On behalf of the Fellows form the Division of Emergency Medicine at Cincinnati Children’s I am delighted to bring you a new series that will highlight what we are learning during our ongoing didactic conferences. The main goal of the Pediatric Emergency Digest series will be to provide concise teaching points to reinforce in-person learning and to further the conversation. As always, feedback is welcome.

Pediatric Vomiting

with Katie Edmunds, MD

Case #1

3mo who presented with vomiting for 1 week. Parents felt she was vomiting her whole feed She was spitting up with every bottle. On exam, she was well-appearing and well-hydrated. She had a reassuring growth curve.

Diagnosis: Reflux “Happy Spitter”

  • Reflux in infants is due to the immaturity of the lower esophageal sphincter
  • The peak age of 3-4 months
  • Diagnosis is based on History and physical exam and the absence of “red flags”
    • Poor weight gain: normal weight gain is 30g/day or 5-7oz per week
    • Bloody diarrhea can be a sign of Milk Protein intolerance (1-2% of babies)


  • Reassurance and patient education regarding signs of dehydration and weight gain.
  • Reflux precautions:
    • Keep baby upright for 20-30min following feeds
  • Avoid overfeeding
  • Safe sleep: ALWAYS sleep on the back with nothing in the crib with them.
  • Medications are not generally indicated for the “happy spitter”
    • Zantac/PPI evidence is poor to prevent reflux
    • Some evidence for use in the fussy infant with reflux
    • Side effects include increased risk of long bone fractures



  • 0.15mg/kg IV or PO
  • 2mg 8-15kg
  • 4mg 15-30kg
  • 8mg >30kg

Side Effects

  • 2013 study showed it does not mask more severe pathology.
  • Prolonged QTc, however, you do not need to screen with EKG for a one time dose in the ED

Youngest Age to dose:

  • Lexicom: 1 mo of age
  • Local Guideline: 2 mo of age

Case 2

6 week old presents from PMD with dehydration. He was seen earlier in an ED with “forceful vomiting.” Having weight loss and periods of apnea.

Diagnosis: Pyloric Stenosis “Hungry vomiters”

  • Due to hypertrophy of the pyloric muscle leading to obstruction between the stomach and the small intestine.
  • 2-3/1000 infants and more commonly seen first-born males (⅓)
  • Usually present between 3-6 weeks of age with a benign exam and a history of “forceful” or “projectile” vomiting.
  • The classic lab abnormality is hypochloremic, hypokalemic, metabolic alkalosis. Less commonly seen due to timely diagnosis of pyloric stenosis.
  • Ultrasound for diagnosis
  • Place PIV
  • Volume resuscitation
  • Obtain lab electrolytes and correct abnormalities
    • Patients with HCO3 >30 or Cl <100 have more difficult time coming off of Anesthesia
    • Apnea or hypoventilation in severe pyloric stenosis is due to respiratory compensation of the metabolic alkalosis.
  • Early Pediatric surgery consultation!

Case 3

7 month old who is vomiting 7-8x/day. Initially, non-bloody and non-bilious emesis but now is green in color. Seen at OSH ED yesterday where he received IV fluid bolus, Zofran and discharged. He is coming back as he still is vomiting at home. Vital signs are stable but he does have a distended abdomen on exam.

Diagnosis: Malrotation and Volvulus

  • Due to malrotation of the intestinal tract during fetal growth. This leads to the the cecum improperly positioning itself in the right upper quadrant and fixing itself to the lateral abdominal wall. This predisposes to twisting of intestines around the mesentery leading to volvulus
  • Epidemiology – 1/500 births
  • 40% seen in the first 1, up to 60% in the first month, and 90% within the first year.
  • Presents similarly to a small bowel obstruction
    • Bilious vomiting
    • Dehydration
  • X-ray abdomen may be helpful but can be normal
  • Do NOT assume there is no pathology if there is a normal x-ray
  • Upper Gastrointestinal tract series is imaging of choice.
    • Fluoroscopic series of images monitoring the movement of swallowed barium through the stomach and the duodenum.. Should be very strongly considered on all infants with true bilious emesis.
    • CT scans are not commonly indicated
  • Management
    • IV fluid resuscitation
    • Obtain electrolytes
    • Place NG/OG
    • Surgical consultation

Case 4

19mo with vomiting and diarrhea a few days. Was seen at an outside facility and diagnosed with gastroenteritis and discharged home following a PO trial. Now has resolution of diarrhea but is not tolerating any PO and vomiting with every attempt. Is tachycardic and uncomfortable appearing on the exam. Appears to be grabbing at her abdomen.

