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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.

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

UMEM Emergency Cardiology Symposium PEARLS

View the recorded lectures here: https://livestream.com/UMEmergencyMed/EMCard2018


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:

https://pdfs.semanticscholar.org/f80b/9983005179f4718bb1326963c722d4f80e58.pdf


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

Traficante

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

PE:
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?

Introduction

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

References: http://hqmeded-ecg.blogspot.com/2018/02/st-elevation-in-avr-with-diffuse-st.html

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.

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

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.

Pediatric Pearls – Bronchiolitis

Pathophysiology
  • Disorder that is commonly caused by a viral lower respiratory tract infection in infants
  • Characterized by acute inflammation, edema and necrosis of epithelial cells lining small airways and increased mucus production

  • Etiology
    • Coronavirus
    • Influenza
    • Rhino virus
    • Adenovirus
    • Parainfluenza virus
    • RSV (respiratory syncytial virus) – MOST COMMON!
  • Incidence – December-March
      • Most infections occur within first 2 years of life
      • About 40% experience lower respiratory infection during initial infection
      • RSV doesn’t grant permanent or long-term immunity – RE-INFECTION COMMON
      • The risk of significant viral or bacterial lower respiratory tract infection or pneumonia in an infant is low
  • Transmission
    • Direct contact with secretions
    • Young children shed virus for >2 weeks
    • 30-70% of household contacts become ill
  • Natural history
    • Begins with URI – Rhinorrhea, congestion, cough
    • Progresses to LRI in 2-6 days – Airway obstruction (tachypnea, wheezing, respiratory distress)
    • Variable and dynamic course
    • Lasts 2-4 weeks

Case

7-month-old male presents to the emergency room with his parents due to cough, runny nose, congestion and SOB that started 3 days ago.

VS: RR – 65, HR – 140, Temp – 99.1°F, O2 sat – 93% on RA


History
  • Typical Presentation of Bronchiolitis
    • Viral URI and cough with signs of lower respiratory tract infection
      • Work of breathing – grunting, nasal flaring, intercostal/subcostal retractions
      • Tachypnea
      • Wheeze
      • Coarse rales

Physical Exam
  • TIPS for a better exam
    • Upper airway obstruction can contribute to work of breathing
    • Suctioning and positioning may decrease the work of breathing and improve the quality of your examination
    • Counting respiratory rate over the course of 1 min is more accurate than shorter observations
  • Assess mental status, respiratory rate, work of breathing, oxygen status, listen to breath sounds, and assess hydration status


Diagnosis
  • DIAGNOSIS IS CLINICAL – NO LABS OR RADIOLOGICIAL STUDIES ARE NEEDED
    • When to consider CXR – if child has had >2 days of fever, an asymmetric chest exam, does not demonstrate improvement or has an unusually high O2 need
    • Diagnostic testing may be considered if:
      • Need cohorting – this is why we get testing for those we admit
      • Uncertain clinical diagnosis
      • Age <2 months
      • To assess for influenza – also needed this for those we admit

Management

Classify patient as mild, moderate, or severe based on the above physical exam

Mild Moderate Severe
1. Consider suction bulb

2. Discharge

1. Suction bulb

2. No bronchodilators

3. Discharge or admit

1. Suction bulb or wall

2. No bronchodilators

3. If no improvement consider starting high flow NC

4. Admit

  • Rehydration
    • IVF – moderately or severely dehydrated, secretions are thick and difficult to mobilize or severe respiratory distress
    • PO feeds – mildly to moderately dehydrated and can tolerate PO
  • Considerations for severely ill patients
    • Consider ONE TIME albuterol MDI trial if:
      • Severe respiratory distress OR
      • Increased risk for asthma
        • >12 months old, wheeze and once of the following
          • personal history of atopy or recurrent wheezing
          • strong family history of atopy or asthma
        • if responds to albuterol then consider switching to asthma pathway
      • Consider HFNC for significant hypoxia OR severe respiratory distress not improving with rigorous supportive care

