What do you mean the cocaine gave me an Asthma Attack!?!?

[Dustdevil]

I thought they used to give a liquid syrup of coccaine to people with respiratory problems. This was before my time, but I remember coccaine bottles on the vintage medicine shelf in our pharmacy/soda shop/general store.

I've used cocaine in the ER for nasal haemostasis, and seen it used for nasal intubation. Of course, it is an ingredient in TAC (c for cocaine) too. Those are the only medicinal uses I have seen for it.

[bandaidpatrol]

I've used cocaine in the ER for nasal haemostasis, and seen it used for nasal intubation. Of course, it is an ingredient in TAC (c for cocaine) too. Those are the only medicinal uses I have seen for it.

I'm talking 1920's. Or is that before your time? I was born about 18 years afterward.

[Ace844]

For those of you here who see a fair amount of OD's I thought you may find this interesting. + the NARCAN threads are all locked?!?!?!?

HTH,

ACE844

(The American Journal of Emergency Medicine

Volume 24 @ Issue 4 , July 2006, Pages 515-516

doi:10.1016/j.ajem.2005.09.008

Copyright © 2006 Elsevier Inc. All rights reserved.

Correspondence

Caution with naloxone use in asthmatic patients

Paul J. Allegretti DO, FACOEPa, Jeff S. Bzdusek DOa, and Jim Leonard DOa

aEmergency Medicine Residency, Midwestern University, Chicago College of Osteopathic Medicine, Chicago, IL 60515, USA

Available online 17 June 2006.)

The city of Chicago has a high prevalence of asthma and is currently in the midst of a heroin abuse epidemic. Higher-purity heroin is readily available and can be easily inhaled. As a result, the emerging pattern in heroin administration is changing, with inhalation being the most commonly reported route of use. This has contributed to a growing perception that heroin is not as dangerous or addictive as it used to be. The population of suburban youth inhaling heroin (younger than 25 years) demonstrates the largest increase. As more are attracted to use it, the incidence of acute asthma triggered by inhaled heroin will increase [1]. Clinicians need to maintain a high level of suspicion that heroin is another trigger for asthma and screen patients appropriately. The association between heroin and asthma exacerbation has been well described in various case studies reported in the literature.

A recent article in Chest described 5 patients with life-threatening asthma that occurred shortly after inhaling heroin. Each patient had history of asthma and received the standard therapy to treat asthma. Mechanical ventilation was required for the treatment for 4 patients for an average of 5 days [2]. This was atypical because asthmatic patients usually require only 24 to 48 hours on a ventilator before they recover. The pulmonary inflammation and bronchospasm are more difficult to treat than in an asthmatic patient who has not used heroin. These cases demonstrate a link between inhaled heroin and asthma exacerbation.

Several other studies have been conducted to elucidate the mechanism of heroin-induced airway inflammation. Investigators have identified that postoperative patients receiving morphine or heroin had significantly elevated histamine levels [3]. The opioids act as an allergen and stimulate this histamine release from the degranulation of mast cells. Histamine causes the contraction of smooth muscle [4]. It also contributes to the inflammatory response by activating the release of cytokines and inflammatory mediators from neighboring leukocytes [5]. Consequently, the muscles surrounding the airways constrict, causing the dyspnea, wheezing, and chest tightness characteristic of an asthma exacerbation. These data suggest that airway inflammation due to heroin use is mediated by an immunological pathway.

Although the symptoms of opioid use are reversed by naloxone, this antidote must be used cautiously. Naloxone competitively binds opioid receptors to inhibit the effects of heroin. Heroin-induced respiratory depression is the primary cause of most opioid-related deaths, and in cases of life threatening heroin toxicity, naloxone is indicated. Naloxone may be given by way of the endotracheal, sublingual, intramuscular, intravenous, nebulized, and subcutaneous routes. Of significant concern is the appearance of characteristic withdrawal symptoms including agitation, nausea, and vomiting after the administration of naloxone. In a recent study, withdrawal was precipitated by injecting naloxone to morphine-dependent mice. The subsequent histological analysis of brain tissue revealed elevated levels of mast cells. The authors concluded that naloxone-induced morphine withdrawal increases the concentration of mast cells in the thalamus [6]. This strongly suggests that opioid withdrawal would exacerbate asthma by increasing mast cell degranulation and histamine release. The increased circulation of histamine would cause the immunologically mediated bronchoconstriction and airway edema. These symptoms have a strong tendency to worsen asthma, especially in asthmatic patients who are already in exacerbation.

