Harm Reduction ⫸CASE STUDIES - It could happen to YOU!⫷
- Thread starter djsim
- Start date
bindingaffinity
Bluelighter
- Joined
- Apr 19, 2012
- Messages
- 150
I found a few interesting and perhaps sobering case studies, which I intend to post here over the next few weeks. Still looking for the full text on some of them.
Yek, C., Li, X., & Mauskar, M. (2017). Painful purpura associated with exposure to levamisole-adulterated cocaine BMJ Case Reports. doi:10.1136/bcr-2016-219077
A 56-year-old man presented with a 2-day history of a painful rash. Examination revealed necrotic retiform purpura over the trunk and extremities (figure 1 (this is a direct image link)). Laboratory testing was notable for leucopenia (3.2 cells/µL) and positive peripheral antineutrophil cytoplasmic antibody (p-ANCA) with antimyeloperoxidase specificity (3.5 U, normal <0.4 U). Skin biopsy showed microvascular thrombosis and fibrinoid necrosis. On questioning, the patient endorsed regular cocaine use.
The patient was diagnosed with levamisole-induced vasculitis. He was discharged after workup but was readmitted a week later with wound superinfection requiring antibiotic therapy, surgical debridement and skin grafting. He recovered well postoperatively with complete resolution of his wounds at 2-month follow-up.
Levamisole is a veterinary antihelminthic previously used as an immunomodulator and cancer adjuvant prior to its withdrawal in 1999 from US markets due to toxicity. In the early 2000s, levamisole began to be used as a cutting agent in cocaine; by 2010 it was detected in up to 80% of cocaine samples seized in the USA.¹ Use of levamisole-containing cocaine has been associated with agranulocytosis, small vessel cutaneous vasculitis and pauci-immune glomerulonephritis.¹ Levamisole-induced vasculitis classically manifests as painful purpura with a predilection for the ears, cheeks, trunk and extremities. Laboratory findings may include leucopenia, high titre ANCAs (p-ANCA and c-ANCA), positive antiphospholipid antibodies and low antinuclear antibody (ANA) titres.² Diagnosis is typically established clinically and may be confirmed by skin biopsy.³ Rapid symptom resolution can be expected in most cases if cocaine is avoided, although complications such as wound superinfection may delay resolution.
Learning points
Yek, C., Li, X., & Mauskar, M. (2017). Painful purpura associated with exposure to levamisole-adulterated cocaine BMJ Case Reports. doi:10.1136/bcr-2016-219077
A 56-year-old man presented with a 2-day history of a painful rash. Examination revealed necrotic retiform purpura over the trunk and extremities (figure 1 (this is a direct image link)). Laboratory testing was notable for leucopenia (3.2 cells/µL) and positive peripheral antineutrophil cytoplasmic antibody (p-ANCA) with antimyeloperoxidase specificity (3.5 U, normal <0.4 U). Skin biopsy showed microvascular thrombosis and fibrinoid necrosis. On questioning, the patient endorsed regular cocaine use.
The patient was diagnosed with levamisole-induced vasculitis. He was discharged after workup but was readmitted a week later with wound superinfection requiring antibiotic therapy, surgical debridement and skin grafting. He recovered well postoperatively with complete resolution of his wounds at 2-month follow-up.
Levamisole is a veterinary antihelminthic previously used as an immunomodulator and cancer adjuvant prior to its withdrawal in 1999 from US markets due to toxicity. In the early 2000s, levamisole began to be used as a cutting agent in cocaine; by 2010 it was detected in up to 80% of cocaine samples seized in the USA.¹ Use of levamisole-containing cocaine has been associated with agranulocytosis, small vessel cutaneous vasculitis and pauci-immune glomerulonephritis.¹ Levamisole-induced vasculitis classically manifests as painful purpura with a predilection for the ears, cheeks, trunk and extremities. Laboratory findings may include leucopenia, high titre ANCAs (p-ANCA and c-ANCA), positive antiphospholipid antibodies and low antinuclear antibody (ANA) titres.² Diagnosis is typically established clinically and may be confirmed by skin biopsy.³ Rapid symptom resolution can be expected in most cases if cocaine is avoided, although complications such as wound superinfection may delay resolution.
Learning points
- Use of levamisole-containing cocaine has been associated with agranulocytosis, small vessel cutaneous vasculitis and rarely pauci-immune glomerulonephritis.
- Levamisole-induced vasculitis classically manifests as rapidly progressive, painful retiform purpura on the ears, cheeks, trunk and extremities.
- Supportive care is the mainstay of treatment, although superinfection is a concern and should be treated early if suspected.
bindingaffinity
Bluelighter
- Joined
- Apr 19, 2012
- Messages
- 150
I'm seeing fewer and fewer reports recently of cocaine cut with (significant amounts of) levamisole on ecstasydata.org, so we can only hope so.
