Pearls

Acute HIV infection can present with fever, rash, pharyngitis, diffuse lymphadenopathy, leukopenia, thrombocytopenia, and elevated LFTs. The rash usually starts on the trunk and spreads to the arms and legs;the face is often spared (NEJM,7/24/14;358)

The Asplenic Patient - What it Means For the Emergency Physician

The asplenic patient population includes patients with surgical asplenia, congenital asplenia, and functional asplenia (as found in patients, for example, with sickle cell anemia, severe celiac disease, and untreated HIV infection). Asplenic patients are at risk for episodes of rapidly progressive septicemia that are fatal in up to 50% of cases (1). Most commonly caused by Streptococcus pneumoniae, such episodes often have a sudden onset and a fulminant course.

Postsplenectomy sepsis should be suspected in an asplenic patient presenting with severe illness or a febrile illness of any severity. If fever develops in an asplenic patient, immediate administration of empirical antimicrobial therapy is indicated, because fever can be the initial manifestation of a fulminant infection and prompt administration of an antibiotic may prevent the development of clinical sepsis (1). Ceftriaxone administered IV or IM with or without vancomycin is a reasonable empirical choice. Outpatient management can be considered for the stable, non-toxic patient if follow-up is ensured and the patient can return promptly if the condition worsens.

Asplenic persons who sustain a dog bite should receive a prophylactic antibiotic (e.g., penicillin) (1). This may help prevent fulminant sepsis caused by C. canimorsus (2).

Of note, prophylactic antimicrobial therapy, typically oral penicillin given twice daily, is generally recommended for asplenic children < 5 years of age and may be considered for older patients during the initial 1 - 2 years after splenectomy, with lifelong prophylaxis for persons who have had an episode of postsplenectomy sepsis.

References:
(1) Rubin LG, et al. N Engl J Med 2014; 371:349-356.
(2) Long SS, et al, eds. Principles and practice of pediatric infectious diseases. 4th ed. Edinburgh: Elsevier Saunders, 2012:880-1.

During the period 2001-2008, a total of 233 cases and 26 deaths from tetanus were reported in the United States. In 2009, a total of 19 tetanus cases and 2 deaths were reported to the national tetanus surveillance system (CDC.gov, 4/1/14).

In the US in 2013, there were 2 reported cases of human rabies, and 4248 cases of animal rabies reported (MMWR Weekly, August 15, 2014).

MRI with gad and renal failure

Gadolinium MRI and the Dialysis Patient

Nephrogenic systemic fibrosis (NSF) is a potentially debilitating and even fatal fibrosing condition that most often affects the skin, but can involve multiple organs. NSF is associated with the administration of gadolinium-based contrast agents (GBCAs) in patients with chronic or acute renal failure.

American College of Radiology guidelines consider GBCAs contraindicated in patients with ESRD on chronic dialysis (1,2). However, there may be occasions when the use of a GBCA is considered to be essential in a dialysis patient presenting to the ED. Although it has not been proven that hemodialysis following GBCA administration can prevent NSF, It is recommended that hemodialysis be performed immediately after GBMCA administration in patients already undergoing hemodialysis - preferably initiated within 2 hours and several dialysis sessions should be conducted with prolonged dialysis times (1). This recommendation is based on the principle of clearing as much of the agent as possible from the patient's circulation to minimize risk.

References:
(1) Besheli DL, et al. Clinical Radiology 2014;69: 661-668.
(2) ACR Manual on Contrast Media. Available at: http://www.acr.org.
(3) Juluru K. RadioGraphics 2009;29: 9-22.

Tympanostomy with Discharge - Treatment?

The insertion of tympanostomy tubes is one of the most frequently performed surgical procedures in children, and acute otorrhea is a common sequela (an incidence of 26% in one meta-analysis) (1,2). Many such patients present to the ED for evaluation. Bacterial infection is the predominant cause of acute tympanostomy-tube otorrhea (1,3).

The few trials comparing topical and oral antibiotics in children with this condition have indicated that antibiotic or antibiotic-glucocorticoid eardrops are as effective as, or more effective than, oral antibiotics. A recent trial of 233 children found that antibiotic-glucocorticoid eardrops were more effective than oral antibiotics in children with tympanostomy tubes who had uncomplicated acute otorrhea (1). In this study, antibiotic-glucocorticoid eardrops were administered for 7 days and was compared to 7 days of PO amoxicillin–clavulanate. Therefore, even though acute tympanostomy-tube otorrhea is a form of acute otitis media, clinicians should recognize that PO antibiotics are not preferred treatment.

