First_Aid_Step2

First_Aid_Step2. Stevens-Johnson syndrome. Bipolar disorder; anticonvulsant. GI (nausea, vomiting), tremor, sedation, alopecia, weight gain. Rarely, pancreatitis, thrombocytopenia, fatal hepatotoxicity, and agranulocytosis. Second-line mood stabilizer; anticonvulsant. Blurred vision, GI distress, Stevens-Johnson syndrome. ↑ dose slowly to monitor for rashes.


First_Aid_Step2

First_Aid_Step2. Characteristics of personality disorders— orders below). Benzodiazepines may be of beneft in refractory agitation. Bipolar depression: Mood stabilizers +/– antidepressants. Start mood stabilizers first (see Table 2.14-6) to avoid inducing mania. ECT may be used to treat refractory cases. In patients with severe depression or bipolar II with predominantly depressive features, antidepressant treatment can be augmented with low-dose lithium—e.g., at blood levels of 0.4–0.6 mEq/L. Personality can be defned as an individual’s set of emotional and behavioral traits, which are generally stable and predictable. Personality disorders are defned when one’s traits become chronically rigid and maladaptive and affect most aspects of one’s life (see the mnemonic MEDIC). Onset occurs by early adulthood. Personality disorders are defned under Axis II in the DSM-IV (see defnition of axes on the following page). Specifc disorders are outlined in Table 2.14-7.


First_Aid_Step2

First_Aid_Step2. TAB LE 2.1 4-7. Signs and Symptoms of Personality Disorders Distrustful, suspicious; interpret others’ motives as malevolent. Isolated, detached “loners.” Restricted emotional expression. Odd behavior, perceptions, and appearance. Magical thinking; ideas of reference. Patients are suspicious and distrustful of psychiatrists, making it diffcult to form therapeutic relationships between patient and psychiatrist. Be clear, honest, noncontrolling, and nondefensive. Unstable mood, relationships, and self-image; feelings of emptiness. Impulsive. History of suicidal ideation or self-harm. Excessively emotional and attention seeking. Sexually provocative; theatrical. Grandiose; need admiration; have sense of entitlement. Lack empathy. Violate rights of others, social norms, and laws. Impulsive; lack remorse. Begins in childhood as conduct disorder. Patients change the rules and demand attention. They are manipulative and demanding and will split staff members.


First_Aid_Step2

First_Aid_Step2. Patients change the rules and demand attention. They are manipulative and demanding and will split staff members. Be frm. Stick to the treatment plan. Be fair. Do not be punitive or derogatory. Be consistent. Do not change rules. Preoccupied with perfectionism, order, and control at the expense of eff ciency. Infexible morals, values. Socially inhibited; rejection sensitive. Fear being disliked or ridiculed. Submissive, clingy; need to be taken care of. Diffculty making decisions. Feel helpless. Patients are controlling and may sabotage their treatment. Words may be inconsistent with actions. Avoid power struggles. Give clear recommendations, but do not push patients into decisions. Ask about attitudes, mood variability, activities, and reaction to stress.


First_Aid_Step2

First_Aid_Step2. Avoid power struggles. Give clear recommendations, but do not push patients into decisions. Ask about attitudes, mood variability, activities, and reaction to stress. Patients have chronic problems dealing with responsibilities, roles, and stressors. They may also deny their behavior, have diff culty understanding the cause of their problems, have diffculty changing their behavior patterns, and frequently refuse psychiatric care. Psychotherapy is the mainstay of therapy. Pharmacotherapy is reserved for cases with comorbid mood, anxiety, or psychotic signs/symptoms. Characterized by hallucinations, delusions, disordered thoughts, behavioral disturbances, and disrupted social functioning with a clear sensorium.


First_Aid_Step2

First_Aid_Step2. Characterized by hallucinations, delusions, disordered thoughts, behavioral disturbances, and disrupted social functioning with a clear sensorium. Epidemiology: Prevalence is approximately 1%; males and females are affected equally. Peak onset is earlier in males (ages 18–25) than in females (ages 25–35), and has an ↑ incidence in those born in winter or early spring. Schizophrenia in frst-degree relatives also ↑ risk. Ten percent of those affected commit suicide. Etiology: Etiologic theories focus on neurotransmitter abnormalities such as dopamine dysregulation (frontal hypoactivity; limbic hyperactivity; effcacy of dopamine antagonists) and brain abnormalities on CT and MRI (enlarged ventricles and ↓ cortical volume). Subtypes are as follows: Paranoid: Delusions (often of persecution of the patient) and/or hallucinations are present. Cognitive function is usually preserved. Associated with the best overall prognosis.


First_Aid_Step2

First_Aid_Step2. Paranoid: Delusions (often of persecution of the patient) and/or hallucinations are present. Cognitive function is usually preserved. Associated with the best overall prognosis. Disorganized: Speech and behavior patterns are highly disordered and disinhibited with fat affect. The thought disorder is pronounced, and the patient has poor contact with reality. Carries the worst prognosis. Catatonic: A rare form characterized by psychomotor disturbance with two or more of the following: excessive motor activity, immobility, extreme negativism, mutism, waxy fexibility, echolalia, or echopraxia. Two or more of the following are present continuously for six or more months with social or occupational dysfunction: symptoms: Hallucinations (most often auditory), delusions, disorganized speech, bizarre behavior, and thought disorder. symptoms: Flat affect, ↓ emotional reactivity, poverty of speech, lack of purposeful actions, and anhedonia. The differential includes the following:


First_Aid_Step2

First_Aid_Step2. symptoms: Flat affect, ↓ emotional reactivity, poverty of speech, lack of purposeful actions, and anhedonia. The differential includes the following: Schizophreniform disorder: Symptoms of schizophrenia with a duration of < 6 months. Schizoaffective disorder: Combines the symptoms of schizophrenia with a major affective disorder (major depressive disorder or bipolar disorder). Five categories are used by the DSM-IV to classify the factors contributing to an individual’s mental state: Axis I: Psychiatric disorders. Axis II: Personality disorders and mental retardation. Axis III: Physical and medical problems. Axis IV: Social and environmental problems/ stressors. Axis V: The Global Assessment of Functioning (GAF), which rates a patient’s overall level of social, occupational, and psychological functioning on a scale of 1 (nonfunctional) to 100 (extremely high functioning across several areas). Antipsychotics (see Table 2.14-8); long-term follow-up.


First_Aid_Step2

First_Aid_Step2. Antipsychotics (see Table 2.14-8); long-term follow-up. Supportive psychotherapy, training in social skills, vocational rehabilita tion, and illness education may help. Terms used to describe ■ symptoms may be more diffcult to treat. components of psychosis: Delusion: A f xed false idiosyncratic belief. Hallucination: Perception of an object or event without an existing external stimulus. Illusion: False perception of an actual external stimulus. A persistent pattern of excessive inattention and/or hyperactivity/impulsivity. More common in males; typically presents between ages 3 and 13. Often shows a familial pattern. Diagnosis requires six or more symptoms from each category listed below for six or more months in at least two settings, leading to signifcant social and academic impairment. Some symptoms must be present in patients before age seven.


First_Aid_Step2

First_Aid_Step2. ■Inattention: Poor attention span in schoolwork/play; poor attention to detail or careless mistakes; does not listen when spoken to; has difficulty T AB LE 2.1 4-8. Antipsychotic Medications Typical antipsychotics Haloperidol, droperidol, f uphenazine, thioridazine, chlorpromazine Atypical antipsychotics Clozapine, risperidone (also available in long-acting depot injection), quetiapine, olanzapine, ziprasidone, aripiprazole Currently frst-line treatment for schizophrenia given fewer EPS and anticholinergic effects. Clozapine is reserved for severe treatment resistance and severe tardive dyskinesia. Weight gain, type 2 DM, somnolence, sedation, and QTc prolongation. Agranulocytosis requiring weekly CBC monitoring (clozapine). Psychotic disorders, acute agitation, acute mania, Tourette’s syndrome. Thought to be more effective for symptoms of schizophrenia; primarily block D2 dopamine receptors.


First_Aid_Step2

First_Aid_Step2. Psychotic disorders, acute agitation, acute mania, Tourette’s syndrome. Thought to be more effective for symptoms of schizophrenia; primarily block D2 dopamine receptors. For patients in whom compliance is a major issue, consider antipsychotics that come in depot forms (haloperidol, f uphenazine). (EPS; see Table 2.14-9), hyperprolactinemia. Anticholinergic effects (dry mouth, urinary retention, constipation). Seizures, hypotension, sedation, and QTc prolongation. (thioridazine). Neuroleptic malignant syndrome: Fever, muscle rigidity, autonomic instability, elevated CK, clouded consciousness. Stop medication; provide supportive care in the ICU; administer dantrolene or bromocriptine (see Table 2.14-9). T AB LE 2.1 4-9. Extrapyramidal Symptoms and Treatment


First_Aid_Step2

First_Aid_Step2. Acute dystonia Involuntary muscle contraction or spasm (e.g., torticollis, oculogyric crisis). Anticholinergics (benztropine or diphenhydramine); some patients on antipsychotics who are prone to dystonic reactions may need regular prophylactic dosing of these. Akathisia Subjective/objective restlessness, which is perceived as being distressing. ↓ neuroleptic and try β-blockers (propranolol). Benzodiazepines or anticholinergics may help. Pseudoparkinsonism (e.g., shuffing gait, cogwheel rigidity). Give an anticholinergic (benztropine) or a dopamine agonist (amantadine). ↓ the dose of neuroleptic or discontinue (if tolerated). Stereotypic oral-facial movements. Likely from dopamine receptor sensitization. Often irreversible (50%). Discontinue or ↓ the dose of neuroleptic; attempt treatment with more appropriate drugs; and consider changing neuroleptic (e.g., to clozapine or risperidone). Giving anticholinergics or decreasing neuroleptics may initially worsen tardive dyskinesia.


First_Aid_Step2

First_Aid_Step2. following instructions or finishing tasks; loses items needed to complete tasks; is forgetful and easily distracted. ■ Hyperactivity/impulsivity: Fidgets; leaves seat in classroom; runs around inappropriately; cannot play quietly; talks excessively; does not wait turn; interrupts others. Initial treatment may be nonpharmacologic (e.g., behavior modif cation). Sugar and food additives are not considered etiologic factors. Pharmacologic treatment includes the following: Psychostimulants: Methylphenidate (Ritalin), dextroamphetamine (Dexedrine), mixed salts of dextroamphetamine and amphetamine (Adderall), atomoxetine (Strattera), pemoline (Cylert). Adverse effects include insomnia, irritability, ↓ appetite, tic exacerbation, and ↓ growth velocity (normalizes when medication is stopped). Antidepressants (e.g., SSRIs, nortriptyline, bupropion) and α2-agonists (e.g., clonidine).