The administration of naloxone is a potentially dangerous practice and does not treat the underlying bronchospasm or inflammation. The authors' concern comes with heroin-using asthmatic patients struggling with pulmonary inflammation and bronchospasm without signs of respiratory depression. Naloxone given to these patients may worsen asthma symptoms because acute withdrawal has a deleterious effect on asthma. Precipitation of acute withdrawal in these patients may lead to a worsening of asthma and, possibly, respiratory failure. We have witnessed asthmatic patients in exacerbation who, after having received naloxone, proceed rapidly into respiratory failure. The judicious use of naloxone is warranted in heroin users and should be limited only to patients with altered mental status along with a respiratory rate less than 12 [7]. Caution should be exercised when administering naloxone in heroin users that present in status asthmaticus without respiratory depression.

References

[1] K. Kane-Willis and Schmitz-Bechteler, A multiple indicator analysis of heroin use in the Chicago metropolitan area from 1995-2002, Institute for Metropolitan Affairs of Roosevelt University (2003).

[2] J. Cygan, M. Trunsky and T. Corbridge, Inhaled heroin–induced status asthmaticus: five cases and a review of the literature, Chest 117 (2000), pp. 272–275. Abstract-MEDLINE | Abstract-EMBASE | Abstract-Elsevier BIOBASE | Full Text via CrossRef

[3] A. Deonicke, J. Moss and W. Lorenz et al., Intravenous morphine and nalbuphine increase histamine and catecholamine release without accompanying hemodynamic changes, Clin Pharmacol Ther 58 (1995), pp. 81–88.

[4] D. Schmidt, E. Ruehlmann and D. Branscheid et al., Passive sensitization of human airways increases responsiveness to leukotriene C4, Eur Res J 14 (1999), pp. 315–319. Abstract-EMBASE | Abstract-MEDLINE | Abstract-Elsevier BIOBASE | Full Text via CrossRef

[5] G. Marone, F. Granata and G. Spadaro et al., Antiinflammatory effects of oxatomide, J Investig Allergol Clin Immunol 9 (1999), pp. 207–214. Abstract-EMBASE | Abstract-MEDLINE

[6] O. Taiwo, K. Kovacs and L. Sperry et al., Naloxone-induced morphine withdrawal increases the number and

[AZCEP]

Another good reason to limit the amount of medications a Basic provider can administer.

[Ace844]

Here's some more great 'crack' info for you also to be aware of...it is a case study..

Abstract

Cocaine and coronary calcification in young adults. The coronary artery risk development in young adults (cardia) study

Pletcher MJ, Kiefe DI, Sidney S, et al. Am Heart J 2005;150:921–6

Mary Westergaard MDa

aDenver Health Medical Center, Denver, CO

Available online 22 June 2006.

This study examined the correlation between cocaine use and coronary calcification in participants enrolled in a longitudinal study of risk factors for coronary artery disease. At the 15-year evaluation of the CARDIA cohort, 3038 participants answered questions about cocaine use and underwent computed tomography (CT) to quantify coronary artery calcification. Before adjustment for age, sex, socioeconomic status, ethnicity, family history, smoking and alcohol use, cocaine exposure was strongly associated with coronary calcification. After adjustment for these factors, however, the correlation disappeared, with adjusted odds ratios for coronary calcification of 0.9 (95% confidence intervals [CI] 0.6–1.3) for 1 to 10 lifetime episodes, 1.2 (95% CI 0.8–1.7) for 11–99 episodes and 1.0 (95% CI 0.6–1.6) for ≥ 100 lifetime episodes of cocaine exposure. Male gender, alcohol and tobacco use were the three most important confounders, whereas systolic blood pressure, LCL-C, and HCL-C remained strong independent predictors of coronary calcification. The authors conclude that the increased rate of myocardial ischemia and infarction seen in cocaine users is due primarily to the acute effects of cocaine rather than accelerated atherogenesis.

