Dont decompensate......

Decompensated Cirrhosis / encephalopathy consider:

• SBP and other infection
• portal vein thrombosis
• variceal haemorrhage / upper GI bleed
• constipation
• narcotics / medications
• dehydration
• hypokalemia
• hepatocellular carcinoma

Here is a link for a recent article on cirrhosis management : Lancet. 2008 Mar 8;371(9615):838-51.

http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6T1B-4S0JSP4-15&_user=1166899&_rdoc=1&_fmt=&_orig=search&_sort=d&view=c&_acct=C000051839&_version=1&_urlVersion=0&_userid=1166899&md5=5581813824abf0c779fe91e89e3be860

Isnt it ELITE!!

Here is a link to the ELITE morning report ..... ILD

http://chiefmedicalresident.blogspot.com/2009/06/day-343-interstitial-lung-disease.html

Pneumocystis jirovecii pneumonia

PJP is the most common AIDS deifining opportunistic infection in HIV-infected individuals. The presentation in most people (>85%) includes fever, progressive cough and dyspnea. It is generally subacute developing over days to weeks. Other constitutional symptoms are common.

Radiology:

A large percent of initial CXR imaging is normal in people with PJP. As the disease progresses diffuse bilateral interstitial or alveolar infiltrates develop. Discrete infiltrates, cysts, nodules and pleural effusions have been described. If a patient suddenly deteriorates dont forget to think about the pnumothorax which is not an uncommon complication of this disease (see above). a HRCT maybe very helpful in times when the CXR is normal.

Diagnosis:

The diagnosis is confirmed based on demonstration of PJP in sputum (sens 50-90%) or BAL (sens >95%). Laboratory data is not particularly helpful for diagnosis but the 2 most common abnormalities are an elevated LDH and low CD4.

Treatment:

Anti-PCP treatment....first line is TMP-SMX - other considerations include tolerance, iv vs oral therapy. Duration 21 days.

Steroids: As people typically worsen 3-5 days into treatment with an inflammatory response, steroids become the standard of treatment in severe infection. This is defined as a PaO2 <70>35 on ABG. The original studies in this area came out of Toronto so check out this link.....

http://ovidsp.tx.ovid.com/spa/ovidweb.cgi?WebLinkFrameset=1&S=ELAFFPJJMDDDNMAANCFLNCJLJICKAA00&returnUrl=http%3a%2f%2fovidsp.tx.ovid.com%2fspa%2fovidweb.cgi%3fMain%2bSearch%2bPage%3d1%26S%3dELAFFPJJMDDDNMAANCFLNCJLJICKAA00&directlink=http%3a%2f%2fgraphics.tx.ovid.com%2fovftpdfs%2fFPDDNCJLNCAAMD00%2ffs047%2fovft%2flive%2fgv039%2f00005220%2f00005220-198808001-00007.pdf&filename=The+Possible+Role+of+Corticosteroid+Therapy+for+Pneumocystis+Pneumonia+in+the+Acquired+Immune+Deficiency+Syndrome+%28AIDS%29.

" The possible role of corticosteroid therapy for pneumocyctis pneumonia in the acquired immune deficiency syndrome" J Acquir Immune Defic Syndr. 1988;1(4):354-60

Milk 'does the body good'

Today we reviewed how to interpret a blood gas. There are many ways to do this but the approach generally follows a few simply steps....here is an example:

6 simple steps…

1. What is the pH?
2. Is the primary disturbance respiratory or metabolic?
3. Is there appropriate compensation?
4. If this is a metabolic acidosis is there an anion gap?

• what is the delta – delta?
• is there an osmolar gap?

5. what is the A-a gradient?

We also had a brief discussion of 'milk alkali syndrome' which is a syndrome characterized by the triad of hypercalcemia, alkalosis and renal insufficiency. This syndrome is most often precipitated by excessive ingestion of calcium carbonate preparations in predisposed individuals. In the acute presentation of this syndrome the patient develops symptoms within a week of the treatment. They have symptoms of hypercalcemia, including nausea, vomiting, weakness, and mental changes with psychosis or depressed sensorium. The also have severe metabolic alkalosis, a normal to elevated plasma phosphate concentration, and acute renal insufficiency. Withdrawal of milk and alkali leads to rapid relief of symptoms and the return of normal renal function.

Acute Yellow Atrophy

Fulminant Hepatic Failure is the acute rapid injury of the liver characterized by dysfunction with impaired synthetic dysfunction and encephalopathy in a person with a previously normal liver or well compensated liver disease. There are a number of etiologies and one easy to remember mnemonic is :

A - Acetaminophen, hepatitis A, autoimmune hepatitis
B - Hepatitis B
C - Cryptogenic, hepatitis C
D - Hepatitis D, drugs
E - Esoteric causes - Wilson's disease, Budd-Chiari syndrome
F - Fatty Infiltration - acute fatty liver of pregnancy, Reye's syndrome

Drugs - either Tylenol or idiosyncratic reactions to other medications - remain the number one cause of FHF (fulminant hepatic failure) in North America. Please see attached link for some additional information about some drugs which have been implicated.

http://emedicine.medscape.com/article/177354-overview

Do you have a sweet tooth??

Hi everyone,

I missed what was undoubtedly a fabulous discussion about insulin resistance on Monday. I have linked the new Diabetes Guidelines and an amazing article on DKA for you to this web page.

http://www.diabetes.ca/for-professionals/resources/2008-cpg/

Diagnosis and treatment of diabetic ketoacidosis and the hyperglycemic hyperosmolar state

CMAJ 2003;168(7):859-66

http://www.cmaj.ca/cgi/reprint/168/7/859