Monteggia fracture dislocation

Typically, Monteggia fracture-dislocations occur as the result of a fall onto an outstretched hand (FOOSH).

The Bado classification is used to subdivide the fracture-dislocation into four types which all have different treatment options and prognoses and is based on the principle that the direction in which the apex of the ulnar fracture points is the same direction as the radial head dislocation 3. The direction of radial head dislocation depends on whether abduction or adduction forces were applied during the fall.

As is usually the case, in everyday practice, describing the fracture-dislocation is far more important than remembering the grade.



AUM Fees and Financial Planning: The Odd Couple

This is a really great article.  If it doesn’t offend you, maybe you are better off with an AUM model for financial advice.


The fact is that it is no mathematically harder to manage $10,000 than it is $10,000,000 from the asset side.  If they are doing a lot more then MAYBE it would be justified to have a decreasing sliding scale of AUM.

For example, let’s say you hit $10M and they start coming up with strategies for retirement.  That would include RMD’s, Social Security, and intervehicle conversions (partial or full conversions to Roth, recategorizing “horse race” funds, etc) to maximize tax efficiency.

Pulmonary vasculitis

  • ANCA associated vasculitides
    • Wegener granulomatosis (WG): ANCA associated pulmonary renal syndrome
    • microscopic polyangiitis (MPA)
    • Churg-Strauss vasculitis (CSV)
  • idiopathic, pauci-immune pulmonary capillaritis (IPIPC): may or may not be ANCA associated
  • non ANCA associated pulmonary renal syndrome: Goodpasture syndrome
  • rheumatoid pulmonary vasculitis: rare
  • cryoglobulinaemic vasculitis (affecting lung)

Mesenteric venous thrombosis part 2

This is an extremely subtle case of mesenteric venous thrombosis that remains to be proven. My diagnostic certainty is in the 90 to 100% range but I will certainly grant that other differential considerations could produce this appearance and it is not uncommon to find ileus in a patient with cirrhosis and ascites. The cirrhosis and ascites can easily account for mural thickening of bowel due to a number of causes, chiefly

The initial CT was performed without contrast about 3 days prior to the follow-up CT which was performed with contrast. I presume (because I get very little clinical information) that the patient was not doing well with ordinary nasogastric decompression. My initial interpretation was a small bowel obstruction without a transition point identified. In retrospect, I think this was probably small bowel venous ischemia associated with mesenteric thrombosis. I have seen more than a few cases of this, and in almost every circumstance, they are missed initially and often missed on subsequent studies.

Because the consequences are disastrous with necrotic ischemic bowel that must be resected if medical management fails, this is an important entity even though it is uncommon.

As I discussed in the previous case even body imagers miss this diagnosis.

The 2nd images below are definitely more suggestive of the diagnosis although this is by no means a “slam dunk”. There appears to be a mesenteric thrombus parked in the Iliocolic branches of the superior mesenteric vein.

Baby heads are hard to read


There is definitely asymmetry here with edema in the left posterior MCA distribution.  Not sure if ischemia, prenatal insult, or some TORCH action going on here.  I considered a venous sinus abnormality but I think the brightness of the dural sinuses is an age thing, given the uniformity.




Since it’s always good to review the TORCHs, here is a bit on HSV:


Given the hospital it came from, I included Neonatal HSV in the diff, but MRI will probably flesh it out.  For reference –

Radiographic features
It is important to appreciate that the radiographic appearance of neonatal HSV encephalitis is different from its more common adult counterpart. Changes are typically diffuse which can be difficult to identify due to normal immature myelin (see normal myelination) and more commonly involving the cerebral cortex, the deep white matter, and thalamus 4. The medial temporal and inferior frontal lobes may be spared and haemorrhagic change is uncommon but can develop later and is best seen on gradient echo/susceptibility sequences

may be negative in the early course of the disease
in advanced stages may present with extensive areas of parenchymal hypoattenuation, predominantly in the white matter, as a result of oedema or necrosis
enhancement usually presents in a gyriform pattern

Lipomatous Hypertrophy of the Interatrial Septum


Lipomatous hypertrophy of the interatrial septum is an exaggerated growth of normal fat existing within the septum and is not a true tumor. Rather, it is a developmental disorder caused by expansion of adipose tissue trapped in the interatrial septum during embryogenesis. The septal hypertrophy may be as large as 2 cm in thickness and is seen primarily in older patients and in those who are obese.

It has been suggested that this disorder is associated with the presence of coronary artery disease in proportion to the degree of atrial septal thickness (possibly true in this case although the patient is a vasculopath).

Lipomatous hypertrophy of the interatrial septum is indistinguishable from lipoma except that the former occurs in the atrial septum with a typical distribution (generally sparing the fossa ovalis). In the absence of symptoms of atrial arrhythmias, heart block, or rare vena caval obstruction, they do not require resection.