Emergency Medicine

Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS) are similar but distinct diabetic emergencies that are frequently encountered in the ED. Patients with DKA or HHS present with hyperglycemia and dehydration and frequently appear quite ill physically. In both syndromes, there is insufficient insulin levels to transport glucose into cells.

As previously noted, although DKA and HHS share similar characteristic signs and symptoms, they are two distinct conditions that must be differentiated in the clinical work-up. One characteristic that helps the emergency physician (EP) to distinguish between the two conditions is the patient age at symptom onset. Although both conditions can occur at any age, diabetic ketoacidosis typically develops in younger patients, less than 45 years, who have little or no endogenous insulin production, whereas HHS usually occurs in much older non-insulin-dependent patients (who are often greater than 60 years old). ^1-3 This review discusses the similarities and differences in the etiology, diagnosis, and treatment of DKA and HHS to guide evaluation and simplify management, highlighting practical tips and clinical pearls. When applicable, information has been organized into groups of five to facilitate retention and recall.

The Etiology of DKA Vs HHS

The fundamental underlying issue in both DKA and HHS is an absolute or relative lack of insulin that results in an increase in counter-regulatory hormones, including glucagon, cortisol, and catecholamines.

Insulin has five main actions: (1) to drive glucose into cells; (2) to drive potassium into cells; (3) to create an anabolic environment; (4) to inhibit breakdown of fat; and (5) to block the breakdown of proteins. (Table 1).

Diagnosis and Workup

Laboratory Evaluation

In addition to hyperglycemia, another key finding in DKA is elevated anion gap metabolic acidosis resulting from ketoacid production. Laboratory evaluation will demonstrate a pH less than 7.3 and serum bicarbonate level less than 18 mEq/L; urinalysis will be positive for ketones.

Though HHS patients also present with hyperglycemia, laboratory evaluation will demonstrate no, or only mild, acidosis, normal pH (typically >7.3), bicarbonate level greater than 18 mEq/L, and a high-serum osmolality (>350 mOsm/kg). While urinalysis may show low or no ketones, patients with HHS do not develop the marked ketoacidosis seen in DKA. Moreover, glucose values are more elevated in patients with HHS, frequently exceeding 1,000 mg/dL.

Signs and Symptoms

Patients with either of these hyperglycemic crises often present with fatigue, polyuria, and polydipsia. They appear dehydrated on examination with dry mucous membranes, tachycardia, and in severe cases, hypotension. Patients with HHS often present with altered mental status, seizures, and even coma, while patients with DKA typically only experience changes in mental status in the most severe cases (Table 2). As many as one-third of patients with a hyperglycemic crisis will have an overlapping DKA/HHS syndrome.^1-3 With respect to patient age, HHS tends to develop in older patients who have type 2 diabetes and several underlying comorbidities.²

Precipitating Causes of DKA and HHS

The five causes of DKA/HHS can be remembered as the “Five I’s”: (1) infection; (2) infarction; (3) infant (pregnancy), (4) indiscretion, and (5) [lack of] insulin (Table 3).

Infection. Infection is one of the most common precipitating factors in both DKA and HHS.¹ During the history intake, the EP should ask the patient if he or she has had any recent urinary and respiratory symptoms, as positive responses prompt further investigation with urinalysis and chest radiography. A thorough dermatological examination should be performed to assess for visible signs of infection, particularly in the extremities and intertriginous areas.

When assessing patients with DKA or HHS for signs of infection, body temperature to assess for the presence of fever is not always a reliable indicator. This is because many patients with DKA/HHS develop tachypnea, which can affect the efficacy of an oral thermometer. In such cases, the rectal temperature is more sensitive for detecting fever. It should be noted, however, that some patients with severe infection or immunocompromised state—regardless of the presence or absence of tachypnea—may be normothermic or even hypothermic due to peripheral vasodilation—a poor prognostic sign.³ Blood and urine cultures should be obtained for all patients in whom infection is suspected.

Laboratory evaluation of patients with DKA may demonstrate a mild leukocytosis, a very common finding in DKA even in the absence of infection; leukocytosis is believed to result from elevated stress hormones such as cortisol and epinephrine.³

Infarction. Infarction is another important underlying cause of DKA/HHS and one that must not be overlooked. Screening for acute coronary syndrome through patient history, electrocardiography, and cardiac biomarkers should be performed in all patients older than age 40 years and in patients in whom there is any suggestion of myocardial ischemia.

A thorough neurological examination should be performed to assess for deficits indicative of stroke. Although neurological deficits can be due to severe hyperglycemia, most patients with focal neurological deficits from hyperglycemia also have altered mental status. Focal neurological deficits without a change in mental status are more likely to represent an actual stroke.⁴

Infant (Pregnancy). Pregnant patients are at an increased risk of developing DKA for several reasons, most notably due to the increased production of insulin-antagonistic hormones, which can lead to higher insulin resistance and thus increased insulin requirements during pregnancy.⁵ A pregnancy test is therefore indicated for all female patients of child-bearing age.

Indiscretion. Non-compliance with diet, such as taking in too many calories without appropriate insulin correction, and the ingestion of significant amounts of alcohol can lead to DKA. Eating disorders, particularly in young patients, may also contribute to recurrent cases.³

[Lack of] Insulin. In insulin-dependent diabetes, skipped insulin doses or insulin pump failure can trigger DKA/HHS. In fact, missed insulin doses are becoming a more frequent cause of DKA than infections.¹

Both DKA and HHS are usually triggered by an underlying illness or event. Therefore, clinicians should always focus on identifying precipitating causes such as acute infection, stroke, or myocardial infarction, as some require immediate treatment. In fact, DKA or HHS is rarely the primary cause of death; patients are much more likely to die from the precipitating event that caused DKA or HHS.^1,3

Assessing Disease Severity

Mental status and pH and serum bicarbonate levels help clinicians determine the extent of disease severity, classifying patients as having mild, moderate, or severe DKA (Table 4).² Patients at the highest risk for poor outcomes include those at the extremes of age, who have severe comorbidities, who have underlying infection, and who are hypotensive and/or in a comatose state.³

Patients who have HHS are much more likely to present with altered mental status, including coma. There is a linear relationship between osmolality and degree of altered mental status. Thus, diabetic patients with major changes in mental status but without high serum osmolality warrant immediate workup for alternative causes of their altered mental status.³ In addition, seizures, especially focal seizures, are relatively common in severe cases of HHS. Finally, highly abnormal blood pressure, pulse, and respiratory rate can also provide additional clues regarding the severity of hyperglycemic crisis.

Arterial Blood Gas Assessment: To Stick or Not to Stick?

In the past, measuring arterial blood gases (ABG) has been considered a mainstay in the evaluation of patients with DKA. But does an arterial stick, which is associated with some risk, really add essential information? One study by Ma et al⁶ evaluated whether ABG results significantly alter how physicians manage patients with DKA. In the study, the authors evaluated 200 ED patients and found that ABG analysis only changed diagnosis in 1% of patients, altered treatment in 3.5% of patients, and changed disposition in only 1% of patients. Arterial stick partial pressure of oxygen and partial pressure of carbon dioxide altered treatment and disposition in only 1% of patients. Furthermore, the study results showed venous pH correlated very strongly with arterial pH (r = 0.95).⁶ These findings demonstrate that ABG measurements rarely affect or alter DKA management, and support the use of venous pH as an adequate substitute for ABG testing.

Euglycemia

Euglycemic DKA has been reported in patients with type 1 diabetes who had been fasting or vomiting or who had received exogenous insulin prior to presentation.¹Euglycemia has also been reported in pregnant patients with type I diabetes.¹ More recently, sodium glucose cotransporter 2 inhibitors (SGLT2) have been shown to cause euglycemic DKA. While the therapeutic mechanism of this drug class is to inhibit proximal tubular resorption of glucose, they can cause DKA by decreasing renal clearance of ketone bodies and increasing glucagon levels and promoting hepatic ketogenesis. Patients with DKA who are on SGLT2 inhibitors may present with only modestly elevated glucose levels (typically in the 200- to 300-mg/dL range), but have profound wide gap metabolic acidosis due to β-hydroxybutyrate acid and acetoacetate accumulation.⁷ When evaluating patients on SGLT2 inhibitors for DKA, EPs should not solely rely on glucose values but rather assess the patient’s overall clinical picture, including the physical examination, vital signs, and pH. Additionally, once resuscitation with intravenous (IV) fluids and insulin is initiated, it may take longer for patients who use SGLT2 inhibitors to clear ketoacids than patients with DKA who do not use these medications.⁸

Treatment

The goal of treatment for DKA and HHS is to correct volume deficits, hyperglycemia, and electrolyte abnormalities (Table 5). Three of the five therapies to manage DKA and HHS are mandatory: IV fluid resuscitation, IV insulin, and IV potassium. The other therapies, IV bicarbonate, and IV phosphate, should be considered, but are rarely required for DKA or HHS.

In general, management of HHS is less aggressive than that of DKA because HHS develops over a period of weeks—unlike DKA, which develops over only 1 to 2 days. Treatment of any underlying causes of HHS should occur simultaneously.

Intravenous Fluids

The goal of IV fluid therapy for patients with DKA is rehydration—not to “wash-out” ketones. Ketone elimination occurs through insulin-stimulated metabolism. When determining volume-replacement goals, it is helpful to keep in mind that patients with moderate-to-mild DKA typically have fluid deficiencies of 3 to 5 L, and patients with severe DKA have fluid deficiencies between 5 and 6 L. Patients with HHS present with significantly higher fluid deficiencies of around 9 to 12 L.

The initial goal of fluid management is to correct hypoperfusion with bolus fluids, followed by a more gradual repletion of remaining deficits. After bolus fluids are administered, the rate and type of subsequent IV fluid infusion varies depending on hemodynamics, hydration state, and serum sodium levels.^2,3

Nonaggressive Vs Aggressive Fluid Management. One study by Adrogué et al⁹ compared the effects of managing DKA with aggressive vs nonaggressive fluid repletion. In the study, one group of patients received normal saline at 1,000 mL per hour for 4 hours, followed by normal saline at 500 mL per hour for 4 hours. The other group of patients received normal saline at a more modest rate of 500 mL per hour for 4 hours, followed by normal saline at 250 mL per hour for 4 hours. The authors found that patients in the less aggressive volume therapy group achieved a prompt and adequate recovery and maintained higher serum bicarbonate levels.⁹

Current recommendations for patients with DKA are to first treat patients with an initial bolus of 1,000 mL or 20 cc/kg of normal saline. Patients without profound dehydration should then receive 500 cc of normal saline per hour for the first 4 hours of treatment, after which the flow rate may be reduced to 250 cc per hour. For patients with mild DKA, therapy can start at 250 cc per hour with a smaller bolus dose or no bolus dose. Patients with profound dehydration and poor perfusion, should receive crystalloid fluids wide open until perfusion has improved. Overall, volume resuscitation in HHS is similar to DKA. However, the EP should be cautious with respect to total fluid volume and infusion rates to avoid fluid overload, since many patients with HHS are elderly and may have congestive heart failure.

Crystalloid Fluid Type for Initial Resuscitation. Normal saline has been the traditional crystalloid fluid of choice for managing DKA and HHS. Recent studies, however, have shown some benefit to using balanced solutions (Ringer’s lactate or PlasmaLyte) instead of normal saline. A recently published large study by Semler et al¹⁰ compared balanced crystalloid, in most cases lactated Ringers solution, to normal saline in critically ill adult patients, some of whom were diagnosed with DKA. The study demonstrated decreased mortality (from any cause) in the group who received balanced crystalloid fluid therapy and reduced need for renal-replacement therapy and reduced incidence of persistent renal dysfunction. The findings by Semler et al¹⁰ and findings from other smaller studies, calls into question whether normal saline is the best crystalloid to manage DKA and HHS.^11,12 It remains to be seen what modification the American Diabetes Association (ADA) will make to its current recommendations for fluid therapy, which were last updated in 2009.

It appears that though the use of Ringers lactate or PlasmaLyte to treat DKA usually raises a patient’s serum bicarbonate level to 18 mEq/L at a more rapid rate than normal saline, the use of balanced solutions may result in longer time to lower blood glucose to 250 mg/dL.¹³ However, by using a balanced solution, the hyperchloremic metabolic acidosis often seen with normal saline treatment will be avoided.¹²

Half-Normal Saline. An initially normal or increased serum sodium level, despite significant hyperglycemia, suggests a substantial free-water deficit. Calculating a corrected serum sodium can help quantify the degree of free-water deficit.³ While isotonic fluids remain the standard for initial volume load, clinicians should consider switching patients to half-normal saline following initial resuscitation if the corrected serum sodium is elevated above normal. The simplest estimation to correct sodium levels in DKA is to expect a decrease in sodium levels at a rate of at least 2 mEq/L per 100-mg/dL increase in glucose levels above 100 mg/dL. For a more accurate calculation, providers can expect a drop in sodium of 1.6 mEq/L per 100 mg/dL increase of glucose up to a level of 400 mg/dL and then a fall of 2.4 mEq/L in sodium per every 100 mg/dL rise in glucose thereafter.¹⁴

Glucose. Patients with DKA require insulin therapy until ketoacidosis resolves. However, the average time to correct ketoacidosis from initiating treatment is about 12 hours compared to only 6 hours for correction of hyperglycemia. Since insulin therapy must be continued despite lower glucose levels, patients are at risk for developing hypoglycemia if glucose is not added to IV fluids. To prevent hypoglycemia and provide an energy source for ketone metabolism, patients should be switched to fluids containing dextrose when their serum glucose approaches 200 to 250 mg/dL.^1,3 Typically, 5% dextrose in half-normal saline at 150 to 250 cc per hour is usually adequate to achieve this goal.

