1. Cold agglutinins are usually due to infections or lymphoproliferative disorders
- Lymphoproliferative disorders: anything involving increased production of antibodies (i.e B-cell cancers), so waldenstrom's macroglobulinemia, lymphoma, CLL, multiple myeloma.
- Viral infections: CMV, EBV (60% of mono pts will have cold agglutinins, but hemolytic anemia is rare), VZV, Mumps, rubella, HIV, influenza
- Bacterial infections: legionella, e.coli, syphilis, listeria
- Parasitic infections: trypanosomes, malaria
- CANOMAD syndrome (chronic ataxic neuropathy ophthalmoplegia M-protein agglutination disialosyl antibodies): gait and upper-limb ataxia, external ophthalmoplegia, cold agglutinins, IgM paraprotein, and anti-disialosyl antibodies. Neurologic and hematologic symptoms respond to rituximab.
2. Warm agglutinins: 
- 80% of all autoimmune hemolytic anemia (AIHA).
- Always polyclonal. IgG1 and IgG3 are the most destructive, and the people with AIHA with a significant component of one or either will have a more advanced, aggressive course. The composition of Ig subtypes is unique and does not always reflect serum composition.
- Usually caused by drugs
- Drugs: cephalosporins (cefotetan most commonly, ceftriaxone next), penicillins (esp piperacillin), NSAIDs,
- Systemic autoimmune diseases: Lupus, RA
- S/p URI
- CLL
3. Acute chest
- Infarctions may lead to secondary infections, so pneumonia in a homozygous sickle cell patient may represent ACS
- Multiple infarctions -> pulmonary congestion, shunting of blood, hypoxia -> more sickling
- Treat with exchange transfusion to goal of HbA > 50% to decrease sickling.
- Hydroxyurea is good to prevent sickle crises (increases Hb F production), but is not an effective treatment in the acute setting.
4. Osteonecrosis (aka avascular necrosis) of the femoral head:
- Common in sickle cell, hypercoagulability (i.e. antiphospholipid), steroid use, gout, alcohol use, lupus, s/p trauma, gout.
- Unclear why alcohol use causes this... but there is a clear relationship. Compared to demographically matched controls, RRs of osteonecrosis of the femoral head were 3.3, 9.8, and 17.9 for current consumers of less than 400, 400-1000, and greater than or equal to 1000 ml/week of alcohol {source}
- CXR: initially will show nothing, later on may show increased density (marrow infarction -> calcification). MRI is >90% sensitive, good for detection in the early phases.
- Can use radionuclide bone scan in people who can't get MRI- although this is not as sensitive.
5. Complex regional pain syndrome/reflex sympathetic dystrophy
- pain in the extremities, swelling, local vasomotor instability (hot flashes), limited range of motion,
- local osteoporosis (bone densitometry scan)
6. Septic arthritis: 
- Always should suspect in acute onset monoarticular arthritis, but is uncommon in the absence of prosthetic hip, recent trauma/surgery, previous hip disease
7. Platelet transfusion should be avoided in consumptive processes unless there is life-threatening bleeding.
8. TTP
- ADAMTS13 normal levels: 65-133%, in fulminant TTP expect to be very low.
- More importantly, ADAMTS13 inhibitor should be positive. No inhibitor = No TTP
9. Evans syndrome: 
- Coombs+ warm AIHA + ITP
- Smear: spherocytes/microspherocytes + decreased platelets + elevated retics
- Tx like TTP: steroids and IVIg. children have a good response to steroids.
10. Thrombocytopenias: 
- Pseudothrombocytopenia: where platelets agglutinate in large clumps, occasionally to neutrophils but sometimes to other cell types. These large platelet clumps are not read by the cell counter and you get a falsely low platelet count. Repeat the test with heparin or sodium citrate (instead of EDTA).
- Gestational: occurs in 5% of pregnancies, appears in late gestation. Platelets are 70-150K. Generally no treatment.
- ITP: no findings other than low platelets. No large spleen, no adenopathy, no abnormal white or red cell morphology. Sometimes you will see giant (i.e. immature) platelets on smear.