Chapter 20: HIV CONDITIONS

Clinical Summary

Establishing a definitive diagnosis in the earliest stage of HIV infection can have significant impact on the patient’s outcome and may serve a public health function as well. Patients are highly infectious during acute seroconversion and may be unaware that they are infected. It is believed that a significant number of the new cases of HIV infection occurring in the United States are acquired from acutely infected individuals. Identifying acute seroconverters could offer the opportunity to discuss transmission reduction behavior. Clinical illness accompanies primary HIV infection in approximately two-thirds of patients. The usual time from HIV exposure to the development of symptoms is approximately 10 to 20 days, with average symptom duration of 1.5 to 2 weeks. The most common symptoms following seroconversion mimic a typical viral syndrome and may include mucocutaneous lesions and a generalized maculopapular rash located over the face, neck, and trunk. The rash is seen in over 50% of persons with symptomatic primary HIV infection. The lesions are typically small, well circumscribed, erythematous, nonpruritic, and nontender. Less frequently, patients may demonstrate neurologic signs and symptoms consistent with meningoencephalitis, myelopathy, and peripheral neuropathy. If obtained, laboratory studies may show lymphopenia and thrombocytopenia.

Management and Disposition

Although rapid HIV testing has become feasible in most emergency department (ED) settings, the diagnosis of acute infection cannot rely solely on rapid antibody-based tests. If the possibility of acute seroconversion is entertained, then a discussion should take place with the patient regarding level of risk behavior. If acute HIV is suspected, HIV-1 ribonucleic acid (RNA) quantitative polymerase chain reaction (PCR) is the appropriate diagnostic test. Patients who are acutely seroconverting should have extremely high levels of HIV RNA. Importantly, a negative HIV antibody test does not rule out HIV infection in these cases. During the “window period” of acute HIV infection, antibodies against the HIV virus have not yet formed and may not be detected for 8 to 10 weeks. If acute HIV is suspected or confirmed, patients should be educated about disease transmission and referred for prompt follow-up and further outpatient testing and evaluation.

Pearls

1. Maintain a high degree of clinical suspicion for acute primary HIV infection, especially when sexually active patients or patients who use intravenous drugs present with mononucleosis-like symptoms, unexplained rash, mucocutaneous ulcers, lymphadenopathy, or aseptic meningitis.

2. Obtain an HIV RNA quantitative PCR (and not just an HIV antibody test) if acute HIV is suspected.

3. Ensure proper follow-up for patients in whom the diagnosis of acute HIV infection is entertained, and counsel patients regarding potential risk of transmission.

Clinical Summary

Effective antiretroviral therapy establishes virologic suppression and can allow the patient’s immune system to rebuild to a near-normal competency. In some patients who develop a rapid immune response after a very advanced degree of immune suppression, the immune reconstitution inflammatory syndrome (IRIS) can develop. In these patients, it is thought that previously subclinical infections manifest with the development of a more robust immune status. IRIS is most often seen in patients who have recently started antiretroviral therapy (usually within 60 days of starting therapy) with an initial CD4 count below 100 cells/mm³. Most common infections that can “trigger” IRIS include mycobacterium (tuberculosis [TB] and mycobacterium avium complex [MAC]), cytomegalovirus (CMV), cryptococcal disease, and histoplasmosis. Patients typically present with fever, malaise, lymphadenopathy, and symptoms associated with the active opportunistic infection.

Management and Disposition

The key for the ED physician is to identify those patients who have recently started antiretroviral therapy and may be presenting with IRIS-related findings. Appropriate evaluation and management depends on the underlying opportunistic infection. Patients will often require admission to the hospital and consultation with an infectious diseases specialist.

Pearl

1. HIV-infected patients who are currently taking antiretroviral therapy and present with a febrile illness should be questioned regarding the duration of antiretroviral therapy and pretreatment CD4 count. Patients with advanced disease who have recently started antiretroviral therapy may be presenting with signs and symptoms of IRIS-related disease.