 

Discharge criteria Admission criteria
–       Oxygen saturation >90%

–       Awake

–       Adequate oral intake

–       Mild/moderate work of breathing

–       Reliable caretaker

–       Able to obtain follow up care

–       MDI/spacer teaching if response to albuterol

–       Admit if discharge criteria not met:

o   Inpatient: Requires 02 or progression expected

o   OBS: Mild disease with expected LOS < 24 hours

o   ICU: Apnea, severe distress; Requires HFNC / CPAP / intubation

–       Infants with these risk factors present early in the illness have higher risk of progression:

o   Gestational age < 34 weeks

o   Respiratory rate ≥ 70

o   Age < 3 months

Additional Notes
  • Differentiate infants with probable viral bronchiolitis from those with other disorders
  • The above management points to do take into consideration patients with significant medical history such as congenital heart disease, anatomic airway defects, neuromuscular disease, immunodeficiency, chronic lung disease – ADMIT, HIGH RISK!
  • The physical exam will vary from minute to minute depending on child’s position, level of alertness, response to treatment – CONSTANTLY RE-EVALUATE!
  • If patient presents within the first couple of days, they may worsen and need admission at a later point – PARENT EDUCATION IS KEY!
    • Viral illness, treated by hydration and suction
    • Signs of respiratory distress
    • How to suction
    • When to suction
    • Frequent feeds and watch hydration status
    • Cough may last 2-4 weeks, do not use OTC cough and cold medications
    • Avoid tobacco smoke
  • NOT RECOMMENDED!
    • Albuterol – Wheezing is due to the airways being clogged with debris not bronchospasm
    • Racemic epinephrine
    • Corticosteroids
    • Chest physiotherapy
    • Montelukast
    • Antibiotics
    • Hypertonic Saline
    • Routine testing
    • Chest X-rays

References

  1. http://pediatrics.aappublications.org/content/134/5/e1474
  2. http://www.chop.edu/clinical-pathway/bronchiolitis-emergent-evaluation-clinical-pathway
  3. http://www.cochrane.org/CD001266/ARI_bronchodilators-for-bronchiolitis-for-infants-with-first-time-wheezing
  4. http://www.seattlechildrens.org/healthcare-professionals/gateway/pathways/

Special thanks to Dr. Hima Khamar, MD PGY-2 for her contribution to this month’s Pediatric Pearls!

Varicella in Pregnancy

Varicella-zoster virus

Varicella (chickenpox) is a highly contagious disease caused by primary infection with varicella-zoster virus (VZV)2 and may cause maternal mortality or serious morbidity

> Reactivation of latent infection, usually many years after the primary infection, may result in herpes zoster (shingles), a painful vesicular eruption in the distribution of sensory nerve roots2

> Both varicella (chickenpox) and zoster (shingles) are notifiable diseases. Notification must be made to the Communicable Disease Control Branch of SA Health as soon as possible and at least within three days of suspicion of diagnosis, by telephone or post.


Route of transmission

> Infection with chickenpox is transmitted through airborne / respiratory droplets and direct contact with vesicle fluid


Incubation period

> 10 to 21 days (may be up to 35 days in contacts given high titre zoster immunoglobulin, ZIG)


 Period of infectivity

> 48 hours before the onset of rash until crusting of all lesions (usually day 6 of rash)

> Infectious period may be prolonged in people with impaired immunity


Infection Control

> Non-immune staff should not care for the woman / baby infected with chickenpox

> Varicella (and herpes zoster) vesicles contain large numbers of virus particles. Ensure appropriate transmission based (standard, contact and airborne) precautions including:

> A negative pressure room with door shut (chickenpox and disseminated shingles)

> Immune staff in attendance

> Gloves, gown

> All dressing materials should be treated as medical waste

> Chickenpox and disseminated shingles use standard, contact and airborne precautions

> Localized shingles use contact precautions (only immune staff in attendance, single room, gloves, gown)

