Tobacco Cessation and Substance Abuse Treatment in Women’s Healthcare

5. Health Effects

Byron C. Calhoun 


Department of Obstetrics and Gynecology, West Virginia University-Charleston, Charleston, WV, USA

Byron C. Calhoun



AddictionsHealth effectsOpioidsBenzodiazepinesStimulantsAlcohol


Tobacco abuse is the leading cause of death in the United States [13]. It is linked to some 440,000 deaths a year with some $100 billion in direct medical costs and nearly $100 billion in lost productivity annually [4]. There have been estimates made that each pack of cigarettes costs an estimated $7.18 in medical care and lost work [5]. Cigarettes increase the risk of developing and amplify respiratory tract infections, influenza, pneumococcal pneumonia, and TB. It has been estimated that adult men lose 13.2 years of life and adult women 14.5 years of life as a result of tobacco abuse. There have also been estimates of passive smoking attributable to some 40,000 deaths, with 35,000 due to cardiovascular disease, 3000 from lung cancer, and some 1000 from perinatal issues [5].

Tobacco consists of volatile and particulate states that contain multiple substances other than nicotine that are responsible for morbidity and mortality. The volatile state contains over 500 gaseous compounds that include: nitrogen, CO, carbon dioxide, ammonia, hydrogen cyanide, and benzene. There are also more than 3500 different compounds in the particulate state consisting of active alkaloids nornicotine, anabasine, anatabine, myosmine, nicotyrine, and nicotine. The tar of the cigarette is the particulate matter minus the alkaloid and water portion. The tar of the cigarette contains the carcinogens of aromatic hydrocarbons, N-nitrosamines, and aromatic amines.

With smoking there over 4000 different chemicals released including some 50 known carcinogens. The increased risk of cardiovascular disease is related to the oxidant chemical exposure and CO along with hydrogen cyanide, carbon disulfide, cadmium, and zinc [6]. Chronic obstructive lung disease appears related to exposure to tar, nitrogen oxide, hydrogen cyanide, and volatile aldehydes. This oxidative stress causes the generation of superoxide radicals and hydrogen peroxide with lung damage. The most significant contribution to lung cancers appears to be the polynuclear aromatic hydrocarbons and tobacco N-nitrosamines with polonium-210 and the volatile aldehydes. Catechol, volatile aldehydes, and nitrogen oxide all increase the formation of N-nitrosamines which are linked to tumorigenesis. The risk of oral, larynx, esophagus, lung, stomach, pancreas, kidney, urinary bladder, uterine cervix, and leukemia are related to the intensity and duration of cigarette smoking. Cigarette smoking also causes skin changes with increased risk of skin cancers, wrinkling, and premature aging of the skin. There have also been links to cataracts and possibly macular degeneration as well. Women who smoke also demonstrate lower estrogen levels with earlier menopause and osteoporosis. In males, smoking may impair penile erection and doubles the likelihood of erectile dysfunction.

Nicotine suppresses appetite and smokers weigh 2.7–4.5 kg less than non-smokers. Nicotine also increases lipolysis and the release of free fatty acids in liver. This may contribute to the decrease in high-density lipoproteins seen in smokers. Smoking is also linked to delayed healing of peptic ulcers with decreased production of endogenous prostaglandins and decrease in the mucous bicarbonate barrier in the stomach.

In summary, tobacco has been linked to the following cardiovascular effects: atherosclerosis, stroke, myocardial infarction, peripheral vascular disease, corpulmonale, erectile dysfunction, hypertension control issues, angina, and dysrhythmias; renal effects: renal failure and hypertension; gastrointestinal effects: peptic ulcers, gastroesophageal reflux, malignancy of stomach and pancreas; pulmonary effects: lung cancer, chronic obstructive lung disease, reactive airway, pneumonia, bronchitis, pulmonary hypertension, interstitial lung disease, and pneumothorax; neurologic effects: stroke, small-vessel ischemia, and cognitive deficits; infectious disease: bronchitis, pneumonia, upper respiratory tract infection; sleep effects: insomnia and increased sleep latency; trauma effects; burns and smoke inhalation; perioperative effects: pulmonary infection, difficulty weaning off ventilators/oxygen, respiratory failure, and reactive airway exacerbations; hematologic effects: hypercoagulability; musculoskeletal: compartment syndromes and fractures; and nutritional lacks.


