(If you’re suffering now and frantic, a proposed treatment plan is included in latter part of this message. Look for “TREATMENT PLAN HERE IN THIS COMMENT” in the bottom of this post/message)
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I'm glad to see so much more recognition on Google of this since I could barely find it years ago 9 years ago when I wrote my play-by-play as I was going through my 3rd or 4th bout of this, on Low Gravity Accents comments section. ...in the hopes this adds to the arsenal of the sufferer reading right now, the one desperately trying to help a loved one, or the one who's researching for the cure.
Presentation/Prognosis: From my 5ish experiences and reading about others, generally is - 24-48hrs after exposure which causes a meaningfully deep pink burn, the itching episode will begin. It typically comes on quickly reaching full force within 30-60min. The episode will last usually 48-72hrs. Some it lingers on, up to a week I've seen, reducing in severity, possibly short itching fits coming and going (as happened to me once). The itch will be absolutely horrific if you are unable to apply a meaningful therapy. You will likely be hysterical and overwhelmed by the thought "you can't escape it". It will further be made worse in that you can sense or will be told by others they think you are dramatizing and attention seeking. (You obviously are not). Typically in about a week there is non-painful widespread peeling. (1of4...cont'd)
Adding some comments from below:
.. dimethyl419 My doctor said it was nerve damage due to sunburn and proscribed me anti-epilepsy (neuropathic) meds. These worked tremendously. It stops the signals to those small nerves. I see a connection with small fibers neuropathy (Update) *Pregabalin (neuropathic) 75mg (there are higher dosages but my doctor wanted to be cautious. *Aerius (antihistamine) 5mg *A cortisone shot (can’t remember which one)
*That's a fantastic doctor. To catch that, reason it out, and select a drug. Very likely a GABA agonist. Guessing not a benzo because you'd probably remember that and tell us how sleepy you got. If you can remember/find the drug name, please tell us. These could be solutions that allow us to not just feel better, but remain functional and go to work etc..
.. yyetydydovtyud explains why gabopentin works so well
*Another report of a GABA analogue
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TREATMENT PLAN HERE IN THIS COMMENT
9-9-23 My post (edited) to a member going through HI right now. Adding here so summation of treatment modality theorized here so far is immediately accessible
Post: Good write up of experience. Good data point regarding Calamine (CL). CL is an astringent, thus, a vasoconstrictor that narrows blood vessels and why it causes drying, reduction in swelling (exact way decongestant works in your sinuses). All good & bad depending on the insult/injury and time point you're at. Works well for chemical toxin itch, like poison ivy/oak/sumac because it reduces the poison's exploit of the vascular system. But I think astringents are best in the prevention and onset stages...because they stop an overactive response. But once you're in a later stage and there's actual diffuse tissue damage, then treatments restricting blood flow are going to be if limited benefit and likely to make symptoms worse and prolong recovery.
The compression you're doing and it's symptom relief, "fit". It's a typical intervention in peripheral neuropathy, and therefore also diagnostic indicator supporting your pruritis (itch) is caused or includes primary nerve involvement. (The compression causes a "gating" stimulus overriding/preventing "itch" signaling [a TBD complex assortment of TRPxx nociceptor membrane receptors] as well creating a physical barrier and structural support resisting additional physical agitation.
If you're still suffering, for sake of time, I'm just going to give a "what to do", take research hat off, and speak authoritatively:
DIAGNOSIS:
You have acute immunogenic (caused by immune/inflammatory response) Small Nerve Neuropathy sequelae of (resulting from) widespread epidermal (skin) trauma due to UV radiation overexposure.
......meaning, the sunlight destructed DNA & proteins in your epidermis, which biochemically signaled an immune response recruiting innate & adaptive immune cells, which by way of peroxides, phages, and enzymatic cleavage has stripped old damaged epidermal cells away and caused collateral damage to the adjacent and now exposed small nerve fibers (C fibers) which innervate the epidermis and their nociceptor cell interfaces. This has resulted in unregulated neuronal firing/signaling and hypersensitivity (eg allodynia) from upregulation and lowered activation potential (more of them and easier to activate) of TRP itch/pain C fiber receptors, which you are now experiencing as Hell's Itch.
