COW #19

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

·       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.
·       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. Accessed September 08, 2018.
·       Laser iridotomy.
·       Murphy-Crews, M. 2017. Angle Closure Glaucoma. Taming the Sru.



Case of the Week COW #18

CC: Shortness of Breath

HPIALS 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

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

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

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.


  • 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).


Case presented by Dr. Daniel Poor

UMEM Emergency Cardiology Symposium PEARLS

View the recorded lectures here:

LBBB and Chest Pain in Acute MI…What Should I Do?

Dr. William Brady – University of Virginia

  • Patients with new LBBB on EKG is not common in the setting of Acute MI (AMI). It is, however, the most common pseudo-infarction pattern.
  • 80% of AMIs with LBBB are not detectable by ECG

Rational approach to AMI in patients with LBBB:

Wonder Women: Exploring the Gender Gap in ACS

Dr. Susanne DeMeester – University of Michigan

  • Average age of women presenting with ACS is 71. This age lags men by about 7-9 years.
  • Women have a higher 1 and 5 year post ACS mortality compared to men
  • 20% of women with acute STEMI on their ECG will have a clean cath
    • Cardiac microvascular dysfunction more common in women
      • Smaller epicardial vessels
      • Increased stiffness
      • Smooth muscle dysfunction
    • Rupture embolic plaque causing STEMI more common in men
    • Coronary vasospasm equal between men and women
  • NSTEMI is more common in women
  • Dyspnea is the most common angina presentation in women and geriatric patients (not chest pain!)
  • Women more likely to complain of chest “discomfort” rather than “chest pain” or “chest pressure”
  • Women have additional risk factors that have a greater association with ACS:
    • Depression, anxiety, psychosocial environment
  • Women with low risk HEART Score have lower risk of 6 week major acute cardiac event (MACE) compared to men (2% vs 6.5%).
  • Women have a smaller degree of ST elevation in acute STEMIs compared to men and are likely to produce lower levels of troponin.
  • Remember the diagnosis of spontaneous coronary artery dissection (SCAD) in the young peripartum woman
    • Risk factors include pregnancy, OCPs, vascular and connective tissue disorders
    • High recurrence rate ~20%
  • Fibrinolytics in ACS – Women are more likely to bleed
  • Women historically have had delays to treatment, and have received non-guideline treatment: Be careful to recognize and appropriately treat ACS in men and women

“Un-Break My Heart”: 2018 NSTEMI Updates

Dr. Tarlan Hedayati – Cook County, Chicago

  • Not all elevated troponin equals ACS
    • PE, dissection, myocarditis, pericarditis
    • History and clinical context are extremely important
  • Some NSTEMIs will have complete vessel occlusion (~25% of the time)
    • These patients are more likely to have higher troponins
  • Main risk factors for ACS: HTN, DM, Hypercholesterolemia (including HDL<40), Family Hx, Tobacco use
    • Others risk factors: Cocaine abuse, HIV/AIDS, ESRD, SLE, RA, stress, exogenous testosterone
  • Clopidogrel (Plavix: pro-drug, needs activation) vs. ticagrelor (Brilinta: works immediately)
    • PLATO trial
      • Lower risk of MACE with Brilinta
      • No difference in bleeding complications between two groups
    • Lovenox vs Heparin
      • No major differences in outcomes
      • Consider using Heparin if patient will be going for upcoming catheterization
  • Three options of NSTEMI management
    • Ischemic guided (conservative management)
      • Wait, trend troponins and serial EKG
      • Better for low risk patients
    • Immediate invasive (Cath ASAP, should be within 1-2 hours)
      • Patients with: refractory angina, recurrent angina, sustained Vtach/Vfib, or those who are clinically or hemodynamically unstable
    • Routine invasive (cath within 24-72 hours)
      • Early (cath within 24 hours)
        • Patients with dynamic EKG changes, new ST depressions or rising troponins
      • Late/delayed (within 72 hours)
        • Patients with DM, CKD/ESRD, LVEF < 40%, CABG/PCI within last 6 months, patients who are post recent MI with chest pain
      • TIMACS study
        • Benefit with early cath only seen with high risk patients

