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

By no means am I arguing with you, but isn't it impossible to OD from free-basing ice? I've overamped where my body has shut down, but have never heard of anyone ODing smoking it.
 
you are right but this is the real world and there r no "IF's". Meth is dangerous and i KNOW this. Convincing myself on bluelight wont change the fact that meth is an evil drug, but lovely nonetheless. Meth being dangerous also doesnt change the fact that heroin also destroys lives. It may not b very toxic but the indirect effects of heroin are mostly always devastating. Heroin users are also PROBABLY the most reckless in their use of the drug.

there is no such thing as a safe drug but when it comes to meth vs heroin, judging by all aspects, heroin wins the most dangerous drug title and my argument is not against meth molecule vs heroin molecule but instead icehead vs dopehead.
 
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I love this thread! It can be hard to find stuff like this in search engines half the time. Good job djsim!
 
Pott Puffy Tumor Associated With Intranasal Methamphetamine

[It's been a while since I've had the time to look for new case reports. Let's keep this thread alive!]

Pott Puffy Tumor Associated With Intranasal Methamphetamine
Author information: University of California, San Diego
Letters Section Editors: Phil B. Fontanarosa, MD, Deputy Editor; Stephen J. Lurie, MD, PhD, Fishbein Fellow.

Pott puffy tumor (PPT) is an anterior extension of a frontal sinus infection that results in frontal bone osteomyelitis and subperiosteal abscess. Since the advent of antibiotics, PPT has been rarely reported and most cases have been described in children and adolescents. We report a case of PPT associated with use of intranasal methamphetamine hydrochloride.

REPORT OF A CASE
A 34-year-old woman presented with fever, chills, photophobia, and neck pain for 9 days. Nine months previously, she had developed swelling on her forehead that gradually enlarged over 5 days and then spontaneously drained purulent material. Over several weeks, a fistula developed at the site of the forehead swelling, and was accompanied by intermittent bloody, purulent drainage for approximately 9 months. The patient had no other contributory medical illnesses. However, she had used intranasal and inhaled methamphetamine weekly for 15 years and reported continued intranasal use immediately prior to the development of the forehead lesion. She reported no history of intravenous or other drug use.

Physical examination revealed a sinocutaneous fistula in the midline of the forehead with seropurulent drainage but no local erythema or tenderness. The patient had nuchal rigidity, but findings of the neurologic examination were within normal limits. The remainder of the physical examination was noncontributory. The white blood cell count was 15.3 × 109/L (77 neutrophils and 9 bands). Examination of cerebrospinal fluid, obtained by lumbar puncture, revealed a white blood cell count of 0.5 × 109/L (91% neutrophils, 2% lymphocytes), glucose level of 63 mg/dL (3.5 mmol/L), and a total protein level of 81 mg/dL. A Gram stain showed no organisms and the cerebrospinal fluid cultures and blood cultures were sterile. Computed tomographic scan of the head showed complete opacification of all sinuses with a 1-cm connection between the anterior frontal sinus and the skin. There were no epidural fluid collections or underlying brain parenchymal lesions.

The patient was treated with intravenous clindamycin and ceftriaxone sodium, and oral ciprofloxacin for osteomyelitis with presumed bacterial meningitis secondary to a contiguous focus of infection. On day 5 of her hospital stay, she underwent endoscopic sinus surgery. A second surgical procedure for debridement of the infected frontal bone, ablation of the frontal sinus, and repair of the frontal sinocutaneous fistula was also performed. Aerobic and anaerobic cultures of the purulent drainage from the maxillary sinuses grew Streptococcus milleri and Candida albicans. At the end of 2 weeks, antibiotics were changed to intravenous cefazolin and oral metronidazole and this therapy was continued for 4 additional weeks at home. No further complications occurred at 2 months. The patient was then lost to follow-up.

COMMENT
Osteomyelitis of the frontal bone is most commonly caused by trauma and frontal sinusitis [1].​ We propose that the use of intranasal methamphetamine by this patient contributed to chronic sinus inflammation, which led to the frontal bone osteomyelitis and subperiosteal abscess. Noskin and Kalish [2] have implicated the use of intranasal cocaine as a cause of chronic sinusitis associated with PPT in a 34-year-old man. The sympathomimetic effects of methamphetamine cause vasoconstriction of the mucosal vessels that may result in ischemic injury to the sinus mucosa, and thereby could provide an environment conducive to bacterial growth. We propose that PPT is a potential complication of methamphetamine use.

