Dr. Charles A. Leale, a 23-year-old assistant surgeon, U.S. Volunteers, reached the patient within minutes of the shooting and was accosted immediately by a distraught First Lady crying: “Oh, physician! Is he dead? Can he recover?” The President was not yet dead. However, after a cursory examination, Leale announced: “His wound is mortal; it is impossible for him to recover.” At 7:20 a.m., Abraham Lincoln, 16th president of the United States of America, breathed his last, and his spirit ﬂed to God who gave it.

Why Lincoln died is no mystery. His wound, as Dr. Leale predicted, was mortal, because in 1865 little could be done for patients with such wounds. Today modern advances in trauma care have greatly expanded our capacity to manage traumatic brain injuries and have radically altered the prognosis of patients with injuries like Lincoln’s. Could these techniques have saved Lincoln if they had been available in 1865, and if so, what would he have been capable of in the aftermath of such care? These questions were addressed in 2007 by Dr. Thomas M. Scalea, director of the R. Adams Cowley Shock Trauma Center, the world’s oldest such center, at the University of Maryland School of Medicine, during the school’s bicentennial celebration. Dr. Scalea believes that recent advancements in trauma care discussed below would not only have saved Lincoln’s life, but would also have restored much of the President’s neurological function.

Lincoln was shot in the left occiput at close range with a relatively low-velocity bullet. Two young physicians, Dr. Charles Leale, who had graduated from medical school only days before the shooting, and Dr. Charles Taft, just 30 years old, cared for Lincoln. In accordance with the medical practice of the day, they repeatedly probed the President’s wound to prevent blood from accumulating within the skull and compressing his brain. For a time, this maneuver relieved Lincoln’s respiratory distress.

Lincoln’s initial symptoms and his dilated left pupil were caused by cerebral herniation—displacement and compression of vital areas of the brain by blood and edema ﬂuid accumulating within his skull. His physicians remarked that “as long as bleeding continued, the President’s condition remained stable. When the ﬂow stopped, the vital signs weakened … It would produce signs of increased compression. The breathing became stertorous and intermittent, and the pulse became more feeble and irregular.” The most likely path of the bullet that killed Lincoln was through the left lateral sinus. As it traveled through the brain, it created pressure waves that damaged the brain stem (the upper spinal cord). It also produced intraventricular hemorrhage (bleeding into the inner cavities of the brain), a deep laceration of the left cerebral hemisphere, and bilateral subdural hematomas (pools of blood collected on the surface of the brain). In time, these primary injuries (i.e., those occurring at the time of impact) were likely magniﬁed by inadequate delivery of oxygen to the brain resulting from repeated episodes of hypotension and the president’s irregular breathing. This, in turn, caused pressure within the skull (the intracranial pressure [ICP]) to rise, producing additional (secondary) damage to the brain.

Lincoln’s intracerebral hemorrhaging would have caused his ICP to soar. Whereas repeated probing of his wound allowed blood to escape from his skull and for a time relieved his elevated ICP, it also contributed to substantial blood loss. The brain is an extremely vascular organ and when injured bleeds profusely. In fact, Lincoln’s attendants commented that his sheets were crimson and his bed surrounded by a pool of blood. Thus, it is likely that he died because of both cerebral herniation and massive hemorrhaging.