Tag Archives: Ultrasound

Conference Notes 08/30/23

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Emergency Management of Dentition and Midface

  • Dentoalveolar trauma can include fractures, avulsions, displacement of teeth
  • An avulsed tooth is only viable within one hour, however, even outside of this window it is still worth replacing the tooth. In some cases, they may then get a root canal with dentistry
  • Alveolar fractures need timely treatment or risk poor cosmetic outcome and infection
  • Most oral abscesses can be drained in the ED with close dental follow-up
  • The need to obtain CT is dependent on the full clinical picture. If pt has significant RFs for deep space infection or cancer, it may warrant a face CT
  • Trismus sometimes can be confused with guarding due to pain. Can be worthwhile to provide analgesia and reassess
  • Buccal and canine space infections can present with significant facial swelling. These should be assessed with CT, drainage should occur from within the oral cavity near the involved tooth, not through the skin of the face
  • Radiology reads will frequently indicate Ludwig’s, however, this is often overread. True Ludwig’s is a surgical emergency. Can cause significant airway compromise
  • As a general approach to anesthetic for oral abscesses, should first infiltrate around the abscess, then can attempt direct injection
  • Inferior alveolar N blocks can be challenging due to surrounding vessels as well as the parotid gland that can be inadvertently damaged

Anti-Arrhythmics

  • Among the sodium channel blockers, they are divided into IA, IB and IC. Procainamide is the common IA, Lidocaine is a IB and Flecanide is IC
  • Class II antiarrhythmics are the beta blockers
  • Class III antiarrhythmics are K channel blockers. Amiodarone is the most common example
  • Class IV antiarrhythmics are the Ca channel blockers
  • Beta-blockers and calcium channel blockers should be used with caution in the setting of CHF exacerbation given their negative inotropic effects
  • Amiodarone has both rate and rhythm-control properties
  • Ibutilide and procainamide are the safest medications to give in the setting of WPW
  • Dr Huecker: Can also consider adding magnesium to any of the aforementioned therapies

Infective Endocarditis

  • Defined by the Modified Duke Criteria
  • Most commonly caused by Staph species
  • Don’t forget about pseudomonal coverage in those with prosthetic valves
  • Valves are at high risk of infection given their lack of robust vasculature as well as the turbulent flow around them
  • IE cases are increasing due to both increased IVDU as well as increased prosthetics being placed
  • The average age of IE is now >65. Majority will require surgical intervention
  • Recall Osler nodes, Janeway lesions, splinter hemorrhages, Roth spots/ conjunctival petechiae
  • IVDU leads to right-sided IE
  • When IE is diagnosed don’t forget to get blood cx from 3 separate sites
  • Empirically give Vancomycin. Add on pseudomonal coverage if pt has a prosthetic valve
  • The biggest RF for IE is prior IE
  • Undomiciled patients are at increased risk of IE due to Bartonella species given flea exposure

Ultrasound in the Unstable Patient

  • CXR sensitivity for edema/ effusions is low
  • Ultrasound has good sensitivity in confirming ETT placement
  • Palpating pulses during ACLS has poor sensitivity/ specificity, another area where ultrasound can be helpful, in addition to checking for reversible causes of a patient’s arrest
  • Ultrasound can be used to find the CO plus the SVR, which together can be very valuable information when resuscitating an undifferentiated shock/ SOA/ hypotensive patient

Conference 07/14/2021

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RSI Pharmacology – Jade Daugherty, PharmD

Sedatives

Etomidate:
– Does not inhibit sympathetic tone or myocardial function. Minimal BP and HR changes|
– RSI: 0.3 mg/kg; Procedural sedation 0.1 – 0.2 mg/kg
– Onset 30 – 60 seconds; Peak 1 minute; Duration 3 – 5 minutes
– Can see myoclonus, dose dependent, can be blunted w/ opioids and benzos. Resolves upon paralysis. May cause difficulty w/ procedural sedation.
– Other adverse effects: N/V, lowers sz threshold, mild decrease in IOP and ICP, adrenal suppression (single dose can cause effects for 24 – 72 hrs)
– Consider avoiding Etomidate in Sepsis patients (see CORTICUS trial)

Ketamine:
– Analgesic and amnestic properties
– Nystagmus with amnestic doses
– RSI: 1 – 2 mg/kg
– Exerts sympathomimetic effects: increased HR, BP, CO by lessens reuptake of catecholamines. May not see this in catecholamine depleted patients
– Also causes bronchodilation and anticonvulsant effects