As it turns out, that's not the worst thing cocaine could be cut with.
Tomassoni AJ, Hawk KF, Jubanyik K, et al. Multiple Fentanyl Overdoses — New Haven, Connecticut, June 23, 2016. MMWR Morb Mortal Wkly Rep 2017;66:107–111. DOI: http://dx.doi.org/10.15585/mm6604a4.
On the evening of June 23, 2016, a white powder advertised as cocaine was purchased off the streets from multiple sources and used by an unknown number of persons in New Haven, Connecticut. During a period of less than 8 hours, 12 patients were brought to the emergency department (ED) at Yale New Haven Hospital, experiencing signs and symptoms consistent with opioid overdose. The route of intoxication was not known, but presumed to be insufflation (“snorting”) in most cases. Some patients required doses of the opioid antidote naloxone exceeding 4 mg (usual initial dose = 0.1–0.2 mg intravenously), and several patients who were alert after receiving naloxone subsequently developed respiratory failure. Nine patients were admitted to the hospital, including four to the intensive care unit (ICU); three required endotracheal intubation, and one required continuous naloxone infusion. Three patients died. The white powder was determined to be fentanyl, a drug 50 times more potent than heroin, and it included trace amounts of cocaine. The episode triggered rapid notification of public health and law enforcement agencies, interviews of patients and their family members to trace and limit further use or distribution of the fentanyl, immediate naloxone resupply and augmentation for emergency medical services (EMS) crews, public health alerts, and plans to accelerate naloxone distribution to opioid users and their friends and families. Effective communication and timely, coordinated, collaborative actions of community partners reduced the harm caused by this event and prevented potential subsequent episodes.
Shortly after 4:00 p.m. on June 23, 2016, four patients with symptoms and signs of opioid overdose, characterized by central nervous system and respiratory depression, miosis (pinpoint pupil constriction), hypotension, and bradycardia, arrived in rapid succession at the York Street Campus (two patients) and St. Raphael Campus (two patients) EDs of Yale New Haven Hospital in downtown New Haven. Within 6 hours, seven additional patients arrived at the York Street Campus ED and one more at the St. Raphael ED; these patients included two who were pronounced dead on arrival and four critically ill patients requiring endotracheal intubation and ICU admission (Figure). The patients represented four geographic clusters (i.e., at least one other victim found in the same vehicle or parking lot, or in the same house or an adjacent house), and were transported by EMS crews responding to bystander 911 calls. All of the patients had clinical signs of opioid overdose and received at least one dose of naloxone from EMS (Table 1). Twelve patients met the case definition for suspected fentanyl exposure (i.e., clinical signs of opioid toxicity and response to naloxone, with laboratory confirmation of fentanyl or fentanyl metabolites in blood, or history of direct association with a laboratory-confirmed fentanyl exposure) (Table 1). Among the four patients admitted to the ICU, three required endotracheal intubation and mechanical ventilation for respiratory failure that was relatively refractory to large doses of naloxone, and one required a continuous naloxone infusion for 12 hours. Two of the three intubated patients suffered acute kidney injury and pulmonary or gastrointestinal hemorrhage, one of whom (patient K) died 3 days later from multisystem organ failure. The third patient survived with permanent cardiac injury. Other intoxicated patients who arrived at the ED with signs or symptoms of the opioid toxidrome were excluded from this analysis because of inconsistent history (e.g., patient reported using a nonfentanyl opioid) or toxicology test results that did not identify fentanyl.
Shortly after arrival in the ED, serum toxicology screens, designed to detect a panel of nonopioid toxins, were performed for all patients, and qualitative urine immunoassay toxicology screens for drugs of abuse were performed for nine patients (A, C, D, F, G, H, J, K, and L) (Table 2). The urine immunoassay screening tests cannot detect fentanyl and its analogs; however, all but one of the nine tested positive for cocaine. The one patient with a negative urine cocaine screen (patient A) acknowledged past cocaine use. Serum and urine specimens were later analyzed at the University of California, San Francisco (UCSF) using liquid chromatography high-resolution mass spectrometry (LC-HRMS) (1) to detect 215 common illicit and pharmaceutical drugs and metabolites, followed by additional analyses in attempts to identify 7,038 novel drugs and metabolites (2,3). Levels of fentanyl, cocaine, benzoylecgonine (a cocaine metabolite that persists in body fluids and is an indicator of cocaine use) and levamisole (a veterinary antihelminthic that has been used as a cocaine adulterant) were quantified. Nine patients (B, C, D, F, G, H, J, K, and L) had fentanyl detected in blood that was collected during their hospitalization and tested at UCSF (Table 2). One patient who reported cocaine use before symptom onset (patient A) and who was found in the vicinity of patients B, C, and D at the time of intoxication, was discharged before the full scope of the outbreak had been recognized and did not receive confirmatory toxicology testing. The Connecticut Medical Examiner’s Office performed postmortem toxicology screens on specimens obtained from two patients who died en route to the hospital (patients E and I).