First_Aid_Step2

First_Aid_Step2. Antidepressants (e.g., SSRIs, nortriptyline, bupropion) and α2-agonists (e.g., clonidine). More common in males. May be associated with tuberous sclerosis and fragile X syndrome. Symptom severity and IQ vary widely. ■Characterized by abnormal or impaired social interaction and communication together with restricted activities and interests, evident before age three. Children must exhibit ADHD symptoms in two or more settings (e.g., home and school). Conduct disorder is seen in Children. Antisocial personality disorder is seen in Adults. Patients fail to develop normal social behaviors (e.g., social smile, eye contact) and lack interest in relationships. The development of spoken language is delayed or absent. Children show stereotyped speech and behavior (e.g., hand f apping) and restricted interests (e.g., preoccupation with parts of objects). Other pervasive developmental disorders include the following:


First_Aid_Step2

First_Aid_Step2. Other pervasive developmental disorders include the following: Asperger’s syndrome: An autism-like disorder of social impairment and repetitive activities, behaviors, and interests without marked language or cognitive delays. Rett’s disorder: A genetic neurodegenerative disorder of females with progressive impairment (e.g., language, head growth, coordination) after five months of normal development. Childhood disintegrative disorder: Severe developmental regression after > 2 years of normal development (e.g., language, motor skills, social skills, bladder/bowel control, play). Intensive special education, behavioral management, and symptom-targeted medications (e.g., neuroleptics for aggression; SSRIs for stereotyped behavior). Family support and counseling are crucial. Include conduct disorder and oppositional def ant disorder. More common among males and in patients with a history of abuse. Hx/PE:


First_Aid_Step2

First_Aid_Step2. Family support and counseling are crucial. Include conduct disorder and oppositional def ant disorder. More common among males and in patients with a history of abuse. Hx/PE: Conduct disorder: A repetitive, persistent pattern of violating the basic rights of others or age-appropriate societal norms or rules for one year or more. Behaviors may be aggressive (e.g., rape, robbery, animal cruelty) or nonaggressive (e.g., stealing, lying, deliberately annoying people). May progress to antisocial personality disorder in adulthood. Oppositional defiant disorder: A pattern of negativistic, defiant, disobedient, and hostile behavior toward authority fgures (e.g., losing temper, arguing) for six or more months. May progress to conduct disorder. Tx: Individual and family therapy. Occur more frequently in males and in those of low socioeconomic status (SES); often exhibit a familial pattern. Hx/PE:


First_Aid_Step2

First_Aid_Step2. Tx: Individual and family therapy. Occur more frequently in males and in those of low socioeconomic status (SES); often exhibit a familial pattern. Hx/PE: Academic functioning is substantially lower than expected for age, intelligence, and education as measured by standardized test achievement in reading, mathematics, or written expression. Learning problems signifcantly interfere with schooling and daily activities. Always rule out physical disorders (e.g., deafness) and social factors (e.g., non–English speakers). Tx: Interventions include remedial classes or individualized learning strategies. Associated with male gender, chromosomal abnormalities, congenital infections, teratogens, inborn errors of metabolism, and alcohol/illicit substances during pregnancy. Hx/PE: Patients have signifcantly subaverage intellectual functioning (an IQ of < 70) with deficits in adaptive functioning (e.g., hygiene, social skills); onset is before the age of 18.


First_Aid_Step2

First_Aid_Step2. Hx/PE: Patients have signifcantly subaverage intellectual functioning (an IQ of < 70) with deficits in adaptive functioning (e.g., hygiene, social skills); onset is before the age of 18. Levels of severity are mild (IQ 50–70; 85% of cases), moderate (IQ 35–49), severe (IQ 20–34), and profound (IQ < 20). Tx: 1° prevention consists of educating the general public about possible causes of mental retardation and providing optimal prenatal screening and health care to mothers and their children. Treatment measures include family counseling and support; speech and language therapy; occupational/physical therapy; behavioral intervention; educational assistance; and social skills training. More common in males; shows a genetic predisposition. Associated with ADHD, learning disorders, and OCD. Hx/PE: Begins prior to age 18.


First_Aid_Step2

First_Aid_Step2. More common in males; shows a genetic predisposition. Associated with ADHD, learning disorders, and OCD. Hx/PE: Begins prior to age 18. Characterized by multiple motor (e.g., blinking, grimacing) and vocal (e.g., grunting, coprolalia) tics occurring many times per day, recurrently, for > 1 year with social or occupational impairment. Tx: Treatments include dopamine receptor antagonists (haloperidol, pimozide) or clonidine. Behavioral therapy may be of beneft, and counseling can aid in social adjustment and coping. Stimulants can worsen or precipitate tics. Fetal alcohol syndrome is the number one avoidable cause of mental retardation. Coprolalia = repetition of obscene words. Features of substance dependence— Both substance abuse and substance dependence are maladaptive patterns of substance use that lead to clinically signifcant impairment. Substance abuse is distinguished from substance dependence as follows:


First_Aid_Step2

First_Aid_Step2. Substance abuse: Requires one or more of the following in one year: Failure to fulfill responsibilities at work, school, or home. Use in physically hazardous situations (e.g., driving while intoxicated). Legal problems during the time of substance use. Continued substance use despite recurrent social or interpersonal problems 2° to the effects of such use (e.g., frequent arguments with spouse over the substance use). Substance dependence: Requires three or more of the following in one year: Tolerance and use of progressively larger amounts to obtain the same desired effect. Withdrawal symptoms when not taking the substance. Failed attempts to cut down use or abstain from the substance. Three or more of seven within a 12-month period: Harm (physical and psychosocial) with continued use Desire to cut down/ control Time spent obtaining/ using the substance is ↑ A diagnosis of substance dependence trumps a diagnosis of substance abuse.


First_Aid_Step2

First_Aid_Step2. Desire to cut down/ control Time spent obtaining/ using the substance is ↑ A diagnosis of substance dependence trumps a diagnosis of substance abuse. Signifcant time spent obtaining the substance (e.g., visiting many doctors to obtain a prescription for pain pills). Isolation from life activities. Taking greater amounts of the substance than intended. Continued substance abuse despite recurrent physical or psychological problems 2° to the effect of the substance use. Substance use is often denied or underreported, so seek out collateral information from family and friends. Check urine and blood toxicology screens, LFTs, and serum EtOH level. The management of intoxication for selected drugs is described in Table 2.14-10. T AB LE 2.1 4-1 0. Signs and Symptoms of Substance Abuse


First_Aid_Step2

First_Aid_Step2. Alcohol Disinhibition, emotional lability, slurred speech, ataxia, aggression, blackouts, hallucinations, memory impairment, impaired judgment, coma. Tremor, tachycardia, hypertension, malaise, nausea, seizures, DTs, agitation. Opioids Euphoria leading to apathy, CNS depression, constipation, pupillary constriction, and respiratory depression (life threatening in overdose). Naloxone/naltrexone will block opioid receptors and reverse effects (beware of antagonist clearing before opioids, particularly with long-acting opioids such as methadone). Dysphoria, insomnia, anorexia, myalgias, fever, lacrimation, diaphoresis, dilated pupils, rhinorrhea, piloerection, nausea, vomiting, stomach cramps, diarrhea, yawning. Opioid withdrawal is not life threatening, “hurts all over,” and does not cause seizures. Amphetamines Psychomotor agitation, impaired judgment, hypertension, pupillary dilation, tachycardia, fever, diaphoresis, anxiety, angina, euphoria, prolonged wakefulness/attention,


First_Aid_Step2

First_Aid_Step2. cause seizures. Amphetamines Psychomotor agitation, impaired judgment, hypertension, pupillary dilation, tachycardia, fever, diaphoresis, anxiety, angina, euphoria, prolonged wakefulness/attention, arrhythmias, delusions, seizures, hallucinations. Haloperidol can be given for severe agitation and symptom-targeted medications (e.g., antiemetics, NSAIDs). Postuse “crash” with anxiety, lethargy, headache, stomach cramps, hunger, fatigue, depression/dysphoria, sleep disturbance, nightmares. Cocaine Psychomotor agitation, euphoria, impaired judgment, tachycardia, pupillary dilation, hypertension, paranoia, hallucinations, sudden death. ECG changes from ischemia are often seen (“cocaine chest pain”). Treat with haloperidol for severe agitation along with symptom-specifc medications (e.g., to control hypertension). Postuse “crash” with hypersomnolence, depression, malaise, severe craving, angina, suicidality, ↑ appetite, nightmares, “cocaine bugs.”


First_Aid_Step2

First_Aid_Step2. T AB LE 2.1 4-1 0. Signs and Symptoms of Substance Abuse (continued)


First_Aid_Step2

First_Aid_Step2. Phencyclidine hydrochloride (PCP) Assaultiveness, belligerence, psychosis, violence, impulsiveness, psychomotor agitation, fever, tachycardia, vertical/horizontal nystagmus, hypertension, impaired judgment, ataxia, seizures, delirium. Give benzodiazepines or haloperidol for severe symptoms; otherwise reassure. Acidifcation of urine or gastric lavage can help eliminate the drug. Recurrence of intoxication symptoms due to reabsorption in the GI tract; sudden onset of severe, random violence. LSD Marked anxiety or depression, delusions, visual hallucinations, fashbacks, pupillary dilation, impaired judgment, diaphoresis, tachycardia, hypertension, heightened senses (e.g., colors become more intense). Supportive counseling; traditional antipsychotics for psychotic symptoms; benzodiazepines for anxiety. Marijuana Euphoria, slowed sense of time, impaired judgment, social withdrawal, ↑ appetite, dry mouth, conjunctival injection, hallucinations, anxiety, paranoia, amotivational syndrome.


First_Aid_Step2

First_Aid_Step2. for anxiety. Marijuana Euphoria, slowed sense of time, impaired judgment, social withdrawal, ↑ appetite, dry mouth, conjunctival injection, hallucinations, anxiety, paranoia, amotivational syndrome. Barbiturates Low safety margin; respiratory depression. Anxiety, seizures, delirium, life-threatening cardiovascular collapse. Benzodiazepines Interactions with alcohol, amnesia, ataxia, somnolence, mild respiratory depression. (Avoid using for insomnia in the elderly; can cause paradoxical agitation even in relatively low doses.) Rebound anxiety, seizures, tremor, insomnia, hypertension, tachycardia, death. Restlessness, insomnia, diuresis, muscle twitching, arrhythmias, tachycardia, fushed face, psychomotor agitation. Headache, lethargy, depression, weight gain, irritability, craving. Restlessness, insomnia, anxiety, arrhythmias. Irritability, headache, anxiety, weight gain, craving, bradycardia, diff culty concentrating, insomnia. Caffeine Nicotine


First_Aid_Step2

First_Aid_Step2. Occurs more often in males (4:1) and in those 21–34 years of age, although the incidence in females is rising. Also associated with a family history. Hx/PE: See Table 2.14-10 for the symptoms of intoxication and withdrawal. Look for palmar erythema or telangiectasias as well as for other signs and symptoms of end-organ complications. Dx: Screen with the CAGE questionnaire. Monitor vital signs for evidence of withdrawal. Labs may reveal ↑ LFTs, LDH, and MCV. Tx: Rule out medical complications; correct electrolyte abnormalities. Start a benzodiazepine taper for withdrawal symptoms. Add haloperidol for hallucinations and psychotic symptoms. Pinpoint pupils are not always a reliable sign of opioid ingestion because coingestions can lead to normal or enlarged pupils. Also look for a ↓ respiratory rate, track marks, and ↓breath sounds. CAGE questionnaire: 1. Have you ever felt the need to Cut down on your drinking? 2. Have you ever felt Annoyed by criticism of your drinking? 3.


First_Aid_Step2

First_Aid_Step2. CAGE questionnaire: 1. Have you ever felt the need to Cut down on your drinking? 2. Have you ever felt Annoyed by criticism of your drinking? 3. Have you ever felt Guilty about drinking? 4. Have you ever had to take a morning Eye opener? More than one “yes” answer makes alcoholism likely. There are two types of anorexia nervosa: Give multivitamins and folic acid; administer thiamine before glucose (which depletes thiamine) to prevent Wernicke’s encephalopathy. Give anticonvulsants to patients with a seizure history. Group therapy, disulfram, or naltrexone can aid patients with dependence. Long-term rehabilitative therapy (e.g., Alcoholic Anonymous). ■ Cx: GI bleeding from gastritis, ulcers, varices, or Mallory-Weiss tears.


First_Aid_Step2

First_Aid_Step2. Long-term rehabilitative therapy (e.g., Alcoholic Anonymous). ■ Cx: GI bleeding from gastritis, ulcers, varices, or Mallory-Weiss tears. Pancreatitis, liver disease, DTs, alcoholic hallucinosis, peripheral neuropathy, Wernicke’s encephalopathy, Korsakoff’s psychosis, fetal alcohol syndrome, cardiomyopathy, anemia, aspiration pneumonia, ↑ risk of sustaining trauma (e.g., subdural hematoma). Risk factors include female gender, low self-esteem, and high SES. Also associated with OCD, major depressive disorder, anxiety, and careers such as modeling, gymnastics, ballet, and running. Hx/PE: Diagnosed as follows (see also Table 2.14-11): Body weight is < 85% of that expected. Patients present with refusal to maintain normal body weight, an intense fear of weight gain, a distorted body image (patients perceive themselves as fat), and amenorrhea. Patients restrict (e.g., fasting, excessive exercise) or binge and purge (through vomiting, laxatives, and diuretics).


