#2 Remember naloxone, glucose, and thiamine (NGT) Original: Consider or give naloxone, glucose and thiamine The number of patients presenting with opioid intoxication is growing, and the gentle reversal of patients without severe respiratory depression with naloxone is in the art of medicine – consider starting with 0.4mg and titrate to effect.
In contrast to empiric administration of glucose in the altered or ill patient, rapid assessment of glucose level with point-of-care testing is recommended.
Thiamine deficiency may be less prevalent than previously thought in intoxicated patients, but we now know that giving 100mg of IV thiamine can benefit other malnourished patients, including those with calorie-malnourishment from cancer, gastric bypass, hyperemesis gravidarum, and eating disorders. Personally, I use the ‘T’ of ‘NGT’ to remind myself not to miss alcohol withdrawal.
Why does this matter? I hear you thinking we underwrite life insurance, we’re not doctors. So true. But if we think like doctors we will get better at what we do by recognizing the subtleties buried within the medical charts we read. Here’s what my eyes/brain picked up.
The bold in the excerpt above are mine to illustrate how the mind of a mortality risk expert works. In Emergency Department records pay attention to the initial treatments provided which in some cases hints to a serious condition impacting mortality. Naloxone and opioids are obvious. But would you have associated the administration of IV thiamine to malnutrition or alcohol withdrawal? I thought so.
So read and research widely. You’ll always find little jewels to improve your skills and to impress your friends with. Or in my case to make Dr. Lee think his old man knows more than he actually does.
Non-alcoholic fatty liver disease (NAFLD) is the leading cause of chronic liver disease worldwide, affecting at least a quarter of the global adult population. It is rapidly becoming one of the most common indications for liver transplantation in Western countries. NAFLD is widely considered as the hepatic manifestation of the metabolic syndrome. It is particularly common among patients with type 2 diabetes and obesity. Nonetheless, emerging data suggest that NAFLD is present in a significant proportion of lean individuals. In a systematic review and meta-analysis of 93 studies (involving over 10 million individuals), Ye et al found that 19.2% and 40.8% of patients with NAFLD were lean and non-obese, respectively, according to ethnic-specific body mass index (BMI) cut-offs.1 However, over 80% of the studies included in this systematic review were from Asia, raising the suspicion that NAFLD in lean individuals is a unique phenomenon among Asians, especially as Asians are known to have more central fat deposition and develop NAFLD and metabolic complications at a lower BMI.2
80% of the studies reviewed were from Asia which helps to explain why NAFLD was found in lean and non-obese people. I wonder how their diets have changed from traditional cuisines to cause this incidence level? Western style fast food?
Alkaline phosphatase 59 U/L, AST 28. ALT 10 as of September 2020. GGTP 36 as of December 2015. Sharing these numbers for all of my friends from the past who thought I would never live long enough to boast about these numbers.
Siopsis et al., JHND Early View Background The management of diabetes costs in excess of $1.3 trillion per annum worldwide. Diet is central to the management of type 2 diabetes. It is not known whether dietetic intervention is cost effective. This scoping review aimed to map the existing literature concerning the cost effectiveness of medical […]
Of 2387 abstracts assessed for eligibility, four studies combining 22 765 adults with type 2 diabetes were included. Dietetic intervention was shown to be cost‐effective in terms of diabetes‐related healthcare costs and hospital charges, at the same time as also reducing the risk of cumulative days at work lost to less than half and the risk of disability ‘sick’ days at work to less than one‐seventh.
Conclusions: The findings highlight the importance of advocacy for medical nutrition therapy for people with type 2 diabetes, with respect to alleviating the great global economic burden from this condition. Further studies are warranted to elucidate the factors that mediate and moderate cost effectiveness and to allow for the generalisation of the findings.
Conclusion All NAFLD histological stages were associated with significantly increased overall mortality, and this risk increased progressively with worsening NAFLD histology. Most of this excess mortality was from extrahepatic cancer and cirrhosis, while in contrast, the contributions of cardiovascular disease and HCC were modest.
Sex Differences in Coronary Artery Calcium and Mortality From Coronary Heart Disease, Cardiovascular Disease, and All Causes in Adults With Diabetes: The Coronary Calcium Consortium
RESULTS Among 4,503 adults with diabetes (32.5% women) aged 21–93 years, 61.2% of women and 80.4% of men had CAC >0. Total, CVD, and CHD mortality rates were directly related to CAC; women had higher total and CVD death rates than men when CAC >100. Age- and risk factor–adjusted hazard ratios (HRs) per log unit CAC were higher among women versus men for total mortality (1.28 vs. 1.18) (interaction P = 0.01) and CVD mortality (1.47 vs. 1.27) (interaction P = 0.04) but were similar for CHD mortality (1.48 and 1.48). For CVD mortality, HRs with CAC scores of 101–400 and >400 were 3.67 and 6.27, respectively, for women and 1.63 and 3.48, respectively, for men (interaction P = 0.04). For total mortality, HRs were 2.56 and 4.05 for women, respectively, and 1.88 and 2.66 for men, respectively (interaction P = 0.01).
