Use of Angiotensin II in Severe Vasoplegia After Left Pneumonectomy Requiring Cardiopulmonary Bypass: A Renin Response Analysis.

OBJECTIVE: Describe a case of post-pneumonectomy vasoplegia managed with angiotensin II. Plasma renin activity was measured at specific time intervals to describe the relationship between endogenous renin activity and exogenous angiotensin II supplementation. DESIGN: Case report. SETTING: Spectrum Health Cardiothoracic Critical Care Unit. PATIENTS: Fifty-seven-year-old male. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Plasma renin activity at five pre-determined time points. Angiotensin II caused a significant increase in mean arterial pressure and a rapid reduction in catecholamine vasopressor doses from 0.75 to 0.31 mcg/kg/min norepinephrine equivalents. Plasma renin activity drawn immediately before angiotensin II initiation was 40 ng/mL/hr (normal, 0.6-3.0 ng/mL/hr) with resultant drop to 22 and 12 ng/mL/hr at 2 and 6 hours after angiotensin II initiation, respectively. The patient suffered no end-organ damage and achieved a positive outcome, discharging home on postoperative day 11. CONCLUSION: Exogenous angiotensin II reduced catecholamine vasopressor doses and had an apparent effect in reducing endogenous renin production in this case. Prospective research is warranted to determine the utility of angiotensin II and to better understand it effects on the dysfunctional renin-angiotensin-aldosterone system during vasoplegic shock.

Faster Transition From Intravenous to Oral Antihypertensives Associated With Improved Outcomes After Aortic Dissection.

Background: After stabilization with intravenous (IV) antihypertensives, the impact of speed-of-transition from IV to enteral (PO) medications in the intensive care unit (ICU) is unknown. Objective: To assess ICU length of stay (LOS) based on transition time from IV to PO antihypertensive therapy. Methods: Retrospective study of aortic dissection patients admitted from June 2013 to July 2017 at a tertiary teaching hospital. Patients were grouped based on achieving full transition to PO medications in either ≤72 hours or >72 hours from the first PO dose. Secondary end points included hospital LOS, IV infusion volume, medication cost, and time spent with arterial/central lines. Results: A total of 56 patients transitioned completely from IV to PO therapy in ≤72 hours, and 72 patients required more than 72 hours. Demographics, IV and PO medication choices, and timing of first PO medication administration were similar between groups. ICU LOS was shorter in the group transitioned in ≤72 hours compared with those who took longer to transition (3.6 vs 10.5 days; P < 0.001). Hospital LOS, IV infusion volume, and cost were also significantly lower in the ≤72-hour group (P < 0.001). The rapid transition group also spent less time with arterial lines (44 vs 156 hours, P < 0.001) and central lines (45 vs 242 hours, P < 0.001). Conclusion and Relevance: In this cohort, transitioning to PO antihypertensives in ≤72 hours was associated with shorter ICU LOS and improvement in other measured outcomes. These observational data are the first to describe a potentially critical juncture in postdissection care; a prospective study is warranted.

Valsartan Effective for Malignant Hypertension after Aortic Dissection with Renal Artery Involvement.

When aortic dissections extend to the renal arteries, reductions in renal blood flow can cause marked increases in renin production. The resultant rise in angiotensin II can lead to difficult-to-control blood pressure, despite normal postdissection antihypertensive agents. We highlight a case of a postdissection patient with malignant hypertension refractory to eight different enteral antihypertensives. Angiotensin-converting enzyme inhibitors and angiotensin receptor blockers had been held due to postoperative acute kidney injury. A single dose of valsartan, administered on day 12, produced a marked drop in blood pressure, alleviation of encephalopathy, and allowed for cancellation of a planned tracheostomy. A serum renin level was found to be 50 times the normal upper limit. In patients with aortic dissection and renal artery involvement, angiotensin-modifying agents may warrant earlier administration to combat this unique cause of hypertension.

Intravenous Chlorothiazide Versus Enteral Metolazone to Augment Loop Diuretic Therapy in the Intensive Care Unit.

BACKGROUND: In cases of loop diuretic resistance in the intensive care unit (ICU), recommendations for a specific second-line thiazide agent are lacking. OBJECTIVE: To compare the effects of intravenous chlorothiazide (CTZ) and enteral metolazone (MET) on urine output (UOP) when added to furosemide monotherapy therapy in critically ill adults. METHODS: This was a retrospective cohort study conducted in the medical, surgical, and cardiothoracic ICUs of a quaternary medical center. The primary outcome was change in UOP induced by the study interventions compared with furosemide alone. Secondary outcomes included onset of diuresis, eventual need for hemodialysis, and incidence of adverse events. RESULTS: A total of 122 patients (58 in CTZ, 64 in MET) were included. When added to furosemide monotherapy, CTZ induced a greater change in UOP at 24 hours compared with MET (2405 vs 1646 mL, respectively; P = 0.01). CTZ also caused a more rapid dieresis: 1463 mL total UOP in the first 6 hours compared with 796 mL in the MET group ( P < 0.01). There were no differences found regarding ICU length of stay, need for renal replacement therapy, or survival to discharge. The CTZ arm required more potassium supplementation to maintain normokalemia (median 100 vs 57 mEq in MET; P = 0.02) and carried a higher cost (mean $97 vs $8, P < 0.01). CONCLUSION: Both CTZ and MET induced significant increases in UOP. CTZ induced a greater and more rapid change and was associated with higher cost and greater need for potassium replacement. Randomized controlled trials are needed to establish whether a preferable thiazide diuretic exists in this setting.

