TRALI

Calvin D. Sun, MD, PGY-3
Follow-Up Rounds 5/12/2017


THE CASE

Triage Vitals: T 97.4F,  BP 137/49, HR 66, RR 18, O2 100% on RA

CC: Lower Back Pain, B/L LE numbness

HPI:

  • 56M
  • No known PMH
  • Lower back pain radiating to BL feet x 1 week
  • Numbness of BL feet since x 1 day
  • Denies fever, LOC, headache, trauma, history of abdominal surgeries, abdominal pain
  • Jehovah’s Witness
  • Nightly AM Advil at home for back pain/sleeping aid also relieves pain.
  • Pt also c/o blood on top of brown stool x months
  • Normal colonoscopy and EGD 3 years ago

PHYSICAL EXAM

  • Gen: AAO x 3, well appearing, NAD
  • HEENT: atraumatic, no cyanosis, no pallor, MMM
  • CV: RRR, no murmurs appreciated
  • Pulm: CTA B/L, no wheezing
  • Abd: S, NT, ND, + BS in all 4 quadrants
  • Extr: pulses palpable bilaterally, no edema
  • Neuro: moving all 4 extremities, no facial droop, no focal deficits, CN II-XII grossly intact

STUDIES

CBC
WBC (/nL) 10.2 (3.5 – 11.0)
Hgb (g/dL) 4.4 (12.0 – 16.0)

 

Coags
aPTT (sec) 23.3 (20.1 – 31.2) sec
PT 13.4 (9.5 – 12.2) sec
INR 1.0 (0.9 – 1.2)

 

CMP
Na 139 (135 – 145) mEq/L
K 7.1 (3.5 – 5.0) mEq/L
Cl 112 (98 – 108) mEq/L
CO2 17 (24 – 30) mEq/L
BUN 18 (5 – 26) mg/dL
Creat 2.27 (0.1 – 1.5) mg/dL
Gluc 111 (70 – 105) mg/dL

INTERVENTIONS

  • Patient begins 1u pRBC transfusion
  • 5 minutes later and after receiving 100 mL of blood, patient begins to feel SOB

INTERVENTIONS – 5 MINUTES LATER

  • Nurse notices acute respiratory distress
  • Patient becomes altered, obtunded, not answering questions, diaphoretic w/ retractions, unable to speak
  • PO2 on NRB mask 79%
  • Patient intubated
  • …and pRBC transfusion stopped

Portable CXR


TRALI

  • Transfusion-related acute lung injury
  • Incidence among patients receiving transfusion
    • 04-0.10% (1 in 5000) in all cases
    • 5-8% in critically ill patients
  • During or within 6 hours after blood product administration
  • Can occur with any blood product
  • Being critically ill is the highest risk factor
  • Pathogenesis (2-hit):
    • Neutrophils primed to respond
    • Neutrophil activation by a factor in the blood product → damage capillary endothileum in lung → pulmonary edema

CLINICAL PRESENTATION OF TRALI

  • Hypoxemia (100%)
  • Bilateral pulmonary infiltrates (100%)
  • Pink frothy airway secretions (56%)
  • Fever (33%)

DIFFERENTIALS RELATED TO TRALI

  • TACO: Transfusion-associated circulatory overload
    • More associated with volume overload
  • Hemolytic transfusion reaction
    • More associated with fever and chills
  • Anaphylaxis
    • More associated with stridor, cough, wheezing
  • Sepsis
    • More associated with fever and hypotension with evidence of an active infectious process

MANAGEMENT OF TRALI

  • O2, Airway management, CXR
  • Stop transfusion immediately
    • Return blood product to the blood bank for a transfusion reaction workshop (CBC, bilirubin, haptoglobin, Coombs)
  • Supportive care
    • Intubation often required (70-80%)
  • Mixed results with steroids; not recommended
  • Patients appear not to be at increased risk for repeat episodes with future transfusions if from other donors

REFERENCES

Fung YL, Silliman CC. The role of neutrophils in the pathogenesis of transfusion-related acute lung injury. Transfus Med Rev 2009; 23:266.

Silliman CC. The two-event model of transfusion-related acute lung injury. Crit Care Med 2006; 34:S124.

Bux J, Sachs UJ. The pathogenesis of transfusion-related acute lung injury (TRALI). Br J Haematol 2007; 136:788.

van Stein D, Beckers EA, Sintnicolaas K, et al. Transfusion-related acute lung injury reports in the Netherlands: an observational study. Transfusion 2010; 50:213.

