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R. Giores, M.B.A., M.D.
Medical Instructor, New York University Long Island School of Medicine
Pregnancy category is "D" for all other indications (high-dose use during first trimester of pregnancy may result in birth defects). Bone marrow suppression in immunosuppressed patients can be irreversible and fatal. Patients with only a partial response to 3 mg may require additional slow titration to a total of 5 mg. If patient does not respond after cumulative 13-mg dose, suspect agent other than benzodiazepines. May precipitate seizures, especially in patients taking benzodiazepines for seizure control or in patients with tricyclic antidepressant overdose. Use normal dose for initial dose and decrease the dosage and frequency for subsequent doses. Do not use a spacer with Aerospan because the product has a self-contained spacer. Use with caution in patients with angle-closure glaucoma, receiving diuretics, or with liver (reduce dose with cirrhosis) or renal impairment. Increased bleeding diathesis with unaltered prothrombin time may occur with warfarin. Delayed-release capsule is currently indicated for depression and is dosed at 90 mg Q7 days. Breast-feeding is not recommended by the manufacturer as adverse events in nursing infants have been reported. Vilanterol is a long-acting 2-adrenergic agonist with a faster onset and longer duration of action compared to salmeterol. Fluticasone propionate and fluticasone furoate do not have equivalent potencies; follow specific dosing regimens for the respective products. Occlusive dressings are not recommended because they may increase local side effects (irritation, folliculitis, acneiform eruptions, hypopigmentation, perioral dermatitis, contact dermatitis, secondary infection, skin atrophy, striae, hypertrichosis, and miliaria). Dose may be increased by 25 mg/24 hr Q714 days (slower titration for minimizing behavioral side effects). Use with caution in hepatic disease (dosage reduction may be necessary); drug is extensively metabolized by the liver. May mask hematologic effects of vitamin B12 deficiency but will not prevent the progression of neurologic abnormalities. Contraindicated in hypersensitivity to any components or other pyrazole compounds. Fomepizole is extensively eliminated by the kidneys (use with caution in renal failure) and removed by hemodialysis. Inhalation solution (Perforomist): 20 mcg/2 mL (60s) 5 yr and adult: Asthma/Bronchodilation (should be used with an inhaled corticosteroid): Foradil Aerolizer: 12 mcg Q12 hr; max. Use with caution in seizures, thyrotoxicosis, diabetes, ketoacidosis, aneurysm, and pheochromocytoma. Hypocalcemia (increased risk if given with pentamidine), hypokalemia, and hypomagnesemia may also occur. For lower foscarnet dosage regimens of 4060 mg/kg, use 50% of the aforementioned hydration recommendations. Oral hydration methods may also be considered in patients who are able to tolerate. Drug is also metabolized to liberate small amounts of formaldehyde, which is considered clinically insignificant with short-term use. May cause hypokalemia, alkalosis, dehydration, hyperuricemia, and increased calcium excretion. Prolonged use in premature infants and in children <4 yr may result in nephrocalcinosis. Some of these patients may have an exaggerated response leading to hypovolemia, tachycardia, and orthostatic hypotension requiring fluid replacement. Usual dosage range: 835 mg/kg/24 hr Maximum daily dose of 3600 mg/24 hr has been suggested but not formally evaluated. Somnolence, dizziness, ataxia, fatigue, and nystagmus were common when used for seizures (12 yr). Viral infections, fever, nausea and/or vomiting, somnolence, and hostility have been reported in patients aged 312 yr receiving other antiepiletics. Drug is not metabolized by the liver and is primarily excreted unchanged in the urine.