Marijuana affects several psychomotor functions in a dose-dependent manner including object distance, shape discrimination, reaction time, information processing, perceptual motor coordination, motor performance, signal detection, tracking behaviors, and slowed time perception [7]. Marijuana particularly affects to a greater extent those tasks that are more complex requiring sustained concentration. There is an additive effect to cannabis with alcohol especially with driving.

Cannabis usage has been linked to “amotivational syndrome” with lack of initiative and decreased executive function. Some authors point to possible confounders with alcohol use, other substances, and social surroundings. It is clear from the scientific literature that adolescent substance abusers suffer from attention, memory, and executive function deficits [8]. Baa and Tapert, 2010 note in their review of the substance body of literature noting alterations in the prefrontal, hippocampal, cerebellar structure and function as well as white matter structural integrity [8]. In line with this there are the subtle decreases in intellectual function and memory, attention, and integration of complicated information. Complex reaction times, perception, reading, arithmetic performance, recall, and memory appear affected as well. One 20-year prospective study found that heavy users lost IQ points (average 6) while nonusers gained (average 1 point) [9]. Further, the persistent users had significant loss in learning, memory, and executive decision making [9].

Effects on major organ systems are also found. The major health effect appears to be the damage to the respiratory system since many of the same carcinogens found in tobacco are also found in marijuana smoke. Marijuana smoking increases airway resistance, decreases pulmonary function, produces chronic cough, airway inflammation, and atypical cell growth. There has not been enough data available at this time to link marijuana to lung cancer. Marijuana appears to suppress macrophage function and natural killer cell activity thus impairing host resistance to infections. Marijuana increases heart rate and produces orthostatic hypotension which are of little effects in healthy young adults but may be significant in older users.

Cannabinoid receptors are significant actors in the development of a variety of liver pathology. The chronic use of THC appears to increase steatosis with increased live fibrosis. There is also inhibition of liver microsomes with prolongation of certain medications (i.e., barbiturates). Renal complications appear only rarely. The effects on the endocrine are significant that virtually every system is affected in some way. THC effects include: inhibition of pituitary luteinizing hormone, prolactin, and growth hormone. The effects on the human thyroid are not well documented. THC use may affect female reproduction including production of galactorrhea.

Marijuana may produce euphoria, hunger, and possible relaxation. There have also been reports of panic, anxiety, nausea, and dizziness. These effects are more likely with oral doses of 20 mg or more in a naïve user.


This includes the chemical substances that alter cognitive, perceptual, and emotional understanding of reality and self. These include classical hallucinogens (mescaline, psilocybin, LSD, dimethyltryptamine); the entactogenic phenylalkylamines (methylenedioxyamphetamine, MDMA, MDE); anticholinergic dissociatives (atropine, hyoscyamine, scopolamine); and dissociative anesthetics (phencyclidine [PCP], ketamine, salvinorin A). Physical effects include mild effects: tachycardia, palpitations, slight hypo or hypertension, diaphoresis, slight hyperthermia, motor incoordination, tremor, hyperreflexia, and altered neuroendocrine functioning; mild to strong physical effects: mydriasis, arousal, and insomnia; and rare physical effects: nausea, vomiting, diarrhea, blurred vision, nystagmus, piloerection, and salivation. Psychological effects include typical effects: intensification and lability of affect with euphoria, anxiety, depression, and/or cathartic expressions, dream state, sensory activation with illusion, pseudohallucinations, hallucinations, and/or synesthesia, altered experience of time and space, altered body image, increased suggestibility, lassitude/indifference/detachment, acute cognitive alterations with loosening of association, inability for goal-directed thinking, and memory disturbance; “positive” psychological effects include: sense of perceiving deeper layers of the world, oneself, and others, mystical experience, and sense of profound discovery/healing; and “negative” psychological effects include: psychosomatic complaints, impaired judgement, derealization, depersonalization, megalomania, impulsivity, odd behaviors, paranoid delusions, and suicidal ideation. The national survey by the National Survey on Drug Use and Health (NSDUH) in 2010 estimated that about 37.5 million (14.8 %) Americans over age 12 years used a hallucinogen at least once in their lifetime [10]. In conclusion, hallucinogens are a heterogeneous class of drugs with diverse effects and mechanisms of action. They are physiologically non-toxic in medium doses with main complications resulting from unsupervised use.