Insulin

As previously noted, insulin therapy is required to treat hyperglycemic crises from DKA and HHS. In DKA there is an absolute insulin deficiency, whereas in HHS, there is a relative insulin deficiency. In HHS, there is not enough endogenous insulin to move glucose into the cells, but there is enough insulin to block a catabolic state. That is why the breakdown of fats and proteins does not occur, and why ketoacidosis and hyperkalemia are not seen in HHS. On the other hand, glucose elevations do occur, and are usually more extreme in HHS than DKA. There are five major therapeutic actions of insulin in DKA (Table 5), and it is imperative to determine serum potassium before starting an insulin infusion as insulin will drive potassium into the cell, worsening hypokalemia and promoting the development of life-threatening arrhythmias, including ventricular fibrillation, ventricular tachycardia, and torsades de pointes. The electrocardiogram does not accurately predict severity of hypokalemia and should not be used as a substitute for direct potassium measurement.

Loading Dose and Drip Rate. When treating adult patients with DKA or HHS, the ADA recommends an IV push loading dose of 0.1 U/kg insulin, followed by an hourly maintenance dose of 0.1 U/kg. Alternatively, a continuous infusion of 0.16 U/kg/hr can be used without a bolus. The rationale behind a bolus is the rapid saturation of insulin receptors, followed by a drip to maintain saturation of receptors. However, a recent prospective observational cohort study by Goyal et al¹⁵ questions the utility of the initial insulin bolus. The study compared DKA patients who received an initial insulin bolus to those who did not. Both groups were similar at baseline and received equivalent IV fluids and insulin drips. They found no statistically significant differences in the incidence of hypoglycemia, rate of serum glucose change, anion gap change, or length of stay in the ED or hospital. The authors concluded that administration of an insulin bolus has no significant benefit to patients and does not change clinically relevant end-points.¹⁵ At this time, there is no proven benefit to giving DKA patients an IV insulin bolus; moreover, doing so may further increase hypoglycemia. The use of an insulin bolus is particularly not recommended for use in pediatric patients with DKA due to a higher incidence of hypoglycemia in this patient population.¹⁶

As with DKA, the ADA³ recommends giving HHS patients an insulin bolus of 0.1 U/ kg followed by a continuous infusion at 0.1 U/kg per hour. It is crucial to monitor patients closely to ensure glucose levels do not fall too rapidly. Glucose levels should be kept between 150 to 200 mg/dL for patients with DKA and 200 to 300 mg/dL for patients with HHS until the conditions resolve; this may necessitate lowering the infusion rate to 0.02 to 0.05 U/kg per hour. In addition to frequent glucose monitoring, a basic metabolic panel and venous pH should be obtained every 2 to 4 hours while a patient is on an insulin drip.³

Subcutaneous Vs Intravenous Insulin for DKA. Several small studies evaluating patients with mild-moderate DKA demonstrated similar outcomes when subcutaneous (SQ) insulin was used instead of IV insulin. However, SQ injections require more frequent dosing (every 1 to 2 hours) and still require close monitoring of blood glucose. This monitoring frequency is usually not feasible on a hospital floor, but may be feasible on step-down units, thus avoiding admission to the intensive care unit (ICU) for patients who do not otherwise require ICU-level of care.¹⁷ Subcutaneous insulin should not be given to patients with severe acidosis, hypotension, or altered mental status. The ADA consensus statement continues to recommend IV infusion of regular insulin as the preferred route due to its short half-life and easy titration.³

Determining When to Switch to Subcutaneous Insulin. Ideally, patients are not in the ED long enough to have their metabolic abnormalities corrected, as this usually requires several hours. In DKA, the insulin drip should continue until the blood glucose is less than 200 and at least two of the following conditions are met: the anion gap is less than 12, venous pH greater than 7.3, and serum bicarbonate >15. In HHS, osmolality and mental status should both return to normal prior to stopping the infusion. In both cases, subcutaneous insulin should be administered at least 1 to 2 hours before stopping the drip to prevent recurrent crisis.^1,3

Refractory Acidosis. First and foremost, refractory acidosis should prompt a diligent source for dead gut, abscess, and underlying sepsis. While vomiting and diffuse abdominal pain are common in DKA and are related to ketoacidosis, these symptoms are atypical of HHS and should raise suspicion for underlying pathology.³ Additionally, a lower than expected bicarbonate level can also occur from resuscitation with large volumes of normal saline, resulting in a hyperchloremic non-gap metabolic acidosis.

Potassium

Both DKA and HHS patients have total body potassium deficits due to osmotic diuresis that require careful repletion. Deficits can be substantial: The average total whole body potassium deficit in DKA is 3 to 5 mEq/kg.² Clinicians should exercise caution, however, since DKA patients may be hyperkalemic initially despite a total body potassium deficit. Early hyperkalemia is due to the transmembrane shift of potassium secondary to acidosis and insulin deficiency as well as hypertonicity. If initial potassium is greater than 5.2 mEq/L, potassium should not be administered but instead rechecked in 1 to 2 hours. If the potassium level is 4.0 to 5.2 mEq/L, then 10 mEq per hour is usually adequate. For levels between 3.3 and 4.0 mEq/L, administer potassium chloride at 20 mEq per hour. For levels less than 3.3 mEq/L, insulin should be held and potassium chloride should be aggressively repleted at 20 to 30 mEq per hour with continuous cardiac monitoring.^1-3 Failure to recognize and act on critical potassium levels is a known cause of unexpected death in DKA. During the first hour of DKA onset, patients are more likely to die from hyperkalemia. Later, while the patient is “stabilizing” on an insulin infusion, potassium levels will fall as insulin drives potassium back into cells.

Bicarbonate

Bicarbonate has many theoretical benefits but also has potential risks (Table 6).

Phosphate

Since there is no proven benefit to giving phosphate to adult patients with DKA, it is rarely used, except in specific situations other than pediatric DKA. Similar to potassium, initial serum phosphate levels do not reflect total body phosphate levels due to transmembrane shifts.^2,3 Phosphate repletionis most beneficial for patients who have cachexia, respiratory depression, anemia, cardiac dysfunction, or phosphate values lower than 1.0 to 1.5. If given, 20 to 30 mEq/L potassium phosphate (K₂PO₄) added to fluids is usually sufficient.³ Overly aggressive phosphate administration (>4.5 mmol/h or 1.5 mL/h potassium phosphate) can cause severe hypocalcemia and should be avoided.^1,3 In pediatric patients, up to one-half of potassium requirements are often given as potassium phosphate, but this may vary by institution.

Conclusion

Both DKA and HHS are diabetic emergencies that must be approached and managed systematically to correct underlying dehydration and metabolic abnormalities. Patient care begins by determining the etiology of these conditions, especially HHS. Once the cause has been identified, patients should be treated with bolus fluids to obtain adequate perfusion, followed by IV fluid infusion. Clinicians should carefully monitor the serum sodium level of patients with DKA or HHS to determine the ideal amount and type of fluid required, and also should measure potassium levels prior to starting patients on insulin. (Tables 7 and 8 summarize important clinical pearls when treating patients with DKA or HHS.)

Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS) are similar but distinct diabetic emergencies that are frequently encountered in the ED. Patients with DKA or HHS present with hyperglycemia and dehydration and frequently appear quite ill physically. In both syndromes, there is insufficient insulin levels to transport glucose into cells.

As previously noted, although DKA and HHS share similar characteristic signs and symptoms, they are two distinct conditions that must be differentiated in the clinical work-up. One characteristic that helps the emergency physician (EP) to distinguish between the two conditions is the patient age at symptom onset. Although both conditions can occur at any age, diabetic ketoacidosis typically develops in younger patients, less than 45 years, who have little or no endogenous insulin production, whereas HHS usually occurs in much older non-insulin-dependent patients (who are often greater than 60 years old). ^1-3 This review discusses the similarities and differences in the etiology, diagnosis, and treatment of DKA and HHS to guide evaluation and simplify management, highlighting practical tips and clinical pearls. When applicable, information has been organized into groups of five to facilitate retention and recall.

The Etiology of DKA Vs HHS

The fundamental underlying issue in both DKA and HHS is an absolute or relative lack of insulin that results in an increase in counter-regulatory hormones, including glucagon, cortisol, and catecholamines.

Insulin has five main actions: (1) to drive glucose into cells; (2) to drive potassium into cells; (3) to create an anabolic environment; (4) to inhibit breakdown of fat; and (5) to block the breakdown of proteins. (Table 1).

Diagnosis and Workup

Laboratory Evaluation

In addition to hyperglycemia, another key finding in DKA is elevated anion gap metabolic acidosis resulting from ketoacid production. Laboratory evaluation will demonstrate a pH less than 7.3 and serum bicarbonate level less than 18 mEq/L; urinalysis will be positive for ketones.

Though HHS patients also present with hyperglycemia, laboratory evaluation will demonstrate no, or only mild, acidosis, normal pH (typically >7.3), bicarbonate level greater than 18 mEq/L, and a high-serum osmolality (>350 mOsm/kg). While urinalysis may show low or no ketones, patients with HHS do not develop the marked ketoacidosis seen in DKA. Moreover, glucose values are more elevated in patients with HHS, frequently exceeding 1,000 mg/dL.

Signs and Symptoms

Patients with either of these hyperglycemic crises often present with fatigue, polyuria, and polydipsia. They appear dehydrated on examination with dry mucous membranes, tachycardia, and in severe cases, hypotension. Patients with HHS often present with altered mental status, seizures, and even coma, while patients with DKA typically only experience changes in mental status in the most severe cases (Table 2). As many as one-third of patients with a hyperglycemic crisis will have an overlapping DKA/HHS syndrome.^1-3 With respect to patient age, HHS tends to develop in older patients who have type 2 diabetes and several underlying comorbidities.²

Precipitating Causes of DKA and HHS

The five causes of DKA/HHS can be remembered as the “Five I’s”: (1) infection; (2) infarction; (3) infant (pregnancy), (4) indiscretion, and (5) [lack of] insulin (Table 3).

Infection. Infection is one of the most common precipitating factors in both DKA and HHS.¹ During the history intake, the EP should ask the patient if he or she has had any recent urinary and respiratory symptoms, as positive responses prompt further investigation with urinalysis and chest radiography. A thorough dermatological examination should be performed to assess for visible signs of infection, particularly in the extremities and intertriginous areas.

When assessing patients with DKA or HHS for signs of infection, body temperature to assess for the presence of fever is not always a reliable indicator. This is because many patients with DKA/HHS develop tachypnea, which can affect the efficacy of an oral thermometer. In such cases, the rectal temperature is more sensitive for detecting fever. It should be noted, however, that some patients with severe infection or immunocompromised state—regardless of the presence or absence of tachypnea—may be normothermic or even hypothermic due to peripheral vasodilation—a poor prognostic sign.³ Blood and urine cultures should be obtained for all patients in whom infection is suspected.

Laboratory evaluation of patients with DKA may demonstrate a mild leukocytosis, a very common finding in DKA even in the absence of infection; leukocytosis is believed to result from elevated stress hormones such as cortisol and epinephrine.³

Infarction. Infarction is another important underlying cause of DKA/HHS and one that must not be overlooked. Screening for acute coronary syndrome through patient history, electrocardiography, and cardiac biomarkers should be performed in all patients older than age 40 years and in patients in whom there is any suggestion of myocardial ischemia.

A thorough neurological examination should be performed to assess for deficits indicative of stroke. Although neurological deficits can be due to severe hyperglycemia, most patients with focal neurological deficits from hyperglycemia also have altered mental status. Focal neurological deficits without a change in mental status are more likely to represent an actual stroke.⁴

Infant (Pregnancy). Pregnant patients are at an increased risk of developing DKA for several reasons, most notably due to the increased production of insulin-antagonistic hormones, which can lead to higher insulin resistance and thus increased insulin requirements during pregnancy.⁵ A pregnancy test is therefore indicated for all female patients of child-bearing age.

Indiscretion. Non-compliance with diet, such as taking in too many calories without appropriate insulin correction, and the ingestion of significant amounts of alcohol can lead to DKA. Eating disorders, particularly in young patients, may also contribute to recurrent cases.³

[Lack of] Insulin. In insulin-dependent diabetes, skipped insulin doses or insulin pump failure can trigger DKA/HHS. In fact, missed insulin doses are becoming a more frequent cause of DKA than infections.¹

Both DKA and HHS are usually triggered by an underlying illness or event. Therefore, clinicians should always focus on identifying precipitating causes such as acute infection, stroke, or myocardial infarction, as some require immediate treatment. In fact, DKA or HHS is rarely the primary cause of death; patients are much more likely to die from the precipitating event that caused DKA or HHS.^1,3

Assessing Disease Severity

Mental status and pH and serum bicarbonate levels help clinicians determine the extent of disease severity, classifying patients as having mild, moderate, or severe DKA (Table 4).² Patients at the highest risk for poor outcomes include those at the extremes of age, who have severe comorbidities, who have underlying infection, and who are hypotensive and/or in a comatose state.³

Patients who have HHS are much more likely to present with altered mental status, including coma. There is a linear relationship between osmolality and degree of altered mental status. Thus, diabetic patients with major changes in mental status but without high serum osmolality warrant immediate workup for alternative causes of their altered mental status.³ In addition, seizures, especially focal seizures, are relatively common in severe cases of HHS. Finally, highly abnormal blood pressure, pulse, and respiratory rate can also provide additional clues regarding the severity of hyperglycemic crisis.

