For ex, meperidine does not change pupils, and often the presence of adulterants or co-ingestants like sympathomimetics and anticholinergics can make the pupils appear nml or even enlarged
The best predictor of opioid toxicity is respiratory rate <12.
Heart rate is typically normal or low normal (60-70).
Look for evidence of trauma, certainly check a fingerstick glucose. An EKG is never a bad idea, especially in cases of suspected self-harm or where LOC occurred.
We do not recommend routinely checking urine toxicologic screens.
In fact, in a young patient where opioid abuse is clinically suspected and responds well the naloxone, no evidence supports further diagnostic workup.
Opioid overdose is a clinical diagnosis!
Ddx: in patients who present obtunded U must consider other sedative-hypnotics like clonidine, ethanol, benzodiazepines, and barbiturates.
Hypoglycemia is a commonly missed medical diagnosis.
Clonidine, which has opioid-like effects, causes miosis w/e bradycardia & hypotension
Management: Naloxone is a pure opioid antagonist, immediately displaces opioids at receptors.
It reverses all respiratory and central nervous system depression within 1 minute.
Reversal effects depend on the type and duration of the opioid(s) taken, from 20 minutes to an hour
Is the patient in respiratory or cardiac arrest or in critical condition (keywords: non-arousable or no spontaneous ventilations)?
Yes. By all means, give large doses of naloxone.
If not, then give smaller doses of naloxone to avoid precipitating withdrawal.
Naloxone in life-threatening situations
If available, intranasal naloxone is recommended in life-threatening situations.
Otherwise, initial dose: 2 mg IV rapid push. You can also do intramuscular or intraosseous for similar effects, but not as predictable as IV.
If the initial dose is partially effective, give the same dose again. If no effects observed, give a 👆dose.
There’s no literature on how many times you should administer naloxone & watch for an effect, but wouldn’t advise >10 mg total of naloxone if no clinical improvement
When an opioid effect is expected to be prolonged (e.g. massive overdose, suicide attempt, methadone usage), a continuous infusion or naloxone should be used.
You likely have this stocked at your hospital, but it’s easy to make: mix 4 mg naloxone in 100 mL D5W.
The initial naloxone infusion rate should be 2/3 of the naloxone dose that reversed the patient’s symptoms.
Example: initial bolus dose which reversed symptoms = 2 mg; Start infusion at 1.3 mg/hr.
Titrate the infusion as needed: increase by 0.1 to 0.2 mg/hr if symptoms return.
To wean off the infusion:
1. Decrease by 0.1 to 0.2 mg/hr every 2 hours. 2. Check the patient for signs/symptoms. 3. If decreased respiratory rate or responsiveness is noted, return to the previous rate and attempt to decrease again in 1 to 2 hours.
Monitoring post-naloxone.
Its controversial how long patients who received naloxone should be watched in the ED.
The underlying concern is that the duration of naloxone is shorter than the duration of most opioids.
So, if naloxone wears off in about 40 minutes, close monitoring is needed for a few hours to be sure there are no recurrent symptoms.
No one really agrees on the amount of time to observe, and that’s honestly never going to happen.
When the choice is made to discharge, bystander-administered naloxone should be prescribed.
Providing the patient, w/ this medication can 👇overdose mortality.
One study showed a comprehensive opioid overdose prevention program 🔽 deaths from 46 to 29 per 100,000.
Complications of opioid toxicity
One unique complication is lung injury and noncardiogenic pulmonary edema; it is rare (<3% of patients receiving naloxone).
The pathophysiology is unclear, but it can be a major adverse effect of narcotic overdose
It seems that the trigger is iatrogenic from reversal of narcotic toxicity with naloxone.
Rapid precipitation of withdrawal in the setting of elevated pCO2 causes a surge of catecholamines, therefore increasing afterload and vascular permeability in the lungs.
This is another reason to use small doses of naloxone if possible.
t has a rapid onset, often with crackles, hypoxia, and frothy sputum. Expect hypertension and tachcardia.
There are no published, evidence-based guidelines on how to manage this. It will not be on board exams.
Supportive management is indicated: supplemental oxygen, likely with NIPPV, is standard of care.
Diuretics have been quoted as helpful, along with nitroglycerin if patients are hypertensive.
Hematogenous dissemination then can occur typically 4 to 10 weeks later, giving rise to secondary syphilis. <40% of pts w/ syphilis have primary syphilis diagnosed. These “Secondary” lesions last for several weeks before spontaneously resolving. Coined “early, latent infection”
What does late infection mean? When syphilitic lesions recur after 1 year from the initial eruption, or seropositivity is detected more than 1 year after the initial eruption, it is termed late latent syphilis.
Some optics neuritis pearls in a short #Medtweetorial 🧵…. We all know that optic neuritis is frequently associated with multiple sclerosis (MS). But optic nerve inflammation can exist from autoimmunity, infection, granulomatous disease, paraneoplastic disorders, & demyelination
Classical ON from MS is unilateral, moderate, painful color vision loss with an afferent pupillary defect & normal fundus examination.
In those with ON, 95% of patients showed unilateral vision loss & 92% had associated retroorbital pain that frequently worsened w/ eye movement.
If you have not listened to the @CuriousClinPod most recent podcast (Episode 10: Why does metronidazole treat both bacterial and parasitic infections?) then I suggest you tune in.
I'll summarize their show notes here in short #medtweetorial
First a question:
Was metronidazole first used as an antibiotic or as an antiparasitic?
If you guessed antiparasitic, then you would be correct!
It was developed in the 1950s to treat the parasite trichomonas & then was used in the 1960s to treat other parasitic infections, like giardia and amoebiasis.
A 31-year-old M born and raised in Brazil w/ no PMH presented with a 3 mon history of worsening DOE, orthopnea, 7kg weight loss, abdominal distention, dry cough, and syncope
An interesting fact from @3owllearning : Depending on the clinical problems, the studies of disease probability for differential diagnosis often show 10 - 25% of cases are unexplained, even after careful examination and testing.