Diagnosis: Appendicitis

  • Important considerations in the young patient
  • Pre-school children make up 2-9% of appendicitis cases – Under 2yo is rare
  • Studies show that misdiagnosis of appendicitis is near 100% in children younger than 2yo.
  • Children <5yo are more likely to present later and with perforation

Take Home Points

  • Not all vomiting is gastroenteritis
  • The differential diagnosis for pediatric vomiting changes with age of the patient
  • Bilious vomiting in the <1yo needs to be taken seriously.
  • Appendicitis is uncommon in the younger patient but will be missed if we don’t think about it
  • Red Flag findings need further work-up
    • Weight loss
    • Severe fussiness
    • Fevers

Pulmonary Embolus

with Tim Murphy, MD, MBA

“The Great Mimicker”

  • Epidemiology: 63,000 cases per year with a 17% Mortality
  • Signs and Symptoms can be vague with Syncope (19%), fever (13%), altered mental status (10%), and even wheezing (9%).

PESIT trial

  • 17% of patients who had new onset syncope had PE
  • Prevalence in patients admitted for first time syncope was 17%
  • Caveats: only looked at admitted patients
  • Follow up studies showed 0.5-1.5% prevalence of PE in syncope pts in the ED


  • Basic lab evaluation (CBC/BMP/Trop/BNP)
  • CXR and EKG
  • D-dimer vs CT-Pulmonary Angiography

Clinical decision rules

Wells Criteria for PE

  • Determine who was LOW RISK enough of PE to rule out further testing with a d-dimer
  • Now many clinicians use it to predict who is low-risk enough to apply the PERC rule to stop work-up for PE.
  • Only applies to patients suspicious for PE
  • Score
    • Three-tier model
      0-1 (1.3%)
      2-6 (16.2%)
      >6 (37.5%)
    • Two-tier model
      </=4 (12.1%) >/=5 (37.1%)
  • Only validated for patients >18yo

Clinical decision rule pitfalls

  • Failure to consider the diagnosis
  • Overestimate risk: not everyone needs a CT
  • Assuming low risk with no risk factors (50% of pts with PT have minimal risk factors)
  • Applying rules incorrectly


  • Low-risk: Heparin and admit to adult
  • Submassive: PE with any evidence of right heart strain, RV dysfunction on Echo, Dilation on CT, Evidence of pulmonary HTN, Elevated BNP or troponin, RV patterns on EKG (RBBB, S1Q3T3, T-wave inversions in V1-V3)
  • Massive: Sustained hypotension, profound bradycardia or signs of shock, Pulselessness


  • Resuscitation
  • Be judicious with volume (generally no more than 1L due to right heart outflow obstruction from PE)
  • Reverse hypoxia and hypercarbia as it leads to further pulmonary vasoconstriction
  • Start pressors early (norepinephrine is pressor of choice)
  • Thrombolytics
    • Controversial on when thrombolytics are indicated
    • Literature shows mixed results
    • Big picture: Likely no mortality benefit with thrombolytics but some improvement in morbidity
  • Embolectomy
    • Decreased risk of systemic bleeding
    • Very high mortality 27%. Studies are generally on very high-risk population
  • EKOS
    • Pulmonary artery catheter with ultrasound capabilities
    • Thrombolytics at the site of PE with ultrasound waves to help “break apart” clot
    • No studies looking at EKOS vs Systemic thrombolytics vs embolectomy

Take home points

  • Only start down PE path if you are willing to go to the finish (CT-PA)
  • Use Wells and PERC keeping in mind they are validated for >18yo
  • Be judicious with fluids and start pressors (norepinephrine) early
  • Team decision regarding targeted therapy

PEM/PICU Joint Conference

with Rachel Bensmen and Denise Hasson

Case Discussion

Grade school age female with renal tubular acidosis on Poly-Citra who presented initially to the emergency department for difficulty walking, UTI, and psych evaluation.  She had been falling over and crawling around at home the day before but the aunt had also seen her walking normally. She also reported having an increase in urinary frequency and burning.  She was being taken care of by another caregiver due to significant social concerns. There has also been bullying at school.

