Gastric feeding intolerance in critically ill patients during sustained pharmacologic neuromuscular blockade.

BACKGROUND: The purpose of this study was to assess gastric feeding intolerance for critically ill patients who received sustained neuromuscular blocker (NMB) pharmacotherapy. METHODS: Adult patients (>17 years of age) admitted to the trauma intensive care unit who received continuous intravenous NMB pharmacotherapy (rocuronium, cisatracurium, vecuronium, or pancuronium) for ≥48 h during continuous intragastric enteral nutrition (EN) were retrospectively evaluated. Gastric feeding intolerance was defined by initiation of a prokinetic agent (metoclopramide, erythromycin, or both) for an elevated gastric residual volume (GRV) >300 ml and with distention of the abdomen by physical examination, observation of regurgitation or emesis, temporary discontinuation of EN with low intermittent gastric suctioning, or initiation of parenteral nutrition (PN). Patients were evaluated for gastric feeding intolerance for the first 3 days of combined EN and NMB pharmacotherapy. A P value < 0.05 was considered statistically significant. RESULTS: Ten patients of the 47 patients (21%) were intolerant to EN during NMB pharmacotherapy. No statistically or clinically relevant differences in patient characteristics were found between patients who tolerated EN vs those who experienced gastric feeding intolerance, except for a higher median maximum GRV of 125 ml (28, 200) vs 300 (250, 400) ml, respectively (P < 0.001). Five patients responded to prokinetic therapy and five required PN. CONCLUSION: Most patients tolerated intragastric EN during sustained NMB pharmacotherapy. Presence of NMB pharmacotherapy is not an absolute contraindication for EN.

Reduction in Hypercalcemia Following Readjustment of Target Serum 25-Hydroxy Vitamin D Concentration during Cholecalciferol Therapy in Vitamin D-Deficient Critically Ill Patients.

The intent of this study was an evaluation of our effort to reduce the incidence of hypercalcemia in critically ill vitamin D-deficient patients with multiple traumatic injuries given cholecalciferol. Vitamin D deficiency was defined as a serum 25-hydroxy vitamin D concentration (25-OH vit D) of <20 ng/mL. Adult patients (>17 years of age) were given 10,000 IU of cholecalciferol daily with an intended target 25-OH vit D of >19.9 ng/mL. These patients were compared to a historical control group that underwent therapy with a higher target of >29.9 ng/mL. Patients received cholecalciferol via the feeding tube along with enteral nutrition (EN) until the target 25-OH vit D was achieved, EN discontinued, the nutrition support service signed off the patient, or the patient was discharged from the TICU. Patients were included if two consecutive weekly 25-OH vit D were measured. One hundred and three critically ill trauma patients were retrospectively studied. Fifty were given cholecalciferol therapy with the new lower target 25-OH vit D, and 53 were from a historical cohort aiming for the higher target. Hypercalcemia (serum ionized calcium concentration > 1.32 mmol/L) was reduced from 40% (21 out of 53 patients) to 4% (2 out of 50 patients; p < 0.001). None of the hypercalcemic patients were symptomatic. Readjustment of target 25-OH vit D concentration resulted in a ten-fold decrease in the rate of hypercalcemia and improved the safety of cholecalciferol therapy for critically ill patients with traumatic injuries.

Hypercalcemia Without Hypervitaminosis D During Cholecalciferol Supplementation in Critically Ill Patients.

BACKGROUND: Vitamin D deficiency during critical illness has been associated with worsened outcomes. Because most critically ill patients with severe traumatic injuries are vitamin D deficient, we investigated the efficacy and safety of cholecalciferol therapy for these patients. METHODS: Fifty-three patients (>17 years of age) admitted to the trauma intensive care unit who had a serum 25-hydroxy vitamin D (25-OH vit D) concentration <20 ng/mL were given 10,000 IU of cholecalciferol daily. Efficacy was defined as achievement of a 25-OH vit D of 30-79.9 ng/mL. Safety was evaluated by the presence of hypercalcemia (serum ionized calcium [iCa] >1.32 mmol/L) or hypervitaminosis D (25-OH vit D >79.9 nmol/L). Patients were monitored for 2 weeks during cholecalciferol therapy. RESULTS: Twenty-four patients (45%) achieved target 25-OH vit D. No patients experienced hypervitaminosis D. Hypercalcemia occurred in 40% (n = 21) of patients; 2 patients experienced an iCa >1.49 nmol/L. 25-OH vit D was significantly greater for those who developed hypercalcemia (37.2 + 11.2 vs 28.4 + 5.6 ng/mL, respectively, P < 0.001) by the second week of cholecalciferol. Of 24 patients who achieved target 25-OH vit D, 14 (58%) experienced hypercalcemia in contrast to 24% of patients (7 out of 29) who did not achieve target 25-OH vit D (P = 0.024). CONCLUSIONS: Cholecalciferol normalized serum 25-OH vit D concentrations in less than half of patients yet was associated with a substantial proportion of patients with hypercalcemia without hypervitaminosis D.

Obesity attenuates serum 25-hydroxyvitamin D response to cholecalciferol therapy in critically ill patients.

OBJECTIVES: The presence of obesity may confound cholecalciferol dosing in vitamin D-deficient patients owing to potentially decreased bioavailability. The aim of this retrospective study was to evaluate cholecalciferol therapy in vitamin D-deficient, critically ill trauma patients with and without obesity. METHODS: Adult patients with severe traumatic injuries who had a serum 25-hydroxyvitamin D (25-OH vit D) <50nmol/L were prescribed 10 000 IU of liquid cholecalciferol daily. Efficacy was defined as achievement of a 25-OH vit D of 75 to 200nmol/L. Safety was evaluated by the presence of hypercalcemia (serum ionized calcium >1.32 mmol/L). Fifty-three patients (18 obese, 35 non-obese) were identified for study. RESULTS: Despite similar baseline concentrations (36 ± 7 versus 37 ± 7 nmol/L; P = NS), 25-OH vit D response was attenuated for those with obesity after 1 and 2 wk of cholecalciferol therapy (51 ± 18 versus 66 ± 27nmol/L, P < 0.01; 68 ± 19 versus 92 ± 25nmol/L, P < 0.01, respectively). Patients with obesity also tended to experience less hypercalcemia (22% versus 49% of patients, respectively) post-cholecalciferol therapy. CONCLUSION: Obesity alters the response to cholecalciferol therapy in critically ill patients with severe traumatic injuries.

Life-threatening ACE inhibitor-induced angioedema after eleven years on lisinopril.

Angiotensin-converting enzyme inhibitors (ACE-Is) are the primary medication class implicated in drug-associated angioedema. Angioedema is most common early in ACE-I therapy, yet episodes can occur late in therapy and have been reported even as late as 10 years after single treatment initiation. We present a case of a 65-year-old African American woman who experienced 2 episodes of angioedema, with the second being life threatening after receiving several concomitant agents known to cause angioedema, most notably lisinopril for 11 years.