Signing off

As it was my last official morning report on Friday, 

I thought i would jsut bring up the topic of safe sign over, as I sign off to Amin.

An effective handover is crucial for safe patient care. 

The mneumonic "SIGNOUT?" can be used to remind us what should be included. See this article for more details.  

S - Is the patient sick? Stable? Code Status? 
I- ID 
G - General Hospital Course 
N - New events of the day 
O - Overall clinical condition 
U - Upcoming possibilities (those that can reasonably anticipated) with plan/rationale 
T - Tasks to complete overnight (explicit instructions) and rationale 
? - Any questions

Thanks for reading, 
I hope this was helpful.

-Alyse

Alyse, Amin & Leslie

joints, kidneys and minimal tsh

Yesterday we discussed approach to a patient with a single angry joint. 

Although the history and physical exam is crucial, there are no physical exam findings that reliably rule in or out septic arthritis according JAMA Rational Clinical Exam paper linked HERE.

For the Joint aspirate:

WBC over 100,000- Positive LR 28

WBC over 25,000- Positive LR 2.9

WBC less than 25,000- Negative LR 0.32

PMN over 90%- Positive LR 3.4; Negative LR 0.34

This isn't perfect either. 

◦    The absolute leukocyte count can be used to differentiate inflammatory from non-inflammatory fluid; however, it cannot be used to differentiate between inflammatory conditions, such as septic arthritis and crystal arthropathy!

◦    Traditional teaching suggests that cell counts greater than 50,000 WBC/mm3 are indicative of septic arthritis. THIS IS NOT TRUE! Crystal arthropathies and rheumatic disorders may present with cell counts this high.

AND septic arthritis may have cell counts < 50,000 WBC/mm³

Polymorphonuclear cell (> 90%) suggests the presence of an inflammatory condition, regardless of the total cell count!!

Also, the culture and sensitivty aren't perfect either.

Gram stain: sensitivity is  75%; Culture up to 90%

--> A special thanks to Dr. Ali Kara for discussing a case of AKI this morning. Click here for a NEJM CPC that goes over the approach to ARF

-->Although we didn't talk about it today, a patient was admitted last night with thyroid storm.
Here is a previous post on Thyrotoxicosis, with a good article on thyroid emergencies. 

DKA

Today we reviewed a case of ?syncope which turned out to also involve DKA.


We reviewed: What are the problems going on in DKA: (and how to manage)

1.     dehydrationà3-6L deficit: Must restore extravascular and intravascular fluid, increase renal perfusions and clearance of glucose

2.     electrolytes (K!!!!) Total body depletion! (initially may be shifted because of hypo-insulin)

3.     hyperglycemia: insulin  to get rid of ketones and stop lypolisis

4.     acidosis

Treat:

1.     Iv NS à a lot!!!!

2.     Replace K when <5.3 and run in fluid, Hold insulin if until K>3.0;

3.     Insulin drip at 0.1 U/kg; add sugar to your saline if AC<15

4.     Acidosis: don’t give bicarb if >6.9; not helpful (? Increase in intracellular CNS acid)

*** keep a close eye on sugar (q1h), lytes and gas (q2-4h) ****

What can KILL in DKA:

1.     Low K

2.     Too MUCH insulinàhypoglycemia

3.     UNDERLYING cause

(Ischemia, iatrogenic, intoxication, insulin non compliance, initial presentation, intra-abdominal process)

When to consider transitioning to subcut insulin:

·      -->follow AG since takes longer to stop ketogenesis and clear ketone than correct glucose

·      -(Bicarb will trail behind because non-AG acidosis from the NS)

-->patient is EATING

  Here is a review on DKA. 

anaphylaxis take 3

Today we discussed a case of a women who had an anaphylactic reaction post gold infusion.

Typically we think of the following drugs in association with anaphylaxis (although a lot of drugs can cause rare reactions)

- Antibiotics (75% of all fatal anaphylactic reactions are due to penicillin)

• Non-steroidal anti-inflammatory agents (including aspirin)

• Anesthetics

• Latex

• Iodine (contrast)

Our previous talks on anaphylaxis can be viewed HERE and HERE, review articles and doses can be found on those pages. 

