Tag Archives: Pediatrics

Conference Lectures 1/2020

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Obstetrics and Gynecology Emergencies – Dr. Marques

Normal Vaginal Delivery Key Steps

  • Support the perineum to prevent tearing with delivery of the anterior shoulder
  • Upon delivery of the anterior shoulder, provide upward pressure to deliver the newborn
  • Pull only gentle traction when delivering the placenta, to avoid uterine inversion

Post-Partum Hemorrhage

  • Palpate the uterus to feel for inversion or retained products
  • Provide tone by providing suprapubic pressure with an external hand and uterine pressure with an intravaginal hand
  • Oxytocin can be given IM or IV to treat uterine atony

Shoulder Dystocia

  • Leg hyperflexion and abduction at the hips along with suprapubic pressure (McRobert’s Maneuver) can be done if the anterior shoulder cannot be delivered

Breech Delivery

  • This happens in 3-4% of all deliveries
  • Do not pull traction at any time, as this can lead to entrapment in a cervix that is not dilated
  • A pressure against the popliteal fossa can help flex the leg and deliver each leg

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Oral Boards: Sepsis Due to Spontaneous Bacterial Peritonitis – Hugh, Shoff, MD

  • The CMS Core Measures (SEP-1) provide quality measures for providers to follow in sepsis
  • Severe Sepsis is defined as Lactate >2 or organ dysfunction
  • Septic Shock is defined as severe sepsis with hypoperfusion despite fluid resuscitation or lactate>4
  • Within 3 hours of presentation, obtain a lactate, blood cultures prior to broad spectrum antibiotics, and 30cc/kg fluid resuscitation
  • Within 6 hours, lactate must be repeated if >2

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CCU Follow-Up – Phil Giddings, MD

Myocardial bridging- coronary arteries travel deep into myocardium as opposed to laying upon the muscle

The vessels are occluded but when there is demand ischemia it can look like a STEMI

Myocardial bridging is fairly common in the general population, but usually isn’t symptomatic or pathologic.

If it is symptomatic- you could do Ca2+ channel blockers, beta blockers, and even myotomy or CABG if you’re feeling wild.

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Urology Review- Isaac Shaw, MD

Priapism-

  • Normal tumescence- veins constrict so the corpus cavernosum engorges because blood flows in
  • Ischemic= low flow, less venous outflow, rigid, painful
  • Nonsichemic= high flow, more arterial inflow, half rigid
  • (Distinguish w/ a blood gas)
  • Treatment
  • anesthetize by blocking the dorsal nerve of the penis (2 & 10 o’clock) w/o epi
  • then aspirate at 3 or 9 o’clock from the corpus cavernosum
  • Use a phenylephrine stick from Room 9, 100mcg-500mcg Q1-5min

Fournier’s Gangrene

  • polymicrobial
  • assoc w/ DM
  • 22-40% mortality
  • empiric + clindamycin (clinda first because it’s addressing the toxins)

consult surgery before imaging

Paraphimosis

  • foreskin trapped proximal to glans so the tip can get ischemic
  • Treatment: manually reduce, dextrose, lube, may have to incise the dorsal foreskin

Phimosis

  • foreskin can’t be retracted over the glans 2/2 inflammation
  • Treatment in ED: topical steroids with urology follow-up

Urinary Retention

  • often have hesitancy, nocturia, frequency, urgency
  • >200cc PVR
  • d/c w/ Foley à Uro will keep that in for 2 weeks prior to void trial

Renal Stones

  • remember that 10-15% don’t have hematuria
  • CT w/o contrast is still the standard for diagnosis, but some emergent literature exists that US alone is sufficient in young, healthy patients
  • if <5mm, 90% pass; but if >8mm, 5% pass
  • admit for intractable vomiting, pain, urinary extravasation, infection & obstruction

Balanitis

  • Candida on the glans
  • Associated with DM or uncircumcised

Torsion

  • twisted around the spermatic cord
  • if actively torsed, you will NOT have a cremasteric reflex
  • ultrasound 88-100% sensitive because they can torse and untorse
  • consult before imaging

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Breaking Bad News– Frank Woggon, PhD

  • insensitive truth telling can have similar effects as lying
  • goals include gathering info, provide info, support patient, strategy for care
  • keep it simple, no jargon, talk slow, repeat PRN, use neutral language, be honest, allow emotions, consider cultural differences
  • “compassion is the willingness to let yourself be affected by the life and suffering of others”

SPIKES

  • Setting- privacy, sit down, eye contact, turn off pager
  • Perception- don’t combat denial at first, interpret first
  • Invitation- ask how much they want to know first
  • Knowledge- “what I’m about to say is not good,” be direct but not blunt, use their language
  • Empathize- ok to validate the emotions, silence is ok
  • Strategy & Summary- what comes next

GRIEV_ING Protocol

  • Gather the family
  • Resources- call for support
  • Identify yourself & staff, those in the room
  • Educate the family about what happened
  • Verify that the patient died by using that word
  • SPACE- silence is ok, let them have their gut reaction
  • Inquire whether they have questions
  • Nuts & bolts- organ donation, funeral arrangements, personal belongings, etc.
  • Give contact info for f/u questions

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STEMI Mimicks – Frank Shary, MD

