Tracey Newell BSN,RN,CCRN



Comprehensive Case StudyTracey NewellWright State University Comprehensive Case StudyFocused History and PhysicalSourcePatient, reliable sourceChief Complaint“Headache”History of Present IllnessMr. SM is a 21 year old African American male with a history of acquired immune deficiency syndrome (AIDS) diagnosed three months ago after feeling fatigued for a couple of months. His CD4 count was < 100/mcL at the time of diagnosis. He was to follow-up with infectious disease, and is currently not receiving antiretroviral therapy (ART). He recently was seen in the emergency department (ED) on for a rash and itching. He was on amoxicillin four days prior to presentation for an ear infection and was discharged home with a prednisone taper and hydroxyzine 25 mg every four hours as needed for itching. Two weeks later he presented and was diagnosed with varicella virus (VZV)/shingles and discharged on valacyclovir 1000 mg three times a day for 10 days. Today he presents with a chief complaint of bilateral frontal headache for the past week associated with weakness, fever (100.9), and gait instability. Vitals: Temp 98.8, B/P 115/54, HR 100, RR 18, oxygen saturation 98%. He denies visual changes, seizures, cough, hemoptysis, night sweats, weight loss, abdominal pain, skin changes (other than shingles), or exposure to tuberculosis (TB). Patient denies recent travel or sick contacts. In the ED a head computed tomography (CT) scan revealed multiple contrast-enhancing lesions in the basal ganglia with mass effect. Pending labs include: CSF, blood, and fungal cultures. Patient tested positive for serum toxoplasmosis IgG, and negative for serum cryptococcal antigen, and rapid plasma regain (RPR). CBC results: WBC 3.6, H/H 10.5/32, and platelets 251 per mcL. All other labs were within normal limits. Medical HistoryRecently diagnosed with AIDS, CD4 count <100/mcL.Past Surgical HistoryNo past surgical historyFamily HistoryFather- HTN, DMMother- bipolar, HTNSister- bipolarSocial HistoryPatient is currently a senior at the University of Cincinnati majoring in law and lives with his significant other. He denies tobacco, alcohol or illicit drug use. AllergiesNo known allergiesMedicationsPatient takes no prescriptive, herbal or over the counter meds.Review of SystemsGeneral:Patient reports a non-relenting bilateral frontal headache for the past week associated with weakness, fever, and balance instability. Height 6’1” and current weight 77.7 kg. Skin/hair: Reports painful lesions right side. HEENT:Complains of bilateral frontal headache. Denies blurred vision or diplopia. Denies any eye drainage or pain. Reports left ear pain, but denies tinnitus, or hearing difficulties. Denies nasal discharge. Neck: Denies neck pain or stiffness. Denies any enlarged neck, axilla, or inguinal lymph nodes or tenderness.Chest:Denies dyspnea, cough, or hemoptysis.CV:Denies CP, palpitations, or lower extremity edema. GI: Denies abdominal pain /nausea /vomiting /diarrhea/constipation, or rectal bleeding. GU:Denies dysuria, urgency, frequency, and hesitancy. M/S:Complains of generalized weakness. Denies joint stiffness, redness, or swelling. Full ROM of extremities.Neuro:Positive for headache and balance coordination. Denies confusion, numbness, and tingling.Physical ExamVital Signs:B/P 115/54 mmHg, T- 100.9 orally, HR 100, RR-18 , Sats: 98% on RA, Ht. 6 ' 1" Wt.-77 kg.General:21-year-old well-groomed cachectic, African American male appears stated age and anxious. Patient is alert and oriented.Skin/Hair: Skin is brown, warm, and non-tenting. Mucous membranes dry and pale pink.Hair is coarse, short, and well distributed. Open draining lesions noted over nerve pathways right side.Nails:Nailbeds pale, smooth, and thick. No clubbing or cyanosis.HEENT: Head is normocephalic and atraumatic. Face is symmetrical. PERRLA 2mm sluggish, mm pink and dry. Eyes symmetrical and aligned. Eye brows and lashes well distributed. Conjunctiva free of discharge. Sclera white. Nares patent without discharge. Turbinates visualized. Neck: Supple and trachea