PDA

View Full Version : Case Studies (It could happen to YOU...)



Pages : 1 2 3 4 5 [6] 7 8

InvisibleEye
22-03-2010, 03:20
Intravenous Neck Injections in a Drug Abuser Resulting in Infection of a Laryngocele

Jeevanan Jahendran, Abdullah Sani, Philip Rajan, Gurdeep Singh Mann and Balachandran Appoo (2005)

A 40-year-old Sikh male lorry driver presented with a progressively enlarging, painless left neck mass over a 2-month period. Subsequently, he developed hoarseness followed by worsening
stridor over the next month. There was associated lowgrade fever for which he was prescribed oral antibiotics. However, this did not resolve his symptoms. In the previous year, he had noticed a similar swelling, but that had resolved spontaneously after a course of antibiotics without any complications. A point of interest was that he had been an intravenous drug abuser for more then 10 years andhad injected drugs directly into the major vessels of the neck (jugular veins) and lower limbs (femoral veins), as all other peripheral veins were already difficult to access. A soft, cystic swelling measuring about 5 X? 4 cm was palpable on the left lateral aspect of the neck anterior to thesternomastoid but displacing the muscle posteriorly. The mass and the skin overlying it did not show any signs of inflammation, but there was tenderness on deep palpation. Laryngeal endoscopy revealed a smooth bulging mass in the left supraglottic region, which probably arose from the ventricle, extending superiorly. This caused the epiglottis and the laryngeal inlet to be pushed to the right and resulted in partial obstruction of the airway. The appearance of the true cords as well as the subglottic region was normal except that movement of the left vocal cord was hindered due to the presence of the mass. Routine blood investigations were essentially normal except for leucocytosis; hepatitis and retroviral screening were also negative. Computed tomography (CT) showed a fluidfilled mass arising from the larynx and extending through the thyrohyoid membrane into the external soft tissue plane (Figures 1 & 2).

He was started on intravenous antibiotics and surgery was performed after 48 hours as there was no clinical improvement. During the watchful waiting period, there was no further deterioration in airway obstruction. Diagnosis of a pyolaryngocele was made and the mass was excised using a transcervical approach. The mass was separated from the surrounding structures up to the thyroid cartilage. The upper half of the ala of the thyroid cartilage was excised to gain access to the internal component. The entire sac was removed without breaching the laryngeal mucosa or damaging the superior laryngeal neurovascular bundle. Direct laryngoscopy after closure of the external wound showed that the larynx and the surrounding structures had almost retained their normal anatomy except for minimal oedema over the left supraglottic area. On opening the sac, we found it filled with thick yellowish material (Figure 3). Histological examination showed a fibrous-walled cyst filled with leucocytic material. There was no evidence of malignancy. Material sent for cultures and test for acid-fast bacilli was negative. The postoperative period was uneventful and the patient was well on subsequent follow-up, with no evidence of recurrence.

http://img265.imageshack.us/img265/1452/figure1.gif (http://img265.imageshack.us/i/figure1.gif/)

http://img249.imageshack.us/img249/999/figure2.gif (http://img249.imageshack.us/i/figure2.gif/)

http://img715.imageshack.us/img715/7993/figure3.gif (http://img715.imageshack.us/i/figure3.gif/)

Captain.Heroin
22-03-2010, 08:29
So I was hoping that for my 1,000th post (yay!) I would make some super awesome thread

But I really don't have anything thread worthy, so I'm gonna dedicate my 1000 posts to this thread

So kudos to djsim and everyone else who has contributed case reports. This thread is truly a great contribution to harm reduction, and it's the kind of thing that makes me proud to be a member of this community!

So...post more case studies! :)

Well designated 1000th post! :)

opiaddict
28-03-2010, 06:00
Thanks This is a great thread. Making me think about not experimenting with IVing suboxone.

HeavyHanded
05-04-2010, 10:28
I've lurked this forum for years and recently decided to join. It's things like this and the serious dedication behind the harm reduction message that make this place so special, along with the dedicated community of course.

I recently came into contact with an old friend that may or may not have access to fent patches. I was SERIOUSLY considering really reestablishing contact for the purpose of acquiring said patches. Upon reading the first few pages of this thread I have reconsidered and decided that it would be a poor choice to do so. Thanks again BL (djism and everyone else). Harm Reduced.

InvisibleEye
06-04-2010, 22:57
Widespread pulmonary granulomatosis following long time intravenous drug abuse—A case report

R.B. Dettmeyera, M.A. Verhoffa, B. Brckelb and D. Walterb
(Feb 2010)

Abstract

Foreign body granulomas in the lungs following acute singular or long time intravenous drug abuse are frequent findings during microscopic investigation of the lungs. Most cases present single granulomas. Cases with multiple foreign body granulomas, already palpable during autopsy and leading to pulmonary granulomatosis with multiple granulomas are less frequent. We report the case of a 32-year old man, dying suddenly and unexpectedly after a well-known history of drug abuse for more than a decade. The granulomas are caused by foreign particle embolization immediately after intravenous injection of not only the drug itself but also of adulterants, e.g. cotton fibers, potato starch or microcrystalline cellulose. At the end, a reduction in the size of the pulmonary bed had occurred followed by pulmonary hypertension. For the first time, lung dust in such a case was characterised by energy dispersive X-ray (EDX).

Case report

A 32-year old man, well known as drug addict for more than a decade, was found lifeless in his apartment. At the time of death, the man attended a program for drug withdrawal. Drug accessories were found in the room near the corpse. A severe lung disease was reported in his medical history but he refused to turn to a doctor.

2.1. Macroscopic autopsy findings

Autopsy revealed long scars in the bend of the elbows and one puncture with a fresh subcutaneous bleeding on the back of the left hand. Additionally, scars were found in the groins. Internal organs presented an edema including the brain (1426 g) and the lungs (left 1282 g, right 1526 g). The heart weighed 411 g with right ventricular hypertrophy (thickness 4–6 mm). Lung tissue presented numerous palpable nodules, first suggesting miliar tuberculosis. The nodules were found in all lobes concentrated near the hilus.

2.2. Histopathology

Histological investigations using conventional stainings presented round and oval granulomas in the lungs with often multiple giant cells in the centre and a surrounding fibrosis with lymphocytes and macrophages (Fig. 1 and Fig. 2). The deposits with foreign body giant cell reaction were located perivascular and included birefringent crystals, easy to detect by polarized light (Fig. 3). Inside the granulomas, capillaries with congestion were found first suggesting organized and recanalized microthrombi, also sometimes seen in intravenous drug users. In addition, liver tissues showed a chronic hepatitis and samples from the heart with microfocal lympho-monocytic infiltrations demonstrating a myocarditis.

