bottom line is I'm a big proponent of NIV in the treatment of acute CHF exacerbation with respiratory symptoms and pulmonary edema. It has kept me from intubating quite a few patients and given in conjunction with lasix, NTG gtts, and Morphine usually will turn around extremely ill patients within 30-45 minutes. Again, from the "Journal of Mattison Anectdotal Evidence"...
  • Chen, W.L., et al, Emerg Med J 23:e01, January 2006: A case report (so take it with a grain of salt) of a patient with vertebral artery dissection AFTER chiropractic manipulation. Some info to provide your patients who are interested in this option.
  • Taddio, A., et al, Can Med Assoc J 172(13):1691, June 2005: Topical liposomal lidocaine provides equal anesthetic relief in 30 minutes when compared to subQ lidocaine. It takes about 30 minutes to be effective (quicker than EMLA) and would be a nice choice in peds.
  • Kim, T.Y., et al, Ped Emerg Care 22(1):28, January 2006: Lethargy and swelling around the shunt size are the only statistically significant signs of ventricular shunt malfunction (that correlate with CT). Also look for headaches, N/V and seizures. Obviously you'll do a CT (to look for enlarged ventricles). The other films you can order our shunt series (plain film x-rays). I personally have never seen a shunt series that was beneficial. General opinion also agrees with the fact that this does not offer much in the way of work-up (the CT is the key).
  • Benson, P.C., et al, Ann Emerg Med 47(1):100, January 2006: Emirical IV acyclovir is indicated in suspected cases of viral ENCEPHALITIS. In the cases of viral meningitis, it's not warranted, but if you suspect encephalitis (AMS), go ahead and give it.
  • Iosif, A., et al, Can Med Assoc J 173(12):1498, December 6, 2005: Not an important study, but it's interesting to note that there appears to be no correlation between lunar cycles and increasing mania or "madness". Thus there is no true "full moon effect".
  • Lang, E., et al, Can Med Assoc J 174(3):313, January 2006: An interesting study from Montreal where family practice doctors received an emailed transcript of the ED visit, labs, etc. the day AFTER the ED visit. Sounds like a great idea that would improve communication, follow-up, etc. Actually there was an INCREASE in multiple consultations and other factors that you'd assume were improved with this information. It sure sounds like a nice idea though and it'd be interesting if the primary doctors could receive an email of the WEBMEDX typed charts of their patients after the ED visits. Something to consider if feasible.
  • One CT of the Abd/pelvis is equivalent to 500 CXR's in the pediatric population. A fun fact for parents who are adament about a CT when you don't think it's warranted.
  • Ozucelik, D.N., et al, Int J Clin Pract 59(12):1422, December 2005: A Turkish study (have to plug that) that utilized Reglan 10 mg IV 15 minutes before NGT placement showed a significant decrease in discomfort and nausea. Consider it the next time you have a patient who's not tolerating or doesn't think they'll tolerate an NGT well.
  • Jefferson, T., et al, Lancet 367:303, January 28, 2006: Antivirals (neuraminidase inhibitors) for influenza are only efficacious in the acute illness, when treated early and may shorten the course by only 24 hours.
  • Shafi, S., et al, J Trauma 59:1140, November 2005: An interesting study that supports my experience that intubation with positive pressure ventilation (PPV) in hypotensive trauma patients caused an increase in hypotension and overall lower survival. Obviously there's a selection bias in that the sicker patients needed to be intubated. The take home point is be careful with PPV in hypotensive patients (even if they aren't trauma patients, i.e. COPD).
  • Christopher Study Investigators JAMA 295(2):172, January 11, 2006: This is a new algorithm looking at PE: a little bit more simple in that you're either a) low-risk or b) non-low risk. You perform a D-dimer in low-risk only and don't treat them if negative. You do a CT angiogram in all the others and treat if positive. There were some technical problems with the study and follow-up stats, but you may be hearing more about this.
  • Evans, R., Emerg Med J 23:64, January 2006: Very interesting study that examined the use of absorbable sutures in the pediatric population. There was no difference in cosmesis or complications, PLUS there was an actual decrease in dehiscence. The bottom line is that absorbable sutures will do just as well and parents don't have to bring back the child for suture removal. The only question I would have is with regards to facial wounds where you want the sutures out at an exact time frame (5 days) in order to diminish scarring. Other than that any other sutures should be absorbable in pediatrics.
  • One last reminder for all docs and PA's- when writing for cipro or levaquin (any fluorquinolone) remember that the PO form has 100% bioavailability. Thus if the patient can swallow a pill, give it to them PO. It's much cheaper than IV and works just as well. Also consider how much easier and quicker it is to administer.
  • That's it for right now. The first case study should be out in a few days.