Often when we think of hypoglycemia, our first thought is diabetes. Often times, we are right. Most people that present to the emergency department with hypoglycemia are diabetics and the derangement in their blood glucose is related to medication mismanagement. However, hypoglycemia can occur for other reasons and we should be able to consider a wider differential diagnosis in a patient when an etiology is unclear.

Hypoglycemia is usually considered a blood glucose below 70 mg/dl, however some patients (mainly diabetics) can have symptoms of hypoglycemia above this level because their bodies are used to higher baseline blood glucose levels. This is important to recognize because relative hypoglycemia may be a sign of another pathology and requires treatment and workup depending on the clinical scenario.

We always start out with a thorough history and physical exam. Special attention should be paid to timing of the hypoglycemia related to meals and when medications are taken. In addition, past medical history, medication lists, social history, daily nutrition, and other concurrent symptoms should be obtained to attempt to find the cause.

The differential diagnosis for hypoglycemia in the non-diabetic patient is extensive but includes medications other than those taken by diabetics (fluoroquinolones, beta blockers, pentamidine, valproic acid, and ethanol among others), renal failure, infection/sepsis, starvation, hypothyroidism, pituitary insufficiency, islet and non-islet cell tumors. This is not an exhaustive list and a more complete list can be found on the Life in the Fast Lane website below as well as a mnemonic to help remember this differential.

As far as evaluation of this patient population, it depends on the clinical scenario. If a cause is identified and the patient is safe to have further evaluation by an endocrinologist or primary care physician as an outpatient, then discharge is appropriate. But, if the hypoglycemia is unpredictable or continues to occur despite treatment, the patient requires inpatient admission. Work-up is directed toward the differential diagnosis discussed above with addition of other testing including insulin levels, c-peptide levels, BHOB, and pro-insulin levels which can be undertaken as an outpatient or by the inpatient team. For further information, some resources/ sources for the information above can be found below.

Resources:

https://lifeinthefastlane.com/resources/hypoglycemia-ddx/

https://www.uptodate.com/contents/hypoglycemia-in-adults-without-diabetes-mellitus-diagnostic-approach?search=hypoglycemia&source=search_result&selectedTitle=1~150&usage_type=default&display_rank=1

There is rarely a shift in the emergency department where we aren’t asked to evaluate an STI-related complaint.  We frequently test for gonorrhea, chlamydia, and trichomoniasis, and we frequently treat for these as well. While the vast majority of these cases are not “emergencies” per se, we recognize how important to public health these diseases can be. Occasionally, I’ve seen people test for hepatitis if there’s an unexplained jaundice, right upper quadrant pain, or GI upset. However, there are two STI’s which we don’t frequently test for in the department, namely HIV and syphilis. Despite their clear dangers to public heath, we don’t test for these often. I’ve heard people give different reasons for this. “We aren’t primary care”, “they can just go to the health department”, or “I don’t want to have to wait on those tests” are some of the most common. We’ve touched on HIV testing at room9er previously, so I’ll limit this post to syphilis and what we can do in the Emergency Department.

Syphilis, which can cause significant morbidity and mortality, has been increasing in prevalence in recent years. In Louisville, there were 73 cases diagnosed in 2014. In 2016, this number increased to 89. There are many different factors that contribute to this, including decreased condom use, availability of new partners on dating apps, and cuts to public health initiatives and clinics. Regardless of the cause, syphilis rates are increasing and we undoubtedly have seen patients who are affected by it during our residency.

Risk factors for syphilis are similar to those of other STI’s. Men who have sex with men, those with multiple sexual partners, patients diagnosed with other STI’s including HIV, pregnant women, patients taking pre-exposure prophylaxis for HIV, and those with partners known or suspected to have syphilis are at increased risk.

So what can we do if a patient comes in with a chief complaint of GU discomfort or STI exposure? Firstly, we need to think about all of the potential diseases, not just the ones we routinely treat such as gonorrhea and chlamydia. Evaluate for risk factors during the history. Look for chancres or other sores during the GU exam, and test and treat as necessary. For those with known exposure, empiric treatment is recommended  by the CDC.  For patients presenting with known exposure, primary, or secondary syphilis,  benzathine penicillin G, 2.4 million units IM is currently recommended. Alternative regimens exist for those who have allergies to penicillin. In other words, testing and treatment are relatively simple and straightforward in the early stages.

