Malpractice Counsel

Hypoglycemia

mrfiza/ Shutterstock

A 44-year-old-man with type 1 diabetes mellitus (DM) was transported to the ED via emergency medical services (EMS) with a chief complaint of hypoglycemia. His wife stated the patient had been acting strangely prior to presentation. She further noted that after checking his blood sugar, which was 19 mg/dL, she gave her husband an oral glucose tablet with some water before calling EMS.

Upon arrival to the ED, the patient was triaged and designated as an urgent level III. At that time, he was alert and oriented, with a blood glucose level of 66 mg/dL. The patient was examined by a physician assistant (PA) within 15 minutes of his arrival. When interviewed by the PA, the patient described feelings of weakness, dizziness, and lightheadedness. The PA attributed these symptoms to the patient’s hypoglycemic state and ordered him a food tray. The patient was then observed for approximately 2 hours, during which time repeat blood-glucose testing revealed a level of 438 mg/dL. Approximately 20 minutes later, another blood-glucose test showed a level of 400 mg/dL. The patient felt well, appeared back to baseline, and expressed the desire to go home. At discharge, the PA instructed the patient to reduce his insulin by 20% and to follow up with his primary care physician (PCP) that same week.

Approximately 3 hours after discharge, the patient was found unresponsive by his wife, and EMS was again called. When EMS arrived at the patient’s house, his blood glucose level was 85 mg/dL. At presentation to the ED, the patient was unresponsive and without a pulse. Despite approximately 30 minutes of intensive resuscitative efforts, the code was called and the patient was pronounced dead.

The family sued the hospital, the emergency physician (EP), and the PA. They claimed the triage nurse failed to obtain an adequate history of the patient’s recent glucometer checks, previous hypoglycemic episodes, the amount and time of his last dose of insulin, and when and how much food he had recently ingested. The plaintiff further argued that that PA failed to obtain an electrocardiogram (ECG) to determine if the patient’s heart rhythm had been affected by his hypoglycemic state. The plaintiff also claimed the PA should have notified the patient’s PCP that the patient was in the ED, so that he could be admitted.

The defendants denied any negligence and argued the patient’s death was due to a sudden cardiac event, which was unrelated to the low-blood sugar levels. The defense contended that the patient’s enlarged heart and preexisting cardiovascular disease, hypertension, hypercholesterolemia, poorly controlled type 1 DM, history of alcohol abuse, and documented evidence of medication noncompliance were the cause of death. According to published accounts, a defense verdict was returned.

Discussion

It seems that rarely a shift goes by without a patient presenting with diabetes-associated complications such as hyperglycemia or hypoglycemia. While the jury reached the correct conclusion in this case, it does serve as a reminder that cases of hypoglycemia should not be treated lightly, and the EP must attempt to determine its cause.

The most commonly accepted definition of hypoglycemia is a blood-glucose level <50 mg/dL with associated symptoms. The causes of hypoglycemia in patients treated with insulin typically involves inadequate or no food intake, or accidental administration of too much insulin or the wrong type of insulin.¹

The differential diagnosis, however, needs to be more than just these two conditions. Since insulin is cleared by the kidneys, and patients with DM are at increased risk for kidney disease, acute renal failure should be considered in the differential. Other conditions to consider include infection, acute coronary syndromes, or unusual physical or mental stress.²

As with every patient presenting to the ED, patients with DM require a good history taking and physical examination. Additional testing, such as an ECG, troponin level, and kidney function test, should be performed based on the history and physical examination. Once the cause is determined, the majority of these patients can be treated with either intravenous (IV) or oral medications, observed, and discharged home with follow-up instructions.

