Cocaine: quick review

PATHOPHYSIOLOGY:

• Release of NE, blocks NE reuptake
• Release & reuptake blockade of serotonin and dopamine
• Na channel blockade – local anesthetic effect
• Fat soluble - crosses blood brain barrier
• Stimulates CNS, especially limbic system, which potentiates dopaminergic transmission - pleasurable behavioral effects
• REMINDER: don't treat with a beta-blocker (shunts to unopposed alpha receptors)

NOTABLE NUMBERS:

Route	Onset	Peak(min)	Duration(min)	Half-life (min)
Inhalation	7s	1-5	20	40-60
IV	15s	3-5	20-30	40-60
Nasal	3min	15	45-90	60-90
Oral	10min	60	60	60-90

DEATH BY...

• Tachydysrhythmias cause most non-traumatic deaths
• Stroke
• SAH
• Hyperthermia
• MI (acute vasospasm, dysrhythmia, chronic accelerate atherogenic disease)

HEART BREAKER:

• Patients with cocaine-related MI often have fixed atherosclerotic lesions.
• Cocaine can induce increased heart rate and BP, resulting in increased myocardial oxygen demand.
• effects of cocaine also include myocarditis and dilated cardiomyopathy.

10-SECOND RECAP:
--stims norepi, serotonin, dopa release, blocks reuptake; also Na+ channel blocker
--DON'T treat with beta-blocker (unopposed alpha-receptor action)
--inhaled/IV works in seconds, nasal/oral works in minutes, lasts hour(s)
--sympathomimetic response, and resulting problems (dysrhythmias, MI, stroke, SAH, hypertherm, etc.)
--say NO to drugs.


Submitted by J. Gullo. 

Reference(s): emedicine.com: cocaine toxicity in emergency medicine, picture

Intussusception: quick review

(scroll to bottom for 10-second version)

DEMOGRAPHICS

--most common cause of intestinal obstruction in kids 3 months-6 years of age.

--male:female ratio is 4:1

--Seasonal variation with peaks after GI viral illness seasons.

PATHOPHYSIOLOGY
--In younger children, the ileum invaginates into the upper colon, bringing the mesentery with it (ileocolic).

--lead point is often lymphoid hyperplasia from viral gastroenteritis. 

--In older children, ileo-ileo intussusceptions are more common. 

--lead point causes include intestinal polyps, Meckel diverticulum, lymphosarcoma, or even HSP

--Constriction of the mesentery obstructs venous return, leading to bowel ischemia and bloody stools leading to the classic “currant jelly” stool, which is a late finding occurring in about 50% of cases. 

CLINICAL FEATURES

--Sudden colicky abdominal pain (child will stop, cry, draw up their legs, and then after a few minutes the child appears well). 

--As the condition progresses the time between episodes decreases.   
--Stool is generally guaiac positive even in the absence of gross blood. 
--A palpable sausage shaped mass can be found on the right side of the abdomen in about 2/3 of cases

DIAGNOSIS
--Diagnosis often made by history alone
--KUB may suggest a filling defect in the right lower quadrant of the abdomen or can be normal
--US can often show the classic target appearance of bowel within bowel (donut sign (transverse); sandwich sign (longitudinal)

TREATMENT
--Air contrast enema is preferred over barium enema because it enables better control over colonic pressure and in the case of perforation prevents barium spillage into the peritoneum.
--Children generally admitted for observation because of the 5-10% recurrence rate.  A second attempt at air reduction is usually successful, but if further recurrences occur surgical reduction may be necessary.  

10-SECOND RECAP:

--most common in kids 3 mo-6 yrs old; male:female 4:1

--ileocolic (younger), ileo-ileo (older), or wherever

--common lead points (lympoid hyperplasia from gastroenteritis, polyps, meckel's, cancer, HSP, etc.)

--bowel ischemia -> guaiac+ stool -> occasionally currant jelly stool

--history is key, palpable sausage in RLQ in 2/3, KUB maybe, ultrasound (donut/sandwich signs)

--air contrast enema = diagnostic + therapeutic; surgery if that doesn't work

Submitted by J. Grover.

