Cortical effects lead to pressure
of speech, excitation, and a reduced feeling of fatigue; stimulation of
lower centers leads to tremor and tonic-clonic convulsion; brain stem
effects lead to stimulation and then depression of the respiratory
vasomotor and vomiting centres. Cocaine causes hyperthermia as a result of
two mechanisms: the increase in muscular activity and a direct effect on
thermal regulatory centers. The visceral effects on liver and kidney are
due to dopaminergic action of cocaine, or its metabolites, or to
impurities. The abrupt increase intra-alveolar pressure can cause alveolar
rupture and pneumomediastinum. Rhabdomyolysis occurs as a result of
several different mechanisms: direct effect on muscle and muscle
metabolism, tissue ischemia, the effects of drugs taken with cocaine, such
as alcohol and heroin.
Pharmacodynamics:
The principle effects of cocaine
are the result of its sympathetic action:
cocaine prevents the re-uptake
of dopamine and noradrenaline, which accumulate and stimulate neuronal
receptors. At the same time, the release of serotonin a sedative
neurotransmitter, is inhibited.
The inhibition of catecholamine re-uptake
does not explain the duration of action of cocaine, which may also result
from an increase in calcium flux, potentiating cellular responses and
causing receptor hypersensitivity. There may also be a direct effect on
peripheral organs.
Applied locally, cocaine blocks neuronal transmission:
this results in a powerful local anaesthetic action at the level of
sensory nerve terminals. Teratogenicity: A recent meta-analysis shows an
increase in congenital malformation rate in the offspring of
cocaine-users, particularly for abnormalities of the limbs, the
genito-urinary tract, and the cardiovascular, neurological, and digestive
systems.
Patients with choline esterase deficiency may develop severe
reactions. Interactions can occur with adrenaline, alpha- and
beta-blockers, vasoactive amines, antidepressants, chlorpromazine,
guanethidine, indomethacin, monoamine oxidase inhibitors, methyldopa,
naloxone, psychotropic medicines, and reserpine. There are metabolic
interactions with other local anaesthetics, cholinesterase inhibitors and
cytotoxic drugs. Chronic poisoning: Ingestion: Chronic ingestion of
cocaine can cause thoracic pain, changes on the electrocardiogram with
transient elevation of the ST segments and re-polarisation abnormalities;
and convulsions). Erosion of the teeth has been noted with chronic oral
ingestion. Inhalation: During inhalation of crack cocaine, chest pain
with changes on the electrocardiogram (re-polarization abnormalities and
transient ST segment elevation), and convulsions can occur. Reversible
cardiomyopathy with hypotension, hypoxemia and tachycardia, has been
described. A number of other symptoms have been described, though their
aetiology is not always clear. Cough, black or blood-stained sputum,
dyspnoea, thoracic pain, spontaneous pneumothorax, spontaneous
pneumomediastinum, and asthma (in a few cases) or immunoallergic lung
disease, have been described. Pulmonary granulomas and fibrosis,
bronchiolitis obliterans, and isolated arterial hypertension have also
been observed. Chronic cocaine intoxication causes anorexia, which leads
to weight loss, physical exhaustion, behavioral problems, and depression.
Skin exposure: Application of cocaine to skin or mucous membrane can cause
necrotic lesions. Eye contact: Repeated application of cocaine can cause
necrotic lesions. Other: Intranasal administration of cocaine can cause
necrosis and perforation of the nasal septum, atrophy of the nasal mucosa,
chronic sinusitis, and anosmia. Course, prognosis, cause of death: In
patients who are moderately poisoned, the symptoms have often
spontaneously resolved before emergency admission, and most patients leave
hospital within 36 hours.
Serious cocaine intoxication evolves in 3
phases: an early phase of stimulation, a second phase of hyper-stimulation
with tonic-clonic convulsions, tachyarrhythmias, and dyspnea, a third
phase of depression of the central nervous system, with loss of vital
function, paralysis, coma, and respiratory and circulatory collapse.