The Crashing Kid

Dr. Mimi Lu – University of Maryland

  • There are 1 million adults with congenital heart defects.
  • 60% of congenital defects are missed on prenatal ultrasounds
  • Clinical findings of pediatric patients with congenital heart defects:
    • Central cyanosis, diastolic murmurs, delayed or difference pulses
    • Hepatomegaly is more common physical exam finding in pediatric patients with CHF (more common than lower extremity edema which is typically seen in adults)
    • Grunting = BAD in children
  • Cyanosis, poor feeding and/or tachypnea in first 7-14 days
    • Think sepsis, sepsis, sepsis (most common cause)
    • But also consider if this is a ductal dependent lesion
      • Typically present within the first 2 weeks of life
      • Hyperoxia test – check ABG on RA à apply 100% FiO2 for 10-15 min à recheck ABG
        • If PaO2 > 150mmHg = Lung problem
        • If PaO2 < 150mmHg = Cardiac problem
      • Quick and dirty hyperoxia test
        • Apply supplemental O2
        • If sats increase at least 5-10% = think Lung problem
        • If sats remain the same = think Cardiac problem
    • Workup
      • EKG – look for hypertrophy, abnormal axis, arrhythmias
      • CXR – look for cardiomegaly or pulmonary edema
        • It can be difficult to appreciate cardiomegaly in neonates (because of thymus, etc.)
        • Get a lateral film and use the anterior tracheal line to help determine if cardiomegaly
          • line parallel to anterior tracheal wall inferiorly to diaphragm – should NOT intersect heart; should NOT be pushed back to “hit” spine above diaphragm
      • Labs
        • BNP literature is weak, but can be considered
    • Initial Management of the Congenital Heart Disease pediatric patient
      • IV fluids – 10cc/kg
      • Maintain SpO2 80-85%
      • Prostaglandin (PGE-1) if considering ductal dependent lesion
        • Dose is 0.1mcg/kg/hr
        • Works within 10-15 minutes
        • Side effects: apnea, hypotension, fever
        • Historically most pts receiving PGE-1 are intubated however recent data supports watch and wait to see how the patients respond, but have RSI equipment ready
          • If transferring the patient to another facility after starting PGE-1 you should secure airway to avoid pt becoming apneic en route
      • Inotropes if shock (did not get into detail on which to use)
      • Furosemide if pulmonary edema (1mg/kg/dose)
      • Make sure to check blood sugar
      • Correct acidosis – early bicarb!
      • Optimize ionized calcium 

Diuretics in Acute Heart Failure: The Dark Side of the Force?

Dr. Peter Pang – Indianapolis EMS

  • Treatment of heart failure has not changed much over the past 40 years
    • Only additions are use of inotropes and nesiritide (recombinant BNP)
  • Patient outcomes have only slightly improved over past 40 years
    • Current data:
      • 75% = 5 yr mortality for patients admitted for CHF
      • 22% = 30 day rehospitalization rate of patients admitted for CHF
      • 8% = 30 day mortality for patients admitted for CHF
  • DOSE trial (2011)
    • No difference in patient outcomes using bolus vs. infusion of Lasix
    • Doubling (2-2.5x) the dose of patients home dose of Lasix ( continuing patients home dose) was associated with better symptom improvement and increased weight change at 72 hours. However there was no difference in mortality, hospital readmission, or ED visit. And there was increased risk of worsening renal failure with the higher dose.
  • Best practice appears to be doubling the oral dose of Lasix. You achieve better sx improvement and better urine output.  You may get a bump in the Creatine but this doesn’t seem to be worrisome as the patients do well.
  • Prospective Cohort Study ~1300 pts.  Loops that were given within 60 mins of arrival have less in Hosp mortality then delayed therapy. This study is suggestive that early therapy may benefit and is at least safe. Will need more studies to duplicate this finding.
  • The addition of captopril to combat the RAA system does not have sufficient evidence out at this time to recommend it.

