Thanks to Anne Montgomery for presenting a fascinating case of 30M with HIV/AIDS who presented with AMS and fever found to have hypercalcemia and disseminated MAC.
- All lymphocytes, including CD4 cells, are reduced in acute infection. The CD4% is a more accurate measure of the degree of immunosuppression in patients with HIV presenting with an acute infection.
- Bacterial infections are the most common cause of infectious syndromes in patients with HIV and therefore, are the focus of the initial diagnosis and treatment. CrAg, AFB blood culture (moderate sensitivity for disseminated MAC), and B-D-Glucan + LDH (sensitive, but not specific markers of PCP) are also important considerations in the first/second pass work up.
- Both solid and liquid tumors occur with higher frequency in patients with HIV. Many of these tumors are related to an oncogenic virus: squamous cell carcinoma (HPV), lymphoma (EBV) and kaposi sarcoma (HHV-8). See below for more details.
- Break up the causes of hypercalcemia into PTH-related and PTH-independent causes. Remember that a “normal” PTH is ABnormal in a hypercalcemic patient.
Non-infectious complications of HIV
Thanks to Geoff, Lurit and Jessica for presenting a fascinating case of a 60M with DM who presents with cough and B symptoms found to have diffuse pulmonary nodules, mediastinal LAD and a possible cavitary lung lesion.
- While a detailed exposure history is not necessary in every infectious syndrome (e.g., CAP) a travel history is informative in certain clinical situations (e.g., cavitary lung lesion, persistent fever despite broad spectrum Abx)
- Exposures can be elicited directly (swimming in freshwater) OR
- Inferred from other activities (presumed tick bite from a lot of outdoor activities).
- A cavitary lung lesion is not always easily distinguished from normal pulmonary parenchyma [e.g. normal course of an airway]. However, when truly present, a cavitary lesion influences the DDx significantly. See below for details.
- Cryptococcus Gattii is distinct from the more commonly encountered Cryptococcus Neoformans by:
- Geographic Restriction: Gattii limited to New Zealand, Australia and Pacific NW
- Incidence in immunocompetent patients: 40% of patients with C. Gattii are immunocompetent. Most C. Neoformans infections occur in immunocompromised patients.
- Propensity to form masses: High incidence of Cryptococcoma [pulmonary and brain] in C.Gattii
- Dx testing: CrAg is also positive in C. Gattii- culture is the most reliable means of distinguishing between the two different species.
Approach to Cavitary Lung Lesions
Thanks to Theresa for presenting an interesting case of a 83 M–>F with metastatic RCC and newly diagnosed non-small cell lung cancer who presents with cough and dyspnea found to have RSV pneumonia.
- The distinction between productive and non-productive cough is rarely diagnostically informative. In cases of chronic cough, a productive cough points to bronchiectasis or chronic bronchitis in the right clinical context.
- The negative predictive value of a BNP in the diagnosis of CHF is most informative. A positive BNP level supports the diagnosis of CHF in the right clinical context, but an isolated elevation is more likely to be noise.
- The respiratory viral panel is changing our illness scripts for viral lower respiratory tract infections. In short, with the exception of an empyema, a viral pneumonia can do anything [severity of illness, radiographic findings, sepsis physiology] that a bacterial pneumonia does.
Thanks to LT and Bharat for two great cases today.
LT told us about an 86M who was out of care who was found wandering the streets by the police but appeared well-groomed and well-nourished.
Bharat shared a case of a 64M with osteomyelitis who had a transient episode of LOC and then had a PEA arrest of unclear etiology.
Here are some pearls that came up during our discussion:
- Aphasia and dysarthria can mimic altered mental status – pay close attention to these possibilities.
- While AMS may be unrecognized dementia, a work up to exclude other causes [MISTO!] is always indicated
- CT has limited sensitivity for many causes of AMS, it can assess for:
- Hemorrhage [intraparenchymal or subdural]
- Global atrophy —> initial clue to underlying dementia
- Enable a safe LP in patients who need an LP before CT
- By the time dementia has set in, “reversible” causes [e.g., B12 deficiency, neurosyphilis] are rarely fully reversible, but halting disease progression is usually possible.
- PICC -line associated DVT:
- If the line is necessary, you don’t need to remove it!
- Anticoagulate for 3 months from the day of diagnosis [regardless of when the line was taken out]
- In patients who cannot get a CTPE [AKI or hemodynamic instability], 4-extremity ultrasound and transthoracic ECHO are helpful but imperfect tests in assessing the possibility of PE.
Thanks to Gladys for presenting a fascinating case of a 40F with HIV who presents with fever, oral ulcers found to have retroperitoneal lymphadenopathy and ultimately diagnosed with disseminated histoplasmosis.
1.The most common causes of oral ulcers are aphthous ulcers and HSV infection. A second pass work up includes investigation for a wide variety of infectious, autoimmune, malignancy, drug-induced or autoimmune blistering conditions.
2. Granulomas are caused by a wide variety of infectious, autoimmune, malignant processes. Immunodeficiency [e.g., chronic granulomatous disease] and foreign bodies [e.g, TALC granulomatosis] are other considerations. Owing to their morbidity and the possible need for immunsuppression/chemotherapy if a autoimmune or malignant cause is found, an initial focus on infections [usually intracellular bugs] is important.