Arterial Blood Gas Assessment: To Stick or Not to Stick?

In the past, measuring arterial blood gases (ABG) has been considered a mainstay in the evaluation of patients with DKA. But does an arterial stick, which is associated with some risk, really add essential information? One study by Ma et al⁶ evaluated whether ABG results significantly alter how physicians manage patients with DKA. In the study, the authors evaluated 200 ED patients and found that ABG analysis only changed diagnosis in 1% of patients, altered treatment in 3.5% of patients, and changed disposition in only 1% of patients. Arterial stick partial pressure of oxygen and partial pressure of carbon dioxide altered treatment and disposition in only 1% of patients. Furthermore, the study results showed venous pH correlated very strongly with arterial pH (r = 0.95).⁶ These findings demonstrate that ABG measurements rarely affect or alter DKA management, and support the use of venous pH as an adequate substitute for ABG testing.

Euglycemia

Euglycemic DKA has been reported in patients with type 1 diabetes who had been fasting or vomiting or who had received exogenous insulin prior to presentation.¹Euglycemia has also been reported in pregnant patients with type I diabetes.¹ More recently, sodium glucose cotransporter 2 inhibitors (SGLT2) have been shown to cause euglycemic DKA. While the therapeutic mechanism of this drug class is to inhibit proximal tubular resorption of glucose, they can cause DKA by decreasing renal clearance of ketone bodies and increasing glucagon levels and promoting hepatic ketogenesis. Patients with DKA who are on SGLT2 inhibitors may present with only modestly elevated glucose levels (typically in the 200- to 300-mg/dL range), but have profound wide gap metabolic acidosis due to β-hydroxybutyrate acid and acetoacetate accumulation.⁷ When evaluating patients on SGLT2 inhibitors for DKA, EPs should not solely rely on glucose values but rather assess the patient’s overall clinical picture, including the physical examination, vital signs, and pH. Additionally, once resuscitation with intravenous (IV) fluids and insulin is initiated, it may take longer for patients who use SGLT2 inhibitors to clear ketoacids than patients with DKA who do not use these medications.⁸

Treatment

The goal of treatment for DKA and HHS is to correct volume deficits, hyperglycemia, and electrolyte abnormalities (Table 5). Three of the five therapies to manage DKA and HHS are mandatory: IV fluid resuscitation, IV insulin, and IV potassium. The other therapies, IV bicarbonate, and IV phosphate, should be considered, but are rarely required for DKA or HHS.

In general, management of HHS is less aggressive than that of DKA because HHS develops over a period of weeks—unlike DKA, which develops over only 1 to 2 days. Treatment of any underlying causes of HHS should occur simultaneously.

Intravenous Fluids

The goal of IV fluid therapy for patients with DKA is rehydration—not to “wash-out” ketones. Ketone elimination occurs through insulin-stimulated metabolism. When determining volume-replacement goals, it is helpful to keep in mind that patients with moderate-to-mild DKA typically have fluid deficiencies of 3 to 5 L, and patients with severe DKA have fluid deficiencies between 5 and 6 L. Patients with HHS present with significantly higher fluid deficiencies of around 9 to 12 L.

The initial goal of fluid management is to correct hypoperfusion with bolus fluids, followed by a more gradual repletion of remaining deficits. After bolus fluids are administered, the rate and type of subsequent IV fluid infusion varies depending on hemodynamics, hydration state, and serum sodium levels.^2,3

Nonaggressive Vs Aggressive Fluid Management. One study by Adrogué et al⁹ compared the effects of managing DKA with aggressive vs nonaggressive fluid repletion. In the study, one group of patients received normal saline at 1,000 mL per hour for 4 hours, followed by normal saline at 500 mL per hour for 4 hours. The other group of patients received normal saline at a more modest rate of 500 mL per hour for 4 hours, followed by normal saline at 250 mL per hour for 4 hours. The authors found that patients in the less aggressive volume therapy group achieved a prompt and adequate recovery and maintained higher serum bicarbonate levels.⁹

Current recommendations for patients with DKA are to first treat patients with an initial bolus of 1,000 mL or 20 cc/kg of normal saline. Patients without profound dehydration should then receive 500 cc of normal saline per hour for the first 4 hours of treatment, after which the flow rate may be reduced to 250 cc per hour. For patients with mild DKA, therapy can start at 250 cc per hour with a smaller bolus dose or no bolus dose. Patients with profound dehydration and poor perfusion, should receive crystalloid fluids wide open until perfusion has improved. Overall, volume resuscitation in HHS is similar to DKA. However, the EP should be cautious with respect to total fluid volume and infusion rates to avoid fluid overload, since many patients with HHS are elderly and may have congestive heart failure.

Crystalloid Fluid Type for Initial Resuscitation. Normal saline has been the traditional crystalloid fluid of choice for managing DKA and HHS. Recent studies, however, have shown some benefit to using balanced solutions (Ringer’s lactate or PlasmaLyte) instead of normal saline. A recently published large study by Semler et al¹⁰ compared balanced crystalloid, in most cases lactated Ringers solution, to normal saline in critically ill adult patients, some of whom were diagnosed with DKA. The study demonstrated decreased mortality (from any cause) in the group who received balanced crystalloid fluid therapy and reduced need for renal-replacement therapy and reduced incidence of persistent renal dysfunction. The findings by Semler et al¹⁰ and findings from other smaller studies, calls into question whether normal saline is the best crystalloid to manage DKA and HHS.^11,12 It remains to be seen what modification the American Diabetes Association (ADA) will make to its current recommendations for fluid therapy, which were last updated in 2009.

It appears that though the use of Ringers lactate or PlasmaLyte to treat DKA usually raises a patient’s serum bicarbonate level to 18 mEq/L at a more rapid rate than normal saline, the use of balanced solutions may result in longer time to lower blood glucose to 250 mg/dL.¹³ However, by using a balanced solution, the hyperchloremic metabolic acidosis often seen with normal saline treatment will be avoided.¹²

Half-Normal Saline. An initially normal or increased serum sodium level, despite significant hyperglycemia, suggests a substantial free-water deficit. Calculating a corrected serum sodium can help quantify the degree of free-water deficit.³ While isotonic fluids remain the standard for initial volume load, clinicians should consider switching patients to half-normal saline following initial resuscitation if the corrected serum sodium is elevated above normal. The simplest estimation to correct sodium levels in DKA is to expect a decrease in sodium levels at a rate of at least 2 mEq/L per 100-mg/dL increase in glucose levels above 100 mg/dL. For a more accurate calculation, providers can expect a drop in sodium of 1.6 mEq/L per 100 mg/dL increase of glucose up to a level of 400 mg/dL and then a fall of 2.4 mEq/L in sodium per every 100 mg/dL rise in glucose thereafter.¹⁴

Glucose. Patients with DKA require insulin therapy until ketoacidosis resolves. However, the average time to correct ketoacidosis from initiating treatment is about 12 hours compared to only 6 hours for correction of hyperglycemia. Since insulin therapy must be continued despite lower glucose levels, patients are at risk for developing hypoglycemia if glucose is not added to IV fluids. To prevent hypoglycemia and provide an energy source for ketone metabolism, patients should be switched to fluids containing dextrose when their serum glucose approaches 200 to 250 mg/dL.^1,3 Typically, 5% dextrose in half-normal saline at 150 to 250 cc per hour is usually adequate to achieve this goal.

Insulin

As previously noted, insulin therapy is required to treat hyperglycemic crises from DKA and HHS. In DKA there is an absolute insulin deficiency, whereas in HHS, there is a relative insulin deficiency. In HHS, there is not enough endogenous insulin to move glucose into the cells, but there is enough insulin to block a catabolic state. That is why the breakdown of fats and proteins does not occur, and why ketoacidosis and hyperkalemia are not seen in HHS. On the other hand, glucose elevations do occur, and are usually more extreme in HHS than DKA. There are five major therapeutic actions of insulin in DKA (Table 5), and it is imperative to determine serum potassium before starting an insulin infusion as insulin will drive potassium into the cell, worsening hypokalemia and promoting the development of life-threatening arrhythmias, including ventricular fibrillation, ventricular tachycardia, and torsades de pointes. The electrocardiogram does not accurately predict severity of hypokalemia and should not be used as a substitute for direct potassium measurement.

Loading Dose and Drip Rate. When treating adult patients with DKA or HHS, the ADA recommends an IV push loading dose of 0.1 U/kg insulin, followed by an hourly maintenance dose of 0.1 U/kg. Alternatively, a continuous infusion of 0.16 U/kg/hr can be used without a bolus. The rationale behind a bolus is the rapid saturation of insulin receptors, followed by a drip to maintain saturation of receptors. However, a recent prospective observational cohort study by Goyal et al¹⁵ questions the utility of the initial insulin bolus. The study compared DKA patients who received an initial insulin bolus to those who did not. Both groups were similar at baseline and received equivalent IV fluids and insulin drips. They found no statistically significant differences in the incidence of hypoglycemia, rate of serum glucose change, anion gap change, or length of stay in the ED or hospital. The authors concluded that administration of an insulin bolus has no significant benefit to patients and does not change clinically relevant end-points.¹⁵ At this time, there is no proven benefit to giving DKA patients an IV insulin bolus; moreover, doing so may further increase hypoglycemia. The use of an insulin bolus is particularly not recommended for use in pediatric patients with DKA due to a higher incidence of hypoglycemia in this patient population.¹⁶

As with DKA, the ADA³ recommends giving HHS patients an insulin bolus of 0.1 U/ kg followed by a continuous infusion at 0.1 U/kg per hour. It is crucial to monitor patients closely to ensure glucose levels do not fall too rapidly. Glucose levels should be kept between 150 to 200 mg/dL for patients with DKA and 200 to 300 mg/dL for patients with HHS until the conditions resolve; this may necessitate lowering the infusion rate to 0.02 to 0.05 U/kg per hour. In addition to frequent glucose monitoring, a basic metabolic panel and venous pH should be obtained every 2 to 4 hours while a patient is on an insulin drip.³

Subcutaneous Vs Intravenous Insulin for DKA. Several small studies evaluating patients with mild-moderate DKA demonstrated similar outcomes when subcutaneous (SQ) insulin was used instead of IV insulin. However, SQ injections require more frequent dosing (every 1 to 2 hours) and still require close monitoring of blood glucose. This monitoring frequency is usually not feasible on a hospital floor, but may be feasible on step-down units, thus avoiding admission to the intensive care unit (ICU) for patients who do not otherwise require ICU-level of care.¹⁷ Subcutaneous insulin should not be given to patients with severe acidosis, hypotension, or altered mental status. The ADA consensus statement continues to recommend IV infusion of regular insulin as the preferred route due to its short half-life and easy titration.³

Determining When to Switch to Subcutaneous Insulin. Ideally, patients are not in the ED long enough to have their metabolic abnormalities corrected, as this usually requires several hours. In DKA, the insulin drip should continue until the blood glucose is less than 200 and at least two of the following conditions are met: the anion gap is less than 12, venous pH greater than 7.3, and serum bicarbonate >15. In HHS, osmolality and mental status should both return to normal prior to stopping the infusion. In both cases, subcutaneous insulin should be administered at least 1 to 2 hours before stopping the drip to prevent recurrent crisis.^1,3

Refractory Acidosis. First and foremost, refractory acidosis should prompt a diligent source for dead gut, abscess, and underlying sepsis. While vomiting and diffuse abdominal pain are common in DKA and are related to ketoacidosis, these symptoms are atypical of HHS and should raise suspicion for underlying pathology.³ Additionally, a lower than expected bicarbonate level can also occur from resuscitation with large volumes of normal saline, resulting in a hyperchloremic non-gap metabolic acidosis.

Potassium

Both DKA and HHS patients have total body potassium deficits due to osmotic diuresis that require careful repletion. Deficits can be substantial: The average total whole body potassium deficit in DKA is 3 to 5 mEq/kg.² Clinicians should exercise caution, however, since DKA patients may be hyperkalemic initially despite a total body potassium deficit. Early hyperkalemia is due to the transmembrane shift of potassium secondary to acidosis and insulin deficiency as well as hypertonicity. If initial potassium is greater than 5.2 mEq/L, potassium should not be administered but instead rechecked in 1 to 2 hours. If the potassium level is 4.0 to 5.2 mEq/L, then 10 mEq per hour is usually adequate. For levels between 3.3 and 4.0 mEq/L, administer potassium chloride at 20 mEq per hour. For levels less than 3.3 mEq/L, insulin should be held and potassium chloride should be aggressively repleted at 20 to 30 mEq per hour with continuous cardiac monitoring.^1-3 Failure to recognize and act on critical potassium levels is a known cause of unexpected death in DKA. During the first hour of DKA onset, patients are more likely to die from hyperkalemia. Later, while the patient is “stabilizing” on an insulin infusion, potassium levels will fall as insulin drives potassium back into cells.