Comment: This longitudinal study provides unique insight into the causes of coronary disease in people who

Crack cocaine causing fatal vasoconstriction of the aorta

Joanne Williams MD, FAAEM, a and Jonathan Wasserberger FACEP, FACMT, FAAEMa

aDepartment of Emergency Medicine, Martin Luther King, Jr./Charles R. Drew Medical Center, Charles R. Drew University of Medicine and Science, Los Angeles, California

Received 10 December 2004; revised 22 April 2005; accepted 4 August 2005. Available online 20 July 2006.

Abstract

Cocaine is the most powerful central nervous stimulant found in nature. All forms of cocaine cause tachycardia and vasoconstriction. A smokable, rapidly reacting form of cocaine base, “crack,” is highly addictive. Smoking crack introduces a high concentration of cocaine into the bloodstream, rendering it especially dangerous. We report a case that visually demonstrates severe aortic vasoconstriction from the suprarenal aorta and extending to both femoral arteries and beyond, resulting in renal failure and fatal bowel ischemia after a 5-day binge of crack cocaine.

Keywords: crack binge; vasoconstriction; renal failure; bowel ischemia

Article Outline

Introduction

Case report

Emergency Department Course

Bedside ultrasound

Laboratory data

Aortogram with run-off (Figure 3)

ICU Course

Cause of death

Discussion

References

Introduction

One of the most powerful addictive drugs of abuse, cocaine was first isolated from the leaves of the coca plant, Erythoxylon coca, in the late 1800s. The coca plant is indigenous to the highlands of the Andean mountains of South America. As a part of their religious rituals, the Incas used coca leaves thousands of years ago. As early as 3000 B.C., coca chewing was practiced throughout South America. Coca was believed to be a gift from God (1). Laborers in the Andes either chewed coca leaves or brewed tea from the coca leaves to relieve hypoxia, hunger, fatigue, and for refreshment over the centuries.

Albert Niemann was the first to isolate the active ingredient of the coca plant around 1860 (2). The Viennese neurologist Sigmund Freud wrote several papers “to the glory” of cocaine. In Uber Coca, written in 1884, Freud speaks of “the most gorgeous excitement” animals display after receiving injection of cocaine “offering.” The fictional detective Sherlock Holmes thought of cocaine as “so transcendentally stimulating and clarifying to the mind that its secondary action is a matter of no small moment” (3). Robert Louis Stephenson was said to have written The Strange Case of Dr. Jekyll and Mr. Hyde during a 6-day cocaine binge. The polar adventurer Ernest Shackleton was said to have explored Antarctica through the use of tablets of “Forced March” (3).

Cocaine is the most powerful central nervous stimulant found in nature. In addition, all forms of cocaine cause tachycardia and vasoconstriction. After its isolation, cocaine became a popular ingredient in patent medicines, Coca-Cola, and other products. The Harrison Act of 1914 outlawed the use of cocaine and opiates in over-the-counter products, making these drugs available only by prescription.

A smokable, rapidly reacting form of cocaine base, “crack,” is highly addictive, and some first-time users have become addicted. Crack cocaine is made by heating ordinary cocaine hydrochloride in a solution of baking soda until the water evaporates. This type of base-cocaine makes a cracking sound when heated; hence the name, “crack” cocaine. The resulting paste is then baked and broken into small pieces (“rocks”). Because base-cocaine vaporizes at a low temperature, it can be easily inhaled through a heated pipe. This method of use introduces a high concentration of cocaine into the bloodstream, rendering it an especially dangerous form of the drug.

Before the development of crack, smokable cocaine was consumed in the form of “free-basing”. Free-base was produced using highly volatile solvents, most notably ether. Because free-basing is physically dangerous to make and flammable, crack has replaced free-basing in popularity. The U.S. Drug Enforcement Administration figures reflect that crack has been weighing in at 75%–90% potency in recent years. This is up from 34% in 1987! These high concentrations may overtax the cardiovascular system, causing sudden death.

