Cocaine Adverse Reactions
- abdominal pain
- agitation
- agnosia
- anxiety
- apnea
- bowel ischemia
- cardiac arrest
- Cheyne-Stokes respiration
- confusion
- delirium
- diaphoresis
- dizziness
- dysphoria
- emotional lability
- encephalopathy
- erythrocytosis
- euphoria
- exophthalmos
- fecal incontinence
- fetal abortion
- fetal death
- fetal distress
- formication
- hallucinations
- headache
- heart failure
- hyperemia
- hyperreflexia
- hypertension
- hyperthermia
- hyporeflexia
- infection
- intracranial bleeding
- irritability
- muscle paralysis
- mydriasis
- myocardial infarction
- myoglobinuria
- nasal congestion
- nasal septum perforation
- nausea/vomiting
- neonatal abstinence syndrome
- ocular irritation
- premature labor
- premature ventricular contractions (PVCs)
- psychological dependence
- psychosis
- pulmonary edema
- renal tubular obstruction
- restlessness
- rhabdomyolysis
- rhinitis
- seizures
- serotonin syndrome
- sinus bradycardia
- sinus tachycardia
- sinusitis
- sneezing
- tachypnea
- tolerance
- tremor
- urinary incontinence
- ventricular fibrillation
- ventricular tachycardia
- withdrawal
Cocaine Adverse Reactions
In general, the adverse effects of cocaine are a result of excessive sympathetic activity and may be caused by rapid absorption, decreased patient tolerance, or, rarely, hypersensitivity. Adverse reactions can occur with as little as 20 mg; the fatal dose has been reported to be 1.2 gm orally. Patient sensitivity to cocaine is highly variable. Toxicity typically occurs in three stages: early stimulation, advanced stimulation, and depression. Progression to more advanced stages is largely dose-dependent.
Initial adverse cardiovascular effects (i.e. early stimulation) of cocaine include hypertension, premature ventricular contractions (PVCs), generalized vasoconstriction, and sinus tachycardia or ventricular tachycardia. Low doses can cause sinus bradycardia due to prolonged central vagal stimulation, but after moderate doses the heart rate is increased by cocaine’s central and peripheral effects on the sympathetic nervous system. Cardiac toxicities associated with advanced stimulation include cardiac arrhythmias, such as ventricular tachycardia and ventricular fibrillation, myocardial ischemia, myocardial infarction, and congestive heart failure. Late depressive cardiovascular effects include cardiac arrest and circulatory collapse.
Long-term or repeated intranasal use of cocaine can result in rebound hyperemia (nasal congestion) and chronic rhinitis, including sneezing or sniffling, which may lead to chronic sinusitis and increased risk of upper respiratory infection. With repeated or prolonged intranasal use, ischemic damage to the mucosa may occur and may lead to atrophy of the nasal mucosa, necrosis of septal tissue and nasal septum perforation.
CNS toxicity is extremely common with cocaine use, and, initially, patients present with symptoms of CNS stimulation such as agitation, anxiety, apprehension, confusion, dizziness, emotional lability, a feeling of well-being or euphoria (or sometimes dysphoria), excitement, exophthalmos, formication (especially during withdrawal), hallucinations (may be auditory, gustatory, olfactory, tactile, or visual), headache, urinary incontinence, fecal incontinence, irritability, lightheadedness, mydriasis, nervousness, preconvulsive movements, pressured speech, psychosis, restlessness, and/or generalized tics or twitching of small muscles. CNS effects seen with advanced stimulation include delirium, malignant encephalopathy, hyperreflexia, intracranial bleeding, psychosis, seizures, and status epilepticus. Late depressive effects include hyporeflexia, muscle paralysis, mydriasis, and death. First-time use of cocaine can result in seizure, with single generalized motor seizures being most common, but multiple seizures and status epilepticus can occur immediately or within 2 hours of ingestion (coinciding with peak blood levels). Long-term use can result in agnosia and ageusia. Concurrent use of cocaine with CNS stimulants can cause excessive anxiety, irritability, seizures, and/or cardiac arrhythmias.