The Evidence For and Against Epinephrine in CPR

Dr. Corey Slovis – Vanderbilt

  • Epi is a potent alpha and beta agonist
  • The evidence for use of epinephrine in cardiac arrest is weak and incomplete!
    • The case for or against epinephrine in CPR is embarrassingly not based on large randomized double-blind studies
    • Its use stems from a 1968 JAMA study on the use of epi in cardiac arrest of n=15 dogs
    • There is not good objective evidence, in controlled studies, that epinephrine is more effective than placebo
  • “High dose” epinephrine, of more than 1 mg per dose, significantly improves ROSC but not survival to discharge
    • The more you look into the data, the more higher dose of epinephrine looks bad
    • Also, reduced dose of epinephrine appears to offer no benefits
  • Early v. late use of epinephrine in cardiac arrest
    • Use epi as soon as possible (until its effectiveness is proven or disproven)
    • However, if patient is in VF/pVT, data supports waiting for the second shock prior to giving epi (better outcomes when compared to using after the first shock)
  • Try to space your repeat doses of epinephrine by longer intervals, not shorter ones
    • ACLS recommends epinephrine q3-5 min
    • It appears spacing doses out up to 8-10 minutes may be optimal, however this is a violation of current guidelines and no randomized study exists
    • Err on spacing out closer to the q5 minute mark
  • Epi given in shockable rhythms was 1/3 as effective in those patients that did not get epi in a post hoc analysis of a large trial (12% vs 32%)
  • Resuscitation 2018: 2255 pts got low dose epi in out-of-hospital cardiac arrest (0.5 mg).  Reduced dose didn’t cause a difference.
  • There is a London study coming out soon over >8,000 patients comparing epi vs. no epi for OHCA – should provide some useful information for use of epi in cardiac arrest.

Panel Discussion

  • RBBB does not prevent our ability to read an EKG like the LBBB does. You just have to look closely for the st elevation in that it can be more subtle. New RBBB in setting of an acute Mi is a bad prognostic sign.
  • Small group of pts who had pacers were studied with Sgarbossa criteria thus far. Seemed applicable to date. Bigger study by Dr Smith to be out soon that further looks into application of Sgarbossa criteria to paced individuals.
  • No data on continuous drip of epi verses bolus dose epi in cardiac arrest although some centers are doing this.
  • Cardiac Arrest with ROSC + NSTEMI – Should be indication for emergent cath (Also, Arrest with ROSC plus any of following: witnessed arrest with bystander CPR, initial rhythm VF/pVT)

Case of the Week COW #14

Presenting Resident


Chief Complaint

Cardiac arrest

Brief HPI

Hispanic male in his mid 30s who presented to the ED as John Doe after he was found unresponsive in the field with cardiac arrest. Unknown downtime. As per EMS endorsement from bystanders, the patient allegedly had a witnessed syncopal episode followed by seizure-like activity after which he became unresponsive. No bystander CPR. EMS arrived at the scene and found him pulseless, CPR started. On ALS arrival patient found to be in PEA. CPR, intubated, epi x 2, bicarb then ROSC achieved. Initial rhythm in ED was sinus tach on monitor. After 5 min in ED patient became bradycardic and went into PEA, compressions started, received epi x 1 w ROSC. Pt then went into wide complex tachycardia on monitor – SVT vs Vtach – pt was cardioverted 200J and given Amiodarone 150mg. Post cardioversion, rhythm changed to afib v aflutter. EKG was obtained after 10 min (below).

Pertinent PE and Vitals

On arrival: BP 81/50; P113; SpO2 95% ambubag 100% FiO2; Temp 37.0; BS 136

Gen: Unresponsive, intubated, occasional myoclonic jerks
HEENT: 2 cm hematoma right occiput, pupils constricted 1-2 mm b/l and non-reactive CV: tachycardic, s1/s2, no murmurs
Resp: Assisted breathing, good air entry b/l
Abd: Soft, NT
Neuro: GCS 3, has occasional myoclonic jerks

On admission: BP 153/83; P153; SpO2 98% on vent 100% FiO2

Pertinent Labs

ABG done on patient arrival = 6.80/86/253/14; Na+ 133; K+ 4.4, Ca++ 1.04; Glu 246, Lac 8.8, BE -10.2 These were the only labs available at the time of admission.

Pertinent Imaging/EKG

Case d/w Cardio fellow who came to evaluate pt at bedside, decision made to transfer pt directly to cath lab. EKG was repeated after 5 minutes prior to patient being transferred, which is shown below.

Working Diagnosis at time of Disposition

Cardiac Arrest
STEMI – possible LMCA, LAD or Triple vessel dx

ED & Hospital Course

Interventional cardiologist advised immediate transfer to cath lab for diagnostic cath (did not want to wait for CT Head). Cath showed normal coronaries with LVEF 75%.

Patient transferred to the CCU post cath. He was noted to have no brainstem reflexes off sedation. CT Head showed findings c/w anoxic encephalopathy, no bleed. Neuro was consulted who stated patient’s exams and further diagnostic studies were significant for loss of all cortical and brain stem function, consistent with brain death. Patient was pronounced on Day 10 (delay with identifying patient and determining NOK).

Pearls & Takeaways

Is ST-Segment Elevation in Lead aVR Getting Too Much Respect?


