1.24.19 Conference Summary

Morbidity & Mortality - Dr. Leah Carter

Case #1

Young female 32 wks pregnant presenting with headache, blurred vision, n/v, abd pain. Severe-range BP consistent. Pre-eclampsia treatment started in the ED. Transferred to L&D. Tracing showing decels with severe fetal bradycardia; patient having painful contractions. Emergently taken to OR for placental abruption, >2L EBL.


Placental Abruption

  • Separation of the placenta from the uterus

  • Leading cause of pathological bleeding in 2nd half of pregnancy

  • Relatively high maternal and fetal mortality

  • Rupture of uterine artery associated with severe hemorrhage

  • How does abruption present?

    • Symptoms:

      • Vaginal bleeding 70-80% cases; those without bleeding have worse prognosis

      • Abdominal pain

    • Clinical findings:

      • Tender, hard uterus

      • High frequency/low amplitude contractions

      • Variable late decels, bradycardia, reduced variability

  • Risk factors: chronic hypertension and preeclampsia, cocaine, tobacco use

  • Abruption on ultrasound

    • 2-25% of abruption can be detected; in acute setting, ultrasound may be normal

    • Findings include: retroplacental hemorrhage, intraplacental anechoic areas, placental thickening >5.5cm, separation and rounding of placental edge

  • Complications: coagulopathy and DIC, fetal/maternal death

  • Workup should include type & screen/cross, coags, DIC labs

  • Treatment: resuscitate! (if needing blood, consider adding cryo to correct for fibrinogen), Rho-Gam if Rh neg, emergent c-section if unstable

Case #2

Young male with sickle cell disease presented for cough, fever. Had low grade fever in ED, workup unremarkable. Thought to have URI, patient discharged home. Returned later that day, now more febrile. Tested positive for influenza A, chest x-ray clear. Received tamiflu and empiric 2g ceftriaxone per hematology and admitted. Hospital course unremarkable



Sickle Cell Disease

  • Epidemiology

    • Sickle cell is the most common inherited disease in U.S.

    • Median survival is 40-45 yrs of age

    • 3x more common than CF with slightly higher medial survival age but has significantly less NIH funding

  • How high risk is fever in sickle cell patients?

    • No great evidence for sickle cell population in general (high risk in asplenic patients)

    • Most mortality related to vaso-occlusive complications

    • Obtain cultures and have low threshold for antibiotics and admission

  • Asplenia + fever

    • Treat similarly to immunocompromised patient

    • Strep pneumoniae is most common pathogen (n.mening, h.flu, ecoli, s.aureus less common)

    • Usually vague presentation — fever, malaise, headache, GI sx, etc.

    • Ceftriaxone is good empiric antibiotic choice (good strep pneumo coverage)

  • Pain control in sickle cell

    • Pain associated with increased vasoconstriction —> Adequate pain control important

    • Skill-based therapy good adjunct to meds

      • Cognitive behavioral therapy proven with RCT

      • Also support groups, massage, hypnosis, accupuncture

Case #3

60s yo patient with alcoholic cirrhosis s/p liver transplant a few years ago, complicated by recurrent ascites requiring frequent paracentesis, presented for abdominal pain/distention and dyspnea. Workup concerning for hepatorenal syndrome, hyperkalemia, marked leukocytosis, thrombocytosis, mild coagulopathy. Received empiric ceftriaxone and treatment for hyperkalemia. Diagnostic paracentesis not consistent with SBP. Initially hemodynamically stable but tachycardic then became hypotensive during ED course. Given fluids and albumin, declined pressors. Antibiotic coverage broadened. Had prolonged stay in ED and ultimately admitted to MICU where he expired after opting for comfort care.


Spontaneous Bacterial Peritonitis

  • Diagnosing SBP (need paracentesis)

    • Absolute PMN > 250 cells/mm3

    —Absolute PMN = total nucleated cells x % neutrophil); correction for RBCs: subtract 1 PMN per 250 RBCs—

  • Indications for a tap?

    • Anyone with new onset grade 2 or 3 ascites, all patients hospitalized for worsening ascites, any complication of cirrhosis (level 1A recommendation)…. so basically everyone with ascites and abdominal pain, fever, etc. (dyspnea alone not an indication)

  • When is albumin indicated?