Two-thirds of deaths occur within five hours of administration, and
one-third within one hour after absorption of the drug, whatever the route
of administration. Systematic description of clinical effects:
Hematological: Disseminated intravascular coagulation has been observed in
subjects: platelet aggregation and thromboxane A2 levels are increased and
prostacyclin inhibited by cocaine. Immunological: Opportunist infections
such as cerebral mycosis, and infectious lung disease, have been described
in intravenous cocaine users. Metabolic: Acid-base disturbances;
electrolyte disturbances. Special risks: Pregnancy: cocaine causes
uterine hypercontractility, a reduced uterine blood flow, and placental
vasoconstriction. Thus, women cocaine addicts can develop hypertension of
pregnancy, spontaneous abortion, placental abruption, premature delivery,
and complications at delivery. Risks in the fetus: The offspring of
mothers who are cocaine addicts has an increased risk of genito-urinary,
cardiovascular, gastrointestinal, and neurological malformations; even a
single exposure to cocaine during pregnancy can lead to cerebral
infarction or hematoma, or to failure of development of the blood supply
or nerve supply to fetal structures. In the new-born: Ventricular
tachycardia, cerebral infarction, convulsion, hypertension, and unilateral
hypotonia are seen with increased frequency. Sudden, unexplained death in
the babies of cocaine addicted mothers can occur during the first few
weeks of life. Breast feeding: Cocaine and benzoylecgonine are found in
maternal milk up to 36 hours after the use of cocaine. Enzyme
deficiencies: Subjects who are deficient in pseudocholinesterase can die
suddenly after cocaine. ANIMAL/PLANT STUDIES: Anabolic experiments have
shown that there is no true physical tolerance to the effects of cocaine,
but a very marked psychic tolerance which leads animals to auto-inject
cocaine to obtain the desired psychological effects, even though this may
lead to death. Teratogenicity: The studies in animals are contradictory
International Programme on Chemical Safety; Poisons Information
Monograph: Cocaine (PIM 139) (1999) Available from, as of May 19, 2005:
http://www.inchem.org/pages/pims.html
HUMAN TOXICITY EXCERPTS:
The subjective effects of CNS sympathomimetics, /amphetamine, cocaine,
& related drugs/, like those of all centrally active drugs, are
dependent on the user, the environment, the dose of the drug, & the
route of administration. For example, moderate doses of amphetamine given
orally to normal subjects commonly produce an elevation of mood, a sense
of increased energy & alertness, & decreased appetite; task
performance that has been impaired by fatigue or boredom is improved. Some
individuals may become anxious, irritable, or loquacious. A few may
experience transient drowsiness, but insomnia is more common. As the dose
is increased toward toxic levels, the effects of individual experiences
& of environment become less significant.
[Gilman, A.G., L.S.Goodman,and A. Gilman. (eds.). Goodman and Gilman's The Pharmacological Basis of
Therapeutics. 7th ed. New York: Macmillan Publishing Co., Inc., 1985., p.550]
Four to 8 hours after a single intranasal dose of cocaine (96 mg),
subjects report a decreased sense of energy & increased feelings of
tiredness & sedation.
Cocaine ... causes transient irregularity of the corneal epithelium,
pupillary dilation with the attendant hazard of precipitating acute
glaucoma in individuals having abnormally shallow anterior chambers, and
in overdosage may cause death. Many cases of acute glaucoma were reported
around 1900 from cocaine eyedrops, presumably representing angle closure
glaucoma secondary to mydriasis. ... The epithelium and stroma of the
cornea can be injured by repeated application of cocaine ... and in one
bizarre case corneal ulceration and scarring have been reported in an
addict who used the conjunctival sac as the route for self administration.
... Systemically, cocaine has no selective ocular toxic action, but there
have been instances of transient blackouts of vision with the onset of
unconsciousness in systemic poisoning. In association with pupillary
dilation, the lids become elevated and the eyes appear staring, owing to
the contraction of sympathetically innervated smooth muscle attached to
the lid. [Grant, W.M. Toxicology of the Eye. 3rd ed. Springfield, IL:
Charles C. Thomas Publisher, 1986., p. 248]
Cocaine does not produce the classical addiction pattern seen with opiates
& sedative hypnotics, despite the fact that heavy users develop acute
tolerance to the euphoric effects of cocaine as well as physical
withdrawal symptoms (eg, depression, insomnia, headaches, fatigue,
irritability, GI distress). Major physiological changes & strong
tolerance do not characteristically accompany medical or casual cocaine
use. Nevertheless, cocaine use definitely can lead to compulsive, drug
oriented behavior that causes social, economic, & physical
deterioration. [Ellenhorn, M.J. and D.G. Barceloux. Medical Toxicology -
Diagnosis and Treatment of Human Poisoning. New York, NY: Elsevier Science
Publishing Co., Inc. 1988., p. 647] **PEER REVIEWED**
Reports of withdrawal like symptoms similar to those which occur in adults
exist. Neonates exhibit jitteriness, abnormal sleep patterns, poor feeding
& irritability. [Knoben, J.E. and P.O. Anderson (eds.) Handbook of
Clinical Drug Data. 6th ed. Bethesda, MD: Drug Intelligence Publications,
Inc. 1988., p. 207]
... /It is believed/ that with chronic use, cocaine users may manifest an
orderly progression of clinical syndromes from euphoria to paranoid
psychosis. The cocaine user normally develops a depressive aftermath &
often will use the drug again to dispel the depression. Thus, while
cocaine does not cause physical addiction, as does heroin, it causes
psychologic addiction ... [Haddad, L.M. and Winchester, J.F. Clinical
Management of Poisoning and Drug Overdosage. Philadelphia, PA: W.B.
