https://novaprd-lb.newcastle.edu.au/vital/access/manager/Index ${session.getAttribute("locale")} 5 https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:38473 Wed 29 Sep 2021 15:27:47 AEST ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:14403 2 years) recruited to the Australian snakebite project with VICC (International Normalized Ratio [INR] > 3) were eligible. Patients were randomized 2 : 1 to receive FFP or no FFP. The primary outcome was the proportion with an INR of < 2 at 6 h after antivenom administration. Secondary outcomes included time from antivenom administration to discharge, adverse effects, major hemorrhage, and death. Results: Of 70 eligible patients, 65 consented to be randomized: 41 to FFP, and 24 to no FFP. Six hours after antivenom administration, more patients randomized to FFP had an INR of < 2 (30/41 [73%] vs. 6/24 [25%]; absolute difference, 48%; 95% confidence interval 23–73%; P = 0.0002). The median time from antivenom administration to discharge was similar (34 h, range 14–230 h vs. 39 h, range 14–321 h; P = 0.44). Seven patients developed systemic hypersensitivity reactions after antivenom administration – two mild and one severe (FFP arm), and three mild and one severe (no FFP). One serious adverse event (intracranial hemorrhage and death) occurred in an FFP patient with preexisting hypertension, who was hypertensive on admission, and developed a headache 6 h after FFP administration. Post hoc analysis showed that the median time from bite to FFP administration was significantly shorter for nonresponders to FFP than for responders (4.7 h, interquartile range [IQR] 4.2–6.7 h vs. 7.3 h, IQR 6.1–8 h; P = 0.002). Conclusions: FFP administration after antivenom administration results in more rapid restoration of clotting function in most patients, but no decrease in discharge time. Early FFP administration (< 6–8 h) post-bite is less likely to be effective.]]> Wed 11 Apr 2018 15:48:26 AEST ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:14506 Wed 11 Apr 2018 15:30:33 AEST ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:14505 Wed 11 Apr 2018 15:19:38 AEST ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:14376 12 and partial VICC, with only incomplete fibrinogen consumption, occurred in three patients. Systemic symptoms occurred in eight patients. Myotoxicity and neurotoxicity did not occur. H. stephensi venom was detected in all three H. stephensi envenomings (1.1, 44 and 81 ng/mL) for whom pre-antivenom blood samples were available, and not detected in one without envenoming. In two cases with post-antivenom blood samples, venom was not detected after tiger snake antivenom (TSAV) was given. In vitro binding studies demonstrated that TSAV concentrations of 50mU/mL are sufficient to bind the majority of free H. stephensi venom components at concentrations above those detected in envenomed patients (100 ng/mL). Eleven patients received antivenom, median dose 2 vials (Range: 1 to 5 vials), which was TSAV in all but one case, where polyvalent antivenom was used. Immediate hypersensitivity reactions occurred in six cases including one case of anaphylaxis. Envenoming by Hoplocephalus spp. causes VICC and systemic symptoms, making it clinically similar to brown snake (Pseudonaja spp.) envenoming. Based on in vitro studies reported here, patients may be treated with one vial of TSAV, although one vial of brown snake antivenom may also be sufficient.]]> Wed 11 Apr 2018 15:19:00 AEST ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:14876 Wed 11 Apr 2018 15:03:25 AEST ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:14537 Wed 11 Apr 2018 14:02:42 AEST ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:14380 Wed 11 Apr 2018 13:23:18 AEST ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:14550 Wed 11 Apr 2018 12:16:41 AEST ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:14507 1.5) in Russell’s viper envenoming, the specificity of negative WBCT20 in non-envenomed patients and directly compared paired WBCT20 and INR. Results: Admission WBCT20 was done in 140 Russell’s viper bites with coagulopathy and was positive in 56/140 [sensitivity 40% (95% confidence interval (CI): 32–49%)]. A negative WBCT20 led to delayed antivenom administration [WBCT20−ve tests: median delay, 1.78 h (interquartile range (IQR): 0.83–3.7 h) vs. WBCT20 + ve tests: median delay, 0.82 h (IQR: 0.58–1.48 h); P = 0.0007]. Delays to antivenom were largely a consequence of further WBCT20 being performed and more common if the first test was negative (41/84 vs. 12/56). Initial WBCT20 was negative in 9 non-envenomed patients and 48 non-venomous snakebites [specificity: 100% (95% CI: 94–100%)]. In 221 paired tests with INR > 1.5, the WBCT20 was positive in 91(41%). The proportion of positive WBCT20 only increased slightly with higher INR. Conclusions: In clinical practice, the WBCT20 has low sensitivity for detecting coagulopathy in snake envenoming and should not over-ride clinical assessment-based decisions about antivenom administration. There is an urgent need to develop a simple bedside test for coagulopathy in snake envenoming.]]> Wed 11 Apr 2018 11:31:16 AEST ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:14545 Wed 11 Apr 2018 10:59:06 AEST ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:4914 20% was only 10%. In 55 patients with systemic effects, these improved in 58% after IV antivenom vs. 65% after IM antivenom (-8%; 95% CrI: -32% to +17%). Twenty-four hours after antivenom pain had improved in 84% in the IV group vs. 71% in the IM group (+13%; 95% CrI: -2% to +27%). A meta-analysis including data from a previous trial found no difference in the primary outcome between IV and IM administration. Discussion: The difference between IV and IM routes of administration of widow spider antivenom is, at best, small and does not justify routinely choosing one route over the other. Furthermore, antivenom may provide no benefit over placebo.]]> Sat 24 Mar 2018 10:14:08 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:7558 Sat 24 Mar 2018 08:42:05 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:7361 100) occurred on 44 occasions (56%) and hypotension only twice. There were no seizures, dysrhythmias or deaths. Multivariate analysis of 215 presentations (in 181 patients) where dose of promethazine ingested was known demonstrated that dose, administration of charcoal within 2 h and co-ingestants predicted whether patients developed delirium. No relationship was shown for sex and age. A plot of probability that a patient will develop delirium vs. dose was constructed which showed the probability of delirium for 250 mg was 31%, 500 mg was 42% and for 1 g was 55% for promethazine alone overdoses. Conclusion: The main feature of promethazine toxicity is delirium, the probability of which can be predicted from the dose ingested. The administration of charcoal and the presence of co-ingestants appears to reduce the probability of delirium in a predictable manner.]]> Sat 24 Mar 2018 08:40:19 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:7163 Sat 24 Mar 2018 08:34:20 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:1442 24 h. Of these, only 6 (11%) received antivenom. One severe neurotoxic envenoming by an Australian funnelweb spider required antivenom. No definite spider bites resulted in necrotic ulcers (0%, 99%CI 0–0.7%). There were no early allergic reactions and secondary infection occurred in seven cases (0.9%, 95%CI 0.4–1.9%). Circumstances and early clinical effects were strongly associated with taxonomic spider identification, with positive predictive values >0.95 for common groups of spiders. Conclusions: Australian spider bite caused minor effects in most cases and is unlikely to cause necrotic ulcers, allergic reactions or infection. Redback spider bite (widow spider) caused prolonged pain, and antivenom could have been used more frequently. The circumstances and early clinical features of spider bites may allow early appropriate advice and treatment of spider bite without taxonomic identification.]]> Sat 24 Mar 2018 08:28:07 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:2481 38°C were universal in such patients; these features were therefore added. Using these seven clinical features, decision rules (the Hunter Serotonin Toxicity Criteria) were developed. These new criteria were simpler, more sensitive (84% vs. 75%) and more specific (97% vs. 96%) than Sternbach’s criteria. DISCUSSION: These redefined criteria for serotonin toxicity should be more sensitive to serotonin toxicity and less likely to yield false positives.]]