The VIP syndrome occurs in healthcare when a celebrity or other well-connected “important” person receives a level of care that the average person does not. This situation was first documented in a paper published in the 1960s which noted that VIP patients have worse outcomes.
VIPs have the expectation that they can get special access to care and that the care will be of higher quality than that provided to others. Healthcare providers often grant this extra access, in the form of returned phone calls and preferential access to their clinic or office. The provider tries to provide a higher quality of care by ordering additional tests and involving more consultants. This idea ignores the fact that we already provide the best care we know how, and money or fame can’t buy any better.
Unfortunately, trying to provide better care sets up the VIP for a higher complication rate and a greater chance of death. Healthcare consists of a number of intertwined systems that, in general, have found their most efficient processes and lowest complication rates. Any disturbance in this equilibrium of tests, consultants, or nursing care moves this equilibrium away from its safety point.
Every test has its own set of possible complications. Each consultant feels compelled to add something to the evaluation, which usually means even more tests, and more possible complications. And once too many consultants are involved, there is no “captain of the ship” and care can become fragmented and even more inefficient and dangerous.
How do we avoid the VIP Syndrome? First, explain these facts to the VIP, making sure to impress upon them that requesting or receiving care that is “different” may be dangerous to their health. Explain the same things to allproviders who will be involved in their care. Finally, do not stray from the way you “normally” do things. Order the same tests you usually would, use the same consultants, and take control of all of their recommendations, trying to do things in your usual way. This will provide the VIP with the best care possible, which is actually the same as what everybody else gets.
Reference: “The VIP Syndrome”: A Clinical Study in Hospital Psychiatry. Weintraub, Journal of Mental and Nervious Disease, 138(2): 181-193, 1964.
Today is the first day of the Eastern Association for the Surgery of Trauma’s Annual Scientific Assembly. I’ll be sitting in the front row taking it all in so I can share the good stuff with you.
I’ll be tweeting important info continuously using the hash tag #east2011, as well as #traumapro. I will also be blogging about the best papers over the next 10 days or so. I like to see the presentation to find out the nitty gritty about the work, because we all know that the little bit of info posted in the abstract can be misleading. It also gives me an opportunity to add some historical perspective.
Stay tuned, and as always, please leave comments or questions.
Bleeding from scalp wounds may seem like a trivial problem, but I have personally seen someone die from unrecognized hemorrhage over time from one. All too often, these are covered up with a crude dressing when the patient arrives in the ED and is not looked at for some time.
Here are some tips to stop scalp bleeding:
Use direct pressure. This seems obvious but is frequently done incorrectly. Direct pressure involves a small diameter piece of gauze (stack of 2x2s or double folded 4×4) and only one or two fingers. Larger dressings or the palm of the hand do not provide enough pressure to stop all the bleeding. Direct pressure for 5 minutes (no peeking) will stop all bleeding that doesn’t need more advanced techniques.
Inject local anesthetic with epinephrine. This increases vasoconstriction and helps the direct pressure work even better. Be cautious if there is a large skin flap that does not have a nice pink color. Degloved skin has been crushed and small vessel vascular injury has occurred. Further reducing blood flow with epinephrine may kill the skin flap in this type of injury.
Apply Raney clips. Neurosurgeons use these to stop scalp bleeding during brain procedures. Caution! Only apply to unconscious patients, and only to the scalp (not face)! These hurt!
Oversew the scalp. Use a large silk or nylon suture and insert a large running stitch to close the wound. This will stop all bleeding from the skin edges. However, any arterial bleeders underneath will continue to be a problem.
Ligate individual bleeders. Use a small absorbable suture and attack each small arterial bleeder with a figure of 8 stitch. Don’t suture large chunks of tissue; make sure that you are attacking just the artery and not any adjacent nerves.
We have long assumed that pulmonary emboli start as clots in the deep veins of the legs (or pelvis), then break off and float into the branches of the pulmonary artery in the lungs. A huge industry has developed around how best to deal with or prevent this problem, including mechanical devices (sequential compression devices), chemical prophylaxis (heparin products), and physical devices (IVC filters).
The really interesting thing is that less than half of patients who are diagnosed with a pulmonary embolism have identifiable clots in their leg veins. In one study, 26 of 200 patients developed DVT and 4 had a PE. However, none of the DVT patients developed an embolism, and none of the embolism patients had a DVT! How can this kind of disparity be explained?
Researchers at the Massachusetts General Hospital retrospectively looked at the correlation between DVT and PE in trauma patients over a 3 year period. DVT was screened for on a weekly basis by duplex venous ultrsonagraphy. PE was diagnoses exclusively using CT scan of the chest, but also included the pelvic and leg veins to look for a source. A total of 247 patients underwent the CT study for PE and were included in the study.
Forty six patients had PE (39% central, 61% peripheral pulmonary arterial branches) and 18 had DVT (16 seen on the PE CT and 2 found by duplex). Of the 46 patients with PE, only 15% had DVT. All patient groups were similar with respect to injuries, injury severity, sex, anticoagulation and lengths of stay. Interestingly, 71% of PE patients with DVT had a central PE, but only 33% of patients without DVT had a central PE.
The authors propose 4 possible explanations for their findings:
The diagnostics tools for detecting DVT are not very good. FALSE: CT evaluation is probably the “gold standard”, since venography has long since been abandoned
Many clots originate in the upper extremities. FALSE: most centers do not detect many DVTs in the arms
Leg clots do not break off to throw a PE, they dislodge cleanly and completely. FALSE: cadaver studies have not show this to be true
Some clots may form on their own in the pulmonary artery due to endothelial inflammation or other unknown mechanisms. POSSIBLE
An invited critique scrutinizes the study’s use of diagnostics and the lack of hard evidence of clot formation in the lungs.
The bottom line: this is a very intriguing study that questions our assumptions about deep venous thrombosis and pulmonary embolism. More work will be done on this question, and I think the result will be a radical change in our use of anticoagulation and IVC filters over the next 3-5 years.
Reference: Velmahos, Spaniolas, Tabbara et al. Arch Surg. 2009; 144(10):928-932.
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