Clinical Summary

Oral hairy leukoplakia (OHL) is a disease of the lingual squamous epithelium caused by the Epstein-Barr virus (EBV). OHL generally affects the lateral portion of the tongue, although the floor of the mouth, palate, or buccal mucosa may also be involved. The lesions are white corrugated plaques that, unlike Candida, cannot be scraped from the surface to which they adhere. Most often OHL is asymptomatic, although occasionally this condition can be painful. Diagnosis is usually clinical, though definitive diagnosis can be made by biopsy characteristically revealing acanthosis and parakeratosis.

Management and Disposition

Patients who are known to be HIV-seropositive can be educated about the disease and reassured. OHL is not considered to be a premalignant lesion. If the patient is not known to be infected with HIV, primary care provider referral and HIV screening, if available, should be offered.

Pearls

1. Oral candidiasis can be distinguished from OHL by utilizing a swab in an attempt to remove the exudate characteristic of thrush and by observing pseudohyphal elements microscopically with candida. OHL cannot be scraped off and usually involves the lateral aspect of the tongue.

2. OHL is fairly specific for HIV infection as it is rarely observed in patients with other immunodeficiencies. If OHL is identified in a patient not known to be HIV infected, risk factors and HIV screening options should be discussed.

Clinical Summary

Oral candida infections are seen in over half of all HIV patients, with the severity of infection often correlating with the degree of immunosuppression. Oral candidiasis can occur at all stages of HIV disease. The usual causative agent is Candida albicans, but other Candida species have been isolated. Oral candidiasis, or “thrush,” can be classified as pseudomembranous, angular, or erythematous. Pseudomembranous candidiasis can be diagnosed by identifying removable whitish plaques on the tongue, uvula, and buccal mucosa. Erythematous or atrophic candidiasis appears as smooth red patches along the soft and hard palate. Although isolated oral candidiasis is not an AIDS-defining illness (though esophageal candidiasis is), oral candidiasis is an indication for pneumocystis prophylaxis regardless of CD4+ cell count.

Vaginal candidiasis is common in HIV positive patients and can cause a severe whitish discharge with vulvar erythema.

Management and Disposition

Patients presenting to the ED for dysphagia or odynophagia thought to be due to candidiasis should be evaluated for dehydration and may require inpatient admission. Most cases of minimally symptomatic oral candidiasis respond well to nystatin suspension or clotrimazole troches. More symptomatic oral or esophageal candidiasis usually responds to fluconazole. Rare cases of resistant candidiasis may require intravenous echinocandin therapy.

Pearls

1. Symptomatic oral and esophageal candidiasis is still a common ED presentation in HIV patients who are not receiving or are not compliant with effective antiretroviral therapy.

2. The diagnosis of oral candidiasis in a patient not already diagnosed with HIV infection should lead to a discussion of risk factors and should prompt HIV screening.

3. Mildly symptomatic oral, esophageal, or vaginal candidiasis usually responds to a one-time oral dose of fluconazole. Close clinical follow-up should be arranged.

Clinical Summary

Kaposi sarcoma (KS) is a low-grade vascular tumor associated with human herpesvirus 8 (HHV-8). Since the introduction of highly active antiretroviral therapy (HAART), the incidence of KS in HIV-infected persons has significantly declined. Skin involvement is characteristic but extracutaneous spread of KS is common, particularly to the oral cavity, gastrointestinal (GI) tract, and respiratory tract. The skin lesions appear most often on the lower extremities, face (especially the nose), oral mucosa, and genitalia. Most commonly, the lesions are papular, ranging in size from several millimeters to centimeters in diameter. Less commonly, the lesions may be plaque-like, especially on the soles of the feet, or exophytic and fungating with breakdown of overlying skin. Papular lesions may resemble lesions associated with bacillary angiomatosis or herpesvirus infections.

Pulmonary involvement can occur in AIDS-related KS. Affected persons may present with shortness of breath, fever, cough, hemoptysis, or chest pain or as an asymptomatic finding on chest x-ray. Diagnosis can be confirmed via bronchoscopy.

Management and Disposition

All HIV-infected patients with KS should receive antiretroviral therapy, which is generally effective in treating most cutaneous lesions. Systemic chemotherapy and newer immunomodulator therapy (interleukin-12, angiogenesis inhibitors) are reserved for more extensive disease including patients with visceral involvement.

