At the turn of the last century, a 10-year-old child diagnosed with diabetes could not reasonably expect to live long enough to celebrate his 12th birthday.[1] Diabetes care has significantly improved since then, but is still the seventh leading cause of death in the United States.[2]
Diabetes mellitus is a chronic disease caused by the body’s inability to metabolize glucose in a normal way. This form of diabetes, type 2, is most commonly found in people who are older, overweight, or physically inactive, or of a minority ethnicity and those with a family history of diabetes. By 2050, estimates are that one-fifth to one-third of the United States population will suffer from diabetes.[3]
What happens in diabetes
At some level, all cells in the human body utilize glucose for energy production. Very soon after eating, the bloodstream absorbs glucose from the gastrointestinal tract and plasma levels rise. The circulatory system then distributes glucose to all tissues of the body.
At the tissue level, insulin serves as a carrier protein to help transport glucose across the cellular membrane so that cellular organelles can convert the molecule into energy. Glucose movement into the cellular environment lowers glucose levels in the bloodstream.
In diabetes mellitus, the patient’s body is unable to manufacture insulin or stops responding to the insulin produced by the pancreas. Without insulin, the circulating glucose molecules cannot cross the cellular membrane, resulting in elevated plasma but lowered intracellular glucose levels. Without glucose, the cells cannot manufacture enough energy to remain alive.
Falling intracellular glucose levels trigger the pancreas to secrete glucagon, which causes the liver and muscles to convert stored glycogen into glucose, which then enters the bloodstream, elevating the circulating glucose levels even further. As this glucose-rich blood flows into the kidney, some of the glucose spills over into the urine, carrying with it higher than normal volumes of fluid. The result is overproduction of urine (polyuria) and loss of plasma volume (hypovolemia).
Cardiovascular effects
Excess urine production produces thicker-than-normal blood, which becomes increasingly harder for the circulatory system to pump. This results in circulatory impairment and becomes especially noticeable in the capillary beds of the tissues early in the disease process.
Later, the impairment affects larger blood vessels, which leads to many cardiovascular problems, including high blood pressure, heart attack, and stroke. Although these conditions also occur in non-diabetic individuals, people with diabetes are two to four times more likely to develop cardiovascular disorders.
As the cells lose access to glucose, adipose tissue begins releasing free fatty acids to be used as a source of energy.[4] The breakdown of the free fatty acids within the liver results in the formation of ketone bodies, which spill over into the urine, and produces metabolic acidosis.
Renal effects
Long-term elevated glucose levels in the kidneys damage the capillaries that filter blood. This results in the movement of large molecules (such as protein) out of the blood stream and into the urine.
Large protein molecules passing through the tubules in the nephron (filtering subunit of the kidney) create inflammation and scarring of the tubules with eventual loss of function. When enough nephrons are damaged, kidney failure will occur.
In fact, almost half of all patients placed on renal dialysis developed end-stage renal disease because of diabetes.[5]
Diabetic renal patients and cardiac arrest
First-year mortality rates in the United States for patients who begin renal dialysis is about 20%, with sudden cardiac arrest accounting for almost 60% of those deaths.[5] Most patients undergoing hemodialysis receive treatment three times per week. The risk of cardiac arrest is about 4.5 times higher during a hemodialysis treatment compared to the period between sessions.
Between dialysis sessions, the greatest incidence of cardiac arrest within this population occurs during the three-day break in treatment.[6-8] Hyperkalemia is the most common electrolyte problem associated with life-threatening arrhythmias and hemodialysis-associated cardiac arrest.[9]
Cardiac arrest during the hemodialysis session can be difficult to differentiate from circulatory collapse caused by excessive fluid removal resulting from ultrafiltration. Once the arrest is confirmed, however, experts recommend no specific alterations to standard basic life support measures when managing the electrolyte imbalance.[10]
It is standing policy in many dialysis centers to disconnect patients from hemodialysis machines before defibrillation. However, most of the concerns about defibrillation while the patient is still attached — such as alternative defibrillation energy pathways, current leakage, and damage to the hemodialysis hardware — appear largely theoretical.[9]
ALS treatment in the out-of-hospital setting
Immediate advanced life support treatment of hyperkalemia associated with cardiac arrest in patients suffering from renal failure is twofold: protect the myocardium from the harmful effects of the elevated extracellular potassium levels and lower those potassium levels by forcing potassium to the intracellular space.[10] Administration of a 10% calcium preparation either in the form of calcium chloride or calcium gluconate is very effective at stabilizing the myocardial cell membrane.
