Treat a patient with PE as an outpatient? Insanity! But where is the evidence that says we’re doing the right treatment with all of the PEs we diagnose? The original publications that launched our current way of thinking about PEs are not what I would call practice changing, and if published today, would probably be interesting anecdotes rather than news makers.

The question: Do we need to hospitalize all patients diagnosed with pulmonary embolism in the ED? Can some be discharged and managed as outpatients?

Currently, the diagnosis of PE in the United States means admission to the hospital. This is much easier than setting up outpatient anticoagulation and risk stratifying patients. Setting up a patient to go home on low molecular weight heparin (LMWH) and warfarin, getting lab rechecks, connecting them with follow up, etc, takes time. In the case of PE, is that going to be time well spent? Read on.

When we’re talking about the outpatient treatment of  PE, there are several factors to consider.

 1.Is this safe for our patient?

The corollary to that is: Is the patient going to benefit from hospitalization? If they are unstable, they may need critical or at least very closely monitored care. But for the majority of PEs, that’s not the case. What else do they get? They get definite medication. In this case LMWH and warfarin and perhaps connection with follow-up. Although I suspect that many patients are discharged from the hospital before their INR is therapeutic, so in a way, they are also being treated as outpatients.

2. Is outpatient treatment inferior to inpatient  and are there systems in place to make outpatient treatment work?

If you’re talking about a treatment  that doesn't require monitoring, like antibiotics for pneumonia, there’s no need get doxycycline levels checked. But with PE, close and continued monitoring is critical.

3.Are we going to cause any harm? 

Patients are going to get the same anticoagulants whether they’re in the hospital or at home. This was the magic of LMWH in treating DVT-we no longer had to admit patients to give them heparin.

The main complication/iatrogenic effect we worry about is bleeding. An argument in favor of hospitalization could be that some hemorrhage risk factor was missed and we can observe for serious hemorrhage. Also, hospitalized patients will have their blood monitored frequently. As we’ll see, this could mean a shorter time on dual anticoagulation (shots and pills) and subsequently lower risk of bleeding. But no matter where where patients are dispositioned, bleeding is going to happen.  If you thin enough people’s blood, some of them are going to bleed.

What are the key points to tease out from the literature?

1) Is outpatient treatment inferior to inpatient?

2) Will we cause our patients harm?

3) What are the inclusion and exclusion criteria we can replicate them in our clinical practice?

4) Is the treatment strategy feasible and something we can and should be doing?

Outpatient versus inpatient treatment for patients with acute pulmonary embolism: an international, open label, randomized, non inferiority trial. Lancet July 2011.

Design: 344 patients with acute, symptomatic pulmonary embolism and low risk of death as determined by a PESI (pulmonary embolism risk severity index) score of 1 or 2, randomized to either outpatient or 5 days of inpatient treatment. Primary outcomes:  symptomatic, recurrent venous thromboembolism (VTE) within 90 days. Safety outcomes: mortality within 90 days and major bleeding.

 1) Is outpatient treatment inferior to inpatient? There was one recurrent VTE in the outpatient group versus zero for the inpatients. Outpatient therapy was deemed non inferior to inpatient.

 2) Will we cause our patients harm? Outpatients were treated with LMWH for 11.5 days versus 8.9 days for inpatients. Could longer treatment with dual anticoagulation lead to increased bleeding? It surely doesn’t help. Two outpatients and no inpatients had major bleeding with 14 days. At 90 days, 3 outpatients and no inpatients had major bleeding. There was one death in each group.

 3) What are the inclusion/exclusion criteria and can we replicate them in our clinical practice?  PESI is an 11 point scoring system used to predict 30 day mortality in patients with PE. No special testing beyond a good H and P and a little bit of diagnostic data is needed to populate the pieces of PESI. Patients were deemed low risk and appropriate for outpatient management if they were PESI class 1 or 2. There were also several exclusion criteria that are easy to determine in the ED. This can be replicated in clinical practice.

The Hestia study. Outpatient treatment in patients with acute pulmonary embolism. Journal of Thrombosis and Hemostasis 2011.

A single treatment arm study with 297 patients managed as outpatients. There was no control group.

1) Is outpatient treatment inferior to inpatient? Since there was no control arm in this study, non-inferiority cannot be directly determined. The authors used a 7% recurrence rate of VTE as the efficacy cutoff (based on previous publications). Six patients (2%, 95% CI 0.8-4.3) had recurrent VTE. Based on a goal efficacy of 7%, outpatient therapy was deemed non-inferior to inpatient.