 

 

 

Grand Rounds: Point of Care Ultrasound in Cardiac Arrest

Dr. Felipe Teran, MD (@FTeranmd), Faculty and Fellow in the Divisions of Emergency US and Emergency Critical Care at Mount Sinai, Co-Director of the Resuscitate NYC 2017 EMCrit Conference, discusses the role of ultrasound in cardiac arrest (02/08/2017).



VT Storm

Brian Gilberti, MD, PGY-3
Follow-Up Rounds 3/3/2017

CASE
Triage Vitals: T 98.0, HR 152, BP 66/48, RR 20, SpO2 97%
CC: Dizziness

HPI
  • 75 yo M
  • PMH CAD s/p CABG, HFrEF (25%, AICD), HTN, DM
  • Worsening over past two days
  • Denied fevers, vertigo, CP, SOB
  • Compliant with medications
PHYSICAL EXAM
Vitals: HR 152, BP 66/48
General: In no acute distress
HEENT: no JVD
CV: Tachycardic, no murmurs
Pulm: Mild rales at bases bilaterally
Abd: Soft, NT
Extremities: Trace pitting edema

STUDIES

ECG on presentation

ECG 3 months prior

Labs: Unremarkable
ICD Interrogation

  • Episodes
    • Today: VT
    • 2 days prior: VT >18 hrs
    • 3 days prior: VT > 18 hrs

Definition

  • Without ICD
    • ≥2 episodes of VT within 24 horus
    • Recurrence of VT within 5 mins of termination of prior episode
    • >24 hour episode
  • With ICD
    • ≥3 episodes requiring device intervention
  • Incidence 2-10% per year in patients with ICDs

 

Triggers

  • Structural abnormality
  • Myocardial ischemia
  • Heart failure
  • Thyrotoxicosis
  • Hypomagnesemia
  • Hypokalemia
  • QT prolongation

 

Indicators of Ventricular Tachycardia on ECG (vs SVT with aberrancy)

  • Regular
  • Northwest axis (-90 to +/-180)
  • Compared to sinus rhythm, axis shift >40 during wide-complex tachycardia
  • QRS duration >160 msec
  • Negative concordance of QRS morphology in V1-V6
    • Positive concordance as well, but not as strongly suggestive of VT
  • Fusion beats (diagnostic of VT)

 

Treatment

  • Unstable
    • Cardiovert
  • Stable
    • Antiarrhythmics
      • Procainamide
        • Procainamide was more effective than Amiodarone in terminating VT within 20 mins (67% vs 38%) and had fewer MACE (9% vs 41%).1
          • NB: This was not a study of pts with electrical storm
        • AHA Class IIa for stable monomorphic VT
        • Contraindicated in patients with impaired renal function because its active metabolite, N-acetylprocainamide, is excreted by the kidneys
        • Administer until:
          • Max dose of 17 mg/kg or 1 g
          • Arrhythmia resolves
          • QRS widens by >50%
          • Pt bradycardic
          • Pt hypotensive
      • Amiodarone
        • Reduces frequency of recurrent episodes of ventricular arrhythmia2,3
        • Mexiletine/Purkinje catheter ablation4
          • Effective in relatively narrow QRS refractory to Amiodarone
        • Acute side effects5
          • Hypotension (diluent)
          • Bradycardia
          • AV block
          • QT prolongation
          • Interstitial lung disease/pulmonary fibrosis
          • Hepatitis
        • Lidocaine6,7
          • Most efficacious in ischemic myocardium
          • Conversion rates from VT = 8-30%

Beta Blockers6,7

  • Provides competitive sympathetic blockade
  • Metoprolol preferred
  • Propranolol reasonable but no studies supporting the use of one over the other
    • Use with caution in patients with HFrEF

Catheterization8

  • Electrical storm often seen in ischemic heart disease
  • Urgent cath if MI considered etiology

Catheter Ablation6,9

  • Recommended if VT persists despite amiodarone/beta blocker
  • Superior to escalating medical therapy10

References

1)    Ortiz M, Martín A, Arribas F, et al. Randomized comparison of intravenous procainamide vs. intravenous amiodarone for the acute treatment of tolerated wide QRS tachycardia: the PROCAMIO study. Eur Heart J. 2016 Jun 28.

