Category Archives: Cases

“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.

Cervical seatbelt sign and CTA

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Summary: No CTA for isolated cervical seatbelt sign.

Good blog post.
http://wueverydayebm.blogspot.com/2014/07/does-cervical-seatbelt-sign-mandate.html
Take Home:
CT-angiogram is not necessarily indicated based on the finding of a cervical seatbelt sign alone in the absence of significant hematoma, neurologic symptoms, or other traumatic injuries.

EAST Guideline:
https://www.east.org/education/practice-management-guidelines/blunt-cerebrovascular-injury
What patients are of high enough risk, so that diagnostic evaluation should be pursued for the screening and diagnosis of BCVI?
1. Patients presenting with any neurologic abnormality that is unexplained by a diagnosed injury should be evaluated for BCVI.
2. Blunt trauma patients presenting with epistaxis from a suspected arterial source after trauma should be evaluated for BCVI.
3. Asymptomatic patients with significant blunt head trauma as defined below are at significantly increased risk for BCVI and screening should be considered. Risk factors are as follows:
* Glasgow Coma Scale score ≤8;
* Petrous bone fracture;
* Diffuse axonal injury;
* Cervical spine fracture particularly those with (i) fracture of C1 to C3 and (ii) fracture through the foramen transversarium;
* Cervical spine fracture with subluxation or rotational component; and
* Lefort II or III facial fractures

From EAST Guideline:
An isolated cervical seat belt sign without other risk factors and normal physical examination has failed to be identified as an independent risk factor in two retrospective studies and should not be used as the sole criteria to stratify patients for screening.
References:
https://www.ncbi.nlm.nih.gov/pubmed/12013287
https://www.ncbi.nlm.nih.gov/pubmed/12013287

Alternate Screening Guidelines:

Screening Criteria for BCVI adapted from Biffl et al[10] (with permission)
Screening Criteria for BCVIInjury mechanism

  • Severe cervical hyperextension/rotation or hyperflexion, particularly if associated with
    • Displaced midface or complex mandibular fracture
    • Closed head injury consistent with diffuse axonal injury
  • Near hanging resulting in anoxic brain injury Physical signs
  • Seat belt abrasion or other soft tissue injury of the anterior neck resulting in significant swelling or altered mental status

Fracture in proximity to internal carotid or vertebral artery

  • Basilar skull fracture involving the carotid canal
  • Cervical vertebral body fracture
Denver Modification of Screening Criteria for BCVI adapted from Cothren et al[51] (with permission)
Denver Modification of Screening CriteriaSigns/symptoms of BCVI

  • Arterial hemorrhage
  • Cervical bruit
  • Expanding cervical hematoma
  • Focal neurological deficit
  • Neurologic examination incongruous with CAT scan findings
  • Ischemic stroke on secondary CAT scan

Risk factors for BCVI

  • High-energy transfer mechanism with
    • Lefort II or III fracture
    • Cervical spine fracture patterns: subluxation, fractures extending into the transverse foramen, fractures of C1-C3
    • Basilar skull fracture with carotid canal involvement
    • Diffuse axonal injury with GCS =6
    • Near hanging with anoxic brain injury

Decreased Survival with Intubation During Cardiac Arrest

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Quick Read on something I feel like comes up a lot with our cardiac arrest patients. They don’t typically need intubated, they need good CPR. Bag or put an LMA in and stop at that. While the numbers aren’t astounding, given the differences in such a large amount of patients think these make sense.

http://www.healio.com/cardiology/arrhythmia-disorders/news/online/%7B5396b1a2-0167-4a2d-885c-0e1bc527398e%7D/findings-do-not-support-early-tracheal-intubation-for-in-hospital-cardiac-arrest-in-adults

Top Ten UTI Myths

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Good 5-10 minute read on myths regarding UTI and asymptomatic bacteriuria. Hope you’ll take a look as this is a common problem in many EDs, not just ours with regards to over-diagnosis and over-treatment.
http://www.medscape.com/viewarticle/865175
Ross

