seizures and tongue lacs

QUESTION:

--my patient had some sort of 'episode', story is unclear
--does their tongue lac tell me anything? was this a seizure?


PUBMED BIOPSY (not a ton out there):
STUDY 1: "Value of tongue biting in the diagnosis of seizures"
--study of 106 patients admitted to epilepsy unit + 45 patients with syncope
--small sample size, but interesting

--8/106 seizure patients had a tongue lac: all on the side
--1/45 syncope patients had a tongue lac: at the tip.

--sensitivity of 24% and a specificity of 99% for the diagnosis of generalized tonic-clonic seizures.
--Lateral tongue biting was 100% specific to grand mal seizures.

STUDY 2: The diagnostic value of oral lacerations and incontinence during convulsive "seizures".

--84 patients on EEG
--trying to tell seizure from pseudoseizure (a.k.a. psychogenic non-epileptic seizure, or PNES)

--oral lacs: (p=0.01)

• seizure: 26% (17/66) --14 side of tongue, 1 tip of tongue, 2 cheek, 3 lip
• not a seizure: 0% (0/18)
• sensitivity 26%, specificity 100%

--Incontinence: (p = 0.09)

• seizure: 23% (15/66)
• not a seizure: 6% (1/18) --!!! (now that's commitment)
• sensitivity 23%, specificity 94%

BOTTOM LINE:
--side-of-tongue lac is near 100% specific for seizure, not very sensitive
--if the story fits, and you bit the side of your tongue and/or pissed yourself, you probably earned a seizure workup


Reference(s): tongue biting, oral lacs and incontinence, picture

PE and the ECG

STUDY:
--retrospective chart review, 130 patients with diagnosed PEs, 140 controls with negative CTPAs
--checked 15 different ECG parameters between the groups, to see if people with PEs had particular ECG findings that normals didn't


NOTABLE NUMBERS:
--Sinus tachycardia (found in 39% of PE group vs. 24% of control group, P <0.01)
--S1 Q3 T3 pattern (12% vs. 3%, P <0.01)
--atrial tachyarrhythmias (15% vs. 4%, P <0.005)
--Q wave in lead III (40% vs. 26%, P <0.02)
--Q3 T3 pattern (8% vs. 1%, P <0.02)


NICE RECAP:
--"We conclude that 1) standard 12-lead ECG findings can increase the pretest probability of pulmonary embolism before performing CT pulmonary angiography; and that 2) the ECG findings have relatively low likelihood ratios to have clinical use."


Reference(s): study, picture

orthostatic vital signs in the ED: not so useful

THEORY:

--normally, standing leads to a small fall in systolic BP (5 to 10 mmHg), an increase in diastolic BP (5 to 10 mmHg) and a compensatory increase in pulse rate (10 to 25 beats per minute)

--traditional criteria for orthostatic hypotension

• > 20 mmHg decreased SBP
• > 10 mmHg decreased DBP
• Symptoms of cerebral hypoperfusion

--also seen:

• >20 increased HR

NOT TOO USEFUL:

--study of 132 random, presumed euvolemic ED patients

--took lying & standing vitals

--HR range was from decreases 5.0 to increases 39.4 beats per minute

--SBP range was decreases 20 to increases 25.7 mm Hg

--DBP range was decreases 6.4 to increases 24.9 mm Hg

--43% had "positive" orthostatic vital signs according to currently accepted values

TO REITERATE:

--43% of likely euvolemic random ED patients had +orthostatic vitals by numbers

--43% suspected false positive, essentially

--probably not a useful test, this orthostatic vital signs thing

  

Reference(s): uptodate.com: Mechanisms, causes, and evaluation of orthostatic and postprandial hypotension; study from 1991, picture

audio podcast: the knee

INAUGURAL PODCAST!
--trying something here, taking the audio from one of our excellent resident lectures, and posting it up as an audio file/podcast for everyone to enjoy
--if you missed this conference, need a refresher, or just want something to put in your ipod for your next workout or for the drive home, here it is!
--the goal is to make this a semi-regular thing; haven't decided yet how frequent