    • In sicker patients (renal impairment, AMS, bacteremic/septic, positive ascitic cultures)

    • Albumin associated with lower incidence of renal impairment and mortality, though no significant increase in MAP with hypotension

  • SBP vs secondary peritonitis in cirrhosis patients

    • Peritonitis more likely if polymicrobial gram stain/culture, higher elevations in serum wbc and ascitic LDH/protein/ neutrophils, low ascitic glucose, etc, or poor response to standard treatment for SBP

Pediatric Endocrine Emergencies - Dr. Ryan Farrell, Pediatric Endocrinologist

Diabetic ketoacidosis

  • DKA is most common initial presentation of DM, usually under age 5

    • D: (Dextrose) Glucose >200

    • K: Ketonemia: >3 mmol/L or higher

    • A: Acidosis pH <7.3, bicarb <15

  • Clinical features: polyuria, polydipsia, vomiting, dehydration, AMS

  • Principles of DKA management = fluid, electrolytes, insulin, monitoring, post-acidotic transition

  • Fluid Therapy

    • Initial hydration with NS +KCl first 4 hours 10cc/kg 1st hr, 20cc/kg if severe dehydratied

    • Subsequent fluid 0.45% NS + KCl; add dextrose when glucose <300 mg/dL

    • Avoid rapid hydration to prevent cerebral edema (see below)

  • Electrolytes in DKA

    • Serum sodium — total body sodium depleted + hyperglycemia falsely lowers serum sodium

      • Corrected sodium = add 1.6 mEq/L for every 100mg glucose about 100 mg/dL

    • Serum potassium normal to slightly elevated due to shifts, though total body K is low

      • Risk of hypokalemia with glucose and insulin therapy —> give 20-40 mEq/L KCl in fluids

    • Bicarb — only use as absolute last resort, i.e. severe acidemia

    • Phosphate therapy is controversial

  • Insulin

    • Continuous regular insulin infusion 0.1 units/kg/hr; avoid bolus !

    • Monitor closely while on insulin drip (strict I/Os, neuro checks, q1h glucose + pH, q2-3h BMP)

    ***if rapid drop in glucose, do not stop insulin, just give more glucose

  • Cerebral edema in DKA

    • Risk factors: younger children, severe acidemia, new onset, excessive fluid administration, etc

    • Symptoms: headache, AMS, bradycardia most common

    • Tx = decrease IV fluid rate, elevate HOB, mannitol 1 gm/kg IV, or hypertonic saline; hyperventilation not indicated

  • Transition to subcutaneous insulin — ok once ketoacidosis has resolve and patient able to tolerate PO

    • New onset diabetes: glargine and homolog 0.5-1u/kg/day

    • Known diabetics: transition to home doses

Hypoglycemic disorders

  • Associated with neurologic sequelae (brain growth relies heavily on glucose)

  • Normal to have glucose <50 in first 24 hours of life (transition phase); only address if symptomatic; hypoglycemia after the first day is pathologic

  • Symptoms

    • Adrenergic: anxiety, tachycardia, perspiration, pallor

    • Neuroglycopenic: tremor, seizures, unresponsiveness

  • Causes (there are many!!)

    • Infants of diabetic mothers is most common

      • High insulin, low beta hydroxybutyrate, low fatty acids

      • Treatment: glucose infusion (+/- continuous feeds)

  • Persistent hypoglycemia — increased glucose utilization

    • Diagnosis = glucose < 50mg/dl; usually low FFA and beta hydroxybutyrate, insulin is often detectable

    • Tx: diazoxide (suppresses insulin production, resulting in higher glucose levels)

  • Hypopituitarism

    • Cholestatic jaundice and hypoglycemia

    • Tx = GH, cortisol, levothyroxine

  • Ketotic hypoglycemia

    • Usually seen with concurrent illness between age 18 mos to 5 yrs, remits spontaneously by 8-9 yrs of age

    • Check urine ketones during illness

    • Tx = frequent feeds of high carb/protein diet

  • Diagnostic approach for undifferentiated hypoglycemia

    • Age at presentation, risk factors, association with fasting

    • Look for clues on physical exam

    • Differentiate ketotic vs non-ketotic hypoglycemia

  • Treatment

    • If less than 1 yr: 5 cc/kg D10 —> 6-8 mg/kg/min; if older can give 2cc/kg D25 bolus

    • If hyperinsulinemic, give diazoxide, somatostatin analogs

Adrenal emergencies

  • Mineralocorticoids (aldosterone), cortisol, androgens — regulated by HPA axis, negative feedback mechanisms

  • CAH

    • 21-hydroxylase deficiency most common

    • Severe ‘classic’ form can be life-threatening; associated with salt-wasting (1st-2nd week of life)

    • Adrenal insufficiency/crisis (fatigue, obtundation, waning hypotension, can appear septic, salt wasting) + ambiguous genitalia

  • Adrenal insufficiency

    • Primary (involves both aldosterone and cortisol deficiency) vs secondary (only cortisol)

    • Symptoms: fatigue, n/v, anorexia, weight loss, dehydration

  • Adrenal Crisis

    • Treatment:

      • Fluid first!!