If a patient is high-risk, please resist the urge to pass the tasks of testing and treating to their primary doctor. Many of our patients have poor follow up and do not understand the threat this disease poses to public health.

Here is some bonus material from Essentials of EM/ LITFL. A couple of lectures from Dr. Mattu from some of his favorite topics. It includes a lecture reviewing some of the hyperkalemia stuff we went over today.

Primum non killem

Also, I received a reply with some additional info from Dr. Coleman regarding epiglottitis and a sign called the vallecula sign which sometimes accompanies the thumbprint sign on a lateral neck x-ray.

From Dr. Coleman:

Good discussion from Steve Smith on T wave inversions: something we see a lot of. Check it out.

http://hqmeded-ecg.blogspot.com/2015/05/new-40-minute-lecture-on-t-wave.html

Quick read by Ryan Radecki on Medical Expulsion Therapy for Ureterolithiasis.

https://www.acepnow.com/article/medical-expulsive-therapy-no-longer-recommended-for-ureterolithiasis/?elq_mid=30116&elq_cid=10110279

All,

As promised during my lecture. See below for the links to the videos I referenced as well as a few others for joint reduction techniques. Hope these help. Also, I’m open to any feedback you have regarding the talk: things you liked, didn’t like, would like to see more of. Thanks.

https://www.youtube.com/watch?v=UxUhW4Zac74 Whistler Technique Hip Reduction Video

https://www.emrap.org/episode/reduction/reduction Multiple Techniques Hip Reduction

https://www.emrap.org/episode/hipreductionby/hipreductionby East Baltimore Lift- Hip

Larry Mellick Posterior Shoulder Reduction: https://www.youtube.com/watch?v=KRCqVekNEKc

Larry Mellick Inferior Shoulder Reduction https://www.youtube.com/watch?v=C8Irt39KBgk

Shorter version of Mellick’s Posterior Reduction w/o sound https://www.youtube.com/watch?v=MWb1OKkDDwE

Larry Mellick: 10 ways of reducing shoulder (10min) https://www.youtube.com/watch?v=HtOnreM7heg

Larry Mellick: Intra-articular injection/Ant Shoulder Reduction https://www.youtube.com/watch?v=HzROgg-HWPk

Larry Mellick: Davos Technique Shoulder Reduction https://www.youtube.com/watch?v=u2MsnjVNoPM

Jess Mason EMRAP: good explanation of Inf Shoulder Reduction https://www.youtube.com/watch?v=k_ORI51luFI

https://coreem.net/core/true-knee-patellar-dislocations/ Nice little summary on knee/patella dislocations

Larry Mellick Knee Dislocation: https://www.youtube.com/watch?v=aN7zDxtyHy8

Not Actual patients but good 2 minute video on techniques/exam: https://www.youtube.com/watch?v=vdrfY3K7yR4

https://www.youtube.com/watch?v=A91TWNbSEOQ – Silent Posterior Elbow Reduction Video

https://www.youtube.com/watch?v=IcrmMAxLnp8 – Interlocking Hands Technique for Posterior Reduction

https://www.youtube.com/watch?v=s9GVdF6v9xQ Posterior Elbow Reduction- 2 providers

Everyone gets a little nervous when we start talking about the legal implications of HIV testing in the emergency department. Happily, a quick review of the law in the state of Kentucky is reassuring. The first two paragraphs really set the tone for the law, which is essentially quite pro-healthcare provider:

“(1) The General Assembly finds that the use of tests designed to reveal a condition indicative of human immunodeficiency virus (HIV) infection can be a valuable tool in protecting the public health. The General Assembly finds that knowledge of HIV status is increasingly important for all persons since treatment using antiretroviral medications can slow disease progression, prolong and improve the lives of HIV positive individuals, and reduce the likelihood of perinatal mother-to-child transmission. Many members of the public are deterred from seeking testing because they misunderstand the nature of the test or fear that test results will be disclosed without their consent. The General Assembly finds that the public health will be served by facilitating informed, voluntary, and confidential use of tests designed to detect human immunodeficiency virus infection.

