Alcohol-induced dilated cardiomyopathy

Note the enlarged ventricular chambers - the increased size causes the appearance of thinned ventricular walls. Assumption that there is decreased musculature in heart walls can cause incorrect diagnosis of cause-of-death.

Dilated cardiomyopathy can cause systolic dysfunction and atrial fibrilation, as well as being a source of thromboembolism.

DVT In Children: How Old Is Old Enough?

Adult trauma patients are at risk for venous thromboembolism (VTE). Children seem not to be. The big question is, when do children become adults? Or, at what age do we need to think about screening and providing prophylaxis to kids? As of yet, there are no national guidelines for dealing with DVT in children.

Researchers at Johns Hopkins went to the NTDB to try to answer this question. They looked at the records of over 400,000 trauma patients aged 21 or less who were admitted to the hospital. 

Here are the interesting factoids:

  • Only 1,655 patients (0.4%) had VTE (1,249 DVT, 332 PE, 74 DVT+PE)
  • VTE patients were older, male, and frequently obese
  • VTE patients were more severely injured, with higher ISS and lower GCS
  • Patients with VTE were more likely to be intubated and receive blood transfusions, and had longer hospital and ICU stays

The risk of VTE stratified by age was as follows:

Bottom line: Risk of VTE in pediatric trauma patients follows the usual injury severity pattern. But it also demonstrates a predictable age distribution. Risk increases as the teen years begin (13), and rapidly becomes adult-like at age 16. Begin your standard surveillance practices on all 16 year olds, and consider it in 13+ year olds if their injury severity warrants.

Related post:

Reference: Venous thromboembolism after trauma: when do children become adults. JAMA Surgery online first October 31, 2013.

More On DVT In Children

Deep venous thrombosis has been a problem in adult trauma patients for some time. Turns out, it’s a problem in injured children as well although much less common (<1%). However, the subset of kids admitted to the ICU for trauma have a much higher rate if not given prophylaxis (approx. 6%). Most trauma centers have protocols for chemical prophylaxis of adult patients, but not many have similar protocols for children.

The Medical College of Wisconsin looked at trends prior to and after implementation of a DVT protocol for patients < 19 years old. They used the following protocol to assess risk in patients admitted to the PICU and to determine what type of prophylaxis was warranted:

The need for and type of prophylaxis was balanced against the risk for significant bleeding, and this was accounted for in the protocol. The following significant findings were noted:

  • The overall incidence of DVT decreased significantly (65%) after the protocol was introduced, from 5.2% to 1.8%
  • The 1.8% incidence after protocol use is still higher than most other non-trauma pediatric populations 
  • After the protocol was used, all DVT was detected via screening. Suspicion based on clinical findings (edema, pain) only occurred pre-implementation.
  • Use of the protocol did not increase use of anticoagulation, it standardized management in pediatric patients

Bottom line: DVT does occur in injured children, particularly in severely injured ones who require admission to the ICU. Implementation of a regimented system of monitoring and prophylaxis decreases the overall DVT rate and standardizes care in this group of patients. This is another example of how the use of a well thought out protocol can benefit our patients and provide a more uniform way of managing them.

Related posts:

Reference: Effectiveness of clinical guidelines for deep vein thrombosis prophylaxis in reducing the incidence of venous thromboembolism in critically ill children after trauma. J Trauma 72(5):1292-1297, 2012.
Largest Study to Date: Transgender Hormone Treatment Safe

A study of nearly 1,600 transgender patients (1,073 MTF, 523 FTM) found that cross-sex hormone therapy is associated with low health risks, the worst of which being venous thromboembolism, occurring in just 1% of MTF patients. The study also finds that transitioning vastly lowers rates of depression.

“Some side effects are expected, such as venous thromboembolism with estrogen use, but most of the results are really reassuring,” says Dr. Nelson.

“The take-home message,” Dr. Asscheman said, “is that when using the guidelines from the Endocrine Society [“Endocrine Treatment of Transsexual Persons”], you are not going to see a lot of comorbidities with cross-sex hormone treatment.”


Pulmonary emboli usually arise from thrombi that originate in the deep venous system of the lower extremities; however, they rarely also originate in the pelvic, renal, upper extremity veins, or the right heart chambers. After traveling to the lung, large thrombi can lodge at the bifurcation of the main pulmonary artery or the lobar branches and cause hemodynamic compromise.

Pulmonary thromboembolism is not a disease in and of itself. Rather, it is a complication of underlying venous thrombosis. Under normal conditions, microthrombi (tiny aggregates of red cells, platelets, and fibrin) are formed and lysed continually within the venous circulatory system.

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 got this mnemonic online and found it very helpful.

I added some more information to it, my theory being, if I forget one manifestation; I have another one for backup.


Arthritis, Ankylosing spondylitis

Pyoderma gangrenosum, Pyoderma vegetans, Perianal skin tags, Psoriasis, Pleuritis, Pericarditis, Pancreatitis

I for eye signs: Iritis, uveitis, episcleritis, conjunctivitis

Erythema nodosum

Sclerosing cholangitis, Sacroilitis

Aphthous ulcers

Clubbing of fingers, Cholelithiasis, renal Calculi

Other manifestations include thromboembolism, vitamin and calcium deficiency due to involvement of the ileum and myocarditis. 

How I remember pANCA is associated with ulcerative colitis: nUCLEAR is an anagram for ULCER so ulcerative colitis is associated with pANCA. 

Is it too much? xD


valerie-volatile  asked:

Saw your comment, about HRT thromboembolism risk being overblown, in post about progesterone, estradiol cypionate, bicalutamide. Wondered if you could comment/point me in the right direction/help get this question out there for someone else to answer: My understanding: spiro prevents T from ever being produced, while bicalutamide prevents it from finding its way to receptors. What happens to the T that bicalutamide allows to be produced? Any risks? Can it interfere with development?

Spironolactone functions as an anti-androgen because it both prevents the production of testosterone and because it blocks the testosterone that’s already made from interacting with the androgen receptor. However, doctors tend to [wrongfully] ignore the latter activity and dose spironolactone such that the patient’s testosterone is suppressed all the way to typical, cis female levels.

Unfortunately I don’t have any good answers as to how much lower dosages of spironolactone can be to still be effective.

Bicalutamide works by out-competing testosterone and thus blocking it from interacting with the androgen receptor. It does not lower the amount of testosterone in your body. The testosterone in your body is handled the same way as it would normally be: it’s broken down by enzymes and excreted or recycled.

The main thing you need to know if you’re thinking about using bicalutamide is that it can be pretty toxic to the liver but we don’t really have a clear picture as to how toxic it actually is. In either case you should definitely not be taking it without the help of a doctor to monitor your liver health. This isn’t a drug you should self-medicate. This standards of care suggests that the drug should be avoided entirely until more research is done to demonstrate it’s hepatic safety.