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.
Falls from a height can be either accidental or intentional (suicide attempt). There are several prognostic factors for survival that have been identified:
Type of surface
Body part that touches the ground first
Two other factors are important, but do not have a significant effect on mortality:
Circumstances of the fall (suicide, accident, escape)
Initial impact with an object before impacting the ground
Height. Overall, about half of victims die at the scene, and a total of 70% die before they reach the hospital. The median height leading to death is about 49 feet, or about 4 to 5 storeys. 100% of victims die after falling 85 feet, or about 8 storeys.
Age. Mortality increases with age due to pre-existing medical conditions and decreased physiologic reserve.
Type of surface. The type of surface struck (i.e. grass, water, construction debris) can also have an effect on secondary injuries and survival. Mortality after striking a hard surface is nearly double that of hitting a soft one (39% vs 22%)
Body part touching the ground first. The highest mortality is seen when the victim lands in a prone position (57%). Striking head first has the next highest mortality at 44%. The best striking position is feet first, with a mortality of 6%.
Circumstances of the fall. Suicide attempts have the highest death rate at 46%. This may be attributable to pre-planning, and the increased likelihood that the fall may lead to additional trauma mechanisms (struck by car after jumping from land bridge, drowning after jumping from bridge over water). Accidental falls have a lower 17% mortality.
Initial impact before final impact. Striking wires or scaffolding before the final impact is protective, decreasing the death rate from 37% to 15%.
It is important for the trauma professional to obtain as much information from bystanders or EMS as possible about the fall details. This will ultimately enable to trauma physician to pursue appropriate diagnostic techniques to pinpoint specific injuries associated with various types of falls.
Frequently, radiologists and trauma professionals are coerced into describing the size of a pneumothorax seen on chest xray in percentage terms. They may something like “the patient has a 30% pneumothorax.”
The truth is that one cannot estimate a 3D volume based on a 2D study like a conventional chest xray. Everyone has seen the patient who has no or a minimal pneumothorax on a supine chest xray, only to discover one of significant size with CT scan.
Very few centers have the software that can determine the percentage of chest volume taken up with air. There are only two percentages that can be determined by viewing a regular chest xray: 0% and 100%. Obviously, 0% means no visible pneumothorax, and 100% means complete collapse. Even 100% doesn’t really look like 100% because the completely collapsed lung takes up some space. See the xray at the top for a 100% pneumothorax.
If you line up 10 trauma professionals and show them a chest xray with a pneumothorax, you will get 10 different estimates of their size. And there aren’t any guidelines as to what size demands chest tube insertion and what size can be watched.
The solution is to be as quantitative as possible. Describe the pneumothorax in terms of the maximum distance the edge of the lung is from the inside of the chest wall, and which intercostal space the pneumothorax extends to. So instead of saying “the patient has a 25% pneumo,” say “the pneumothorax is 1 cm wide and extends from the apex to the fifth intercostal space on an upright film.”
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