Level 1 Rapid Infuser & Autotransfusion

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All,
Couple videos on what was covered today with Level 1 Infuser and Autotransfusion. They’re not bad, definitely get the overall setup at least. With the autotransfusion videos, there are a few small differences in their setup vs ours I think, but overall for your purposes is mostly the same. Hope this helps.
Ross

Level 1 Infuser
https://www.youtube.com/watch?v=9YIROsYE_Yo

Autotransfusion
https://www.youtube.com/watch?v=WmLs-43jaR4

QTc

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Yesterday I had a 21 yo female come in by BLS crew, tachycardic with a GCS of 3, spontaneously breathing with equal and reactive pupils bilaterally at ~ 6mm, with vomitus around her airway.  She was found down at home after her significant other called EMS due to concern that she was going to attempt suicide.  Report received that she was found with multiple empty pill bottles nearby.  No response to Narcan either in the field or in Room 9.

Here is her ECG: Calculated QTc (automated) is 401 ms, rate is 143.   The accepted normal value for QTc is: below 450ms for men and below 460ms for women.  The 99th percentile of normal: 470ms (men) and 480 ms (women).

ecg_case_micu

Just how does the computer calculate this?

By using the Bazett formula: QTc = QT / sqrt( R-R interval in seconds)

This means of course that if our rate is 60 BPM, then our R-R interval would be 1000ms, (or 1 second), and thus our QTc = QT/sqrt(1); and therefore in this situation QTc equals QT.

In our particular case: the R to R interval is 10.5 boxes (thus 420 ms, or in seconds: 0.420).  The QT was autocalculated at 260 ms, and when using the Bazett equation, this gives us a QTc of 401 ms.

What if you cannot rely on the computer calculated QT (which certainly can be inaccurate)? Then calculate the QT yourself by finding the tangential intersection of the T wave downslope with the ECG baseline, and measuring the intersection distance from the start of the QRS.  See the diagram below:

qt_picture

Using this measurement principal, and (in our case) using the lead V2 where the p wave and T wave are 180 degrees out of phase, we obtain a QT ranging from 8-9 boxes (320-360 ms).  When using the Bazett, this gives us a calculated QTc of 493-555. Of course qualitatively we can tell the QTc seems long as it exceeds half the R-R interval, quantitatively this is an increased QTc of 38% from the auto calculated, and is certainly in the significantly prolonged QTc range.

Follow-up: TCAs and benzos positive on her drug screen.  She was started on a bicarb drip in the ED (placed 3 amps of bicarb in a bag of D5); pH 7.34, lactic acid 1.2.  She is supposedly on Flexeril (similar in structure to TCA and will light up as TCAs on the drug screen), treated the same, however appears to be less cardiogenic in toxicity:J Emerg Med 1995;13(6):781-5.  Pt is intubated and stable currently.

Click here for the EMCrit on TCAs (overview below):

  1. Bicarb drip:  Goals: QRS duration <100, hemodynamically stable, Na ~150, pH ~7.5.  Sodium and bicarb don’t rise significantly in severe toxicity, her repeat showed no change in either.
  2. Magnesium: may help, though risk of Torsades is low as long as the patient remains tachycardic.
  3. Lidocaine: even though lidocaine is another Na-Channel Blocker, it will antagonize the effects of the TCA-like medications.
  4. Watch the electrolytes (decreases expected in both K+ and Ca+):  Lytes and ABG Q1H; (My pt’s Ca+ dropped from 9.8->8.5 over 4 hours).
  5. Intubation: hyperventilate to ensure no hypercapnia (want alkalosis).  Sedate with versed or propofol to raise seizure threshold.
  6. ECMO: If everything else fails.

Name that Disease?

