Iodine Deficiency

Severe iodine deficiency results in impaired thyroid hormone synthesis and/or thyroid enlargement (goiter). Population effects of severe iodine deficiency, termed iodine deficiency disorders (IDDs), include endemic goiter, hypothyroidism, cretinism, decreased fertility rate, increased infant mortality, and mental retardation. (See Pathophysiology and Presentation.)[1]

Iodine is a chemical element. It is found in trace amounts in the human body, in which its only known function is in the synthesis of thyroid hormones. Iodine is obtained primarily through the diet but is also a component of some medications, such as radiology contrast agents, iodophor cleansers, and amiodarone. (See Etiology.)

Worldwide, the soil in large geographic areas is deficient in iodine. Twenty-nine percent of the world’s population, living in approximately 130 countries, is estimated to live in areas of deficiency (see the Table).[2] This occurs primarily in mountainous regions such as the Himalayas, the European Alps, and the Andes, where iodine has been washed away by glaciation and flooding. Iodine deficiency also occurs in lowland regions far from the oceans, such as central Africa and Eastern Europe. Persons who consume only locally produced foods in these areas are at risk for IDD. See the distribution of iodine deficiency in the image below. (See Epidemiology.)

Iodine Deficiency	None	Mild	Moderate	Severe
Median urine iodine, mcg/L	>100	50-99	20-49	< 20
Goiter prevalence	< 5%	5-20%	20-30%	>30%
Neonatal thyroid stimulating hormone (TSH), >5 IU/mL whole blood	< 3%	3-20%	20-40%	>40%
Cretinism	0	0	+	+

Normal dietary iodine intake is 100-150 mcg/day. The US Institute of Medicine’s (IOM’s) recommended dietary allowance (RDA) of iodine is as follows:

Adults and adolescents - 150 mcg/day
Pregnant women - 220 mcg/day
Lactating women - 290 mcg/day
Children aged 1-11 years - 90-120 mcg/day
Infants - Adequate intake is 110-130 mcg/day
WHO’s recommendations are similar, although the organization recommends 200 mcg/day for pregnant or lactating women and 50-90 mcg/day for infants younger than 1 year.

Sources of dietary iodine
In areas where iodine is not added to the water supply or food products meant for humans or domesticated animals, the primary sources of dietary iodine are saltwater fish, seaweed, and trace amounts in grains. The upper limit of safe daily iodine intake is 1100 mcg/day for adults; it is lower for children.[3, 4, 5, 6]

In the United States, iodine has been voluntarily supplemented in table salt (70 mcg/g). Salt was selected as the medium for iodine supplementation because intake is uniform across all socioeconomic strata and across seasons of the year, supplementation is achieved using simple technology, and the program is inexpensive. The estimated annual cost of iodine supplementation of salt in the United States is $0.04 per person. (See Treatment and Medication.)

Other major sources of dietary iodine in the United States are egg yolks, milk, and milk products because of iodine supplementation in chicken feed, the treatment of milk cows and cattle with supplemental dietary iodine to prevent hoof rot and increase fertility, and the use of iodophor cleaners by the dairy industry.[7]

Changes in US iodine intake
In the early 1900s, the Great Lakes, Appalachian, and northwestern regions of the United States were endemic regions for IDD, but since the iodization of salt and other foods in the 1920s, dietary iodine levels generally have been adequate. However, sustaining these iodization programs has become a concern.

Data collected in the United States by National Health and Nutrition Examination Survey I (NHANES I) for the years 1971-1974 showed that the median urinary iodine level was 320 mcg/L, reflecting adequate dietary iodine intake.[8] However, by the time of NHANES III (1988-1994), the median urinary iodine value had fallen to 145 mcg/L.

The reduction in US dietary iodine intake since the 1970s has likely been the result of the removal of iodate conditioners in store-bought breads, widely publicized recommendations for reduced salt and egg intake for blood pressure and cholesterol control, the increasing use of noniodized salt in manufactured or premade convenience foods, decreased iodine supplementation of cattle feed, poor education about the medical necessity of using iodized salt, and reduction in the number of meals made at home.[8, 9, 10]

The NHANES surveys of 2001-2002, 2005-2006, and 2007-2008 showed that US dietary iodine intake has stabilized.[9, 10] Although the most recent NHANES survey reveals adequate iodine intake in the general US population, certain groups have an insufficient intake of iodine, such as pregnant women, who were found to have a median urinary iodine concentration of 125 mcg/L).[11]

Population-based assessment and treatment
In population-based assessments, iodine sufficiency can be determined based on the results of a spot urine test for iodine and creatinine.[9] Supplementation can be achieved by using iodized salt in cooking or a once-daily multiple vitamin containing sodium iodide. (See Workup, Treatment, and Medication.)[3, 12]

Pediatric considerations
Iodine stores within the thyroid increase with age in pediatric patients. Therefore, infants and young children tend to have higher131 I uptake than do adults. Additionally, newborns and young infants are much more severely affected by iodine deficiency than are adults and are more likely to become overtly hypothyroid. (See Presentation.)