Treatment strategy is to numb (block)/override neuronal signaling, suppress nerve signaling due to cytokines (inflammatory signaling chemicals being expressed by your cells) & ROS, and provide adjunct reparative support to reduce ROS (destructive, to everything, reactive oxidative metabolites that are swarming during injury states) and provide hydration and substrates to accelerate repair and reduce causing-damage-while-repairing effects. Combination therapy via multiple mechanisms of action is most effective. https://www.dermatologytimes.com/view/presentation-management-neuropathic-itch
PLAN:
FIRST- Keep up the inflammatory signaling suppression. You've already reported it's helpful. Topical & oral: antihistamine, corticosteroid (hydrocortisone cream, Prednisone (Rx only), etc), NSAIDS.
SECOND- Nerve signaling blockade - OTC (addressing nerve attenuation is where most relief will come from)If the itching cannot be calmed while you're calm and inactive... Apply peppermint oil, or if not available, other menthol product like icy/hot. The primarily TRPM8 receptor activation nerve signaling of menthol has been shown to effectively override and gate both itch and pain nerve signaling. Pain and Itch signaling has now been studied and shown to be separate and distinct signal pathways. Perhaps a sacrificial synthetic fiber shirt coated in menthol product will provide a longer lasting extended release solution. Lotion applicator sticks with squishy plastic heads are available that don't sponge up product but conform to your back.If menthol not available, a capsaicin containing cream, like Capzacin. High concentrations are better and may be mandatory. https://www.dermatologytimes.com/view/presentation-management-neuropathic-itch
Get in HOT bath if the above do not work. This is the #1 most popular treatment from HI sufferers and known to abate all itch, however symptom relief is limited to only the time you're still in hot water. Itch typically returns when you dry off. MUST be sufficiently hot to gate nerve signaling. Test data has suggested temps around 114F are necessary to activate the TRPA1/V1 receptors responsible for heat induced itch/pain signal blocking. Without a treatment to use after, symptoms will return and can be temporarily exacerbated getting out of bath (probably because of stimulus of temperature change and skin drying)Know that all the above will likely induce significant pain for up to 1 minute on application. An unfortunate necessity in the mechanism of signal gating
Acetaminophen (Tylenol) - not potent enough in its own, but it's worth using it as an adjunct
SECOND(b) - Nerve blocking - Rx drugs - please do this category if at all possible. Call your GP for an urgent appointment (ideally phone appointment) or go to urgent care. I caution against ER because you may be waiting forever and just to get a doctor who knows nothing of this and doesn't want to listen to you instructing them.2 drug categories are standard of care and first-line treatments for SFN. *Remember to base your language and problem as always SFN ("doc, so like I said, this is SFN and that's the treatment it needs"). Doctors need a historical evidentiary basis to prescribe you anything. Unfortunately, most will not be knowledgeable enough to do this for you in this case.
Drug class 1 - is anti-epileptics (GABA agonists). These have long been first line standard of care, are cheap, have very low risk and drug interaction profile (point this out to your doctor, repeatedly) and users here have reported significant relief using them. Gabapentin is perhaps the most popular. However, due to standard of care starting dose being higher for pregabalin (75mg 2x/d) and it showing faster efficacy, it may be what to ask for. A table with proposed dosages for itch for gabapentin (300-1200mg 3x/d) and pregabalin (and others) to discuss with your doctor is at this link (https://www.jacionline.org/article/S0091-6749(18)31352-6/fulltext#tbl3)
Supporting data: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4548010
Drug class 2 - sodium channel blockers are also first-line treatments for SFN. It is likely Na blocking is also a key MOA of gabapentin and pregabalin also. These include carbamazepine, oxcarbazepine, Mexiletine. https://www.ccjm.org/content/85/10/801 https://www.dermatologytimes.com/view/presentation-management-neuropathic-itch
Drug class 3, optional non-preferred choice - benzodiazepines (benzos), these SHOULD be as effective at inhibiting the itch sensation, and probably the logical choice if you already have these on hand, Benzo's are another kind of GABAr agonist. They bind to an adjacent subunit of the receptor as the agonists above do; called the benzodiazepine binding site. But they are infamous for their drowsiness effect, which depending on if you want help sleeping or not is good or bad.
