phentolamine
Regulatory sources consulted
Approved indications
- OraVerse: reversal of soft-tissue anesthesia of the lip and tongue and associated functional deficits after intraoral submucosal injection of a local anesthetic containing a vasoconstrictor, in adults and children aged 3 years and older.
- Ryzumvi: treatment of pharmacologically induced mydriasis produced by adrenergic agonists such as phenylephrine or parasympatholytic agents such as tropicamide.
Contraindications
Absolute
- OraVerse: hypersensitivity to phentolamine or any formulation component.
Clinical warnings
- Major warning · Parenteral phentolamine has been associated with marked hypotension or shock-like states, myocardial infarction, cerebrovascular spasm or occlusion, tachycardia, and arrhythmias; monitor patients with cardiovascular history carefully, although these effects are uncommon with OraVerse. — openFDA OraVerse set_id 4025cf98-ea87-4531-b0fc-6283c84f63f3
Adverse events
Common (≥1%)
OraVerse: injection-site pain (5%) · Ryzumvi: instillation-site discomfort (16%) · Ryzumvi: conjunctival hyperemia (12%) · Ryzumvi: dysgeusia (6%)
Rare but serious
Acute or prolonged hypotension · Cardiac arrhythmias · Myocardial infarction · Cerebrovascular spasm or occlusion
Pregnancy and lactation
FDA category: C
OraVerse: adequate pregnancy data are unavailable; animal studies showed skeletal immaturity, decreased growth, and lower implantation at high exposures, without malformations or embryofetal death. Its presence in human milk and effects on the infant or milk production are unknown; consider breastfeeding benefits, the mother's clinical need, and potential adverse effects.
Recent literature (PubMed)
Extravasation is the leakage of intravenous solutions into surrounding tissues, which can be influenced by drug properties, infusion techniques, and patient-related risk factors. Although peripheral administration of vesicants may increase the risk of extravasation injuries, the time and resources required for central venous catheter placement may delay administration of time-sensitive therapies. Recent literature gathered from the growing use of peripheral vasopressors and hypertonic sodium suggests low risk of harm for initiating these emergent therapies peripherally, which may prevent delays and improve patient outcomes. Physiochemical causes of tissue injury include vasoconstriction, pH-mediated, osmolar-mediated, and cytotoxic mechanisms of extravasation injuries. Acidic agents, such as promethazine, amiodarone, and vancomycin, may cause edema, sloughing, and necrosis secondary to cellular desiccation. Alternatively, basic agents, such as phenytoin and acyclovir, may be more caustic due to deeper tissue penetration of the dissociated hydroxide ions. Osmotically active agents cause cellular damage as a result of osmotic shifts across cellular membranes in addition to agent-specific toxicities, such as calcium-induced vasoconstriction and calcifications or arginine-induced leakage of potassium causing apoptosis. A new category has been proposed to identify absorption-refractory mechanisms of injury in which agents such as propofol and lipids may persist in the extravasated space and cause necrosis or compartment syndrome. Pharmacological antidotes may be useful in select extravasations but requires prompt recognition and frequently complex administration strategies. Historically, intradermal phentolamine has been the preferred agent for vasopressor extravasations, but frequent supply shortages have led to the emergence of terbutaline, a β2 -agonist, as an acceptable alternative treatment option. For hyperosmolar and pH-related mechanisms of injuries, hyaluronidas
The adrenal glands drive physiologic homeostasis, with dysregulation in any direction causing multisystem dysfunction. Adrenal excess states include hyperaldosteronism which manifests with refractory hypertension and electrolyte abnormalities including hypernatremia and hypokalemia. Paragangliomas including pheochromocytoma can cause multisystem end-organ dysfunction due to catecholaminergic storm, which require rapid blood pressure control with phentolamine and identification of lesions amenable to surgical resection. Adrenal insufficiency states in contrast can result in hypotension and decompensation refractory to vasopressor administration, requiring adrenal supplementation via hydrocortisone.
A hypertensive crisis is defined as a sudden and significant rise in blood pressure. The blood pressure reading is 180/120 mmHg or higher. A hypertensive crisis is a medical emergency. It can lead to a heart attack, stroke, or other life-threatening medical problems. Investigating the management of the hypertensive crisis was the goal of this study. English-language articles were collected from 2010 to 2024 demonstrating the management of the hypertensive crisis. Overall, there were 15 articles. Surveys and analyses of national databases were the most widely used methods (n=15). The scientific studies documented (1) all investigative studies or reports that included a hypertensive crisis diagnosis, (2) data integrity and reproducibility, and (3) management studies. Other studies show that acute severe hypertension in the hospital is associated with high rates of mortality and morbidity, particularly with new or worsening end-organ damage. The problem is linked to poor medical adherence, but alarmingly low follow-up rates are likely to contribute to a high recurrence rate. The treatment of acute severe hypertension varies according to the hospital unit (medical ward or intensive care unit), medication, and blood pressure targets or thresholds. Because of a lack of evidence-based guidance, arbitrary blood pressure control targets are used, or blood pressure targets are crudely extrapolated from guidelines intended primarily for outpatient management. Patients with acute aortic dissection need to be administered intravenous esmolol within 5 to 10 minutes in order to lower their blood pressure right away. The goal is to maintain a systolic reading of less than 120 mm Hg. Vasodilators such as nitroglycerin or nitroprusside may be administered if the blood pressure persists following beta blocking. Intravenous administration of clevidipine, nicardipine, or phentolamine is required; the initial dose is 5 mg, with subsequent doses given every 10 minutes as necessary to achi
The adrenal glands drive physiologic homeostasis, with dysregulation in any direction causing multisystem dysfunction. Adrenal excess states include hyperaldosteronism which manifests with refractory hypertension and electrolyte abnormalities including hypernatremia and hypokalemia. Paragangliomas including pheochromocytoma can cause multisystem end-organ dysfunction due to catecholaminergic storm, which require rapid blood pressure control with phentolamine and identification of lesions amenable to surgical resection. Adrenal insufficiency states in contrast can result in hypotension and decompensation refractory to vasopressor administration, requiring adrenal supplementation via hydrocortisone.
Cocaine is one of the most commonly abused drugs and represents a major public health concern. Cocaine users frequently present to the emergency department, with chest pain being the most common presenting complaint. The incidence of acute myocardial infarction in patients with cocaine-associated chest pain is often quoted as 6%, but it is highly variable depending on the included population. Risk assessment can be challenging in these patients; serial assessment of electrocardiograms and troponins is often required. This review focuses on the assessment and management of patients presenting with cocaine-associated chest pain and cardiotoxicity. Specific treatments are discussed, including benzodiazepines, nitroglycerin, calcium channel blockers, and phentolamine, and how treatment priorities differ from patients with noncocaine presentations. The use of beta-blockers in this population remains controversial, and the literature around its use is reviewed. The most recent literature and recommendations for the use of percutaneous coronary intervention and fibrinolytics in cocaine-associated myocardial infarction is discussed as well. Cocaine-associated dysrhythmias are suggested to be the cause of sudden cardiac death in some users. The pathophysiology and evidence-based treatments for dysrhythmias are reviewed. This review provides evidence-based recommendations for the assessment and management of patients presenting with cocaine-associated cardiovascular toxicity.