can also provide information on whether there is ongoing over‐ or underfeeding.
A RQ of <0.8 signifies a considerable catabolic state where fats and proteins are being utilized as the source of energy. Conversely, in patients with a RQ >1.0 this signifies overfeeding. The goal RQ for patients on TPN is between 0.8 and 1.0.
Complications
Catheter infections remain the major infectious complication of parenteral nutrition. Common pathogens include Staphylococcus epidermidis, Candida, and S. aureus. For patients on TPN, an established catheter monitoring and maintenance protocol is essential. In patients with suspected infection, replacement of the central catheter at a different site is necessary.
Hyperglycemia can occur as a result of increased parenteral carbohydrate availability along with concomitant insulin resistance. This can be avoided by gradual titration to the patient’s carbohydrate goal as well as regular glucose monitoring. Goal blood glucose should be between 140 and 180 mg/dL.
Hypertriglyceridemia can occur as a result of lipids infusion, the underlying stress hormone production, and renal insufficiency. In severe cases (triglycerides >1000 mg/dL) this can lead to precipitation of acute pancreatitis. Lipids should be removed from TPN if the plasma triglyceride concentration exceeds 400 mg/dL.
Hepatic steatosis and cholestasis are known complications of long‐term parenteral nutrition. More often seen in children, the exact etiology of fatty liver remains unclear. In the absence of enteral nutrition it is also common for development of cholestasis and biliary sludge. Early resumption of enteral feeding is the definitive treatment. Experimental use of ursodeoxycholic acid and cholecystokinin have shown mixed results.
Refeeding syndrome can occur when TPN is introduced to patients who are severely malnourished. A rapid intracellular shift of potassium phosphorous and magnesium can precipitate rhabdomyolysis heart failure and cardiac arrhythmias. Careful monitoring and timely replacement of electrolytes can help avoid this complication.
Intestinal mucosal atrophy can occur in the absence of enteral nutrition. There is risk for bacterial overgrowth and translocation of bacteria in the setting of mucosal denudation and impaired local immunity. The early initiation of trophic feeds helps reduce the risk of infection and translocation. The role of antibiotic agents such as neomycin to inhibit bacterial growth remains poorly defined.
Reading list
1 Hartl WH, Jauch KW, Parhofer K, Rittler P. Complications and monitoring – guidelines on parenteral nutrition, chapter 11. Ger Med Sci. 2009; 7:Doc17.
2 Neuman T, Kohli‐Seth R, Wilson S, Bassily‐Marcus A. Total parenteral nutrition in the ICU: the Mount Sinai Hospital experience. ICU Director 2010; 1(4):203–9.
3 Plauth M, et al. ESPEN Guidelines on Parenteral Nutrition: hepatology. Clin Nutr 2009; 28(4):436–44.
4 Singer P, Pichard C. Reconciling divergent results of the latest parenteral nutrition studies in the ICU. Curr Opin Clin Nutr Metab Care 2013; 16(2):187–93.
5 Thibault R, Pichard C. Parenteral nutrition. World Rev Nutr Diet 2013; 105:59–68.
Additional material for this chapter can be found online at:
www.wiley.com/go/mayer/mountsinai/criticalcare
This includes multiple choice questions.
CHAPTER 8 Glycemic Control
Amira Mohamed1 and Adel Bassily‐Marcus2
1 Albert Einstein College of Medicine, New York, NY, USA
2 Icahn School of Medicine at Mount Sinai, New York, NY, USA
OVERALL BOTTOM LINE
Intravenous insulin is recommended in hyperglycemic patients in the ICU.
When on intravenous insulin infusion, glucose should be checked every hour until it is at goal for at least 4 hours.
Once stable, patients on PO diet should be started on long‐acting and meal time insulin; patients on continuous feeds should be started on NPH insulin every 6 hours.
When converting to long‐acting insulin, total insulin dose is calculated using the insulin requirement in the last 6 hours of insulin infusion.
Background
The last decades have witnessed great changes in the definition of glycemic control in the ICU. In the 1990s, stringent glucose control was encouraged. However, later studies have reported the complications of hypoglycemia.
After the NICE‐SUGAR trial demonstrated increased mortality with intensive control, current guidelines recommend a more lenient approach with a target blood glucose level of approximately 140–180 mg/dL. The prevalence of diabetes in the USA has greatly increased to an astonishing 23.9% of the population, 40% of whom are still undiagnosed. The prevalence of diabetes in hospitalized patients appears to be as high as 25%. However, because inpatient diabetes studies are not routinely performed this number is likely underestimated. It is estimated that about 3160 dollars per patient are saved in health care costs as a result of decreased ICU length of stay, sepsis, renal failure, and even mechanical ventilation.
The causes of hyperglycemia in the ICU are complex and not limited to diabetes but are also caused by the impact of stress hormones such as cortisol including both stress‐induced or iatrogenic increases in steroid levels. Differentiation between the causes of hyperglycemia is challenging which is why the exact incidence of each is not yet known.
Pathogenesis
There is a substantial amount of evidence to suggest that stress‐induced hyperglycemia or hospital‐related hyperglycemia is an independent risk factor for increased morbidity and mortality when compared with hyperglycemia in diabetic patients.
Multiple factors contribute to hyperglycemia in the critically ill non‐diabetic patient such as stress hormones and inflammatory mediators causing insulin resistance and an increase in the rate of gluconeogenesis. Nonetheless, the question that remains unanswered is whether the resultant hyperglycemia is a direct cause of mortality or simply an indicator of the severity of illness.
The effects of hyperglycemia in the critically ill patient include leukocyte dysfunction, increased oxidative stress, and hypercoagulability and have also been associated with myocardial injury and increase in stroke size.
Recent evidence has suggested that stress‐induced hyperglycemia and hyperglycemia secondary to diabetes do not have the same mortality risk. Stress‐induced hyperglycemia is associated with worse outcome, including increased risk of infection and increased length of stay compared with diabetic
