Acute Peptic Ulceration and Cerebral Fat Embolism after Fracture

The relationship between acute intracerebral lesions and oesophago-gastro-duodenal ulceration has long been recognised, first by Rokitansky (1849), later by Pomorski (1891) and L#{233}pine(1895), and in more recent years by Opper and Zimmerman (1938), Strassmann (1947), Globus and Ralston (1951), Schlumberger (1951) and Dalgaard (1960). Strassmann found fifty-six instances of peptic ulceration in 14,000 necropsies on mental hospital patients and for medico-legal purposes ; all but two had intracranial lesions and twenty-six showed acute haemorrhagic ulceration of the stomach, oesophagus and duodenum. In addition thirty perforating lesions of the upper gastro-intestinal tract were noticed. In 1960 Dalgaard reported his observations from 4,317 necropsies, one-third performed for medico-legal purposes. He found 208 cases of acute peptic ulceration including so-called oesophago-malacia and gastro-malacia and mucosal erosions. In 32 per cent cerebral vascular lesions were evident, compared with 12 per cent for the entire necropsy series. Other causes of ulceration in Dalgaard’s cases were intracranial injuries (thirty-five cases), cerebral tumours (fifteen cases), craniotomy (twenty-three cases), infections (eleven cases), as well as burns (four cases), intoxication (twenty cases), cerebral hypoxia (nine cases) and acute stress (fifteen cases). Microscopical examination confirmed the acute nature of the lesions, with necrosis, haemorrhagic and cellular response within the layers of the stomach wall. Despite the variety of reported intracranial pathology that may give rise to acute peptic ulceration, we have been unable to find any instance or reference to fat embolism as a causative factor. This report is of three instances in which skeletal injury led to fat embolism, followed in two cases by perforation, and in the other by haemorrhage. All proved fatal and were recognised only at necropsy.