Delayed emesis following anticancer chemotherapy.

As the control of acute chemotherapy-induced emesis has improved, delayed emesis (occurring 24 h or more after treatment) has become the most bothersome vomiting problem. Delayed vomiting occurs after treatment with many anticancer drugs, but has been most often studied following cisplatin or combinations of cyclophosphamide and anthracyclines. The mechanism of this phenomenon is unknown. Empirical trials of antiemetic agents effective in controlling acute emesis identified the combination of metoclopramide and dexamethasone as useful in lessening delayed emesis after displatin in a randomized, placebo-controlled study. The specific serotonin receptor (5-HT3) antagonist ondansetron yielded results equivalent to the prior placebo results in a phase II trial using identical methodology in similar patients given cisplatin. Following anthracycline and cyclophosphamide combination chemotherapy, the delayed vomiting prevention observed with dexamethasone alone exceeds that of ondansetron. These observations suggest that delayed emesis is primarily mediated by neurotransmitters other than serotonin. Since delayed emesis occurs more frequently in patients who experience nausea and vomiting on the day they receive chemotherapy, tested combination antiemetic regimens, employing a 5-HT3 antagonist (either granisetron, metoclopramide, ondansetron or tropisetron), dexamethasone, and a benzodiazepine (lorazepam and alprazolam) should be routinely employed. This approach provides the best protection for acute and delayed emesis. Further research, looking beyond the specific 5-HT3 antagonists, provides the best strategy to improve the control of delayed symptoms.

The Yankton Model Program.

Changes in medical education towards a student-centered, problem-based learning, with continuity care experience in ambulatory settings have been recommended. The University of South Dakota School of Medicine has developed such an educational model for third year medical students named the Yankton Model Program and is herein described.

The diagnosis and prevalence of subclinical hepatic encephalopathy in apparently healthy, ambulant, non-shunted patients with cirrhosis.

Thirty-seven patients, all with histologic evidence of cirrhosis and with a normal neurological examination and normal mental status were evaluated by psychometric testing for subclinical hepatic encephalopathy. They were all regarded as having well compensated cirrhosis, not requiring any treatment or dietary restrictions and they were working, and many of them driving. A group of 19 patients with a history of alcoholism, or medical disorders, but without clinical or biochemical evidence of cirrhosis, served as controls. They were matched by age, sex, education, and alcohol consumption. Investigations performed were an EEG, fasting arterial ammonia, liver biochemical tests and a series of verbal and performance psychometric tests. The EEG was abnormal in 3 (8.3%) of patients, the ammonia elevated in 17 (45.9%) of patients and 26 patients (70.3%) failed 2 or more psychometric tests, as compared to 2 (10.5%) of the control group. It is concluded that 2 out of 3 patients with stable, well compensated cirrhosis were suffering from subclinical hepatic encephalopathy and that impairment of performance rather than verbal skills occurred. The digital symbol test, trail test (number connection test) and block design tests readily identified the patients with subclinical hepatic encephalopathy. The implication of these observations in patients with cirrhosis, especially those working in mechanical or skilled occupations, needs consideration.