Diabetic Ketoacidosis

Today we discussed a case of Diabetic Ketoacidosis.

• You can read more about precipitants to DKA here.


• Check out the management of DKA/HONK here.

Preeclampsia

Preeclamsia

What is it? Hypertension that develops after 20 weeks gestational age which is associated with proteinuria.

Breifly, what is the pathophysiology? The release of placental/fetal factors that alter maternal endothelial function. Ultimately there may be less vascular endothelial growth factor (VEGF) - possible from VEGF antagonists released by the placenta.

What are the diagnostic criteria?

• systolic BP >140 mmHg, or
• diastolic BP >90 mmHg, and
• proteinuria >0.3 grams in 24-hours, and
• gestational age >20 weeks

What are some of the other clinical manifestations of preeclampsia? this will relate to complications of endothelial damage and severe hypertension. Think about headaches, blurred vision, peripheral edema which may include the hands and face, pulmonary edema, and fetal compromise. Also think about end-organ damage from hypertension - you can read more at this link.

Are there risk factors? Yes, some of these include nulliparity, previous or family history of preeclampsia, preexisting hypertension, APLA syndrome or other connective tissue disease, multiple gestation, or 'extremes' of age (>40, <20). style="font-weight: bold;">Dreaded complications? Yep. Eclampsia (aka seizure), and the HELLP syndrome. HELLP stands for Hemolysis, Elevated Liver enzymes, and Low Platelets.

Okay, so what do I do? well, it's kind of complicated. First, remember that the only 'cure' is delivery. Also remember that cases can still present in the early post partum period. Get the obstetrical service involved early and ensure that the unborn child is well with a biophysical profile. Sometimes this is severe and an urgent delivery is necessary - so predelivery sterioids may be necessary to decrease fetal pulmonary complications. Otherwise, hypertension can be managed with a few drugs that are safe in pregnancy. Women with this condition should be watched very closely and there should be a very low threshold for admission to hospital.

Drugs commonly used in preeclampsia include labetolol, hydralazine, methyldopa, and nifedipine. The target blood pressure is debated, but many would agree on 130 to 150 mmHg systolic and 80 to 100 mmHg diastolic.

In severe preeclampsia, where eclampsia is a very real risk, Magnesium Sulfate is administered to reduce the seizure threshold. It is generally administered during labour and delivery, and is continued for 24-48 hours afterwards.

Here is a link on the utility of Magnesium in preventing eclampsia.
Here is a cool case of preeclampsia with a twist.

HoPingKong-isms

(a helicopter?)

1. "....my favorite topic in obstetrics...the men are 'he' and the women are 'she'..." Huh? What? He is referring to Sheehan's syndrome - pituitary infarction as a result of hypotension from postpartum hemorrhage.

2. "...you've got abdominal pain, and did you hear that buzz...it sounded like a helicopter...." Okay, this one isn't too tough. helicopter = Helicobacter, as in Helicobacter pylori infection as a common cause of peptic ulcer disease.

3. "....you've got abdominal pain and I'm pointing my finger at you..." Referring to Inglefinger's sign in pancreatitis, where patients are more comfortable sitting up and leaning forward.


4. "...this patient has pancreatitis...are you from Trinidad? Are there scorpions there?..." referring to scorpion bites as an unusual cause of pancreatitis. More common etiologies include

• Gallstones,
• Alcohol use
• Hypertriglyceridemia

Other causes include hypercalcemia, viral infections (eg. mumps, vzv, HIV), bacterial infections (mycoplasma, legionella, salmonella), parasitic infections (toxoplasma, cryptosporidium, Ascaris), traumatic (like post ERCP), congenital, and yes, scorpion bites too.

5. "....hmmm....you know, in pancreatitis, no man is an island..." referring to the pancreatic Islets of Langerhans. Here, the alpha cells produce glucagon, beta cells produce insulin, and delta cells produce somatostatin.

You can read more on pancreatitis here.

Who is Chad anyways?

Atrial Fibrillation. And the CHADS2 score. What's the deal?

Well, essentially this is a very simple scoring system to determine your patients risk of thromboembolism with atrial fibrillation.

• Congestive heart failure (any history): 1 point
• Hypertension (including prior history): 1 point
  
• Age > 75: 1 point
• Diabetes mellitus: 1 point
• Stroke: 2 points

Simple as that. Add up the points. A higher number of points means that the risk of thromboembolism is more likely. Low risk patients have a score of 0 - 1, where the annual incidence of stroke is less than 2.5%. A score of 2 carries a Moderate risk (4% per year) of stroke, and anything greater than 2 is High risk.

Essentially, Aspirin can be used to treat low risk patients, Aspirin or Warfarin in moderate risk patients, and Warfarin in high risk patients. Warfarin will reduce the risk of embolic stroke by about 2/3.

Here is a link to the original article published in JAMA in 2001

Parapneumonic Effusions

When a patient is found to have a pleural effusion, it is important to determine whether this is a transudate or an exudate. You can read more about that here.

