Case study: Idiopathic hemothorax in a patient with status asthmaticus.

INTRODUCTION: Idiopathic spontaneous hemothorax has been rarely described in the literature. CASE STUDY: A case of status asthmaticus and spontaneous hemothorax is described in a 29-year-old female of African descent who presented to the emergency room after 2 days of severe cough productive of yellow sputum, otalgia, sore throat, subjective fevers, chills, headache, progressive wheezing, chest tightness and dyspnea. She had a history of 7 years of asthma and was non-adherent with her controller asthma medications. Prophylactic subcutaneous administration of enoxaparin 40 milligrams was initiated upon hospitalization. The patient initially had a normal chest radiograph but subsequently developed a large, left hemothorax that required tube thoracostomy placement followed by video-assisted thoracoscopic surgery (VATS). RESULTS: The patient was transferred to the Intensive Care Unit (ICU) and tube thoracostomy resulted in evacuation of 1,400 milliliters of blood-like fluid, which had a pleural fluid hematocrit greater than 50% of the serum hematocrit. A contrast-enhanced computed tomography (CT) scan of the chest did not reveal any source for the bleeding and a technetium bone scan of the chest was normal. The patient required transfusion of 5 units of packed red blood cells. She was then taken to the operating room for VATS because of continued chest tube drainage (3,200 milliliters of fluid over a 48-hour period). CONCLUSION: The etiology of the hemothorax was unknown despite surgical exploration but was felt to be secondary to cough and bronchospasm associated with status asthmaticus.

Central serous chorioretinopathy secondary to corticosteroids in patients with atopic disease.

Central serous chorioretinopathy (CSCR) is of unknown etiology and is the most common cause of retinopathy after age-related macular degeneration, diabetic retinopathy, and retinal vein occlusion. Vision loss results from fluid leakage and serous detachment in the macula. Five percent of patients develop chronic CSCR. It is predominantly found in middle-aged men (age-adjusted rates per 100,000: 9.9 for men and 1.7 for women) and is usually unilateral and reversible. Three-quarters of CSCR patients resolve within 3 months but 45% have recurrences, usually with only minor visual acuity changes. Risk factors include type A personality, emotional stress, elevated catecholamines, hypertension, pregnancy, organ transplantation, increased levels of endogenous cortisol, psychopharmacologic medication, use of phosphodiesterase 5 inhibitors, obstructive sleep apnea, Helicobacter pylori infection, or treatment with corticosteroids. Five percent of patients develop chronic disease as a result of subretinal fibrin formation within the blister. CSCR is often bilateral, multifocal, and recurrent, and may be associated with subretinal fibrin formation within the blister. Permanent loss of vision may result from subretinal fibrin-fibrosis with scarring of the macula. Corticosteroid-associated CSCR occurs bilaterally in 20% of patients. Steroid-associated therapy may begin days to years after therapy with any form of drug delivery. We present three atopic patients who presented at various times after oral, inhaled, intranasal, and topical corticosteroid therapy. One patient developed CSCR after three separate types of administration of corticosteroids, which, to our knowledge, has not been observed in the literature.

A 15-year old girl with asthma and lower lobe bronchiectasis.

Wet cough, wheeze, and sputum in an adolescent with evidence for bronchiectasis is an uncommon presentation. The differential diagnosis includes cystic fibrosis (CF), immunodeficiency disorders, complement deficiency, allergic bronchopulmonary aspergillosis, alpha-1 antitrypsin disease, repeated aspiration pneumonia, foreign body, bronchial carcinoid, unresolved right middle lobe pneumonia, and primary ciliary dyskinesia (PCD). The likely diagnosis proceeds from the more to less common in patients with these symptoms. The location of disease on computed tomography scanning, nasal and bronchial exhaled nitric oxide, identification of ultrastructural defects on electron microscopy, and specific genetic mutation help separate CF and PCD. Although differentiating these conditions is vital, the chronic management of the bronchiectasis usually includes clearance mechanisms, bronchodilators, regular exercise, appropriate vaccinations, and judicious antibiotics for airway infections.

A 44-year-old man with bilateral eyelid swelling.

Swollen eyelids are commonly ascribed to allergic conjunctivitis, contact dermatitis, eczema, angioedema, or acute sinusitis. The differential diagnosis extends to thyroid eye disease; blepharitis; Sjögren's syndrome; Churg-Strauss vasculitis; Wegener's granulomatosis; Gleich syndrome; orbital and ocular lymphoid hyperplasia or adnexal lymphoma; idiopathic orbital inflammatory disease/idiopathic sclerosing orbital inflammation; rarely, orbital parasitosis; and IgG4-related diseases. The likely diagnosis proceeds from the more to the less common in patients without a history of allergy or infection. Both ocular lymphoid hyperplasia and ocular adnexal lymphoma must be considered in the differential diagnosis of persistent disease, and neither of these entities can be recognized or differentiated from one another clinically or radiologically. Early diagnosis is essential because therapy may consist of frequent follow-up and/or active intervention. Outcomes in patients treated early and appropriately are often favorable.