Respiratory adverse reactions to cocaine include tachypnea, pulmonary edema, Cheyne-Stokes respiration, respiratory depression, and apnea.
Cocaine causes hyperthermia, rigors (tremor), and diaphoresis by increasing muscular activity in the presence of vasoconstriction. Rhabdomyolysis can occur with myoglobinuria causing renal tubular obstruction.
Gastrointestinal adverse reactions to cocaine include bowel ischemia, abdominal pain, and nausea/vomiting.
Clinicians should consult standard textbooks or a Poison Control Center for the management of cocaine overdose and severe adverse effects, although treatment is primarily supportive and symptomatic. Airway management and assisted pulmonary ventilation may be necessary. Oral ingestion can be treated with gastric lavage or induction of emesis. Seizures can be treated with IV diazepam, lorazepam, or a short-acting barbiturate, and IV beta-blockers may be helpful in treating tachycardia or other arrhythmias. Use of labetalol can prevent beta-blockade-associated adverse effects because it also has some alpha-blocking activity. IV fluids should be used as needed. Use vasopressors with extreme caution.
Cocaine stimulates the release of serotonin (5-HT) and may inhibit serotonin reuptake. Thus, cocaine enhances serotonin activity in the CNS. Cocaine may cause symptoms consistent with the serotonin syndrome when used with other medications (e.g., SSRIs) that enhance serotonin activity within the CNS.
Application of cocaine topical solution to the eye has caused ocular irritation and sloughing of the corneal epithelium with clouding, pitting, and occasionally ulceration of the cornea.
Cocaine may cause a transient erythrocytosis, increasing blood viscosity while maintaining tissue oxygenation during vasoconstriction. Ten to 30 minutes following cocaine administration hemoglobin, hematocrit, and red blood cell counts have been found to increase compared to baseline, with no change in white blood cell counts. There may also be an increase in von Willebrand factor within 30 - 240 minutes following cocaine administration.
Cocaine, as a drug with the potential for abuse, may lead to tolerance, dependence and drug addiction. Tolerance refers to the diminishing effect of a drug after repeated administration at a given dosage, or the need for increasing doses to produce the desired effect. Many of the responses to cocaine exhibit tolerance. Cocaine does not produce physical dependence, since the drug does not have receptors on neurons that regulate peripheral physical functions like heart rate, bowel function or blood pressure. However, psychological dependence, or the compulsive use of a drug to experience emotion, motivation or behavior, does occur. A cocaine withdrawal syndrome is not observed with all patients and is more likely to include depressed mood, drug cravings and other behavioral effects rather than physical symptoms on abrupt discontinuation of the drug.
Cocaine readily crosses the placenta and has been associated with premature labor, spontaneous fetal abortion, and a multitude of adverse effects on the fetus and infant. Cocaine causes placental vasoconstriction, decreasing the blood flow to the fetus, and may cause an increase in uterine contractility. Use of cocaine during pregnancy is associated with shorter gestation, premature delivery, spontaneous abortion, abruptio placentae, and fetal death. Infants who were exposed to cocaine in utero have exhibited depression of interactive behavior and a poor organizational response to environmental stimuli. Infants whose mothers used cocaine regularly during pregnancy are likely to be born having a birth weight and head circumference below the tenth percentile for their gestational age. Other fetal effects noted following maternal cocaine use include growth retardation, fetal distress, cerebrovascular accidents and congenital anomalies. While the presence of a true neonatal abstinence syndrome has been debated (because cocaine dose not have effects on neurons that regulate physical functions), abnormal mild behavioral symptoms (i.e. irritability, muscular rigidity, tremulousness, increased startle response) are prevalent after birth in cocaine-exposed neonates, and GI symptoms (e.g., vomiting) have occurred.
Cocaine is excreted in breast-milk and has caused seizures, hypertension, tachycardia, tremors, respiratory difficulty, and unusual irritability in nursing infants. It is recommended that nursing be discontinued during cocaine use.
[ Last revised: 9/19/2002 5:25:00 PM ]
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