> Sat 24 Mar 2018 08:27:43 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:14407 Sat 24 Mar 2018 08:24:54 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:14405 1000 U/L) and treatment (single dose-activated charcoal [SDAC] and NAC) were analysed. Data were analysed within a repeated measures logistic regression framework using NONMEM (ver 7.2). The primary outcome was administration of NAC, which was determined based on a serum paracetamol concentration greater than the nomogram line. Result.: There were 1571 admissions in 1303 patients, with a median age of 27 years (12–96 years) and 1140 (73%) were females. The median dose was 10 g (1–100 g). The paracetamol concentration was above the nomogram line in 337 of 1571 (22%) patients. Patients presenting later (first paracetamol concentration between 7 and 16 h post-overdose) compared to those presenting earlier (4–7 h post-overdose) were more likely to have hepatotoxicity (5.5% vs. 0.4%; p < 0.0001), have a toxic paracetamol concentration (34% vs. 18%; p  0.0001) and receive NAC (48% vs. 23%; p < 0.0001). SDAC reduced the probability of the paracetamol concentration being above the nomogram. Based on SDAC not being administered there was a 5% probability of requiring NAC at a dose of 6–9 g, a 10% chance of requiring NAC at a dose of 13–16 g, a 50% chance of requiring NAC at a dose of 30–34 g and a 90% chance for needing NAC at 48–50 g. Conclusion. Reported dose was a good predictor of a toxic paracetamol concentration and SDAC reduced the probability of the concentration being above the nomogram. These predictions may assist in determining which patients could be started on NAC immediately.]]> Sat 24 Mar 2018 08:24:53 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:14378 1 Despite the availability of numerous methods for assessing the risk of TdP on the basis of the presence of QT prolongation,^2-5few studies have investigated the direct relationship between the magnitude of QT prolongation and the risk of TdP. Previous studies have generally considered the presence or absence of QT prolongation as a marker of the potential risk for TdP. In addition, they investigated data arising from a range of different drugs, with differing intrinsic cardiotoxic effects. This carries the potential for confounding of the relationship between the magnitude of prolongation of the QT interval and the inherent cardiotoxicity of the drug. Amisulpride is an atypical antipsychotic drug used to treat both the positive and negative symptoms of schizophrenia. It has affinity for limbic D₂ and D₃ receptors and only slight affinity for serotonergic, cholinergic, adrenergic, and histaminergic receptors.⁶ An overdose of the drug has been reported to cause QT prolongation and TdP.⁷ The aim of this study was to investigate whether the magnitude of QT prolongation is a better predictor of TdP than either the occurrence of QT prolongation per se or the dose of the drug. This was investigated in a case series of drug overdose events involving amisulpride.]]> Sat 24 Mar 2018 08:23:08 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:14431 12) and median highest aPTT was 54 s (46 – 72 s; Range: 35 – 170 s). There was low fibrinogen [median: 1.3 g/L;1, – 1.8 g/L; Range: < 0.2 – 2.9], low factor VIII levels [median: 23%; 16 – 37%] and low factor V levels [median: 43%; 23 – 74%]. D-Dimer concentrations [median: 3.4 mg/L; 2 – 7.4 mg/L] were slightly elevated. Factors II, VII and X and vWF antigen concentrations were normal. Discussion and Conclusions: Hump-nosed pit viper bites result in a mild coagulopathy which is usually not detected by a WBCT20. It is characterised by mild elevation of INR, low fibrinogen and Factors V and VIII which may be consistent with the venom containing a thrombin-like enzyme.]]