A 55-year-old man with severe persistent asthma poorly responsive to asthma therapy.

Asthma is often triggered by allergic and nonallergic factors in atopic individuals and readily responds to anti-inflammatory and bronchodilator therapy. The differential diagnosis for poorly responsive disease includes severe persistent asthma with associated allergic rhinitis, cardiac disorders such as left ventricular failure or mitral stenosis, vocal cord dysfunction, gastroesophageal reflux disease, recurrent aspiration, chronic obstructive pulmonary disease, emphysema, alpha-1-antitrypsin deficiency, sarcoidosis, hypersensitivity pneumonitis, bronchiectasis, allergic bronchopulmonary aspergillosis, airway neoplasm, and Churg-Strauss vasculitis. A careful history and physical in conjunction with appropriate screening of laboratory information will usually direct the clinician to the correct diagnosis.

Biological terrorism and the allergist's office practice.

During the anthrax outbreak and threat in Trenton (2001), our allergy practice experienced increased visits from approximately 50 of our regular patients with symptoms they believed resulted from anthrax exposure. In all cases, their symptoms were caused by a combination of an exacerbation of their underlying allergic disease and anxiety because of possible exposure to anthrax. Our objective is to present an orderly approach to the allergist's outpatients presenting with possible exposure to a bioterrorist's agent. The 10 precepts of approach to the management of a biological casualty (index of suspicion, protect yourself, patient assessment, decontaminate, diagnose, treat, infection control, alert authorities, assist in investigation, and maintain proficiency) and the epidemiological characteristics of a biological attack are discussed. In table form, we compared the signs and symptoms of the most common outpatient consultations to an allergist's office practice (chronic rhinitis, asthma, food allergy, venom allergy, atopic dermatitis, drug allergy, chronic urticaria, acute urticaria, immunodeficiency, and anaphylaxis) with those of likely bioterrorism threats. Descriptions of smallpox, plague, tularemia, anthrax, viral hemorrhagic fevers, Q fever, brucellosis, Venezuelan equine encephalitis, glanders, and melioidosis are presented. Patients may readily mistake their allergic symptoms with those of infection with a bioterrorist's agent. At the same time, the allergist may be faced with one of his own chronic patients presenting with symptoms resembling their allergic disease but actually caused by one of the aforementioned pathogens.

A 41-year-old male with cough, wheeze, and dyspnea poorly responsive to asthma therapy.

Reactive airway disease is often triggered by an upper respiratory viral infection and readily responds to anti-inflammatory and bronchodilator therapy. The differential diagnosis for unresponsive disease includes poorly controlled asthma, noncompliance with medical regimen, vocal cord dysfunction, rhinosinusitis, gastroesophageal reflux disease or recurrent aspiration, foreign body aspiration, allergic bronchopulmonary aspergillosis, Churg-Strauss vasculitis, cardiac disorders such as congestive heart failure or mitral stenosis, or other pulmonary disorders such as chronic obstructive pulmonary disease, alpha-1 antitrypsin deficiency, interstitial lung disease, bronchiectasis, sarcoidosis, hypersensitivity pneumonitis, pulmonary embolism, cystic fibrosis, airway neoplasms, or laryngotracheomalacia. As is often the case, a meticulous history can expeditiously direct the clinician to the diagnosis, especially in a patient without a smoking, asthmatic, or atopic history.

Severe acute respiratory syndrome (SARS).

This article reviews the virology, history, pathology, epidemiology, clinical presentations, complications, radiology, laboratory testing, diagnosis, treatment, and prevention of severe respiratory distress syndrome, with reference to documented outbreaks of the disease.

An HIV-infected patient with Nocardia asteroides bilateral pneumonia.

Pneumonia remains a concern for persons with long-standing HIV infection. We present a case of a 43-year-old HIV-infected woman with bilateral pneumonia whose presentation suggested the cause was a bacterial pathogen. A chest of radiograph and CT scan of the chest revealed infiltrates and adenopathies, but this did not help in the differential diagnosis. A Gram stain of a sputum specimen revealed gram-positive filamentous rods, and infection with Nocardia asteroides was diagnosed. The patient was started on a regimen of ceftriaxone and trimethoprim/sulfamethoxazole and experienced significant improvement within a few days.