(2) A person who has signed a general consent form for the performance of medical procedures and tests is not required to also sign or be presented with a specific consent form relating to medical procedures or tests to determine human immunodeficiency virus infection, antibodies to human immunodeficiency virus, or infection with any other causative agent of acquired immunodeficiency syndrome that will be performed on the person during the time in which the general consent form is in effect. However, a general consent form shall instruct the patient that, as part of the medical procedures or tests, the patient may be tested for human immunodeficiency virus infection, hepatitis, or any other blood-borne infectious disease if a doctor or advanced practice registered nurse orders the test for diagnostic purposes. Except as otherwise provided in subsection (5)(d) of this section, the results of a test or procedure to determine human immunodeficiency virus infection, antibodies to human immunodeficiency virus, or infection with any probable causative agent of acquired immunodeficiency syndrome performed under the authorization of a general consent form shall be used only for diagnostic or other purposes directly related to medical treatment.

(3) In any emergency situation where informed consent of the patient cannot reasonably be obtained before providing health-care services, there, is no requirement that a health-care provider obtain a previous informed consent.”

The law seems to poise HIV testing as no different from any other medical testing – if the provider has reasonable suspicion for HIV infection in a patient he or she should order appropriate testing. The law goes on to enumerate appropriate outpatient followup post testing, listing county health departments and primary care providers – seemingly to reiterate that yes, follow up should be arranged but in no manner terribly different from any other infection.

Previously healthy, middle aged male; presenting to room 9 via ground EMS.

Unrestrained single-occupant, rollover MVA. Pt found “partially ejected” through the sunroof of the car.

Awake and oriented with EMS. Hemodynamically stable en route to the hospital. EMS report called and patient room 9ed by the mechanism.

Patient arrives on a backboard and c-collared. He is awake and oriented, GCS 15. ABCs intact. Vital signs all normal.

Exam significant for abrasion/contusion to the R central forehead (skin otherwise intact), bilateral wrist tenderness without deformity.

Photo 1; Photographed with patient permission specifically for academic posting

Chest, abdomen, pelvis without acute traumatic findings.

And… weakness in all extremities; upper worse than lower; distal much worse than proximal. He actually has pretty well-maintained movement about the shoulders but his forearms, hands, wrist fling wildly and uncontrolled.

Motor exam:

            Delt       Bi       Tri       WrFl      WrExt       Grip

RUE:     5          4        2            1             1             1

LUE:      5          4        2            1             1             1

             HipFl    HipExt    KnFl       KnExt     DorsiF      PlantF

RLE:       4            4            3             3              2             2

LLE:        4            4            3             3              2             2

The diagnosis is probably already fairly certain at this point (if not read along).

CT man-scan is obtained by mechanism.

Sagittal CT scan

Still image from CT scan. Demonstrating congenital fusion of C2 and C3 (Klippel-Feil syndrome). There is congenital narrowing of the spinal canal. There are multilevel degenerative changes. There is an avulsion fracture of the anterior-inferior “tip” of the C5 vertebral body. THIS “teardrop” avulsion fracture is associated with extension injury (also evidenced by the forehead abrasion/contusion).

Neurosurgery had already been consulted. The MRI of the cervical spine was ordered and pending.

A Foley catheter was placed for urinary retention.

“IMPRESSION: 1. Posterior disc osteophyte complexes at C4-C5 and C5-C6 in conjunction with a diffusely congenitally narrowed spinal canal cause severe spinal canal stenosis and mass effect on the underlying spinal cord which shows signal abnormality consistent with contusion/edema, possibly superimposed upon myelomalacia.2. Redemonstrated acute mildly displaced fracture along the anterior aspect of the C5 lower endplate. Possible C5 vertebral body bony contusion noted. Associated mild anterior paraspinal edema. Small amount of heterogeneous T1 signal posterior to the C5 and C6 vertebral bodies may represent a combination of blood products, edema, and disc material.3. Mild increased STIR signal intensity within the interspinous spaces from C3 through C7, which could indicate interspinous ligament sprain injury”

The patient was taken to the operative room with neurosurgery for spinal cord decompression. He was maintained on pressors to maintain high MAPs (>85mmHg).