2)    Levine JH, Massumi A, Scheinman MM, et al. Intravenous amiodarone for recurrent sustained hypotensive ventricular tachyarrhythmias. Intravenous Amiodarone Multicenter Trial Group. J Am Coll Cardiol 1996; 27:67.

3)    Scheinman MM, Levine JH, Cannom DS, et al. Dose-ranging study of intravenous amiodarone in patients with life-threatening ventricular tachyarrhythmias. The Intravenous Amiodarone Multicenter Investigators Group. Circulation 1995; 92:3264.

4)    Murata H, Miyauchi Y, Hayashi M, et al. Clinical and Electrocardiographic Characteristics of Electrical Storms Due to Monomorphic Ventricular Tachycardia Refractory to Intravenous Amiodarone. Circ J 2015; 79:2130.

5)    Long B, Koyfman A. Best Clinical Practice: Emergency Medicine Management of Stable Monomorphic Ventricular Tachycardia. J Emerg Med. 2016 Oct 14. pii: S0736-4679(16)30721-1.

6)    Zipes DP, Camm AJ, Borggrefe M, et al. ACC/AHA/ESC 2006 Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death: a report of the American College of Cardiology/American Heart Association Task Force and the European Society of Cardiology Committee for Practice Guidelines (writing committee to develop Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death): developed in collaboration with the European Heart Rhythm Association and the Heart Rhythm Society. Circulation 2006; 114:e385.

7)    Eifling M, Razavi M, Massumi A. The evaluation and management of electrical storm. Tex Heart Inst J 2011; 38:111.

8)    Authors/Task Force members, Windecker S, Kolh P, et al. 2014 ESC/EACTS Guidelines on myocardial revascularization: The Task Force on Myocardial Revascularization of the European Society of Cardiology (ESC) and the European Association for Cardio-Thoracic Surgery (EACTS)Developed with the special contribution of the European Association of Percutaneous Cardiovascular Interventions (EAPCI). Eur Heart J 2014; 35:2541.

9)    Nayyar S, Ganesan AN, Brooks AG, et al. Venturing into ventricular arrhythmia storm: a systematic review and meta-analysis. Eur Heart J 2013; 34:560.

10)   Sapp JL, Wells GA, Parkash R, et al. Ventricular Tachycardia Ablation versus Escalation of Antiarrhythmic Drugs. Circulation. N Engl J Med. 2016 Jul 14;375(2):111-21.

Boerhaave Syndrome

Case presented by Dr. Jordan Smedresman
Follow-up Rounds 11/6/2015

CASE
Triage Vitals: T 98.0, HR 92, BP 150/102, RR 20, SpO2 92%
CC: Back pain

HPI
  • 72 yo M with PMH HTN BIBEMS for L sided back pain
  • Started after eating
  • Denied antecedent vomiting
  • Pain associated with dyspnea
PHYSICAL EXAM
Vitals: SpO2 88% on RA, 96% on 2L NC, BP 146/94
General: In acute distress
CV: RRR, no murmurs
Pulm: Diminished breath sounds on L

Abd: Soft, NT

STUDIES
EKG: NSR, no TWIs or ST deviations
POCUS: Possible L-sided pneumothorax
Labs: Unremarkable
CXR: L-sided hydropneumothorax, pneumomediastinum
CT Thorax: Boerhaave syndrome with L-sided pneumothorax, extensive pneumomediastinum


BACKGROUND
  • From sudden increase in esophageal pressure/decrease in intrathoracic pressure
    • Vomiting
    • Childbirth
    • Seizure
    • Prolonged coughing/laughing
    • Weightlifting
  • 15% of esophageal perforations
    • Most iatrogenic > FB or malignancy
  • Most common location of perforation: L posterolateral aspect of distal intrathoracic esophagus
  • Gastric contents in mediastinal cavity → chemical mediastinitis → bacterial infection
  • Pleural cavity may be violated from inflammation or initial perforation
  • ~100% mortality if untreated
CLINICAL MANIFESTATIONS
  • Symptoms (% of pts)
    • Chest pain (89%)
    • Dyspnea (67%)
    • Dysphagia (3%)
    • Neck pain (11%)
    • Neck swelling (6%)
    • Hoarse voice (6%)
  • History of retching (NB: 25-45% don’t have history of vomiting)
  • Crepitus with palpation of chest wall
  • Hamman’s sign: mediastinal crackling with heartbeat
  • Within hours:
    • Odynophagia, dyspnea, mediastinitis, sepsis
DIAGNOSIS
  • CXR
    • Not sensitive; may require hours for signs to develop
    • Findings
      • Mediastinal/free peritoneal air/SQ emphysema
      • Pleural effusion
      • Mediastinal widening