Prenatal considerations
Women with severe iodine deficiency are more likely to experience infertility, and pregnancy in this group is more likely to result in miscarriage or congenital anomalies. Thyroid hormones are essential for fetal brain growth and development, and severe maternal iodine deficiency may lead to mental and growth retardation or cretinism in offspring. Even in areas of borderline iodine intake, as many as 10% of women may develop goiter during pregnancy. (See Presentation.)

Patient education
The public must understand the importance of using iodized salt, especially in the United States, where iodization of salt is not mandated by law. Several areas of the world, including the United States, Australia, and the Netherlands, where iodine deficiency was eradicated by voluntary methods, have later shown a significant decrease in iodine intake.

For patient education information, see the Thyroid and Metabolism Center and the Pregnancy Center, as well as Thyroid Problems and Miscarriage.

Alcoholic Ketoacidosis

In 1940, Dillon and colleagues first described alcoholic ketoacidosis (AKA) as a distinct syndrome. AKA is characterized by metabolic acidosis with an elevated anion gap, elevated serum ketone levels, and a normal or low glucose concentration.[1, 2]

Although AKA most commonly occurs in adults with alcoholism, it has been reported in less-experienced drinkers of all ages. Patients typically have a recent history of binge drinking, little or no food intake, and persistent vomiting.[3, 4, 5] A concomitant metabolic alkalosis is common, secondary to vomiting and volume depletion (see Workup).[6]

Treatment of AKA is directed toward reversing the 3 major pathophysiologic causes of the syndrome, which are:

Extracellular fluid volume depletion
Glycogen depletion
An elevated ratio of the reduced form of nicotinamide adenine dinucleotide (NADH) to nicotinamide adenine dinucleotide (NAD+)
This goal can usually be achieved through the administration of dextrose and saline solutions (see Treatment).

Pharyngitis in Emergency Medicine

Pharyngitis is defined as an infection or irritation of the pharynx and/or tonsils. The etiology is usually infectious, with most cases being of viral origin. These cases are benign and self-limiting for the most part. Bacterial causes of pharyngitis are also self-limiting, but are concerning because of suppurative and nonsuppurative complications. Other causes include allergy, trauma, toxins, and neoplasia.[1]

The most significant bacterial agent causing pharyngitis in both adults and children is GAS infection (Streptococcus pyogenes); this is shown in the image below.

 Physical findings of GAS are shown in the image below.

The main ED concerns with pharyngitis are to rule out more serious conditions, such as epiglottitis or peritonsillar abscess, and to diagnose group A beta-hemolytic streptococcal (GAS) infections. Airway obstruction is also of utmost importance for the ED physician treating pharyngitis.

Acute Necrotizing Ulcerative Gingivitis Empiric Therapy

Empiric Therapy Regimens
Empiric therapeutic regimens for acute necrotizing ulcerative gingivitis (ANUG) are outlined below, including those for antimicrobial treatment and for adjunctive therapy.

Proper oral hygiene is the primary treatment, and referral should be made to a dentist or periodontist. Topical therapy is all that most patients will require, with systemic antibiotics being required only for patients with systemic signs of infection.

Antimicrobial treatment recommendations
Amoxicillin 500 mg PO TID for 10d plus  metronidazole 250 mg PO TID for 10d[1] or
Amoxicillin-clavulanate 500 mg/125 mg PO TID or 875 mg/125 mg PO BID for 10d or
Clindamycin 150-300 mg PO TID for 10d or
Doxycycline 100 mg PO BID for 10d[1]
Adjunctive therapy
Saline rinses can help to speed resolution; oral rinses with a hydrogen peroxide 3% solution may be of benefit[2]
Chlorhexidine 0.12% oral rinse 15 mL BID[3]
For human immunodeficiency virus (HIV)-positive patients, consider nystatin rinse 5 mL QID or fluconazole 200 mg PO daily for 7-14d
Patients with ANUG should be given a topical anesthetic and nonsteroidal anti-inflammatory drugs (NSAIDs), because pain control is very important in allowing the patient to perform good oral hygiene

Hidradenitis Suppurativa in Emergency Medicine

Hidradenitis suppurativa is a chronic condition caused by a defect of the follicular epithelium leading to follicular occlusion and subsequent follicular rupture. It is characterized by large, painful, inflamed nodules, sterile abscesses and sinus tracts in the axillae, groin, and other parts of the body that contain apocrine glands. Velpeau first described the condition in 1839.