Pearls

1. HIV patients who present with new papular lesions should be referred for dermatologic evaluation and biopsy.

2. A careful examination of the skin and oral cavity is appropriate in HIV-infected patients presenting with GI or respiratory complaints.

3. Half of patients with oral involvement have other GI tract lesions as well. Hemoccult testing of stool is a good preliminary screen.

Clinical Summary

Toxoplasma gondii is a widespread intracellular protozoan parasite with a definitive host stage in cats. Immunocompetent persons are usually asymptomatic, but immunocompromised persons (especially HIV-positive persons with <100 CD4 cells/μL) are susceptible to reactivation of latent disease with considerable morbidity and mortality.

Patients with central nervous system (CNS) toxoplasmosis most often present with symptoms consistent with intracranial mass lesions (headache, focal neurologic deficit, nausea/emesis, and/or seizure) or, less likely, encephalitis (fever, confusion, altered mental status). Contrasted computed tomography (CT) of the head typically reveals ring-enhancing lesions with a predilection for the basal ganglia. Magnetic resonance imaging (MRI) of the head is more sensitive than CT for identifying these lesions. Serological tests for T gondii antibodies (IgG) are usually positive. Other causes of mass lesions in the brain in HIV-infected individuals include CNS lymphoma, cryptococcoma, tuberculoma, and brain abscess.

Ocular toxoplasmosis is a less frequent complication of HIV disease. Patients typically present with eye pain and decreased visual acuity. Retinitis may be diagnosed by ophthalmoscopic evaluation revealing characteristic exudates and hemorrhage. Toxoplasmosis retinitis appears as raised yellow-white, cottony lesions in a nonvascular distribution, unlike the edematous perivascular exudates of CMV retinitis.

Management and Disposition

There are two combination regimens considered to be first choice for the treatment of toxoplasmosis. The most commonly used regimen is pyrimethamine and sulfadiazine for 6 weeks or until neurological findings have resolved; however, for those with sulfa allergies, pyrimethamine and clindamycin is an alternative. If the patient presents with seizures, loading doses of antiepileptics such as fosphenytoin or levatiracetam should be administered along with benzodiazepines. All patients with acute symptomatic CNS toxoplasmosis infection should be admitted for treatment.

In cases of suspected ocular toxoplasmosis, a complete eye examination including slit-lamp examination and measurements of intraocular pressure should be performed before consulting ophthalmology.

Pearls

1. HIV-infected patients presenting with focal neurologic findings or seizures should be evaluated for meningitis and space-occupying lesions in the brain. AIDS-specific differential includes toxoplasmic encephalitis, CNS lymphoma, and cryptococcal disease.

2. All HIV-infected patients should have a CNS space–occupying lesion excluded by imaging prior to lumbar puncture (LP).

3. Initial evaluation of the HIV-infected patient with possible CNS lesions should include CT or MRI imaging, LP, and triage management for bacterial meningitis. Further workup will require admission and infectious diseases consultation.

Clinical Summary

Pneumocystis jirovecii (formerly carinii) pneumonia (PCP) is the most common opportunistic infection in HIV-infected patients. Clinical suspicion for PCP pneumonia in any HIV patient presenting with complaints of dyspnea and nonproductive cough should remain high. Presentations can be indolent, acute, or subacute, with associated symptoms including fever, fatigue, anorexia, weight loss, and chest pain. The complete blood count (CBC) is usually normal except for lymphopenia, while serum lactate dehydrogenase (LDH) is often elevated. Arterial blood gases (ABGs) most often reveal a respiratory alkalosis, Po₂ of 70 mm Hg or less, and an increased A-a gradient of 35 mm Hg or more. Radiographic chest findings are variable with diffuse interstitial alveolar infiltrates being common.