Propofol:
– Short acting sedative hypnotic that enhances GABA activity
– No analgesia; amnestic effects
– Onset 30 sec; Duration 3-10 min
– RSI 1 mg/kg
– Safer in pregnancy
– Adverse effects: hypotension
– Decreased cerebral O2, decrease in IOP and ICP, bronchodilation and anticonvulsant effects

Benzos:
– No analgesia. It does possess anxiolysis, anterograde amnesia, anti-convulsant properties
– Onset 2 – 3 min; Duration 45 – 60 min
– Midazolam preferred: RSI 0.1 – 0.3 mg/kg

Paralytics

Depolarizing Blockers – Succinylcholine:
– Be aware of hyperkalemia; therapeutic dose can raise serum potassium 0.5 – 1 mEq/L
– Consider avoiding in burns and crush injuries (delayed rise in serum K), as well as ESRD on HD, sepsis
– Small increase in ICP
** Special considerations: may require higher doses in Myasthenia gravis
** Pseudocholinesterase deficiency -> results in prolonged paralysis (several hours). NDMB (Roc/Vec) are safe for use

Rocuronium – non-depolarizing neuromuscular blocker:
– Dose 0.6 – 1.2 mg/kg (~1.0 mg/kg)
– Onset 60 – 90 seconds; Duration 30 – 60 minutes

Vecuronium – non-depolarizing neuromuscular blocker:
Needs to be reconstituted
– Dose 0.08 – 0.1 mg/kg (~ 0.1 mg/kg)
– Onset 2 – 3 minutes; Duration 25 – 45 minutes

If you use the longer acting paralytics, sedate appropriately

Guide to Pediatric ED – Dr. Penrod
– EPIC Order Sets: “Peds ED Treatment ____”
Examples: Neonatal Fever (0 – 7 d, 7 – 28 d, > 28 d), Sepsis, Status Epilepticus, Asthma, NAT, Trauma, DKA, more

– Discharge teachings: Get dot phrases from other attendings (i.e. Sandy Herr)

– Admission: bed request > .admitresidentnotification > TigerText (login: phys___@Norton) > ask admit resident when they call if it is ok to put in “ready for dispo” order

– Tylenol 15 mg/kg q6 hrs; Ibuprofen 10 mg/kg q 6 hrs – can alternate q3 hrs
– Versed: PO 1 mg/kg/dose, IN 0.2-0.3 mg/kg/dose, IV 0.1 mg/kg/dose
– CTX: Meningitis 50mg/kg/dose q12hrs, non-meningitis 75 mg/kg/dose daily
– Amox: 50 mg/kg/day, daily for GAS pharyngitis; 90 mg/kg/day divided BID for PNA and AOM

– IVF bolus: 22 cc/kg over 1 hr
– mIVF “4-2-1”: 4 cc/kg/hr for first 10 kg, 2 cc/kg/hr for second 10 kg, 1 cc/kg/hr for each additional kg

Abdominal Ultrasound – Dr. Baker
RUQ US: just below the R costal margin, or X minus 7 mm (7 mm to right of xiphoid process)
Maneuvers to assist: deep breath, left lateral decub
Portal triad (portal vein, hepatic artery, CBD < 7mm normal & > 10 mm + 1mm/decade life abn) makes an exclamation point w/ GB

Cholecystitis: gallstones, anterior* wall > 3mm, sonographic Murphy’s, pericholecystic fluid

Choledocolithiasis: “double barrel” sign

*important to measure anterior wall as posterior acoustic enhancement makes the posterior wall appear thicker due to fluid filled structure enhancing conduction of sound waves

SANE Lecture – Amanda Corzine, MSN, SANE-A
Assault exams/kits done within 96 hours/4 days, sometimes up to 5 days
All male/females 12 yrs and older

Center for Women and Familes (CWF) respond to SA and DV victims as an advocate

Patient may choose to report or not to police. Kit will be destroyed in 1 year if they choose to not report.

Dry swabs for wet surfaces, wet swabs for dry surfaces. Don’t package wet evidence, allow it to fully dry.

Place swab in envelope cotton part down. Do not lick envelope.

EMS Radio Calls Part 2: Dr. Orthober
– Discontinuing IV after Dextrose given: is patient now AAOx4, decisional, clear reason for hypoglycemia, have family members

“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.

Sick PEs

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We had a very ill patient recently. She was found down upstairs visiting her family member. She was calmly altered, not agitated but was in mild distress. Consciousness fluctuated. Tachycardic and hypertensive initially, then had more labile BP and some hypotension.

We had to intubate her due to poor MS and clinical condition. She coded in CT, we placed a central line on the CT table between her noncontrast head CT and her CT chest. We pushed an amp of Epi and ran out of the room for the CT chest. We were worried about dissection and PE in equal amounts. We could not get good cardiac windows on bedside Echo in room 9 prior to the CT.