OMI= occlusive MI

  • V2 & V3 2mm elev = STEMI; Everywhere else 1mm
  • Wellens: biphasic T wave, they recently had an OMI, symptoms may have gotten somewhat better by the time of the EKG, they need a cath
    • Deep T Wellens- deep and wide
  • LV aneurysm- deep Q wave w/ biphasic T wave, static
  • Sgarbossa criteria- OMI in the setting of LBBB and/or paced rhythm
    • look at vector of QRS and vector of ST segment
    • concordant elevation or depression greater than 1mm
    • discordant greater than 5mm
  • Hyperacute T waves- early into the ischemia, before ST elevation, cath soon because you have potential to save more myocardium, large area under the curve especially in proportion to the QRS complex
    • L circumflex is the vessel most likely to be silent
  • aVR- if it’s the only lead elevated and everywhere else is diffusely depressed, you might have diffuse subendocardial ischemia
    • could be bad triple vessel disease

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Managing the Bleeding Patient Without Blood Products – Chase, PharmD

There are 6 Jehovah’s Witness churches in Louisville

  • Plasma Derivatives are technically not Blood products… so whether or not a patient wants that is up to the individual
  • albumin, clotting factors, PCC, Immunoglobulins (including Rhogam and vaccines)
  • equine Ig and Crofab could also be iffy
  • ECMO, cardiopulmonary bypass, dialysis are allowed generally

Source Control

  • bone wax/putty- use in NES and long bone fx, high infection rate though
  • oxidized regenerated cellulose- ex. Surgicell, promotes rebuilding of proteins to heal & achieve hemostasis, like a mesh
  • gelatin matrix- ex. Floseal, more like a gel
  • there is a powder too but it’s $$$ and causes microemboli so don’t use
  • thombin- apply w/ 4×4’s
  • TXA- derivative of lysine THIS IS NOT A PLASMA DERIVATIVE SO THEY SHOULD BE OK WITH IT, 1g over 10min à another 1g over 8-10 hours
  • have a lower threshold to give TXA since there is a decrease in mortality, even if you wouldn’t have given TXA to a non-Jehovah’s witness

Usable Therapies:

  • Cell Saver
    • blood is collected, washed, centrifuged, returned to patient
    • example indications: AAA, TKA, THA, cardiac surgeries
  • Vitamin K
  • PCC- most efficacious
    • 4 factor is better than 3 factor, but if you try to give 3 factor and then just add Factor VII a la carte, more thromboembolic events
  • FFP- prep time is longer, tonzo volume
  • Adnexanet Alpha- new antidote for rivaroxaban and apixaban, we don’t have that
  • Novo7- directly activates Factor VIII, black box warning for thromboembolic events, no difference in mortality but there was a reduction in transfusions
  • Dabigatran reversal- idarucizumab, dialysis, charcoal
  • Antiplatelet reversal- ASA and Plavix are irreversible, but ticagrelor is reversible
    • DDAVP- indicated for DI, von Willebrand disease, uremic bleeding (renal failure), nocturnal enuresis
    • 0.4mcg/kg over 10min

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Pediatric Environmental Emergencies- Dr. Said

Drowning

  • fresh or salt water doesn’t matter, you’re ruining your surfactant
  • if you are anoxic you get brain damage in 4-6min, irreversible
  • cold temp is only helpful if it happens really quickly
  • outcomes depend on initial resuscitation, degree of pulmonary damage, time submerged
  • poor prognosis- coma, apnea, submersion >9min
  • can try vapotherm for positive pressure, albuterol can treat bronchospasm
  • steroids don’t help
  • goal warming 32C
  • if asymptomatic, obs for 8 hours! Oy vey
  • admit if prolonged submersion, respiratory or neuro symptoms, abnormal CXR

Electrical Injuries

  • lightning strikes carry 30% mortality risk, it causes asystole
  • doesn’t cause renal failure or burns/compartment syndrome
  • thicker tissue less damaged
  • tissue between entry and exit wounds could be more damaged interiorly than it appears
  • AC worse than DC because AC at low voltage causes tetany so you’re holding on longer
  • we use DC for defib, countershock, pacing but you get thrown off
  • oral electrical injury – monitor for progressive edema
  • could have delayed bleeding from labial artery

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EMTALA- Melissa Platt, MD

  • in court, all are case-by-case
  • we have to provide a medical screening exam and treat and stabilize an emergency medical condition
  • transferring physician assumes the risk if the patient crumps en route to accepting hospital

Limping toddler

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Nothing crazy here, just some EM bread and butter. I’ve had a couple of these at Children’s, and each time (with two different attendings), I’ve been told that the adult EM residents seem to overlook this, or not have any idea that it’s a thing, which is kind of embarrassing.

The patient is a 22-month-old male who presents with difficulty walking. Mom states that the child was walking fine until this morning. Since then, he has not been wanting to put weight on his right leg. Mom does not recall any injury. The child is otherwise well, no signs/symptoms of illness, and he has no medical problems.

On exam, the child will not put weight on his right leg when forced to stand. The extremity is well perfused, and there are no signs of trauma. He has no point tenderness, so it is not clear where he is hurting, but does seem to have pain when the foot is grasped and rotated internally and externally.

Discussion: In the toddler with a possible lower extremity injury, it may be difficult to localize where the child is having pain. If there is a question, the entire extremity should be imaged (though you should try to localize the problem area if possible). In this case, we suspected a toddler’s fracture, so a 3 view tib/fib was obtained. This is an important learning point: many times, the fracture line will only be visible on the oblique view, so it is necessary to get 3 views. In this patient, the xray was negative (as were other films of the leg). We diagnosed the child with a toddler’s fracture, placed him in a short leg splint with stirrups, and discharged him with orthopedics follow up.

