Dermatomes, chickens, and pneumonia

AM Report Pearls: Approach to Patients with Rashes & Hypoxemia
Many ways to think about disease processes with rashes & hypoxemia, and it comes down to: what is the morphology of the rash?
  • Infectious: Viral – VZV, influenza can have non-specific rash, Fungal pneumonias with infiltrative skin lesions, TB or NTM with infiltrative skin lesions, bacterial superinfection of viral processes
  • Autoimmune: Pulmonary predominant vasculitis such as GPA (Wegener’s) and EGPA (Churg-Strauss), many pulmonary manifestations of SLE including effusions, pleuritis
  • Embolic disease: Cholesterol atheroembolic disease – look for the characteristic rash of livedo reticularis
  • Malignancy: Sweet’s syndrome can have pulmonary manifestations & skin rash (can be bullous or non-specific)
  • Allergy: DRESS /DISH can have pulmonary involvement but it is rare,  CT can show interstitial pneumonitis or pleural effusions
 
AM Report Pearls: Disseminated Zoster & VZV Pneumonia
  • To review, Varicella-zoster virus (VZV) primary infection = varicella (chickenpox), secondary infection/reactivation = herpes zoster/shingles
  • The rash starts as erythematous papules which evolve to grouped vesicles or bullae, crust within 7-10 days
  • Usually limited to one dermatome<20% of pts have systemic symptoms
  • Disseminated zoster usually seen in organ transplant patients, patients with heme malignancies undergoing chemo
  • VZV pneumonitis has a very high mortality and usually seen in bone marrow transplant patients – rare!
  • Usually VZV pneumonia is characterized by nodular opacities with scattered necrotic foci
  • IV Acyclovir is treatment of choice for severe VZV pneumonitis/pneumonia
 

Eat your vitamins Ileum!

Take Home Points: Vitamin & Elemental Absorption and Clinical Deficiency Syndromes
 
To know what deficiencies a patient may be at risk for, you have to know where each nutrient is absorbed.
 
Stomach – stomach acid cleaves protein-bound elements (B12, copper, Iron) and produces intrinsic factor (IF)
 -> Affected in: gastrectomy, Roux-en-Y, atrophic gastritis
 -> Deficiency Syndromes
  • B12 – megaloblastic anemia, peripheral neuropathy, impaired proprioception, slowed mentation
  • Copper – needed for WBC, RBC, and nervous system – results in anemia, usually microcytic (as Rabih pointed out, may help distinguish from B12 deficiency!), neutropenia, ataxia
  • Iron – anemia
 
Duodenum/Proximal jejunum – responsible for absorption of most water-soluble vitamins and elements
-> Affected in: Roux-en-Y and duodenal switch bypasses, Crohn’s affecting this area
-> Deficiency Syndromes
  • Thiamine – Beriberi, “dry” – aphonia, peripheral neuropathy, wernicke’s encephalopathy (nystagms, ophthalmoplegia, ataxia), confusion, coma, “wet” = neuro changes ­+ cardiomyopathy, cardiomegaly, CHF
  • Zinc – delayed growth, impotence, impaired wound healing, dysgeusia and loss of taste, skin lesions
  • Selenium – skeletal muscle dysfunction and cardiomyopathy
  • Copper –anemia, usually microcytic, neutropenia, ataxia
  • Iron – anemia  
 
Jejunum – absorption of fat AND the fat soluble vitamins ADEK
-> Affected in: Roux-en-Y and duodenal switch as well as fat malabsorptive states (Celiac, CF, pancreatic insufficiency, Crohn’s)
-> Deficiency Syndromes
  • A – xerophthalmia, night blindness
  • D – rickets, osteoporosis
  • E – spinocerebellar neuromyopathy, hemolytic anemia in infants
  • K – impaired coagulation
 
Ileum – notable for B12 and bile acid absorption
-> Affected in: ileal resections (>100cm) and ileal disease stats (Crohn’s, lymphoma, etc)
->Deficiency Syndromes
  • Bile acids – may lead to fat malabsorption and deficiency of Vit ADEK + watery diarrhea from bile salt wasting
  • B12 – megaloblastic anemia, peripheral neuropathy, impaired prorprioception, slowed mentation

