POTD: Trauma Tuesday! Blunt Thoracic Aortic Trauma

"Level 1 trauma...high speed car crash...GCS 6, was intubated in the field...ETA 5 minutes."

The patient arrives. You start your ABCs. The patient is intubated with BL breath sounds. You start circulation when you notice the pulses on BL lower extremities are absent with no obvious injury below the waist. You trace it up and notice decreased femoral pulses. The patient is getting exposed and you see a significant seatbelt sign on the chest. There’s a high suspicion for aortic injury. Let’s talk about blunt thoracic aortic injuries.

Background: Right off the bat: 80% of these patients do not make it to the hospital. Most of these patients die on the scene, however you may be able to do something for the 20% that make it to your ED. Up to 2 percent of patient who sustain blunt trauma to the thorax sustain a blunt thoracic aortic injury. 70% of patients are male. 

Associated with rapid deceleration events, aortic injury occurs with MVC most of the time, followed by pedestrian struck, followed by fall from significant height. Sudden deceleration causes the injury at the aortic isthmus.

Where is the isthmus? Why is the isthmus? Good questions. So I looked it up:

Why do injuries occur at this spot of the aorta? Well there are several theories. 1. The aortic isthmus is a transition zone between the unfixed aortic arch and the fixed descending aorta; sudden deceleration causes the two parts to go in different directions leading to tearing. 2. The tissue surrounding the isthmus is weaker compared to the rest of the aorta. 3. The Osseous Pinch (new band name 2021): the aorta is trapped between the bones of anterior chest and the vertebral column during deceleration force.

An initial tear in the intima then leads to more intimate pathology- that of aortic dissection. A tear in the intima in a high pressure vessel leads to bleeding which can penetrate the adventitia, worsening until the point of pseudoaneurysm and free rupture. This is one of the main reasons you're not out of the woods if they're among the lucky 20% of folks to make it to the hospital. 

Diagnosis: Gotta be on your A game. It won't always be apparent from the history and physical that you're dealing with an aortic injury. High speed injury, patient complaining of chest pain, back pain, SOB, trouble swallowing- all good places to start thinking about aortic injury in the setting of trauma. Good luck getting the patient to tell you any of these things, because a GCS <8 is present in up to 41% of patients with blunt thoracic aortic injury.

Physical exam findings that can tip you off include finding seatbelt sign across the chest, steering wheel sign, new murmur on auscultation. On the rarer side of things, you may see subclavicular hematoma or pseudocoarctation leading to increased pulses and hypertension of upper extremities, and decreased pulses and hypotension of the lower extremities.

CXR can show a widened mediastinum. One study by Bruckner et al found that the positive predictive value of a CXR with widened mediastinum is only 5%, but a cxr with the absence of widened mediastinum has a NEGATIVE predictor value of 99%.

Get a CTA of the chest if possible.

Aortagraphy is technically the gold standard for diagnosing blunt aortic injury. I'll be sure to get those right alongside my cardiac biopsies to diagnose myocarditis. Jokes aside, angiography is invasive and comes with its own complications and risks. And our wonderful CT techs and their wonderful machine is just calling to us from down the hall.

An alternative in a more unstable patient who is intubated is TEE. Like CTA, it also has a high sensitivity and specificity for detecting injury.

Grading is based on findings found on CTA. Let's breakdown the classification:

Type 1: Intimal Tear

Type 2: Intramural hematoma

Type 3: Pseudoaneurysm

Type 4: Rupture


Work up and management:

A 👏T👏 L 👏S. This is still a trauma, through and through when this arrives to your ED. Primary survey with ABCDEFast. Two large bore IVs. Fluid and blood. Secondary and tertiary surveys, imaging performed based on patient's clinic status.

For hemodynamically unstable patients, in the setting of trauma, go to the OR.

For the (initially) hemodynamically stable patient

Type 1 injuries may be managed conservatively- this means medical management- treat it like an aortic dissection. Aggressive HR control and BP control. HR below 100 and goal SBP 100. Esmolol is drug of choice, if another drug needed, can use diltiazem, nitroglycerin, nitroprusside.

Grades 2-4 require repair. Options include open repair with thoracotomy vs endovascular repair with aortic stent graft.

Oftentimes there are associated injuries. Injuries strong enough to hurt the aorta via deceleration is usually associated with blunt head, cardiac, lung, and bone injury. In fact, up to 81% of patients have an associated injury. The reason this is important, aside from having more things to treat in the ED, is that these can be distracting injuries to the true big bad laying in hiding.

Note: Thoracic aortic injury is a contraindication for REBOA therapy.

