hypoglycemia-can be deadly

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Dr. Tanenberg

Beware the Perils of Severe Hypoglycemia

J. Tanenberg, MD, FACP - Diabetes Health Advisory Board Member

May 13, 2010

Over 80 years ago, famed diabetologist Elliot Joslin said about the

treatment of patients with

type 1 diabetes

: " Ketoacidosis may kill a patient, but frequent hypoglycemic reactions will

ruin him. " Unfortunately,

hypoglycemia

continues to be the most difficult problem facing most patients, families,

and caregivers who deal with the management of

type 1

diabetes on a daily basis. Frequent hypoglycemia episodes not only can

" ruin, " or adversely impact the quality of life for patients, but also, when

severe,

can cause seizures, coma, and even death.

A Tragic Case

Recently, our group published a case report in the journal Endocrine

Practice describing a tragic death from hypoglycemia that occurred while the

patient

slept in his own bed. Our patient, a 23-year-old man with type 1 diabetes

who had a history of recurrent severe hypoglycemia, was using an older model

insulin pump

and wearing a separate, non-real-time continuous glucose monitoring (

CGM

) system. He was given the CGM in 2005 for the purpose of tracking his

nocturnal (nighttime) blood glucose values and making further

insulin

pump adjustments. After he was pronounced dead in the emergency room, our

diabetes nurse removed the pump and CGM to help us understand what happened.

His insulin pump was found to have been working correctly. What we learned

was that after supper, he had a heavy workout at a gym, followed by a late

snack.

Between 8 pm and midnight, he " stacked " five boluses of insulin, totaling

7.35 units (33% of his basal dose), in an attempt to keep his glucose values

in " tight " control. The downloaded sensor demonstrated that his glucose

values fell from about 200 mg/dL at midnight to under 50 mg/dL by 2:00 am,

and

to under 30 mg/dL by 5:00 am - three hours before he was found by his

parents.

Sadly, this is not a rare occurrence. In 1991, two British diabetes

specialists, describing 22 cases of unexplained sudden death in young

patients with

type 1 diabetes, coined the term " dead-in-bed syndrome. " Studies from Europe

estimate that the " dead-in-bed " syndrome is responsible for six percent of

the deaths of patients under age 40 with type 1 diabetes.

To better understand how these tragedies may occur, one needs to first

understand hypoglycemia as a biological event. When

blood sugars

fall below normal, there are two important consequences, which are

identified by the blood sugar level at which they occur and the type of

symptoms involved.

Mild and Moderate Hypoglycemia

The first consequence triggers a prompt release of hormones that work to

raise the blood sugar. These so-called counter-regulatory hormones include

epinephrine

(adrenaline), glucagon, cortisol, and growth hormone. The clinical responses

to these hormones, which are well known to patients who have had

hypoglycemic

reactions, include sweating, palpitations, tremor, hunger, nervousness, and

tingling sensations. These " fight, or flight " symptoms are often called

sympathetic

or adrenergic to emphasize their origin in the autonomic nervous system and

from the adrenal gland. They are non-specific and may also occur in response

to other stressors.

When hormones are released normally (in response to a low or rapid fall in

blood sugar), patients experience the symptoms and usually take action by

eating

or drinking

carbohydrates

.. Typically, the symptoms resolve within five minutes as the blood sugar

rises.

Severe Hypoglycemia

However, if the hormones are not released and there are no warning symptoms,

the blood sugar will continue to fall. As the blood sugar drops below 55

mg/dL,

the second consequence of hypoglycemia occurs. The brain becomes deprived of

glucose and can no longer function normally. This condition, called

neuroglycopenia,

leads to cognitive dysfunction that presents as confusion. There is a

slowing of reflexes, and the hypoglycemic individual loses the ability to

comprehend

and act appropriately. The patient is no longer able to treat the

hypoglycemia himself. The need for assistance from another person to treat

the hypoglycemia

fulfills the definition of severe hypoglycemia. When driving a car, for

example, patients with severe hypoglycemia often become lost even in a

familiar

neighborhood. If they are not able to quickly recognize the insulin reaction

and pull off the road, they may lose control of their vehicle, with

potentially

catastrophic consequences.

Loss of Protective Hormones

Several hormonal changes occur in patients with type 1 diabetes. Usually

within a few years of the onset of the disease, the patient's pancreas fails

to

secrete glucagon when the blood sugar falls below 70 mg/dL. When this

happens, only epinephrine is left to respond to the

low blood sugar

until it drops below 60 mg/dL. At that level, cortisol and growth hormone

are secreted. Unfortunately, these hormones are " too little, too late " to

help

during the first 10 minutes of the insulin reaction.

Patients with both a diminished glucagon and a diminished epinephrine

response have a 25-fold increase in the frequency of severe hypoglycemia.

