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First_Aid_Step2. Presents with fever, facial pain/pressure, headache, nasal congestion, and discharge. Exam may reveal tenderness, erythema, and swelling over the affected area. High fever, leukocytosis, and a purulent nasal discharge are suggestive of acute bacterial sinusitis. A clinical diagnosis. Culture and radiography are generally not required for acute sinusitis but may guide the management of chronic cases. Transillumination shows opacifcation of the sinuses (low sensitivity). CT is the test of choice for sinus imaging (see Figure 2.8-5) but is usually necessary only if symptoms persist after treatment. MRI is useful for differentiating soft tissue (as in a tumor) from mucus. FIGURE 2.8-5. Sinusitis.


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First_Aid_Step2. FIGURE 2.8-5. Sinusitis. Compare the opacifed left maxillary sinus and normal air-flled right sinus on this coronal CT scan. (Reproduced, with permission, from Lalwani AK. Current Diagnosis & Treatment in Oto laryngology: Head and Neck Surgery, 2nd ed. New York: McGraw-Hill, 2008: Fig. 14-2.) ■Bacterial culture by sinus tap is the gold standard for diagnosis but is not routinely performed because of discomfort. Endoscopically guided cultures from the middle meatus are gaining popularity. Most cases of acute sinusitis are viral and/or self-limited and can thus be treated with symptomatic therapy (decongestants, antihistamines, pain relief). Acute bacterial sinusitis (usually < 7 days): Consider amoxicillin/clavulanate 500 mg PO TID × 10 days or, alternatively, clarithromycin, azithromycin, TMP-SMX, fuoroquinolone, or a second-generation cephalosporin × 10 days.


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First_Aid_Step2. Chronic sinusitis (4–12 weeks): Adjuvant therapy with intranasal corticosteroids, decongestants, and antihistamines may be useful in combating the allergic/infammatory component of the disease. Antibiotics given are similar to those used for acute disease, although a longer course (3–6 weeks) may be necessary. Surgical intervention may also be required. A pulmonary fungal infection endemic to the southwestern United States (e.g., San Joaquin Valley, California). Can present as an acute or subacute pneumonia or as a fulike illness, and may involve extrapulmonary sites, including bone, CNS, and skin. The incubation period is 1–4 weeks after exposure. Filipino, African-American, pregnant, and HIV-patients are at ↑ risk. Potential complications of sinusitis include meningitis, frontal bone osteomyelitis, cavernous sinus thrombosis, and abscess formation.


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First_Aid_Step2. Potential complications of sinusitis include meningitis, frontal bone osteomyelitis, cavernous sinus thrombosis, and abscess formation. Consider coccidioidomycosis in the HIV-, Filipino, African-American, or pregnant patient from the southwestern United States with respiratory infection. Patients present with fever, anorexia, headache, chest pain, cough, dyspnea, arthralgias, and night sweats. Disseminated infection can present with meningitis, bone lesions, and soft tissue abscesses. Obtain bronchoalveolar lavage along with fungal cultures of sputum, wound exudate, or other affected tissue. Identify Coccidioides immitis spherules on H&E or other special stains of sputum or tissue. Precipitin antibodies (IgM) ↑ within two weeks and disappear after two months; complement fxation antibodies (IgG) ↑ at 1–3 months. Titers > 1:16 indicate disseminated infection. CXR fndings may be normal or may show infltrates, nodules, cavity, mediastinal or hilar adenopathy, or pleural effusion.


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First_Aid_Step2. CXR fndings may be normal or may show infltrates, nodules, cavity, mediastinal or hilar adenopathy, or pleural effusion. Consider bronchoscopy, fne-needle biopsy, open lung biopsy, or pleural biopsy if serology is indeterminate. Acute: IV therapy is rarely necessary; however, consider IV amphotericin B for severe or protracted 1° pulmonary infection and disseminated disease. PO fuconazole or itraconazole may be used for mild infection or continuation therapy once the patient is stable. Chronic: No treatment is needed for asymptomatic chronic pulmonary nodules or cavities. Progressive cavitary or symptomatic disease usually requires surgery plus long-term azole therapy for 8–12 months. A highly contagious orthomyxovirus transmitted by droplet nuclei. There are three types of infuenza: A, B, and C. Subtypes of infuenza A (e.g., H5N1, H1N1) are classifed on the basis of glycoproteins (hemagglutinin and neuraminidase). Relevant terms are as follows:


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First_Aid_Step2. Antigenic drift: Refers to small, gradual changes in surface proteins through point mutations. These small changes are suffcient to allow the virus to escape immune recognition, accounting for the fact that individuals can be infected with infuenza multiple times. Antigenic shift: Refers to an acute, major change in the infuenza A subtype (signifcant genetic reassortment) circulating among humans; leads to pandemics. In the United States, the typical infuenza season begins in November and lasts until March. Vaccination with inactivated infuenza virus is recommended for patients > 50 years of age, children 6 months to 19 years of age, patients of any age with chronic medical problems (e.g., diabetes, heart disease, renal failure, HIV), pregnant women, nursing home residents, and contacts of high-risk groups (e.g., health care workers).


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First_Aid_Step2. Patients typically present with abrupt onset of fevers, myalgias, chills, cough, coryza, and weakness. Elderly patients may have atypical presentations characterized only by confusion. Leukopenia is a common fnding. Rapid infuenza tests of viral antigens from nasopharyngeal swabs are available. More defnitive diagnosis can be made with DFA tests or viral culture. Symptomatic care with analgesics and cough medicine. Antivirals such as oseltamivir or zanamivir are most effective when used within two days of onset and may shorten the course of infection by 1–2 days. Severe 1° viral pneumonia, 2° bacterial pneumonia, sinusitis, bronchitis, and exacerbation of COPD and asthma can occur. Reye’s syndrome, or fatty liver encephalopathy, has been associated with ASA use in children with viral infections, including inf uenza. A live attenuated, nasally delivered inﬂ uenza vaccine is available for healthy people 2–49 years of age who are not pregnant or severely immunocompromised.


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First_Aid_Step2. A live attenuated, nasally delivered inﬂ uenza vaccine is available for healthy people 2–49 years of age who are not pregnant or severely immunocompromised. Risk factors for meningitis include recent ear infection, sinusitis, immunodef ciencies, recent neurosurgical procedures, and sick contacts. Causes are listed in Table 2.8-3. Patients present with fever, malaise, headache, neck stiffness, photophobia, altered mental status, nausea/vomiting, seizures, or signs of meningeal irritation ( Kernig’s and Brudzinski’s signs). Obtain blood cultures. LP for CSF Gram stain and culture; obtain glucose, protein, WBC count plus differential, RBC count, and opening pressure (in the absence of papilledema or focal neurologic def cits). Viral PCRs (e.g., HSV); cryptococcal antigen (for HIV patients). CT or MRI to rule out other diagnoses. CBC may reveal leukocytosis; CSF fndings vary (see Table 2.8-4). TAB LE 2.8-3. Causes of Meningitisa,b


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First_Aid_Step2. CT or MRI to rule out other diagnoses. CBC may reveal leukocytosis; CSF fndings vary (see Table 2.8-4). TAB LE 2.8-3. Causes of Meningitisa,b GBS E. coli/GNRs Listeria S. pneumoniae Neisseria meningitidis H. inﬂ uenzae type b Enteroviruses N. meningitidis Enteroviruses S. pneumoniae HSV S. pneumoniae GNRs Listeria N. meningitidis a Causes in HIV include Cryptococcus, CMV, HSV, VZV, TB, toxoplasmosis (brain abscess), and JC virus (PML). b Note: The incidence of H. inﬂ uenzae meningitis has ↓ greatly with the introduction of the H. inﬂ uenzae vaccine in the last 10–15 years. TABLE 2.8-4. CSF Prof les


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First_Aid_Step2. TABLE 2.8-4. CSF Prof les Normal < 10 < 5 ∼2/3 of serum 15–45 10–20 Clear 3–12 Bacterial meningitis ↔ ↑ (> 1000 PMNs) ↓ ↑ ↑ Cloudy ↔ or ↑ Viral meningitis ↔ ↑ (monos/ lymphs) ↔ ↔ or ↑ ↔ or ↑ Most often clear ↔ or ↑ Aseptic meningitis ↔ ↑ ↔ ↔ or ↑ ↔ Clear ↔ SAH ↑↑ ↑ ↔ ↑ ↔ or ↑ Yellow/red ↔ or ↑ Guillain-Barré syndrome ↔ ↔ ↔ or ↑ ↑↑ ↔ Clear or yellow (high protein) ↔ MS ↔ ↔ or ↑ ↔ ↔ ↔ Clear ↑↑ Pseudotumor cerebri ↔ ↔ ↔ ↔ ↑↑↑ Clear ↔ Antibiotics should be administered rapidly (see Table 2.8-5) and may be given empirically up to two hours before an LP is performed. Some cases of viral meningitis can be treated with supportive care and close follow-up. Close contacts of patients with meningococcal meningitis should receive rifampin, ciprofoxacin, or ceftriaxone prophylaxis.


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First_Aid_Step2. Close contacts of patients with meningococcal meningitis should receive rifampin, ciprofoxacin, or ceftriaxone prophylaxis. T AB LE 2.8-5. Empiric Treatment of Bacterial Meningitis < 1 month GBS, E. coli/GNRs, Listeria. Ampicillin + cefotaxime or gentamicin. 1–3 months Pneumococci, meningococci, H. inﬂ uenzae. Vancomycin IV + ceftriaxone or cefotaxime. 3 months – adulthood Pneumococci, meningococci. Vancomycin IV + ceftriaxone or cefotaxime. > 60 years/alcoholism/ chronic illness Pneumococci, gram-bacilli, Listeria, meningococci. Ampicillin + vancomycin + cefotaxime or ceftriaxone. ■ Dexamethasone may be benefcial in bacterial meningitis, especially S. pneumoniae, if given 15–20 minutes before antibiotics. Cerebral edema: Visible on CT/MRI. Presents with loss of oculocephalic refex. Treat with IV mannitol. Subdural effusions: May be seen on CT scan. Occur in 50% of infants with H. inﬂ uenzae meningitis. No treatment is necessary.


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First_Aid_Step2. Subdural effusions: May be seen on CT scan. Occur in 50% of infants with H. inﬂ uenzae meningitis. No treatment is necessary. Ventriculitis/hydrocephalus: Presents as a worsening clinical picture with improved CSF fndings. Requires ventriculostomy and possibly intraventricular antibiotics. Seizures: Treat with benzodiazepines and phenytoin. Hyponatremia: Administer fuids and monitor sodium concentration. Subdural empyema: Presents with intractable seizures. Requires surgical evacuation. Other: Cranial nerve palsies, sensorineural hearing loss, coma, death. HSV and arboviruses are the most common causes of encephalitis. Rarer etiologies include CMV, toxoplasmosis, West Nile virus, VZV, Borrelia, Rickettsia, Legionella, enterovirus, Mycoplasma, and cerebral malaria. Children and the elderly are the most vulnerable.


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First_Aid_Step2. Presents with altered consciousness, headache, fever, and seizures. Lethargy, confusion, coma, and focal neurologic defcits (cranial nerve def cits, accentuated DTRs) may also be present. The differential includes brain abscess or malignancy, toxic-metabolic encephalopathy, subdural hematoma, and SAH. CSF shows lymphocytic pleocytosis and moderately ↑ protein. RBCs without evidence of trauma suggest HSV encephalitis. The glucose level is low in tuberculous, fungal, bacterial, and amebic infections. Obtain a CSF Gram stain (bacteria), acid-fast stain (mycobacteria), India ink (Cryptococcus), wet preparation (free-living amebae), and Giemsa stain (trypanosomes). PCR for HSV, CMV, EBV, VZV, and enterovirus. MRI may demonstrate a contrast-enhancing lesion in the temporal lobe (in HSV).