REFERENCES
1. Koch SE, Wintroub BU. Pott's puffy tumor: a clinical marker for osteomyelitis of the skull. Arch Dermatol. 1985;121:548-549.
2. Noskin GA, Kalish SB. Pott's puffy tumor: a complication of intranasal cocaine abuse. Rev Infect Dis. 1991;13:606-608.
 
Case report: Midfacial osteomyelitis in a chronic cocaine abuser

Author: Koch, R. James (2001)

Nasal inhalation is the most popular method of cocaine administration in the United States. [1] The adverse effects of intranasal cocaine abuse are well documented. Otolaryngologic complications are numerous, with one of the most common being nasal septal perforation. [2] Other complications include osteocartilaginous necrosis of the sinonasal tract, nasal septal necrosis mimicking Wegener's granulomatosis, and perforation of the hard palate. [2-4]

Nasopharyngeal destruction is a result of cocaine's vasoconstrictive properties. Cocaine produces sympathetic-nervous-system-mediated vasoconstriction by preventing the reuptake of presynaptic norepinephrine and dopamine. [5] The initial vasoconstriction is followed by a rebound vasodilation, which leads to atrophic changes in the mucosal lining. Mechanical destruction resulting from the forceful inhalation of powder or crystalline cocaine and the concomitant vasoconstrictive effect results in the formation of a nasal septal defect. [6] Such chronic intranasal abuse results in nasal crusting, epistaxis, and septal perforation. [7] A decrease in the oxygen tension of intranasal tissue can facilitate the growth of anaerobic pathogens and render the patient susceptible to infection. [8]

In this article, we describe the case of a chronic cocaine abuser who experienced a severe septal perforation. A complete loss of cartilage and bone of the midface was attributed to osteomyelitis. To our knowledge, this is the first documented case of midfacial osteomyelitis directly attributable to cocaine abuse.

CASE REPORT
A 56-year-old man with a conspicuous nasal defect and a history of chronic intranasal cocaine abuse had been admitted to the ENT clinic in 1994 for treatment of a hole in the roof of his mouth, which he said he had noticed 5 weeks earlier. The man claimed to have been alcohol and drug-free for 2 weeks.

Computed tomography (CT) of the paranasal sinuses without intravenous contrast showed a bilateral mucoperiosteal thickening of the sphenoid sinuses and what remained of the maxillary sinuses, along with evidence of a markedly erosive process that had destroyed the nasal septum, turbinates, and part of the antrum. CT also showed a bilateral residual soft-tissue opacity in the inferior aspect of the frontal sinuses, ethmoid sinuses, and the entire maxillary sinuses. Analysis of biopsy specimens revealed some exposed bone and an absence of quadrangular cartilage. Extensive destruction of his maxillary walls was also noted. Physical examination revealed an oronasal fistula with black necrotic areas around the edges, accompanied by a foul odor. This pattern is unusual in cocaine-induced erosion.

The patient was given antibiotics and had a prosthesis plate constructed to cover the defect. The patient was dismissed as having a septal and palatal perforation that was caused by his cocaine abuse. Two months later, a palatal and left nasal cavity biopsy revealed no evidence of carcinoma or fungal growth.

The patient was not seen again until April 1996, when he was hospitalized for destructive midfacial osteomyelitis that was marked by a slow and progressive destruction of his midface. Upon physical examination, he was noted to have septal destruction with fistula between his oral and nasal cavity and a saddle-nose deformity with columellar and alar retraction secondary to total cartilage loss. In addition, he now had a complete palatal defect.

Nasal septal biopsy revealed acute osteomyelitis with an extensive overgrowth of bacteria, including Serratia, Streptococcus, and Staphylococcus spp. There was no evidence of granuloma or neoplasm. A peripherally inserted central catheter was placed on day 3 of hospitalization to provide long-term outpatient intravenous antibiotic delivery. The patient was treated with intravenous ampicillin/sulbactam for 6 weeks followed by lifetime oral amoxicillin. He was discharged on day 7.