Lupus in the Lungs

AM Report Pearls: Pulmonary Manifestations of SLE
Think anatomically: SLE can involve the the pleura, the lung parenchyma, and the vasculature.
Pleural disease:
  • SLE patients can get chest pain from pleural inflammation/pleuritis with a normal CXR and without pleural rub
  • Pleural effusions are usually exudative, bilateral, high LDH but lower WBC (either PMN or lymph predominant), low protein
  • Pleural disease often responds to treatment with NSAIDs and if refractory, consider steroids
  • Remember, pleural effusions in SLE still need to be evaluated and SLE as the cause is a dx of exclusion!
Parenchymal disease:
  • ILD noted in ~9% of patients with SLE, with PFTs showing a restrictive pattern and decreased DLCO
  • Often CT can be seen with ground-glass opacities which on biopsy are often associated with the NSIP patternreticulate pattern can also be seen and associated with UIP on pathology
  • SLE-associated ILD treatment involves steroids +/- immunomodulators such as cyclophosphamide
  • Acute lupus pneumonitis/alveolitis can present with fever, cough, dyspnea, and pulmonary infiltrates & CT findings of alveolitis/ground glass – hard to distinguish between DAH and acute lupus pneumonitis!
Vascular disease:
  • Severe pulmonary HTN is rarely associated with SLE, we think of it as more associated with other connective-tissue diseases
  • SLE patients can have acute PE or chronic thromboembolic disease from hypercoagulability from antiphospholipid antibodies
  • Diffuse aleveolar hemorrhage is a rare complication of SLE, diagnosed by bronchoscopy, and treated with high-dose steroids + cycylophosphamide
  • PVOD (pulmonary venoocclusive disease) is a rare cause of pulmonary hypertension in SLE caused by fibrosis leading to occlusion of pulmonary veins and interlobular septal edema
We also had some pretty good pearls from HH & Dr. Gluck from Nephrology on antibiotics and kidneys that I also wanted to pass along!
 
5 Random Pearls from today’s AM Intersection of Nephrology + ID!
  • Tobramycin causes AKI but usually non-oliguric and usually after 5 days (not after first dose)
  • High-dose nafcillin can cause hypokalemia because it is a non-reabsorbable anion that causes potassium excretion 
  • You can also see hypokalemia with the anti-pseudomonal antibiotics such as piperacillin from the same mechanism
  • Vancomycin nephrotoxicity is less common now than it was with past formulations, but supratherapeutic troughs can be associated with nephrotoxicity
  • The combination of vancomycin + aminoglycoside is HIGHLY associated with AKI  – up to 20-30% of patients on this combination can get AKI!

I don’t want no Scrub (Typhus!)

Some Pearls as we ramp up this site:
1. An approach for evaluation of fever in a returned traveler from a tropical area (think about exposures and incubation period)
  • Always consider common causes such as UTIs or URIs, as well as non-travel related causes
  • Take a detailed travel history with info on exposures and risk factors
  • If the incubation period is < 21 days, majority of patients with have malriatyphoid fever, or dengue fever, but also want to think about Rickettsial diseases in this group
  • If the incubation perioid is > 21 days, the majority of patients will have malaria or TB
  • If Altered Mental Statuscall ID early for help as this could be a life threatening infection (i.e. meningococcemia or a viral hemorrhagic fever). 
2. Differential diagnosis for Lymphadenopathy in a returned traveler
·         Localized Lymphadenopathy
o    Bacterial Infection: bartonellosis (cat scratch disease), plague, staphylococcal infection, streptococcal infection, tuberculosis (scrofula), tularemia, typhus
o    Parasitic Infection: African trypanosomiasis, American trypanosomiasis, filariasis, toxoplasmosis
·         Generalized Lymphadenopathy
o    Bacterial Infection: brucellosis, leptospirosis, meliodosis, secondary syphilis, TB, enteric fever
o    Viral Infection: acute HIV, dengue fever, hepatitis B, Lassa fever, measles, mononucleosis (EBV, CMV), rubella
o    Fungal Infection: blastomycosis, coccidioidomycosis, histoplasmosis
o    Parasitic Infetion: visceral leishmaniasis
o    Noninfectious causes
§  Malignancy (lymphoma, melanoma, metastatic carcinoma)
§  Autoimmune (RA, SLE, sarcoid)
§  Medications (Phenytoin, Carbamazepine, allopurinol, sulfonamides)
 