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First_Aid_Step2. MRI may demonstrate a contrast-enhancing lesion in the temporal lobe (in HSV). HSV encephalitis requires immediate IV acyclovir. CMV encephalitis is treated with IV ganciclovir +/– foscarnet. Give doxycycline for suspected Rocky Mountain spotted fever, Lyme disease, or ehrlichiosis. A focal, suppurative infection of the brain parenchyma, usually with a “ringenhancing” appearance due to fbrous capsule. The most common infective organisms are streptococci, staphylococci, and anaerobes; multiple organisms are often implicated (80–90% of cases are polymicrobial). Nonbacterial Although other medications may be used, rifampin is the frequently tested prophylaxis of choice for close contacts of patients with meningococcal meningitis. The presence of RBCs in CSF without a history of trauma indicates HSV encephalitis. HSV encephalitis is associated with high morbidity. PCR is highly sensitive and specific. A full course of IV acyclovir is mandatory.


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First_Aid_Step2. HSV encephalitis is associated with high morbidity. PCR is highly sensitive and specific. A full course of IV acyclovir is mandatory. The classic clinical triad of headache, fever, and a focal neurologic deficit is present in 50% of cases of brain abscess. When fever is absent, 1° and metastatic brain tumors become the major differential diagnoses. In general, do not LP a patient with a mass lesion in the brain. Some commonly tested AIDS-defining illnesses: causes include Toxoplasma, Aspergillus, and Candida; zygomycosis should be contemplated in immunocompromised hosts, and neurocysticercosis should be considered in relevant epidemiologic settings. Modes of transmission include the following: Direct spread: Due to paranasal sinusitis (10% of cases; frequently affects young males; often due to Streptococcus milleri), otitis media or mastoiditis (33%), or dental infection (2%). Direct inoculation: Affects patients with a history of head trauma or neurosurgical procedures.


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First_Aid_Step2. Direct inoculation: Affects patients with a history of head trauma or neurosurgical procedures. Hematogenous spread (25% of cases): Often shows an MCA distribution with multiple abscesses that are poorly encapsulated and located at the gray-white junction. Headache, drowsiness, inattention, confusion, and seizures are early symptoms, followed by signs of increasing ICP and then a focal neurologic def cit. Headache is the most common symptom and is often dull, constant, and refractory to treatment. ↑ ICP leads to CN III and CN VI def cits. CT scan will show a ring-enhancing lesion with a low-density core. MRI has higher sensitivity for early abscesses and posterior fossa lesions. CSF analysis is not necessary and may precipitate a herniation syndrome. Lab values may show peripheral leukocytosis, ↑ ESR, and ↑ CRP.


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First_Aid_Step2. CSF analysis is not necessary and may precipitate a herniation syndrome. Lab values may show peripheral leukocytosis, ↑ ESR, and ↑ CRP. Initiate broad-spectrum IV antibiotics and surgical drainage (aspiration or excision) if necessary for diagnostic and/or therapeutic purposes. Lesions < 2 cm can often be treated medically. Administer a third-generation cephalosporin + metronidazole +/– vancomycin; give IV therapy for 6–8 weeks followed by 2–3 weeks PO. Obtain serial CT/MRIs to follow resolution. Dexamethasone with taper may be used in severe cases to ↓ cerebral edema; IV mannitol may be used to ↓ ICP. CNS lymphoma, toxoplasmosis, or PML P. jiroveci pneumonia or recurrent bacterial pneumonia A retrovirus that targets and destroys CD4+ T lymphocytes. Infection is characterized by a progressively high rate of viral replication that leads to a progressive decline in CD4+ count (see Figure 2.8-6).


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First_Aid_Step2. CD4+ count: Indicates the degree of immunosuppression; guides therapy and prophylaxis and helps determine prognosis. Viral load: May predict the rate of disease progression; provides indications for treatment and gauges response to antiretroviral therapy. ■In acute HIV (acute infection/seroconversion, acute retroviral syndrome), the initial infection is often asymptomatic, but patients may also present with mononucleosis-like or f ulike symptoms (e.g., fever, lymphadenop ACUTE LATENT IMMUNODEFICIENCY Acute symptoms Opportunistic infections and malignancies CD4 lymphocytes Anti-p24 antibodies Anti-gp120 antibodies Virus, p24 antigen FIGURE 2.8-6. Time course of HIV infection. (Adapted, with permission, from Levinson W, Jawetz E. Medical Microbiology and Immunol ogy: Examination & Board Review, 6th ed. New York: McGraw-Hill, 2000: 276.) athy, maculopapular rash, pharyngitis, diarrhea, nausea/vomiting, weight loss, headache).


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First_Aid_Step2. ■HIV may later present as night sweats, weight loss, thrush, recurrent infections, or opportunistic infections. Complications are inversely correlated with CD4+ count (see Figure 2.8-7). F IGU R E 2.8-7. Relationship of CD4+ count to development of opportunistic infections. (Reproduced, with permission, from McPhee SJ et al. Current Medical Diagnosis & Treatment, 48th ed. New York: McGraw-Hill, 2009: Fig. 31-1.) The homozygous CCR5 mutation may confer resistance to HIV infection. HIVpatients who are pregnant should avoid efavirenz. If the patient is not on antiretroviral therapy at the time of delivery, she should be treated with zidovudine (AZT) intrapartum. Infants should receive AZT for six weeks after birth. MMR is the only live vaccine that should be given to HIV patients. Do not give oral polio vaccine to HIV-patients or their contacts. The Major Pathogens Concerning Complete T-Cell Collapse


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First_Aid_Step2. MMR is the only live vaccine that should be given to HIV patients. Do not give oral polio vaccine to HIV-patients or their contacts. The Major Pathogens Concerning Complete T-Cell Collapse ELISA test (high sensitivity, moderate specifcity): Detects anti-HIV antibodies in the bloodstream (can take up to six months to appear after exposure). Western blot (low sensitivity, high specif city): Conf rmatory. Rapid HIV tests are now available. Baseline evaluation should include HIV RNA PCR (viral load), CD4+ cell count, CXR, PPD skin testing, Pap smear, VDRL/RPR, and serologies for CMV, hepatitis, toxoplasmosis, and VZV. Evaluation for acute retroviral syndrome (acute HIV) should include HIV RNA PCR (viral load); ELISA may be .


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First_Aid_Step2. Evaluation for acute retroviral syndrome (acute HIV) should include HIV RNA PCR (viral load); ELISA may be . Initiate antiretroviral therapy for the following: (1) symptomatic patients (i.e., those with AIDS-defning illness) regardless of CD4+ count or viral load; (2) asymptomatic patients with a CD4+ count < 350; (3) pregnant patients; and (4) those with specifc HIV-related conditions (e.g., HIV-associated nephropathy). The initial regimen should generally consist of some combination of two nucleoside/nucleotide reverse transcriptase inhibitors (RTIs) plus either one non-nucleoside RTI (NNRTI) or one protease inhibitor. The most important principle is to select multiple medications (usually at least three) in order to achieve durable treatment response and limit the emergence of resistance. The choice of regimen depends on drug-drug interactions, drug tolerance, patient adherence, and comorbid conditions (e.g., hyperlipidemia, refux). Monotherapy/dual therapy should not be used.


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First_Aid_Step2. The choice of regimen depends on drug-drug interactions, drug tolerance, patient adherence, and comorbid conditions (e.g., hyperlipidemia, refux). Monotherapy/dual therapy should not be used. The goal of therapy is viral suppression (< 50 copies), which usually occurs more rapidly than immune reconstitution. CD4+ count and viral load should thus be carefully monitored. An HIV genotype should be obtained before the initiation of therapy and when resistance is suspected, as such testing can provide mutation information and identify resistance to specif c antiretrovirals. Table 2.8-6 outlines prophylactic measures against opportunistic infections. Figure 2.8-8 illustrates the microscopic appearance of some common opportunistic organisms. Risk factors include xerostomia, antibiotic use, denture use, and immunosuppressed states (e.g., HIV, leukemias, lymphomas, cancer, diabetes, corticosteroid inhaler use, immunosuppressive treatment).


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First_Aid_Step2. Hx/PE: Presents with soft white plaques that can be rubbed off, with an erythematous base and possible mucosal burning. The differential includes oral hairy leukoplakia (lateral borders of the tongue; not easily rubbed off). Odynophagia is characteristic of candidal esophagitis. Dx: Usually clinical. KOH or Gram stain shows budding yeast and/or pseudohyphae. Tx: Treat thrush with local therapy (e.g., nystatin suspension or clotrimazole tablets, or a PO azole such as fuconazole). Treat candidal esophagitis with PO azole therapy. T AB LE 2.8-6. Prophylaxis for HIV-Related Opportunistic Infections


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First_Aid_Step2. P. jiroveci pneumonia CD4+ < 200/mm3, prior P. jiroveci infection, unexplained fever × 2 weeks, or HIV-related oral candidiasis. Single-strength TMP-SMX or dapsone +/– pyrimethamine. Discontinue prophylaxis when CD4+ is > 200 for ≥ 3 months. Mycobacterium avium complex (MAC) CD4+ < 50–100/mm3. Weekly azithromycin or daily clarithromycin. Discontinue prophylaxis when CD4+ is > 100/mm3 for > 6 months. Toxoplasma gondii CD4+ < 100/mm3 + IgG serologies. Double-strength TMP-SMX. — M. tuberculosis PPD > 5 mm or “high risk” (see TB section). Sensitive: INH × 9 months (+ pyridoxine) or rifampin +/– pyrazinamide × 2 months. Include pyridoxine with INH-containing regimens. Candida Multiple recurrences. Esophagitis: Fluconazole. Oral: Nystatin swish and swallow. — HSV Multiple recurrences. Acyclovir, famciclovir, or valacyclovir. — All patients. Pneumovax. Give every fve years or when CD4+ is < 200. All patients. Infuenza vaccine annually. — S. pneumoniae Inf uenza


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First_Aid_Step2. Pseudohyphae + budding yeasts Rare fruiting bodies45° angle branching septate hyphae 5–10 μm yeasts with wide capsular halo Narrow-based unequal budding Germ tubes at 37°C Irregular broad (empty-looking) nonseptate hyphae, wide-angle branching F IGU R E 2.8-8. Common opportunistic organisms. The CSF antigen test for cryptococcal meningitis is highly sensitive and specific. Risk factors include AIDS and exposure to pigeon droppings. Hx/PE: Presents with headache, fever, impaired mentation, and absent meningismus. The differential includes toxoplasmosis, lymphoma, TB meningitis, AIDS dementia complex, PML, HSV encephalitis, and other fungal disease. Dx: LP (↓ CSF glucose; ↑ protein; ↑ leukocyte count with monocytic predominance, ↑↑ opening pressure); CSF cryptococcal antigen test, India ink stain, and fungal culture.


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First_Aid_Step2. Dx: LP (↓ CSF glucose; ↑ protein; ↑ leukocyte count with monocytic predominance, ↑↑ opening pressure); CSF cryptococcal antigen test, India ink stain, and fungal culture. Tx: ■IV amphotericin B + f ucytosine × 2 weeks; then give f uconazole 400 mg × 8 weeks. Lifelong maintenance therapy should be administered with fuconazole 200 mg QD, or until CD4+ is > 200 for > 6 months. ■↑ opening pressure may require serial LPs or VP shunt for management. Risk factors include AIDS, spelunking, and exposure to bird or bat excrement, especially in the Ohio and Mississippi river valleys. 1° exposure is often asymptomatic or causes a f ulike illness. Presentation may range from no symptoms to fulminant disease with pulmonary or extrapulmonary manifestations. Fever, weight loss, hepatosplenomegaly, lymphadenopathy, nonproductive cough, and pancytopenia indicate disseminated infection (most often within 14 days).


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First_Aid_Step2. Fever, weight loss, hepatosplenomegaly, lymphadenopathy, nonproductive cough, and pancytopenia indicate disseminated infection (most often within 14 days). The differential includes atypical bacterial pneumonias, blastomycosis, coccidioidomycosis, TB, sarcoidosis, pneumoconiosis, and lymphoma. CXR shows diffuse nodular densities, focal infltrate, cavity, or hilar lymphadenopathy (chronic infection is usually cavitary). The urine and serum polysaccharide antigen test is the most sensitive test for making the initial diagnosis, monitoring response to therapy, and diagnosing relapse. Culture is also diagnostic (blood, sputum, bone marrow, CSF). The yeast form is seen with silver stain on biopsy (bone marrow, lymph node, liver) or bronchoalveolar lavage. Depends on the severity of disease and the host: Mild pulmonary disease or stable nodules: Treat supportively in the immunocompromised host. Chronic cavitary lesions: Give itraconazole for > 1 year.


