moving day

we are transitioning over to a new website:

dailyem.wordpress.com

update your readers!

New format is a work in progress, so feedback is appreciated.  check it out!

stevens johnson syndrome...without a rash

STEVENS-JOHNSON SYNDROME:
--severe idiosyncratic reactions, most commonly triggered by medications, which are characterized by fever and mucocutaneous lesions leading to necrosis and sloughing


--less severe disease on the same spectrum as TEN (toxic epidermal necrolysis)


DIAGNOSIS: NOT FAIR
--apparently, you can have Stevens-Johnson syndrome without a rash


PMID:  22041607
The Stevens-Johnson syndrome (SJS) classically involves a rash, conjunctivitis and mucositis.

case report of isolated mucositis and conjunctivitis.

Previous rare reports of severe SJS like syndromes without a rash are confined to children, usually with mycoplasma pnemoniae infection


PMID:  22012144
The commonest infections associated with SJS have been HSV and Mycoplasma pneumoniae. 

Less than 10% cases of Mycoplasma pneumonia develop extra pulmonary complications like hemolytic anemia, hepatitis, arthritis, meningitis and SJS.  

unclear from existing literature whether antibiotic treatment of M. pneumoniae infection decreases the risk for SJS. 


PMID:  20678095
another case report of mucocutaneous involvement without skin lesions. 

Oral lesions are present in all cases with SJS associated with M. pneumoniae infection, ocular lesions only in two-thirds and genital lesions in three-fourths of all cases. 

That SJS in association with M. pneumoniae infection is predominantly mucosal is reflected by few reports of SJS presenting without skin lesions. Even when skin lesions are present, mucocutaneous lesions predominate.


BOTTOM LINE:
--stevens johnson syndrome: skin and mucosal involvement, can progress to sloughing (e.g. TEN)
--can present withOUT rash. Mycoplasma pneumonia is common source.


Submitted by J. Gullo.




Reference(s): uptodate.com: Stevens-Johnson syndrome and toxic epidermal necrolysis: Clinical manifestations; pathogenesis; and diagnosis; article 1, article 2, article 3; picture

when not to use succinylcholine

BLATANT REDIRECT:

--check out EMCrit's handy slide

--good quick review of when you can (or can't) use succinylcholine

BOTTOM LINE:

--check out the slide on EMCrit

--if you can't or are lazy, remember succinylcholine causes K+ release

--also, hyperkalemia is bad

--first do no harm

Reference(s): emcrit.org; picture

loop abscess

Looking for a fun and interesting new way to treat an abscess?

(I've done it once, with good success.)

You tube video - only 2 minutes long, worth watching, and worth reviewing in the ED before actually trying this:

Dr. Tsoriades and colleagues found using a vessel loop (see picture) was a safe and effective treatment for subcutaneous abscesses in children when studied in comparison with traditional incision and drainage with packing. 

Children in the study were under general anesthesia or conscious sedation. (I used a traditional field block using 2% lidocaine with epinephrine in an adult.)

Pros:

• no repeat packing
• better tolerated by patients
• less wound care materials
• much smaller incision - less scarring

Discharge instructions:

• apply warm compresses
• expect drainage
• move loop back and forth 2 times daily 
• return if worse/fever/increasing redness

Submitted by S. Morris.

Reference(s): A.P. Ladd, M.S. Levy, J. Quilty. Minimally invasive technique in treatment of complex, subcutaneous abscesses in children. J Pediatr Surg, 45 (2010), pp. 1562–1566;  S.S. Tsoraides, R.H. Pearl, A.B. Stanfill, L.J. Wallace, R.K. VeguntaIncision and loop drainage: A minimally invasive technique for subcutaneous abscess management in children J Pediatr Surg, 45 (2010), pp. 606–609; picture

laws of the house of god

from THE HOUSE OF GOD, by Samuel Shem, M.D.
--haven't read this in a few years, but came upon this list again recently.
--my favorites are #'s 3 & 6.
--enjoy