Six months later, in October 1996, the patient underwent open surgery for nasal reconstruction with a cranial bone graft. The graft, which measured approximately 9 X 2 cm, was harvested in the anteroposterior direction along the flattest portion of the parietal bone. Two glabellar furrows were used to camouflage the incision site. The incision was made in the shape of a teepee and used for placement of the bone graft. The nasal bones were dissected free, leaving the periosteum down. The periosteum was very carefully divided in the midline. With one finger in the nose and one finger on the skin of the nasal surface, the surgeon (R.J.K.) created a pocket in the nasal skin. A columellar strut, fashioned from calvarial bone, was placed via the glabellar incision. Next, the nasal tip of the dorsal graft was rounded to form an inverted shape. This graft was then placed in the pocket. A lag-screw technique was performed to enter the graft between 5 and 6 mm below the most superior cranial aspect of the gr aft. Once placement was determined to be adequate, the wound was closed and the patient was taken to the recovery room in stable condition.

Three months later, in January 1997, the patient underwent the second stage of his surgery. For external nasal valve reconstruction, a conchal graft was taken from the right conchal bowl by making a postauricular incision and elevating the flaps on either side of the conchal cartilage. The graft was obtained, and the wound was closed primarily in the postauricular region.

An incision was made in the right nasoalar crease, and a pocket was created anteriorly toward the nasal tip and posteriorly toward the piriform aperture. Then a conchal cartilage graft with the proper curvature and shape was fashioned and placed in this bed. The wound was irrigated and closed.

For premaxillary augmentation, a sublabial incision was made, and then a periosteal plane was elevated up to the anterior maxillary spine. A small hole was drilled through the anterior portion of the spine from left to right, allowing for an area of fixation. A piece of the calvarial bone graft from the previous harvest, which had been stored under the postauricular skin, was drilled with two holes as well, and 4-0 Ethilon suture was used to fix it in the anterior maxillary spine region. The sublabial wound was then irrigated with clindamycin solution and closed.

A small excisional wedge was made at the right alar base near the aperture, where the ala was seen to be rotated far medially, causing collapse of the nostril. This was then closed and lateralized, providing a much more adequate nasal aperture.

DISCUSSION
Cocaine is an alkaloid obtained from the leaves of the coca plant. Used medicinally as an anesthetic, it is also widely abused as a drug. Early natives of the Incan Empire experienced mild euphoria, stimulation, and alertness by chewing the coca leaves. [1] Cocaine was first isolated in 1855. In 1912, Owens reported the first case of nasal septal perforation caused by cocaine abuse. [3] Since then, cocaine abuse has been implicated in multiple complications affecting almost every system in the human body.

According to estimates, 30 million Americans have experimented with cocaine, and 5 million use it on a regular basis. [1] Despite the tremendous number of individuals who use intranasal cocaine and the numerous reports of nasopharyngeal destruction attributed to its abuse, our case is unique. Noskin and Kalish also described a rare case of chronic cocaine abuse in which a patient developed Pott's puffy tumor, which is a subperiosteal abscess of the frontal bone that is associated with frontal osteomyelitis. [8]

To our knowledge, ours is the first reported case of midfacial osteomyelitis caused by chronic cocaine abuse. The devascularized nasal tissue served as a breeding ground for secondary bacterial infection. The severity of our patient's complications, coupled with the success of his reconstructive surgery, makes this case particularly interesting. We believe that it is important for physicians to understand that septal perforation in a cocaine abuser should not be underestimated, because midfacial osteomyelitis might result.

REFERENCES
(1.) Cregler LL, Mark H. Medical complications of cocaine abuse. N Engl J Med 1986;315:1495-500.
(2.) Kuriloff DB, Kimmelman CP. Osteocartilaginous necrosis of the sinonasal tract following cocaine abuse. Laryngoscope 1989; 99:918-24.
(3.) Armstrong M, Jr., Shikani AH. Nasal septal necrosis mimicking Wegener's granulomatosis in a cocaine abuser. Ear Nose Throat J 1996;75:623-6.
(4.) Mattson-Gates G, Jabs AD, Hugo NE. Perforation of the hard palate associated with cocaine abuse. Ann Plast Surg 1991;26:466-8.
(5.) Daggelt RB, Haghighi P, Terkeltaub RA. Nasal cocaine abuse causing an aggressive midline intranasal and pharyngeal destructive process mimicking midline reticulosis and limited Wegener's granulomatosis. J Rheumatol 1990;17:838-40.
(6.) Sastry RC, Lee D, Har-EI G. Palate perforation from cocaine abuse, Otolaryngol Head Neck Surg 1997:116:565-6.
(7.) Schwartz RH, Grundfast KM. Nasal septal perforation from illicit drug use. Am Fam Physician 1956;34:187-8.
(8.) Noskin GA, Kalish SB. Pott's puffy tumor: A complication of intranasal cocaine abuse. Rev Infect Dis 1991;13:606-8.
 