Serum samples from the hospitalized patients analyzed at UCSF demonstrated fentanyl levels of 0.5–9.5 ng/mL (Table 2) (therapeutic range for analgesia = 0.6–3.0 ng/mL) (4); postmortem levels in the first two patients who died were 11 ng/mL (patient E) and 13 ng/mL (patient I). Norfentanyl, a major metabolite of fentanyl, was detected in the serum of nine patients; norfentanyl was not detected in postmortem testing of patients E and I, presumably because death occurred before metabolism of fentanyl to norfentanyl. All hospitalized patients had detectable serum levels of cocaine, cocaine metabolites (benzoylecgonine and ecgonine methyl ester), cocaethylene (a compound formed in vivo when ethanol is ingested in the presence of cocaine), or levamisole by LC-HRMS confirmatory testing (Table 2), all suggesting recent cocaine use. The absence of other opioids, such as heroin, methadone, or oxycodone, in serum (only one patient [D] was hydrocodone positive) was consistent with reports by the patients that most were not habitual opioid users.
Additional substances detected in serum and urine were reported qualitatively (Table 2) and reflected nicotine (cotinine), cannabinoid (tetrahydrocannabinol), and hydroxyzine (antihistamine) use, or receipt of naloxone. Postmortem toxicology screens identified fentanyl as a cause of death for patients E and I, both of whom arrived in the ED in cardiac arrest. In addition to the clinical specimens, one 32-mg forensic sample of the illicit drug material collected by law enforcement was tested at the Drug Enforcement Administration laboratory. Analysis of that product recovered from an involved crime scene found 6.6% (± 0.8% ) fentanyl by weight with trace amounts of cocaine and an inert adulterant.
Within a few hours of recognition of the outbreak, a multiagency response involving the New Haven Office of Emergency Management, New Haven and Connecticut Departments of Public Health, the Drug Enforcement Administration, local police, Connecticut Poison Control Center, and the New Haven Mayor’s Office was undertaken. Initial actions included 1) rapid notification of public health and law enforcement agencies by ED and EMS personnel; 2) real-time interviews of patients and family members in an attempt to trace and limit further use or distribution of the fentanyl; 3) advice to EMS crews to increase naloxone doses in treating suspected cases; 4) public health alerts regarding the event, including notices of the sale of a high potency opioid marketed as cocaine causing deaths in the region; and 5) plans to accelerate distribution of naloxone to opioid users and their friends and families. The high naloxone requirements necessitated both immediate naloxone resupply and augmentation for local EMS crews, including the transfer of 700 naloxone kits from the Connecticut Department of Public Health to hospitals and EMS crews the following morning. Actions of multiple partners led to the arrest 4 days later of three persons allegedly responsible for the illicit fentanyl sales.
As it turns out, that's not the worst thing cocaine could be cut with.
Tomassoni AJ, Hawk KF, Jubanyik K, et al. Multiple Fentanyl Overdoses — New Haven, Connecticut, June 23, 2016. MMWR Morb Mortal Wkly Rep 2017;66:107–111. DOI: http://dx.doi.org/10.15585/mm6604a4.
On the evening of June 23, 2016, a white powder advertised as cocaine was purchased off the streets from multiple sources and used by an unknown number of persons in New Haven, Connecticut. During a period of less than 8 hours, 12 patients were brought to the emergency department (ED) at Yale New Haven Hospital, experiencing signs and symptoms consistent with opioid overdose. The route of intoxication was not known, but presumed to be insufflation (“snorting”) in most cases. Some patients required doses of the opioid antidote naloxone exceeding 4 mg (usual initial dose = 0.1–0.2 mg intravenously), and several patients who were alert after receiving naloxone subsequently developed respiratory failure. Nine patients were admitted to the hospital, including four to the intensive care unit (ICU); three required endotracheal intubation, and one required continuous naloxone infusion. Three patients died. The white powder was determined to be fentanyl, a drug 50 times more potent than heroin, and it included trace amounts of cocaine. The episode triggered rapid notification of public health and law enforcement agencies, interviews of patients and their family members to trace and limit further use or distribution of the fentanyl, immediate naloxone resupply and augmentation for emergency medical services (EMS) crews, public health alerts, and plans to accelerate naloxone distribution to opioid users and their friends and families. Effective communication and timely, coordinated, collaborative actions of community partners reduced the harm caused by this event and prevented potential subsequent episodes.