Bicarbonate

Bicarbonate has many theoretical benefits but also has potential risks (Table 6).

Phosphate

Since there is no proven benefit to giving phosphate to adult patients with DKA, it is rarely used, except in specific situations other than pediatric DKA. Similar to potassium, initial serum phosphate levels do not reflect total body phosphate levels due to transmembrane shifts.^2,3 Phosphate repletionis most beneficial for patients who have cachexia, respiratory depression, anemia, cardiac dysfunction, or phosphate values lower than 1.0 to 1.5. If given, 20 to 30 mEq/L potassium phosphate (K₂PO₄) added to fluids is usually sufficient.³ Overly aggressive phosphate administration (>4.5 mmol/h or 1.5 mL/h potassium phosphate) can cause severe hypocalcemia and should be avoided.^1,3 In pediatric patients, up to one-half of potassium requirements are often given as potassium phosphate, but this may vary by institution.

Conclusion

Both DKA and HHS are diabetic emergencies that must be approached and managed systematically to correct underlying dehydration and metabolic abnormalities. Patient care begins by determining the etiology of these conditions, especially HHS. Once the cause has been identified, patients should be treated with bolus fluids to obtain adequate perfusion, followed by IV fluid infusion. Clinicians should carefully monitor the serum sodium level of patients with DKA or HHS to determine the ideal amount and type of fluid required, and also should measure potassium levels prior to starting patients on insulin. (Tables 7 and 8 summarize important clinical pearls when treating patients with DKA or HHS.)

Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS) are similar but distinct diabetic emergencies that are frequently encountered in the ED. Patients with DKA or HHS present with hyperglycemia and dehydration and frequently appear quite ill physically. In both syndromes, there is insufficient insulin levels to transport glucose into cells.

As previously noted, although DKA and HHS share similar characteristic signs and symptoms, they are two distinct conditions that must be differentiated in the clinical work-up. One characteristic that helps the emergency physician (EP) to distinguish between the two conditions is the patient age at symptom onset. Although both conditions can occur at any age, diabetic ketoacidosis typically develops in younger patients, less than 45 years, who have little or no endogenous insulin production, whereas HHS usually occurs in much older non-insulin-dependent patients (who are often greater than 60 years old). ^1-3 This review discusses the similarities and differences in the etiology, diagnosis, and treatment of DKA and HHS to guide evaluation and simplify management, highlighting practical tips and clinical pearls. When applicable, information has been organized into groups of five to facilitate retention and recall.

The Etiology of DKA Vs HHS

The fundamental underlying issue in both DKA and HHS is an absolute or relative lack of insulin that results in an increase in counter-regulatory hormones, including glucagon, cortisol, and catecholamines.

Insulin has five main actions: (1) to drive glucose into cells; (2) to drive potassium into cells; (3) to create an anabolic environment; (4) to inhibit breakdown of fat; and (5) to block the breakdown of proteins. (Table 1).

Diagnosis and Workup

Laboratory Evaluation

In addition to hyperglycemia, another key finding in DKA is elevated anion gap metabolic acidosis resulting from ketoacid production. Laboratory evaluation will demonstrate a pH less than 7.3 and serum bicarbonate level less than 18 mEq/L; urinalysis will be positive for ketones.

Though HHS patients also present with hyperglycemia, laboratory evaluation will demonstrate no, or only mild, acidosis, normal pH (typically >7.3), bicarbonate level greater than 18 mEq/L, and a high-serum osmolality (>350 mOsm/kg). While urinalysis may show low or no ketones, patients with HHS do not develop the marked ketoacidosis seen in DKA. Moreover, glucose values are more elevated in patients with HHS, frequently exceeding 1,000 mg/dL.

Signs and Symptoms

Patients with either of these hyperglycemic crises often present with fatigue, polyuria, and polydipsia. They appear dehydrated on examination with dry mucous membranes, tachycardia, and in severe cases, hypotension. Patients with HHS often present with altered mental status, seizures, and even coma, while patients with DKA typically only experience changes in mental status in the most severe cases (Table 2). As many as one-third of patients with a hyperglycemic crisis will have an overlapping DKA/HHS syndrome.^1-3 With respect to patient age, HHS tends to develop in older patients who have type 2 diabetes and several underlying comorbidities.²

Precipitating Causes of DKA and HHS

The five causes of DKA/HHS can be remembered as the “Five I’s”: (1) infection; (2) infarction; (3) infant (pregnancy), (4) indiscretion, and (5) [lack of] insulin (Table 3).

Infection. Infection is one of the most common precipitating factors in both DKA and HHS.¹ During the history intake, the EP should ask the patient if he or she has had any recent urinary and respiratory symptoms, as positive responses prompt further investigation with urinalysis and chest radiography. A thorough dermatological examination should be performed to assess for visible signs of infection, particularly in the extremities and intertriginous areas.

When assessing patients with DKA or HHS for signs of infection, body temperature to assess for the presence of fever is not always a reliable indicator. This is because many patients with DKA/HHS develop tachypnea, which can affect the efficacy of an oral thermometer. In such cases, the rectal temperature is more sensitive for detecting fever. It should be noted, however, that some patients with severe infection or immunocompromised state—regardless of the presence or absence of tachypnea—may be normothermic or even hypothermic due to peripheral vasodilation—a poor prognostic sign.³ Blood and urine cultures should be obtained for all patients in whom infection is suspected.

Laboratory evaluation of patients with DKA may demonstrate a mild leukocytosis, a very common finding in DKA even in the absence of infection; leukocytosis is believed to result from elevated stress hormones such as cortisol and epinephrine.³

Infarction. Infarction is another important underlying cause of DKA/HHS and one that must not be overlooked. Screening for acute coronary syndrome through patient history, electrocardiography, and cardiac biomarkers should be performed in all patients older than age 40 years and in patients in whom there is any suggestion of myocardial ischemia.

A thorough neurological examination should be performed to assess for deficits indicative of stroke. Although neurological deficits can be due to severe hyperglycemia, most patients with focal neurological deficits from hyperglycemia also have altered mental status. Focal neurological deficits without a change in mental status are more likely to represent an actual stroke.⁴

Infant (Pregnancy). Pregnant patients are at an increased risk of developing DKA for several reasons, most notably due to the increased production of insulin-antagonistic hormones, which can lead to higher insulin resistance and thus increased insulin requirements during pregnancy.⁵ A pregnancy test is therefore indicated for all female patients of child-bearing age.

Indiscretion. Non-compliance with diet, such as taking in too many calories without appropriate insulin correction, and the ingestion of significant amounts of alcohol can lead to DKA. Eating disorders, particularly in young patients, may also contribute to recurrent cases.³

[Lack of] Insulin. In insulin-dependent diabetes, skipped insulin doses or insulin pump failure can trigger DKA/HHS. In fact, missed insulin doses are becoming a more frequent cause of DKA than infections.¹

Both DKA and HHS are usually triggered by an underlying illness or event. Therefore, clinicians should always focus on identifying precipitating causes such as acute infection, stroke, or myocardial infarction, as some require immediate treatment. In fact, DKA or HHS is rarely the primary cause of death; patients are much more likely to die from the precipitating event that caused DKA or HHS.^1,3

Assessing Disease Severity

Mental status and pH and serum bicarbonate levels help clinicians determine the extent of disease severity, classifying patients as having mild, moderate, or severe DKA (Table 4).² Patients at the highest risk for poor outcomes include those at the extremes of age, who have severe comorbidities, who have underlying infection, and who are hypotensive and/or in a comatose state.³

Patients who have HHS are much more likely to present with altered mental status, including coma. There is a linear relationship between osmolality and degree of altered mental status. Thus, diabetic patients with major changes in mental status but without high serum osmolality warrant immediate workup for alternative causes of their altered mental status.³ In addition, seizures, especially focal seizures, are relatively common in severe cases of HHS. Finally, highly abnormal blood pressure, pulse, and respiratory rate can also provide additional clues regarding the severity of hyperglycemic crisis.

Arterial Blood Gas Assessment: To Stick or Not to Stick?

In the past, measuring arterial blood gases (ABG) has been considered a mainstay in the evaluation of patients with DKA. But does an arterial stick, which is associated with some risk, really add essential information? One study by Ma et al⁶ evaluated whether ABG results significantly alter how physicians manage patients with DKA. In the study, the authors evaluated 200 ED patients and found that ABG analysis only changed diagnosis in 1% of patients, altered treatment in 3.5% of patients, and changed disposition in only 1% of patients. Arterial stick partial pressure of oxygen and partial pressure of carbon dioxide altered treatment and disposition in only 1% of patients. Furthermore, the study results showed venous pH correlated very strongly with arterial pH (r = 0.95).⁶ These findings demonstrate that ABG measurements rarely affect or alter DKA management, and support the use of venous pH as an adequate substitute for ABG testing.

Euglycemia

Euglycemic DKA has been reported in patients with type 1 diabetes who had been fasting or vomiting or who had received exogenous insulin prior to presentation.¹Euglycemia has also been reported in pregnant patients with type I diabetes.¹ More recently, sodium glucose cotransporter 2 inhibitors (SGLT2) have been shown to cause euglycemic DKA. While the therapeutic mechanism of this drug class is to inhibit proximal tubular resorption of glucose, they can cause DKA by decreasing renal clearance of ketone bodies and increasing glucagon levels and promoting hepatic ketogenesis. Patients with DKA who are on SGLT2 inhibitors may present with only modestly elevated glucose levels (typically in the 200- to 300-mg/dL range), but have profound wide gap metabolic acidosis due to β-hydroxybutyrate acid and acetoacetate accumulation.⁷ When evaluating patients on SGLT2 inhibitors for DKA, EPs should not solely rely on glucose values but rather assess the patient’s overall clinical picture, including the physical examination, vital signs, and pH. Additionally, once resuscitation with intravenous (IV) fluids and insulin is initiated, it may take longer for patients who use SGLT2 inhibitors to clear ketoacids than patients with DKA who do not use these medications.⁸

Treatment

The goal of treatment for DKA and HHS is to correct volume deficits, hyperglycemia, and electrolyte abnormalities (Table 5). Three of the five therapies to manage DKA and HHS are mandatory: IV fluid resuscitation, IV insulin, and IV potassium. The other therapies, IV bicarbonate, and IV phosphate, should be considered, but are rarely required for DKA or HHS.

In general, management of HHS is less aggressive than that of DKA because HHS develops over a period of weeks—unlike DKA, which develops over only 1 to 2 days. Treatment of any underlying causes of HHS should occur simultaneously.

Intravenous Fluids

The goal of IV fluid therapy for patients with DKA is rehydration—not to “wash-out” ketones. Ketone elimination occurs through insulin-stimulated metabolism. When determining volume-replacement goals, it is helpful to keep in mind that patients with moderate-to-mild DKA typically have fluid deficiencies of 3 to 5 L, and patients with severe DKA have fluid deficiencies between 5 and 6 L. Patients with HHS present with significantly higher fluid deficiencies of around 9 to 12 L.

The initial goal of fluid management is to correct hypoperfusion with bolus fluids, followed by a more gradual repletion of remaining deficits. After bolus fluids are administered, the rate and type of subsequent IV fluid infusion varies depending on hemodynamics, hydration state, and serum sodium levels.^2,3

Nonaggressive Vs Aggressive Fluid Management. One study by Adrogué et al⁹ compared the effects of managing DKA with aggressive vs nonaggressive fluid repletion. In the study, one group of patients received normal saline at 1,000 mL per hour for 4 hours, followed by normal saline at 500 mL per hour for 4 hours. The other group of patients received normal saline at a more modest rate of 500 mL per hour for 4 hours, followed by normal saline at 250 mL per hour for 4 hours. The authors found that patients in the less aggressive volume therapy group achieved a prompt and adequate recovery and maintained higher serum bicarbonate levels.⁹

Current recommendations for patients with DKA are to first treat patients with an initial bolus of 1,000 mL or 20 cc/kg of normal saline. Patients without profound dehydration should then receive 500 cc of normal saline per hour for the first 4 hours of treatment, after which the flow rate may be reduced to 250 cc per hour. For patients with mild DKA, therapy can start at 250 cc per hour with a smaller bolus dose or no bolus dose. Patients with profound dehydration and poor perfusion, should receive crystalloid fluids wide open until perfusion has improved. Overall, volume resuscitation in HHS is similar to DKA. However, the EP should be cautious with respect to total fluid volume and infusion rates to avoid fluid overload, since many patients with HHS are elderly and may have congestive heart failure.

Crystalloid Fluid Type for Initial Resuscitation. Normal saline has been the traditional crystalloid fluid of choice for managing DKA and HHS. Recent studies, however, have shown some benefit to using balanced solutions (Ringer’s lactate or PlasmaLyte) instead of normal saline. A recently published large study by Semler et al¹⁰ compared balanced crystalloid, in most cases lactated Ringers solution, to normal saline in critically ill adult patients, some of whom were diagnosed with DKA. The study demonstrated decreased mortality (from any cause) in the group who received balanced crystalloid fluid therapy and reduced need for renal-replacement therapy and reduced incidence of persistent renal dysfunction. The findings by Semler et al¹⁰ and findings from other smaller studies, calls into question whether normal saline is the best crystalloid to manage DKA and HHS.^11,12 It remains to be seen what modification the American Diabetes Association (ADA) will make to its current recommendations for fluid therapy, which were last updated in 2009.