Fig. 1. Numerous pulmonary granuloma, partly with an accompanying perifocal emphysema and located beside peripheral vessels
Fig. 2. Pulmonary granuloma contains giant cells, amorph crystal material, and fibrosis in the circumference a lympho-monocytic infiltrate
Fig. 3. Birefringent crystal material inside the granuloma

http://www.sciencedirect.com/cache/MiamiImageURL/B6T6W-4YB27T1-1-2/0?wchp=dGLzVlb-zSkzV

http://www.sciencedirect.com/cache/MiamiImageURL/B6T6W-4YB27T1-1-4/0?wchp=dGLzVlb-zSkzV

http://www.sciencedirect.com/cache/MiamiImageURL/B6T6W-4YB27T1-1-6/0?wchp=dGLzVlb-zSkzV

InvisibleEye
06-04-2010, 23:06
Trauma and Substance Abuse: Deadly Consequences of Intravenous Percocet Tablets

Joseph M. Galante MD, Salman Ahmad MD, Elizabeth A. Albers MD and Matthew J. Sena MD
(Jan. 2010)

Introduction
There are an estimated 20.6 million adults and teenagers classified as being addicted to or dependent on drugs or alcohol (1). The United Nations Office on Drugs and Crimes estimates that there are 1.3 million intravenous drug abusers in the United States (2). The use of drugs and alcohol is high among the trauma population. A single-center study suggests that as many as 40% of traumatic deaths may be related to drug or alcohol use (3). A large number of trauma patients who are discharged from the hospital receive a prescription for oral narcotics. The combination of addiction and prescription of narcotics can have deadly consequences.

Case Report

A 20-year-old man was initially evaluated in the Emergency Department after an assault to the head and face with a brief loss of consciousness. Trauma evaluation demonstrated a left anterior maxillary sinus fracture, and left posterolateral and inferior orbital wall fractures, with no evidence of intracranial injury on head computed tomography (CT). Further evaluation included a CT scan of the cervical spine and abdomen as well as plain radiographs of the chest and pelvis, all of which were negative. The patient's past medical history was significant only for an anxiety disorder and a history of polysubstance abuse, including intravenous drug use. He was admitted for 24 h of observation as well as evaluation of his maxillofacial injuries by Ophthalmology and Plastic Surgery. He was discharged home approximately 24 h after admission and given a prescription for 30 Percocet (Endo Pharmaceuticals, Newark, DE) (acetaminophen/oxycodone) for a severe headache. He had received instruction for appropriate follow-up of his injuries.

Twenty-four hours after discharge, emergency medical services (EMS) were called to the patient's residence for a complaint of decreased level of consciousness. The patient's significant other stated that he had been complaining of a worsening headache since the date of discharge. Per EMS, the patient was in severe respiratory distress with a large amount of pink, frothy sputum. During transport he became unresponsive and was orally intubated. Cardiac rhythm rapidly deteriorated to pulseless electrical activity, and cardiopulmonary resuscitation was started and the patient was given atropine and epinephrine, according to advanced cardiac life support guidelines. Narcan (1 mg) and D50 were also administered, given the uncertainty in diagnosis. With his history of recent trauma, he was immediately evaluated by the on-call trauma team upon arrival. Bilateral chest decompression was performed to exclude tension pneumothorax, and a focused abdominal ultrasound for trauma did not identify fluid in the peritoneum or pericardium. Neither of these demonstrated the etiology of his electrical rhythm. Resuscitative efforts were continued for approximately 30 min without restoration of spontaneous circulation, at which point the patient was pronounced dead.

A postmortem examination was performed. The patient's oxycodone level was 330 ng/mL, which is higher than the toxic level of 200 ng/mL. Needle track marks were identified in the patient's right antecubital fossa, with associated hemorrhage and polarizable foreign material within the subcutaneous tissue.

After hematoxylin and eosin staining of lung tissue, polarizable foreign material was also identified, occluding several pulmonary arterioles. There were acute inflammatory cells, necrotic debris, and fibrin associated with interstitial pulmonary congestion in each lung (Figure 1).

Figure 1. Pathology specimen of lung tissue from the patient showing polarizable foreign material occluding several pulmonary arterioles (arrows). There were acute inflammatory cells, necrotic debris, and fibrin associated with interstitial pulmonary congestion consistent with an acute event.

http://www.sciencedirect.com/cache/MiamiImageURL/B6T8B-4Y5GVFW-4-2/0?wchp=dGLbVtz-zSkWb

InvisibleEye
06-04-2010, 23:17
A fatality involving an unusual route of fentanyl delivery: Chewing and aspirating the transdermal patch

Henry J. Carsona, Laura D. Knightb, Mary H. Dudleya and Uttam Garge
(April 2010)

Most opioid abuse is of a conventional type, e.g. injection, insufflation, or oral ingestion. However, novel forms of opioid abuse have developed with the development of new drug delivery systems, particularly the fentanyl patch. This potent opioid is intended for time-released transdermal drug delivery, but in abuse situations the drug can be delivered by intravenous injection of patch contents, oral or transmucosal application, volatilization and inhalation, insufflation, or application of heat to the patch to enhance and hasten drug absorption.

Most victims of fentanyl overdose die from the direct toxic effects. We recently encountered a subject who died from an uncommon misuse of the patch, chewing, followed by complications of aspiration of the patch, in combination with other illicit drugs.

Case report

The decedent was a 28-year-old white male with a past medical history of prescription drug abuse who was found unresponsive in bed by his girlfriend. Emergency personnel transported him to the hospital, but he was pronounced dead in the emergency department shortly after arrival. The decedent’s girlfriend reported that she had last seen him the night before, lying in bed with her chewing a drug patch, the type of which she was unaware.

The body was that of a normally developed, well-nourished 158 lb adult man with numerous tattoos and a tongue piercing. The only evidence of injury was a small abrasion on the right bridge of the nose. Internal examination revealed the presence of a 2.2 0.8 cm wadded, beige, tough but somewhat stretchy, foreign material in the primary branch of the right mainstem bronchus (Fig. 1). The heart weighed 468 g (normal range 251–437 g), consistent with hypertrophy, suggestive of chronic stimulant abuse in hindsight. The remaining organs were unremarkable.

Fig. 1: Chewed transdermal fentanyl patch recovered from right middle lobe bronchus (arrow). The patch is comprised of clear flexible crushed plastic that lodged in the bronchus as a result of unintentional aspiration.

http://www.sciencedirect.com/cache/MiamiImageURL/B6W7W-4YRR0S7-1-2/0?wchp=dGLbVtb-zSkzS

Cloudburst
16-04-2010, 07:41
I was just too scared to read this thread when I was using the needle. Now that I've come pretty damn close to being a case report myself makes it all the more potent.

Advice to whoever is reluctant to read into this: don't make my mistake and grow some balls, stare reality at its ugly face.

ThePharmicist
24-04-2010, 08:36
Holy shit, sorry to hear that man. What'd the docs have to say about it?



So true. 10mg of fentanyl (equivalent to ~2grams of morphine) in a pouch which is easier to open than a TV dinner... hmmm, wonder what will happen 8) I wonder how the fuck something with so much fentanyl got thru when at the same time junkies were dying from China White? Obviously the FDA knew how strong fent (and analogs) were, and more importantly, that people would inject it to get high. Incredibly stupid.
I haven't seen the gel patches for so long.... what kind of dimensions are we talking (for the biggest one)? ie how many mL of gel in the 100mcg/hr?

According to the pouch,

"Each transdermal system contains: 10mg fentanyl and 0.4mL alcohol USP"

Honestly, I'm wearing one right now, it has the gel in it, and I'm looking at it thinking "Hmm, so when is all this fent gonna leak out."

So abusable, almost designed for abuse alone. I mean, it's seriously like wearing a band-aid with a big bag of fentanyl attached to it.