THIS MONTH:
THE KNEE: ORTHOPEDIC INJURIES & ED MANAGEMENT
--tough to imagine an ortho lecture being good without pictures, but actually some good talking points if you stick with it. give it a listen. feedback is appreciated.

download link

Lecture by E. Hawkins.

ethylene glycol ingestion and Wood's lamp-ing urine

NICE IDEA:
--most antifreeze (which contains ethylene glycol) has fluorescein added to it
--fluorescein should light up with a Wood's lamp (=blacklight = UV)
--can you light up a patient's face (to see if they drank some) and/or urine (to see if they're peeing it out) to help your diagnosis?


NOT THAT USEFUL, SADLY:
STUDY 1: 60 docs in 2 groups; 150 urine specimens, all of which were fluorescent by flow cytometry
--Group 1 reported fluorescence in 80.7% of urine specimens
--group 2 reported fluorescence in 69.3%
--Interrater agreement was poor (72.5%)

STUDY 2: 2 docs, 27-30 urine specimens; shown sequentially or together on a test tube rack
--sequential: sensitivity 35%, specificity 75%, accuracy 48% for detecting florescein
--grouped:  sensitivity 42%, specificity 66%, accuracy 50%


BOTTOM LINE:
--urine fluorescence for ethylene glycol ingestion, nice idea, not too clinically useful
--not very sensitive, specific, or accurate
--we suck at eyeballing fluorescence, apparently
--stick with anion/osmol gaps, clinical judgement, etc.


Reference(s): study 1, study 2, another study that agrees, picture

Dexamethasone Instead of Prednisone for Acute Asthma

EMERGENCY MEDICINE NEWS:

--this month's journal had a nice breakdown of a couple articles about using dex instead of prednisone to treat asthma exacerbations. head over there for details, its a decent read

10-SECOND VERSION:

--corticosteroids (with bronchodilators) help avoid admission & ED relapse in acute asthma exacerbations

--dexamethasone has longer half-life (days) than prednisone (hours)

--dex 0.6mg/kg daily (x 2 days) vs. prednisone 1mg/kg daily (x 5 days)

--adult size: dex 16mg/day vs. pred 60mg/day

--limited studies, but generally dex was same or slightly better
--dex is probably ok alternative to pred

Reference(s): emergency medicine news: article, uptodate.com: prednisone, dexamethasone, picture

heliox for acute asthma

COCHRANE REVIEW:

--10 small RCT’s (7 adults, 3 children), 544 acute asthma patients comparing inhaled heliox vs placebo (O2, air) in addition to standard treatment found no difference in PFT’s or admission to hospital (1)

--However, in subgroup of patients with severe baseline pulmonary function, heliox did improve PFT so may be some benefit to use in patients w/severe airway obstruction

PEARLS:

--Should be considered after 1st (albuterol, Duoneb, steroid) and 2nd (mag, terbutaline, epi) line therapies fail and patient still has some reserve

--“Heliox-driven albuterol nebulization may be considered for patients who have life- threatening exacerbation or who remain in severe exacerbation after intensive conventional adjunctive therapy” (2)

--Since generally given in mixtures of 70:30 (helium:O2) CANNOT use in patients who are hypoxemic (i.e. need 50% FiO2)

--If the patient needs to be intubated, INTUBATE!

Submitted by F. DiFranco.

Reference(s): (1) i.Rodrigo GJ, Pollack CV, Rodrigo C, Rowe BH. Heliox for non-intubated acute asthma patients. Cochrane Database of Systematic Reviews 2006, Issue 4; (2) Cincinnati Children's Hospital Medical Center. Evidence-based care guideline for management of acute asthma exacerbation in children. Cincinnati (OH): Cincinnati Children's Hospital Medical Center; INFO@GUIDELINES.GOV 2011, picture

thyroid storm treatment

Treat symptoms with Beta blocker:

--propranolol: also slows peripheral conversion of T4 to T3

--lesser options: esmolol, metoprolol, calcium channel blockers (diltiazem)