A toddler’s fracture is a spiral fracture of the distal tibia which usually occurs by the same mechanism as an adult spraining an ankle. Sometimes it is a clinical diagnosis, not visible on X-ray. There is debate in the literature about immobilization in this case; some say it is necessary, some say it’s not. The culture at Norton Children’s seems to be immobilization. Regardless, the child should follow up in 1 week for definitive diagnosis, either with repeat plain films, or possibly MRI or bone scan. If there is a visible fracture on plain films in the ER, the child should be placed in a short leg splint with knee immobilizer and follow up with orthopedics in 72 hours.

It’s my asthma

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An interesting case from the Pediatric ED:

A mid teen female with a reported two year history of mild persistent asthma, presented with asthma exacerbation. She presented to an outside ED with two days of cough, wheezing and shortness of air which acutely worsened three hours prior to arrival. Upon initial presentation there, the patient was reported to be in moderate respiratory distress with increased work of  breathing, tachypnea, and an O2 saturation in the 80%’s on room air. Lung auscultation revealed diminished breath sounds on the left with faint wheezing at left and right apices. She was placed on 3L nasal cannula with normalization of her O2 sats. She received an hour long course of albuterol and dose of Solu-Medrol, with moderate improvement in her symptoms. She subsequently received a chest X-ray which was concerning for a large left sided bleb/cyst with mediastinal shift to the right. Patient was subsequently transferred to us.

Further HPI and PMHx revealed that patient was diagnosed with allergic rhinitis in her early teens and diagnosed with asthma two years ago. She reported no history of ever being evaluated with a chest x-ray prior to current presentation. Over the course of the past two years she had been prescribed 3 courses of steroids and used albuterol approximately 2x per week PRN. Patient denied any other medical problems or smoking history.

A CT scan of the chest confirmed presence of large left sided pulmonary cyst.

Patient was admitted and followed by both pediatric pulmonology and surgery. Inpatient workup included PFT’s and alpha-1-anti-trypsin (negative). She was eventually diagnosed with idiopathic giant bullous emphysema, otherwise known as vanishing lung syndrome. She later underwent bullectomy with improvement of her symptoms.

Bullous emphysema is often seen as a complication of COPD in adults, but rarely diagnosed in children with few case reports in the literature. Giant bullae can present asymptomatically, with progressive dyspnea, hypoxia or hemoptysis. Giant bullous emphysema is classified as occupying more than one third of a hemi-thorax, and is often initially mistaken as a pneumothorax on initial chest radiograph. As disease progresses, enlargement of the bullae fill with air and loss of lung function results as fibrous membranous surface of the bullae result in poor gas exchange. Bullae are at high risk for rupture and tension pneumothorax should be suspected if a patient develops worsening respiratory distress.

The learning point I took from this case is to step back and re-evaluate a patient’s presentation when things do not exactly add up, as in this case a teen with worsening asthma not responding to conventional treatment and little pcp workup in the past. This point is particularly exemplified in the pediatric population where we often see several low acuity cases each shift, often drifting into “auto pilot” mode, employing little critical thinking. Don’t forget, rare or more complex pathology may actually be responsible for the patients symptoms.

Neonatal Airway

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I’m currently on peds anesthesia and behind on reading Annals, which worked out in my favor.  I was looking through the February 2017 issue and there’s an EM:RAP commentary about the neonatal airway.  So I figured I would give you all the highlights from that article.

  • At birth, an oxygen level of 60% is normal.  There’s a nice chart showing the oxygen saturation and how it increases after birth.
    • 1 minute- 60-65%
    • 2 minutes- 65-70%
    • 3 minutes 70-75%
    • 4 minutes 75-80%
    • 5 minutes 80-85%
    • 10 minutes 85-95%
  • Remember when doing BVM on a neonate, not to press too hard on their face.  Their nose is not stiff and they are obligate nose breathers.  So don’t close off their airway by pressing too hard.
  • Don’t worry about using a paralytic in the neonate.  You can either time passing the tube through the cords or just push it through.
  • Tube size/Blade size
    • Normally in peds we use the formula (age in yrs/4) + 4
    • For neonates, they suggest the 0-1-2-3 rule: Use a 0 straight blade in a 1-2 kg newborn with a 3.0 mm uncuffed tube
    • They also recommend resting your pinky on the cric to provide your own cric pressure since neonatal airways can be very anterior
  • How far to pass the tube
    • 1 kg neonate- 7 cm
    • 2 kg neonate- 8 cm
    • 3 kg neonate- 9 cm

Baffling Neurology Pathology Strikes Again…

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…forever seeking the unsuspecting emergency medicine intern.

A previously healthy teenage male presented to the emergency department via emergency medical services with the complaint of weakness, sensory changes, and increasing difficulty of breathing.  Family reported the patient went outside to mow the grass approximately 10 hours prior to presentation.  After two passes in the yard with a push mower, the patient had sudden onset occipital headache, fatigue, parasthesias described as tingling in both lower extremities, and generalized weakness.  Patient reported these symptoms to parents and laid down to rest.  After an hour long nap, patient was encouraged to take a shower to see if symptoms improved.  During shower, patient became weaker, had one episode of vomiting and was no longer able to stand on legs.  The patient’s father reports patient was able to make small movements but unable to ambulate or push against resistance.  Emergency medical services were contacted at this point, however, after assessment, the symptoms were deemed related to anxiety and patient was not transported.  Over the course of the day, the patient’s weakness progressed to the complete inability to move legs, followed by inability to move arms, with continued paresthesias in all extremities. After patient demonstrated worsening respiratory distress, EMS was called again.  Parents denied history of asthma, prior wheeze, fevers, recent illness or trauma, recent travel or drug abuse.  Family reports patient went camping one week prior but denies tick exposure.