Saunders Co., 1983., p. 445]
Cocaine addicts describe the euphoric effects of cocaine in terms that are
almost indistinguishable from those used by amphetamine addicts. In the
laboratory, subjects familiar with cocaine cannot distinguish between the
subjective effects of 16 mg of cocaine & those of 10 mg of
dextroamphetamine when both are given intravenously. Like amphetamine,
cocaine reduces the sense of fatigue & decrement in performance caused
by sleep deprivation. The toxic syndrome seen with cocaine seems
clinically indistinguishable from that produced by amphetamines. [Gilman,
A.G., L.S.Goodman, and A. Gilman. (eds.). Goodman and Gilman's The
Pharmacological Basis of Therapeutics. 7th ed. New York: Macmillan
Publishing Co., Inc., 1985., p. 550]
While cocaine is commonly perceived as a sexual stimulant, its use is
assoc with difficulty in establishing an erection & delayed
ejaculation. [Knoben, J.E. and P.O. Anderson (eds.) Handbook of Clinical
Drug Data. 6th ed. Bethesda, MD: Drug Intelligence Publications, Inc.
1988., p. 114]
A recent survey of cocaine abusers suggests a link between cocaine abuse
and eating disorders (anorexia nervosa, bulimia). [Ellenhorn, M.J. and
D.G. Barceloux. Medical Toxicology - Diagnosis and Treatment of Human
Poisoning. New York, NY: Elsevier Science Publishing Co., Inc. 1988., p.
647]
With time, tolerance develops to the euphorigenic effects of amphetamine;
higher & more frequent doses are used, & toxic symptoms &
signs then appear. These include bruxism, touching, & picking of the
face & extremities, suspiciousness, & a feeling of being watched.
Perceptual changes & pseudohallucinations may also occur with cocaine.
The most common of these are tactile ("cocaine bugs" in the skin) &
visual ("snow lights"). In addn, the user seems facinated or preoccupied
with his own thinking processes & with philosophical concerns about
"meanings" & "essences". Stereotypical, repetitious behavior is
common. Many patients who later show a full-blown toxic psychosis exhibit
a compulsion to take apart mechanical objects. They also have a compulsion
to put them together, but are usually too disorganized to do so. [Gilman,
A.G., L.S.Goodman, and A. Gilman. (eds.). Goodman and Gilman's The
Pharmacological Basis of Therapeutics. 7th ed. New York: Macmillan
Publishing Co., Inc., 1985., p. 552]
Cocaine occurs in abundance in the leaves of the coca shrub (Erythroxylon
coca). For centuries, Andean natives have chewed an alkali extract of
these leaves for its stimulatory and euphoric actions.
[Hardman, J.G.,L.E. Limbird, P.B. Molinoff, R.W. Ruddon, A.G. Goodman (eds.). Goodman and Gilman's The Pharmacological Basis of Therapeutics. 9th ed. New York, NY:McGraw-Hill, 1996., p. 331]
In contrast /to the chewing of coca leaves by the natives of the Andes/,
the smoking of coca paste (60-80% cocaine sulfate) by younger people
living in urban areas of Peru is assoc with a variety of
psychopathological states (euphoria, hypertalkativeness, irritability,
stereotypical behaviors, insomnia, wt loss, & toxic psychosis),
neglect of work, & a preoccupation with obtaining money to purchase
coca paste. ... Some users may smoke more than 40 g each day ... /Coca
paste (60-80% cocaine sulfate)/ [Gilman, A.G., L.S.Goodman, and A. Gilman.
(eds.). Goodman and Gilman's The Pharmacological Basis of Therapeutics.
