Huong Van Nguyen

Serum C-reactive protein as a biomarker for early detection of bacterial infection in the older patient

BACKGROUND although C-reactive protein (CRP) is widely used in younger populations, its value for diagnosing bacterial infection in older population is not well established. This study examined the usefulness of serum CRP level in the early detection of bacterial infection in older patients. METHODS in a prospective cohort study, consecutive patients aged 70 years or over admitted to Aged Care wards were recruited. CRP levels were measured within 24 h of presentation, and their significance in predicting bacterial infections was analysed. The relationship between CRP and other clinical features of diagnosing bacterial infections (e.g. temperature, white cell count, neutrophil count, oxygen saturation, blood pressure and heart rate) was also examined. RESULTS a total of 232 patients were recruited over a period of 3 months. CRP levels were 21.3 +/- 36.0 and 150.5 +/- 114.1 mg/l (mean +/- SD) in the non-infection and infection groups, respectively (P < 0.001). We found that the CRP cut-off value of 60 mg/l had the best combination of sensitivity and specificity. At this level, the sensitivity of diagnosing bacterial infection was 80.7%, specificity 96.0%, positive predictive value 91.9% and negative predictive value 89.8%. CRP and temperature had higher sensitivity and specificity than white cell count and neutrophil count in the diagnosis of infection. For every 1-mg/l increment in CRP, the risk of bacterial infection increases by 2.9%. CONCLUSION CRP is a convenient and useful biomarker to predict early bacterial infection in older patients especially when other markers are atypical or not present.

Quality of life in a random sample of community dwelling older patients with essential tremor.

Study Objective –  Nested case‐control study aimed to assess the quality of life of community dwelling participants aged 65 years or over with newly diagnosed Essential Tremor (ET).

Recurrent diabetic ketoalkalosis in a patient with Type 1 diabetes mellitus and severe gastroparesis.

Diabetic ketoalkalosis is a rare complication of diabetes and results from a combination of diabetic ketosis and metabolic alkalosis as a result of vomiting and contraction alkalosis from dehydration. Our patient is a 24-year-old man with poorly controlled Type 1 diabetes mellitus, who was brought to the emergency department by ambulance after his mother found him collapsed. He had been vomiting every hour for 2 days, causing him to omit his insulin, but denied any preceding illness or recent alcohol intake. On examination he was lethargic, dehydrated, hypotensive (systolic blood pressure 70 mmHg) and tachycardic (pulse rate 124 ⁄ min), and his respiratory rate was 16 ⁄ min. His Type 1 diabetes mellitus was diagnosed at age 16 years and was complicated by severe gastroparesis, peripheral neuropathy, microalbuminuria and frequent episodes of diabetic ketosis (see Table 1). He had previously suffered spontaneous pneumomediastinum and pneumothorax during an episode of protracted vomiting and also had severe erosive reflux oesophagitis and alcohol-related gastritis. Medications prescribed were twice-daily insulin aspart–protamine suspension (NovoMix 30 ; NovoNordisk Pharmaceuticals Pty Ltd, Baulkham Hills, NSW, Australia), omeprazole, metoclopramide pre-meals, perindopril and atorvastatin. He was an unemployed panel beater, smoked 20 cigarettes ⁄ day, used regular cannabis and drank on average 100 g of alcohol twice weekly. He admitted to frequently omitting his medications. At this presentation, he had an elevated random blood glucose of 20.6 mmol ⁄ l, ketonuria and a raised anion gap of 20 mmol ⁄ l, consistent with diabetic ketoacidosis (DKA); however, his arterial blood gas showed marked metabolic alkalosis: pH 7.69, PaCO2 55.8 mmHg, HCO3 68.1 mmol ⁄ l and base excess > 30 mmol ⁄ l. Blood biochemistry profile (see Table 1, results II) showed acute renal failure, marked hyponatraemia, hypokalaemia and hypochloraemia, consistent with vomiting and contraction alkalosis. Lactate was normal at 1.3 mmol ⁄ l (reference range 0.7–2.1). Glycated haemoglobin was 11.3%. He required intensive care admission, but recovered fully with intravenous fluid, electrolyte replacement and an insulin infusion, although it took 3 days for the alkalosis to resolve. He experienced a milder ketoalkalosis episode with similar

Subcutaneous unfractionated heparin-induced hyperkalaemia in an elderly patient.

Admission biochemistry were: sodium 132 mmol/L (135–145), potassium (K) 5.0 mmol/L (3.5–5.0), urea 11.2 mmol/L (3.0–8.0), creatinine 119 mmol/L (70–110). The raised urea/creatinine ratio, high normal-range plasma K and mild hyponatraemia were initially thought to be due to a combination of dehydration from poor oral intake, the use of frusemide and ramipril. Frusemide and ramipril were withheld shortly after admission. Potassium initially fell over the next 3 days to 4.7 mmol/L. Despite stable renal and cardiac function, potassium then rose again peaking at 6.9 mmol/L 3 days later. The hyperkalaemia was managed with an intravenous bolus of insulin/dextrose and oral resonium. As expected, potassium fell over the next 48 hours but remained high at 5.8 mmol/L. Other possible causes of hyperkalaemia were considered, including diabetic nephropathy; inadequate insulin dosing; adrenal insufficiency in the context of concomitant mild hyponatraemia; and subcutaneous heparin injection. The rapidity of the potassium rise in the setting of improving renal function made diabetic renal failure a less likely cause. Significant insulin deficiency was also unlikely with blood glucose levels ranging from 6 to 9 mmol/L. Adrenal insufficiency was excluded by an adequate response to short Synacthen test. Heparin was then discontinued. Potassium gradually returned to 4.5 mmol/L over the next 5 days. A rechallenge of heparin 5000 units twice daily subcutaneously a day later resulted in recurrence of hyperkalaemia (K 5.5 mmol/L).

Venous thromboembolism in psychogeriatric in-patients – A study of risk assessment, incidence, and current prophylaxis prescribing

BACKGROUND While venous thromboembolism (VTE) risk assessment and prophylaxis is well established for medical and surgical in-patients, there is a paucity of evidence, and therefore guidelines, in this area for psychogeriatric in-patients. We wished to determine VTE incidence, risk, and use of prophylaxis, in a psychogeriatric in-patient population. METHODS Retrospective audit of consecutive psychogeriatric patients aged 65 years and over admitted to Bankstown Hospital over a 3-year period, 2007-2009. Using an adapted VTE risk scoring system, patients were assigned as low, medium, or high VTE risk. RESULTS A total of 192 patients were included in the study. Mean age was 79.1 ± 7.0 years. Out of the total, 55.2% of patients had diagnosis of dementia, and 33.3% had depression. Overall, 81.8% (157/192) were assessed as low risk, and 18.2% (35/192) as medium risk. Also, 16.7% (32/192) received VTE prophylaxis. Four new VTE events occurred in medium-risk group, and one in low-risk group (p = 0.004). Overall VTE incidence was 10.5/10,000 patient-days, but 44.2 per 10,000 in medium-risk group. VTE risk score was predictive of VTE events - IRR 6.02 (95% Confidence Intervals (CI) = 1.76-20.7, p = 0.004) for every one-point increment in risk. Depression was associated with significantly higher VTE occurrence (6.3% in those with diagnosis vs. 0.8% without, p = 0.043). CONCLUSION Using a VTE risk scoring system adapted for psychogeriatric in-patients, those assessed to be at medium risk had a significantly increased rate of VTE. On this basis, we would recommend VTE prophylaxis be prescribed for psychogeriatric in-patients assessed to be at medium and high level of risk.