Case of the Week COW #20

Posted on by Yenis Paez-Perez

Resident: D’Amore/Clayton

CC: “My heart is racing.”

HPI: 26 year old male with no past medical history presents to the Emergency Room with complaints of palpitations. Patient states that while exercising at the gym just prior to arrival, he suddenly developed palpitations along with associated lightheadedness. He reported one similar episode in the past that self-remitted. He denies chest pain, shortness of breath, nausea or vomiting but was experiencing intermittent lightheadedness. He denies taking any medication prior to arrival. Patient states he drinks ETOH infrequently with his last drink several days ago. He denies tobacco or illicit drug use. Patient also denies any family history of heart disease or arrhythmias.

Physical Exam:
Vitals: HR: 221 BP: 117/74 RR: 20 T: 98.8 Pulse Ox 100% on Room Air
General: Patient is awake, appears uncomfortable
Respiratory: No respiratory distress. Lungs are clear to auscultation.
Cardiovascular: +S1/+S2, tachycardic, irregular. No murmurs, rubs or gallops.
Abdomen: Soft, non-tender, non-distended
Extremities: Palpable, rapid pulses. No cyanosis, clubbing, or edema.
Neurological: Alert and oriented to person, place, time, and situation, following all commands, strength and sensation intact and equal bilaterally.

Laboratory Data:
Lab work and radiography including troponins, complete blood count, complete metabolic panel, thyroid stimulating hormone, chest x-ray, and urine drug screen were all within normal limits. Image 1 is the EKG on presentation. The patient quickly became hypotensive 90/52 and complained of lightheadedness. The patient was quickly sedated and cardioverted with 150 joules. He returned to sinus rhythm at which time the underlying conduction was more apparent.

Questions

  1. What EKG abnormalities do you notice?
  2. EMS requests permission to administer 6mg of Adenosine to treat the arrhythmia.

What is your recommended treatment plan?

Answers:

  1. This EKG demonstrates Wolff-Parkinson-White Syndrome with Atrial Fibrillation.
  2. Advise EMS not to treat with Adenosine or other A-V nodal blocking agents as this may precipitate ventricular tachycardia or ventricular fibrillation.

Discussion:

Wolff-Parkinson-White Syndrome is a pre-excitation syndrome where myogenic bundles known as the Bundles of Kent directly link the atria to the ventricles, bypassing the atrioventricular (AV) node and the organized infranodal system [source: Tintinalli]. Atrial Fibrillation (AFib) in Wolff-Parkinson-White Syndrome (WPW) is a presentation of this syndrome in up to 20% of cases.

Features include an irregularly irregular rhythm, very rapid ventricular rates often in the range of 250 to 300, and widened QRS complexes that differ in duration and morphology from one to the next.The accessory pathway present in patients with WPW allow for the multitude of additional ectopic atrial impulses present in AFib to bypass the AV node and conduct to the ventricles, accounting for the unusually rapid ventricular rates. The variation in QRS duration and morphology can also be attributed to simultaneous conduction through the traditional AV node-His-Purkinje pathway as well as the Bundle of Kent-Ventricle route.

WPW with AFib is often misdiagnosed as a supraventricular tachycardia (SVT), ventricular tachycardia (VT) or atrial fibrillation with a bundle branch block, all of which can be safely treated with AV nodal blockers such as Adenosine, Diltiazem, and Amiodarone. WPW in the presence of atrial fibrillation makes degeneration into ventricular fibrillation more likely and thus synchronized cardioversion, delivering 0.5 – 2 Joules/kilogram, is the first-line treatment. Second-line treatments include Procainamide or Ibutilide whose mechanism prolongs the refractory period of the accessory pathway and whose dosing is weight-based. Stable WPW in the presence of narrow-complex SVT can be treated with the traditional vagal maneuvers, adenosine, and calcium channel- or betablockers [source: Tintinalli]. Patients with WPW should undergo ablation as this syndrome can lead to sudden cardiac death by means of ventricular fibrillation.

Take Home Pearls:

  • Wolff-Parkinson-White with Atrial Fibrillation presents as an irregularly irregular tachycardia with widened QRS complexes that vary in morphology and result in ventricular rates often greater than 250.
  • If the QRS complex is widened, avoid use of any AV nodal blockers as they can precipitated ventricular arrhythmias.
  • Procainamide and synchronized Cardioversion are the treatment of choice for WPW with AFib.

COW #19

Posted on by Nick Mota
Presenting Resident Nicholas Mota, DO PGY3
Chief Complaint Double vision
Brief HPI 30-year-old male with no past medical history presented with acute onset left ocular pain and double vision x1d. Patient states that last night he turned off the light and had immediate symptoms. Patient denies using glasses or contact lenses. Patient has never felt this before. Patient has not taken anything for the symptoms. No primary care physician. Denies any associated fever, chills, blurry vision, redness of the eye, discharge from the eye, nausea or vomiting, focal weakness, dysphagia, dysarthria, parasthesias, sob, chest pain, cough, abd pain, trauma.
Pertinent PE and Vitals T: 36.4 °C HR: 86 RR: 20 BP: 146/79 SpO2: 98%

Constitutional: Alert, awake, comfortable
Head/Face: Normocephalic, atraumatic, no temporal artery tenderness
Eye: OD 2 mm reactive, OS 6 mm nonreactive; APD present; EOMI, no nystagmus; intraocular pressure OD 21, OS error ×3; acuity OD 20/20, OS 20/40
ENT: Moist mucous membranes; Posterior Pharynx is without erythema and exudates, Airway is patent

Neck: ROM is full and without pain, no spinous process tenderness, trachea midline
Cardiovascular: Regular rate, regular rhythm, S1, S2, no murmurs, gallops, or rubs
Respiratory: No respiratory distress, breath sounds are equal bilaterally, no rales, no rhonchi, no wheezing.
Abdomen/Gi: Appears normal, Bowel Sounds present; Soft, non-tender, no guarding or rigidity.
Neuro: Oriented to person, place and time, Lucid thought process, follows commands. Strength 5/5 all extremities, Sensation intact, cerebellar signs absent
Musculoskeletal: Full active ROM without pain, 2+ b/l DP, PT.
Skin: Warm, dry, no rash or injuries
Pertinent Labs, Pertinent Imaging/EKG (if any) n/a
Working Diagnosis Acute Angle Closure Glaucoma
ED & Hospital Course Ophthalmology was consulted and requested acetazolamide 500 mg IV, mannitol 50 g IV, Combigan gtt (brimonidine/timolol), and pilocarpine gtt. Pt to f/u in office for YAG iridotomy. Patient was given drops with resultant resolution of anisocoria and APD. Patient had brother pick him up and drive him to ophthalmology office.
Pearls & Takeaways Ø  Glaucoma is characterized by increased intraocular pressure which will compress the optic nerve and can cause vision disturbances and, if left untreated, blindness.