On exam, the patient had significant respiratory distress with poor air movement and was only able to answer questions with one word responses secondary to respiratory distress.  Neurological exam revealed 0/5 strength in all extremities, areflexic biceps and brachioradialis reflexes, areflexic patellar and Achilles reflexes, and downward going Babinski bilaterally.  Sensation to light touch was intact but diminished in all extremities.  There were no rashes or lesions on skin exam.

Initial differential included but was not limited to:

  • Organophosphate toxicity – although patient self-decontaminated earlier in the afternoon and did not have diarrhea, salivation, or lacrimation
  • Guillain Barre – although acute time course without report of recent URI or GI syndromes
  • Tick paralysis – although no known exposure or lesions identified on skin or scalp
  • Transverse Myletitis – although no personal history of recent illness, no family history of multiple sclerosis or other autoimmune disease
  • Spinal Cord Infarct – although patient and family deny trauma, recent surgery, or history of coagulation disorder
  • Conversion Disorder – although no anxiety or other psychiatric history

As concern for bronchospasm, the patient was given IM epinephrine and started on a hour long albuterol while history was being obtained.  Bedside ultrasound demonstrated grossly normal myocardial contractility without effusion, normal lung sliding, and a collapsible IVC.  Chest x-ray was unrevealing. After lack of improvement with initial intervention, second dose of epinephrine and fluid bolus begun.  Intial VBG demonstrated hypercapnea and patient was started on BiPAP.  Within minutes, patient showed improvement in respiratory status and appeared more comfortable.  Initial CMP, CBC, CRP, and ESR were unrevealing.   Lumbar puncture was performed after head CT revealed only an arachnoid cyst.  CSF studies demonstrated mildly elevated segs, mildly elevated glucose, negative gram stain and normal protein.  Foley catheter was placed after patient complained of bladder fullness (confirmed by bladder scan) with inability to void.  Neurology and Neurosurgery were consulted from the emergency department, who requested urgent MRI on admission.  Patient was admitted to PICU with ED diagnoses of acute flaccid paralysis and acute neuromuscular respiratory failure.   After admission, MRI was obtained and demonstrated (drum roll please) ischemia vs. infarct from approximately C2-T5 with predominance in the anterior horns.

The literature review of non-traumatic spinal cord infarction is as rare as the pathology itself in the pediatric population and predominately consists of case studies.  Causes typically include but are not limited to hypotension, vascular injury, thrombus, embolus or compression.  Considering many of these etiologies are already scarce in the pediatric population, finding cause proves to be a difficult task.   Pain in neck, back or legs, weakness, tingling, and numbness are commonly described symptoms in pediatric case studies and were present in the patient that presented to us.   Prognosis studies have been performed on primarily adult patients; one such study demonstrated >40% recovery in ambulation amongst the 37 patients that left the hospital wheelchair bound through aggressive physical therapy and rehabilitation programs.[1]   Poor prognostic factors include female sex, advanced age, severity of symptoms, and lack of improvement within 24 hours after infarction.[2]   It appears as though outcomes are primarily dependent on access to physical therapy and supportive care including psychological treatment.   Workup and treatment recommendations if suspicious of atraumatic spinal cord infarct include obtaining an MRI for definitive diagnosis, followed by autoimmune, hypercoagulable, and infectious evaluations. Treatment in the emergency department is mostly supportive and includes addressing any contributory conditions and the management of respiratory concerns.[3]

On follow up, I found that the patient required intubation after exhibiting respiratory decompensation after the MRI was obtained.  Initial treatment with high-dose steroids and IVIG were discontinued when infectious and immunologic work-ups were unrevealing.  The hospital course was complicated by neurogenic bowel and bladder, neuropathic pain, anxiety, intermittent autonomic instability with hypotension, pneumonia and a urinary tract infection.  The patient required tracheostomy and percutaneous gastric tube placement during his hospital stay.  The patient continued to exhibit flaccid paralysis of all four extremities and ventilator dependence on discharge to acute rehabilitation.

Per my own investigation, I was relieved to find that Frazier has both success managing these cases and many unique resources that may positively impact this patient’s course (if you are curious here is some video evidence https://www.youtube.com/watch?v=8o_w174rI3s).  Needless to say, my differential for motor weakness, particularly in pediatrics, will forever be haunted by this case.

 

[1] Robertson CE, Brown RD Jr, Wijdicks EF, et al. Recovery after spinal cord infarcts: long-term outcome in 115 patients.  Neurology. 2012; 78: 114–121.

[2]Cheshire WP, Santos CC, Massey EW, Howard JF Jr .  Spinal cord infarction: etiology and outcome.  Neurology. 1996;47(2):321.

[3] Spencer, Sandra P. MD; Brock, Timothy D. MD; Matthews, Rebecca R. MD; Stevens, Wendy K. MD.  Three Unique Presentations of Atraumatic Spinal Cord Infarction in the Pediatric Emergency Department Pediatric Emergency Care. 30(5):354-357, May 2014.

Facial Edema

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This was an interesting presentation from a Peds shift.

