Friday, January 30, 2009
(dorsal fat pad pictured above)
Many patients with require corticosteroid treatment for their underlying medical condition. Unfortunately, there are many complications of these drugs - a discussion with patients of the risks, benefits, and alternatives of corticosteroid therapy should be performed prior to starting therapy.
Skin & Soft Tissue: thinning of the skin and easy bruising. Cushingoid features are common, which include central obesity, dorsal fat pad, weight gain, purple striae, and moon facies.
Eyes: cataract formation and glaucoma.
Metabolic: hyperglycemia and hyperlipidemia.
Central Nervous System: sleep disturbances, mood changes, hypomania, and overt psychosis.
Cardiovascular: Increased risk of myocardial infarction and stroke - likely stemming from the metabolic abnormalities. Patients may be at an increased risk of hypertension and congestive heart failure from fluid-retention.
Gastrointestinal: Patients are at an increased risk of developing gastritis, ulcer formation, and GI bleeding - especially when concomitantly taking NSAIDS.
Musculoskeletal: There is the rare but dreaded avascular necrosis of the hip, and commonly osteopenia and osteoporosis which can result in fragility fractures. Patients may also develop proximal muscle weakness from a steroid-induced myopathy.
Infection: Steroids are immune modulators and patients are at an increased risk of infection - perhaps from decreased phygocytic function or a blunted cytokine response.
Pregnancy: Steroids may be a risk factor for cleft-palate development in the fetus.
(another complication of steroids pictured to the left)
Thursday, January 29, 2009
Wednesday, January 28, 2009
- Chest pain
- New pulmonary infiltrate
- Tachypnea, wheezing, or a cough
Treatment of this condition is pretty much supportive and includes:
- Maintaining a PaO2 between 70 to 100 mmHg
- Attaining and maintaining Euvolemia - crystalloids are best
- Pain management - typically will require opioid analgesics
- Coverage for community acquired pneumonia
- Exchange transfusion - if there are progressive pulmonary infiltrates or severe dyspnea that is not responding to the above therapy.
Wednesday, January 21, 2009
- Check out the treatment of Status Epilepticus here.
- We also talked about TB meningitis, and you can read a bit more about the diagnosis and treatment of that over here.
- Check out Alcohol Withdrawal syndromes over here.
Tuesday, January 20, 2009
Look for mucocutaneous bleeding: gingival bleeding after brushing teeth, epistaxis, menorrhagia, metrorrhagia, and easy bruising. Also look for petichiae (non-palpable, non-blanchable) in dependent areas, like the shins and feet. These should not be on the soles of the feet as there is a thick protective layer of subcutaneous tissue. You may see them on the palate as well. Check out the photos at the bottom.
Decreased Production of platelets:
- Hypocellular bone marrow: from aplastic anemia of which there are many causes(idiopathic, radiation, chemo, medications, viruses). Other cell lines will also be decreased.
- Cellular bone marrow: myelodysplastic syndromes, leukemia
- Replacement of marrow: with primary or secondary malignancies, myelofibrosis, or granuloma (eg. TB, sarcoid).
Increased Destruction of platelets:
- Immune mediated: Idiopathic Throbocytopenia Purpura (primary), or secondary to Collagen Vascular Diseases (eg. SLE), Infections (eg. HIV, Hep C), Drugs (eg. heparin, sulfa), Lymphoproliferative diseases (CLL, lymphoma), and the Antiphospholipid Antibody Syndrome.
- Non-Immune mediated: Think about things like Disseminated Intravascular Coagulation, Thrombotic Thrombocytopenia Purpura and it's cousin the Hemolytic Uremic Syndrome, HELLP syndrome in pre-eclampsia, and malignant hypertension.
- Mostly in a large spleen.
- Very rarely, blood collected in the tube will react to a chemical (EDTA) and cause platelet clumping - this may cause 'spurious' thrombocytopenia. The platelets work just fine, they just react to the EDTA.
(petichiae to the left, and palatal petichia + gingival bleeding below)
Monday, January 19, 2009
Thursday, January 15, 2009
Today we talked about a few issues. Firstly, the difference between a Transudate and Exudate in the analysis of pleural effusions. You can read more about this here.
We also discussed Endocarditis - and went through many of the peripheral stigmata of this condition. Have a look over here for more info.
Let's talk about the diagnosis of endocarditis for a minute...and think about the Duke Criteria. These are divided into major and minor criteria. For a Definite diagnosis of endocarditis, we require 2 major, 1 major + 3 minor, or 5 minor criteria. Alternatively, you can be confient in your diagnosis if you have pathologic evidence of endocarditis (eg. you have microbiologic evidence grown directly from a valve vegetation). Possible infective endocarditis is defined by 1 major + 1 minor criteria, or 3 minor criteria.
Okay...so what are the Major and Minor criteria? We will discuss these below, but here is a good link for details on the diagnosis and managment of Infective Endocarditis from the American Heart Association.