1. GOMERS DON’T DIE.
2. GOMERS GO TO GROUND.
3. AT A CARDIAC ARREST, THE FIRST PROCEDURE IS TO TAKE YOUR OWN PULSE.
4. THE PATIENT IS THE ONE WITH THE DISEASE.
5. PLACEMENT COMES FIRST.
6. THERE IS NO BODY CAVITY THAT CANNOT BE REACHED WITH A #14G NEEDLE AND A GOOD STRONG ARM.
7. AGE + BUN = LASIX DOSE.
8. THEY CAN ALWAYS HURT YOU MORE.
9. THE ONLY GOOD ADMISSION IS A DEAD ADMISSION.
10. IF YOU DON’T TAKE A TEMPERATURE, YOU CAN’T FIND A FEVER.
11. SHOW ME A BMS (Best Medical Student, a student at the Best Medical School) WHO ONLY TRIPLES MY WORK AND I WILL KISS HIS FEET.
12. IF THE RADIOLOGY RESIDENT AND THE MEDICAL STUDENT BOTH SEE A LESION ON THE CHEST X-RAY, THERE CAN BE NO LESION THERE.
13. THE DELIVERY OF GOOD MEDICAL CARE IS TO DO AS MUCH NOTHING AS POSSIBLE.  

Reference(s): thanks, dr. wikipedia; picture

Antibiotics for MRSA abscesses? NO.

STUDY #1:

Schmitz et al. Randomized Controlled Trial of Trimethoprim-Sulfamethoxazole for Uncomplicated Skin Abscesses in Patients at Risk for Community-Associated Methicillin-Resistant Staphylococcus aureus Infection. Annals of Emergency Medicine, Vol 56, Sept 2010

Bactrim vs. placebo after incision and drainage.  

Multicenter, double-blind, RCT in 4 military ED's

outcome: treatment failure after 7 days or reduction of new lesion formation in 30 days

results:

                        Tx failure 7 days              New lesion within 30 days      

Placebo                     26%                                          28%

TMP/SMX                  17%                                           9%

Difference (95%CI)      9% (-2 to 21%)                         19% (4-34%)

As shown above, there was a significant difference of new lesions in 30 days.  only 45% were available at 30 days.  big confidence intervals.

STUDY #2

Duong et al. Randomized, Controlled Trial of Antibiotics in the Management of Community-Acquired Skin Abscesses in the Pediatric Patient. Annals of Emergency Medicine, Vol 55, May 2010

Bactrim vs. placebo after incision and drainage. 

double-bind RCT in pediatric patients

outcome: treatment failure within 10 days (need for second incision, IV antibiotics, continued erythema, warmth, fluctuance at 10 day follow up).

results:

              Failure to improve            10 day new lesions    90 day new lesions**
Placebo          5.3%                         26.4%                     28.8%
TMP/SMX       4.1%                         12.9%                     28.3%

** Note that only around 60% were effectively followed up at 90 days.

Conclusion: no difference in failure rates with or without antibiotics. 

Of note,  in treatment arm, only 46% of patients were compliant with antibiotics, taking at least half of the pills. 

Note that there are many other studies showing that antibiotic use does NOT eradicate MRSA.

BOTTOM LINE:

Immunocompetent patients with MRSA abscesses can be treated with I & D alone. Not enough data to support consistent antibiotic use. 

Consider addition of antibiotics in diabetics, immunocompromised, or systemically ill. 

Submitted by S. Morris.

Reference(s): study 1, study 2, picture

passive preoxygenation - a radical concept

Next time you intubate someone...

consider putting them on a nasal cannula at 15L per min under the NRB.  

this article advocates it as a form of "apneic oxygenation" which can prevent desaturation during intubation. 

Awake patients will not tolerate it at 15L/min, so you can start with 4-5 L and then increase to 15 after giving your induction and paralytic medications.

The point: Apneic oxygenation can extend the duration of safe apnea.

Note: High O2 could decrease the respiratory drive, but this is for people who you are committed to intubating already.  

I would love to hear your success stories with this new method!

Submitted by S. Morris.

Reference(s): Weingart, S., Levitan, R.  Preoxygenation and Prevention of Desaturation During Emergency Airway Management. Annals of Emergency Medicine. Nov 2011. Vol 9. Iss 3. ; picture

steroids for pharyngitis + Centor criteria refresher

STUDY HIGHLIGHTS:

Meta-analysis of 9 RCT's of adults and children using steroids for tonsillitis or pharyngitis 

did find more patients with resolution of pain with steroids at 24 or 48 hours.

All patients received antibiotics, which may have been confounding.

