Experiments to determine the effect of furnishing an ample supply of sodium chloride on the toxemia of pyloric and intestinal obstruction are reported.
A fall in chlorides is the first and seemingly most significant change to take place in the blood after pyloric and intestinal obstruction.
The chloride is apparently utilized by the body as a protective measure against the primary toxic substance.
Two dogs with pyloric obstruction were given 50 cc. of 10 per cent NaCl subcutaneously daily. One lived 3 days, the other 4. The blood showed little change, except a marked terminal rise in chlorides. Animals given a like amount of distilled water or 25 per cent glucose showed the changes typical of untreated animals.
The obstruction of the pylorus was released in six dogs 48 to 72 hours after the initial operation. Two died within 24 hours after the second operation with a high non-protein nitrogen in the blood. Two survived but showed a high level of non-protein nitrogen in the blood and a high nitrogen excretion in the urine, low blood chlorides, and a marked alkalosis. One dog in such a state died on the 13th day from peritonitis, arising in a wound infection. The other showed a marked fall in non-protein nitrogen in the blood following the administration of 10 gm. of sodium chloride by mouth, but died following the intravenous injection of 25 per cent sodium chloride. Two animals were given 50 cc. of 10 per cent NaCl subcutaneously, at the time of the second operation. The blood rapidly returned to normal and complete recovery followed.
Two dogs with the duodenum obstructed by section and inversion of the cut ends were treated with 10 per cent sodium chloride after the obstruction had existed for 48 hours and the characteristic blood changes had developed. The non-protein nitrogen returned to normal within 48 hours after treatment was begun. One dog died following a lateral anastomosis for relief of the obstruction. A second operation was not attempted in the other animal.
Two dogs in which the duodenum was obstructed by section and inversion of the cut ends were given 500 cc. of 0.85 per cent NaCl subcutaneously on the day of operation and each day thereafter until death. One dog lived 21 days, the other 28. Both dogs showed a marked alkalosis, but never any rise in the non-protein nitrogen of the blood. The animals at autopsy showed intussusception of the ileum with extensive ulceration. In one there was a perforation and terminal peritonitis. The operation wounds healed normally.
Three dogs with section of the duodenum were given 500 cc. of distilled water every day. One died in 24 hours, one in 48 hours, and the third in 72 hours. Autopsy showed no cause for death other than toxemia.
One dog with section of the duodenum was given 500 cc. of 2 per cent glucose every day. The blood showed a rapid rise in non-protein nitrogen and carbon dioxide-combining power, and a fall in chlorides. The animal died 72 hours after operation.
Three dogs with section of the duodenum were given 500 cc. of 1 per cent sodium bicarbonate every day. One dog died in 72 hours, one lived 7 days, and the third lived 9 days. All developed a high non-protein nitrogen in the blood and two showed marked clinical symptoms of an alkalosis.
These results demonstrate that solutions of sodium chloride have a marked effect in preventing and controlling the toxemia of pyloric and intestinal obstruction as shown in clinical symptoms and in chemical changes in the blood.
Dogs given an abundant supply of distilled water died more quickly than untreated control animals. Solutions of glucose have no specific value, and sodium bicarbonate solutions prolong life only a short while. Good therapeutic results have been obtained with very concentrated sodium chloride solutions, and with dry sodium chloride given by mouth.
It seems evident that sodium chloride has a specific action in preventing and possibly in controlling the changes produced by the toxic body.
Sodium chloride is a valuable therapeutic agent in pyloric and high intestinal obstruction.