Of note, although initial observation is often recommended as an initial strategy for the treatment of acute otitis media, initial observation is not an adequate management strategy for children with acute tympanostomy-tube otorrhea. In the study cited above, half of children who were assigned to initial observation still had otorrhea at 2 weeks.

References:
(1) Van Dongen T, et al. N Engl J Med 2014; 370:723-733.
(2) Kay DJ, et al. Otolaryngol Head Neck Surg 2001;124:374-380.
(3) Peters BM, et al. Clin Microbiol Rev 2012;25:193-213.

Current Management of ICH after tPA

The most feared complication of IV thrombolysis for acute stroke is ICH, which occurs most commonly in older patients with severe deficits and large areas of ischemia at presentation (1,2). Most symptomatic ICHs after IV thrombolysis for stroke occur in the first 24 hours. Generally, small petechial hemorrhages do not require active intervention (1).

There is no universally accepted standardized guideline for reversal of thrombolysis-associated hemorrhage. Management algorithms are empirical rather than data based.

Administer cryoprecipitate (0.15 U/kg) if fibrinogen level <150 mg/dL
Antifibrinolytics (e.g. tranexamic acid 1000 mg) have not been well studied, but their use is backed by solid pathophysiologic rationale. Tranexamic acid competitively inhibits the activation of plasminogen and may stabilize hemorrhage expansion (1,3)
Consider platelet transfusion if platelet count < 100 x 109 or platelet dysfunction is suspected.

A suggested management algorithm may be found in the EMedHome.com PDF Database.

References:
(1) Fugate JE, et al. Mayo Clin Proc, epub, April 28 2014.
(2) Saver JL. Stroke 2007;38(8):2279-2283.
(3) French KF, et al. Neurocrit Care 2012;17(1):107-111.

The Potential Harm of Oxygen in ED Patients

Most physicians believe that high oxygen concentrations are life-saving (2). Yet, an abundance of evidence suggests the contrary even though it is common practice to administer high flow oxygen to unstable ED patients. We thought this would make for a thought-provoking clinical pearl:

ACS & CHF
In both acute ischemic cardiac syndromes and CHF, experimental evidence argues against the use of supplemental oxygen. Administration of oxygen induces a variety of potentially hazardous hemodynamic changes, largely because it induces coronary and systemic vasoconstriction. As early as 1950 it was suggested that oxygen might be deleterious, as it prolonged ECG changes during exercise tolerance testing (2). In patients with severe triple-vessel disease, administration of 6 minutes of high-flow oxygen was demonstrated to reduce coronary blood flow sufficiently to induce myocardial ischemia (3). It appears that only when patient oxygen saturations are < 85- 90%, does oxygen administration increase myocardial oxygen delivery (2).

COPD
A 2010 trial of 405 patients with COPD exacerbations compared treatment with high-concentration oxygen with titrated oxygen in a pre-hospital setting. Mortality was significantly lower in COPD patients receiving titrated oxygen rather than high-concentration oxygen (4).

Stroke
Hyperoxia can cause vasoconstriction of the carotid and downstream cerebral arteries. 3 randomized trials have looked at the effect of supplemental oxygen in ischemic stroke. One showed no benefit, one showed a lower survival in non-hypoxic patients and one showed excess mortality in the hyperoxia group (2). Guidelines from the American Stroke Association do not support the use of supplemental oxygen for most patients with acute ischemic stroke.

Cardiopulmonary Resuscitation
There is evidence that patients might be managed more safely after ROSC with 30% oxygen rather than 100% (2). Clinically, hyperoxia is associated with poor neurological outcome following resuscitation (2,5).

Septic and Hemorrhagic Shock
Hyperoxia may impair oxygen delivery in patients with sepsis, and hyperoxia decreases whole-body oxygen consumption in critically ill patients (2,6). In hemorrhagic shock, data from animal studies suggest that increasing the fraction of inspired oxygen compromises hemodynamics (2).

References:
(1) Burls A, et al. Emerg Med J 2010, 27:283-286.
(2) Cornet AD, et al. Crit Care 2013 Apr 18;17:313.
(3) Bourassa MG, et al. Am J Cardiol 1969, 24:172-177.
(4) Austin MA, et al. BMJ 2010, 341:c5462.
(5) Janz DR, et al. Crit Care Med 2012, 40:3135-3139.
(6) Rossi P, et al. Clin Physiol Funct Imaging 2007, 27:180-184.