Diabetic patients presenting with hypoglycemia due to a sulfonylurea agent or a long-acting insulin are in a completely different category. Because of the longer half-life of these agents, such patients will usually require admission to the hospital for serial glucose monitoring and treatment.² On occasion, patients with diabetic hypoglycemia and who are on a regular form of insulin will also require hospital admission. Those at highest risk are patients with DM aged 80 years and older.¹

Hyperkalemia

A 59-year-old man presented to the ED complaining of generalized weakness, the onset of which he stated had developed gradually over the previous 3 days. He denied chest pain, shortness of breath, or nausea and vomiting. His medical history was significant only for renal insufficiency. The patient was on no medications and denied alcohol or tobacco use.

Monkey Business Images/ Shutterstock

On physical examination, the patient had normal vital signs, including normal pulse oximetry. Similarly, the heart, lung, and abdominal examinations were all normal. On neurological examination, the patient had 5/5 motor strength in all four extremities and exhibited a normal gait.

The EP ordered an ECG, complete blood count (CBC), basic metabolic panel, urinalysis, and a chest X-ray (CXR). Laboratory evaluation showed an elevated potassium level of 6 mEq/L. The results of the CBC, urinalysis, and CXR were all reported as normal. (Unfortunately, there was no published information on the results of the BUN, creatinine, serum bicarbonate, or ECG findings.)

Based on the patient’s elevated potassium level, the EP ordered sodium polystyrene (Kayexalate) orally and arranged for admission to the hospital. The sodium polystyrene was administered to the patient approximately 1 hour after it was ordered.  While waiting for an inpatient bed, the patient experienced a cardiac arrest and died in the ED.

The family sued the EP and hospital for failure to properly respond to the patient’s elevated potassium level. The hospital denied any negligence, and the defense argued that the death was not related to any electrolyte abnormality, but was due to a respiratory arrest that led to the cardiac arrest. The defendants also maintained the sodium polystyrene had been administered in a timely manner. At trial, a defense verdict was returned.

Discussion

Hyperkalemia has been variably defined as serum potassium concentrations >5 mEq/L, >5.5 mEq/L, or >6 mEq/L.¹ Symptoms of hyperkalemia include generalized muscle weakness (as seen in this patient), muscle cramps, paresthesias, nausea, vomiting, and/or diarrhea. However, it is the cardiac manifestations (eg, ventricular arrhythmias, complete heart block, asystole) associated with hyperkalemia that are most concerning.

There are numerous causes of hyperkalemia, including medications, renal failure, digitalis toxicity, and metabolic acidosis. Therefore, it is important for the EP to identify the etiology in order to definitively treat the hyperkalemia.

Traditionally, it has been taught that hyperkalemia only requires treatment if abnormalities on the ECG are noted. Classic findings seen on ECG include prolonged PR interval, peaked T waves,² shortened QT interval, QRS widening, and a sinusoidal wave pattern. Once fictitious or hemolysis has been ruled out as the etiology, most EPs will initiate treatment above a specific threshold value (frequently 6 mEq/L),

Since it is the cardiac effects of hyperkalemia that can result in death, the initial treatment must be directed toward cardiac membrane stabilization. This is best accomplished by the administration of calcium gluconate 10% IV. This medication has a rapid onset of action (typically 1-3 minutes) and helps prevent the development of cardiac arrhythmias. Additional measures, which involve moving potassium intracellullarly, include sodium bicarbonate IV and insulin with glucose IV.

Actual removal of potassium from the body involves either the administration sodium polystyrene sulfonate or hemodialysis. Sodium polystyrene sulfonate, which is an ion-exchange resin designed to exchange sodium for potassium in the colon, can be given either orally or as an enema. Even though sodium polystyrene sulfonate has been approved for the treatment of hyperkalemia since 1958, it does not take effect for 1 to 2 hours after administration; there is also growing evidence questioning its efficacy and safety.³ In addition, sodium polystyrene sulfonate can exacerbate volume overload due to the associated increase in serum sodium. Therefore, hemodialysis is the most effective treatment for hyperkalemia, and is the treatment of choice for unstable patients with hyperkalemia and acute or chronic renal failure.