15 y/o AAM with no significant medical history who presents with facial swelling. Patient noticed significant swelling to the left side of his face upon awakening in the morning. The swelling involved his entire left cheek, inferior lid of his left eye, upper lip and part of his right cheek. The patient denies any pain, tongue swelling, voice change, difficulty breathing or swallowing, fevers, recent ill symptoms (cough, congestion, vomiting, diarrhea), dysuria, hematuria, rectal bleeding, sore throat, ear complaints. He denies any new exposures including new medications, new soaps, detergents, animal exposures, environmental exposures, recent travel, insect bites.

PMH:none. PShx: had 4 wisdom teeth removal 1 month prior (finished antibiotics), no other recent surgeries or dental work. No EtOH, drugs. No current medications. No known allergies.

Vitals: 97.8, 90, 110/70, 18, 99 % on RA

Exam: HEENT- moderate swelling of the left buccal area, inferior lid of the left eye, upper lip. Mild swelling to the right buccal area. No erythema or palpable areas of fluctuance. No swelling surrounding the right eye. No conjunctival injection. No erythema within the ears, TMs normal. No mastoid tenderness. No lingual swelling, no erythema within the mouth or palpable areas of fluctuance. No signs of infection from previously removed wisdom teeth. No posterior oropharyngeal swelling or uvular deviation. No lymphadenopathy.

Heart- normal. Lungs- clear, no wheezing or stridor. Abdomen- normal. No CVA tenderness.

Treatment started with Benadryl for possible allergic reaction. Basic labs obtained and urine for possible nephrotic syndrome. WBC-17, otherwise normal. Urine with 200 protein, no RBC or WBC- nephrology consulted and recommended repeat POC labs as outpatient and follow-up in clinic, but no intervention at this time. Patient had mild improvement with Benadryl. Discharged home with Benadryl and steroids.

Patient re-presents 6 hours later (just came back for my shift the next day)

Facial swelling has worsened. Now involves bilateral buccal areas, bilateral lower eyelids and upper lip. No fevers, no difficulty breathing, no dysphagia. Patient had taken 1 repeat dose of Benadryl at home and had not started steroids yet. No other changes in HPI except patient mentions some bleeding from the inside of his upper lip. Upon exam, patient has some bleeding and purulent drainage from the gumline of his left central incisor. No palpable fluctuance, but able to express drainage with pressure to upper lip.

Labs obtained: WBC 17, CRP 1.6, ESR 41. UA- minimal protein. All other labs unremarkable. CT face with contrast obtained showing left central incisor periapical abscess with cortical erosion as well as extensive cellulitis of the midface. Also some concern for phlegmon within the paranasal sinus. ENT, OMFS, and finally pediatric dentistry consulted. Patient admitted for IV clindamycin, Unasyn for cellulitis and dentistry consult for possible root canal versus tooth extraction.

Bottom line: Odontogenic infections can cause orofacial infections and rarely but more importantly peripharyngeal space infections as well as jaw osteomyelitis. If concerned about deep facial infection, CT face is warranted. Treatment includes draining of pus from abscesses (either through I&D or needle aspiration) and culture as well as antibiotic therapy. Common regimens include a penicillin plus metronidazole, clindamycin, augmentin, or unasyn depending on disposition. Dentistry should be involved whether through consult or outpatient follow-up for root canal versus tooth extraction.

“Knot in my Throat”

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Recently had a patient while on a Peds EM shift with an interesting presentation. Not sure how many of us have had this case, so this should serve as a helpful reminder for management.

 

15yF with no significant PMHx presenting with a “knot in my throat.” Per patient report, she woke up the morning of presenting to the ED with a palpable knot. Unsure how long it had been present, but she happened to notice it that morning. Denies hx of fever, chills, changes in energy level, palpitations, shortness of breath, odonyphagia, dysphagia, changes in menstrual cycle, recent URI, changes in hair or nail quality nor irradiation to the neck. Mother was really concerned because 2 people in her family had either thyroid carcinoma or nodules removed. One was diagnosed in her 20s.

 

On physical exam:
General: AFVSS
HEENT: NCAT, EOMI, PERRLA, no evidence of exophthalmos
Neck: Supple, Trachea midline, R anterio-lateral neck mass – approx 1.5cm x 2cm. Firm to palpation and located anatomically near superior pole of R thyroid lobe. Moves with swallowing. No associated erythema or fluctuance. No cervical lymphadenopathy.
Lungs: CTAB,
CVS: RRR, no m/r/g. Pulses equal. No peripheral edema.

 

So you get labs: CBC,TSH, Free T4
All within normal limits

 

Beside USN revealed what appeared to a multicystic nodule in the R thyroid lobe where the patient’s palpable mass was located. So let’s get a formal USN.

 

Formal reveals that patient actually has multiple nodules. The largest being approx 3cm x 2cm x 2cm, and read as a colloid nodule.

Let’s recap:

We have a 15yF presenting with an asymptomatic thyroid nodule, who is euthyroid based on hx, physical exam, and labs. What’s next??

 

1. Discuss the case with a Pediatric Endocrinologist. Nothing acutely needs to be done; however, she should have outpatient followup with an endocrinologist to help keep surveillance of her nodules.

 

2. Add testing for Thyroid specific antibodies to rule out Hashimoto’s thyroiditis and other autoimmune inflammatory processes. Consider adding Anti thyroid peroxidase (Anti-TPO) and Anti-Thyroglobulin antibodies.