2 ) Will we cause our patients harm? Three patients died in the three month follow up period, but none of the deaths were felt to be caused by PE. One patient had  a fatal intracranial hemorrhage (0.3%) and two had major bleeding events.

3 ) What are the inclusion/exclusion criteria and can we  replicate them in our clinical practice? The exclusion criteria are an 11 point yes/no checklist. This can be replicated in clinical practice. There is nothing here that requires special testing beyond what is regularly asked or evaluated in an emergency department chest pain workup.

The Hestia Checklist

1. Is the patient hemodynamically unstable?
2. Is thrombolysis or embolectomy necessary?
3. Active bleeding or high risk of bleeding?
4. More than 24 h of oxygen supply to maintain oxygen saturation > 90%?
5. Is pulmonary embolism diagnosed during anticoagulant treatment?
6. Severe pain needing intravenous pain medication for more than 24 h?
7. Medical or social reason for treatment in the hospital for more than 24 h (infection, malignancy, no support system)?
8. Does the patient have a creatinine clearance of < 30 mL min)?
9. Does the patient have severe liver impairment?
10. Is the patient pregnant?
11. Does the patient have a documented history of heparin-induced thrombocytopenia?

The Big Question

Should we manage select ED patients with PE as outpatients?

All pulmonary emboli are not created equal. The elderly patient with a saddle embolus and a history of heart failure is different from the otherwise healthy 30 year old with a small peripheral clot, no medical problems and stable vital signs. The irony is that, beyond thrombolysis in the hemodynamically unstable, all PEs are treated as equals. Evidence is mounting that we should think of PEs along a spectrum of risk and treat accordingly. Do all patients with PE need to be admitted to the hospital? Probably not. But there are a few qualifiers if you are thinking of discharging your patient from the ED...

 Easy access to outpatient resources and clearly defined follow up are essential to making this work. In the Lancet study, outpatients were on dual anticoagulants 2.5 days longer, and this was in a setting where it can be inferred that there was close monitoring and follow up.  Whether the 2.5 days of extra treatment was significant is unclear, but it stresses the importance of close monitoring.

Risk stratify to select the appropriate patients. The criteria used in these two studies do not require any special testing.

Shared decision making: Like most of the decisions made in medicine, the final call is up to the patient. Our job is to diagnose, educate and treat- with emphasis on educate.

Decide in your group/hospital/community if this is going to be the standard practice. Are systems in place to assure close follow-up and monitoring?

Links

Emergency Medicine Literature of Note

Basics of Emergency Medicine Pocket Guide by Joe Habboushe

Electrophysiologist, cyclist, and philosopher Dr. John Mandrola from The Dr. John M blog joins ERcast to discuss the intersection of sports and cardiology.

In this podcast, John gives his take on....

• Are marathons bad for you?
• Sudden death in sports
• How should you counsel patients before they start a fitness program?
• What are the important things to watch for on a sports physical?
• Early repolarization: harbinger of death or no big deal
• Managing atrial fibrillation in the athlete

Important links

Cardiac Arrest during Long-Distance Running Races

The EKG of an athlete

In this episode we talk with Dr. Scott Weingart about new developments in caring for patients in cardiac arrest including:

• End tidal CO2 monitoring
• Therapeutic hypothermia
• Should all post arrest patients with return of spontaneous circulation go to the cath lab?
• A logical approach to managing the airway during cardiac arrest resuscitation

Airway control in a cardiac arrest

What’s one of the first things that happens when a patient gets transferred from the paramedic stretcher to the ED bed? The extraglottic airway comes out and the patient gets intubated. Considering the circumstances, is doing this action within the first few minutes of a resuscitation the best use of your time, and more importantly, the patient’s time? We have a tendency to think of non-endotracheal tube airway devices as inferior and often that is the case. But is it the case here? What advantage do you get from changing out a functioning supraglottic/extraglottic airway device in the early stages of cardiac arrest resuscitation? Probably not much.

What do we always fret about when rushed placing an ET tube? Esophageal intubation. If that happens, things just went from under control to FUBAR in a hurry. At a time when you want to focus in getting good uninterrupted chest compressions, giving electricity, and sorting out what’s going on, getting definitive tracheal airway control has a low return on investment. If the patient is just being bagged with a BVM (bag valve mask), go ahead and put in a device that doesn’t require an all stop - such as an extraglottic airway device. That DOES have a return on investment because it gives you an extra set of hands now that the person who had to hold the BVM on the face is now free. Perhaps more importantly - getting a good, consistent BVM facial seal in a code is challenging. It seems easy in practice, but in the heat of battle it is not. it’s hard.