Ø  Aqueous humor normally drains from the posterior chamber, through the iris/lens interface into the anterior chamber, through the trabecular meshwork and out through the canal of Schlemm and into the episcleral vein.
Individuals with shallow anterior chambers are more susceptible to closure of the angle because the iris and lens have a greater area of contact with subsequent bowing of the iris, blocking drainage.

Ø  Acute angle closure attacks are mostly precipitated by pupillary dilation, increased iris/lens contact, blocked aqueous flow into the anterior chamber and increased posterior chamber pressure that causes worsening bowing or the iris against the canal.
o   Pupillary dilators: dim light, mydriatics, antihistamines, anticholinergics, TCAs, adrenergics, emotional stress, antiparkinsonians
Ø  Far-sightedness is a risk factor due to anatomic flatter corneas, narrower angles, and shorter Anterior to Posterior lengths.
Ø  Family history, Asian descent, female, age (lenses thicken and anterior chambers narrow) are additional risk factors
Ø  The increase in IOP will cause corneal edema and cause the cornea to appear hazy and the patient to complain of blurred vision and/or halos.
Ø  Conjunctival injection, mid-dilated (5-6mm) pupil, hardness of globe (may use contralateral eye or nose as reference), decreased acuity are some exam findings
Ø  Fundoscopic exams are more difficult due to corneal edema but may show a pale, cupped optic disc with cup-to-disc ration > 0.6
Ø  Slit lamp will show shallow anterior chamber and corneal cloudiness
Ø  Oblique flashlight test: if shadow appears on nasal iris when penlight shone from temporal side with beam parallel to iris angle is narrow (sensitivity 76%, specificity 81%)
Ø  IOP > 22 is hallmark.

o   Tonopen: Be kind and anesthetize the eye. Instruct patient to look straight ahead. Contact cornea for 10 applanations; you do not need to indent the cornea and it may lead to incorrect readings and corneal injury. Error codes are displayed. Two numbers will appear: the first is the IOP measurement and the second (smaller) number is the statistical confidence indicator (95 is acceptable, repeat if 80 or 80-). Tonopen tip should be cleaned with canned air for 3 seconds and should occur monthly if 10 pts/week.

o   Shiotz: Measures via indentation tonometry and is dependent upon scleral rigidity.

§  Check calibration by testing tonometer against spherical mould and 5.5g weight: pointer should read 0.
§  Clean, anesthetize, have patient look straight at fixed point (their own outstretched finger)
§  With 5.5g weight, gently lower tonometer disc onto corneal surface and note reading.
§  If 2 or less, replace weight with 7.5g weight and repeat. If again 2 or less, use 10g weight.

o   Goldmann applanation: gold standard

§  Calibrate with the dial at 0mmHg, insert control weight. Set measuring drum at 0mmHg. If prism does not tilt forward and backward with the turning of the measuring drum up to +2 and -2, then calibration required. (Beyond the scope of this review)
§  Anesthetize and instill fluorescein, dab the eyes dry.
§  Patient positions into slit lamp with eyes level with black alignment marker
§  Maximum brightness of light
§  Blue light
§  Touch central surface of cornea with prism and then pull back
§  View cornea through miscroscope. 2 semicircular rings (mires) will be seen.
§  Adjust drum until mires line up. IOP is 10x the drum reading.

Ø  TREATMENT: should be in co-ordination with specialist but based on following principle:
o   Decrease production
§  Topical Beta-blocker: timolol 0.5% 3 drops q15m x3
§  Topical alpha-2 agonist: brimonidine 0.15% or apraclonidine 1% 3                        drops q15m x3
§  Topical CA inhibitor: dorzolamide 2% 3 drops q15m x3
§  Systemic CA inhibitor: acetazolamide 500mg IV/PO
§  Topical anti-inflammatory: prednisolone acetate 1%
o   Increase drainage
§  Topical prostaglandin: latanoprost 0.005%
§  Systemic diuretic: mannitol 50g IV
§  Topical muscarinic (miotic): pilocarpine 1-2%
§  Surgical iridotomy (YAG laser typically) is typically curative if done early

References
·       Cordero I. Understanding and caring for a Schiotz tonometer. Community Eye Health. 2014;27(87):57.
·       Stevens S. How to measure intraocular pressure: Schiötz tonometry. Community Eye Health. 2008;21(66):34.
·       TonoPen Avia User Guide. http://doclibrary.com/MSC167/PRM/68E3892-Rev-J-UG-AVIA4540.pdf
·       Shikino K, Hirose Y, Ikusaka M. Oblique Flashlight Test: Lighting Up Acute Angle-Closure Glaucoma. Journal of General Internal Medicine. 2016;31(12):1538. doi:10.1007/s11606-016-3737-8.
·       Chang DF. Chapter 2. Ophthalmologic Examination. In: Riordan-Eva P, Cunningham ET, Jr. eds. Vaughan & Asbury’s General Ophthalmology, 18e New York, NY: McGraw-Hill; 2011. http://accessmedicine.mhmedical.com/content.aspx?bookid=387&sectionid=40229319. Accessed September 08, 2018.
·       Laser iridotomy. http://www.littlerockeye.com/laser-iridotomy/
·       Murphy-Crews, M. 2017. Angle Closure Glaucoma. Taming the Sru. http://www.tamingthesru.com/blog/annals-of-b-pod/b-pod-case/angle-closure-glaucoma

 

 

Case of the Week COW #18

Posted on by Yenis Paez-Perez

CC: Shortness of Breath

HPI: ALS box call to St. Joseph Wayne ED # 1: 92 year old female from nursing home with PMH of Alzheimer Disease and failure to thrive, RUE DVT on Eliquis with complaints of SOB. BiPAP was initiated in the nursing home with minimal improvement. On arrival, Patient was in severe respiratory distress, tripoding and with an O2 saturation of 75% on BiPAP. Patient was tachycardic with initial HR of 130bpm, BP 100/80 with a RR of 30.