Drugs act as antagonists of the N-methyl-D-aspartate (NMDA) receptor subtypes of the major excitatory neurotransmitter, glutamic acid, of the brain. This includes phencyclidine (PCP), ketamine dizocilpine, dextromethorphan (DXM), and nitrous oxide. The clinical effects are the dissociative state of intoxication. The major effects are impairments in working and episodic memory along with cognitive task problems. PCP may cause an acute reaction similar to catatonic schizophrenia. PCP may also induce an organic brain syndrome along with cardiovascular and renal toxicity. DXM abuse may cause brain damage, seizures, loss of consciousness, irregular heart rate, and even death. It may even cause respiratory depression.


Alcohol affects all tissue and organ systems and in heavy drinkers there is skeletal fragility, brain/liver/heart damage and susceptibility to cancers. Moderate alcohol use (<2 drinks per day) have been associated with some benefits, including decreased risk of coronary artery disease.

In summary, alcohol has been linked to the following cardiovascular effects: cardiomyopathy, atrial fibrillation (holiday heart), hypertension, dysrhythmia, masking angina symptoms, coronary artery spasm, myocardial ischemia, high-output states, coronary artery disease, and sudden death; liver effects: steatosis (fatty liver), acute and chronic hepatitis infection [B or C] or toxic [acetaminophen], alcoholic hepatitis, cirrhosis, portal hypertension and varices, spontaneous bacterial peritonitis; renal effects: hepatorenal syndrome, rhabdomyolysis and acute renal failure, volume depletion and prerenal failure, acidosis, hypokalemia, hypophosphatemia; gastrointestinal effects: gastritis, pancreatitis, diarrhea, malabsorption (pancreatic insufficiency or folate/lactase deficiency, parotid enlargement, malignancy, colitis, Barrett’s esophagus, gastroesophageal reflux, Mallory-Weiss syndrome, and GI bleeding; pulmonary: aspiration, sleep apnea, respiratory depression, apnea, chemical or infectious pneumonitis; neurologic effects: peripheral and autonomic neuropathy, seizure, hepatic encephalopathy, Korsakoff dementia, Wernicke syndrome, cerebellar dysfunction, Marchiafava–Bignami syndrome, central pontine myelinolysis, myopathy, amblyopia, stroke, withdrawal delirium, hallucinations, toxic leukoencephalopathy, subdural hematoma, intracranial hemorrhage; infectious problems: Hepatitis C, pneumonia, TB, HIV, sexually transmitted diseases, spontaneous bacterial peritonitis, brain abscess, and meningitis; sleep effects: apnea, periodic limb movements of sleep, insomnia, disrupted sleep, daytime fatigue; trauma: MVA’s fatal and nonfatal injuries, physical and sexual abuse; perioperative issues: withdrawal, perioperative complications (delirium, infection, bleeding, pneumonia, delayed wound healing, dysrhythmia), hepatic decompensation, hepatorenal syndrome, and death; hematologic effects include: macrocytic anemia, pancytopenia due to marrow toxicity and or splenic sequestration, leucopenia, thrombocytopenia, coagulopathy because of liver disease, iron deficiency anemia, folate deficiency, spur cell anemia, and burr cell anemia; musculoskeletal effects include: rhabdomyolysis, compartment syndromes, gout, saturnine gout, fracture, osteopenia, osteonecrosis; and nutritional effects including vitamin and mineral deficiencies (B vitamins, riboflavin, niacin, vitamin D, magnesium, calcium, folate, phosphate, and zinc).

Nonalcohol Sedative Hypnotics

These drugs include the benzodiazepines, nonbenzodiazepine hypnotics, barbiturates, and related compounds. These compounds produce effects from sedation to frank obtundation. The barbiturates are the most risk for respiratory depression. Benzodiazepine toxicity usually includes an impaired gag reflex and ataxia. Benzodiazepines withdrawal varies based upon length of administration. Short periods of use will have mild anxiety, headache, insomnia, dysphoria, tremor, and muscle twitching. Chronic long-term use may lead to autonomic dysfunction, nausea, vomiting, depersonalization, derealization, delirium, hallucinations, illusions, agitation, and grand mal seizures. Barbiturate withdrawal with acute discontinuation may lead to apprehension, uneasiness, muscular weakness, coarse tremors, postural hypotension, anorexia, vomiting, and myoclonic jerks that may last for up to 2 weeks. Grand mal seizures may occur within 2–3 days of stopping barbiturates and last for up to 8 days and delirium develops 3–8 days and may last up to 2 weeks.


Medical complications of opioids include central nervous system, pulmonary, cardiovascular, gastrointestinal, renal, musculoskeletal, and infectious diseases. The central effects of the opioids are well-known with the overdosing of the medications varying from mild sedation to coma. Along with this effect is the suppression of the gag reflex with subsequent aspiration of stomach contents with the centrally mediated nausea and vomiting. Overdosing of opioids results in the central depression of respiration but also may lead to noncardiogenic pulmonary edema (NCPE) with bronchospasm. NCPE presents with frothy, pick bronchial secretions, cyanosis, and rales. It is most commonly associated with intravenous or inhalational use of heroin. Cardiovascular effects usually result from the hypoxia due to respiratory depression. Opioids are thought to cause a release of histamine with vasodilation with subsequent orthostatic hypotension. Propoxyphene may cause direct myocardial toxicity. Further, high doses of methadone (>300 mg/day) have been linked to prolongation of the QT interval with torsades de pointes [11]. Gastrointestinal effects include nausea and vomiting, slowing of GI motility with constipation and possible fecal impaction. Morphine may also cause spasm of sphincter of Oddi and should not be used in biliary colic. Renal effects include rare cases of rhabdomyolysis with heroin, illicit methadone, and propoxyphene. Heroin, morphine, and pentazocine have been liked to nephropathy when used intravenously with subsequent glomerulonephritis. High doses of opioids may induce centrally mediated muscle rigidity of the chest and abdominal wall. Intravenous use may also lead to osteomyelitis, septic arthritis, polymyositis, and fibrous myopathy. Well-known infectious complications from intravenous abuse with needle sharing include HIV, hepatitis B, hepatitis C, and bacterial infections.

In summary, opioids have been linked to the following liver effects: granulomatosis; kidney effects: rhabdomyolysis, acute renal failure, and factitious hematuria; gastrointestinal effects: constipation, ileus, and intestinal pseudoobstruction; pulmonary complications: respiratory depression/failure, emphysema, bronchospasm, exacerbation of sleep apnea, and pulmonary edema; neurologic effects: seizure (overdose) and compression neuropathy; infectious complications: aspiration pneumonia; sleep problems: insomnia; trauma: MVAs and other accidental death; perioperative complications: withdrawal and problems with pain control; and musculoskeletal which includes osteopenia.

Cocaine, Amphetamines, and Other Stimulants

These compounds include the naturally occurring plant alkaloids including cocaine, ephedra, khat, and synthetic compounds such as amphetamines and methylphenidate. Virtually, all systems of the body are affected by stimulants.

Adverse neurologic effects consist of dysphoric effects like anxiety, irritability, panic attacks, interpersonal sensitivity, hypervigilance, suspiciousness, paranoia, grandiosity, impaired judgment, and psychotic symptoms like delusions and hallucinations. The stimulant psychosis may resemble acute schizophrenia. Hallucinations may be auditory, visual, somatosensory (tactile sensation of “skin crawling”). Physiologic effects may include tachycardia, dilated pupils, diaphoresis, and nausea. Chronic cocaine use may result in cognitive impairment that persists for several months after last use. Amphetamine abuse may lead to persistent paranoia and hallucinations that may last for several years. There have been psychotic flashbacks seen in methamphetamine abusers up to 2 years after last use. Cocaine and amphetamine abuse have been linked to cerebral vasoconstriction, cerebrovascular atherosclerosis, cerebrovascular disease, and strokes [12]. There are also a number of movement disorders found with stimulant abuse. These include: repetitive stereotyped behaviors (such as repeated dismantling of objects, cleaning, doodling, and searching for imaginary objects), acute dystonic reactions, choreoathetosis, and akathisa (“crack dancers”), buccolingual dyskinesias (“twisted mouth”), exacerbation of Tourette syndrome, and tardive dyskinesia.

Stimulants have direct and central nervous system effects. The direct effects include increasing adrenergic activity at sympathetic nerve terminals and in the CNS increasing heart rate, blood pressure, and systemic vascular resistance. Cocaine-induced tachycardia results in an increased oxygen demand with decreased blood flow may cause acute myocardial infarction even in a young person even without atherosclerosis. Cocaine also increases activated platelets, platelet aggregation, and thromboxane synthesis. Cocaine use has been attributed to about 25 % of nonfatal heart attacks in patients younger than 45 years of age [13]. Frequent cocaine users are up to seven times more likely to have a nonfatal heart attack than nonusers [13]. Cocaine is also associated with cardiac arrhythmias including ventricular tachycardia or ventricular fibrillation as well as sudden death. Chronic cocaine or amphetamine use is further associated with cardiomyopathy and myocarditis [14]. Cocaine-associated cases of dilated cardiomyopathy and myocardial fibrosis may be due to direct toxic effects of high concentrations of circulating norepinephrine. Cocaine-associated myocarditis may be a direct toxic effect of cocaine or hypersensitivity effect.

The effects of smoked cocaine cause both acute and chronic pulmonary toxicity [15]. Acute respiratory symptoms may develop in up to half of users within minutes to several hours after smoking. Symptoms include productive cough, shortness of breath, wheezing, chest pain, hemoptysis, and exacerbation of asthma. Severe effects include pulmonary edema, pulmonary hemorrhage, pneumothorax, pneumomediastinum, and thermal airway injury. Pulmonary edema has been reported after intravenous cocaine use. Chronic use may lead to interstitial pneumonitis and bronchiolitis obliterans.

Stimulants have no direct toxic effects on the kidneys. Acute renal failure may occur from renal ischemia or infarction, malignant hypertension, or rhabdomyolysis. Intrarenal artery constriction may cause medullary ischemia and renal tubular damage.

Cocaine reduces gastric motility and delays gastric emptying with effects on the medullary centers controlling these functions. The most serious effects of cocaine use are due to vasoconstriction and ischemia: gastroduodenal ulceration and perforation, intestinal infarction, and perforation, and ischemic colitis. Ulceration is found in the greater curvature and prepyloric region of the stomach, pyloric canal, and first portion of the duodenum. Cocaine is hepatotoxic due to the oxidative metabolism to norcocaine by the cytochrome P450 microsomal enzyme system in the liver with further changes in the hepatotoxic compound of N-hyroxynorcocaine.

Cocaine use activates the hypothalamic–pituitary–adrenal (HPA) center, stimulating the secretion of epinephrine, adrenocorticotropin releasing hormone, adrenocorticotrophic hormone (ACTH), and cortisol. Prolactin is decreased in acute cocaine use as well. Chronic cocaine has normal, increased, or decreased prolactin levels. Acute cocaine also increases plasma luteinizing hormone. Chronic cocaine users have normal testosterone, cortisol, luteinizing hormone, and thyroid hormones.

Stimulants may cause rhabdomyolysis by several mechanisms: a direct toxic effect causing myofibrillar degeneration, indirectly by vasoconstriction of intramuscular arteries resulting in ischemia, and secondary to stimulant-induced hyperthermia or seizures. Some one-third of patients with rhabdomyolysis will develop acute renal failure with occasional DIC and liver damage.

Head and neck problems with cocaine use are dependent on the route of administration. Intranasal cocaine is associated with chronic rhinitis, perforated nasal septum and nasal collapse, oropharyngeal ulcers, and osteolytic sinusitis due to vasoconstriction and necrosis. Oral cocaine is associated with gingival ulceration and erosion of dental enamel. Both cocaine and methamphetamine reduce salivary secretions and causes bruxism. Chronic use causes caries, cracking of enamel, and loss of teeth.

Cocaine has been linked with several vasculitic syndromes usually affecting skin and muscle. They may mimic Henoch–Schönlein purpura, Stevens–Johnson syndrome, or Raynaud phenomenon. Cocaine impairs the response of monocytes to bacterial infection (lipopolysaccharides).

Cocaine with chronic use reduces libido and impairs sexual function. Men may experience erectile dysfunction or delayed or inhibited ejaculation. Cocaine has been applied to the penis or clitoris as a local anesthetic effect to delay orgasm.