midline. No lymphadenopathy noted. No thyromegaly. Full ROM. No nuchal rigidity.CV: S1 and S2 noted. Rhythm regular and tachycardic. PMI noted at the 5th intercostal space. No gallops/rubs/murmur. No palpable heaves or thrills. No peripheral edema. Radial and DP pulses + 2. Negative carotid bruits noted. Chest: Symmetrical, AP diameter 2:1. Chest expansion equal. Breath sounds equal without crackles. Respirations regular and unlabored.GI: Abdomen flat/soft/ND. Bowel sounds hypoactive x 4 quads. No venous hums, rubs or bruits noted. No organomegaly.M/S: Full ROM and strength 4/5 all extremities. No tenderness, crepitus, erythema, edema or warmth noted of joints. Neuro: Alert and oriented to person, place, time and situation. Positive Romberg.Differential DiagnosisThe list of differentials for this patient include: toxoplasmosis encephalitis, progressive multifocal leukoencephalopathy (PML), and primary central nervous system (CNS) lymphoma (PCL). The most likely diagnosis based on presenting symptoms, physical exam, laboratory, and diagnostic findings is toxoplasmosis encephalitis. There is a three step approach in determining the cause of headache in a patient with human immunodeficiency virus infection and acquired immune deficiency syndrome (HIV/AIDS): initially determine severity of the situation, evaluate the degree of immunosuppression (CD4 T lymphocyte count), and determine whether there is a mass lesion on neuroimaging (Stern, Cifu, & Altkorn, 2014). HIV-patients with a CD4 T lymphocyte (CD4) count > 200/mcL are at a markedly reduced risk for developing opportunistic infections (OIs) (Katz, 2016). However as the CD4 count drops < 200/mcL the immunosuppression worsens, the differential diagnosis broadens including OIs and PCL (Katz, 2016). In this case the patient presented with subacute complaints of a non-relenting frontal headache, fever (100.9), and gait instability. Toxoplasmosis is a protozoal disease caused by Toxoplasma gondii, a tiny obligate, parasite that is intracellular and identified in Wright or Giemsa-stained preparations (Roppers, Samuels, & Klein, 2014). Toxoplasmosis has become more recognized over the past decades due to prevalence in the AIDS population (Roppers et al., 2014). Toxoplasmosis is the most common cause of focal cerebral lesions in the AIDS population (Roppers et al., 2014). Humans may contract congenital or post-nasally (Roppers et al., 2014). Congenital refers to mother fetal transmission. Other sources of transmission include: eating raw beef, handling uncooked mutton, and contact with cat feces (Roppers et al., 2014). However, in most cases of the AIDS population the source remains a mystery (Roppers et al., 2014). Based on serologic surveys approximately 40% of American city dwellers have the antibodies, but active infection is rare and generally seen in the immunocompromised population (Roppers et al., 2014). Most cases in adults are reactivation of the congenital form (Katz, 2016). The clinical picture in the AIDS population varies from those who are not immunocompromised (Katz, 2016). Headache, focal neurologic deficits, seizures, and altered mental status may be the initial presentation (Katz, 2016). A positive toxoplasmosis serologic test does not secure the diagnosis, numerous HIV/AIDS patients have measureable titers without exhibiting active disease (Katz, 2016). A small percentage of patients with toxoplasmosis have negative titers (Katz, 2016). Consequently, negative toxoplasmosis titers in an HIV/AIDS patient with a single space-occupying lesion should raise suspicion for an alternate differential (Katz, 2016). Toxoplasmosis encephalitis is most likely in this case based on neuroimaging (multiple mass lesions), positive serum toxoplasmosis IgG titers, CD4 count < 100/mcL, mental status changes, and focal neurological findings. However, further work-up is warranted to rule out the other differentials.PML is a progressive degenerative disorder caused by the JC virus, a human polyoma virus (Longo et al., 2014). The disorder is characterized pathologically by