ECG reading is all about pattern recognition. And this particular pattern of ST-Elevation in aVR with diffuse ST Depression is a very important ECG pattern that you must be able to recognize. But what’s probably more important than being able to recognize the pattern, is understanding what it represents. There appears to be a common misconception that the ST-Elevation in aVR always represents “STEMI”, or acute transmural (full- thickness) ischemia. If this were the case the patient would most likely be dead or at the very least in profound cardiogenic shock. The key to understanding what this pattern represents lies in understanding that the ST-Elevation in aVR is reciprocal to the diffuse ST-Depression – and that this diffuse ST-Depression represents global subendocardial ischemia. So the real question that you must answer is: What is causing the global subendocardial ischemia?

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

Worrisome Diagnoses:

  • –  Thoracic Aortic Dissection
  • –  Massive Pulmonary Embolism
  • –  Massive Gastro Intestinal Hemorrhage

Non-Worrisome Diagnoses:

  • –  Left Bundle Branch Block (LBBB)
  • –  Left Ventricular Hypertrophy (LVH) with Strain Pattern
  • –  Severe Atrial Tachydysrhythmias (i.e. SVT)

It is critical to realize that more often than not the cause is global myocardial strain from a Non-ACS etiology! (profound sepsis, tachycardia, anemia, hypoxemia, etc). In our patient above it may have been because of the SVT he was in during the code in addition to being in Afib w/ RVR at the time of the ECG. It is also very important to understand that in these Non-ACS settings, you can see this pattern with or without underlying coronary artery disease.

But of course it could be ACS. And if it is, then you are dealing with Left Main, Proximal LAD, or even multi-vessel plaque instability. But keep in mind that even if it is ACS you are still dealing with subendocardial and not transmural ischemia.

Take Home Points

    1. STE in aVR Should be Concerning IF you have a patient with:
      1. Worrisome/Concerning Symptoms (Cardiopulmonary Symptoms) AND…
      2. ST-Segment Depression in Several Other Leads

    2. 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

    3. Patients with ACS due to LMCA Blockage, Triple Vessel Disease, or Proximal LAD Blockage will look “sick” due to global cardiac ischemia. This narrows the number of patients we would consider activating the cath lab for with STE in aVR.

    4. The key to ECG reading is pattern recognition. The pattern of ST-Elevation of at least 1mm in lead aVR + diffuse ST-Depression with a maximal depression vector towards leads II & V5 is a pattern you must know. It represents global subendocardial ischemia.

    5. When you see this pattern you should divide the differential for the diffuse subendocardial ischemia into two main categories: ACS vs Non-ACS. Do not automatically assume that it is ACS. I have seen this mistake made many times as ACS becomes the focus, at the expense of appropriate resuscitation addressing the underlying cause. It is very important to keep in mind that the etiology is far more likely to be Non-ACS than ACS!

    6. The key to determining the etiology is through history, physical exam, clinical picture, laboratory data, Echo, and vigilant monitoring and frequent reassessment. If you have identified and addressed potentially reversible causes of the ischemia, and the ECG pattern persists then you are dealing with ACS until proven otherwise.

    7. Refrain from using dual-antiplatelet therapy in these patients as there is a high likelihood they will require CABG.

    8. Remember that if this ECG pattern does represent ACS, the ST-Elevation in aVR is not the result of direct injury (or transmural ischemia) and that the ST-Elevation in aVR is reciprocal to the diffuse ST-Depression. Therefore these ACS cases do not represent a clear “STEMI”. However, while there is not great data to guide the timing of cath for these patients, I would advocate going to the cath lab with a much stronger sense of urgency than for other “NSTEMIs”. The reasoning is that ACS is a very dynamic process and without the advantage of optimal medical therapy (a second platelet inhibitor should be withheld) there is a higher chance of the culprit vessel suddenly occluding and evolving to transmural ischemia. If this happens in the Proximal LAD, Left Main, or in the setting of Multi-vessel involvement the myocardial territory in jeopardy is so large that there is a good chance the patient will arrest and die before any reperfusion can be established! If your patient looks sick or has persistent chest pain, they should be going to the cath lab ASAP.

    9. With diffuse subendocardial ischemia, you may not see any wall motion abnormality. Global function can even be normal, although it may be globally depressed as well. A normal bedside echo does not help in:
      1. differentiating the cause of the STE in aVR
      2. ruling out ACS


Pediatric Pneumonia

 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.

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 


 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


+ 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


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


Ceftriaxone 50 mg/kg Q24hrs

Consider Vancomycin for seriously ill patients

*Refer to AAP guideline on management of pediatric pneumonia below


  • 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