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Harm Reduction ⫸CASE STUDIES - It could happen to YOU!⫷

I have been an opiate addict for 6 or 7 years now (H for the last year...) and have a sky-high tolerance....pretty much the only 2 opiates i never tried is dilaudid and fentanyl. In the 'case report' i am referencing (its an old one..on page 2..from 6/16/09 titled "Inhalation Abuse of Fentanyl Patch) ...the guy OD'd from ONE (1!) lungful of smoke from a patch. Now, the fact that this guy scraped the patch, used aluminum foil, etc, etc...i am assuming he had *some* level of opiate experience and tolerance.... is fentanyl THAT strong to where ONE hit can make someone OD?? and since ONE hit did THAT..will further assume that when he fatally OD'd...probably wasn't that many more hits past the 1st one. Again..have never tried it and do not know a whole lot about it other than is incredibly strong. but WOW...1 hit = OD in this guy?? thats crazy


Also curious....what type of opiate is fentanyl? i mean...Oxycontin is oxycodone, Opana is oxymorphone, Dilaudid is hydromorphone, etc, etc ....what kind of 'done' or 'phone' or whatever is fentanyl?

i take 300mg-360mg oxy ir daily, and a few monthsd ago i was taking 4-5 50micrograms fetpatch gel squirted up my butthole and was getting ripped, not nodding but def like a kite. so there ya go bro bro brody!
 
Your tool or your habit!

That pic is scary and like you said "NASTY"! I've been in healthcare for 25 years, seen a lot of crazy shit, but that dick pic is just awful. Thank God I never got to the point of having to shoot dope in my dick veins...fuck that...I like my dick. When it's all said and done my manhood is more important than having to look at a dick like that. I had to IM some dope when all the "normal" veins were tore up...sure no rush, but when you're sick you gotta do something. It was scary injecting muscle, but I was very careful, good saline, needles, filters, everything, no shortcuts...pissed me off, but took my time and did everything the right way. Never got an infection or abscess, but I knew my dope days were coming to an end. Great thread, good info...but I seriously have no appetite after seeing that.
Goddamn that pic is nasty 8o . The only people i have seen resort to shooting up into their dick where all IV coke users. Coke is probably the most commonly IVed drug where i live followed by dilaudid and morphine. I did more damage to my veins from a few weeks of IV coke use then i did with 3 years of IV opiate use. I get some pretty nasty pills such as MScontins and hydromorph contins so i have to be extra careful when shooting those things. Thankfully i haven't had any complications despite 3 years of IV drug use. If i ever got so bad that i started shooting into me cock id fucking well go to detox or get on methadone.
 
I believe the gel patch has been discontinued...a few dozen OD's and other weird stuff, it has been replaced by the matrix design. Don't ask me what a matrix design is, but it's "safer", which means to many addicts figured out how to use and abuse the old one.
 
Femoral sticks

For any one considering a femoral vein shot...you better know your anatomy and know it well, otherwise don't do it. I work as a cardiac catheterization tech, we stick femoral veins and arteries all day and yes we miss and hit vein when trying for the artery and vis versa. There's a rule that goes...Artery first, vein second. The acronym is NAVE, which stands for nerve, artery, vein and empty space starting from the outside of the leg inward. But, sometimes the anatomy is different i:e vein on top of artery or artery overlapping vein. Those 2 vessels are so close to each other that should you mess it up, the pressure differences will create a false channel or pseudoaneurysm. That is where the artery and vein are now communicating or falsely connected...high pressure (artery) goes to low pressure (vein)...bad shit when you are pumping 120/80 pressure into vein designed for 15/05 pressure. A whole list of bad things happen and outcomes are usually not good.
Don't do it or your dick for that matter...the loss of limb and even mortality rates are high. Be safe.

Oh. My. Dear. God. The picture of that guy's penis is absolutely horrific. Poor guy. :( A friend of mine couldn't find a vein and I JOKINGLY told him to shoot in his penis vein. He actually did it and missed a good portion of the shot. Luckily he ended up being OK aside from having a giant lump on his penis for almost a week. I can totally see how shooting there could go wrong so quickly though. I was considering shooting in my femoral but I'm definitely not interested after reading/seeing this. Great harm reduction thread!!
 