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First_Aid_Step2. Mild pulmonary disease or stable nodules: Treat supportively in the immunocompromised host. Chronic cavitary lesions: Give itraconazole for > 1 year. Severe acute pulmonary disease or disseminated disease: Amphotericin B or amphotericin B liposomal × 3–10 days followed by itraconazole × 12 weeks or longer. Maintenance therapy with daily itraconazole. Formerly known as Pneumocystis carinii pneumonia, or PCP. Risk factors include impaired cellular immunity and AIDS. Presents with dyspnea on exertion, fever, nonproductive cough, tachypnea, weight loss, fatigue, and impaired oxygenation. Can also present as disseminated disease or as local disease in other organ systems. The differential includes TB, histoplasmosis, and coccidioidomycosis. Diagnosed by cytology of induced sputum or bronchoscopy specimen with silver stain and immunofuorescence. Obtain an ABG to check PaO2.


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First_Aid_Step2. Diagnosed by cytology of induced sputum or bronchoscopy specimen with silver stain and immunofuorescence. Obtain an ABG to check PaO2. CXR may show diffuse, bilateral interstitial infltrates with a ground-glass appearance, but any presentation is possible. Treat with high-dose TMP-SMX × 21 days. Clindamycin and primaquine constitute an alternative regimen for patients with sulfa allergy. A prednisone taper should be used in patients with moderate to severe hypoxemia (PaO2 < 70 mm or an arterial-alveolar oxygen gradient > 35).


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First_Aid_Step2. A prednisone taper should be used in patients with moderate to severe hypoxemia (PaO2 < 70 mm or an arterial-alveolar oxygen gradient > 35). Most 1° CMV infections are asymptomatic; serious reactivation generally occurs only in immunocompromised patients. Seventy percent of adults in the United States have been infected. Transmission occurs via sexual contact, in breast milk, via respiratory droplets in nursery or day care facilities, and through blood transfusions. Risk factors for reactivation include the f rst 100 days status post tissue or bone marrow transplant and HIV positivity with a CD4+ < 100 or a viral load > 10,000. Systemic infection may resemble EBV mononucleosis (see the discussion of infectious mononucleosis). Specifc manifestations are as follows: CMV retinitis: Has a high rate of retinal detachment (“pizza pie” retinopathy), and presents with foaters and visual feld changes (CD4+ < 50).


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First_Aid_Step2. Specifc manifestations are as follows: CMV retinitis: Has a high rate of retinal detachment (“pizza pie” retinopathy), and presents with foaters and visual feld changes (CD4+ < 50). GI and hepatobiliary involvement: Can present with multiple nonspecifc GI symptoms, including bloody diarrhea. CMV, microsporidia, and cryptosporidia have been implicated in the development of AIDS cholangiopathy. CMV pneumonitis: Presents with cough, fever, and sparse sputum production; associated with a high mortality rate. Much more common in patients with hematologic malignancies and transplant patients than in those with AIDS. CNS involvement: Can include polyradiculopathy, transverse myelitis, and subacute encephalitis (CD4+ < 50; periventricular calcif cations). Suspect P. jiroveci pneumonia in any HIV patient who presents with nonproductive cough and dyspnea. Treat CMV infection with ganciclovir. Virus isolation, culture, tissue examination, serum PCR.


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First_Aid_Step2. Suspect P. jiroveci pneumonia in any HIV patient who presents with nonproductive cough and dyspnea. Treat CMV infection with ganciclovir. Virus isolation, culture, tissue examination, serum PCR. Treat with ganciclovir or foscarnet. Treat underlying disease if the patient is immunocompromised. Ubiquitous organisms causing pulmonary and disseminated infection in several demographic groups. The 1° form occurs in apparently healthy nonsmokers (Lady Windermere syndrome); a 2° pulmonary form affects patients with preexisting pulmonary disease such as COPD, TB, or CF. Disseminated infection occurs in AIDS patients with a CD4+ < 50. There is no evidence that behavioral change affects exposure. Disseminated M. avium infection in AIDS is associated with fever, weakness, and weight loss in patients who are not on HAART or chemoprophylaxis for MAC. Hepatosplenomegaly and lymphadenopathy are occasionally seen.


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First_Aid_Step2. Hepatosplenomegaly and lymphadenopathy are occasionally seen. Adrenal insuffciency is possible in the setting of infltration into the adrenals. Obtain mycobacterial blood cultures ( in 2–3 weeks). Labs show anemia, hypoalbuminemia, and ↑ serum alkaline phosphatase and LDH. Biopsy of bone marrow, intestine, or liver reveals foamy macrophages with acid-fast bacilli. Typical granulomas may be absent in immunocompromised patients. Treat with clarithromycin and ethambutol +/– rifabutin and HAART. Continue for > 12 months and until CD4+ is > 100 for > 6 months. Weekly azithromycin for those with a CD4+ < 50 or AIDS-def ning opportunistic infection. Risk factors include ingesting raw or undercooked meat and changing cat litter. Worldwide, exposure is highest in France. 1° infection is usually asymptomatic. Reactivated toxoplasmosis occurs in immunosuppressed patients and may present in specif c organs (brain, lung, and eye > heart, skin, GI tract, and liver).


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First_Aid_Step2. 1° infection is usually asymptomatic. Reactivated toxoplasmosis occurs in immunosuppressed patients and may present in specif c organs (brain, lung, and eye > heart, skin, GI tract, and liver). ■Encephalitis is common in seropositive AIDS patients. Classically, CNS lesions present with fever, headache, altered mental status, seizures, and focal neurologic def cits. Serology, PCR (indicates exposure and risk for reactivation); tissue examination for histology, isolation of the organism in mice, or tissue culture. In the setting of CNS involvement, obtain a CT scan (can show multiple isodense or hypodense, ring-enhancing mass lesions) or an MRI (predilection for basal ganglia; more sensitive). Induction with high-dose PO pyrimethamine + sulfadiazine and leukovorin × 4–8 weeks; maintenance with low-dose pyrimethamine + sulfadiazine and leukovorin until the disease has resolved clinically and radio-graphically.


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First_Aid_Step2. TMP-SMX (Bactrim DS) or pyrimethamine + dapsone can be used for prophylaxis in patients with a CD4+ < 100 and a toxoplasmosis IgG. The two most likely differential diagnoses of ring-enhancing lesions in AIDS patients are toxoplasmosis and CNS lymphoma. The most common bacterial STD in the United States. Caused by Chlamydia trachomatis, which can infect the genital tract, urethra, anus, and eye. Risk factors include unprotected sexual intercourse, new or multiple partners, and frequent douching. Often coexists with or mimics N. gonorrhoeae infection (known as nongonococcal urethritis when gonorrhea is absent). LGV serovars of Chlamydia cause lymphogranuloma venereum, an emerging cause of proctocolitis. Infection is often asymptomatic but may present with urethritis, mucopurulent cervicitis, or PID. Exam may reveal cervical/adnexal tenderness in women or penile discharge and testicular tenderness in men.


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First_Aid_Step2. Exam may reveal cervical/adnexal tenderness in women or penile discharge and testicular tenderness in men. The differential includes gonorrhea, endometriosis, PID, orchitis, vaginitis, and UTI. Lymphogranuloma venereum presents in its 1° form as a painless, transient papule or shallow ulcer. In its 2° form, it presents as painful swelling of the inguinal nodes, and in its 3° form it can present as an “anogenital syndrome” (anal pruritus with discharge, rectal strictures, rectovaginal f stula, and elephantiasis). Diagnosis is usually clinical. Culture is the gold standard. Urine tests (PCR or ligase chain reaction) are a rapid means of detection, while DNA probes and immunofuorescence (for gonorrhea/chlamydia) take 48–72 hours. Gram stain of urethral or genital discharge may show PMNs but no bacteria (intracellular). Chlamydia infection is a common cause of nongonococcal urethritis in men.


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First_Aid_Step2. Gram stain of urethral or genital discharge may show PMNs but no bacteria (intracellular). Chlamydia infection is a common cause of nongonococcal urethritis in men. Chlamydia species cause arthritis, neonatal conjunctivitis, pneumonia, nongonococcal urethritis/ PID, and lymphogranuloma venereum. Treat for gonorrhea and chlamydia in light of the high prevalence of coinfection. Syphilis is the “great imitator” because its dermatologic findings resemble those of many other diseases. Doxycycline 100 mg PO BID × 7 days or azithromycin 1 g PO × 1 day. Use erythromycin in pregnant patients. Treat sexual partners, and maintain a low threshold to treat for N. gonorrhoeae. LGV serovars require prolonged therapy for 21 days. Chronic infection and pelvic pain, Reiter’s syndrome (urethritis, conjunctivitis, arthritis), Fitz-Hugh–Curtis syndrome (perihepatic inf ammation and f brosis). Ectopic pregnancy/infertility can result from PID (in women) and epididymitis (in men).


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First_Aid_Step2. Ectopic pregnancy/infertility can result from PID (in women) and epididymitis (in men). A gramintracellular diplococcus that can infect almost any site in the female reproductive tract. Infection in men tends to be limited to the urethra. Presents with a greenish-yellow discharge, pelvic or adnexal pain, and swollen Bartholin’s glands. Men experience a purulent urethral discharge, dysuria, and erythema of the urethral meatus. The differential includes chlamydia, endometriosis, pharyngitis, PID, vaginitis, UTI, salpingitis, and tubo-ovarian abscess. Gram stain and culture is the gold standard for any site (i.e., pharynx, cervix, urethra, or anus). Nucleic acid amplif cation tests can be sent on penile/vaginal tissue or from urine. Disseminated disease may present with monoarticular septic arthritis, rash, and/or tenosynovitis.


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First_Aid_Step2. Disseminated disease may present with monoarticular septic arthritis, rash, and/or tenosynovitis. Ceftriaxone IM or cefepime PO × 1 dose. Also treat for presumptive chlamydia coinfection (doxycycline × 7 days or macrolide × 1 dose). Condoms are effective prophylaxis. Treat the sexual partner or partners if possible. Fluoroquinolones should not be used because of emerging resistance. Disseminated disease requires IV ceftriaxone for at least 24 hours. Persistent infection with pain; infertility; tubo-ovarian abscess with rupture; disseminated gonococcal infection (see Figure 2.8-9). Caused by Treponema pallidum, a spirochete. AIDS can accelerate the course of disease progression. ■1° (10–90 days after infection): Presents with a painless ulcer (chancre; see Figure 2.8-10). F IGU R E 2.8-9. Disseminated gonococcal infection. Hemorrhagic, painful pustules on erythematous bases. (Reproduced, with permission, from


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First_Aid_Step2. F IGU R E 2.8-9. Disseminated gonococcal infection. Hemorrhagic, painful pustules on erythematous bases. (Reproduced, with permission, from Wolff K et al. Fitzpatrick’s Color Atlas & Synopsis of Clinical Dermatology, 5th ed. New York: McGraw-Hill, 2005: Fig. 27-17.) 2° (4–8 weeks after chancre): Presents with low-grade fever, headache, malaise, and generalized lymphadenopathy with a diffuse, symmetric, asymptomatic (nonpruritic) maculopapular rash on the soles and palms. Highly infective 2° eruptions include mucous patches or condylomata lata (see Figure 2.8-11). Meningitis, hepatitis, nephropathy, and eye involvement may also be seen. Early latent (period from resolution of 1° or 2° syphilis to end of f rst year of infection): No symptoms; serology. Late latent (period of asymptomatic infection beyond the f rst year): No symptoms; or serology. One-third progress to 3° syphilis. FIGURE 2.8-10. 1° syphilis.


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First_Aid_Step2. Late latent (period of asymptomatic infection beyond the f rst year): No symptoms; or serology. One-third progress to 3° syphilis. FIGURE 2.8-10. 1° syphilis. The chancre is an ulcerated papule with a smooth, clean base; raised, indurated borders; and scant discharge. (Reproduced, with permission, from Bondi EE. Dermatology: Diagnosis and Therapy, 1st ed. Stamford, CT: Appleton & Lange, 1991: 394.) FIGURE 2.8-11. Condylomata lata.