7th ed. New York: Macmillan Publishing Co., Inc., 1985., p. 552]
Many of those who use amphetamine & cocaine are best described as
"recreational" or occasional users, but some become dependent. A small
percentage of the latter ... seem able to restrict drug intake &
function productively (stabilized addicts). Others show progressive social
& occupational deterioration, punctuated by periods of hospitalization
for toxic psychosis. In terms of the compulsion to continue use, the
degree to which a drug pervades the life of the user, & the tendency
to relapse following withdrawal, some compulsive users of amphetamine or
cocaine are addicts. The risk of developing patterns of compulsive use is
not limited to those who use drugs intravenously or smoke cocaine as the
base. Severe dependence with psychological, physical, & vocational
impairment is also seen among those who use cocaine intranasally. It is
not clear whether the dependence syndromes caused by amphetamine or
cocaine are as persistent as that produced by opioids. ... Very little is
known of the natural history of cocaine dependence. [Gilman, A.G.,
L.S.Goodman, and A. Gilman. (eds.). Goodman and Gilman's The
Pharmacological Basis of Therapeutics. 7th ed. New York: Macmillan
Publishing Co., Inc., 1985., p. 552]
A case of perinatal cerebral infarction assoc with maternal cocaine use
has been reported. The mother used cocaine intranasally during her first 5
weeks of pregnancy & then discontinued until the 3 days just prior to
delivery, during which time she used 5 g of cocaine intranasally. The
infant's initial exam was within normal limits except for mild decreased
muscle tone of the right upper extremity & tachycardia as high as 180
beats per minute. He later had several episodes of apnea & cyanosis
& suffering multiple focal seizures. A CT scan at 24 hours of life
showed a cerebral hemorrhage. At 3 months of age the infant's head
circumference had fallen from the 50th percentile at birth to the 5th
percentile. [Knoben, J.E. and P.O. Anderson (eds.) Handbook of Clinical
Drug Data. 6th ed. Bethesda, MD: Drug Intelligence Publications, Inc.
1988., p. 207]
In one small study of pregnant cocaine addicts, one mother delivered a
child manifesting the prune belly syndrome, which was similar to the
cryptorchidism and hydronephrosis produced in gravid mice. Spontaneous
abortion rates and the incidence of abruptio placentae (especially after
iv cocaine injection) were increased in the group of pregnant cocaine
addicts, perhaps because of placental constriction and incr uterine
contractility that occur after cocaine use. Neonates exposed to cocaine
from this group of mothers displayed significant depression of interactive
behavior and poor organizational response to external stimuli. In a case
control study of 50 cocaine abusing mothers, reduced birth weight, incr
malformation rates, and higher incidences of abruptio placentae and
stillbirths were detected. [Ellenhorn, M.J. and D.G. Barceloux. Medical
Toxicology - Diagnosis and Treatment of Human Poisoning. New York, NY:
Elsevier Science Publishing Co., Inc. 1988., p. 649]
There is no strong evidence to suggest that intrauterine cocaine exposure
causes fetal malformation. [Knoben, J.E. and P.O. Anderson (eds.) Handbook
of Clinical Drug Data. 6th ed. Bethesda, MD: Drug Intelligence
Publications, Inc. 1988., p. 207]
/In a controlled study/, a 25 mg intranasal cocaine dose produces slight
elevations in systolic pressure & subjective feeling of euphoria. A 16
mg intravenous dose simulates the effects of the average dose that
subjects self inject on the street. Both intravenous & intranasal
doses produce significant physiological & psychological changes. ...
Toxic reactions are difficult to predict, because of variations in street
impurities, adulterants, cocaine content, & individual tolerance.
[Ellenhorn, M.J. and D.G. Barceloux. Medical Toxicology - Diagnosis and
Treatment of Human Poisoning. New York, NY: Elsevier Science Publishing
Co., Inc. 1988., p. 648]
... The two most common presentations to an emergency department from
cocaine overdose have been seizures and cardiac arrhythmias. ...
Hypertension or hyperthermia or both also may be present. ... In critical
cases, cardiac or respiratory arrest may be the presenting picture.
[Haddad, L.M. and Winchester, J.F. Clinical Management of Poisoning and
Drug Overdosage. Philadelphia, PA: W.B. Saunders Co., 1983., p. 446]
Cocaine-related deaths result from all routes of admin, incl intravenous,
nasal, vaginal, and oral, as well as from accidental and inflicted trauma.
[Ellenhorn, M.J. and D.G. Barceloux. Medical Toxicology - Diagnosis and
Treatment of Human Poisoning. New York, NY: Elsevier Science Publishing
Co., Inc. 1988., p. 644]
Although the oral lethal dose of cocaine is usually given as 1200 mg,
death has been reported to follow as little as 20 mg of parenterally admin
cocaine. [Haddad, L.M., Clinical Management of Poisoning and Drug
Overdose. 2nd ed. Philadelphia, PA: W.B. Saunders Co., 1990., p. 731]
/Exposure by insufflation causes a/ reactive hyperemia of nasal mucosa ...
/which produces/ a peristent rhinitis. Erosions and, less often, nasal
perforation complicate chronic use. ... Deep inhalation may deposit
adulterants near the ethmoid sinuses, leading to sinusitis. ... In
addition, pulmonary granulomas, abdominal colic, dyspnea on exertion,
cough, pulmonary opacities, & cerebrospinal fluid rhinorrhea have been
reported after admin via the nasal route. [Ellenhorn, M.J., S. Schonwald,
G. Ordog, J. Wasserberger. Ellenhorn's Medical Toxicology: Diagnosis and
Treatment of Human Poisoning. 2nd ed. Baltimore, MD: Williams and Wilkins,
1997., p. 372]
Chronic cough and bronchitis productive of black or blood-tinged sputum
frequently result from habitual freebase smoking. Pneumomediastinum and
pneumothoraces have been reported after the prolonged Valsalva maneuvers
associated with freebasing. [Ellenhorn, M.J., S. Schonwald, G. Ordog, J.