Sources:

https://www.annalsthoracicsurgery.org/article/S0003-4975(10)65322-2/pdf

https://cardiothoracicsurgery.biomedcentral.com/articles/10.1186/s13019-020-01101-6

https://pubmed.ncbi.nlm.nih.gov/16564268/

https://wikem.org/wiki/Traumatic_aortic_transection

https://www.ncbi.nlm.nih.gov/books/NBK555980/

https://pubmed.ncbi.nlm.nih.gov/21217494/

https://www.ncbi.nlm.nih.gov/books/NBK459138/

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The Fish Diseases

Hey all,

Scombroid. Ciguatera. Tetrodotoxin. Histamine poisoning.

Tired of getting these questions wrong on Rosh Review? Didn't realize that scombroid and histamine poisoning are the same thing?

Then this POTD is for you. Let's break down this topic together.

Scombroid: Think of histamine, and you'll get most questions correct regarding scombroid poisoning.

Background: Accounts for 40% of seafood borne illness in the US and Europe, most common states in Hawaii, California, Florida. Occur in outbreaks where everyone is eating the same batch of fish.

Symptoms: Flushing of face and neck, urticaria/pruritic erythematous rash, palpitations, dizziness, perioral burning and itching, edema, diarrhea, headache. Length of symptoms: 1-12 hours. Involves other members of family/friends who all ate the same food. Patients note that the fish has a "peppery" taste.

Rarely, upper airway edema, hypotension, or bronchospasm. 

Delicious Jerks Responsible: Typically fish of the Scombridae families, including tuna, mackeral, bonito, skip jack. Also happens with mahi mahi, swordfish, marlin, herring, sardine, anchovies, salmon, tilapia, and trout. Also swiss cheese for some reason (more on that later).

Pathophysiology: Caused by consuming fish which have not been properly refrigerated after being caught. Poor refrigeration leads to bacterial overgrowth in the fish capable of decarboxylating histidine into histamine. Histamine builds up in the fish over time, and post ingestion gives the histaminergic symptoms described above. Foods with histamine concentrations exceeding 50mg/100g of food are considered to be hazardous. Accumulation of histamine oftentimes happens before the fish becomes "spoiled" and thus is approved for consumption. Scombroid is associated with swiss cheese because it is thought the raw milk used in the production of the cheese can be contaminated with the same bacteria able to produce histamine from histidine.

Histamine is NOT destroyed when cooking the fish.

Treatment: Antihistamines- H1 and H2 Antihistamines

Treatment is focused on combating the excess histamine-

H1: Diphenhydramine

H2 for moderate to severe symptoms: famotidine/cimetidine

For patients presenting with enough histamine to appear as if they are in anaphylaxis, treat them as your would any anaphylaxis patient. 

Who is at risk for anaphylaxis like reaction? Patients taking something that inhibit histamine metabolism. This includes patients on isoniazid and MAO inhibitors.

Contact local public health to report scombroid poisoning.

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Ciguatera: Why do my teeth hurt? Why is my ice cream so HOT? The one with all the weird neuro-symptoms

Background:

Common on coastal regions; accounts for 20% of fish related foodborne illness in the US.

Fish containing ciguatera toxin appear normal. They do not taste or smell different than their non-ciguatera containing counterparts.

Symptoms: Vomiting, diarrhea, abdominal pain;

paresthesias, painful teeth, reversal of hot and cold sensation, perioral paresthesias, painful urination, cerebellar dysfunction including ataxia and vertigo, ;

rarely cardiorespiratory symptoms of bradycardia, heart block, hypotension, shortness of breath, respiratory distress.

Patients in multiple case studies report relapsing of symptoms. Though symptoms usually resolve in days to weeks, some report relapsing symptoms months and years down the line. 

Delicious Jerks Responsible: The reefers (moray eel, amberjack, grouper, snapper, parrot fish, sea bass, and ooh, barracuda).

Pathophysiology: Fish eat dinoflagellates of the Gambierdiscus family that grow on coral reefs. These dinoflagellates produce ciguatera toxin that accumulates in the fish. The fish are not affected by the ciguatera. The toxin is also heat stable, meaning it will not be destroyed during cooking.

The toxin works by opening voltage-dependent sodium channels on cell membranes, triggering cell depolarization.

Treatment: Symptomatic treatment.

Start at your ABCs as always, as these patients rarely, though sometimes, require airway maintenance. Atropine if needed for bradycardia, pacing. 

Antiemetics, IV hydration.

Sometimes recommended to use mannitol if neurological symptoms are present, though in an RCT of 50 patients by Schnorf et al, mannitol shown to have no benefit over normal saline in treating symptoms.