Concomitant use of other topical acne products may lead to significant skin irritation. Onset of therapeutic benefits may be experienced within 23 wk with optimal effects in 6 wk. Injection as acetonide: 10 mg/mL (Kenalog-10) (5 mL), 40 mg/mL (Kenalog-40) (1, 5, 10 mL); contains benzyl alcohol and polysorbate 80 Kits (all contain benzyl alcohol and polysorbate 80): ReadySharp Triamcinolone: 40 mg/mL (1 Ч 1 mL) Pro-C-Dure 5: 40 mg/mL (2 x 1 mL) Arze-Ject-A, Pro-C-Dure 6: 40 mg/mL (3 Ч 1 mL) Intranasal (titrate to lowest effective dose after symptoms are controlled; discontinue use if no relief of symptoms occur after 3 wk of use): Child 25 yr: 1 spray in each nostril once daily (110 mcg/24 hr; starting and max. Topical steroids should be used with caution on the face and in intertriginous areas. With systemic use, pregnancy category changes to "D" if used in the first trimester. Reduce dose when there is reepithelialization of the corneal ulcer Continued Yes Yes? Avoid touching the applicator tip to eyes, fingers, or other surfaces and do not wear contact lenses during treatment of ocular infections. Use with caution in patients with nonvisualizing gallbladder and chronic liver disease. Aluminum-containing antacids, cholestyramine, and oral contraceptives decrease ursodiol effectiveness. This prodrug is metabolized to acyclovir and L-valine with better oral absorption than acyclovir. For initial episodes of genital herpes, therapy is most effective when initiated within 48 hr of symptom onset. Therapy should be initiated immediately after the onset of symptoms in recurrent episodes (no efficacy data when initiating therapy > 24 hr after onset of symptoms). Use with caution in renal insufficiency (adjust dose; see Chapter 30), preexisting bone marrow suppression, or in those receiving myelosupressive drugs or irradiation. Use effective contraception during and for at least 90 days after therapy; may impair fertility in men and women. If using divalproex sodium extended-release tablets, administer daily dose once daily. Idiosyncratic life-threatening pancreatitis has been reported in children and adults. Hyperammonemic encephalopathy has been reported in patients with urea cycle disorders. It increases amitriptyline/nortriptyline, rufinamide, phenytoin, diazepam, and phenobarbital levels. Concomitant phenytoin, phenobarbital, topiramate, meropenem, cholestyramine, and carbamazepine may decrease valproic acid levels. Use with caution in renal and liver insufficiency (no data are available), heart failure, postmyocardial infarction, renal artery stenosis, renal function changes, and volume depletion. Onset of initial antihypertensive effects is 2 hr with maximum effects after 24 wk of chronic use. Patients may require higher doses of oral tablet dosage form than with the oral suspension due to increased bioavailability with the oral suspension. Greater nephrotoxicity risk has been associated with higher therapeutic serum trough concentrations (15 mg/mL), concurrent piperacillin/tazobactam therapy, and receiving furosemide in the intensive care unit. Although current extrapolated adult guidelines suggest measuring only trough levels, an additional postdistributional level may be useful in characterizing enhanced/altered drug clearance for quicker dosage modification to attain target levels; this may be useful for infants with known faster clearance and patients in renal compromise. Recommended serum sampling time at steady-state: Trough within 30 min prior to the fourth consecutive dose and peak 60 min after the administration of the fourth consecutive dose. Infants with faster elimination (shorter T1/2) may be sampled around the third consecutive dose. Common adverse effects with oral vancomycin capsules in adults include nausea, abdominal pain, and hypokalemia. Pregnancy category "C" for the intravenous route and "B" for the oral route of administration. Local discomfort, redness and swelling at the injection site, and headache may occur. Cardiac arrest, ventricular fibrillation, and pulseless ventricular tachycardia: Child (use following 2 doses of epinephrine; limited data): 0. Use with caution in seizures; migrane; asthma; and renal, cardiac, or vascular diseases.
