Occipital Neuralgia

http://www.dizziness-and-balance.com/disorders/central/migraine/images/FIG3-MG.jpg

What is it?
Irritation to the greater or lesser occipital nerves

How does it present?
I. sudden onset stabbing/shooting/shock-like/electric pain that starts in the nuchal region and spreads
II. patient can complain of diminished sensation when not feeling

How can you diagnose?
The International Classification of Headache Disorders-2 definition:
A. paroxysmal stabbing pain, with or without persistent aching between paroxysms, in the distribution of the greater, lesser, and/or third occipital nerves
B. tenderness over the affected area
C. pain is eased temporarily by local anesthetic block of the nerve.

This being said, it is important to make sure the pain isn't coming from the neck. Palpate and range the neckHow to treat?

Nerve block!! Here are the key points:
Great occipital nerve: Identify the inion (it's the bony part of the back of the skull). The greater occipital nerve runs 2cm lateral to this bony prominence.

Lesser occipital nerve: Runs close to the mastoid process, just medial to it

http://www.ankoorclinic.com/images/OccipitalNeuralgia.jpg

Medicine: 0.5% Marcaine (1.7ml) + 40mg/ml methyprednisolone (0.3ml). Or 2% Lidocaine (1.7ml) + 10mg triamcinolone (0.3ml).

Technique: Have patient flex neck, chin to chest. Inject and spread. Make sure you aspirate to avoid a superficial artery. Infiltrate at the point of maximal tenderness and surrounding areas. Then wait 10-15min.

PEARL: Alleviation of symptoms by nerve block is both therapeutic and diagnostic!


Practical Pain Management offers a nice tutorial with cool skull pictures:

References:
Garza, I. Occipital Neuralgia. In: UpToDate, Basow, DS (Ed), UpToDate, Waltham, MA, 2013.

Ward, JB.(2003). Greater Occipital Nerve Block. Seminars in Neurology 23(1):59-61

Steroids for asthma

https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhzvGQ4LxkC0DaijKca3dXqvWBa_zxQJe0JtwxRFqH_TDa2RN7tSrUIyiI4VQXNv524McT3uFOoWAXUgF-KwjrHD7vLwuK8Oa2YNsvphue6kRfAPtjIr1cnprOfSqe-80rZ9517YhuK864E/s320/arnold_schwarzenegger.jpg

I'm going to pump you up!

When it comes to asthma, steroids are a life-saver.
Early intervention of steroids in acute asthma exacerbation not only reduces hospital admission rates but reduces relapse rates as well.

Does it matter what type of steroid I give?
Hmmm....

Let's break that question down. It has been the standard to give prednisone 2mg/kg, max 60mg x 5 days for outpatient treatment of asthma exacerbation, and it works. However, new studies are substituting prednisone with dexamethasone (Decadron) 0.6mg/kg, max16mg x 2. Here's the breakdown:
   I. dexamethasone has a longer half-life, thus will require fewer doses
  II. dexamethasone may have less vomiting?
 III. dexamethasone tastes better than prednisone, which could help increase compliance (especially kids)

So far the studies have shown dexamethasone to be just as effective!

http://library.med.utah.edu/WebPath/jpeg1/LUNG051.jpg

Check out that mucus plug!!!!→

Now there's even research suggesting a SINGLE IM dose of dexamethasone is just as effective (in children)! Will it be validated?! Stay tuned....






References:
Kravitz, J., Dominici, P., Ufberg, J., Fisher, J., & Giraldo, P. (August 2011). Two Days of Dexamethasone versus 5 day of Prednisone in the Treatment of Acute Asthma: A Randomized Controlled Trial. Ann Emerg Med, 58(2):200-4. doi: 10.1016/j.annemergmed.2011.01.004. 

Qureshi, F., Zaritsky, A., & Poirer, M.P. (Jul 2001) Comparative Efficacy of Oral Dexamethasone versus Oral Prednisone in Acute Pediatric Asthma. J Pediatr, 139(1): 20-6. 

Shefrin, A.E., Goldman, R.D. (July 2009). Use of Dexamethasone and Prednisone in Acute Asthma Exacerbations in Pediatric Patients. Can Fam Phys 55(7):704-706

dizzy dizzy

http://www.hitrecord.org/records/813005

This is tough one, I would love to discredit all dizziness but there's that sinking feeling in my gut that I just killed my patient...

Here's the low down:

Acute Vestibular Syndrome vs. Stroke

What is an acute vestibular syndrome?