Reference(s): Tintinalli's Emergency Medicine, picture 1, KUB, donut, sandwich

hyoid bone fracture

QUICK OVERVIEW:
--rare, due to protected location of the larynx (mandible is superior and anterior and spine is posterior)

--Hyoid bone fractures from blunt trauma other than strangulation = 0.002%

--Respiratory distress can progress rapidly: hematoma formation and soft tissue swelling leads to airway compromise and hypoxia

--Laryngeal injuries occur more commonly in males (77% vs 33%)

--Women have slimmer longer necks so they are more prone to hyoid bone fractures

--symptoms: horseness, neck pain, dyspnea, dysphonia, aphonia, dysphasia, odynophonia/phagia, stridor (inspiratory), hemoptysis, subcutaneous emphysema, hematoma, ecchymosis, crepitus, loss of landmarks

--Associated injuries w/laryngeal fractures: intracranial injury (13%), open neck injury (9%), C-spine fx (8%), esophageal injury (3%)

BOTTOM LINE:

--hyoid bone fractures are rare

--most are from strangulation, few from blunt trauma

--respiratory compromise is the big issue (duh)

--associated with other head & neck badness

Submitted by J. Gullo.

Reference(s): PMID: 21397138; PMID: 10484094; emedicine: laryngeal fractures, picture

brace vs. cast for Salter I & II distal fibula fractures

QUICK OVERVIEW:

--Isolated non-displaced Salter type I & II distal fibula fx’s and avulsion fx’s are very low risk for long-term complications (i.e. growth arrest – no reports found after lit review)

--For an unstable ankle, the ligaments connecting the tibia, fibula and talus must be broken in 2 places; with Salter I/II fibula fx ligament only broken in 1 place

--removable ankle brace (e.g. Air-Stirrup) vs. traditional casts: in a non-inferiority RCT single blind study, removable ankle brace patients had...

• less functional morbidity
• more rapid return to baseline activity (~80% back to baseline activity with brace in 4 wks, vs ~60% of those with cast)
• preferred by patient and families
• more cost-effective

--Can advise parents/patient to expect pain for next 2-4 weeks, full return to competitive sports usually in 6-12 weeks

Submitted by F. DiFranco. 

Reference(s): Boutis, K., et al. A randomized controlled trial of removable brace versus casting in children with low-risk ankle fractures. Pediatrics. 119(6):1256-1263, June 2007; Boutis, K., et al. Common pediatric fractures treated with minimal intervention. Pediatric Emergency Care. 26(2):152-157, Feb. 2010., picture

steroids and sore throat

(scroll to bottom for 10-second version)

REVIEW ARTICLE:

--includes 5 adult trials of IM vs oral steroids for acute pharyngitis

--suggested earlier reduction of pain and shorter time to complete relief as well as 3 pediatric trials using oral dex (0.6 mg/kg to a max of 10 mg) as a single dose or given over 3 days showed earlier pain reduction compared to controls

--no benefit to 3 day vs. single dose

META-ANALYSIS:

--includes 8 RCT’s comparing systemic corticosteroids and placebo

--when given with antibiotics, patients who received steroids had an average onset of pain relief 6.3 hours earlier

INTRAMUSCULAR STEROIDS:

--turkish study; single dose IM dex vs. placebo for patients with 2+ Centor criteria

--average onset to pain relief of 8.1 hrs in steroid group vs. 19.9 hrs in placebo group

--complete pain relief of 28.9 hrs (steroid) vs 53.7 hrs (placebo)

PO vs. IM STEROIDS:

--single dose oral prednisone vs IM dexamethasone

--no difference in pain scores or number of hours to relief of pain

10-SECOND RECAP:

--steroids in acute pharyngitis: hastens pain relief by about 6-24 hours (vs. placebo)

--single dose probably just as good as 3-day course

--dexamethasone IM vs. prednisone PO: works about the same

Submitted by F. DiFranco.

Reference(s): Hayward, G., et al. Corticosteroids for pain relief in sore throat: systematic review and meta-analysis. British Medical Journal. 339:b2976, Aug. 2009; Korb, K., et al. Steroids as adjuvant therapy for acute pharyngitis in ambulatory patients: a systematic review. Annals of Family Medicine. 8(1):58, Jan.-Feb. 2010; Marvez-Valls, E., et al. A randomized clinical trial of oral versus intramuscular delivery of steroids in acute exudative pharyngitis. Academic Emergency Medicine. 9(1):1, Jan. 2002; Tasar, A., et al. Clinical efficacy of dexamethasone for acute exudative pharyngitis. Journal of Emergency Medicine. 35(4):363, Nov. 2008; picture

where do patient’s with Marfan Syndrome dissect?