Hypoglycemia

mrfiza/ Shutterstock

A 44-year-old-man with type 1 diabetes mellitus (DM) was transported to the ED via emergency medical services (EMS) with a chief complaint of hypoglycemia. His wife stated the patient had been acting strangely prior to presentation. She further noted that after checking his blood sugar, which was 19 mg/dL, she gave her husband an oral glucose tablet with some water before calling EMS.

Upon arrival to the ED, the patient was triaged and designated as an urgent level III. At that time, he was alert and oriented, with a blood glucose level of 66 mg/dL. The patient was examined by a physician assistant (PA) within 15 minutes of his arrival. When interviewed by the PA, the patient described feelings of weakness, dizziness, and lightheadedness. The PA attributed these symptoms to the patient’s hypoglycemic state and ordered him a food tray. The patient was then observed for approximately 2 hours, during which time repeat blood-glucose testing revealed a level of 438 mg/dL. Approximately 20 minutes later, another blood-glucose test showed a level of 400 mg/dL. The patient felt well, appeared back to baseline, and expressed the desire to go home. At discharge, the PA instructed the patient to reduce his insulin by 20% and to follow up with his primary care physician (PCP) that same week.

Approximately 3 hours after discharge, the patient was found unresponsive by his wife, and EMS was again called. When EMS arrived at the patient’s house, his blood glucose level was 85 mg/dL. At presentation to the ED, the patient was unresponsive and without a pulse. Despite approximately 30 minutes of intensive resuscitative efforts, the code was called and the patient was pronounced dead.

The family sued the hospital, the emergency physician (EP), and the PA. They claimed the triage nurse failed to obtain an adequate history of the patient’s recent glucometer checks, previous hypoglycemic episodes, the amount and time of his last dose of insulin, and when and how much food he had recently ingested. The plaintiff further argued that that PA failed to obtain an electrocardiogram (ECG) to determine if the patient’s heart rhythm had been affected by his hypoglycemic state. The plaintiff also claimed the PA should have notified the patient’s PCP that the patient was in the ED, so that he could be admitted.

The defendants denied any negligence and argued the patient’s death was due to a sudden cardiac event, which was unrelated to the low-blood sugar levels. The defense contended that the patient’s enlarged heart and preexisting cardiovascular disease, hypertension, hypercholesterolemia, poorly controlled type 1 DM, history of alcohol abuse, and documented evidence of medication noncompliance were the cause of death. According to published accounts, a defense verdict was returned.

Discussion

It seems that rarely a shift goes by without a patient presenting with diabetes-associated complications such as hyperglycemia or hypoglycemia. While the jury reached the correct conclusion in this case, it does serve as a reminder that cases of hypoglycemia should not be treated lightly, and the EP must attempt to determine its cause.

The most commonly accepted definition of hypoglycemia is a blood-glucose level <50 mg/dL with associated symptoms. The causes of hypoglycemia in patients treated with insulin typically involves inadequate or no food intake, or accidental administration of too much insulin or the wrong type of insulin.¹

The differential diagnosis, however, needs to be more than just these two conditions. Since insulin is cleared by the kidneys, and patients with DM are at increased risk for kidney disease, acute renal failure should be considered in the differential. Other conditions to consider include infection, acute coronary syndromes, or unusual physical or mental stress.²

As with every patient presenting to the ED, patients with DM require a good history taking and physical examination. Additional testing, such as an ECG, troponin level, and kidney function test, should be performed based on the history and physical examination. Once the cause is determined, the majority of these patients can be treated with either intravenous (IV) or oral medications, observed, and discharged home with follow-up instructions.