Important links:

• The ERcast Emergency Orthopedic Conference is  being held on April 21,2011, click HERE for the brochure PDF file
• More on therapeutic hypothermia: August 2010, ERcast
• Interested in learning more about current decisions from the US Supreme Court? Check out Rich Orman's new podcast US Supreme Court Review
• A good primer on "Post Cardiac Arrest Syndrome" can be found HERE

An article published Feb 27, 2012 in the British Medical Journal titled Hypnotics' association with mortality or cancer: a matched cohort study is something we should know about for a few reasons. First, many of us take some form of sedative hypnotic before night shifts and second, it’s been in the news. Your patients are going to want to know what to do.

Read it: http://bmjopen.bmj.com/content/2/1/e000850.full.pdf+html

This was a population based study that found those prescribed sedative hypnotics (most commonly zolpidem and temazepam) for sleep issues had a greater than threefold increase of death during the study period as well as an increased risk for cancer.

When I first saw this study, my eyes just about popped out of my head. My first job out of residency was all nights and I could never fall asleep before shifts, so by the 4th night in a row, I was really tired. Then I took a zolpidem at 5pm, woke up at 10pm,  and it was night shift 2.0. Wide awake and ready to roll. It was like a cold glass of water on a hot summer day. But just as the Joe Jackson song goes, everything, it seems, gives you cancer.

This paper suggests a correlation between death/cancer and sedative hypnotics prescribed for sleep, but the real question is whether these drugs were directly responsible for the outcome or a marker for higher likelihood of underlying disease.

As a  side note, the group studied was not a bunch of shift working, hard charging emergency providers who were taking these meds strategically to feel rested for a particular interval. There may have been some that cohort (us) scattered in the mix, but this was the general population, who were likely prescribed these meds for the usual reasons.

Back to the first question: Were the insomniacs just sicker to start with? They were compared to a cohort with similar demographics and problem list comorbidities who were followed in the same clinics. The main body of the study says that there were not significant differences between the two groups but, the supplemental data, which is several mouse clicks away, shows that that is not the case. The prescription group had significantly higher incidence of prior disease (including coronary artery disease, chronic kidney disease, asthma, obesity, GERD, etc).

The next question is why. Why would these drugs cause higher mortality and risk of cancer?

Death: There’s the obvious answer that they impair thinking. If used during activities such as driving, or mixed with other meds or alcohol, could lead to death. They may also worsen sleep apnea which in turn could exacerbate other underlying comorbidities. Cause of death was not given in the study, so one can only surmise. I doubt there will be a controlled double blinded trial to see if they directly kill people.

Cancer: Many factors may be at play with malignancy. Zolpidem increases risk of GERD, which increases risk of Barrett’s esophagus which can lead to esophageal cancer. But that is a stretch. Lymphoma, lung, colon and prostate cancer were also increased with the hazard ratio for sedative hypnotics being greater than that of smoking. It may be, however, that patients on these meds were also more likely to have more medical care and disease surveillance (detection bias).

There are many problems with this study and I don’t think we can say the sky is falling based on the author’s conclusions alone. Correlation does not equal causation. One huge omission is that cause of death was not included.   When looking at the supplemental data of the study, I get a sense of confirmation bias where some data was plucked out to support the hypotheses that these drugs are deadly. While not a perfect study by any stretch, it gives food for thought. There does appear to be a correlation with bad outcome and sedative-hypnotic prescriptions, even at low frequency (<18 pills per year). I’d say, just know that these drugs have potential consequences, much like many of the meds we prescribe.

Rapid fire...

Should we black box them? No.

Do they help some people? Yes.

Are they overused? Yes.

Should we encourage better sleep hygiene and healthier lifestyle? Yes.

Should you stop taking Ambien? Long term, daily use - I think so.  Short term, PRN - remains to be seen.

How do you treat an uncomplicated urinary tract infection? What is your go to agent? There’s no best answer because much of it depends on your local resistance and susceptibility patterns. But one drug that causes some confusion is nitrofurantoin. For the most part, it’s a great first line agent for uncomplicated cystitis, but what about pyelonephritis? What about the elderly? There‘s a great paper from 2011 in the journal Clinical infectious disease called:

Clinical Practice Guidelines for the Treatment of Acute Uncomplicated Cystitis and Pyelonephritis in Women: A 2010 Update by the Infectious Diseases Society of America and the European Society for Microbiology and Infectious Diseases

http://www.uphs.upenn.edu/bugdrug/antibiotic_manual/idsa-cystitispyelo-2010.pdf

Here's a brief summary of the paper

Cystitis-

1st choice Nitrofurantoin monohydrate/macrocrystals (100 mg twice daily for 5 days)

2nd choice Trimethoprim-sulfamethoxazole (160/800 mg [1 double- strength tablet] twice-daily for 3 days) if resistance is less than 20%

Quinolones are not the best first choice because of what's known as 'collateral damage'.  Here's what the guidelines have to say: Use of fluoroquinolones has been linked to infection with methicillin-resistant S. aureus and with increasing fluoroquinolone resistance in gram-negative bacilli, such as Pseudomonas aeruginosa. 

Bottom line: Quinolones certainly work, but may cause complications down the road. Granted, sometimes a quinolone is needed such as in cases of resistance, treatment failure, drug interaction or allergy.

Beta lactams can be used if none of the above are options, but have inferior efficacy and more adverse effects, compared with other UTI antimicrobials.

Amoxicillin, although still prescribed for some UTIs, especially in peds, is not a good choice for empiric management. 

Pyelonephritis:

1st choice Ciprofloxacin.

Oral TMP-sulfa and Beta Lactams are distant seconds

 Nitrofurantoin, although great for cystitis, is not recommended for pyelonephritis

Admitted patients: IV ceftriaxone, ciprofloxacin and aminoglycosides are all good choices.

A 2009 study from the Canadian Pharmacists Journal called :A retrospective review assessing the efficacy and safety of nitrofurantoin in renal impairment

http://www.cpjournal.ca/doi/pdf/10.3821/1913-701X-142.5.248

casts doubt on the dangers of nitrofurantoin, finding that it is just as effective in patients with renal insufficiency without an increase of adverse events.

Since there is conflicting data, I'd say don't use nitrofurantoin as your first line in elderly patients with deceased gfr or those with renal insufficiency in general. But if it's your only option because of resistance, med interactions or allergies, there is some (retrospective, limited) evidence to say its ok. 

There are many paths to laxation, below are my management strategies.

Patient is on narcotics and you want to prevent constipation

1. Polyethylene glycol (PEG) 17g/1 glass per day. Up to 3 doses daily if needed

2. PEG + fecal inotrope/stimulant. Senna first choice

3. Docusate  + Senna

Docusate alone is probably not sufficient to prevent constipation in a patient on narcotics. The problem with narcotics is that they slow gut motility. Docusate works by breaking down fats, making stool soft/slick and also works as a weak osmotic laxative. This creates a soft stool that is still sitting in the colon. It's like a fast car propped up on cinderblocks. If docusate is used in combination with a stimulant like senna, laxation improves significantly.

Warning: Bulking agents are often recommended as constipation prophylaxis for patients on narcotics. This may expand the diameter of the colonic lumen without moving anything though.

Patient is on narcotics and is now constipated

Step 1. Manually disimpact if needed and place an enema in the ED.

Step 2. 2mg PO naloxone before ED discharge

Step 3. Disimpaction dose of PEG  (1.5g/kg/day or easy dosing 4 glasses per day). Take for 6 days or until soft stool passes, whichever comes first

Step 4. Maintenance PEG. (0.3-0.8g/kg/day or easy dosing 1 glass per day). Take for 2 weeks and slowly taper

Need a soft stool because of a sore anus (fissure, hemorrhoids, abscess, etc)

Choice 1. Bulking agent like methylcellulose or psyllium. Must drink at least 1.5 liters of water per day, or the stool will become a colon shaped piece of concrete.

Choice 2. Docusate

Constipated kids older than 1

1. I will often place a saline enema while the patient is in the ED.

2. Another option in the ED, especially for younger kids who may not be able to hold in an enema, is a glycerin suppository. Glycerin softens stool and makes the passageway slick, but more importantly, acts as a stimulant and increases intestinal propulsion. See The Suppository Conundrum for details on how to place an suppository.

3. Outpatient treatment: PEG disimpaction dose (1.5g/kg/day) for 6 days or until soft stool passes, followed by a maintenance dose of 0.3-0.8g/kg/day for two weeks followed by a slow taper

4. Lactulose also a laxative option

5. Stress a diet with lots of fiber and water

6. Don’t hold it in Kids should defecate when the urge strikes. Waiting may make the urge pass with the result being a harder, drier, more impacted stool. Then, like  an overdue baby, it won’t want to leave its happy home.  Kids will keep playing rather than going to the bathroom, and some have angst with pooping so they hold it in. We need to talk to our patients/parents about this.

Disimpaction Action

Below is Whit Fisher's famous Disimpaction Action video. One thing I do differently than Whit is that I don't tape my wrists (you'll know what this means after watching the video). I realize the risk of 'debris' getting up the sleeve, but there is often need to remove the outer glove during or after the procedure. Also, I don't want to unwind tape around my wrists using a glove smeared with fecal matter, which is inevitable in this procedure. Enjoy.

httpvh://www.youtube.com/watch?v=mqg8C5dltug

The Constipation Manifesto Cast of Characters

Joe Lex - Free Emergency Medicine Talks

Andy Sloas - PEM ED podcast

zdoggMD -zdoggMD.com

Graham Walker- The NNT, MD Calc, Emergency Medicine News

Mike Phillips

Aaron Wohl

Related Links

The Suppository Conundrum

References and Recommended Reading for this Podcast and Post

Procedurettes by Whit Fisher, MD

EMRAP

Is NEXUS dead? Are we admitting too many patients with pneumonia? How useful is the PERC rule? It's all about decision rules on this episode of ERcast. Ryan Radecki from EM LIterature of Note joins us for a review of four papers:

1. Hospital admission decision for patients with community-acquired pneumonia: variability among physicians in an emergency department

2. Diagnostic Accuracy of Pulmonary Embolism Rule-Out Criteria: A Systematic Review and Meta-analysis.

3. National Emergency X-Radiography Utilization Study criteria is inadequate to rule out fracture after significant blunt trauma compared with computed tomography.

4. Are Steroids Effective for Treating Bell's Palsy?

 

Scott Weingart from emcrit.org gives his 2 cents worth on how we should be using the PERC rule. The question is, "How do we decide if a patient has a low pretest probability so that we can select the proper patients in whom to apply PERC?" Scott recommends using the Well's score to decide if the patient is low risk. This gives you validated method of establishing a pretest probability rather than guessing. Although guessing/gestalt works pretty well too. Here is a link to Scott's algorithm.

 NEXUS Criteria

1. No posterior midline neck tenderness

2. No evidence of intoxication

3. Oriented to person, place, time, and event

4. No focal neurological deficit

5. No painful distracting injury

Canadian C-Spine Rules

PERC Rule

Age < 50 years
Pulse < 100 bpm
SaO2 > 94%
No unilateral leg swelling
No hemoptysis
No recent trauma or surgery
No prior PE or DVT
No hormone use

MD Calc Wells Score Calculation Engine

 Bonus Section: Shoulder Dislocation

The Cunningham Technique for shoulder reduction is all the rage. Check out the ERcast tutorial on how it's done. Even though this method can get some dislocated shoulders in like a hot knife through butter, remember that all shoulder dislocations are not the same, nor will all patients be relaxed enough to make it work. I think every emergency provider should be proficient with several reduction techniques.

Here are my top 6

1. Cunningham technique

2. Scapular manipulation

3. Milch/Modified Milch

4. Kocher method

5. Spaso Technique

6. Traction/counter traction with my elbow hooked inside the patients AC fossa while their arm is bent.

The best way to keep up on hot topics in emergency medicine: R and R in the Fastlane 

One of the most important factors driving the medical workup on a well appearing, febrile infant is the prevalence of serious bacterial infection (SBI) . This number changes depending on age and immunization status (pneumococcus vaccine having the most impact in North America.) The higher the likelihood of disease, the more aggressive the workup and treatment.

Prevalence of serious bacterial infection/meningitis by age

• 0-14 days    (pre-vaccine)                             1/10
• 14-28 days                                                       1/20
• 28-60 days (pre-vaccine)                              1/100
• 28-60 days (post-vaccine)                            1/1,000
• 60-90 days                                                       1/1,000-1/10,000
• >90 days                                                           1/>10,000

Pediatric Fever Trivia

Many parents will bring their febrile infant to the emergency department because the fever is not responding to antipyretics. Does response to antipyretics make SBI less likely?

