VA ICU Report 5.26.17

Morning, some good neuro critical care action at the VA this week, thought we’d cover something today not yet covered on the blog: non-invasive estimations of elevated ICP, namely fundoscopy and ocular ultrasound

Dan Reiss correctly pointed out the acute finding in elevated ICP on an ocular ultrasound is the optic nerve sheath diameter, a handful of smaller studies (n in each about 40-60) have evaluated the correlation between nerve sheath diameter and MRI/CT findings of elevated CT, Sensitivity and Specificy depends on the cutoff chosen, in adults typically a ONSD of >4.5mm is considered too high, which yields a sens and spec of around 70-80% for the detection of elevated ICP. The challenge here, as with fundoscopy, is inter-observer variability presumably due to operator characteristics. Here is a review paper on non-invasive determination of ICP.

Other quick pearls

#generally opt for beta blockers and ccb in the acute treatment of hypertensive emergency due to the theoretical concern for cerebral vasodilation with nitro/hydral, nicardipine and esmolol are good options

#PRES, covered elswhere, stands for posterior reversible encephalopathy syndrome, though not always posterior or reversible. Remember, MRI is the diagnostic test for PRES.


Filed under: Morning Report, Neurology, Pulmonary and Critical Care Medicine

VA Intern Report 5.25.17-Last one of the GJ/CVG era!

Big thanks to all the interns who survived intern report out at the VA, what a year. It was a fitting end to the year as we ranged from heat stroke, to cobalt-beer cardiomyopathy, and that was before we even got to the cases! (JK) Anyway here are the top pearls, and thanks again we will miss you guys.

#Cobalt beer cardiomyopathy: We got here by talking about cobalt toxicity in the s/o hip prostheses, not the metallosis associated w/ the hip resurfacing (see here) but acute heart failure! Seems some hearty Quebecois and midwesterners who liked to drink a case of cheap beer after a hard day of work were turning up in acute cardiogenic shock and LV failure. In a case review from 1972 28 patients were profiled, seems that cobalt improves the foamy head of a glass of beer and so was added for aesthetic reasons. It was an old treatment for aplastic anemia because it boosts red cell counts, unfortunately cobalt is toxic to hemoglobin and causes it to tightly bind oxygen, resulting in hypoxia and ischemic injury, it also disrupts the conversion of pyruvate to acetyl-coA (krebs cycle shenanigans) leading to a disruption in oxidative metabolism similar to thiamine deficiency. Needless to say, no more adding cobalt to cheap beer.

#Heat stroke/Heat illness: Something we don’t often cover in inpatient medicine in San Francisco but those of us who will practice in warmer climes (ahem yours truly) should know the basics of the spectrum of heat-related illness. Basics, remember when you are exercising you generate heat. A lot of heat. Heat can be dissipated through evaporation, i.e. sweat evaporates on contact with cooler air which helps cool the skin, conduction direct transfer of heat from a hotter to cooler object, like your fancy “sweat wicking” workout clothes, radiation, heat just flowing as energy from hotter to colder areas of space, and convection, or cold air flowing across a surface absorbing heat continuously. You’ll notice all these processes require that the surrounding temperature is lower than that of the bodies surface and core temperature, when that’s not the case, the potential for ineffective heat removal arises and can progress to the most dangerous stage of heat illness: heat stroke.

Generally to distinguish when the weather is more predisposing to heat illness, we use the wet-bulb globe temperature, which takes into account both ambient air temperature as well as radiant heat (from the sun duh) and humidity. This technique provides a heat index which is more useful than just temperature in determining the safety of participating in outdoor activities. Note that older patients are at risk of developing heat illness at baseline regardless of activity level. The main culprit in the progression of heat related illness is inadequate fluid intake, so staying hydrated is key. You can lose up to 2L of sweat in an hour in a hot enough environment.

Heat exhaustion vs. Heat stroke: The distinguishing factor is a breakdown in thermoregulatory mechanisms, in heat exhaustion you can feel crummy: GI upset, dizziness, maybe even some headache or vertigo, but once you become altered you worry more about heat stroke. Patients with heat stroke actually stop sweating due to volume depletion and peripheral vasoconstriction, a compensatory response to the lowered MAP, unfortunately this eliminates radiation and evaporation as heat removal strategies, and also causes a subsequent spike in core temp, in fact temp > 40.5 plus encephalopathy should raise the suspicion for heat stroke to the top of your list. Early and aggressive fluid resuscitation is key, as well as active cooling.

Interestingly, some younger patients can present diphoretic even though they meet the above criteria for eat stroke, can also present with rhabdo and acute kidney injury, and can even see thermal injury to the myocardium resulting in ST changes and trop elevation!

Above temps of 42 direct cellular injury occurs and multi-organ failure ensues, often resulting in death.

Evaporative cooling is most useful in these settings, constantly changing cool wet blankets or spraying the skin with cool water and placing fans at the bedside is another strategy, cold IV fluids are less effective due to the changes described above. ECMO can be used but is often not practical.

Filed under: Morning Report


Poaching from Moffitt at VA report. Mini case of a young patient presenting with palpitations with the 1st EKG above.

Several things: Notice the extremely fast rate (>200 BPM!), wide complex, irregularly irregular rhythm, and variable QRS amplitudes and morphologies.

AFIB w/ BBB is certainly on the differential, as is VT (more commonly regular, but can look irregular with fusion/capture beats making their way down the AVN). However, notice how the QRS morphology changes. This makes AFIB w/ BBB less likely. Polymorphic VT is also less likely given that the axis of the QRS complexes does not change with this different beats!

This is a case of AFIB w/ a WPW bypass tract! Treatment of choice? Procainamide which preferentially slows the fast conduction down the bypass tract.

In this case, procainamide failed and cardioversion resulted in the second EKG. Notice the clear delta-waves  in the precordial leads! (Also RBBB morphology that may have been leading to some of the QRS morphology variability in the 1st EKG).

AFIB w/ WPW is a dangerous rhythm that may degenerate into VF.

It is important to recognize as nodal blocking agents should be avoided since it would result in conduction only down the fast bypass pathway and an unstable rhythm!


Filed under: Morning Report