Management and Disposition

The initial treatment of PCP is often based on a presumptive diagnosis pending definitive results, usually a stained bronchial lavage sample obtained through bronchoscopy. It is essential that any HIV-infected patient who may have a CD4 count below 200 cells/mm³ or CD4 cell percent less than 14 presenting with respiratory signs or symptoms be evaluated for PCP. Initial evaluation should include history of medications, especially adherence with prophylactic medications, clinical exam, chest x-ray, and room air ABG. Trimethoprim-sulfamethoxazole, orally or intravenously, is the first-line standard treatment. Clindamycin-primaquine, pentamidine, trimetrexate-leucovorin, atovaquone, and trimethoprim-dapsone are less effective alternatives. Treatment with corticosteroids should be initiated if the Po₂ is less than 70 or the A-a gradient is greater than 35. Any patient treated with steroids for presumptive PCP must have a definitive diagnosis made before discharge. Other pathogens that can cause pneumonia in HIV-infected patients may initially respond to steroid therapy.

Pearls

1. Include PCP in the differential diagnosis of any HIV patient who presents with a persistent fever or respiratory complaint.

2. Patients with significant dyspnea should have a room air ABG obtained. Oxygen saturation measures are not adequate to evaluate neither the oxygenation level nor the need for adjunct steroid therapy in a patient with suspected PCP.

3. The classic clinical presentation of PCP is a quiet patient with an increased respiratory rate, poor air movement, and a nonproductive cough on deep inspiration.

4. Over 30% of patients with PCP will have a normal chest x-ray. CT scanning of the chest is much more sensitive to reveal the classic interstitial ground glass pattern.

Clinical Summary

Cryptococcus neoformans is the most common cause of meningitis in patients with AIDS. Cryptococcal meningoencephalitis typically manifests itself in patients whose CD4 cell counts are less than 50/μL. The onset tends to be insidious with fairly nonspecific symptoms such as fever, nausea, and headache. Symptoms may be present for several weeks. Seizures or focal neurological presentations are rare and neck stiffness and/or photophobia are usually absent. Diagnosis is usually made on examination of cerebrospinal fluid (CSF). Opening pressures may be quite elevated on LP, and CSF values usually reveal a normal CSF glucose concentration, a mildly elevated CSF protein concentration, and a CSF leukocyte count of less than 20/mL. India ink staining shows the organisms directly with an approximate sensitivity of 70%, while CSF cryptococcal latex antigen testing has a sensitivity approaching 90%. Fungal CSF cultures should also be sent. Cutaneous manifestations are seen in disseminated disease.

Management and Disposition

Treatment should begin for presumptive meningitis pending completion of CSF studies. Most often, the decision to treat for cryptococcal meningitis will be based on the results of CSF studies, along with consultation with infectious disease specialists. Cryptococcus can also cause pneumonia and skin lesions. Treatment regimens are usually based on amphotericin preparations followed by fluconazole.

Pearls

1. Perform the LP only after CT with contrast rules out space-occupying lesions, and do so with the patient in a lateral decubitus position so as to obtain an accurate opening pressure.

2. “False-positive” India ink stains can occur with other encapsulated organisms such as Klebsiella pneumoniae, Rhodotorula, Candida, and Proteus species.

Clinical Summary

Disseminated histoplasmosis most commonly occurs in immunocompromised patients living in the Ohio and Mississippi River Valleys. HIV-infected patients usually have a CD4 count <200 cells/mm³ and present with fever, weight loss, malaise, and pulmonary symptoms such as cough and dyspnea. Pulmonary symptoms predominate and in severe cases patients may present with acute respiratory distress syndrome. Patients may present with a diffuse papular rash in disseminated disease. Mediastinitis is a rare but serious complication of histoplasmosis. Urine and serum antigen testing carries a high sensitivity, but bronchoalveolar lavage may be needed to make the diagnosis. Serum LDH and alkaline phosphatase levels may be markedly elevated as well.

Management and Disposition

Disseminated histoplasmosis should be considered in any patient with moderate to advanced HIV infection and constitutional symptoms. Acutely ill patients with fever, weight loss, and functional decline should be admitted for evaluation treatment. Some patients with less severe disease may be treated with oral itraconazole but should be referred for evaluation and a definitive diagnosis.

Pearls

1. Consider disseminated histoplasmosis in any patient with moderate to advanced HIV infection and constitutional symptoms, rash, and appropriate geographic exposure.