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First_Aid_Step2. FIGURE 2.8-11. Condylomata lata. Typical appearance of the verrucous heaped-up lesions of condylomata lata. (Reproduced, with permission, from Wolff K et al. Fitzpatrick’s Color Atlas & Synopsis of Clinical Dermatology, 5th ed. New York: McGraw-Hill, 2005: Fig. 27-27.) ■ 3° (late manifestations appearing 1–20 years after initial infection): Presents with destructive, granulomatous gummas. Neurosyphilis includes tabes dorsalis (posterior column degeneration), meningitis, and Argyll Robertson pupil (constricts with accommodation but not reactive to light). Cardiovascular fndings include dilated aortic root, aortitis, aortic root aneurysms, and aortic regurgitation. ■See Table 2.8-7. VDRL false positives are seen with Viruses (mononucleosis, HSV, HIV, hepatitis), Drugs/IV drug use, Rheumatic fever/Rheumatoid arthritis, and SLE/Leprosy. TABLE 2.8-7.


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First_Aid_Step2. ■See Table 2.8-7. VDRL false positives are seen with Viruses (mononucleosis, HSV, HIV, hepatitis), Drugs/IV drug use, Rheumatic fever/Rheumatoid arthritis, and SLE/Leprosy. TABLE 2.8-7. Dark-f eld microscopy Identifes motile spirochetes (only 1° and 2° lesions). VDRL/RPR Rapid and cheap, but sensitivity is only 60–75% in 1° disease. Many false positives. FTA-ABS Sensitive and specifc. Used as a 2° diagnostic test. TPPAa Sensitivity and specifcity similar to FTA-ABS but easier to use. Becoming the 2° test of choice. a TPPA = T. pallidum particle agglutination test. ■Neurosyphilis should be suspected and ruled out in any AIDS patient with neurologic symptoms and a RPR. 1°/2°: Benzathine penicillin IM × 1 day. Tetracycline or doxycycline × 14 days may be used for patients with penicillin allergies. Latent infection: Treat with benzathine penicillin once weekly × 3 weeks. Neurosyphilis: Treat with penicillin IV; penicillin-allergic patients should be desensitized prior to therapy.


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First_Aid_Step2. Latent infection: Treat with benzathine penicillin once weekly × 3 weeks. Neurosyphilis: Treat with penicillin IV; penicillin-allergic patients should be desensitized prior to therapy. See Table 2.8-8 for a description of common sexually transmitted genital lesions along with an outline of their diagnosis and treatment. Remember that treatment of syphilis can result in an acute ﬂ ulike illness known as the Jarisch-Herxheimer reaction. Affect females more frequently than males, and E. coli cultures are obtained in 80% of cases. See the mnemonic SEEKS PP for other pathogens. Risk factors include the presence of catheters or other urologic instrumentation, anatomic abnormalities (e.g., BPH, vesicoureteral ref ux), previous UTIs or pyelonephritis, diabetes mellitus (DM), recent antibiotic use, immunosuppression, and pregnancy.


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First_Aid_Step2. Present with dysuria, urgency, frequency, suprapubic pain, and possibly hematuria. Children may present with bed-wetting, poor feeding, recurrent fevers, and foul-smelling urine. The differential includes vaginitis, STDs, urethritis or acute urethral syndrome, and prostatitis. Diagnosed by clinical symptoms. In the absence of symptoms, treatment is warranted only for children, those with anatomical GU tract anomalies, pregnant women, those with instrumented urinary tracts, patients scheduled for GU surgery, and renal transplant patients. Urine dipstick/UA: ↑ leukocyte esterase (a marker of WBCs) is 75% sensitive and up to 95% specif c. ↑ nitrites (a marker of bacteria), ↑ urine pH (Proteus infections), and hematuria (seen with cystitis) are also commonly seen. Microscopic analysis: Pyuria (> 5 WBCs/hpf) and bacteriuria (1 organism/hpf = 106 organisms/mL) are suggestive. Urine culture: The gold standard is > 105 CFU/mL.


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First_Aid_Step2. Microscopic analysis: Pyuria (> 5 WBCs/hpf) and bacteriuria (1 organism/hpf = 106 organisms/mL) are suggestive. Urine culture: The gold standard is > 105 CFU/mL. Uncomplicated UTI: Treat on an outpatient basis with PO TMP-SMX or a f uoroquinolone × 3 days, or nitrofurantoin × 7 days. Note that resistance to TMP-SMX and fuoroquinolones has been increasing. Complicated UTI (urinary obstruction, men, renal transplant, catheters, instrumentation): Administer the same antibiotics as above, but for 7–14 days. Common UTI bugs— SEEKS PP Serratia E. coli Enterobacter Klebsiella pneumoniae S. saprophyticus Pseudomonas Proteus mirabilis T AB LE 2.8-8. Sexually Transmitted Genital Lesions


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First_Aid_Step2. Lesion Papule becomes a beefy-red ulcer with a characteristic rolled edge of granulation tissue Papule or pustule (chancroid; see Figure 2.8-12) Vesicle (3–7 days postexposure) Papule (condylomata acuminata; warts) Papule (chancre) Appearance Raised red lesions with a white border Irregular, deep, well demarcated, necrotic Regular, red, shallow ulcer Irregular, pink or white, raised; caulif ower Regular, red, round, raised Number 1 or multiple 1–3 Multiple Multiple Single Size 5–10 mm 10–20 mm 1–3 mm 1–5 mm 1 cm Pain No Yes Yes No No Concurrent signs and symptoms Granulomatous ulcers Inguinal lymphadenopathy Malaise, myalgias, and fever with vulvar burning and pruritus Pruritus Regional adenopathy Clinical exam, biopsy (Donovan bodies) Diffcult to culture; diagnosis is made on clinical grounds Tzanck smear shows multinucleated giant cells; viral cultures; DFA or serology Clinical exam; biopsy for conf rmation Spirochetes seen under dark-f eld microscopy; T. pallidum identifed by serum


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First_Aid_Step2. Tzanck smear shows multinucleated giant cells; viral cultures; DFA or serology Clinical exam; biopsy for conf rmation Spirochetes seen under dark-f eld microscopy; T. pallidum identifed by serum antibody test Doxycycline (100 mg BID) or azithromycin (1 g weekly) × 3 weeks Doxycycline (100 mg BID) or azithromycin (1 g weekly) × 3 weeks Acyclovir or valacyclovir for 1° infection Cryotherapy; topical agents such as podophyllin, trichloroacetic acid, or 5-FU cream Penicillin IM Diagnosis Treatmentd a Previously known as Calymmatobacterium granulomatis. b Some 85% of genital herpes lesions are caused by HSV-2. c HPV serotypes 6 and 11 are associated with genital warts; types 16, 18, and 31 are associated with cervical cancer. d For all, treat sexual partners.


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First_Aid_Step2. FIGURE 2.8-12. Chancroid. Multiple, painful ulcers. (Reproduced, with permission, from Wolff K et al. Fitzpatrick’s Color Atlas & Synopsis of Clinical Dermatology, 5th ed. New York: McGraw-Hill, 2005: Fig. 27-31.) Pregnant patients: Treat asymptomatic bacteruria or symptomatic UTI with nitrofurantoin or cephalosporin × 3–7 days. Avoid f uoroquinolones. Confrm clearance with a repeat culture post-treatment. Patients with urosepsis should be hospitalized and initially treated with IV antibiotics. Consider broader coverage to include resistant GNRs or enterococcus. Prophylactic antibiotics may be given to women with uncomplicated recurrent UTIs. Check for prostatitis in men. Nearly 85% of community-acquired cases of pyelonephritis result from the same pathogens that cause cystitis. Cystitis and pyelonephritis have similar risk factors. ■Signs and symptoms are similar to those of cystitis but show evidence of upper urinary tract disease.


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First_Aid_Step2. ■Signs and symptoms are similar to those of cystitis but show evidence of upper urinary tract disease. ■ Symptoms include f ank pain, fever/chills, and nausea/vomiting. Dysuria, frequency, and urgency are also possible. ■UA and culture: Results are similar to those of cystitis, but with WBC casts. Send blood cultures to rule out urosepsis. Pyelonephritis is the most common serious medical complication of pregnancy. Twenty to thirty percent of patients with untreated bacteriuria will develop pyelonephritis. When in doubt, admit a patient with pyelonephritis and administer IV antibiotics. Urosepsis must be considered in any elderly patient with altered mental status. SIRS = two or more of the following: 1. Temperature: Either < 36°C or > 38°C (i.e., hypothermia or fever). 2. Tachypnea: > 20 breaths per minute or PaCO2 < 32 mmHg on ABG. 3. Tachycardia: HR > 90 bpm. 4. Leukocytosis/leukopenia: WBC < 4000 cells/mm3 or > 12,000 cells/mm3. CBC: Reveals leukocytosis.


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First_Aid_Step2. 2. Tachypnea: > 20 breaths per minute or PaCO2 < 32 mmHg on ABG. 3. Tachycardia: HR > 90 bpm. 4. Leukocytosis/leukopenia: WBC < 4000 cells/mm3 or > 12,000 cells/mm3. CBC: Reveals leukocytosis. Imaging: In general, imaging is not necessary. Ultrasound can be used to rule out obstruction and calculi and can often confrm the diagnosis noninvasively, but CT is becoming the test of choice in patients with adequate renal function who are not responding to therapy. In recurrent cases, IVP may demonstrate renal scarring. For mild cases, patients may be treated on an outpatient basis for 10–14 days. Fluoroquinolones are frst-line therapy. Encourage ↑ PO f uids and monitor closely.


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First_Aid_Step2. For mild cases, patients may be treated on an outpatient basis for 10–14 days. Fluoroquinolones are frst-line therapy. Encourage ↑ PO f uids and monitor closely. Admit and administer IV antibiotics to patients who have serious medical complications or systemic symptoms, are pregnant, present with severe nausea and vomiting, or have suspected bacteremia. Fluoroquinolones, thirdor fourth-generation cephalosporins, β-lactam/β-lactamase inhibitors, and carbapenem may be used depending on disease severity. Defned as the presence of systemic infammatory response syndrome (SIRS) with a documented infection, induced by microbial invasion or toxins in the bloodstream. Severe sepsis refers to sepsis with end-organ dysfunction due to poor perfusion. Septic shock refers to sepsis with hypotension and organ dysfunction from vasodilation. Examples include the following: Gram-shock (e.g., staphylococci and streptococci) 2° to f uid loss caused by exotoxins.


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First_Aid_Step2. Gram-shock (e.g., staphylococci and streptococci) 2° to f uid loss caused by exotoxins. Gram-shock (e.g., E. coli, Klebsiella, Proteus, and Pseudomonas) 2° to vasodilation caused by endotoxins (lipopolysaccharide). Neonates: GBS, E. coli, Listeria monocytogenes, H. inﬂ uenzae. Children: H. inﬂ uenzae, pneumococcus, meningococcus. Adults: Gramcocci, aerobic grambacilli, anaerobes (dependent on the presumed site of infection). IV drug users/indwelling lines: S. aureus, coagulase-Staphylococcus species. Asplenic patients: Pneumococcus, H. inﬂ uenzae, meningococcus (encapsulated organisms). Presents with abrupt onset of fever and chills, altered mental status, tachycardia, and tachypnea. Severe sepsis is seen in end-organ dysfunction. Hypotension occurs in cases of septic shock. Septic shock is typically a warm shock with warm skin and extremities. This contrasts with cardiogenic shock, which typically presents with cool skin and extremities.


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First_Aid_Step2. Septic shock is typically a warm shock with warm skin and extremities. This contrasts with cardiogenic shock, which typically presents with cool skin and extremities. Petechiae, ecchymoses, or abnormal coagulation tests suggest DIC (2–3% of cases). A clinical diagnosis. Labs show leukocytosis or leukopenia with ↑ bands, thrombocytopenia (50% of cases), evidence of ↓ tissue perfusion (↑ creatinine, ↑ LFTs), and abnormal coagulation studies (↑ INR). It is critical to obtain cultures of all appropriate sites (e.g., blood, sputum, CSF, wound, urine). Imaging (CXR, CT) may aid in establishing the etiology or site of infection. ICU admission may be required. Treat aggressively with IV f uids, pressors, and empiric antibiotics (based on the likely source of infection). Treat underlying factors (e.g., remove Foley catheter or infected lines). The 1° goal is to maintain BP and perfusion to end organs.


