Day #131 - Upper GI Bleed secondary to Gastric Mass

Today we talked about upper GI bleeding in a young patient. We highlighted the epidemiology of upper GI bleeds and discussed the history/physical examination pertinent to Upper GI bleeding.

There is a great article here (and an article on the value of omeprazole/PPI in acute peptic ulcer bleeding here)

I have previously blogged on upper GI bleeding here.

Remember, the most common causes of significant upper GI bleeding at our hospital are peptic ulcer disease and esophageal varices. These will account for greater than 90%. The keys on the history are to look for signs/symptoms/risk factors for portal hypertension so that you can

Remember, there is not a reliable way to predict risk from a GI bleed without endoscopy for most patients. Patients with a low risk would have all of the following:

• Age less than 60
• HR less than 100 pre-volume
• BP greater than 100 pre-volume
• No postural changes (BP drop 20mm, HR increase 20, symptoms)
  
• No CHF, heart disease or other major illness
• No renal failure, cirrhosis or metastatic cancer
• Hemoglobin greater than 100
• No coagulopathy
• Reliable follow up

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This is an interesting article on the pathology of GIST. Another review is located here.

Day #126 - Hepatitis B

Today we discussed a patient with acute hepatitis on the backgroud of hepatitis B chronic infection. I have previously discussed acute hepatitis, cirrhosis and complications thereof.

I wanted to talk about hepatitis B -- Firstly, this is a great review article and so is this.

Secondly - Serologies:

• Early in infection you have the production of Hepatitis B Surface Antigen and Hepatitis B Envelope Antigen which represents active infection
• The you develop hepatitis B core IgM then core IgG. These antibodies are not protective
• If you are going to clear your infection you will next develop anti-hepatitis B-EAg antibodies, clear your E antigen and then start to clear your S-Antigen
• You then make hepatitis B surface antibodies
• There can be a window period in between clearing the S-Ag and developing the anti-HepB surface antibody where the only way you will know if they are infected is by the core antibody.

An immunized person will only have hepatitis B surface antibody

A natural, but cleared infection will have positive HepB surface antibody and core antibody and no surface antigen

A patient with chronic active hepatitis will have core antibody and in most cases hepatitis B surface antigen. They may also have E antigen (or E antibody). They will not have surface antibody.

For chronic carriers treatment depends on a number of factors -- this table provides an excellent summary:

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Note that I link to a lot of NEJM articles. This is my preferred journal. Those of you with a U of T library account have NEJM access via e-journal search in the gerstein library website. We pay for an institutional license @ U of T which you can access at home and there is a licence here at the hospital.

Those of you who would like their own subscription (b/c above don't work) can obtain one here ($~60/year for electronic only ~ $150 for print copy too)

Day #125 - Polycythemia and Hypoxemia

Today we discussed a case of a patient with polycythemia and acute hypoxemia. The most likely diagnosis was pulmonary embolism and the discussant detailed an excellent approach to the diagnosis of PE.

I have previously blogged about DVT and PE here. The article the discussant mentioned is available here

I wanted to focus on the approach to polycythemia in more detail (review article here):

Definition: Hemoglobin greater than 165 in women (hematocrit 48%) or 185 in men (hematocrit 52%).

Relative polycythemia, related to volume contraction, needs to be differentiated from absolute polycythemia in which there is an increased red cell mass.

Primary

• Polycythemia vera
• High oxygen affinity hemoglobins
• Epo receptor activating mutations
• Other

Secondary

• Chronic hypoxemia from:
  
  • Cyanotic heart disease
  • Right to left shunts (i.e. AVMs in HHT, other)
    
  • Chronic hypoxemic lung disease
  • Obstructive sleep apnea
  • Pickwickian syndrome (obesity hypoventillation)
  • Living at altitude
  • Chronic carbon monoxide poisoning! (Including smoker's polycythemia)
    
• EPO overproduction (think highly vascular tumors):
  
  • Renal cell carcinoma
  • HCC
  • Uterine cancer
  • Hemangioblastoma
    

Uptodate has a good algorithm for the diagnosis of polycythemia (adaped below):


Treatment of PRV:

• ASA to prevent ischemic events
• Phlebotomy to hematocrit less than 45% in men and 42% in women
• Failing phlebotomy add hydroxyurea
• Add allopurinol in patients with symptomatic hyperuricemia or very high uric acid excretion (greater than 1100mg/day)
  

Day #124 - Pretibial Septic Bursitis

Today's case was of a painter, who did a lot of work on his hands and knees, presenting with acute onset knee pain. We discussed the differential diagnosis in detail and then focused on septic arthritis. I have previously blogged about this here and had linked to an excellent article that I recommend you reading.

In this case, the diagnosis was pretibial septic bursitis, which can mimic septic arthritis and is commonly seen in people who do labor on their hands and knees and is associated with minor traumas. The most common infectious aetiology is stapylococcus aureus.

Day #120 - Pleural Effusion and Anemia

Today we discussed a case of progressive dyspnea on exertion related to severe iron deficiency anemia and an exudative pleural effusion.

Please see my previous blogs on the evaluation of a pleural effusion here and here.

Day #119 - Adult Onset Still's Disease

This was a great case which the discussant enjoyed taking us through. I have previously blogged about fever of unknown origin here, here and here.

There was a previous special guest blog about FUO here.

Here are articles suggested by the discussant on rheumatologic causes of FUO, Adult Onset Still's Disease, and the use of IL-1 antagonists in the treatment of Still's.

Here is another review on Stills.

Day #118 - Probable Leptospirosis

Today we heard a case of a returning traveller who suffered complete cardiorespiratory collapse as part of a sepsis syndrome. In this syndrome the patient was hypotensive requiring inopressors, hypoxemic/hypercapnic requiring ventillation, coagulopathic with a microangiopathic hemolytic anemia (see TTP blog and previous anemia/thrombocytopenia blogs) from DIC, and in acute renal failure. In the context of this illness he suffered either myocarditis or a myocardial infarction related to hypoperfusion.

This was as sick as anyone can be and survive and it is a testiment to our critical care system that he did indeed survive.

We spent time discussing the approach to diarrhea, which was his initial presenting symptom.

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We then defined sepsis

SIRS Criteria:

• Fever or hypothermia
  
• WBC >12,000 or less than 4,000
• HR >90
• RR >20

Sepsis = 2 or more SIRS criteria of presumed infective etiology
Severe sepsis includes sepsis with end organ dysfunction or lactate >4
Septic shock includes severe sepsis with refractory hypotension requiring inopressors

We then talked about the approach to early goal directed therapy in sepsis.

In this case, I believe early appropriate antibiotic therapy would include:

• Vancomycin (in case of community associated MRSA in a young man)
• Meropenem (to cover streptococcus, gram negatives including ESBL/drug resistant)
• Doxycycline to cover leptospirosis

In general, in a critically ill patient like this, I will draw cultures and then use very broad spectrum coverage empirically with a plan to de-escallate when culture results are available

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The etiology in this case is unclear but I wonder about leptospirosis. I didn't really want to talk about leptospirosis in detail during the case presentation.... This is the case of leptospirosis in NEJM that I elluded to.

I have provided you with a copy of a talk I once gave on leptospirosis here.

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Free tidbits:

Here is an article on fever in the returning traveller
A good review of typhoid fever is here.