She continued to intermittently lose her pulse and drop her BP. We confirmed bilat PEs on the CT when we saw NO contrast left her right ventricle. The CT tech noticed first and became worried the patient had no cardiac output (ie pulseless).

We rushed the patient back to room 9 and gave a tPA bolus (50mg) followed by infusion of 40mg. She was on pressors and heparin and improving. Dr Smith accepted her to Jewish for possible EKOS or even ECMO if needed. On arrival to Jewish a few hours later she coded and died.

I was surprised when I found out she had died. Her O2 sat was improving, HR was decreasing, blood pressure was stable (though dependent on pressors). She received a large amount of crystalloid IV which according to some data might not have been optimal management. She also had the following ECG:

FullSizeRender

I think she was infarcting her myocardium. She likely had pulmonary infarction considering her poor oxygenation. She had coded a few times. She had a lot of strikes against her. Her BEST SHOT was going to a place with catheter assisted treatment for PE and ECMO if needed.

I am posting the case to let everyone know:

  1. How to manage sick PE patients (see post below)
  2. To use tPA in massive and in many cases of submassive PE
  3. TRANSFER sick PE patients to Jewish for EKOS/ECMO
  4. The decision to diagnose PE with RV strain on BEDSIDE Echo with no formal Radiologic testing will depend on your attending

This post from EmCrit / PulmCrit is a beautiful summary with potential dogmalysis related to PE management (see take home points below but do read the post).

In addition, here is a nice review article on catheter-based reperfusion treatment for PE with nice references for further reading.

Take home points from the Emcrit post:

  • The only evidence-based intervention that seems to improve mortality in massive PE is thrombolysis.   The primary goal of therapy should be administration of thrombolysis as soon as possible to patients without contraindication.
  • Consider early stabilization of blood pressure using a norepinephrine infusion, administered peripherally if necessary.
  • Volume administration may facilitate dilation of the right ventricle and hemodynamic deterioration.
  • Intubation is very hazardous and should be avoided if possible.   Patients die from cardiovascular collapse, and intubation may worsen this.
  • For a coding PE patient consider 50mg alteplase bolus as well as an infusion of epinephrine.  Patients can do well despite requiring CPR and high dose vasopressor infusions.

Interesting Ultrasound

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A late 20s F G4P3003 at approximately 6 weeks gestation by LMP presents with a chief complaint of vaginal bleeding. A few hours PTA, patient states she felt a “gush of blood” with some mild abdominal cramping. VSS. On exam, noted to have a moderate amount of vaginal bleeding per the os. On our bedside ultrasound we note what appears to be a viable IUP with cardiac activity.  However, the uterus appears septate, with half containing the IUP and the other half more hyperechoic/solid in nature. We were concerned for a possible subchorionic hemorrhage and consulted OB/GYN. Our bedside US image is below:

BS US

OB came down with their Cadillac ultrasound and confirmed our findings.  For comparison, here is their much clearer image:

OB US

For this patient, with this large of a subchorionic bleed, the likelihood of her carrying this pregnancy to term was low. They planned to have her follow up in clinic for a repeat ultrasound in 2 weeks to reassess viability. Per our OB colleagues, other things on the differential included a fibroid. However, as this patient had 3 very healthy and rambunctious boys at the bedside with her, OB commented that a fibroid that large would likely have resulted in infertility.

And from UptoDate:

“A subchorionic hemorrhage or hematoma is a risk factor for spontaneous abortion, particularly when it amounts to 25 percent or more of the volume of the gestational sac. A meta-analysis of seven comparative studies found that women having a subchorionic hematoma had a significantly increased risk of spontaneous abortion, compared to women without such findings (18 versus 9 percent; OR 2.18, 95% CI 1.29–3.68). The findings also are associated with an increased risk of placental abruption (4 versus 1 percent; OR 5.71, 95% CI 3.91–8.33) and preterm premature rupture of membranes (4 versus 2 percent; OR 1.64, 95% CI 1.22–2.21). The increased risks of preterm labor and stillbirth appeared to be dependent upon the presence of vaginal bleeding.

Pregnancy outcome associated with subchorionic hematoma also relates to location, with worse outcomes observed for retroplacental hematomas, compared to marginal hematomas. The location, rather than the size, of a subchorionic hematoma may be the most important predictor of pregnancy outcome. Evidence relating to the size of the hematoma and the risk of adverse outcomes is inconclusive.