First_Aid_Step2

First_Aid_Step2. Patients restrict (e.g., fasting, excessive exercise) or binge and purge (through vomiting, laxatives, and diuretics). Signs and symptoms include lanugo, dry skin, bradycardia, lethargy, hypotension, cold intolerance, and hypothermia (as low as 35°C). Dx: Measure height and weight; check CBC, electrolytes, endocrine levels, and ECG. Perform a psychiatric evaluation to screen patients for co-morbid conditions. Tx: Initially, monitor caloric intake to restore nutritional status and to stabilize weight; then focus on weight gain. Hospitalize if necessary to restore nutritional status, rehydrate, and correct electrolyte imbalances. Once the patient is medically stable, initiate individual, family, and group psychotherapy. Treat comorbid depression and anxiety. Cx: Mitral valve prolapse, arrhythmias, hypotension, bradycardia, amenor- TABLE 2.14-11. Anorexia vs. Bulimia


First_Aid_Step2

First_Aid_Step2. Cx: Mitral valve prolapse, arrhythmias, hypotension, bradycardia, amenor- TABLE 2.14-11. Anorexia vs. Bulimia Body image Disturbed body image; use extensive measures to avoid weight gain (e.g., purging, excess exercise). Same. Binge eating May occur. Same. Patients are underweight (≥ 15% below expected weight). Patients are of normal weight or are overweight. Patients are typically not distressed by their illness and may thus be resistant to treatment. Patients are typically distressed about their symptoms and are thus easier to treat. Weight Attitude toward illness rhea (missing three consecutive cycles), nephrolithiasis, osteoporosis, multiple stress fractures, pancytopenia, thyroid abnormalities (see Table 2.1412). Mortality from suicide or medical complications is > 10%. More common among women; associated with low self-esteem, mood disorders, and OCD. Hx/PE: Diagnostic criteria are as follows (see also Table 2.14-11):


First_Aid_Step2

First_Aid_Step2. More common among women; associated with low self-esteem, mood disorders, and OCD. Hx/PE: Diagnostic criteria are as follows (see also Table 2.14-11): Patients have normal weight or are overweight. For at least two times a week for three or more months, patients have episodes of binge eating and compensatory behaviors that include purging or fasting. Patients are usually ashamed and conceal their behaviors. Signs include dental enamel erosion, enlarged parotid glands, and scars on the dorsal hand surfaces (from inducing vomiting). Patients usually have normal body weight. Tx: Psychotherapy focuses on behavior modifcation and body image. Antidepressants may be effective for both depressed and nondepressed patients. Cx: See Table 2.14-12. Interest in sexual activity usually does not ↓ with aging. Men usually require ↑ stimulation of the genitalia for longer periods of time to reach orgasm; intensity of orgasm ↓, and the length of the refractory period before the next orgasm ↑.


First_Aid_Step2

First_Aid_Step2. Men usually require ↑ stimulation of the genitalia for longer periods of time to reach orgasm; intensity of orgasm ↓, and the length of the refractory period before the next orgasm ↑. In women, estrogen levels ↓ after menopause, leading to vaginal dryness and thinning, which may result in discomfort during coitus. May be treated with HRT, estrogen vaginal suppositories, or other vaginal creams. Preoccupation with or engagement in unusual sexual fantasies, urges, or behaviors for > 6 months with clinically signifcant impairment in one’s life. Includes criminal sex offenders (e.g., pedophilia); see Table 2.14-13. Found almost exclusively in men, and usually begins before or during puberty. Sexual excitement is derived from unique exposures to certain situations, individuals, or objects.


First_Aid_Step2

First_Aid_Step2. Sexual excitement is derived from unique exposures to certain situations, individuals, or objects. T AB LE 2.1 4-1 2. Medical Complications of Eating Disorders be more disturbed by their behavior than anorexics and are more easily engaged in therapy. Anorexic patients deny health risks associated with their behavior, making them resistant to treatment. Bupropion should be avoided in the treatment of patients with eating disorders, as it is associated with a ↓ seizure threshold. Cachexia Hypothermia Fatigue Electrolyte abnormalities Arrhythmias Sudden death Hypotension Bradycardia Prolonged QT interval Dental erosions and decay Abdominal pain Delayed gastric emptying Amenorrhea Nephrolithiasis Dermatologic: Lanugo Hematologic: Leukopenia Neurologic: Seizures Musculoskeletal: Osteoporosis, stress fractures T AB LE 2.1 4-1 3. Features of Common Paraphilias


First_Aid_Step2

First_Aid_Step2. T AB LE 2.1 4-1 3. Features of Common Paraphilias Exhibitionism Sexual arousal from exposing one’s genitals to a stranger. Pedophilia Urges or behaviors involving sexual activities with children. Voyeurism Observing unsuspecting persons unclothed or involved in sex. Fetishism Use of nonliving objects (often clothing) for sexual arousal. Transvestic fetishism Cross-dressing for sexual arousal. Frotteurism Touching or rubbing one’s genitalia against a nonconsenting person (common in subways). Sexual sadism Sexual arousal from inficting suffering on sexual partner. Sexual masochism Sexual arousal from being hurt, humiliated, bound, or threatened. ■ Tx: Treatment includes insight-oriented psychotherapy and behavioral therapy. Antiandrogens (e.g., Depo-Provera) have been used for hypersexual paraphilic activity.


First_Aid_Step2

First_Aid_Step2. ■ Tx: Treatment includes insight-oriented psychotherapy and behavioral therapy. Antiandrogens (e.g., Depo-Provera) have been used for hypersexual paraphilic activity. Strong, persistent cross-gender identification and discomfort with one’s assigned sex or gender role of the assigned sex in the absence of intersexual disorders. Patients may have a history of dressing like the opposite sex, taking sex hormones, or pursuing surgeries to reassign their sex. More common in males than in females. Associated with depression, anxiety, substance abuse, and personality disorders, which may be addressed and treated. Tx: Treatment is complex and includes educating the patient about culturally acceptable behavior patterns. Other options include sex-reassignment surgery or hormonal treatment (e.g., estrogen for males, testosterone for females). Supportive psychotherapy is helpful. Problems in sexual arousal, desire, or orgasm or pain with sexual intercourse.


First_Aid_Step2

First_Aid_Step2. Problems in sexual arousal, desire, or orgasm or pain with sexual intercourse. Prevalence is 30%; one-third of cases are attributable to biological factors and another third to psychological factors. Tx: Treatment depends on the particular condition. Pharmacologic strategies include sildenafl (Viagra) and bupropion (Wellbutrin). Psychotherapeutic strategies include sensate focusing. Up to one-third of all American adults suffer from some type of sleep disorder during their lives. The term dyssomnia describes any condition that leads to a disturbance in the normal rhythm or pattern of sleep. Insomnia is the most common example. Risk factors include female gender, the presence of mental and medical disorders, substance abuse, and advanced age. Affects up to 30% of the general population; causes sleep disturbance that is not attributable to physical or mental conditions. Often exacerbated by anxiety, and patients may become preoccupied with getting enough sleep.


First_Aid_Step2

First_Aid_Step2. Dx: Patients present with a history of nonrestorative sleep or difficulty initiating or maintaining sleep that is present at least three times a week for one month. Tx: First-line therapy includes the initiation of good sleep hygiene measures, which include the following: Establishment of a regular sleep schedule Limiting of caffeine intake Avoidance of daytime naps Warm baths in the evening Use of the bedroom for sleep and sexual activity only Exercising early in the day Avoidance of large meals near bedtime Pharmacotherapy is considered second-line therapy and should be initiated with care for short periods of time (< 2 weeks). Pharmacologic agents include diphenhydramine (Benadryl), zolpidem (Ambien), zaleplon (Sonata), and trazodone (Desyrel).


First_Aid_Step2

First_Aid_Step2. Dx: Diagnosed when a patient complains of excessive daytime sleepiness or nighttime sleep that occurs for > 1 month. The excessive somnolence cannot be attributable to medical or mental illness, medications, poor sleep hygiene, insuffcient sleep, or narcolepsy. Tx: First-line therapy includes stimulant drugs such as amphetamines. Antidepressants such as SSRIs may be useful in some patients. May affect up to 0.16% of the population. Onset typically occurs by young adulthood, generally before the age of 30. Some forms of narcolepsy may have a genetic component. Dx: Manifestations include excessive daytime somnolence and ↓REM sleep latency on a daily basis for at least three months. Sleep attacks are the classic symptom; patients cannot avoid falling asleep. Factitious disorders and malingering are distinct from somatoform disorders in that they involve conscious and intentional processes. ■The characteristic excessive sleepiness may be associated with the following:


First_Aid_Step2

First_Aid_Step2. ■The characteristic excessive sleepiness may be associated with the following: Cataplexy: Sudden loss of muscle tone that leads to collapse. Hypnagogic hallucinations: Occur as the patient is falling asleep. Hypnopompic hallucinations: Occur as the patient awakens. Sleep paralysis: Brief paralysis upon awakening. ■ Tx: Treat with a regimen of scheduled daily naps plus stimulant drugs such as amphetamines; give SSRIs for cataplexy. Occurs 2° to disturbances in breathing during sleep that lead to excessive daytime somnolence and sleep disruption. Etiologies can be either central or peripheral. Central sleep apnea (CSA): A condition in which both airf ow and respiratory effort cease. CSA is linked to morning headaches, mood changes, and repeated awakenings during the night.


First_Aid_Step2

First_Aid_Step2. Central sleep apnea (CSA): A condition in which both airf ow and respiratory effort cease. CSA is linked to morning headaches, mood changes, and repeated awakenings during the night. Obstructive sleep apnea (OSA): A condition in which airf ow ceases as a result of obstruction along the respiratory passages. OSA is strongly associated with snoring. Risk factors include male gender, obesity, prior upper airway surgeries, a deviated nasal septum, a large uvula or tongue, and retrognathia (recession of the mandible). In both forms, arousal results in cessation of the apneic event. Associated with sudden death in infants and elderly, headaches, depression, ↑ systolic blood pressure, and pulmonary hypertension. Dx: Sleep studies (polysomnography) document the number of arousals, obstructions, and episodes of ↓ O2 saturation; distinguish OSA from CSA; and identify possible movement disorders, seizures, or other sleep disorders. Tx:


First_Aid_Step2

First_Aid_Step2. Tx: OSA: Nasal continuous positive airway pressure (CPAP). Weight loss if obese. In children, most cases are due to tonsillar/adenoidal hypertrophy, which is corrected surgically. CSA: Mechanical ventilation (e.g., BPAP) with a backup rate for severe cases. A spectrum of disorders characterized by a misalignment between desired and actual sleep periods. Subtypes include jet-lag type, shift-work type, delayed sleep-phase type, and unspecif ed. Tx: Jet-lag type usually resolves within 2–7 days without specific treatment. Shift-work type may respond to light therapy. Oral melatonin may be useful if given 5½ hours prior to the desired bedtime. Patients often present with medically unexplained somatic symptoms, generally with varying etiologies. Somatoform disorders: Patients have no conscious control over symptoms. The fve main categories are outlined in Table 2.14-14.


First_Aid_Step2

First_Aid_Step2. Somatoform disorders: Patients have no conscious control over symptoms. The fve main categories are outlined in Table 2.14-14. Factitious disorders: Patients fabricate symptoms or cause self-injury to assume the sick role (1° gain). More common in males. Munchausen’s syndrome: Common among health care workers. Munchausen’s syndrome by proxy: A “caregiver” makes someone else ill and enjoys taking on the role of concerned onlooker. Malingering: Patients intentionally cause or feign symptoms for 2° gain of financial benefit or housing. Most frequently affects women < 35 years of age who f ll the following criteria: Are experiencing marital discord and are substance abusers or have a partner who is a substance abuser; or Are pregnant, are of low SES, or have obtained a restraining order. In malingering, patients intentionally simulate illness for personal gain. Sexual abusers are usually male and are often known to the victim (and are often family members). TABLE 2.14-14.


First_Aid_Step2

First_Aid_Step2. Somatization disorder Multiple, chronic somatic symptoms from different organ systems with multiple GI, sexual, neurologic, and pain complaints. Frequent clinical contacts and/or surgeries; signif cant functional impairment. The male-to-female ratio is 1:20; onset is usually before age of 30. Schedule regular appointments with the identifed 1° caregiver who maintains communication with consultants and specialists; psychotherapy. Conversion disorder Symptoms or defcits of voluntary motor or sensory function (e.g., blindness, seizure-like movements, paralysis) incompatible with medical processes. Close temporal relationship to stress or intense emotion. More common in young females and in lower socioeconomic and less educated groups. Usually resolves spontaneously, but psychotherapy may help. Hypochondriasis Preoccupation with or fear of having a serious disease despite medical reassurance, leading to signifcant distress/impairment. Often involves a history of prior physical disease.