Crack first appeared in the early to mid-1980s and has reached epidemic standing in the United States. Three factors have contributed to the escalating usage of crack cocaine, namely, 1) it is cheap and affordable, 2) it is easy to smoke, and 3) its effect is rapid and intense.

We report a case that visually demonstrates severe aortic vasoconstriction after a 5-day use of crack cocaine.

Case report

A 32-year-old woman presented to the Emergency Department (ED) complaining of severe bilateral lower extremity pain and inability to walk. She stated that she had been “doin’ crack” for 5 days straight when the pain developed. When the pain started, she stopped “smokin’” and drank several cans of beer in an effort to quell the pain. When she was no longer able to walk, her friends brought her to the ED.

She had no significant past medical history. She said that she had been “speed balling” (injecting a mixture of cocaine and heroin) for years but recently began “doin’ crack.”

Emergency Department Course

The patient had a blood pressure of 70/systolic, heart rate 172 beats/min, respiratory rate 22 breaths/min, and an oral temperature 36.1°C (97°F). She was a well-developed, well-nourished, ill-appearing female in moderate distress due to pain, lethargic yet arousable to verbal stimuli, oriented × 4 when aroused. At the time it was felt that the lethargy was due either to cocaine washout syndrome or concomitant heroin use. The chest was clear to auscultation and the heart was tachycardic without murmurs or gallops. The trunk was mottled circumferentially below the umbilicus, and the abdomen had mild diffuse tenderness and no bowel sounds were appreciated on auscultation. There was moderate bilateral costovertebral angle tenderness. The extremities were mottled, pale, cold to the touch right more than left and the femoral pulses were faintly audible with doppler. No pulses were appreciated distally. There was a marked decrease in sensation bilaterally in the lower extremities and multiple old and new “tracks” were noted on both upper extremities.

She was placed on supplemental oxygen. A subclavian intravenous line was placed and 4 L of normal saline were infused rapidly. Blood pressure rose to 110/systolic and pulse rate decreased to 110 beats/min and the patient felt subjectively better. A foley catheter to gravity was placed with negligible urinary output. A nitroglycerin infusion was begun at 20 μg/min in concert with continued infusion of normal saline.

The Ultrasound Technician performed a bedside ultrasound in the ED in an attempt to rule out any abdominal aorta obstruction.

Bedside ultrasound

Figure 1 and Figure 2 show portions of the abdominal aorta seen in the bedside ultrasound. Note the lack of vasoconstriction in Figure 1 showing the abdominal aorta above the renal arteries after a 7-L infusion of normal saline. Figure 2 reveals the beginning of the vasoconstriction that persists after a 7-L infusion of normal saline.

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Figure 1. Patient’s aorta above the renals.

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Figure 2. Beginning of vasoconstriction (just above the renal arteries).

Laboratory data

The CPK was 5600, BUN 156, Cr 6.2, K 4.0, CBC and remaining electrolytes were within normal limits.

Aortogram with run-off (Figure 3)

This study demonstrates severe vasoconstriction that begins just above the renal arteries and continues to both lower extremities. This study was done after the patient had received more than 10 L of normal saline intravenously. Figure 4 demonstrates a normal aortogram (note the size of the vessels and the branches on this study).

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Figure 3. Aortogram showing persistent vasoconstriction even after 7 L of rapid normal saline infusion.

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Figure 4. Normal aortogram (note the abundance of branching vessels) for comparison.

ICU Course

The patient continued to improve subjectively and was transferred to the intensive care unit (ICU). The patient’s initial treatment was continued in the ICU. One day later she had normal skin consistency, color and normal pulses in the lower extremities. Early in the morning on day 3 she developed fever, acute septic shock, and disseminated intravascular coagulopathy. She suffered a cardiopulmonary arrest and failed to respond to Advanced Cardiac Life Support measures and was subsequently pronounced dead.

Cause of death

The speculated cause of death was diffuse dead bowel, i.e., mesenteric ischemia, secondary to prolonged vasoconstriction, and ischemic renal failure due to prolonged vasoconstriction.

