Tag Archives: groth

A case of a chest pain zebra

16 Jun

Case: A 32 yo female 2 weeks post-partum who presents with sudden onset dull left anterior chest pressure and mild shortness of breath. No trauma or other sx. No PMH or significant FH.


Other than HR 105, vitals are normal including bilateral BP’s.  Her exam is unremarkable.


Your Ddx is broad- you consider pericarditis, myocarditis, PE, cardiomyopathy, aortic dissection, ACS, gastritis, esophageal disruption, pneumothorax, pneumonia, substance use…

Her CXR is normal.

EKG is below:


Her Tn returns at 4.58 and her other labs are unremarkable (including a negative d-dimer). Cardiology admits her, brings her to the cath lab and she is found to have a…




Spontaneous coronary artery dissection

This is very rare- about 300 documented cases according to 1 journal article in 2008, 70-90% reported cases are in women

Risk factors: Female, pregnancy or post-partum, fibromuscular dysplasia, extreme exercise, connective tissue disorder, cocaine use, marked HTN

Sx/presentation: Chest pain, diaphoresis, palpitations, shortness of breath- symptoms of ACS. Patients may present with an NSTEMI, STEMI, CHF, unstable angina, or even a pericarditis clinical syndrome.  Traditionally, patients will have ST elevation in the leads corresponding to the dissecting artery, but this is not always the case.

Dx: Many options for diagnostic studies: cardiac cath, coronary angiogram, intravascular US, optical coherence tomography, CTA

Tx: Given the low incidence, there is a significant amount of variability. Main options include medical management, coronary bypass, and stenting.

Bottom line: SCA is a very rare diagnosis with a high mortality. Consider in the ddx, particularly in young female patients with chest pain and an ACS picture. Classically, you will see ST elevations and an elevated troponin. For me the take away is keeping a high index of suspicion in patients with concerning histories or exams.


Submitted by Heather Groth.



Cleveland Clinic http://my.clevelandclinic.org/services/heart/disorders/spontaneous-coronary-artery-dissection

Tweet, et al. Clinical Features, Management, and Prognosis of Spontaneous Coronary Artery Dissection. Circulation. 2012;126:667-670.

Vanzetto, et al. Prevalence, therapeutic management and medium-term prognosis of spontaneous coronary artery dissection: results from a database of 11,605 patients. European Journal of Cardio-thoracic Surgery. 2008: 35 (3), 205-254. 

Zampieri et al. Follow up after spontaneous coronary artery dissection: a report of five case series; Heart.1996: 75, 206-209.

picture 1, 2.


Rapid Bedside Diagnosis of Massive PE (Looking for R heart strain)

8 Jan


-RV failure can be seen in massive PE but also in RV infarct and other conditions therefore this is NOT specific for a PE.

-Echo findings NOT sensitive for PE. Increased PA pressure not seen until >30 % obstruction (beyond my US skills- looking at tricuspid regurg jets…) and RV failure not seen until >50% ACUTE obstruction.

-BUT this is a good tool to have for the unstable patient in whom you have a high clinical suspicion for a PE.


US findings of increased RV pressure:

  1. Large RV
  2. Underfilled LV
  3. Paradoxical septal wall motion
  4. RV apex dominance
  5. McConnell’s sign


Findings by US view:

  1. Parasternal Long
    1. Large RV



Note: Normal ratio of RV: Aortic outflow: LV should be 1:1:1.


  1. Underfilled LV



  1. Parasternal Short
    1. Large RV
    2. Underfilled LV
    3. Paradoxical septal wall motion (“D” sign)


 The LV should be circular. Increased RV pressure pushes on the LV, causing it to look more like a “D”. Also, will see bowing of the septum toward the LV or flattening of the septum during diastole.


  1. Apical 4 Chamber
    1. RV apex dominance



  1. McConnell’s sign
    • Acute RV failure, 77% sensitive and 94% specific for PE in RV failure
    • Hypokinetic free wall and hyperkinetic apex (looks like a little person is jumping on a trampoline at the apex)
    • Here is an example: McConnell’s Sign


Submitted by Heather Groth.









Management of Cutaneous Anthrax

6 Jan

*Most commonly from contact with infected animals or animal products. Keep bioterrorism in mind and look for evidence of inhalation or GI tract exposure.  

*Incubation period of 1-12 days

***Call the State Department of Health. This is a reportable disease.***


Physical exam: Small, painless, pruritic papules -> central vesicle/bulla -> erosion with painless necrotic ulcer/black eschar

 anthrax1 anthrax2

*Oftentimes there is extensive surrounding edema and lymphadenopathy (from toxin release).