Penile and scrotal skin necrosis after injection of crushed buprenorphine tablets

Authors: Nicolas Kluger, Céline Girard, Bernard Guillot, Didier Bessis; Service de dermatologie, hôpital Saint-Éloi, Université Montpellier I.

Intravenous drug abuse is responsible for complications ranging from minor to life-threatening and lethal [1]. Cutaneous complications vary according to the properties, formulation, and dose of the injected drug, as well as the method of delivery, injection site, and presence of foreign bodies, adulterants and infectious agents [1 and 2]. When the usual accessible peripheral veins (hands, arms, and legs) become sclerosed, addicts use alternative, and sometimes imaginative, locations, including the neck, armpits, inguinal folds (groins), or penis for drug injection. Thus, several cases of localized gangrene of the genitalia have been reported after injection of heroin, temazepam, or buprenorphine into the femoral vessels [2, 3, 4 and 5]. We report a new case of penoscrotal necrosis after injection into the groin of crushed buprenorphine tablets intended for sublingual administration (Subutex®).

CASE REPORT
A 31-year-old white man, with a 10-year history of heroin abuse, presented with a black necrotic eschar involving the scrotum and the base of the penis and painful ulcerations of the inguinal folds. He has been treated by oral buprenorphine chlorhydrate tablets (Subutex®) for a year. He acknowledged that the day before the consultation, he had injected crushed buprenorphine tablets into the right inguinal fold and experienced sudden pain immediately after injection. He denied any direct injection into the scrotum or the penis. Progressive worsening of the lesions and pain led to admission (at which time he was apyretic). Examination showed a black necrotic eschar of the scrotum and the base of the penis and painful fibrinous lesions with irregular borders along the inguinal folds (Figure 1). No laboratory test could be performed because of the poor condition of the peripheral veins. An isolate of a cutaneous swab sample was positive for Streptococcus sanguinis . The patient was treated with oral pristinamycin (1g, 3 times a day) for 2 weeks and local applications of sulfadiazine. The lesions improved markedly, but the remaining necrotic scrotal lesion necessitated surgical debridement, excision, and a full skin graft.

gr1.jpg

Figure 1.
Necrotic eschar of the scrotum and cutaneous ulcerations on the inguinal folds and the base of the penis after several days of local treatment and oral antibiotherapy


DISCUSSION
Repeated intravenous drug injections are usually followed by progressive sclerosis of the peripheral veins, which prompts drug abusers to choose new sites for injection, and the groin (the so-called “groin hit”) is a well-known alternative. Some abusers may use the femoral vessels routinely for years before any complication occur [3]. They may, however, deliberately inject directly into the femoral artery, which is the cause of several cases of penoscrotal necrosis after heroin injection into the groins reported in the literature [3, 4 and 5]. Femoral injections lead to embolization through the superficial and deep external pudendal artery. The superficial external pudendal artery provides branches to the penis, which explains the penile necrosis in our case.

This patient’s clinical presentation is typical of the natural history of this entity, as previously described by Somers et al. : soon after injecting the drug in the groin, the patient experienced severe localized pain and edema, followed by the development of a leathery black necrotic eschar and lastly loss of the scrotal skin. Surgery may be necessary to excise the remaining necrosis [3]. All but one of the cases reported have involved men, but women addicts may also use this site for injection. Del Giudice et al . reported a similar case of cutaneous necrosis after buprenorphine injection into the pudendal artery in a 25-year-old woman [2]. Other reported complications after groin/genitalia drug injection include ecthyma gangrenosum [4], Fournier’s gangrene [3], and penile ulcers [6, 7 and 8]. In the latter situation, drug abusers may have tried to inject heroin directly in the dorsal vein of the penis. Extravasation of the material is then complicated by penile ulcer [6, 7 and 8].

Buprenorphine chlorhydrate is a semisynthetic partial opioid agonist designed for sublingual administration, used in Europe for substitution treatment in opiate addiction. However, drug addicts rapidly started to misuse buprenorphine with subcutaneous or intravenous injections [9]. Such misuse may be followed by various cutaneous complications such as abscesses, cellulitis, thrombophlebitis, and necrotizing livedo [2 and 10].