AORTIC DISSECTION & MARFAN SYNDROME:
--The major cardiovascular manifestation in Marfan Syndrome is a progressive dilatation of the ascending aorta, leading to aortic aneurysm formation and eventually to fatal aortic rupture or dissection. Aortic dissection in early adult life is the leading cause of death.

--The ascending and descending aorta are both abnormal in Marfan Syndrome.

· The descending aorta is affected in two out of three patients during aortic dissection, and is the site of most complications which occur during follow-up.

· Aortic dissection limited to the descending aorta can occur in patients without dilatation of the ascending aorta.

--Dissection of the descending aorta was associated with dissection of ascending aorta in 43% and was isolated in 20% of cases.

BOTTOM LINE:

--dissections in Marfan involve descending aorta ~2/3 of the time, but these frequently involve the ascending aorta also

--if you have a patient with Marfan, and are worried about a dissection...worry about both (ascending/descending)

Submitted by J. Gullo.

Reference(s): PMID: 20232788, medscape article, picture

how often is manual testicular detorsion successful?

STUDY 1:

--over 10 years, looked at 35 of 104 patients who underwent pre-op manual detorsion. 

--of the 34 evaluable patients, all the testes were salvaged (i.e. 100%)

STUDY 2:

--16 Total cases of acute torsion, 15 underwent successful detorsion

--93% testicular salvage in the 15 who underwent detorsion

STUDY 3:

--14 of 17 patients had successful manual detorsion with no testicular atrophy noted after 22 months

BOTTOM LINE:

--manual testicular detorsion works pretty well

--most torsion is medial, so to detors, twist 180 degrees laterally (like opening a book); should relieve symptoms

--then call urology

Submitted by J. Gullo.

Reference(s): study 1, study 2, study 3, picture

elevated troponin: what if its not an MI?

QUICK REVIEW:
--Myocardial necrosis indicated by elevated troponin is NOT always due to atherosclerotic CAD

--Troponin has high sensitivity for detecting very small amount of myocardial cell death

--Troponin is released in the blood due to irreversible as well as reversible cell damage AND does ≠ permanent myocyte damage


EXPANDED DIFFERENTIAL:
--Demand ischemia: sepsis/SIRS, hypotension, hypovolemia, SVT/afib, LVH

--Myocardial ischemia: coronary vasospasm, ICH/stroke, ingestion of sympathomimetic agents

--Direct myocardial damage: cardiac contusion, ICD shock, cardiac infiltrative d/o (amyloidosis), chemotherapy, myocarditis/pericarditis, heart transplant

--Myocardial strain: CHF, PE, PHTN, COPD, strenuous exercise

--Chronic renal insufficiency


Submitted by F. DiFranco.


Reference(s): Jeremias A. & Gibson M. Narrative review: alternative causes for elevated cardiac troponin levels when acute coronary syndromes are excluded. Annals of Internal Medicine. 142(9):786-791, May 2005.

ultrasound in testicular torsion

WHAT TO LOOK FOR:

Submitted by F. DiFranco.


Reference(s): www.sonoguide.com; Images from: Adhikari, S.R. MD. Testicular Ultrasound. Fig 5&6. Retreived from http://www.sonoguide.com; Baldisserotto, M. Scrotal emergencies. Pediatr Radiol 2009; 39:516.

How to tell a traumatic tap vs. SAH

QUICK REVIEW:

--There is no criteria for how many RBCs in the CSF are needed to diagnose SAH

--One of the best methods to distinguish traumatic tap vs SAH is by looking for xanthochromia

--Can measure xanthochromia by visual inspection (subjective, human error) OR spectrophotometry (very sensitive but not very specific, not widely available at most hospitals)

--Occurs via breakdown of Hgb -> oxyhemoglobin (pink-orange, can happen in vitro) -> bilirubin (yellow, only happens in vivo)

PEARLS:

--False positive xanthochromia can occur from jaundice (usually total serum bili of at least 10-15 mg/dL), rifampin, high CSF protein concentration (>150 mg/dL), or excess carotenoid intake

--Oxyhemoglobin can be present in traumatic tap and appear faintly yellow

--Formation of bilirubin takes time, but after 12 hrs from onset of aneurysm rupture (i.e. “worst HA of my life”), CSF should show xanthochromia in patients with SAH

--Elevated opening pressure (> 20 cm H2O) + bloody CSF strongly suggests SAH

--When all else fails, you may repeat the LP at a higher interspace

Submitted by F. DiFranco.