Med control: Intubation was advised with 50 mcg of Fentanyl, 18 mg of Etomidate, 75 mg of Succinylcholine, and 1 mg of Ativan for post-intubation sedation. NS IV Fluids were started and patient was to be transported to PCI Center St. Joseph Regional Center Paterson for Cardiac catheterization.

ALS box call to St. Joseph Wayne (SJW) ED #2: Patient los pulses after intubation. CPR was in progress.

Med control: Transfer to SJW, continue ACLS

Patient arrives in SJW with return of spontaneous circulation (ROSC) status-post Epinephrine x 2 and total CPR time 3-4 minutes.

Physical Exam:

Palpable Carotid Pulses. Endotracheal Tube (ETT) was confirmed
BP 81 / 68      HR140      RR20       T: 96.5 F         SaO2 94%.
Intubated, GCS 3T, Pupils 4mm equal and reactive bilaterally
Respiratory exam: Equal but diminished breath sounds throughout.
GI: Abdomen soft
Extremities: 2+ femoral pulses B/L, no peripheral edema.

Pertinent Labs (if any):

Na: 138    K: 3.7    CL: 116     CO2: 10   BUN: 37   Cr: 1.14   Platelet: 195
WBC: 10   Hg: 6.6   Platelet: 265
INR 6.3
ABG: 7.17/28/62/11
UA: nitrite +, large LE, WBC 6-10, Moderate bacteria, Large blood, RBC TNTC
Troponin: 0.042
Lactic Acid: 6.3

Pertinent Imaging/EKG: Bedside Cardiac Echocardiogram: Severe pericardial effusion with diastolic RV collapse.

 

Initial EKG post intervention: Sinus tachycardia, low voltage

Working Diagnosis at time of Disposition: Urinary Tract Infection and Pneumonia with Sepsis

Acute Respiratory Failure
Cardiac Arrest with ROSC
Cardiac Tamponade, possibly iatrogenic
Supratherapeutic INR

ED/Hospital course: 

A blind subxiphoid pericardiocentesis was performed. 50cc of frank blood was aspirated and no coagulation of aspirate was noted. Repeat vitals signs were BP 94 /74; Pulse 103; RR 20; Pulse Ox 98%.

Ultrasound was used to confirm the presence of the guide wire in the pericardial space. A triple lumen was passed over the guide wire and secured into placed. A total of 350cc was aspirated with repeat vitals: BP 111/73; Pulse 74; RR 20; Temp 97.6; Pulse Ox 99%.

A subclavian triple lumen catheter was placed and patient was given 2 PRBCs, 2 FFPs, 10mg IV Vitamin K, and 1L NS. Cardiologist from St. Joseph in Paterson was called and he accepted the transferred to their CCU. Patient was started on Fentanyl and Ativan Drip. Levophed gtt was also started for transport.

While in the CCU, patient was continued on antibiotics and vasopressors for septic shock.

Cardiac ECHO showed LV EF 65 to 70%, impaired relaxation pattern of LV diastolic filling, moderate concentric LVH, moderate pericardial effusion is present, no hemodynamic compromise, echogenic material adherent to the visceral pericardium, especially anteriorly measuring approximately 0.5 cm in thickness.

On Hospital day 2 (HOD), Cardiothoracic was consulted. They determined “patient currently very ill and unable to tolerate OR. Not stable for OR at this time.” Pericardial fluid was sent for evaluation.

Pericardial fluid results: Exudative as LDH 1613 with RBC count 1 million; ANA positive, RF negative.

Patient was additionally seen by palliative care. It was also determined there was no surgical interventions needed for the effusion. Sputum culture grew MRSA.

On Hospital day #4, Patient was following commands and was taken off the vasopressors. She self extubated and failed a trial on BiPAP and was re-intubated.

Patient was extubated on HOD #9 and discharged back to Nursing Home on HOD#15.

EKG post ER interventions: NSR, improved amplitude, prolonged QT

CXR post procedure: Enlarged heart, LLL infiltrate with obscured L hemi-diaphragm, ETT above carina, R subclavian central line, Pericardardial drain

 

Pearls & Takeaways ·       Tamponade:

o   Obstructive shock from impaired cardiac filling due to pericardial accumulation

o   As fluid accumulates, pericardial pressure become greater than the cardiac relaxing pressures

o   Incidence 2/10,000 in USA.

o   TB #1 cause in developing countries. Viral and postsurgical complications #1 cause in developed countries. Differential includes malignancy, infectious including HIV, idiopathic, atrogenic, trauma, uremia, hypothyroid, rheumatologic, and post radiation.

o   Symptom development depends on rate of fluid accumulation and amount. Pericardial compliance accommodates a slower rate of volume expansion.

o   Signs include persistent tachycardia, JVD, muffled heart sounds, pericardial friction rub, hepatomegaly, peripheral edema, pulsus paradoxus. Hypotension and bradycardia precede cardiac arrest.

o   Pulsus paradoxus reportedly present in 98% of tamponade cases even prior to onset of hypotension.

o   Pulsus paradoxus (decrease in SBP >10% during inspiration) occurs because the negative intrathoracic pressure during inspiration increases venous return and pulmonary vasculature compliance with subsequent pulmonary vascular pooling. RV engorges with septal shift causing decreased LV filling, SV, and SBP.

o   Pulsus paradoxus can be seen on plethysmogram. 1998 study by Frey of 57 PICU patients shows sensitivity of 89% and specificity of 90% to detect pulsus paradoxus 10% change with a pleth variation of 8mm.