ALS3232
04-05-2010, 08:02
Great thread. Good info Thank you

Anglokraut
18-06-2010, 19:43
Is this thread only for "official" case studies from external sources or is it okay to relate the sad effects of long-term iv drug use to a friend? That would include acute troubles like blood poisoning/toxaemia and long term consequences to the state of used veins and the term effects everyday effects after a single occurrance of severe thrombosis with blood clots blocking multiple large veins of both legs at the same time? I can't provide photos or links, but the symptomatology isn't extremely rare anyway, more something that happens, in this or similar form, to a not insignificant percentage of long term iv users. With chances more like a car accident, as opposed to a plane crash.

marione
19-06-2010, 19:17
This is more common than you may think. My ex knew a guy who had a butterfly needle stuck in his arm 24/7; all he had to do was mix a shot in a needle-less syringe, stick it onto the butterfly needle and inject. No prodding for a vein.

However it certainly isn't a good idea to expose your blood stream to whatever bacterial/viral/fungal microbes are hanging out in the air.


That is very strange, do the butterfly really never clogged keeping it 24/7 with no constant drip of a water solution ?

I use similar technique but with a saline solution dripping during all the process to keep the needle clean, I prep. the shoot then close the drip, open the butterfly tube and insert the prepared rig, shoot, and back with saline solution again.
It is a good HR way when you're doing coke and don't want to shoot 5-10 or more in a session, veins will thank you.

jazzyhope
20-06-2010, 06:47
I have a quick injecting question... please feel free to move this post if it's not in the correct place.
I ran out of BS water today so I gotta use something else tomorrow. I have used both distilled water and plain tap water in the past. Why does the tap water burn like crazy and the distilled doesn't? Seriously it hurts something terrible- bad... like a severe cramp when I inject tap water, & yes I boil it first. Are there minerals or something in there that hurt muscles? I should probably mention that I inject suboxone IM ..NOT IV. Anybody know? Thanks Jazzy

Newmorfan
30-06-2010, 11:12
^^^^^
Injecting Suboxone IM is fucking RETARDED

did you read this thread at all??!!!?

stuckinaloop
30-06-2010, 16:33
I have a quick injecting question... please feel free to move this post if it's not in the correct place.
I ran out of BS water today so I gotta use something else tomorrow. I have used both distilled water and plain tap water in the past. Why does the tap water burn like crazy and the distilled doesn't? Seriously it hurts something terrible- bad... like a severe cramp when I inject tap water, & yes I boil it first. Are there minerals or something in there that hurt muscles? I should probably mention that I inject suboxone IM ..NOT IV. Anybody know? Thanks Jazzy


Holy crap you are dumb. I feel bad for you man..

DO NOT IM SUBOXONE

The only way of injecting suboxone that could be considered safe would be IVing it after having filtered with a micron filter

fm1983
30-06-2010, 18:28
I have a quick injecting question... please feel free to move this post if it's not in the correct place.
I ran out of BS water today so I gotta use something else tomorrow. I have used both distilled water and plain tap water in the past. Why does the tap water burn like crazy and the distilled doesn't? Seriously it hurts something terrible- bad... like a severe cramp when I inject tap water, & yes I boil it first. Are there minerals or something in there that hurt muscles? I should probably mention that I inject suboxone IM ..NOT IV. Anybody know? Thanks Jazzy

It's funny you ask this question in the cases studies thread. Why the hell are you IM'ing subs? Jesus chirst man, do yourself a favor and read this thread.

Levvytation
19-08-2010, 21:06
Sorry if this article is rather long (I've copy/pasted it), but it literally contains EVERYTHING about codeine...potentiation the lot. No need to read it all in one go, just scroll down until you find the info you are looking for.:) *EDIT* My bad, this is the SECOND part of the article....best read my second post below which is more relevant & less technical...

*


The LD50 for codeine is 800mg for average weighed non-tolerant adult person. The lowest reported lethal dose is 12mg/kg. The lethal dose varies and depends on many factors including weight, gender and developed tolerance to the drug.
Codeine Metabolism

Codeine is readily absorbed from the gastrointestinal tract. It is rapidly distributed from the intravascular spaces to the various body tissues, with preferential uptake by the liver, spleen, and kidneys.
Conversion of codeine to morphine

CYP2D6 and CodeineTo experience the effects of codeine, human body must convert the drug to morphine. "Codeine is metabolized by glucuronidation, by O-demethylation to morphine, and by N-demethylation to norcodeine. The enzyme responsible for the O-demethylation to morphine has been identified as cytochrome P4502D6 (CYP2D6)." - Microsomal codeine N-demethylation: cosegregation with cytochrome P4503A4 activity. In most humans, about 10% of codeine is transformed to morphine. Very small number of people is missing cytochrome 2D6 and therefore cannot experience the effects of codeine. The deficiency of the enzyme CYP2D6 is estimated at around 5-10% for Caucasians, 2% for Asians, and 1% for Arabic. On the other hand, between 0.5% and 2% of the population has multiple copies of the 2D6 gene and will metabolise 2D6-dependent drugs much more quickly and efficiently than others. Codeine tends to saturate the cytochrome 2D6 in effect making it work less efficiently; i.e. each dose of codeine lowers the effects of latter doses (during short period of time, eg 0-6 hours between doses). You may need to assess whether it's a waste for you.
Codeine analgesia is due to codeine-6-glucuronide, not morphine

Professionals Vree TB, van Dongen RT, Koopman-Kimenai PM from Netherlands has established a different theory on codeine action: "Eighty per cent of codeine is conjugated with glucuronic acid to codeine-6-glucuronide. Only 5% of the dose is O-demethylated to morphine, which in turn is immediately glucuronidated at the 3- and 6-position and excreted renally. Based on the structural requirement of the opiate molecule for interaction with the mu-receptor to result in analgesia, codeine-6-glucuronide in analogy to morphine-6-glucuronide must be the active constituent of codeine. Poor metabolisers of codeine, those who lack the CYP450 2D6 isoenzyme for the O-demethylation to morphine, experience analgesia from codeine-6-glucuronide. Analgesia of codeine does not depend on the formation of morphine and the metaboliser phenotype."

The plasma half-life is about 2.9 hours. The elimination of codeine is primarily via the kidneys, and about 90% of an oral dose is excreted by the kidneys within 24 hours of dosing. The urinary secretion products consist of free and glucuronide conjugated codeine (about 70%), free and conjugated norcodeine (about 10%), free and conjugated morphine (about 10%), normorphine (4%), and hydrocodone (1%). Negligible amounts are excreted in the faeces.
Mechanism of action

Opiate receptors in actionOpiate agonists and antagonists interact with stereospecific, saturable receptors in the brain and other tissues. These receptors are widely but unevenly distributed throughout the Central Nervous System. Opiate receptors include (mu), kappa, and delta, which have been reclassified by an International Union of Pharmacology subcommittee as OP1 (delta), OP2 (kappa), and OP3 (). Distribution of these receptors varies according to the presence in the CNS. Mu receptors are located widely throughout the CNS, especially in the limbic system (frontal cortex, temporal cortex, amygdala, and hippocampus); thalamus; striatum; hypothalamus; and midbrain. Kappa receptors are located primarily in the spinal cord and cerebral cortex. Opiate receptors are coupled with G-protein (guanine-nucleotide-binding protein) receptors and function as modulators, both positive and negative, of synaptic transmission via G-proteins that activate effector proteins.