Giant cell arteritis presenting as facial swelling.

Facial swelling is commonly ascribed to angioedema and a host of other causes. Temporal arteritis (TA), a disease most often diagnosed in patients over the age of 50 years, frequently presents with nonspecific and often ignored complaints (headache, symptoms of polymyalgia rheumatica, low-grade fever, fever of unknown origin, loss of appetite, depression, joint pains, weight loss, hair loss, and even respiratory symptoms). The diagnosis of TA is highly likely in the presence of new-onset headaches, polymyalgia rheumatica, and a tender, cord-like, or swollen temporal artery. Facial swelling must be appreciated as another presentation of TA, especially when accompanied by other nonspecific symptoms. High clinical suspicion, immediate treatment, and definitive diagnosis by temporal artery biopsy are necessary to prevent the most severe vascular complications of blindness and cerebrovascular accidents. Treatment with corticosteroids is most often successful. Because this treatment is fraught with all the risks of high-dose and prolonged steroid therapy, it should only be initiated in cases of significant clinical suspicion, followed by a timely temporal artery biopsy to confirm the diagnosis. Delay in therapy increases the risk of a vascular catastrophe. Delay in obtaining a temporal artery biopsy after therapy has been initiated decreases the diagnostic sensitivity of the test. Other modalities of immunosuppressive therapy remain either unsuccessful or unproven. Concomitant low-dose aspirin therapy appears to hold promise.

Fever of unknown origin due to zoonoses.

Fevers of unknown origin have been classified as classic, nosocomial, immune-deficient, and HIV-related. More than half of the 1407 human pathogens are zoonotic, making zoonotic infections an important subcategory in each of the classifications. This article describes both common and unusual zoonoses causing fevers of unknown origin. Simian immune virus is considered as a possible emerging infection. For special populations (the homeless, zoophiliacs, those whose occupation or leisure brings them in close contact with oceans or lakes, and veterinarians), zoonotic infection potentials are discussed.

Hereditary angioedema presenting in late middle age after angiotensin-converting enzyme inhibitor treatment.

BACKGROUND: Angioedema due to Cl esterase inhibitor (CI-INH) deficiency may be hereditary (HAE), commonly first occurring in childhood, or acquired (AAE), with onset usually in middle age. Type I HAE exhibits low levels of functionally normal C1-INH. Dysfunctional Cl-INH typifies type II HAE. Patients with type I AAE have low levels of Cl-INH, Clq complement, and C4 complement. In type II AAE, there is immune blockade of C1-INH. OBJECTIVE: To describe a man who first presented at the age of 52 years with type I HAE triggered by the administration of an angiotensin-converting enzyme (ACE) inhibitor. METHODS: The patient had C1-INH levels, a complement profile, and a lack of underlying co-pathology that led to the diagnosis of type I HAE triggered by the administration of an ACE inhibitor. RESULTS: The patient presented with life-threatening angioedema. His C4 complement and Cl-INH serum levels were below the reference ranges, and his C3 complement, total hemolytic complement assay, and Clq complement levels remained within the reference ranges. During the 10 years between his initial episode of angioedema and the second, he had not developed any secondary medical conditions, and he had been taking the ACE inhibitor lisinopril for 7 years. CONCLUSION: Physicians must remain aware of the possibility of unmasking HAE in the adult and geriatric population with the common use of ACE inhibitors for the treatment of hypertension, cardiovascular diseases, and metabolic diseases.

Cerebrospinal fluid leak mimicking allergic rhinitis.

Rhinitis and rhinorrhea are common clinical complaints that may be allergic or nonallergic in etiology. Distinguishing between allergic and nonallergic etiologies can be difficult but necessary for treatment. Here, we present a case of a 50-year-old woman with > 20 years of rhinorrhea before a diagnosis of cerebrospinal fluid leak and a life-threatening complication occurred. It is essential that no symptom, especially that which persists and resists treatment, is trivialized. Here, we establish how a careful history and evaluation will direct the clinician to the correct diagnosis.

Pulmonary aspergillosis and central nervous system hemorrhage as complications of autoimmune hemolytic anemia treated with corticosteroids.

Warm, active antibody adult autoimmune hemolytic anemia is the most common form of hemolytic anemia not related to drug therapy. Mortality in adult autoimmune hemolytic anemia is related to the inability to successfully treat patients' underlying disease, or the infectious complications of splenectomy and prolonged steroid therapy. Predisposing factors for invasive aspergillosis are neutropenia and steroid therapy. We present a fatal case of aspergillosis complicating a nonneutropenic case of warm active antibody adult autoimmune hemolytic anemia treated with prolonged steroid therapy.