screen-shot-2016-11-29-at-4-51-24-pm

  • CT
    • Findings
      • Esophageal wall edema/thickening
      • Mediastinal widening
      • Air/fluid in pleural spaces/retroperitoneum

screen-shot-2016-11-29-at-4-50-53-pm

MANAGEMENT
  • NPO
  • Broad spectrum abx
  • Protonix gtt
  • CT Surgery consult
    • Surgical candidates:
      • Diffuse extravasation
      • Extension of perforation
      • Sepsis
      • Progression of pneumomediastinum or pneumothorax
      • Patients with empyema

REFERENCES

Blencowe NS, Strong S, Hollowood AD. Spontaneous oesophageal rupture. BMJ 2013;346:f3095.

Carrott PW, Jr., Low DE. Advances in the management of esophageal perforation. Thorac Surg Clin 2011;21:541-55.

Henderson JA, Peloquin AJ. Boerhaave revisited: spontaneous esophageal perforation as a diagnostic masquerader. Am J Med 1989;86:559-67.

Newcomb AE, Clarke CP. Spontaneous pneumomediastinum: a benign curiosity or a significant problem? Chest 2005;128:3298-302.

Triadafilopoulos G. “Boerhaave syndrome: Effort rupture of the esophagus.” Up To Date. http://www.uptodate.com, 26 Apr. 2016. Web. 28 Nov. 2016. https://www.uptodate.com/contents/boerhaave-syndrome-effort-rupture-of-the-esophagus

Spider Bites

Author: Dr. Neil McCormack, PGY-4


Sometimes it IS a spider bite

Trigger warning: Pictures of spiders (But, seriously, did you expect something different?)

Cutaneous skin abscesses are a common complaint in emergency rooms and have become more prevalent as the years continue.1 According to bacteriology studies, the majority of these abscesses are caused by skin flora, primarily Staphylococcus and Streptococcus species.2, 3 If you ask the patients, however, abscesses are caused by spider bites approximately 100% of the time. Is this reputation warranted? Are spiders the bane of Emergency Medicine’s existence and the source of all of our abscesses all these years?

Information on the clinical presentation of spider bites continues to be unreliable, being based on case reports, case series and databases. For instance, the Bureau of labor 2014 statistics reported 1,470 incidents involving spider bites. The listed symptoms include 230 incidents of “cuts or lacerations,” 300 incidents of “soreness and pain,” and 900 “other” incidents. The data, however, represents only spider bites reported from the workplace, and lack expert confirmation of the actual spider involved.

Before we discuss the various venomous spiders, let’s define the terms. Many individuals use the terms “poisonous” and “venomous” interchangeably but they’re not exactly the same. Poisons are typically secreted by a plant/animal (think poison dart frogs of the tropics) and are introduced into the body by ingestion or absorption through the skin. Venom, by contrast, is a substance that is actively injected into the body by the animal in question.

There is controversy regarding the number of venomous spiders in the United States. Some sources list only the black widow and the brown recluse spiders; other sources will also include the hobo spider. The CDC, for example, only lists two species; however, we will discuss the three classically considered venomous spiders.4

Black Widow

The black widow spider (genus: Latrodectus) is probably the most recognized spider on this list. There are three subspecies in the US named for their primary residence. The Northern black widow (spp variolus) spans primarily northeast from Canada to Florida and as far West as Texas. The Southern black widow (spp mactans) is found throughout the southeastern states. The Western black widow (spp hesperus) is found from Canada to Mexico along the West coast and as far East as Texas.

Adult_Female_Black_Widow

Black Widow Spider

The black widow spider grows to approximately 0.5 inches in body length as an adult. They can be identified by their distinctive black body with red hourglass marking.

