Day #140 - Adrenal Insufficiency

Today we talked about a case of a patient with symptomatic hypotension, that was not initially fluid responsive with a known history of intrabdominal malignancy and hyponatremia with hyperkalemia. The combination of these things led to the suspicion of adrenal insufficiency.

This is a classic (now 12 year old) review of adrenal insufficiency from nejm.

I have previously blogged about adrenal insufficiency here.

Day #139 - Atrial Fibrillation

Today we talked about a case of rapid atrial fibrillation.

The ACC guidelines for atrial fibrillation are here, and the ACLS tachycardia algorithm is here.

Is the AF causing severe CHF, hypotension or angina? If so manage as unstable. Otherwise manage as stable.

Unstable:

• DC Cardioversion

Stable:

• Does the patient have pre-excitation or a grade III/IV LV?
  
  • Amiodarone 150mg IV over 10 minutes, can repeat, then give 360mg IV over 6h then 540mg IV over 18h loading. Risk of cardioversion.
• No WPW or grade III/IV LV:
  
  • IV beta blocker (like metoprolol 5mg IV over 2 mins, can repeat q 5 mins x 3)
  • IV calcium channel blocker (diltiazem 0.25mg/kg IV over 2 mins, can repeat in 10 mins with 0.35mg/kg IV)
  • Follow up with oral agent of same class
• There is evidence that IV magnesium can be effective as a rate control agent, either alone or in combination.
  
• Afib of less than 48h duration (or no thrombus on TEE) can consider cardioversion either electrical or chemical.
• Does this patient need anticoagulation?
  
  • CHADS2 score if greater than or equal to 2, yes. Otherwise anti-platelet agents.
    

Consider the cause of the AF:

• Hypertension
• Structural Heart Disease
• Hyper/hypo thyroidism
• Alcohol/Stimulants
• Ischemia
• PE
• Infection
• Other stressor

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We have previously talked about septic bursitis and septic arthritis here.

I will expand on that by saying that one of the keys in effective management is source control. The septic joint should be repeatedly tapped until there is a negative culture and the cell count is dramatically decreased. If it isn't improving -- they will need surgical management. If you can't tap the joint, they will need surgical management. This is particularly a problem with "difficult" to aspirate joints like the shoulder or hip. These patients should have orthopedic surgery to wash out the joint.

Failure to drain the joint can lead to treatment failure and joint damage.

Here is a good review of the diagnosis and management of acute septic arthritis.

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1. For the record, ciprofloxacin monotherapy is a totally inappropriate empiric choice for the treatment of community acquired cellulitis (even if the patient is penicillin allergic)
   
   • Penicillin allergy is one of the bains of my existance. I direct you to this article on trying to determine if a history of penicillin allergy is "real".

Day #138 - Massive Upper GI Bleed

Today was a great case of massive upper GI bleeding. I have previously blogged about GI bleeding here and here.

The initial approach is usually endoscopic therapy. If this isn't an option, you are left with interventional radiology (angioembolization) or emergent surgery. In this case, angioembolization localized and stopped the bleeding.

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Everything you ever wanted to know about myelodysplastic syndromes and classification of the leukemias, myelodysplastic syndromes, and myeloproliferative disorders.

Day #137 - Thrombocytopenia

Today we discussed a case of a patient who has presumed immune mediated thrombocytopenia.

We discussed the approach to thrombocytopenia and then the management of ITP.

I have previously blogged about this here (including references and discussion of management).

Note that today's patient, by virtue of his cirrhosis is at a very high risk of peri-operative death from splenectomy -- he may be a candidate for rituximab if steroids fail.

Day #134 - Thrombophilia

Fantastic case today. A young woman with recurrant thromboses including one on LMWH (in the context of thrombocytopenia) manifesting as a cardiac mass! I have previously blogged about DVT/PE here.

There are a good set of clinical guidelines for DVT/PE here.

The utility of the thrombophilia workup (or possible lack thereof) will be debated at next week's medical grand rounds. You should attend.