First_Aid_Step2

First_Aid_Step2. Hypochondriasis Preoccupation with or fear of having a serious disease despite medical reassurance, leading to signifcant distress/impairment. Often involves a history of prior physical disease. Men and women are equally affected. Onset is in adulthood. Manage with group therapy and schedule regular appointments with the patient’s 1° caregiver. Body dysmorphic disorder Preoccupation with an imagined physical defect or abnormality that leads to signif cant distress/impairment. Patients often present to dermatologists or plastic surgeons. Has a slight female predominance. May be associated with depression. SSRIs may be of benef t. Somatoform pain disorder Intensity or profle of pain symptoms is inconsistent with physiologic processes. Close temporal relationship with psychological factors. More common in females; peak onset is at 40–50 years of age. May be associated with depression. Treatment includes rehabilitation (e.g., physical therapy), psychotherapy, and behavioral therapy.


First_Aid_Step2

First_Aid_Step2. More common in females; peak onset is at 40–50 years of age. May be associated with depression. Treatment includes rehabilitation (e.g., physical therapy), psychotherapy, and behavioral therapy. Analgesia is usually not helpful. TCAs and SNRIs (venlafaxine and duloxetine) may be therapeutic.


First_Aid_Step2

First_Aid_Step2. Suicide is the third leading cause of death (after homicide and accidents) among 15to 24-year-olds in the United States. Emergent inpatient hospitalization is required for patients with suicidal intentions. Victims of childhood abuse are more likely to become adult victims of abuse. Hx/PE: Patients typically have multiple somatic complaints, frequent ER visits, and unexplained injuries with delayed medical treatment. They may also avoid eye contact or act afraid or hostile. Children may exhibit precocious sexual behavior, genital or anal trauma, STDs, UTIs, and psychiatric problems. Other clues include a partner who answers questions for the patient or refuses to leave the exam room. Tx: Perform a screening assessment of the patient’s safety domestically and in their close personal relationships. Provide medical care, emotional support, and counseling; educate the patient about support services and refer appropriately. Documentation is crucial.


First_Aid_Step2

First_Aid_Step2. Accounts for 30,000 deaths per year in the United States; the eighth overall cause of death in the United States. One suicide occurs every 20 minutes. Risk factors include male gender, age greater than 45 years, psychiatric disorders (major depression, presence of psychotic symptoms), a history of an admission to a psychiatric institution, a previous suicide attempt, a history of violent behavior, ethanol or substance abuse, recent severe stressors, and a family suicide history (see the mnemonic SAD PERSONS). Women are more likely to attempt suicide, whereas men are more likely to succeed by virtue of their ↑ use of more lethal methods. Dx: Perform a comprehensive psychiatric evaluation. Ask about family history, previous attempts, ambivalence toward death, and hopelessness. Ask directly about suicidal ideation, intent, and plan, and look for available means.


First_Aid_Step2

First_Aid_Step2. Ask about family history, previous attempts, ambivalence toward death, and hopelessness. Ask directly about suicidal ideation, intent, and plan, and look for available means. Tx: A patient who endorses suicidality requires emergent inpatient hospitalization even against his will. Suicide risk may ↑ after antidepressant therapy is initiated because a patient’s energy to act on suicidal thoughts can return before the depressed mood lifts. Neoplasms of the Lungs 469 LUNG NODULES 469 LUNG CANCER 470 Beware—all that wheezes is not asthma! Asthma should be suspected in children with multiple episodes of croup and URIs associated with dyspnea.


First_Aid_Step2

First_Aid_Step2. Beware—all that wheezes is not asthma! Asthma should be suspected in children with multiple episodes of croup and URIs associated with dyspnea. Characterized by airway narrowing, obstructive lung diseases restrict air movement and often cause air trapping. The etiologies of obstructive lung disease are described in the mnemonic ABCT. Figure 2.15-1 illustrates the role of lung volume measurements in the diagnosis of lung disease; Table 2.15-1 and Figure 2.15-2 contrast obstructive with restrictive lung disease. Reversible airway obstruction 2° to bronchial hyperreactivity, airway inﬂ ammation, mucous plugging, and smooth muscle hypertrophy. Presents with cough, episodic wheezing, dyspnea, and/or chest tightness. Symptoms often worsen at night or early in the morning.


First_Aid_Step2

First_Aid_Step2. Presents with cough, episodic wheezing, dyspnea, and/or chest tightness. Symptoms often worsen at night or early in the morning. Exam reveals wheezing, prolonged expiratory duration (↓ I/E ratio), accessory muscle use, tachypnea, tachycardia, ↓ breath sounds (late sign), ↓O2 saturation (late sign), hyperresonance, and possible pulsus paradoxus. ■ABGs: Mild hypoxia and respiratory alkalosis. Normalizing PCO2, respiratory acidosis, and more severe hypoxia in an acute exacerbation warrant close observation, as they may indicate fatigue and impending respiratory failure. F IGU R E 2.1 5-1. Lung volumes in the interpretation of pulmonary function tests. (Reproduced, with permission, from Gomella LG et al. Clinician’s Pocket Reference, 11th ed. New York: McGraw-Hill, 2006: Fig. 18-1.) T AB LE 2.1 5-1. Obstructive vs. Restrictive Lung Diseasea a FEV1 = forced expiratory volume in one second; FVC = forced vital capacity.


First_Aid_Step2

First_Aid_Step2. T AB LE 2.1 5-1. Obstructive vs. Restrictive Lung Diseasea a FEV1 = forced expiratory volume in one second; FVC = forced vital capacity. Spirometry/PFTs: ↓ FEV1/FVC; peak fow is diminished acutely; ↑ RV and total lung capacity (TLC). CBC: Possible eosinophilia. CXR: Hyperinf ation. Methacholine challenge: Tests for bronchial hyperresponsiveness; useful when PFTs are normal but asthma is still suspected. In general, avoid allergens or any potential triggers. Management is as follows (see also Tables 2.15-2 and 2.15-3): Asthma triggers include allergens, URIs, cold air, exercise, drugs, and stress. F IGU R E 2.1 5-2. Obstructive vs. restrictive lung disease. Note: Obstructive lung volumes > normal (↑ TLC, ↑ FRC, ↑ RV); restrictive lung volumes < normal. In both obstructive and restrictive disease, FEV1 and FVC are reduced, but in obstructive disease, FEV1 is more dramatically reduced, resulting in a ↓FEV1/FVC ratio.


First_Aid_Step2

First_Aid_Step2. T AB LE 2.1 5-2. Common Asthma Medications and Their Mechanisms β2-agonists Albuterol: Relaxes bronchial smooth muscle (β2-adrenoceptors). Give during acute exacerbations. Salmeterol: Long-acting agent for prophylaxis. Corticosteroids Beclomethasone, prednisone: Inhibit the synthesis of virtually all cytokines; inactivate NF-κB, a transcription factor for TNF-α, among other inﬂ ammatory agents. Inhaled corticosteroids are the first-line treatment for long-term control of asthma. Muscarinic antagonists Ipratropium: Competitively blocks muscarinic receptors, preventing bronchoconstriction. Methylxanthines Theophylline: Likely causes bronchodilation by inhibiting phosphodiesterase, thereby ↓ cAMP hydrolysis and ↑ cAMP levels. Usage is limited because of its narrow therapeutic-toxic index (cardiotoxicity, neurotoxicity). Cromolyn Prevents release of vasoactive mediators from mast cells. Useful for exercise-induced bronchospasm. Effective only for the prophylaxis of asthma; not effective


First_Aid_Step2

First_Aid_Step2. neurotoxicity). Cromolyn Prevents release of vasoactive mediators from mast cells. Useful for exercise-induced bronchospasm. Effective only for the prophylaxis of asthma; not effective during an acute asthmatic attack. Toxicity is rare. Antileukotrienes Zileuton: A 5-lipoxygenase pathway inhibitor. Blocks conversion of arachidonic acid to leukotrienes. Montelukast, zafirlukast: Blocks leukotriene receptors.


First_Aid_Step2

First_Aid_Step2. TABLE 2.15-3. Acute: O2, bronchodilating agents (short-acting inhaled β2-agonists are f rst-line therapy), ipratropium (never use alone for asthma), systemic corticosteroids, magnesium (for severe exacerbations). Maintain a low threshold for intubation in severe cases or acutely in patients with PCO2 > 50 mmHg or PO2 < 50 mmHg. Chronic: Measure lung function (FEV1, peak fow, and sometimes ABGs) to guide management. Administer long-acting inhaled bronchodilators and/ or inhaled corticosteroids, systemic corticosteroids, cromolyn, or, rarely, Medications for Chronic Treatment of Asthma


First_Aid_Step2

First_Aid_Step2. Medications for Chronic Treatment of Asthma Mild intermittent ≤ 2 days/week ≤ 2 nights/month ≥ 80% No daily medications. PRN short-acting bronchodilator. Mild persistent > 2/week but < 1/day > 2 nights/month ≥ 80% Daily low-dose inhaled corticosteroids. PRN short-acting bronchodilator. Moderate persistent Daily > 1 night/week 60–80% Lowto medium-dose inhaled corticosteroids + long-acting inhaled β2-agonists. Severe persistent Continual, frequent ≤ 60% High-dose inhaled corticosteroids + long-acting inhaled β2-agonists. Possible PO corticosteroids. PRN short-acting bronchodilator. theophylline. Montelukast and other leukotriene antagonists are oral adjuncts to inhalant therapy. A disease caused by cycles of infection and infammation in the bronchi/bronchioles that lead to permanent fbrosis, remodeling, and dilation of bronchi. Presents with chronic cough accompanied by frequent bouts of yellow or green sputum production, dyspnea, and possible hemoptysis and halitosis.


First_Aid_Step2

First_Aid_Step2. Presents with chronic cough accompanied by frequent bouts of yellow or green sputum production, dyspnea, and possible hemoptysis and halitosis. Associated with a history of pulmonary infections (e.g., Pseudomonas, Haemophilus, TB), hypersensitivity (allergic bronchopulmonary aspergillosis), cystic f brosis, immunodefciency, localized airway obstruction (foreign body, tumor), aspiration, autoimmune disease (e.g., rheumatoid arthritis, SLE), or IBD. Exam reveals rales, wheezes, rhonchi, purulent mucus, and occasional hemoptysis. CXR: ↑ bronchovascular markings; tram lines (parallel lines outlining dilated bronchi as a result of peribronchial inf ammation and f brosis); areas of honeycombing. High-resolution CT: Dilated airways and ballooned cysts at the end of the bronchus (mostly lower lobes). Spirometry shows a ↓ FEV1/FVC ratio. Antibiotics for bacterial infections; consider inhaled corticosteroids.


First_Aid_Step2

First_Aid_Step2. Antibiotics for bacterial infections; consider inhaled corticosteroids. Maintain bronchopulmonary hygiene (cough control, postural drainage, chest physiotherapy). Consider lobectomy for localized disease or lung transplantation for severe disease. Characterized by ↓ lung function with airfow obstruction. Generally 2° to chronic bronchitis or emphysema, which are distinguished as follows: Chronic bronchitis: Productive cough for > 3 months per year for two consecutive years. Emphysema: Terminal airway destruction and dilation that may be 2° to smoking (centrilobular) or to α1-antitrypsin deficiency (panlobular). Symptoms are minimal or nonspecifc until the disease is advanced. The clinical spectrum includes the following (most patients are a combination of the two phenotypes):


First_Aid_Step2

First_Aid_Step2. Symptoms are minimal or nonspecifc until the disease is advanced. The clinical spectrum includes the following (most patients are a combination of the two phenotypes): Emphysema (“pink puffer”): Dyspnea, pursed lips, minimal cough, ↓ breath sounds, late hypercarbia/hypoxia. Patients often have a thin, wasted appearance. Pure emphysematous patients tend to have few reactive episodes between exacerbations. aspiration Or 2° to foreign bodies Necrotizing pneumonia Chemical corrosive smoking cessation, pneumococcal and inﬂ uenza vaccines) Dilators (β2-agonists, anticholinergics) In COPD patients with chronic hypercapnia, high concentrations of O2 may suppress patients’ hypoxic respiratory drive. Supplemental oxygen titrated to > 90% SaO2 for > 15 hours a day and smoking cessation are the only interventions proven to improve survival in patients with COPD.