To the poster asking about oding off one fent patch hit, yes it can happen and ive watched it happen. Have smoked a ton of those things...really because this guy and his wife were pharm techs that stole unused returned meds from the bins where they worked and got literally everything cII imaginable, and scored boxes of various dose patches. This was back when the brand name jaansen duragesics had the gel resevoir. Id smoke a 25mcg/hr in a few hits off foil. The guy i was getting them from had a tiny tolerance, like 1/8th mine probably. Well he squeezed a pea sized glob out of the patch hit it off foil, and after he exhaled his head kind of started to slowly go down and within a matter of seconds his head was down and he was fucked. His wife and i were able to get him on the floor laid out, his breathing was really slow as was everything else, but after a few minutes he came around more. I think had he smoked a few mcgs more we would have had to narcan him. I was just waiting for him to turn blue. It was frightening. Then the opposite thing happened, his wife got her tits done and he was giving her all sorts of drugs for pain, im morphine shots, oral oxy, then put a patch on her and she was way too fucked in an hour so we had to take the patch off but she stayed really trashed for like 6 hours, i guess bc by the time the patch was affecting her she had absorbed a bunch of it. Goes to show how strong fent is. I used to do dope with these two, so they didnt really have low opi tolerance. No wonder so many ppl overdosed on the gel patches and died alone in the bath tub or under an electric blanket. Even after wearing a 100 patch for 3 days there was still a good amount of gel in the patch. Only one of a number of times where i actually woke up high, really disorienting actually lol.
 
They DO still make Fentanyl gel patches; I'm wearing one, and have two five-pack 100mcg boxes made by Watson Labs right here! Neither my pain doctors nor my pharmacists have hinted that the jellies will be discontinued.
 
For any one considering a femoral vein shot...you better know your anatomy and know it well, otherwise don't do it. I work as a cardiac catheterization tech, we stick femoral veins and arteries all day and yes we miss and hit vein when trying for the artery and vis versa. There's a rule that goes...Artery first, vein second. The acronym is NAVE, which stands for nerve, artery, vein and empty space starting from the outside of the leg inward. But, sometimes the anatomy is different i:e vein on top of artery or artery overlapping vein. Those 2 vessels are so close to each other that should you mess it up, the pressure differences will create a false channel or pseudoaneurysm. That is where the artery and vein are now communicating or falsely connected...high pressure (artery) goes to low pressure (vein)...bad shit when you are pumping 120/80 pressure into vein designed for 15/05 pressure. A whole list of bad things happen and outcomes are usually not good.
Don't do it or your dick for that matter...the loss of limb and even mortality rates are high. Be safe.

I'm just wondering what procedure required that you hit an artery? I was under the impression that it's dangerous and should be avoided, but it seems like there are some medical procedures that you do it for.
 
I was insanely stupid when i was injecting. (Please dont laugh) when my veins collapsed i purposely injected into an artery in my arm. (The drug was subutex). I could feel the shot burning into the tiny veins in my hand, an itchy, molten heat.

I managed to quit iv before i started hitting the groin. "Needle fixation" isnt recognized by any doctor ive spoken to, but i believe its very real and is a powerful compulsion.
 
I had something similar from similar drug to my arm, a subcutaneous cyst which had to be removed with surgery. Wld love to attach my post op picture. Thank God for early intervention on my part in disclosing the truth..
 
What caused the abscess in the first place and how did it contain multiple pockets of gas. Eiteology of this process.
Big title implicating Ritalin, so could this happen with any IV drug? As for the contents and pathology, I'd guess this also cld be caused by any drug.
so why aren't the dangers and exactly what happened more emphasised than the drug itself, because that is quite scary!!!
 
Acetaminophen/Paracetamol is demonic shit. It is way, way too easy to cross the line, especially when you are having a good time and your judgement is impaired. My state bans anything anyone has the nerve to post a Youtube video of themselves having some fun with, but this poison, apparently not. This ingredient is in most common CIII pain combos. Give a listen.

http://www.thisamericanlife.org/radio-archives/episode/505/use-only-as-directed
 
...."Needle fixation" isnt recognized by any doctor ive spoken to, but i believe its very real and is a powerful compulsion.

(Firstly, I'm no addiction psychologist....) What you're describing as "Needle fixation" I personally haven't heard as single issue (which I'm assuming here why your doctors haven't heard of this specifically). However the complexity and totality of an (IV ROA) addiction is multifactorial - an addiction, and the process of removing oneself from the addiction is a lot more involved than simply (maybe "simply") quitting ingestion of x substance! In any addiction there is a huge psychological aspect which needs to be addressed. You've mentioned one; that feeling and entire process of scoring, setting up, finding a vein, seeing the flashback and knowing "what's to come". There is others, another influencer is termed "CPP" or "Conditioned Place Preferences". This is where if say you alway shoot up at one particular place, just by the mere fact of visiting there (even if there was no intention of using drugs) can (sometimes quite vividly) bring back all those thoughts, feelings and emotions.