o   EKG findings include low voltage, tachycardia, electrical alternans, PR depression, nonspecific ST/T changes

o   CXR may show enlarged silhouette

o   Bedside ECHO

§  Effusion

·       Trivial is seen only in systole

·       Mild < 10mm

·       Moderate 10-20mm

·       Severe >20mm

§  Collapse of chambers during relaxation

·       Atrial collapse precedes ventricular collapse

·       Atrial collapse longer than 1/3 of cardiac cycle has 100% sensitivity and specificity of tamponade

·       M Mode with EKG tracing through collapsing wall

·       RV indentation is more sensitive and specific than pulsus paradoxus

§  IVC size > 20mm is 92% sensitive

·       Pericardiocentesis: Indicated when hemodynamic compromise is present

§  US may guide you if necessary: if only RA collapse and RV unaffected, may wait to CTS consult

o   Needle aspiration with drain placement for repeat aspiration if re-accumulation occurs

§  Triple lumen catheter is most readily available in the ER though CTS prefers pigtail catheters due to decreased clotting

o   Subxiphoid approach (blind or US guided)

§  Insert needle at xiphoid process at 45 degree angle and aim towards tip of left scapula/left areola. Advance slowly until fluid aspirated.

§  US guided may be limited by habitus. Needle will enter pericardium inferior to the RV.

o   Parasternal (US)

§  Probe on left parasternal position at 4th intercostal space (Long axis view). Needle should be inserted in-plane with probe at a 45 degree angle. Will enter pericardial space anterior to RV.

§  Preferred over subxiphoid due to closer proximity to effusion and better ability to avoid liver and lung

o   Confirmation

§  Aspirated blood should not clot due to anticoagulative factors in space

§  Agitated saline flush showing “snow-storm appearance”

§  Repeat vitals after aspiration

o   Complications

§  PTX

§  Myocardial, coronary artery injury

§  Arrhythmias

§  Cardiac arrest

§  Liver injury

Case presented by Nick

Case of the Week COW#17

Posted on by Yenis Paez-Perez

CC: Hand Injury-Job Related

HPI: 35 yo otherwise healthy male presents to the Emergency Dept. (ED) with a laceration over the palmar surface of the left hand, proximal to the PIP joint and extending over the MCP joints of the 4th and 5th digit. He sustained this injury at work one hour ago. He is a firefighter and was responding to a house fire when he accidently tripped over an object in a smoke filled room while putting on his glove. He states his left hand went through a glass door. At the scene, patient washed it out with sterile saline and a dressing was applied. Pt also complaints of decreased sensation to the distal aspect of his left 5th digit. He denies any other trauma, preceding symptoms of chest pain, dizziness, feeling lightheaded, palpitations, inhalation injury or difficulty breathing. Denies head injury, neck pain or LOC. Last tetanus is unknown.

Physical Exam:

Vitals: BP 155/97   Pulse 97   RR 15     T 98.6F   SpO2 100% on RA
MSK/extremities: 2.5cm complex “V” shaped laceration over the palmar MCP of the left 5th digit that is oozing blood; no arterial bleeding noted. Tissue flap noted. 1.5 cm laceration over the left palmar aspect of the 4th digit between the MCP and PIP joint. Hemostasis noted. Small tissue flap noted. Sensation intact over the distal left 4th digit; Sensation mildly decreased over the distal left 5th digit. Cap refill brisk both digits. Pt is able to flex and extend both digits.

Location of laceration

:

Pertinent Labs (if any): N/A
Pertinent Imaging/EKG: No displaced fracture or dislocation. No radiopaque foreign body is identified.


Working Diagnosis: Prior to x-rays: possible FB, dislocation/subluxation, fracture. Possible Partial flexor tendon laceration.

 ED/Hospital course: Pt received Toradol for pain and a tetanus shot

  • Digital block was performed on the 4th and 5th digits of the left hand by injecting lidocaine into the web spaces as well as local was performed on the palm where the digital block was ineffective.
  • Moderate bleeding/oozing noted of the 5th left finger laceration. Upon lifting the tissue flap of the 5th digit the flexor tendon was exposed but not lacerated. The 4th left digit wound more superficial. No tendon exposed. No FB found in either laceration.
  • 4th finger closed w/ six 4-0 Ethilon sutures
  • 5th finger closed w/ ten 4-0 Ethilon sutures
  • Pt discharged w/ Rx for: Bacitracin Ibuprofen Keflex F/u w/ employee health F/u in 7-10 days for suture removal

 Pearls & Takeaways:

  • For lacerations to the hand or other injuries that may or may not involve a tendon always ask:
    • Position of hand injury?
    • Crush, burn, injection, chemical injury?
    • Other trauma or preceding symptoms?
  • Exam for hand/wrist lacerations
    • Check and compare Bilateral grip strength
    • Check sensation
      • Compare bilaterally with 2 point discrimination to the volar aspect of each fingertip
      • Normal 2 point discrimination on the hand is 5-6 mm
      • Review of nerve distribution :
    • Check Motor function
      • Ask them to make a clenched fist— The middle and distal phalanges should all be parallel to each other with the nails positioned in the same plane and pointing toward the Scaphoid when fist is clenched
      • Ulnar Nerve innervates the Lumbricals and Adductor Pollices Muscles
        • Lumbricals: Have patient abduct their fingers and have them resist the force of you pushing their fingers back to midline
        • Adductor Pollices Test: Have patient hold a piece of paper with the volar pulp of the thumb and PIP of index finger. If you pull away at the paper, and pt is able to maintain the key pinch of paper against resistance then adductor pollicis is strong.
  • Median Nerve
    • Make the “OK” Sign (Flexor Pollicus Longus)
    • Opposition (Thenar Muscles): As them to touch their pinky with their thumb
    • Ask pt to abduct their thumb with palm up and have the pt resist a force to redirect the thumb toward the palm (Abductor Pollicis longus)
  • Radial Nerve
    • With palm on the table, hyperextend all fingers against resistance from can have them lay their palm flat on a table, and lift each digit straight up and extend up from the table while keeping the palm flat
  • Vascular
    • Check for capillary refill and pulses
  • Flexor Tendor Testing
    • 90% of the tendon can be severed/lacerated with preservation of ROM without RESISTANCE.
    • Apply resistance when testing for tendon function
    • Pain along course of tendon during resistance testing suggest partial laceration even if pt has FULL ROM
    • Test for Flexor Digitalis Profundus (FDP): Ask the to flex their DIP joint against resistance while holding their MCP and PIP joint in extension
    • Test for Flexor Digitalis Superficialis (FDS): Ask to flex their PIP joint against resistance while ALL the rest of the fingers are held in full extension (Hyperextension disengages FDP and the FDS function is isolated).
  • Imaging
    • If isolated fingers involved, get a AP, oblique and lateral view of the designated finger as well as the hand
  • Digital Blocks
    • Web Space– Inject 1-3 mL of Anesthetic
    • Transthecal
      • Inject into flexor Tendon sheath
      • ID distal palmar crease and tendon
      • Insert needle at 45 degrees just distal to crease
      • Inject
      • If resistance, withdraw slightly
      • Apply proximal pressure
      • Pros: Only 1 poke and numbs entire finger
      • Cons: It’s over most sensitive part of the hand
    • Method to get a bloodless field
      • Use tourniquet or Penrose drain at base of finger secured by hemostat
      • Use another tourniquet or gauze to wrap around distal end of finger and wrap w/ moderate compression down from most distal part to laceration milking out the blood in the distal finger
      • Do not leave tourniquet on for >20 minutes
    • What If there is a stellate laceration?
    • When to refer tendon lacerations:
    • Splinting tendon Injuries:
      • General rule is to splint in the direction of function
        • Extensor tendons splinted in extension
        • Flexor tendons splinted in flexion
      • Flexor Tendon Injuries specifically:
        • Dorsal splint
        • Wrist flexed to 30 degrees
        • 70 degree MCP flexion
        • 30-45 degree PIP flexion
      • Antibiotics
        • NO Great guidelines
        • ACEP Clinical guidelines
          • Looks ok-à No ABX
          • Looks bad-à ABX
        • If simple laceration -à no ABX
        • If not simple (contaminated, infected, bone, tendon, joint involvement)-à ABX
          • 1st line: Cephalosporin
          • Consider Context:
            • Human, Cat, Dog Bites: Amoxicilin/Clavulanic Acid (Augmentin)
            • Open fractures: Cefazolin (Ancef)
            • Visibly dirty and open wound: Ancef + Gentamycin

Case presented by Dr. Jessica Williams

Case of the Week COW#16

Posted on by Yenis Paez-Perez

CC: BIB BLS for “Psych Evaluation”

HPI: 46-year-old female w/ PMH of asthma, SLE, RA and seizure disorder presents to the emergency department by BLS for evaluation. Patient states, “I don’t like people accusing me of doing things I didn’t do, I only took 2 Percocet and that’s it!” Patient states that she has been feeling depressed and “everything I do is never good enough for my kids, I buy them car, and I don’t even have car myself.” Patient appears to have multiple scratches over her face and left wrist, but is not willing to elaborate how she sustained them or provide any additional history. Denies any suicidal ideations, homicidal ideations, or hallucinations. There is no known psychiatric history.

Per family and EMS, patient was in her bedroom with the door shut, “not acting right, she was asking for us to pass her the key under the door to get out of the room but there is no lock on the door. She did this once before but it went away, today is more severe.” Pt was found in her bedroom by EMS with 2 empty beer cans and bottles of Percocet nearby. She had a recent URI for which she was taking Zzz-quil.

Medications: oxycotin 60mg q12h prn, Percocet 10/325mg q4-6h prn, toradol 10mg TID, ambien CR 12.5mg qHS, ProAir HFA 2 puffs q6h, Zzz-quil

 Physical Exam:

VS: 148/101, HR 111, RR 18, T 99.1, SpO2 95% on RA
General: Awake, alert, coherent, intermittently tearful
HEENT: superficial abrasions over face, otherwise NCAT; moist mucous membranes
Eyes: 3mm PERRL
Cardiac: tachycardic, regular rhythm, no M/R/G
Lungs: CTA b/l
Abd: soft, NT, ND, normal active bowel sounds
Neuro: AAOx3, lucid, following commands, moving all 4 extremities, no gross deficits, steady gait w/o difficulty
Skin: multiple superficial abrasions over face and L wrist, normal moisture
Extremities: 2+ distal pulses, warm, normal color
Psych: Anxious appearing, depressed mood, emotionally labile, intermittently tearful; denies SI/HI

Pertinent Labs (if any)
CBC: 11.7>16.5/50.1<324
CMP (@15:09 hours): Na 135, K 4.6, Cl 106, CO2 5, Glucose 132, BUN 9, Cr 0.98, GFR >60
Alk phosphate 77, AST 59, ALT 66
UA: Moderate blood, 0-3 RBCs, occasional calcium oxalate crystals, otherwise WNL
Alcohol: <10 mg/dl
UDS: (+) cocaine
Acetaminophen: <10.0 ug/ml
Salicylate: <2.5 mg/dl
Repeat CMP (@ 17:30 hours): Na 138, K 5.4, Cl 109, CO2 <2, Glucose 143, BUN 9, Cr 1.10 GFR:53, Alk phos 77, AST 69, ALT 74
Serum Osmolality: 334 mOsm/kg (N: 283-299)
Calculated osmolar gap: 53.0 mOsm/kg
ABG: pH 7.00 / pCO2 13 / pO2 151 / HCO3 – 3.2
ABG Lactate: 20.0 mmol/L
Serum lactic acid: 1.2 mmol/L
Acetone: Negative

ECG in the ED

Working Diagnosis: Anion gap metabolic acidosis, most likely due to ethylene glycol poisoning

ED/Hospital course:  In the ED patient became increasingly altered. Upon arrival patient was coherent, AAOx3, tearful. Upon reevaluation she was found in room shaking back and forth talking to herself and banging her hands on the bed rails, more confused, inappropriate in her thoughts and actions. A short time later she was found on the floor next to stretcher and was AAOx1, agitated, combative, not following commands, fighting with staff, incontinent of urine. Lab results returned at this time and the patient was subsequently intubated, received 1 amp sodium bicarbonate prior to intubation and admitted to MICU. Repeat labs in MICU showed persistent anion gap metabolic acidosis with Bicarbonate of 5 and anion gap of 26. She was placed on bicarbonate drip and received emergent HD. After HD, the acidosis improved with a bicarbonate value of 19 afterwards. Additionally placed on fomepizole. Received 2 rounds of HD. Subsequently extubated and transferred to floor. Upon extubation she continued to deny any SI or toxic ingestion. Methanol and ethylene glycol levels (-), however, they were drawn after HD was performed.

