Cutaneous-hemolytic loxoscelism following brown recluse spider envenomation: new understandings.

Background: Brown recluse spider (BRS) (Loxosceles reclusa) envenomation can cause local dermonecrotic lesions, constitutional symptoms, and potentially fatal hemolysis (i.e., cutaneous-hemolytic loxoscelism). As the incidence of hemolysis is low and the spider habitat is limited, little is known regarding the clinical course of cutaneous-hemolytic loxoscelism.Methods: We performed a retrospective observational study of patients following BRS envenomation over an eight-year period. Demographics, clinical course, laboratories, and interventions were assessed. Wilcoxon rank-sum tests and Pearson chi-square tests were used in the univariate analyses. Logistic regression assessed the independent contribution of symptoms in a multivariate analysis.Results: Of the 97 patients, 40.2% (n = 39) developed hemolysis; the majority (66.7%) were 18 years old or younger. Univariate analysis revealed that constitutional symptoms were associated with hemolysis, but multivariate analysis showed only myalgia (aOR: 7.1; 95% CI: 2.2-22.7; p < .001) and malaise (aOR: 12.76; 95% CI: 1.4-119.9; p = .026) were independently associated with hemolysis. The median time to hemolysis onset was 1.0 days (IQR: 1.0-2.5) and all occurred within a week of envenomation. Hemolysis durations were longer in patients DAT positive for IGG antibodies (7.5 vs. 4.0 days; p = .042). Most (76.9%) of hemolyzing patients received blood. In patients with cutaneous-hemolytic loxoscelism, hematuria occurred in 32.4%, rhabdomyolysis occurred in 60.9%, and elevated transaminases with normal hepatic synthetic function occurred in 29.4% but all of these patients developed rhabdomyolysis. Hemolysis was both intravascular and extravascular. Complications (hyperkalemia, INR ≥2.0, metabolic acidosis requiring bicarbonate, hypotension requiring vasopressors, and hypoxia requiring intubation) occurred only in patients with profound hemolytic anemia (hemoglobin <4 g/dL); one patient died.Conclusions: Constitutional symptoms occur in both cutaneous and cutaneous-hemolytic loxoscelism, although they occur more frequently in patients who develop hemolysis. Children may be at a higher risk of hemolysis after envenomation. Renal involvement (as evidenced by hematuria) and rhabdomyolysis may occur more frequently than has been previously reported. Hemolysis was both intravascular and extravascular.

Naloxone reversal of clonidine toxicity: dose, dose, dose.

CONTEXT: Following clonidine ingestion, naloxone is seldom administered as it is considered ineffective in reversing somnolence, bradycardia, or hypotension. However, this conclusion has been based on administration of small doses (2 mg or less) of naloxone. The somnolence is frequently treated with endotracheal intubation (ETI), a procedure with significant morbidity. OBJECTIVE: We aimed to determine if naloxone administration reversed the effects of clonidine or caused any adverse effects. METHODS: We performed a retrospective descriptive cohort (IRB approved) of hospital medical records for pediatric patients (6 months-16 years) with clonidine exposure. Demographics, history, co-ingestants, clinical data, treatments, and outcome were recorded in a de-identified database. RESULTS: The most common clinical findings in the 52 patients were sedation (n = 51), bradycardia (n = 44), and hypotension (n = 11). Of 51 somnolent patients, naloxone administration awoke 40 patients, five of which had co-ingestants. Nine patients experienced recurrent sedation that resolved with a repeat bolus of naloxone. Twenty somnolent bradycardic patients (11 less than 3 years old) received 10 mg naloxone via intravenous bolus. Thirteen awoke; bradycardia persisted in six of the awake patients. Of the remaining 31 patients, 22 awoke following 6 mg or less of naloxone. Naloxone reversed hypotension in 7 of 11 hypotensive patients. Only one hypotensive patient (with a coingestion) received vasopressors for hypotension. Three awake normotensive patients received vasopressors for bradycardia. Seven patients awoke and had normal vital signs following naloxone administration, but were chemically sedated and intubated for transport. There were no adverse events following the administration of any dose of naloxone. CONCLUSIONS: Administration of naloxone to somnolent pediatric patients with clonidine toxicity awoke the majority (40/51) and resolved bradycardia and hypotension in some. Persistent bradycardia was benign. Hypotension was rare and clinically insignificant. No adverse effects occurred in any patient including the 21 patients who received 10 mg naloxone. Morbidity in this overdose may be due to ETI, a procedure that could be prevented if high-dose naloxone (10 mg) were administered. Administration of high-dose naloxone should be considered in all children with clonidine toxicity.