Wasserberger. Ellenhorn's Medical Toxicology: Diagnosis and Treatment of
Human Poisoning. 2nd ed. Baltimore, MD: Williams and Wilkins, 1997., p.
373]
Anorexia, wt loss, malnutrition, water soluble vitamin deficiencies,
dehydration, pallor, tremor, & isolated convulsions are seen in
habitual cocaine users. [Ellenhorn, M.J. and D.G. Barceloux. Medical
Toxicology - Diagnosis and Treatment of Human Poisoning. New York, NY:
Elsevier Science Publishing Co., Inc. 1988., p. 653]
The practice of inhaling or smoking cocaine is reported to produce a
significant reduction of carbon monoxide diffusing capacity /pulmonary
function test/, suggesting that depositing cocaine alkaloid in the alveoli
damages the pulmonary gas exchange surface. This alteration in respiratory
function was found during the cocaine free interval, indicating that long
term effects of regular use of freebase may lead to sustained pulmonary
damage. Clinical reports of hoarseness, bronchitis, and bloody
expectoration are increasing. [Weiss RD et al; Am J Psychiatry 138 (8):
110-2 (1981) as cited in DHHS/NIDA; Research Monograph Series 61: Cocaine
Use in America: Epidemiologic and Clinical Perspectives p.155 (1985) DHHS
Pub No. (ADM)87-1414]
The risk for acute overdose reactions increases with speedballing, either
because of the stimulant effect or the depressant effect. [DHHS/NIDA;
Research Monograph Series 61: Cocaine Use in America: Epidemiologic and
Clinical Perspectives p.197 (1985) DHHS Pub No. (ADM)87-1414]
Serious mental and physical consequences can result from the intense
reinforcing nature of the drug. With intravenous use, coca paste smoking,
or the inhalation of cocaine alkaloid vapors (freebasing), the desired
mood altering effects are detectable in seconds and disappear in a few
minutes. This means an immediate reward with a rapid decline to baseline
mood levels or below. Both the positive and the negative reinforcers drive
the person to consume more cocaine. When cocaine is sniffed, the curve has
a lower peak and a longer duration, but compulsive, incessant patterns of
usage with nasal absorption are increasingly recorded in the literature.
[DHHS/NIDA; Research Monograph Series 61: Cocaine Use in America:
Epidemiologic and Clinical Perspectives p.152 (1985) DHHS Pub No.
(ADM)87-1414]
Based on the procaine data, ... /it was suggested/ that some of the acute
effects of cocaine normally associated with its psychomotor stimulant
properties could, in fact, be related to its local anesthetic effects.
These might include mood lability and, in some instances, euphoria,
profound anxiety and dysphoria, tinnitus, sensory distortions,
hallucinations, and even seizures should the dose be high enough. Based on
the extrapolation from the pharmacological kindling effects that have been
demonstrated in preclinical studies with repeated administration, ... /it
was suggested/ that some of the chronic effects of cocaine could also be
attributed to its local anesthetic properties, including sensitization to
bizarre behavior, seizure sensitization (pharmacological kindling),
irritability and aggression (particularly in subjects who have shown local
anesthetic induced seizures), cognitive impairment, and even panic
attacks. Fifty percent of the first 500 patients calling the Cocaine
Hotline to report adverse psychological effects reported experiencing
cocaine-induced panic attacks. [DHHS/NIDA; Research Monograph Series 88:
Mechanisms of Cocaine Abuse and Toxicity p.230 (1988) DHHS Pub No.
(ADM)89-1585]
As clinical observations accumulate, the existence of a true withdrawal
syndrome following cocaine use seems compelling. The depression, social
withdrawal, craving, tremor, muscle pain, eating disturbance,
electroencephalographic changes, and changes in sleep patterns must be
more than simply the consequence of what traditionally has been termed
"psychological dependence." When listening to descriptions of this state
by cocaine using patients, these dysphoric and often dramatic symptoms
must be viewed as negative reinforcers. For many patients it appears that
the withdrawal symptoms are a major consideration that makes discontinuing
cocaine almost impossible so long as the drug is available. Yet continuing
the drug produces unacceptable irritability, paranoid and delusional
thinking, and other unpleasant effects. [DHHS/NIDA; Research Monograph
Series 50: Cocaine: Pharmacology Effects and Treatment of Abuse p.47
(1984) DHHS Pub No. ADM(87)-1326]
Studies were carried out in order to find a sensitive in vitro model which
investigated cocaine-mediated hepatotoxicity. Precision-cut slices were
prepared from human /liver/. ... Slices were cultured for up to 6 hr in
the presence of 0-5 mM cocaine. Indices of toxicity consisted of K+
retention and Ca2+ uptake. Minimal effects and no clear dose-response
relationships were observed. ... [Connors S et al; Toxicology 61 (2):
171-83 (1990)]
Widespread use and abuse of cocaine have increased the frequency with
which health professionals must manage acute and chronic intoxication and
the complications stemming from drug ingestion. Acute intoxication from
catecholamine excess progessess through three stages, affecting the
cardiovascular, respiratory, and central nervous systems. Management is to
support or return these systems to normal with sedation, beta blockade,
and antiarrhythmics. Casual cocaine use is no longer considered benign,
and numerous related medical complications are now recognized.