Impact of Quetiapine Treatment on Duration of Hypoactive Delirium in Critically Ill Adults: A Retrospective Analysis.

STUDY OBJECTIVE: Because delirium remains a common consequence of critical illness, and reducing its duration has been shown to have a positive impact on patient outcomes during and after an intensive care unit (ICU) stay, we sought to determine whether treatment of hypoactive delirium with quetiapine reduces the duration of delirium compared with no pharmacologic treatment. DESIGN: Retrospective cohort study. SETTING: Three medical-surgical ICUs within the two main campuses of an academic tertiary care hospital system. PATIENTS: A total of 113 adults with documented hypoactive delirium during an ICU length of stay (LOS) of at least 72 hours between August 2013 and September 2014; 52 patients received at least one dose of quetiapine during their hypoactive delirium course, and 61 patients received no pharmacologic delirium treatment. MEASUREMENTS AND MAIN RESULTS: Patients were screened for hypoactive delirium using the Confusion Assessment Method-ICU (CAM-ICU) and the Richmond Agitation Sedation Scale (RASS). The primary outcome was time to first resolution of delirium, and secondary outcomes included ICU and hospital LOS, and duration of mechanical ventilation. To assess potential adverse effects of quetiapine, the number of RASS assessments deeper than goal and the total number of RASS assessments documented during the delirium course were recorded for all patients. Daily progress notes and discharge documentation were surveyed to assess for new onset of extrapyramidal symptoms or torsade de pointes. Median duration of hypoactive delirium was shorter in the quetiapine-treated group compared with the no-quetiapine group (1.5 vs 2.0 days, p=0.04), and time to extubation after screening positive for delirium trended favorably toward quetiapine-treated patients (3 vs 5 days, p=0.08). There were no significant differences in ICU or hospital LOS, and safety outcomes were similar between groups. CONCLUSION: In this mixed ICU population, treatment of hypoactive delirium with quetiapine was safe and reduced the duration of delirium compared with standard care alone. Prospective placebo-controlled studies are needed to further assess the role of antipsychotics in hypoactive delirium.

Diagnosis of exclusion: a case report of probable glatiramer acetate-induced eosinophilic myocarditis.

Importance. Medication-induced eosinophilia is an acknowledged, often self-limiting occurrence. Glatiramer acetate, a biologic injection used in the management of relapsing-remitting multiple sclerosis, is widely regarded as a safe and effective medication and lists eosinophilia as an infrequent side effect in its package insert. Contrary to reports of transient, benign drug-induced eosinophilia, we describe a case of probable glatiramer acetate-induced eosinophilia that ultimately culminated in respiratory distress, shock, and eosinophilic myocarditis. Observations. A 59-year-old female was admitted to the hospital after routine outpatient labs revealed leukocytosis (43,000 cells/mm(3)) with pronounced hypereosinophilia (63%). This patient had been using glatiramer acetate without complication for over 10 years prior to admission. Leukocytosis and hypereosinophilia persisted as a myriad of diagnostic evaluations returned negative, ultimately leading to respiratory depression, shock, and myocarditis. Glatiramer acetate was held for the first time on day 6 of the hospital stay with subsequent resolution of leukocytosis, hypereosinophilia, respiratory distress, and shock. Conclusions and Relevance. Glatiramer acetate was probably the cause of this observed hypereosinophilia and the resulting complications. Reports of glatiramer-induced eosinophilia are rare, and few case reports regarding medication-induced hypereosinophilia describe the severe systemic manifestations seen in this patient.

Early pharmacological treatment of delirium may reduce physical restraint use: a retrospective study.

INTRODUCTION: Evidence surrounding pharmacological treatment of delirium is limited. The negative impact of physical restraints on patient outcomes in the intensive care unit (ICU), however, is well published. The objective of this study was to evaluate whether initiating pharmacologic delirium treatment within 24 hours of a positive screen reduces the number of days in physical restraints and improves patient outcomes compared with delayed or no treatment. METHODS: Patients from a mixed ICU with a documented positive delirium score using the Intensive Care Delirium Screening Checklist were retrospectively grouped based on having received pharmacologic treatment within 24 hours of the first positive screen or not. Primary end points were number of days spent in physical restraints and time to extubation after delirium onset. Secondary end points included hospital and ICU length of stay (LOS) and survival to discharge. RESULTS: Two hundred intubated patients were either pharmacologically treated (n = 98) or not treated (n = 102) within 24 hours of the first positive delirium score. Patients receiving treatment spent a shorter median time in restraints compared with patients who were not treated (3 vs 6 days; P < .001), and had a shorter median time to extubation (3 vs 6.5 days; P < .001). The treatment group also experienced a shorter ICU LOS (9.5 vs 16 days; P < .001) and hospital LOS (14.5 vs 22 days; P < .001) compared with the no-treatment group. CONCLUSIONS: Delirious patients who received pharmacological treatment within 24 hours of the first positive screen spent fewer days in physical restraints and less time receiving mechanical ventilation compared with those who did not. Although delirium management is multifactorial, early pharmacological therapy may benefit patients diagnosed with delirium.