Diabetic patients presenting with hypoglycemia due to a sulfonylurea agent or a long-acting insulin are in a completely different category. Because of the longer half-life of these agents, such patients will usually require admission to the hospital for serial glucose monitoring and treatment.² On occasion, patients with diabetic hypoglycemia and who are on a regular form of insulin will also require hospital admission. Those at highest risk are patients with DM aged 80 years and older.¹

Hyperkalemia

A 59-year-old man presented to the ED complaining of generalized weakness, the onset of which he stated had developed gradually over the previous 3 days. He denied chest pain, shortness of breath, or nausea and vomiting. His medical history was significant only for renal insufficiency. The patient was on no medications and denied alcohol or tobacco use.

Monkey Business Images/ Shutterstock

On physical examination, the patient had normal vital signs, including normal pulse oximetry. Similarly, the heart, lung, and abdominal examinations were all normal. On neurological examination, the patient had 5/5 motor strength in all four extremities and exhibited a normal gait.

The EP ordered an ECG, complete blood count (CBC), basic metabolic panel, urinalysis, and a chest X-ray (CXR). Laboratory evaluation showed an elevated potassium level of 6 mEq/L. The results of the CBC, urinalysis, and CXR were all reported as normal. (Unfortunately, there was no published information on the results of the BUN, creatinine, serum bicarbonate, or ECG findings.)

Based on the patient’s elevated potassium level, the EP ordered sodium polystyrene (Kayexalate) orally and arranged for admission to the hospital. The sodium polystyrene was administered to the patient approximately 1 hour after it was ordered.  While waiting for an inpatient bed, the patient experienced a cardiac arrest and died in the ED.

The family sued the EP and hospital for failure to properly respond to the patient’s elevated potassium level. The hospital denied any negligence, and the defense argued that the death was not related to any electrolyte abnormality, but was due to a respiratory arrest that led to the cardiac arrest. The defendants also maintained the sodium polystyrene had been administered in a timely manner. At trial, a defense verdict was returned.

Discussion

Hyperkalemia has been variably defined as serum potassium concentrations >5 mEq/L, >5.5 mEq/L, or >6 mEq/L.¹ Symptoms of hyperkalemia include generalized muscle weakness (as seen in this patient), muscle cramps, paresthesias, nausea, vomiting, and/or diarrhea. However, it is the cardiac manifestations (eg, ventricular arrhythmias, complete heart block, asystole) associated with hyperkalemia that are most concerning.

There are numerous causes of hyperkalemia, including medications, renal failure, digitalis toxicity, and metabolic acidosis. Therefore, it is important for the EP to identify the etiology in order to definitively treat the hyperkalemia.

Traditionally, it has been taught that hyperkalemia only requires treatment if abnormalities on the ECG are noted. Classic findings seen on ECG include prolonged PR interval, peaked T waves,² shortened QT interval, QRS widening, and a sinusoidal wave pattern. Once fictitious or hemolysis has been ruled out as the etiology, most EPs will initiate treatment above a specific threshold value (frequently 6 mEq/L),

Since it is the cardiac effects of hyperkalemia that can result in death, the initial treatment must be directed toward cardiac membrane stabilization. This is best accomplished by the administration of calcium gluconate 10% IV. This medication has a rapid onset of action (typically 1-3 minutes) and helps prevent the development of cardiac arrhythmias. Additional measures, which involve moving potassium intracellullarly, include sodium bicarbonate IV and insulin with glucose IV.

Actual removal of potassium from the body involves either the administration sodium polystyrene sulfonate or hemodialysis. Sodium polystyrene sulfonate, which is an ion-exchange resin designed to exchange sodium for potassium in the colon, can be given either orally or as an enema. Even though sodium polystyrene sulfonate has been approved for the treatment of hyperkalemia since 1958, it does not take effect for 1 to 2 hours after administration; there is also growing evidence questioning its efficacy and safety.³ In addition, sodium polystyrene sulfonate can exacerbate volume overload due to the associated increase in serum sodium. Therefore, hemodialysis is the most effective treatment for hyperkalemia, and is the treatment of choice for unstable patients with hyperkalemia and acute or chronic renal failure.