-vestibular neuritis

-vestibular migraine

-multiple sclerosis

I. Auditory symptoms aren’t as helpful

  A. non-specific to central vs. peripheral

      1. hearing changes could be related to infarction of anterior inferior cerebellar artery (AICA)

II. Onset is important

  A. sudden onset suggest neuritis

III. Trauma

  A. concern for dissection of vertebral artery

IV. Neck Pain

  A. associated with stroke

V. Neuro deficits

  A. trouble swallowing

  B. slurred speech

  C. diplopia are concerning symptoms: posterior circulation syndrome

VI. Age > 50 is concerning

VII. Vascular risk factors (I know I know, this is risk stratification rather than clinically significant for disease)

  A, age

  B.  bp

  C. smoking

  D. H/O CVA or MI

  E. DM

  F. a-fib

  G. atherosclerosis

  H. CHF

PEARL: Dizziness, neck pain, headache= 3 most common complaints in dissecting vertebral artery

HPI: H/O otitis, Rx (aminoglycosides, etc.), HIV, depression, recent viral syndrome

This next part is going to blow your mind, in 2011 some smart people over at John Hopskins found that physical exam is just as sensitive as imaging!!!

HINTS exam (head impulse/head thrust, nystagmus, test of skew)

-Impulse Normal (patient is able to fixate)= stroke ; abnormal means vestibular cause

   This one is a little hard to do, and even hard to see the results. I like Scott Weingart's idea of using your phone to slow down the action

-Fast-Alternating: gaze evoked nystagmus (look right, beat right; look left, beat left)= stroke

-Refixation on Cover Test: ocular misalignment (skew)= stroke

-INFARCTS= if any 1 of the 3 is found on exam, think stroke!

CT is not helpful, but is 1^st line of defense

MRI is only 83% sensitive…and if you do get an MRI, go big and get a MRA with neck.

http://www.webmm.ahrq.gov/case.aspx?caseID=63

Dix-Hallpike- not helpful. It doesn’t really confirm peripheral vertigo, and it DOES NOT rule-out central causes. 

Dr Michelle Lin's blog offers a great flash card you can print out as well as videos (can you tell I REALLY like her blog yet?)

References: 

Kerber, KA, Brown, DL, Lisabeth, LD, Smith, MA, Morgenstern, LB. Stroke Among Patients with Dizziness, Vertigo, and Imbalance in the Emergency Department. Stroke, 2006 August 31; 37:2484-2487. doi: 10.1161/​01.STR.0000240329.48263.0d

Tarnutzer AA, Berkowitz AL, Robinson KA, Hsieh YH, Newman-Toker DE. Does my dizzy patient have a stroke? A systematic review of bedside diagnosis in acute vestibular syndrome. CMAJ. 2011 Jun 14;183(9):E571-92.

PERC? ...What?!

Remember me?

This confused the crap out of me, and apparently I'm not the only one.
Pulmonary Embolisms are scary, the presentation is highly variable but the test for diagnosis comes with a high dose of radiation. That being said, the D-Dimer is the first line of defense in diagnosing PE, but isn't very specific.




The Pulmonary Embolism Rule-out Criteria was designed by some very smart people in 2004 to help justify NOT getting a D-Dimer in low and very low risk groups. The goal is if the patient meets ALL of the 8 criteria listed, and is in the low/very low risk group. THEN you can justify NOT getting the D-Dimer.

1. < 50 y/o
2. HR < 100
3.SpO2 > 94% RA
4. No H/O DVT/PE
5. No recent surgery
6. No hemoptysis
7. No exogenous estrogen (i.e. birth control)
8. No clinical signs suggesting DVT

Now for the hard part; this only applies if the pre-test probability is LESS or equal to 15%. This is where gestalt takes over, it's up to YOU as the provider to decide what the risk of a PE is. If you feel it is less than 15%, then apply PERC and call it a day. If you risk stratify and feel it is higher, then I would get the D-Dimer and go from there. Scott Weingart provides a nice algorithm if you are a visual learner.





What is the low risk group?
Essentially these are the people who do NOT have the classic complaints that make PE suspicious:
-NO C.C. of shortness of breath, syncope, pleuritic chest pain, substernal chest pain
-NO H/O cancer/malignancy
-NO H/O thrombophilia
-NO H/O smoking
-NOT postpartum



Life in the Fast Lane also provides a great review on the topic.

References:
Kline JA, et al. Clinical criteria to prevent unnecessary diagnostic testing in emergency department patients with suspected pulmonary embolism. J Thromb Haemost 2004; 2: 1247–55.

Kline JA, et al. Prospective multicenter evaluation of the pulmonary embolism rule-out criteria. J Thromb Haemost 2008; 6: 772–80. (PMID: 18318689).

Back pain. It happens to everyone, and it sucks.

It's also one of the most non-specific complaints, ranging from lumbar strain to aortic aneurysm.