 

3. Ultrasound simply characterizes the mass that we’ve palpated. Yes, the nodule was read as a “colloid nodule,” which is fairly common regarding thyroid nodules; however, this needs to be confirmed by Cytopathology. Nuclear studies can be done but not recommended in isolation. Such studies can be helpful when determining whether a nodule is “hot” or “cold.” Simply speaking, is there increased thyroid uptake or not. CT and MRI imaging is not cost effective in the initial stages of evaluation.

 

4. Lastly, the best way to determine whether a nodule is benign or malignant, you have to sample the source via Fine Needle Aspiration Biopsy (FNAB). Await the cytopathology results and return to #1.

Approach to the Fussy Infant

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There are many different types of challenging patients that we all dread seeing when they pop up on the board. Whether the patient’s chief complaint is headache, back pain, or pregnant female with abdominal pain. Another very challenging patient presentation is the crying infant. The differential when evaluating a crying infant is broad. In this post I will include a list of differential diagnosis to consider based on organ system and then a patient I had that presented in this way.

CNS- Meningitis, epidural hematoma, subdural hematoma, hydrocephalus

HEENT- Skull fracture (accidental or non- accidental trauma), ocular foreign body, corneal abrasion, otitis media, nasal foreign body.

Cardiovascular- SVT, myocarditis, congestive heart failure

Pulmonary- foreign body in airway, bronchiolitis, pneumonia

GI- Malrotation/volvulus, pyloric stenosis, appendicitis, gastro-esophageal reflux, intussusceptions, anal fissure

GU- Testicular torsion, UTI, incarcerated inguinal hernia, soap vaginitis, phimosis, paraphimosis

Musculoskeletal- Fracture, septic arthritis, dislocation, hair tourniquet

My patient presented as a 1 month old male with his Spanish speaking Hispanic parents. Mom stated that he has been crying consistently for the past 4 days. She does not remember a specific time when the crying started but she states it has not improved.

Mom is breastfeeding the baby and denies any dietary changes. The baby was full term and mom had no complications with the pregnancy. Patient up to date on all vaccinations. Baby has been afebrile and per mom has not been lethargic. Baby is still feeding well and gaining weight appropriately and mom denies any projectile vomiting after feeds, denies any change in stooling, and notes good urine output. Baby lives at home with mom and dad and I have no red flags to suspect non-accidental trauma.

On exam he is overall well-appearing and does not appear to be in any type of distress: crying but consolable. He appeared to be healthy. He was interactive, tracking me with his eye movements, and did not appear to be meningitic or lethargic. Heart and lungs were unremarkable and abdomen was soft, nontender and non distended. GU exam (make sure you do this) was unremarkable. Baby was moving all extremities while lying on the oversized adult bed in the middle of the hallway and on inital exam did not appear to have any outward bruising or signs of trauma.

Upon removing the patient’s socks I noticed something odd on his second toe of his right foot. Just distal to his PIP joint he had a circumferential red line. As soon as I started to examine that toe his crying increased substantially. On further examination he had a hair tourniquet that had eroded its way all the way down to the bone of the middle phalanx of the second toe.

At this point the baby was still in the hallway and we took him to Room 9 to attempt to try any remove it. I am sure you can imagine how awesome this was on a crying kicking 1 month old. We attempted to unwind the hair but ultimately were unable to do so as it was just to deep into the tissue. I called Kosair and the patient was transferred and I do not yet follow up on the final outcome.

This just re-enforces the importance of a good head to ahem, toe physical exam on patient’s that are not straight forward. Mom had been with the infant 24/7 for the past 4 days and had not noticed this; not to mention who knows when the hair tourniquet actually started. Just something to keep in mind and hopefully this helps next time you all have to examine a crying baby.

 

5 day old with “seizures”

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Recently I had an interesting case at Kosair of a 5 day old male who presented with jerking movements of his arms and legs. He always had “twitches,” which the parents had been assured were normal for a newborn, but the episodes were getting worse. Since the day before, he had had several episodes where both arms would shake and seize up and his legs would curl up under him, lasting about a minute. He is sleepy afterwards, but mom thinks he’s always pretty drowsy. Overall it was unclear if what mom was describing was a seizure. Even her helpful phone videos were not 100% clear, but we proceeded as though they were real seizures. In a 5 day old.

Mom had 3 UTIs during pregnancy, and her labor was likely precipitated by an episode of pyelo. She and baby were briefly tachy during labor but pain meds helped, and the SVD was otherwise uneventful. No STIs, GBS negative.

Baby was afebrile, normal VS. Appeared drowsy until the usual screeching during the cath urine, so overall, well-appearing baby. He did twitch sometimes, but he never had one of the spells while he was in the ER.

Differential diagnosis for neonatal seizures? Bacterial meningitis, viral encephalitis, intraventricular hemorrhage, SAH, SDH, hypoxia, hypoglycemia, hyponatremia, inborn errors of metabolism, etc.

Our patient wasn’t actively seizing and labs were WNL.

Subdural hematoma (from birth) and meningitis were high on our differential. We went ahead and gave antibiotics but got a CT head before proceeding with the LP, and I’m glad we did.  It turned out that he did have a subdural hematoma, likely parturitional. We elected to forego the LP, since he was afebrile and we already had a reasonable explanation for his symptoms. Neurosurgery wanted a repeat CT in 6 hours (surprise!), and neuro wanted an EEG (surprise!). He never had any of the episodes in the ER, so neuro didn’t start any antiepileptic medications.  He was admitted to the PICU.