Codeine is a weak opiate agonist in the Central Nervous System. Opiates do not alter the pain threshold of afferent nerve endings to noxious stimuli, nor do they affect the conductance of impulses along peripheral nerves. Analgesia is mediated through changes in the perception of pain at the spinal cord and higher levels in the Central Nervous System. There is no ceiling effect of analgesia for opiates, except for codeine, which effects has an estimated ceiling at 7mg/kg. The emotional response to pain is also altered. Opioids also modulate the endocrine and immune systems. Opioids inhibit the release of vasopressin, somatostatin, insulin and glucagon.

The stimulatory effects of opioids are the result of "disinhibition" as the release of inhibitory neurotransmitters such as GABA and acetylcholine is blocked. The exact mechanism how opioid agonists cause both inhibitory and stimulatory processes is not well understood.

THE BRAINClinically, stimulation of -receptors produces analgesia, euphoria, respiratory depression, miosis, decreased gastrointestinal motility, and physical dependence. Kappa-receptor stimulation also produces analgesia, miosis, respiratory depression, as well as, dysphoria and some psychomimetic effects (i.e. disorientation and/or depersonalisation). Miosis is produced by an excitatory action on the autonomic segment of the nucleus of the oculomotor nerve. Opiate-induced respiratory depression is caused by direct action on respiratory centres in the brain stem. The combination of effects of opiate agonists on the gastrointestinal tract results in constipation and delayed digestion. The urinary smooth muscle tone is increased by opiate agonists. The tone of the bladder detrusor muscle, ureters, and vesical sphincter is increased, which sometimes causes urinary retention.

Several other clinical effects occur with opiate agonists including cough suppression, hypotension, and nausea/vomiting. The antitussive effects of codeine are mediated through direct action on receptors in the cough centre of the medulla. Codeine also has a drying effect on the respiratory tract and increases the viscosity of bronchial secretions. Cough suppression can be achieved at lower doses than those required to produce analgesia. Hypotension is possibly due to an increase in histamine release and/or depression of the vasomotor centre in the medulla. Induction of nausea and vomiting possibly occurs from direct stimulation of the vestibular system and/or the chemoreceptor trigger zone.
Effects

The list below includes all possible effects of codeine, dihydrocodeine, hydrocodone and oxycodone, including side effects.

* Duration

Effects of codeine start at 10-30 minutes after ingestion, peak within 1 to 2 hours and may last 4-6 hours, depending on dose administered.


* Central Nervous System, Behavioural, Subjective

Suppression of the sensation of and emotional response to pain, euphoria, drowsiness, lethargy, relaxation, dizziness, difficulty in concentrating, decreased physical activity in some users and increased physical activity in others, mild anxiety or fear, nervousness or restlessness, pupillary constriction (pinpoint pupils), confusion, blurred vision, impaired night vision, hallucinations (eg 'corner-eye' hallucinations, seeing 'spiders' and 'bugs'), suppression of cough reflex.


* Respiratory

Reduced respiratory rate.


* Gastrointestinal

Nausea and vomiting, constipation, loss of appetite and decreased gastric motility, hiccups, difficulties with urination.


* Other

Dry mouth, allergic reaction (difficulty breathing, closing of throat, swelling of lips, tongue or face), slight drop in body temperature, sweating, reduced libido (women may experience amenorrhea and infertility and men may be unable to attain or maintain an erection), prickly or tingling sensation on the skin (itching), coma in lethal doses.


* Dependency Potential

Moderately low, continued use results in both psychological and physical dependency.


* Tolerance

Tolerance to the drug usually appears in chronic use.



Drug testing

Following the administration of codeine, the following substances can be detected up to 48 hours after (depends upon the dose, its frequency, route of administration and urine excretion/dilution): codeine, morphine, and hydrocodone.

Opioids can be detected in urine, blood, bile, hair, nails and sweat.
Chemical properties

Codeine can be synthesised from morphine by methylation of the 3-hydroxyl group (found on the second non-aromatic ring of morphine).

Orange beaker
Name Codeine
Chemical name (5alpha,6alpha)-7,8-didehydro-4,5-epoxy-3
-methoxy-17-methylmorphinan-6-ol
Alternative names methylmorphine, morphine monomethyl ether
CAS Number 76-57-3
Chemical formula C18H21NO3
Molecular weight 299.37
Boiling point 250C (480F) at 22mm/Hg
Melting point 154-156C (309.2-312.8F) (monohydrate)
Flash point 75C (167F)


Name Codeine phosphate
Chemical name (5alpha,6alpha)-7,8-didehydro-4,5-epoxy-3
-methoxy-17-methylmorphinan-6-ol dihydrogen orthophosphate hemihydrate
Alternative names (-)-Codeine phosphate
CAS Number 52-28-8
Chemical formula C18H21NO3.H3PO4
Molecular weight 397.40

Name Codeine sulphate
Chemical name (5alpha,6alpha)-7,8-didehydro-4,5-epoxy-3
-methoxy-17-methylmorphinan-6-ol sulphate
Alternative names
CAS Number 1420-53-7
Chemical formula C36H42N2O6.SO4
Molecular weight 694.86

Codeine 2D moleculeCodeine is a phenanthrene-derivative opiate agonist. Codeine occurs as colourless or white crystals or as a white, crystalline powder; the drug is slightly soluble in water and freely soluble in alcohol. Codeine phosphate occurs as fine, white, needle-shaped crystals or as a white, crystalline powder and is freely soluble in water and slightly soluble in alcohol. Codeine sulphate occurs as white needle shaped crystals, or as a white, crystalline powder and is soluble in water and very slightly soluble in alcohol.

Codeine phosphate and sulphate tablets should be stored in well-closed, light-resistant containers at a temperature less than 40C (104F), preferably between 15-30C (59-86F). Codeine phosphate and sulphate soluble tablets should be stored in tight, light-resistant containers at 15-30C (59-86F). Codeine phosphate injection should be protected from light and stored at a temperature less than 40C (104F), preferably between 15-30C (59-86F); freezing should be avoided.

Related information: 3D codeine molecule
Solubility of miscellaneous substances in 100ml of pure water

Syringe from mid 1800's
Name 87.8F water 69.8F water
Aspirin 1g 0.33g
Ibuprofen <1g <1g
Paracetamol 1.43g 0.66g
Codeine 43.48g 142.86g

Levvytation
19-08-2010, 21:27
=D Ah, here we go. this is the FIRST part of the article, more informative & less technical....


Codeine is an opiate agonist - sedative and analgesic narcotic substance found in opium in concentrations between 0.1% and 2%. Codeine was first isolated from opium by the French chemist Pierre-Jean Robiquet in 1832. Because of the small concentration found in nature, most codeine found in medical products is synthesized from morphine.

When injected, 120mg of codeine phosphate produces an analgesic response equivalent to that from 10mg of morphine. Codeine can be converted to morphine.