First_Aid_Step2

First_Aid_Step2. Supplemental oxygen titrated to > 90% SaO2 for > 15 hours a day and smoking cessation are the only interventions proven to improve survival in patients with COPD. ■Chronic bronchitis (“blue bloater”): Cyanosis with mild dyspnea; productive cough. Patients are often overweight with peripheral edema, rhonchi, and early signs of hypercarbia/hypoxia. Look for the classic barrel chest, use of accessory chest muscles, JVD, end-expiratory wheezing, and muffed breath sounds. CXR: Hyperinﬂ ated lungs, ↓ lung markings with fat diaphragms, and a thin-appearing heart and mediastinum. Parenchymal bullae or subpleural blebs (pathognomonic of emphysema) are also seen (see Figure 2.15-3). PFTs: ↓ FEV1/FVC; normal or ↓ FVC; normal or ↑ TLC (emphysema, asthma); ↓ DLCO (in emphysema). ABGs: Hypoxemia with acute or chronic respiratory acidosis (↑ PCO2). Blood cultures: Obtain if the patient is febrile.


First_Aid_Step2

First_Aid_Step2. ABGs: Hypoxemia with acute or chronic respiratory acidosis (↑ PCO2). Blood cultures: Obtain if the patient is febrile. Gram stain and sputum culture: Consider in the setting of fever or productive cough, especially if infltrate is seen on CXR. Acute exacerbations: O2, inhaled β-agonists (albuterol) and anticholinergics (ipratropium, tiotropium), IV +/− inhaled corticosteroids, antibiotics. Severe cases may beneft from noninvasive ventilation. Consider intubation in the setting of severe hypoxemia or hypercapnia, impending respiratory fatigue, or changes in mental status. Chronic: Smoking cessation, supplemental O2 (if resting PaO2 is ≤ 55 mmHg or SaO2 is ≤ 89%, or in the setting of cor pulmonale, pulmonary hypertension, a hematocrit > 55%, or nocturnal hypoxia), inhaled β-agonists, AB F IGU R E 2.1 5-3. Chronic obstructive pulmonary disease.


First_Aid_Step2

First_Aid_Step2. AB F IGU R E 2.1 5-3. Chronic obstructive pulmonary disease. Note the hyperinfated and hyperlucent lungs, f at diaphragms, ↑ AP diameter, narrow mediastinum, and large upper bullae on (A) AP and (B) lateral CXRs. (Reproduced, with permission, from Stobo J et al. The Principles and Practice of Medicine, 23rd ed. Stamford, CT: Appleton & Lange, 1996: 135.) anticholinergics (tiotropium), systemic or inhaled corticosteroids. Give pneumococcal and ﬂ u vaccines. Characterized by a loss of lung compliance, restrictive lung diseases result in ↑ lung stiffness and ↓ lung expansion. Table 2.15-1 and Figure 2.15-2 contrast obstructive with restrictive lung disease. The etiologies of restrictive lung disease are shown in the mnemonic PAINT.


First_Aid_Step2

First_Aid_Step2. A heterogeneous group of disorders characterized by inﬂ ammation and/or fibrosis of the interalveolar septum. In advanced disease, cystic spaces develop in the lung periphery (“honeycombing”). Causes include idiopathic interstitial pneumonias, collagen vascular disease, granulomatous disorders, drugs, hypersensitivity disorders, pneumoconiosis, and eosinophilic pulmonary syndromes. Presents with shallow, rapid breathing; dyspnea with exercise; and a nonproductive cough. Patients may have cyanosis, inspiratory squeaks, fne or “Velcro-like” crackles, fnger clubbing, or right heart failure. ■ CXR: Reticular, nodular, or ground-glass pattern; “honeycomb” pattern (severe disease). ■↓TLC, ↓FVC, ↓DLCO (may be normal if the cause is extrapulmonary), normal FEV1/FVC. Serum markers of connective tissue diseases should be obtained if clinically indicated.


First_Aid_Step2

First_Aid_Step2. ■↓TLC, ↓FVC, ↓DLCO (may be normal if the cause is extrapulmonary), normal FEV1/FVC. Serum markers of connective tissue diseases should be obtained if clinically indicated. Supportive. Avoid exposure to causative agents. Some inf ammatory diseases respond to corticosteroids or other anti-inf ammatory/immunosuppressive agents. A multisystem disease of unknown etiology characterized by noncaseating granulomas. Most commonly found in African-American females and northern European Caucasians; most often arises in the third or fourth decade of life. Presents with fever, cough, malaise, weight loss, dyspnea, and arthritis. The lungs, liver, eyes, skin (erythema nodosum, violaceous skin plaques), nervous system, heart, and kidney may be affected. Symptoms may be GRUELING (see mnemonic). Causes of restrictive lung disease— Pleural (fibrosis, effusions, empyema, pneumothorax) Alveolar (edema, hemorrhage, pus)


First_Aid_Step2

First_Aid_Step2. Causes of restrictive lung disease— Pleural (fibrosis, effusions, empyema, pneumothorax) Alveolar (edema, hemorrhage, pus) Interstitial lung disease (idiopathic interstitial pneumonias), Inﬂ ammatory (sarcoid, cryptogenic organizing pneumonitis), Idiopathic Neuromuscular (myasthenia, phrenic nerve palsy, myopathy) Thoracic wall (kyphoscoliosis, obesity, ascites, pregnancy, ankylosing spondylitis) Medications that can cause or contribute to interstitial lung disease include busulfan, nitrofurantoin, amiodarone, bleomycin, radiation, and long-term high O2 concentration (e.g., ventilators). CXR: Radiographic fndings are used to stage the disease. Biopsy: Lymph node biopsy or transbronchial/video-assisted thoracoscopic lung biopsy reveals noncaseating granulomas. PFTs: Restrictive or obstructive pattern and ↓ diffusion capacity.


First_Aid_Step2

First_Aid_Step2. Biopsy: Lymph node biopsy or transbronchial/video-assisted thoracoscopic lung biopsy reveals noncaseating granulomas. PFTs: Restrictive or obstructive pattern and ↓ diffusion capacity. Other findings: ↑serum ACE levels (neither sensitive nor specif c), hypercalcemia, hypercalciuria, ↑ alkaline phosphatase (with liver involvement), lymphopenia, cranial nerve defects, arrhythmias. Systemic corticosteroids are indicated for constitutional symptoms, hypercalcemia, or extrathoracic organ involvement. Risk factors include environmental exposure to antigens leading to alveolar thickening and granulomas. Types and etiologies are listed in Table 2.15-4. Acute: Dyspnea, fever, malaise, shivering, and cough starting 4–6 hours after exposure. Chronic: Patients present with progressive dyspnea; exam reveals f ne bilateral rales. CXR is normal or shows miliary nodular infltrate (acute); fbrosis is seen in the upper lobes (chronic).


First_Aid_Step2

First_Aid_Step2. Chronic: Patients present with progressive dyspnea; exam reveals f ne bilateral rales. CXR is normal or shows miliary nodular infltrate (acute); fbrosis is seen in the upper lobes (chronic). Avoid ongoing exposure to inciting agents; give corticosteroids to ↓ chronic inf ammation. T AB LE 2.1 5-4. Antigens of Hypersensitivity Pneumonitis Farmer’s lung Spores of actinomycetes from moldy hay. Bird fancier’s lung Antigens from feathers, excreta, serum. Mushroom worker’s lung Spores of actinomycetes from compost. Malt worker’s lung Spores of Aspergillus clavatus in grain. Grain handler’s lung Grain weevil dust. Bagassosis Spores of actinomycetes from sugarcane. Air conditioner lung Spores of actinomycetes from air conditioners. Risk factors include prolonged occupational exposure and inhalation of small inorganic dust particles. Table 2.15-5 outlines the f ndings and diagnostic criteria associated with common pneumoconioses. Avoid triggers; supportive therapy and supplemental O2.


First_Aid_Step2

First_Aid_Step2. Table 2.15-5 outlines the f ndings and diagnostic criteria associated with common pneumoconioses. Avoid triggers; supportive therapy and supplemental O2. The most common form of idiopathic interstitial pneumonia. Has an unrelenting progression, with death usually occurring within 5–10 years. Exertional dyspnea and a nonproductive cough. Inspiratory crackles and/or clubbing on exam. T AB LE 2.1 5-5. Diagnosis of Pneumoconioses Usual interstitial pneumonia is one of the most common forms of interstitial pneumonia.


First_Aid_Step2

First_Aid_Step2. Asbestosis Work involving manufacture of tile or brake linings, insulation, construction, demolition, or shipbuilding. Presents 15–20 years after initial exposure. CXR: Linear opacities at lung bases and interstitial fibrosis; calcified pleural plaques are indicative of benign pleural disease. ↑ risk of mesothelioma (rare) and lung cancer; risk of lung cancer is higher in smokers. Coal miner’s disease Work in underground coal mines. CXR: Small nodular opacities (< 1 cm) in upper lung zones. Spirometry: Consistent with restrictive disease. Progressive massive fibrosis. Work in mines or quarries or with glass, pottery, or silica. CXR: Small (< 1-cm) nodular opacities in upper lung zones. Eggshell calcifications. Spirometry: Consistent with restrictive disease. ↑ risk of TB; need annual TB skin test. Progressive massive fibrosis. Work in high-technology fields such as aerospace, nuclear, and electronics plants; ceramics industries; foundries; plating facilities; dental material sites;


First_Aid_Step2

First_Aid_Step2. skin test. Progressive massive fibrosis. Work in high-technology fields such as aerospace, nuclear, and electronics plants; ceramics industries; foundries; plating facilities; dental material sites; and dye manufacturing. CXR: Diffuse infiltrates; hilar adenopathy. Requires chronic corticosteroid treatment. Silicosis Berylliosis


First_Aid_Step2

First_Aid_Step2. High-resolution CT: Patchy opacities at the lung bases, often with honeycombing. PFTs: Restrictive pattern. Surgical biopsy (usually required to confrm the diagnosis): Interstitial in-f ammation, fbrosis, and honeycombing. Options include corticosteroids, cytotoxic agents (azathioprine, cyclophosphamide), antifbrotic agents (have not been shown to improve survival), and lung transplantation. A diverse group of disorders characterized by eosinophilic pulmonary infiltrates and peripheral blood eosinophilia. Includes allergic bronchopulmonary aspergillosis, Löfﬂ er’s syndrome, and acute eosinophilic pneumonia. Presents with dyspnea, cough, and/or fever. CBC reveals peripheral eosinophilia; CXR shows pulmonary inf ltrates. Removal of the extrinsic cause or treatment of underlying infection if identifed. Corticosteroid treatment may be used if no cause is identif ed.


First_Aid_Step2

First_Aid_Step2. Removal of the extrinsic cause or treatment of underlying infection if identifed. Corticosteroid treatment may be used if no cause is identif ed. Causes include ventilation-perfusion (V/Q) mismatch, right-to-left shunt, hypoventilation, low inspired O2 content (important at altitudes), and diffusion impairment. Findings depend on the etiology. ↓HbO2 saturation, cyanosis, tachypnea, shortness of breath, pleuritic chest pain, and altered mental status may be seen. Pulse oximetry: Demonstrates ↓ HbO2 saturation. CXR: To rule out ARDS, atelectasis, or an infltrative process (e.g., pneumonia) and to look for signs of pulmonary embolism. ABGs: To evaluate PaO2 and to calculate the alveolar-arterial (A-a) oxygen gradient ([(Patm − 47) × FiO2 − (PaCO2/0.8)] − PaO2). An ↑ A-a gradient suggests a V/Q mismatch or a diffusion impairment. Figure 2.15-4 summarizes the approach toward hypoxemic patients. Is PaCO2 increased? Hypoventilation Yes Yes No No Is PAO2 − PaO2 increased?