Hypoglycemia

mrfiza/ Shutterstock

A 44-year-old-man with type 1 diabetes mellitus (DM) was transported to the ED via emergency medical services (EMS) with a chief complaint of hypoglycemia. His wife stated the patient had been acting strangely prior to presentation. She further noted that after checking his blood sugar, which was 19 mg/dL, she gave her husband an oral glucose tablet with some water before calling EMS.

Upon arrival to the ED, the patient was triaged and designated as an urgent level III. At that time, he was alert and oriented, with a blood glucose level of 66 mg/dL. The patient was examined by a physician assistant (PA) within 15 minutes of his arrival. When interviewed by the PA, the patient described feelings of weakness, dizziness, and lightheadedness. The PA attributed these symptoms to the patient’s hypoglycemic state and ordered him a food tray. The patient was then observed for approximately 2 hours, during which time repeat blood-glucose testing revealed a level of 438 mg/dL. Approximately 20 minutes later, another blood-glucose test showed a level of 400 mg/dL. The patient felt well, appeared back to baseline, and expressed the desire to go home. At discharge, the PA instructed the patient to reduce his insulin by 20% and to follow up with his primary care physician (PCP) that same week.

Approximately 3 hours after discharge, the patient was found unresponsive by his wife, and EMS was again called. When EMS arrived at the patient’s house, his blood glucose level was 85 mg/dL. At presentation to the ED, the patient was unresponsive and without a pulse. Despite approximately 30 minutes of intensive resuscitative efforts, the code was called and the patient was pronounced dead.

The family sued the hospital, the emergency physician (EP), and the PA. They claimed the triage nurse failed to obtain an adequate history of the patient’s recent glucometer checks, previous hypoglycemic episodes, the amount and time of his last dose of insulin, and when and how much food he had recently ingested. The plaintiff further argued that that PA failed to obtain an electrocardiogram (ECG) to determine if the patient’s heart rhythm had been affected by his hypoglycemic state. The plaintiff also claimed the PA should have notified the patient’s PCP that the patient was in the ED, so that he could be admitted.

The defendants denied any negligence and argued the patient’s death was due to a sudden cardiac event, which was unrelated to the low-blood sugar levels. The defense contended that the patient’s enlarged heart and preexisting cardiovascular disease, hypertension, hypercholesterolemia, poorly controlled type 1 DM, history of alcohol abuse, and documented evidence of medication noncompliance were the cause of death. According to published accounts, a defense verdict was returned.

Discussion

It seems that rarely a shift goes by without a patient presenting with diabetes-associated complications such as hyperglycemia or hypoglycemia. While the jury reached the correct conclusion in this case, it does serve as a reminder that cases of hypoglycemia should not be treated lightly, and the EP must attempt to determine its cause.

The most commonly accepted definition of hypoglycemia is a blood-glucose level <50 mg/dL with associated symptoms. The causes of hypoglycemia in patients treated with insulin typically involves inadequate or no food intake, or accidental administration of too much insulin or the wrong type of insulin.¹

The differential diagnosis, however, needs to be more than just these two conditions. Since insulin is cleared by the kidneys, and patients with DM are at increased risk for kidney disease, acute renal failure should be considered in the differential. Other conditions to consider include infection, acute coronary syndromes, or unusual physical or mental stress.²

As with every patient presenting to the ED, patients with DM require a good history taking and physical examination. Additional testing, such as an ECG, troponin level, and kidney function test, should be performed based on the history and physical examination. Once the cause is determined, the majority of these patients can be treated with either intravenous (IV) or oral medications, observed, and discharged home with follow-up instructions.