At the time of hospital discharge, he had regained some function including wrist flexion and extension (although still weak), plantar and dorsiflexion returning. He was discharged to rehab.

CENTRAL CORD SYNDROME

 As the name implied Central Cord Syndrome is an incomplete spinal cord injury.

Of the incomplete syndromes, it is the most common.

Most commonly occurring in hyperextension injuries of the neck.

Mostly in those with pre-existing degenerative disease of the cervical spine.

The classic presentation of upper limb weakness >> lower limb weakness. Distal >> proximal motor loss.

Variable sensory loss of primarily pain and temperature.

Urinary retention!! (place a foley catheter early!)

Some require neurosurgical intervention (worsening exam, acute cord compression (herniated disk), or have unstable fractures of the cervical spine)

Admit to ICU for neuro-checks.

Key words: Central cord syndrome, spinal cord injury, neurosurgery, trauma

A Cautionary Tale from “The Tank”

Let this serve as a cautionary tale for our rising residents.

“EXI” or “The Tank” is our holding area for acutely intoxicated patients or those requiring direct, constant observation for de-compensated psychiatric disease, suicidal/homicidal thoughts/actions. The 6 beds housed there see a rapid turnover of patients, most of whom are simply intoxicated and need time to sober. The general “tank” patient meets several requirements for safe discharge, a fairly basic list including: ‘clinical sobriety’, insight into the reason for hospitalization, (1) tolerating oral intake, (2) ambulating with steady gait, and (3) clear communication.

Heed this warning: sick patients do end up in “the tank”.

I will present a recent case and discuss the circumstances under which a patient’s disposition was delayed.

It was an unusually busy Thursday afternoon; the room 9 buzzer seemed to go off every ten minutes for several hours straight. Presenting to triage was a 30’s yo female registered with a chief complaint of “visual changes, SOB that all started after using meth” (directly quoted from the patient’s registration). She was placed in a recliner in bay 24 and connected to a bedside monitor which includes cardiac monitoring, pulse oximetry, and a traditionally less accurate measure of respiratory rate.

On my initial interview the patient states she had injected intravenously a “standard” quantity of methamphetamine. This occurred approximately 1 hour prior to triage intake. Keeping with her triage complaint; the patient relays a history of relatively quick onset SOA, not associated with cough or chest pain, that began after using methamphetamine. She also noted some blurring of her vision. She denied a history of either of these complaints. She denied any medical problems. She states that she takes no medications at home.

The initial exam was fairly unimpressive. The patient was awake, she was talking (at times nonsensical and tangential), and I would document her as “anxious” but in no acute distress. She demonstrated some degree of psychomotor agitation but no hostility towards staff. She was tachycardic to 130 bpm on the bedside monitor, regular, with the appears of sinus tachycardia. She had strong palpable peripheral pulses, a brachial blood pressure was 179/89. Her lungs were clear to auscultation. She was mildly tachypneic to the mid 20’s. Her abdomen was soft and nontender. Her skin showed evidence of peripheral IV drug use with multiple track marks and sclerosed veins. Her mucus membranes were tacky and she requested a glass of water (1 of the 3 basic “sober” requirements checked).

Her initial plan of care was “water” and “time”, planned sober re-evaluation.

“ROOM 9”. Several unstable patients later, several procedures and I re-evaluate the patient. She is sleeping but rousable. Her mentation is stable but not improving. She remains tachycardic, but mildly improved on bedside monitor to the 120s bpm.

A peripheral line and IV fluid bolus were ordered. Initial palpation/landmark guided attempts at peripheral IV were unsuccessful. An ultrasound was placed at bedside for attempts at deeper peripheral venous access.