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55 y/o  F with hx of HTN,COPD and recurrent indurative lesion on her left foot, last event was a yr or so ago, presented to the ED for worsening pain and increased size of her lesion for the last few wks now. No fever, chills, or fatigue. On exam, the cutaneous lesion is mildly tender and erythematous, non-fluctuant, no warmth noted. Pt is immunocompetent.

img_7436

 

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Answer:

Pyoderma Gangrenosum.  Take home point is to not I&D this lesion. It is not an abscess. It is a rare autoimmune disease that affects pts in their 40s-50s. These pts will have hx of other autoimmune diseases–lupus, crohns etc.  An I&D would lead to phenomenon known as pathergy,  the formation of new lesions following a trauma.

Tx: High dose steroids and pain meds. Refer to podiatry. Pt in this case was already well known to podiatry on arrival and was discharged with steroids and pain meds after podiatry consult in the ED.

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.

 

Central Line Insertion Choice

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All,
I know this came up during conference today so thought I’d send the article I think was cited. At least this is the one I found from EMRAP, below is their summary of this article. Long and short of it, complication rates are really low, when done in sterile fashion in a controlled environment.
This was done in the ICU, not in the emergency department.
Overall they didn’t say that one site was absolutely the best.

nejm-2015-central-line-site-complications

Take Home Points
No central line site is superior.
Femoral lines are fastest and most successful. Subclavian lines have a lower infection risk but higher rate of pneumothorax.

Parienti, JJ et al. Intravascular complications of central venous catheterization by insertion site. N Engl J Med. 2015 Sep 24;373(13):1220-9. PMID: 26398070

Bottom line: no line was superior. Femoral lines were the fastest to place and had the highest success rates. Subclavian lines had the lowest infection risk but had a higher rate of pneumothorax.

A patient needs central line access. Which should we choose? Which is best? There are multiple complications; infection, mechanical complications like artery puncture or pneumothorax and thrombotic complications.

The authors of this study conducted a randomized, controlled trial in 10 French ICUs. They enrolled adult patients with at least two accessible sites. Patients with all three sites accessible were randomized in a 1:1:1 fashion while those with only two sites were randomized in a 1:1 fashion. The doctors had all performed at least fifty central lines. However, they were all aware of the study and probably tried harder to reduce complications.

They looked for symptomatic clots and/or infection from the time of insertion up to 48 hours after removal. This was a large study; 3471 catheters were placed in 3027 patients. Catheters were assigned to a randomly assigned site and side; placement was successful approximately 91% of the time. 85% of subclavian lines were successfully placed, 91% of the jugular lines were placed and 95% of the femoral lines were placed. Femoral lines were most successful and subclavian lines were least likely successful.

Placement of femoral lines was also more rapid, by about a minute.

The primary outcome was a composite of infection, symptomatic clot and mechanical complications such as pneumothorax and bladder puncture. The jugular line performed the worst followed by the femoral line, then subclavian line. However, it is important to look at the individual components.
For mechanical complications, the subclavian line performed the worse. 2% had a complication versus 1.5% of jugular lines and less than 1% of femoral lines.
All lines were fairly low for symptomatic clots; 0.5% for subclavian, 1% for jugular and 1.4% for the femoral group.
In terms of infection, the subclavian group was the lowest (0.5%). The highest? Surprisingly, jugular lines had a 1.4% rate of infection versus 1.2% in the femoral line group.
Overall, there were fairly low rates of complications. These were performed in very sterile conditions in the ICU. These were not placements in crashing or coding ED patients.

Placement of central lines, including femoral lines, when done carefully under sterile conditions has a low rate of complications. This article does not identify one superior line placement.

Headache in a post-neurosurgical patient

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Earlier this month while moonlighting I had an approximately 40yM present for a headache (9/10 pain) for 3 days.

I know, this is an everyday occurrence.

But in his case he had a craniotomy with removal of a meningioma 1 month prior. He also noted 2 weeks of swelling on the left side of his head along the surgical scar.
ROS: denied fevers, chills, changes in vision, weakness, numbness, or tingling, etc.