Venous Air Embolism

Venous air embolism (VAE), a subset of gas embolism, is an entity with the potential for severe morbidity and mortality. Venous air embolism is a predominantly iatrogenic complication[1, 2] that occurs when atmospheric gas is introduced into the systemic venous system[3] . In the past, this medical condition was mostly associated with neurosurgical procedures conducted in the sitting position.[4, 5] More recently, venous air embolism has been associated with central venous catheterization,[3, 6, 7] penetrating and blunt chest trauma,[8, 9] high-pressure mechanical ventilation,[3] thoracocentesis,[1] hemodialysis,[3, 7] and several other invasive vascular procedures.

Venous air embolism (VAE) has also been observed during diagnostic studies, such as during radiocontrast injection for computerized tomography.[10, 11] The use of gases such as carbon dioxide and nitrous oxide during medical procedures and exposure to nitrogen during diving accidents can also result in VAE.[2] Many cases of VAE are subclinical with no adverse outcome and thus go unreported. Usually, when symptoms are present, they are nonspecific, and a high index of clinical suspicion of possible venous air embolism is required to prompt investigations and initiate appropriate therapy.

Latex Allergy

Background

Allergy to natural rubber latex is increasingly common and serious in children and adults. Latex is the milky fluid derived from the lactiferous cells of the rubber tree,Hevea brasiliensis. It is composed primarily of cis -1,4-polyisoprene, a benign organic polymer that confers most of the strength and elasticity of latex. It also contains a large variety of sugars, lipids, nucleic acids, and highly allergenic proteins.

More than 200 polypeptides have been isolated from latex. Latex proteins vary in their allergenic potential. Protein content varies with harvest location and manufacturing process. Basic knowledge of the manufacturing processes aids in understanding the medical problems related to latex exposure.^[1]

Freshly harvested latex from Malaysia, Indonesia, Thailand, and South America is treated with ammonia and other preservatives to prevent deterioration during transport to factories. Latex is treated with antioxidants and accelerators including thiurams, carbamates, and mercaptobenzothiazoles. It is then shaped into the desired object and vulcanized to produce disulfide cross-linking of latex molecules.

After being dried and rinsed to reduce proteins and impurities, the product frequently is dry-lubricated with cornstarch or talc powder. Powder particles rapidly adsorb residual latex proteins; other proteins remain in soluble form on the surface of finished products.

Latex is ubiquitous in modern society and particularly in health care. William Halstead first used latex surgical gloves in 1890. Latex has been used in a myriad of medical devices for decades. In the late 1980s, however, its use skyrocketed as latex gloves were widely recommended to prevent transmission of blood-borne pathogens, including the human immunodeficiency virus (HIV). Billions of pairs of medical gloves are imported to the United States in annually, often as powdered, nonsterile examination gloves.

In the 1980s and 1990s, heightened demand for latex to manufacture gloves and other objects resulted in hundreds of new, poorly regulated latex factories in tropical countries. The incidence of minor and serious allergic reactions to latex began to rise rapidly among patients and health care workers (HCWs).^{[2, 3, 4]} Latex sensitization can occur after skin or mucosal contact, after peritoneal contact during surgery, and possibly after inhalation of aerosolized particles with latex on their surfaces.

Syncope

Syncope is defined as a transient, self-limited loss of consciousness with an inability to maintain postural tone that is followed by spontaneous recovery. This definition excludes seizures, coma, shock, or other states of altered consciousness. Although most causes of syncope are benign, this symptom presages a life-threatening event in a small subset of patients.