BOTTOM LINE:

consider steroids (maybe prednisone 60mg x1 or 2 days) for adult patients with severe exudative sore throat in conjunction with antibiotics.

Of course, steroids have complications, so consider them when prescribing.

Hayward, G. et.al. (2009). Corticosteroids for pain relief in sore throat: systematic review and meta-analysis. British Medical Journal. 

-----

P.S.

a reminder of the Centor criteria (if you believe in them)

The 4 criteria are: 

• fever
• pharyngeal exudates
• anterior cervical adenopathy
• absence of a cough. 

The presence of a cough, hoarse voice, or conjunctivitis, suggests a viral etiology and is not considered a risk factor for group A beta-hemolytic strep. 

Centor criteria should not be used to predict GABS in children.

• <2 points — No antibiotic or throat culture necessary.
  (Risk of strep infection <10%)
• 2-3 points — Should receive a throat culture and treat with an antibiotic if culture is positive.
• >3 points — Treat empirically with an antibiotic.
  (Risk of strep infection >50%)

Singer JI, Gebhart ME: Sore throat, in Marx JA, Hockberger RS, Walls RM (eds): Rosen's Emergency Medicine Concepts and Clinical Practice, ed 6, St. Louis: Mosby, 2006: 274

Submitted by S. Morris.

Reference(s): hayward study; rosen's chapter (listed above); picture

broaden your horizons (a.k.a. good luck diagnosing this one in the ED): EE

RAGING HYPOTHETICAL:
--patient with esophageal foreign body, mobilizing for GI swallow/scope
--foreign body resolved by the time GI swallow is done
--GI consult requests IgE... why?




Eosinophilic Esophagitis (EE) 


--mimics GERD and may result in narrowing or stricture of the esophagus.  


--differentiated from GERD by the amount of mucosal eosinophilia and lack of response to acid suppression.  


--In a cohort, 71% percent of patients with EE were male with a mean age of 10.5+/-5.4 years.  


--strong familial pattern 


--sometimes first presents with lodged food boluses 2/2 stricture.  




Submitted by T. Boyd.




Reference(s): Noel et al. Eosinophilic Esophagitis Correspondence. NEJM. 351:940-941. Aug 2004. picture

broaden your horizons (a.k.a. good luck diagnosing this one in the ED): HLH

HLH (Hemophagocytic LymphoHistiocytosis)


--a condition where there is uncontrolled activation of the cellular immune system. 


--Diagnostic criteria include:

• idiopathic fever
• spleenomegaly
• cytopenias
• hypertriglyceridemia
• hypofibrinogenemia
• lymphadenopathy
• rash
• presence of hemophagaocytosis

--Varied skin manifestations:

• erythroderma
• generalized purpuric macules and papules
• morbilliform eruptions. 

--You’re falling asleep right now reading this aren’t you?  


--Basically this is a rare but potentially fatal disease that no Emergency Physician will ever diagnose. 


--BUT if a patient comes in with this in their medical history, now you (sort of) know what to expect




Submitted by T. Boyd.




Reference(s): Favara BE. Hemophagocytic Lymphohistiocytosis: A He mophagocytic Syndrome. Smnr Diag Path. 1992. Schwartz et al. Lymphohistiocytosis. Emedicine. May 2011, picture

cervical artery dissection: quick review

CAROTID (AND VERTEBRAL) DISSECTIONS: QUICK HITS


--first consult call to Neurologists (less commonly Vascular Surgeons)


--Vascular imaging is a must, but CTA is more sensitive than MRA.  


--To catch on MRI, specific sequences are required so check with your Neurologist/Radiologist to figure out which.  


--Dissections that extend intracranially have a high incidence of forming SAH, especially when heparin is started, thus making heparin have higher mortality than anti-platelet drugs.  


--Extracranial dissections are usually treated with antiplatelet drugs and anticoagulation. 

Submitted by T. Boyd.



Reference(s): Shea et al. Carotid and Vertebral Artery Dissections in the Emergency Department. Emergency Medicine Practice.14;4. April 2012; picture

possible open joint: how much do I infuse?

RAGING HYPOTHETICAL:
--patient arrives with wound around the knee
--want to inject saline in the joint capsule to see if it is open (if it leaks)
--how much saline do I put in there?


Keese et al. The Accuracy of the Saline Load Test in the Diagnosis of Traumatic Knee Arthrotomies. J. Orthop Trauma. 21;7. Aug 2007.