numerous areas of demyelination scattered throughout the CNS, sparing the spinal cord and optic nerves (Longo et al., 2014). Furthermore, there are distinct cytologic changes in astrocytes and oligodendrocytes (Longo et al., 2014). PML is most commonly seen in the immunocompromised patient, 80% of the cases are found in the AIDS population (Longo et al., 2014). PML usually presents with neurological focal deficits: aphasia, mental status changes, hemiparesis, and visual deficits (Katz, 2016). Neuroimaging studies will display non-ring enhancing white matter lesions varying in size, location, and multiplicity making diagnosis more contingent on viral double-stranded nucleic acid (DNA) isolation from the cerebral spinal fluid (CSF) (Roppers et al., 2014). In most cases the CSF is normal, but may have an elevated protein and and/or IgG (Longo et al., 2014). CSF positive for polymerase chain reaction (PCR) or JC virus DNA with typical neuroimaging and clinical presentation is diagnostic in PML (Longo et al., 2014). In this case PML is unlikely based on diagnostic, clinical, and laboratory findings. PCL is a primary brain tumor of the parenchyma mainly found in immunocompromised adults (Armao & Bouldin, 2015). PCL is associated with the Epstein-Barr virus and is a primarily large B cell lymphoma identified by a characteristic feature, an angiocentric pattern (Armao & Bouldin, 2015). Pathogenesis is likely due to activation of dormant Epstein-Barr virus genes secondary to immunodeficiency (Stern et al., 2014). The tumor is aggressive and associated with a high incidence of mortality with a median survival of one year without treatment and seven years with treatment (Stern et al., 2014). Typical focal presentation in the advanced HIV population is weakness (Stern et al., 2014). However, many present with seizure and mental status changes (Stern et al., 2014). Other symptoms may include: fever, night sweats, weight loss, and headache (Stern et al., 2014). In CSF positive for the Epstein-Barr virus the PCR is 87% sensitive and 98% specific in diagnosing PCL (Stern et al., 2014). Neuroimaging studies such as a computerized tomography (CT) scan is 90% sensitive and usually shows contrast enhancement of single or multiple lesions along with mass effect similar to toxoplasmosis (Stern et al., 2014). PCL is unlikely in this case based on the lack of ring enhancing lesions and clinical findings inconsistent with the differential. The CSF is pending.Laboratory TestingA complete blood count (CBC) is useful in evaluating for infection and hematologic complications associated with HIV (Jaffe & Ratcliffe, 2011). In the absence of a CD4 count, an absolute lymphocyte count may be beneficial (Jaffe & Ratcliffe, 2011). Typically, if the total lymphocyte count is less than 1000/mcL, then the CD4 is more than likely > 200/mcL (Jaffe & Ratcliffe, 2011). In this case the CD4 count is < 100/mcL. The CD4 count allows the provider to concentrate on the diagnoses most likely to be seen at each stage of immunodeficiency (Katz, 2016). Certain infections may occur at any CD4 count, while others are uncommon unless the CD4 count has fallen below a specified level (Katz, 2015). For example, a CD4 count < 200 /mcL pneumocystis pneumonia (PCP) may occur, a CD4 count < 100/mcL Toxoplasma gondii, candida esophagitis, cryptococcus neoformans meningitis, disseminated histoplasmosis, and meningeal coccidioidomycosis may occur, and a CD4 count < 50 /mcL cytomegalovirus (CMV) retinitis, disseminated mycobacterium avium/intracellular (MAI), or mycobacterium avium complex (MAC) may occur (Stern et al., 2014). In this case the CD4 count is < 100/mcL and significant in securing the diagnosis of toxoplasmosis encephalitis in conjunction with the clinical and diagnostic findings. Labs and diagnostics to consider when there is a high suspicion for toxoplasmosis encephalitis in the HIV/AIDS population include: a head CT, CD4 count, toxoplasmosis IgG, serum crypticoccal antigen, rapid plasma reagin (RPR), CSF, blood, and fungal cultures. Computerized Tomography (CT)A