Essential update: Predicting serious outcome and death in patients with syncope
Peak troponin concentration is associated with an increased risk of serious outcome and death in patients with syncope, and this risk increases with higher concentrations, according to a prospective cohort study of 338 patients who had plasma troponin levels measured 12 hours after syncope with the ARCHITECT STAT sensitive troponin I assay.[1] The percentage of patients with a serious outcome increased across patients divided into quintiles on the basis of peak troponin concentration at 1 month (0%, 9%, 13%, 26%, 70%) and at 1 year (10%, 22%, 26%, 52%, 85%).[1]

Signs and symptoms
History and physical examination are the most specific and sensitive ways of evaluating syncope. These measures, along with 12-lead electrocardiography (ECG), are the only current level A recommendations listed in the 2007 American College of Emergency Physicians (ACEP) Clinical Policy on Syncope.[2]

A detailed account of the event must be obtained from the patient, including the following:

Precipitant factors
Activity the patient was involved in before the event
Position the patient was in when the event occurred
The following questions should be asked:

Was loss of consciousness complete?
Was loss of consciousness with rapid onset and short duration?
Was recovery spontaneous, complete, and without sequelae?
Was postural tone lost?
If the answers are positive, syncope is highly likely; if 1 or more are negative, other forms of loss of consciousness should be considered.[3]

Presyncopal symptoms reported may include the following:

Prior faintness, dizziness, or light-headedness (70% of cases of true syncope)
Prior vertigo, weakness, diaphoresis, epigastric discomfort, nausea, blurred or faded vision, pallor, or paresthesias
Red flag symptoms: Exertional onset, chest pain, dyspnea, low back pain, palpitations, severe headache, focal neurologic deficits, diplopia, ataxia, or dysarthria
Other information that should be obtained includes the following:

Detailed account of the event from any available witnesses (eg, whether patient experienced postevent confusion)
Patient’s medication history
Patient’s personal or familial medical history of cardiac disease
A complete physical examination is required, with particular attention to the following:

Analysis of vital signs
Measurement of the glucose level by rapid fingerstick
Detailed cardiopulmonary examination
Detailed neurologic examination
Assessment for signs of trauma
Stool guaiac examination
Bedside examinations to help elucidate the origin of syncope (eg, Hallpike maneuver)
See Clinical Presentation for more detail.

Diagnosis
No specific laboratory testing has sufficient power to be absolutely indicated for evaluation of syncope. Research-based and consensus guideline recommendations are as follows:

Serum glucose
Complete blood count
Serum electrolytes
Cardiac enzymes
Total creatine kinase
Urinalysis/dipstick
Imaging studies that may be helpful include the following:

Chest radiography: May serve to identify pneumonia, congestive heart failure (CHF), lung mass, effusion, or widened mediastinum
Computed tomography (CT) of the head (noncontrast): Has a low diagnostic yield in syncope but may be clinically indicated in patients with new neurologic deficits or in patients with head trauma secondary to syncope
CT of the chest and abdomen: Indicated only in select cases (eg, suspected aortic dissection, ruptured abdominal aortic aneurysm, or pulmonary embolism [PE])
Magnetic resonance imaging (MRI) of the brain and magnetic resonance arteriography (MRA): May be required in select cases to evaluate vertebrobasilar vasculature
Ventilation-perfusion (V/Q) scanning: Appropriate for suspected PE
Echocardiography: The test of choice for evaluating suspected mechanical cardiac causes of syncope
A standard 12-lead ECG is a level A recommendation in the 2007 ACEP consensus guidelines for syncope.[2] The following considerations are relevant:

Normal ECG findings are a good prognostic sign
ECG can be diagnostic for acute myocardial infarction or myocardial ischemia and can provide objective evidence of preexisting cardiac disease or dysrhythmia
Bradycardia, sinus pauses, nonsustained ventricular tachycardia and sustained ventricular tachycardia, and atrioventricular conduction defects are truly diagnostic only when they coincide with symptoms
Loop recorders have a higher diagnostic yield than Holter monitor evaluation, with a marginal cost savings[4]
Ambulatory monitoring appears to have a higher negative than positive diagnostic yield[5]
Other diagnostic tests and procedures include the following:

Head-up tilt-table test: Useful for confirming autonomic dysfunction and can generally be safely arranged on an outpatient basis
Electroencephalography (EEG): Can be performed at the discretion of a neurologist if seizure is considered a likely alternative diagnosis
Stress test: A cardiac stress test is appropriate for patients in whom cardiac syncope is suspected and who have risk factors for coronary atherosclerosis
Carotid sinus massage (to diagnose carotid sinus syncope)
See Workup for more detail.

Management
Prehospital management of syncope may require the following:

Intravenous access
Oxygen administration
Advanced airway techniques
Glucose administration
Pharmacologic circulatory support
Pharmacologic or mechanical restraints
Defibrillation or temporary pacing
Advanced triage decisions, such as direct transport to multispecialty tertiary care centers, may be required in select cases.