Pharmaceutical products from Codeine

Different forms of codeineCodeine can be found in many pharmaceutical products all around the world, it's found in many forms including tablets, capsules, syrups, etc. The sulphate and phosphate salts are used most frequently in medicine. Although there are internet pharmacies that sell pure codeine, in most countries codeine is a scheduled (controlled) substance not available as a sole product. Codeine is usually given orally as an ingredient in syrups to relieve non-productive cough. It is also combined with non-narcotic analgesics (eg tylenol, aspirin, ibuprofen, and others) and is used orally to relieve pain. Generic injection is also available. Some products are available over the counter outside the USA, but they usually contain limited amounts of codeine (eg 10mg). Products containing higher quantities of codeine require a prescription. The usual amount of codeine in over the counter tablets is too small to enjoy the effects and make it possible to overdose other substances (eg tylenol, aspirin, etc.) contained in these tablets as well.


Codeine Indications

Codeine's common medical uses include relief of mild to moderate pain (eg arthralgia, back pain, bone pain, dental pain, headache, migraine, myalgia and surgical pain), relief of non-productive (dry) cough, and relief of diarrhea.


Codeine Precautions

* All opiate/opioid agonists may impair the mental and/or physical abilities required for the performance of potentially hazardous tasks such as driving a motor vehicle or operating machinery.



* Codeine must be avoided in persons with chronic heart failure, advanced respiratory insufficiency, bronchial asthma, and raised intracranial pressure.



* Persons with severe kidney or liver disease should avoid taking opioids orally because of the possibility of drug accumulation or prolonged duration.


* The respiratory depressant effects of opioids and their capacity to elevate cerebrospinal-fluid pressure may be markedly exaggerated in the presence of head injury, other intracranial lesions, or a pre-existing increase in intracranial pressure.


* Caution and a dose reduction are necessary in the elderly and debilitated users. Also caution in myasthenia gravis, and Addison's disease.


* Opioids can cause urinary retention and oliguria, due to increasing the tension of the detrusor muscle. Patients more prone to these effects include those with prostatic hypertrophy (enlarged prostate), urethral stricture, bladder obstruction, or pelvic tumors.


* Convulsions can be precipitated by opiate agonists in users with pre-existing seizure disorder, eg epilepsy.


* In pregnant women codeine has been connected to respiratory malformations of the foetus and there are risks for the foetus towards the end of pregnancy. Also infant withdrawal syndrome has been reported in mothers who have used the drug during pregnancy. Some studies have reported clinically important amounts of codeine being excreted in breast milk. If you are pregnant or nursing mother, you must not use codeine.


Codeine Interactions

Most of the activity of codeine is believed to be due to its conversion to morphine via the CYP2D6 hepatic isoenzyme. Codeine has a low affinity for CYP2D6; therefore, its analgesic activity may vary greatly when it is combined with any other drug that may affect CYP2D6. Several drugs can inhibit this enzyme.


* Effects increase


o Administration of CYP2D6 enzyme inducers will increase the amount of codeine converted into morphine. Inducers of CYP2D6 include gluthethimide, rifampin and ritonavir. In vitro studies have shown no effect of carbamazepine and phenytoin on the conversion of codeine to morphine.


o Concurrent administration of an opiate agonist with other Central Nervous System (CNS) depressants listed below can potentiate the CNS effects (eg increased sedation, respiratory depression, or hypotensive responses) of either drug.


+ Alcohol increases the respiratory depressant effects of opioids and tends to worsen the euphoric effects.


+ Antihistamines (eg brompheniramine, carbinoxamine, chlorpheniramine, clemastine, cyproheptadine, dimenhydrinate, diphenhydramine, doxylamine, methdilazine, promethazine, trimeprazine)


+ phenothiazines (eg trifluoperazine)


+ general anesthetics


+ tricyclic antidepressants (eg dothiepin)


+ anxiolytics (eg meprobamate)


+ sedatives


+ skeletal muscle relaxants


+ hypnotics (eg zolpidem).


+ butorphanol


+ nalbuphine


+ pentazocine


+ tramadol


+ entacapone


o Large doses of Loperamide (Immodium) seem to have additive positive effects when administered with other opioids.


o Marijuana seems to increase the euphoric effects of all opioids, although it's not scientifically proved.


o Consumption of carbonated beverages tends to accelerate the absorption of orally administered opiates.


o Tropane alkaloids obtained from Belladonna (Atropa belladonna), Henbane (Hyoscyamus niger) or Thornapple (Datura stramonium) such as atropine, hyoscine (scopolamine) and hyoscyamine, can greatly potentiate the effects of opioids. The combination of the two produces a tranquillized state of consciousness known as twilight sleep. Remember that these alkaloids can be very poisonous and sometimes fatal in large doses.


* Codeine Side Effects


o Quinidine has been shown to interfere with the conversion of codeine to morphine; a corresponding decrease in the analgesic effect of codeine was seen.


o Selective Serotonin Reuptake Inhibitors (SSRI) also inhibit the CYP2D6. Among SSRIs are: citalopram (Celexa), fluoxetine (Prozac, Sarafem), fluvoxamine (Luvox), paroxetine (Paxil), sertraline (Zoloft). Remember that half-life of fluoxetine (Prozac) may be up to seven days.


o Other inhibitors of CYP2D6 may also decrease the analgesic effect of codeine include amiodarone, methadone, metoclopramide, cimetidine, haloperidol, mibefradil, propafenone, thioridazine, and tricyclic antidepressants.


o Opiate antagonists, such as nalmefene, naloxone and naltrexone, are pharmacologic opposites of opiate agonists (such as codeine, dihydrocodeine, hydrocodone and oxycodone). These drugs can block the actions of opiate agonists and, if applied to chronic users, they can produce acute withdrawal and/or eliminate the euphoria.


o Amphetamines and some sympathomimetics will generally counteract the sedative effects of opiates.


o Herbs high in tannins reduce the absorption of codeine (tannins are a group of unrelated chemicals that give plants an astringent taste). Herbs containing high levels of tannins include green tea (Camellia sinensis), black tea, uva ursi (Arctostaphylos uva-ursi), black walnut (Juglans nigra), red raspberry (Rubus idaeus), oak (Quercus spp.), and witch hazel (Hamamelis virginiana).


o Herbs high in salicylates may also reduce absorption of codeine. Herbs containing high amounts of salicylates include Sweet Birch (Betula lenta), Black Cohosh (Cimicifuga racemosa), Meadowsweet (Filipendula ulmaria), Wintergreen (Gaultheria procumbens), Popular bark and/or buds (Populus canadensis), and Willow (Salix spp.).


* Adverse reactions


o The results of concurrent use of opiates and mono amino oxidase inhibitors may be fatal. Avoid taking opioids if you have used mono amino oxidase inhibitors (MAOI) such as isocarboxazid (Marplan), phenelzine (Nardil), tranylcypromine (Parnate), in the past 14 days.



Codeine Administration

Codeine cough syrupCodeine can be administered orally (PO), subcutaneously (SC), intramuscularly (IM) and rectally (PR). Rectal administration is considered as more efficient than oral (up to 125%).

Codeine cannot be safely administered by an intravenous (IV) injection as it may result in pulmonary oedema, facial swelling, dangerous release of histamines, and various cardiovascular effects. It cannot be administered intranasally (snorting).