It appears that though the use of Ringers lactate or PlasmaLyte to treat DKA usually raises a patient’s serum bicarbonate level to 18 mEq/L at a more rapid rate than normal saline, the use of balanced solutions may result in longer time to lower blood glucose to 250 mg/dL.¹³ However, by using a balanced solution, the hyperchloremic metabolic acidosis often seen with normal saline treatment will be avoided.¹²

Half-Normal Saline. An initially normal or increased serum sodium level, despite significant hyperglycemia, suggests a substantial free-water deficit. Calculating a corrected serum sodium can help quantify the degree of free-water deficit.³ While isotonic fluids remain the standard for initial volume load, clinicians should consider switching patients to half-normal saline following initial resuscitation if the corrected serum sodium is elevated above normal. The simplest estimation to correct sodium levels in DKA is to expect a decrease in sodium levels at a rate of at least 2 mEq/L per 100-mg/dL increase in glucose levels above 100 mg/dL. For a more accurate calculation, providers can expect a drop in sodium of 1.6 mEq/L per 100 mg/dL increase of glucose up to a level of 400 mg/dL and then a fall of 2.4 mEq/L in sodium per every 100 mg/dL rise in glucose thereafter.¹⁴

Glucose. Patients with DKA require insulin therapy until ketoacidosis resolves. However, the average time to correct ketoacidosis from initiating treatment is about 12 hours compared to only 6 hours for correction of hyperglycemia. Since insulin therapy must be continued despite lower glucose levels, patients are at risk for developing hypoglycemia if glucose is not added to IV fluids. To prevent hypoglycemia and provide an energy source for ketone metabolism, patients should be switched to fluids containing dextrose when their serum glucose approaches 200 to 250 mg/dL.^1,3 Typically, 5% dextrose in half-normal saline at 150 to 250 cc per hour is usually adequate to achieve this goal.

Insulin

As previously noted, insulin therapy is required to treat hyperglycemic crises from DKA and HHS. In DKA there is an absolute insulin deficiency, whereas in HHS, there is a relative insulin deficiency. In HHS, there is not enough endogenous insulin to move glucose into the cells, but there is enough insulin to block a catabolic state. That is why the breakdown of fats and proteins does not occur, and why ketoacidosis and hyperkalemia are not seen in HHS. On the other hand, glucose elevations do occur, and are usually more extreme in HHS than DKA. There are five major therapeutic actions of insulin in DKA (Table 5), and it is imperative to determine serum potassium before starting an insulin infusion as insulin will drive potassium into the cell, worsening hypokalemia and promoting the development of life-threatening arrhythmias, including ventricular fibrillation, ventricular tachycardia, and torsades de pointes. The electrocardiogram does not accurately predict severity of hypokalemia and should not be used as a substitute for direct potassium measurement.

Loading Dose and Drip Rate. When treating adult patients with DKA or HHS, the ADA recommends an IV push loading dose of 0.1 U/kg insulin, followed by an hourly maintenance dose of 0.1 U/kg. Alternatively, a continuous infusion of 0.16 U/kg/hr can be used without a bolus. The rationale behind a bolus is the rapid saturation of insulin receptors, followed by a drip to maintain saturation of receptors. However, a recent prospective observational cohort study by Goyal et al¹⁵ questions the utility of the initial insulin bolus. The study compared DKA patients who received an initial insulin bolus to those who did not. Both groups were similar at baseline and received equivalent IV fluids and insulin drips. They found no statistically significant differences in the incidence of hypoglycemia, rate of serum glucose change, anion gap change, or length of stay in the ED or hospital. The authors concluded that administration of an insulin bolus has no significant benefit to patients and does not change clinically relevant end-points.¹⁵ At this time, there is no proven benefit to giving DKA patients an IV insulin bolus; moreover, doing so may further increase hypoglycemia. The use of an insulin bolus is particularly not recommended for use in pediatric patients with DKA due to a higher incidence of hypoglycemia in this patient population.¹⁶

As with DKA, the ADA³ recommends giving HHS patients an insulin bolus of 0.1 U/ kg followed by a continuous infusion at 0.1 U/kg per hour. It is crucial to monitor patients closely to ensure glucose levels do not fall too rapidly. Glucose levels should be kept between 150 to 200 mg/dL for patients with DKA and 200 to 300 mg/dL for patients with HHS until the conditions resolve; this may necessitate lowering the infusion rate to 0.02 to 0.05 U/kg per hour. In addition to frequent glucose monitoring, a basic metabolic panel and venous pH should be obtained every 2 to 4 hours while a patient is on an insulin drip.³

Subcutaneous Vs Intravenous Insulin for DKA. Several small studies evaluating patients with mild-moderate DKA demonstrated similar outcomes when subcutaneous (SQ) insulin was used instead of IV insulin. However, SQ injections require more frequent dosing (every 1 to 2 hours) and still require close monitoring of blood glucose. This monitoring frequency is usually not feasible on a hospital floor, but may be feasible on step-down units, thus avoiding admission to the intensive care unit (ICU) for patients who do not otherwise require ICU-level of care.¹⁷ Subcutaneous insulin should not be given to patients with severe acidosis, hypotension, or altered mental status. The ADA consensus statement continues to recommend IV infusion of regular insulin as the preferred route due to its short half-life and easy titration.³

Determining When to Switch to Subcutaneous Insulin. Ideally, patients are not in the ED long enough to have their metabolic abnormalities corrected, as this usually requires several hours. In DKA, the insulin drip should continue until the blood glucose is less than 200 and at least two of the following conditions are met: the anion gap is less than 12, venous pH greater than 7.3, and serum bicarbonate >15. In HHS, osmolality and mental status should both return to normal prior to stopping the infusion. In both cases, subcutaneous insulin should be administered at least 1 to 2 hours before stopping the drip to prevent recurrent crisis.^1,3

Refractory Acidosis. First and foremost, refractory acidosis should prompt a diligent source for dead gut, abscess, and underlying sepsis. While vomiting and diffuse abdominal pain are common in DKA and are related to ketoacidosis, these symptoms are atypical of HHS and should raise suspicion for underlying pathology.³ Additionally, a lower than expected bicarbonate level can also occur from resuscitation with large volumes of normal saline, resulting in a hyperchloremic non-gap metabolic acidosis.

Potassium

Both DKA and HHS patients have total body potassium deficits due to osmotic diuresis that require careful repletion. Deficits can be substantial: The average total whole body potassium deficit in DKA is 3 to 5 mEq/kg.² Clinicians should exercise caution, however, since DKA patients may be hyperkalemic initially despite a total body potassium deficit. Early hyperkalemia is due to the transmembrane shift of potassium secondary to acidosis and insulin deficiency as well as hypertonicity. If initial potassium is greater than 5.2 mEq/L, potassium should not be administered but instead rechecked in 1 to 2 hours. If the potassium level is 4.0 to 5.2 mEq/L, then 10 mEq per hour is usually adequate. For levels between 3.3 and 4.0 mEq/L, administer potassium chloride at 20 mEq per hour. For levels less than 3.3 mEq/L, insulin should be held and potassium chloride should be aggressively repleted at 20 to 30 mEq per hour with continuous cardiac monitoring.^1-3 Failure to recognize and act on critical potassium levels is a known cause of unexpected death in DKA. During the first hour of DKA onset, patients are more likely to die from hyperkalemia. Later, while the patient is “stabilizing” on an insulin infusion, potassium levels will fall as insulin drives potassium back into cells.

Bicarbonate

Bicarbonate has many theoretical benefits but also has potential risks (Table 6).

Phosphate

Since there is no proven benefit to giving phosphate to adult patients with DKA, it is rarely used, except in specific situations other than pediatric DKA. Similar to potassium, initial serum phosphate levels do not reflect total body phosphate levels due to transmembrane shifts.^2,3 Phosphate repletionis most beneficial for patients who have cachexia, respiratory depression, anemia, cardiac dysfunction, or phosphate values lower than 1.0 to 1.5. If given, 20 to 30 mEq/L potassium phosphate (K₂PO₄) added to fluids is usually sufficient.³ Overly aggressive phosphate administration (>4.5 mmol/h or 1.5 mL/h potassium phosphate) can cause severe hypocalcemia and should be avoided.^1,3 In pediatric patients, up to one-half of potassium requirements are often given as potassium phosphate, but this may vary by institution.

Conclusion

Both DKA and HHS are diabetic emergencies that must be approached and managed systematically to correct underlying dehydration and metabolic abnormalities. Patient care begins by determining the etiology of these conditions, especially HHS. Once the cause has been identified, patients should be treated with bolus fluids to obtain adequate perfusion, followed by IV fluid infusion. Clinicians should carefully monitor the serum sodium level of patients with DKA or HHS to determine the ideal amount and type of fluid required, and also should measure potassium levels prior to starting patients on insulin. (Tables 7 and 8 summarize important clinical pearls when treating patients with DKA or HHS.)

ANSWER

The chest radiograph shows an approximately 3-cm cavitary lesion in the right upper lobe. Such a lesion can indicate lung abscess, neoplasm, or tuberculosis. 

Subsequent workup determined that he did, in fact, have tuberculosis, with involvement in his spine (known as Pott disease).

ANSWER

The chest radiograph shows an approximately 3-cm cavitary lesion in the right upper lobe. Such a lesion can indicate lung abscess, neoplasm, or tuberculosis. 

Subsequent workup determined that he did, in fact, have tuberculosis, with involvement in his spine (known as Pott disease).

ANSWER

The chest radiograph shows an approximately 3-cm cavitary lesion in the right upper lobe. Such a lesion can indicate lung abscess, neoplasm, or tuberculosis. 

Subsequent workup determined that he did, in fact, have tuberculosis, with involvement in his spine (known as Pott disease).

The number of U.S. emergency department visits for acute pancreatitis associated with alcohol abuse, chronic pancreatitis history, and younger age was on the rise in recent years, an analysis of a nationally representative database has suggested.

Katarzyna Bialasiewicz/Thinkstock

Help your patients better understand pancreatitis and available tests and treatments by using AGA patient education materials, https://www.gastro.org/practice-guidance/gi-patient-center/topic/pancreatitis.

SOURCE: Garg SK et al. J Clin Gastroenterol. 2018 Apr 6. doi: 10.1097/MCG.0000000000001030.

The number of U.S. emergency department visits for acute pancreatitis associated with alcohol abuse, chronic pancreatitis history, and younger age was on the rise in recent years, an analysis of a nationally representative database has suggested.

Katarzyna Bialasiewicz/Thinkstock

Help your patients better understand pancreatitis and available tests and treatments by using AGA patient education materials, https://www.gastro.org/practice-guidance/gi-patient-center/topic/pancreatitis.

SOURCE: Garg SK et al. J Clin Gastroenterol. 2018 Apr 6. doi: 10.1097/MCG.0000000000001030.

The number of U.S. emergency department visits for acute pancreatitis associated with alcohol abuse, chronic pancreatitis history, and younger age was on the rise in recent years, an analysis of a nationally representative database has suggested.

Katarzyna Bialasiewicz/Thinkstock

Help your patients better understand pancreatitis and available tests and treatments by using AGA patient education materials, https://www.gastro.org/practice-guidance/gi-patient-center/topic/pancreatitis.

SOURCE: Garg SK et al. J Clin Gastroenterol. 2018 Apr 6. doi: 10.1097/MCG.0000000000001030.

A 51-year-old man with end-stage renal disease, on peritoneal dialysis for the past 4 years, presented to the emergency department with severe pain in both legs. The pain had started 2 months previously and had progressively worsened. After multiple admissions in the past for hyperkalemia and volume overload due to noncompliance, he had been advised to switch to hemodialysis.

See related article and editorial

Laboratory analysis revealed the following values:

• Serum creatinine 12.62 mg/dL (reference range 0.73–1.22)
• Blood urea nitrogen 159 mg/dL (9–24)
• Serum calcium corrected for serum albumin 8.1 mg/dL (8.4–10.0)
• Serum phosphorus 10.6 mg/dL (2.7–4.8).

His history of end-stage renal disease, failure of peritoneal dialysis, high calcium-phosphorus product (8.1 mg/dL × 10.6 mg/dL = 85.9 mg²/dL ², reference range ≤ 55), and characteristic physical findings led to the diagnosis of calcific uremic arteriolopathy.

CALCIFIC UREMIC ARTERIOLOPATHY

Calcific uremic arteriolopathy or “calciphylaxis,” seen most often in patients with end-stage renal disease, is caused by calcium deposition in the media of the dermo-hypodermic arterioles, leading to infarction of adjacent tissue.^1–3 A high calcium-phosphorus product (> 55) has been implicated in its development; however, the calcium-phosphorus product can be normal despite hyperphosphatemia, which itself may promote ectopic calcification.

Early ischemic manifestations include livedo reticularis and painful retiform purpura on the thighs and other areas of high adiposity. Lesions evolve into violaceous plaquelike subcutaneous nodules that can infarct, become necrotic, ulcerate, and become infected. Punch biopsy demonstrating arteriolar calcification, subintimal fibrosis, and thrombosis confirms the diagnosis.

Differential diagnosis

Warfarin necrosis can cause large, irregular, bloody bullae that ulcerate and turn into eschar that may resemble lesions of calcific uremic arteriolopathy. Our patient, however, had no exposure to warfarin.

