Day #9 - I see two people....

Great case today about headache and diplopia. My feeling about the case was that this represented a lacunar stroke that just wasn't seen on the MRI. Treatment would involve modification of the vascular risk factors.

The discussant very methodically went over an approach to diplopia. I think his anatomical approach was excellent:

• Neurological -- i.e. ischemia/vasculitis, demyelination, tumour (including leptomenegeal), infection (TB, syphilis, listeria, lyme), toxic/metabolic (alcohol/wernike's)
  
• NMJ - mysesthenia and other myesthenic syndromes
  
• Muscular/Structural - Graves, masses in the muscles, muscular impingement
  
• Opthomologic -- monocular diplopia -- think corneal or lens problem
  

In this case I think it was important to think about temporal arteritis because of the diplopia and headache. Temporal arteritis will lead to blindness if not diagnosed and treated. Clues on history and physical include:

• Diplopia
• Jaw/Tongue claudication
• Temporal artery beading and tenderness

Excluding subarachnoid hemorrhage is important given the right clinical context (i.e. in the context of the characteristic thunderclap headache). A normal CT scan and negative lumbar puncture are sufficient to exclude with high sensitivity and low negative likelihood ratio provided there are no gross neurological deficits.

Also, remember syphilis is the 'great mimicker' and in "young" patients with stroke/stroke-like syndromes one should think about excluding this diagnosis.

ACC cardiology guidelines

As mentioned at noon rounds today, the ACC has some excellent guidelines available for you to learn from. I have used them extensively during my residency.

The pocket guidelines are the most succinct and easy to read.

I also really like the BMJ series called the ABCs of clinical electrocardiography which really helped me improve my skill at reading ECGs.

Day #7 - Sickle Cell Anemia

Today's case was on sickle cell anemia presenting with vaso-occlusive bony crisis. The take home big picture points include:

• IV hydration and correction of hypoxemia
• Exclude or treat infection
• Appropriate analgesia (morphine, hydromorphone) using narcotic sparing treatments such as ketorolac (5 days maximum ketorolac, use with H2/PPI)
• Avoid transfusions unless symptomatic or <50-60.>
• Chest crisis, stroke, splenic crisis should be considered for exchange transfusion
  
• All patients should be on folic acid
• Consider hydroxyurea in those with >=3 episodes/year. See this article.
  

Up to Date has an excellent review of sickle cell anemia that is very comprehensive. We will also have a noon rounds session on sickle cell anemia on August 26th.

Management of DKA

Thank you to those who participated in our small group discussion on management of DKA. This was a first attempt at running such a session, so hopefully the next one will be even more effective.

The takeaway points (as I see them are):
* Stabilize the patient first while doing everything else

• large bore IVs with NS for hypovolemia
• foley as required
• think about arterial line in the sicker patients
  

* History/Px/Labs to look for volume status and precipitant
* Insulin:

• When you know the K+ isn't very low start the insulin
• 0.1u/kg bolus then rate 0.1u/hr titrated to IV sliding scale
  
• If glucose not falling can increase the dose, but be sure they are volume replete
• Add dextrose (D5W or 2/3-1/3) when glucose <~13
• Continue until patient has normal glucose and no anion gap and is ready to eat

* Potassium

• Add K+ to the IV as soon as they are urinating and K+ <5
• Oral repletion for hypokalemia in addition to IV.
  
• Hold insulin when K+ <3.3

* Sodium/Water Balance

• Use IV NS until you have reversed the signs of shock
• Then change to a hypotonic fluid like 1/2NS or 2/3-1/3 or D5W

* Treat the precipitant

As promised, here is my favorite article on the management of DKA/HONK.

This is my favorite figure from the article if you don't want to read it all:

Day #4 - Acute Monoarthritis

Today the discussant spoke about the approach to acute monoarthritis. It was a very articulate presentation and your participation was excellent.

To clarify the point on treatment:

• CEFTRIAXONE 2g IV q24h will cover most organisms including GC, most streptococci, Staph. aureus and many gram negatives. It is not the ideal agent for Staph. aureus, so if it turns out to be methicillin *sensitive* staph. aureus you should change to ANCEF (1g IV q8) or CLOXAILLIN (2g IV q6)
• Is MRSA a possibility or is this a prosthetic joint? --> ADD VANCOMYCIN (renal dose)
• Is there reason to worry about pseudomonas? --> I would suggest VANCO+CEFTAZADIME and ID consult.

• Prosthetic Joint = Call ortho. Probably should not be admitted to medicine if septic prosthetic joint is the main reason they are in hospital -- they need to go to the OR for wash-out and, in my experience, this is much less likely if they are admitted to GIM instead of orthopedics. Should get ID consult as well.

This article from JAMA is an excellent reference on making an evidence based diagnosis of septic arthritis on history, physical and laboratory examination.
VIDEO: How to do an arthrocentesis of the knee

Highlights include:

Risk Factors: Age, DM, rheumatoid arthritis, joint surgery, hip/knee prosthesis, HIV infection, skin infection, (unprotected sexual intercourse for GC)

History: Pain and swelling are present >80% of the time; fever is present only 60% rigors and chills less than that.

Synovial Fluid Exam (LR less than 0.1 rules out; LR >10 rules it in)

• WBC <=25,000 unlikely septic arthritis (LR 0.32) unless immunosuppressed
• WBC >=25,000 LR 2.9
• WBC >=50,000 LR 7.7
• WBC >100,000 LR 28

• PMNs <90%>
• PMNs >90% LR 3.4

Important to note that measurement of glucose, protein, lactate do not appear to be helpful according to the literature. Also note that LDH in the joint may have some utility in ruling out as LDH less than 250 has a good NPV; but the number included in the studies are small

Day#3 - Congestive Heart Failure

Today in morning report the team presented a case of presumed decompensated congestive heart failure. The discussant reviewed a good approach to the diagnosis and etiology of CHF. He also talked about constrictive pericarditis and quoted an article "Undercover and Overlooked"

**You can access NEJM online for free @ the UHN. At home you can access it for free if you have a U of T library card using this link.

Regarding CHF management:

In the acute setting treatment can be loosely summarized by the nmemonic LMNOP:

L = lasix --> usually IV, dose dependent on whether they are
M = morphine --> small IV doses help with the sensation of dyspnea and can also venodilate reducing preload
N = nitrates --> as the discussant pointed out, often patients are hypertensive related to sympathetic drive. Adding nitrates will reduce preload and afterload through veno/arteriodilation
O = oxygen --> this can include Non-Invasive Positive Pressure Ventillation (NIPPV) which can be helpful in acute CHF as the positive pressure can help reduce preload as well as help overcome resistance in the lung caused by fluids
P = position --> sit the patient upright, swing their legs over the side of the bed. This will decrease preload.

The ACC has a fantastic series of pocket guidelines for many cardiac conditions. I have always liked their ACC Chronic Congestive Heart Failure Guidelines.