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The treatment of patients poisoned with drugs and pharmaceuticals can be quite challenging. Diverse exposure circumstances, varied clinical presentations, unique patientspecific factors, and inconsistent diagnostic and therapeutic infrastructure support, coupled with relatively few definitive antidotes, may complicate evaluation and management. The historical approach to poisoned patients (patient arousal, toxin elimination, and toxin identification) has given way to rigorous attention to the fundamental aspects of basic life supportairway management, oxygenation and ventilation, circulatory competence, thermoregulation, and substrate availability. Selected patients may benefit from methods to alter toxin pharmacokinetics to minimize systemic, target organ, or tissue compartment exposure (either by decreasing absorption or increasing elimination). These may include syrup of ipecac, orogastric lavage, activated single-or multi-dose charcoal, whole bowel irrigation, endoscopy and surgery, urinary alkalinization, saline diuresis, or extracorporeal methods (hemodialysis, charcoal hemoperfusion, continuous venovenous hemofiltration, and exchange transfusion). Pharmaceutical adjuncts and antidotes may be useful in toxicant-induced hyperthermias. In the context of analgesic, anti-inflammatory, anticholinergic, anticonvulsant, antihyperglycemic, antimicrobial, antineoplastic, cardiovascular, opioid, or sedative-hypnotic agents overdose, N-acetylcysteine, physostigmine, L-carnitine, dextrose, octreotide, pyridoxine, dexrazoxane, leucovorin, glucarpidase, atropine, calcium, digoxin-specific antibody fragments, glucagon, high-dose insulin euglycemia therapy, lipid emulsion, magnesium, sodium bicarbonate, naloxone, and flumazenil are specifically reviewed. In summary, patients generally benefit from aggressive support of vital functions, careful history and physical examination, specific laboratory analyses, a thoughtful consideration of the risks and benefits of decontamination and enhanced elimination, and the use of specific antidotes where warranted. Data supporting antidotes effectiveness vary considerably. Clinicians are encouraged to utilize consultation with regional poison centers or those with toxicology training to assist with diagnosis, management, and administration of antidotes, particularly in unfamiliar cases.
The treatment of patients poisoned with drugs and pharmaceuticals can be quite challenging. Diverse exposure circumstances, varied clinical presentations, unique patientspecific factors, and inconsistent diagnostic and therapeutic infrastructure support, coupled with relatively few definitive antidotes, may complicate evaluation and management. The historical approach to poisoned patients (patient arousal, toxin elimination, and toxin identification) has given way to rigorous attention to the fundamental aspects of basic life supportairway management, oxygenation and ventilation, circulatory competence, thermoregulation, and substrate availability. Selected patients may benefit from methods to alter toxin pharmacokinetics to minimize systemic, target organ, or tissue compartment exposure (either by decreasing absorption or increasing elimination). These may include syrup of ipecac, orogastric lavage, activated single-or multi-dose charcoal, whole bowel irrigation, endoscopy and surgery, urinary alkalinization, saline diuresis, or extracorporeal methods (hemodialysis, charcoal hemoperfusion, continuous venovenous hemofiltration, and exchange transfusion). Pharmaceutical adjuncts and antidotes may be useful in toxicant-induced hyperthermias. In the context of analgesic, anti-inflammatory, anticholinergic, anticonvulsant, antihyperglycemic, antimicrobial, antineoplastic, cardiovascular, opioid, or sedative-hypnotic agents overdose, N-acetylcysteine, physostigmine, L-carnitine, dextrose, octreotide, pyridoxine, dexrazoxane, leucovorin, glucarpidase, atropine, calcium, digoxin-specific antibody fragments, glucagon, high-dose insulin euglycemia therapy, lipid emulsion, magnesium, sodium bicarbonate, naloxone, and flumazenil are specifically reviewed. In summary, patients generally benefit from aggressive support of vital functions, careful history and physical examination, specific laboratory analyses, a thoughtful consideration of the risks and benefits of decontamination and enhanced elimination, and the use of specific antidotes where warranted. Data supporting antidotes effectiveness vary considerably. Clinicians are encouraged to utilize consultation with regional poison centers or those with toxicology training to assist with diagnosis, management, and administration of antidotes, particularly in unfamiliar cases.
Purpose To review and discuss the epidemiology, contributing factors, and approach to clinical management of disorders of sodium and water balance in hospitalized patients. Source An electronic search of the MEDLINE, Embase, and Cochrane Central Register of Controlled Trials databases and a search of the bibliographies of all relevant studies and review articles for recent reports on hyponatremia and hypernatremia with a focus on critically ill patients. Principal findings Disorders of sodium and water balance are exceedingly common in hospitalized patients, particularly those with critical illness and are often iatrogenic. These disorders are broadly categorized as hypo-osmolar or hyper-osmolar, depending on the balance (i.e., excess or deficit) of total body water relative to total body sodium content and are classically recognized as either hyponatremia or hypernatremia. These disorders may represent a surrogate for increased neurohormonal activation, organ dysfunction, worsening severity of illness, or progression of underlying chronic disease. Hyponatremic disorders may be caused by appropriately elevated (volume depletion) or inappropriately elevated (SIADH) arginine vasopressin levels, appropriately suppressed arginine vasopressin levels (kidney dysfunction), or alterations in plasma osmolality (drugs or body cavity irrigation with hypotonic solutions). Hypernatremia is most commonly due to unreplaced hypotonic water depletion (impaired mental status and/or access to free water), but it may also be caused by transient water shift into cells (from convulsive seizures) and iatrogenic sodium loading (from salt intake or administration of hypertonic solutions). Conclusion In hospitalized patients, hyponatremia and hypernatremia are often iatrogenic and may contribute to serious morbidity and increased risk of death. These disorders require timely recognition and can often be reversed with appropriate intervention and treatment of underlying predisposing factors.
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