Administration of sodium bicarbonate is an easy way for prehospital providers to begin forcing potassium from the extracellular into the intracellular space. Other effective methods include administration of a glucose and insulin mixture and nebulized albuterol. However, the most effective long-term treatment is removal of the potassium from the body.
Patients with indwelling catheters, such as the central venous catheters used to deliver dialysis treatment, have a higher incidence of infection than can be found in the general population.[9] This includes infection from multiple drug-resistant bacteria. Hospitalization rates and bacteremia are disproportionately high in patients receiving hemodialysis.[11]
Patients with renal failure often require blood transfusions during the course of their therapy, which places them at an increased risk for blood-borne disease transmission and transfusion reactions.
Diabetes prevalence rates in the United States continue to increase. Diabetes is a significant risk factor for the development of renal failure and the need for hemodialysis, which places a tremendous burden on the health care system. Once on dialysis, the patient faces new threats — and unfortunately, a significant number of those patients dies shortly after beginning treatment.
References
1. MacCracken, J., & Hoel, D. (1997). From ants to analogues: Puzzles and promises in diabetes management. Postgraduate Medicine, 101(4), 138-140.
2. Centers for Disease Control and Prevention. (2013). National diabetes fact sheet, 2011. Retrieved from http://www.cdc.gov/diabetes/pubs/pdf/ndfs_2011.pdf
3. Boyle, J. P., Thompson, T. J., Gregg, E. W., Barker, L. E., & Williamson, D. F. (2010). Projection of the year 2050 burden of diabetes in the US adult population: dynamic modeling of incidence, mortality, and prediabetes prevalence. Population Health Metrics, 8, 29. doi: 10.1186/1478-7954-8-29
4. Miles, J. M., Haymond, M. W., Nissen, S., & Gerich, J. E. (1983). Effects of free fatty acid availability, glucagon excess and insulin deficiency on ketone body production in postabsorptive man. Journal of Clinical Investigation, 71(6), 15544-1561. doi:10.1172/JCI110911
5. National Institutes of Health, National Institute of Diabetes and Digestive and Kidney Diseases. (2013). U.S. renal data system, USRDS 2013 annual data report: Atlas of chronic kidney disease and end-stage renal disease in the United States. Bethesda, MD.
6. Bleyer, A. J., Russell, G. B., & Satko, S. G. (1999). Sudden and cardiac death rates in haemodialysis patients. Kidney International, 55(4), 1553-1559. doi:10.1046/j.1523-1755.1999.00391.x
7. Karnik, J., Young, B. S., Lew, N. L., Herget, M., Dubinsky, C., Lazarus, J. M., & Chertow, G. M. (2001). Cardiac arrest and sudden death in dialysis units. Kidney International, 60(1), 350-357. doi:10.1046/j.1523-1755.2001.00806.x
8. Lafrance, J. P., Nolin, L., Sene ́cal, L., & Leblanc, M. (2006). Predictors and outcome of cardiopulmonary (CPR) calls in a large haemodialysis unit over a seven-year period. Nephrology, Dialysis and Transplantation, 21(4), 1006-1012. doi:10.1093/ndt/gfk007
9. Alfonzo, A. V., Simpson, K., Deighan, C., Campbell, S., & Fox, J. (2007). Modifications to advanced life support in renal failure. Resuscitation, 73(1), 12-28. doi:10.1016/j.resuscitation.2006.07.019
10. Vanden Hoek, T. L., Morrison, L. J., Shuster, M., Donnino, M., Sinz, E., Lavonas, E. J., Jeejeebhoy, F. M., & Gabrielli, A. (2010). Part 12: Cardiac arrest in special situations: 2010 American Heart Association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care. Circulation, 122(suppl 3), S829-S861. doi:10.1161/CIRCULATIONAHA.110.971069
Ramanathan, V., & Darouiche, R. O. (2012). Prevention and management of hemodialysis catheter infections. Expert Review of Anti-infective Therapy, 10(12), 1447-1455. doi:10.1586/eri.12.134