Our case should serve as a reminder that acute groin and genital-necrotizing ulcers in drug addicts should prompt questioning about potential femoral drug injection. Drug addicts usually acknowledge drug injection, which facilitates the diagnosis. Otherwise, the presence of linear cord-like hypo- or hyperpigmented scars on the arms, reflecting repeated injections along superficial veins (“tracks”) [1 and 3], should suggest the possibility of drug injection in the groin.

REFERENCES
[1] Del Giudice P. Cutaneous complications of intravenous drug abuse Br J Dermatol 2004 ; 150 : 1-10.
[2] Del Giudice P., Vandenbos F., Boissy C., Cua E., Marion B., Bernard E., et al. Cutaneous complications of direct intra-arterial injections in drug addicts Acta Derm Venereol 2005 ; 85 : 451-452
[3] Somers W.J., Lowe F.C. Localized gangrene of the scrotum and penis: a complication of heroin injection into the femoral vessels J Urol 1986 ; 136 : 111-113
[4] Cunningham D.L., Persky L. Penile ecthyma gangrenosum Complication of drug addiction Urology 1989 ; 34 : 109-110.
[5] Bahia H., Moazzam A., Ramakrishnan V. Penoscrotal necrosis complicating intravenous drug abuse Br J Plast Surg 1999 ; 52 : 324-325
[6] Minkin W., Cohen H.J. Dermatologic complications of heroin addiction N Engl J Med 1967 ; 277 : 473-475
[7] Bennett R.G., Leyden J.J., Decherd J.W. The heroin ulcer New addition to the differential diagnosis of ulcers of the penis Arch Dermatol 1973 ; 107 : 121-122
[8] White W.B., Barrett S. Penile ulcer in heroin abuse: a case report Cutis 1982 ; 29 : 62-63.
[9] Vidal-Trecan G., Varescon I., Nabet N., Boissonnas A. Intravenous use of prescribed sublingual buprenorphine tablets by drug users receiving maintenance therapy in France Drug Alcohol Depend 2003 ; 69 : 175-181.
[10] Potier A., Leclech C., Croue A., Chappard D., Verret J.L. Necrotic livedo after injection of buprenorphine (Subutex) Ann Dermatol Venereol 2007 ; 134 : 148-150.
 
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....
there is no such thing as a safe drug but when it comes to meth vs heroin, judging by all aspects, heroin wins the most dangerous drug title and my argument is not against meth molecule vs heroin molecule but instead icehead vs dopehead.

I agree, however all drugs are poisons! Generally (and tbh probably over simply) your med professional ways up the negative (and all drugs produce negative) effects versus any positive effects which may be produced - if the positive outweighs the negative, the drug is taken - it's a cost/benefit analysis.

I don't think one can really "rank" a methamphet addict* ("icehead") with, say, a diacetylmorphine addict* ("dopehead") - both are addicts by definition and hence display the same/similar destructive behaviours.




* by an "addict" here I'm referring to a pathological (physiological/physical/emotional/etc) dependence resulting in extreme destructive behaviours, preventing living a healthy, active life....I'm sure I don't need to explain addiction to anyone here just wanted to clarify I'm referring to a "final line" dependence! lol :)
 
Uhh gross.. if you can't afford micron filters just use sterfilts. Way cheaper and easier than microns. I've been doing tec at least 10 times a day for 5 years straight without issue with my veins. Still have dozens of places to hit. I've always used 31G rigs and never use them more than 3 or 4 times. I can't believe people that say that say they have no veins left. Amazes me that they would have to resort to shooting down there. Maybe this guy lost a bet?
 
FDA warns about serious blood disorder resulting from misuse of Opana ER

[10-11-2012] The U.S. Food and Drug Administration (FDA) recently became aware of cases of a serious blood disorder that occurred in individuals abusing the prescription pain medicine Opana ER (oxymorphone hydrochloride extended-release tablets) by injecting the drug into their bloodstream. This serious blood disorder, called thrombotic thrombocytopenic purpura (TTP), resulted in kidney failure requiring dialysis in some cases, and at least one death.