Diabetic patients presenting with hypoglycemia due to a sulfonylurea agent or a long-acting insulin are in a completely different category. Because of the longer half-life of these agents, such patients will usually require admission to the hospital for serial glucose monitoring and treatment.² On occasion, patients with diabetic hypoglycemia and who are on a regular form of insulin will also require hospital admission. Those at highest risk are patients with DM aged 80 years and older.¹

Hyperkalemia

A 59-year-old man presented to the ED complaining of generalized weakness, the onset of which he stated had developed gradually over the previous 3 days. He denied chest pain, shortness of breath, or nausea and vomiting. His medical history was significant only for renal insufficiency. The patient was on no medications and denied alcohol or tobacco use.

Monkey Business Images/ Shutterstock

On physical examination, the patient had normal vital signs, including normal pulse oximetry. Similarly, the heart, lung, and abdominal examinations were all normal. On neurological examination, the patient had 5/5 motor strength in all four extremities and exhibited a normal gait.

The EP ordered an ECG, complete blood count (CBC), basic metabolic panel, urinalysis, and a chest X-ray (CXR). Laboratory evaluation showed an elevated potassium level of 6 mEq/L. The results of the CBC, urinalysis, and CXR were all reported as normal. (Unfortunately, there was no published information on the results of the BUN, creatinine, serum bicarbonate, or ECG findings.)

Based on the patient’s elevated potassium level, the EP ordered sodium polystyrene (Kayexalate) orally and arranged for admission to the hospital. The sodium polystyrene was administered to the patient approximately 1 hour after it was ordered.  While waiting for an inpatient bed, the patient experienced a cardiac arrest and died in the ED.

The family sued the EP and hospital for failure to properly respond to the patient’s elevated potassium level. The hospital denied any negligence, and the defense argued that the death was not related to any electrolyte abnormality, but was due to a respiratory arrest that led to the cardiac arrest. The defendants also maintained the sodium polystyrene had been administered in a timely manner. At trial, a defense verdict was returned.

Discussion

Hyperkalemia has been variably defined as serum potassium concentrations >5 mEq/L, >5.5 mEq/L, or >6 mEq/L.¹ Symptoms of hyperkalemia include generalized muscle weakness (as seen in this patient), muscle cramps, paresthesias, nausea, vomiting, and/or diarrhea. However, it is the cardiac manifestations (eg, ventricular arrhythmias, complete heart block, asystole) associated with hyperkalemia that are most concerning.

There are numerous causes of hyperkalemia, including medications, renal failure, digitalis toxicity, and metabolic acidosis. Therefore, it is important for the EP to identify the etiology in order to definitively treat the hyperkalemia.

Traditionally, it has been taught that hyperkalemia only requires treatment if abnormalities on the ECG are noted. Classic findings seen on ECG include prolonged PR interval, peaked T waves,² shortened QT interval, QRS widening, and a sinusoidal wave pattern. Once fictitious or hemolysis has been ruled out as the etiology, most EPs will initiate treatment above a specific threshold value (frequently 6 mEq/L),

Since it is the cardiac effects of hyperkalemia that can result in death, the initial treatment must be directed toward cardiac membrane stabilization. This is best accomplished by the administration of calcium gluconate 10% IV. This medication has a rapid onset of action (typically 1-3 minutes) and helps prevent the development of cardiac arrhythmias. Additional measures, which involve moving potassium intracellullarly, include sodium bicarbonate IV and insulin with glucose IV.

Actual removal of potassium from the body involves either the administration sodium polystyrene sulfonate or hemodialysis. Sodium polystyrene sulfonate, which is an ion-exchange resin designed to exchange sodium for potassium in the colon, can be given either orally or as an enema. Even though sodium polystyrene sulfonate has been approved for the treatment of hyperkalemia since 1958, it does not take effect for 1 to 2 hours after administration; there is also growing evidence questioning its efficacy and safety.³ In addition, sodium polystyrene sulfonate can exacerbate volume overload due to the associated increase in serum sodium. Therefore, hemodialysis is the most effective treatment for hyperkalemia, and is the treatment of choice for unstable patients with hyperkalemia and acute or chronic renal failure.