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First_Aid_Step2. Treat underlying factors (e.g., remove Foley catheter or infected lines). The 1° goal is to maintain BP and perfusion to end organs. A protozoal disease caused by four strains of the genus Plasmodium (P. falciparum, P. vivax, P. ovale, and P. malariae) and transmitted by the bite of an infected female Anopheles mosquito. P. falciparum has the highest morbidity and causes the largest number of deaths, occasionally within 24 hours of symptom onset. Recent outbreaks have occurred in parts of the southern and eastern United States and in Europe, mainly through the arrival of infected travelers and immigrants from endemic areas. Travelers to endemic areas should take chemoprophylaxis and use mosquito repellent and bed nets to minimize exposure.


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First_Aid_Step2. Patients have a history of exposure in a malaria-endemic area, with periodic attacks of sequential chills, fever (> 41°C), and diaphoresis occurring over 4–6 hours. Splenomegaly often appears four or more days after onset of symptoms. Patients are often asymptomatic between attacks, which recur every 2–3 days, depending on the Plasmodium strain. Severely ill patients may present with hyperpyrexia, prostration, impaired consciousness, agitation, hyperventilation, and bleeding. The presence of rash, lymphadenopathy, neck stiffness, or photophobia suggests a different or additional diagnosis. Timely diagnosis of the correct strain is essential because P. falciparum can be fatal and is often resistant to standard chloroquine treatment.


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First_Aid_Step2. Timely diagnosis of the correct strain is essential because P. falciparum can be fatal and is often resistant to standard chloroquine treatment. Giemsa-or Wright-stained thick and thin blood f lms should be sent for expert microscopic evaluation to determine the strain as well as the degree of parasitemia. Specimens should be obtained at eight-hour intervals for three days, including during and between febrile periods. CBC usually demonstrates normochromic, normocytic anemia with reticulocytosis. If resources allow, more sensitive serologic tests are available, including rapid antigen detection methods, fuorescent antibody methods, and PCR. Malaria should be considered in the differential for any patient who has emigrated from or recently traveled to tropical locations and presents with fever. P. vivax, P. ovale, and P. malariae can all cause symptoms months to years after initial infection.


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First_Aid_Step2. P. vivax, P. ovale, and P. malariae can all cause symptoms months to years after initial infection. Obtain a finger stick in a patient with malaria and mental status changes to rule out hypoglycemia. ■Uncomplicated malarial infection can be treated orally, with the choice of medication determined by the Plasmodium strain. Chloroquine has been the standard antimalarial medication, but increasing resistance has led to A young adult who presents with the triad of fever, sore throat, and lymphadenopathy may have infectious mononucleosis. The lymphocytosis in EBV infection is predominantly due to B-cell proliferation, but the atypical cells are T lymphocytes. the use of other medications, including quinine with clindamycin or doxycycline, atovaquone, mefoquine, artesunate, and halofantrine.


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First_Aid_Step2. the use of other medications, including quinine with clindamycin or doxycycline, atovaquone, mefoquine, artesunate, and halofantrine. The life cycles of P. vivax and P. ovale strains include dormant liver hypnozoite forms, which are resistant to treatment with chloroquine. Thus, in cases of P. vivax, P. ovale, or an unknown strain, primaquine is added to eradicate the hypnozoites in the liver. Severe infections can be treated with parenteral antimalarial medications (IV quinidine) with transition to oral regimens as tolerated. Newer combinations such as proguanil/atovaquone (Malarone) eliminate the need for multiple medications. Symptoms can be treated with supportive care. Cerebral malaria: Headache, change in mental status, neurologic signs, retinal hemorrhages, convulsions, delirium, coma. Severe hemolytic anemia: Usually associated with P. falciparum infection. Acute tubular necrosis and renal failure: Associated with blackwater fever (dark urine due to hemoglobinuria).


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First_Aid_Step2. Severe hemolytic anemia: Usually associated with P. falciparum infection. Acute tubular necrosis and renal failure: Associated with blackwater fever (dark urine due to hemoglobinuria). Noncardiogenic pulmonary edema: Often precipitated by overly rapid re-hydration. Other: Additional complications include grambacteremia, acute hepatopathy, hypoglycemia, cardiac dysrhythmias, secretory diarrhea, lactic acidosis, DIC, and a low birth rate in children of infected mothers. Most commonly occurs in young adult patients; usually due to acute EBV infection. Transmission most often occurs through exchange of body f uids, including saliva. Presents with fever and pharyngitis. Fatigue invariably accompanies initial illness and may persist for 3–6 months. Exam may reveal low-grade fever, generalized lymphadenopathy (especially posterior cervical), tonsillar exudate and enlargement, palatal petechiae, a generalized maculopapular rash, splenomegaly, and bilateral upper eyelid edema.


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First_Aid_Step2. Patients who present with pharyngitis as their 1° symptom may be misdiagnosed as having streptococcal pharyngitis (30% of patients with infectious mononucleosis are asymptomatic carriers of group A strep in their oropharynx). Treatment of patients with ampicillin (for streptococcal pharyngitis) during acute EBV infection can cause a prolonged, pruritic, drug-related maculopapular rash. This rash does not portend future sensitivity to β-lactams and will remit with discontinuation of ampicillin. The differential also includes CMV, toxoplasmosis, HIV, HHV-6, other causes of viral hepatitis, and lymphoma. Diagnosed by the heterophil antibody (Monospot) test (may be in the frst few weeks after symptoms begin). The EBV-infected proliferating B cells produce a characteristic antibody that agglutinates the horse and sheep RBCs that are the basis for the Monospot test.


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First_Aid_Step2. EBV-specif c antibodies can be ordered in patients with suspected mono nucleosis and a Monospot test. Infectious mononucleosis syndromes that are Monospot and EBV-antibody are most often due to CMV infection. Acute HIV and other viral etiologies should be considered. CBC with differential often reveals mild thrombocytopenia with relative lymphocytosis and > 10% atypical T lymphocytes. CMP usually reveals mildly elevated transaminases, alkaline phosphatase, and total bilirubin. Treatment is mostly supportive, as there is no effective antiviral therapy. Corticosteroids are indicated for airway compromise due to tonsillar enlargement, severe thrombocytopenia, or severe autoimmune hemolytic anemia. CNS infection: Can present as aseptic meningitis, encephalitis, meningoencephalitis, cranial nerve palsies (particularly CN VII), optic and peripheral neuritis, transverse myelitis, or Guillain-Barré syndrome.


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First_Aid_Step2. Splenic rupture: Occurs in < 0.5% of cases. More common in males, and presents with abdominal pain, referred shoulder pain, or hemodynamic compromise. Upper airway obstruction: Treat with steroids. Bacterial superinfection: Ten percent of patients develop streptococcal pharyngitis secondarily. Fulminant hepatic necrosis: More common in males; the most common cause of death in affected males. Autoimmune hemolytic anemia: Occurs in 2% of patients during the f rst two weeks. Coombs . Mild anemia lasts 1–2 months. Treat with corticosteroids if severe. Other: Rare complications associated with acute EBV infection include hepatitis (which can be fulminant), myocarditis or pericarditis with electrocardiographic changes, pneumonia with pleural effusion, interstitial nephritis, genital ulcerations, and vasculitis. About one-third of patients with infectious mononucleosis have coexisting streptococcal pharyngitis that requires treatment. Fever of Unknown Origin (FUO)


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First_Aid_Step2. About one-third of patients with infectious mononucleosis have coexisting streptococcal pharyngitis that requires treatment. Fever of Unknown Origin (FUO) A temperature of > 38.3°C of at least three weeks’ duration that remains undiagnosed following three outpatient visits or three days of hospitalization. Presents with fever, headache, myalgia, and malaise. The differential includes the following: Infectious: TB, endocarditis (e.g., HACEK organisms; see the discussion of infective endocarditis), occult abscess, osteomyelitis, catheter infections. In HIV patients, consider MAC, histoplasmosis, CMV, or lymphoma. Neoplastic: Lymphomas, leukemias, hepatic and renal cell carcinomas. Autoimmune: Still’s disease, SLE, cryoglobulinemia, polyarteritis nodosa, connective tissue disease, granulomatous disease (including sarcoidosis). Miscellaneous: Pulmonary emboli, alcoholic hepatitis, drug fever, familial Mediterranean fever, factitious fever. ■ Undiagnosed (10–15%).


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First_Aid_Step2. Miscellaneous: Pulmonary emboli, alcoholic hepatitis, drug fever, familial Mediterranean fever, factitious fever. ■ Undiagnosed (10–15%). Overall, infections and cancer account for the majority of cases of FUO (> 60%). Autoimmune diseases account for ~15%. In the elderly, rheumatic diseases account for one-third of cases. FUO patients without other symptoms do not require empiric antibiotic therapy. With fever and rash, think— Lyme disease is the most common vector-borne disease in North America. Labs: Confrm the presence of fever and take a detailed history (including family, social, sexual, occupational, dietary, exposures [pets/animals], and travel); obtain a CXR, CBC with differential, ESR, multiple blood cultures, sputum Gram stain and culture, UA and culture, and PPD. Specifc tests (ANA, RF, viral cultures, viral serologies/antigen tests) can be obtained if an infectious or autoimmune etiology is suspected.


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First_Aid_Step2. Imaging: CT of the chest and abdomen should be done early in the workup of a true FUO. Rule out drug fever. Invasive testing (marrow/liver biopsy) is generally low yield. Laparoscopy and colonoscopy are higher yield as second-line tests (after CT). Stop unnecessary medications. Give empiric antibiotics to severely ill patients until the etiology has been determined. Stop antibiotics if there is no response. Defned as a single oral temperature of ≥ 38.3°C (101°F) or a temperature of ≥ 38.0°C (100.4°F) for ≥ 1 hour in a neutropenic patient (i.e., an absolute neutrophil count of < 500 cells/mm3). Hx/PE: Common in cancer patients undergoing chemotherapy (neutropenic nadir 7–10 days postchemotherapy). Infammation may be minimal or absent. Dx: Send appropriate cultures, including blood, urine, sputum, and wound. Consider testing for viruses, fungi, and mycobacteria.


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First_Aid_Step2. Dx: Send appropriate cultures, including blood, urine, sputum, and wound. Consider testing for viruses, fungi, and mycobacteria. Conduct a thorough physical exam, but avoid a rectal exam in light of the bleeding risk if the patient is thrombocytopenic. Obtain a CBC with differential, serum creatinine, BUN, and transaminases; order blood, urine, lesion, and stool cultures. CXR for patients with respiratory symptoms; CT scan to evaluate for abscesses or other occult infection. Tx: Empiric antibiotic therapy (see Figure 2.8-13). Routine use of colony-stimulating factors is not indicated. If fevers persist after 72 hours despite antibiotic therapy, start antifungal treatment. A tick-borne disease caused by the spirochete Borrelia burgdorferi. Usually seen during the summer months, and carried by Ixodes ticks on white-tailed deer and white-footed mice. Endemic to the Northeast, northern Midwest, and Pacif c coast.


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First_Aid_Step2. Hx/PE: Presents with the onset of rash with fever, malaise, fatigue, headache, myalgias, and/or arthralgias. Infection usually occurs after a tick feeds for > 18 hours. ■1° (early localized disease): Erythema migrans begins as a small erythematous macule or papule that is found at the tick-feeding site and expands slowly over days to weeks. The border may be macular or raised, often with central clearing (“bull’s eye”).