In TTP, blood clots form in small blood vessels throughout the body. The clots can limit or block blood flow to the body’s organs, such as the kidneys, brain, and heart. Certain blood cells called platelets help the blood to clot. In TTP, as platelets clump together in the blood clots, fewer platelets are available in the blood in other parts of the body to help with clotting there. This can lead to bleeding under the skin and purple-colored spots called purpura, or to bleeding inside the body. TTP can cause death or lead to other complications with permanent damage, such as kidney failure, brain damage, or stroke.

TTP appears to occur with Opana ER only when it is abused and injected intravenously. Opana ER is meant to be taken orally, and should only be taken when prescribed and as directed. Taking it any other way may result in serious adverse events, including death (source).


If anyone finds any articles on specific cases on this please post them here.
 
Isn't it interesting that the 2 major drugs the pharma industry has introduced (and sometimes forced on) to IV heroin addicts, are causing serious medical issues???

I'm sure that they don't have to, or say that they don't, test these drugs (using this ROA and procedure) on less fortunate animals (rats) to see what the possible side effects of the drugs are...but, one may speculate that they do in fact do these tests...

Just a thought... Because, once this information gets out, as it is now, people won't abuse these drugs in said manner.

This inability to abuse prescription drugs has a twofold result (or advantage?);
1. It protects the pharma industry from prosecution
2. It only re-advertises the safer(?) alternative: illegal drugs...

BTW - Great Thread!

Keep it going folks,

C_P
 
They aren't going to test pill form drug injections on animals. That's just cruel. Opana is causing this problem because of the polymers/plastics in it that make it extended release, not the drug itself. They use oxymorphone IV in hospitals all the time without problems.
 
Ok, how's this for on topic...don't inject drugs in your genitalia and don't inject pills...and it "won't happen to you!" 8o Sorry, but I had a valid point that totally related to the thread...
 
Introduction

Fentanyl is a potent synthetic opioid with large abuse potential. Fentanyl prescriptions in the United States increased from 0.5 million in 1994 to 7.04 million in 2006 (1). Furthermore, the number of case fatalities from fentanyl overdose in southwestern Virginia increased from three in 2000 to 12 in 2003, and in 2000 the state of North Carolina reported a twofold increase in fentanyl fatalities over the previous 3-year period (2).

A common preparation of fentanyl is a sustained-release transdermal patch. Methods of fentanyl patch abuse include transdermal application, buccal absorption, rectal insertion, removal of the drug from the patch for injection or inhalation, and whole patch ingestion (3). To our knowledge, there are only two published case reports of whole patch ingestion: one of a 38-year-old man who was hospitalized multiple times after ingesting patches and was ultimately found dead in a correctional facility, and another of an accidental ingestion of a used patch by a 1-year-old girl resulting in death [4] and [5]. However, there has not been a clinical case series describing the ingestion of intact patches. A case series of 76 patients with a history of whole patch ingestion is reported.

Materials and Methods


This was an Institutional Review Board-approved retrospective review of all patients who ingested intact fentanyl patches as reported to three regional poison information centers (RPIC) between 2000 and 2008. The three RPIC medical record databases were queried for all exposures with a substance code matching the Micromedex® (Thomson Reuters, New York, NY) fentanyl product codes. The history was reviewed by the investigators, and all cases in which the patient had a history of whole fentanyl patch ingestion were included. Collected data included: age, gender, reason for the exposure, number of patches ingested, dose (μg/h), symptoms, symptom onset and duration, treatment hospital flow (level of care), and outcome (all defined by the American Association of Poison Control Centers National Poison Data System). Symptoms coded as unrelated to the exposure were excluded from the analysis. Descriptive statistics were used to characterize the data.

Results

A total of 76 patients met the inclusion criteria. Ages ranged from 15 to 56 years, with a mean of 32.6 years. Four patients were under the age of 18 years. There were 31 (40.8%) women and 45 (59.2%) men. The number of patches ingested ranged from one to five, with the majority ingesting one patch (Table 1). No patients were reported to have any coingestants. There were 26 different signs and symptoms coded as related to the exposure (Table 2). Fifteen patients had symptoms documented as unknown whether they were related to fentanyl patch ingestion: agitation/irritation occurred in 5/76 (6.6%), and hypertension, vomiting, hyperglycemia, numbness, and other symptoms each occurred in 2/76 (2.6%). Five patients (6.6%) were asymptomatic. The most common related sign was coma.[46%] One hundred ninety-eight (198) therapies were administered, the most common of which were naloxone, oxygen, and intravenous fluids.

