meningitis

Today we talked about a case of bacterial meningitis.

Some key points addressed:

- Empiric antibiotics can be started as soon as the diagnosis is suspected since it takes a few hours for them to penetrate the CSF and obscure the LP finding
- AB include: Ceftriaxone, Vancomycin, and Ampicillin and HIGHER doses
- CT head should be done before LP if patient is >60, recent new seizure (1 week), focal neuro findings  like papilledema, abnormal level of consciousness, history of CNS mass/stroke

Here is a good review on bacterial meningitis.

http://www.proceduresconsult.com/lhsc/ is our online access to procedure videos. NEJM also has free videos.

Happy reading.

thyrotoxicosis

Today we talked about thyrotoxicosis in morning report.. and then again in lunch rounds... (this keeps happening to me)

If patient presents with a combination of 1. fever 2. cns manifestations 3. cardiac instability and 4. gi side effects, 
dont forget to consider the thyroid as a cause, (if you don't think of thyroid storm then you can't diagnose or treat it)

The treatment consists of:
- decrease thyroid hormone production and release
- decrease bodies response to hormone
- supportive therapy
- treat the cause

Here is a review on thyroid emergencies.

PE

Welcome to Block 3!

today we reviewed diagnosis and treatment of PE.

The wells criteria for PE include:

• Clinical findings suggestive of DVT: 3
• No other more likely alternative diagnosis: 3
• Immobilization (bedridden ³ 3 days) or major surgery within past 4 wks: 1.5
• HR > 100: 1.5
• Previous DVT/PE: 1.5
• Active malignancy: 1
• Hemoptysis: 1

Treatment:

Evidence-based, graded summary of recommendations regarding acute and chronic antithrombotic treatment of DVT and PE.  Can be found HERE.  The most helpful sections are 4.1, 4.6, and 5.0-5.1.

anaphylaxis

Today's Morning report was on Anaphylaxis.

We covered the vague presenting symptoms such as abdominal pain and sweating, in addition to the expected signs of urticaria, macular papular rash, andgioedema and bronchospasm.

Important immediate management consists of:

Airway (?intubate)

EPI - Be careful! the doses are tricky! 0.5mg EPI-->careful the suspension.

IV access and fluids (there is impending cardiovascular compromise)

O2

Use your resources and dont waste time with steroids and anti histamines acutely

An article about lessons from failed treatment can be found here. 

A review article about anaphylaxis can be found here. 

Happy last day of block 2.

aki

I would like to thank our special guest Dr. Seychelle Yohanna for doing morning report Tuesday morning while I was post call.

She addressed key considerations of AKI.

Here is a NEJM article goes through the approach.

Also here is an article suggested by Dr. Kane regarding CT scans and autoimmune disease.

Happy reading.

See you tomorrow.

sepsis and feb neut

Hi.

Today we chatted about the spectrum that is SIRS, SEPSIS, SEVER SEPSIS and SEPTIC SHOCK,  including the principles of GOAL DIRECTED THERAPY, and source control. 

Here is the seminal Rivers Trial. 

We also discussed Febrile neutropenia (fever>38.3 once, or persistent >38.0) and neutrophil <0.5

The key points beings examine the patient "gum to bum" as mucositis is the most likely cause of infection. Thorough investigation should be sent including cultures.

Yet in 30-40% of 'feb neuts' no infection is discovered.

They should be treated with broad spectrum AB as per hospital protocol.

LHSC protocol is Pip tazo.

There are some stable patients that can be sent home. Here is an article outlining criteria for Low risk feb neuts that can be managed as an outpatient. 

Happy hump day.

poor pizza delivery man

Happy friday.

Today we went through a sad but packed case of a hip fracture with MULTIPLE medical problems.

We discussed the approach to syncope and reviewed the JAMA and JCIM finding in severe aortic stensosis.

We also reviewed the differential to Macrocytic anemia:
which includes reticulocytes, hypothyroid, etoh, liver disease, folate, b12 and MDS

And which Cancers met to bone:
thyroid, breast, kidneys, lung, prostate and testicular.
(mm causes lytic lesions)

Lastly we touched upon the POISE trial about the questionable role for beta blocker in the preoperative setting. ALthough it may help prevent cardiac death, there wasn't a clear role for prevention of overall death... so likely not a clear cut answer if someone has a risk of getting infected.