Among black widow spiders, the larger female is the one who can bite and cause symptoms — males and juveniles have fangs that are too small to cause harm to humans. The black widow injects latrotoxins that attack nerves leading to episodic release of neurotransmitters acetylcholine, norepinephrine and GABA.5 This leads to a constellation of symptoms known as latrodectism. Symptoms start at the site of the bite (a pair of red spots, although the bite is commonly unnoticed), then spread contiguously. They initially include severe pain starting within 5-10 minutes of the bite and increasing in intensity over the first hour. Secondarily, generalized muscle pain, abdominal cramps, nausea and vomiting are seen. Piloerection and profuse diaphoresis at the site are also common. Some victims will see symptoms spread to more diffuse pain, muscle cramping, and diaphoresis/piloerection distant from the bite site, though this is rare. The symptoms in pregnant women can sometimes be severe enough to be confused with contractions.6

Treatment involves symptomatic management of pain and cramping with analgesics and muscle relaxants. For severe symptoms, there is an antivenin available,7,8 though the antivenin is generally limited to envenomation treatment center.9,10,11 Symptoms (and here is the part you don’t want to hear) typically resolve in several days but some people can have lingering symptoms for several weeks.12

Brown Recluse

The brown recluse (Loxosceles reclusa) is a spider native to the Southern US. Their distribution lies along the Southern states from Texas to the East coast and as far North as the Ohio valley.  How are you, a well-mannered “keep to yourself” kind of person likely to encounter a brown recluse if you live outside of this spider’s habitat? Unfortunately for you, there are reports of brown recluse spiders being transported to other areas of the country via shipping of goods throughout the US. The reports are of singular incidents and not always verified as brown recluse spiders. But it is something to consider, albeit it is exceedingly rare if you do not live in recluse country. This species has a reputation for being dangerous though, like most spiders, they are rarely aggressive towards humans and many bites are defensive.

Brown_Recluse

Brown Recluse Spider

The brown recluse spider is, as the name suggests, a brown colored spider that can grow to upwards of 0.75 inches. Their shade can range from dark grey/brown to the lighter color seen in the figure. Luckily for us, the brown recluse has short fangs and are not overly powerful. Thus, most bites require direct skin contact without clothing interference.

The bite of a brown recluse is typically painless initially. The dangerous aspect of this species is that they use a hemotoxin as their venom.  This can cause local necrosis of the skin (loxoscelism) due to the toxic protein actions. These main constituents of the venom are hyaluronidase, sphingomyelinase-D, alkaline phosphatase, esterase, and ATPase.13 The clinical manifestations can range from a localized urticarial response only, to forming a blistering, bleeding, ulcerating lesion. The lesion may increase in size and the central blister may become necrotic over the next few days.14 Systemic symptoms, which are rare in the US, include nausea, vomiting, rashes, fevers and joint pains.14 Once necrosis has set in, what do you do now? The most prudent management of these lesions starts with wound care, immobilization, tetanus prophylaxis, and analgesics. Local tissue damage and destruction may be surgically debrided though this will leave a large wound (which may need grafting and prolonged healing) or allowing the wound to for an eschar then heal by secondary intention. One thing to remember when dealing with suspected recluse bites outside of their natural habitat is that if the spider was not caught red-handed there are numerous other causes of skin lesions/necrosis in the medical literature.

Hobo Spider

The hobo spider (Eratigena agrestis) is known as the “aggressive house spider.” I will include this spider here but here is a disclaimer: There is currently debate on whether or not this spider is truly venomous or not. That being said, the hobo spider is native to Europe but in the US it resides in the upper Northwestern US from Canada to Northern California and West towards the Rocky Mountains.

Hobo spider

Hobo Spider

The hobo spider is a small brown spider mostly living in fields and outdoors. They grow to approximately 0.5-0.75 inches in length.

Are their bites venomous to humans though? The classic hobo spider bite is described as a small (several cm) painful bite with central erythema leading to blistering within 24 hours. This blistering then often times ruptures leaving a small necrotic lesion which typically will heal within 1-2 months. Only supportive treatment is available for these situations.

There is controversy regarding whether or not this truly happens with hobo spider bites or if this is misattributed to other causes. Some researchers suggest that the bites are caused by MRSA.15 One author reports that out of 33 confirmed Hobo Spider bites, none showed dermatonecrosis.16 The possibility of misattribution of Hobo bites to Recluse spiders or other causes of dermonecrosis leaves us, as well as other researchers,8,15,17,18,19,20 questioning the true nature of hobo spider bites and their medical importance. At this time, if you live in the Northwestern US, let’s just say older reports implicate the hobo spider though this may be an unlikely cause of your patient’s necrosis and should be taken with a certain degree of skepticism.

