Michael J. Cawley

Electrolyte imbalances are common in critically ill patients. Although multiple disease states typically encountered in the intensive care unit may be responsible for the development of electrolyte disorders, medications may contribute to these disturbances as well. Medications can interfere with the absorption of electrolytes, alter hormonal responses affecting homeostasis, as well as directly impact organ function responsible for maintaining electrolyte balance. The focus on this review is to identify commonly prescribed medications in the intensive care unit and potential electrolyte disturbances that may occur as a result of their use. This review will also discuss the postulated mechanisms associated with these drug-induced disorders. The specific drug-induced electrolyte disorders discussed in this review involve abnormalities in sodium, potassium, calcium, phosphate, and magnesium. Clinicians encountering electrolyte disturbances should be vigilant in monitoring the patient's medications as a potential etiology. Insight into these drug-induced disorders should allow the clinician to provide optimal medical management for the critically ill patient, thus improving overall healthcare outcomes.

A 34-year-old woman with a history of renal insufficiency induced by long-term cocaine use was admitted with acute shortness of breath remarkable for submandibular and anterior throat swelling. She required intubation, mechanical ventilation, and sedation. Sedation was administered with daily infusions of intravenous lorazepam 65, 313, and 305 mg for 3 days, respectively. Forty-eight hours into the infusion the patient experienced anion gap metabolic acidosis with hyperlactatemia, hyperosmolality, and increased osmolal gap. Propylene glycol (PG), a component of lorazepam intravenous formulation, was considered the potential source of the metabolic abnormality. The patient received greater than 40 times the acceptable recommended amount of PG over 72 hours. Cessation of lorazepam produced major improvements in lactic acid, serum osmolality, and anion and osmolal gaps. The large PG exposure associated with long-term cocaine-induced renal insufficiency produced a toxic metabolic state. Agents containing PG should be avoided in patients with compromised renal function (creatinine clearance < or = 30 ml/min) induced by cocaine use.

Streptococcal toxic shock syndrome (STSS) is caused by infection with a toxicogenic strain of Streptococcus pyogenes. Clinical manifestations may be those of a mild illness, characterized by malaise, fever, and muscle pain, to severe sepsis and multisystem organ failure. The syndrome may be associated with several invasive infections including necrotizing fasciitis. Treatment is primarily surgical debridement of infected tissue with supportive care, antibiotics, and hemodynamic monitoring. Intravenous immunoglobulin (IVIG) is reported to have beneficial effects in the management of STSS associated with necrotizing fasciitis. The agent was successful in conjunction with surgical excision and antibiotics in a patient with necrotizing fasciitis, toxic shock, and multisystem organ failure. On the basis of this experience and a thorough literature review, we concur that IVIG may be a useful adjunct in the treatment of STSS associated with necrotizing fasciitis.

We conducted a retrospective chart review of 193 patients admitted during a 3-month period to determine the frequency of and potential risk factors associated with thrombocytopenia, and the association of acquired thrombocytopenia with length of stay in a surgical-trauma intensive care unit (SICU) and mortality. All records were reviewed beginning 24 hours after admission. Patients were followed for the duration of SICU stay or until death. Data collected and analyzed as potential risk factors for thrombocytopenia were age, gender, admitting diagnosis, classification (trauma, surgical, medical), APACHE II score, medical history, all scheduled drugs with start and stop dates, select laboratory values, arterial or central line placement, and complications. Thrombocytopenia occurred in 25 (13%) patients. These patients were more likely (p<0.05) than those without thrombocytopenia to have the following potential risk factors: presence of a central or arterial line (76% vs 46%, p<0.025), nonsurgical diagnosis (60% vs 37%, p<0.05), diagnosis of sepsis (p<0.001), and administration of phenytoin (p<0.01), piperacillin (p<0.005), imipenem-cilastatin (p<0.001), and vancomycin (p<0.005). A longer SICU stay (mean 21 vs 4.5 days, p<0.05) and increased mortality (16% vs 4%, p<0.05) were significantly associated with thrombocytopenia. Cefazolin administration was significantly associated with nonthrombocytopenia (p<0.05). Factors not associated with thrombocytopenia were age, gender, and administration of histamine2-receptor antagonists, heparin, enoxaparin, penicillins, ceftazidime, ceftriaxone, chloramphenicol, and amphotericin B. A central or arterial line was the only factor associated with the development of thrombocytopenia in a multiple linear regression analysis (p=0.0003, multiple r=0.2580). Thrombocytopenia is not a common occurrence in the SICU, but is associated with a longer SICU stay and increased mortality.