head CT is usually performed prior to a lumbar puncture (LP) because it quickly rules out a large mass lesion that may lead to LP herniation (Jaffe & Ratcliffe, 2011). A head CT with contrast typically shows mass lesions in approximately 87–96% of patients with toxoplasmosis encephalitis (Stern et al., 2014). Single photon emission CT (SPECT) thallium 201 imaging may reveal reduced isotope activity in patients with toxoplasmosis encephalitis versus increased uptake in patients with PCL (Stern et al., 2014). However this diagnostic is less reliable in patients receiving antiretroviral therapy (ART), because 50% of this population has an increased uptake (Stern et al., 2014).Magnetic Resonance Imaging (MRI)MRI is the diagnostic neuroimaging of choice and recommended in patients with a normal head CT or single lesion mass (Jaffe & Ratcliffe, 2011). Typical findings on MRI: one or more ring-enhancing lesions with mass effect and edema located in basal ganglia, thalamus, and cortex (Jaffe & Ratcliffe, 2011). Only 14% of cases are single lesions making toxoplasmosis less likely (Stern et al., 2014). The presence of a single lesion increases the likely hood of PCL and less likely existence of toxoplasmosis encephalitis (Stern et al., 2014).Lumbar Puncture (LP)An LP should precede the head CT if mental status changes are present in the HIV/AIDS population secondary to complications that may occur if a large mass lesion is present (Jaffe & Ratcliffe, 2011). Platelet count, prothrombin time, and partial thromboplastin time must be evaluated prior to an LP to rule out risk for a spinal epidural hemorrhage (Stern et al, 2014). CSF should be sent for cell count, glucose, protein, India ink, viral culture, fungal culture, toxoplasmosis, cryptococci antigens, coccidioidomycosis titer, gram stain, and culture (Jaffe & Ratcliffe, 2011). Brain BiopsyA brain biopsy is not performed routinely due to risk for complications and faulty sensitivity results (Stern et al., 2014). A brain biopsy is warranted in those who did not have an early biopsy, those who have clinical or radiologic deterioration during the first week of treatment, and in non-responders to initial empiric treatment (Centers for Disease Control, (CDC, 2015).Prioritized Moinzadeh, P., et al.Plan The prioritized plan will be based on the most recent guidelines for the treatment of AIDS patients with opportunistic infections not currently on ART. Empiric therapy for toxoplasmosis encephalitis should be initiated in this triad of presumptive findings: a CD4 count < 100/mcL, opportunistic infection without ART, and positive serology for toxoplasmosis (Stern et al., 2014).The acute care nurse practitioner (ACNP) will admit for observation to observe the patient for focal neurologic deficits and initial response to therapy. The initial treatment regimen for this patient will consist of combination therapy a class AI recommendation: pyrimethamineb 200 mg once by mouth, then based on body weight > 60 kg will dose: pyrimethamineb 50 mg daily, plus sulfadiazine 1000 mg every six hours, plus leucovorin 10–25 mg daily (CDC, 2015). Pyrimethamine is effective in penetrating the blood brain barrier and leucovorin alleviates the hematologic toxicities associated with pyrimethamine treatment (CDC, 2015). This will also allow for prophylaxis of other opportunistic infections associated with a CD4 count < 200/mcL (Hull, Linder, Montaner, & Russell, 2015). Dexamethasone four milligrams every six hours is recommended in cases where the patient has a midline shift, signs of increased intracranial pressure, or a dramatic decline in mental status within the first 48 hours of presentation (Hull et al., 2015). In this case there was no evidence of a midline shift, but the head CT revealed multiple contrast-enhancing lesions in the basal ganglia with mass effect so corticosteroid therapy was initiated. This patient will need monitoring for clinical improvement. Clinical improvement has been witnessed in > 90% of responders within the first two weeks of empiric therapy (Stern et al., 2014). Crucial