a case a metabolic acidosis

Hope everyone had a good good weekend

Friday, we started with a good example of Anion Gap Metabolic acidosis and reveiwed how to approach acid base problems.

1. pH: acidemia vs alkalosis
2. is it primary met or resp:

3. is there compensation? and is it appropriate? (for acute met acidosis compensation should be ~1:1)
For met acidosis:
4. is there an anion gap? (what is the albumin- if low then anion gap is bigger than appears)--> for every drop of albumin by 10, add 3 to your AG
5. What caused the anion gap? Really the 4 things to think about are:
- Lactic acidosis (hypoperfusion or liver disease)
-Ketone (diabetes, alcohol or starvation)
-Uremia
-Poison/Toxin- ethanol, methanol, ethylene glycol, ASA, isopropyl alcohol

(Think about how many AG points each of the above would raise your gap!!-- Ketone 1:1, Creatitinine 100:1, Lactate 1:2)

6. is there an osmole gap? 

7.Check the delta delta to see if another disorder is also going on.
Basically you just compare the delta AG (e.g. 6 if your AG is 18) to the delta bicarb (e.g. 8 if the bicarb is 17). If they are equal then this is a pure met acidosis.
If delta AG is bigger than delta bicarb: also met ALKALOSIS
if delta AG is smaller than delta bicarb: there is also a non AG met acidosis 

I will review DKA in another post soon.

:O)

MDS and PE

Thank you Dr. Ann George for yesterday's talk on anemia secondary to MDS.
Here is a good reference for MDS.

Today we went through a case of recurrent PE.

Here is a link to our last talk on PE where we reviewed wells criteria. 


This NEJM study compared Heparin and ALEPLASE (a TPA) vs heparin alone and showed that in SUBMASSIVE PE (and RV dysfunction) but NO hypotention (since that would be the definition of Massive PE) that there was less escalation in therapy with TPA... no change in death.... IE this is still an area of uncertainty.

Indications for thrombolysis is hypotension (sBP<90 mmHg)

Review of acute PE is HERE

c dif diarrhea

Welcome block 4!

Today we talked about a case of acute non bloody diarrhea, that turned out to be recurrent cdif. 

Here is a review of acute contagious diarrhea

We focused on the treatment of c dif which is as follows:

First Episode

***If possible stop offending antibiotics***

IF: Mild/Moderate Disease --> Metronidazole OR Vancomycin (PO) duration 10-14d

IF: Severe Disease ( Defined as:   Two of (Age above 60, Febrile, WBC above 15, Albumin below 25)   OR hypotension/shock or Cr greater than 1.5x normal, or toxic megacolon, peritoneal signs, perforated bowel)

consider- Infectious Disease +/- General Surgery Consultation

 Vancomycin (PO) unless severe illeus/toxic megacolon, then vanco PR and Metronidazole (IV) duration 10-14d (Vanco has more rapid symptom resolution and a lower risk of treatment failure).

Relapse

•   First relapse --> can repeat last treatment depending on severity

•   Second relapse --> vancomycin taper. ID consult.

New drug:  Fidaxomicin .. expensive, but targeted bactericidal drug.

Here is a review on C DIF from NEJM. and HERE is an article form annals thats good too. 

Here is the small study that gives hope to probiotics. 

SBP

Today we talked about a young patient who came in with abdominal pain and encephalopathy in the setting of cirrhosis and ascites.

See the previous post on the approach to this patient's Ascites from block 2



Today we discussed the importance of considering SBP on the differential when:
- any cirrhotic pt is admitted to the hospital (regardless of reason)
- pt wiht ascites has a GI bleed
-pt with ascites  has abdo pain, nausea/vomiting/diarrhea, leukocytosis, encephlopathy

thus do a diagnostic tap
look for: Ascites PMN > 250 or WBC > 500 

BUT--If WBC > 1000 or polymicrobial culture or protein > 10g/L, suspect secondary peritonitis, perforation, abscess etc

Treatment of SBP includes antibiotics (3rd gen cephlosporin or cipro) and albumin if renal failure is a concern (see this NEJM article on use of albumin in SBP)

some more respirology

Firstly, thanks again to Dr. Stephanie Leung who taught about chronic cough yesterday. 
Here is a link to a review on cough. (who knew there was a journal called "cough"?)


Today we went through a case that presented with dysphagia. Here is a good decision tree to direct your history.

He ended up having a large pleural effusion. This led us to a discussion on the classification of pleural effusion (transudative and excitative) as per Light's criteria (this wil take you to the reveiw article by Lights himself).

Reminder lights criteria predicts exudative effusion if ONE of:

• pleural protein / serum protien >0.5
• pleural LDH/ serum LDH >0.6
• pleural LDH > 2/3 upper limit of normal serum LDH

SPAG (serum-pleural albumin gradient) >12 points towards a transudative effusion in cases that clinically seem transudative but based on chemistry of the pleural tap have a exudative picture. (such as after diuresis)

This is the LINK to our procedure website that has a video and tips about thoracentesis.

special guest week

Thank you special guests Dr. Julie Brophy and Dr. Amanda Brahm for doing morning today and yesterday on Monoarthritis and anemia.

