1. Most missed injuries in abdominal survey during trauma:
-G-E junction
-Ureters
-Ligament of treitz
-Mesenteric borders of small bowel
-Posterior wall of transverse colon
-Extraperitoneal rectum
2. "Bail out injuries": i.e. injuries such that if you see these intra-op, do not attempt to completely fix everything in one go. Convert to damage control surgery. Depending on how stable they are, either fix the most life-threatening injuries, or just pack it and get out. Either way, leave the abdomen open and go the ICU. Resuscitate, wait until they are more stable, then go back to the OR to fix things.
-Significant vascular injury plus hollow viscus injury
-Penetrating injury to aorta or IVC
-High grade liver injury
-Pelvic fracture with expanding hematoma
-Injuries requiring simultaneous surgery elsewhere-- thorax, head, neck.
3. Trauma triad of death: hypothermia, coagulopathy, acidosis. These signs are an extremely poor prognosis. If you wait for these to come on before you decide to close and go to the ICU, it will be too late.
4. Intraoperative cues of impending hostile physiology (i.e. precursors to trauma triad of death): if you see these signs, stop operating as quickly as possible, get to the ICU.
-Diffuse oozing
-Bowel mucosa edema
-Midgut distention
-Dusky serosa
-Noncompliant, swollen abdominal wall
5. Options for bleeding vessel control:
-sutures
-packing
-packing + hemostasis agents (surgicel, floseal, thrombin)
-if is a big vessel, you can insert a foley catheter into it, blow up the cuff and pull up
6. If you're operating a long time on an extremity and doing vascular surgery, consider a presumptive fasciotomy to stave off compartment syndrome.
7. Postop fever etiology mnemonic 
-POD 1-2 wind (pneumonia)
-POD 3-4 water (UTI)
-POD 4-5 walking (DVT/PE)
-POD 5-7 wound
-POD 7+ wonder drugs (drug fever - esp anticonvulsants & bactrim)
8. On the pupillary light reflex: {source}
"Because of the different paths these two nerve supplies take, brain and brainstem
trauma interrupt the sympathetic and parasympathetic tracts in different patterns.
Consequently, the pupillary reflex can be a valuable assessment tool. For example,
damage to the hypothalamus destroys only the sympathetic branch allowing the
parasympathetic to predominate. Parasympathetic nerve supply causes constriction with
reaction to light. In the lower brainstem (pons and medulla), damage causes a similar
response, but more exaggerated. In this case, the pupils are tightly constricted
(“pinpoint”) and unreactive or “fixed.” Notice that midbrain, mesencephalon, damage
disrupts both the sympathetic and the parasympathetic pathways resulting in pupils being
midposition and “fixed.”

In usual situations, both pupils respond similarly (bilaterally). However, if the
parasympathetic occulomotor nerve is damaged outside the brain and at some point along
its course to the eye, parasympathetic supply is disrupted only to that one eye. In the affected eye sympathetic predominates and the pupil dilates while the other eye remains
normal. This condition is common with temporal lobe herniation as the protruding lobe
of the brain presses on the occulomotor nerve on the herniated side. Thus, the dilated
(“blown”) pupil indicates the side of herniation."

9. Fixed, dilated pupils are possibly due to brainstem ischemia, as well as to cranial nerve III compression by uncal hernation. {Neurosurgery, 162 patients GCS<8 underwent xenon CT scans to determine blood flow, found significantly higher brainstem  blood flow among those with fixed, dilated pupils vs reactive pupils; pupil reactivity/size did not correlate with ICP or the presence of a brainstem lesion} 

10. Uretopelvic junction obstruction: able to tolerate normal urine outflow without trouble, but fails when there is a large diuresis-- hence the adolescent presenting symptomatically (with colicky flank pain) after their first binge-drinking session