 Pearls: Brief differential diagnosis of anion gap metabolic acidosis:

  • Methanol, metformin
  • Uremia
  • Diabetic or alcoholic ketoacidosis
  • Paraldehyde
  • Isoniazid, Iron, Inhalants (carbon monoxide, cyanide, hydrogen sulfide)
  • Lactic acid
  • Ethylene glycol (ethanol may produce a small gap)
  • Salicylates, solvents

Osmolar gap:

  • Calculated osmolar gap ≥10 is consistent with poisoning by alcohols (ethanol, methanol, ethylene glycol, isopropanol, propylene glycol), glycerol or mannitol
  •  Absence of osmolar gap does not exclude toxic alcohol poisoning.
  • Normal osmolar gap: ±10
  • Normal serum osmolality: 280-295 mOsm
  • Osmolar gap formula: (2 x Na) + BUN/2.8 + Glucose/18 + Ethanol/4.6
  • Labs for this calculation (i.e. serum osmolality, ethanol, and SMA-7) must be drawn at the same time for accuracy

Toxic Alcohol Poisonings:

  1. Methanol
  • Found in windshield washing fluids, solvents, paint thinners and canned fuels
  • Converted by alcohol dehydrogenase to formaldehyde then to formic acid
  • Accumulation of formic acid correlates with the decrease in bicarbonate, the increase in anion gap, and the severity of the metabolic acidosis
  • Formic acid affects optic nerve function, causing optic papillitis and retinal edemaà “blind drunk”
  • Visual symptoms include photophobia, “snowstorm” vision, and blindness
    • Management:
      • Supportive measures including airway management
      • Severe acidosis is treated with bicarbonate to reduce diffusion of formate into the CNS and protect the optic nerve
      • Alcohol dehydrogenase inhibitor (ethanol or fomepizole) to block further metabolism of methanol
      • Fomepizole Fomepizole (4-methylpyrazole) is preferred iv.
      • Hemodialysis to remove methanol and formic acid indicated if methanol level >50 mg/dL, metabolic acidosis (arterial pH ≤ 7.25), severe visual or CNS symptoms
  1. Ethylene glycol
  • Found in antifreeze and brake fluids
  • Converted by alcohol dehydrogenase to glycolaldehyde which is metabolized to glycolic acid
  • Glycolic acid is primarily responsible for the anion gap metabolic acidosis; it is metabolized to multiple metabolites including oxalic acid
  • Oxalic acid forms calcium oxalate crystals in the kidney, brain and liver
  • Initial CNS changes suggestive of ethanol intoxication progressing over 9-12 hours to possible seizures, stupor, coma; toxicity may progress to pulmonary edema and myocardial dysfunction
  • Late toxicity is characterized by renal failure
  • Positive birefringent calcium oxalate crystals in the urine; often absent initially commonly described as “envelope-shaped”
  • May see hypocalcemia although not always present
  • Management:
    • Alcohol dehydrogenase inhibitors: Fomepizole or ethanol
    • Hemodialysis with same indications as methanol above
    • Thiamine and pyridoxine can be administered to decrease production of oxalic acid
    1. Isopropanol
  • Isopropyl (rubbing) alcohol
  • More intoxication/CNS depression but generally less severe sequlae than methanol and ethylene glycol 80% is absorbed from the stomach within 30 minutes and metabolized by alcohol dehydrogenase to acetone
  • Presentation: CNS depression, hypotension in severe cases, hemorrhagic gastritis/tracheobronchitis
  • Positive serum acetone and acetonuria
  • Anion gap metabolic acidosis is generally not a feature of isopropanol toxicity (unless you have significant hypotension with subsequent lactic acidosis)
  • Management:
    • Supportive care, including airway management
    • Alcohol dehydrogenase inhibitors are not indicated
    • Hemodialysis indicated for refractory hypotension or serum levels >400-500 mg/dL

Some Additional Points:

      • Lactic acid on lab analysis may be falsely elevated and vary depending on how the sample is analyzed. You will note that ABG lactic acid and serum lactic acid analyzed by lab are very different values, this is due to the fact that a metabolite of ethylene glycol’s metabolism has a very similar chemical structure to lactic acid, causing a falsely positive elevated lactic acid
      • The differential diagnosis of anion gap metabolic acidosis listed above is a limited list of the most commonly noted causes of AG metabolic acidosis; a comprehensive list is much broader
      • An osmolar gap >50 is highly suggestive of toxic alcohol ingestion; a level >100 is virtually pathognomonic—there is really nothing else that can cause such a severely elevated osmolar gap other than toxic alcohol

Case presented by Dr. GregnCassidy

Special thanks to Dr. Kashani for his guidance in preparing this case.

Case of the week COW #15

Posted on by Yenis Paez-Perez

CC: Shortness of breath

HPI: 7 day old female presents to the Emergency Dept. (ED) after being seen earlier in clinic. Mother is rom Nigeria and arrived to the U.S a few weeks prior to delivery. Prenatal care is unclear. Patient was delivered via C-Section at 39 weeks at another nearby hospital. Both mother and baby spent one day in the hospital after delivery being discharged home. Mother states that since last night, the baby appears to “ not breathing right.” She also hasn’t’ been eating much and is crying more often than usual, during which her lips start to turn blue.

Physical Exam:
Obvious respiratory distress, hypoxic on RA, saturating in the middle to low 80’s on NC 3 L
HR 176,   RR 60.    Accuchek 96.
BP: (RA) 69/45    BP (LA) 91/64     BP (LL) 84/64     BP (RL) 71/58

Pertinent Imaging/ECG

ECG in the ED:

Working Diagnosis: Shock secondary to congenital cardiac pathology.

ED/Hospital course:  Patient was admitted to PICU, underwent Echocardiogram and further imaging and was diagnosed with Coarctation of the Aorta. The patient was transferred to Mt. Sinai for operative repair.

