Niftymedi911 Posted June 16, 2008 Posted June 16, 2008 My thoughts: Hyperglycemic Hyperosmolar Nonketotic Syndrome (HHNS) with New onset DM Type II Type 2 diabetics often retain enough pancreas function to avoid ketones. In this case, blood acidity does not occur, hence the absent kussmaul breathing. Whereas highs in Type 1 diabetics lead to ketones and blood acidity that causes DKA, Type 2 diabetics tend to get highs without ketones leading to HHNS. HHNS is a form of high blood sugars that occurs with Type 2 diabetes, whereas ketosis is more common with Type 1 diabetes. It is quite different from the "ketosis" or "ketoacidosis" that occurs from ketones in highs, but almost as dangerous. HHNS occurs more commonly in Type 2 diabetics who retain enough pancreas function to avoid ketones, but who can still go dangerously high. Being high for prolonged periods causes severe dehydration from frequent urination. Because of the frequent urination and overactive kidney function, the mensenteric arteries and vessels are still profusing thus resulting in a normotensive blood pressure. The decreased repiratory effort is caused by the extremly high blood sugar count and causing the brain to shut down. Which is also causing the lack of a gag reflex. The elevated pulse is a compensentory mechanism for the apena. Hope this helps.
AZCEP Posted June 16, 2008 Posted June 16, 2008 HHNS typically will have a much higher BGL than 560 mg% associated with it. There is still the little matter of the reduced respiratory rate that isn't being accounted for. HHNS won't usually cause a drop in the respiratory drive. The tachycardia is a compensation for hypovolemia, not apnea. Hyperglycemia does not induce apnea without another cause being present.
chbare Posted June 16, 2008 Posted June 16, 2008 My thoughts: Hyperglycemic Hyperosmolar Nonketotic Syndrome (HHNS) with New onset DM Type II Type 2 diabetics often retain enough pancreas function to avoid ketones. In this case, blood acidity does not occur, hence the absent kussmaul breathing. Whereas highs in Type 1 diabetics lead to ketones and blood acidity that causes DKA, Type 2 diabetics tend to get highs without ketones leading to HHNS. HHNS is a form of high blood sugars that occurs with Type 2 diabetes, whereas ketosis is more common with Type 1 diabetes. It is quite different from the "ketosis" or "ketoacidosis" that occurs from ketones in highs, but almost as dangerous. HHNS occurs more commonly in Type 2 diabetics who retain enough pancreas function to avoid ketones, but who can still go dangerously high. Being high for prolonged periods causes severe dehydration from frequent urination. Because of the frequent urination and overactive kidney function, the mensenteric arteries and vessels are still profusing thus resulting in a normotensive blood pressure. The decreased repiratory effort is caused by the extremly high blood sugar count and causing the brain to shut down. Which is also causing the lack of a gag reflex. The elevated pulse is a compensentory mechanism for the apena. Hope this helps. Well...a fee considerations if I may? First: People who do not make insulin typically do not develop HHNKC. You see, the patient above is most likely a type I or insulin dependant diabetic. So, their body actually starts burning fats before the sugars climb to the levels seen in a HHNKC patient. The cells are simply not getting glucose by conventional means and the body begins breaking down fats. This process is generally messy and leaves behind allot of waste. Hence, this is where we get the ketone bodies. Hence, the term diabetic ketoacidosis. Second: People who still produce insulin are much more likely to develop HHNKC. You see, we still have some glucose movement into the cells; however, not enough to counter the increasing levels within the blood. The cells are still getting glucose, so, the body does not break down fat; however, the glucose levels continue to raise unchecked. The initial therapy for both HHNKC and DKA will be the same in most cases however. Supportive care and isotonic fluid resuscitation. In fact, nondiabetic people hospitalized with conditions such as pancreatitis and other disorders are prone to develop HHNKC. Take care, chbare.
Niftymedi911 Posted June 17, 2008 Posted June 17, 2008 Yes, but true DKA patient's do not have a rerspiratory rate of 4. I was merely trying to account for the respiratory (lack of) drive. When did my research, the article which I read had stated a decreased respiratory drive or effort would also be included because of the lack of acidosis. If there are not any indications of Kussmaul breathing, (which from what I was reading) there was no evidence of that type of breathing. Now, I might be missing it totally, which I'm starting to realize that I might be. but never the less, one cannot learn until they try it for themselves. Possible Closed Head Injury.........?????
p3medic Posted June 17, 2008 Posted June 17, 2008 Hyperventilating to blow off CO2 in an effort to buffer the acidosis eventually results in the tiring of the muscles involved in breathing, and eventual respiratory failure. Not saying thats what is going on in this particular case, but the lack of deep, rapid respiration in a hypoglycemic patient is very worisome, and probably needs prompt airway management unless a easily reversed cause is identified (opiate ingestion).
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