In summary, cocaine has been linked to the following cardiovascular effects: hypertension, myocardial infarction, angina, chest pain, supraventricular tachycardia, ventricular dysrhythmias, cardiomyopathy, myocarditis, sudden death, and aortic dissection; liver effects include ischemic necrosis and hepatitis; kidney issues include: rhabdomyolysis, acute renal failure, vasculitis, necrotizing angiitis, accelerated hypertension, nephrosclerosis, and ischemia; gastrointestinal problems include ischemic bowel and colitis; pulmonary complications include: nasal septum perforation, gingival ulceration, perennial rhinitis, sinusitis, hemoptysis, upper airway obstruction, fibrosis, hypersensitivity pneumonitis, epiglottitis, pulmonary hemorrhage, pulmonary hypertension, pulmonary edema, emphysema, interstitial fibrosis, and hypersensitivity pneumonia; neurologic complications: stroke, seizure, status epilepticus, headache, delirium, depression, hypersomnia, and cognitive defects; sleep issues include hypersomnia in withdrawal; perioperative effects consist of: hypersomnia and depression in withdrawal, inability to separate postoperative neurologic complications from drug effects, and complications due to underlying pulmonary disease; and musculoskeletal effects of rhabdomyolysis.


These include three classes of compounds: volatile alkyl nitrites, nitrous oxide, and volatile solvents/fuels/anesthetics. Deaths as a result of abuse are well known. Death results from behavioral toxicity and overdose. The solvents as a class produce significant intoxication and anesthetic effects at high concentrations. The usual scenario is loss of consciousness with overdose and lethal concentrations of the compounds. The proximate cause of death is CNS depression with respiratory arrest. There are also reports of acute cardiotoxicity with cardiac arrest. The major areas of effects are the brain, nose/mouth, lungs, liver, and kidneys. The classic neurotoxins are hexane and methyl-n-butylketone (MBK). These solvents produce axonopathies. Leaded gasoline causes demyelination. The inhalants show significant neuropathies with loss of white matter, brain atrophy, and damage to neural pathways. Coupled with these physiologic effects are the high rates of psychiatric disorders with inhalant abuse. One recent study found that 70 % of inhalant abusers met criteria for at least one lifetime mood, anxiety, or personality disorder, and 38 % had a mood disorder in the last year of study [16].

Chronic solvent abusers demonstrate irritation of the eyes, nose, and mouth with rhinitis, nose bleeds, conjunctivitis, and skin rash. Chronic use also leads to inflammation of the lungs with chronic cough. There may also be pulmonary edema, bronchospasm, bronchitis, granulomatosis, and even airway burns. The liver may be damaged particularly with the halogenated hydrocarbons like carbon tetrachloride. Glomerulonephritis and kidney stones have been reported and even acute tubular necrosis with toluene. Benzene and vinyl chloride are known carcinogens. Nitrites and methylene chloride can cause methemoglobinemia.


No discussion of substance abuse would be complete without discussion of prevention. There are several excellent screening tools for initiating discussion of the risk for and prevention of substance abuse. One such tool is the “SBIRT” or “Screening, Brief Intervention, Referral to Treatment” tool. SBIRT is an all-encompassing, integrated means to assess for early intervention and treatment for individuals with substance abuse disorders, and those who are at risk for developing these disorders. The SBIRT may be utilized in primary care offices, ERs, trauma centers, public health clinics, and other healthcare settings to allow opportunity for early intervention for at-risk individuals before significant consequences.

Screening involves the quick assessment of the severity of the substance use and identifies appropriate levels of treatment.

Brief intervention provides emphasis on increasing insight and awareness about substance use and motivation for behavioral changes.

Referral to treatment provides those identified as needing more extensive treatment with access to specialty care.

Provider involvement is key to the success of the interventions. More complete information may be obtained at www.​samhsa.​gov/​sbirt/​resources (Accessed 10/30/2015).

Screening for alcohol abuse may be done with the simple “CAGE” questionnaire. Two “yes responses” indicate that there is a possibility of alcoholism and possible abuse investigated further. The questions are as follows:





Screening for drugs may be accomplished with the “Drug Abuse Screening Test-10” or DAST-10. This tool consists of ten questions to help score the level of drug abuse. The questions are (yes or no, and, refer to previous 12 months):











Once these items have been scored, the interpretation involves how high the scoring of the questions answered is for the individual. The scoring is as follows:

DAST-10 score

Drug abuse

Suggested action


No problems reported

None at this time


Low level

Monitor, reassess


Moderate level

Further investigation


Substantial level

Intensive assessment


Severe level

Intensive assessment

The most important part of screening remains the initiation of frank conversation with our patients regarding substance and alcohol abuse. As screening becomes a part of routine care, it becomes more and more comfortable to the providers and the patients. Our patients will be grateful we cared enough to begin this serious and potentially life-saving discussion.



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