First_Aid_Step2

First_Aid_Step2. Is PaCO2 increased? Hypoventilation Yes Yes No No Is PAO2 − PaO2 increased? Is PAO2 − PaO2 increased? Yes Yes NoNo Is low PO2 correctable with O2? 1. High altitude 2. ↓ FiO2 HIGH-YIELD FACTS Hypoventilation plus another mechanism Shunt 1. Alveolar collapse (asthma, COPD) 2. Intra-alveolar filling (pneumonia, pulmonary edema) 3. Intracardiac shunt 4. Vascular shunt within lungs 1. Airways disease (asthma, COPD) 2. Interstitial lung disease 3. Alveolar disease 4. Pulmonary vascular disease V/Q mismatch 1. ↓ respiratory drive 2. Neuromuscular disease Hypoventilation alone F IGU R E 2.1 5-4. Determination of the mechanism of hypoxia. (Reproduced, with permission, from Kasper DL et al. Harrison’s Principles of Internal Medicine, 16th ed. New York: McGraw- Hill, 2005.) Address the underlying etiology. Administer O2 before initiating evaluation.


First_Aid_Step2

First_Aid_Step2. Hill, 2005.) Address the underlying etiology. Administer O2 before initiating evaluation. If the patient is on a ventilator, ↑ O2 saturation by increasing FiO2, positive end-expiratory pressure (PEEP), or the I/E ratio. Hypercapnic patients: ↑ minute ventilation. Acute respiratory failure with refractory hypoxemia, ↓lung compliance, and noncardiogenic pulmonary edema. The pathogenesis is thought to be endothelial injury. Common triggers include sepsis, pneumonia, aspiration, multiple blood transfusions, inhaled/ingested toxins, and trauma. Overall mortality is 30–40%. Presents with acute-onset (12–48 hours) tachypnea, dyspnea, and tachycardia +/− fever, cyanosis, labored breathing, diffuse high-pitched rales, and hypoxemia in the setting of one of the systemic infammatory causes or exposure. Additional fndings are as follows: Phase 1 (acute injury): Normal physical exam; possible respiratory alkalosis.


First_Aid_Step2

First_Aid_Step2. Phase 1 (acute injury): Normal physical exam; possible respiratory alkalosis. Phase 2 (6–48 hours): Hyperventilation, hypocapnia, widening A-a oxygen gradient. Phase 3: Acute respiratory failure, tachypnea, dyspnea, ↓ lung compliance, scattered rales, diffuse chest infltrates on CXR (see Figure 2.15-5). F IGU R E 2.1 5-5. AP CXR showing a diffuse alveolar filling pattern 2° to ARDS. (Reproduced, with permission, from Kasper DL et al. Harrison’s Principles of Internal Medicine, 16th ed. New York: McGraw-Hill, 2005: 1497.) ■ Phase 4: Severe hypoxemia unresponsive to therapy; ↑ intrapulmonary shunting; metabolic and respiratory acidosis. The criteria for ARDS diagnosis (according to the American-European Consensus Conference defnition) are as follows: Acute onset of respiratory distress. PaO2/FiO2 ratio ≤ 200 mmHg. Bilateral pulmonary infltrates on CXR. No evidence of cardiac origin (capillary wedge pressure < 18 mmHg or no clinical evidence of elevated left atrial pressure).


First_Aid_Step2

First_Aid_Step2. PaO2/FiO2 ratio ≤ 200 mmHg. Bilateral pulmonary infltrates on CXR. No evidence of cardiac origin (capillary wedge pressure < 18 mmHg or no clinical evidence of elevated left atrial pressure). There is no standard treatment. Treat the underlying disease and maintain adequate perfusion to prevent end organ damage. Minimize injury induced by mechanical ventilation by ventilating with low tidal volumes. Use PEEP to recruit collapsed alveoli and titrate PEEP and FiO2 to achieve adequate oxygenation. Goal oxygenation is PaO2 > 60 mmHg or SaO2 > 90% on FiO2 ≤ 0.6. Slowly wean patients from ventilation, and follow with extubation trials (see Table 2.15-6). Pulmonary hypertension is defned as a mean pulmonary arterial pressure of > 25 mmHg (normal = 15 mmHg). It is classifed as either 1° (if the etiology


First_Aid_Step2

First_Aid_Step2. Pulmonary hypertension is defned as a mean pulmonary arterial pressure of > 25 mmHg (normal = 15 mmHg). It is classifed as either 1° (if the etiology T AB LE 2.1 5-6. Criteria for Extubation from Mechanical Ventilationa a Patients who meet these criteria are typically given a weaning (T-piece) trial to determine if they are ready for extubation. is unknown) or 2°. 1° pulmonary hypertension most often occurs in young or middle-aged women. The main causes of 2° pulmonary hypertension include the following: ■↑ pulmonary venous pressure from left-sided heart failure or mitral valve disease. ■↑ pulmonary blood fow 2° to congenital heart disease with left-to-right shunt. Hypoxic vasoconstriction 2° to chronic lung disease (e.g., COPD). Thromboembolic disease. Remodeling of pulmonary vessels 2° to structural lung disease. Presents with dyspnea on exertion, fatigue, lethargy, syncope with exertion, chest pain, and symptoms of right-sided CHF (edema, abdominal distention, JVD).


First_Aid_Step2

First_Aid_Step2. Presents with dyspnea on exertion, fatigue, lethargy, syncope with exertion, chest pain, and symptoms of right-sided CHF (edema, abdominal distention, JVD). Inquire about a history of COPD, interstitial lung disease, heart disease, sickle cell anemia, emphysema, and pulmonary emboli. Exam reveals a loud, palpable S2 (often split), a systolic ejection murmur, an S4, or a parasternal heave. CXR shows enlargement of central pulmonary arteries. ECG demonstrates RVH. Echocardiogram and right heart catheterization may show signs of right ventricular overload and may aid in the diagnosis of the underlying cause. Supplemental O2, anticoagulation, vasodilators, and diuretics if symptoms of right-sided CHF are present. Treat underlying causes of 2° pulmonary hypertension. Causes of pulmonary hypertension include left heart failure, mitral valve disease, and ↑ resistance in the pulmonary veins, including hypoxic vasoconstriction.


First_Aid_Step2

First_Aid_Step2. Causes of pulmonary hypertension include left heart failure, mitral valve disease, and ↑ resistance in the pulmonary veins, including hypoxic vasoconstriction. Other etiologies of embolic disease include postpartum status (amniotic f uid emboli), fracture (fat emboli), and cardiac surgery (air emboli). Dyspnea, tachycardia, and a normal CXR in a hospitalized and/or bedridden patient should raise suspicion of pulmonary embolism. Occlusion of the pulmonary vasculature by a blood clot. Ninety-f ve percent of emboli originate from DVTs in the deep leg veins. Often leads to pulmonary infarction, right heart failure, and hypoxemia. Virchow’s triad consists of the following: Stasis: Immobility, CHF, obesity, surgery, ↑ central venous pressure. Endothelial injury: Trauma, surgery, recent fracture, previous DVT. Hypercoagulable states: Pregnancy/postpartum, OCP use, coagulation disorders (e.g., protein C/protein S defciency, factor V Leiden), malignancy, severe burns.


First_Aid_Step2

First_Aid_Step2. Hypercoagulable states: Pregnancy/postpartum, OCP use, coagulation disorders (e.g., protein C/protein S defciency, factor V Leiden), malignancy, severe burns. Presents with sudden-onset dyspnea, pleuritic chest pain, low-grade fever, cough, and, rarely, hemoptysis. Pulmonary embolism: Hypoxia and hypocarbia with resulting respiratory alkalosis. Tachypnea, tachycardia, and fever. Exam may reveal a loud P2 and prominent jugular A waves with right heart failure. Venous thrombosis: Unilateral swelling; cords on the calf. ABGs: Respiratory alkalosis (2° hyperventilation) with PO2 < 80 mmHg. CXR: Usually normal, but may show atelectasis, pleural effusion, Hampton’s hump (a wedge-shaped infarct), or Westermark’s sign (oligemia in the affected lung zone). ECG: Not diagnostic; most commonly reveals sinus tachycardia. The classic triad of S1Q3T3—acute right heart strain with an S wave in lead I, a Q wave in lead III, and an inverted T wave in lead III—is uncommon.


First_Aid_Step2

First_Aid_Step2. Helical (spiral) CT with IV contrast: Sensitive for pulmonary embolism. V/Q scan: May reveal segmental areas of mismatch. Results are reported with a designated probability of pulmonary embolism (low, indeterminate, or high) and are interpreted in combination with clinical suspicion. Angiogram: The gold standard, but more invasive and rarely done today (see Figure 2.15-6). D-dimer: Sensitive but not specifc in patients at risk for DVT or pulmonary embolism (a useful “rule-out” test in patients with a low clinical suspicion, but it cannot rule out DVT or pulmonary embolism alone in patients with an intermediate or high clinical suspicion of clot). Venous ultrasound of the lower extremity: Can detect a clot that may have given off the pulmonary embolism. Serial ultrasounds have high diagnostic specif city. Heparin: Bolus followed by weight-based continuous infusion of unfractioned heparin or low-molecular-weight heparin (LMWH) SQ.


First_Aid_Step2

First_Aid_Step2. Heparin: Bolus followed by weight-based continuous infusion of unfractioned heparin or low-molecular-weight heparin (LMWH) SQ. Warfarin: For long-term anticoagulation, usually given for at least six months unless the underlying predisposing factor persists (and is then given indefnitely). Follow INR (goal = 2–3). IVC filter: Indicated for patients with documented DVT in a lower extremity if anticoagulation is contraindicated or if patients experience recurrent emboli while anticoagulated. FIGURE 2.15-6. Pulmonary embolus. A large flling defect in the pulmonary artery is evident on pulmonary angiogram. Thrombolysis: Indicated only in cases of massive DVT or pulmonary embolism causing right heart failure and hemodynamic instability (contraindicated in patients with recent surgery or bleeding). DVT prophylaxis: Treat all immobile patients; give SQ heparin, LMWH, intermittent pneumatic compression of the lower extremities (less effective), and early ambulation (most effective).


First_Aid_Step2

First_Aid_Step2. DVT prophylaxis: Treat all immobile patients; give SQ heparin, LMWH, intermittent pneumatic compression of the lower extremities (less effective), and early ambulation (most effective). Often asymptomatic, or patients may present with chronic cough, dyspnea, and shortness of breath. Always inquire about smoking and exposure history. Serial CXRs: Determine the location, progression, and extent of the nodule. Chest CT: Determine the nature, extent, and infltrating nature of the nodule. Characteristics favoring carcinoma: Age > 45–50; smoking history; history of malignancy; new or enlarging (unless very rapidly enlarging) lesions; absence of calcifcation or irregular calcifcation; size > 2 cm; irregular margins. Lung nodule clues based on the history: Recent immigrant: Think TB. From the southwestern United States: Think coccidioidomycosis. From the Ohio River Valley: Think histoplasmosis. Squamous and Small cell cancers are Central lesions.


First_Aid_Step2

First_Aid_Step2. Recent immigrant: Think TB. From the southwestern United States: Think coccidioidomycosis. From the Ohio River Valley: Think histoplasmosis. Squamous and Small cell cancers are Central lesions. ■Characteristics favoring a benign lesion: Age < 35; no change from old flms; central/uniform/laminated/popcorn calcifcation; size < 2 cm; smooth margins. Surgical resection is indicated for nodules at high risk for malignancy. Low-risk nodules can be followed with CXR or CT every three months for one year and then every six months for another year. An invasive diagnostic procedure is indicated if the size of the nodule ↑. The leading cause of cancer death in the United States. Risk factors include tobacco smoke (except for bronchoalveolar carcinoma) and radon or asbestos exposure. Types are as follows: Small cell lung cancer (SCLC): Highly correlated with cigarette exposure. Central location. Neuroendocrine origin; associated with paraneoplastic syndromes (see Table 2.15-7).


First_Aid_Step2

First_Aid_Step2. Small cell lung cancer (SCLC): Highly correlated with cigarette exposure. Central location. Neuroendocrine origin; associated with paraneoplastic syndromes (see Table 2.15-7). Metastases are often found on presentation (intrathoracic and extrathoracic sites such as brain, liver, and bone). Non–small cell lung cancer (NSCLC): Less likely to metastasize. TAB LE 2.1 5-7. Paraneoplastic Syndromes of Lung Cancer Adenocarcinoma: The most common lung cancer; peripheral location. Includes bronchoalveolar carcinoma, which is associated with multiple nodules, interstitial infltration, and prolifc sputum production but is not associated with smoking. Squamous cell carcinoma: Central location; 98% are seen in smokers. Large cell/neuroendocrine carcinomas: Least common; associated with a poor prognosis. Presents with cough, hemoptysis, dyspnea, wheezing, postobstructive pneumonia, chest pain, weight loss, and possible abnormalities on respiratory exam (crackles, atelectasis).