--study of 30 patients undergoing arthroscopy


--after arthroscopy hole was made each knee was injected with saline and measure how much it took until extravasation was seen.


--50ml of saline gave 46% sensitivity
--194ml of saline gave 95% sensitivity. 




FOOD FOR THOUGHT:
--standard 50ml injection not great sensitivity in this small study
--200cc NS seemed to do the trick




Submitted by T. Boyd.




Reference(s): article, picture

d-dimer and aortic dissection

RAGING HYPOTHETICAL:

--your patient arrives complaining of severe chest pain radiating to the back
--you fear aortic dissection
--you've heard about this d-dimer thing...but is it ready for prime-time?




HIGH IN PE/DISSECTION, NOT SO MUCH IN MI: (PMID: 21478122)
--purpose of this research was to define the D-dimer value for discrimination between AAD, PE and AMI.
--consecutive series of 35 AAD, 22 PE and 206 AMI patients


--D-dimer values of patients with AAD (32.9 ± 66.7 g/ml, p<0.001) and PE (28.5 ± 23.6 g/ ml, p<0.001) were significantly higher than those of AMI patients (2.1 ± 3.7 g/ml).
--A cutoff value of 5.0 g/ ml was effective in distinguishing AAD and PE from AMI, with a sensitivity of 68% and a specificity of 90% (ok, but not great)




GOOD SENSITIVITY IS PROMISING... (PMID: 21296332)
--Review and meta-analysis to examine use of d-dimer as screening tool for aortic dissection.
--A value of 500 ng/ml was defined as the threshold for a positive plasma DD finding because it is widely used for ruling out pulmonary emboli.
--Identified 7 studies involving 298 subjects with aortic dissection and 436 without.


--When data were pooled across studies:

• sensitivity high (0.97, 95% confidence interval [CI] 0.94 to 0.99)
• negative predictive value high (0.96, 95% CI 0.93 to 0.98)
• specificity low (0.56, 95% CI 0.51 to 0.60)
• positive predictive value low (0.60, 95% CI 0.55 to 0.66) 

--In conclusion, our meta-analysis suggests that plasma DD <500 ng/ml is a useful screening tool to identify patients who do not have AAD.




NOT QUITE READY?  (PMID: 21546117)
--There is inadequate evidence to support the use of D-dimer to exclude acute aortic dissection.


--registry data reported by Suzuki et al provide the most valid estimates for D-dimer sensitivity and specificity; however, the relatively small sample size (N=220) resulted in imprecise estimates, with a lower limit of the 95% confidence interval (CI) of 0.90 for sensitivity and 0.38 for specificity.


--A conservative estimate based on these results indicates that the negative likelihood ratio for D-dimer is approximately 0.2 and the positive likelihood ratio is 1.5. If these approximations are validated in a larger prospective study, a positive D-dimer result would have no value in clinical decisionmaking, but a negative D-dimer result may decrease the probability of aortic dissection to a moderate degree.


--However, to rule out aortic dissection with a negative D-dimer result, the pretest probability would have to be very low. 


--Unfortunately, unlike pulmonary embolism or acute myocardial infarction, there are no validated clinical prediction rules to aid clinicians with establishing a pretest probability of aortic dissection.

BOTTOM LINE:

--studies used d-dimer cutoff of 500ng/ml

--high (but not perfect) sensitivity (90+%), low specificity

--potentially useful with patients with low pretest probability for aortic dissection

--since no validated prediction rules (like Wells/PERC for PE) for dissection, not quite ready for primetime

Submitted by J. Gullo.




Reference(s): PMID: 21478122; PMID: 21296332; PMID: 21546117; picture

fallopian tube torsion

WHAT IS FALLOPIAN TUBE TORSION?