Imo, if one wants to truely kick their addiction, treatment itself should include a variety of modalities to increase the chances of success. By this I mean; pharmacotherapy for help with the physical w/d symptoms, seeing a therapist (psychologist/-chiatrist) to understand why the addiction began and why it couldn't be stopped/got out of control (etc.), making sure you have a firm, supportive foundation of friends/family/peer-to-peer sponser, making sure you're generally living health (eating well, exercising) etc.

In all honesty, suffering through and making it past that initial w/d stage is just the begging.

I don't want to scare you off trying to quit. I'm just trying to supply as much info as I can to help. Either a sponser or rehab clinic would definitely be the best places to start.


Good luck dopemegently!
 
....Wld love to attach my post op picture. Thank God for early intervention on my part in disclosing the truth..

Do you have pics? A bit of hard truth might sway someone thinking of using the parenteral ROA for the first time. :\


Acetaminophen/Paracetamol is demonic shit. It is way, way too easy to cross the line, especially when you are having a good time and your judgement is impaired....

This is a naive thing to say (imo knee-jerk reactions like this regarding any drug is at the least naive).

All things are poison, and nothing is without poison; only the dose permits something not to be poisonous.
--Paracelsus

One of the first things one learns studying any form of medicine!



I think the interviewer basically said it simple and clear....
....Now I want to be very clear about what I'm saying here. Taken as recommended, Tylenol-- or any drug containing the active ingredient in Tylenol, acetaminophen-- is considered safe by most doctors and experts. The problems that we're talking about with the drug probably affect much less than 1% of all the people taking acetaminophen and Tylenol....

Some people may be shocked by this 1% statistic .... these choices of risk (ADRs/ADEs) versus overall benefit to the individual/society are well known (before release to market) and with a drug such as this having been on the shelves for as long as it has the drug profile is extremely well documented!

Paracetamol's TI is extremely safe and does have a large margin of error. Additionally, (especially in this case) the benefits paracetamol brings as an analgesic/antipyretic do outweigh these edge (or idiopathic) cases. Which unfortunately occur, of course, however when these situation do occur it does absolutely no body any help screaming death. These very few cases of course should be looked at and if possible the etiology investigated. But I'm sorry Xerolad, your post was an extreme overreaction.
 
Necrotising myositis after intravenous methylphenidat (Ritalin) injection

A 30 year old male intravenous drug user was admitted with a swollen painful left thigh after injection of 30 mg methylphenidat (Ritalin). On examination, we found a softball-sized abscess in his left thigh. Striking lab results were a CK of 18 100 U/l, a CRP of 177 mg/l, and a WCC of 20.0x109/l. A CT scan revealed a large abscess that contained multiple pockets of gas, extending from the lesser trochanter to the distal femoral condyle (fig 1). The patient went to theatre and the abscess was excised and drained and an extensive debridement was performed. Macro- and microscopic analysis showed acute necrotising myositis and extensive abscess formation. The patient was re-examined 2 days later and the wound was closed. Thereafter, healing of the wound progressed well. The patient was discharged home 15 days postoperatively.

I wanna take this ocasion to remind everyone how complete shit Ritalin is for recreation. I've gotten IR pills and it sucks. It's NOT an anphetamine, it's a synthetic lab made thing that's like coke with worst side effects and a 10 min duration if snorted that makes you euphoric and afterwards let's you really down and depressed wanting to do more. I heard of people IV'ing it every 10 mins over and over again because of this. In the end when you stop you're left with depression and tired, not able to fall asleep for a good while.
I did take 40mg orally right before playing soccer once and it worked seems physical energy it does give at least. Tried ER once and noticed nothing.

EDIT: Also you need more dramatic endings to the cases lol. There was this stupid Brazillian kid who injected coke into his dick to see if he would get a better boner, they had to amputate it. NOPLS.JPG True story...
 