Reference(s): Shah, K.H., & Edlow, J.A. Distinguishing traumatic lumbar puncture from true subarachnoid hemorrhage. The Journal of Emergency Medicine. 23(1), 67-74, 2002. picture

seizure vs. syncope: is creatine kinase (CK) useful?

STUDY 1:
--37 syncope and 26 generalized tonic–clonic seizure patients
--tested serum CK and myoglobin at ED presentation and 4 hrs after the event

--no statistically significant different in myoglobin at any time
--no statistically significant different in CK at ED presentation
--CK drawn 4 hrs after the event:

• elevated in four of 37 (10.8%) patients with syncope
• elevated in nine of 26 (34.6%) patients with seizure activity
• statistically significant difference in CK between seizure and syncope groups (P<0.05)
• sensitivity 34%
• specificity 89%

STUDY 2:
--Sequential sample of 205 patients with transient loss of consciousness. The study group consisted of 96 patients who had CK measurements in the ED

--Mean (+/- SE) CK significantly higher in the seizure group (231.1 +/- 34.8 U/L vs. 70.5 +/- 5.6 U/L, p less than 0.001).
--elevated CK: sensitivity of 0.43, specificity of 0.98--elevated CK >3hrs after event: sensitivity was 0.80, specificity was 0.94


10-SECOND TAKEAWAY:
--serum CK level after seizure: not too sensitive (better after 3 hrs), pretty specific
--may be useful to confirm suspected seizure if elevated >3-4 hours s/p event


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

Humidified air for treatment of croup: does it work?

WELL, DOES IT?

--Treatment of croup with humidified air is not effective according to multiple studies

--In a JAMA article, 140 children with moderate-severe croup either received humidified blow-by O2, 40% humidified O2 or 100% humidified O2 with no difference found in croup score, treatment with epi or dex, hospital admission, or additional medical care between groups

--Another study of 71 children age 3 months – 6 yrs with moderate croup received either mist stick or no mist for 2 hours showed no difference in croup score, O2 sat, HR or RR between groups

--Some risks of humidified air include scald injuries, dispension of molds and fungus from improperly cleaned mist tents

BOTTOM LINE:
--Treatment of croup with humidified air is not effective in improving vitals or need for further treatment


Submitted by F. DiFranco.


Reference(s):  Bjornson C., Johnson D.W. Croup. The Lancet. 371:329-339, Jan. 2008.; Neto G., Kentab O., Klassen T., Osmond M. A randomized controlled trial of mist in the acute treatment of moderate croup. Academic Emergency Medicine. 9:873-879, 2002.; Scolnik D., Coates A., Stephens D., DaSilva Z., Lavine E., Schuh S. Controlled delivery of high vs low humidity vs mist therapy for croup in emergency departments. JAMA. 295:1274-80, 2006. , picture

audio podcast: respiratory distress

THIS MONTH:

RESPIRATORY DISTRESS
--round 2 of these resident lecture podcasts. feedback, as always, is appreciated.

download link

Lecture by P. Morse.

valproic acid toxicity and ammonia

RAGING HYPOTHETICAL:
--wacky/altered patient, happens to be on valproate, what could be going on?


VALPROIC ACID TOXICITY
--if you're worried about this, your differential for secondary problems/causes can include: cerebral edema, electrolyte abnormalities, hepatotoxicity, and hyperammonemia/encephalopathy


HYPERAMMONEMIA w/VALPROIC ACID:
--can occur after acute toxicity or chronic use
--not always associated with elevated liver function tests
--happens 'cause a metabolite of valproic acid inhibits an enzyme needed for ammonia elimination by the urea cycle (you can look up the names if you really want to)
--valproate may also mess with carnitine, elevate ammonia that way too


BOTTOM LINE:
--wacky patient with valproate on their med list, consider sending an ammonia level and/or checking for asterixis


Reference(s): uptodate.com: valproic acid poisoning, picture

seizure or not: is prolactin useful?