References

  1. Taira, B.R., Singer, A.J., Thode Jr, H.C., and Lee, C.C. (2009). National epidemiology of cutaneous abscesses: 1996 to 2005. The American Journal of Emergency Medicine 27, 289–292.
  2. MEISLIN, H.W., LERNER, S.A., GRAVES, M.H., McGEHEE, M.D., KOCKA, F.E., MORELLO, J.A., and ROSEN, P. (1977). Cutaneous AbscessesAnaerobic and Aerobic Bacteriology and Outpatient Management. Ann Intern Med 87, 145–149.
  3. Summanen, P.H., Talan, D.A., Strong, C., McTeague, M., Bennion, R., Thompson, J.E., Väisänen, M.-L., Moran, G., Winer, M., and Finegold, S.M. (1995). Bacteriology of Skin and Soft-Tissue Infections: Comparison of Infections in Intravenous Drug Users and Individuals with No History of Intravenous Drug Use. Clin Infect Dis. 20, S279–S282.
  4. CDC – Venomous Spiders – NIOSH Workplace Safety and Health Topic.
  5. Ushkaryov, Y.A., Rohou, A., and Sugita, S. (2008). α-Latrotoxin and Its Receptors. Handb Exp Pharmacol 171–206.
  6. Wolfe, M.D., Myers, O., Caravati, E.M., Rayburn, W.F., and Seifert, S.A. (2011). Black widow spider envenomation in pregnancy. J. Matern. Fetal. Neonatal. Med. 24, 122–126 (2005).
  7. Singletary, E.M., Rochman, A.S., Bodmer, J.C.A., and Holstege, C.P. (2005). Envenomations. Med. Clin. North Am. 89, 1195–1224.
  8. Weinstein, S., Dart, R., Staples, A., and White, J. (2009). Envenomations: an overview of clinical toxinology for the primary care physician. Am Fam Physician 80, 793–802.
  9. Heard, K., O’Malley, G.F., and Dart, R.C. (1999). Antivenom therapy in the Americas. Drugs 58, 5–15.
  10. Kunkel, D.B. (1984). Arthropod envenomations. Emerg. Med. Clin. North Am. 2, 579–586.
  11. Quan, D. (2012). North American poisonous bites and stings. Crit Care Clin 28, 633–659.
  12. Peterson, M.E. (2006). Black widow spider envenomation. Clin Tech Small Anim Pract 21, 187–190.
  13. Swanson, D.L., and Vetter, R.S. (2006). Loxoscelism. Clinics in Dermatology 24, 213–221.
  14. Wasserman, G.S., and Anderson, P.C. (1983). Loxoscelism and Necrotic Arachnidism. Journal of Toxicology: Clinical Toxicology 21, 451–472.
  15. Gaver-Wainwright, M.M., Zack, R.S., Foradori, M.J., and Lavine, L.C. (2011). Misdiagnosis of spider bites: bacterial associates, mechanical pathogen transfer, and hemolytic potential of venom from the hobo spider, Tegenaria agrestis (Araneae: Agelenidae). J. Med. Entomol. 48, 382–388.
  16. McKeown, N., Vetter, R.S., and Hendrickson, R.G. (2014). Verified spider bites in Oregon (USA) with the intent to assess hobo spider venom toxicity. Toxicon 84, 51–55.
  17. Bennett, R.G., and Vetter, R.S. (2004). An approach to spider bites. Erroneous attribution of dermonecrotic lesions to brown recluse or hobo spider bites in Canada. Can Fam Physician 50, 1098–1101.
  18. Fisher, R.G., Kelly, P., Krober, M.S., Weir, M.R., and Jones, R. (1994). Necrotic arachnidism. West J Med 160, 570–572.
  19. Vetter, R. (2008). Medical aspects of spider bites. Annual Review of Entomology 53, 409–429.
  20. Vetter, R.S., Roe, A.H., Bennett, R.G., Baird, C.R., Royce, L.A., Lanier, W.T., Antonelli, A.L., and Cushing, P.E. (2003). Distribution of the medically-implicated hobo spider (Araneae: Agelenidae) and a benign congener, Tegenaria duellica, in the United States and Canada. J. Med. Entomol. 40, 159–164.

