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Nicardipine extravasation treatment:
Definition Field Listing
Dihydropyridine calcium channel blockers can produce negative inotropic effects and exacerbate heart failure. Monitor heart failure patients carefully. 2018 Chiesi USA, Inc. All rights reserved. Created in the USA. 07/2018 PP‑CP‑0021 V3.0. IV: Use with caution; guidelines for dose adjustments not available; monitor and adjust as necessary. CLEVIPREX is not a beta-blocker, does not reduce heart rate, and gives no protection against the effects of abrupt beta-blocker withdrawal. Beta-blockers should be withdrawn only after a gradual reduction in dose. Note: Cardene SR has not been available in the US for more than a year. Defective lipid metabolism seen in conditions such as pathologic hyperlipemia, lipoid nephrosis, or acute pancreatitis if it is accompanied by hyperlipidemia; and. CARDENE I.V. (nicardipine hydrochloride) Premixed Injection is indicated for the short-term treatment of hypertension when oral therapy is not feasible or not desirable. For prolonged control of blood pressure, transfer patients to oral medication as soon as their clinical condition permits. (clevidipine) Prescribing Information. 2017. 6. Brevibloc [package insert]. Deerfield, IL: Baxter Healthcare Corporation; 2014. 7. Grillo P, Bruder N, Auquier P, et al. Esmolol blunts the cerebral blood flow velocity increase during emergence from anesthesia in neurosurgical patients. Anesth Analg. 2003;96(4):1145-1149. 8. Singh PP, Dimich I, Sampson I, Sonnenklar N. A comparison of esmolol and labetalol for the treatment of perioperative hypertension in geriatric ambulatory surgical patients. Can J Anaesth. 1992;39(6):559-562. 9. Ezri T, Szmuk P, Warters RD, et al. Changes in onset time of rocuronium in patients pretreated with ephedrine and esmolol–the role of cardiac output. Acta Anaesthesiol Scand. 2003;47(9):1067-1072. 10. Nitropress [package insert]. Bridgewater, NJ: Valeant Pharmaceuticals North America, LLC; 2015. 11. van Wezel HB, Koolen JJ, Visser CA, et al. Antihypertensive and anti-ischemic effects of nicardipine and nitroprusside in patients undergoing coronary artery bypass grafting. Amer J Cardiol. 1989;64:22H-27H. 12. van Wezel HB, Koolen JJ, Visser CA, et al. The efficacy of nicardipine and nitroprusside in preventing poststernotomy hypertension. J Cardiothorac Anesth. 1989;3(6):700-706. 13. Nitroglycerin Injection [package insert]. Shirley, NY: American Regent Laboratories, Inc; 2005. 14. Cooke CR, Wall BM, Huch KM, Mangold T. Cardiovascular effects of vasopressin following V 1 receptor blockade compared to effects of nitroglycerin. Am J Physiol Regul Integr Comp Physiol. 2001;281(3):R887-R893. 15. Loh E, Elkayam U, Cody R, et al. A randomized multicenter study comparing the efficacy and safety of intravenous milrinone and intravenous nitroglycerin in patients with advanced heart failure. J Card Fail. 2001;7(2):114-121. 16. Hydralazine hydrochloride [package insert]. Lake Forest, IL: Akorn Inc.; 2012. 17. Labetalol [package insert]. Bedford, OH: Bedford Laboratories; 2012. 18. Sladen RN, Klamerus KJ, Swafford MWG, et al. Labetalol for the control of elevated blood pressure following coronary art. PO dose: 40 mg q8hr; equivalent IV infusion: 2.2 mg/hr. Low rate of overshoot in acute severe hypertension patients in the VELOCITY trial 5. Defective lipid metabolism seen in conditions such as pathologic hyperlipemia, lipoid nephrosis, or acute pancreatitis if it is accompanied by hyperlipidemia; and. CLEVIPREX (clevidipine) is a dihydropyridine calcium channel blocker indicated for the reduction of blood pressure (BP) when oral therapy is not feasible or not desirable. There is no information to guide use of CLEVIPREX in treating hypertension associated with pheochromocytoma. Acute hypertensive emergencies may result from an abrupt increase in systemic vascular resistance (SVR). 2,3. 2018 Chiesi USA, Inc. All rights reserved. Created in the USA. PP-CI-0006 V5.0. PO dose: 20 mg q8hr; equivalent IV infusion: 0.5 mg/hr. IV: Use with caution; guidelines for dose adjustments not available; monitor and adjust as necessary. Allergies to soybeans, soy products, eggs, or egg products;. Start at 20 mg, and allow 3 days between dose increases to achieve steady-state plasma drug concentration; usual dosage range, 60-120 mg/day. CLEVIPREX (clevidipine) Injectable Emulsion is contraindicated in patients with:. Use with caution; initiate at low end of adult dosing range; monitor closely. CLEVIPREX is not a beta-blocker, does not reduce heart rate, and gives no protection against the effects of abrupt beta-blocker withdrawal. Beta-blockers should be withdrawn only after a gradual reduction in dose. . Second, the FUNC score (FUNCtional outcome risk stratification) predicts functional independence rather than mortality at 90-days (Table 2) 9). . While lowering blood pressure may reduce the risk of expansion, it may theoretically also reduce cerebral perfusion. One randomized clinical trial found that lowering systolic blood pressure to 140mmHg compared to 180mmHg reduced the risk of hematoma expansion but had no effect on outcomes 73). A is the largest hemorrhage diameter on the selected slice (in centimeters [cm]). B is the largest diameter perpendicular to A on the same slice. C is the approximate number of slices in which the hemorrhage is seen multiplied by the slice thickness (often 0.5cm slices). A, B, and C are then multiplied and the product divided by 2 [A x B x C/2]. . The steps to follow using this technique are: . The most common cause of intracranial hemorrhage is high blood pressure (hypertension). Since high blood pressure by itself often causes no symptoms, many people with intracranial hemorrhage are not aware that they have high blood pressure, or that it needs to be treated. Less common causes of intracranial hemorrhage include trauma, infections, tumors, blood clotting deficiencies, and abnormalities in blood vessels (such as arteriovenous malformations). Intracranial hemorrhage occurs at all ages. The average age is lower than for ischemic stroke. Less common than ischemic strokes, intracranial hemorrhage or hemorrhagic strokes make up about 12 percent of all strokes. . Despite the differences in clinical presentation between hemorrhagic and ischemic strokes, brain imaging is required to definitively diagnose intracerebral hemorrhage. CT Angiography (CTA) is gaining increasing acceptance as a diagnostic tool in the acute setting 64). , highlighting the critical importance of early and effective treatment in the emergency department. Death at 1 year for intracranial hemorrhage varies by location of intracranial hemorrhage: 51% for deep hemorrhage, 57% for lobar, 42% for cerebellar, and 65% for brain stem 6). Recommended Guidelines from the American Heart Association and American Stroke Association for Treating Elevated BP in Spontaneous intracranial hemorrhage. Spontaneous intracranial hemorrhage is a serious form of stroke which appears suddenly without warning, unlike ischemic strokes that are often preceded by a transient ischemic attack. Spontaneous intracranial hemorrhage accounts for 10-15% of stroke but it is one of the most disabling forms of stroke 1). . Intracranial hemorrhage refers to any bleeding within the intracranial vault, including the brain parenchyma and surrounding meningeal spaces 2). . Of the estimated 67,000 patients who had an intracranial hemorrhage in the United States during 2002, only 20% are expected to be functionally independent at 6 months 7). Noncontrast computerized tomography (CT) is the most rapid and readily available tool for the diagnosis of intracranial hemorrhage 62). . Intracranial hemorrhage remains the most devastating form of stroke with the 30-day mortality rate ranges from 35% to 52% with only 20% of survivors expected to have full functional recovery at 6 months 4). . MRI can also detect underlying secondary causes of intracranial hemorrhage such as tumor and hemorrhagic transformation of ischemic stroke. Finally, for patients with poor TEENney function or contrast allergies, the cerebral vasculature can be analyzed without contrast using Time-of-Flight MR angiography (MRA) 70). . Neurologic deficits are related to the site of parenchymal hemorrhage. Thus, ataxia is the initial deficit noted in cerebellar hemorrhage, whereas weakness may be the initial symptom with a basal ganglia hemorrhage. Early progression of neurologic deficits and decreased level of consciousness can be expected in 50% of patients with intracranial hemorrhage. The progression of neurological deficits in many patients with an intracranial hemorrhage is frequently due to ongoing bleeding and enlargement of the hematoma during the first few hours. Compared with patients with ischemic stroke, headache and vomiting at onset of symptoms is observed three times more often in patients with intracranial hemorrhage 61). Elevated blood pressure (BP) is common in the acute setting after an intracranial hemorrhage, and higher blood pressure levels are associated with hematoma expansion and poor prognosis. However, it is not clear that reducing blood pressure improves outcomes 72). If systolic blood pressure is >200 mm Hg or mean arterial pressure is >150 mm Hg, then consider aggressive reduction of blood pressure with continuous intravenous infusion, with frequent blood pressure monitoring every 5 min. If systolic blood pressure is >180 mm Hg or mean arterial pressure is >130 mm Hg and there is the possibility of elevated intracranial pressure, then consider monitoring intracranial pressure and reducing blood pressure using intermittent or continuous intravenous medications while maintaining a cerebral perfusion pressure≥60 mm Hg. If systolic blood pressure is >180 mm Hg or mean arterial pressure is >130 mm Hg and there is no evidence of elevated intracranial pressure, then consider a modest reduction of blood pressure (e.g., mean arterial pressure of 110 mm Hg or target blood pressure of 160/90 mm Hg) using intermittent or continuous intravenous medications to control blood pressure and clinically reexamine the patient every 15 min. Recommendations from European Stroke Initiative for blood pressure management in intracranial hemorrhage. . The imaging characteristics of intracranial hemorrhage vary with time as the hemoglobin passes through different stages during the pathological process. In the acute phase, gradient recalled-echo (GRE) imaging techniques with T2*weighting are the best option to detect the presence of intracranial hemorrhage 69). The classic presentation of intracranial hemorrhage is sudden onset of a focal or generalized neurological deficit that progresses over minutes to hours with accompanying headache, nausea, vomiting, decreased consciousness, and elevated blood pressure. The acute presentation of intracranial hemorrhage can be difficult to distinguish from ischemic stroke. Additional symptom may include seizures. Findings such as coma, headache, vomiting, seizures, neck stiffness and raised diastolic blood pressure increase the likelihood of intracranial hemorrhage compared to ischemic stroke, but only neuroimaging can provide a definitive diagnosis 60). Recommended Guidelines from the American Heart Association and American Stroke Association for Treating Elevated BP in Spontaneous intracranial hemorrhage. Patients with intracranial hemorrhage are often unable to protect the airway. Endotracheal intubation may be necessary but this decision should be balanced against the risk of losing the neurologic examination. Rapid sequence intubation is typically the preferred approach in the acute setting. Pretreatment with lidocaine may be considered as it may blunt a rise in intracranial pressure (ICP) associated with intubation. Paralytic agents include succinylcholine, rocuronium or vecuronium, and for postintubation sedation, propofol is a reasonable choice given its short half-life 71).