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First_Aid_Step2. Fever (≥ 38.3°C) + Neutropenia (< 500 neutrophils/mm3) PO IV (outpatient) Vancomycin not needed Reassess after 3–5 days Vancomycin needed Intermediate/High Risk High-dose chemo? Hematologic malignancy? Neutropenia > 14 days? Combination Therapy: Aminoglycosides + antipseudomonal, penicillin, cefepime, ceftazidime, or carbapenem Vancomycin + cefepime, ceftazidime, or carbapenem ± aminoglycoside Monotherapy: Cefepime, ceftazidine, or carbapenem Ciprofloxacin + amoxicillin/clavulanate (adults only) Low Risk Solid tumors treated as outpatient with conventional chemotherapy? Minimal comorbidity? Neutropenia < 7 days? F IGU R E 2.8-1 3. Empiric treatment algorithm for a neutropenic fever patient. 2° (early disseminated disease): Presents with migratory polyarthropathies, neurologic phenomena (e.g., Bell’s palsy), meningitis and/or myocarditis, and conduction abnormalities (third-degree heart block). 3° (late disease): Arthritis and subacute encephalitis (memory loss and mood change).


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First_Aid_Step2. 3° (late disease): Arthritis and subacute encephalitis (memory loss and mood change). Dx: Clinical diagnosis of erythema migrans is as follows: ELISA and Western blot: Use the Western blot to conf rm a or indeterminate ELISA. A ELISA denotes exposure but is not specif c for active disease. Western blots sent without ELISA have high rates of false positives. Tissue culture/PCR: Extremely diffcult to obtain; not routinely done. Tx: Treat early disease with doxycycline and more advanced disease (e.g., CNS or arthritic disease) with ceftriaxone. Consider empiric therapy for patients with the characteristic rash, arthralgias, or a tick bite acquired in an endemic area. Prevent with tick bite avoidance. A disease caused by Rickettsia rickettsii and carried by the American dog tick (Dermacentor variabilis). The organism invades the endothelial lining of capillaries and causes small vessel vasculitis.


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First_Aid_Step2. Hx/PE: Presents with headache, fever, malaise, and rash. The characteristic rash is initially macular (beginning on the wrists and ankles) but becomes petechial/purpuric as it spreads centrally (see Figure 2.8-14). Altered mental status or DIC may develop in severe cases. Dx: Clinical diagnosis should be confrmed with indirect immunof uorescence of rash biopsy. Tx: Doxycycline or chloramphenicol (for multidrug-resistant organisms). Lyme arthritis can be very subtle and minimally inﬂ ammatory and can wax and wane. Rocky Mountain spotted fever starts on the wrists and ankles and then spreads centrally. FIGURE 2.8-14. Rocky Mountain spotted fever. These erythematous macular lesions will evolve into a petechial rash that will spread centrally. (Courtesy of Daniel Noltkamper, MD, as published in Knoop KJ et al. Atlas of Emergency Medicine, 2nd ed. New York: McGraw-Hill, 2002: 382.)


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First_Aid_Step2. The condition can be rapidly fatal if left untreated. If clinical suspicion is high, begin treatment while awaiting testing. Prevent by avoiding tick bites. Causes of red eye: A common complaint in the emergency room setting, inf ammation of the conjunctiva is most often bacterial or viral but can also be fungal, parasitic, allergic, or chemical. It is essential to differentiate potentially vision-threatening infectious etiologies from allergic or other causes of conjunctivitis, as well as to identify other vision-threatening conditions that may mimic conjunctivitis. See Table 2.8-9 for the common etiologies of infectious conjunctivitis. Commonly due to infection of the paranasal sinuses; can lead to endophthalmitis and blindness. Usually caused by streptococci, staphylococci (including MRSA), and H. inﬂ uenzae (in children). In diabetic and immunocompromised patients, mucormycosis and Rhizopus are in the differential.


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First_Aid_Step2. Hx/PE: Presents with acute-onset fever, proptosis, ↓ EOM, ocular pain, and ↓ visual acuity. Look for a history of ocular trauma or sinusitis. Pala T AB LE 2.8-9. Common Causes of Infectious Conjunctivitis


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First_Aid_Step2. T AB LE 2.8-9. Common Causes of Infectious Conjunctivitis Bacterial Staphylococci, streptococci, Haemophilus, Pseudomonas, Moraxella Foreign body sensation, purulent discharge. Gram stain and culture if severe. Antibiotic drops/ ointment. N. gonorrhoeae An emergency! Corneal involvement can lead to perforation and blindness. Gram stain shows gram-intracellular diplococci. IM ceftriaxone, PO ciprofoxacin or of oxacin. Inpatient treatment if complicated. C. trachomatis A–C Recurrent epithelial keratitis in childhood, trichiasis, corneal scarring, and entropion. The leading cause of preventable blindness worldwide. Giemsa stain, chlamydial cultures. Azithromycin, tetracycline, or erythromycin × 3–4 weeks. Viral Adenovirus (most common) Copious watery discharge, severe ocular irritation, preauricular lymphadenopathy. Occurs in epidemics. Contagious; self-limited. Topical corticosteroids with supervision of an ophthalmologist.


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First_Aid_Step2. tal or nasal mucosal ulceration with coexisting maxillary and/or ethmoid sinusitis suggests mucormycosis or Rhizopus. Dx: Mostly clinical. Blood and tissue fuid culture; CT scan (to rule out orbital abscess and intracranial involvement). Tx: Admit. Immediate IV antibiotics; request an ophthalmologic/ENT consult. Abscess formation may necessitate surgery. Diabetic and immunocompromised patients should be treated with amphotericin B and surgical debride ment (often associated with cavernous sinus thrombosis) if Mucor or Rhizopus is diagnosed. An inf ammation of the external auditory canal, also known as “swimmer’s ear.” Pseudomonas (from poorly chlorinated pools) and Enterobacteriaceae are the most common etiologic agents. Both grow in the presence of excess moisture.


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First_Aid_Step2. Hx/PE: Presents with pain, pruritus, and possible purulent discharge. Exam reveals pain with movement of the tragus/pinna (unlike otitis media) and an edematous and erythematous ear canal. See the Pediatrics chapter for a discussion of otitis media. Dx: A clinical diagnosis. Gram stain and culture are helpful if a fungal etiology is suspected. CT scan if the patient is toxic appearing. Neisseria conjunctivitis is an ocular emergency often requiring inpatient parenteral antibiotic therapy. Diabetics are at risk for malignant otitis externa. ■ Tx: Antibiotic and steroid eardrops. Use systemic antibiotics in patients with severe disease. Diabetics are at risk for malignant otitis externa and osteomyelitis of the skull base and thus require hospitalization and IV antibiotics. pain with movement of the tragus/pinna.


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First_Aid_Step2. pain with movement of the tragus/pinna. Infection of the endocardium, usually 2° to bacterial or other infectious causes. Most commonly affects the heart valves, especially the mitral valve. Risk factors include rheumatic, congenital, or valvular heart disease; prosthetic heart valves; IV drug abuse; and immunosuppression. Etiologies are as follows: S. aureus (both methicillin-sensitive and methicillin-resistant): The causative agent in > 80% of cases of acute bacterial endocarditis in patients with a history of IV drug abuse. Viridans streptococci: The most common pathogens for left-sided sub-acute bacterial endocarditis. Coagulase-Staphylococcus: The most common infecting organism in prosthetic valve endocarditis. Streptococcus bovis: S. bovis endocarditis is associated with coexisting GI malignancy.


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First_Aid_Step2. Coagulase-Staphylococcus: The most common infecting organism in prosthetic valve endocarditis. Streptococcus bovis: S. bovis endocarditis is associated with coexisting GI malignancy. Candida and Aspergillus species: Account for most cases of fungal endocarditis. Predisposing factors include long-term indwelling IV catheters, malignancy, AIDS, organ transplantation, and IV drug use. Table 2.8-10 lists the causes of endocarditis. Constitutional symptoms are common (fever/FUO, weight loss, fatigue). Exam reveals a heart murmur. The mitral valve is more commonly affected than the aortic valve in non–IV drug users; more right-sided involvement is found in IV drug users (tricuspid valve > mitral valve > aortic valve).


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First_Aid_Step2. Osler’s nodes (small, tender nodules on the f nger and toe pads), Janeway lesions (small peripheral hemorrhages; see Figure 2.8-15), splinter hemorrhages (subungual petechiae; see Figure 2.8-16), Roth’s spots (retinal hemorrhages), focal neurologic defcits from embolic stroke, and other embolic phenomena are also seen. TABLE 2.8-10. Causes of Endocarditis S. aureus (IV drug abuse) S. pneumoniae N. gonorrhoeae Viridans streptococci (native valve) Enterococcus S. epidermidis (prosthetic valve) S. bovis (GI insult) Fungi Cancer (poor prognosis). Mets seed valves; emboli can cause cerebral infarcts. Haemophilus parainﬂ uenzae Actinobacillus Cardiobacterium Eikenella Kingella Coxiella burnetii Brucella Bartonella Libman-Sacks endocarditis (autoantibody to valve) FIGURE 2.8-15. Janeway lesions.


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First_Aid_Step2. FIGURE 2.8-15. Janeway lesions. Peripheral embolization to the sole leads to a cluster of erythematous macules known as Janeway lesions. (Courtesy of the Department of Dermatology, Wilford Hall USAF Medical Center and Brooke Army Medical Center, San Antonio, TX, as published in Knoop KJ et al. Atlas of Emergency Medicine, 2nd ed. New York: McGraw-Hill, 2002: 384.) Diagnosis is guided by risk factors, clinical symptoms, and the Duke criteria (see Table 2.8-11). CBC with leukocytosis and left shift; ↑ ESR and CRP. ■Early empiric IV antibiotic treatment includes vancomycin or nafcillin + gentamicin. Ampicillin/sulbactam or ceftriaxone are alternative choices depending on the suspected organism. Tailor antibiotics once the causative agent is known. Acute valve replacement is sometimes necessary. The FIGURE 2.8-16. Splinter hemorrhages.


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First_Aid_Step2. FIGURE 2.8-16. Splinter hemorrhages. Note the splinter hemorrhages along the distal aspect of the nail plate, due to emboli from sub-acute bacterial endocarditis. (Courtesy of the Armed Forces Institute of Pathology, Bethesda, MD, as published in Knoop KJ et al. Atlas of Emergency Medicine, 2nd ed. New York: McGraw-Hill, 2002: 384.) T AB LE 2.8-1 1. Duke Criteria for the Diagnosis of Endocarditis Endocarditis: indications for surgery— Suppurative local complications with conduction abnormalities Resection of mycotic aneurysm Ineffective antimicrobial therapy (e.g., vs. fungi) The anthrax-associated pruritic papule forms an ulcer with an edematous halo and then a black eschar. At least two separate blood cultures for a typical organism, persistent bacteremia with any organism, or a single culture of Coxiella burnetii. Evidence of endocardial involvement (via transesophageal echocardiography or new murmur).


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First_Aid_Step2. Predisposing risk factors. Fever ≥ 38.3°C. Vascular phenomena: Septic emboli, septic infarcts, mycotic aneurysm, Janeway lesions. Immunologic phenomena: Glomerulonephritis, Osler’s nodes. Roth’s spots. Microbiological evidence that does not meet major criteria. prognosis for prosthetic valve endocarditis is poor. See the mnemonic PUS RIVER for indications for surgery. ■Give antibiotic prophylaxis before dental work in patients with high-risk valvular disease (e.g., those with previous endocarditis or a prosthetic valve). Caused by the spore-forming gram-bacterium Bacillus anthracis. Its natural incidence is rare, but infection is an occupational hazard for veterinarians, farmers, and individuals who handle animal wool, hair, hides, or bone meal products. Also a biological weapon. B. anthracis can cause cutaneous (most common), inhalation (most deadly), or GI anthrax.


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First_Aid_Step2. Cutaneous: Presents 1–7 days after skin exposure and penetration of spores. The lesion begins as a pruritic papule that enlarges to form an ulcer surrounded by a satellite bulbus/lesion with an edematous halo and a round, regular, and raised edge. Regional lymphadenopathy is also characteristic. The lesion evolves into a black eschar within 7–10 days. Inhalational: Presents with fever, dyspnea, hypoxia, hypotension, or symptoms of pneumonia (1–3 days after exposure), classically due to hemorrhagic mediastinitis. GI: Occurs after the ingestion of poorly cooked, contaminated meat; can present with dysphagia, nausea/vomiting, bloody diarrhea, and abdominal pain. CXR is the most sensitive test for inhalational disease (widened mediastinum, pleural effusions, infltrates). Aerobic culture and Gram stain of ulcer exudate show nonmotile short chains of bacilli. Antibody tests are also useful in confrming the diagnosis.


