Saturday, February 7, 2015

Allergic Rhinitis in the ED... makes a difference !

OK... I know that runny nose, congestion and sneezing is not a sexy EM topic. However, we often see these patients in the ED complaining of "sinus infections" and not infrequently, get inappropriate prescriptions for antibiotics when what they need is a nasal steroid. Patients with AR are also likely to suffer asthma and atopic dermatitis. So let's review the basics on this topic and how they related to other common problems seen in the emergency department.


The presence of allergic rhinitis (seasonal or perennial) significantly increases the probability of asthma: up to 40% of people with allergic rhinitis have or will have asthma. Atopic eczema frequently precedes allergic rhinitis. Patients with allergic rhinitis usually have allergic conjunctivitis as well. The factors determining which atopic disease will develop in an individual person and the reasons why some people have only rhinitis and others have rhinitis after eczema or with asthma remain unclear.

The differential diagnosis includes forms of rhinitis that are nonallergic in origin such as a noninflammatory rhinopathy (also known as vasomotor rhinitis) and nonallergic chronic rhinosinusitis. Seasonal symptoms can be caused by viral infections, especially if the patient is a child or lives with children; rhinovirus has a marked peak in incidence in September and a smaller peak in the spring. The diagnosis of allergic rhinitis is often made clinically on the basis of characteristic symptoms and a good response to empirical treatment with an antihistamine or nasal glucocorticoid. Formal diagnosis is based on evidence of sensitization, measured either by the presence of allergen-specific IgE in the serum or by positive epicutaneous skin tests (i.e., wheal and flare responses to allergen extracts) and a history of symptoms that correspond with exposure to the sensitizing allergen. Epicutaneous skin testing and testing for allergen-specific IgE have similar sensitivity, although they do not identify sensitization in an entirely overlapping group of patients.


Pharmacologic treatment options include H1-antihistamines, intranasal glucocorticoids, and leukotriene-receptor antagonists. Therapy usually starts with oral antihistamines, frequently initiated by the patient. H1-antihistamines are also available as nasal sprays by prescription. The intranasal preparations appear to be similar to oral preparations in efficacy but may be less acceptable to patients owing to a bitter taste. The effect of antihistamines on symptoms, especially nasal congestion, is modest. They can be combined with oral decongestants, and the combination can improve nasal airflow in the short term (on the basis of data from trials lasting 2 to 6 weeks), at the cost of some side effects. Topical nasal decongestants are more effective than oral agents, but there are reports of rebound congestion (rhinitis medicamentosa) or reduced effectiveness beginning as early as 3 days after treatment, and only short-term use is recommended. In one study, adding an intranasal glucocorticoid reversed the reduced effectiveness of a topical decongestant. Intranasal glucocorticoids are the most effective pharmacotherapy for seasonal allergic rhinitis, yet the overall efficacy is moderate. Although the clinical effects appear within a day, the peak effect in cases of perennial rhinitis is not reached for several weeks. The superiority of intranasal glucocorticoids over antihistamines in the treatment of perennial allergic rhinitis is uncertain. The effect of leukotriene-receptor antagonists on the symptoms of allergic rhinitis is similar to or slightly less than that of oral antihistamines, and some randomized trials have shown a benefit of adding the leukotriene-receptor antagonist montelukast to an antihistamine. Although the majority of trials have favored intranasal glucocorticoids over this combination, data are inconsistent; this combination should be considered for patients whose symptoms are inadequately controlled with an antihistamine and who do not wish to use a glucocorticoid nasal spray. There is no significant benefit of adding an oral antihistamine or montelukast to a nasal glucocorticoid. However, in randomized trials, the combination of an intranasal antihistamine plus an intranasal glucocorticoid has been shown to be superior to either agent alone.

Although allergen immunotherapy has traditionally been administered subcutaneously in the United States, rapidly dissolving tablets for sublingual administration were recently approved by the FDA for treatment of grass and ragweed allergy. With immunotherapy, unlike pharmacotherapy, the effect persists after the discontinuation of therapy. If there is improvement in the first year, injections are generally continued for at least 3 years. Data from randomized trials are lacking to guide decisions about the duration of therapy. Subcutaneous immunotherapy carries a risk of systemic reactions, which occur in 0.1% of injection visits, in rare cases leading to life-threatening anaphylaxis (1 reaction per 1 million injection visits). Although subcutaneous immunotherapy has not been compared with sublingual immunotherapy in large head-to-head trials, indirect comparisons suggest that subcutaneous immunotherapy is more effective for symptom relief. However, sublingual immunotherapy has a clear advantage in terms of safety, with very few reports of anaphylactic reactions.


In summary:
- Treat allergic rhinitis aggressively. Oral H1 antihistaminics +/- nasal steroids is a good first line approach.
- Oral or topical decongestants help to alleviate symptoms, but with some side effects and risk of tachyphylaxis and rebound effect. Therefore, use with caution and for short periods of time.
- Refer to allergy testing patient with severe symptoms, combination with asthma and/or atopic dermatitis. 


Wednesday, January 7, 2015

Could that chest pain be Pericarditis?

Chest pain is, the pain of our existence in the ED (one of many). Pericarditis is one of the long list of possible etiologies and it's important we recognize it because the therapy is very different from other common causes of chest pain. So let's review the basics.



Chest pain is the presenting symptom in virtually all patients for whom a diagnosis of pericarditis would be considered. Although the differential diagnosis of chest pain is extensive, certain features point strongly to pericarditis, especially pleuritic pain that is relieved by sitting forward and that radiates to the trapezius ridge (the latter feature is virtually pathognomonic). Many patients have premonitory symptoms suggestive of a viral illness, and an abrupt onset is not unusual. Sinus tachycardia and low-grade fever are also common. The diagnosis of acute pericarditis is established when a patient has at least two of the following symptoms or signs: chest pain consistent with pericarditis, pericardial friction rub, typical ECG changes, or a pericardial effusion of more than trivial size. Because the rub and ECG findings may be transient, frequent auscultation and ECG recordings can be helpful in establishing the diagnosis.


The electrocardiographic signs of pericarditis are distinctive to the trained eye, but they can also be subtle. It is important to recognize that the fibrous tissue of the pericardium is electrically silent; therefore, the presence of electrocardiographic changes indicates a degree of myocarditis. There are some who suggest that the correct name should be myopericarditis. In any case, the "classic" EKG changes in pericarditis described are diffuse ST elevation in leads I, II, aVL, aVF & V1. Some myocarditis can occur specially in the atria causing an exaggerated atrial T wave and PR segment depression, which is seen only in viral pericarditis.



Some refer to the concave upwards ST elevation as the "smily face" of pericarditis compared with the"frown face" of STEMI.

Another EKG finding is the Spodick sign, which is a downsloping of the TP segment. When you see it and there are not other worrying findings, you may feel a bit more comfortable calling it pericarditis



Another example: 



Now, changes NOT seen in pericarditis that are worrisome: Q waves (specially if new), conduction abnormalities (BBB's, AVB's), T wave inversion following ST elevation, dysrhythmias and reciprocal ST depression. If you see any of this, you cannot call it pericarditis, at least not based on electrocardiographic findings.



Nonsteroidal antiinflammatory drugs (NSAIDs) have long been the mainstay of the initial treatment of acute pericarditis. The most commonly used agents are ibuprofen (600 to 800 mg every 6 to 8 hours), indomethacin (25 to 50 mg every 8 hours), and aspirin (2 to 4 g daily in divided doses). Patients receiving these drugs should also receive a proton pump inhibitor for gastric protection. On the basis of observational data from a relatively small number of patients with recurrent pericarditis, the European Society of Cardiology concluded in its 2004 guidelines that there was sufficient evidence to recommend colchicine combined with an NSAID for initial treatment of a first bout of pericarditis. More recently, evidence from the Investigation on Colchicine for Acute Pericarditis (ICAP) randomized clinical trial, involving patients with a first episode of pericarditis, strongly supported this recommendation. The optimal duration of treatment is uncertain. For colchicine, a 3-month course is reasonable on the basis of results from the ICAP trial. The usual duration of NSAID treatment, supported by expert opinion, is 1 to 2 weeks, with the actual duration driven by clinical response.

In 70 to 90% of patients, acute idiopathic pericarditis is self-limited, responds promptly to initial treatment, and completely resolves. In a small number of patients, probably less than 5%, the condition does not respond satisfactorily to initial treatment, and in 10 to 30% of patients, recurrences develop after a satisfactory initial response. Most patients have only one or two recurrences, but a small fraction (probably less than 5% of the total population with acute pericarditis) have multiple recurrences with considerable disability. Ultimately, recurrences cease in the majority of cases.

In Summary:
- Think pericarditis in the differential diagnosis of CP.
- EKG findings: Diffuse concave upwards STE, PR depression, downsloping TP segment (Spodick's sign) 
- Consider ischemia if there are Q waves, arrhythmias, conduction abnormalities, ST depression.
- If still not clear diagnosis, get an echo and look for pericardial effusion vs wall motion abnormalities.
- Labs are not particularly useful, but elevated trops indicate myocarditis and these patients should be admitted to monitor bed as they have increased risk for complications.
- NSAID's and ASA first line. Colchicine for prevent recurrence