On her first visit to the ED she had an evaluation by neurology who noted astasia/abasia on their exam (normal motor exam but unable to walk normally), 5/5 strength on extremities, and an abnormal gait on exam.  Urinalysis at that time revealed positive blood but negative RBC’s. Neurology offered admission for these symptoms but aunt felt comfortable with discharge home.  She was discharged home on Bactrim and follow-up

She returned to the emergency department with continued symptoms and at that time had labs and repeat urinalysis that revealed:

  • Cr: 2.19
  • K 1.8,
  • Na 128.
  • VBG: 7.07/25/7.4/-23
  • UA: large blood with minimal RBC

She was admitted to the PICU after nephrology consultation and electrolyte supplementation. Her hospital course revealed non-sustained wide complex beats Labs at the time of the wide complex beats showed a grossly hemolyzed K of 6.2 from 1.8.  She was given Ca continuation of wide complex ectopy but it responded and resolved with sodium bicarbonate bolus. She was in the ICU and improving and on hospital day 3 she developed pain in her hands secondary to hypocalcemia. Her diagnosis was thought to be hypokalemic paralysis secondary to poor medication compliance for her renal tubular acidosis.

Learning Points


  • Weakness
  • Ascending paralysis
  • Can lead to muscle cramps and rhabdomyolysis
    • Secondary to ischemia from inappropriate vasoconstriction to muscles
  • Resp: failure from muscle involvement
  • GI: ileus/emesis
  • Hypokalemic Paralysis:
  • Periodic Paralysis
    • Primary Channelopathy. Autosomal dominant
    • Precipitated by heavy exercise, fasting, or high-carb meals
    • Not due to a total body deficit of potassium
  • Hypokalemia paralysis
    • Due to severe total body deficit secondary to losses.
    • A common cause is Renal Tubular Acidosis as they have no compensatory mechanism

Renal Tubular Acidosis – Courtesy MedComic

The OTHER parts of the UA

  • Specific gravity
    • Normal: 1.010 (isosthenuria)
    • Excessively dilute or concentrated urine can lead to false negative results of other portions of the UA
    • Cells and molecules falsely elevate specific gravity
  • Proteinuria: means albuminuria
    • 1+ = 30-100mg/dl
    • 2+ = 100-1000mg/dl
    • 3+ = >1000mg/dl
  • Glycosuria
    • When Blood glucose is >180mg/dL, it starts to spill out in urine
    • Isolated glycosuria
  • Hematuria
    • >2rbcs/hpf
    • Positive blood without RBC’s is hemoglobinuria or myoglobinuria
  • Casts/Crystals
    • RBC: Glomerulonephritis
    • WBC: Pyelonephritis, Acute interstitial nephritis (ATN)
    • Muddy Brown: ATN

Take Home Points

  • Be more diligent when a patient with a chronic condition presents:
    • Is it related to the progression of the disease or complications of the disease
    • Is this related to the treatment of the disease
    • Is this unrelated process
  • Consider the possibility with a specialist
  • Don’t anchor on the psych diagnosis

Journal Club

with James Gray, MD

Investigators looked at infants <12mo old with the clinical diagnosis of bronchiolitis who were hypoxic (not work of breathing)

Intervention groups infants were randomized to:

  • HFNC at a rate of 2L/kg/min on optiflo system
  • Standard oxygen therapy up to 2L/min

Primary Outcome: Treatment failure as defined by the escalation of care in the standard therapy group (standard oxygen therapy) vs high flow oxygen therapy during the treatment of bronchiolitis.

  • Escalation of care for the standard therapy group was escalation to HFNC.

Methods: Multicenter randomized control trial


  • 12% of HFNC group had escalation of care
  • 23% of Standard Therapy Group had escalation of care to HFNC
  • NNT = 9
    • In other words: We need to treat 9 hypoxic children with HFNC to prevent 1 hypoxic child from needing escalation to…HFNC
  • Secondary outcomes
    • No significant difference in duration of hospital stay, duration of O2 therapy, or duration of ICU stay.


  • Unblinded study: People knew if child was receiving HFNC or standard therapy at the bedside
  • They used HFNC for hypoxia where we generally use it for work of breathing as well
  • Did not stratify based on severity of illness (HFNC group had a higher RR vs Standard group so in theory could have had a more severe population)

This is overall looking at hypoxia treatment with HFNC vs standard oxygen therapy.  We commonly use HFNC for work of breathing. We conclude that using HFNC to treat hypoxia is not cost effective, and overall does not affect LOS, ICU admission or intubation.