Pemphigus foliaceus, an immunoglobulin G4-mediated autoimmune disorder targeted against desmoglein-1, leads to the formation of fragile blisters that easily rupture when rubbed (Nikolsky sign). Lesions evolve into scaling, crusty erosions on an erythematous base. With tender blisters and lack of mucous membrane involvement, pemphigus foliaceus shares similarities with calcific uremic arteriolopathy, but the presence of necrotic eschar surrounded by violaceous plaques in our patient made it an unlikely diagnosis.

Cryofibrinogenemia. In the right clinical scenario, ie, in a patient with vasculitis, malignancy, infection, cryoglobulinemia, or collagen diseases, cryofibrinogen-mediated cold-induced occlusive lesions may mimic calcific uremic arteriolopathy, with painful or pruritic erythema, purpura, livedo reticularis, necrosis, and ulceration.⁴ Our patient had no color changes with exposure to cold, nor any history of Raynaud phenomenon or joint pain, making the diagnosis of cryofibrinogenemia less likely.

Nephrogenic systemic fibrosis. Gadolinium contrast medium in magnetic resonance imaging can cause nephrogenic systemic fibrosis, characterized by erythematous papules that coalesce into brawny plaques with surrounding woody induration, which may resemble lesions of calcific uremic arteriolopathy.⁵ However, our patient had not been exposed to gadolinium.

Management

Management is multidisciplinary and includes the following¹:

• Hemodialysis, modified to optimize calcium balance²
• Intravenous sodium thiosulfate: the exact mechanism of action remains unclear, but it is thought to play a role in chelating calcium from tissue deposits, thus decreasing pain and promoting regression of skin lesions³
• Wound care, including chemical debridement agents, negative-pressure wound therapy, and surgical debridement for infected wounds⁶
• Pain management with opioid analgesics.

The patient was treated with all these measures. However, he died of sudden cardiac arrest during the same admission.

A 51-year-old man with end-stage renal disease, on peritoneal dialysis for the past 4 years, presented to the emergency department with severe pain in both legs. The pain had started 2 months previously and had progressively worsened. After multiple admissions in the past for hyperkalemia and volume overload due to noncompliance, he had been advised to switch to hemodialysis.

See related article and editorial

Laboratory analysis revealed the following values:

• Serum creatinine 12.62 mg/dL (reference range 0.73–1.22)
• Blood urea nitrogen 159 mg/dL (9–24)
• Serum calcium corrected for serum albumin 8.1 mg/dL (8.4–10.0)
• Serum phosphorus 10.6 mg/dL (2.7–4.8).

His history of end-stage renal disease, failure of peritoneal dialysis, high calcium-phosphorus product (8.1 mg/dL × 10.6 mg/dL = 85.9 mg²/dL ², reference range ≤ 55), and characteristic physical findings led to the diagnosis of calcific uremic arteriolopathy.

CALCIFIC UREMIC ARTERIOLOPATHY

Calcific uremic arteriolopathy or “calciphylaxis,” seen most often in patients with end-stage renal disease, is caused by calcium deposition in the media of the dermo-hypodermic arterioles, leading to infarction of adjacent tissue.^1–3 A high calcium-phosphorus product (> 55) has been implicated in its development; however, the calcium-phosphorus product can be normal despite hyperphosphatemia, which itself may promote ectopic calcification.

Early ischemic manifestations include livedo reticularis and painful retiform purpura on the thighs and other areas of high adiposity. Lesions evolve into violaceous plaquelike subcutaneous nodules that can infarct, become necrotic, ulcerate, and become infected. Punch biopsy demonstrating arteriolar calcification, subintimal fibrosis, and thrombosis confirms the diagnosis.

Differential diagnosis

Warfarin necrosis can cause large, irregular, bloody bullae that ulcerate and turn into eschar that may resemble lesions of calcific uremic arteriolopathy. Our patient, however, had no exposure to warfarin.

Pemphigus foliaceus, an immunoglobulin G4-mediated autoimmune disorder targeted against desmoglein-1, leads to the formation of fragile blisters that easily rupture when rubbed (Nikolsky sign). Lesions evolve into scaling, crusty erosions on an erythematous base. With tender blisters and lack of mucous membrane involvement, pemphigus foliaceus shares similarities with calcific uremic arteriolopathy, but the presence of necrotic eschar surrounded by violaceous plaques in our patient made it an unlikely diagnosis.

Cryofibrinogenemia. In the right clinical scenario, ie, in a patient with vasculitis, malignancy, infection, cryoglobulinemia, or collagen diseases, cryofibrinogen-mediated cold-induced occlusive lesions may mimic calcific uremic arteriolopathy, with painful or pruritic erythema, purpura, livedo reticularis, necrosis, and ulceration.⁴ Our patient had no color changes with exposure to cold, nor any history of Raynaud phenomenon or joint pain, making the diagnosis of cryofibrinogenemia less likely.

Nephrogenic systemic fibrosis. Gadolinium contrast medium in magnetic resonance imaging can cause nephrogenic systemic fibrosis, characterized by erythematous papules that coalesce into brawny plaques with surrounding woody induration, which may resemble lesions of calcific uremic arteriolopathy.⁵ However, our patient had not been exposed to gadolinium.

Management

Management is multidisciplinary and includes the following¹:

• Hemodialysis, modified to optimize calcium balance²
• Intravenous sodium thiosulfate: the exact mechanism of action remains unclear, but it is thought to play a role in chelating calcium from tissue deposits, thus decreasing pain and promoting regression of skin lesions³
• Wound care, including chemical debridement agents, negative-pressure wound therapy, and surgical debridement for infected wounds⁶
• Pain management with opioid analgesics.

The patient was treated with all these measures. However, he died of sudden cardiac arrest during the same admission.

A 51-year-old man with end-stage renal disease, on peritoneal dialysis for the past 4 years, presented to the emergency department with severe pain in both legs. The pain had started 2 months previously and had progressively worsened. After multiple admissions in the past for hyperkalemia and volume overload due to noncompliance, he had been advised to switch to hemodialysis.

See related article and editorial

Laboratory analysis revealed the following values:

• Serum creatinine 12.62 mg/dL (reference range 0.73–1.22)
• Blood urea nitrogen 159 mg/dL (9–24)
• Serum calcium corrected for serum albumin 8.1 mg/dL (8.4–10.0)
• Serum phosphorus 10.6 mg/dL (2.7–4.8).

His history of end-stage renal disease, failure of peritoneal dialysis, high calcium-phosphorus product (8.1 mg/dL × 10.6 mg/dL = 85.9 mg²/dL ², reference range ≤ 55), and characteristic physical findings led to the diagnosis of calcific uremic arteriolopathy.

CALCIFIC UREMIC ARTERIOLOPATHY

Calcific uremic arteriolopathy or “calciphylaxis,” seen most often in patients with end-stage renal disease, is caused by calcium deposition in the media of the dermo-hypodermic arterioles, leading to infarction of adjacent tissue.^1–3 A high calcium-phosphorus product (> 55) has been implicated in its development; however, the calcium-phosphorus product can be normal despite hyperphosphatemia, which itself may promote ectopic calcification.

Early ischemic manifestations include livedo reticularis and painful retiform purpura on the thighs and other areas of high adiposity. Lesions evolve into violaceous plaquelike subcutaneous nodules that can infarct, become necrotic, ulcerate, and become infected. Punch biopsy demonstrating arteriolar calcification, subintimal fibrosis, and thrombosis confirms the diagnosis.

Differential diagnosis

Warfarin necrosis can cause large, irregular, bloody bullae that ulcerate and turn into eschar that may resemble lesions of calcific uremic arteriolopathy. Our patient, however, had no exposure to warfarin.

Pemphigus foliaceus, an immunoglobulin G4-mediated autoimmune disorder targeted against desmoglein-1, leads to the formation of fragile blisters that easily rupture when rubbed (Nikolsky sign). Lesions evolve into scaling, crusty erosions on an erythematous base. With tender blisters and lack of mucous membrane involvement, pemphigus foliaceus shares similarities with calcific uremic arteriolopathy, but the presence of necrotic eschar surrounded by violaceous plaques in our patient made it an unlikely diagnosis.

Cryofibrinogenemia. In the right clinical scenario, ie, in a patient with vasculitis, malignancy, infection, cryoglobulinemia, or collagen diseases, cryofibrinogen-mediated cold-induced occlusive lesions may mimic calcific uremic arteriolopathy, with painful or pruritic erythema, purpura, livedo reticularis, necrosis, and ulceration.⁴ Our patient had no color changes with exposure to cold, nor any history of Raynaud phenomenon or joint pain, making the diagnosis of cryofibrinogenemia less likely.

Nephrogenic systemic fibrosis. Gadolinium contrast medium in magnetic resonance imaging can cause nephrogenic systemic fibrosis, characterized by erythematous papules that coalesce into brawny plaques with surrounding woody induration, which may resemble lesions of calcific uremic arteriolopathy.⁵ However, our patient had not been exposed to gadolinium.

Management

Management is multidisciplinary and includes the following¹:

• Hemodialysis, modified to optimize calcium balance²
• Intravenous sodium thiosulfate: the exact mechanism of action remains unclear, but it is thought to play a role in chelating calcium from tissue deposits, thus decreasing pain and promoting regression of skin lesions³
• Wound care, including chemical debridement agents, negative-pressure wound therapy, and surgical debridement for infected wounds⁶
• Pain management with opioid analgesics.

The patient was treated with all these measures. However, he died of sudden cardiac arrest during the same admission.

Neuroimaging may be appropriate only for specific types of patients with recurrent seizures who present at emergency departments because the scans are otherwise unlikely to prompt acute changes in treatment, a new multicenter study suggests.

Spotmatik/Thinkstock

“Going forward, our results should help ED providers determine which patients are more likely to derive benefit from neuroimaging and which patients are not likely to benefit,” lead author Martin Salinsky, MD, of Oregon Health & Science University, Portland, said in an interview. “They can be more selective in ordering scans and reduce the total number obtained.”

As the study authors noted in their report, published July 18 in Epilepsia, “head CT is generally considered a benign procedure. However, overuse is problematic.”

The scans are costly and expose patients to radiation equivalent to 10 chest x-rays, the authors wrote. Scans can complicate care by clogging ED work flow and producing false positives, and patients often seize while undergoing scans, creating even more complications, they added.

“There is very little information in the medical literature that would help guide ED providers in their decision of whether to obtain neuroimaging on a patient who presents with a recurrent seizure,” Dr. Salinsky said. “Without this information, the tendency is to be cautious and obtain scans in more patients.”

For the study, the researchers tracked 822 consecutive ED visits for nonindex – recurrent – epileptic seizures at Oregon Health & Science University and VA Portland Health Care medical centers. (Nonindex seizures accounted for 78% of the total seizures that prompted ED care.)

The study subjects were adults treated for seizure as the main complaint. Patients who had a history of seizures but hadn’t had one for at least 5 years were excluded.

Of the total nonindex seizures, 46% of those resulted in neuroimaging.

“The overall yield of neuroimaging in this patient group was 2%-3%,” Dr. Salinsky said, referring to the percentage of patients whose scans resulted in an acute change in management.

False positives due to imaging artifacts were subsequently discovered in 3 of the 11 patients whose neuroimaging prompted an acute change in management. When the false positives were removed, the yield of acute management changes prompted by neuroimaging decreased to 2.1% overall.

“Three clinical factors – acute head trauma, prolonged alteration of consciousness, and focal neurological examination [at presentation] – were associated with an increased yield of imaging,” he said. “Absent all three factors, the yield in our patients was zero.”

At the two medical centers, the percentages of patients with acute head trauma were 10% and 15%. Prolonged alteration of consciousness occurred in 6% at both centers, and focal neurological examination at presentation was observed in 12% and 14%.

A fourth factor, presentation with status epilepticus/acute repetitive seizures, “bordered on statistical significance and might have reached significance in a larger series,” the authors wrote.

As they put it, “these results support a more conservative use of ED neuroimaging for nonindex seizures, based on clinical factors at the time of presentation. ... without specific indications, ED neuroimaging for nonindex seizures is unlikely to result in an acute change in care.”

The study authors estimated that hundreds of millions of dollars could be saved annually in the United States if neuroimaging in these ED patients could be cut in half.

No study funding was reported, and the authors reported no relevant disclosures.

SOURCE: Salinsky M et al. Epilepsia. 2018 July 18. doi: 10.1111/epi.14518

Neuroimaging may be appropriate only for specific types of patients with recurrent seizures who present at emergency departments because the scans are otherwise unlikely to prompt acute changes in treatment, a new multicenter study suggests.

Spotmatik/Thinkstock

“Going forward, our results should help ED providers determine which patients are more likely to derive benefit from neuroimaging and which patients are not likely to benefit,” lead author Martin Salinsky, MD, of Oregon Health & Science University, Portland, said in an interview. “They can be more selective in ordering scans and reduce the total number obtained.”

As the study authors noted in their report, published July 18 in Epilepsia, “head CT is generally considered a benign procedure. However, overuse is problematic.”

The scans are costly and expose patients to radiation equivalent to 10 chest x-rays, the authors wrote. Scans can complicate care by clogging ED work flow and producing false positives, and patients often seize while undergoing scans, creating even more complications, they added.