Inhibit thyroid hormone synthesis (works in 1-2 hrs):

--propylthiouracil (PTU): blocks thyroidal peroxidase, also inhibits T4 to T3 conversion

--lesser options: methimazole

Block release of thyroid hormone:

--iodine: give ~1 hour AFTER other stuff, otherwise it’ll form MORE thyroid hormone

Steroids (thyroid storm can precipitate adrenal insufficiency, maybe autoimmune effects if Grave's disease):

--dexamethasone: also blocks T4 to T3 conversion

--other options: hydrocortisone

10-SECOND RECAP:

--thyroid storm is not awesome

--treat symptoms, stop thyroid hormone synthesis, inhibit release, give steroids

--ideally: propranolol, PTU, waaaaaiiit an hour, iodine, dexamethasone

Reference(s): uptodate.com: thyroid storm, Tintinalli p. 1312-3, picture

costal margin tenderness: indication for abdominal CT?

STUDY 1:
--Do patients with pain or tenderness to the left lower ribs after blunt traumatic injury require abdominal computed tomography (CT) scanning for the detection of splenic injury?

875 patients had left lower rib pain or tenderness
--63 (7.2%; 95% confidence interval [CI] 5.6% to 9.1%) patients had splenic injuries
--20 (2.3%; 95% CI 1.4% to 3.5%) patients had left renal injuries

301 (of 875 total) patients had "isolated" left lower rib injury (i.e. no other reason to get a CT)
--9 (3.0%; 95% CI 1.4% to 5.6%) had splenic injuries
--All 9 patients had a pleuritic component to their rib tenderness, and 3 (33%) patients underwent splenectomy

--"A small but important percentage of patients with pain or tenderness to the left lower ribs has splenic injuries. All patients with splenic injury had pleuritic pain."


STUDY 2:
--derive and validate clinical prediction rules to identify adult patients at very low risk for intra-abdominal injuries after blunt torso trauma

derived rule for the presence of any intra-abdominal injury:

• GCS < 14
• costal margin tenderness
• abdominal tenderness
• femur fracture
• hematuria >= 25 RBCs/HPF
• hematocrit < 30%
• abnormal CXR (pneumothorax or rib fracture)

--sensitivity 137 of 143 (95.8%; 95% CI 91.1% to 98.4%)
--specificity 434 of 1,452 (29.9%; 95% CI 27.5% to 32.3%)
--negative predictive value 434 of 440 (98.6%; 95% CI 97.1% to 99.5%).

--"Patients without any of these variables are at very low risk for having intra-abdominal injury, particularly intra-abdominal injury requiring acute intervention, and are unlikely to benefit from abdominal computed tomography scanning"


BOTTOM LINE:
--2-7% those with left lower rib/costal margin pain can had splenic injury
--consider abdominal CT if patient with blunt trauma has left costal margin pain, particularly if pleuritic


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

blood pressure control guidelines (head bleed, dissection, AAA)

RAGING HYPOTHETICAL:

--you have a patient with a vessel somewhere that has either ruptured or is about to

--you call the appropriate surgeon, who is on the way, but in the meantime, what can you do?

MINIMIZE THE DAMAGE:

ICH:

--lowering to SBP 140-160 probably safe

--theory: less/slower hematoma growth

--options: nicardipine (less cerebral vasospasm)

AORTIC DISSECTION:

--SBP 100-120, HR <60

--theory: reduce shear forces

--options: beta blocker (labetolol push, esmolol drip), nitroprusside

RUPTURED AAA:

--goal SBP 80-100

--theory: permissive hypotension; bleed slower, less likely to blow out the few clots they're making

Reference(s): uptodate.com: Ruptured abdominal aortic aneurysm, management of aortic dissection, Spontaneous intracerebral hemorrhage: Prognosis and treatment, Kodama K, et al. Tight heart rate control reduces secondary adverse events in patients with type B acute aortic dissection, picture

serum glucose and calcium channel blocker and beta blocker overdose

RAGING HYPOTHETICAL:
--you have a patient that is bradycardic/hypotensive/unresponsive/dead
--you suspect calcium channel blocker or beta blocker overdose
--nurse has done a fingerstick glucose--how does this help you?