Risks for Peri-Intubation Cardiac Arrest

Kristi L. Koenig, MD, FACEP, FIFEM Reviewing Heffner AC et al., Resuscitation 2013 Aug 5;
In a retrospective analysis, patients in shock were at higher risk for peri-intubation cardiac arrest, which usually had an initial rhythm of pulseless electrical activity.
Peri-intubation hypotension and even cardiac arrest are concerns in patients undergoing emergency resuscitation. To determine the incidence of peri-intubation cardiac arrest and factors associated with it, researchers retrospectively analyzed records for 410 adult patients who underwent rapid sequence intubation (RSI) at a single urban emergency department during 2007.

Peri-intubation cardiac arrest (defined as occurring within 60 minutes after initiation of airway management) was documented on the standardized data collection tool in 17 patients (4.2%), at a median 6 minutes after intubation. Nearly two thirds of cardiac arrests occurred within 10 minutes. Pulseless electrical activity was the initial arrest rhythm in most cases. Arrest was more common in patients with pre-intubation hypotension (12% vs. 3%) and in those with pre-intubation oxygen saturation (<92%).

In multivariate logistic regression analysis, higher pre-RSI shock index and body weight were independently associated with peri-intubation cardiac arrest. Although more than half of patients were initially resuscitated, peri-intubation cardiac arrest portended a 14-fold increase in the odds of in-hospital death.

COMMENT

The association of peri-intubation cardiac arrest with higher pre-intubation shock index, and the finding that nearly all cardiac arrest patients had pulseless electrical activity, highlights the precarious state of hypotensive critically ill patients, especially those with higher body mass index. We are subjecting these fragile patients to a combination of induction agents, airway manipulation, and, especially, positive pressure ventilation. The take-home message? Intubate earlier, if possible, before the patient deteriorates; optimize hemodynamic parameters with pressors, fluids, or blood; and carefully control mechanical ventilation to minimize ventilation pressures.

Factor IX Complex Profilnine SD for Emergent Warfarin Reversal

Profilnine SD comes in vial sizes expressed in international units of Factor IX. (In either 500, 1,000, or 1,500 IU vials.) It is FDA approved for treatment of bleeding associated with Hemophilia B, or Factor IX deficiency.

However, each vial also contains factors II, VII and X – so, all of the Vitamin K-dependent factors inactivated by Warfarin. Therefore, Profilnine and other “prothrombin complex concentrates” are routinely used off-label for the emergent reversal of Warfarin-induced coagulopathy.

A 1,000 IU vial of Profilnine will (per the drug information packet) contain:

Factor International Units

II 1,500
VII 350
IX 1,000
X 1,000

For comparison, a 250 mL unit of FFP contains 1 unit of coagulation factors per 1 mL. So one unit of FFP will contain:

Factor International Units

II 250

VII 250

IX 250

X 250

Methods of Dosing:

Dosing for hemophilia-associated bleeding can be looked up in a pharmacopia or discussed with a hematologist.

Dosing for emergent Warfarin reversal is 25-50 international units/kg; may round up or down within this range dependent on product on hand. (It is sometimes given with 1-2 units of FFP for additional Factor VII.)

Dosing can be a flat 25 units/kg, or it may be INR-based:

25units/kg (INR 2-4)

35 units/kg (INR 4-6)

50 units/kg (INR > 6)

Reconstitution:

It comes with a vial of sterile water and a vial of powder, the two vials screw together to allow reconstitution of the powder:

Rate of administration: No greater than 10 ml/minute

Adverse Reactions: According to 2010 guidelines from the American Heart / American Stroke Association for managing Warfarin-associated intracranial hemorrhages, “Although PCCs may theoretically increase the risk of thrombotic complications, this risk appears relatively low.” Because this is a powderized blood product, there is also theoretical risk of transmission of viral infection or prion-associated disease. More common reactions, according to ePocrates, include urticaria, fever, nausea, headache, lethargy, flushing or tingling.

Stability: Once mixed stable for 3 hours

Onset: Reversal of Warfarin-induced coagulopathy within minutes.

Half-life: 24.68 hours ± 8.29

“Factor IX Complex Profilnine® SD.” HYPERLINK "http://www.grifolsusa.com/Controller?_fb=pfch&pAction=_factory&file=profil9-ft.pdf&_fp=0&idPortlet=15341&idval=385714"http://www.grifolsusa.com/Controller?_fb=pfch&pAction=_factory&file=profil9-ft.pdf&_fp=0&idPortlet=15341&idval=385714

Hubbard AR. “International biological standards for coagulation factors and inhibitors.” HYPERLINK "http://www.ncbi.nlm.nih.gov/pubmed/17427063" \o "Seminars in thrombosis and hemostasis."Semin Thromb Hemost. 2007 Apr;33(3):283-9. HYPERLINK "http://www.ncbi.nlm.nih.gov/pubmed/17427063" http://www.ncbi.nlm.nih.gov/pubmed/17427063

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