3. Scrub typhus is a disease caused by the bacteria Orienta tsutsugamushi, which is in the rickettsia family. Transmitted by the bite an infected larval mite, which live in grassland areas at the edge of dense monsoon forests.  Found in Asia and the Pacific region including northern Australia. Sx occur in 1-2 weeks and include fever, chills, diaphoresis, headache, lymphadenopathy, and occasionally a dull red skin rash.  Treatment is 14 days of doxycycline.

That’s a mean gradient ya got there

More pearls!:
1. Aortic Stenosis, the most common valvular heart disease in the Western World, is a narrowing of the aortic valve opening with presentations that can range from assymptomatic to angina (5 year mortality of 50% if AV not replaced), syncopy (3 year mortality at 50% if AV not replaced), or CHF (2 year mortality at 50% if AV not replaced).
Severity of Aortic Stenosis
Degree of aortic stenosis Mean gradient
(mmHg)
Aortic valve area
(cm
2)
Mild aortic stenosis <25 >1.5
Moderate aortic stenosis 25 – 40 1.0 – 1.5
Severe aortic stenosis >40 < 1.0
Critical aortic stenosis >70 < 0.6
2. Patients with supravavlular aortic stenosis (SVAS) often present with unequal blood pressures in the upper extremities, which is thought to be explained by the Coanda effect. The Coanda effect is the tendency of a jet stream to adhere to a wall, and in supravalvular AS, the high velocity stream tends to adhere to the right aortic wall, causing disproportionately high pressure in the right arm.
3. Recommendation for treating Community Acquired PNA in a patient admitted to the ICU include givein Ceftriaxone and Azithromycinwith or without Vancomycin (add Vanc if patient has risk factors for MRSA infection including prior influenza, presence of cavitary disease, or empyema.

Reticulocytes don’t grow on trees!

Some pearls from a recent M&M as we ramp up the site:
1.    Paroxysmal Nocturnal Hemoglobinuria (PNH) is a rare, genetically acquired disease characterized by complement-induced intravascular hemolytic anemiared urine, and thrombosis. Patients generally present with red discoloration of the urine (from hemoglobin and hemosiderin), with a small proportion of patients presenting with abdominal pain and odynophagia. Forty percent of patients present with thrombosis. Diagnosis is made with flow cytometry for CD55 and CD59 on white and red blood cells. Treatment is with eculizumab with definitive tx being a allogenic bone marrow transplant.
2.     A quick and general way to determine if your patient has appropriate reticulocyte production in the setting of anemia. Just remember,“4, 14, 40, 400.”
3.     Differential Diagnosis for Iron Deficiency Anemia (Remember: Tiny TAILS)
·         Thalassemia
·         Anemia of Chronic Disease
·         Iron Deficiency
·         Lead Poisoning
·         Sideroblastic Anemia

PCP, Mycoses, and the biliary tree: Low CD4 Pearls

Some pearls from a past morning report as we ramp up this site:
1.       In evaluating a patient for PCP, a High Resolution CT scan with no evidence of ground glass opacities has a close to 100% negative predictive value for the presence of PCP.  Initially reported by our very own Dr. Hopewell (paper attached). 
 
2.       Color coated map of Endemic Mycoses in the United States
 
3.       AIDS Cholangiopathy is a syndrome of biliary obstruction from infection related strictures of the biliary tract.  Etiologies include Cryptosporidium parvum (most common), Microsporidium, and CMV. Very rare since the advent of HAART and seen when CD4 < 100.  Pt’s present with RUQ and epigastric pain with diarrhea, and rarely have fever or jaundice. Treatment is HAART with obstruction reliefwith sphincterotomy or biliary stenting if there are clinical signs of obstruction.