to this prioritized plan is education and emphasis on follow-up care: to ensure continuation of therapy at lower doses for suppressive therapy, prophylaxis for opportunistic infections, and initiation of ART based on current treatment guidelines to inhibit progressive immunologic deterioration (Hull et al., 2015).Follow UpPrior to discharge it is important for the patient to understand the importance of follow-up care with an infectious disease specialist for prophylactic prevention of other opportunistic infections, chronic maintenance therapy after toxoplasmosis treatment, and initiation of ART based on the most current guidelines (CDC, 2015). There are no recommendations in the most recent guidelines on when to initiate ART therapy in a patient currently infected with toxoplasmosis. However, based on a class CIII recommendation many providers initiate ART within two to three weeks of diagnosis, based on the considerable reduction in the incidence of AIDS progression or mortality witnessed in a controlled trial of 282 patients with opportunistic infections (CDC, 2015). It is crucial the patient receives education regarding the diagnosis, transmission, management of his disease process on ART, and the natural history of the disease progression if left untreated (Stern et al., 2014). Outpatient testing and follow-up should include: baseline labs, HIV isolate baseline, HIV viral load, test for co-infections, and HIV genotyping to identify transmitted resistance-associated mutations before any ART therapy is initiated (Stern et al., 2014). The guidelines recommend surveillance of the CD4 count and viral load every three months with a goal of an undetectable viral load within four to six months of therapy initiation (CDC, 2015). Follow-up also includes non-live immunizations if indicated and monitoring of adherence to ART. Non-compliance will lead to failure achieving viral suppression and HIV drug resistance (CDC, 2015). Other follow up considerations includes: effectiveness of empiric therapy, assessment for improvement in clinical findings, and follow-up neuroimaging for radiologic improvements (CDC, 2015).ReferencesArmao, D., & Bouldin, T. (2015). Pathology of the nervous system. In Reisner, H.M. (Eds), Pathology: A modern case study. Retrieved from for Disease Control. (2015). Guidelines for the prevention and treatment of opportunisticinfections in HIV-infected adults and adolescents. AIDSinfo. Retrieved from lines/0Hull, M., Linder, A.M., Montaner, J., & Russell, J.A. Hull, Mark, et al.(2015). Human immunodeficiency virus (HIV) and AIDS in the intensive care unit. In Hall JB, Schmidt GA, Kress JP. Hall, J.B., Schmidt, G.A., Kress, J.P. Eds. Jesse B. Hall, et al.(Eds),Principles of critical care, (4th ed., Ch. 69). Retrieved from .ezproxy.libraries.wright.edu/content.aspx?bookid=1340&Sectionid=80034609.Jaffe, J., & Ratcliff, T. (2011). Infectious disease emergencies. In Stone, C., Humphries, R.L.,(Eds), CURRENT diagnosis & treatment emergency medicine, (7th ed., Ch. 42). Retrievedfrom . libraries.wright.edu/content.aspx?bookid=385&Sectionid=40357258.Katz, M.H. (2016). HIV infection & AIDS. In Papadakis, M.A., McPhee, S.J., Rabow, M.W.(Eds), Current medical diagnosis & treatment 2016, (55th ed., Ch. 31). Retrieved from , D.L., Fauci, A.S., Kasper, D.L., Hauser, S.L., Jameson, J., & Loscalzo, J. (2014). Acute meningitis and encephalitis. In Longo, D.L., Fauci, A.S., Kasper, D.L., Hauser, S.L.,Jameson, J., Loscalzo, J. (Eds), Harrison's manual of medicine, (18th ed., Ch. 203)Retrieved from , A.H., Samuels, M.A., & Klein, J.P. (2014). Infections of the nervous system (bacterial, fungal, psirochetal, parasitic) and sarcoidosis. In Ropper, A.H., Samuels, M.A., Klein, J.P. (Eds), Adams & Victor's principles of neurology, (10th ed., Ch. 42). Retrieved from , S.C., Cifu, A.S., & Altkorn, D. (2014). AIDS/HIV infection. In Stern, S.C., Cifu, A.S., Altkorn, D. (Eds), Symptom to diagnosis: An evidence-based guide, (3rd ed, Ch. 5). Retrieved from . ................
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