PE: VSS, HEENT: Left side of head extending from his surgical scar and wrapping around to even under his L eyebrow was swollen and firm. NEURO: WNL

So, I know something isn’t right and my guess is that he either had a bleed or infection associated with his surgery. I order a CT head. For his headache I give him a migraine cocktail (IVF, compazine, and benadryl, minus the toradol).

img_1534

img_1535

After I see the CT images, I rush to check on the patient as the CT obviously shows quite a bit of midline shift and the patient states his headache is drastically improved (2/10 down from 9/10). Apparently migraine cocktails work on all causes of headache.

I consulted Neurosurgery who promptly admitted the patient to the ICU with plans to go to the OR. Approximately 45 minutes later, after the NES nurse practioner has seen the patient and he is getting packed up to go to the ICU, the radiologist calls to notify me of the CT findings.

This is a reminder to ALWAYS look at CT images yourself, especially if you’re expecting a life threatening finding.

Chest pain?

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Yesterday, 10 minutes before the end of a very busy shift in the middle of nowhere:
Nurse hand’s me an EKG for the mom of one of our best young medics. Ischemic STD in II, III, aVF, V5, V6. No STE. Maybe some LVH. No other EKG on file, she hasn’t been here before. I get up to see her right away.
In the room is a 50 yo lady in severe distress. BP 250/140. Describes “tearing” L sided CP radiating to her upper back. I ask her if she has a family hx of sudden death or aneurysms, her son says yes. No SOA. No N/V. Lungs are clear. Can’t palpate pulses in her feet. Slightly obese. She is sweating. There isn’t a CT surgeon in this county; I am sweating, too.
The nurse gets CT ready and I start the ball rolling for big IVs, blood, helicopter, etc. She gets dilaudid 1 mg then 0.5 then 0.5 again for pain and hopefully BP control. I tell everyone she’s now the ED’s top priority. The family of another patient grabs me twice in the hallway and asks why their mom, who fell, hasn’t gotten her home dose of lisinopril yet.
~30 minutes from door to imaging – CTAs = no dissection. Great, I have some time. Pain is well controlled now and BP 150s/80s. Repeat EKG w ischemia resolved completely, normal. Hypertensive emergency? She has a bit of a headache so I scan her head because we’re in CT, but it’s not useful due to the residual contrast. Trops, CBC, CMP, urine, tox, etc. all negative. Now looks great and feeling much better. Wants to go home.
Her son, her nurse, and I spend a long time convincing her she needs to stay overnight. She doesn’t want to be admitted, as she’s starting a new job Tuesday and can’t miss it. Eventually, she agrees to stay. Then we have to convince her to be transferred, since ED MD is the only MD in house overnight and she had me straight terrified. Reluctantly, she agrees to the transfer as long as her son will bring her home Monday night, no matter what. Hospitalist at the local mothership accepts readily. At that hospital, she’d had a negative stress 8 months ago and NES had placed her shunt (pseudotumor, she has a lot of headaches); hospitalist will consult cards and NES when she gets in.
I arrive back to work this morning to find out she’d made it upstate only to be transferred again overnight. She’d been flown to a bigger center after repeat CT head demonstrated SAH. She had 2 aneurysms, 1 was bleeding, both were definitively addressed. 24 hours after walking in the door, at the time of this writing, she is extubated and thriving.
Found this article from 1988 with a similar presentation, but I can’t say I’d ever heard of it before. Something else for your differential. Really consider that admission for observation when something seems wrong, even if you don’t know what it is.
Going to change my drawers now.

Delivery in the Emergency Department

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I will apologize for the wall of text in advance but I thought I to share an experience from last May that fits pretty well with the first 2 weeks of lectures this month. I think it definitely highlights the importance of  feeling comfortable with both delivery and newborn resuscitation in case they actually happen to you. I’ve also tried to point out all problems that came about but I am sure I didn’t hit them all and I am positive that I could have handled some of them better. 

It was nearly the end of a pretty typical shift at Jewish Downtown. For those of you who haven’t been there or don’t know there is zero OB coverage at Jewish. I was finishing my charts when I hear the secretary say “pregnant woman in labor” over the phone. That is a pretty unusual thing to hear at Jewish so I immediately asked the attending who was sitting closer if I heard that correctly. I also half-jokingly said I definitely wanted in on the patient if they were serious because I still needed a few more deliveries. The attending chuckles and replied that she thought the secretary was only joking because there shouldn’t be any reason for a laboring patient to come to Jewish, so I returned to my charts.