Twisting of the fallopian tube on itself -- similar to closed loop bowel obstruction

Ovarian torsion is more of an end tube twist, Fallopian tube torsion is proximal to ovarian torsion

Much more rare cause of LQ abd pain/pelvic pain than ovarian torsion

                Prevalence: one in 1.5 million women

                Population at risk: pre-menopausal women, 80% are <50 yo

Risk factors: Most commonly benign etiology (89%)

                Intrinsic factors:  long mesosalpinx, tortuous dilated tube (hydro- or hemato-salpinx), tubal mass, tubal ligation, PID, abnormal peristalsis/periovulatory spasm

                Extrinsic factors:  adhesions, adnexal venous congestion, adjacent ovarian or paraovarian masses, uterine masses, gravid uterus, trauma, sudden body position changes (Sellheim theory)

Proposed mechanism: Mechanical obstruction of adnexal veins/lymphatics --> pelvic congestion/edema --> enlargement of fimbrial end --> partial/complete torsion of tube

                Since vascular supply to adnexa comes from ovarian + uterine vessels --> can get isolated tubal necrosis w/o ovarian vascular compromise

DDx: ovarian torsion, ruptured ovarian cyst, PID, ectopic, appy, urolithiasis, cystitis, SBO/perf

Difficult diagnosis -- non-specific findings, pain is only universal feature

Clinical presentation

Sudden onset lower quadrant abdominal pain / pelvic pain

                May be more intermittent than ovarian torsion (53% had previous attacks of undx’d abd pain)

Slightly more common on the right (3:2 R:L)

Labs: Leukocytosis is mild, and late finding (>24 hrs after onset) -- tube likely unsalvageable

Ultrasound findings

Normal ovaries + uterus with normal blood flow

Free pelvic fluid

Dilated adnexal tubular structure that flares at one end, with thickened echogenic walls, suspicious for hydrosalpinx

A beaked, tapering appearance of the tube, with its vertex pointing toward the affected adnexa

Internal debris/convoluted echogenic mass, which may represent thickened torsed tube

Difficult to visualize vascular compromise of tubal wall

CT findings

Adnexal mass, twisted appearance to fallopian tube, dilated tube >15 mm, thickened enhancing tubal wall, luminal attenuation >50 H c/w hemorrhage

Free pelvic fluid, peritubular fat stranding, enhancement + thickening of broad ligament, regional ileus

Treatment options

Surgical detorsion, salpingotomy

Salpingectomy frequently performed 2/2 irreversible damage

Submitted by S. Eucker.

Reference(s): Gross, M et al, “Isolated Fallopian Tube Torsion: A Rare Twist on a Common Theme”, AJR 2005; 185: 1590-1592.  (Also the reference for the images); Ho, P et al, “Isolated Torsion Of The Fallopian Tube: A Rare Diagnosis In An Adolescent Without Sexual Experience” Taiwan J Obstet Gynecol 2008; 47(2):235-237. Ferrera, P et al, “Torsion of the Fallopian Tube”, Am J Emerg Med 1995; 13:312-314. Weir, CD and Brown, S, “Torsion of the Normal Fallopian Tube in a Premenarcheal Girl: A Case Report”, J Pediatr Surg 1990; 25(6):685-686.

Kanavel signs for flexor tenosynovitis

CLASSIC TEACHING:
--Kanavel signs for flexor tenosynovitis

• pain on passive extension (early finding)
• finger held in flexion
• uniform swelling of finger
• tenderness to percussion along flexor tendon sheath (late finding)

HOW GOOD IS OUR H&P?
--study of 75 patients with flexor tenosynovitis


--incidence of H&P findings 

• fusiform swelling (97%)
• pain on passive extension (72%)
• semiflexed posture (69%)
• subcutaneous purulence (68%)
• tenderness along flexor sheath (64%)
• elevated WBC (59%)
• diabetes mellitus (35%)
• skin necrosis (23%)
• fever (17%)

--overall, the 4 signs aren't perfect, but are there individually in at least 2/3rds of patients

--hard to find data on sensitivity/specificity of these signs combined on brief pubmed biopsy

TREATMENT TOOLBOX:
--IV antibiotics: staph and strep coverage, think pasturella for bite-associated infections

--surgery: consult your hand surgeon ASAP

Kanavel signs for flexor tenosynovitis (REVISITED)

• pain on passive extension (early finding)
• finger held in flexion
• uniform swelling of finger
• tenderness to percussion along flexor tendon sheath (late finding)

Reference(s): uptodate.com: infectious tenosynovitis; study; picture.

to CT or not CT?: Canadian CT Head Rule & New Orleans Criteria

CT or NOT?