In patients brought to the emergency department with a presumptive diagnosis of syncope, appropriate initial interventions include the following:

IV access, oxygen administration, and cardiac monitoring
ECG and rapid blood glucose evaluation
The treatment choice for syncope depends on the cause or precipitant of the syncope, as follows:

Situational syncope: Patient education regarding the condition

Orthostatic syncope: Patient education; additional therapy in the form of thromboembolic disease (TED) stockings, mineralocorticoids, and other drugs (eg, midodrine); elimination of drugs associated with hypotension; intentional oral fluid consumption
Cardiac arrhythmic syncope: Antiarrhythmic drugs or pacemaker placement
Cardiac mechanical syncope: Beta blockade; if valvular disease is present, surgical correction
See Treatment and Medication for more detail

Deep Venous Thrombosis Risk Stratification

Clinical Parameter	Score
Active cancer (treatment ongoing, or within 6 mo or palliative)	+1
Paralysis or recent plaster immobilization of the lower extremities	+1
Recently bedridden for >3 d or major surgery < 4 wk	+1
Localized tenderness along the distribution of the deep venous system	+1
Entire leg swelling	+1
Calf swelling >3 cm compared with the asymptomatic leg	+1
Pitting edema (greater in the symptomatic leg)	+1
Previous DVT documented	+1
Collateral superficial veins (nonvaricose)	+1
Alternative diagnosis (as likely or greater than that of DVT)	-2
Total of Above Score
High probability	≥3
Moderate probability	1 or 2
Low probability	≤0
*Adapted from JAMA. 1998 Apr 8;279(14):1094-9.[1]

Deep Venous Thrombosis Risk Stratification
The Wells clinical prediction guide quantifies the pretest probability of deep venous thrombosis (DVT) (see Table). The model enables physicians to reliably stratify patients into high-, moderate-, or low-risk categories. Combining the pretest probability with the results of objective testing greatly simplifies the clinical workup of patients with suspected DVT. The Wells clinical prediction guide incorporates risk factors, clinical signs, and the presence or absence of alternative diagnoses.

To see complete information on Deep Venous Thrombosis, please go to the main article by clicking here.

Table. Wells Clinical Score for Deep Venous Thrombosis* (Open Table in a new window)

Clinical Parameter Score
Active cancer (treatment ongoing, or within 6 mo or palliative) +1
Paralysis or recent plaster immobilization of the lower extremities +1
Recently bedridden for >3 d or major surgery < 4 wk +1
Localized tenderness along the distribution of the deep venous system +1
Entire leg swelling +1
Calf swelling >3 cm compared with the asymptomatic leg +1
Pitting edema (greater in the symptomatic leg) +1
Previous DVT documented +1
Collateral superficial veins (nonvaricose) +1
Alternative diagnosis (as likely or greater than that of DVT) -2
Total of Above Score
High probability ≥3
Moderate probability 1 or 2
Low probability ≤0
*Adapted from JAMA. 1998 Apr 8;279(14):1094-9.[1]
Using the pretest probability score calculated from the Wells DVT score, patients are stratified into 2 risk groups: DVT unlikely (DVT score < 2) or DVT likely (DVT score ≥2).

This risk group stratification is then considered in concert with the results of a sensitive D-dimer assay such as the VIDAS rapid enzyme-linked immunoabsorbent assay (ELISA). A negative D-dimer result rules out DVT in the unlikely group (low-to-moderate risk of DVT). Even if the D-dimer test is negative, patients in the likely group (moderate-to-high risk of DVT) require a diagnostic study (ie, duplex ultrasonography), as do all patients with a positive D-dimer result.

In a patient who is scored as unlikely to have DVT, a negative duplex ultrasonographic study result rules out DVT, even if the D-dimer assay is positive. If the duplex findings are positive in a patient who is scored as likely, treat for DVT. When discordance exists between the pretest probability and the duplex ultrasonographic study result, further evaluation is required.

If the patient is scored as likely to have DVT (DVT score ≥2) but the ultrasonographic findings are negative, the patient still has a significant probability of DVT. Duplex ultrasonography is relatively insensitive for calf vein thrombosis, so some authors recommend venography to rule out a calf vein DVT that ultrasonography did not detect. Most recommend surveillance with repeat clinical evaluation and ultrasonography in 1 week. Others use the results of the D-dimer assay to guide management. A negative D-dimer assay in combination with negative ultrasonographic findings rules out DVT. A positive D-dimer assay in this group mandates surveillance and repeat ultrasonography in 1 week.

If the patient is scored as unlikely to have DVT (DVT score < 2) but the ultrasonographic findings are positive, some authors recommend a second confirmatory study such as venography before treating for DVT and committing the patient to the risks of anticoagulation. Most, however, treat the patient for DVT.

If the patient is scored as likely to have DVT (DVT score ≥2) and had a positive D-dimer assay result but the ultrasonographic findings are negative, repeat clinical evaluation and ultrasonography in 1 week is recommended.

The DVT score was developed in a specific subgroup of patients. Excluded from the model were patients with suspected coexistent PE and patients already taking anticoagulants. Therefore, the evaluation and subsequent treatment of these excluded subgroups must be individualized.

For more information, see Deep Venous Thrombosis.

Hypogammaglobulinemia

Hypogammaglobulinemia refers to a set of clinicolaboratory entities with varied causes and manifestations. The common clinical feature of hypogammaglobulinemia relates to a predisposition toward infections that normally are defended against by antibody responses (including Streptococcus pneumoniae and Haemophilus influenzae infections).

Essential update: Rituximab increases incidence of hypogammaglobulinemia
In a retrospective study from Memorial Sloan-Kettering Cancer Center, Casulo et al examined the relation between rituximab and hypogammaglobulinemia in 211 patients with B-cell lymphoma who were treated with rituximab and assessed with serial quantitative serum immunoglobulin (SIgG) concentrations before and after treatment.[1] Of the 211 patients, 179 (85%) had normal SIgG values before rituximab therapy; after rituximab therapy, 39% of these 179 patients had hypogammaglobulinemia. The risk was greater in patients who received maintenance rituximab.[1]

Signs and symptoms
Most patients with hypogammaglobulinemia present with a history of recurrent infections. A detailed clinical history should emphasize the following:

Family history
Age of onset
Site of infections
Type of microorganisms
Blood product reactions
Recurrent infections
Gastrointestinal symptoms
Musculoskeletal symptoms
Autoimmune and collagen vascular diseases
Physical findings may include the following:

Growth retardation
Abnormalities of lymphoid tissue and organs (eg, a paucity of tonsillar tissue, adenoids, and peripheral lymph nodes)
Developmental abnormalities (eg, of skeleton or chest wall)
Abnormalities of skin and mucous membranes (eg, scars, rash, or livedo reticularis)
Ear, nose, and throat abnormalities (eg, tympanic membrane perforation, purulent nasal discharge, cobblestone pattern of pharyngeal mucosa, and nasal exudate)
Pulmonary abnormalities (eg, bronchiectasis and lung fibrosis with rales, rhonchi, and wheezing)
Cardiovascular abnormalities (eg, a loud pulmonic heart sound, right ventricular heave, and tricuspid regurgitation murmur suggesting pulmonary hypertension; jugular venous distention, tender hepatomegaly, and lower-extremity edema suggesting cor pulmonale)
Neurologic abnormalities (eg, paralytic poliomyelitis or deep sensory loss with decreased vibratory and position sense of limb segments)
See Clinical Presentation for more detail.

Diagnosis
Laboratory studies that may be helpful include the following:

Serum immunoglobulin
Antibody response after immunization
Isohemagglutinins
Peripheral blood lymphocyte immunophenotyping
Evaluation of cellular immunity (cutaneous delayed-type hypersensitivity)
Complete blood count
Renal studies
GI studies (eg, alpha1 -antitrypsin)
Imaging studies that may be useful include the following:

Chest radiography
High-resolution computed tomography (HRCT) and nuclear scanning
The following tests may be considered as circumstances warrant:

Adenosine deaminase (ADA) levels and mutations in purine nucleoside phosphorylase
Flow cytometry or Western blotting
Restriction fragment length polymorphism (RFLP)
The following biopsy procedures may also be considered:

Lymph node biopsy (for rapidly enlarging lymph nodes to rule out infection or malignancy)
Rectal biopsy (for common variable immunodeficiency [CVID] and immunoglobulin A [IgA] deficiency)
Thymus biopsy (indicated only for thymoma)
See Workup for more detail.