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Respiratory Arrest caused by abuse of Fentanyl Patch: A Case Report

Respiratory Arrest caused by abuse of Fentanyl Patch: A Case Report
Arif Duran, Osman Ylldırım, Tarık Ocak, Ümit Tekelioğlu
National Journal of Physiology, Pharmacy & Pharmacology | 2014 | Vol 4 | Issue 1 | 89 – 91

ABSTRACT
Fentanyl is a pure and selective μ opioid receptor agonist that was discovered to identify an improved analgesic over morphine, an opioid frequently associated with histamine-release, bradycardia, hyper- or hypotension, and prolonged postoperative respiratory depression. It is 80-100 times more potent and has less adverse effect than morphine. The formulations are intravenous, transmucosal, and transdermal. Besides its efficacy, the transdermal route is safe, since with it the plasma concentration of fentanyl can be adequately maintained at a steady level. Transdermal fentanyl patch has been increasingly used recently for the management of chronic pain. This brings about increased rates of misuse or addiction in general population. Transdermal fentanyl patch may produce respiratory arrest as all other opioids do. Herein, we describe a woman with meperidine dependence who developed respiratory arrest after cutaneous application of 4 transdermal fentanyl patches, with relevant literature review.

CASE REPORT
A 26 year-old female patient has been found unconscious in her room by her relatives and was transferred to the emergency unit by their own means. The respiration has been associated to a mechanical ventilator by intubating the patient because of her unconsciousness. While the patient’s clothes were removed, 4 fentanyl 10 mg transdermal patches were observed on her abdominal region and those were immediately removed. The incoming brachial tension arterial was 85/55 mmHg, heart rate was 120 /minutes, fever was 36.5˚ C axillary. No light reflex was observed in systemic physical examination and there was a spot pupil. The Glaskow coma scale (GKS) was 3 (E1V1M1). In the electrocardiography, there was no other pathology than a sinus tachycardia at a rate of 120/ minutes. No pathology was observed in brain tomography. The relatives explained that the patient was a nurse in a private medical care center, that she had severe headache approximately 9 months ago, and that one of her nurse friend applied to her on dose of intramuscular drug containing meperidin, and that our patient always asked for that drug. Besides, 2 weeks ago, our patient has been suspended from the hospital where she was working because the stock of drug decreased due to her 5-6 weekly doses. As she could not get meperidin, the patient used 4 transdermal fentanyl patches with a 100 μ/ hour release rate from one of her relatives having a cancer treatment. The patient has been transferred to intensive care unit. She was monitored in SIMVVC mode of the mechanical ventilator and woke up after 16 hours. She was monitored for 8 hours in intubated state after she woke up, and then was extubated. After 48 hours in intensive care unit, the patient who did not present any complication has been transferred to the psychiatric unit.

DISCUSSION
Nowadays, morphine and fentanyl, which is a newly developed synthetic group member are widely used and easily prescribed, thus leading to serious health problems. Fentanyl transdermal products are frequently used for pain management in cancer patients, especially in chronic pain treatment. Fentanyl transdermal system may provide a 72 hours pain control with regular absorption. In Turkey, 2.5, 5, 7.5, and 10mg versions of the drug are on sale and provide release at 25, 50, 75, 100 μ/hour. In our patient, 4 fentanyl 10 mg transdermal patches with a 100 μ/hour release rate were observed on her abdominal region. Fentanyl, like other opium derivatives, may lead to side effects such as the inhibition of central nervous system, loss of consciousness, respiratory depression, hypotension, bradycardia, hypothermia. In our case also, the patient developed nervous system inhibition, coma (GKS:3) and respiratory arrest. The blasting of the transdermal system, the utilization of too many patches, the inhalation, the suction of this drug may lead to toxicity. In literature, cases of death due to oral absorption of transdermal system or many patches at 100μ/hour rate have been observed. The active utilization of fentanyl transdermal system in our country only for the last 10 years may explain the absence of such cases. The only case of transdermal fentanyl misuse or addiction declared in our country is the fentanyl transdermal system addiction from Geçici et al.

[Full article and references available here: http://www.scopemed.org/?mno=31555]
 
Ocular Complications in IV Drug Users

Ocular Complications in IV Drug Users
Two case reports illustrate the visually devastating risks associated with the use of injectable street drugs.
By Amanda S. Legge, O.D.
Review of Optometry, 11/19/2012

Intravenous drug use is directly associated with a variety of localized and systemic complications. In addition, it can yield numerous ophthalmological consequences. The most devastating ocular side effects of intravenous drug use include the formation of choroidal and retinal nodules, infarction and inflammation. Typically, such associated lesions form in the posterior pole near the macula.
Eliciting a thorough patient history is crucial for appropriate testing, culturing and treatment. Prompt diagnosis and management is of utmost importance to decrease both ocular and systemic morbidity.
The following case reports describe complicated infections and potential posterior segment damage secondary to intravenous drug abuse.