“There is very little information in the medical literature that would help guide ED providers in their decision of whether to obtain neuroimaging on a patient who presents with a recurrent seizure,” Dr. Salinsky said. “Without this information, the tendency is to be cautious and obtain scans in more patients.”

For the study, the researchers tracked 822 consecutive ED visits for nonindex – recurrent – epileptic seizures at Oregon Health & Science University and VA Portland Health Care medical centers. (Nonindex seizures accounted for 78% of the total seizures that prompted ED care.)

The study subjects were adults treated for seizure as the main complaint. Patients who had a history of seizures but hadn’t had one for at least 5 years were excluded.

Of the total nonindex seizures, 46% of those resulted in neuroimaging.

“The overall yield of neuroimaging in this patient group was 2%-3%,” Dr. Salinsky said, referring to the percentage of patients whose scans resulted in an acute change in management.

False positives due to imaging artifacts were subsequently discovered in 3 of the 11 patients whose neuroimaging prompted an acute change in management. When the false positives were removed, the yield of acute management changes prompted by neuroimaging decreased to 2.1% overall.

“Three clinical factors – acute head trauma, prolonged alteration of consciousness, and focal neurological examination [at presentation] – were associated with an increased yield of imaging,” he said. “Absent all three factors, the yield in our patients was zero.”

At the two medical centers, the percentages of patients with acute head trauma were 10% and 15%. Prolonged alteration of consciousness occurred in 6% at both centers, and focal neurological examination at presentation was observed in 12% and 14%.

A fourth factor, presentation with status epilepticus/acute repetitive seizures, “bordered on statistical significance and might have reached significance in a larger series,” the authors wrote.

As they put it, “these results support a more conservative use of ED neuroimaging for nonindex seizures, based on clinical factors at the time of presentation. ... without specific indications, ED neuroimaging for nonindex seizures is unlikely to result in an acute change in care.”

The study authors estimated that hundreds of millions of dollars could be saved annually in the United States if neuroimaging in these ED patients could be cut in half.

No study funding was reported, and the authors reported no relevant disclosures.

SOURCE: Salinsky M et al. Epilepsia. 2018 July 18. doi: 10.1111/epi.14518

Neuroimaging may be appropriate only for specific types of patients with recurrent seizures who present at emergency departments because the scans are otherwise unlikely to prompt acute changes in treatment, a new multicenter study suggests.

Spotmatik/Thinkstock

“Going forward, our results should help ED providers determine which patients are more likely to derive benefit from neuroimaging and which patients are not likely to benefit,” lead author Martin Salinsky, MD, of Oregon Health & Science University, Portland, said in an interview. “They can be more selective in ordering scans and reduce the total number obtained.”

As the study authors noted in their report, published July 18 in Epilepsia, “head CT is generally considered a benign procedure. However, overuse is problematic.”

The scans are costly and expose patients to radiation equivalent to 10 chest x-rays, the authors wrote. Scans can complicate care by clogging ED work flow and producing false positives, and patients often seize while undergoing scans, creating even more complications, they added.

“There is very little information in the medical literature that would help guide ED providers in their decision of whether to obtain neuroimaging on a patient who presents with a recurrent seizure,” Dr. Salinsky said. “Without this information, the tendency is to be cautious and obtain scans in more patients.”

For the study, the researchers tracked 822 consecutive ED visits for nonindex – recurrent – epileptic seizures at Oregon Health & Science University and VA Portland Health Care medical centers. (Nonindex seizures accounted for 78% of the total seizures that prompted ED care.)

The study subjects were adults treated for seizure as the main complaint. Patients who had a history of seizures but hadn’t had one for at least 5 years were excluded.

Of the total nonindex seizures, 46% of those resulted in neuroimaging.

“The overall yield of neuroimaging in this patient group was 2%-3%,” Dr. Salinsky said, referring to the percentage of patients whose scans resulted in an acute change in management.

False positives due to imaging artifacts were subsequently discovered in 3 of the 11 patients whose neuroimaging prompted an acute change in management. When the false positives were removed, the yield of acute management changes prompted by neuroimaging decreased to 2.1% overall.

“Three clinical factors – acute head trauma, prolonged alteration of consciousness, and focal neurological examination [at presentation] – were associated with an increased yield of imaging,” he said. “Absent all three factors, the yield in our patients was zero.”

At the two medical centers, the percentages of patients with acute head trauma were 10% and 15%. Prolonged alteration of consciousness occurred in 6% at both centers, and focal neurological examination at presentation was observed in 12% and 14%.

A fourth factor, presentation with status epilepticus/acute repetitive seizures, “bordered on statistical significance and might have reached significance in a larger series,” the authors wrote.

As they put it, “these results support a more conservative use of ED neuroimaging for nonindex seizures, based on clinical factors at the time of presentation. ... without specific indications, ED neuroimaging for nonindex seizures is unlikely to result in an acute change in care.”

The study authors estimated that hundreds of millions of dollars could be saved annually in the United States if neuroimaging in these ED patients could be cut in half.

No study funding was reported, and the authors reported no relevant disclosures.

SOURCE: Salinsky M et al. Epilepsia. 2018 July 18. doi: 10.1111/epi.14518

From the Department of Psychiatry, Brigham and Women’s Hospital, and Harvard Medical School, Boston, MA.

Abstract

• Objective: To provide a review of emergency department (ED)-based psychosocial interventions that support adult patients with an identified suicide risk towards a goal of reducing subsequent suicidal behavior through the period after discharge, which is known to be a time of high risk for suicidal behavior.
• Methods: Non-systematic review of the literature.
• Results: Multiple methods of engaging patients after discharge from the ED have been shown to reduce subsequent suicidal behaviors. These methods include sending caring letters in the mail, facilitating supportive phone conversations, case management, and protocols that combine different services. Overall, the existing literature is insufficient to recommend widespread adoption of any individual strategy or protocol. However, providing psychosocial and emotional support to patients with an identified suicide risk after they are discharged from the ED is feasible and may reduce subsequent suicidal behaviors. Templates for providing supportive outreach using different modalities now exist, and these may help guide the ongoing development and widespread adoption of more effective and cost-effective solutions.
• Conclusion: Many ED–based interventions that provide enhanced support to patients with suicide risk after they are discharged have demonstrated a potential to reduce the risk of future suicidal behavior.

Key words: suicide; emergency department.

Despite the fact that emergency department (ED) providers often feel unprepared to manage suicide risk, patients with significant suicide risk frequently receive care in EDs, whether or not they have sustained physical injuries resulting from suicidal behavior [1,2]. Patients make greater than 400,000 visits to EDs in the United States each year for suicidal and self-injurious behaviors (suicide attempts and self-injurious behaviors are typically coded in ways that make them indistinguishable from each other in retrospective analyses) [3], and it is estimated that 6% to 10% of all patients in EDs endorse suicidal ideation when asked, regardless of their original chief complaints [4]. Meanwhile, suicide has become the 10th leading cause of death in the United States [5], and the Joint Commission has charged all accredited health care organizations with providing comprehensive treatment to suicidal patients, which may range from immediately containing an acute risk to ensuring continuity of care in follow-up [5].

When an acute suicide risk is identified in the ED, the provider’s immediate next steps should be to place the patient in a safe area under constant observation and to provide an emergency assessment [5,6]. Although psychiatric consultation and/or psychiatric admission may follow this assessment, suicide risk does not require admission in all cases; and some patients with suicide risk may be discharged to an outpatient setting even without receiving a psychiatric consultation [1]. Regardless of whether an outpatient disposition from the ED is appropriate, however, the period that immediately follows discharge is a time of high risk for repeated suicidal behavior and suicide death [7–9], and only 30% to 50% of patients who are discharged from EDs after a self-harm incident actually keep a follow-up mental health appointment [9,10]. Therefore, any support given to patients through this transition out of the emergency care setting could be especially high-yield.

The Joint Commission recommends that all patients with suicidal ideation receive, at minimum, a referral to treatment, telephone numbers for local and national crisis support resources (including the National Suicide Prevention Lifeline 1-800-273-TALK), collaborative safety planning, and counseling to restrict access to lethal means upon discharge [5]. However, some programs have demonstrated the capacity to provide enhanced support to patients beyond discharge from the ED, with some success in reducing the rates of subsequent suicidal behaviors. This non-systematic review describes interventions that can be initiated in the context of an ED encounter with the purpose of reducing future suicidal behavior among adult patients. They are primarily psychosocial rather than clinical. Clinical interventions that apply psychotherapy [11–13] psychopharmacology [14], and specialized inpatient treatments [15] have been studied as well but are beyond the scope of this review.

[polldaddy:10107269]

Interventions to Support Patients At Risk of Suicide After Discharge from the ED

Brief Contact Interventions

The idea that maintaining written correspondence with patients who have a known suicide risk after discharge can reduce subsequent suicide rates originated with a study of psychiatric inpatients conducted by Motto and Bostrom, in which patients who had been admitted for depression but had declined outpatient treatment were randomly assigned to periodically receive letters containing supportive messages from staff members over a period of 5 years [16]. This study remarkably found that these so-called brief contact interventions (BCIs), which were personalized to each recipient but did not contain psychotherapy per se, were associated with a reduced rate of suicide throughout the duration of the program compared with no written contacts [16].

BCIs have since been adapted to other communication formats and have been studied in patients who were discharged directly from the ED after an evaluation of suicide risk or suicidal behavior. Typically, BCIs consist of short, supportive messages that are delivered at regular intervals (often once every 1–2 months) over a period of 1 to 5 years [17,18]. They notably do not contain psychotherapy content, although they may reinforce coping strategies or remind recipients of how to access help if needed [17,19]. They may arrive as postcards [20,21], letters [22], telephone outreach [23–25], or a combination of modalities [26].

Protocols that rely on BCIs alone vary in their structure and have yielded mixed results [18]. A meta-analysis of 12 BCI protocols conducted by Milner et al found that, overall, BCIs administered after a presentation to the ED for self-harm have been associated with a significant reduction in repeat suicide attempts per recipient but not in total suicide deaths [27]. Milner’s group did not recommend large-scale promotion of BCIs based on the inadequacy of data so far, but suggested that this strategy may yet show promise upon further study [27]. A key advantage of BCIs is that they are inexpensive to implement, particularly if they do not include a telephone outreach component [28]. Thus, even if the potential benefit to patients is small, administering BCIs can be cost-effective [28].

It should not come as a surprise, therefore, that the potential for incorporation of BCIs into mobile smartphone technology is currently under investigation. Individuals who own mobile phones typically keep them on their persons and turned on continuously, and thus this is a reliable platform for maintaining contact with a wide range of patients in real-time [17,29]. Developers of at least 2 BCI smartphone programs that rely on mobile text messaging have published their protocols [17,30]. However, whether these programs will succeed in meaningfully reducing suicide rates remains to be determined by future research.

Green Cards

Morgan et al conducted a study in the United Kingdom in which individuals who presented to EDs after a self-harm event received a “green card,” which contained encouraging messages about seeking help and provided contact information for emergency services with 24-hour availability [31]. The green card also facilitated access to a crisis admission if necessary. The green card was distributed first in the ED and a second time by mail 3 weeks later. No suicides occurred in either the intervention or control group, which received usual care, and no statistically significant differences in suicide reattempt rate were found between groups after 1 year [31].

Evans et al studied an updated version of the green card intervention in which the green card facilitated access to an on-call psychiatrist with 24-hour availability by telephone [32]. The updated card included encouraging messages about seeking help similar to the original green card described by Morgan; however, the psychiatry consultation via telephone replaced the offer of hospital admission [32]. This second trial of green cards also failed to show a reduction in the rate of suicide reattempts among green card recipients at 6 months and 1 year [32,33].

Brief Intervention and Contact

The World Health Organization’s Brief Intervention and Contact (BIC) protocol is a standardized, multi-step suicide prevention program that has been studied primarily in patients who present to EDs after a suicide attempt in middle-income countries [34]. BIC includes a 1-hour information session that is administered shortly prior to discharge, and subsequently provides 9 follow-up contact interventions at specified intervals over an 18-month period. Unlike in a typical BCI, the contacts in BIC are conducted by a clinician either face-to-face or over the phone and include standardized assessments of the patient’s condition, although they still do not include psychotherapy. BIC has been shown to reduce suicide attempts, suicide deaths, or both in India [34–36], Iran [34,36,37], China [34,36], Brazil [34,36], and Sri Lanka [34,36] but was not found to directly improve clinical outcomes in a study conducted in French Polynesia [38]. A meta-analysis conducted by Riblet et al concluded that BIC is effective in reducing suicide risk overall [39].

ED-SAFE

The Emergency Department Safety Assessment and Follow-up Evaluation (ED-SAFE) protocol was validated in 8 EDs in 7 states in the US that did not already provide psychiatric services internally [40]. Under this model, all patients in the ED receive a screening for suicide risk, and those with an initial positive screen receive a secondary screen administered by the ED physician, a self-administered safety plan, and a series of up to 11 phone contacts over the following year that are administered by trained mental health clinicians in a central location. The ED-SAFE phone contacts follow the Coping Long Term with Active Suicide Program (CLASP) protocol [41] and provide support around safety planning and treatment engagement. They have the capacity to engage the patients’ significant others directly if a significant other is available and the patient chooses to involve that person.