When dealing with a parapnumonic effusion, it is important to categorize it into one of three types:

• Uncomplicated Parapneumonic Effusions: These resolve on their own with antibiotic therapy.
• Complicated Parapneumonic Effusions: This will require drainage to prevent progression to an empyema.
• Empyema: pus in the pleural space, with cellular debris and fibrin deposition. This certainly requires drainage.
  

Below is a table with recommended definitions of parapneumonic effusions:










Managment issues: Complicated parapneumonic effusions should be drained to prevent conversion to an empmyema. A pig-tail catheter may suffice, but sometimes something larger like a chest tube may be necessary. An empyema may be difficult to drain even with chest tubes/empyema tubes in place. Sometimes thrombolytic therapy is given through the tube to help break up the contents and ease drainage. Other times, Video-assisted thoracoscopic surgery is used. In a recent trial published in NEJM , it was found that "intrapleural administration of streptokinase does not improve mortality, the rate of surgery, or the length of the hospital stay among patients with pleural infection".

Here is a link to a good review on the diagnosis and management of parapneumonic effusions from Clinical Infectious Diseases.

Some liver related issues

(a Black Howler Monkey aka Alouatta pigra pictured left)

We discussed a number of issues today in morning report around Wilson's disease, the managment of ascites, and bacterial peritonitis.

• You can read more about the serum-ascites albumin gradient here.
• We discussed Wilson's disease here.
• Want to know about the underlying causes of liver disease? Try looking here.
• Infections in hemochromatosis can be found here.
  

Complications of Steroids

(Purple striae to the left)


(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)

Polymyalgia Rheumatica

(rainbow trout)

Polymyalgia Rheumatica is characterized by the subacute onset of aching in the shoulders, hips, and neck, in a symmetrical pattern - and almost exclusively occurs in those over the age of 50. Weakness should not a feature - the limitations in physical activity are typically due to pain. Patients may also feel fatigued. The history may appear to be a bit vague.

On exam, you may find a limited range of motion - but weakness should not be present (unless the symptoms have been going on for a long time and there is atrophy). The symptoms are typically arthralgias rather than arthridites.

Investigations should be mostly normal however inflammatory markers like the Erythrocyte Sedimentation Rate will almost always be elevated. Radiographs of affected joints should also be normal, but ultrasonography or MRI can show bursitis.

Other Important Items: PMR is exquisitely responsive to steroids at low-to-moderate doses, and symptoms may dissolve quickly on as little as 15-20 mg of prednisone. Treatment usually lasts for a few weeks followed by a slow taper. Some patients relapse when tapering, and this is relieved by bumping up the prednisone again. Do not forget to counsel your patient on the side effects of steroid therapy, and to protect their bones.

Relationship to Giant Cell Arteritis: Yes, the two conditions are intimately linked. You can read more about GCA here.

A fantastic review article from Annals of Internal Medicine on PMR and GCA here.

Acute Chest Syndrome in Sickle Cell Disease

The Acute Chest Syndrome will unfortunately occur in up to 50% of patients with sickle cell disease. It is defined by:

• Fever
• Chest pain
• New pulmonary infiltrate
• Tachypnea, wheezing, or a cough

Underlying etiologies include Infection (community acquired pneumonia), viral infection, pulmonary infarction, fat embolism, but mostly this is idiopathic (over 40%). The infarction stems from RBC's sickling and clogging up the pulmonary microvasculature.

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

Other things to consider:

• Exchange transfusion - if there are progressive pulmonary infiltrates or severe dyspnea that is not responding to the above therapy.

One last word: patients should be vaccinated against encapsulated organisms (Pneumococcus, Meningococcus, H. Flu), and consideration should be given to placing patients on Hydroxyurea for the prevention of subsequent sickle cell crises.

Links:

• a good review of hydroxyurea here.
• the original article of hydroxyurea's effects from NEJM here.
  

Seizure-Related Topics

• 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.
  

Thrombocytopenia: an approach

(a megakaryocyte pictured on the left)

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).

you can read more about related issues here.

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.

Sequestration:

• Mostly in a large spleen.

Other:

• 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)

Saturday Night Fever of Unknown Origin

The classic definition of FUO from the early 1960s was: fever greater than 38 degrees Celsius on several occasions over a 3 week period of time with week worth of hospital investigations. Due to advances in our diagnostic capabilities, the definition of FUO has been changed to a 3 week duration of occasional fever over 38 degrees, but the 1 week of hospital investigations has been replaced with a "first wave" of investigations (history, physical exam, basic blood work, ANA, RF, HIV, CMV, urinalysis, blood and urine cultures, chest imaging, and possibly viral hepatitis serology). I should note that there are a few definitions out there - some say 2 weeks, others say 3...you get the picture.