Presumptive diagnosis can be made from history, changes on chest x-ray, blood and sputum culture and sputum Gram stains. Response In mildly ill patients who are treated early, fever subsides in 24 to 48 hrs. If a patient does not improve, the following factors should be considered: Wrong etiologic diagnosis Adverse drug reaction Far advanced case or superinfection Inadequate host defenses due to associated condition Non-compliance to the drug regimen in outpatients Antibiotic resistance of the strain and Complications like empyema requiring drainage, or metastatic foci of infection requiring higher doses. Choice of Antibiotics may be modified based on culture and sensitivity results, if available. Pathogens like Streptococcus pneumonia, which cause pneumonia in immunocompetent people, are still responsible for the majority of pneumonia in compromised patients. Diagnosis: · · · Sputum examination and culture are used but they are not specific. Transtracheal aspirate, bronchoscopy and biopsy have high accuracy; however these are done only in specialized hospitals. High index of suspicion from clinical presentation is important to diagnose pneumonia in immunocompromised hosts. Treatment: · Acutely ill patients who have suspected bacterial infections are often treated with antibiotics selected on the basis of probabilities and the findings with sputum gram stain and culture. Later treatment is adjusted on the basis of more definitive diagnostic evaluation. Bronchial Asthma Learning Objective: At the end of this unit the student will be able to 1. Definition: Bronchial asthma is defined as chronic inflammatory disease of airways characterized by increased responsiveness of the tracheobronchial tree to a multiplicity of stimuli. It is associated with widespread airway obstruction that is reversible (but not completely in some patients), either spontaneously or with treatment Epidemiology: · · · Asthma is a common disease the prevalence of asthma is rising in different parts of the world. About 50% of patients develop asthma before the age of 10 and another 35% before the age of 40. Males are affected twice as common as females in early life; this sex difference equalizes by age 30. Most cases of asthma are associated with personal or family history of allergic disease such as eczema, rhinitis and urticaria. Etiology Asthma is a heterogeneous disease and genetic (atopic) and environmental factors such as viruses, occupational exposure and allegens contribute to its initiation and continuance. In general asthma which has its onset early in life tends to have strong allergic component, where as asthma that develops late in life tends to be nonallergic or to have mixed etiology. Factors important for the genesis of asthma · Genetic factors o · · · · Asthma has strong genetic predisposition or familial tendency Elevated positive Normal Negative Negative skin test injection of allergens Early in life Present Late in life Absent Non Allergic (idiosyncratic) Stimuli that incite Asthma Allergens: Seasonal allergens such as pollen green Non seasonal animal feathers, dust mites, molds Pharmacologic stimuli: Aspirin, Tatrazin (coloring agent), Beta blockers such as Propranolol etc Environmental and air pollution: in industrial and heavily populated areas. Infections: Respiratory infections are the most common of the stimuli that evoke acute exacerbation of asthma. The cells thought to play important part in the inflammatory response are mast cells, eosinophils, lymphocytes and airway epithelial cells. These cells release inflammatory mediators which may result · · · · · · Bronchoconstriction (spasm of airways smooth muscles) Vascular congestion and edema of airways mucosa Increased mucus production Injury and desquamation of the airways epithelium and impaired muco-ciliary transport the symptoms of each asthmatic patient differ greatly in frequency and degree. Some asthmatics are symptom free, with an occasional episode that is mild and brief; others have mild coughing and wheezing much of the time, punctuated by severe exacerbations of symptoms following exposure to known allergens, viral infection, exercise etc. Psychological factors particularly those associated with crying, screaming or hard laughing may precipitate symptoms. The asthmatic first notices dyspnea, tachypnea, cough and tightness in the chest and may even notice audible wheezes. On physical examination · · · · · · Varying degrees of respiratory distress tachypnea, tachycardia, and audible wheezes are often present. Chest examination shows a prolonged expiratory phase with relatively high pitched wheezes throughout inspiration and most of expiration. In more severe episodes, patients may be unable to speak more than a few words without stopping for breath.