*May see systemic signs of fever, malaise, HA. If there are any systemic signs or if the lesions involve the head or neck, treatment must be inpatient. These patients need antitoxin, IV antibiotics, usually an LP, infection control (drainage of effusions…)



-For vesicular lesions- 2 swabs of fluid from an unopened vesicle. Send 1 for Gram stain/culture and the other for PCR.

-For eschars, the edge should be lifted and 2 swabs rotated underneath. Send 1 for Gram stain/culture and the other for PCR.

-For ulcers, the base of the lesion should be sampled with 2 saline moistened swabs. Send 1 for Gram stain/culture and the other for PCR.

-For all lesions, send a full thickness punch biopsy of the lesion in 10% formalin for histopathology and immunohistochemistry. If the patient is not on antibiotics or has been on antibiotics <24 hours, take a second biopsy for Gram stain, culture, and PCR testing.


Isolation: Standard precautions (unless there is continued drainage from wound- then contact precautions).

Treatment: (of cutaneous anthrax without systemic s/sx that does not involve the head or neck)=Generally outpatient.  

7-10 days of ciprofloxacin 500 mg q12 hours

OR doxycycline 100 mg q12 hours OR

clindamycin 600 mg q12.

Follow-up in 1-2 days.


Submitted by Heather Groth. 


Sources: CDC website, Up-To-Date, Vanderbilt Department of Infectious Disease website

Understanding Insulin Pumps

14 Aug

Basic function:pump1

~200-300 units of short acting insulin is in the insulin reservoir. This connects through the tubing to be infused via the cannula to the subcutaneous tissue of the patient.

Frequent BG monitoring is still required.  In fact more these patients check more frequently than patients without pumps d/t the possibility of pump problems.

-Patients have a basal rate they get continuously and then type in their desired bolus amount with meals.

-Patients need to move the needle site every 2-3 days (otherwise increased risk of infection and decrease in glycemic control)



  1. Local reactions to adhesive or insulin preparation
  2. Lipohypertrophy or lipoatrophy
  3. Cellulitis at the needle insertion site
  4. Pump failure. Any part of the device can fail- dead batteries, kinked/cracked tubing, depleted or broken reservoir…
  5. Air in tubing causing missed insulin
  6. Insulin leakage (at insertion site or infusion set connection site causing missed insulin


* Pumps frequently will not given any indication that there is a problem

* As the patient is getting only short-acting insulin, device failure can rapidly lead to DKA. 


Submitted by Heather Groth.



Academic Life in Emergency Medicine

Pickup, John. “Insulin-Pump Therapy for Type I Diabetes Mellitus” N Engl J Med 2012; 366:1616-1624

UCSF Website: http://dtc.ucsf.edu/types-of-diabetes/type2/treatment-of-type-2-diabetes/medications-and-therapies/type-2-pump-rx/

Treatment of Primary Spontaneous Pneumothoraces

12 Aug


Primary= No apparent lung disease   vs   Secondary= Underlying lung disease

 –Spontaneous= No precipitating event (no traumatic/iatrogenic cause)

-The definition of a “small” pneumothorax can vary. For the most part, this means the distance between the lung and chest wall on CXR is <3cm. 


3 Senarios:

  1. Stable patient, small pneumothorax

-Give supplemental O2

-Observe in the ED 3-6 hours

-Repeat x-ray. If no progression and patient is asymptomatic, discharge with follow up in 12 hrs- 2 days.     Otherwise admit.

  1. Stable patient, large pneumothorax

                -Small-bore catheter (<14F/pigtail)    OR    16-22F chest tube and admit

Note: Some physicians have discharged patients with a chest tube in place and a Heimlich valve with follow up in 1-2 days if the patients refuse hospitalization but are reliable. This makes me nervous.


                -Needle aspiration

-There is pretty good data (multiple recent articles) behind needle aspiration of pneumothoraces instead of placing a chest tube. This is the recommended treatment in England but this is not in the American College of Chest Physicians guidelines.  A 2008 Annals review shows no difference in rate of failure/recurrence but lower rates of hospitalization, length of stay, comfort.  HRD has a prior blog post about this.

-You can watch a video of this procedure on the NEJM site under the article: Pasquier et al. “Needle Aspiration of Primary Spontaneous Pneumothoraces” NEJM 2013; 368:e24

  1. Unstable patient

                -Large chest tube.  Could use 16F-22F chest tube but will likely use 24F-28F chest tube as PPV is likely required.


Submitted by Heather Groth.


Baumann et al. “Management of Spontaneous Pneumothorax: An American College of Chest Physicians Delphi           Consensus Statement” Chest. 2001;119(2):590-602.

Bintcliffe et al. “Spontaneous Pneumothorax” BMJ 2014; 348:g2928

Pasquier et al. “Needle Aspiration of Primary Spontaneous Pneumothoraces” NEJM 2013; 368:e24


Up to Date

Zehtabchi S, Rios C L. Management of emergency department patients with primary spontaneous pneumothorax: needle aspiration or tube thoracostomy? Annals of Emergency Medicine 2008; 51(1): 91-100.