        • NS bolus 20cc/kg —> maintenance D5 NS or D5 1/2 NS using 4-2-1 rule

        • Avoid rapid rise in serum Na, check glucose and VBG q1h for at least the first few. hours

      • Stress-dose steroids

        • IV hydrocortisone preferred (both mineralocorticoid and glucocorticoid)

          • Neonate-3yo: 25mg IV initial dose

          • 3-12 yrs: 50 mg

          • >12 yrs: 100mg

      • Treat hypoglycemia. (see above)

      • Treat hyperkalemia — if K > 7 and/or EKG changes — usually Ca + steroids works

        • Calcium chloride 0.1-0.2cc/kg (central access) / gluconate 0.5cc/kg — stop if pt becomes bradycardic

        • Only in peri-arrest situations (especially at an OSH), can consider insulin 0.1 units/kg/hr… but must closely monitor for hypoglycemia and discuss with the nearest PICU

      • Long term therapy: maintenance hydrocortisone, fludricortisone, +/- salt tabs, counsel families on stress dosing when ill or perioperative

Power Half Hour - Dr. Lauren McCafferty

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Case #1: Eczema herpeticum

Young child presented with this pruritic rash. Seen in the ED the day prior for erythematous rash.

  • HSV1 infection

  • Associated with atopic dermatitis 

  • Most commonly affects infants, young children

  • Spread via skin-to-skin contact

  • Symptoms

    • Painful, pruritic, discolored fluid-filled blisters on face/neck

    • High fever, chills, malaise, LAD

  • Clinical diagnosis +/- culture

  • Treatment: antiviral

  • Complications: scarring, herpetic keratitis àblindness, organ failure/

  • Potentially serious —- if concerned, treat immediately!

Case #2: Three-column spinal fracture + ankylosing spondylitis

Middle aged male fell while drinking several days prior to presentation. Developed progressive weakness in upper and lower extremities.


3-column fracture

  • Denis Classification

    • Anterior column = anterior longitudinal ligament, 2/3 vertebral body/discs

      Middle column = posterior 1/3 vertebral body/discs, posterior longitudinal ligament (PLL)

      Posterior column = anything posterior to PLL

  • May be stable if isolated column injury

  • Unstable if two contiguous column injury or 3-column injury

Ankylosing spondylitis

  • Multisystem Inflammatory disorder, primarily joints (SI) and spine 

  • Inflammation may ultimately cause vertebrae to fuse —> ‘bamboo spine’

  • SI/low back pain and stiffness are most common symptoms

  • More common in younger males 

  • HLA-B27 positive

  • Diagnosis: clinical + imaging 

  • Treatment: supportive care (NSAIDs, therapy, etc)


Case #3: Heterotopic pregnancy

Young female prior ectopic presented for lower abdominal cramping and vaginal bleeding for a few days. POCUS nondiagnostic. Transvaginal ultrasound showed heterotopic pregnancy.

  • Heterotopic = extrauterine+ intrauterine pregnancy 

  • Very rare; more commonly seen in pts undergoing assisted reproduction techniques ( in-vitro fertilization), ovulation induction, etc.

  • Extrauterine pregnancies are non-viable with high risk to the mother

  • Management = resuscitate as indicated, call OB!

    • Definitive treatment = salpingectomy (in most cases)

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Case #4: Achilles tendon rupture

Young healthy male slipped on ice and heard/felt a ‘pop’ in ankle with immediate pain over posterior lower leg above heel. Barely able to bear weight, unable to walk. POCUS findings below. MRI obtained at outpatient follow-up.

  • “Loud pop, “ often when exercising

  • Posterior leg/ankle pain, swelling, difficulty plantar flexing

  • Positive Thompson test = inability to plantarflex when calf is squeezed

  • Clinical diagnosis, consider POCUS (edema/hematoma, loss of organized fibers)

  • Management = short leg posterior splint (slight plantar flexion), NWB, ortho follow up +/- non-emergent MRI

    • Surgery is definitive repair

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