I. Red Flags for Imaging
  A. > 50 y/o
  B. trauma
  C. immunocompromised with fever

iStock

  D. IVDA
  E. saddle anesthesia
  F. persistent/unrelenting pain at night OR rest
  G. anti-coagulant use
  H. urinary retention/incontinence
  I. stool incontinence
  J. bilateral radiculopathy

In the ED, what are we looking for?
 I.   Cauda Equina
 II.  Epidural Abscess
III.  Epidural Hematoma
IV.  Spinal Cord Compression
V.   Osteomyelitis
VI. Vertebral Fracture
VII.Thoracic Aneurysm

Now the question is, which imaging?
X-Ray:fracture, tumor, infection
MRI: neurological deficits

Some significant exam findings:
Lhermitte's sign: shock like pain down spine during spine flexion. You can ask patient from standing to touch their toes. In school, this was pathopneumonic for multiple sclerosis.
Straight leg (supine): pain along nerve root when patient flexes hip with leg straight
Extensor Babinski sign: (I was taught there was no such thing as a positive Babinski sign, rather you have to describe the response from the great toe) run a blunt instrument from the heel to the metatarsal pads in a curve. (Remember this is a normal response in infants)
Hoffman's reflex: flicking the nailbed of the middle finger illicits flexion of thumb.

Remember Waddell's sign? 3 or more findings are suggestive of a "non-organic" cause of back pain (aka crazy)
I. Tenderness
   A. Superficial
   B. Non-anatomic
II. Simulation
   A. Axial loading- neck pain
   B. Rotation- during rotation c/o leg pain
III. Distraction
   A. Straight Leg Raise- done in the traditional supine and then sitting.
IV. Regional
   A. Sensory- not conforming to neuroanatomy
   B. Weakness
V. Over-reaction

Labs: If you are worried about infection, get a CBC, ESR, CRP. Otherwise, get a UA.

Treatment:
I think this is the hardest part, people are not going to be satisfied because of the back pain and loss of function. You tell the patient about NSAIDs but they will tell you it doesn't do a thing. Then you go towards muscle relaxants (Robaxin, Baclofen, etc.) maybe even with narcotics. That is an acceptable treatment and given the limited duration of therapy in the ED setting. I would limit to no more than 3-4 days.

Muscle Relaxants:
 I.  Baclofen (Gablofen) 5mg TID
 II. Cyclobenzaprine (Flexeril) 5-10mg TID
III. Methocarbamol (Robaxin) 1500mg QID
IV. Metaxalone (Skelaxin) 800mg TID

Surgical consultation if cord compression, infection, tumor.
Epidural Abscess: Vancomycin 60mg/kg IV plus Flagyl 500mg
Osteomyelitis: Vancomycin works too!

References:
Cline, D.M., Ma, O.J., Cydulka, R.K., Meckler, G.D., Handel, D.A., & Thomas, S.H. (2012). Tintinalli's Emergency Medicine Manual (7th ed.) McGraw Hill Professional: Columbus, OH.

needle decompression

I think it's well understood that anyone with a tension pneumothorax needs decompression, and definitive treatment is a chest thoracostomy. There's also the life-saving intervention of the needle thoracostomy; take a 14G angiocath, 2nd ICS, mid-clavicular line, and "pssshhhtt". The lung inflates, and you save Mark Wahlberg's life (click below in case I lost you):

Warner Bros.

Well turns out the 2nd ICS may not be the most reliable position. There have been multiple studies in Japan, Turkey, Netherlands, and US that  have found the 5th ICS place has a better chance of penetrating the chest cavity. Also, the larger your BMI, the less likely a angiocath can make it into the chest cavity. Although...I think it's a fair trade-off, who wants to be cold all the time?

Matt McAllister is my hero

 Check out Dr. Michelle Lin's blog for more info:

sagittal sinus thrombosis

This was a new one to me...

So let's say you have a patient present to the ED, she had a new onset H/A 2 days ago that was "the worst ever" and went to another ED. No history of migraines. Not responsive to migraine cocktail. Ancillary workup unremarkable, CT and LP unremarkable. Patient was D/C home with pain control.
She presents to you now in obvious distress. Physical exam reveals no focal deficits. What's your differential?
Differential Diagnosis:
Pseudotumor Cerebri (Idiopathic Intracranial Hypertension)
Spinal Headache
Sagittal Sinus Thrombosis (What?!?!)

Quick and dirty:
A. rare, and presentations are variable
B. most common among female, 30ish year olds
C. venous structures in the brain get obstructed, this can lead to increased pressure of capillary beds and end up with cerebral edema.
D. Risk Factors:
   1. prothrombic conditions (MOST COMMON)
   2. head injury
   3. all those things that put you at risk for hypercoagulable states
       a. OCP
       b. pregnancy
       c. malignancy
       d. infection
E. MRI-venous
  1. CT is normal in 30% of cases
F. D-Dimer is not specific (if elevated it can support, but negative does not rule-out)


References:

Ferro, JM, & Canhão , P. Etiology, clinical features, and diagnosis of cerebral venous thrombosis. In: UpToDate, Basow, DS (Ed), UpToDate,Waltham, MA, 2012.

Pathak, V, Rendon, ISH, Freddo, L, Dangal, MM. Sagittal Sinus Thrombosis in a Young Migraineur. New York Medical Journal, Fall 2009.