Dopaminergic systems are the principal sites of reward and participate in
abstinence symptomatology, putatively through depletion of dopamine and
changes in receptor sensitivity and responsiveness. Long-term treatment
approaches have focused on psychologic strategies of behavior modification
and supportive psycotherapy. Pharmacotherapy with desipramine, amantadine,
and bromocriptine was shown in preliminary studies to minimize the
symptoms of cocaine withdrawal when used adjunctively with psychotheraphy.
The response to treatment may depend on the patient's premorbid
psychiatric status. [Hall WC et al; Pharmacotherapy 10 (1): 47-65 (1990)]
http://www.ncbi.nlm.nih.gov/entrez/quer ... ds=2179901
... The effectiveness of the cocaine test for diagnosing Horner's syndrome
/was evaluated/. The test was administered to 119 patients with a
diagnosis of Horner's syndrome and to 50 normal subjects ... the
cocaine-induced anisocoria in the two groups /was compared/ by measuring
photographs of the pupils. ... The cocaine test /was found/ to be highly
effective in separating normal subjects from patients with Horner's
syndrome. The chances of having Horner's syndrome increased with the
amount of cocaine-induced anisocoria. Through the use of logistic
regression analysis, ... the odds ratio of having Horner's /were
determined/. [Kardon RH et al; Arch Ophthamol 108 (3): 384-7 (1990)]
A case of pulmonary edema following smoking freebase cocaine is described.
... This case is unique since adulterants and contaminants were excluded
unlike all previously reported patients. [Kline JN, Hirasuna JD; Chest 97
(4): 1009-10 (1990)]
http://www.ncbi.nlm.nih.gov/entrez/quer ... ds=2323234
... 474 patients seen at Hennepin County Medical Center /were studied/
because of medical complications related to acute cocaine intoxication. Of
the 474, 403 had no history of seizures. Seizures within 90 minutes of
cocaine use was the primary diagnosis in 32 (7.9%) of the 403. The
majority of seizures were single, generalized, induced by intravenous or
crack cocaine, and not associated with any lasting neurologic deficits.
Most that were focal, multiple, or induced by nasal cocaine were
associated with an acute intracerebral complication or concurrent use of
other drugs. Of 71 patients with a history of non-cocaine related
seizures, 12 (16.9%) presented with cocaine-induced seizures; most of
these were multiple, of the same type as those in their history, and
induced by even nasal cocaine. In the 44 cocaine-induced seizure patients,
a pattern of habitual cocaine abuse was associated with diffuse brain
atrophy on CT and diffuse slowing on EEG. [Pascual-Leone A et al;
Neurology 40 (3 pt 1): 404-7 (1990)]
http://www.ncbi.nlm.nih.gov/entrez/quer ... ds=2107459
... The acute in vitro effects of cocaine on cell membrane potentials and
contractility of 12-16 week old human fetal heart, /were examined/ to
better assess the potential for the induction of serious arrhythmia, in
utero, by this abused substance. Ventricular preparations were maintained
in a tissue bath, and continuously provided with oxygen and glucose during
the measurement of membrane potentials with microelectrodes, and developed
force of contractions with microforce transducers. Cocaine (600 ng/ml) had
a significant effect on the ability of the heart to produce action
potentials of normal rising velocity, amplitude, and duration. Within 90
min all electromechanical activity had ceased. ... The effects of cocaine
were reversible, however, reversibility in vitro may have no counterpart
in utero, and irreversible loss of cardiac function may result. [Richards
IS et al; Pharmacol Toxicol 66 (2): 150-4(1990)]
http://www.ncbi.nlm.nih.gov/entrez/quer ... ds=2315267
... The symptomatology, clinical, and laboratory findings in four patients
following oral ingestion of crack cocaine have been reported. All of the
patients had a positive urine test for cocaine metabolites measured by gas
chromatography-mass spectroscopy. Retrospective analysis of the four
patients revealed alterations in function of the cardiovascular system
(4), the autonomic nervous system (4), the central nervous system (3), and
the gastrointestinal system (1). Three patients ingested crack cocaine as
a direct result of confrontation with law enforcement officers. The
symptomatologies of acute toxicity from oral ingestion of crack cocaine
are related to its effect on the cardiovascular system and the brain.
