For those of you who are still new to the splendor of these weekly emails, one recurring theme is that the EMS approach to trauma in NYC is all about ABCs and rapid transport to the appropriate hospital, often a trauma center. As such, most trauma jobs in the city can be performed at the BLS (EMT) level, with CFRs (FDNY firefighters) able to perform many (if not most) of the interventions.
This is well illustrated in the EMS protocol for bleeding, hemorrhage control, and impaled objects, where the bulk of care is in direct pressure (with hemostatic dressings, if available) and tourniquets (one initially for an uncontrolled bleed, with a second one that can be placed proximal to the first for continued bleeding). Note that, as per the Key Points section, tourniquets can also be used for bleeding dialysis access sites, if the bleed is life threatening and refractory to direct pressure. Impaled objects, briefly referenced, are to be left in place unless they are contributing to airway compromise.
That’s it! Stop the bleed! But don’t stop the learning! www.nycremsco.org or the protocol binder for more.
Dave
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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.
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
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.
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
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/
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://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