Management
Replacement therapy with immunoglobulin G (IgG), administered intravenously (IVIG) or subcutaneously (SCIG), is the treatment of choice for most primary immunodeficiency syndromes, including the following:

X-linked agammaglobulinemia (Bruton disease; XLA)
CVID
Severe combined immunodeficiency (SCID)
Hyper-IgM
ADA deficiency
Wiskott-Aldrich syndrome (WAS)
Treatment of secondary hypogammaglobulinemia is directed at the underlying cause, as follows:

IVIG is not indicated for lymphoproliferative disorders unless immunoglobulin levels are low in association with recurrent infections or if IVIG is being used for autoimmune conditions that may accompany these disorders
Live vaccines should not be given to patients with T-cell disorders, XLA, or other severe B-cell disorders or to the family members of such patients
High doses of IVIG or intrathecal immunoglobulin may be beneficial in patients with XLA who have enteroviral meningoencephalitis
Hematopoietic stem cell transplantation (HSCT) is the treatment of choice for SCID and, if a matched donor is available, for ADA deficiency[2]
Enzyme replacement with polyethylene glycol-ADA (PEG-ADA) may be an effective alternative for patients with ADA deficiency who lack an HLA-identical sibling
Tumor necrosis factor (TNF) inhibitors have been used to treat granulomatous diseases in patients with CVID
Gene therapy has been shown to be successful in reconstituting immune function in infants with X-linked SCID, but efficacy is less proven in older children and young adults[3]

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A Duo Ting - Oral Mucolytic Adult: 300 mg bid. Max duration: 10 days. Indications: Mucolytic. Oral As a mucolytic in the treatment of respiratory tract disorders and productive cough Adult: 300 mg bid. Max duration: 10 days. Active ingredients: Erdosteine Unit description, dosage Price, USD List of interchangeable brand or generic drugs Aldosten (South Korea) Amuctol Biopulmin (Chile) Capsule; Oral; Erdosteine 300 mg Granules for Suspension; Oral; Erdosteine 70 mg / g Dostein Capsule; Oral; Erdosteine 300 mg Powder for Suspension; Oral; Erdosteine 175 mg / 5 ml Dostein Disper Tablet, Dispersible; Oral; Erdosteine 300 mg Dostol (Peru) Ectrin (Philippines) Ectrin 300 mg x 20's $ 8.53 Ectrin 300 mg x 100's $ 42.66 Ectrin 175 mg/5 mL x 60 mL $ 3.00 Ectrin 175 mg/5 mL x 100 mL $ 4.50 Edirel Edopect (Indonesia) Edopect 300 mg x 20's $ 6.12 Edotin (Indonesia) Edotin 300 mg x 2 x 10's $ 7.45 Eldotein (Vietnam) Eldotein 300 mg x 3 Blister x 10 Tablet Elstein (South Korea) Erdine (South Korea) Erdobat (Indonesia) Erdobat 300 mg x 2 x 10's $ 0.33 Erdoce (South Korea) Erdocough (South Korea) Erdoin (South Korea) Erdolant (South Korea) ERDOMAC (India) 300 mg x 10's Erdomed (Austria, Bulgaria, Czech Republic, Hungary, Romania, Slovakia) Erdopect (Finland) Erdos (South Korea) Erdosteine (China) Erdostin (Turkey) Erdotin (Brazil, Denmark, Ireland, Italy, United Kingdom) Capsule; Oral; Erdosteine 300 mg ERDOZET (India) 300 mg x 10's $ 1.49 Erdozet 300mg CAP / 10 $ 1.49 Erpect (South Korea) Erstant (South Korea) Esteclin (Mexico) Capsule; Oral; Erdosteine Suspension; Oral; Erdosteine Tablet; Oral; Erdosteine Esteclin Distab Tablet, Dispersible; Oral; Erdosteine Flusten He Tan (China) Ilvico (Ireland) Ilvico 20's