When administered orally, Codeine can be taken with full glass of water and/or food to minimise gastrointestinal irritation.
Codeine Dosage

The average recreational dose for non-tolerant adult users starts at about 200mg. Although effects start from 30mg to 60mg, some people may experience euphoria only in higher doses, usually greater than 150mg.

avcpl
19-08-2010, 22:18
That is an impressive find. Any chance of similar articles on:

oxycodone
hydrocodone
hydromorphone
oxymorphone
morphine

Thanks for posting!

phrozen
20-08-2010, 04:16
Yeah, thanks for posting.

I found this especially interesting:


Professionals Vree TB, van Dongen RT, Koopman-Kimenai PM from Netherlands has established a different theory on codeine action: "Eighty per cent of codeine is conjugated with glucuronic acid to codeine-6-glucuronide. Only 5% of the dose is O-demethylated to morphine, which in turn is immediately glucuronidated at the 3- and 6-position and excreted renally. Based on the structural requirement of the opiate molecule for interaction with the mu-receptor to result in analgesia, codeine-6-glucuronide in analogy to morphine-6-glucuronide must be the active constituent of codeine. Poor metabolisers of codeine, those who lack the CYP450 2D6 isoenzyme for the O-demethylation to morphine, experience analgesia from codeine-6-glucuronide. Analgesia of codeine does not depend on the formation of morphine and the metaboliser phenotype."

Vaya
20-08-2010, 07:29
Neat! It would be great to find such comprehensive information on "better" opiates, too - I don't use codeine, primarily b/c of it's high side effects profile and very limited euphoria relative to morphine and the opiods. I'd also love to find one such comprehensive article on ketamine, too.

Nice post though!

~ vaya

monstanoodle
20-08-2010, 08:25
Yeah, thanks for posting.

I found this especially interesting:

Professionals Vree TB, van Dongen RT, Koopman-Kimenai PM from Netherlands has established a different theory on codeine action: "Eighty per cent of codeine is conjugated with glucuronic acid to codeine-6-glucuronide. Only 5% of the dose is O-demethylated to morphine, which in turn is immediately glucuronidated at the 3- and 6-position and excreted renally. Based on the structural requirement of the opiate molecule for interaction with the mu-receptor to result in analgesia, codeine-6-glucuronide in analogy to morphine-6-glucuronide must be the active constituent of codeine. Poor metabolisers of codeine, those who lack the CYP450 2D6 isoenzyme for the O-demethylation to morphine, experience analgesia from codeine-6-glucuronide. Analgesia of codeine does not depend on the formation of morphine and the metaboliser phenotype."

Yea this has been speculated for some time but I've never seen a "strong theory" placed anywhere, just "slight speculation" :)
Good find Levvy!

leftwing
20-08-2010, 08:44
thanks for posting levvy:)

Levvytation
21-08-2010, 00:14
:)Thanx guys, you're welcome. I've learnt a lot from this forum, and its nice to be able to give some useful info back now & again.

I'm going to post an article from the same source below this post, (much shorter) about Hydrocodone. It deals specifically with hydro dealing with depression. I think there is a thread somewhere about opiates/depression already, so if you mods think it would be better suited there then please feel to move it.

Cheers, Levvy.

*edit* Unfortunately I cannot post a link to the website where these articles are coming from because, although it doesn't sell any drugs itself, it does have its own links to sites that do. Which of course would count as sourcing, hence the copy/pasting. Sorry guys.

Levvytation
21-08-2010, 00:22
Here we go....


Hydrocodone has proven to be one of the only effective medications for patients that do not find relieve from traditional antidepressants.



BUYING HYDROCODONE PRESCRIPTIONS ONLINE

Hydrocodone is one of the most frequently bought pain killers in the USA. Only online the amount of hydrocodone that people buy exceeds several millions of tablets each year and many more millions in sales. Hydrocodone containing medications such as Vicodin ES and Lortab are often bought to treat pain after surgeries or tooth extractions and for chronic pain management. Using hydrocodone will not only numb physical feelings but also emotions and although often not admitted by health care providers it can be used as treatment against depression. Buying Hydrocodone is not always easy if you have a doctor that doesn't believe in narcotics for pain management or if you use it to treat depression because other medications are not effective. Fortunately you can still locate compassionate doctors online that are willing to treat legit patients with Hydrocodone so you can buy these medications at affordable prices.
HYDROCODONE AND DEPRESSION
Studies show that severely depressed patients experience improvement in their condition when using hydrocodone containing products. Most patients buy hydrocodone online because it is quick, easy and convenient and it offers more privacy. Patients who can not find compassionate doctors and those with busy lifestyles or without insurance can benefit from telemedicine, a growing major industry that has just started to develop. A phone consultation can be bought for only $<snips> and you will deal with licensed US doctors that will prescribe high quantities with 2 or 3 refills if appropriate. They surely will not under-prescribe whereas many local doctor charge over $<snips> and only give you a prescription for 30 tablets of a low strength medication. Buying Hydrocodone Bitrate for the use against depression is a sensitive and difficult issue that not many doctors are willing to approve. Treating depressed people with hydrocodone containing products should always be done under strict supervision because of the increased risk that the patient will start self medicating or even overdose. On the other hand it is clear that pain and depression are often related as people with severe chronic pain will usually get depressed and depressed people are more sensitive to pain.

HYDROCODONE Vs. TRADITIONAL ANTIDEPRESSANTS

Patients that suffer from depression have a higher risk of becoming dependant on hydrocodone because they relief emotional pain, sadness or other emotions such as anger. When hydrocodone treatment is abruptly stopped depressed patients are more likely to experience withdrawal symptoms. Most likely this is one of the reasons why doctors will not recognize hydrocodone as a suitable anti-depressant. On the other hand Hydrocodone has proven to be one of the only effective medications for patients that do not find relieve from traditional antidepressants such as Prozac, Celexa, Zoloft and older tri-cyclic medications.

Hydrocodone intake increases the dopamine levels in the brain which can cause a pleasant feeling of well being also called euphoria. If taken by people who are not in pain it will often produce this euphoric effect, people in extreme pain may also experience this sensation although it is less likely to occur. The largest group of people buying Hydrocodone are patients over the age of 40 and mainly seniors older than 60 years of age.

HYDROCODONE AND TOLERANCE
When using Hydrocodone over longer periods of time you will built up tolerance and when abruptly discontinuing hydrocodone you will likely experience withdrawl symptoms. Building up tolerance and experiencing withdrawl is a natural reaction of the body after usage of hydrocodone and this does not mean that you are a junkie. When you buy hydrocodone online with a valid prescription for a legit reason it is not illegal to do so. You can tell when you have built up tolerance when the medication does not work as well or when you need a higher dose to obtain the same functionality. If you start feeling unwell when not taking your medication for more then 12 hours this is also a sign of dependency. If you have become dependent on hydrocodone it is often recommended that you slowly decrease your usage and eventually stop taking the medication for a while. This will prevent will prevent you from starting to buy more hydrocodone to obtain the same effect. Although hydrocodone is very effective against pain it is best to use a low dose when using over longer periods of time. It's important to use Hydrocodone as instructed. When realizing you may have become addicted we recommend visiting Narconon for information on treatment, or to consult a licensed health care professional to become informed regarding accesable treatment options in your area.

**mod edit** removed prices

phrozen
21-08-2010, 03:25
Maybe a better home for this would be in our case studies thread? I bet you guys forgot about that, huh? ;)

leftwing
21-08-2010, 03:52
^well i was going to add it into the CWE extraction threa that blondey made, but realised it's a universal CWE thread, not jst codeine. then thought to ask the guys over in ausdd to add it into the codeine cwe thread over but it's shut down temporarily (fuck, i've forgotten my part in that).

but yeah, case studies thread sounds like as good a place as any other at the moment to give it some more exposure:)

Downloader08
21-08-2010, 08:03
Great thread! Thanks for all the articles!

sweetsurrender
24-08-2010, 08:04
wow!!!

i sat here literally drooling and commenting out loud (might be the speed 8) as i combed through this thread - post by post. i don't think ive ever read every post of a long thread but this is well worth it!!

applause, my friends, applause!!

i iv heroin and ive thought of iving pills but i know a fair amount (im smarter than the average bear ) and im also a science geek. however, you find yourself thinking about some crazy stuff in order to get a better, more intense, whatever, sort of high.

i had a friend that would just smash up anything and draw it up in a syringe. she sat in my closet for hours trying to do god knows what....

anyway, drugs can get desperate but if you are reading this thread and searching for answers in this forum, hopefully you can avoid the tragic mistakes made by the uninformed.

well done!!!
kc

Levvytation
24-08-2010, 08:06
This is an interesting (& scary) article about the use of opiates & benzo's as chemical weapons basically, in an 'aerosolised' form. Agent Orange & teargas spring to mind:\



Background

Few reports describe the use of either benzodiazepines or opioids as incapacitating agents. In August 2002, Alexander Stone authored a brief report in Science titled, "Chemical weapons, US Research on Sedatives in Combat Sets Off Alarms." In this report, Stone highlights the Department of Defense's Joint Non-Lethal Weapons Program and how the funding for studies of nonlethal weapons has jumped from $14 million in 1997 to $36 million in 2001.1 The Institute of Emerging Defense Technologies at Pennsylvania State University is reportedly conducting research on the use of drugs as nonlethal agents and has reportedly urged the Marine Corps to give immediate consideration to weaponizing sedatives such as diazepam.

In October 2002, the Russian Military reportedly used "a fentanyl derivative" to neutralize terrorists holding hostages at the Moscow Dubrovka Theater Center. The Russian Health Minister declared that the "gas" used in that event "cannot by itself be called lethal." Despite that announcement, 127 of the hostages died following the use of that gas in the theater.

In 2005, the3rd European Symposium on Non-Lethal Weapons met in Stadthalle Ettlingen, Germany. At this meeting, an abstract was submitted by Hess and colleagues from the Institute for Clinical and Experimental Medicine and the Military Medical Academy, Czech Republic. In this abstract, they referred to their work using numerous potential pharmacological non-lethal weapons.2

According to the abstract by Hess et al, a major drawback of opioid use is the development of respiratory depression, particularly if administered at higher doses inducing immobilization. In experiments with rabbits, they reportedly tested a combination of alfentanil or remifentanil together with a specific opioid antagonist (naloxone) seeking to identify the optimal agonist/antagonist ratio while maintaining immobilization and markedly reducing respiratory depression. Inhaled administration of opioids was reported to be associated with a very rapid onset of effect. The ultrapotent opioid etorphine, when combined with dimethylsulfoxide, was capable of crossing normal skin and inducing immobilization within 3-8 minutes.2
Pathophysiology

Little has been published regarding the use of aerosolized opioids or benzodiazepines as incapacitating agents. The primary action of benzodiazepines is agonist activity at the g -aminobutyric acid (GABA)–associated benzodiazepine receptors. This activity produces central nervous system depression, which may initially manifest as slurred speech, ataxia, nystagmus, and incoordination. As toxicity increases, the patient may become comatose and develop respiratory depression with airway compromise. In a 1994 article published in Epilepsia by Xi et al, aerosolized diazepam was reported to arrest seizure activity within seconds.3 In Science, Stone reported that diazepam was being given immediate consideration as a weaponized sedative.1

Opioids possess agonist activity at the opioid receptor. The 3 current major classes of opioid receptors are m, k, and d; each has multiple subtypes with differing pharmacologic activity. Numerous opioid agonists also exist; each has varying affinity for each receptor. Fentanyl and its derivatives (ie, sufentanil, alfentanil, remifentanil, carfentanil) are the only opioids that have been described as potential aerosolized opioid agents. In Anesthesiology, Hung et al reported a rapid absorption rate following inhaled liposome-encapsulated fentanyl.4 In Annals of Emergency Medicine, Wax et al provide a comprehensive review of these agents in relation to the Moscow theater event.5 Alfentanil, remifentanil, fentanyl, and carfentanil are 75, 220, 300, and 10,000 times more potent than morphine, respectively.
Frequency
United States

No reports describe the use of aerosolized opioids or benzodiazepines as incapacitating agents in the US population.
International

Only 1 report describes the intentional use of an aerosolized opioid as an incapacitating agent. In the Moscow Dubrovka Theater incident, 50 Chechen rebels stormed the theater and took 800 hostages on October 23, 2002. On October 26, 2002, a gas was introduced into the theater through the ventilation system just before a rescue attempt by Russian Special Forces. Reportedly, 127 (16%) of the 800 hostages in the theater died. Subsequent reports indicated that all had died from complications associated with the gas. The Russian Health Minister announced 4 days after the events that "a fentanyl derivative was used to neutralize the terrorists." This was collaborated by reports that both Moscow and Western Embassy physicians noted signs and symptoms consistent with opiate intoxication. Laboratory confirmation of fentanyl use was not possible in these cases, but blood and urine specimens analyzed from 2 German survivors showed traces of halothane.
Mortality/Morbidity

The mortality and morbidity associated with the use of aerosolized benzodiazepines or opioids as incapacitating agents is unknown. Following the reported use of an aerosolized fentanyl derivative during the 2002 raid on Chechen rebels who had taken hostages in the Moscow Dubrovka Theater Center, 127 (16%) of the 800 hostages in the theater died, and 650 of the survivors required hospitalization. Whether these complications were the result of the use of an aerosolized fentanyl derivative or due to other complications is unclear.
Clinical
History

An event involving an opioid or benzodiazepine aerosolized incapacitating agent would probably create confusion and panic; cause multiple serious injuries or fatalities; and necessitate a major emergency medical service, police, and/or military response.

* Large numbers of casualties could overwhelm any community's emergency response services.
* Chaos may occur following such an event.
* In the early phases of an emergency response, the agent would probably be unknown, and the history may be misleading and inaccurate.
* Physical examination is the key to identifying the causative agent.

Physical

Following exposure to either an aerosolized opioid or benzodiazepine incapacitating agent, the presentation would be a syndrome consistent with opioid or benzodiazepine toxicity, respectively. These syndromes can vary, depending on the opioid or benzodiazepine agent used. In addition, findings may vary, depending on the patient's preexisting medical problems, the treatment provided by first responders, and the potential complications of the intoxication. For example, if hypoxic brain injury occurs, the characteristic miosis seen in an opioid syndrome may be replaced by fixed dilated pupils.

