- Do not analyze a rash and simply call it bed bugs. There is a differential--includes scabies, fleas, bat bugs, dermatitis herpetiformis
- Bite mark: occasionally linear formation where bedbug makes its "path." usually on exposed skin. erythematous wheel with occasional bloody center
- 3/10 people bit will show NO symptoms. The skin changes that appear are an allergic reaction
- They DO NOT transmit disease. Hep B, Hep C, HIV-- die quickly within the bedbug gut
- They love warmth, dark and CO2. If bed bugs are seen in the well-lit ED, the patient likely has a MASSIVE infestation at home
- Hitchhikers: they latch onto anything. at the laundromat, the hotel, your scrubs...
- Oh not, not Diapause! Concept that bedbugs can remain without a meal for months and lie dormant. Even in cold as low as -12C.
- Heat kills: Need 120 F for at least 30 minutes: kills all life forms. Dryer works.
- Studies have shown "bug bombs" have no difference vs. controls
- Treatment for rash: supportive. Rash generally resolves within 7 days spontaneously. Can use antihistamines or topical steroids PRN. However, antihistamines can make it difficult to discern if rash is bed bugs
- Treatment at home: Combination of pest control, Heat, Sealing Cracks and Crevices, Treating Bed frames box springs and mattresses
- Biopsy is of no use.
...now go change your scrubs
1) Afib RVR is often triggered by the same etiologies as sinus tachycardia. Before treating the arrhythmia, treat the most likely etiology.
2) In a person with normal cardiac function and structure, afib RVR is not the cause of the patients shock. Patients that are particularly sensitive to afib RVR include those with cardiomyopathies, recent MIs, severe diastolic dysfunction, HOCM, WPW, severe valvular disease, and severe coronary artery disease. In these populations, afib RVR often manifest as hypotension, pulmonary congestion, and possibly ischemia.
3) Procainamide should be the first line treatment in stable WPW with afib. AV nodal blocking agents should be avoided.
4) Review of recent literature suggest:
- Diltiazem is more effective at controlling rate within 30 minutes when compared to metoprolol (Fromm 2015).
- Beta blockers may have a mortality benefit when used in afib RVR & sepsis (Walkey 2016).
- Use of a rate of rhythm controlling agent in ED patients presenting with an acute underlying illness results in an increase in adverse events compared to patients who did not receive rate or rhythm controlling agents (Scheuremeyer 2015).
5) Physicians should make an effort to optimize care and improve blood pressures before choosing a rate/rhythm controlling agent. Physicians should consider the patient's clinical status and comorbidities when selecting a treatment option.
- Child presents in cariogenic shock = think myocarditis
- There are times Circulation must be addressed before Airway to maximize circulation prior to intubation
- Think beyond tachycardia, symptoms of myocarditis also include: poor perfusion, hepatomegaly, respiratory distress
Case 1 -- Hypotensive Inferior MI
* Mmm bread and butter... Avoid nitroglycerin in the inferior MI. Preload!
* Hypotension prior to RSI drugs? Bad. Crystalloid not helping? Pressors.
* Make your FIRST attempt your best attempt.
* Cath lab is a farther walk than anticipated... and may not have airway resources!
* Be the leader: emphasize closed loop communication especially in code situations
Case 2 -- NAT
* Do not outsmart yourself. Do not talk yourself out of being suspicious for NAT.
* No injury is 100% specific for NAT. Our job is to be sensitive, not necessarily specific.
* Contact DSS! First encounter is mandatory reporter. Otherwise, story may change.
* Just because DSS investigates and clears does not mean NAT is ruled out.
* Be wary of your documentation: be objective, not a detective. Don't write things like "child consoled by mother after trauma"--remember, the victim often returns to the abuser
* Like it or not, we all have inherent bias in the way we approach patients from various backgrounds. Be mindful of your assumptions.
* Be on the same page and contact your colleagues: Social work, CHIPS, Child Abuse team, Trauma
1. Signs and symptoms of an Upper GI bleed in the pediatric patient
-most common presentation is hematemesis
-melena also common presentation
-many things mimic GI bleed -> food coloring, raw meats, swallowed blood from oropharynx
2. Differential diagnosis for acute pediatric upper GI bleed
-determine if variceal vs nonvariceal
-variceal bleed (uncommon but can be life threatening)-> portal HTN from congenital liver pathologies
-mucosal bleed -> gastritis, esophagitis, caustic ingestion, foreign body most common in pediatrics
3. ED diagnostic workup for an upper GI bleed in a pediatric patient
-CBC, BMP, LFT's, and Type/Cross essential to the workup
4. ED Management of Pediatric Upper GI bleed patient
-Place an NG tube
-Get GI, Surgery, and Interventional Radiology Involved early
-Octreotide and vasopressin are important treatments for variceal bleed
-For mucosal bleeds control acid production
“You get to use the word ‘dizzy’ once.” Andrew Asimos
Categories of Dizziness
Posterior Circulation Anatomy
4) Auditory/vestibular structures
5) Visual occipital cortex
Neuro Exam for Posterior Circulation
When should I think about infective endocarditis and septic emboli?
-Consider in patients who raise your suspicion for sepsis and have any of these risk factors:
What exam findings are suggestive of IE?
-Some are more specific than others. Roth’s spots, Osler’s nodes, and Janeway lesions are relatively rare but are essentially illness defining. More sensitive but less specific findings include cardiac murmors, petechiae, splenomegaly, and splinter hemorrhages.
Who gets septic emboli?
-Patients with large lesions, unstable/multiple lesions, and left sided lesions are most likely to embolize secondary to higher left sided pressure gradients.
Where do the emboli go, and what does that look like?
- Right sided lesions (without PFO) go to the lungs, and typically manifest clinically as:
-Left Sided lesions
Take Home Points