Discussion

Animal and human studies have documented cocaine-induced sustained vasoconstriction demonstrated by decrease in epicardial coronary artery diameter ranging from 5% to 30% with various doses of cocaine by various methods of administration (4). Cocaine activates platelets and promotes thrombosis (5). Cocaine is an indirect sympathetic nervous system stimulating agent that has direct toxic effects on the heart and that causes myocardial ischemia. Cocaine induces apoptosis (also known as “programmed cell death”) in a heart muscle (6). This unopposed alpha vasoconstriction of the epicardial coronary arteries may be exacerbated by beta-blockers. Therefore, unopposed alpha stimulation provided by beta-blockers should be avoided (7). Central nervous system hyperexcitability causing this indirect acting sympathomimetic activity from cocaine is treated with benzodiazepines. Coronary artery vasoconstriction is treated with nitroglycerin and calcium channel blockers (7 and 8). Cocaine in the presence of alcohol results in the production of the active metabolite cocaethylene, which has a prolonged half-life of 7 h and thus contributes to the prolonged episodes of vasoconstriction (9).

Up until 1990, only rare instances of intestinal ischemia subsequent to cocaine use were reported, and crack abuse had not been associated with mesenteric ischemia (10 and 11). Only three cases of intestinal ischemia induced by cocaine abuse had been described and actual vasoconstriction of mesenteric vessels had not yet been demonstrated. In these cases, the diagnosis of vasospastic bowel ischemia could not definitely be confirmed. Postmortem examination on those three patients demonstrated the existence of segmental intestinal ischemia. A microscopic study failed to demonstrate any thrombosis of the mesenteric vessels (12). As of 1997, there were only 15 reported cases of cocaine-induced ischemic events of the small bowel and colon (13). Only one case of ischemic colitis was reported in a 36-year-old woman who admitted using crack cocaine twice, 2 days before the onset of her symptoms. Her pathology showed patchy areas of necrosis that were grossly present in the resected transverse colon. On microscopy, multiple small vessel thrombi were present. Colonic mucosa showed ischemic necrosis, and the author has recommended that cocaine abuse should be considered in a differential diagnosis of ischemic colitis, especially in young adults (13).

In 2000, a 33-year-old man developed distal ileum infarction after the abuse of cocaine. He underwent resection of gangrenous bowel segment and survived. He had no previous history of atherosclerosis. This patient suffered cocaine-induced rhabdomyolysis with acute renal failure (14). Renal biopsy findings were inconsistent with thrombotic microangiography and glomerular ischemia. The patient demonstrated renal endothelial injury and vasoconstriction (14). In 1998, perioperative angiography detected occlusive gastrointestinal arterial lesions. These authors emphasized that arterial revascularization should be considered (15).

After self-administering intravenous cocaine, a 45-year-old man developed a sharply demarcated area of small intestinal ischemia with perforation characterized by pseudomembranous colitis. Histologic sections of small bowel resection in this patient showed only rare submucosal arterioles (15).

Since then, two additional women, 29 and 35 years of age, respectively, both presented with occlusion of the celiac plexus axis and the superior mesenteric vessels. A vascular bypass was performed in both cases. Microvascular examination of both arteries and their branches revealed total obstruction by luminal thrombus. Both had a prior history of intravenous cocaine abuse (15).

Most recently, in 2001, three cases were reported of patients presenting with acute onset of abdominal pain after smoking crack cocaine. These three patients required surgical correction of intestinal perforations. The chronological relationship of crack consumption to gastrointestinal perforation led to the hypothesis of a possible crack-induced ischemic event as the cause of the perforations in these patients (16). A warning was emphasized that patients with abdominal pain who have used crack cocaine should be considered as possibly having bowel ischemia (17).

Our present case may be the first that visually demonstrates severe aortic vasoconstriction from the suprarenal aorta and extending to both femoral arteries and beyond after a 5-day use of crack cocaine.

References

1 C.E. Johanson, The encyclopedia of psychoactive drugs cocaine, a new epidemic, Chelsea House Publications, New York, NY (1986).