No. This has been extensively studied and no relationship has been found between response to antipyretics and severity of illness or presence of bacteremia.

Yamamoto LT, Wigder HN, Fligner DJ, et al. Relationship of bacteremia to antipyretic therapy in febrile children. Pediatr Emerg Care. 1987;3:223-227. 

Should a chest X-ray be ordered on a febrile child < 3 months of age without respiratory symptoms?

The data to date would suggest no. The likelihood of finding an infiltrate on CXR is extremely low in the absence of ANY of the following exam findings:

• tachypnea > 50 bpm
• cough
• nasal flaring
• stridor
• grunting
• wheezing
• ronchi
• rales
• hypoxia
• coryza (runny nose)

If you see even one of these criteria in a febrile infant or neonate, it's a mandatory CXR, although I still find runny nose a bit of a hard sell indicating a lower respiratory tract infection. Caveat: a child >3 months with a WBC >20,000 should get a CXR to evaluate for occult pneumonia (even if asymptomatic)

ACEP Policy on Pediatric Fever PDF

Bachur R,Perry H,Harper MB.Occult pneumonias: empiric chest radiographs in febrile children with leukocytosis. Ann Emerg Med. 1999;33:166-173. [II]

What age groups of children are at higher risk for urinary tract infection?

0-6 months circumcised males

0-12 months uncircumcised males

0-24 months females

The term fever without a source implies that a child looks well yet still has a fever. When we want to say that a fever is caused by something we can identify on clinical presentation, what are the recognized/acceptable sources?

1. HSV/Gingivostomatits
2. Herpangina/Ulcerative Stomatits
3. RSV
4. Croup
5. Influenza
6. Varicella
7. Viral Exanthum (rash)
8. Enterovirus, coxsackie HFM dz, echovirus, rhinovirus, enterovirus

In the emergency department, it's virtually impossible to identify the exact type of virus causing an upper respiratory infection or gastroenteritis.  A little sniffle or drop of mucous from one nostril doesn't stop the workup, but a copious river of rhinorrhea and a hacking cough in a febrile 3 month old seal the deal.

 The Workup

It all comes down to what tests to order and what treatment to give for the different age groups. The following age based guidelines are based on Dr. Sloas’ approach to the febrile infant as laid out in the podcast. If you disagree with any of this, send us a note or leave a comment on our google voice line. There's nothing like a feud over pediatric fever.

Reference ABNORMAL values in the febrile infant

• WBC<5 or >15, Band/neutrophil >0.2, Bandemia >1,500 mm3, absolute neutrophil count of >10,000
• CSF > 8 WBC or positive gram stain
• UA  > 10 WBC or positive gram stain
• Stool WBCs or heme
• Infiltrate on CXR

Age 0-28 days

Temp > 100.4  or 38C

Workup

CBC, blood cx, cath UA, CXR (I still do it), lumbar puncture, stool studies if needed

Disposition: Automatic admission and antibiotics

Antibiotics

Ampicillin 50mg/kg plus

Gentamicin - Dose varies by age. Give if child is under 9 days old or

Cefotaxime - 50mg/kg. Give if child is 9-28 days.

Possible add ons

Vancomycin  15-20mg/kg

Acyclovir 60mg/kg/day divided q8hrs

The below presume that the child is well appearing, is on the recommended vaccination schedule and does not have an identifiable source of infection

 Age 29-60 days

temp >100.4 F or 38C

Workup

cbc, blood cx, cath UA, possible CXR, spinal tap, stool studies if needed

Disposition:

Admit for anything positive in workup, unable to get follow-up

Antibiotics:

50mg/kg ceftriaxone or

If Workup completely negative, no antibiotics and next day follow-up

 Age 60-90 days

If the temp is <39C, no testing and followup the next day

Temp >102.2F or 39C

Workup

Start with CBC and UA

If both CBC and UA are normal, no antibiotics. Have patient follow-up next day.

 Option 1

If either the CBC or UA are abnormal then proceed with LP and blood culture. And then...

If just the CBC is abnormal, give 50mg/kg ceftriaxone and follow-up next day

If UA is abnormal, give 50mg/kg ceftriaxone, and prior to discharge, initiate oral antibiotics for urinary pathogens (E. coli is the main player) cefixime orTMP/Sulfa. There are many other antibiotic choices for oral agents. The best choice often depends on resistance patterns in your region.