Source
 
Used one of these case studies in my clinic morning report 'cause there's a patient on my team who has a severe groin abscess as well as what we suspect to be osteomyelitis.

Great forum
 
Ok, how's this for on topic...don't inject drugs in your genitalia and don't inject pills...and it "won't happen to you!" 8o Sorry, but I had a valid point that totally related to the thread...

i've heard that you can die in rare cases from opiate withdrawal nowhere near as common as with alcohol or benzos but still a possibility

The purpose of this thread is to post actual case studies so that we have a scientific article to back it up. If a sentence starts with "I've heard" then it doesn't belong in this thread.
 
I would like for this thread to be only Case Studies and discussion of those studies or on-topic posts. Please do not post second-hand anecdotes.

Motherfuckin science up in this bitch.
 
This is a fantastic thread to demonstrate the problems drug abuse can cause. Although its well established that benzos and opiates are a dangerous mix, many do not believe or think they will die from taking the two together as many other has. This case study I think should be taken into consideration when anyone attempts to mix the two together.

Two cases are reported involving the abuse of extended-release oxymorphone hydrochloride tablets (Opana® ER) in combination with alprazolam (Xanax®). Two juvenile females were discovered unresponsive and hypoxic by a male acquaintance. The trio had reportedly crushed and snorted Opana ER tablets and consumed Xanax for recreational purposes. Emergency personnel were able to stabilize one female. The second female was pronounced dead at the scene. Blood and urine samples from the surviving female were collected at the trauma center between 48 and 96 h post incident. Toxicology results showed the presence of oxymorphone, doxylamine, dextromethorphan, alprazolam, α-hydroxyalprazolam, oxazepam, and temazepam in her urine. No drugs were detected in her blood. Toxicology on the deceased female revealed the presence of 0.13 mg/L oxymorphone and 0.04 mg/L alprazolam in her blood. Gastric contents contained 0.25 and 0.93 mg/L of oxymorphone and alprazolam, respectively. Oxymorphone, alprazolam, and α-hydroxyalprazolam were present in her urine. Quantitative results were achieved by gas chromatography-mass spectrometry monitoring selected ions for the oxime-oxymorphone-trimethylsilyl derivative, alprazolam, and the α-hydroxyalprazolam tert-butyldimethylsilyl derivative. The established linearity ranges for the opiate and benzodiazepine methods were 0.050-3.000 and 0.025-1.000 mg/L, respectively. The cause of death was reported as multiple drug toxicity, and the manner of death was accidental (source).


Another extract on accidental overdose from poppy seed tea and phenazepam respectively.

Phenazepam is a benzodiazepine derivative that has been in clinical use in Russia since 1978 and is not available by prescription in the United States; however, it is attainable through various internet websites, sold either as tablets or as a reference grade crystalline powder. Presented here is the case of a 42-year old Caucasian male who died as the result of combined phenazepam, morphine, codeine, and thebaine intoxication. A vial of white powder labeled "Phenazepam, Purity 99%, CAS No. 51753-57-2, Research Sample", a short straw, and several poppy seed pods were found on the scene. Investigation revealed that the decedent had a history of ordering medications over the internet and that he had consumed poppy seed tea prior to his death. Phenazepam, morphine, codeine, and thebaine were present in the blood at 386, 116, 85, and 72 ng/mL, respectively (source).
 
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This is a fantastic thread to demonstrate the problems drug abuse can cause. Although its well established that benzos and opiates are a dangerous mix, many do not believe or think they will die from taking the two together as many other has. This case study I think should be taken into consideration when anyone attempts to mix the two together.

This is sad! Although a perfect example of how basic drug education may have prevented/mitigate this! :( Although I am usually know to stick up for / totally be on the side of the GP (knowing what they have to deal with, the positions/situations they're put in, responsibilities, pt through-put pressures, etc.), it is one thing I've noticed (possible a result of these things?) GP-pt drug education. Unless for chronic conditions.

Another extract on accidental overdose from poppy seed tea and phenazepam respectively.

Phenzepam OD's do not surprise me (even in terms of any benzo!) tbh - not just due to the very long therapeutic index. There is no wonder why very few places use it therapeutically!
 
poisons in small doses are medicines, medicines in large doses are poisons.

lol, modern medicine hasn't changed that much. we just target smaller body parts, with less collateral damage.
 
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