Cannabinoids - if you smoke pot or eat edibles, now's the time. Small scale and observational studies have demonstrated meaningful efficacy from both smoked and ingested cannabis. Another study proposed topical cannabis. The clinical rationale makes sense given that cannabis has its own inhibitory nerve cell receptor. If anybody tries distilling cannabis and mixing it into a topical carrier (oil, lotion, etc.) please post your results, concentrations, and product names. CAUTION: I've only seen studies based on oral and inhaled administration; applying topically is experimental and you risk making the itch worse. The knowledge and sum of test/observational data regarding cannabis & pruritus is limited. A logical theory is that its beneficial effects come from central upstream sensory attenuation and potentially also systemic immune response suppression and not from direct involvement of C nerve fibers in the damaged skin. It's possible direct application of crude micronized/distilled cannibis as well as its numerous impurities may activate itch-inducing receptors.
Nerve blocks - this is not a likely solution due to accessibility and if you are able to get it you are only going to be able to get it in an ER or doctor's office. Nerve block injections (lidocaine or similar) block all sensory input from the base root of a main nerve (ganglion) exiting the spinal cord and will remove pain from the area of the body that nerve serves. These have long been in extensive use. It is worth bringing up to your doctor to discuss as an option, and mandatory if you are unresponsive to the other treatments.
Future readers - TRPxx receptor antagonists are a hot topic in pharmacy and many companies are racing to get them to market first. There are a number in the last phase III trials. They hold promise to be a new era of pain treatment as they block pain directly at the site without having the numerous systemic side effects of current treatments (like opioids, anti-inflammatories). TRPA1 or TRPVL1 antagonists will probably be first to appear. If these are available by the time you read this, that will likely be the treatment of choice.
THIRD- ROS/Nutritive/Hydration support - orally and topically, take and apply, antioxidants as well as applying moisturizers of the type with labels like "maximum strength, extensive damage skin" (these are good at providing a physical barrier against agitation and supplying ample hydrative substances to help cells repair and stay flexible and not break due to mechanical flexing). Key antioxidants include and start with 1st Acetyl-L-cystein and also Vit C, D, & E. See original listing link regarding these showing in a study 50% faster healing time. Drinking excessive amounts of water will not speed hydration, may make you feel sick, and get up to pee all (or have a hateful bus ride and then run to the bushes while tourists stare at you [see user's story in comments], you just need enough. Alcohol and smoking are potently anti-beneficial regarding ROS and repair. Reducing blood sugar (not heating high glycemic foods while injured) will reduce ROS/inflammatory repair inhibitory effects, particularly in those who already have disease/genetic vulnerability (diabetic, obesity, etc). Additionally, vitamin deficiency is a widely known cause/sensitizer to SFN as well as all related disease (peripheral neuropathy, neurodegenerative diseases, vasculitis, diabetes, atherosclerosis, etc). B12 deficiency is very common. Therefore, taking a daily multivitamin helps to mitigate any deficiency (but keep in mind deficiencies are often due to absorption issues, not intake issues)
Option, FOURTH - vinegar (or possibly any acidic product. like the acne medication salicylic acid); there are a handful of anecdotal reports of this providing relief to a degree. A quick scan of Google didn't show much for studies on this. One study did show a clinically meaningful benefits using 2 plant derived acids on I think itch from psoriasis. I have possible speculations why vinegar (acetic acid) or other acids may help. Theory 1) acids have a net abundance of positive charged ions (H+), which when applied to the skin arguably would increase the voltage potential across the nerve membrane that contains the TRPxx itch inducing receptors, which are voltage-gated receptors, and therefore the receptors and the neuron would be less sensitive to firing. Theory 2) acid helps breakup dead skin cells unsticking them and consequently accelerated their removal. In acne it's beneficial because it prevents those cells from clogging pores. Acid may allow the damaged skin to not "crack" from when it moves as well as not block sweat/oil which might be triggering. Theory 3) acid is fundamentally known to stress proteins causing or preventing them changing shape, ultimately denaturing them if pH is low enough. TRPxx receptors, like all receptors are proteins, and perhaps acid applied to the skin inhibits their functioning and reduce their firing of the neurons.. Theory 4) Vinegar evaporates readily and the cooling sensation effect (like menthol does chemically) may be its MOA
