2. C Snow Blow
AKA
Coke Flake
Often cut with:
• Cornstarch • Sugar
• Talcum Powder • Procaine (anesthetic)
• Baking Soda • Amphetamine (stimulant)
Cocaine + Heroin = Speedball
Crack: freebase cocaine
Refers to crackling sound heard when mixture is smoked
3. Effect on Adults:
Powerful CNS stimulant
Effects last 15 minutes to an
hour, depending on method of
ingestion
Increases alertness, feelings of
well-being & euphoria, energy
& motor activity, feelings of
competence & sexuality
Athletic performance may be
enhanced (attention &
endurance)
4. Schweitzer Case Study
• 18 yo Female
• 3 yr hx of alcohol & drug abuse
• Binged on heroin, benzodiazepine (Xanax), alcohol, and crack
Initial audio:
•Bilateral, severe SNHL (flat)
•Normal tympanometry
•Absent ipsi and contra acoustic reflexes
•Absent DPOAEs
5. Ciorba Case Study
• 30 yo Female
• Heroin addict
• Overdose: IV Cocaine
12 hrs post: Severe symmetrical SNHL
• SRT predictable by pure tone threshold
• WRS 0% @ 80dB HL, 40-50% @ 100 dB HL
• Wave V detectible at 90dB HL
• Tympanometry WNL
• DPOAEs absent
7. Ciorba’s Conclusions
Typically, the basal cochlear turn is most damaged by
vasospasm. More sensitive to hypoxia.
This case showed a flat audiogram initially, equal improvement,
and full recovery- suggests equal dysfunction across cochlea and
hearing loss is not due to hypoxia as that’s permanent
“Perturbation of cochlear homeostasis”
Likely caused by “transient disruption of cochlear K+ recycling
pathway induced by cocaine”
9. DPOAEs
Absent OAEs in the presence of normal out/middle ear function
Tang, 1996
Shivapuia, 1993
Moderate low doses of
cocaine to Chinchillas Newborns of cocaine abusing
every day for 30 days mothers do not have increased
incidence of HL and peak
Little or no difference in latencies normalize by one year of
DPOAEs in chronic and life.
acute groups
12. Works Cited
(2004). Intensive care nursery house staff manual. Retrieved from The Regents of the University of California website:
http://www.ucsfbenioffchildrens.org/health_professionals/intensive_care_nursery_house_staff_manual/index.html
Bauman, J. L., & Didomenico, R. J. (2002). Cocaine-induced channelopathies: Emerging evidence on the multiple mechanisms of sudden death. Journal of Cardiovascular Pharmacol
Therapeut, 7(3), 195-2002.
Ciorba, A., Bovo, R., & Prosser, S. (2009). Considerations on the physiopathological mechanism of inner ear damage induced by intravenous cocaine abuse: Cues from a case report. Auris
Nasus Larynx, 36, 213-217.
Grimmer, I., Buhrer, C., & Aust, G. (1999). Hearing in newborn infants of opiate-addicted mothers. European Journal of Pediatrics, 158, 653-657.
Jospe, N. (2009, December). Prenatal drug exposure. Retrieved from http://www.merckmanuals.com/professional/pediatrics/metabolic_electrolyte_and_toxic_disorders_in_neonates/pre
natal_drug_exposure.html
Ritchie, J.M. and Greene, N.M. (1990) local anesthetics. In:A.G. Gilman, L.S. goodman, T.W. Rall and F. Murad (Eds.), The pharmacological basis of therapeutics. 8th ed., Macmallian, MY,
pp.311-331.
Schweitzer, V. G., Darrat, I., & Stach, B. A. (2011). Sudden bilateral sensorineural hearing loss following polysubstance narcotic overdose. Journal of American Academy of Audiology, 22,
208-214.
Shivapuja, B. G., Gu, Z. P., & Liu, S. Y. (1994). Effects of repeated cocaine injections on cochlear function. Brain Research, 668, 230-238.
Shivapuja, B. G., Gu, Z. P., & Saunders, S. S. (1993). Acute effects of cocaine on cochlear function. Hearing Research, 69, 243-250.