Option 2

There is wide variability in philosophy regarding LP with an abnormal CBC or UA in the 60-90 day age group. Many community ED docs and pediatricians will send blood culture after an abnormal CBC/UA but do not subscribe to the idea that all patients in this cohort need a spinal tap.

Age 3-6 months

Temp >102.2F or 39C

Workup:

Cath UA

Treat if positive

Key Links

The PEM ED Podcast

Andy Sloas' algorithm for pediatric fever

EM BASIC Podcast

Emergency Ultrasound Podcast

Castlefest 2012

As interview with podcast and blogging grandmaster Mark Crislip, MD on vaccinology and influenza.

Mark's website

CDC Flu Site

CDC info for clinicians on antiviral medications and influenza testing

Check out ZdoggMD's video 'Immunize'. Honorable mention winner of the 2011 Disposable Film Festival.

http://youtu.be/-vQOM91C7us

And last, but certainly not least, Mark Crislip's

A Budget of Dumb Asses

I wonder if you are one of those Dumb Asses who do not get the flu shot each year? Yes. Dumb Ass. Big D, big A. You may be allergic to the vaccine, you may have had Guillain Barre, in which case I will cut you some slack. But if you don't have those conditions and you work in health care and you don't get a vaccine for one of the following reasons, you are a dumb ass.

1. The vaccine gives me the flu. Dumb Ass.

It is a killed vaccine. It cannot give you the influenza. It is impossible to get flu from the influenza vaccine.

2. I never get the flu, so I don't need the vaccine. Irresponsible Dumb Ass.

I have never had a head on collision, but I wear my seat belt. And you probably don't use a condom either. So far you have been lucky, and you are a potential winner of a Darwin Award, although since you don't use a condom, you are unfortunately still in the gene pool.

3. Only old people get the flu. Selfish Dumb Ass.

Influenza can infect anyone, and one of the groups who are more likely to die of influenza are the very young. Often those most at risk for dying from influenza are those least able, due to age or underlying diseases, to respond to the vaccine. You can help prevent your old, sickly Grandmother or your newborn daughter from getting influenza by getting the vaccine, so you do not get flu and pass it one to her. Flu, by the way, is highly contagious, with 20 to 50% of contacts with an index case getting the flu.  However, Granny may be sitting on a fortune that will come to you, and killing her off with the flu is a great way to get her out of the way and never be caught.  That would make a good episode of CSI.

4. I can prevent influenza or treat it by taking Echinacea, vitamin C or airborne. Gullible Dumb Ass Cubed Then Squared.

None of these concoctions has any efficacy what so ever against influenza. They neither prevent nor treat influenza. And you can't boost you immune system either. Immunity is not a Jamba Juice. Anyone who says that the immune system can be boosted is also a dumb ass.

5. Flu isn't all that bad a disease. Underestimating Dumb Ass.

Part of the problem with the term flu is that it is used both as a generic term for damn near any viral illness with a fever and is also used for a severe viral pneumonia. Medical people are just as inaccurate about using the term as the general public. The influenza virus directly and indirectly kills 30,000 people and leads to hospitalization of 200,000 in the US each year. Influenza is a nasty lung illness. And what is stomach 'flu'? No such thing, dumb ass.

6. I am not at risk for flu. Denying Dumb Ass.

If you breathe, you are risk for influenza. Here are the groups of people who should not get the flu vaccine (outside of people with severe adverse reactions to the vaccine): Former President Clinton, who evidently doesn't inhale. And people who want to be safe from zombies. If you don't get the vaccine you do not have to worry about the zombie apocalypse, because zombies eat brains.

7. The vaccine is worse than the disease. Dumb Ass AND a Wimp.

What a combination. Your mother must be proud. Unless you think a sore deltoid for a day is too high a price to pay to prevent two weeks of high fevers, severe muscles aches, and intractable cough.

8. I had the vaccine last year, so I do not need it this year. Uneducated Dumb Ass.

Each year new strains of influenza circulate across the world. Last years vaccine at best provides only partial protection. Every year you need a new shot. And we have a new strain this season, H1N1, so you cannot be a parasite on the immunity of others.

9. The vaccine costs too much. Cheap Dumb Ass.

The vaccine costs less than a funeral, less than Tamiflu, less than a week in the hospital.