CASE 1
History
A 30-year-old white male presented to our office for the first time with a chief complaint of decreased visual acuity (O.S.>O.D.). His vision had decreased suddenly about two weeks earlier but had remained stable O.U. since. He denied the presence of floaters, photopsia, diplopia, pain or discomfort.
The patient’s medical history was remarkable for post-traumatic stress disorder, bipolar affective disorder, chronic cluster headaches and depression. He did not take any medications.
The patient’s ocular history was unremarkable because he reported never undergoing a formal eye exam. His family ocular and medical histories were unremarkable.
Prior to vision loss, the patient experienced low-grade fevers, severe cluster headaches and diffuse joint pain for one month. His primary care physician (PCP) performed an extensive lab work-up, which included complete blood count (CBC), partial thromboplastin time, international normalized ratio, lupus anticoagulant, amylase, lipase, fluorescent treponemal antibody (FTA), rheumatoid factor, antinuclear antibodies, rapid plasma reagin (RPR), urinalysis and HIV screening.
All test results returned within normal limits. The patient also had a negative CT scan of the head and chest without contrast. He had not seen his PCP since receiving these results.
Upon further questioning, the patient admitted to injecting crack cocaine dissolved in vinegar intravenously. He said that he had injected the drug approximately 10 to 15 times per week for the past five years. He stated that he was aware of the risks of his behavior, but had not sought any counseling or rehabilitation.

Diagnostic Data
The patient’s uncorrected visual acuity measured 20/40 O.D. and 10/300 O.S. with direct fixation. No improvement was observed upon pinhole testing. He achieved 20/200 O.S. with eccentric fixation. His pupils were equal, round and reactive to light, without evidence of afferent defect O.U. Extraocular motility testing showed no restrictions in muscle movement. Confrontation visual fields were full to finger counting O.U.
Intraocular pressure measured 11mm Hg O.D. and 12mm Hg O.S. Anterior segment examination was unremarkable. We detected no inflammatory cells or protein flare in the anterior chamber.
Gonioscopy revealed that the most posterior structure in all quadrants was the ciliary body face O.U.
No sign of microhyphema, microhypopyon, peripheral anterior synechiae or neovascularization was noted O.U. Posterior segment evaluation revealed multiple choroidal and retinal infarcts of varying duration (figure 1) as well as the presence of Roth’s spots throughout the posterior pole O.U. (figure 2).
Nerve fiber layer hemorrhages and exudates as well as retinal infiltrates were noted, indicating a septic chorioretinitis. The optic nerves appeared flat, pink and distinct, with no sign of disc edema O.U.
The left macula was affected dramatically by multiple infarcts and intraretinal edema, which correlated with the severe visual decrease in that eye.
The right eye exhibited subtle macular edema and exudates, accounting for the mild decrease in vision.
Following the examination, we ordered additional blood work, including another CBC with
platelet count and differential, troponin I, Westergren sedimentation rate, C-reactive protein (CRP) and a blood culture.

Diagnosis and Follow-Up
We tentatively diagnosed our patient with septic chorioretinitis, pending further testing. We educated the patient about the emergent nature of this condition and informed him that it likely was caused by bacterial endocarditis. We made an immediate referral to a local hospital, and indicated the need for a transesophageal echocardiogram (TEE) to confirm the diagnosis and begin prompt administration of intravenous antibiotics.
He did not report to the hospital as recommended. Upon investigation, a relative informed us that he had died from a gunshot wound to the head. Apparently, he was murdered the night of the referral. We later confirmed this report.
The lab results were received within 48 hours, revealing an elevated troponin I, sedimentation rate and CRP. The CBC remained within normal limits. The blood culture revealed growth of Staphylococcus aureus, which may have been methicillin resistant.
Although the TEE could not be obtained to confirm, we presumed the diagnosis to be bacterial endocarditis secondary to S. aureus infection, very likely due to street drug use.