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First_Aid_Step2. ■ Ciprof oxacin or doxycycline plus one or two additional antibiotics for at least 14 days are frst-line therapy for inhalational disease or cutaneous disease of the face, head, or neck. Many strains express β-lactamases that confer resistance to penicillin; therefore, penicillin and amoxicillin are no longer recommended as single agents for inhalational disease. ■For cutaneous disease, treat for 7–10 days. Postexposure prophylaxis (ciprof oxacin) to prevent inhalation anthrax should be continued for 60 days. Bone or bone marrow infection 2° to direct spread from a soft tissue infection (80% of cases) is most common in adults, whereas infection due to hematogenous seeding (20% of cases) is more common in children (metaphyses of the long bones) and IV drug users (vertebral bodies). Common pathogens are outlined in Table 2.8-12.


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First_Aid_Step2. Presents with localized bone pain and tenderness along with warmth, swelling, erythema, and limited motion of the adjacent joint. Systemic symptoms (fevers, chills) and purulent drainage may be present. Labs: ↑ WBC count, ESR (> 100), and CRP levels. Blood cultures may be . Imaging: X-rays are often initially but may show periosteal elevation within 10–14 days. Bone scans are also used and are sensitive for osteomyelitis but lack specif city. MRI (test of choice) will show ↑ signal in the bone marrow and associated soft tissue infection. Defnitive diagnosis is made by bone aspiration with Gram stain and culture. Clinical diagnosis made by probing through the soft tissue to bone is usually suffcient, as aspiration carries a risk of infection. T AB LE 2.8-1 2. Common Pathogens in Osteomyelitis Penicillin and amoxicillin are no longer recommended as single agents for the treatment of disseminated anthrax. Treat with ciproﬂ oxacin plus one or two other antibiotics.


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First_Aid_Step2. Penicillin and amoxicillin are no longer recommended as single agents for the treatment of disseminated anthrax. Treat with ciproﬂ oxacin plus one or two other antibiotics. Osteomyelitis is associated with peripheral vascular disease, diabetes, penetrating soft tissue injuries, chronic decubitus ulcers, and IV drug abuse. Most people S. aureus IV drug user S. aureus or Pseudomonas Sickle cell disease Salmonella Hip replacement S. epidermidis Foot puncture wound Pseudomonas Chronic S. aureus, Pseudomonas, Enterobacteriaceae Diabetic Polymicrobial, Pseudomonas, S. aureus, streptococci, anaerobes Diabetic osteomyelitis should be treated with antibiotics targeting gramorganisms and anaerobes. Surgical debridement of necrotic, infected bone followed by IV antibiotics × 4–6 weeks. Empiric antibiotic selection is based on the suspected organism and Gram stain.


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First_Aid_Step2. Surgical debridement of necrotic, infected bone followed by IV antibiotics × 4–6 weeks. Empiric antibiotic selection is based on the suspected organism and Gram stain. Consider clindamycin + ciprofoxacin, ampicillin/sulbactam, or oxacillin/ nafcillin (for methicillin-sensitive S. aureus); vancomycin (for MRSA); or ceftriaxone or ciprofoxacin (for gram-bacteria). Chronic osteomyelitis, sepsis, septic arthritis. Long-standing chronic osteomyelitis with a draining sinus tract may eventually lead to squamous cell carcinoma (Marjolin’s ulcer). Table 2.9-1 outlines the presentation and treatment of orthopedic injuries that commonly affect adults. Volkmann’s contracture of the wrist and f ngers is caused by compartment syndrome due to supracondylar fractures. Phalen’s maneuver: placing the wrists in f exion reproduces aching and numbness in < 60 seconds. Tinel’s sign: tapping over the median nerve at the wrist elicits tingling in the median nerve distribution.


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First_Aid_Step2. Tinel’s sign: tapping over the median nerve at the wrist elicits tingling in the median nerve distribution. ■↑pressure within a confined space that compromises nerve, muscle, and soft tissue perfusion. Occurs primarily in the anterior compartment of the lower leg and forearm 2° to trauma (fracture or muscle injury) to the affected compartment. Hx/PE: Presents with pain out of proportion to physical findings; pain with passive motion of the fingers and toes; and paresthesias, pallor, poikilothermia, pulselessness, and paralysis. Pulselessness occurs late. Dx: Measure compartment pressures (usually ≥ 30 mmHg); measure delta pressures (diastolic pressure – compartment pressure). Tx: Immediate fasciotomy to ↓ pressures and ↑ tissue perfusion.


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First_Aid_Step2. Dx: Measure compartment pressures (usually ≥ 30 mmHg); measure delta pressures (diastolic pressure – compartment pressure). Tx: Immediate fasciotomy to ↓ pressures and ↑ tissue perfusion. Entrapment of the median nerve at the wrist caused by ↓ size or space of the carpal tunnel, leading to paresthesias, pain, and occasionally paralysis. Can be precipitated by overuse of wrist ﬂexors, diabetes mellitus, or thyroid dysfunction. Commonly occurs in pregnant and middle-aged women. Presents with aching over the thenar area of the hand and proximal forearm. Pain may extend to the shoulder. Paresthesia or numbness is seen in a median nerve distribution. Symptoms worsen at night or when the wrists are held in ﬂexion or extension. Patients may report frequently dropping objects or inability to open jars. Exam shows thenar atrophy (if CTS is long-standing). Phalen’s maneuver and Tinel’s sign are . A clinical diagnosis, although EMG testing can be used to confirm.


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First_Aid_Step2. Exam shows thenar atrophy (if CTS is long-standing). Phalen’s maneuver and Tinel’s sign are . A clinical diagnosis, although EMG testing can be used to confirm. Splint the wrist in a neutral position at night and during the day if possible. Administer NSAIDs. Conservative treatment can include corticosteroid injection of the carpal canal. Work-related CTS may benefit from ergonomic aids. CTS of pregnancy usually resolves after delivery. Surgical release of the carpal tunnel is a widely accepted treatment, particularly for fixed sensory loss, thenar weakness, or intolerable symptoms. Permanent loss of sensation, hand strength, and fine motor skills. T AB LE 2.9-1. Common Adult Orthopedic Injuries


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First_Aid_Step2. Shoulder dislocation Anterior dislocation: Most common; the axillary artery and nerve are at risk. Patients hold the arm in slight abduction and external rotation. Posterior dislocation: Rare; associated with seizure and electrocutions; can injure the radial artery. Patients hold the arm in adduction and internal rotation. Reduction followed by a sling and swath. Recurrent dislocations may need surgical repair. Hip dislocation Posterior dislocation: Most common (> 90%); occurs via a posteriorly directed force on an internally rotated, fexed, adducted hip (“dashboard injury”). Associated with a risk of sciatic nerve injury and avascular necrosis (AVN). Anterior dislocation: Can injure the obturator nerve. Closed reduction followed by abduction pillow/ bracing. Evaluate with CT scan after reduction. Colles’ fracture Involves the distal radius. Often results from a fall onto an outstretched hand, leading to a dorsally displaced, dorsally angulated fracture. Commonly seen in the elderly


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First_Aid_Step2. reduction. Colles’ fracture Involves the distal radius. Often results from a fall onto an outstretched hand, leading to a dorsally displaced, dorsally angulated fracture. Commonly seen in the elderly (osteoporosis) and children. Closed reduction followed by application of a long-arm cast; open reduction if the fracture is intra-articular. Scaphoid fracture The most commonly fractured carpal bone. May take two weeks for radiographs to show the fracture. Assume a fracture if there is tenderness in the anatomical snuff box. Thumb spica cast. If displacement or navicular nonunion is present, treat with open reduction. With proximal third scaphoid fractures, AVN may result from disruption of blood f ow. Boxer’s fracture Fracture of the ffth metacarpal neck. Due to forward trauma of a closed fst (e.g., punching a wall). Closed reduction and ulnar gutter splint; percutaneous pinning if the fracture is excessively angulated. If skin is broken, assume infection by human oral pathogens and


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First_Aid_Step2. fst (e.g., punching a wall). Closed reduction and ulnar gutter splint; percutaneous pinning if the fracture is excessively angulated. If skin is broken, assume infection by human oral pathogens and treat with surgical irrigation, debridement, and IV antibiotics (covering Eikenella). Humerus fracture Direct trauma. May have radial nerve palsy leading to wrist drop and loss of thumb abduction (see Figure 2.9-1). Hanging-arm cast vs. coaptation splint and sling. Functional bracing. “Nightstick fracture” Ulnar shaft fracture resulting from self-defense with the arm against a blunt object. Open reduction and internal fxation (ORIF) if signif cantly displaced. Monteggia’s fracture Diaphyseal fracture of the proximal ulna with subluxation of the radial head. ORIF of the shaft fracture (due to poor fracture diaphyseal blood supply) and closed reduction of the radial head.


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First_Aid_Step2. T AB LE 2.9-1. Common Adult Orthopedic Injuries (continued) Femoral fracture Direct trauma. Beware of fat emboli, which present with fever, change in mental status, dyspnea, hypoxia, petechiae, and ↓ platelets. Intramedullary nailing of the femur. Irrigate and debride open fractures. Tibial fracture Direct trauma. Watch for compartment syndrome. Casting vs. intramedullary nailing. Open fractures An orthopedic emergency; patients must be taken to the OR in < 6 hours owing to ↑ infection risk. OR emergently to repair fracture. Treat with antibiotics and tetanus prophylaxis. Achilles tendon rupture Presents with a sudden “pop” like a rif e shot. More likely with ↓ physical conditioning. Exam shows limited plantar f exion and a Thompson’s test (pressure on the gastrocnemius leading to absent foot plantar f exion). Treat surgically followed by long leg cast for six weeks. Knee injuries


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First_Aid_Step2. Diaphyseal fracture of the radius with dislocation of the distal radioulnar joint. Results from a direct blow to the radius. ORIF of the radius and casting of the fractured forearm in supination to reduce the distal radioulnar joint. ↑ risk with osteoporosis. Presents with a shortened and externally rotated leg. Displaced femoral neck fractures: Associated with an ↑ risk of AVN, nonunion, and DVTs. Present with knee instability, edema, and hematoma. ACL: Results from a noncontact twisting mechanism, forced hyperextension, or impact to an extended knee. anterior drawer and Lachman tests. Rule out a meniscal or MCL injury. PCL: Results from forced hyperextension. posterior drawer test. Meniscal tears: Result from an acute twisting injury or a degenerative tear in elderly patients. Clicking or locking may be present. Exam shows joint line tenderness and a McMurray’s test.


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First_Aid_Step2. Meniscal tears: Result from an acute twisting injury or a degenerative tear in elderly patients. Clicking or locking may be present. Exam shows joint line tenderness and a McMurray’s test. ORIF with parallel pinning of the femoral neck. Displaced fractures in elderly patients may require a hip hemiarthroplasty. Anticoagulate to ↓ the likelihood of DVTs. Treatment of MCL/LCL and meniscal tears is usually conservative. Treatment of ACL injuries is generally surgical with graft from the patellar or hamstring tendons. Operative PCL repair is reserved for highly competitive athletes. Operative meniscal repair is for younger patients with signifcant tears or older patients whose symptoms do not respond to conservative treatment. F IGU R E 2.9-1. Lateral condyle fracture of the humerus. (Reproduced, with permission, from Skinner HB. Current Diagnosis & Treatment in Orthopedics, 2nd ed. Stamford, CT: Appleton & Lange, 2000: 572.)


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First_Aid_Step2. (Reproduced, with permission, from Skinner HB. Current Diagnosis & Treatment in Orthopedics, 2nd ed. Stamford, CT: Appleton & Lange, 2000: 572.) Inf ammation of the bursa by repetitive use, trauma, infection, or systemic inf ammatory disease. A bursa is a ﬂ attened sac filled with a small amount of synovial ﬂuid that serves as a protective buffer between bones and overlapping muscles. Common sites of bursitis include subacromial, olecranon, trochanteric, prepatellar, and infrapatellar bursae. Septic bursitis is more common in superficial bursae (olecranon, prepatellar, and infrapatellar bursae). Presents with localized tenderness, ↓ range of motion (ROM), edema, and erythema; patients may have a history of trauma or inﬂ ammatory disease. Needle aspiration is indicated if septic bursitis is suspected; no labs or imaging is needed. Conservative treatment includes rest, heat and ice, elevation, and NSAIDs.