Cocaine toxicity should be considered in patients with acute and
unexplained cardiovascular, central nervous system, or gastrointestinal
complaints. [Riggs D, Weibley RE; Pediatr Emerg Care 6 (1): 24-6 (1990)]
http://www.ncbi.nlm.nih.gov/entrez/quer ... ds=2320483
For the past 5 years there has been an exponential increase in the use of
cocaine, phencyclidine hydrochloride, and other central nervous system
(CNS) active drugs. A significant amount of this accelerated usage is in
sexually active females, resulting in some urban hospitals reporting
positive drug screens in over 16% of the infants born on their busy
obstetrical service. There is a growing body of data showing that fetal
exposure to cocaine, phencyclidine hydrochloride, and other CNS-active
drugs results in infants and children with abnormal brain wave patterns,
short-term neurologic signs, depression of interactive behavior, and poor
organizational response to environmental stimuli. Whether such neurologic
findings will translate into a significant number of children with
learning and behavioral problems needs to be the focus of long-term
longitudinal studies of children with fetal drug exposure to cocaine,
phencyclidine hydrochloride, and other CNS-active drugs. [Van Dyke DC, Fox
AA; J Learn Disabil 23(3):160-3(1990)]
http://www.ncbi.nlm.nih.gov/entrez/quer ... ds=2179442
High level users were considerably more likely to report a physically
rundown condition, lack of appetite, insomnia, and a lack of sexual
interest. Similarly, persons who used 1 gram or more on each use occasion
were more likely to have experienced each of these health conditions. This
also was true for intravenous users (although differences in insomnia were
not significantly different) and for persons who used more than once a
week. Cocaine has been alleged to possess aphrodisiacal qualities, but
ironically, 3 out of every 10 respondents had experienced a lack of sexual
interest as a result of their use. Users of high levels of cocaine (43%)
were five times more likely than low level users (8%) to have experienced
this symptom. One out of every ten respondents, none of whom were low
level users, reported overdosing on cocaine. High level users were the
most likely group to report an overdose episode. Overdose was much more
common among persons who used intravenously, used more than once a week,
or used 1 gram or more per occasion. [DHHS/NIDA; Research Monograph Series
61: Cocaine Use in America: Epidemiologic and Clinical Perspectives p.124
(1985) DHHS Pub No. (ADM)87-1414]
No significant differences were observed in the proportion of low, medium,
and high level users who reported ever experiencing rhinitis or an
ulcerated (or perforated) nasal septum. These conditions are known to be
produced through intranasal ingestion, and data indicate that persons who
had used cocaine intranasally during their heaviest use period were almost
twice as likely to report rhinitis and three times as likely to report an
ulcerated septum. Abscesses, other skin infections, and hepatitis
(consequences identified with the use of nonsterile needles) were reported
most often by high level users. Route of ingestion was associated with the
presence of these problems; intravenous users were four times more likely
to report these consequences. [DHHS/NIDA; Research Monograph Series 61:
Cocaine Use in America: Epidemiologic and Clinical Perspectives p.121
(1985) DHHS Pub No. (ADM)87-1414]
Cocaine intoxication may occur in infants who are breastfed by mothers
recently exposed to cocaine or by mothers who have rubbed cocaine on their
nipples to relieve soreness. The infant may experience irritability,
vomiting, diarrhea, continuous movements of the extremities. Cocaine
intoxication should be suspected in any infant presenting acutely with
ventricular arrhythmias, hyper- or hypotension, seizures, or respiratory
distress. [Ellenhorn, M.J., S. Schonwald, G. Ordog, J. Wasserberger.
Ellenhorn's Medical Toxicology: Diagnosis and Treatment of Human
Poisoning. 2nd ed. Baltimore, MD: Williams and Wilkins, 1997., p. 356]
Cocaine abuse occurs in both healthy and chronically ill adolescents. Acts
of self-destruction may be observed in both groups including attempted
suicide, a manifestation of cocaine withdrawal, and acts of aggression and
violence, signs of cocaine intoxication. Syndromes of cocaine intoxication
now seen in older children and adolescents include the malignant
hyperthermia or hypermetabolic syndrome and cocaine colitis. Cocaine
abstinence syndrome may include hyperprolactinemia. ... Generalized and
partial seizures, cerebrovascular infarction, and hemorrhage have also
been observed. [Ellenhorn, M.J., S. Schonwald, G. Ordog, J. Wasserberger.