Shortly after 4:00 p.m. on June 23, 2016, four patients with symptoms and signs of opioid overdose, characterized by central nervous system and respiratory depression, miosis (pinpoint pupil constriction), hypotension, and bradycardia, arrived in rapid succession at the York Street Campus (two patients) and St. Raphael Campus (two patients) EDs of Yale New Haven Hospital in downtown New Haven. Within 6 hours, seven additional patients arrived at the York Street Campus ED and one more at the St. Raphael ED; these patients included two who were pronounced dead on arrival and four critically ill patients requiring endotracheal intubation and ICU admission (Figure). The patients represented four geographic clusters (i.e., at least one other victim found in the same vehicle or parking lot, or in the same house or an adjacent house), and were transported by EMS crews responding to bystander 911 calls. All of the patients had clinical signs of opioid overdose and received at least one dose of naloxone from EMS (Table 1). Twelve patients met the case definition for suspected fentanyl exposure (i.e., clinical signs of opioid toxicity and response to naloxone, with laboratory confirmation of fentanyl or fentanyl metabolites in blood, or history of direct association with a laboratory-confirmed fentanyl exposure) (Table 1). Among the four patients admitted to the ICU, three required endotracheal intubation and mechanical ventilation for respiratory failure that was relatively refractory to large doses of naloxone, and one required a continuous naloxone infusion for 12 hours. Two of the three intubated patients suffered acute kidney injury and pulmonary or gastrointestinal hemorrhage, one of whom (patient K) died 3 days later from multisystem organ failure. The third patient survived with permanent cardiac injury. Other intoxicated patients who arrived at the ED with signs or symptoms of the opioid toxidrome were excluded from this analysis because of inconsistent history (e.g., patient reported using a nonfentanyl opioid) or toxicology test results that did not identify fentanyl.
Shortly after arrival in the ED, serum toxicology screens, designed to detect a panel of nonopioid toxins, were performed for all patients, and qualitative urine immunoassay toxicology screens for drugs of abuse were performed for nine patients (A, C, D, F, G, H, J, K, and L) (Table 2). The urine immunoassay screening tests cannot detect fentanyl and its analogs; however, all but one of the nine tested positive for cocaine. The one patient with a negative urine cocaine screen (patient A) acknowledged past cocaine use. Serum and urine specimens were later analyzed at the University of California, San Francisco (UCSF) using liquid chromatography high-resolution mass spectrometry (LC-HRMS) (1) to detect 215 common illicit and pharmaceutical drugs and metabolites, followed by additional analyses in attempts to identify 7,038 novel drugs and metabolites (2,3). Levels of fentanyl, cocaine, benzoylecgonine (a cocaine metabolite that persists in body fluids and is an indicator of cocaine use) and levamisole (a veterinary antihelminthic that has been used as a cocaine adulterant) were quantified. Nine patients (B, C, D, F, G, H, J, K, and L) had fentanyl detected in blood that was collected during their hospitalization and tested at UCSF (Table 2). One patient who reported cocaine use before symptom onset (patient A) and who was found in the vicinity of patients B, C, and D at the time of intoxication, was discharged before the full scope of the outbreak had been recognized and did not receive confirmatory toxicology testing. The Connecticut Medical Examiner’s Office performed postmortem toxicology screens on specimens obtained from two patients who died en route to the hospital (patients E and I).
Serum samples from the hospitalized patients analyzed at UCSF demonstrated fentanyl levels of 0.5–9.5 ng/mL (Table 2) (therapeutic range for analgesia = 0.6–3.0 ng/mL) (4); postmortem levels in the first two patients who died were 11 ng/mL (patient E) and 13 ng/mL (patient I). Norfentanyl, a major metabolite of fentanyl, was detected in the serum of nine patients; norfentanyl was not detected in postmortem testing of patients E and I, presumably because death occurred before metabolism of fentanyl to norfentanyl. All hospitalized patients had detectable serum levels of cocaine, cocaine metabolites (benzoylecgonine and ecgonine methyl ester), cocaethylene (a compound formed in vivo when ethanol is ingested in the presence of cocaine), or levamisole by LC-HRMS confirmatory testing (Table 2), all suggesting recent cocaine use. The absence of other opioids, such as heroin, methadone, or oxycodone, in serum (only one patient [D] was hydrocodone positive) was consistent with reports by the patients that most were not habitual opioid users.
Additional substances detected in serum and urine were reported qualitatively (Table 2) and reflected nicotine (cotinine), cannabinoid (tetrahydrocannabinol), and hydroxyzine (antihistamine) use, or receipt of naloxone. Postmortem toxicology screens identified fentanyl as a cause of death for patients E and I, both of whom arrived in the ED in cardiac arrest. In addition to the clinical specimens, one 32-mg forensic sample of the illicit drug material collected by law enforcement was tested at the Drug Enforcement Administration laboratory. Analysis of that product recovered from an involved crime scene found 6.6% (± 0.8% ) fentanyl by weight with trace amounts of cocaine and an inert adulterant.