Pearls:

  • 7 day olds are terrifying, especially if they are sick.
  • Take a breath! Start with your ABCs.
  • Coarctation of Aorta(CoA) is a congenital aortic narrowing which most commonly occurs at the level of ductus arteriosis. There are Pre-ductal and Post-ductal types. Pre-Ductal CoA is a Truncus dependent lesion and most patients present within 2 weeks of birth once duct closes. Aortic narrowing leads to increased LV function and dilation. Post-ductal are commonly identified in adulthood.
  • Obtain a BP/pulse Ox in all 4 extremities
  • Perform the Hyperoxia test
    • Obtain ABG on RA. Then, apply 100% supplemental oxygen with a NRB for 10-15 minutes. Repeat the ABG on the NRB.
      • On repeat ABG
        If PaO2 > 250mmHg = Lung problem
        If PaO2 < 100mmHg = Congenital Heart Disease
        If PaO2 100-250: Assume the worst situation first
  • You may also apply supplemental oxygen and assess the infant’s response. If saturation increases to at least 5-10%, it’s most likely a Lung problem. If it remains the same, think about Congenital Heart Disease
  • Prostaglandin (pt is less than 4 weeks old typically 1-2 weeks of life) start at 0.05 mcg/kg/min.
  • Dr. Hochman rule #11, call consultants early “don’t be the captain of a sinking ship”
  • Additional medications: Lasix 1 mg/kg if evidence of volume overload.Ductal dependent lesions, pulmonary presentation cyanosis/hypoxia use phenylephrine . If systemic SX, shock, pulmonary congestion on CXR Milrinone (decrease afterload + inotropic support).

The SICK NEONATE!

Case presented by Dr. Daniel Poor

Pediatric Pneumonia

Posted on by Yenis Paez-Perez

 3-year-old boy presents to the ED with a 4-day history of cough and 1-day history of fever. Per family patient has been having rigors and chills with vomiting. He also reports chest pain with coughing. His immunizations are UTD. The child does not appear toxic,

VS: Temp 103.3F,  BP 90/65,  HR 100,  RR 30,  96% O2 Saturation on RA.
Patient has some intercostal retractions, with decreased air entry on the right side with audible crackles.

Questions for EM physician

  • How do you make the diagnosis of pneumonia?
  • Distinguishing patients with bacterial pneumonia, who would benefit from antibiotics, from those with nonbacterial pneumonia who would not.
  • Who requires inpatient management vs. patients that can be safely discharged home on oral antibiotics.
  • Pneumonia is the number 1 killer of children worldwide.
  • Pneumonia occurs more often in early childhood than at any other age and causes significant morbidity and mortality.
  • Identifying the cause of pneumonia in children is difficult due to a lack of rapid, accurate, commercially available laboratory tests for most pathogens. Empirical therapy based on patient’s age, clinical scenario and risk factor is the most common course in most cases.
 Age-specific causes of pneumonia in otherwise healthy children. Pathogen listed in order of frequency
Neonates GBS, E. Coli, Listeria Monocytogenes, Staphylococcus
1 month – 2 years RSV, Parainfluenza virus, Metapneumovirus, Influenza virus, Adenovirus, S. Pneumoniae

 **3 weeks to 3 months of age (Pneumonitis syndrome/Afebrile Pneumonia Syndrome (APS))*: Chlamydia trachomatis, RSV, Parainfluenza virus, Bordetella pertussis
2 – 5 years RSV, S. Pneumoniae, Non-typeable H. Influenzae (NTHi), Group A Streptococcus, Mycoplasma pneumonia, Chlamydia pneumonia
6 – 18 years Mycoplasma pneumonia, Chlamydophila pneumonia, Streptococcus pneumonia, NTHi, Influza virus A , other respiratory viruses
  *Infants (1 – 3 months of age) may present with a characteristic syndrome of cough, tachypnea, progressive respiratory distress, and radiographic evidence of bilateral diffuse pulmonary infiltrates with air trapping. Most are afebrile. This syndrome is also called APS. The most common pathogen included Chlamydia trachomatis and respiratory viruses. Infection of Bordetella pertussis should also be considered due to recent dec. in immunization. Acutely, APS is generally benign and self-limiting disease. In such cases, infants often have viral illness, which does not respond to antibiotic therapy, but differentiating bacterial from viral illness is often difficult. Consider empiric antibiotic therapy.

Diagnosis of pneumonia:

    • Definition: Essentially it is infection of lower respiratory tract in the presence of radiographic abnormalities on CXR.
    • WHO guidelines for pneumonia in children is cough and tachypnea
      • Age < 2 months: Tachypnea is >60 RR
      • Age 2 months to 5 months: Tachypnea is >50 RR
      • Age >12 months: Tachypnea is > 40 RR
    • Clinical features
      • Fever and tachypnea are sensitive but not specific
      • Cough
      • Productive cough is rarely seen before late childhood
      • Consider pneumonia in any child presenting with prolonged fever, prolonged cough, high fever, as well as focal respiratory findings not including wheezing, especially with the presence of multiple symptoms.

Evaluation
Absence of tachypnea, respiratory distress, and rales/decreased breath sound rules-out pneumonia with 100% sensitivity

  • CXR: Cannot differentiate between viral and bacterial (but lobar infiltrate more often bacterial)
      • Consider for:
        • Age 0-3mo (as part of sepsis work up)
        • <5yr with temperature >102.2, WBC >20K and no clear source of infection
        • Ambiguous clinical findings
        • Pneumonia that is prolonged or not responsive to antibiotics
    • Consider RSV, Influenza 

Treatment

 Empiric Antimicrobial Therapy For Children with Pneumonia by Age group
Age group Outpatient Inpatient
Neonates NOT RECOMMENDED Ampicillin 200 mg/kg/d IV divided Q6H

+ Gentamycin 7.5 mg/kg/d IV divided Q8H

OR

+ Cefotaxime 150mg/kg/day IV divided Q8H

Consider Cloxacillin and Nafcillin for patient with S. aureus infection or Vancomycin for MRSA
3 wk – 3 mo NOT RECOMMENDED Azithromycin 10 mg/kg IV first dose, then 5 mg/kg IV QD for 4 days