1. Positive blood cultures for endocarditis.
- typical microorganisms on two separate blood cultures (Strep, Staph, Enterococcus, HACEK etc)
- persistently positive blood cultures that grow an organism that can cause IE (eg. over a 12 hour period).
- Single positive blood culture for Coxiella burnetii or antiphase I IgG antibody titer >1:800.
- Echocardiographic evidence: like an oscillating intracardiac mass, abscess, or dehiscence of a prosthetic valve.
- A NEW regurgitant murmer.
- Fever >38 degrees Celsius
- Predisposing cardiac lesion or IV drug use.
- Vascular phenomena: think about major arterial emboli, septic pulmonary infarcts, mycotic aneurysm, intracranial hemorrhage, conjunctival hemorrhages, Janeway lesions.
- Immunologic phenomena: glomerulonephritis, Osler's nodes, Roth spots, positive rheumatoid factor.
- Microbiologic evidence: positive blood culture but not meeting major criterion as noted previously.
here is the American Heart Assoication 2008 clinical guidelines on valvular heart diseases with a focus in infective endocardits.
Wednesday, January 14, 2009
(Left: PML seen on MRI)
A general approach to a patient with HIV and neurologic findings will be discussed here. We also talked about headaches and a good approach + some links can be found here. It is crucial to get a detailed history - including past CD4 counts/viral loads, a history of antiretroviral therapy and adherence to therapy, and a history of opportunistic infections.
After a detailed history and physical exam are performed, imaging of the head is often done. We typically categorize diseases into Central Nervous System lesions with a mass effect and those with no mass effect. Of note, contrast should be used to obtain the best images, and MRI is preferred over CT.
- Toxoplasmosis: can present with fever, headache, focal deficits, or seizures. Multiple ring enhancing lesions are visualized, and CD4 counts are typically less than 100.
- Primary CNS Lymphoma: can present with focal deficits, confusion, seizure, and constitutional symptoms. There can be one or more lesions, and they may or may not ring enhance (may look like Toxo).
- Abscess: many pathogens can do this including Staphylococcus, Streptococcus, Aspergillus, Nocardia, plus some really strange ones like cryptococcomas, tuberculomas, and syphilitic gummas.
No Mass Effect:
- Progressive multifocal leukoencephalopathy: As the name implies, there are progressive neurologic deficits in this condition. Hemiparesis, ataxia, aphasia, and mental status changes. It is from reactivation of the JC virus, which can be detected in the CSF. Look for asymmetric subcortical and periventricular demylination.
- HIV Encephalopathy: Radiographically, this is more symmetric and diffuse compared to PML. Patients will have mental status changes and likely disordered movement.
- CMV Encephalitis: This represents reactivation of CMV seen when CD4 counts drop below 50. Either subcortical changes or ventricular enlargement are visualized.
- Meningitis: think the usual bacterial causes (Streptococcus, Meningococcus, H. flu, Listeria) to more unusual etiologies like cryptococcus, and tuberculosis.
Here is a link on the general managment of a new HIV infection.
These are the most recent guidelines on the treatment of Opportunistic Infections.
Here is a good review on PML.
Tuesday, January 13, 2009
Today we discussed a number of issues related to communication with our patients, namely in a palliative setting. We focused on the well-being of our patients, their families, and also of the health care team. Below are some helpful links to papers on spiritual care and communication.
Monday, January 12, 2009
1. Decreased Intake: B12 is found primarily in animal products like meat, eggs, and milk. Strict vegans may be at risk.
2. Stomach-Related Conditions: Remember that B12 must bind to Intrinsic Factor (released from gastric parietal cells) to ultimately be absorbed in the terminal ilium. In Pernicious Anemia, autoantibodies attack intrinsic factor - this condition can be diagnosed with the Schillings test or by detecting autoantibodies. Autoimmune Chronic Atrophic Gastritis from autoanitbodies directed against parietal cells will also cause B12 deficiency. Also consider chronic gastritis, gastrectomy or gastric bypass as potential causes.
3. Intestinal Issues: Diphyllobothrium (Fish Tapeworm) is a massive worm...like-the-up-to-10-metres-long kind of massive, that can cause B12 malabsorption. Also consider diseases that will impair B12 absorption in the terminal ilium. Crohn's Disease is common here as is Lymphoma, and depending on the patients geographical past, think about Tuberculosis iliitis. Chronic pancreatitis is another common etiology.
4. Medication: Prolonged usage of proton pump inhibitors may cause B12 deficiency from impared gastric acid secretion, and metformin has been implicated in B12 deficiency from a calcium-mediated process in the ilium.
5. Rare inherited diseases: For example Imerslund-Grasbeck's syndrome, where there is impaired uptake of the B12-Intrinsic Factor complex in the terminal ilium.
Here is a neat case and a good approach to B12 deficiency.
Here is a terrific review on Pernicious Anemia from NEJM.
Here is the Rational Clinical Exam paper for splenomegaly from JAMA.
