Palliative Care of Stroke Patients.

Critical care clinicians frequently care for patients with acute brain injury, such as stroke. Regardless of the severity of the neurologic insult, these patients have life-altering deficits that threaten their personal identity and quality of life. The sudden nature of the injury often means that there has been little discussion between patients and their families about life-sustaining treatments, and most patients are unable to speak for themselves because of impaired cognition and communication. Thus, individuals experiencing stroke and their families present clinicians with unique and complex care needs in the acute care setting. Key professional organizations have endorsed the early integration of palliative care into the treatment of patients with stroke and devastating neurologic injury. Implementing interdisciplinary primary or specialty palliative care helps clinicians adopt a patient-centered approach to care and aids in decision-making.

Choosing the Correct "-ase" in Acute Ischemic Stroke: Alteplase, Tenecteplase, and Reteplase.

Alteplase is a tissue plasminogen activator approved for treating acute ischemic stroke (AIS), acute myocardial infarction (AMI), and acute massive pulmonary embolism. Two additional tissue plasminogen activators, tenecteplase and reteplase, are also approved for AMI treatment. However, neither tenecteplase nor reteplase is approved for AIS treatment. The U.S. Food and Drug Administration has received reports of accidental administration of tenecteplase or reteplase instead of alteplase in patients with AIS, which can lead to potential overdose. Primary factors contributing to medication errors include use of the abbreviations "TPA," "tPA," or "TNK" in written or verbal orders and use of these agents in similar settings. Steps to reduce the likelihood of accidental substitution include use of full brand or generic names and inclusion of the indication in written and verbal orders, addition of alerts in automated dispensing machines and ordering systems, and use of stroke boxes containing alteplase and materials for administration.

Physiological evaluation of the severity of pancreatic exocrine dysfunction during endoscopy.

OBJECTIVES: Despite the advances in pancreatic imaging, there continues to be a need to measure exocrine function to determine which patient requires enzyme supplementation. To evaluate the potential use of a rapid endoscopic test that can be conducted by nonacademic centers, we investigated whether concentration of trypsin in food-stimulated secretion is related to trypsin synthesis and secretion. METHODS: Subjects include 22 chronic pancreatitis patients (10 mild, 5 moderate, and 7 severe radiological disease) and 11 healthy controls. During upper gastrointestinal endoscopy, pancreatic secretion was stimulated by a single 30-mL duodenal injection of an enteral diet, followed 5 minutes later by periampullary juice aspiration (endoscopic pancreatic function test [ePFT]). This was followed by a conventional 2-hour marker-perfusion diet-stimulated pancreatic trypsin secretion and synthesis study (2-hour PFT [2hPFT]). RESULTS: Severity of radiological disease was associated with a progressive loss of enzyme secretion measured by the 2hPFT. The endoscopic PFT correlated positively with 2hPFT (r2 = 0.48; P < 0.0001) and an activity of less than 5% of the average normal had a 96% specificity and 75% sensitivity for the detection of pancreatic insufficiency as defined by a loss of greater than 90% of pancreatic secretion. CONCLUSIONS: The diagnostic power of endoscopy may be enhanced by the collection of a pancreatic juice sample after enteral feed stimulation because measurement of the trypsin content will identify chronic pancreatitis patients who will be benefited by enzyme supplementation.

Recurrent flares of pancreatitis predict development of exocrine insufficiency in chronic pancreatitis.