> Sat 24 Mar 2018 08:21:03 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:14457 120 mg) identified from admissions to a toxicology unit between January 1987 and August 2013. Demographic information, details of ingestion, clinical effects, ECG parameters (HR, QT and QRS), and length of stay were extracted from a clinical database. Results: From 267 mirtazapine overdoses, there were 89 single-agent mirtazapine ingestions and 178 cases where mirtazapine was taken with at least one other drug. The median age of the 89 single-agent mirtazapine ingestions was 36 years [interquartile range (IQR): 26 – 49 years; Range: 15 – 81 years]; 45 were female (51%). The median ingested dose was 420 mg (IQR: 270 – 750 mg; Range: 150 – 1350 mg) and 41 patients (46%) had a Glasgow coma score (GCS) < 15, but the minimum GCS was 10. There were no seizures, serotonin toxicity or delirium. Tachycardia occurred in 29 patients (33%) and hypertension in 32 patients (36%). The median QRS was 80 ms (Range: 80 – 120 ms) and there were no cases with QT prolongation. There were no arrhythmias and no deaths. The median length of stay was 14 h (IQR: 8.8 – 18.2 h; Range:2.2 – 75 h). No single-agent mirtazapine patient was admitted to intensive care. The 178 patients taking co-ingestants had more severe toxicity depending on the co-ingested drug. Conclusion: Mirtazapine appears to be relatively benign in overdose, associated with tachycardia, mild hypertension and mild CNS depression not requiring intervention.]]> Sat 24 Mar 2018 08:19:18 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:14549 Sat 24 Mar 2018 08:18:49 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:10169 Sat 24 Mar 2018 08:12:31 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:11219 3, and 18 with partial VICC. Serial citrated plasma samples were collected from 0.5 to 60 h post-bite. INR, activated partial thromboplastin time (aPTT), coagulation factors (F)I, II, V, VII, VIII, IX, X, von Willebrand factor antigen (VWF:Ag) and D-dimer concentrations were measured. Results: Complete VICC was characterized by near/total depletion of fibrinogen, FV and FVIII, with an INR and aPTT that exceeded the upper limits of detection, within 2 h of snakebite. Prothrombin levels never fell below 60% of normal, suggesting that the toxins were rapidly eliminated or inactivated and re-synthesis of clotting factors occurred irrespective of antivenom. Partial VICC caused limited depletion of fibrinogen and FV, and almost complete consumption of FVIII. Onset of VICC was more rapid with brown snake (Pseudonaja spp.) venom, which contains a group C prothrombin activator toxin, compared with the tiger snake group, which contains a group D prothrombin activator toxin and requires human FVa formation. Resolution of VICC occurred within 24-36 h irrespective of snake type. Conclusions: These results suggest that Australasian elapid prothrombin activators have a potent but short duration of action. Antivenom is unlikely to be administered in time to prevent VICC.]]> Sat 24 Mar 2018 08:11:13 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:11220 3, and 18 with partial VICC. Serial citrated plasma samples were collected from 0.5 to 60 h post-bite. INR, activated partial thromboplastin time (aPTT), coagulation factors (F)I, II, V, VII, VIII, IX, X, von Willebrand factor antigen (VWF:Ag) and D-dimer concentrations were measured. Results: Complete VICC was characterized by near/total depletion of fibrinogen, FV and FVIII, with an INR and aPTT that exceeded the upper limits of detection, within 2 h of snakebite. Prothrombin levels never fell below 60% of normal, suggesting that the toxins were rapidly eliminated or inactivated and re-synthesis of clotting factors occurred irrespective of antivenom. Partial VICC caused limited depletion of fibrinogen and FV, and almost complete consumption of FVIII. Onset of VICC was more rapid with brown snake (Pseudonaja spp.) venom, which contains a group C prothrombin activator toxin, compared with the tiger snake group, which contains a group D prothrombin activator toxin and requires human FVa formation. Resolution of VICC occurred within 24-36 h irrespective of snake type. Conclusions: These results suggest that Australasian elapid prothrombin activators have a potent but short duration of action. Antivenom is unlikely to be administered in time to prevent VICC.]]