BLOOD GLUCOSE (in a non-diabetic=helpful):
--calcium channel blocker OD:  hyperglycemia (BG is high)
--beta blocker OD: hypoglycemia (BG is low)


WHY?
--calcium channel blockers:

• hyperglycemia caused by inhibition of calcium-mediated insulin release 

--beta blockers:

• epinephrine, acting via the beta-adrenergic receptors, has important effects on glucose metabolism
• increases glucose production by stimulating both glycogenolysis and gluconeogenesis
• increases the delivery of these gluconeogenic substrates from the periphery
• inhibits glucose utilization by several tissues
• via the alpha-2-receptors, inhibits insulin secretion
• BLOCK all these, glucose gets low

TREATMENT OPTIONS:
--ABCs, IVF
--calcium
--glucagon
--high dose insulin/glucose
--pressors
--lipid emulsion


10-SECOND TAKEAWAY:
--calcium channel blocker OD: glucose is high
--beta blocker OD: glucose is low
--treatment toolbox: calcium, glucagon, insulin/glucose, pressors, lipid emulsion


Reference(s): uptodate.com: calcium channel blocker poisoning, beta blocker poisoning, major side effects of beta blockers, picture

retinal detachment

KEY POINTS:

--can be traumatic or non-traumatic

--often present with 'floaters' in one eye, peripheral visual field defect

--can lead to loss of vision

--need optho consultation, dilated eye exam, may need retinopexy (something I can't do in the ED)


OCULAR ULTRASOUND:
--high-frequency linear (7.5-10 MHz) transducer
--retinal detachment: a prominent, continuous linear density rising from the fundus


Reference(s): uptodate.com: retinal tear and detachment, ACEP Focus on ocular ultrasound for retinal detachment (picture also)

perforated tympanic membrane

HOW DID THIS HAPPEN?

--barotrauma of all sorts (pressure changes with airplanes, diving, etc)

--self-induced/foreign bodies (q-tips, paper clips, etc)

--otitis

WHAT DO I DO?:

--most heal on their own

--antibiotics only if infectious etiology

--antibiotic choice: oral + topical; avoid antiseptic/acidic drops with perf'd TM (e.g. ofloxacin ok, corticosporin NOT ok)

--pain meds

--no evidence for decongestants, antihistimines, steroids

Reference(s): uptodate.com: ear barotrauma, acute otitis media in adults, nice pics, picture

photokeratitis

WHAT IS IT?

--UV (ultraviolet) keratitis
--UV light damages corneal epithelium
--often presents some time after exposure (latent period 6-12 hours)
--generally self-limited with complete resolution in 1-3 days


COMMON PRESENTATIONS:
--welders
--snowblindness

--bilateral eye pain, injection, photophobia, foreign body sensation
--can have associated facial erythema/edema


MANAGEMENT:
--analgesics (photokeratitis hurts)
--antibiotic ointments (prophylaxis and lubrication)
--optho follow-up
--advise proper protective eyewear


10-SECOND RECAP:
--photokeratitis=corneal epithelial damage from UV light
--often from welding, snowblindness
--bilateral pain, photophobia, injection; often presents after a 6-12 hr latent period
--treatment toolbox: pain meds, antibiotic oinments, optho follow-up, better goggles

Reference(s): uptodate.com: photokeratitis, photo

hypotension and valvular dysfunction: chicken or the egg?

CASE PARTICULARS:

--SOB, hypotension

--labs notable for slightly elevated troponin, AKI

DIAGNOSTICS:

--could not undergo CTPA to r/o PE due to AKI
--ECHO in ED shows no RV dilation but did show severe MR and TR.
--pt intubated secondary to massive fluid resuscitation

--ECHO following day was normal. 

--Once rehydrated, pt did much better.  No PE was found on CTPA.

WHAT HAPPENED?