What is the etiology of FUO? Roughly half of patients do not end up with a diagnosis. About 20% have an underlying inflammatory condition (eg. vasculitis, SLE), 15% have an infectious diagnosis, 7% have an underlying malignancy, and the rest are a hodge-podge (yes, hodge-podge) of miscellaneous conditions - this is from a prospective Dutch study that did not involve immunocompromised patients.

So how do we investigate? A proposed algorithm based on existing evidence was created by local talent and published in Archives of Internal Medicine.

Diagnosis of Endocarditis

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.

Major Criteria:

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.

2. Evidence of endocardial involvment

• Echocardiographic evidence: like an oscillating intracardiac mass, abscess, or dehiscence of a prosthetic valve.
• A NEW regurgitant murmer.

Minor Criteria:

1. Fever >38 degrees Celsius
   
2. Predisposing cardiac lesion or IV drug use.
3. Vascular phenomena: think about major arterial emboli, septic pulmonary infarcts, mycotic aneurysm, intracranial hemorrhage, conjunctival hemorrhages, Janeway lesions.
4. Immunologic phenomena: glomerulonephritis, Osler's nodes, Roth spots, positive rheumatoid factor.
5. Microbiologic evidence: positive blood culture but not meeting major criterion as noted previously.

Some other useful links:
here is the American Heart Assoication 2008 clinical guidelines on valvular heart diseases with a focus in infective endocardits.

HIV with Neurological Findings

(Left: Cerebral Toxoplasmosis in AIDS)












(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.

Mass Effect:

• 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.

Communication Issues

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.

This is an interesting article on the interaction of religion with medicine.

Here is an article on how to enhance the mechanisms of communication.

Here is a good paper (by our Chair of Medicine at the U of T) on how some mechanisms of communication-training for physicians may not be helpful in improving patient satisfaction.

Causes of Vitamin B12 Deficiency

No, not D12 (the Detroit rap group - former member: Eminem), we're talking about B12 today. B12 deficiency is kind of neat...there are interesting causes and consequences to this condition. We will focus on causes here.

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)

HoPingKong-isms

(W. bancrofti...this little guy can cause some big problems)

1. "...Diseases in Guyana?...Think big like a tiger, big like a giraffe, big like an elephant..." Okay, not too tough I guess. He was referring to lymphatic filariasis, from the nematode Wuchereria bancrofti seen in the adjacent picture. Colloquially this is often called elephantiasis - as the parasites (transmitted via mosquito) destroy lymphatic drainage causing lymphedema which can sometimes be quite profound.

2. "...No wrong answers here...there are only right answers with this arthritis...". Yep, he is referring to Reactive Arthritis, formerly known as Reiter's Syndrome (get it??? '...only right answers...' and Reiter's?) . This is a seronegative spondyloarthropathy (along with Psoriasis, Ankylosing Spondylitis, and Inflammatory Bowel Disease). It can follow infection with Chlamydia trachomatis, Yersinia, Salmonella, Shigella and Campylobacter, and is associated with the HLA-B27 haplotype. It is manifested by oligoarthritis, enthesitis, uveitis, urethritis and sometimes keratoderma blennorrhagica (hyperkeratotic skin lesions on soles and palms)....hence the mnemonic "can't see, can't pee, can't climb a tree".

3. "...It's a steal for you...how your kidneys are damaged in diabetes..." referring to Kimmelstiel-Wilson lesions commonly seen in diabetic nephropathy.

4. "...Does she have hyperthyroidism? Don't lag behind me here...." referring to the lid lag seen in Graves' disease. Other extra-thyroid manifestations include lid retraction, pretibial myxedema, and acropatchy. Here is a recent review on Graves' Disease.

(massive lymphededma in filariasis)

(keratoderma blennorrhagicum in Reactive Arthritis)

Clinical features of Multiple Myeloma

(rouleaux formation on blood film)

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)

Interstitial Lung Disease

(Do you fancy this bird?)

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.

1. Organic: aka hypersensitivity pneumonitis. Think about Bird Fancier's Lung (proteins in bird excrement), Cheese Washers Lung, Farmer's Lung, and many many more.


2. 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.

This cheese looks dirty....it may need a good washing.

An Approach to the Confused Patient

An approach to the confused patient...think about 4 major categories.

1. Drugs/Toxins: make sure you ask about both prescribed and non-prescribed drugs - like herbal supplements, traditional medications, and street drugs. Also, remember to ask about both intoxication and withdrawal effects (eg. Alcohol, Benzodiazepines).

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.

3. Metabolic: "pick an organ and make it fail". Common things include hyper/hyponatremia, hyper/hypoglycemia, hypercalcemia, hepatic or uremic encephalopathy, hyper/hypothyroidism, hypercarbia or hypoxia, etc.

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.

Other rare stuff: today we talked about other rare causes of confusion, including CNS vasculidities, Creutzfeldt–Jakob Disease (a good link here), tertiary syphilis, and paraneoplastic syndromes (remember the anti-Hu antibodies - check out this link)