--Papa et al. study looked at both decision rules (link below)

--314 patients (73%) had a GCS of 15

--22 of the 314 (7%) had evidence of a traumatic intracranial lesion on CT

--3 of 314 (1.0%) required neurosurgical intervention

NEW ORLEANS CRITERIA (if ANY of these are true, then do a CT ):

• headache
• vomiting
• age > 60 years
• drug or alcohol intoxication
• deficits in short-term memory
• evidence of trauma above the clavicles
• seizure

CANADIAN CT HEAD RULES (if ANY of these are true, then do a CT):

• GCS < 13
• failure to reach GCS of 15 within 2 h
• suspected open skull fracture
• any sign of basal skull fracture
• vomiting >2 episodes
• age >65 years
• amnesia before impact >30 min 
• dangerous mechanism of injury (pedestrian struck by car, ejection from MVC, fall > 3 feet or > 5 stairs)

--NOC and CCHR both had 100% sensitivity (95% confidence interval [CI] = 82% to 100%)

--CCHR was more specific (36.3% specificity) for detecting any traumatic intracranial lesion on CT vs. NOC (10.2% specificity)

Reference(s): study; mdcalc: canadian; mdcalc: new orleans; picture

stress dose steroids

RAGING HYPOTHETICAL:
--septic patient
--poured in lots of fluid, still hypotensive
--dripping in lots of pressors, still hypotensive
--um, what now?




POSSIBLE OPTION: STEROIDS (quick hits)
--'stress dose' steroids have been used for fluid/pressor unresponsive patients in septic shock


--hydrocortisone 50mg IV q6h, or 100mg IV bolus + drip (adults)


--not highly recommended in kids, unless known adrenal insufficiency
--rule of thumb stress dose for those on chronic steroids: 2-3x normal daily dose


--seems to have quicker resolution of shock, but not much mortality benefit


--slow taper later (thanks for taking care of this, ICU colleagues)




Reference(s): surviving sepsis recs, meta-analysis, uptodate.com: Hydrocortisone (systemic): Drug information, Corticosteroid therapy in septic shock, picture

epileptic vs. non-epileptic seizure: what are the signs?

WHAT ARE THE SIGNS?

--review by Avbersek & Sisodiya in J Neurol Neurosurg Psychiatry (link below)
--looked at 34 studies
--tried to tease out what signs distinguish epileptic vs. non-epileptic seizure


WHAT DID THEY FIND?

--signs that favor psychogenic non-epileptic seizures (specificity)

• fluctuating course (96%)
• asynchronous movements (93-96%)
• pelvic thrusting (96-100%)
• side-to-side head/body movement (96-100%)
• closed eyes (74-100%)
• ictal crying (100%)
• memory recall (96%)

--signs that favor epileptic seizures (specificity)

• occurance from sleep (100%)
• post-ictal confusion (88%)
• stertorous (snoring) breathing (100%)

FYI:
--the sensitivities for all of these signs were horrible, so can't use them to rule anything out
--sometimes excluded frontal lobe partial seizures
--insufficient evidence: gradual onset, flailing/thrasing, opisthotonus, tongue biting, urinary incontinence


Reference(s): review article, picture

Spontaneous Cervical and Intracranial Arterial Dissections

(scroll to bottom for quick hits)

Background
-Arterial dissections can cause stroke in both young in old populations, and is the most common cause of stroke in the young

-Extracranial dissection is more common than intracranial dissection

-Stroke is generally caused by either diminished blood flow from intraluminal thrombus or embolized clot


Pathogenesis (stick with it)
-Dissection are believed to begin with a tear in the media of the vessel wall, leading to bleeding in the wall itself

-partially coagulated intramural blood can enter the lumen which activates platelets and
the coagulation cascade leading to intraluminal thrombus.

-Intramural blood can accumulate leading to compression of the lumen



Risk Factors
-Connective tissue and vascular disorders are thought to be main risk factors:
(e.g. Ehlers-Danlos Syndrome (type IV), Marfan Syndrome, Polycystic kidney disease, cystic medial necrosis, Fibromuscular dysplasia)

-many are caused by trauma




Diagnosis
-based on radiologic criteria taken from the Strategies Against Stroke Study for Young Adults in Japan (SASSY) using CTA or MRI/MRA

-Primary rules are based on finding an intimal flap or double lumen on Angiogram or MRI/MRA, or repeated non-specific findings associated with dissection on multiple studies.



Symptoms
-Head or neck pain

-Horner Syndrome - occurs when the sympathetic fibers on the ICA are stretched. It is usually just partial with ptosis and miosis but no anhidrosis.