He never had any seizure activity on EEG, so neuro diagnosed him with neonatal myoclonus. Hypocoagulability workup by hematology was negative. Neurosurgery will follow up in 3 weeks as an outpatient. He was discharged after 4 days.

The other interesting discussion on this patient involved whether or not to involve CPS, since this type of injury could be seen with a shaken baby syndrome. The parents were very appropriate and there was no sign of any other trauma and negative skeletal survey, so CPS was not contacted. The overall assumption was that the SDH was secondary to birth trauma rather than any non-accidental trauma.

It’s a rash, I think??

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Meet little Jimmy. No, this isn’t his real name. Jimmy has been relatively healthy for his 17 months of life. Eating and drinking has been great. No recent diarrhea or vomiting; however, Mom became worried when she noticed a rash. Yes, I said it….a rash. Initially it began as a few bumps that started to spread along his arms and legs. Sounds a little strange, eh? Here’s more background…

Let’s go back about 6 weeks prior to me seeing little Jimmy in the pediatric ED. He was prescribed Amoxicillin for otitis media. It’s a standard medication that’s given; however, he began to develop this rash around that time. No other associated symptoms though. Not pruritic and did not seem to bother him. Intermittent tactile fevers, but Mom did not associate the rash and fever. Thinking the antibiotic was the culprit, she saw the Pediatrician who said to stop taking the medication [Amoxicillin]. Pediatrician thought this could be a drug reaction.. Little Jimmy was given some OraPred and Benadryl. Told to follow up in the next several days…

Rash begins to improve over the next week or so; however, a week prior to coming to the ED, the rash returns. This time, the rash is all over the body: face, arms, legs, torso, diaper area. Continues to have the intermittent tactile fevers but the child overall seems relatively well. By this time, Mom is fed up. She’s seen the Pediatrician multiple times and has not gotten a definite answer about the rash’s etiology.

Oh yea… Mom is on a deadline too. She’s moving across the country in 1 week and NEEDS an answer.
What’s that? Describe the rash.. oh yea!

Vitals: Stable, Afebrile
General: Child is mildly fussy but consolable on examination.

Skin: Diffuse, erythematous rash along bilateral upper and lower extremities.
Scattered vesicles with occasional patches throughout extremities, most noted to the legs.
Diaper area appears erythematous, however no vesicles.
When looking at the face, a peri-oral rash is present consisting of crusted, opened vesicles. Crusting is a yellowish-golden color.

Yellowish-golden crust ….. Impetigo?
Vesicular rash along extremties with patches ….. Eczema herpeticum?
Periorificial rash affecting both mouth and diaper areae ….. Acrodermatitis enterohepathica?

Impetigo:
Causative agent(s): Staphylococci and Streptococci
Appearance: Erythematous sores that can rupture, releasing fluid or pus, and covered by a yellowish-golden crust
Treatment: Topical cream vs Systemic antibiotic treatment [Penicillins, 1st gen Cephalosporins, Doxycycline, Clindamycine]

Eczema herpeticum:
Causative agent (s): Herpes Simplex Virus, both 1 and 2, Coxsackievirus.
Appearance: Vesicles superimposed on healing atopic dermatitis
Commonly associated s/s: Fever, Lymphadenopathy
Treatment: Supportive Care, Antiviral therapy [Acyclovir]

Acrodermatitis enterohepathica
Appearance: Erythematous plaques that can evolve into vesicles and bullae
Pathophysiology: Autosomal recessive; Zinc deficiency
Treatment: Supportive care, Zinc supplementation

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We see many rashes in the ED. Not all of them are “Viral Exanthems.” All of the mentioned “rashes” can be treated. It’s helpful to get exposure to these dermatological presentations, and it’s even more helpful to know that you can’t apply steroid cream to everything hoping that it solves the problem.

So what happened to little Jimmy?
He received IV fluids and a dose of Acyclovir. Leading diagnosis: Eczema herpeticum

What about his Zinc level? What about the wound culture?
…..Stay tuned!

NRP

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This is just a little reference card that goes along with what we learned on our last Peds Sim. I found that the Neonatal Resuscitation Program obviously has a different algorithm than with most of our resuscitation algorithms.  Take a look at it, memorize it or just forget about it. Ether way here is a quick reference for everyone.

 

 

NRP

Interesting case from the weekend – thoughts?

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Hey guys, I was hoping to get your input on an interesting case I had at Kosair over the weekend.

16 yo F (6 ft, 150 lb…so basically an adult) with a PMH of depression, self injury, and prior suicide attempt presents after ingesting citalopram 40 mg x 90 pills (her prescription, just filled 2 days ago) and concerta 10 mg x 8-9 pills (her brother’s). Patient had been at a party the night before, admitted to EtOH.  Parents found out about the party the morning of admission and they had a big fight, took away car keys, etc. Patient decides to retaliate by swallowing pills, doesn’t tell anyone. Parents find her altered about 10:30, at Kosair at 11:40. Best guess is ingestion occurred sometime around 9-9:30am.  Had one seizure at home per family, and one en route per EMS. Generalized, tonic-clonic, brief.

Initial exam shows a drowsy but arousable patient. Answers orientation questions x3. Initial vitals show HR 147, BP 135/70, RR 25, 93% on some oxygen (can’t remember if NC or nonrebreather). Patient denies CP, palpitations, SOB, abd pain, N/V, weakness/numbness.  4mm, PERRL. MAE equally. Old self injury scars noted on wrists bilaterally. Exam otherwise unremarkable.

