Intestinal obstruction, as a rule, is associated with an increasing amount of non-coagulable nitrogen in the blood. With acute intoxication the rise in non-coagulable nitrogen may be rapid and reach as high as three or even ten times normal. With more chronic intoxication there may be little or no rise in the blood non-coagulable nitrogen.

Closed intestinal loops show exactly the same picture, and, when combined with obstruction, may give very high nitrogen readings.

Acute proteose intoxication due to injection of a pure proteose will show a prompt rise in blood non-coagulable nitrogen, even an increase of 100 per cent within 3 or 4 hours.

These intoxications also show a high blood content of creatinine and urea. The residual or undetermined nitrogen may be very high.

A human case of intestinal obstruction with autopsy presents blood findings exactly similar to those observed in many animal experiments.

Clinically the non-coagulable nitrogen of the blood may give information of value in intestinal obstruction. A high reading means a grave intoxication, but a low reading may be observed in some fatal cases and gives no assurance that a fatal intoxication may not supervene.

The kidneys in practically all these experiments are normal in all respects.

It is possible that protein or tissue destruction rather than impaired eliminative function is responsible for the rise in non-coagulable nitrogen of the blood in these acute intoxications.

Transfusions of dextrose solutions often benefit intestinal obstruction, and may depress the level of the non-coagulable nitrogen in the blood. Some cases show no change in non-coagulable nitrogen following transfusions and diuresis, and, as a rule, such cases present the most severe intoxication.

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