--hypovolemia exacerbated systolic anterior motion of mitral valve causing severe dynamic MR and TR, causing cardiogenic shock. 

TEACHING POINTS:
--This patient had LV outflow tract obstruction by a hyperdynamic anterior motion of the mitral valve leaflets during systole, causing a severe mitral regurgitation due to the blockage of the outflow tract as well as opening of the mitral valve during systole. 

--This mimics HOCM, but was in a structurally normal heart. 
--Obstructive physiology, and especially systolic anterior motion of the mitral valve, can be caused by various disorders including hypercontractile states such as hypovolemia, anemia, beta agonist drugs, D-transposition of the great arteries, congenital/acquired abnormalities of the mitral valve/papillary muscles, and immediately after aortic valve surgery for aortic stenosis (due to acute afterload reduction).

10-SECOND TAKEAWAY:

--suspect massive PE, can’t to CTPA, think of bedside echo to look for RV dilation/strain

--severe hypercontractile states (e.g. hypovolemia) can result in obstructive physiology, including valvular dysfunction

--can be transient, should improve with fluids (good idea for treatment)

Submitted by T. Boyd.

Refence(s): Rosen B et al. “Hypovolemia-Induced Reversible Severe Mitral Regurgitation Due to Left Ventricular Outflow Tract Obstruction.” Echocardiography. 19:8; Nov. 2002.

acute appendicitis: how good are your diagnostic skills?

AAFP REVIEW ARTICLE KEY POINTS:

COMMON SYMPTOMS (frequency in %):

• abdominal pain ~100%
• anorexia ~100%
• nausea 90%
• vomiting 75%
• pain migration 50%
• Classic symptom sequence (vague periumbilical pain to anorexia/nausea/unsustained vomiting to migration of pain to right lower quadrant to low-grade fever) 50%

SYMPTOM/SIGN (positive likelihood ratio--increased likelihood you have an appy if you have this):

• RLQ pain (8.0)
• pain migration (3.2)
• pain before vomiting (2.8)
• anorexia, nausea & vomiting (<2.8)
• psoas sign (2.38)
• rebound tenderness (variable, 1.1 to 6.3)
• fever (1.9)

IMAGING:

• ultrasound: sensitivity 85%, specificity 92%
• CT: sensitivity 90-100%, specificity 95-97%

BOTTOM LINE:
--most common: abd pain, anorexia, nausea/vomiting, migratory pain
--most useful: RLQ pain, migratory pain, pain before vomiting
--ultrasound is pretty accurate, CT is really accurate, but neither are perfect
--none are truly absolute, think of appy, but also think past appy

Reference(s): AAFP review on appendicitis, tangential craziness

haldol and QTc

RAGING HYPOTHETICAL:

--You are working overnight and get called about an elderly lady who is agitated. Your patient has IV access and the nurse wants to know what to give. What do you order?

HALDOL (one option):

--can prolong QT interval; should be avoided if QTc is already prolonged

--Haldol is actually FDA approved for IM, not IV. (but we use it IV all the time)

--peaks in the serum in about 20min

OTHER OPTIONS:

--Seroquel is a good PO option (consider 12.5 mg or 25 mg)

--Ativan can worsen delerium (avoid if possible, especially in elderly)

QT  FACTOIDS:

--normal QTc is less than or equal to ~440ms (males borderline long at 431-450, females 451 to 470)

--  >450 is abnormal for males and >470 is abnormal for females.

--the QT interval can be prolonged with hypoKalemia, low Mg, or hypothyroidism (and many, many drugs)

--remember Bazett's formula (or look it up)

QTc=^QT⁄_√RR

--cheater's way: QTc should be less than 1/2 of the R-R interval.

10-SECOND RECAP:

--agitation tx options: haldol, seroquel, ativan

--haldol can prolong QT, as with MANY other drugs

--QTc=^QT⁄_√RR   (or 1/2 the R-R interval)

--normal QTc is less than 440ms(ish)

Submitted by R. Morris.

Reference(s): uptodate: haldol, picture