A couple of things I wanted to highlight:

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Thrombophilias:

• Factor V Leiden/Activated Protein C resistance
• Prothrombin mutation
• Protein C and S deficiencies
• Antithrombin III deficiency
• Elevated Factor VIII
• Antiphospholipid Antibody Syndrome
• Hyperhomocysteinemia
• Heparin Induced Thrombocytopenia

Our patient had none of these for her first ~5 embolic events -- but clearly she has some underlying thrombophilia which we probably have not discovered yet. A malignancy search has been negative.

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Use of D-Dimer in established thromboembolic disease

This can be used to assist in risk stratification. A positive D-dimer (1 month post stopping warfarin) predicts patients who have a high risk of recurrent thromboembolism (original NEJM article and meta-analysis)

A Canadian study sought to identify risk factors for recurrent DVT/PE in patients with one previous idiopathic DVT/PE and found that they could predict women at low risk who could safely stop anticoagulation. These women had 0 or 1 of the following:

• Post thrombotic signs (hyperpigmentation of limb, edema, redness)
• D-Dimer greater than 250
• BMI greater than 30
• Age greater than 65

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Heparin Induced Thrombocytopenia

This is a prothrombotic condition caused by anti-PF4 antibodies which bind to heparin-platelet complexes and activate platelets. This causes platelet consumption and activation with thrombosis (arterial or venous).

If you see a patient on heparin who develops thrombocytopenia and thrombosis you had better think about this diagnosis.
The diagnosis can be challenging; however, there is a clinical prediction rule, which in association with laboratory testing can be helpful in ruling out HIT. This is called the 4 T's.

1. Thrombocytopenia:
   • Greater than 50% drop in PLT and nadir greater than 20 = 2 points
   • 30-50% drop OR nadir 10-20 = 1 point
   • less than 30% drop OR nadir less than 10 = 0 points
2. Timing:
   
   • Drop @ 5-10 days (or less than 1 day with previous heparin within 30d) = 2 points
   • Drop after day 10, or unclear when drop, or less than 1 day with previous heparin greater than 30d ago = 1 point
   • Fall less than four days without previous exposure = 0 points
3. Thrombosis
   
   • New thrombosis = 2 points
   • Progressive or recurrant thrombosis or suspected (not proven) thrombosis = 1 point
   • None = 0 points
4. oTher cause of thrombocytopenia
   
   • None = 2 points
   • Possible = 1 point
   • Definite = 0 points

Total score:

• 0-3 low (0%)
  
• 4-5 intermediate (10%)
  
• 6-8 high (80%)

NB: our patient would score a minimum of 6 (if you assume there is a possible other cause of thrombocytopenia)

The authors suggest the following algorithm for diagnosis and management of HIT using the 4T's coupled with the widely available sensitive but non-specific anti-PF4 antibody assay to screen and the difficult to obtain serotonin release assay (SRA) to confirm.

Day #133 - Unstable Angina

Today we heard a case of a female patient presenting with typical angina (although atypically described by her on the history) which was escallating in frequency. A diagnosis of unstable angina was made and she was treated according to the guidelines.

(The unstable angina/NSTEMI pocket guideline is here)

Patients should be started on:

• antiplatelet -- i.e. ASA +/-clopidogrel
• anticoagulant -- i.e. IV heparin or LMWH. In high risk patients, consider gpIIaIIIb inhibitor
• statin
• oral beta-blocker within 24 hours for patients without contraindications
• oral calcium channel blocker if contraindication to beta-blocker
• oral ACEi within 24h for patients with heart failure or LVEF less than 40%
• oxygen if hypoxemic
• nitroglycerin 0.4mg SL spray/tablets q5 mins prn (max 3 doses) for symptoms of ischemia

When admitting a patient with UA/NSTEMI, I always find it helpful to estimate their risk of complications (i.e. death/MI) using the TIMI risk score.

Patients with probable ACS of ischemic origin should have (if appropriate) early (<72h) cardiac risk stratification. If high risk patients, they should be considered for early angiography +/- angioplasty (early invasive strategy).

She then went on to have non-invasive risk stratification, which was felt to be positive and then went on to coronary angiography. This showed triple vessel disease, for which she ultimately should consider coronary artery bypass surgery.

Physical Exam - Ascites

With great thanks to a previous CMR.