2 J. Biscoping and M.B. Bachmann-Mennenga, Local anesthetics from ester to isomer, Anasthesiol Intensivmed Notfallmed Schmerzther 35 (2000), pp. 285–292. Abstract-MEDLINE | Full Text via CrossRef

3 J.R. Maltby, Sherlock Holmes and anaesthesia, Can J Anaesth 35 (1988), pp. 58–62. Abstract-EMBASE | Abstract-MEDLINE

4 B.S. Benzquen, Effects of cocaine on the coronary arteries, Am Heart J 142 (2001), pp. 402–410.

5 L. Zhang, Y. Xlao and J. He, Cocaine and apoptosis in myocardial cells, Anat Rec 257 (1999), pp. 208–216. Abstract-MEDLINE | Abstract-EMBASE | Abstract-Elsevier BIOBASE | Full Text via CrossRef

6 R.A. Lange and L.D. Hillis, Cardiovascular complications of cocaine use, N Engl J Med 345 (2001), pp. 351–358. Abstract-EMBASE | Abstract-Elsevier BIOBASE | Full Text via CrossRef

7 R.G. Williams, K.M. Kavanagh and K.K. Teo, Pathophysiology and treatment of cocaine toxicity implications for the heart and cardiovascular system, Can J Cardiol 12 (1996), pp. 1295–1301. Abstract-MEDLINE | Abstract-EMBASE

8 W.R. Pitts, R.A. Lange, J.C. Cigarroa and L.D. Hillis, Cocaine-induced myocardial ischemia and infarction pathophysiology, recognition and management, Prog Cardiovasc Dis 40 (1997), pp. 65–76. Abstract | PDF (1099 K)

9 M.J. Landry, An overview of cocaethylene, an alcohol-derived, psychoactive, cocaine metabolite, J Psychoactive Drugs 24 (1992), pp. 273–276. Abstract-EMBASE | Abstract-MEDLINE

10 A. Tun and I.A. Khan, Myocardial infarction with normal coronary arteries the pathologic and clinical perspectives, Angiology 52 (2001), pp. 299–304. Abstract-EMBASE | Abstract-MEDLINE

11 D.C. Hon, L.J. Salloum, H.W. Hardy III and J.E. Barone, Crack-induced enteric ischemia, N J Med 87 (1990), pp. 1001–1002. Abstract-MEDLINE

12 A. Garfia, J.L. Valverde, J.C. Borondo and I. Candenas, Vascular lesions in intestinal ischemia induced by cocaine-alcohol abuse report of a fatal case due to overdose, J Forensic Sci 35 (1990), pp. 740–745. Abstract-MEDLINE | Abstract-EMBASE

13 H.H. Bsutros, S. Paulter and S. Chaskrabarti, Cocaine-induced ischemic colitis with small vessel thrombosis of colon and gallbladder, J Clin Gastroenterol 24 (1997), pp. 49–53.

14 J. Volcy, C.M. Nzery, A. Oderinde and K. Hewan-Iowe, Cocaine-induced acute renal failure, hemolysis, and thrombocytopenia mimicking thrombotic thrombocytopenic purpura, Am J Kidney Dis 35 (2000), p. E3. Abstract-MEDLINE

15 M.P. Hoang, E.L. Lee and A. Anand, Histologic spectrum of arterial and arteriolar lesions in acute and chronic cocaine-induced mesenteric ischemia report of three cases and literature review, Am J Surg 22 (1998), pp. 1404–1410. Abstract-EMBASE | Abstract-MEDLINE | Full Text via CrossRef

16 A.E. Muniz and T. Evans, Acute gastrointestinal manifestations associated with use of crack, Am J Emerg Med 19 (2001), pp. 61–63. Abstract | PDF (49 K)

17 J. Osorio, N. Farreras, L. Ortiz de Zarate and E. Bachs, Cocaine-induced mesenteric ischaemia, Dig Surg 17 (2000), pp. 648–651. Abstract-MEDLINE | Abstract-EMBASE | Full Text via CrossRef