Within a few hours of recognition of the outbreak, a multiagency response involving the New Haven Office of Emergency Management, New Haven and Connecticut Departments of Public Health, the Drug Enforcement Administration, local police, Connecticut Poison Control Center, and the New Haven Mayor’s Office was undertaken. Initial actions included 1) rapid notification of public health and law enforcement agencies by ED and EMS personnel; 2) real-time interviews of patients and family members in an attempt to trace and limit further use or distribution of the fentanyl; 3) advice to EMS crews to increase naloxone doses in treating suspected cases; 4) public health alerts regarding the event, including notices of the sale of a high potency opioid marketed as cocaine causing deaths in the region; and 5) plans to accelerate distribution of naloxone to opioid users and their friends and families. The high naloxone requirements necessitated both immediate naloxone resupply and augmentation for local EMS crews, including the transfer of 700 naloxone kits from the Connecticut Department of Public Health to hospitals and EMS crews the following morning. Actions of multiple partners led to the arrest 4 days later of three persons allegedly responsible for the illicit fentanyl sales.
RedXIII
Greenlighter
- Joined
- Sep 26, 2017
- Messages
- 37
If yall havent heard of the case of the frozen addicts, its a hell of a read. One of my favorites.
Hope you enjoy!
https://arstechnica.com/science/201...g-people-but-kickstarted-parkinsons-research/
Hope you enjoy!
https://arstechnica.com/science/201...g-people-but-kickstarted-parkinsons-research/
BeachBum4u
Bluelighter
- Joined
- Feb 9, 2012
- Messages
- 1,678
To the poster who robbed the pharmacy but ended up in the hospital, did (and how, I suppose) you end up getting caught for it or did all the craziness of your acute medical condition cover things up for you? I mean, it sounds like you probably had pharmacy pill containers laying around everywhere. Not too sure getting caught would be a totally bad thing in the long run. Thanks in advance for the follow-up!
Jabberwocky
Frumious Bandersnatch
- Joined
- Nov 3, 1999
- Messages
- 84,998
Old post, but have you ever thought of trying methadone? It would probably be much more helpful than buprenorphine for your needs.
Early in the ‘Injecting Methodone’ box reply, you said, “...you might end up hanging out, and many users don’t get a rush anyway.” I’m not sure what is meant by “hanging out.” (Where I live, that means visiting with friends in a casual way. That doesn’t seem to fit this, contextually...)
Acetylated
Greenlighter
- Joined
- Jan 2, 2018
- Messages
- 5
Seizures on high doses of dissociatives? specifically O-PCE, Diphenidine
TL;DR
Accidental O-PCE overdose presented in emergency room after full body seizures on/off for 15 mins. Doctors did not seem interested in what the substance was so I focused on explaining it's a dissociative blah blah. They wanted to rule out a tumor or other cause of seizures. CT scan clean. Discharged given nothing and told to lay off the obscure shit.
I have no history of seizures and have never had one that was not apparently drug induced. This does not mean the specific drug(s) mentioned cause seizures but they may lower seizure threshold. Ethanol, benzos, and gabapentin withdrawal lower seizure threshold a bit and speculatively anything that puts one in a state with less synaptic GABA will increase chance of seizure and/or convulsions.
8 AM: Following the tail end of 1 out of too many hexen binges, I found a sample of O-PCE and throughout the night periodically took tiny bumps to take the edge off. I have a lot of experience with dissociatives including O-PCE but have not taken both together. Neither substance resulted in a seizure in the past even in binge mode.
9-10 AM: As the hexen doses get smaller and spaced out due to supply, O-PCE doses get bigger. Nothing crazy with regard to effects. I was chasing the stim high. I should mention hexen usage was very high. 7g/day. Average build, bell ringer (hit) maybe every 2 mins then 3 mins then every 5 mins etc - as I ran out I paced it out. By the end it was 1 hit every 10-20 mins. O-PCE's initial comeup was soothing but the energy it brings into the mix was not welcome nor appreciated at that time. No gabaergics in the home at the time but now I won't touch O-PCE or sleep deprivation without gabapentin or benzos.
11 AM: Somewhat irritated that I ran out. No real crash from hex. Over the hour I basically hydrated and relaxed, stretched, felt OK. Near afternoon I take maybe 20mg O-PCE. I can't recall time much after this but for some idiotic reason I wanted to hole and put a big dose out. It could of been 100-150mg. Insufflated like the earlier doses. Knew I been done did fucked up when the comeup was as fast and potent as a big hit of vaped O-PCE freebase. I wasn't expecting a rush, but it wasn't unpleasant.
Other dissociative that gave me seizures: MXE doses were extremely high for months with no problems whatsoever minus maybe having to pee more frequently. Same with K. This was many years ago. In retrospect, the Mrs would tell me that I had maybe 5 seizures that weren't as long lasting but would qualify medically as seizures on vaped Diphenidine. I had used this for months with seemingly no problems but towards the end of the obsession doses were high and binges lasted days. An SSRI was taken daily at medicinal doses at that time with no ethanol, stims or benzos minus the occasional etizolam though that usage would not be considered abuse or recreational imo. Seizures on Diphenidine would only occur when vaping very high quantities and in the early hours of the day (AM) following a binge with notable sleep deprivation.