Diabetes

specialists use the term hypoglycemic unawareness to describe patients who

have lost the ability to trigger the classic sympathetic symptoms. Sleep,

which

naturally suppresses epinephrine, makes the patient vulnerable to severe

nocturnal hypoglycemia.

If the blood sugar drops falls below 30 mg/dL, it may lead to seizures,

coma, and ultimately death (as it did in our patient). Occasionally,

patients with

tightly controlled type1 diabetes (e.g.,

A1c

under 6.5%) may be reasonably lucid with blood sugars below 40 mg/dL.

Apparently, the brain has a capability to lower the natural clinical set

point. This

situation places the patient in great danger. The only treatment is to back

off on glycemic control (in other words, raise the target blood sugars),

which

should raise the set point back to normal. In fact, it is well known that

each episode of severe hypoglycemia increases the possibility of a future

episode

occurring at an even lower blood glucose level. Our patient had experienced

an earlier episode of severe hypoglycemia that was successfully treated with

intravenous dextrose by the local rescue squad. It was for this reason that

the CGM study was ordered.

Causes of Hypoglycemia

In type 1 diabetes, the most common cause of hypoglycemia is a mismatch of

insulin, food intake, and physical activity. Whenever there is a change in

the

amount of food or

exercise

in a nondiabetic individual, the body adjusts by changing the hormones to

keep the glucose as close to normal as possible. This is why people without

diabetes

rarely become hypoglycemic when fasting or running marathons. In patients

taking insulin, however, vigorous physical activity may cause hypoglycemia

both

during the activity and for several hours afterward. In fact, late afternoon

exercise is a well known cause of nocturnal hypoglycemia. Regimens using the

newer analogue insulins (e.g., glargine and lispro) reduce the incidence of

hypoglycemia compared to those using regular and NPH insulin. But any

insulin,

even when dosed correctly, can cause severe hypoglycemia. If patients taking

insulin increase their physical activity, they must either eat more or

reduce

the insulin dose before and after their activity. Similarly, patients on

insulin who eat much less than usual need to reduce their insulin dose to

prevent

hypoglycemia. Furthermore, the indiscriminate use of alcohol can also lead

to severe hypoglycemia.

Treatment of Hypoglycemia

Mild hypoglycemia should be treated with 15 grams of fast-acting

carbohydrate, such as four ounces of juice or three to four dextrose

tablets. If the blood

sugar is still low in 10 to 15 minutes another 15 grams of carbohydrate

should be given (known as the Rule of 15). Moderate hypoglycemia typically

responds

to oral carbohydrates, but may take as long as 30 minutes to fully resolve.

Frequent fingerstick blood glucose testing is mandatory to be sure the

glucose

does not continue to fall.

Patients with severe hypoglycemia who are not yet comatose may respond to

liquid or buccal oral carbohydrates, but injectable glucagon is the best

treatment

in the home setting. Since glucagon may not raise the glucose levels to

normal, giving fast-acting carbohydrates after the patient becomes more

responsive

is essential. Rescue squads and emergency room physicians administer

50-percent dextrose intravenously, which usually reverses the condition very

quickly.

In some cases, repeated doses of intravenous dextrose are needed.

Prevention of Severe Hypoglycemia

To help prevent severe hypoglycemia, diabetes specialists recommend the

following:

list of 5 items

.. For physically active persons, it is important to check fingerstick blood

sugars after exercise in anticipation of possible hypoglycemia. It is

especially

important to check at bedtime and 3:00 am if the activity is after 4:00 pm.

.. Bedtime insulin should be decreased after exercise.

.. Physicians should be cautious about recommending near-normal blood glucose

control and A1c targets to patients with type 1 diabetes and a history of

hypoglycemia,

particularly if they sleep alone.

.. If severe hypoglycemia occurs, the physician should raise the glucose

targets immediately to prevent another episode.

.. Patients with nocturnal hypoglycemia, hypoglycemic unawareness, and/or a

history of seizures are candidates for the newer real-time subcutaneous

sensors

with low glucose alarms.

list end

Final Thoughts

Our purpose in publishing this tragic case is twofold. First, we want to

better inform physicians and patients of this potential danger. Severe

hypoglycemia,

in very rare cases, can lead to death while driving a car, swimming in the

ocean, or even sleeping in ones' own bed. If patients who take insulin learn

nothing else, they should learn to always test their blood sugar at bedtime,

before driving, and any time there is a change in activity or food intake.

Early treatment of mild hypoglycemia must be emphasized so that progression

to more severe consequences can be avoided. As physicians and diabetes

educators

learn more about the hazards of nocturnal hypoglycemia, they will educate

their patients to anticipate and prevent it.

Second, my colleagues and I are hoping that this tragic case report will add

to the growing literature that supports the need for real-time glucose

sensors

in all patients on insulin with a history of hypoglycemia. These data are

essential to convince all insurance carriers to reimburse this new

life-saving

technology. In my opinion, if our patient had been wearing a real-time

sensor four years ago, he would be alive today.

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