Tan-Laxa, M. A., Sison-Switala, C., & Rintelman, W. (2004). Abnormal auditory brainstem response among infants with prenatal cocaine exposure. American Academy of Pediatrics, 113,
357-360.
Tang, W. X., Shivapuja, B. G., & Salvi, R. J. (1996). Effects of cocaine on distortion-product otoacoustic emissions in the chinchillas. Association for Research in Otolaryngology, 103(B5).
Trigueiros-Cunha, N., Ledo, P., & Renard, N. (2006). Prenatal cocaine exposure accelerates morphological changes and transient expression of tyrosine hydroxyls in the cochlea of developing
rats. Brain Research, 1086, 55-64.
Volkow, N. D. (2010). Cocaine: Abuse and addiction. Retrieved from National institute on drug abuse website: http://www.nida.nih.gov/researchreports/cocaine/cocaine.html
2 chemical forms of abused cocaine: 1) Water-soluble hydrochloride salt Injected or snorted 2) Water-insoluble: freebase Processed with ammonia or sodium bicarbonate (baking soda) and water, then heated to remove the hydrochloride to produce a smokable substance
CNS Stimulant, appetite suppressant, & topical anesthetic Serotonin-norepinephrine-dopamine reuptake inhibitor. Addictive: effects mesolimbic reward pathway Crosses blood-brain barrier Second most popular recreational drug in U.S (behind marijuana). U.S. is world’s largest consumer of cocaine. NHSDA (National Household Survey on Drug Abuse) reported that 3.7 million Americans or 1.7% of the household population age 12+ reports use in 1999.
Tx: prednisone, anti-viral initially (little improvement). Then 6d later steroids and vasoactive therapy (pentoxifulline- increases tissue oxygenation). 6 mo later: Minimal HL thru 2kHz, moderate HL at HF (initial audio unknown)- no addl follow up, P overdosed 2 mo later.
Tx: Betamethason (corticosteroid for inflammation) and Mannitolo (renal diurretic) DPOAEs also returned
Vasospasm refers to a condition in which blood vessels spasm , leadin g to vasoconstriction .
Within the cochlea, potassium channels are responsible for maintaining endolymphatic and cellular resting potential, which contributes to hair cell excitability. Within a cardiac model, cocaine behaves like a local anesthetic by rendering the sodium ion channel non-conducting, and prolonging neuronal repolarization. Additionally, at lower concentration levels, cocaine blocks potassium channels, which results in prolonged action potential duration It is highly possible that cocaine exposure results in a transient disruption of the cochlear K+ recycling pathway and hearing loss.
Dependent on OHC status & independent of neural status. Cocaine has known effect on neural status- not discussed here. Was the case caused by something else?
Inhibits reuptake of the neurotransmitters norepinephrine and epinephrine; it crosses the placenta and causes vasoconstriction and hypertension in the fetus. Increases maternal arterial blood pressure, decreases uterine blood flow, and transiently increases fetal systemic blood pressure. Neonates born to addicted mothers have low birth weight, reduced body length and head circumference, and lower Apgar scores. intestinal atresia or necrosis, limb amputations, -VASCULAR DISRUPTION a pattern of mild neurobehavioral effects has also been observed, including decreases in attention and alertness, lower IQ, and impaired gross and fine motor skills. Some neonates may show withdrawal symptoms if the mother used cocaine shortly before delivery, but symptoms are less common and less severe than for opioid withdrawal, and signs and treatment are the same. After birth: Hypertonicity, irritability, tremors, abnormal cry/sleep/feeding patterns, tachycardia, tachypnea, apnea. Treat with behavioral and soothing methods. My question: do babies who would have hearing loss die before birth? They’re smaller and an overdose is easier for them vs the mom who would survive smaller doses.
Research is extremely limited Effects vary depending on cocaine concentration, vessel, age, species, and route of administration (Ciorba, 2009 In surviving neonatally exposed infants, the auditory system does not seem to be grossly impacted, long term.
