Two Diabetics Suffer Premanent Brain Damage

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Two older diabetics suffer permanent brain damage, one from human insulin, one

from glipizide caused hypoglycemia in hospital.

Iatrogenic Hypoglycemia and Malpractice Claims

 

SIDNEY FINK, MD, and TAPAN K. CHAUDHURI, MD, Hampton, Va

 

ABSTRACT: Iatrogenic neuroglycopenia represents a medical emergency for

which accepted and usually effective treatment exists. Treating physicians face

a malpractice risk if there is permanent neurologic damage and there is a

perception of failure to act prudently both before and after the damaging

episode. We report two cases to illustrate the medical and legal issues that may

be raised in such claims. [strangely, the known Humulin/human insulin problems

aren't even raised in defense in either of these two cases, but then far more of

the elderly are forced to take synthetic insulins than any of the various oral

anti-diabetic agents such as the glipizide in case 2 We refer interested readers

to the article on the bad record of human insulin with older diabetics.

Naturally, both settled out of court to prevent publicity. Ed]

 

A REVIEW of Indiana malpractice claims involving care of diabetic patients

during a 13-year period (35 claims) found none based directly on hypoglycemic

brain damage.1 We report two malpractice claims brought against internists in

the southeastern United States after insulin- and glipizide-induced

neuroglycopenia with permanent sequelae occurred.

 

CASE REPORTS

 

Case 1. A 75-year-old man with insulin-treated [ diabetes was hospitalized

after an episode of disorientation. He was taking 50 units of NPH insulin at 8

AM and 30 units at 7 PM. He had a 10-year history of hypertension controlled by

a low-salt diet and 250 mg of chlorothiazide daily. There was no history of

neurologic or ophthalmologic abnormality. On admission, he was described as

malnourished. His vital signs were normal. He was alert and in no distress.

Neurologic and ophthalmologic examinations were unremarkable apart from absent

ankle reflexes. There were no sensory abnormalities. No carotid bruits or

cardiac murmurs were heard. Laboratory studies showed a fasting blood glucose

level of 90 mg/dL, serum albumin value of 2.6 mg/dL, BUN value of 35 mg/dL, and

creatinine value of 2.4 mg/dL, with 1+ albuminuria.

 

The next day computed tomography (CT) of the brain showed an old right

temporal cerebral infarct. That afternoon the patient had an episode of slurred

speech, which cleared with the administration of orange juice. The blood glucose

concentration was not measured. The next evening at 8 o'clock he became

lethargic, speech was again slurred, and his face was drawn to one side. A blood

glucose value of 32 mg/dL was obtained before the administration of a bolus of

50% glucose. His mentation cleared immediately and neurologic signs disappeared.

An order was written to continue 5% glucose in water at 100 mL/hour overnight.

However, the intravenous infusion infiltrated at midnight and was discontinued

by the nursing staff. The physician was not called.

 

At 6:30 the next morning, the patient could not be aroused. The blood

glucose value was 45 mg/dL, and a bolus of 50% glucose was given intravenously,

followed by a constant infusion of 5% glucose. During the next 30 minutes, he

gradually became alert and after 1 hour was able to eat breakfast. He complained

of partial loss of vision bilaterally and color blindness. These losses were

permanent. An ophthalmologist later documented abnormal visual evoked potentials

and suggested neuronal degeneration due to hypoglycemia as the cause.2 Repeated

CT of the brain was unchanged at 6 weeks. A claim citing failure to protect

against recurrent hypoglycemia and substandard treatment after it occurred was

made against the attending physician and the hospital. The case was settled

before trial.

 

Case 2. A thin 69-year-old woman required nursing home placement due to

Alzheimerís disease. She had a history of diabetes controlled by diet, mild

hypertension, and stable angina. She had renal insufficiency with a BUN value of

40 mg/dL and creatinine value of 2.2 mg/dL. During her second year in the home,

her fasting blood glucose values rose to 150 to 180 mg/dL, and 2.5 mg daily of

glipizide was prescribed. Two weeks later, she had a hypoglycemic episode

manifested by confusion and upper respiratory distress. She did not lose

consciousness. The blood glucose value was found to be 19 mg/dL, and an

intravenous bolus of 50% glucose was administered, followed by an infusion of

glucose for 4 hours. She responded immediately to the IV bolus of glucose with a

return to normal mental state. Glipizide therapy was discontinued, and she

remained in the nursing home. Two days later, she was hospitalized because of a

fecal impaction with rectal bleeding. At midnight of the next day, she was found

to be confused with slurred speech. Blood glucose measured 30 mg/dL. She

responded to a bolus of 50% glucose followed by 5% glucose in water through the

night. There were no recognized sequelae to these episodes.

 

Four months later, a random blood glucose value of 278 mg/dL was reported

to a physician providing weekend call to the nursing home. He was unaware of the

earlier hypoglycemic episodes and gave a telephone order for 5 mg of glipizide

daily, to be followed by a fasting blood glucose measurement in 1 week. In the

late afternoon 3 days later, the patient became unresponsive to verbal stimuli.

She was given 1 unit of glucagon subcutaneously and became alert. She ate dinner

and a late snack, but at 6 oíclock the next morning she was again unresponsive.