A and C Tablets with Codeine

A and C Tablets with Codeine - for the relief of the symptom complex of tension (or muscle contraction) headache. Active ingredients: Caffeine/Codeine/Aspirin Unit description, dosage Price, USD Tablet; Oral; Aspirin 375 mg; Caffeine 15 mg; Codeine Phosphate 15 mg Tablet; Oral; Aspirin 375 mg; Caffeine 15 mg; Codeine Phosphate 30 mg Tablets; Oral; Aspirin 375 mg; Caffeine 15 mg; Codeine Phosphate 15 mg Tablets; Oral; Aspirin 375 mg; Caffeine 15 mg; Codeine Phosphate 30 mg List of interchangeable brand or generic drugs 222 Tablet Tablet; Oral; Aspirin 375 mg; Caffeine Citrate 30 mg; Codeine Phosphate 8 mg Tablets; Oral; Aspirin 375 mg; Caffeine Citrate 30 mg; Codeine Phosphate 8 mg A C and C Tablet; Oral; Aspirin 375 mg; Caffeine 30 mg; Codeine Phosphate 8 mg Tablets; Oral; Aspirin 375 mg; Caffeine 30 mg; Codeine Phosphate 8 mg AC and C Tablet; Oral; Aspirin 375 mg; Caffeine 30 mg; Codeine Phosphate 8 mg Tablet; Oral; Aspirin 325 mg; Caffeine 15 mg; Codeine Phosphate 8 mg Tablets; Oral; Aspirin 375 mg; Caffeine 30 mg; Codeine Phosphate 8 mg Tablets; Oral; Aspirin 325 mg; Caffeine 15 mg; Codeine Phosphate 8 mg Acetylsalicylic Acid; Caffeine; Codeine Tablet; Oral; Aspirin 375 mg; Caffeine 15 mg; Codeine Phosphate 8 mg Tablets; Oral; Aspirin 375 mg; Caffeine 15 mg; Codeine Phosphate 8 mg Anacin with Codeine Tablet; Oral; Aspirin 325 mg; Caffeine 32 mg; Codeine Phosphate 8 mg Ancasal Antoin ASA and Codeine Compound No. 3 ASA with codeine ASA, Caffeine and Codeine Phosphate Tablet; Oral; Aspirin 325 mg; Caffeine 15 mg; Codeine Phosphate 8 mg Aspirin; Caffeine; Codeine Tablet; Oral; Aspirin 325 mg; Caffeine 15 mg; Codeine Phosphate 8 mg C T Acetylsalicylic Acid Codeine and Caffeine Tablet; Oral; Aspirin 325 mg; Caffeine 16 mg; Codeine Phosphate 8 mg C T Aspirin Codeine and Caffeine Tablet; Oral; Aspirin 325 mg; Caffeine 15 mg; Codeine Phosphate 8 mg C-2 Buffered with Codeine Tablet; Oral; Aspirin 325 mg; Caffeine 15 mg; Codeine Phosphate 8 mg C2 with Codeine Tablet; Oral; Aspirin 325 mg; Caffeine 15 mg; Codeine Phosphate 8 mg Cofena Cojene Dynalgic Fonal N Hypon Mega-Dolor Miophen Novo AC and C Tablet; Oral; Aspirin 400 mg; Caffeine 15 mg; Codeine Phosphate 8 mg Rokal Caplets; Oral; Aspirin 400 mg; Caffeine Anhydrous 50 mg; Codeine Phosphate 10 mg Tablet; Oral; Aspirin 400 mg; Caffeine Anhydrous 50 mg; Codeine Phosphate 10 mg Rokal Plus Tablet; Oral; Aspirin 400 mg; Caffeine Anhydrous 50 mg; Codeine Phosphate 15 mg Sedaspir Tablet; Oral; Aspirin 500 mg; Caffeine 50 mg; Codeine Phosphate Hemihydrate 20 mg More: http://www.igenericdrugs.com/?s=A%20and%20C%20Tablets%20with%20Codeine

A & D Ointment

A. D. N. consists of Multivitamins, Coconut Oil, Maltodextrin, Calcium Caseinate, Multiminerals, Soybean Oil, Sodium Caseinate. Multivitamins - Used for: Treating or preventing low levels of vitamins in the body. It may also be used for other conditions as determined by your doctor. A. D. N. (Multivitamins) is a vitamin supplement. It works by providing extra vitamins to the body. Coconut Oil - Indications: pediculosis treatment of pediculosis. Maltodextrin - Nutritionally complete enteral diet w/ high protein for patients requiring enteral nutritional support. For short- or long-term feeding of patients w/ normal or near normal GI function; for prevention & correction of malnutrition. Suitable to use as the sole-source nutrition. Calcium Caseinate - Indications: dietary protein supplement Multiminerals - Indications: mineral deficiency Phosphorus is a naturally occurring substance that is important in every cell in the body. The majority of phosphorus in the body is found in the bones. The potassium and sodium salt forms of phosphorus are called phosphates. Potassium phosphate and sodium phosphate is used to acidify the urine and lower the urinary calcium concentration. This may reduce rash and odor caused by ammonium in the urine. Potassium phosphate and sodium phosphate may also increase the antibiotic effect of methenamine (Hiprex, Urex). Potassium phosphate and sodium phosphate is also used as a phosphorus supplement to prevent and/or treat a phosphorus deficiency. Active ingredients: Multivitamins/Coconut Oil/Maltodextrin/Calcium Caseinate/Multiminerals/Soybean Oil/Sodium Caseinate Unit description, dosage Price, USD Powder; Oral; Calcium Caseinate; Coconut Oil; Maltodextrin; Multiminerals; Multivitamins; Sodium Caseinate; Soybean Oil