Prefrontal regions, especially area 6, and parietal areas 5 and 7 also contribute to the corticospinal tract. Neurotransmitters: Acetylcholine, gamma-aminobutyric acid (), and substance P (, plus other peptides) are found in small cortical neurons presumed to function as local circuit cells or in corticocortical connections. Glutamate () is present in cortical efferent fibers that project to the spinal cord. Glutaminergic corticospinal fibers and terminals are found in all spinal levels but are especially concentrated in cervical and lumbosacral enlargements. This correlates with the fact that approximately 55% of all corticospinal fibers terminate in cervical levels of the spinal cord, approximately 20% in thoracic levels, and approximately 25% in lumbosacral levels. Lower motor neurons are influenced by corticospinal fibers either directly or indirectly via interneurons. Acetylcholine and calcitonin gene-related peptides are present in these large motor cells and in their endings in skeletal muscle. Clinical Correlations: Myasthenia gravis, a disease characterized by moderate to profound weakness of skeletal muscles, is caused by circulating antibodies that react with postsynaptic nicotinic acetylcholine receptors. Ocular muscles are usually affected first (diplopia, ptosis), and in approximately 50% of patients, facial and oropharyngeal muscles are commonly affected (facial weakness, dysphagia, dysarthria). Weakness may also be seen in limb muscles but almost always in combination with facial/oral weaknesses. Injury to corticospinal fibers on one side of the cervical spinal cord (as in the Brown-Sequard syndrome) results in weakness (hemiparesis) or paralysis (hemiplegia) of the ipsilateral upper and lower extremities. In addition, and with time, these patients may exhibit features of an upper motor neuron lesion (hyperreflexia, spasticity, loss of superficial abdominal reflexes, and the Babinski sign). Bilateral cervical spinal cord damage above C4C5 may result in paralysis of all four extremities (quadriplegia). Unilateral spinal cord lesions in thoracic levels may result in paralysis of the ipsilateral lower extremity (monoplegia). If the thoracic spinal cord damage is bilateral both lower extremities may be paralyzed (paraplegia). Small lesions within the decussation of the pyramids may result in a bilateral paresis of the upper extremities (lesion in rostral portions) or a bilateral paresis of the lower extremities (lesion in caudal portions) based on the crossing patterns of fibers within the decussation. Rostral to the pyramidal decussation, vascular lesions in the medulla (the medial medullary syndrome), pons (the Millard-Gubler or Foville syndromes), or midbrain (the Weber syndrome) all produce alternating (crossed) hemiplegias. These present as a contralateral hemiplegia of the upper and lower extremities, coupled with an ipsilateral paralysis of the tongue (medulla), facial muscles or lateral rectus muscle (pons), and most eye movements (midbrain). Lesions in the internal capsule (lacunar strokes) produce contralateral hemiparesis sometimes coupled with various cranial nerve signs due to corticonuclear (corticobulbar) fiber involvement. Bilateral weakness, indicative of corticospinal involvement, is also present in amyotrophic lateral sclerosis. These fibers influence-either directly or through neurons in the immediately adjacent reticular formation-the motor nuclei of oculomotor, trochlear, trigeminal, abducens, facial, glossopharyngeal and vagus (both via nucleus ambiguus), spinal accessory, and hypoglossal nerves. Corticonuclear (corticobulbar) fibers arise in the frontal eye fields (areas 6 and 8 in caudal portions of the middle frontal gyrus), the precentral gyrus (somatomotor cortex, area 4), and some originate from the postcentral gyrus (areas 3,1, 2). Fibers from area 4 occupy the genu of the internal capsule, but those from the frontal eye fields (areas 8,6) may traverse caudal portions of the anterior limb, and some (from areas 3,1,2), may occupy the most rostral portions of the posterior limb. In addition, it is important to note that descending cortical fibers (many arising in areas 3, 1, 2) project to sensory relay nuclei of some cranial nerves and to other sensory relay nuclei in the brainstem, such as those of the posterior column system. Neurotransmitters: Glutamate () is found in many corticofugal axons that directly innervate cranial nerve motor nuclei and in those fibers that terminate near (indirect), but not in, the various motor nuclei. Clinical Correlations: Lesions involving the motor cortex (as in cerebral artery occlusion) or the internal capsule (as in lacunar strokes or occlusion of lenticulostriate branches of M1) give rise to a contralateral hemiplegia of the arm and leg (corticospinal fiber involvement) coupled with certain cranial nerve signs. Strictly cortical lesions may produce a transient gaze palsy in which the eyes deviate toward the lesioned side and away from the side of the hemiplegia. In addition to a contralateral hemiplegia, common cranial nerve findings in capsular lesions may include 1) deviation of the tongue toward the side of the weakness and away from the side of the lesion when protruded and 2) paralysis of facial muscles on the contralateral lower half of the face (central facial palsy). This reflects the fact that corticonuclear (corticobulbar) fibers to genioglossus motor neurons and to facial motor neurons serving the lower face are primarily crossed. Interruption of corticonuclear fibers to the nucleus ambiguus may result in weakness of palatal muscles contralateral to the lesion; the uvula will deviate towards the ipsilateral (lesioned) side on attempted phonation. In addition, a lesion involving corticonuclear fibers to the accessory nucleus may result in drooping of the ipsilateral shoulder (or an inability to elevate the shoulder against resistance) due to trapezius weakness, and difficulty in turning the head (against resistance) to the contralateral side due to weakness of the sternocleidomastoid muscle. In contrast to the alternating hemiplegia seen in some brainstem lesions, hemisphere lesions result in spinal and cranial nerve deficits that are generally, but not exclusively, contralateral to the cerebral injury.
