Fromm D

Secretory state of gastric mucosa and resistance to injury by exogenous acid

The capacity of the stomach to resist the effects of highly acid solutions was assessed by comparing the effects of such solutions on spontaneously secreting, stimulated, and inhibited gastric mucosae of rabbits in vivo and frogs in vitro. Exposure of unstimulated resting mucosa to HC1, 120 mM, for 60 minutes produced superficial erosions in all rabbits, whereas such lesions were observed in only one of ten animals stimulated with histamine. Metiamide obviated the protective effect of histamine against ulcerations even though it did not reduce H+ secretion to zero. Exposure of inhibited isolated frog fundic mucosa to HC1 resulted in significant deterioration of electrical parameters, suggesting impairment of active transport processes and increased tissue permeability. These data are consistent with the hypothesis that actively secreting gastric mucosae from two species resist injury to exogenous acid more effectively than do resting or inhibited tissues, perhaps in part as a result of a greater alkaline tide.

Anastomotic dehiscence after low anterior resection of the rectum

Thirty-two patients who had anastomoses to the extraperitoneal rectum underwent radiographic contrast studies about two weeks after operation in order to determine the incidence of anastomotic dehiscence. No extravasation occurred in the sixteen anastomoses in which the middle hemorrhoidal arteries were intact, but partial disruption occurred in four of seventeen (24%) anastomoses in which the middle hemorrhoidal arteries were sacrificed. Since not all patients with anastomotic dehiscence after low anterior resection are symptomatic, the incidence of anastomotic breakdown will be under-estimated unless x-ray studies are performed. More data are required for a better understanding of the technical features of operation which will reduce the incidence of leakage from anastomoses to the extraperitoneal rectum.

Recognition of adrenal insufficiency in the postoperative patient

The signs and symptoms of adrenal insufficiency in the postoperative patient are generally nonspecific, and the diagnosis is usually made at postmortem examination. Two patients in whom adrenal insufficiency developed in the postoperative period are reported on (one had metastatic carcinoma to the adrenal glands and in the other bilateral adrenal hemorrhage developed during anticoagulant treatment). Both patients survived multiple, successive stressful episodes before the diagnosis of adrenal insufficiency was established by the alpha1-24 corticotropin stimulation test.

Mechanism of the Inhibitory Action of Electric Current on H+ Secretion by Frog Gastric Mucosa

The mechanism of the inhibitory action of electric current on gastric H+ secretion was studied using isolated frog gastric mucosa. Electric current, 500 μA/cm2, passed from mucosa to serosa (mucoso positive with respect to serosa), reversibly inhibited net H+ secretion, leading to complete cessation of luminal H+ appearance usually within 1 hr. The decrease in luminal H+ appearance was associated with an almost equal decrease in serosal HCO3− appearance. This is consistent with the suggestion that the inhibition of net H+ secretion was due to decrease in active H+ transport rather than to passive electrochemical back flux of the secreted H+ from the luminal bathing solution. Ultrastructural analysis of the tissues supported this view by demonstrating conversion of oxyntic cells into the resting (nonsecreting) morphologic configuration during the passage of current. Blocking of the conductive pathways for K+ in the nutrient (serosal) cell membrane by adding Ba++ to the serosal bathing solution significantly opposed the inhibitory action of electric current on H+ secretion. When electric current was passed through a mucosal solution containing a high concentration of K+, slight stimulation rather than inhibition of active H+ transport occurred (as judged from serosal HCO3− appearance). In this circumstance, the oxyntic cells retained their active secretory configuration despite the opposing current. The data indicate that electric current, passed from mucosa to serosa, inhibits active H+ transport by oxyntic cells. The data also suggest that the inhibitory action of an opposing current may be accomplished by electrolytic removal of K+ from an intracellular compartment essential for the function of the H+ secretory pump.

Postoperative clostridial sepsis of the abdominal wall

Abstract 1. 1. The diagnosis of clostridial sepsis after abdominal operation is difficult prior to the development of signs and wound infection. Hypotension, fever, tachycardia out of proportion to the fever, jaundice, renal failure, or mental changes may precede signs of wound infection. 2. 2. A review of the literature reveals that the average time between operation and the first indication of wound infection was twenty-four to forty-eight hours (ranging from four hours to eighteen days). The over-all mortality of clostridial infection of the abdominal wall is 60 per cent; in the presence of peritonitis (20 to 36 per cent of cases) the mortality is 86 per cent. 3. 3. Wound crepitus is a late sign not essential for the diagnosis of clostridial sepsis. 4. 4. A high index of suspicion is required to make the diagnosis of clostridial sepsis before obvious signs of wound infection occur. Once the diagnosis is suspected, the wound must be opened and inspected and material obtained for gram stain and culture. 5. 5. Despite reluctance to undertake unnecessary radical excision of a wound, treatment must be instituted rapidly if the clinical picture is compatible with the diagnosis and if organisms resembling Clostridia are present on gram stain. Treatment should consist of antibiotics and radical debridement with or without hyperbaric oxygen therapy.

Gastric mucosal defense mechanisms: Effects of salicylate and histamine

Some of the recent concepts about the gastric mucosal defense mechanisms against damage by luminal acid and the effects of histamine and salicylate on these mechanisms are reviewed. The mucosal barrier to acid appears to consist of at least two physiologic components: a permeability mechanism and a metabolic mechanism related to cellular bicarbonate production as a result of acid secretion. In the absence of salicylate, histamine appears to exert some protection by affecting both mechanisms, but in the presence of salicylate, histamines protective effect is limited to altering mucosal permeability. The actions of salicylate on the gastric mucosa are complex, related in part to the concentration of salicylate and the pH of the luminal fluid. The damaging effects of salicylate appear to be related more to the concentration of acid in the lumen than to the lipid solubility of the drug. Salicylate increases permeability regardless of pH; the increase is initially selective for cations and subsequently becomes nonselective, involving both cations and anions. Although both low and high concentrations of salicylate increase mucosal permeability to hydrogen ions, only high concentrations of salicylate affect cellular bicarbonate production.

Pseudo-Crohn's disease

Fistulization and abscess formation are hallmarks of Crohn’s disease. It is axiomatic that the development of these complications in patients previously operated on represents prima facie evidence of recurrence of inflammatory bowel disease. Many investigators have demonstrated that Crohn’s disease has a high incidence of recurrence after operation, especially if patients are followed up for ten to fifteen years [I]. Despite the frequency of recurrence, most patients with Crohn’s disease ultimately require operation for complications of the disease and for chronic invalidism [2], a position justified by the long symptom-free intervals produced by surgical therapy 131. Because of the complications of the primary disease such as abscess and fistula, postoperative morbidity tends to be higher in these difficult cases than in other types of uncomplicated intestinal operations. We have encountered ten patients during the past eight years in whom postoperative complications masqueraded as recurrent Crohn’s disease. In many instances morbidity was prolonged for months or years because the symptoms were falsely attributed to recurrent disease. Correction of the complication usually led to complete rehabilitation of the patient.