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First_Aid_Step2. Needle aspiration is indicated if septic bursitis is suspected; no labs or imaging is needed. Conservative treatment includes rest, heat and ice, elevation, and NSAIDs. Intrabursal corticosteroid injection can be considered (contraindicated if septic bursitis is suspected). Septic bursitis should be treated with 7–10 days of antibiotics. Oral f uoroquinolones are An inf ammatory condition characterized by pain at tendinous insertions associated with an ↑ risk of into bone associated with swelling or impaired function. It commonly occurs tendon rupture and tendinitis. Most lower back pain is mechanical; bed rest is contraindicated. Red f ags for lower back pain include age > 50, > 6 weeks of pain, previous cancer history, severe pain, constitutional symptoms, and loss of anal sphincter tone.


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First_Aid_Step2. Red f ags for lower back pain include age > 50, > 6 weeks of pain, previous cancer history, severe pain, constitutional symptoms, and loss of anal sphincter tone. in the supraspinatus, biceps, wrist extensor, patellar, iliotibial band, posterior tibial, and Achilles tendons. Overuse is the most common cause and includes work-related activities or an ↑ in activity level. Presents with pain at a tendinous insertion that worsens with repetitive stress and resisted strength testing of the affected muscle group. Wrist ﬂexor tendinitis (lateral epicondylitis, or tennis elbow) worsens with resisted dorsiﬂexion of the wrist. A clinical diagnosis. Consider a radiograph if there is a history of trauma. Treat with rest and NSAIDs; apply ice for the first 24–48 hours. Consider splinting or immobilization. Begin strengthening exercises once pain has subsided.


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First_Aid_Step2. Treat with rest and NSAIDs; apply ice for the first 24–48 hours. Consider splinting or immobilization. Begin strengthening exercises once pain has subsided. If conservative treatment fails, consider peritendinous injection of lidocaine and corticosteroids. Never inject the Achilles tendon in view of the ↑ risk of rupture. Avoid repetitive injection. Table 2.9-2 outlines the motor, reﬂex, and sensory deficits with which low back pain is associated. Causes include degenerative changes, trauma, or neck/back strain or sprain. Most common (95%) in the lumbar region, especially at L4–L5 and L5–S1. Presents with sudden onset of severe, electricity-like LBP, usually preceded by several months of aching, “discogenic” pain. Common among middle-aged and older men. Exacerbated by ↑ intra-abdominal pressure or Valsalva (e.g., coughing). Associated with sciatica, paresthesias, muscle weakness, atrophy, contractions, or spasms. T AB LE 2.9-2. Motor and Sensory Deficits in Back Pain


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First_Aid_Step2. Associated with sciatica, paresthesias, muscle weakness, atrophy, contractions, or spasms. T AB LE 2.9-2. Motor and Sensory Deficits in Back Pain L4 L5 S1 Foot dorsifexion (tibialis anterior) Patellar Medial aspect of the lower leg. Big toe dorsifexion (extensor hallucis longus), foot eversion (peroneus muscles) None Dorsum of the foot and lateral aspect of the lower leg. Plantar fexion (gastrocnemius/soleus), hip extension (gluteus maximus). Achilles Plantar and lateral aspects of the foot. A passive straight leg raise ↑pain (highly sensitive but not specific). A crossed straight leg raise ↑ pain (highly specific but not sensitive). Large midline herniations can cause cauda equina syndrome. Obtain an ESR and a plain radiograph if other causes of back pain are suspected (e.g., infection, trauma, compression fracture). Order a stat MRI for cauda equina syndrome or for a severe or rapidly progressing neurologic deficit.


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First_Aid_Step2. Order a stat MRI for cauda equina syndrome or for a severe or rapidly progressing neurologic deficit. Order an MRI if symptoms are refractory to conservative management. MRI may show disk herniation (see Figure 2.9-2). NSAIDs in scheduled doses, physical therapy, and local heat lead to resolution within four weeks in 80% of cases. Epidural or nerve block may be of benefit. Severe or rapidly evolving neurologic deficits and cauda equina syndrome are indications for discectomy. Narrowing of the lumbar or cervical spinal canal, leading to compression of the nerve roots. Most commonly due to degenerative joint disease; typically occurs in middle-aged or elderly patients. ■Presents with neck pain, back pain that radiates to the buttocks and legs, and leg numbness/weakness. Lung, breast, and prostate cancer can metastasize to the vertebrae and cause back pain.


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First_Aid_Step2. ■Presents with neck pain, back pain that radiates to the buttocks and legs, and leg numbness/weakness. Lung, breast, and prostate cancer can metastasize to the vertebrae and cause back pain. Bowel or bladder dysfunction (urinary overf ow incontinence), impotence, and saddle-area anesthesia are consistent with cauda equina syndrome, which is a surgical emergency. FIGURE 2.9-2. Disk herniation. MRI reveals herniations of L4–L5 and L5–S1. (Reproduced, with permission, from Skinner HB. Current Diagnosis & Treatment in Orthopedics, 1st ed. Stamford, CT: Appleton & Lange, 1995: 186.) The most common benign bone tumor is osteochondroma. Leg cramping is worse at rest, with standing, and with walking (pseudoor neurogenic claudication). Symptoms improve with fexion at the hips and bending forward. Radiographs show degenerative changes that include disk space narrowing, facet hypertrophy, and spondylolisthesis, leading to a narrowed spinal canal. MRI or CT shows spinal stenosis.


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First_Aid_Step2. Radiographs show degenerative changes that include disk space narrowing, facet hypertrophy, and spondylolisthesis, leading to a narrowed spinal canal. MRI or CT shows spinal stenosis. Mild to moderate: NSAIDs and abdominal muscle strengthening. Advanced: Epidural corticosteroid injections can provide relief. Refractory: Surgical laminectomy may achieve significant short-term success, but many patients will have a recurrence of symptoms. The second most common 1° malignant tumor of bone (after multiple myeloma). Tends to occur in the metaphyseal regions of the distal femur, proximal tibia, and proximal humerus; often metastasizes to the lungs. Some cases are preceded by Paget’s disease. Risk factors include male gender and age 20– 30. Presents as progressive and eventually intractable pain that is worse at night. Constitutional symptoms such as fever, weight loss, and night sweats may be present. Erythema and enlargement over the site of the tumor may be seen.


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First_Aid_Step2. Constitutional symptoms such as fever, weight loss, and night sweats may be present. Erythema and enlargement over the site of the tumor may be seen. See the Endocrinology chapter for a discussion of osteosarcoma vs. Paget’s disease. Radiographs show Codman’s triangle (periosteal new bone formation at the diaphyseal end of the lesion) or a “sunburst pattern” of the osteosarcoma (see Figure 2.9-3)—in contrast to multilayered “onion skinning,” which is classic for Ewing’s sarcoma. MRI and CT facilitate staging (soft tissue and bony invasion) and planning for surgery. Limb-sparing surgical procedures and preand postoperative chemotherapy (e.g., methotrexate, doxorubicin, cisplatin, ifosfamide). Amputation may be necessary. A common, chronic, noninﬂ ammatory arthritis of the synovial joints. Characterized by deterioration of the articular cartilage and osteophyte bone formation at the joint surfaces. Risk factors include a family history, obesity, and a history of joint trauma.


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First_Aid_Step2. FIGURE 2.9-3. Osteosarcoma. “Sunburst” appearance of neoplastic bone formation in the femur of a 15-year-old girl. Amputation was required owing to the size of the tumor. (Reproduced, with permission, from Skinner HB. Current Diagnosis & Treatment in Orthopedics, 2nd ed. Stamford, CT: Appleton & Lange, 2000: 272.) Presents with crepitus, ↓ ROM, and initially pain that worsens with activity and weight bearing but improves with rest. Morning stiffness lasts for < 30 minutes. Stiffness is also experienced after periods of rest (“gelling”). Radiographs show joint space narrowing, osteophytes, subchondral sclerosis, and subchondral bone cysts (see Figure 2.9-4). Radiograph severity does not correlate with symptomatology. Synovial ﬂuid shows straw-colored ﬂuid, normal viscosity, and a WBC count < 2000 cells/μL.


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First_Aid_Step2. Synovial ﬂuid shows straw-colored ﬂuid, normal viscosity, and a WBC count < 2000 cells/μL. Physical therapy, weight reduction, and NSAIDs. Intra-articular corticosteroid injections may provide temporary relief. Consider joint replacement (e.g., total hip/knee arthroplasty) in advanced cases. FIGURE 2.9-4. Osteoarthritis. Plain radiographs show joint space narrowing, osteophytes, and subchondral degenerative cysts involving the DIP and PIP joints, with sparing of the MCP. (Reproduced, with permission, from USMLERx.com.) A pain syndrome accompanied by loss of function and autonomic dysfunction, usually occurring after trauma. Formerly known as reﬂ ex sympathetic dystrophy. The disease has three phases: acute sympathetic denervation and underactivity → dystrophic phase → atrophic phase. Diffuse pain occurs out of proportion to the initial injury, often in a nonanatomic distribution. Pain can occur at any time relative to the initial injury.


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First_Aid_Step2. Diffuse pain occurs out of proportion to the initial injury, often in a nonanatomic distribution. Pain can occur at any time relative to the initial injury. Loss of function of the affected limb is seen. Sympathetic dysfunction occurs and may be documented by skin, soft tissue, or blood ﬂ ow changes. Skin temperature, hair growth, and nail growth may ↑ or ↓. Edema may be present. A clinical diagnosis, but objective evidence of changes in skin temperature, hair growth, or nail growth may be present. Medications include NSAIDs, corticosteroids, low-dose TCAs, gabapentin, pregabalin, and calcitonin (no oral medications are consistently effective). Physical therapy modalities such as heat, ice, desensitization techniques, and gentle ROM exercises may be helpful. Chemical sympathetic blockade may relieve symptoms. Referral to a chronic pain specialist is appropriate for complicated cases.


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First_Aid_Step2. Chemical sympathetic blockade may relieve symptoms. Referral to a chronic pain specialist is appropriate for complicated cases. A centrally mediated chronic pain disorder characterized by soft tissue and axial skeletal pain in the absence of joint pain. Inﬂammation is notably absent. Hx/PE: Most common in women 30–50 years of age; associated with depression, anxiety, sleep disorders, IBS, and cognitive disorders (“fibro fog”). Dx: Multiple (≥ 11 of 18), diffuse tender points over all four body quadrants and the axial skeleton must be present for diagnosis (see Figure 2.9-5). The presence of < 11 of 18 tender points or non-fibromyalgiaassociated tender points is known as myofascial pain syndrome. Tx: Antidepressants (an SSRI/TCA combination has proven efficacy), gabapentin, pregabalin, muscle relaxants, and physical therapy (stretching, heat application, hydrotherapy). Avoid narcotics.


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First_Aid_Step2. Tx: Antidepressants (an SSRI/TCA combination has proven efficacy), gabapentin, pregabalin, muscle relaxants, and physical therapy (stretching, heat application, hydrotherapy). Avoid narcotics. Recurrent attacks of acute monoarticular arthritis resulting from intra-articular deposition of monosodium urate crystals due to disorders of urate metabolism. Risk factors include male gender, obesity, and postmenopausal status in females. ■Presents with excruciating joint pain of sudden onset that can awaken the patient from sleep. F IGU R E 2.9-5. Tender points characteristic of fibromyalgia. Gout crystals appear yeLLow when paraLLel to the condenser. Causes of hyperuricemia: ↑ cell turnover (hemolysis, blast crisis, tumor lysis, myelodysplasia, psoriasis) Cyclosporine Dehydration Diabetes insipidus Diet (e.g., ↑ red meat, Colchicine inhibits neutrophil chemotaxis and is most effective when used early during a gout f are (use is limited by a narrow therapeutic window).