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.

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.

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 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.

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.

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.

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.

Heparin-induced thrombocytopenia.

Each year, 25% of all hospitalized patients are affected by venous thromboembolism, a disease comprising deep vein thrombosis and pulmonary embolism, that is responsible for up to 10% of all inpatient deaths (Alikhan, Peters, Wilmott, Cohen, 2004). Used in both the treatment and the prevention of venous thromboembolism, heparin is administered to more than 12 million patients each year in the United States, making it one of the most widely prescribed medications and the leading intravenous anticoagulant. Heparin-induced thrombocytopenia is an antibody-mediated adverse drug reaction to heparin therapy with potentially life-threatening complications. This article discusses the pathogenesis, diagnosis, and treatment of patients with heparin-induced thrombocytopenia.