* Opioid intoxication
o Respiratory depression manifesting as hypoventilation, apnea, and airway occlusion may be present.
o Central nervous system depression manifesting as fatigue, somnolence, ataxia, and/or coma may be present.
o Miosis may be present. Intoxication with the opioids meperidine and propoxyphene does not typically cause miosis, and normal pupillary size is regularly maintained; however, neither of these agents has been associated with aerosolization. Mydriasis may occur in patients with severe toxicity because of anoxic brain injury. Miosis may be limited by preexisting medical conditions, such as a history of previous cataract surgery.
o Cardiovascular manifestations of opioid toxicity may include hypotension secondary to arteriolar and venous dilation. Both tachycardia secondary to hypotension or hypoxia and bradycardia secondary to a reduction of direct central nervous system stimulation may be observed. If hypoventilation becomes prominent, hypoxia-induced cardiac arrhythmias may occur.
* Benzodiazepine intoxication
o Respiratory depression manifesting as hypoventilation, apnea, and airway occlusion may be present.
o Central nervous system depression manifesting as drowsiness, somnolence, ataxia, nystagmus, and/or coma may be present.
o Cardiovascular manifestations of benzodiazepines may include hypotension, tachycardia, and bradycardia. Hypoxia-induced cardiac arrhythmias may occur.

Arobskittle
24-08-2010, 10:35
i hope someday there are "drug terrorists" who bomb a building and everyone inside ends up high as fuck on opiates.......while i am there....

Levvytation
24-08-2010, 20:17
i hope someday there are "drug terrorists" who bomb a building and everyone inside ends up high as fuck on opiates.......while i am there....

^lol

I'd like to know how these drugs are 'aerosolized', ie converted into a gas (& obviously a very potent one).

Any ideas/info from our more scientific Bluelighters on this?

Vaya
25-08-2010, 07:19
^lol

I'd like to know how these drugs are 'aerosolized', ie converted into a gas (& obviously a very potent one).

Any ideas/info from our more scientific Bluelighters on this?

I definitely don't know the answer to this, Levvy, but am dying to know as well! Thanks for putting the question out there. I'm no scientist, but have an understanding of chemistry (relative to your typical layman) such that I had two thoughts I'd like to throw out there on the subject.

In order to convert the opioid/benzodiazepine chemical compound itself into a gaseous state, that would require the compound being heated to its vaporization point, would it not? And obviously, this temperature has the potential to be exceedingly hot, especially if the intended aerosolized drug is meant to be non-lethal. So, in my somewhat informed opinion, I do not think that it could be a pure form of the opioid/benzodiazepine in its gaseous state.

Alternatively, might one (through knowledge of various chemical affinities for other molecules) bind these compounds to molecules of a gas that is gaseous at non-lethal temperatures? I cannot imagine that the addition of a chemical compound (opioid/benzo) to a gaseous molecule wouldn't affect the latter's ability to retain its gaseous composition at the same temperature.

This is really intriguing; and now, back to your scientists...
=D

~ vaya

Static_Color
25-08-2010, 09:47
Curious to see of any case studies of IMed Ketamine?

Traumadoll
29-08-2010, 01:18
Carafentanyl. Wiki it. A lot of the hostages died as well, keep in mind, bc the medics didn't show up with enough opiate agonists...

svacheme3
29-08-2010, 10:41
It's not as official as medical records, but my girlfriend became septic and experienced acute renal failure (couldn't pee for 3 days despite above normal fluid intake), and was too weak to even lift herself in and out of the car getting to the hospital, and was found to have endocarditis and had to stay in the hospital 3 weeks followed by an additional 6 weeks of daily vancomycin infusions. Was informed had we waited even another day and she wouldn't have made it; which given her state I don't doubt.

Don't inject old wash from pills, especially from a big cap of it that sits in the drawer moist for a week.

specneck
29-08-2010, 19:39
I dont know if anyone has posted this case study - I'm working my way through all 12 incredible pages so sorry in advance if it has been shown already...

http://www.rcsed.ac.uk/journal/svol2_3/2030002.html

That leg.....

doIhavePotential
27-10-2010, 21:02
bump so others have a chance to see this great thread.

RedThorn
28-10-2010, 14:19
Fantastic eye-opener, thanks for such a great thread.

CaPoNe.
05-02-2011, 21:38
Im not exactly sure where this would go so mods move if needed. I felt the need to post this because it has a large value in harm reduction. So a good friend of mine doesnt have a problem but like to snort his drugs sometimes it was coke sometimes mephedrone or anyting else really. He had a sinus infection at the time but continued to snort different drugs. Well a couple of weeks later he was sent to the hospital he had 3 small strokes and wound up in a coma. I was just informed this morning that he has died. I felt others should know this because the doctors said he snorted the sinus infection right up into his brain where the infection rapidly spread throughout eventually killing him. So please people if you have a sinus infection wait until its gone before snorting any drugs.

CaPoNe.

monstanoodle
05-02-2011, 23:16
Jeezus man :( I'm so, so sorry to hear this....
That's fucked :(
((((((((( CaPoNe, his friends and family )))))))))

This is a very valuable piece of harm reduction information. It might very well be more useful as a permanent fixture in the "Case Studies" thread as that's where such cases are posted but usually when they have an article to back it up.
Ofcourse I'm not saying that this isn't true!!!! Please don't think that (yer probably not and I'm just being paranoid).

Anyway, I'll ask the mods of OD if they want to move it anywhere.

Again, my ultimate condolences ♥

Alice_D
06-02-2011, 00:00
wow I had no idea that could happen! I am so sorry for your loss brother, I know the feeling of losing a friend to drugs. I think we have all lost a few too many good ones.

Vader
06-02-2011, 02:48
I'm sorry for your loss man, but I don't understand how you could snort something into your brain. That just doesn't sound plausible.

Mora Fiend
06-02-2011, 02:53
This needs a bump for sure.

Very, very sorry to hear that man, I am sure he meant a lot to you. You have to realize something though and I think I should tell you because I had a friend that died when I was 18 due to drugs and I blamed myself for it.

It's not your fault he's gone, wether or not you were there to stop it he would of done it anyway. Any guilt you may feel, remember it's not your fault.

Much love man, sorry to hear it and thanks for posting. Others on here who use their nose to get high should take heed.

dokomo
06-02-2011, 02:58
Merged into case studies thread.

So sorry for your loss man :( , and thanks for sharing this information with us

monstanoodle
06-02-2011, 03:03
Thanks for doing this Dokomo

Vader
06-02-2011, 03:12
I though this thread was meant to be a collection of journal articles rather than anecdotal evidence:

I'm just posting some relevant journal articles at the moment. I could share some of my experiences -- like the junky who robbed the pharmacy and was found dead later in the day with 5+ durogesics on his arm -- but at the end of the day it's just another 2nd hand experience which people can easily dismiss as being irrelevant. It's harder to do so when the facts (and more importanly the pictures in this case) are staring you in the face.
said djsim

monstanoodle
06-02-2011, 03:46
Yea this is why I made sure to question the OD mods if it should be put here or not.
But I think it's important enough to warrent adding. If you like, you could do a little research and see if you can find any sources that back up the anecdotal evidence :)
It'd be of great use.

CaPoNe.
06-02-2011, 07:31
Thanks everyone i know he would want this to be done to warn people of his mistake. I never thought it could happen either i will do some research and post my findings I just hope people can find this and read it before it is to late for anybody else.

Mora Fiend
07-02-2011, 09:31
Bumping because I feel this thread should be on the front page.