About 2 minutes later they call for a physician from the room behind the doctors area and we walk into what is in fact a laboring patient. The nurses state she seems to be contracting every 3-4 minutes but they don’t know much else at this point. While the attending checks her cervix, I grab the ultrasound and check the fetal position. She was about 8cm dilated and the best I could tell the baby was vertex but the head was so far down I gather this from the rest of the anatomy. Immediately calls start going out to the neonatologist at Kosair while we attempt to talk to the family and figure out how the patient ended up at Jewish. Here comes out first problem:

Problem 1: Neither the patient nor the family speak a word of english. Not only that but there is no translator phone in the room so the family has to be taken to another room to try to get some questions answered.

In the meantime I attempt to get a fetal heart rate to assess how the fetus is doing.

Problem 2: The only doppler is a pen style for checking pulses that doesn’t actually display a pulse number.

I go back to the ultrasound, find the heart and count the beats on the screen while a nurse counts for 15 seconds to get a FHR of about 144, which is always reassuring. In the mean time we are able to obtain some more information from the family.  

Apparently, the patient’s water broke during her office visit around 2pm (it’s now almost 11pm) and she was told to go to the hospital. For whatever reason they decided to wait and they got mixed up between Norton’s and Jewish hence our current situation. There are calls being made to Norton’s L&D informing them of the situation and transport is on the way. The neonatologist is also en route as a safety precaution in case she actually delivers here. The patient and fetus appear to be stable, and while still contracting around every 3-4 minutes she still isn’t fully dilated. I make the mistake of leaving the room assuming that the patient will soon be swept away to have her baby properly on an L&D floor. About 5 minutes later another call from the room and I walk in to see the beginning of this baby crowning.

The nurses wheel in their delivery kit as I gown and glove up. I apply a few packets of lubricant jelly, have the nurses move the patient closer to the end of the bed and attempt to create a semi-sterile field with the supplies available.

Problem 3: It’s nice and easy to set up to deliver in a room with a bed designed to deliver a baby. Unfortunately for me this situation involved a nurse/tech on each leg and the patient mostly laying flat in a bed with bag to collect fluid half hanging off the table but mostly just shoved under her bottom as best as I can with no real drainage.

Problems 4 & 5: Did I mention she didn’t speak english, also I have no idea what the word for “push” is in her language.  Also when you are on the L&D floor you have all kinds of cool toys such a tocometer to help you know when to tell the patient to push. I do not have that luxury.

I attempt to put a hand on her abdomen to feel her uterus contract so I know when to tell her to push and hope that she figures out what we want from her. Maybe it was a good thought but I have no idea, good thing she does and she is pushing every few minutes and the head is progressing it’s way out.. After a few good pushes the progress seems to slow a little bit and I start to worry a little bit that this 2 week post-dates baby may be stuck. What was that mnemonic for shoulder dystocia again? All I can remember is McRobert’s maneuver, but for anyone curious, Rosen’s has a nice one:

Help: Obstetrics, neonatology, anesthesia

Episiotomy: Generous, possibly even episioproctotomy

Legs flexed: McRoberts’ maneuver

Pressure Suprapubic pressure: shoulder pressure

Enter the vagina: Rubin’s maneuver or Wood’s maneuver

Remove posterior arm Splint, sweep, grasp, and pull to extension

Luckily, I have the nurses holding onto each leg (because this bed doesn’t have stirrups) so they flex her legs towards her as much as they can and everything continues to progress smoothly. Eventually the head is out and the rest of this baby boy delivers quickly. He is suctioned, wrapped in a warm blanket and the nurses begin assessing him. I think we put his APGAR at a 7 at 1 minute.

So I am done right? Baby is out, nothing more to see or do, lets ship them out. Right?……

Turning back to the patient I realize she seems still be bleeding a little more than I expected. It’s hard to figure out where she is bleeding from so I deliver the placenta which appears to be intact. I even sweep and massage the uterus just to be sure which seems to be contracting well.