Have a lovely weekend.

HypoNA

Yesterday we went through Hyponatremia, a WATER problem.

Here is the approach we went through:
1. Is the hypoNA real? (i.e. is there glucose or manitol on board, or is there high lipid or paraprotiens)
2. Is it acute and symptomatic- if so this should be treated immediate with 50cc/h of high concentration. Often this needs ICU 
3. What is the volume status? (hypo/hyper or euvolemic)

The urine lyte are the kidneys ways of telling you if its hypo or hypervolemic vs euvolemic and the physical exam tells you hypo or hyper. 

When treating with volume (for hypovolemia) or fluid restriction, the lytes should be checked every 4-6 hours to be sure there is no overcorrection (over 8 in 24 hour... we say over 12 to be safe). 

We discussed the dangers of the acute treatment of a chronic problem, and how to avoid complications like CPM with use of d5w or DDAVP if you exceed 0.5 meq/hr.
  (DDAVP is often given as 1-2mcg SC/IV) 

Here is the article discussing using DDAVP to prevent rapid correction.

end of life communication

Today we did something a little different for MR and discussed some challenges of determining code status.

Some key tips from todays talk:
-Try to get an idea of goals of care at admission
-Determine if the patient is capable of making own decisions and guide family discussions towards what the patient would like (possible what this patient at their time of health would feel about their current status)
-Be clear that DNR does NOT equal do not treat, but instead means will not try aggressive means of resuscitation when the patients medical state is so far gone that there is little chance of returning to baseline

This is always a tricky conversation and requires practice and honesty.

Here is a A nice NEJM article to read.

hyperCA

Yesterday we discussed a case of hypercalcemia, likely secondary to malignancy.

We reviewed an approach to determining the aetiology of hypercalcemia, with first break point being PTH level.

If PTH appropriately low:
-Malignancy (PTHrP which is hard to order at LHSC without permission)- associated with squamous cell CA
-Mets to bone
-Myelomoa
-hyperVitamin D from lymphoma, or granulmaotous disease
-Medications (HCTZ, tums-->milk alkali )
-Endocrine causes (hyperthyroid, AI, pheo, acromegaly)- often NOT the way these conditions present
-Rhabdo

If PTH normal or HIGH:
-Primary/secondary/tertitatry hyper PTH (likely in outpatients)
-lithium
-familial hypercalcemic hypocalciuria

Malignancy can cause hypercalemia in 4 ways:
1. PTHP
2. Mets to bone
3. Vit D production
4. Rarely PTH production

 Malignancy associated hypercalcemia is summarized in THIS NEJM article.

The TREATMENT of elevated calcium:
FLUID!!! and lots of it
Lasix ONLY if volume overloaded
Consider bisphospinate if cancer but take time to work
Calcitonin is fast but there is tachiphalaxis.
Hyper V causes- consider steroids

HERE is a review looking at the use of lasix for treatment of hyperCA

IE

Hope everyone had a good weekend

Today we started off the week talking about a blue team patient who was admitted last week with a high suspicion of endocarditis. We discussed how although our patients are often IVDU, most commonly IE occurs in older patients who are not drug users.

We reviewed the DUKE's CRITERIA: since to make a diagnosis you need 2 major criteria, or 1 major and 2 minor, or 5 minor. 


Major Criteria:

1. Positive blood cultures for endocarditis.

• high risk microorganisms on 2 blood cultures (separated by time) (Strep, Staph, Enterococcus, HACEK etc). THese should be persistent (i.e. over a 12 hour period) and positive for typical IE organisms

• Single positive blood culture for Coxiella burnetii 

2. Evidence of endocardial involvment

• Echocardiographic evidence

• A NEW regurgitant murmer.