> Sat 24 Mar 2018 08:11:12 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:20541 Sat 24 Mar 2018 08:02:39 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:5774 Sat 24 Mar 2018 07:47:18 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:1 Sat 24 Mar 2018 07:42:10 AEDT ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:33115 95 % on FiO2 25 %, and a GS of 8. She was admitted to intensive care and had a normal non-contrast CT brain. She was treated with a glyceryl trinitrate patch (5 mg) and observed for 36 h with subsequent BP reduction to 124/81 mmHg and improved in conscious state. Midodrine and desglymidodrine concentrations were measured with liquid chromatography tandem mass spectrometry and were detected with 2-h post-ingestion at concentrations of 158.4 and 169.7 ng/mL, respectively. The parent drug concentrations rapidly decreased with an elimination of half-life of 1.6 h, and the metabolite initially increased and then decreased. The peak in blood pressure appeared to coincide with peak metabolite concentrations. Midodrine in overdose can potentially cause severe hypertension and reflex bradycardia but given its short half-life treatment with vasodilator agents and supportive care is sufficient.]]> Mon 27 Aug 2018 15:49:46 AEST ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:32381 140-180 mmHg) occurred in 23/71 patients (32%), and tachycardia occurred in 29/74 (39%) patients. There were no abnormal QT intervals and no QRS > 120 m s. Serotonin toxicity was diagnosed by the treating physician in 7/75 (9%) patients, but only one of these met the Hunter Serotonin Toxicity Criteria. None of the 75 patients who took desvenlafaxine only (± alcohol) had seizures, were admitted to intensive care or died. In comparison, the 107 patients taking desvenlafaxine in overdose with other medications developed more pronounced toxicity. Generalised seizures occurred in 5/107 (5%), but in three of these cases co-ingestants were possible proconvulsants. Fifteen patients had a GCS ≤9 and none had an abnormal QT or QRS. Severe effects appeared to be associated with coingestants. Conclusion: Desvenlafaxine overdose causes minor effects with mild hypertension and tachycardia. The risk of seizures or serotonin toxicity is low.]]> Mon 23 Sep 2019 12:11:51 AEST ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:27226 D-dimer may assist in early diagnosis, but fibrinogen levels often add little in the clinical setting. Bedside investigations would be ideal, but point-of-care testing international normalized ratio and whole blood clotting tests have been shown to be unreliable in VICC. The major complication of VICC is hemorrhage, including intracranial hemorrhage which is often fatal. The role of antivenom in VICC is controversial and may only be beneficial for some types of snakes including Echis spp where the duration of abnormal clotting is reduced from more than a week to 24 to 48 hours. In contrast, antivenom does not appear to speed the recovery of VICC in Australian snake envenoming. Other treatments for VICC include factor replacement, observation and prevention of trauma, and heparin. An Australian study showed that fresh-frozen plasma speeds recovery of VICC, but early use may increase consumption. There is no evidence to support heparin.]]> Mon 23 Jul 2018 13:17:15 AEST ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:23876 3 g) admitted to a toxicology unit over 20 years. Cases were identified from a prospective database and data extracted included demographics, dose, coingestants, clinical effects, investigations, treatment and outcomes. Results: There were 36 acute metformin overdose cases. Median age 41 years old (15–68 years old); 25 were female. Median ingested dose was 10 g (interquartile range (IQR): 5–16.1 g; range: 3.5–50 g), with coingestants taken in 34 presentations. Gastrointestinal symptoms were present in 12/36, tachycardia in 10, bradycardia in three, hypotension in four and hypoglycaemia in eight. Hypotension and bradycardia were consistent with coingestants taken. Blood pH and lactate levels were available in 25/36. Median lowest pH was 7.35 (IQR: 7.28–7.38) and acidosis (pH < 7.35) occurred in 11/25. Median peak lactate was 3.9 mmol/L (IQR: 2.6–5.2 mmol/L). There was a statistical association between dose and lactate (r = 0.51; P = 0.01) and dose and pH (r = −0.70; P = 0.0001). Hyperlactataemia (lactate >2 mmol/L) without acidosis occurred in 10/25, and hyperlactataemia with acidosis in 11/25; five had lactic acidosis. The median time to peak lactate in 10 presentations with peak lactate >2 was 6 h (2–19 h). There were six intensive care unit admissions, one for lactic acidosis, and five related to coingestants. There were no deaths. Conclusion: Metformin overdose is characterised by hyperlactataemia and minor gastrointestinal effects, with a few large ingestions progressing to lactic acidosis. Coingestants are common and may dominate toxicity.]]