Hartmann's gallbladder pouch revisited 60 years later.

BACKGROUND: Hartmann's gallbladder pouch was the subject of an article in The Lancet 60 years ago. It has regained new interest in view of laparoscopic cholecystectomy. However, different opinions exist with regard to its incidence and nature. To elucidate these discrepancies, a descriptive study was performed with regard to the incidence and morphology of Hartmann's pouch. METHODS: Gallbladders were obtained after elective laparoscopic cholecystectomy. In addition, gallbladders were obtained during routine postmortem examination. The gallbladders were divided in two groups: those with Hartmann's pouch and those without Hartmann's pouch. All the gallbladders were examined macroscopically and microscopically. Fisher's Exact Probability Test (p < 0.05, two-tailed) was used to analyze the data. RESULTS: A total of 98 gallbladders were examined: 49 obtained after laparoscopic or open cholecystectomy and 49 obtained after postmortem examination. Among the gallbladders with Hartmann's pouch (n = 51), 65% contained stones and 35% had no stones. Among the gallbladders without Hartmann's pouch, 43% contained stones and 57% had no stones. Macroscopically, in all the gallbladders with Hartmann's pouch, the pouch was observed to result from adhesions between the cystic duct and the neck of the gallbladder. After cleavage of these adhesions, the phenomenon of Hartmann's pouch was abolished in all cases. CONCLUSIONS: Hartmann's gallbladder pouch is a frequent but inconstant feature of normal and pathologic human gallbladders. There is a significant association between the presence of Hartmann's pouch and stones (p < 0.05). Adhesions between the cystic duct and the neck of the gallbladder are responsible for Hartmann's pouch. Consequently, Hartmann's gallbladder pouch is a morphologic rather than an anatomic entity.

Endocrine and metabolic responses in children with meningoccocal sepsis: striking differences between survivors and nonsurvivors.

To get insight in the endocrine and metabolic responses in children with meningococcal sepsis 26 children were studied the first 48 h after admission. On admission there was a significant difference in cortisol/ACTH levels between nonsurvivors (n = 8) and survivors (n = 18). Nonsurvivors showed an inadequate cortisol stress response in combination to very high ACTH levels, whereas survivors showed a normal stress response with significantly higher cortisol levels (0.62 vs. 0.89 micromol/L) in combination with moderately increased ACTH levels (1234 vs. 231 ng/L). Furthermore, there was a significant difference between nonsurvivors and survivors regarding pediatric risk of mortality score (31 vs. 17), TSH (0.97 vs. 0.29 mE/L), T3 (0.53 vs. 0.38 nmol/L), reverse T3 (rT3) (0.75 vs. 1.44 nmol/L), C-reactive protein (34 vs. 78 mg/L), nonesterified fatty acids (0.32 vs. 0.95 mmol/L), and lactate (7.3 vs. 3.2 mmol/L). In those who survived, the most important changes within 48 h were seen in a normalization of cortisol and ACTH levels, but without a circadian rhythm; a decrease of rT3 and an increase in the T3/rT3 ratio; and a decrease in the levels of the nonesterified free fatty acids and an unaltered high urinary nitrogen excretion. At this moment, it is yet unknown whether the hormonal abnormalities are determining factors in the outcome of acute meningococcal sepsis or merely represent secondary effects. Understanding the metabolic and endocrine alterations is required to design possible therapeutic approaches. The striking difference between nonsurvivors and survivors calls for reconsideration of corticosteroid treatment in children with meningococcal sepsis.