Gabapentin for neuropathic pain.

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Tetrodotoxin: The dangerous one; the one that can kill you

Background: Also known as pufferfish poisoning. Question stems usually involve someone eating fugu at a sushi restaurant.

Symptoms: Occur shortly after ingestion: parasthesia, headache, vomiting, diarrhea, abdominal pain

dysarthria, dysphagia, ascending paralysis, respiratory failure, and death.

Delicious Jerks Responsible: Pufferfish, angelfish, blue ringed octopus.

Pathophysiology: Produced by an endosymbiotic bacteria, tetrodotoxin is a neurotoxin that binds sodium channels, preventing sodium influx and preventing depolarization. Can cause paralysis; affects skeletal muscle interfering with respiration, causing respiratory failure, and with vascular smooth muscle, causing hypotension.

Treatment: Supportive care. ABCs, and if progressing to respiratory failure: intubation.

IVF

Can consider GI decontamination with stomach lavage and WBI if presenting to ED soon enough.

Some evidence suggests using anticholinesterases like neostigmine, though the evidence is weak and not shown to be effective in all patients.

Sources:

https://pubmed.ncbi.nlm.nih.gov/2689658/

https://wikem.org/wiki/Scombroid

https://pubmed.ncbi.nlm.nih.gov/11914401/

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4626696/

https://pubmed.ncbi.nlm.nih.gov/25410493/




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POTD: Droperidol

CODE WHITE AMBULANCE TRIAGE. The patient is at imminent risk of harming themselves and your staff. Verbal deescalation was attempted but has failed. Everyone is looking to you for your OK for chemical sedation. You dig your heels in and are about to mutter the first thing that comes to mind: "5 of haldol and 2 of ativan."

But hold up. Because this POTD is about droperidol.

Background: Droperidol is a dopamine antagonist, and is a first generation antipsychotic. It used to be a favorite of ED doctors to treat agitation in the ED and was used for more than 30 years for acute agitation. It was removed from market 20 years ago because of a black box warning due to QTC prolongation and risk of torsades/sudden cardiac death. This was based off a study looking at 273 case reports over a 4 year period. In the deaths reported, the doses used were 25mg-250mg per dose, doses MUCH higher than what we would typically give in the ED for agitation. Adverse cardiac events or death occurred in 10 patients who received a dose less than 2.5mg. From this study, the FDA placed a black box warning on droperidol. Upon further review of these cases by multiple authors, all of these cases had confounding factors that could have accounted for the adverse event. Overwhelming evidence after the FDA black box warning was issued has showed that droperidol is both safe and effective, especially when used at typical dosing for agitation.

Why Droperidol: Comparatively to other sedatives, namely haloperidol, droperidol is more potent, is faster onset, and has a shorter duration. According to Cressman et. al who examined absorption, metabolism, and excretion of droperidol, absorption via IM is near equivalent to IV administration. Onset of action is 3-10 minutes, and peaks at 30 minutes. Duration of effect is 2-4 hours, and effects may last up to 12 hours. Undergoes hepatic metabolism.

In the DORM study, 10mg droperidol IM was compared to 10mg IM Midazolam. Droperidol, compared to Midazolam, reduced the duration of violent behavior (20 min vs 24 min), required less additional sedation (33% vs 62%), and has less respiratory distress among intoxicated agitated patients.

If single agent droperidol is not enough, it was found in a study authored by Taylor et al that combination 5+5 droperidol and midazolam was more effective at sedation than droperidol or olanzapine alone.

Uses: Typical dosing ranges between 5mg -10mg for agitation, and can be administered IM or IV.

In addition, it can be used to treat headaches, vertigo, nausea, and pain, usually at half the agitation dose.

Side effects: Sedation, extrapyramidal effects, hypotension, prolongation of QT interval. Obtain an EKG if possible before administration, but if not possible, can be obtained after if the patient is agitated. Be mindful of using droperidol in the setting of patients with known prolonged QT interval and patients at risk given their medication history (e.g. methadone).

Sources:

https://vimeo.com/180991859

https://pubmed.ncbi.nlm.nih.gov/4707581/

http://www.emdocs.net/droperidol-use-in-the-emergency-department-whats-old-is-new-again/

http://www.emdocs.net/the-art-of-the-ed-takedown/

https://www.tamingthesru.com/blog/2019/4/20/the-return-of-droperidol

https://pubmed.ncbi.nlm.nih.gov/12707137/

https://dailymed.nlm.nih.gov/dailymed/fda/fdaDrugXsl.cfm?setid=147e033d-d997-4ef6-8bb5-a9ba372590b2&type=display

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