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Monographs of Topical Drugs that Have Caused Contact Allergy/Allergic Contact Dermatitis
Published in Anton C. de Groot, Monographs in Contact Allergy, 2021
Diltiazem is a benzothiazepine calcium channel blocking agent and vasodilator, which is used in the management of angina pectoris and hypertension. Topical diltiazem creams are used to treat anal fissures and Raynaud’s syndrome. They are antipruritic and relieve ischemia by relaxing the muscles (anal sphincter in the case of fissures) and dilating small blood vessels in the affected areas of skin and mucosa (9). In pharmaceutical products, diltiazem is employed as diltiazem hydrochloride (CAS number 33286-22-5, EC number 251-443-3, molecular formula C22H27ClN2O4S) (1).
Introduction to the clinical stations
Published in Sukhpreet Singh Dubb, Core Surgical Training Interviews, 2020
I would first ensure that the patient was made comfortable with appropriate analgesic. Following this, I would offer conservative treatment first which would include a high fibre diet and elevated fluid intake. I would recommend sitz baths as well as stool softeners. For topical analgesic, I would offer GTN but avoid it for pregnant or lactating patients. I would warn the patient about headaches with this therapy and recommend paracetamol which is often helpful. Diltiazem is an alternative if headaches do not abate.
Dermatomyositis and its associated complications
Published in Biju Vasudevan, Rajesh Verma, Dermatological Emergencies, 2019
Iffat Hassan Shah, Saniya Akhtar
Calcinosis cutis is a troublesome complication of severe DM with poor response to treatment, although spontaneous improvement can occur. Diltiazem has been used successfully [69]. Surgical excision is another option. Table 42.7 summarizes the treatment strategy in specific situations seen in DM.
Pathobiology and evolving therapies of coronary artery vasospasm
Published in Baylor University Medical Center Proceedings, 2021
Monish A. Sheth, Robert J. Widmer, Hari K. Dandapantula
Calcium channel blockers are the main line of therapy in patients with CAV. It is recommended to start with a low dose and titrate upwards while watching for the side effects of hypotension, bradycardia, and heart block. Based on their relative affinities for arterial smooth muscle and myocardium, CCBs may be classified into the following groups38: dihydropyridines (drug name ends in “pine”), which are relatively selective for arteries; non-dihydropyridines, which include diltiazem (benzothiazepines), which possess equally potent myocardial and arterial effects; and verapamil (phenylalkylamines), which predominantly affect the myocardium. By having both cardiac depressant and vasodilator actions, diltiazem can reduce arterial pressure without producing the same degree of reflex cardiac stimulation caused by dihydropyridines. Nifedipine is mainly used in acute attacks and recurrent attacks, being a rapid-acting first-generation CCB. Amlodipine, because of its longer half-life and experimental evidence suggesting that it may also bind to non-dihydropyridine binding sites, is used for prophylaxis of CAV.39
Anticoagulation strategy in patients with atrial fibrillation after carotid endarterectomy
Published in Acta Chirurgica Belgica, 2019
Murat Ugurlucan, Hakki Tankut Akay, Ibrahim Erdinc, Didem Melis Oztas, Cenk Conkbayir, Erdal Aslim, Cenk Eray Yildiz, Kubilay Aydin, Ufuk Alpagut
The operations were performed with deep or superficial regional anesthesia. Superficial cervical block was performed with the injection of 10 cc bupivacaine 0.05%, 6 cc lidocaine 2% and 4 cc saline combination along the lateral border of the sternocleidomastoid muscle subcutaneously. Deep cervical plexus block was performed at the level of the transverse processes of cervical vertebrae C2, C3, and C4. A combination of lidocaine hydrochloride and bupivacaine hydrochloride was injected after negative aspiration result for blood. A total amount of bupivacaine hydrochloride 2–3 mg/kg was allowed. Additional prilocaine hydrochloride was used subcutaneously at the incision line as infiltration anesthesia. Additional doses of prilocaine hydrochloride were injected intraoperatively if the patient complained of pain during the procedure. The allowed total dose of prilocaine was 5 mg/kg. Intraoperative remifentanil (0.025–0.05 mg/kg/min) maintained an adequate level of comfort, responsiveness, and cooperation. Continuous infusion of nitroglycerin was used for blood pressure control. Additional diltiazem or metoprolol was administered if needed. After de-clamping occasionally midazolam was given. Systemic heparin (100 IU/kg) was injected before clamping and was not antagonized after the procedure. A shunt was selectively used in the case of neurologic deterioration at cross-clamping test at duration of 2–3 min.
High-dose intravenous lipid emulsion affecting successful initiation of continuous venovenous hemofiltration and extracorporeal membrane oxygenation
Published in Clinical Toxicology, 2018
Jonathan H. Sin, Andrew Tom, Alexander Toyoda, Nathalie Roy, Bryan D. Hayes
An unidentified middle-aged female suffered a pulseless electrical activity (PEA) arrest after presumably ingesting unknown amounts of diltiazem extended-release, digoxin, and alprazolam. Toxicology results were notable for a serum digoxin concentration of 4.8 ng/mL (reference range: 0.9–2 ng/mL) and alprazolam concentration of 1084 mcg/L (reference range: 19–55 mcg/L). A qualitative toxicology analysis confirmed the presence of diltiazem in the serum, but a diltiazem concentration was not performed. The patient received calcium chloride 2 g, glucagon 3 mg, antidigitalis antibody fragments 400 mg, and hyperinsulinemia-euglycemia therapy with a regular insulin bolus of 80 units (1 unit/kg), followed by an infusion of 80 units/hr (1 unit/kg/hr). Despite another calcium chloride 2 g bolus and uptitration of the insulin to 180 units/hr (2.25 units/kg/hr), the patient remained in presumed toxin-induced cardiogenic shock, prompting a 20% intravenous lipid emulsion (ILE) bolus of 120 mL (1.5 mL/kg), followed by an infusion of 20 mL/min (0.25 mL/kg/min). Even after the ILE bolus and the initiation of the infusion, vasopressor/inotrope requirements continued to escalate rapidly in order to maintain a mean arterial pressure >65 mmHg. Due to the concern that diltiazem extended-release was still being enterally absorbed, it was an informed decision to continue the ILE infusion after assessing the risk-versus-benefit profile. The infusion was maintained at 20 mL/min (0.25 mL/kg/min) for a total of 3.5 hours. The patient received an estimated total of 4200 mL (52.5 mL/kg) of 20% ILE, which correlated to ∼850 g of lipid.