A good review on mono-arthritis on found HERE. Remember, gout and infection CAN coexist so be sure to rule out infection before using steroids to treat gout. Also, gram stains and cultures are not perfectly sensitive, so beware the worsening gout after being treated with steroids.

A contemporary approach to anemia can be found HERE, a concise but good approaches are outlined in this article 


Looking forward to Dr. Leung's morning report tomorrow.


See you thursday!

CAP

Yesterday we reviewed the differential for shortness of breath and spoke about CAP.

The diagnosis of pneumonia is a clinical one with the history being the most important factor. 
A chest xray will help confirm the clinical suspicion.

The clinical Prediction rule CURB65 is a simple scale to help decide if a patient needs to be admitted.

• C: confusion
• U: urea >7 mmol/l
• R: resp rate> 30
• B: BP: systolic <90 ; diastolic <60
• 65: age over 65

Each gives you 1 point. and the sum correlated to a 30 day mortatily rate: 0.6% if socare of 0, 1.7% with a score of 1, 

Scores of 4 have a 15% 30 day mortality rate (this is High).

The general suggestion is score of 3 or more needs to be admitted, and 4 or more needs the ICU

This however, illustrated by our case, is just a tool, but NON a substitution for clinical judgment.

A newer study showed that  a presenting O2 saturday of <92% in itself is a strong predictor of need for hospitalition . 

The patient we discussed had presented with diarreah, AKI, elevated liver enzymes, and a slightly lowered sodium, which made the team suspicious of Legionnaires disease. Although these may be clues to consider this diagnosis, no clinical data can accurately predict this pathogen.
Here is a review article on legionnaires disease

Have a great weekend.
(Happy new year for those celebrating)

lots of talking about salt

Yesterday we talked about approach to diagnosis of Hyponatremia

See the previous post on this : HERE

Also: take a lot at a review on hyponatremia.

Its important to note that volume depletion should results in HYPERnatremia. Hypovolemic hyponatremia is a result of replacing your loss with hypo-osmolar fluid (ie water or juice)

A special thanks to Dr. Amna Ahmed for reviewing the treatment of hyponatremia this morning as well as discussing HYPERnatremia.

HERE is a review on hypernatremia.

Acetaminophen TOX

Today we talked about a case from the weekend who was admitted with overdose of tylenol and effexor.

At time of presentations, there were not acute symptoms of an OD, but after being admitted the patients liver enzymes dramatically increased to >6000 and INR rose to 3.8.

When liver enzymes are over 1000, always consider tylenol as one of the causes (the others include shock liver, autoimmune, viral hepatitis, and wilsons- although wilsons typically a chronic problem)

Acetaminophen pathway requires glutathione for  the toxic metabolite (napq) to be metabolized. When glutathione runs out you are left with liver toxicity. NAC repeats it.

See this article for a good summary of acetaminophen pathway and treatment.

At presentation: high risk features include: pH <7.3. As well, elevated INR, encephaolopaty, Cr>300, high bili and  hypoglycaemia are predictors of fulminent liver failure.

another cause of hypercalcemia

Welcome new clerks!!

I hope you will have a chance to look at the attachments here to complement your exposure at the hospial.


We started off this week with a case of serious hypercalcemia (3.78!!, normal albumin)  that was managed with fluids, pamidronate, calcitriol .. and was still high in the morning.
See the previous post on hypercalcemia HERE.

Along with the : CALCIUM,
there was RENAL FAILURE, ANEMIA, BONY PAIN.
thus very suggestive of Multiple myeloma. 

Multiple Myeloma is a hematologic malignancy that arises from a single clone of plasma cells producing a monoclonal immunoglobulin (usually IgG or IgA). 

A lot of the clinical features arise from the proliferation of these cells, and the immunoglobulins which are released.

Renal disease: there are MANY causes such as: 1) light chain or cast nephropathy,  2)amyloidosis, 3)light chain deposition disease, 4)Fanconi’s syndrome (proximal tubular dysfunction), and 5)hypercalcemia with acute renal failure. Less commonly, one might see 6)heavy chain deposition disease, 7)cryoglobulinemia, 8)uric acid nephropathy and 9)renal plasma cell invasion.

Anemia:  due to plasma cells proliferating, displacing the normal bone marrow. 

Bone Pain: secondary to lytic lesions or pathologic fractures. (increased osteoclast and decreased osteoblast activity because of cytokine RANKL)

Recurrent Infection: secondary to hypogammaglobulinemia and impaired plasma cell function. (most commonly: Pneumonia and pyelonephritis)

For more information, here is a Review on MM.