Clinical Summary

Cytomegalovirus (CMV) can be a cause of considerable morbidity in severely immunocompromised HIV-infected individuals. The major problems encountered are, in order of frequency, retinitis, colitis, esophageal ulceration, encephalitis, and pneumonitis.

CMV retinitis is the most common cause of blindness and eye disease in patients with AIDS. Patients typically present with loss of vision, floaters, scotoma, or visual field loss. Fundoscopic examination reveals exudates and hemorrhages, which follow the vasculature of the retina, giving it the typical “pizza pie” or “cottage cheese and ketchup” appearance.

CMV colitis is an uncommon but serious complication of HIV. The usual presenting features include generalized abdominal pain, diarrhea which may be bloody, and a low-grade fever. Loops of dilated large bowel may be seen on abdominal imaging, but definitive diagnosis is made with mucosal biopsy revealing characteristic “owls eye” inclusion bodies.

Management and Disposition

Treatment for CMV retinitis can be sight saving and should be started as soon as the diagnosis is considered. Emergent ophthalmologic consultation is needed. Treatment can be initiated with intravenous, intravitreal, or oral ganciclovir formulations. Relapse is common with CMV retinitis and if left untreated may progress to complete blindness.

Pearls

1. Ocular complaints in HIV patients require a comprehensive eye examination along with ophthalmology involvement if lesions are observed or complaints are significant.

2. Patients with CMV esophagitis often complain of odynophagia, but rarely complain of dysphagia, which may help clinically differentiate between CMV and candidal esophagitis.

Clinical Summary

Varicella zoster virus (VZV) infection presents as shingles in HIV-infected patients at a greater frequency and severity than the general population. Despite the high incidence of shingles in this population, severe disseminated disease is rare.

The diagnosis of herpes zoster in the ED is often made clinically, by either recognizing the pain syndrome or visualizing the rash. Patients can present with a well-defined area of hyperesthesia for days prior to an outbreak of the characteristic lesions. Immunocompromised patients may demonstrate multidermatomal distribution or scattered vesicles at a distant site. Approximately 20% of patients will have systemic symptoms such as malaise, fever, headache, or fatigue. Culture, serologic testing, or PCR confirms the diagnosis. A Tzanck test can be obtained by scraping the base of a lesion in an attempt to demonstrate multinucleated giant cells.

Management and Disposition

Three antiviral drugs are used to treat herpes zoster infections: acyclovir, famciclovir, and valacyclovir. Patients with severe disseminated disease or ophthalmic zoster should receive intravenous acyclovir (10-12.5 mg/kg IV q 8 h for 10-14 days). Treatment of zoster ophthalmicus should include topical antibiotics and immediate ophthalmology consultation. Providing treatment of the disease within 72 hours of rash onset will result in a more rapid resolution of cutaneous lesions and decrease viral shedding, but will not change the incidence of postherpetic neuralgia. Immunocompromised patients should not be placed on glucocorticoids. Narcotics, capsaicin cream, and tricyclic antidepressants can be used for pain control.

Pearls

1. Worsening cases of herpes zoster, complicated herpes zoster, or ophthalmic zoster all require intravenous acyclovir and admission.

2. Herpes zoster encephalitis is rare, but can occur months after the cutaneous phase and can be difficult to diagnose. Common presenting symptoms include mental status changes, headache, fever, photophobia, vomiting, or even focal neurological deficits.

3. Patients presenting with localized hyperesthesia may have a zoster-related prodrome and treatment should be initiated if clinical suspicion is high.

4. The presence of vesicles on the tip of the nose (Hutchinson sign) indicates involvement of the nasociliary branch of cranial nerve V and is associated with a higher risk of ocular involvement.

Clinical Summary

Eosinophilic folliculitis, commonly seen in advanced HIV patients, is a pruritic skin eruption usually involving the face, neck, trunk, and extremities manifesting in the form of pustules and papules. The skin lesions usually start as small pustular groups that later coalesce to create irregular erosions and plaques with central hyperpigmentation. The associated pruritus is often so intense that the lesions become excoriated. Most patients with this condition will demonstrate CD4 cell counts of less than 250/μL. The etiology of eosinophilic folliculitis is unknown, but is commonly thought of as an inflammatory process associated with immune dysfunction. It has become less common with the advent of HAART.

