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Question about D50


ambodriver

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I recall reading an article several years ago that stated BS level directly effected mortatily rates in AMI. I couldn't find the exact article, but here is another that stated much the same.

http://content.onlinejacc.org/cgi/content/abstract/40/10/1748

http://www.ncbi.nlm.nih.gov/pubmed/15136307

PS- a link to the full study can be found for the first one on the right hand side.

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  • 1 month later...

Regarding the OP's question, a single amp of D50 in a nondiabetic will do no appreciable harm. You cannot compare patients with impaired glucose tolerance, as the studies cited here did, with a nondiabetic patient with a functioning insulin axis getting a single 100 KCal challenge.

Regarding whether or not this was an error, the patient was exhibiting altered mental status as part of the picture. So it would seem that they took the reading, interpreted it in the setting of the patient's condition, and gave the drug. And it sounds appropriate.

Third, hypoglycemia causes adrenergic output, and may cause the patient to feel a lot of things that we don't expect: nauseated, short of breath, anxious. So someone who presents as an apparent MI can in fact have hypoglycemia. I had a 31 yo in thyroid storm code in front of me from hypoglycemia and catecholamine depletion, so essentially a cardiac problem begat by a glucose problem.

Just find a labtech who is over age 50, and ask them their opinion of today's doctors who can not make a diagnosis without a minimum of 7 labtests. As we become more technologically advanced, many in our profession rely on that technology way to much.

Therein is another problem with asking the lab tech what they think of the tests being ordered. Ask the doctor WHY he is doing the test, and the answer may not stick with what the lab tech thinks. It may not be needed to make the diagnosis, but for other reasons:

- to rule out the less likely but possible diagnosis that may be more life-threatening, i.e., the PE that lurks, masked by symptoms that just sound cardiac

- to establish a baseline in a patient for later comparison to monitor response to therapy, i.e., getting lfts in a known hepatitis patient

- to establish nutritional status, i.e., the CBC in the chronic alcoholic who can't make a RBC MCV above 60 or get the albumin above 2

- to help interpret other labs, i.r., using albumin to estimate the real calcium level when it comes back low on the BMP

- to seek extra-organ sequelae of a disease process, i.e., the renal failure that accompanies a pneumonia, liver failure that accompanies septic shock.

- to seek extra-organ causes of the primary problem, i.e., the PE or electrolyte disturbance that led to the a-fib

- to establish the safety of doing another test, i.e., checking the renal function before doing a CT

- to hone in on a diagnosis among 2 or 3 that are not as likely. Is the pain from appendicitis, an ectopic pregnancy, PID, UTI, or a kidney stone?

- to get a prognosis on a disease process. LFTs may tell us how irritated the liver is, but coags will tell us if it is truly working or not. Elevated PT or PTT in a liver patient is a bad sign. Or elevated cardiac enzymes that portend a poor prognosis in PE. Or the various labs needed for Ranson's criteria in acute pancreatitis.

- getting to a prognosis for discharge home. The elderly guy with weakness, no sign of infection, a normal chest xray, and a WBC of 23K doesn't go home. The middle aged gal with single lobe community acquired pneumonia and acute renal failure doesn't either. The vag bleeder with dizziness and SOB on standing and a hemoglobin of 11 can go.

- getting to the bottom of a vague complaint, i.e., the COPD/CHF patient who is short of breath and coughing up greenish sputum but doesn't have a fever, and maybe has some wheezes, and has a bilateral vaguely interstitial pattern on chest xray that could be pneumonia or pulmonary edema or fibrosis.

- to get a sample prior to treatment in case the patient worsens, i.e., the urine cultures on the somewhat puny looking little old lady with a UTI that I'm sending home with antibiotics and outpatient follow-up. If she crumps and comes back, that culture data may be useful.

You don't want to order labs on just anyone. It's like picking your nose; you can do it, but you better know what you're going to do with it. The more tests you order, the greater the chances are that one or more will be abnormal. Shotgunning the labs will leave you scratching your head with a completely-unrelated-to-the-chief-complaint sodium level of 125 that you don't know what to do with. That said, in the prehospital setting, BGL is a lab that will never hurt you.

The fact is, the patients don't read the book, and a good doctor (and medic) knows this. Some patients show up looking like one disease process, but turn out to be another. At best, a patient fits "many aspects of a pattern of a disease process", essentially, connects most of the dots but never all. Exam findings can be unreliable, and a good doctor knows not to trust all of them. An objective lab value may help sort out the weirdness. There are a few diagnoses I make each day on sight with no testing required, but most patients come with some amount of diagnostic mystery. Even if it's not a mystery, there are so many reasons above why lab tests are useful. We understand that the human body is not a series of organs in isolation, but interconnected, and true badness can lurk unseen in cases which seem straightforward. Don't think only one organ system can bite you.

'zilla

Edited by Doczilla
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Since we're discussing hyperglycemia here, my question is this: How do we treat the hyperglycemic patient in the field? Do we even attempt to treat it in the field?

Since one of the symptoms of hyperglycemia is polyuria, would NS IV (KVO) be a consideration?

Since the cause of the polyuria is the body trying to rid itself of the elevated glucose, would we 'assist this' by using lasix as well?

I'm not trying to be a wise arse here, and I'm not trying to stir the pot; this is an honest quest for information for someone who doesn't know.

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Since we're discussing hyperglycemia here, my question is this: How do we treat the hyperglycemic patient in the field? Do we even attempt to treat it in the field?

It depends on how hyperglycaemic they are. We went to an old lady who was non compliant with her insulin for about two days her BGL was 11.7mmol/l which is just on the high side of normal (or about 200 mg/dl) but other than a little thirst and some nausea she was fine. Didn't do anything but transport her.

Since one of the symptoms of hyperglycemia is polyuria, would NS IV (KVO) be a consideration?

Yes, if the patient is very dehydrated.

Since the cause of the polyuria is the body trying to rid itself of the elevated glucose, would we 'assist this' by using lasix as well?

No. Prehospital fruisemide needs to be forever banished.

The problem with hyperglyceamia is the hyperosmolar state which shifts free body water from the interstitium to intravascular space. This causes a change in the gradient with the intravascular space being on the high end meaning the kidneys percieve as problematic and act to lower what is reabsored thru the DCT/loop of Henle in an effort to rid the body of the fluid imbalance via the urine.

This is why a very hyperglyceamic patient will be dehydrated and may have an electrolyte imbalance.

We give IV fluid in an attempt to rehydrate the patient, anything you give (such as lasix) that is going to make them piss more is only going to make the problem worse.

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Since we're discussing hyperglycemia here, my question is this: How do we treat the hyperglycemic patient in the field? Do we even attempt to treat it in the field?

Since one of the symptoms of hyperglycemia is polyuria, would NS IV (KVO) be a consideration?

Hyperglycemia itself is not immediately hazardous, but as Kiwi said, it's the dehydration that accompanies it from increased renal output that is problematic. Even DKA would fail to be that problematic if it weren't for the renal insufficiency that results from the severe dehydration (healthy, hydrated kidneys are very good at handling excess acids as well as excess glucose). For this reason, the first measure of treatment in DKA is always volume resuscitation. Insulin is a secondary concern, and I will usually wait until I have a potassium level back before starting the insulin drip in DKA.

Asymptomatic hyperglycemia does not require any prehospital treatment, but anyone showing signs of dehydration (tachycardia, dry mucous membranes, nausea, poor urine output, sunken eyes) should be hydrated with IV fluid. This applies for the Type 1 diabetics in DKA as well as type 2 diabetics in a hyperosmolar nonketotic state. NS at KVO rate really won't help in any way, as it is a negligible amount of fluid. I start with fluid boluses, dose dependent on other comorbidities. If they have renal failure and are on dialysis, or are known brittle CHF patients, I'm pretty careful with the fluid, going 250-500cc at a time with reassessment each time. If not, I'll hit them with a liter of fluid. In children with DKA, overly aggressive fluid resuscitation is a risk factor for cerebral edema, so I'll hit them with 20cc/kg of NS IV bolus, followed by a maintenance rate + rehydration rate, which requires a bit of calculation.

Remember that the dehydrated hyperglycemic patient didn't get that way overnight, so you shouldn't expect to fix it in a short period of time. Most people I plan to rehydrate over 48 hours. The initial bolus is helpful, but they will continue getting hydrated in the hospital over that time, or if sent home, will have instructions regarding aggressive hydration with PO fluids.

'zilla

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Regarding the OP's question, a single amp of D50 in a nondiabetic will do no appreciable harm. You cannot compare patients with impaired glucose tolerance, as the studies cited here did, with a nondiabetic patient with a functioning insulin axis getting a single 100 KCal challenge.

Regarding whether or not this was an error, the patient was exhibiting altered mental status as part of the picture. So it would seem that they took the reading, interpreted it in the setting of the patient's condition, and gave the drug. And it sounds appropriate.

Third, hypoglycemia causes adrenergic output, and may cause the patient to feel a lot of things that we don't expect: nauseated, short of breath, anxious. So someone who presents as an apparent MI can in fact have hypoglycemia. I had a 31 yo in thyroid storm code in front of me from hypoglycemia and catecholamine depletion, so essentially a cardiac problem begat by a glucose problem.

Therein is another problem with asking the lab tech what they think of the tests being ordered. Ask the doctor WHY he is doing the test, and the answer may not stick with what the lab tech thinks. It may not be needed to make the diagnosis, but for other reasons:

- to rule out the less likely but possible diagnosis that may be more life-threatening, i.e., the PE that lurks, masked by symptoms that just sound cardiac

- to establish a baseline in a patient for later comparison to monitor response to therapy, i.e., getting lfts in a known hepatitis patient

- to establish nutritional status, i.e., the CBC in the chronic alcoholic who can't make a RBC MCV above 60 or get the albumin above 2

- to help interpret other labs, i.r., using albumin to estimate the real calcium level when it comes back low on the BMP

- to seek extra-organ sequelae of a disease process, i.e., the renal failure that accompanies a pneumonia, liver failure that accompanies septic shock.

- to seek extra-organ causes of the primary problem, i.e., the PE or electrolyte disturbance that led to the a-fib

- to establish the safety of doing another test, i.e., checking the renal function before doing a CT

- to hone in on a diagnosis among 2 or 3 that are not as likely. Is the pain from appendicitis, an ectopic pregnancy, PID, UTI, or a kidney stone?

- to get a prognosis on a disease process. LFTs may tell us how irritated the liver is, but coags will tell us if it is truly working or not. Elevated PT or PTT in a liver patient is a bad sign. Or elevated cardiac enzymes that portend a poor prognosis in PE. Or the various labs needed for Ranson's criteria in acute pancreatitis.

- getting to a prognosis for discharge home. The elderly guy with weakness, no sign of infection, a normal chest xray, and a WBC of 23K doesn't go home. The middle aged gal with single lobe community acquired pneumonia and acute renal failure doesn't either. The vag bleeder with dizziness and SOB on standing and a hemoglobin of 11 can go.

- getting to the bottom of a vague complaint, i.e., the COPD/CHF patient who is short of breath and coughing up greenish sputum but doesn't have a fever, and maybe has some wheezes, and has a bilateral vaguely interstitial pattern on chest xray that could be pneumonia or pulmonary edema or fibrosis.

- to get a sample prior to treatment in case the patient worsens, i.e., the urine cultures on the somewhat puny looking little old lady with a UTI that I'm sending home with antibiotics and outpatient follow-up. If she crumps and comes back, that culture data may be useful.

You don't want to order labs on just anyone. It's like picking your nose; you can do it, but you better know what you're going to do with it. The more tests you order, the greater the chances are that one or more will be abnormal. Shotgunning the labs will leave you scratching your head with a completely-unrelated-to-the-chief-complaint sodium level of 125 that you don't know what to do with. That said, in the prehospital setting, BGL is a lab that will never hurt you.

The fact is, the patients don't read the book, and a good doctor (and medic) knows this. Some patients show up looking like one disease process, but turn out to be another. At best, a patient fits "many aspects of a pattern of a disease process", essentially, connects most of the dots but never all. Exam findings can be unreliable, and a good doctor knows not to trust all of them. An objective lab value may help sort out the weirdness. There are a few diagnoses I make each day on sight with no testing required, but most patients come with some amount of diagnostic mystery. Even if it's not a mystery, there are so many reasons above why lab tests are useful. We understand that the human body is not a series of organs in isolation, but interconnected, and true badness can lurk unseen in cases which seem straightforward. Don't think only one organ system can bite you.

'zilla

excellent post sir. thank you for confirming my initial thoughts...and also understanding the crews' judgment call w/o being snarky or condescending. I appreciate it. :closed:

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