CASE 2
History
A 42-year-old white female presented with a chief complaint of severe blurred vision in her right eye that had persisted for a week. Her vision decreased rapidly and painlessly over the course of two to four days and had remained stable since that time. She did not complain of pain, irritation, diplopia, photopsia or floaters. Additionally, she exhibited no associated systemic signs or symptoms.
The patient’s medical history was unremarkable, but she admitted that she had not seen a PCP in at least 10 years. Her ocular history was unremarkable; however, she reported wearing glasses since age 12. Her current prescription was at least four to five years old. The patient’s family ocular and medical histories were unremarkable.
Upon additional questioning, the patient admitted to intravenous heroin use since age 15. She reported that, during the past year, she had reduced her drug usage to “just a few times a month.” However, she admitted to using heroin up to six times per day in the past. She acknowledged the risks of her behavior, and had attended multiple counseling sessions during the last five years. Still, she never enrolled in a formal rehabilitation program.

Diagnostic Data
Upon evaluation, the patient’s corrected visual acuity measured 20/100 O.D. and 20/20 O.S. No improvement was documented upon pinhole testing. Her pupils were equal, round and reactive to light, with no evidence of afferent defect. Extraocular motility testing showed no restrictions in muscle movement. Confrontation visual fields were full to finger counting O.U.
On color vision testing, the patient correctly identified 14/14 Ishihara plates O.U. No red desaturation was detected.
Her intraocular pressure measured 18mm Hg O.D. and 19mm Hg O.S. The anterior segment examination was unremarkable, with no evidence of inflammatory cells or protein flare in the anterior chamber. Gonioscopy revealed that the most posterior structure in all quadrants was the ciliary body face O.U. We documented no sign of microhyphema, microhypopyon, peripheral anterior synechiae or neovascularization O.U.
The posterior segment evaluation revealed a round, yellow-white pre-retinal lesion (figure 3) with surrounding telangiectasia (figure 4) and 2+ posterior vitreous cells in her right eye. Furthermore, we noted trace to 1+ cells in the anterior vitreous.
The right optic nerve had blurred margins. This presentation likely was caused by traction and vitreal inflammation rather than true disc edema, because no afferent defect was noted on pupil testing and color vision was normal.
The fundus examination of the left eye was unremarkable.

Diagnosis and Follow-Up
Immediately, we referred her to the hospital for blood work and intravenous antimicrobial therapy. The patient received an MRI of the brain and orbits, both with and without contrast. Additionally, she underwent FTA, RPR, HIV screening, Lyme titer, angiotensin-converting enzyme, Toxocara screening, purified protein derivative, chest X-ray, CBC testing and a blood culture.
Further, a vitreal culture was taken the following day. A mold infection of unknown species was identified in the vitreal cultures. All other blood testing was negative. The patient was started on intravenous amphotericin B, because of its broad-spectrum coverage. The mold did not reproduce in the mycology lab, which was necessary for species identification.
Because amphotericin B has poor vitreal penetration when prescribed orally, the patient also was started on 5µg/0.1mL intravitreal injection of the drug. She received two in-patient intravitreal injections during the five-week hospitalization period. Following discharge, the patient was transitioned from intravenous to oral amphotericin B by her infectious disease specialist. Recently, she reported a moderate improvement in vision with mild distortion. Approximately five and a half weeks after the initial diagnosis, her visual acuity measured 20/50 O.D. and 20/20 O.S.
Vitreous cells were not observed at follow-up. The pre-retinal nodule had formed into a fibrotic scar, causing retinal traction and striae (figure 5). Blood cultures were performed again both two and four weeks after hospital admittance; all cultures returned negative. Eight weeks after initial culture, we identified the mold as a Malbranchea species.
During the next year, we will closely monitor the patient for advancing retinal traction and a potential detachment O.D. We educated her extensively on the risks associated with intravenous drug abuse, and she promised to begin an official rehabilitation program as soon as possible.

DISCUSSION (abridged)
Recreational injection of street drugs directly is associated with a variety of local and systemic complications. It is also linked to the transmission of infectious diseases through needle sharing and sexual activity. The most serious ocular complications have been reported from the use of crack or crack-cocaine, methylenedioxymethamphetamine or diamorphine (heroin) injections.
Ophthalmological complications include corneal ulcers, reduced corneal sensitivity, microtalc retinopathy, retinal or choroidal infarcts, central retinal artery or vein occlusion, endophthalmitis, nystagmus, and cerebrovascular accidents that cause neuro-ophthalmic manifestations.
Retinal or choroidal infarct, inflammation or infiltrates cause some of the most devastating visual sequelae, because they typically are located in the posterior pole. These signs are indicative of general septic chorioretinopathy. The underlying cause is bacterial or fungal (or, less commonly, parasitic). Inflammatory causes of chorioretinopathy must also be ruled out.