Problem 6(?): Not really a problem because it seems her bleeding was not coming from the uterus but I have no access to the medications typically used to help control uterine bleeding after a deliver such a pitocin. Not that it matters because I didn’t know what the dose would be anyway. Just another interesting thought that I had during this whole process.

Since the placenta is whole, and seems to be firm I look for other sources of bleeding. This is when I realize the patient has a nice 2nd or 3rd degree tear (Dr Sterrett would be very disappointed I didn’t control the head well enough). I check to make sure it isn’t a 4th (thankfully it’s not), and start contemplating my next course of action. The attending asks what kind of suture I want to use to repair her tear. My only reaction was to smile and say “nothing”, followed by explaining that since the bleeding is slowing it’d probably be better to let the OB-GYNs fix her. I plan to pack her to make sure she doesn’t bleed too much in transport. 

Problem 7: No one had even seen a vaginal packing kit in the ED before, so we improvised and used some kerlex with a tail for easy removal.
By the time this had finished the neonatologist had arrived and began assessing the newborn. I think we ended up giving him apgars of 7 and 9. I started the patient on some fluids (because we didn’t have an IV when all of this started, another mistake I didn’t realize until it was all over) and within another 2 minutes transport had arrived to take the patient to Norton’s and she was actually swept away. Hopefully the OBs she finally got to didn’t think I botch the whole thing too much. Overall it was a pretty intimidating and adrenaline pumping situation. Not sure if I will ever have an experience quite like this again but if it does happen at least it will not be the first. 

Any comments, critiques, criticism or otherwise are welcome.

1.4% Observed Adverse Reaction Treated With Flumazenil

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Flumazenil (Rx: Romazicon) has recently been described as coming into favor for two unique purposes: (1) hepatic encephalopathy and (2) paradoxical reactions to benzodiazepines.

Regarding the first, flumazenil’s use in hepatic encephalopathy has been well described recently in a Cochrane review of 113 RCTs with a total n = 805, wherein flumazenil had a significant beneficial effect on short term improvement of hepatic encephalopathy.1 This is thought to occur physiologically secondary to reversal of the origin of hepatic encephalopathy—i.e., an accumulation of substances that bind to a receptor-complex in the brain resulting in neural inhibition1 (principally GABA receptors which are forefront in the stimulation of sedation). Therefore GABA receptor antagonists (such as flumazenil) can be used to directly oppose this mechanism. Effect on full recovery and survival has still not been proven with flumazenil administration.1

Secondly, flumazenil can be used for paradoxical reactions to benzodiazepines2,4 and in a 10 year review of its use, published in the Journal of Emergency Medicine,3 the real safety of this drug has once again come into question, as there were relatively few adverse outcomes even in the highest of seizure provocation risk—which occurred with co administration of pro-convulsant (e.g., TCAs) at a 2.7 % incidence (8/293)—the total incidence including all subjects bore a rate of 1.4% of seizure activity (n = 904).3

I present an example of administration in the second of indications above. I took care of a 26 yo WF with PMH of asthma, a prior severe dental cavity pending root canal and an IV heroin addiction, currently sober and progressing through the the 12 Steps program at the Healing Place. She presented in sepsis, afebrile with qSOFA of 0/3 (Labs: WBC 21.2 with left shift, procal 1.33, ESR 83, CRP 201, lactic acid 0.8 s/p 2 L NS IVFs), and AKI (Cr. 1.6) with dental as well as urinary possible sources. She was eventually discharged on day 3 with Dx of urosepsis, creatinine returned to normal, and had a negative echo for routine endocarditis rule out in the setting of PMH of IVDA.