Time is hazy now and I have a few frames of memory to reference. The rest is what I was told by witnesses afterwards. First frame is waking up in bed with a dozen paramedics, cops, firefighters in my bedroom. Scene felt serene, calm with the only noises being beeps from the medical machines and occasional chatter between checking my vitals. Next was in the ambulance. I was asked some questions and my answers were "good enough" but I "opted in" for going to the ER. I was asked if I wanted to go and I said "yea! let's go!" ecstatically. I don't recall any of this. Next I recall being in the ER. Vitals were fine throughout the entire ordeal. I was high as fuck. I felt bad that tax payer money was being wasted.
Doctors noticed double nystagmus. Hand-eye coordination was slightly off but the nystagmus given my age (early 30s) alarmed them. I casually explained the situation and politely asked if I can bounce. They said I was free to go but they highly suggest a CT scan as the symptoms may be due to a tumor. I had a full charge on my phone, was in an excellent mood and did not desire anything specific, but mostly was also interested in the CT scan so I remained there. After waiting for close to 7 hours-I suppose when the O-PCE wore off-I became somewhat annoyed that the CT scan results was taking so long to process and asked for things to be expedited, and explained that the symptoms are reversible from previous experience, and that I doubted this was a stroke. "Text me a sad emoji if it's a tumor." I believed they had the CT scan result already. I personally knew the state of things and seriously doubted it would be a tumor. Given how much time elapsed, the machine/algorithm would have flagged irregularities in the results and my situation would of been a higher priority. Instead I was in bed next to somebody who was in the ER for having a hangover (seriously.)
I am NOT downplaying the situation nor the hospital's response. I was sleep deprived a few days and hungry and wanted out. After asking for the discharge forms against medical advice my doctor checked the results and said I was fine. What was somewhat unsettling was how many symptoms the doctors were unable to see or figure out because they don't have a baseline. My speech was wrecked beyond repair for example. Forming words was possible but quite a feat. I kept asking the Mrs how I sound, because forming words was difficult and I know from experience with dissocs they can make you seem OK to talk and walk when in reality it's obvious to the world you're incapable of either in the slightest. I "just sounded like I have a speech impediment" she said.
Note: The hospital setting was stimulating enough to overcome the usual dissociative amnesia. At home the entire experience would be a blur, naturally. Focusing on updating setting could be a potential way to reduce dissociative-induced amnesia. I also do not have much amnesia when I am with many friends vs alone on these things.
(The previous O-PCE experiences years ago at very high doses may have caused seizures. I doubt it but of course can't be sure. I was alone.)
TL;DR
Accidental O-PCE overdose presented in emergency room after full body seizures on/off for 15 mins. Doctors did not seem interested in what the substance was so I focused on explaining it's a dissociative blah blah. They wanted to rule out a tumor or other cause of seizures. CT scan clean. Discharged given nothing and told to lay off the obscure shit.
I have no history of seizures and have never had one that was not apparently drug induced. This does not mean the specific drug(s) mentioned cause seizures but they may lower seizure threshold. Ethanol, benzos, and gabapentin withdrawal lower seizure threshold a bit and speculatively anything that puts one in a state with less synaptic GABA will increase chance of seizure and/or convulsions.
8 AM: Following the tail end of 1 out of too many hexen binges, I found a sample of O-PCE and throughout the night periodically took tiny bumps to take the edge off. I have a lot of experience with dissociatives including O-PCE but have not taken both together. Neither substance resulted in a seizure in the past even in binge mode.
9-10 AM: As the hexen doses get smaller and spaced out due to supply, O-PCE doses get bigger. Nothing crazy with regard to effects. I was chasing the stim high. I should mention hexen usage was very high. 7g/day. Average build, bell ringer (hit) maybe every 2 mins then 3 mins then every 5 mins etc - as I ran out I paced it out. By the end it was 1 hit every 10-20 mins. O-PCE's initial comeup was soothing but the energy it brings into the mix was not welcome nor appreciated at that time. No gabaergics in the home at the time but now I won't touch O-PCE or sleep deprivation without gabapentin or benzos.
11 AM: Somewhat irritated that I ran out. No real crash from hex. Over the hour I basically hydrated and relaxed, stretched, felt OK. Near afternoon I take maybe 20mg O-PCE. I can't recall time much after this but for some idiotic reason I wanted to hole and put a big dose out. It could of been 100-150mg. Insufflated like the earlier doses. Knew I been done did fucked up when the comeup was as fast and potent as a big hit of vaped O-PCE freebase. I wasn't expecting a rush, but it wasn't unpleasant.