BACKGROUND & AIMS: The natural history of specific morphologic stages of chronic pancreatitis (CP) is not well defined. The aim of this study was to determine if worsening morphologic stages of CP are associated with poorer clinical outcomes. METHODS: A retrospective analysis of 159 subjects with CP was performed. The baseline stage of CP was categorized according to the Cambridge classification. Pain was categorized as type A (intermittent acute), B (continuous), or combined. Exocrine failure was defined by steatorrhea; endocrine failure was characterized as diabetes mellitus. Complications were defined clinically. RESULTS: Pancreatic duct (PD) morphology was equivocal in 37.1%, minimal in 12.6%, moderate in 7.5%, and severe in 42.8% of the patients. Over a median follow-up period of 3.7 years, the risk of developing exocrine insufficiency and diabetes was 28% and 19%, respectively. Recurrent acute flares of pancreatitis predicted the development of exocrine insufficiency (P = .004). Severe PD morphology predicted the likelihood of having persistent pain (P = .008). Patients with concurrent type A and B pain and older age at diagnosis had a greater likelihood of having persistent pain (P = .021). The risk of developing bile duct stricture was higher in the advanced morphologic stages of CP (P = .005). CONCLUSIONS: Recurrent flares of pancreatitis predispose to the development of exocrine insufficiency in CP. Patients with complex-type pain, older age at diagnosis, and advanced morphologic stage are more likely to have persistent pain. PD morphology does not correlate with the risk of developing exocrine failure and/or diabetes. Pain does not necessarily decrease or disappear with the onset of exocrine insufficiency and diabetes.

Trypsin secretion and turnover in patients with acute pancreatitis.

Studies in humans have shown that pancreatic enzyme secretion is reduced during acute pancreatitis. It is not known, however, whether the reduction is due to impaired synthesis or disruption of the secretory pathway. The rate of secretion and turnover of trypsin was measured in 12 patients with acute pancreatitis of variable etiology and severity (median Ranson's score 2.5, range 0-5, 4 with severe necrotizing disease) and eight healthy volunteers by 4-h primed/continuous intravenous infusions of 1-(13)C-labeled l-leucine, and collection of pancreatic secretions by duodenal perfusion and sampling. Trypsin secretion was reduced from 476 +/- 73 to 153 +/- 60 U/h (means +/- SE, P = 0.005) in acute pancreatitis, with the greatest reductions being observed in patients with necrotizing disease (32 +/- 7 U/h, P = 0.003). The time for newly labeled trypsin to first appear in digestive juice was not, however, delayed in pancreatitis patients (87.2 +/- 11.1 vs. 94.7 +/- 4.9 min); on the contrary, there was an early appearance of newly labeled trypsin at 30 min in patients with severe necrotizing pancreatitis (P < 0.05). Calculated zymogen pool turnover was unchanged, but pool size was decreased (P = 0.01). Despite low rates of luminal secretion, trypsin continues to be synthesized in patients with acute pancreatitis. Our findings could be explained by post-Golgi leakage of enzymes from acinar cells or by loss of synthetic function in some cells with preservation in others.

Nutrition in the management of necrotizing pancreatitis.

Comparative trials have shown that enteral feeding (EN) is better than total parenteral nutrition (TPN) in acute pancreatitis. However, the following case report of a 64-year-old man with necrotizing pancreatitis suggests that EN may cause complications in patients with ductular damage. In the second week, this patient with acute pancreatitis developed >50% pancreatic necrosis, resulting in gastroduodenal obstruction and pain, leading to the use of TPN. A trial of EN delivered past the obstruction was associated with increased abdominal pain, leukocytosis, and pancreatic fluid accumulation. Measurement of the pancreatic response to feeding showed a 90% reduction in enzyme secretion compared to healthy volunteers, but no change in the uptake of stable isotope labeled amino acids into secreted trypsin. This suggests that enzymes were being synthesized by the remaining pancreatic tissue, but that some of the secretions were leaking into the inflammatory mass. Symptoms resolved after reinstitution of TPN and bowel rest. A further trial of EN was successful when the tube was advanced to the distal jejunum to avoid pancreatic stimulation. After 3 weeks of home EN, he was readmitted for surgical evacuation of an infected fluid collection. Although enteral feeding is generally better than TPN in the nutritional management of acute pancreatitis, there may be a subgroup of patients with ductular damage due to necrotizing disease in whom TPN and pancreatic rest may be safer.