Minor Criteria:

1. Fever >38 degrees C

1. High risk- e.g. cardiac lesion or IV drug use.

1. Vascular phenomena: arterial emboli, septic pulmonary infarcts, mycotic aneurysm, intracranial hemorrhage, conjunctival hemorrhages, Janeway lesions.

1. Immunologic phenomena: glomerulonephritis, Osler's nodes, Roth spots, positive rheumatoid factor.

1. Microbiologic evidence: positive blood culture not meeting major criterion 

Remember: Dukes is for LEFT sided lesions and right sides lesions do not have the same presentation in terms of vascular phenomena or easily heard murmur.



Here is a link the american heart association recommendations 

Happy monday.

acute panc

Today we discussed the etiology and prognostic considerations in acute pancreatitis.

A great article that addressees the prognostic scores and some guidelines is here.

This includes a newer predictive score:

BUN>9

Impaired mental status

Sirs (2 criteria)

Age >60

Pleural effusion

A score of 3 or more correlates with high risk of death or sever pancreatitis.

Less than 3 had a 99% NPV for death (WOW).

Those are hopefully the ones we see more often on the ward.

The RANSON"s score, which is more often referred to, does point out some important complications to watch for, such as hypoglycaemia and hypocalcemia.

The NEJM review can be found here.

tamponade

Hope everyone had a nice long weekend,

Today we talked about pericardial effusions, and ruling out tamponade.

Here is the JAMA physical exam paper for assessing for tamponade in a patient with pericardial effusion.

Of course we also alluded to the 'ever important' Ewart's sign: of dullness to percussion, egophony and bronchial breath sounds at the inferior angle of the scapula when the effusion is large enough to compress the left lower lobe. (thank you Drs. Willie, McIntosh.... and Dr. Wikipedia)

Here is a NEJM review.

happy tuesday.
:O)

dementia and ttp

On thursday we discussed a case of dementia and decreased ambulating

We touched on some reversible causes:
-B12 deficiency (which may manifest as subacute combined degeneration)
-NPH-(imparied reabsorption of CSF by the arachnoid granules)--> classic triad: cognitive changes, incontinence and trouble walking (may have a 'magnetic gate')

NPH is treated by large volume CSF drainage, and possiblly a shunt placement. 

here is a good review article on dementia from CMAJ, including when CT head should be included in the workup.



On Friday, Dr Thompson taught us about TTP that has many possible aetiologies.

TTP's Classic pentad:

1) Thrombocytopenia

2) Microangiopathic hemolytic anemia (MAHA; recognized by hemolysis with RBC fragments-shown above)

3) Neurological signs/symptoms

4) Renal failure

5) Fever

But our take home message was: 

Thrombocytopenia and MAHA without another cause is enough to start therapy!!

Here is a link to a review article on TTP. 

have a good long weekend :o)

hypoglycemia and ascites

Tuesday we started off the block with talking about hypoglycaemia in a non diabetic patient.

Our key "testable" points in the work up:

1. Cpeptide and insulin are BOTH high if endogenous insulin is secreted. 

2. Cpeptide is LOW if when insulin level is high, exogenous insulin. 

2. Sulphonurea increase ENDO insulin so this has to be ruled out before you go searching for a rare tumour

Remember; glucagon 1mg sub cut or IM or IV is a good treatment of hypoglycaemia. 

Today we talked about a case of a young lady with liver disease and ascites.

Some key points for ascites physical exam:

Most sensitive findings (if they are not there, may be able to rule out)

On history:

1. increased abdo girth, 

2. weight gain, 

3. ankle swelling

On exam:

1. flank dullness

2. shifting dullness

3. bulging flanks

4. leg edema

In looking at a patient with new ascites look for:

1) signs of decompensated liver disease : scleral icterus, jaundice, edema (low albumin), asterixis (encepalopathy)

2) signs of chronic liver disease: parotid changes, temporal wasting, muscle wasting, spider nevi, gynecomastia

3) Causes of the livery disease: cardiac exam such  as TR murmur, chf, Lymph nodes, 

CNS (wilson's disorder movement disorder),etc - this is a pretty wide differential.

Here is a reminder of how liver function tests decline over time:

Here is a link to the jama article on ascites.