Other dissociative that gave me seizures: MXE doses were extremely high for months with no problems whatsoever minus maybe having to pee more frequently. Same with K. This was many years ago. In retrospect, the Mrs would tell me that I had maybe 5 seizures that weren't as long lasting but would qualify medically as seizures on vaped Diphenidine. I had used this for months with seemingly no problems but towards the end of the obsession doses were high and binges lasted days. An SSRI was taken daily at medicinal doses at that time with no ethanol, stims or benzos minus the occasional etizolam though that usage would not be considered abuse or recreational imo. Seizures on Diphenidine would only occur when vaping very high quantities and in the early hours of the day (AM) following a binge with notable sleep deprivation.
Time is hazy now and I have a few frames of memory to reference. The rest is what I was told by witnesses afterwards. First frame is waking up in bed with a dozen paramedics, cops, firefighters in my bedroom. Scene felt serene, calm with the only noises being beeps from the medical machines and occasional chatter between checking my vitals. Next was in the ambulance. I was asked some questions and my answers were "good enough" but I "opted in" for going to the ER. I was asked if I wanted to go and I said "yea! let's go!" ecstatically. I don't recall any of this. Next I recall being in the ER. Vitals were fine throughout the entire ordeal. I was high as fuck. I felt bad that tax payer money was being wasted.
Doctors noticed double nystagmus. Hand-eye coordination was slightly off but the nystagmus given my age (early 30s) alarmed them. I casually explained the situation and politely asked if I can bounce. They said I was free to go but they highly suggest a CT scan as the symptoms may be due to a tumor. I had a full charge on my phone, was in an excellent mood and did not desire anything specific, but mostly was also interested in the CT scan so I remained there. After waiting for close to 7 hours-I suppose when the O-PCE wore off-I became somewhat annoyed that the CT scan results was taking so long to process and asked for things to be expedited, and explained that the symptoms are reversible from previous experience, and that I doubted this was a stroke. "Text me a sad emoji if it's a tumor." I believed they had the CT scan result already. I personally knew the state of things and seriously doubted it would be a tumor. Given how much time elapsed, the machine/algorithm would have flagged irregularities in the results and my situation would of been a higher priority. Instead I was in bed next to somebody who was in the ER for having a hangover (seriously.)
I am NOT downplaying the situation nor the hospital's response. I was sleep deprived a few days and hungry and wanted out. After asking for the discharge forms against medical advice my doctor checked the results and said I was fine. What was somewhat unsettling was how many symptoms the doctors were unable to see or figure out because they don't have a baseline. My speech was wrecked beyond repair for example. Forming words was possible but quite a feat. I kept asking the Mrs how I sound, because forming words was difficult and I know from experience with dissocs they can make you seem OK to talk and walk when in reality it's obvious to the world you're incapable of either in the slightest. I "just sounded like I have a speech impediment" she said.
Note: The hospital setting was stimulating enough to overcome the usual dissociative amnesia. At home the entire experience would be a blur, naturally. Focusing on updating setting could be a potential way to reduce dissociative-induced amnesia. I also do not have much amnesia when I am with many friends vs alone on these things.
(The previous O-PCE experiences years ago at very high doses may have caused seizures. I doubt it but of course can't be sure. I was alone.)
Slow_Mobius
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^^moved to case studies megathread
crOOk
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Increase seizure threshold*
Slow_Mobius
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Lowering seizure threshold was the correct thing to say. A lower threshold means it's easier to trigger a seizure
crOOk
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Please read the quote again.
EDIT: Oh lol he said "withdrawals". :D
"Ethanol, benzos, and gabapentin withdrawal lower seizure threshold a bit"
EDIT2: It should be withdrawals or lowers though, so I win. :D :D
NickyBoy613
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- Jul 6, 2018
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- 11
So before i type up a novel i just want to know if this is the right place to discuss personal stories and discuss long term effects our using has caused us etc maybe we can Get some insight from people actually going thru it not some flimsy booklet of sorts written by people who have no real experience lol if this is not the right place then i apologize in advance. Thanks.
fairnymph
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Only halfway through but great thread. It was around back when I was active briefly in 2012 but I assume I didn't look at it bc I generally don't do stupid shit & highly value my health. Or maybe it hadn't been stickied then?
What about accounts we've personally witnessed? Also, re long term nasal use, I've been using heroin hcl (& for about 6yrs the citric acid salt - never from lemon juice, wtf!) in solution nasally for 9.5yrs. It has definitely substantially if not dramatically reduced my formerly very acute sense of smell but I've had no other problems, & when I've taken breaks I regain much of my SOS so I'm hopeful the damage isn't permanent or at least not fully. It's worse since moving to Europe bc it's all freebase here & it's difficult not to over-acidify my solution, especially if I want to fully extract the h from the cut. I do gravity & micron filter my solution, though. No health problems at all from my use. I have IVed it only 3-4x over the years & I had others hit me after I prepped as I was out of practice & I hate shooting one handed. I also had an unfortunate EPS tremor for years from being on max dose Prozac for 6yrs.