(Diphyllobothrium...aka Fish Tapeworm aka Gross)
Friday, January 9, 2009
(massive lymphededma in filariasis)
Thursday, January 8, 2009
Multiple Myeloma is a hematologic malignancy that arises from a single clone of plasma cells producing a monoclonal immunoglobulin (usually IgG or IgA). The plasma cells proliferate in the bone marrow - many of the clinical features and complications of this disease arise from the proliferation of these cells, and the immunoglobulins which are released.
Anemia: Very common. Essentially, the plasma cells proliferate and displace the normal bone marrow. An autoimmune destruction of RBC's can also occur.
Bone Pain: Also very common, and usually secondary to lytic lesions or pathologic fractures. Nerve compression may result from this . There is increased osteoclast and decreased osteoblast activity. A cytokine known as RANKL is likely responsible for the osteoclast activity.
Renal disease: there are many mechanisms for this to occur including deposition of filtered light chains in the glomerulus, acute tubular necrosis from light chain deposition, amyloidosis, hypercalcemia, type II renal tubular acidosis...or Fanconi's syndrome, urate nephropathy, or pyelonephritis.
Recurrent Infection: this is also very common and is likely secondary to hypogammaglobulinemia and impaired plasma cell function. Pneumonia and pyelonephritis are common.
Laboratory examination may reveal anemia. Rouleaux will be frequently seen on blood film secondary to the high burden of protein (immunoglubulins) expelled by the plasma cells. Hypercalcemia and renal failure are also common (here is a link to hypercalcemia in malignancy). Serum protein electrophoresis will often detect a an M Spike - this is the immunoglubulin that is being overproduced by the clonal plasma cells. You can determine which immunoglobulin it is via immunofixation. In about 15% of cases, only a light chain of the immunoglubulin is secreted, and these can be detected in the urine as Bence-Jones proteins via urine protein electrophoresis and immunofixation. Rarely (less than 5% of the time) plasma cells will not secrete immunoglobulins.
Bone marrow biopsy is essential to confirm the diagnosis of multiple myeloma, and by definition would require more than 10% clonal plasma cells.
Unfortunately this disease has a poor prognosis with survival ranging between 2 to 5 years.
Here is a good paper on malignancy related hypercalcemia.
Here is a review for the various treatments of multiple myeloma.
(lytic bone lesions on the skull of a patient with multiple myeloma)
Wednesday, January 7, 2009
An organised approach to Interstitial lung diseases:
Systemic Diseases: the most common of these are sarcoidosis and the Collagen Vascular Diseases - with scleroderma being the prototype. Also consider mixed connective tissue diseases. ILD is not as commonly in SLE and Rheumatoid arthritis.
Here is a good review article on sarcoidosis.
Exposures: these are classically divided up into organic and inorganic.
- Organic: aka hypersensitivity pneumonitis. Think about Bird Fancier's Lung (proteins in bird excrement), Cheese Washers Lung, Farmer's Lung, and many many more.
- Inorganic: aka pneumoconiosis. This would include exposure to dust from asbestos, silica, and coal.
Drugs: Exposure to alkylating chemotherapeutic agents (eg bleomycin), and commonly used meds like amiodarone, methotrexate, nitrofurantoin, and sulfa drugs.
Idiopathic: This is a strange category with bizarre acronyms. It doesn't help that there are new and old acronyms for some of the pathologies, but all are still commonly used. Here's a sample.
- Usual Interstitial Pneumonia (UIP), also known as Interstitial Pulmonary Fibrosis (IPF). This is the most common of the idiopathic interstitial lung diseases. Here is a good review article.
- Acute Interstitial Pneumonia (AIP) also known as the Hamman-Rich Syndrome. Just like UIP, but more rapid and severe.
- Cryptogenic Organising Pneumonia (COP), but if the etiology is known, it will be called Bronchiolitis Obliterans with Organizing Pneumonia (BOOP). Lots of granulation tissue in the small airways here.
- Desquamative Interstitial Pneumonia (DIP). Many macrophages in alveoli. Common in middle-aged smokers. A milder version of this may be referred to as Respiratory Bronchilitis-Associated Interstitial Lung Disease (RBILD).
- Others: Lymphocytic Interstitail Pneumonia (LIP), Nonspecific Interstitial Pneumonia (NSIP).
Other Rare Causes: Alveolar hemmorhage, Pulmonary Infiltrates with Eosinophilia (PIE), Pulmonary Alveolar Proteinosis (PAP), Lymphangioleiomyomatosis (LAM).
Mimickers of ILD: Congestive heart failure, certain infections like Pneumocystis Carini Pneumonia, and lymphangitic carcinomatosis can cause interstitial pattersns on chest X-rays.
Tuesday, January 6, 2009
2. Infection: think about common sites - like urinary tract, pneumonia, intra-abdominal, and endovascular sources of infection. Also consider less common areas like meningitis and cerebritis.
4. Structural: think big, like heart (eg. myocardial infarction), gut (eg. ischemia, obstruction), brain (eg. mass, infarct), muscle (eg. rhabdo), lung (eg. pulmonary embolus), etc.