I was called to the patient’s bedside. She had attempted to ambulate to the bathroom (2 of the 3 basic “sober” requirements checked?) but had stumbled around wildly and needed assistance with ambulation. The clinical condition had deteriorated. She remained tachycardic. Her mental status was waning. Her breathing pattern was deep and labored (Kussmaul-type). A finger stick blood glucose returned at >600 mg/dL. Just like that, everything clicked. This patient wasn’t acutely intoxicated on methamphetamine; which can cause tachycardia, tachypnea, and anxiety; she was in DKA.

She was surprisingly still conscious. She did endorse a history of insulin dependent diabetes when asked directly about the condition. She was unsure of her last insulin use as she had been on an amphetamine binge, her best estimate was “a week ago”.

She had no peripheral venous access after several failed attempts. Phlebotomy was able to obtain blood from her. Screening labs were sent including a serum and urine tox.

She was taken to room 9 where an internal jugular central venous catheter was placed for aggressive volume resuscitation. The MICU service was consulted for admission. Potassium supplementation was started. IV insulin therapy was ordered. Venous blood gas showed a pH <6.7, pCO2 <22.0, undetectable bicarb, uncalculated base excess (extraordinarily negative I’m sure). Broad spectrum abx were initiated pending completion of her laboratory workup. WBC 50k. Urinary tract infection with ESBL E coli. AKI. NSTEMI. Transaminitis (diagnosed with hepatitis C).

Total time between triage arrival and ICU consultation… 4 hours.

We read frequently about hang-ups in diagnosis. In the post-encounter review of this patient I identified several hang-ups in my own medical decision making.

1) The first I will call “triage level” in lieu of some other established name. I urge caution when patients are placed in “the tank”, the hallways, or when the intake nurse/bedside nurse suggests a patient will be a “quick” or “easy” dispo (they rarely are). Also, the assigned triage level 1-5 is not infallible. Do not let the level 5 patient in the hallway put you at ease or lower your guard.

2) Anchoring bias. This patient threw the anchor when she presented with “visual changes, SOB that all started after using meth”. It was easy in the middle of a busy shift to anchor on the provided information. After all, a lot of this patient’s history and exam findings suggested acute methamphetamine intoxication.

3) Provider fatigue. This was an unusually busy weekday shift. Be sure to take time to breath. Don’t rush to pick up the next patient. Focus on the task at hand.

Luckily this patient suffered no long term consequence of her delayed diagnosis. After an brief ICU and inpatient stay the patient was successfully discharged to her home with her boyfriend.

Sick patients do end up in “The Tank”, in the hallways, and in First Care/Fast Tracks. Use caution, keep a broad differential, and re-evaluate frequently.

I recently had two patients that presented with similar yet vague symptoms with two very different outcomes.

The first patient was a 70s-year-old female with a history of rheumatoid arthritis and hypertension who presented after finding dried blood in her mouth throughout the day. She denied any oral and dental injury or pain. She could not identify a source of the bleeding and did not feel any active bleeding. She had no associated symptoms, no melena or any other evidence of bleeding. She had no changes in her medications, but she is on methotrexate for her RA. Her physical exam was significant for dried blood in her oropharynx without an identifiable source. Her exam was otherwise benign. Lab work was significant for platelet count of 3, but otherwise normal. She was admitted for suspected ITP. On follow-up, she was later diagnosed with methotrexate toxicity. Her platelets improved after holding her home medications.

Second patient was an 80s-year-old female with severe dementia and hypertension. She was brought in by her son with whom she lives. The patient was unable to participate in her history or exam. He stated that when he went to get her out of bed that morning, he noticed dried blood in her mouth. Again, no trauma or source of bleeding was identified. She had no observed hematemesis or hemoptysis. Otherwise, history was unremarkable other than gradual weight loss secondary to poor intake. Exam was only significant for small amounts of dried blood in the oropharynx. Her mental status was at baseline. Lab work was insignificant. However, a chest x-ray showed a previously unknown left middle lobe mass. After a long discussion about goals of care with the son, the patient went home with plans for hospice care.

I found the juxtaposition of these two patients interesting as both had a vague, non-classic complaint with a generally benign exam.

Thought I’d post this. Saw it on Twitter. Cool little infographic on tox related syndromes.