I always end up with some super acidic, dilute, probably mostly morphine solution eventually (I do several extractions in 10g batches), that I either give away bc morphine is hyperalgesic for me, or I plug. But recently I've been extra desperate (temporary due to bad luck) & I've been IMing that super acidic last bit. It burns soooo fucking much but so far, almost a month since I started doing this (4x total alternating sides of my glutes), no problems. I micron filter it freshly & ofc always fresh gear, but I worry about cuts that can't be broken down. So far no lumps but I do feel occasional twinges of pain for around 1wk after. But seriously - don't read this thread right before IMing street shit. It didn't dissuade me but damn it made me nervous.
I'm SHOCKED that djsm believes in global warming! That's been debunked...in fact we are about to enter a minor ice age. Also the thought that Obama did a single good thing for the US, lmfao. All drugs should definitely be legal but socialism in all forms is shit. I want to stab the rich Germans who want higher taxes - how DARE they speak for us all? Fortunately little of my income is taxable here but the damn 19% sales tax is bad enough. Not that taxes matter since they just print money. Everyone go research fiat currency. The US makes a shitload off the the WOD; very possibly more than if drugs were legalised.
Wtf is hexen? Not up on my research chems...
What about accounts we've personally witnessed? Also, re long term nasal use, I've been using heroin hcl (& for about 6yrs the citric acid salt - never from lemon juice, wtf!) in solution nasally for 9.5yrs. It has definitely substantially if not dramatically reduced my formerly very acute sense of smell but I've had no other problems, & when I've taken breaks I regain much of my SOS so I'm hopeful the damage isn't permanent or at least not fully. It's worse since moving to Europe bc it's all freebase here & it's difficult not to over-acidify my solution, especially if I want to fully extract the h from the cut. I do gravity & micron filter my solution, though. No health problems at all from my use. I have IVed it only 3-4x over the years & I had others hit me after I prepped as I was out of practice & I hate shooting one handed. I also had an unfortunate EPS tremor for years from being on max dose Prozac for 6yrs.
I always end up with some super acidic, dilute, probably mostly morphine solution eventually (I do several extractions in 10g batches), that I either give away bc morphine is hyperalgesic for me, or I plug. But recently I've been extra desperate (temporary due to bad luck) & I've been IMing that super acidic last bit. It burns soooo fucking much but so far, almost a month since I started doing this (4x total alternating sides of my glutes), no problems. I micron filter it freshly & ofc always fresh gear, but I worry about cuts that can't be broken down. So far no lumps but I do feel occasional twinges of pain for around 1wk after. But seriously - don't read this thread right before IMing street shit. It didn't dissuade me but damn it made me nervous.
I'm SHOCKED that djsm believes in global warming! That's been debunked...in fact we are about to enter a minor ice age. Also the thought that Obama did a single good thing for the US, lmfao. All drugs should definitely be legal but socialism in all forms is shit. I want to stab the rich Germans who want higher taxes - how DARE they speak for us all? Fortunately little of my income is taxable here but the damn 19% sales tax is bad enough. Not that taxes matter since they just print money. Everyone go research fiat currency. The US makes a shitload off the the WOD; very possibly more than if drugs were legalised.
Wtf is hexen? Not up on my research chems...
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fairnymph
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I have a crazy fast metabolism & very unusual CYP profile (some like 2d6 I have none or almost none of, others I have extra by 3-4x). So keep that in mind, but, I've been combining a strong MAOI (tranylcypromine), in doses up to 90mg/day, with all kinds of meds & drugs, including the no no tyramine foods, with no problems THOUGH I do find it scary how it potentiates crack/cocaine & will no longer use them together as the combined effect makes me sleepy & wacked out for 4+hrs. More on point, I've used my tranyl with high dose heroin, hydromorphone, codeine & morphine with absolutely no effects, good or bad. Just nothing. Same with red wine & Parmesan cheese. I've even combined my tranyl with DL-phenylalanine & l-tyrosine, usually 1-3grams, and find that a nice combo; likewise with caffeine 200mg & street speed (dexamphetamine). The effects are overall stronger & longer lasting, as one would expect. I am on high dose strong opiates & diazepam 24/7 for severe chronic pain btw so often these are multidrug combos, though I never combine stims or alcohol w/ anything but my normal meds. NOT that I am recommending people try this or advising it as safe, but my friend with normal metabolism has also combined tranyl w/ morphine, clonazepam, heroin, crack, caffeine & DA precursors (also large quantities of red wine) with no ill effects. Tranyl has no effect on the first 4 drugs for him, interestingly, so my weird response to tranyl + crack could be due to the meds in my system, a multidrug interaction. But the lack of effects combined with opiates & benzos is at least true for 2 people. And my friend is my opposite - hypersensitive to meds & generally needs only the minimum dose.