First_Aid_Step2

First_Aid_Step2. Presents with cough, hemoptysis, dyspnea, wheezing, postobstructive pneumonia, chest pain, weight loss, and possible abnormalities on respiratory exam (crackles, atelectasis). Other f ndings include Horner’s syndrome (miosis, ptosis, anhidrosis) in patients with Pancoast’s tumor at the apex of the lung; superior vena cava syndrome (obstruction of the SVC with supraclavicular venous engorgement); hoarseness (2° to recurrent laryngeal nerve involvement); and many paraneoplastic syndromes (see Table 2.15-7). CXR or chest CT. Fine-needle aspiration (CT guided) for peripheral lesions and bronchoscopy (biopsy or brushing) for central lesions. Thoracoscopic biopsy may be performed, with conversion to open thoracotomy if the lesion is found to be malignant. ■ SCLC: Unresectable. Often responds to radiation and chemotherapy initially but always recurs; has a lower median survival rate than NSCLC. Has usually metastasized at the time of diagnosis.


First_Aid_Step2

First_Aid_Step2. ■ SCLC: Unresectable. Often responds to radiation and chemotherapy initially but always recurs; has a lower median survival rate than NSCLC. Has usually metastasized at the time of diagnosis. Chemotherapy is the mainstay ■NSCLC: Surgical resection in early stages (IA, IB, IIA, IIB, and possibly IIIA). The extent of resection is based on lesion size; the presence of me-of treatment for small cell tastases; and the patient’s age, general health, and lung function. Supple- lung cancer. ment surgery with radiation or chemotherapy (depending on the stage). Palliative radiation and/or chemotherapy is appropriate for symptomatic but unresectable disease. An abnormal accumulation of ﬂuid in the pleural space. Classifed as follows: Transudate: 2° to ↑ pulmonary capillary wedge pressure (PCWP) or ↓ oncotic pressure. Exudate: 2° to ↑ pleural vascular permeability. Table 2.15-8 lists the possible causes of both transudates and exudates.


First_Aid_Step2

First_Aid_Step2. Exudate: 2° to ↑ pleural vascular permeability. Table 2.15-8 lists the possible causes of both transudates and exudates. Presents with dyspnea, pleuritic chest pain, and/or cough. Exam reveals dullness to percussion and ↓breath sounds over the effusion. A pleural friction rub may be present. TABLE 2.15-8. Causes of Pleural Effusions CHF Cirrhosis Nephrotic syndrome Pneumonia (parapneumonic effusion) TB Malignancy Pulmonary embolism Collagen vascular disease (rheumatoid arthritis, SLE) Pancreatitis Trauma Complicated parapneumonic effusions necessitate chest tube drainage. Presentation of pneumothorax: CXR shows costophrenic angle blunting. Thoracentesis is indicated for new effusions > 1 cm in decubitus view, except with bilateral effusions and other clinical evidence of CHF. The effusion is an exudate if it meets Light’s criteria: The ratio of pleural to serum protein is > 0.5 or The ratio of pleural to serum LDH is > 0.6 or


First_Aid_Step2

First_Aid_Step2. The effusion is an exudate if it meets Light’s criteria: The ratio of pleural to serum protein is > 0.5 or The ratio of pleural to serum LDH is > 0.6 or Pleural fuid LDH is more than two-thirds the upper normal limit of serum LDH A parapneumonic effusion is classifed as complicated in the setting of a Gram stain or culture or a pH < 7.2 (normal is 7.6) or a glucose level of < 60. The presence of pus indicates an empyema. Treatment is directed toward the underlying condition causing the effusion. Complicated parapneumonic effusions and empyemas require chest tube drainage in addition to antibiotic therapy. A collection of air in the pleural space that can lead to pulmonary collapse. Subtypes are as follows: 1° spontaneous pneumothorax: 2° to rupture of subpleural apical blebs (usually found in tall, thin young males).


First_Aid_Step2

First_Aid_Step2. 2° pneumothorax: 2° to COPD, TB, trauma, Pneumocystis jiroveci (formerly P. carinii) pneumonia, and iatrogenic factors (thoracentesis, subclavian line placement, positive-pressure mechanical ventilation, bronchoscopy). Tension pneumothorax: A pulmonary or chest wall defect acts as a one-way valve, drawing air into the pleural space during inspiration but trapping air during expiration. Etiologies include penetrating trauma, infection, and positive-pressure mechanical ventilation. Shock and death result unless the condition is immediately recognized and treated. Presents with acute onset of unilateral pleuritic chest pain and dyspnea. Exam reveals tachypnea, diminished or absent breath sounds, hyperreso F IGU R E 2.1 5-7. Tension pneumothorax. Note the hyperlucent lung feld, hyperexpanded lower diaphragm, collapsed lung, tracheal de viation, mediastinal shift, and compression of the opposite lung on AP CXR.


First_Aid_Step2

First_Aid_Step2. Note the hyperlucent lung feld, hyperexpanded lower diaphragm, collapsed lung, tracheal de viation, mediastinal shift, and compression of the opposite lung on AP CXR. nance, ↓tactile fremitus, and JVD 2° to compression of the superior vena cava. ■Suspect tension pneumothorax in the presence of tracheal deviation, respiratory distress, falling O2 saturation, hypotension, and distended neck veins. CXR shows the presence of a visceral pleural line and/or lung retraction from the chest wall (best seen in end-expiratory flms; see Figure 2.15-7). Small pneumothoraces may resorb spontaneously. Supplemental O2 therapy is helpful. Large, symptomatic pneumothoraces require chest tube placement. Tension pneumothorax requires immediate needle decompression (second intercostal space at the midclavicular line) followed by chest tube placement.


First_Aid_Step2

First_Aid_Step2. Tension pneumothorax requires immediate needle decompression (second intercostal space at the midclavicular line) followed by chest tube placement. In hypernatremia, certain patients (e.g., infants, intubated patients, those with a change in mental status) may not drink enough free water to replace insensible losses. Hypernatremia causes— The 6 D’s Diuresis Dehydration Diabetes insipidus Docs (iatrogenic) Diarrhea Disease (e.g., kidney, sickle cell) Serum sodium > 145 mEq/L. Usually due to water loss rather than sodium gain. Presents with thirst (due to hypertonicity) as well as with oliguria or polyuria (depending on the etiology). Neurologic symptoms include mental status changes, weakness, focal neurologic deficits, and seizures. Exam reveals “doughy” skin and signs of volume depletion. Assess volume status by conducting a clinical exam and measuring urine volume and osmolality. Hypertonic Na+ gain: Due to hypertonic saline/tube feeds or ↑aldosterone (suppresses ADH).


First_Aid_Step2

First_Aid_Step2. Assess volume status by conducting a clinical exam and measuring urine volume and osmolality. Hypertonic Na+ gain: Due to hypertonic saline/tube feeds or ↑aldosterone (suppresses ADH). Pure water loss: Due to central or nephrogenic diabetes insipidus; characterized by large volumes of dilute urine. Do not neglect dermal and respiratory insensible losses. Hypotonic f uid loss: Due to ↓ intake, diuretics, intrinsic renal disease, GI losses (diarrhea), burns, and osmotic diuresis (mannitol, glucose in DKA, urea with high protein feeds). A minimal volume (approximately 500 ml/day) of maximally concentrated urine (> 800 mOsm/kg) suggests adequate renal response without adequate free-water replacement. Treat the underlying causes and replace free-water deficit with hypotonic saline, D5W, or oral water, depending on volume status.


First_Aid_Step2

First_Aid_Step2. Treat the underlying causes and replace free-water deficit with hypotonic saline, D5W, or oral water, depending on volume status. Correction of chronic hypernatremia (> 36–48 hours) should be accomplished gradually over 48–72 hours (≤ 0.5 mEq/L/hr) to prevent neurologic damage 2° to cerebral edema. Serum sodium < 135 mEq/L. Almost always due to ↑ ADH. May be asymptomatic or may present with confusion, lethargy, muscle cramps, hyporeﬂexia, and nausea. Can progress to seizures, coma, or brain stem herniation. Hyponatremia can be categorized according to serum and urine osmolality as well as by volume status (i.e., by clinical exam). Osmolality is classified as follows: High (> 295 mEq/L): Hyperglycemia, hypertonic infusion (e.g., mannitol). Normal (280–295 mEq/L): Hypertriglyceridemia, paraproteinemia (pseudohyponatremia).


First_Aid_Step2

First_Aid_Step2. High (> 295 mEq/L): Hyperglycemia, hypertonic infusion (e.g., mannitol). Normal (280–295 mEq/L): Hypertriglyceridemia, paraproteinemia (pseudohyponatremia). Hypervolemic hyponatremia is caused by “nephrOSIS, cirrhOSIS, and cardiOSIS.” ■ Low (< 280 mEq/L): Applies to the majority of cases. Hypotonic etiolog ies are listed in Table 2.16-1. Specific treatments are outlined in Table 2.16-1. Chronic hyponatremia (> 72 hours’ duration) should be corrected slowly (no more than 0.5 mEq/L/hr) in order to prevent central pontine myelinolysis (symptoms include paraparesis/quadriparesis, dysarthria, and coma). Serum potassium > 5 mEq/L. Etiologies are as follows: Spurious: Hemolysis of blood samples, fist clenching during blood draws, delays in sample analysis, extreme leukocytosis or thrombocytosis. ■↓excretion: Renal insufficiency, drugs (e.g., spironolactone, triamterene, ACEIs, trimethoprim, NSAIDs), hypoaldosteronism, type IV renal tubular acidosis (RTA).


First_Aid_Step2

First_Aid_Step2. ■↓excretion: Renal insufficiency, drugs (e.g., spironolactone, triamterene, ACEIs, trimethoprim, NSAIDs), hypoaldosteronism, type IV renal tubular acidosis (RTA). Cellular shifts: Cell lysis, tissue injury (rhabdomyolysis), insulin deficiency, acidosis, drugs (e.g., succinylcholine, digitalis, arginine, β-blockers), exercise. Iatrogenic. May be asymptomatic or may present with nausea, vomiting, intestinal colic, aref exia, weakness, ﬂaccid paralysis, and paresthesias. Confirm hyperkalemia with a repeat blood draw. In the setting of extreme leukocytosis or thrombocytosis, check plasma potassium. ECG findings include tall, peaked T waves; a wide QRS; PR prolongation; and loss of P waves (see Figure 2.16-1). Can progress to sine waves, ventricular fibrillation, and cardiac arrest. T AB LE 2.1 6-1. Evaluation and Treatment of Hypotonic Hyponatremia


First_Aid_Step2

First_Aid_Step2. T AB LE 2.1 6-1. Evaluation and Treatment of Hypotonic Hyponatremia Consider using hypertonic saline only if a patient has seizures due to hyponatremia, and use it cautiously and brief y. In most instances, normal saline is the best replacement f uid. What dreaded complication can arise from treating hyponatremia too rapidly? Central pontine myelinolysis. Hypervolemic Renal failure, nephrotic syndrome, cirrhosis, CHF, hypothyroidism, 2° or 3° adrenal insuff ciency. Water restriction; consider diuretics; cortisol replacement with adrenal insuff ciency; thyroid replacement with hypothyroidism. Euvolemic SIADH, renal failure, drugs, psychogenic polydipsia, oxytocin use. Water restriction. Hypovolemic Diuretics (especially thiazides), vomiting, diarrhea, bleeding, third spacing, dehydration, DKA, 1° adrenal insuff ciency. Replete volume with normal saline. FIGURE 2.16-1. Hyperkalemia on ECG. Hypokalemia is usually due to renal or GI losses


First_Aid_Step2

First_Aid_Step2. FIGURE 2.16-1. Hyperkalemia on ECG. Hypokalemia is usually due to renal or GI losses Hypokalemia sensitizes the heart to digitalis toxicity because K+ and digitalis compete for the same sites on the Na+/K+ pump, so if a patient is on digitalis, potassium levels must be carefully monitored. Electrocardiographic manifestations include peaked T waves, PR prolongation, and a widened QRS complex. (Reproduced, with permission, from Cogan MG. Fluid and Electrolytes, 1st ed. Stamford, CT: Appleton & Lange, 1991: 170.) Values of > 6.5 mEq/L or ECG changes (especially PR prolongation or wide QRS) require emergent treatment. The mnemonic C BIG K summarizes the treatment of hyperkalemia. First give calcium gluconate for cardiac cell membrane stabilization. Give bicarbonate and/or insulin and glucose to temporarily shift potassium into cells. β-agonists (e.g., albuterol) promote cellular reuptake of potassium. Eliminate potassium from diet and IV ﬂ uids.