An infusion of glucose in half-normal saline was begun, which led to pulmonary

edema. She was hospitalized, and the admitting chest film showed pulmonary

congestion and a pneumonic infiltrate at the left base. She never regained

consciousness and died 5 days later. The autopsy showed patchy areas of necrosis

in the brain with the distribution characteristic of neuroglycopenic damage.3,4

There was evidence of coronary artery disease, with a healed myocardial

infarction, and bilateral bronchopneumonia. A claim of malpractice was made

against the attending physician, the nursing home director, and the nursing

home. It cited the manner in which glipizide therapy was reinstituted despite

the patient's history of vulnerability, and the failure to provide adequate

treatment, including timely hospitalization. The case was settled during the

trial.

 

DISCUSSION

 

Both cases raised legal issues involving alleged negligence and causation.

Negligence was cited first in the failure to protect these patients from

neuroglycopenia. Juries are easily educated about the lesser importance of a

hormonal response to hypoglycemia as contrasted with one eliciting neurologic

signs, and the plaintiff experts cited the general vulnerability of both

patients to neuroglycopenia due to their age, poor nutritional status, and renal

insufficiency. Equally harmful to the defense were the episodes of hypoglycemia

with neurologic signs that preceded the permanent damage. Physicians are not

expected to anticipate every complication, but once harbingers are present, as

in these cases, physicians have difficulty in proving that they continued to

provide prudent care. Both cases also cited substandard care after the

appearance of neurologic signs in the final episodes. Substandard care is

readily recognized when a physicianís orders are not followed (Case 1).

Substandard treatment in Case 2 was the failure to provide an immediate bolus of

50% glucose and provide the conditions for a constant glucose infusion given

that the patient had already shown a tendency to relapse 3 days after

discontinuance of glipizide therapy. Pertinently, the court exhibits included a

page from a standard textbook,5 which stated that all cases of

sulfonylurea-induced severe hypoglycemia require hospital admission with blood

glucose monitoring for at least 3 days.

 

It has been known for decades that neuroglycopenia has specific

deleterious effects on the central nervous system after administration of

insulin6 and sulfonylurea.3,7 The retina (Case 2) is vulnerable to hypoglycemia

because it has an unusually active metabolism, particularly on the part of the

photoreceptor cells. As in the brain, these needs are met by the circulating

blood glucose, with only a limited quantity of glycogen available (most of it in

the Müller cells). The defense in both cases conceded the importance of adequate

cerebral access to glucose but emphasized the element of causation and the

possibility that the iatrogenic falls in blood glucose played no role in the

adverse outcomes. Proximate cause requires reasonable foreseeability and cause

in fact, and the possibility that the damages were due to ischemia rather than

hypoglycemia was raised in both patients. This defense was supported by the

patientsí histories of hypertension and cardiovascular disease, as well as the

CT evidence of a past stroke in Case 1. However, this defense was weakened by

the temporal relationship between the neurologic damage and the hypoglycemia and

by the findings on ophthalmologic and autopsy examinations. Brain damage due to

neuroglycopenia shows a distribution pattern that differs from that of ischemia,

with greatest neuronal loss in the superficial and paraventricular layers of the

cerebral cortex and hippocampus, especially the dentate gyrus of the latter.

Ischemia, on the other hand, causes selective loss of one type of neuron

depending on the brain region involved and also affects glial and endothelial

cells.8 Although not pertinent in our cases, it has been pointed out that the

presence of ischemic change does not in itself rule out hypoglycemic brain

damage; infarction may well develop secondarily in the recovery period after

hypoglycemia due to tissue lactic acidosis after rapid glucose

administration.4,8

 

Physicians who treat patients with diabetes may face claims that involve

hypoglycemia indirectly. The Indiana claims review1 included three patients who

had indirect complications (eg, falls) attributed to hypoglycemia. An

interesting example of indirect legal exposure is Pittman v Upjohn C.9 Without

his grandmotherís knowledge, 26-year-old Pittman mistook her prescription

Micronase (glyburide) tablets for aspirin and had neuroglycopenic brain damage

as a result. The patientís representative sued the prescribing physician for

failure to warn the grandmother of the danger of Micronase if it were to be

consumed by someone other than herself.

 

We see narrow limits to the risk management steps physicians can take for

these indirect claims. However, our cases do illustrate the risk management

value of a prompt, complete, and well-documented medical response when a

physician is called to treat neuroglycopenia. In the cases we have reported,

neither party made reference to current guidelines for the management of

hypoglycemia,10 and it remains to be seen what role guidelines will play in

future suits.

 

References

 

1. Clark CM Jr, Kinney ED: The potential role of diabetes guidelines in

the reduction of medical injury and malpractice claims involving diabetes.

Diabetes Care 1994; 17:155-159

 

2. Harrad RA, Cockram CS, Plumb AP, et al: The effect of hypoglycaemia on

visual function: a clinical and electrophysiological study. Clin Sci 1985;

69:673-679

 

3. Kalimo H, Olsson Y: Effects of severe hypoglycemia on the human

brain-neuropathological case reports. Acta Neurol Scand 1980; 62:345-356

 

4. Auer RN: Progress review: hypoglycemic brain damage. Stroke 1986;

17:699-708

 

 

 

 

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