Eliciting a history of illicit intravenous drug abuse is imperative when septic chorioretinopathy is suspected. This helps to facilitate prompt testing for the most commonly associated pathogens and also could help guide the most appropriate treatment regimen.

Bacterial pathogens, specifically those of the Staphylococcus genus, are the most common cause of infection in intravenous drug users. Without question, eye care clinicians should be most concerned about the potential for methicillin-resistant Staphylococcus aureus. Other common pathogens associated with this behavior include streptococci, gram-negative bacilli, enterococci, Fusarium, Aspergillus and Candida.
The development of Roth’s spots is one of the most serious presentations in intravenous drug users who are suspected of bacterial chorioretinitis or endocarditis. Roth’s spots are white-centered hemorrhages that classically are indicative of bacteremia and bacterial endocarditis; however, they also are seen in diseases such as leukemia, pernicious anemia, sickle cell disease and connective tissue disorder.
In bacterial endocarditis, Roth’s spots are formed as a result of thrombocytopenia and a low-grade, disseminated, intravascular coagulopathy. The clinically viewed, white-centered hemorrhages are most likely caused by anoxia, which causes a sudden increase in venous pressure. This causes capillary rupture and extrusion of whole blood. Platelet release causes the coagulation cascade to initiate, eventually causing a platelet-fibrin thrombus surrounded by heme.

Because of this specific pathology, Roth’s spots are now part of the standard used to determine a diagnosis of bacterial endocarditis.

[Full article with pics and references here: http://www.revoptom.com/content/c/37817/]
 
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Myofibrosis in a pentazocine addict

Myofibrosis in a pentazocine addict
By Paresh Zanzmera, Manoj Somasekharan, Achal Srivastava
Indian Journal of Pain, 2013, 27, 3, 185-188

ABSTRACT
Pentazocine, a synthetic narcotic analgesic, is commonly used for the relief of moderate to severe pain, but has been rarely abused also. It is usually well tolerated; however, adverse effects are not uncommon, when higher doses are used, especially in a dependent fashion. There are reports of various complications associated with its use, including skin fibrosis, skin ulceration, abnormal skin pigmentation and symmetrical myopathy with fibrous myopathy. Fibrosis has usually been reported in the muscles at the site of injection of the drug. Being opioid in nature, it has a high abuse potential. We report a case of pentazocine-induced myofibrosis in a 33-year-old man involving muscles which were not injected with pentazocine. This case highlights the care that needs to be taken when prescribing opioid analgesics, such as pentazocine, as routine painkillers. Rare consequences such as myofibrosis are devastating and can cause significant lifelong disability.

CASE REPORT
A 33-year-old man presented with complaints of painless and progressive bilaterally symmetrical toe walking with stiffness and wasting of the muscles of both calves, followed by bilateral elbow contracture and then stiffness and wasting of back and proximal muscles of both upper limbs for the previous 3½ years. There was significant impairment of his daily activities including walking, bending, lifting, or straightening arms. Patient had retained ambulation till now and due to contracture of the bilateral shoulder, elbow, hip, knee and ankle joints along with lordosis of lumbar spine; resulting in characteristic 'robotic' posture with 'toe walking'. There was no associated weakness.

At 17 years of age, he was prescribed long-acting benzodiazepines, valium (Diazepam) 10 mg and nitravate (Nitrazepam) 10 mg by general practitioner for pain relief and insomnia. Over a period of time, he developed drug dependency. From 23 years onwards, he started self-injecting Fortwin (Pentazocine) and Phenergan (Promethazine) combination in a dependent fashion, around two ampules every day in divided doses, into the buttocks and upper arms. He never injected into thighs, calves, abdominal, shoulder girdle or forearm muscles. He would develop generalized tonic-clonic seizures and restlessness in absence of drugs.

On examination, his vitals were stable but he had great difficulty in dorsiflexion of ankles and extension of elbow, along with overhead abduction and complete adduction of shoulders. There was wasting and hardening of the muscles of the back, arms, thighs, forearm, and calf muscles [Figure 1] and [Figure 2]. He walked with a lordotic posture and robotic gait and had marked woody indurations of the deltoids, biceps, glutei and quadriceps, and gastrocnemius. The range of movements was decreased markedly. His arms could not be actively abducted beyond 75° and the legs not more than 60°. Both elbows were semi-flexed with no more than a 25° range of movement. He was unable to touch heels on floor with ankle range of movement nearly 10°. There was associated bilateral wrist joint contracture with range of movement not more than 40°. Movements at the distal joints in both upper and lower limbs were significantly affected as compared to proximal muscles. Muscle power was normal within the limited range of movements, and there was no sensory deficit. Examination of the rest of the nervous and other systems did not reveal any other abnormalities.