For example, the combination of olanzapine and fluoxetine has been extensively studied (449452) and is typically initiated with 6 mg of olanzapine and 25 mg of fluoxetine daily and titrated upward as tolerated to a maximum of 18 mg of olanzapine and 75 mg of fluoxetine daily. With quetiapine, doses of 25 to 400 mg/day have been used, with benefits for depressive symptoms found in some (454, 455) but 55 not all (456) clinical trials. Risperidone augmentation, in doses of up to 3 mg daily (457, 458) also appears to improve the response to antidepressant agents. In most of these trials, the onset of the effect of second-generation antipsychotic augmentation has been rapid, although the magnitude of the advantage relative to placebo has been relatively modest. In the only two trials to utilize active comparison groups, the combination of olanzapine and fluoxetine was not significantly more effective at study endpoint than continued therapy with nortriptyline (450) or venlafaxine (451). Naturalistic follow-up data also suggest that long-term weight gain can be problematic for many patients receiving second-generation antipsychotic augmentation therapy, particularly with the olanzapine-fluoxetine combination (459). When compared with other strategies for antidepressant nonresponders, augmentation with a second-generation antipsychotic carries disadvantages: the high cost of many agents, the significant risk of weight gain and other metabolic complications. Thus, the advantages and disadvantages of antipsychotic medications should be considered when choosing this augmentation strategy. In addition, when augmentation with a second-generation antipsychotic is effective, it is uncertain how long augmentation therapy should be maintained. Many clinicians find that augmentation of antidepressants with low doses of stimulants such as methylphenidate or dextroamphetamine may help ameliorate otherwise suboptimally responsive depression (460462), although not all clinical trials have shown benefits from this strategy (463). Although there are no clear guidelines regarding the length of time stimulants or modafinil should be coadministered, in one extension study the effects of modafinil were maintained across 12 weeks of additional therapy (468). Physicians prescribing modafinil for this off-label use should become familiar with rare but dangerous cutaneous reactions to it, including reported instances of Stevens-Johnson syndrome, toxic epidermal necrolysis, drug rash with eosinophilia and systemic symptoms (469), and cytochrome P450 interactions. As with any surgical device implantation, there is a small risk of postsurgical infection (482). A majority of individuals experience hoarseness or voice alteration during stimulation, and coughing, dyspnea, and neck discomfort are common (281, 481) but generally are tolerable to patients (282, 479). The possibility of relapse should be carefully monitored during the continuation phase as this is when risk of relapse is highest (483). There is evidence that patients who do not completely recover during acute treatment have a significantly higher risk of relapse (and a greater need for continuation treatment) than those who have no residual symptoms (227, 491, 492). Similarly, patients who have not fully achieved remission with psychotherapy are at greater risk of relapse in the near term (364, 365, 367, 493, 494). To reduce the risk of relapse during the continuation phase, treatment should generally continue at the same dose, intensity, and frequency that were effective during the acute phase. Although the number of randomized controlled trials of antidepressant medications in the continuation phase is limited, the available data indicate that patients treated for a first episode of uncomplicated major depressive disorder who exhibit a satisfactory response to an antidepressant medication should continue to receive a full therapeutic dose of that agent for at least 49 months after achieving full remission (105, 225, 495). Cognitive-behavioral therapy may prevent relapse of depression when used as augmentation to medication treatment. It may also bestow an enduring, protective ben- Copyright 2010, American Psychiatric Association. Practice Guideline for the Treatment of Patients With Major Depressive Disorder, Third Edition efit that reduces the risk of relapse after the treatment has ended (363). Cognitive group therapy helps to prevent relapse and recurrence for patients in remission after a major depressive episode (497). Mindfulness-based cognitive therapy is a variant of cognitive therapy that encourages patients to pay attention to their thoughts and feelings in the moment and to accept them rather than judging or trying to change or disprove them. Among patients with remitted depression, mindfulness-based cognitive therapy groups may reduce risk of relapse for patients who have already experienced three or more episodes (498). Given the significant risk of relapse during the continuation phase of treatment, it is essential to assess depressive symptoms, functional status, and quality of life in a systematic fashion, which can be facilitated by the use of periodic, standardized measurements. Furthermore, any sign of symptom persistence, exacerbation, or reemergence or of increased psychosocial dysfunction during the continuation period should be viewed as a harbinger of possible relapse. If a relapse does occur during the continuation phase, a return to the acute phase of treatment is required. For patients receiving psychotherapy, an increased frequency of sessions or a shift in the psychotherapeutic focus may be needed. It is also essential to de- 57 termine whether any specific precipitants are contributing to the relapse of depression. For example, the onset or worsening of psychosocial stressors, substance use disorders, or general medical conditions can contribute to increased depressive symptoms. In addition, decreased treatment adherence or reductions in medication blood levels.
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