What is MELAS???

8 Aug


Otherwise healthy male in his 30’s presents to the ED very anxious-appearing with vague episodic neurologic complaints.  His neurologic exam is completely normal.  Later, his R index finger starts wiggling and he says he can’t control it. He then contorts his face saying he cannot control this. They both stop as you talk with him.  Then he tells you his mother died of MELAS and is worried about this.  You go back to your desk and Google MELAS…


What is MELAS???

Mitochondrial Encephalomyopathy, Lactic Acidosis, and Stroke-like episodes

(exact incidence unknown)


Mitochondrial genetic mutation affecting muscles and the nervous system



Usually presents in childhood 

-can include muscle weakness/pain, recurrent HA’s, loss of appetite, emesis, seizures

Can present any time but usually affected people have stroke-like episodes before 40 y.o.

-Patients often times have elevated lactate causing pain, fatigue, muscle weakness, possible involuntary muscle spasms. Patients can also develop renal impairment and DM.



-Usually clinical with supporting lab work. Confirmation by mitochondrial DNA studies.



-No currently known specific treatment. Treatment is targeted to affected organ system/sx.  Various antioxidants and vitamins have been used without consistent success. This is a progressive and fatal diagnosis at this point.


Submitted by Heather Groth.



-NLM/NIH website: http://ghr.nlm.nih.gov/condition/mitochondrial-encephalomyopathy-lactic-acidosis-and-stroke-like-episodes

-Thambisetty, et al. “A practical approach to the diagnosis and management of MELAS: a case report and review.” Neurologist. 2002 Sep;8(5):302-12.



Not just an foot/ankle sprain: Lisfranc Injuries

17 Dec

 Lisfranc joint complex= the entire tarsometatarsal articulationlis1


Lisfranc joint= articulation of the 1st and 2nd metatarsals with the 1st and 2nd cuneiforms


Why we should care:

*Up to 20-40% of these injuries are missed on initial visit. 

*Chronic pain and disability are fairly common with Lisfranc injuries. 

*Operative management is sometimes needed.


History: Direct or indirect trauma, can be low energy.  Most have midfoot pain, swelling and difficulty bearing weight. These are not sensitive features.



* TTP at the 1st and 2nd metatarsal bases or remainder of Lisfranc joint complex

* Pain with passive abduction and pronation of forefoot when hindfoot is held flexed (specific for tarsometatarsal injuries)

* Plantar ecchymosis

* Of course perform neurologic and vascular exams.  Also consider and evaluate for a compartment syndrome of the foot.


XR findings (order AP, lateral, and oblique views):

 lis2AP or oblique views:

  1. 1.    Medial border of the 2nd metatarsal base and 2nd cuneiform (red line) form a straight line (as do the medial border of the 4th metatarsal base and cuboid)
  2. 2.    Lateral border of the 3rd metatarsal base and lateral border of the lateral cuneiform should form a straight line.
  3. 3.    >2 mm diastasis or >1 mm side to side difference between the metatarsal bases is abnormal (yellow asterix)
  4. 4.    “Fleck sign” or an avulsed bone fragment is a sign of ligamentous injury (yellow asterix)
  5. 5.    Cuneiform or metatarsal fracture



lis3Lateral views:

  1. 1.    A metatarsal shaft should never be more dorsal than its respective tarsal bone (red arrow)

*** If initial x-ray is normal but suspicion is high, order a weight bearing AP view to assess the 1-2 interval of the metatarsals and/or obtain a comparison x-ray of the contralateral foot. 



* If available, orthopedics consultation

* If not available, consider closed reduction if appropriate.  Then apply bulky dressing and posterior splint with very close ortho follow up

* Some mild lisfranc injuries are treated with casting and non-weight-bearing.  Others go on to require surgery such as reduction and fixation (2 mm of displacement and/or greater than 15 deg of talometatarsal angulation typically require surgery). 


Submitted by H. Groth.


Sources: Cvetanovich, Greg; Lieberman, Gillian. “Imaging of Lisfranc Injury”. Lecture at Beth Isreal Deaconess Medical Center November 2011; Nunley, JA. “Classification, investigation, and management of midfoot sprains: lisfranc injuries in the athlete”. Am J Sports Med 2002; 30:871-878; Perron, Andrew D; Brady, William J.; Keat, Theodore E. “Orthopedic pitfalls in the ED: Lisfranc fracture-dislocation” Amer J of Emerg Med 2001; 19(1): 71-75; Tintinalli’s Emergency Medicine; Wheeless’ Textbook of Orthopedics.