Ellenhorn's Medical Toxicology: Diagnosis and Treatment of Human
Poisoning. 2nd ed. Baltimore, MD: Williams and Wilkins, 1997., p. 357]
... Fetal growth appears to be decreased in women who use cocaine
throughout pregnancy. These effects are not manifest in the infants of
women who use cocaine only in the first trimester of pregnancy.
[Ellenhorn, M.J., S. Schonwald, G. Ordog, J. Wasserberger. Ellenhorn's
Medical Toxicology: Diagnosis and Treatment of Human Poisoning. 2nd ed.
Baltimore, MD: Williams and Wilkins, 1997., p. 362]
_________________________________________________________
Crack users, probably via sexual exposure, may be at increased risk of
developing hepatitis B and D infection. /Crack/ [Ellenhorn, M.J., S.
Schonwald, G. Ordog, J. Wasserberger. Ellenhorn's Medical Toxicology:
Diagnosis and Treatment of Human Poisoning. 2nd ed. Baltimore, MD:
Williams and Wilkins, 1997., p. 366] **PEER REVIEWED**
Cocaine-induced myocardial infarction may follow cocaine abuse by the
intranasal, intravenous, and inhalation routes. About half of these
patients who experience a myocardial infarction have had previous chest
pain; 9 of 10 have been cigarette smokers and two thirds have had their
myocardial infarcts within 3 hours of use of cocaine (range, 1 minute to 4
days). [Ellenhorn, M.J., S. Schonwald, G. Ordog, J. Wasserberger.
Ellenhorn's Medical Toxicology: Diagnosis and Treatment of Human
Poisoning. 2nd ed. Baltimore, MD: Williams and Wilkins, 1997., p. 368]
Cocaine-associated strokes occur in both first-time users and long-time
users and are independent of the route of administration. [Ellenhorn,
M.J., S. Schonwald, G. Ordog, J. Wasserberger. Ellenhorn's Medical
Toxicology: Diagnosis and Treatment of Human Poisoning. 2nd ed. Baltimore,
MD: Williams and Wilkins, 1997., p. 369]
The alkaloid form of cocaine has been associated with both occlusive and
hemorrhagic strokes. The hydrochloride form has been related mainly to
hemorrhagic strokes. Both subarachnoid and intracerebral hemorrhages have
been associated with cocaine use. In about 80% an aneurysm or
arteriovenous malformation has been detected. [Ellenhorn, M.J., S.
Schonwald, G. Ordog, J. Wasserberger. Ellenhorn's Medical Toxicology:
Diagnosis and Treatment of Human Poisoning. 2nd ed. Baltimore, MD:
Williams and Wilkins, 1997., p. 369]
A newborn developed a cerebral infarction shortly after delivery. The
mother had used 5 g of cocaine over a 3-day period prior to delivery and 1
g in the 15 hours preceding birth. At about 16 hours of age the child
became apneic and cyanotic and experienced multiple focal seizures and a
right-sided hemiparesis. [Ellenhorn, M.J., S. Schonwald, G. Ordog, J.
Wasserberger. Ellenhorn's Medical Toxicology: Diagnosis and Treatment of
Human Poisoning. 2nd ed. Baltimore, MD: Williams and Wilkins, 1997., p.
370]
______________________________________________________________
Intravenous cocaine users have experienced fungal cerebritis, and such
cases have usually terminated fatally. [Ellenhorn, M.J., S. Schonwald, G.
Ordog, J. Wasserberger. Ellenhorn's Medical Toxicology: Diagnosis and
Treatment of Human Poisoning. 2nd ed. Baltimore, MD: Williams and Wilkins,
1997., p. 371]
Cocaine snorting leading to frontal sinusitis may subsequently be followed
by a lethal brain abscess. [Ellenhorn, M.J., S. Schonwald, G. Ordog, J.
Wasserberger. Ellenhorn's Medical Toxicology: Diagnosis and Treatment of
Human Poisoning. 2nd ed. Baltimore, MD: Williams and Wilkins, 1997., p.
371]
An increasing number of people who inject cocaine intravenously are at
risk of HIV infection through needle sharing, perhaps because of the
frequency of injection during binges of cocaine use - up to 15-25 times in
a single day. ... In South America, HIV infection is now seen in 36-57% of
cocaine injectors. Those who smoke cocaine in the form of crack are at
higher risk of HIV infection (and sexually transmitted diseases) from
sex-for-drug transactions. [Ellenhorn, M.J., S. Schonwald, G. Ordog, J.
Wasserberger. Ellenhorn's Medical Toxicology: Diagnosis and Treatment of
Human Poisoning. 2nd ed. Baltimore, MD: Williams and Wilkins, 1997., p.
372]