Management and Disposition

The diagnosis requires dermatology consultation and referral for biopsy. Antihistamines, potent topical steroids, itraconazole, topical permethrin, retinoids, metronidazole, dapsone, and ultraviolet B phototherapy have all shown variable levels of efficacy.

Pearls

1. The severe pruritus associated with this condition helps distinguish it from bacterial folliculitis. Symptomatic treatment for pruritus is necessary, and the disease generally improves with effective antiretroviral therapy.

2. Dermatological referral is warranted prior to initiating definitive therapy.

3. Patients with eosinophilic folliculitis may present with prurigo nodularis and lichen simplex chronicus as a result of severe itching and rubbing.

4. Secondary syphilis should be considered in all HIV-infected patients presenting with rash.

Clinical Summary

Infection with herpes simplex virus (HSV) is extremely common in HIV-infected patients and may present with oral, genital, anal, esophageal, or ophthalmologic involvement. The hallmark for most clinical presentations of HSV outbreaks is an inflammatory cutaneous eruption, with or without vesicles and pain. HSV esophagitis is seen in immunocompromised HIV-infected patients and presents as dysphagia and odynophagia with or without oral lesions. Idiopathic apthous ulcerations in HIV-infected patients are indistinguishable from HSV lesions. Perirectal lesions are often erythematous, ulcerative, and extremely tender, with a predilection for the gluteal cleft. Perirectal HSV may also be associated with proctitis and anal fissures.

Ocular HSV may be demonstrated by observing dendritic lesions after fluorescein staining. HSV is associated with a syndrome of acute retinal necrosis characterized by pain, keratitis, and iritis that may lead to retinal detachment. The diagnosis is usually made clinically but can be confirmed by a Tzanck test, biopsy, or culture.

Management and Disposition

Multiple oral treatment regimens are available to treat HSV. Duration of treatment is usually increased for immunocompromised patients. Ocular HSV requires prompt ophthalmology consultation.

Pearls

1. Anticipate involvement of multiple sites in HIV patients; presentations of HSV may be atypical compared to HSV in immunocompetent individuals.

2. Suspect HSV in any HIV patient with a chronic painful ulcerative lesion.

3. Perirectal HSV outbreaks may be missed on a superficial history and physical examination. Ask if it is painful to wipe after stool and examine the perianal area. Do not assume hemorrhoids in HIV-infected patients at risk for HSV.

Clinical Summary

Human scabies, caused by the Sarcoptes scabiei mite, is one of the most common contagious dermatoses. In HIV patients, this organism can cause “crusted scabies,” also known as Norwegian scabies, which denotes an overwhelming scabies infestation. In typical scabies, the mites cause extremely pruritic burrows, vesicles, and papules in a characteristic distribution involving the finger webs, sides of the hands and feet, breasts, waist, and groin. Pruritus is most intense at night. In contrast, crusted scabies typically affects the hands and the feet with asymptomatic crusting and does not cause significant pruritus. Transmission through infected linens or clothing is common in cases of Norwegian scabies. Risk factors include poor hygiene, crowding, and exposure to pets.

Most often the diagnosis of scabies is made clinically, with evidence of burrows and severe pruritus in a characteristic distribution. Definitive diagnosis is made from examination of shavings from the lesions. Placing mineral oil over a suspected lesion and then shaving it with a number 15 blade can demonstrate the mites, which are usually 0.3 to 0.4 mm in length.

Management and Disposition

Topical permethrin 5% cream has a low toxicity and is the treatment of choice for scabies. Patients are instructed to apply the cream from the neck down and leave it on for 8 to 14 hours before removal. One application is usually sufficient for treatment in nonimmunocompromised patients. The patient’s clothes and bedding should be washed in hot water. Antihistamines should be prescribed to alleviate the pruritus. Often the pruritus persists after treatment as a hypersensitivity reaction to the mites and their feces and eggs. Any complicating secondary skin infection should be treated with appropriate systemic antibiotics. Localized infections can be treated with topical steroids.