10.  I received the vaccine and I got the flu anyway.  Inexact Dumb Ass.

The vaccine is not perfect and you may have indeed had the flu.  More likely you called one of the many colds people get each year the flu.  Remember there are hundreds of potential causes of a respiratory infection circulating, the vaccine only covers influenza, the virus most likely to kill you and yours.

11. I don't believe in the flu vaccine.  Superstitious, Premodern, Magical Thinking Dumb Ass.

What is there to believe in?  Belief is what you do when there is no data. Probably don't believe in gravity or germ theory either. Everyone, I suppose, has to believe in something, and I believe I will have a beer.

12. The government puts tracking nanobots in the vaccine as well as RFID chips as part of the mark of the beast, and the vaccine doesn't work since it is part of a big government sponsored conspiracy to line the pockets of big pharma and inject the American sheeple with exotic new infections in an attempt to control population growth and help usher in a New World Order. Well, that excuse is at least reasonable. Paranoid Dumb Ass.

The list of potential badness in the pregnant patient with right lower quadrant pain is long and distinguished, but it often comes down to a simple question, "Does this patient have appendicitis?" The subtext of this question is, "Is this patient going to need a CT scan?" Nobody likes ordering am abdominal CT on a pregnant patient because, no matter how low the statistical risk of damage to the fetus, there is still potential harm from ionizing radiation. As you will see below, the risk of immediate  maternal and fetal harm is far greater than the long term risk of ionizing radiation exposure.

Interview with Ingrid Lim MD at ACEP 2011

Risk of mortality with appendicitis in pregnancy:

In a pregnant patient with unperforated appendicitis, fetal loss is 3-5%. With perforation, fetal loss skyrockets: -30% in trimesters 1 and 2 -70% in trimester 3

Maternal mortality is 1% without  perforation and 4% with perforation

Diagnosis:

Step 1: Ultrasound- more sensitive in the 1st vs. 3rd trimester. Even though it may be inconclusive as far as appendicitis, ultrasound can give valuable information about the fetus, uterus, ovaries, kidneys and gallbladder. If ultrasound doesn't give the answer....

Step 2: MRI without contrast DO NOT USE GADOLINIUM:CONTRAINDICATED IN PREGNANCY If no MRI available...

Step 3: CT with or without contrast depends on your local radiologist. Contrast (IV or PO) is considered safe in pregnancy. Research has shown that contrast does not harm fetal thyroid

RADIATION PRIMER for CT Appy protocol 

Fetal background radiation exposure during 9 months of pregnancy 0.1 rad (1mGy) Teratogenesis threshold: 5 rad (50mGy)

Estimated fetal radiation exposure from CT Appy protocol:

Trimester 1: 2.4 rad (24mGy)

Trimesters 2 and 3: 3 rad (30mGy)

Teratogenesis - fetal death. malformation or developmental delay from in utero radiation exposure. The threshold for a <1% teratogenesis risk is 5 rad (50mGy). The highest risk period is 3-15 weeks. The amount of radiation absorbed from a CT appy protocol is less than the 5 rad teratogenic threshold.   Even with exposure to 10 rads,  there is a 99% chance of no fetal teratogenic effects.

Carcinogenesis-    Most worrisome for childhood cancers such as leukemia. The baseline risk of dying from childhood cancer is  1 in 2000. A 5 rad exposure is believed to increase that risk to 2 in 2000. While that is a doubling of the relative risk, it is still small compared the rate of fetal loss from a ruptured appendix.

Bonus section: Ectopic Pregnancy and HCG levels

Traditional teaching holds that if the HCG does not double in the first 48 hours, consider ectopic. But many patients do not follow this curve. With  the development of more sensitive assays, a minimum rise of 53% over 48 hrs is acceptable. 3% of ectopic pregnancies can have a negative serum HCG

Two theories: 1.     Have to have a viable trophoblast to produce HCG, no trophoblast…no HCG    2.  Ectopic died then ruptured

Bottom line, if patient looks sick and there is a lot of free fluid in the pelvis –go to surgery

Written Summary:  Justin Arambasick MD  Akron General  Medical Center and Rob Orman MD

A good article on MRI uses in pregnancy

Research and Reviews in Emergency Medicine and Critical Care is an amazing project thatbrings together physicians from across the globe to find the hottest medical articles on the planet. This is an international collaboration with  contributers  from Ireland, UK, South Africa, Australia and the United States. If you want to see what's making waves in the medical world and stay up to date on current trends in emergency medicine and critical care,  click here to go to R and R post 1.