The only management option for subchorionic hematoma is expectant. There is insufficient evidence regarding whether bed rest decreases the risk of pregnancy loss when a subchorionic hematoma is present. Some clinicians repeat an ultrasound in one to two weeks to confirm fetal viability and assess any change in size of the hematoma, primarily to provide reassurance to the patient. A subchorionic hematoma is not an indication to conduct a diagnostic evaluation for an acquired or inherited thrombophilia.”

A large red herring

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The patient is a 20s y/o AAF, multip, last normal period 3 weeks ago (definite date), who presented to another facility with spotting and occasional moderate bleeding for about a week with 4 days of crampy pelvic pain, worse on the left than the right.  There, she was diagnosed with trichomonas and treated empirically for gonorrhea and chlamydia.  She had a positive pregnancy test and reportedly had transabdominal and transvaginal ultrasounds.  She stated they told her she definitely had a pregnancy in her left tube.  She was given instructions to see her regular doctor in 48 hours for a repeat evaluation and discharged.

It is at this point that the big red flashing lights in my head go off and I think to myself “Wait, WHAT?  Someone DISCHARGED a confirmed ectopic?  No way.  Maybe they said it was a possibility and she misinterpreted.”  Whatever the sequence of events, all that mattered was that I get the records and do an ultrasound myself.

Her records came in from the other ED after a couple of attempts (as per usual).  A few things that I learned from her records:
1. she was indeed told that she had an ectopic and that she should see her regular doctor or OB in 48 hours.
2. she did get treated for STDs.
3. sure, she had an ultrasound, but there wasn’t any interpretation available unless I called and had them hold the phone up to the speaker (didn’t have time to do this).
4. my dislike for paper charts is warranted when I can’t read what someone says about my patient.

Initial vitals normal with a HR 100, BP 118/78
She was tender in the LLQ and suprapubic areas without peritoneal signs.  Cervix was closed, she had a small to moderate amount of dark blood in the vaginal vault, and had uterine and left adnexal tenderness on bimanual exam.

I started fluids, gave her some meds for her nausea, and put in all the usual orders.

Labs:
-WBC 13.8 (88% Neut)
-Hb 9.6
-CMP unremarkable
-U/A positive for blood/protein/ketones but micro negative
-Quant 12000+
-Swabs + for trich

And then came the ultrasound:

transverse view, abdominal probe

transverse view, abdominal probe

longitudinal view, abdominal probe

longitudinal view, abdominal probe

A few things about this caused even more red light flashing: first, how could a gestational sac be THAT SIZE in someone whose last period was 3 weeks ago?  Second, what was that OTHER thing behind the uterus on the left?  Third, if the sac was really that big, why was there no pole?

The transvaginal exam was more or less to confirm my suspicions that this was not normal.  I knew that my plan was now to call the specialists with the fancy machine and adnexal expertise.  I couldn’t actually get a GOOD view in two planes (sorry, Dr. O’Brien!) due to patient discomfort, but this one was good enough.

longitudinal view, transvaginal probe

longitudinal view, transvaginal probe

I hadn’t seen any free fluid in her pelvis on either exam.  However, when OB came down, they found some.  They confirmed my suspicions and admitted the patient to go to the OR.

In my brief lit search just prior to posting, I found that this pseudosac finding is not extremely common (the average reported frequency is about 10% of cases).  I feel like this patient’s story would have raised enough red flags to make me uncomfortable sending her home without OB involvement even without the ultrasound, but the date/quant discrepancy coupled with a sac that was definitely not consistent (even though it WAS in the uterus) clinched the diagnosis for me.

Positioning is Everything

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When using a chest x-ray to look for a pneumothorax, positioning of the patient is everything.  The first chest x-ray below is an upright chest x-ray from an OSH of a patient that fell 30 feet from deer stand and was found to have a right pneumothorax.  The OSH didn’t do any other imaging and didn’t even send the patient with a c-collar.

When the patient arrived we laid him down and placed a c-collar and assumed that his spines weren’t cleared yet.  When we shot the portable, supine chest x-ray in our ED we couldn’t see a pneumothorax and our radiologist actually read it as no pneumothorax.

Using the US, an EFAST was performed and showed a pneumothorax and the subsequent Chest CT verified it.  Therefore the next time you get an ED, supine chest xray on someone, remember that just because you don’t see a pneumothorax on a supine CXR, doesn’t mean they don’t have one.  The optimal xray is an upright chest xray (expiratory if possible)!

Upright OSH xrayUpright Chest x-ray from OSH

Supine UofL portable Xray

Portable, supine Chest X-ray in our ED

CT scan

CT showing the Right Pneumothorax