Objective Delirium affects 60– 80% of ventilated patients and is associated with worse clinical outcomes including death. Unfortunately there are limited data regarding the prevalence and risk factors of delirium in critically ill burn patients. The objectives of this study were to evaluate the prevalence of delirium in ventilated burn patients, using validated instruments, and to identify its risk factors. Methods Adult ventilated burn patients at 2 tertiary centers were prospectively evaluated for delirium using the Confusion Assessment Method in the ICU for 30 days or until ICU discharge. Patients with neurological injuries, severe dementia and those not expected to survive > 24 hours, were excluded. Markov logistic regression was used to identify risk factors of delirium, adjusting for clinically relevant covariates. Results The 82 ventilated burn patients had a median (interquartile range) age of 48 (38, 62), APACHE II scores 27 (21, 30) and percent burns of 20 (7, 32). Prevalence of delirium was 77% with a median duration of 3 (1, 6) days. Exposure to benzodiazepines was an independent risk factor for the development of delirium [Odds Ratio 6.8, (confidence interval 3.1, 15), p <0.001) while exposure to intravenous opiates [0.5 (0.4, 0.6), p <0.001] and methadone [0.7 (0.5, 9), p=0.02] were both associated with a lower risk of delirium. Conclusion Delirium occurred atleast once in approximately 80% of ventilated burn patients. Exposure to benzodiazepines was an independent risk factor for delirium while opiates and methadone reduced the risk of developing delirium, possibly through reduction of pain in these patients.
The degree of correction of acidosis during the first 24 h of haemofiltration was determined by patients outcome but was not affected by the substitution of bicarbonate- for lactate-containing replacement fluids.
In an earlier study, we reported a significantly increased risk of pressure ulcer hospital discharge diagnoses in African Americans, higher age groups, and those with certain medical conditions. The objectives of the present study were to: (a) investigate the demographics associated with a higher odds ratio (OR) in African Americans and (b) determine whether African Americans have different rates of medical risk factors. The 2003 Nationwide Inpatient Sample database was queried. Patients with pressure ulcers were identified by discharge diagnoses using ICD-9 codes 707.0-707.09. Discharge diagnosis was examined using the agency for healthcare research and quality clinical classifications software (CCS). The present study used identified CCS discharge diagnoses present in at least 5% of all patients, with an OR>2. African Americans exhibited a higher incidence of an OR>2 for 28 identified CCS risk factors for pressure ulcers. The pressure ulcer diagnoses tended to occur at younger ages in African Americans. No significant differences were noted in African Americans with pressure ulcers when a subanalysis was conducted by zip code income quartile, region of the country, or teaching status of the hospital. Hospitalized African Americans exhibit an age-dependent, higher prevalence of pressure ulcers compared with Caucasians. Socioeconomic factors tracked within the Nationwide Inpatient Sample do not provide an explanation for this phenomenon.
SUMMARY. The occurrence of hypophosphataemia in paracetamol overdose suggests that nephrotoxicity is common, impaired renal tubular reabsorption of phosphate indicating renal damage. To investigate the potential nephrotoxicity of paracetamol, we studied 148 consecutive patients with paracetamol overdose. Serial clinical and biochemical measurements were made, and a fasting overnight urine collection was obtained for creatinine (Cr), phosphate and retinol-binding protein (RBP) determination. Renal threshold phosphate concentration (TmP0 4/GFR) was determined from urinary parameters by an established nomogram. The degree of hypophosphataemia correlated with the severity of overdose, and with TmP0 4/GFR. The median RBP/Cr ratio was higher in those patients exhibiting biochemical hepatotoxicity compared with those without hepatotoxicity, in whom median RBP/Cr was not significantly higher than controls. Within the group of patients showing biochemical hepatotoxicity, there was a correlation between log RBP/Cr and TmP0 4/GFR. RBP/Cr ratio is a less sensitive marker of renal tubular toxicity than phosphaturia in these patients, and may indicate a different mechanism of toxicity.
SUMMARY. We have measured the urinary excretion of total protein, albumin and retinol binding protein (RBP) in random urine specimens obtained from 40 female patients with systemic lupus erythematosus (SLE). Thirty-three of these patients had no clinical evidence of any renal impairment (non-renal SLE); seven had overt renal disease (renal SLE). RBP: creatinine ratios were significantly higher in non-renal SLE patients compared with female controls (P = 0,002). There was no significant difference between urine total protein concentrations, albumin: creatinine or total protein: creatinine ratios in non-renal SLE patients when compared with controls, despite approximately 20% of these patients having elevated excretion of total protein or albumin. All seven renal SLE patients had elevated albumin: creatinine ratios but only four of them had an increased RBP: creatinine ratio. Of 29 non-renal SLE patients who had urinary total protein concentrations below 0·2 giL, (i.e. approximating to a negative protein dipstick), 14 had increases in either albumin: or RPB: creatinine ratios. Only two patients had increases in both. In the absence of clinical evidence of renal disease, increases in urinary albumin or RBP excretion could indicate subclinical nephropathy and measurements may have a role in the early diagnosis and subsequent monitoring of renal disease in SLE.
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