> Mon 23 Jul 2018 12:56:16 AEST ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:30614 Daboia russelii) envenoming is a major health issue in South Asia and causes venom-induced consumption coagulopathy (VICC). Objectives: To investigate the effects of fresh frozen plasma (FFP) and two antivenom doses in correcting VICC. Methods: We undertook an open-label randomized controlled trial in patients with VICC attwo Sri Lankan hospitals. Patients with suspected Russell’s viper bites and coagulopathy were randomly allocated (1 : 1) to high-dose antivenom (20 vials) or low-dose antivenom (10 vials) plus 4 U of FFP. The primary outcome was the proportion of patients with an International Normalized Ratio (INR) of < 2 at 6 h after antivenom administration. Secondary outcomes included anaphylaxis, major hemorrhage, death, and clotting factor recovery. Results: From 214 eligible patients, 141 were randomized: 71 to high-dose antivenom, and 70 to low-dose antivenom/FFP; five had no post-antivenom blood tests. The groups were similar except for a delay of 1 h in antivenom administration for FFP patients. Six hours after antivenom administration, 23 of 69 (33%) patients allocated to high-dose antivenom had an INR of < 2, as compared with 28 of 67 (42%) allocated to low-dose antivenom/FFP (absolute difference 8%; 95% confidence interval - 8% to 25%). Fifteen patients allocated to FFP did not receive it. Severe anaphylaxis occurred equally frequently in each group. One patient given FFP developed transfusion-related acute lung injury. Three deaths occurred in low-dose antivenom/FFP patients, including one intracranial hemorrhage. There was no difference in recovery rates of INR or fibrinogen, but there was more rapid initial recovery of factor V and FX in FFP patients. Conclusion: FFP after antivenom administration in patients with Russell’s viper bites did not hasten recovery of coagulopathy. Low-dose antivenom/FFP did not worsen VICC, suggesting that low-dose antivenom is sufficient.]]> Fri 24 Aug 2018 09:01:46 AEST ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:45740  3000 mg were identified in each unit’s database. Excluded were cases of chronic exposure, hospital presentation > 24 hours after ingestion, and cases without a salicylate concentration. Included in our analysis was demographic data, clinical effects, investigations, complications, and treatment. Results: There were 132 presentations in 108 patients (79 females (73%)). The median age was 28 years (range: 13–93 years). The median dose ingested was 7750 mg (IQR: 6000–14,400 mg). There were 44 aspirin-only ingestions. Mild toxicity (nausea, vomiting, tinnitus or hyperventilation) occurred in 22 with a median dose of 160 mg/kg. Moderate toxicity (acid–base disturbance, confusion) occurred in 16 with a median ingested dose of 297 mg/kg. There were no cases of severe toxicity (coma or seizures) due to aspirin alone. The median peak salicylate concentration was 276 mg/L (IQR: 175–400 mg/L, range: 14–814 mg/L). There was a moderate association between dose ingested and peak concentration (Pearson r = 0.58; 95% CI 0.45–0.68). Activated charcoal was administered in 36 (27%) cases, which decreased the median peak salicylate concentration (34.2 to 24.8 mg/L/g (difference: 9.4, 95% CI: 1.0–13.1)). Bicarbonate was administered in 34 (26%) presentations, decreasing the median apparent elimination half-life from 13.4 to 9.3 h (difference: 4.2 h, 95% CI: 1.0–6.5 h). Conclusions: Acute aspirin overdose caused only mild to moderate effects in this series. Early administration of activated charcoal decreased absorption and use of bicarbonate enhanced elimination.]]> Fri 19 Apr 2024 12:58:48 AEST ]]> https://novaprd-lb.newcastle.edu.au/vital/access/manager/Repository/uon:15310 Fri 09 Sep 2016 16:08:51 AEST ]]>