For HIV patients with Norwegian scabies, permethrin should be applied to the face, scalp, behind the ears, and from the neck downward. Repeat treatments may be needed. For severe or refractory cases, oral ivermectin (200 mg/kg for one dose) can be tried with the exception of pregnant or lactating women.

Pearls

1. Often secondary staphylococcal infections complicate the diagnosis, including impetigo, ecthyma, paronychia and furunculosis.

2. Oral antibiotics are often indicated for Norwegian scabies because of skin breakdown.

3. Close contacts of infected patients should be treated simultaneously. Inform patients that although the scabicide will kill the mites, itching may last for weeks. Patients often seek repeat treatments and inappropriately receive additional scabicides, which can cause contact dermatitis.

Clinical Summary

Molluscum contagiosum is caused by a poxvirus that presents flesh-colored, dome-shaped lesions on affected individuals. Usually, molluscum contagiosum is an asymptomatic benign disease, but may become severe in HIV patients. Typical presentations consist of groups of 2 to 20 small, discrete, shiny lesions with central umbilication.

Management and Disposition

If the diagnosis is suspected in the ED, the patient should be reassured and referred to a dermatologist. Usually self-limited with spontaneous remission, treatment outside of genital lesions is for cosmetic reasons only.

Pearl

1. Clinically, it may be difficult to distinguish between cutaneous Cryptococcus and molluscum contagiosum. Dermatology or infectious disease consultation and biopsy may be required if the patient is clinically ill.

Clinical Summary

Dermatophyte infections are common superficial fungal infections involving the scalp (tinea capitis), body (tinea corporis), feet (tinea pedis), crural fold (tinea cruris), and nails (onychomycosis). Infection is very common in healthy individuals, but can be varied and atypical in patients with HIV. HIV patients also can demonstrate a much more severe and extensive form of disease. Three different dermatophytes are the usual source of infection: epidermophyton, trichophyton, and microsporum.

Tinea capitis is seen as an enlarging scaling patch on the scalp that may progress to a kerion. The initial lesion can be overlooked until alopecia is present. Untreated permanent scarring can occur. Tinea pedis is the most common dermatophyte infection seen in practice. Usually self-limited, intermittent, recurrent, and intensely pruritic, these lesions can often be secondarily infected due to mechanical irritation. Tinea corporis is the most common fungal infection seen in HIV patients. Usually, it begins as an intensely pruritic, oval scaling erythematous lesion that spreads centrifugally and can merge with other lesions. Tinea cruris is an infection involving the crural fold, much more common in men than women. It usually begins as a macular patch on the inner thigh, opposite the scrotal sac.

Management and Disposition

Tinea capitis responds to griseofulvin; however, other oral agents that can be effective include terbinafine, itraconazole, or fluconazole. Treatment usually is carried out for at least 3 weeks, with topical treatments ineffective. Tinea pedis can usually be treated with a topical antifungal cream for 4 weeks. Often patients have tried outpatient, over-the-counter antifungal medications without success. Extensive treatment can be initiated with griseofulvin, terbinafine, or itraconazole orally. Tinea corporis often responds to daily application of topical antifungal medications; however, systemic oral agents described above are also effective. Tinea cruris usually responds to topical antifungal medications.

Pearls

1. Confirming the diagnosis with a KOH preparation is important before initiating therapy, especially in diffuse disease. Often HIV patients suffer from a variety of skin infections that mimic dermatophyte lesions (eczema).

2. Athletes are especially at risk when close skin-to-skin contact occurs (wrestling, football). Oral treatment in these cases is preferred, with restriction in sports for 2 weeks or until lesions heal.

3. Some dermatophyte infections fluoresce under the Wood lamp examination.

Clinical Summary

Thrombocytopenia occurs in 40% to 70% of all HIV patients. It can occur independently at all stages of HIV infection and may be encountered as the initial presentation of disease. HIV-associated anemia and granulocytopenia can occur concomitantly as course of the HIV infection worsens, with thrombocytopenia seen in 30% of patients with CD4 counts less than 200/μL. HIV patients with thrombocytopenia often present to the ED with bleeding (especially from the oral mucosa), ecchymosis, and petechiae. Secondary causes of thrombocytopenia are generally seen as the result of opportunistic infections, malignancy, or medications.