 
3 mo – 5 yr* Amoxicillin 80 – 100mg/kg/day in 2 divided doses Ampicillin 200 mg/kg/d IV divided Q6H

OR

Ceftriaxone 50 mg/kg Q24hrs

Consider Azithromycin 10 mg/kg IV first dose, then 5 mg/kg IV QD for 4 days

Consider Vancomycin for seriously ill patients
6yr – 18yr* Azithromycin 10 mg/kg for first dose, then 5 mg/kg daily for 4 days Azithromycin 10 mg/kg IV first dose, then 5 mg/kg IV QD for 4 days

PLUS

Ceftriaxone 50 mg/kg Q24hrs

Consider Vancomycin for seriously ill patients
*Refer to AAP guideline on management of pediatric pneumonia below

Disposition

  • Consider Admission For
    • Age: <2-3 months old (Consider up to 6 months)
    • History of severe or relevant congenital disorders (Cystic fibrosis)
    • Suspected complication (Empyema)
    • Vomiting, dehydration, unable to tolerate PO
    • Immune suppression (HIV, SCD, malignancy)
    • Toxic appearance/respiratory distress
    • SpO2 <90-93%
    • Social circumstances

Post by Dr. Michael Hong

Case of the Week COW#13

Posted on by Yenis Paez-Perez

CC: Chest Pain

HPI: 49-year-old female brought in via ALS presents complaining of Chest pain. As per the Paramedics, the patient was found to be in no acute distress, stating she had exertional chest pain, which had subsided. The pre-hospital ECG was suspicious for ischemia and she was given ASA. Patient states she was walking home from the store when she began to have a pressure like pain on the left side of her chest, which was non-radiating and persisted when she laid down. She admits to feeling similar symptoms over the past few months, but today was the most severe. Upon arrival to Emergency Department, she denied chest pain, SOB, palpitations, abdominal pain, nausea or vomiting. Denied ETOH or illicit drugs use

 Physical Exam:
BP:128/91, Hr:88, RR: 14, Temp: 98.0, Pulse O2: 100% RA
General: Patient lying comfortably in bed, in no distress
HEENT: NCAT, pupils PERRLA, neck supple
Respiratory: non-labored, CTA B/L, no wheezing, rales or rhonchi
Cardiac: +S1/S2, no MRG, regular rate and rhythm
Abdomen: soft NT ND, + BS
Neuro exam: AAO X 3, lucid, strength is 5/5 in all extremities, muscle tone is intact,
Skin: No rash or peripheral edema.

Pertinent Labs:
CBC: Unremarkable
CMP: Unremarkable
Troponin: Negative (< 0.010)

Pertinent Imaging/ECG
CXR: no acute infiltrate, No Pneumothorax or cardiomegaly. Normal Chest X-ray
Pre-Hospital ECG

ECG in the ED

Working Diagnosis: Left Main Insufficiency

ED Course: Repeat ECG in ED showed NSR and had completely normalized. Case was discussed with Interventional cardiologist on call. A Code STEMI was activated and patient was taken emergently to the Cath lab. She was given a Heparin bolus as well as Plavix.

ED/Hospital course:  The catheterization report revealed 80-90% Distal left main, 30 % mid LAD, and LM stenosis improved partially during catheterization with nitroglycerin. Patient admitted to recently using cocaine. CT surgery was called due to the fact that patient had recent cocaine use and it was believed she might have had Left Main Coronary spasm. On hospital day 2, patient went back for repeat catheterization, which revealed Left main distal 30% and LAD mid 30% stenosis. Patient was transferred to telemetry, and discharged on hospital day 4.

Pearls:

aVR in ACS
Typical ECG findings with left main coronary artery (LMCA) occlusion:

  1. Widespread horizontal ST depression, most prominent in Leads I, II and V4-6
  2. ST elevation in aVR ≥ 1mm
  3. ST elevation in aVR ≥ V1

(Don’t worry so much about STE 0.5mm or less in lead aVR, because it lacks specificity. Using 1.0mm or greater in lead aVR, has better specificity)

ST-Segment Elevation in lead aVR foreshadows a worse prognosis in ACS and often predicts the need for CABG. Patients with NSTEMI and ST elevation ≥ 1mm in aVR are likely to have multi-vessel or LMCA disease and are likely to require CABG, therefore withholding Clopidogrel may be prudent. ST-segment elevation in aVR can be caused by any of the following 4 mechanisms

  1. Critical narrowing of the LMCA causing sub-endocardial ischemia due to insufficient blood flow. (LMCA insufficiency)
  2. Transmural infarction of the basal septum due to a very proximal LAD occlusion or complete LMCA occlusion (patient will be VERY sick)
  3. Severe multi-vessel coronary artery disease.
  4. Diffuse sub-endocardial ischemia from oxygen supply/demand mismatch.

Patients with complete occlusion of the LMCA (mechanism 2), often present in cardiogenic shock and require immediate revascularization. Patients with acute coronary occlusions typically will have active symptoms and look sick!

There is an estimated 70% mortality without immediate PCI. Medical therapy (including thrombolytic) does not improve mortality. Emergency PCI may decrease mortality to 40%.

 What Else can Cause STE in aVR that Won’t Benefit from Going to the Cath Lab?

Other causes of global cardiac ischemia
o Thoracic aortic dissection
o Large pulmonary embolism
o Severe anemia
o Post-arrest (within 15 min. of epinephrine or defibrillation)

oMiscellaneous causes
o Supraventricular Tachycardia (esp. AVRT)
o Left bundle branch block (LBBB) & paced rhythms
o LVH with strain (from severe hypertension)
o Severe hypokalemia
o Na+ channel blockade (TCA toxicity, hyperkalemia, Brugada, etc.)

REMEMBER: ST-Segment Elevation in Lead aVR is NOT SPECIFIC for an acute LMCA Lesion, Acute Proximal LAD Lesion, or Acute Triple Vessel DiseasE

    • Correlate Your ECG with the Patient’s Clinical Status
    • Patients with ACS due to LMCA Blockage, Triple Vessel Disease, or Proximal LAD blockage will look “sick” due to global cardiac ischemia

Case presented by Dr. Kerri Clayton.