First_Aid_Step2

First_Aid_Step2. β-agonists (e.g., albuterol) promote cellular reuptake of potassium. Eliminate potassium from diet and IV ﬂ uids. Kayexalate to remove potassium from the body. Dialysis is appropriate for patients with renal failure or for severe, refractory cases. Serum potassium < 3.6 mEq/L. Etiologies are as follows: Transcellular shifts: Insulin, β2-agonists, alkalosis, familial hypokalemic periodic paralysis. GI losses: Diarrhea, chronic laxative abuse, vomiting, NG suction. Renal losses: Diuretics (e.g., loop or thiazide), 1° mineralocorticoid excess or 2° hyperaldosteronism, ↓ circulating volume, Bartter’s and Gitelman’s syndromes, drugs (e.g., gentamicin, amphotericin), DKA, hypomagnesemia, type I RTA (defective distal H+ secretion), polyuria. Presents with fatigue, muscle weakness or cramps, ileus, hypotension, hyporeﬂexia, paresthesias, rhabdomyolysis, and ascending paralysis. Twenty-four-hour or spot urine potassium may distinguish renal from GI losses.


First_Aid_Step2

First_Aid_Step2. Twenty-four-hour or spot urine potassium may distinguish renal from GI losses. ECG may show T-wave fattening, U waves (an additional wave after the T wave), and ST-segment depression, leading to AV block and subsequent cardiac arrest. Consider RTA in the setting of metabolic acidosis. Treat the underlying disorder. Oral and/or IV potassium repletion. Do not exceed 20 mEq/L/hr. Replace magnesium, as this deficiency complicates potassium repletion. Monitor ECG and plasma potassium levels frequently during replacement. Serum calcium > 10.2 mg/dL. The most common causes are hyperparathyroidism and malignancy (e.g., breast cancer, squamous cell carcinoma, multiple myeloma). Other causes are summarized in the mnemonic CHIMPANZEES. Usually asymptomatic and discovered by routine labs, but may present with bones (osteopenia, fractures), stones (kidney stones), abdominal groans (anorexia, constipation), and psychiatric overtones (weakness, fatigue, altered mental status).


First_Aid_Step2

First_Aid_Step2. Order a total/ionized calcium, albumin, phosphate, PTH, parathyroid hormone–related peptide (PTHrP), vitamin D, and ECG (may show a short QT interval). IV hydration followed by furosemide to ↑ calcium excretion. Calcitonin, bisphosphonates (e.g., pamidronate), glucocorticoids, calcimimetics, and dialysis are used for severe or refractory cases. Avoid thiazide diuretics, which ↑ tubular reabsorption of calcium. Serum calcium < 8.5 mg/dL. Etiologies include hypoparathyroidism (postsurgical, idiopathic), malnutrition, hypomagnesemia, acute pancreatitis, vitamin D deficiency, and pseudohypoparathyroidism. In infants, consider DiGeorge’s syndrome (tetany shortly after birth; absence of thymic shadow). Presents with abdominal muscle cramps, dyspnea, tetany, perioral and acral paresthesias, and convulsions.


First_Aid_Step2

First_Aid_Step2. Presents with abdominal muscle cramps, dyspnea, tetany, perioral and acral paresthesias, and convulsions. Facial spasm elicited from tapping of the facial nerve (Chvostek’s sign) and carpal spasm after arterial occlusion by a BP cuff (Trousseau’s sign) are classic findings that are most commonly seen in severe hypocalcemia. Order an ionized Ca2+, Mg+, PTH, albumin, and possibly calcitonin. If the patient is post-thyroidectomy, review the operative note to determine the number of parathyroid glands removed. ECG may show a prolonged QT interval. Causes of hypercalcemia— Hyperthyroidism Iatrogenic (e.g., thiazides, parenteral (e.g., MEN 1) Excess vitamin A Excess vitamin D Sarcoidosis and other Loops (furosemide) Lose calcium. A classic case of hypocalcemia is a patient who develops cramps and tetany following thyroidectomy. Serum calcium may be falsely low in hypoalbuminemia; check ionized calcium. Treat the underlying disorder. Magnesium repletion.


First_Aid_Step2

First_Aid_Step2. Serum calcium may be falsely low in hypoalbuminemia; check ionized calcium. Treat the underlying disorder. Magnesium repletion. Administer oral calcium supplements; give IV calcium for severe symptoms. Serum magnesium < 1.5 mEq/L. Etiologies are as follows: ■↓intake: Malnutrition, malabsorption, short bowel syndrome, TPN. ■↑loss: Diuretics, diarrhea, vomiting, hypercalcemia, drugs (e.g., aminoglycosides, amphotericin), alcoholism, kidney losses (e.g., recovering ATN, postobstructive diuresis). ■ Miscellaneous: DKA, pancreatitis, extracellular ﬂuid volume expansion. Symptoms are generally related to concurrent hypocalcemia and hypokalemia; they include anorexia, nausea, vomiting, muscle cramps, and weakness. In severe cases, symptoms may also include hyperactive reﬂ exes, tetany, paresthesias, irritability, confusion, lethargy, seizures, and arrhythmias. Labs may show concurrent hypocalcemia and hypokalemia. ECG may reveal prolonged PR and QT intervals.


First_Aid_Step2

First_Aid_Step2. Labs may show concurrent hypocalcemia and hypokalemia. ECG may reveal prolonged PR and QT intervals. IV and oral supplements. Hypokalemia and hypocalcemia will not correct without magnesium correction. See Figure 2.16-2 for a diagnostic algorithm of acid-base disorders. A net ↓ in either tubular H+ secretion or HCO3 reabsorption that leads to a non–anion gap metabolic acidosis. There are three main types of RTA; type IV (distal) is the most common form (see Table 2.16-2). An abrupt ↓ in renal function leading to the retention of creatinine and BUN. ↓ urine output (oliguria, defined as < 500 cc/day) is not required for ARF. ARF is categorized as follows (see also Table 2.16-3): Prerenal: ↓ renal perfusion. Intrinsic: Injury within the nephron unit. Postrenal: Urinary outﬂow obstruction. Generally, both kidneys must be obstructed before one can see a significant ↑ in BUN and creatinine. Alcoholics are the most common patient population with hypomagnesemia.


First_Aid_Step2

First_Aid_Step2. Alcoholics are the most common patient population with hypomagnesemia. Aspirin (salicylate) overdose can cause both a metabolic acidosis and a respiratory alkalosis. If an asthmatic patient’s blood gas goes from alkalotic to normal, it can be a sign of respiratory muscle fatigue, which requires urgent intubation. pH < 7.4 pH > 7.4 Acidosis Alkalosis Respiratory Metabolic Respiratory alkalosis acidosis acidosis with –Hyperventilation compensation –Aspirin ingestion (early) –Chronic lung disease –Opioids, narcotics, sedatives –Weakening of F IGU R E 2.1 6-2. Diagnostic algorithm for acid-base disorders. Metabolic alkalosis with compensation –Vomiting –Diuretic use –Antacid use –Hyperaldosteronism Symptoms of uremia include malaise, fatigue, confusion, oliguria, anorexia, and nausea. Exam may show a pericardial rub, asterixis, hypertension, ↓ urine output, and an ↑ respiratory rate (compensation of metabolic acidosis or from pulmonary edema 2° to volume overload)


First_Aid_Step2

First_Aid_Step2. Exam may show a pericardial rub, asterixis, hypertension, ↓ urine output, and an ↑ respiratory rate (compensation of metabolic acidosis or from pulmonary edema 2° to volume overload) Category-specific symptoms are as follows: Prerenal: Thirst, orthostatic hypotension, tachycardia, ↓ skin turgor, dry mucous membranes, reduced axillary sweating, stigmata of comorbid conditions. Intrinsic: Associated with a history of drug exposure (aminoglycosides, NSAIDs), infection, or exposure to contrast media or toxins (e.g., myoglobin, myeloma protein). Hematuria or tea-colored urine, foamy urine (from proteinuria), hypertension, and/or edema may also be present. Atheroemboli: Subcutaneous nodules, livedo reticularis, digital ischemia. Postrenal: Prostatic disease, ↓ urine output leading to suprapubic pain, distended bladder and ﬂ ank pain. Check serum electrolytes. Examine the urine for RBCs, WBCs, casts (see Table 2.16-4), and urine eosinophils.


First_Aid_Step2

First_Aid_Step2. Check serum electrolytes. Examine the urine for RBCs, WBCs, casts (see Table 2.16-4), and urine eosinophils. An FeNa < 1%, a UNa < 20, a urine specifc gravity > 1.020, or a BUN/Cr ratio > 20 suggests a prerenal etiology. A urinary catheter and renal ultrasound can help rule out obstruction. Ultrasound can also identify kidneys that are ↓ in size, as occurs with chronic kidney disease. Patients with ARF may have a normal urine volume. An FeNa < 1% indicates that the kidneys are trying to conserve sodium, suggesting a prerenal etiology. TABLE 2.16-2. Types of Renal Tubular Acidosis


First_Aid_Step2

First_Aid_Step2. Defect H+ secretion HCO3 – reabsorption Aldosterone def ciency or resistance, leading to defects in Na+ reabsorption and H+ and K+ excretion Serum K+ Low Low High Urinary pH > 5.3 5.3 initially; < 5.3 once serum is acidic < 5.3 Etiologies (most common) Hereditary, cirrhosis, autoimmune disorders (Sjren’s syndrome, SLE), hypercalciuria, sickle cell disease, drugs (lithium, amphotericin) Hereditary (idiopathic or part of syndromes such as Fanconi’s syndrome or cystinosis), drugs (carbonic anhydrase inhibitors), multiple myeloma, amyloidosis, heavy metal poisoning, vitamin D def ciency 1° aldosterone def ciency, hyporeninemic hypoaldosteronism (e.g., from kidney disease, ACEIs, NSAIDs), drugs (e.g., amiloride, spironolactone, heparin), pseudohypoaldosteronism Potassium citrate Potassium citrate Furosemide, mineralocorticoid +/– glucocorticoid replacement, and low-potassium diet in patients with aldosterone def ciency Nephrolithiasis Rickets, osteomalacia Hyperkalemia Treatment


First_Aid_Step2

First_Aid_Step2. citrate Furosemide, mineralocorticoid +/– glucocorticoid replacement, and low-potassium diet in patients with aldosterone def ciency Nephrolithiasis Rickets, osteomalacia Hyperkalemia Treatment Complications


First_Aid_Step2

First_Aid_Step2. TABLE 2.16-3. Causes of Acute Renal Failure Acute tubular necrosis (ATN) Acute/allergic interstitial nephritis Glomerulonephritis Thromboembolism Renovascular disease (HUS/TTP, scleroderma) Prostatic disease Nephrolithiasis Pelvic tumors Recent pelvic surgery Retroperitoneal f brosis Hypovolemia (hemorrhage, dehydration, burns) Cardiogenic shock (↓ CO) Systemic vasodilation (sepsis, burns) Anaphylaxis Drugs (ACEIs, ARBs, NSAIDs) Renal artery stenosis Cirrhosis with ascites T AB LE 2.1 6-4. Findings on Microscopic Urine Examination in Acute Renal Failure Hyaline casts Normal fnding, but an ↑ amount suggests volume depletion Prerenal Red cell casts, dysmorphic red cells Glomerulonephritis Intrinsic White cells, eosinophils Allergic interstitial nephritis, atheroembolic disease Intrinsic Granular casts, renal tubular cells, “muddy-brown cast” ATN Intrinsic White cells, white cell casts Pyelonephritis Postrenal