STUDY:
--200 patients with seizure-like activity, 109 ultimately diagnosed with seizure
--31% (of 200 patients) had abnormal prolactin (upper limit of normal ~30mg/dL)

--the numbers:

• sensitivity of this serum prolactin was 42%
• specificity was 82%
• positive predictive value (PPV) of 74%
• negative predictive value (NPV) of 54%
• overall accuracy of 60% in the diagnosis of seizure,
• likelihood ratio of 2.4

--their conclusion: "The measurement of serum prolactin is helpful as a confirmatory test, but not as screening test in the emergency department setting."


REVIEW ARTICLE:
--most studies used 2x baseline serum prolactin level as 'elevated'
--the numbers:

• pooled sensitivity for generalized tonic-clonic seizures (60.0%); for complex partial seizures (46.1%)
• pooled specificity was similar for both (approximately 96%)
• 2 Class II studies were consistent in showing prolactin elevation after tilt-test-induced syncope.

--their conclusion: "Elevated serum prolactin assay, when measured in the appropriate clinical setting at 10 to 20 minutes after a suspected event, is a useful adjunct for the differentiation of generalized tonic-clonic or complex partial seizure from psychogenic nonepileptic seizure among adults and older children (Level B). Serum prolactin assay does not distinguish epileptic seizures from syncope (Level B)"


META-ANALYSIS:
--usefulness of raised serum prolactin in diagnosing generalised tonic-clonic seizures (GTSC) in patients presenting to the ED after a single episode of syncope
--13 relevant studies only 3 met the criteria for evaluation

--the numbers: if a serum prolactin concentration is > 3x the baseline when taken within one hour of syncope, then...

• LR (likelihood ratio) of GTSC vs pseudoseizure = 8.92, sensitivity 0.62, specificity 0.89
• LR of GTSC vs. syncope = 4.60, sensitivity 0.71, specificity 0.85

10-SECOND TAKEAWAY:
--serum prolactin in seizure: not too useful in the ED
--generally poor sensitivity, better specificity, but only if tested early (~10-60 min s/p episode)

--so if you can draw it fast, and if its significantly elevated, it might be useful (a lot of if's), but if its low, doesn't mean it's not a seizure

--serum prolactin in seizure: not too useful in the ED

Reference(s): study, review, meta-analysis, picture

are antibiotics really helpful in nasal packing after epistaxis?

STUDY #1: questionnaire to UK docs asking about their clinical practice with nasal packing

--preferred nasal packing materials: merocel (72%), rapid rhino (17%), either merocel or rapid rhino (5%), BIPP pack (3%) and no preference (3%).

--antibiotics used if: packing in >24 hrs (37%), packing >48 hrs (28%), NOT used routinely (22%), for all packing (5%), no preference (8%)

--length of antibiotic course: while the pack was in (37%), 5 days (43%), 7 days (14%), no preference (6%)

--antibiotic choice: amoxycillin/clavulanic acid (73%), amoxycillin alone (17%), cephalosporin (10%)

--tangents: 78% of the interviewees believed prophylactic antibiotics reduce the incidence of infection (toxic shock syndrome – TSS, sinonasal infection and middle ear infection). Physicians (6%) suggested prophylactic antibiotics may help to reduce incidence of re-bleeding. The remainder (16%) stated they were unsure of the benefit of antibiotic use.


STUDY #2: small prospective pilot study in the UK looking at how antibiotics affected infection rates. 

--21 patients admitted over a six month period for unilateral anterior nasal packing for epistaxis.  Augmentin was started per hospital protocol if the packing remained in for greater than 24 hours.  After the packing was removed, nasal swabs were taken of both nares and cultured.  

--All 21 patients have the same microbiological growth patterns in the packed and non-packed sides of the nasal cavities.  Only 9 of those patients received antibiotics.  So the antibiotics don’t seem to affect bacteria growth.  Also, there were no clinical signs of infections.


10-SECOND TAKEAWAY:
--nasal packing perceived to increase infection risk (similar to tampon w/toxic shock)
--antibiotics tend to be prescribed, but no dramatic consensus on when to use or for how long
--small study suggests the antibiotics don't change nasal flora
--toxic shock would suck (incidence in post-op packing is 16 per 100,000 packing), but not much evidence prophylactic antibiotics do much to change that. need more data, but judge accordingly.