CONCLUSIONS CAC predicts CHD, CVD, and all-cause mortality in patients with diabetes; however, greater CAC predicts CVD and total mortality more strongly in women.
Sex Differences in Coronary Artery Calcium and Mortality From Coronary Heart Disease, Cardiovascular Disease, and All Causes in Adults With Diabetes: The Coronary Calcium Consortium — Diabetes Care 2020 Oct; 43(10): 2597-2606. https://doi.org/10.2337/dc20-0166
The current investigators analyzed national healthcare claims from the US Medicaid program from 2001 to 2010 for 39,582 Medicaid beneficiaries (mean age, 44.5 years; 78.5% women) diagnosed with depression. Patients with alternative indications for anti-psychotic therapy, such as schizophrenia, psychotic depression or bipolar disorder, were excluded.
After a period of at least 3 months of treatment with a single antidepressant, more than half of the patients (56.6%) augmented their treatment with one of these atypical anti-psychotics: quetiapine, risperidone, aripiprazole or olanzapine. The remaining patients (43.4%) added a second antidepressant. The average chlorpromazine-equivalent starting dose for all atypical anti-psychotics was 68 mg/day, which increased to 100 mg/day during follow-up.
A total of 153 patients died during 13,328 person-years of follow-up, including 105 who augmented with an atypical anti-psychotic and 48 who augmented with a second antidepressant.
Compared with those who added a second antidepressant, those who added an anti-psychotic had a 45% increased risk of dying during follow up (adjusted hazard ratio,1.45; 95% CI, 1.02 – 2.06).
Many widely used medications may cause or exacerbate a variety of arrhythmias. Numerous antiarrhythmic agents, antimicrobial drugs, psychotropic medications, and methadone, as well as a growing list of drugs from other therapeutic classes (neurological drugs, anticancer agents, and many others), can prolong the QT interval and provoke torsades de pointes. Perhaps less familiar to clinicians is the fact that drugs can also trigger other arrhythmias, including bradyarrhythmias, atrial fibrillation/atrial flutter, atrial tachycardia, atrioventricular nodal reentrant tachycardia, monomorphic ventricular tachycardia, and Brugada syndrome. Some drug-induced arrhythmias (bradyarrhythmias, atrial tachycardia, atrioventricular node reentrant tachycardia) are significant predominantly because of their symptoms; others (monomorphic ventricular tachycardia, Brugada syndrome, torsades de pointes) may result in serious consequences, including sudden cardiac death. Mechanisms of arrhythmias are well known for some medications but, in other instances, remain poorly understood. For some drug-induced arrhythmias, particularly torsades de pointes, risk factors are well defined. Modification of risk factors, when possible, is important for prevention and risk reduction. In patients with nonmodifiable risk factors who require a potentially arrhythmia-inducing drug, enhanced electrocardiographic and other monitoring strategies may be beneficial for early detection and treatment. Management of drug-induced arrhythmias includes discontinuation of the offending medication and following treatment guidelines for the specific arrhythmia. In overdose situations, targeted detoxification strategies may be needed. Awareness of drugs that may cause arrhythmias and knowledge of distinct arrhythmias that may be drug-induced are essential for clinicians. Consideration of the possibility that a patient’s arrythmia could be drug-induced is important.
To evaluate the association between ischemic stroke and metabolic syndrome, DeBoer and Gurka reviewed more than 13,000 participants in prior studies and their stroke outcomes. Among that group, there were 709 ischemic strokes over a mean period of 18.6 years assessed in the studies. (Ischemic strokes are caused when blood flow to the brain is obstructed by blood clots or clogged arteries. Hemorrhagic strokes, on the other hand, are caused when blood vessels rupture.)
DeBoer developed the scoring tool, an online calculator to assess the severity of metabolic syndrome, with Matthew J. Gurka, PhD, of the Department of Health Outcomes and Biomedical Informatics at the University of Florida, Gainesville. The tool is available for free at https://metscalc.org/.
Journal Reference: Mark D. DeBoer, Stephanie L. Filipp, Mario Sims, Solomon K. Musani, Matthew J. Gurka. Risk of Ischemic Stroke Increases Over the Spectrum of Metabolic Syndrome Severity. Stroke, 2020; 51 (8): 2548 DOI: 10.1161/STROKEAHA.120.028944