On investigation, hemogram, liver and renal function tests, serum calcium, phosphate, and creatinine phosphokinase were within the normal ranges. Roentgenogram of the lumbar-sacral spine, thigh, knee, chest, shoulder, elbow, and cervical spine showed multiple soft tissue calcifications with hyperdensity of muscles [Figure 3]. MRI thigh [Figure 4] revealed non-descript reduced signal intensities in subcutaneous fascia and myofascium in all groups of muscles of thigh. There was no articular abnormality. Electromyographic examination of muscles was normal. Muscle biopsy showed atrophy with features suggestive of neurogenic involvement without active inflammatory signs.

DISCUSSION
The differential diagnoses considered were ankylosing spondylitis, Stiff-man syndrome, myositis ossificans, and parathyroid disease. In view of normal joints, diagnosis of ankylosing spondylitis was not considered further. Stiff-man syndrome presents with spasms and cramps, and usual presentation is after middle age. The possibility of myositis ossificans was unlikely, as the present case was of late onset and was characterized by the absence of skeletal abnormality. Normal serum calcium and phosphate levels excluded hypoparathyroidism. Pentazocine-induced myofibrosis was a strong possibility in view of the history of pentazocine abuse, hardened muscles and the clinical presentation.

Previous case reports described complications of pentazocine injections in form of browny induration of skin and under-lying tissues [2],[9] and fibrous myopathy [4],[5] with patients having woody induration of muscles with secondary contractures.

The exact mechanism of this condition is unknown. Pentazocine is acidic (pH 4.3) in nature and its crystals gets precipitated in neutral or alkaline medium. This property, along with the muscle trauma caused by repeated needling and rapid injections of large boluses of drugs, may be responsible for this or other types of drug-induced myopathy. [10] This remains the most acceptable hypothesis for explanation of the condition. The use of pentazocine in this case was along with phenergan injection. This could have played a contributory role to the pathogenesis, phenomenon, although we do not consider it as the primary causative agent since its use has not been associated with such lesions in the literature.

Previous reports [8] of pentazocine-induced myofibrosis had predominant involvement of proximal muscles, as contrast to predominant distal muscles involvement in our case. Specifically, toe walking due to pentazocine-induced myofibrosis is novel presentation. Another interesting aspect of this case is the involvement of muscle groups which were not injected with pentazocine. The patient's self-reported history and the inaccessibility of the muscle groups involved (those of the shoulder blade, back muscles) support the claim that these muscle groups were not directly injected by the patient. Hence, the local action of pentazocine seems to be an unlikely explanation of the condition. The possible mechanism could be a direct action of the drug once it enters into the circulation or the release of an independent factor from the site of injection that leads to widespread involvement of the muscles.

Moreover, the onset of the fibrotic changes correlated to the use of the injection pentazocine and was temporally unrelated to the past use of benzodiazepam, as the patient and his family members corroborated that he had stopped benzodiazepam use at least 8 years ago. Moreover, we could find no complications caused by long-term dependence of benzodiazepam.

The abuse of prescription opioids, such as pentazocine, is being increasingly reported across globe [11] including India. [10],[12],[13] With easily over-the-counter access to these drugs in India and many developing countries, awareness of this complication is important so that unwanted side effects can be avoided. Moreover, the drugs are initially prescribed for a medical indication and subsequent use by the patient continues without the advice of a physician. Clinicians should be aware of addictive property of such medicine, and extra caution should be exercised when dealing with individuals with a history of substance abuse and/or dependence. This will help in preventing such drug abuse and its complications.

In conclusion, this case highlights the rare consequence such as myofibrosis following pentazocine addiction resulting in to lifelong disability. Physician should be aware and vigilant about prescribing potentially addictive painkillers.

Figure 1: Front view of patient. Note partly abducted shoulders, semifl exed elbows, and planter flexed ankles
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Figure 2: Lateral view of patient. Note lumbar lordosis, incomplete extension of knees and planter flexed ankles. Figure 1 and 2 shows robot-like posture of patient
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Figure 3: X-ray right elbow AP view showing hyperdensity of muscles. There is no body abnormality seen
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Figure 4: MRI of right thigh, axial section showed non-descript reduced signal intensities in subcutaneous fascia and myofascium in all groups of muscles of thigh
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