We start IVs, get her on a non-rebreather, get IV fluids going. Agree that charcoal seems like a bad idea with her mental status and seizures. Mom has shown up, and as we’re getting some additional history from her, respiratory is placing EKG leads. I’ve talked to poison control. Then, about 20 minutes into her stay, she seizes again. We bag her through the seizure, again generalized tonic-clonic, and just as we’re pushing 2 mg of IV Ativan she comes out of it. She appears post-ictal, but is maintaining her airway. We load her with Keppra, and as I glance at the monitor behind the attending’s head, I notice that her rhythm has changed and she looks like she’s got a wide QRS. We confirm she still has good pulses, still out of it mentally, and since she’s already connected to the EKG leads we grab one (time stamp 12:04):

EKG 1

By the time we get this printed off (!!!!) she appears to have spontaneously converted back to sinus on the monitor. But woah, holy wide QRS/long QT batman! As the attending and I are pouring over the first EKG we get another one immediately (time stamp 12:08):

EKG 2

Thankfully, the QRS appears to have normalized, but we’ve still got a loooong QT, one of the things poison control definitely told us to look out for. Having seen a few similar ingestions at University, I suggest it’s time for bicarb. The attending wants to confirm and we quickly call poison control back, they agree and suggest starting a bicarb gtt, with pH goal of 7.45-7.55.  Now we look back at the monitor and she’s throwing a ton of PVCs, captured here on EKG #3 (time stamp 12:12):

EKG 3

At this point, we opt to push an amp of bicarb while we’re waiting for pharmacy to tube up the bicarb gtt. I have to say, we see it start to work pretty darn quickly. The PVCs slow down, and her rate really starts to head back towards normal. We get an iStat (shot me down when I suggested one earlier), and a few minutes after we’ve pushed the bicarb we get an initial pH of 7.15, pCO2 of 51.5, HCO3 of 18, BE -11, and AG of 21. Electrolytes were WNL. By this time we also know her pregnancy is negative, and her serum tox is negative, no acetaminophen/salicylates on board.  At this point, we talk about intubation as the patient’s mental status is still waxing/waning and she’s breathing shallowly with brief periods of apnea, almost like an opiate overdose. Attending wants to hold off, so I go off to call the PICU resident…and end up having to hang up the conversation halfway through when he changes his mind.

So we intubate her (finally got a peds tube…in an adult), the bicarb gtt comes up from pharmacy, they’re cleaning the PICU bed her, the last EKG looks 1000x better, and all’s well that ends well (time stamp 13:08):

EKG 6

So I’m curious to see what your all’s suggestions/thoughts are on this case.  Looking back at that first EKG, how would you classify it? We’ve got a wide complex, monomorphic tachycardia that to me looks like sustained V tach (with a pulse).  The long QT doesn’t surprise me, but this rhythm does as you’d typically you’d worry about it devolving into Torsades, but that’s not what this is.

Looking back, things I would have done differently:  get a temperature sooner/order a total CK (serotonin syndrome could have been a factor and we don’t have a recorded temp until she’d almost 2 hours into her stay, no one ever ordered a CK), intubate sooner, loading her with keppra when she hit the door after 2 witnessed seizures, maybe could have prevented the 3rd?

Also, if you’re curious, I found this “Toxicology Conundrum” on LITFL that specifically discusses citalopram overdose. Has some good info, citalopram is definitely one of the more potent SSRIs, and QT prolongation is dose dependent and can be seen after ingesting >600 mg (this chick took 3.6 GRAMS). Seizures are also fairly rare, only seen in 2-3% of cases.

RLQ pain and N/V

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15 yr male with hx of hemophilia presenting with 1 day hx of progressively worsening RLQ pain, decreased PO, nausea, and vomiting. Described RLQ as a “small swelling’ that continued to span across the R abdomen as the day progressed. Denies dysuria, hematuria, hematemesis, hematochezia, constipation, diarrhea, abd trauma, or testicular pain. No previous abdominal surgeries. Physical exam is significant for RUQ and RLQ tenderness, no obvious swelling, no ecchymosis seen. He definitely appeared ill and uncomfortable. A&Ox4.

So already…what are we considering?  Appendicitis …. Peritoneal bleed … bowel obstruction …maybe a few others (UTI, Kidney Stones, STI).

While waiting on CT Abd/Pelvis imaging to be completed, patient is found to be anemic with a Hgb of 8. Normal WBCs. Platelets: 300. Elevated PTT: 83. Normal PT/INR. Urinalysis…. negative. IV Fluids have already been started. Zofran for his continued nausea.

Here’s a significant snapshot of the CT

Abdomen

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It spanned from the R kidney down to the bladder. Actively extravasating. Hydronephrosis due to the hematoma compressing the R ureter. It compressed the R renal vasculature as well, and anteriorly displaced the R kidney.

Contacted Hematology, where we decided to administer FEIBA. (He usually takes Alphanate MWF, but had not taken any medicine on day of presentation. Plus, the hospital did not have his particular medication, so we needed to find an alternative.) He was admitted to the Hematology service. They have plans of contacting Surgery for any possible interventions once his Hgb stabilized.

Repeat CBC (after patient had been admitted) showed that the Hgb had fallen to 6.0.

Diagnosis: 15 year old male with non-traumatic R retro peritoneal hematoma. Source currently unknown.