On D/C a good plan would consider the following:

• Ensure that the patient understands she has a serious allergy, and Document it in the medical chart

• EpiPen Rx and instructions for use 
• MedicAlert bracelet 
• Written action plan if anaphylaxis recurs outside the hospital setting6 
• Notification of any outside providers 
• Consideration of referral to an allergist 

CPR or not to CPR

Today we discussed some issues of attaining code status.

Thanks to Allen Greenwald to providing us with video footage that the current R2's did for their holiday rounds.

As we mentioned today, this is a tough discussion, and there are many patient and family factors that complicate this.

Key things to express to the family: 

• DNR does NOT mean do not treat
• Goals of care can be readdressed at ANY time
• decisions should be made as per what the PATIENT's wishes are 

In general this is a hard and complicated discussion to have with families who may never had any exposure to this concept. Giving a 'menu' of options is confusion and typically not helpful.

Encourage discussion between family and patients and try to advise what medically makes sense. 

Some interesting articles:

This is an interesting NEJM article on the influence of television code on people's perceptions.

This article shows how our discussions influence the decisions of our patients.

dem hungry bones

This week we started off by discussing a case of hypocalcemia, post parathyroidectomy.

We reviewed the symptoms to monitor for (ie symptoms of hypocalcemia) post parathyroidectomy:   

• Symptoms:   numbness, tetany, cramps,  
• Signs: Seizures tetany, parasthesias, Chvostek’s sign- facial (think: CH-->Cheek), Trousseau’s sign, (CHECK OUT VIDEO HERE) arrhythmia, prolonged QT

1Its a good time to think about what PTH does to:  Bone, gut, kidneys; and thus the LACK of PTH has important implications. 

a.     Bone: Resorptionàwith lack of stimulation of osteoclasts with lack of mobilization of calcium from bone, there is persisitant osteoblast activity,  and increased urine calcium loss, and resultant hypocalcemia.  (leading to bone FORMATION)

b.     Kidney: 1α-hydroxylase is downregulated, with a resultant decreased production of 1,25-dihydroxy vitamin D.

c.      GUT: This decreased production  of vit D- impairs the absorption of calcium and phosphorus in the gut.

Hungry bone syndrome is the extreme case and is seen when:

-->hypocalcaemia with varying degrees of hypophosphatemia after parathyroid surgery 

-->occurs as a result of retention of calcium by bones  that were previously demineralized from the effects of PTH excess (similar to refeeding syndrome)

-->hypomagnesaemia (a sequelae) can exacerbate hypocalcaemia by inhibiting parathyroid hormone release 

Treatment:

Calcium Gluconate, IV and PO, then continue PO

Vit D

Mg replacement

Prevention can be acheived with vit d and calcium loading prior to surgery

For more info check out THIS article. 

A night of only GI consults...

Not quite sure how I made it through 3 months without reviewing a GI bleed....

Last at least 4 patients were admitted with GI bleed.

We reviewed a gentleman,  unknown to powerchart, with hematemesis a significant etoh history and signs of portal hypertension on physical exam.

After stabilizing the patients with fluids +/- blood

Some of the specific managements:

1. IV PPi- Pantoprazole infusion: 80 mg IV bolus then 8 mg/hr

àWhat does it do? Suppresses gastric acid secretion by inhibiting the parietal cell H⁺/K⁺ ATP pump to↑ pH may improve platelet function

EVIDENCE: - decreases endoscopic stigmata, à NOT decrease mortality, or rebleeding or need for surgery

à most effective for PUD

--> more evidence post bleed (72 hours) (with a NNT of 7!! according to THIS article)

2. Octreotide: 50mcg then 50 mcg/h

--> WHat does it do? somatostatin analogue that reduces splanchnic blood flow and portal pressure.

 EVIDENCE:  modest reduction in the amount of transfused blood, a possible decrease in the rate of rebleeding, with no overall decrease in mortality

-->only evidence for Variceal bleed

3. Correct INR

4. Antibiotic therapy – Ceftriaxone or ciprofloxacin x 7 days

--> What does it do? proph for infection (SBP and bacteremia)

--> Start if patients have cirrhosis

EVIDENCE: Reduced rate of infection (SBP and bacteremia) and mortality

Here is a new JAMA article: Does this patient have an UGIB?