3. Unlike the other endemic mycoses, histoplasmosis is an intracellular organism [lives in macrophages]This changes the clinical behavior and unlike the other endemic mycoses involves the liver, spleen, bone marrow, GI tract [oral ulcers and ileitis], and adrenal glands.
- The most common causes of oral ulcers are aphthous ulcers and HSV infection. A second pass work up includes investigation for a wide variety of infectious, autoimmune, malignancy, drug-induced or autoimmune blistering conditions.
- Here is one approach.
- Granulomas are caused by a wide variety of infectious, autoimmune, and malignant processes. Immunodeficiency [e.g., chronic granulomatous disease] and foreign bodies [e.g, TALC granulomatosis] are other considerations.
- Owing to their morbidity and the subsequent need for immunsuppression/chemotherapy if a autoimmune or malignant cause is found, an initial focus on infectious causes [usually intracellular bugs] is important.
- Epidemiology: worldwide distribution
- Incubation period: 1-3 weeks
- Asymptomatic burden: Like the other endemic mycoses, there is a high rate of asymptomatic disease [around 80% without symptoms]
- Unlike the other endemic mycoses, histoplasmosis is an intracellular organism [lives in macrophages]
- This changes the clinical behavior and unlike the other endemic mycoses involves:
- Liver, spleen, lymph node and bone marrow involvement
- GI tract
- Oral mucosa and ileum are the most common sites of involvement.
- Adrenal glands [similar to Tb involvement]
- Also results in this being hardest to diagnose [like Tb]
- Clinical Symptoms:
- Occur as primary infection or reactivation disease in immunosuppressed hosts
- Pulmonary Symptoms – most common
- Acute or subacute flu like illness occur
- Minority have fulminant pulmonary disease
- Reticulonodular (with effusion) most common
- Erytema nodosum may accompany pulmonary disease
- Extra-Pulmonary disease
- Who? —> immunosuppressed
- Reticuloendothelial system: liver, spleen, lymph nodes, bone marrow
- GI tract
- Like Crohn’s anywhere along the GI tract
- Oral mucosa and ileum most common
- Fibrosing mediastinitis
- Constrictive pericarditis
- A sepsis-like syndrome in AIDS patients
- Of the mycoses this is the hardest to diagnose, because antigen based testing + culture have lower sensitivity [ possibly due to the intracellular nature of the organism]
- Culture: 75% [vs >in other mycoses]
- Urine antigen: Sen, Spec 70%
- Sen, Spec 90%
- Cross-reactivity with blasto
- Mild disease: none
- Moderate: Intraconazole
- Severe: Ampho
Thanks to Michelle from presenting a really interesting case of a 26F with chronic diarrhea of unclear etiology despite an extensive evaluation
1. Divide patients with diarrhea into one of four categories: acute inflammatory, acute non-inflammatory, chronic inflammatory and chronic non-inflammatory. This makes a the long DDx of diarrhea easier to approach.
2. Attempting to classify chronic diarrhea as secretory or osmotic by history alone is unreliable.
3. See below for one approach to chronic non-inflammatory diarrhea
4. Factitious diarrhea accounts for up to 15% of chronic, non-inflammatory diarrhea that remains unexplained. Consider a laxative screen and stool osms in these patients.
An approach to diarrhea
What makes diarrhea inflammatory?
- Abdominal Pain
- Pain alone is insufficient, but in the context of other features may add further support to an inflammatory cause
- Serum tests
- Elevated inflammatory markers
- Stool tests
- Stool WBC
- Fecal calprotectin
- Fecal Lactoferrin
Chronic non-inflammatory diarrhea
This category is often the hardest of diagnose and in many cases, will need the expertise of GI [and other consultants]
Here’s one approach:
- Accounts for up to 15% of chronic, non-inflammatory diarrhea that remains unexplained
- Most patients have a healthcare background
- Factitious diarrhea develops in two clinical contexts
- Laxative use
- Surreptitious or unintentional [e.g herbal tea with osmotic agent]
- Laxative screen – stool, urine, blood
- Stool Mg measurement may be information
- Addition of fluid
- Hyopotonic fluid —> serum Osm < 290
- Consider measuring urine osms (as urine may be accidentally mixed in)
- Consider measuring osms of colonoscopy sample
- Hypertonic fluid —> Serum osm > 600
Thanks to Ashleigh and Katie for presenting a fascinating case of a 55M who p/w flank pain found to have pyelonephritis c/b persistent leukocytosis attributed to candidemia
1. Toxidromes account for the majority of pupillary changes [big and small]. In patients with a dilated pupil consider compression of CN III by  elevated ICP or  PCOM aneurysm. In patients with pinpoint pupils, consider the possibility of a brainstem stroke.
2. First line therapy for candidemia are the echinocandins [e.g caspofungin or micafungin]. Prompt removal of any indwelling lines reduces mortality.
3. 15% of patients with candidemia develop endophthalmitis mandating an dilated eye exam in all these patients.
Here’s one approach to fungi
Here’s an evernote about candidemia: