How do insulin pumps work?

Insulin pump: a game-changer in the management of type I diabetes, allowing for more natural insulin administration, tighter control and patient empowerment; a cause of dread for residents who have never had to manage one before.

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Parts of a pump: the pump itself, the infusion set (the tubing), the cannula (the needle that goes into the skin). While many people do the traditional “check your fingerstick four times a day” thing, some also use continuous glucose monitoring (CGM) with their pumps. 


It’s worth noting that hospital policy (at the hospital I work at, at least) is that patients should be allowed to manage their own insulin pump as long as they have capacity. There are tales passed down about patients who refuse to give up their insulin pump and send themselves into repeated episodes of hypoglycemia…but there is more going on there than just diabetes.

The pump requires a lot of education, and are costly. But they are also pretty cool. Every patient has basal infusions of insulin pre-programmed into their pump.ONLY rapid-acting insulin is used (U100) but it is infusing 24 hours a day.The program is usually reviewed every few months with their endocrinologist based on their sugar logs and adjusted if the blood glucoses are too high or low.

Patients still have to count their carbs, do four times a day fingersticks, and use a correction factor, but they can calculate their own mealtime bolus and adjust accordingly. Here is a general page about diabetes management for patients on the Joslin Center website that includes information about insulin pumps.

Calculating a bolus: 

There’s a patient-version handy guide from Medtronic, which has this example:

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  • hypoglycemia: has the patient been exercising more than usual? Are they drinking alcohol and not eating as much as they should? Is their correction factor too aggressive?
  • hyperglycemia: is the infusion site properly connected? Is the pump itself malfunctioning, and do they need new supplies? Is the infusion site scarred over and not absorbing insulin as well? Is it not calculating the right amount of correction insulin?



Inpatient insulin management and adjustment

Insulin management, in truth, deserves a whole chapter of a textbook, but here are a few quick-and-dirty methods I’ve learned for type 2 diabetics in the hospital:

Selecting a type of insulin:

  • I often try to use lantus over NPH if I have a choice, because lantus is longer-acting and doesn’t have a peak-decrease response
  • I also avoid 70/30 mixed insulin unless a patient uses that at home because 70/30 is more prone to giving people labile blood sugars
  • Short acting insulins, like aspart (lispro) and humalog (humulin) I think of as more interchangeable

Brand Name

(length of time before
insulin reaches bloodstream)
(time period when
insulin is most effective)
(how long insulin
works for)


10 – 30 minutes 30 minutes – 3 hours 3 – 5 hours
Short-acting Regular (R) 30 minutes – 1 hour 2 – 5 hours Up to 12 hours
NPH (N) 1.5 – 4 hours 4 – 12 hours Up to 24 hours
Long-acting Lantus
0.8 – 4 hours Minimal peak Up to 24 hours

(Table credit: The Joslin Center)

Calculating an initial dose of long acting (basal) insulin: Body weight (kg) x 0.2 if insulin naive; and x 0.5 if already on insulin.

Calculating the appropriate sliding scale instead of using your hospital’s predetermined one: 5% of total daily insulin requirement. For example, someone who requires 20 units of basal insulin should start with a sliding scale of 1 unit when glucose 150-200, 3 units when 201-249, etc.

Adjusting insulin on a daily basis: Add up the sliding scale units they received over the last 24 hours. Assign 50% to long-acting insulin and 50% to mealtime insulin. So, if someone is getting 10 units long-acting insulin and 2 units mealtime, and required an extra 12 units yesterday, they should now get 13 units long-acting insulin and 4 units at each mealtime.



Landmark papers in critical care: Insulin

When diabetics get sick, their blood sugars shoot up to ungodly levels. Intuitively, it makes sense to keep their blood sugars within normal range because we like lab values that are normal. But is that really the best thing to do?

The NICE-SUGAR trial set out to examine this question. It enrolled over 6,000 patients in ICUs, almost all of whom were mechanically ventilated. Patients were divided into blood sugar goal groups of 81-108 or <180. Ultimately, the study found 90-day mortality was significantly higher in the 81-108 group, by about 3%, and that severe hypoglycemia was about 7% more common.



How do you adjust insulin therapy?

I was totally befuddled by insulin when starting intern year. Luckily, we were required to do PEAC modules that cleared up a lot of confusing issues.

From: Johns Hopkins modules,

When should insulin be started?
Insulin is recommended when hemoglobin A1C >10% and REQUIRED when >10% and ketonuria or weight loss are present.

HOW exactly is insulin therapy started? 
Insulin therapy will always consist of basal insulin (glargine, detemir, NPH) +/- sliding scale. Aim for a morning fasting glucose of 80-130 mg/dl. Start with 10 U and see how the patient responds. If the glucose is above goal, add 2 U every 3 days until the goal is met. If the glucose is >180 mg/dl, add 4 U.

What if a patient was already on medications for diabetes and then has to switch to insulin? 
The non-insulin medications may be continued UNLESS they’re a sulfonylurea, a DPP-4 inhibitor, or GLP-1 agonist.

What if the patient has good morning fasting glucoses, but their A1C is still high?
The likely cause is hyperglycemia associated with eating. You now have two choices: change to twice-daily premixed insulin (usually basal + short-acting) OR add prandial insulin.
Premixed combination therapy is harder to individualize, results in more hypoglycemia, results in inferior glycemic control. If you go with prandial insulin, start with 4 U with the largest meal of the day and aim to control the pre-prandial glucose of the following meal, or bedtime glucose if you’re targeting dinner time, to <130 mg/dl.

From: Johns Hopkins modules,
From: Johns Hopkins modules,

Tips on choosing meds for diabetes type II

There are a slew of medications available for type II diabetes. The American Association of Clinical Endocrinologists has put together a nice algorithm for management (click on the PPT links).

Rather than go through the pharmacokinetics, mechanism, and granular details of each medication, here are some tips that I thought were important:

Lifestyle changes are the first thing that should be tried. In patients with newly discovered/early diabetes, take a cue from Will Ferrell and be, be, aggressive! Have patients record not only their blood glucose, but also what they ate and how much they exercised.

Screen Shot 2015-07-01 at 10.14.02 PMMetformin is the first go-to medication.

  • You can go up to 2000 mg/day, and it’s cheaper to prescribe 500 mg increments rather than the 1000 mg.
  • Start with 500 mg once daily, and work up to the max dose if you have to
  • Monitor creatinine: avoid prescribing in men with a Cr<1.4 and women with Cr <1.5
  • You may have to add on B12 supplementation, as metformin can interfere with B12 absorption

The max benefit of sulfonylureas (glimepiride, glipizide, etc) are reached at half the max dose….so there’s no need to prescribe above that.

GLP-1 agents (exenatide is an example) have systemic effects on the brain, liver, and pancreas that make it really effective for treating diabetes. Patients can even lose weight! Avoid prescribing in patients with pancreatitis or a family history of medullary thyroid cancer, since this med has a tiny association with both. Barriers to using this med include that it is a subcutaneous injection, and is expensive.

Exenatide was derived from the saliva of these things! (Gila monsters, for those unfamiliar with the fauna of the American Southwest)
Exenatide was derived from the saliva of these things! (Gila monsters, for those unfamiliar with the fauna of the American Southwest)

DPP4 inhibitors (such as Januvia) raise GLP-1 to physiologic levels. They’re pretty decent, but won’t have quite the same effect that GLP-1 agents have. However, they can be taken by mouth, and are cheaper.

TZDs (like pioglitazone and rosaglitazone) may be associated with adverse cardiovascular events and are contraindicated in patients with NYHA class III/IV CHF- there is a black box warning.

SGLT-2 inhibitors (dapafliglozin, for example) block sodium reabsorption in the glomerulus. This results in the patient peeing out more glucose, which, logically, is associated with diuresis, risk of dehydration, and questionably, greater risk of UTIs. The FDA has also recently warned about an increased risk of ketoacidosis.