 

Grand Rounds: Ocular POCUS

Dr. Andrew Shannon, MD, MPH of University of Florida College of Medicine – Jacksonville presents on Ocular Point-of-Care Ultrasound (POCUS) (07/20/2016)



Lecture Notes

Importance of Ocular POCUS
  • Up to 67% of periorbital fractures have associated ocular trauma
  • Periorbital swelling may prevent traditional exam
Eye Anatomy 
  • Medial area includes ducts that may require stents if violated in trauma
  • Temporal region of internal anatomy includes optic disk and nerve; nasal includes fovea and macula
  • Possible to evaluate for pupil diameter in axial cut under ultrasound
  • Retina usually not visible on U/S
  • Optic nerve sheath is visible on ultrasound, not the optic nerve
Equipment
  • Amount of energy required for temperature change in the retina is much less than that required to make a change at other tissue
    • Avoid over-exposing
  • Apply tegaderm as barrier prior to exam
Retinal Detachment
  • Complaint of
    • “blurry vision”
    • “wavy” visual loss
    • curtain comes down/across vision
  • Retina has blood supply from choroid
    • As fluid accumulates between choroid/retina → retinal ischemia
  • Retina is tethered to the choroid at the Ora Serrata and at the optic nerve
    • If you see a detachment that does not respect the optic nerve, consider vitreous detachment instead of retinal detachment
  • Worried about these in setting of trauma
    • May be obscured by vitreous hemorrhage
  • Retina will be hyperechoic and undulating
  • May have vitreous hemorrhage + retinal detachment; can be detected on POCUS
Vitreous Hemorrhage
  • Sudden, painless, floaters, dark spots, flashes
  • 2/2: Trauma vs DM vs sickle cell
  • POCUS: Hyperechoic, clotted blood
    • Looks like clothes in a washer
  • Terson’s Syndrome
    • Vitreous hemorrhage associated with ICH (SAH)
    • Occurs in 13% of patients with SAH
  • Posterior Vitreous Detachment
    • May also appear as hyperechoic linear density “lifted off” posterior globe
    • Thinner, smoother, darker than retinal detachment
    • Crosses optic nerve (unlike RD)
Orbital Wall fracture
  • May present as diplopia and blurry vision
  • Herniation of inferior rectus
Retrobulbar Hematoma 
  • Compartment syndrome of the eye
  • 90-120 min of ischemia → irreversible vision loss
  • Tx: Timolol, pilocarpine, acetazolamide
  • May require lateral canthotomy
    • Indications: APD, loss of vision, IOP >40 mmHg
Penetrating Injury/Globe Rupture 
  • May note extruded uveal tissue (almost always brown)
  • Irregular pupil will point toward area of injury
  • Pt NPO
  • Abx: Cephalosporin or anti-penicillinase PCN (i.e. augmentin)
  • Update tetanus
  • Anti-emetic
  • Shield eye & minimize manipulations
  • Modified Seidel Test
    • Use fluoroscein and cobalt blue filter to note aqueous humor flow
  • Hyphema may be noted
  • Ultrasound
    • Avoid if unnecessary and use gingerly
    • Findings
      • ↓ in globe size
      • AC collapse
      • Buckling of sclera
  • Anterior Chamber Decompression
    • From trauma or eroding corneal ulcer
  • Foreign Body
    • May see in 30% of open globe
Lens Dislocation/Subluxation
  • Edge of lens may be visible in/through pupil
  • Complete dislocation/luxation: Lens displaces into vitreous or rarely into AC
  • Differential dx for monocular diplopia: lens dislocation vs psych
  • Dislocation
    • Posterior more often than anterior
    • Typically s/p replacement (cataracts surgery); may see in Marfan’s and trauma
  • Avoid dilating pupil
Optic Nerve Sheath Measurement 
  • ONS is contiguous with dura mater
  • Papilledema is delayed in comparison to optic nerve sheath diameter change
  • Normal ONS is up to 5.0 mm diameter
    • Measure 3 mm posterior to globe for both eyes
    • Take average 2 or more readings
  • Average ONSD > 5.2 mm is considered abnormal
    • Consider ↑ ICP
  • If ONS <5 mm, unlikely ICP >20 mmHg
  • If >5.8, suspect ↑ ICP
  • Crescent sign: Optic nerve protrudes into the globe
  • Drusen: Optic nerve head drusen; may falsely appear as a FB