Management and Disposition

The emergency physician’s efforts are initially focused on stabilization of the patient with two large intravenous lines, type and cross-match, and crystalloid infusion if significant bleeding has occurred. Because of the complexity of the differential diagnosis and potentially complicated treatment of HIV thrombocytopenia, an infectious disease specialist should be consulted early. In most cases, HIV patients with platelet count greater than 50,000 can be managed conservatively with spontaneous remission of approximately 20%. Zidovudine can increase platelet counts up to twofold in over 50% of patients. If the platelet count is less than 20,000, many infectious disease specialists recommend γ-globulin infusion and parenteral steroids. Other possible treatments include dapsone, danazol, interferon-α vincristine, anti-D immunoglobulin, splenic irradiation, and splenectomy. Even if the patient is to be managed conservatively, bone marrow analysis should be performed to rule out other causes of thrombocytopenia.

Pearls

1. Perform thorough skin and oral examinations in all patients with HIV looking for manifestations of thrombocytopenia.

2. Take a careful drug history and consider other infectious etiologies before assuming the thrombocytopenia is directly secondary to HIV infection.

3. Spontaneous bleeding is rare unless the platelet count is less than 10,000.

Clinical Summary

HIV patients have a 5 to 20 times higher rate of drug reactions than non-HIV patients. Up to 5% of ED visits by HIV patients are due to complications of therapy. Many of these manifest dermatologically, in order of decreasing frequency: (1) exanthems, (2) urticaria/angioedema, (3) fixed drug reactions, (4) erythema multiforme, and (5) photosensitivity reactions. The most common medications associated with rashes are antivirals, antibiotics, and antifungals.

Management and Disposition

The emergency physician may need to consult an infectious disease specialist, a pharmacist, or a dermatologist to help clarify the existence of a drug reaction. Clues besides recent initiation of a new drug are eosinophilia greater than 1000 or elevated liver function tests. Individual treatment varies depending on the situation. The offending agent should be discontinued. Antihistamines and steroids are indicated in certain situations.

Pearls

1. Ask about alternative and nonprescription medicines.

2. Half of all HIV patients will react adversely to sulfa drugs.

3. Beware of serious drug reactions such as Stevens-Johnson syndrome and toxic epidermal necrolysis (TEN).

Clinical Summary

Acute necrotizing ulcerative gingivitis (ANUG), also known as Vincent angina or trench mouth, is commonly seen in HIV patients. It is a distinct and rapidly progressive ulceration typically starting at the tip of the interdental papilla, spreading along the gingival margins, eventually destroying the periodontal tissue. The triad associated with ANUG is oral pain, halitosis, and ulcerations. Other signs and symptoms include “metallic taste,” “wooden teeth” sensation, tooth mobility, fever, adenopathy, and malnutrition. The cause of this aggressive, destructive process in HIV patients is a polymicrobial infection by oral anaerobes (Treponema, Selenomonas, Fusobacterium, Porphyromonas, Prevotella). ANUG represents a spectrum of disease from mild ulcerations to severe cellulitis and spread of the infection to the soft tissues, cheeks, lips, and bones.

Management and Disposition

ANUG is most frequently seen in four population groups: (1) HIV patients, (2) malnourished children, (3) young adults who are under a great deal of stress, and (4) polysubstance abusers. The first steps for the emergency physician are to eliminate other potentially more serious life-threatening infections and to address hydration status. Treatment includes (1) eliminating contributing factors (stress, poor nutrition, poor sleep, alcohol, and tobacco use), (2) chlorhexidine rinses twice a day, (3) surgical debridement by an oral surgeon if needed, and (4) oral penicillin and metronidazole.

Pearls

1. Beware of Ludwig angina (brawny submandibular induration and tongue elevation) associated with severe progression of ANUG as acute airway compromise is possible.

2. Noma (cancrum oris, gangrenous stomatitis), a rare disease of childhood associated with malnutrition, is characterized by an anaerobic destructive infectious process of the orofacial tissues that can clinically resemble ANUG.