Submitted by J. Gullo.


Reference(s): study 1, study 2, uptodate.com: Approach to the adult with epistaxis, picture

lithium and hypothyroidism

LITHIUM & THE THYROID:
--not always best friends

--multiple mechanisms by which Lithium causes hypothyroidism:

• inhibits thyroid hormone release and increases TRH-stimulated TSH. 
• concentrated by the thyroid gland and inhibits iodine uptake.
• interferes with the deiodination of T4 to T3
• may have an immunostimulant effect, either by inducing or exacerbating a preexisting autoimmune disease.

--Rates of overt hypothyroidism can vary from 0 – 47% (average 10%) in people on long term lithium treatment.  


BOTTOM LINE:
--if you have a patient who is taking lithium, and you're sending off labs (lithium level, sodium/lytes, etc) for some [presumably good] reason, might be worth adding a TSH to the mix


Submitted by J. Gullo.


Reference(s): a review, another source, picture

what's a normal alkaline phosphatase level in children?

QUICK TAKE-AWAY:
--This study linked below analyzed nearly 1700 serum samples from children age 0 – 18.  About 80 of the children had liver disease.  They considered an alk phos of 335 to be the upper limit of normal in childhood.  Most of their data topped out at under an alk phos of 250-ish.

--not sure I can post their figures up without permission, but if you have a minute, click the link, look at figures 1 & 2, figure 2 mainly. picture's worth a thousand words.

Submitted by J. Gullo.

Reference(s): Knight JA, Haymond RE. gamma-Glutamyltransferase and alkaline phosphatase activities compared in serum of normal children and children with liver disease. Clin Chem. 1981 Jan;27(1):48-51., picture

ABG vs. VBG

DO I REALLY NEED TO STICK THIS PERSON AGAIN, OR CAN I DRAW OFF A VBG? (scroll down for an even more abridged version)


STUDY #1: (hypothetical: metabolic derangement)
--retrospective review of ABG and VBG’s in stable DKA patients. 


--in patients with DKA, the difference between arterial and venous pH was 0.02 units (-0.009 to +0.021) and the difference between bicarbonate was -1.88 mEq/L. 


--their conclusion: VBGs are fine in a hemodynamically stable DKA patient who isn’t in respiratory distress. 




STUDY #2: (hypothetical: respiratory failure)
--compared ABGs and VBGs in the setting of acute COPD exacerbations. 


--their conclusion: the pH correlates extremely well.  also, when using a cutoff of 45 mmHg, the venous pCO2 will catch all cases of arterial hypercarbia. 


--however, there is a large 95% CI so the authors conclude by saying that a VBG is excellent at detecting hypercarbia (present/absent) and useful for initiating non-invasive ventilation, but it is not good enough to replace the ABG in assess the degree of hypercarbia.




STUDY #3: (hypothetical: the hypotensive patient)
--looked at the difference between values on an ABG and a VBG in the setting of hypotension. 
--about 190 patients, 70 hypotensive and 120 normotensive. 


--the average ABG-VBG difference in hypotensive vs normotensive groups was minimal for pH, small for CO2/bicarb, and larger for PO2/SO2.


--their conclusion: Hypotensive status is associated with an increase in the amount of difference between VBG and ABG analysis regarding pH, HCO(3), and BE, though the amount of increase does not seem to be clinically important




ABRIDGED VERSION: (ABG vs. VBG):
--study 1: in DKA, the pH was very similar, bicarb pretty close
--study 2: in COPD, the pH was very similar, VBG PCO2 > 45mmHg cutoff is 100% sensitive for arterial hypercarbia, but the VBG PCO2 value itself is not as good
--study 3: in hypotension, the pH was very similar, PCO2/bicarb pretty close, not so good for oxygen status




BOTTOM LINE:
--if you care about the pH: VBG seems to work just fine
--if you care about hypercarbia: hypercarbia on VBG (>45) probably means you're hypercarbic
--if you care about the amount of hypercarbia: probably need to get the ABG
--if you care about the P02 or 02 sat: probably need to get the ABG




Submitted by J. Gullo.




Reference(s): Study #1 (PMID:  16454777), Study #2 (PMID:  21908141), STUDY #3 (PMID:  22091230), picture