> In herpes zoster (shingles), transmission of infection usually requires contact with vesicle fluid; however, there is also evidence of respiratory spread. Localized shingles requires standard and contact precautions (not airborne precautions)


Susceptibility to varicella

> Women and babies susceptible to infection with VZV (may be severe or life-threatening) include:

> No history of varicella (chickenpox or shingles)

> Seronegative for varicella antibodies (VZV-IgG negative)

> No documented evidence of varicella vaccination 


Significant Exposure

> For the purpose of infection control and prophylaxis, significant exposure of a susceptible woman who is pregnant to varicella includes:

> Living in the same household as a person with active varicella or herpes zoster

OR

> Direct face to face contact with a person with varicella or herpes zoster for at least 5 minutes

OR

> Being in the same room for at least 1 hour

> Chickenpox cases are infectious from 2 days before rash until lesions crusted


Management of maternal exposure to varicella-zoster virus

History of previous chickenpox

> No action required

No or uncertain history of chickenpox

> Obtain serology for antibody status (VZV-IgG) (if practicable)

> ZIG if required should be given within 96 hours. Testing should only be done if ZIG would still be able to be given, if required, within this window


Within 96 hours from exposure

> Zoster immunoglobulin (ZIG) should be given to all seronegative women within 96 hours (see adult dose under ZIG dosage below)

> However there may be some limited effect out to as late as 10 days post exposure

> Advise to seek medical care immediately if chickenpox develops


More than 96 hours following exposure

> Oral aciclovir or valaciclovir (see dosage below) should be considered for women:

> In the second half of pregnancy

> With a history of an underlying lung disease

> Who are immuno-compromised

> Who are smokers

Note: Advise women to seek medical care immediately if chickenpox develops


Management of varicella-zoster in pregnancy

Less than 24 hours since appearance of rash

> Oral aciclovir 800 mg 5 times a day for 7 days OR oral valaciclovir 1 g three times a day for 7 days]

> Monitor at home

More than 24 hours since onset of rash

> No oral aciclovir / valaciclovir and monitor at home if:

> No underlying lung disease

> Not immunocompromised

> Non-smoker

> Monitor in hospital if any of the above risk factors

> Offer appropriate fetal medicine counselling


Complications

> Advise to seek medical attention for the following complications:

> Respiratory symptoms

> Haemorrhagic rash or bleeding

> New pocks developing after 6 days

> Persistent fever

> 6 days

> Neurological symptoms

> Give aciclovir 10 mg / kg every 8 hours for 7 to 10 days (IV followed by oral [see dosage below]) and administer supportive therapy

Consider caesarean section if:

> Signs of significant fetal compromise

> Evidence of maternal respiratory failure exacerbated by advanced


Risk of fetal varicella syndrome (FVS) after maternal VZV

Timing of maternal infection:

>Less than 12 weeks gestation-  0.55%

>12-28 weeks gestation- 1.4%

>More than 28 weeks gestation- No cases of FVS reported


Refer to maternal fetal specialist for prenatal diagnosis and counselling

> Detailed fetal ultrasound for anomalies is recommended at least five weeks after primary infection

> Repeat ultrasounds until delivery. If abnormal may consider fetal MRI

> VZV fetal serology is unhelpful

> Amniocentesis not routinely advised if ultrasound normal, because risks of FVS low but negative VZV PCR may be reassuring


Management of infants exposed to maternal varicella zoster

Maternal chickenpox > 7 days before delivery

> No zoster immunoglobulin (ZIG) required

> No isolation required

> Encourage breastfeeding

> No other interventions even if baby has chickenpox at or very soon after birth unless preterm < 28 weeks gestation or low birth weight < 1,000 g > Very preterm infants (≤ 28 weeks gestation) born with chickenpox should receive intravenous aciclovir 20 mg / kg / dose every 8 hours as a slow infusion (1-2 hours)

 

Thank you to Christine DeFranco PGY-4 EM Resident for this review of VZV in pregnancy!