Hypoglycemia Coma, Pathophysiology and Clinical Features - Essay Example

? Hypoglycemia Coma Introduction Hypoglycemia refers to a condition of the human body where the blood sugar (glucose) level becomes too low with Topiwala and Zieve (2012) considering sugar levels below 70 mg/dL as low. Hypoglycemia has been commonly associated with patients treated for diabetes using insulin and occasionally among patients who receive treatment through agents of oral hypoglycemic sulfonylurea (Ma, Won, Tang & Lin, 2005). Wolfsthal (2012) notes that hypoglycemic coma could result from excessive dosages of insulin, delay in meal ingestion and excessive physical activities. Mild hypoglycemia occurs with blood sugar levels of below 60 to 70 mg/dl with minimal exhibition of symptoms while severe hypoglycemia would occur with sugar level below 40 mg/dl. With less severe and transient decline in glucose availability, brain function and metabolism reduces before detection of decline in ATP in the tissues. Hypoglycemia leads to deprivation of brain’s major substrates and could interfere with cerebral metabolism through reduction of the energy supply of the brain. This severe deprivation of the brain of glucose due to decreased levels of blood sugar could lead to hypoglycemic coma. Type 1 diabetes patients, having insufficient quantities of counter-regulatory hormones which limit decrease in serum glucose would be more susceptible to hypoglycemic coma (Wolfsthal, 2012). Blood sugar levels would usually be slightly lower in children than adults. The prevalence of hypoglycemia coma has been found to range between 1.5 and 3 among 1000 newborns with the risk being higher among the risk groups. The transient form of hypoglycemia has been found to occur in 2 out of three new born babies. The prevalence stands at between 80 and 90 percent for babies born of mothers suffering from insulin dependent diabetes or those who have a history of gestational diabetes. The children who develop stable and severe hypoglycemia make up between 10 and 20 percent in high risk groups. Pathophysiology and clinical features Hypoglycemia coma has been associated with symptoms which would be produced through the following two mechanisms. First, the fall in the glucose concentration in the serum would stimulate the production of catecholamine and the outflow of the sympathetic nervous system. The resultant adrenergic stimulation would lead to sweating, palpitation, muscular weakness, tremulousness and tachycardia (Wolfsthal, 2012). Secondly, with the prolonged hypoglycemic condition, the central nervous system, CNS continually gets deprived of its major sources of glucose and fuel. These CNS symptoms would normally occur much later after the adrenergic symptoms, and have been considered to be more serious. The progress in the experienced mental changes could develop from somnolence and confusion to the more severe coma. This could be accompanied by slurred speech, headache, seizures and focal neurologic signs. Other symptoms include hypertension, muscle hypertonia and hyperreflexia. The establishment of hypoglycemia and indeed hypoglycemia coma has not been difficult: the challenge has been in establishing the cause (Puente, Tanoli & Fisher, 2008). Diagnosis would be guided by history of the patient which would be gathered from the patient’s diary data and from clinical signs. Causes The major causes of hypoglycemia coma as cited by Ma et al. (2005) include hereditary fructose intolerance, galactosemia and sensitivity to leucine. The exaggerated response to insulin secretion referred to as hyperinsulinism and hypoglycemia without known causes, referred to as idiopathic hypoglycemia have also been attributed to hypoglycemia coma. Insulin overdose, alcohol abuse, intense exercises for prolonged time, inadequate intake of food and suppression of some medications cause hypoglycemia coma in type 1 diabetes. On the other hand, in type 2 diabetes, travelling and limited food intake could cause this condition. In addition, overdosing on insulin and sulfonamides, particularly the generation 2 sulfonamides and additional drugs like b-blockers, coumarin and phenylbutazone could also cause hypoglycemia coma. The risk factors associated with hypoglycemia coma include alcoholism, mental disorders, aging, cardiovascular failure, poor nutrition, gastroenteritis and renal disease. Laboratory investigations would further support this diagnosis with the following indicating the possibility of hypoglycemia coma: high insulin levels, hypoglycemia measuring below 2.8 mmol-1, normal pH and alkaline reserve, increasing peptide levels and glycosuria and cetonuria. Treatment The treatment for hypoglycemia coma and indeed hypoglycemia involves raising the levels of blood sugar through carbohydrate ingestion, identifying the cause and adopting appropriate prevention measures. But this would not always hold as in cases of reactive hypoglycemia where rapid ingestion of carbohydrates could further enhance hypoglycemic situation. The blood glucose levels could be raised within minutes of receiving between 10 and 20 grams of carbohydrates. Conscious persons could take this through drinks or food. But for severe cases such as in hypoglycemic coma, the affected persons would not be able to ingest these by mouth. Such persons would have the medical personnel like paramedics and EMTs give intravenous dextrose whose concentrations would vary depending on the age: 2 ml/kg dextrose 10%, 25% and 50% would be given to infants, children and adults respectively (Wolfsthal, 2012). Caution should be taken as infiltrated IV could cause skin necrosis and electrolyte disturbance. An alternative to this would be a dose of between 1 and 2 mg of glucagon through intramuscular injection. Management and prevention Vast mechanisms exist for preventing hypoglycemic coma severity and frequency. The first step according to Topiwala and Zieve (2012) would be to establish the individual insulin regime which includes mealtime bolus insulin and basal insulin. Consequently, there should be consistent monitoring of these factors before meals, when retiring to bed and before and after exercises. One has to be cautious with carbohydrate intake with cookbooks providing reference for “carb counting” (Puente, Tanoli & Fisher, 2008, p.41). Before moderate 30-minute exercises, a fall in the blood sugar could be prevented by reducing the insulin dose accompanied by consideration of the food intake. Conclusion Hypoglycemia coma describes the severe manifestation of hypoglycemia indicated by palpitation, sweating, tremulousness, muscular weakness and tachycardia and in severe cases, somnolence and even coma. Inadequate food intake and insulin overdose have been cited as major causes of hypoglycemic coma. Though intravenous dextrose could be used to treat this condition, prevention measures through consistent monitoring of blood sugar and dietary considerations have been considered as more effective. References Ma, W., Won, J. G. S., Tang, K. & Lin, H. (2005). Severe hypoglycemic coma due to insulin autoimmune syndrome. Journal of China Medical Association, 68 (2), 82 – 86. Puente, E. C., Tanoli, T. & Fisher, S. J. (2008). Hypoglycemia and the central nervous system. Diabetes Pathophysiology, 38 – 41. Retrieved 27 November 2012 from http://www.touchbriefings.com/pdf/3291/fisher.pdf Topiwala, S. & Zieve, D. (2012). Hypoglycemia. US National Library of Medicine. Retrieved 27 November 2012 from http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001423/ Wolfsthal, S. (2012). NMS medicine. 7th ed. Baltimore, MD: Lippincott Williams & Wilkins. Read More