Difference between Carotid and Vertebral Dissections
-Transient monocular blindness occurred only with internal carotid dissection

-Ischemic stroke is more common in vertebral dissections

-Neck pain and recent minor cervical trauma are more common in vertebral dissections

-Proportion of men and a recent infection are more common in ICA



Treatment
-Antithrombotic therapy (antiplatelet or anticoagulation) is the primary initial treatment for ischemic stroke and TIA caused by arterial dissection

-For intracranial dissection, antiplatelet therapy is often the treatment of choice

-For extracranial dissection, anticoagulation initially followed by 6 months of warfarin therapy as opposed to antiplatet therapy is often chosen

-Endovascular and surgical therapy are generally only reserved for recurrent ischemic events


BOTTOM LINE:
-arterial dissection is more common cause of stroke in the young
-extracranial (vertebral, carotid) more common than intracranial dissection
-sx: headache, neck pain, stroke-like symptoms, Horner's syndrome (for ICA)
-risk factors: connective tissue disorders, trauma
-dx: angiography, MRI/MRA
-tx: antithrombotics/anticoagulation (aspirin, heparin, coumadin, etc.); surgical/endovascular for recurrent events


Submitted by J. Grover.


Reference(s): Caplan, LR and Biousse V. “Cervicocranial Artery Dissections.” J Neuro-Opthalmol. 2004; 24:299-305. Maruyama, H et al. “Spontaneous Cervicocephalic Arterial Dissection with Headache and Neck Pain as the Only Symptom.” J Headache Pain (2012) 13: 247-253. “Spontaneous Cerebral and Cervical Artery Dissection: Treatment and Prognosis”. Uptodate.  “Spontaneous Cerebral and Cervical Artery Dissection: Clinical Features and Diagnosis”. Uptodate., picture

octreotide in sulfonylurea overdose

BASIC IDEA:
--Octreotide inhibits the secretion of several neuropeptides, including insulin
--if someone overdoses on a sulfonylurea (e.g. glipizide), would giving octreotide help reduce the hypoglycemia problem?


(straight to the) BOTTOM LINE:
--limited studies out there, but reviews tend to say the same thing...
--octreotide is probably safe and beneficial in sulfonylurea overdose/hypoglycemia


Reference(s): http://www.ncbi.nlm.nih.gov/pubmed/17764782 , http://www.ncbi.nlm.nih.gov/pubmed/16356235, http://www.ncbi.nlm.nih.gov/pubmed/17652687, http://www.ncbi.nlm.nih.gov/pubmed/20352540

fat pad on x-ray

WHAT IS THE FAT PAD?
--might be only subtle sign of a fracture on x-ray

--broken bones leak fat & blood, which also moves existing soft tissue



COOL TRICK:
--courtesy of EM News article (check out the pic on their website)
--if you're aspirating a joint (e.g. knee effusion), and you aspirate blood, take a look under a light, look for the sheen of fat on top (suggests fracture)

--might want to get a CT or MRI next, if those x-rays were negative



Reference(s): EM News article with picture, x-ray, diagram, oil&water

hydrofloric acid burns

HYDROFLUORIC ACID:
--one of the strongest inorganic acids
--can cause significant systemic toxicity due to fluoride poisoning.

--is used mainly for industrial purposes (eg, glass etching, metal cleaning, electronics manufacturing)--may be found in home rust removers.

 
TREATMENT TOOLBOX:
--can be soaked in magnesium hydroxide containing solutions (e.g. Mylanta) or soaked in ice water to help decrease the amount of absorption. 

--decontaminate appropriately and wash with water. 

--apply 2.5% calcium gluconate gel to burn (10% Ca Gluconate solution in 3 times the volume of KY gel) and place hand into latex glove. 

--if pain persists >30 minutes and not on fingers, infiltrate margins of burn with 10% calcium gluconate solution. 

--if severe burns, can inject 10ml of 10% Ca gluconate in 40ml of D5 intra-arterially over 4 hours. 

--repeat as necessary.  For oral, ocular, or inhalation burns, calcium will also have to be given in different concentrations. 

--Consult Toxicology. 

--Treat pain with opioids.


Submitted by T. Boyd.


Reference(s): http://emedicine.medscape.com/article/773304-treatment, picture