During her ER stay she was uncomfortable, diaphoretic, pale, GCS of 15, but anxious and in pain, professing severe insomnia for 3 days, stating, “I just want to sleep”. A trial of oral Ativan 2 mg was given, as she did not want any pain medication due to her prior addiction. She noted a small temporary improvement; however 2 hours later this beneficial effect was absent. By now she had received cefepime 2g and vancomycin 25 mg/kg (for potential osteomyelitis coverage), and was requesting more anxiety medications, having already received 50 mg IV Benadryl 30 minutes prior with no improvement noted. Clinically she was GCS 15, pleasant in interaction, increasingly pale, uncomfortable, wide awake at 0445, and subjectively in pain. She was then given 2 mg IV Versed.

Immediately following the administration of midazolam she became altered to GCS 12 (E4, V3, M5), eyes wide, extremities tremulous, pulled out all of her IVs, and was trying to jump off the bed. It was clear she was paradoxically agitated and hyper-aroused. Rather than reversing her (though we doubted history of benzodiazepine use), we opted to watch and see if this reaction would subside without intervention since she responded favorably to the oral Ativan; however the rarely seen but well known paradoxical reaction to Versed was suspected. She was observed 1:1 and thereafter 3:1 for 40 minutes, at which time she appeared to be steadily worsening rather than improving. The decision was made to give an IV push of 0.2 mg of flumazenil (Rx: Romazicon). Within 30 seconds after administration she once again returned to her pleasant self, she was GCS 15, appropriate, and had no recollection of the previous hour, and had no seizure activity noted throughout her stay. She maintained a healthy mental status of GCS 15 and was AAOx4 for the rest of her evaluation and admission.

In 2010, Kreshak et al. reported a similar case and treatment. This paradoxical reaction to Versed in their report is thought to occur at less than 1% incidence, however it is described as commonly as 1.4 %.4 In the reported literature this reaction is described as a patient becoming acutely agitated, restless and aggressive2. Stiffening and jerking of the extremities, and shaking of a part of the body are also noted. When observing a patient with this reaction, after ruling out other etiologies of agitated AMS, Kreshak et al. (2010) opted to administer flumazenil 0.5mg IV, and “…immediately after which the patient became conscious, oriented and calm, the paradoxical reaction was terminated”. The patient had no recollection of the events,2 similar to the patient observed in the ULED.

Per Kreshak et al. (2010), there exist “…different theories concerning the mechanism of paradoxical reactions, involving a central cholinergic effect or the serotonin imbalance”.2 Unfortunately the exact mechanism of paradoxical reactions remains unclear.

Although difficult to locate literature, if seizures develop following flumazenil administration, pharmacology guidelines recommend Valium 20-30 mg IV then immediately switching to barbiturates; some soft EM sources also suggest going straight to propofol.5

Thank you for reading my post.

References

  1. Als-Nielsen, B., Kjaergard, L., & Gluud, C. (2001). Benzodiazepine receptor antagonists for acute and chronic hepatic encephalopathy. The Cochrane Database of Systematic Reviews (Complete Reviews). doi:10.1002/14651858.cd002798
  2. Cabrera, L., Santana, A., Robaina, P., & Palacios, M. (2010). Paradoxical reaction to midazolam reversed with flumazenil. Journal of Emergencies, Trauma, and Shock J Emerg Trauma Shock, 3(3), 307. doi:10.4103/0974-2700.66551
  3. Kreshak, A. A., Cantrell, F. L., Clark, R. F., & Tomaszewski, C. A. (2012). A Poison Center’s Ten-year Experience with Flumazenil Administration to Acutely Poisoned Adults. The Journal of Emergency Medicine, 43(4), 677-682. doi:10.1016/j.jemermed.2012.01.059
  4. Tae, C. H., Kang, K. J., Min, B., Ahn, J. H., Kim, S., Lee, J. H., . . . Kim, J. J. (2014). Paradoxical reaction to midazolam in patients undergoing endoscopy under sedation: Incidence, risk factors and the effect of flumazenil. Digestive and Liver Disease, 46(8), 710-715. doi:10.1016/j.dld.2014.04.007
  5. (n.d.). Retrieved August 23, 2016, from http://www.goodfriendem.com/2013/05/flumazenil-romazicon-is-probably-safer.html