In a single multicenter study, ED-SAFE reduced the absolute risk of suicide attempt by 5%, and the relative risk by 20% compared to usual treatment [40]. An intermediate phase of the study compared the universal suicide screening alone (ie, without the safety plan or follow-up contacts) with usual care and did not find this to improve outcomes [40].

Case Management

Kawanishi et al conducted a randomized controlled trial of assertive case management, the ACTION-J study, for patients with psychiatric diagnoses who presented with self-harm to 17 participating EDs in Japan [42]. In the ACTION-J study, case managers were mental health clinicians who provided clinical evaluations, treatment planning, encouragement, and care coordination over the course of 7 scheduled face-to-face or phone contacts in the first 18 months, and additional contacts at 6-month intervals until the completion of the trial (up to a total of 5 years) [43]. The comparison intervention, enhanced usual care, consisted of psychoeducation provided at the time of the encounter in the ED without case management services. The assertive case management intervention was associated with a decrease in suicidal behavior in the first 6 months but not for the duration of the study, except in women, for whom the benefit lasted the full 18 months [42]. A subsequent analysis also found a decrease in the total number of self-harm episodes per person-year compared to enhanced usual care, although there was not a difference in the number of participants who experienced a repeat self-harm episode [43]. The benefit was most strongly pronounced among patients who had presented with an index suicide attempt [43].

Morthorst et al applied an alternative case management model for the assertive intervention for deliberate self harm (AID) trial, which took place in Denmark [44]. Participants were aged 12 and older and could have been recruited from medical or pediatric inpatient units as well as the ED after a self-harm event. AID employed psychiatric nurses to provide crisis intervention, crisis planning, problem solving, motivational support, family mediation, and assistance with keeping appointments over a period of 6 months following discharge. Outreach took place over the phone, by text message, in participants’ homes, in cafes, and at health and social services appointments. The intervention required at least 4 contacts, although additional contacts could be made if appropriate. In comparison with a control group, in which participants received only usual care (which included ready access to short-term psychotherapy), the AID intervention was not associated with statistically significant differences in recurrent suicidal behaviors [44]. Subgroup analyses examining adult participants aged 20–39 and 40 and older also did not find differences in recurrent suicidal behavior between groups [44].

The Baerum Model and OPAC

A municipal suicide prevention team that provides comprehensive social services to suicide attempters has operated in Baerum, Norway, since 1983 [45]. Under the Baerum model, patients who attempt suicide, can be discharged from the general hospital without psychiatric admission, and are determined to have a high level of need for support are connected by a hospital-based suicide prevention team to a community-based team consisting of nurses and a consulting psychologist, who subsequently engage patients in own their homes and through follow-up phone calls. The services they provide include care coordination, encouragement, activation of social networks, psychological first-aid, and counseling focused on problem-solving. The ostensible goal of the suicide prevention team is to provide a bridge between inpatient medical care and outpatient mental health treatment; however, the intervention lasts approximately 1 year regardless of whether the patient connects with a treatment program [45].

A retrospective comparison of outcomes between recipients of the original Baerum program and non-recipients failed to find a difference in suicide attempts or suicide deaths between groups [45]. However, this was not a controlled study, and suicide attempters were preferentially referred to the program based on whether they had a higher level of need at baseline. Hvid and Wang adapted this model to patients who presented to EDs and general hospitals in Amager, Denmark [46] and have since conducted a series of randomized controlled trials comparing their adaptation to usual care. The Danish version of the Baerum model, renamed OPAC (for “outreach, problem solving, adherence, continuity”), provides similar case management and counseling services but for a maximum of 6 months. In their studies, OPAC significantly reduced the number of patients with a repeat suicide attempt and the total number of repeat suicide attempts at a 1-year interval, and this effect on total number of suicide attempts was sustained at 5 years [47,48]. Although the OPAC protocol begins with a patient’s presentation to the ED, the intervention is initiated after admission to the general hospital. Therefore, while this may inspire a model that provides similar services directly from the ED to patients who do not require general hospital admission, the existing model is not entirely based in the ED.

Discussion

The needs of suicidal patients are often multidimensional, and in some cases their risks are driven by psychosocial problems in addition to, or instead of, medically modifiable psychiatric conditions [49]. However, developing an ED-based program to support patients who are at risk of suicide after they are discharged from the ED is possible. Many such programs that provide or facilitate caring contacts, family support, case management, and/or treatment engagement with discharged patients have demonstrated that similar strategies may have the potential to impact future suicidal behavior. Nonetheless, it would be a stretch to say that all hospital systems should immediately begin doing so.

A new post-discharge support program is an investment of financial resources, personnel, and sometimes technology. Successful delivery of support or messages in any format requires that the intended recipient be able to receive it via reliable access to a working address, telephone number, or electronic device. Nonetheless, programs that rely on BCIs alone (excluding those conducted via telephone) cost relatively little to implement and thus would require a smaller investment than programs that require synchronous telephone or face-to-face contacts with staff in addition to or instead of BCIs. Costs for synchronous programs will also vary depending on the frequency and duration of contacts and the licensure and training required of the staff who provide them.

A trend toward better outcomes associating with more resource-intensive programs is easy to imagine but has not been definitively demonstrated. The wide variation between protocols in all types of programs makes comparisons between those that do and do not include synchronous contacts, and between types of synchronous contacts, difficult. Meanwhile, the low cost of BCIs alone could increase their attractiveness as an investment regardless of the magnitude of outcome improvement.

Denchev et al constructed a cost/benefit comparison model that included the postcard BCI study conducted by Carter et al [20], the telephone outreach study conducted by Vaiva et al [23], and a study of cognitive behavioral therapy (CBT) [11], all of which showed a clinical benefit. This model relied upon some numeric estimations and did not account for variation in outcomes between individual studies of each intervention strategy. However, it concluded that both telephone outreach and CBT were likely to be cost-prohibitive compared to asynchronous BCIs, which were associated with a reduction in costs overall [28].

Conclusion

There remains much to learn regarding how best to reduce suicide risk among adult patients in the period after discharge from the ED, during which patients with an identified suicide risk are known to be vulnerable. However, providing psychosocial and emotional support to patients with an identified suicide risk after they are discharged from the ED is feasible and may reduce subsequent suicidal behaviors. Templates for providing supportive outreach using different modalities now exist, and these may help guide the ongoing development and widespread adoption of more effective and cost-effective solutions.

Corresponding author: David S. Kroll, MD, dskroll@bwh.harvard.edu.

Financial disclosure: Dr. Kroll has received research funding from Brigham and Women’s Hospital to study and develop technological solutions for supporting suicidal patients after discharge from the emergency department. He has additionally received research funding and a speaking honorarium from Avasure.

From the Department of Psychiatry, Brigham and Women’s Hospital, and Harvard Medical School, Boston, MA.

Abstract

• Objective: To provide a review of emergency department (ED)-based psychosocial interventions that support adult patients with an identified suicide risk towards a goal of reducing subsequent suicidal behavior through the period after discharge, which is known to be a time of high risk for suicidal behavior.
• Methods: Non-systematic review of the literature.
• Results: Multiple methods of engaging patients after discharge from the ED have been shown to reduce subsequent suicidal behaviors. These methods include sending caring letters in the mail, facilitating supportive phone conversations, case management, and protocols that combine different services. Overall, the existing literature is insufficient to recommend widespread adoption of any individual strategy or protocol. However, providing psychosocial and emotional support to patients with an identified suicide risk after they are discharged from the ED is feasible and may reduce subsequent suicidal behaviors. Templates for providing supportive outreach using different modalities now exist, and these may help guide the ongoing development and widespread adoption of more effective and cost-effective solutions.
• Conclusion: Many ED–based interventions that provide enhanced support to patients with suicide risk after they are discharged have demonstrated a potential to reduce the risk of future suicidal behavior.

Key words: suicide; emergency department.

Despite the fact that emergency department (ED) providers often feel unprepared to manage suicide risk, patients with significant suicide risk frequently receive care in EDs, whether or not they have sustained physical injuries resulting from suicidal behavior [1,2]. Patients make greater than 400,000 visits to EDs in the United States each year for suicidal and self-injurious behaviors (suicide attempts and self-injurious behaviors are typically coded in ways that make them indistinguishable from each other in retrospective analyses) [3], and it is estimated that 6% to 10% of all patients in EDs endorse suicidal ideation when asked, regardless of their original chief complaints [4]. Meanwhile, suicide has become the 10th leading cause of death in the United States [5], and the Joint Commission has charged all accredited health care organizations with providing comprehensive treatment to suicidal patients, which may range from immediately containing an acute risk to ensuring continuity of care in follow-up [5].

When an acute suicide risk is identified in the ED, the provider’s immediate next steps should be to place the patient in a safe area under constant observation and to provide an emergency assessment [5,6]. Although psychiatric consultation and/or psychiatric admission may follow this assessment, suicide risk does not require admission in all cases; and some patients with suicide risk may be discharged to an outpatient setting even without receiving a psychiatric consultation [1]. Regardless of whether an outpatient disposition from the ED is appropriate, however, the period that immediately follows discharge is a time of high risk for repeated suicidal behavior and suicide death [7–9], and only 30% to 50% of patients who are discharged from EDs after a self-harm incident actually keep a follow-up mental health appointment [9,10]. Therefore, any support given to patients through this transition out of the emergency care setting could be especially high-yield.

The Joint Commission recommends that all patients with suicidal ideation receive, at minimum, a referral to treatment, telephone numbers for local and national crisis support resources (including the National Suicide Prevention Lifeline 1-800-273-TALK), collaborative safety planning, and counseling to restrict access to lethal means upon discharge [5]. However, some programs have demonstrated the capacity to provide enhanced support to patients beyond discharge from the ED, with some success in reducing the rates of subsequent suicidal behaviors. This non-systematic review describes interventions that can be initiated in the context of an ED encounter with the purpose of reducing future suicidal behavior among adult patients. They are primarily psychosocial rather than clinical. Clinical interventions that apply psychotherapy [11–13] psychopharmacology [14], and specialized inpatient treatments [15] have been studied as well but are beyond the scope of this review.

[polldaddy:10107269]

Interventions to Support Patients At Risk of Suicide After Discharge from the ED

Brief Contact Interventions

The idea that maintaining written correspondence with patients who have a known suicide risk after discharge can reduce subsequent suicide rates originated with a study of psychiatric inpatients conducted by Motto and Bostrom, in which patients who had been admitted for depression but had declined outpatient treatment were randomly assigned to periodically receive letters containing supportive messages from staff members over a period of 5 years [16]. This study remarkably found that these so-called brief contact interventions (BCIs), which were personalized to each recipient but did not contain psychotherapy per se, were associated with a reduced rate of suicide throughout the duration of the program compared with no written contacts [16].

BCIs have since been adapted to other communication formats and have been studied in patients who were discharged directly from the ED after an evaluation of suicide risk or suicidal behavior. Typically, BCIs consist of short, supportive messages that are delivered at regular intervals (often once every 1–2 months) over a period of 1 to 5 years [17,18]. They notably do not contain psychotherapy content, although they may reinforce coping strategies or remind recipients of how to access help if needed [17,19]. They may arrive as postcards [20,21], letters [22], telephone outreach [23–25], or a combination of modalities [26].

Protocols that rely on BCIs alone vary in their structure and have yielded mixed results [18]. A meta-analysis of 12 BCI protocols conducted by Milner et al found that, overall, BCIs administered after a presentation to the ED for self-harm have been associated with a significant reduction in repeat suicide attempts per recipient but not in total suicide deaths [27]. Milner’s group did not recommend large-scale promotion of BCIs based on the inadequacy of data so far, but suggested that this strategy may yet show promise upon further study [27]. A key advantage of BCIs is that they are inexpensive to implement, particularly if they do not include a telephone outreach component [28]. Thus, even if the potential benefit to patients is small, administering BCIs can be cost-effective [28].

It should not come as a surprise, therefore, that the potential for incorporation of BCIs into mobile smartphone technology is currently under investigation. Individuals who own mobile phones typically keep them on their persons and turned on continuously, and thus this is a reliable platform for maintaining contact with a wide range of patients in real-time [17,29]. Developers of at least 2 BCI smartphone programs that rely on mobile text messaging have published their protocols [17,30]. However, whether these programs will succeed in meaningfully reducing suicide rates remains to be determined by future research.

Green Cards

Morgan et al conducted a study in the United Kingdom in which individuals who presented to EDs after a self-harm event received a “green card,” which contained encouraging messages about seeking help and provided contact information for emergency services with 24-hour availability [31]. The green card also facilitated access to a crisis admission if necessary. The green card was distributed first in the ED and a second time by mail 3 weeks later. No suicides occurred in either the intervention or control group, which received usual care, and no statistically significant differences in suicide reattempt rate were found between groups after 1 year [31].

Evans et al studied an updated version of the green card intervention in which the green card facilitated access to an on-call psychiatrist with 24-hour availability by telephone [32]. The updated card included encouraging messages about seeking help similar to the original green card described by Morgan; however, the psychiatry consultation via telephone replaced the offer of hospital admission [32]. This second trial of green cards also failed to show a reduction in the rate of suicide reattempts among green card recipients at 6 months and 1 year [32,33].

Brief Intervention and Contact

The World Health Organization’s Brief Intervention and Contact (BIC) protocol is a standardized, multi-step suicide prevention program that has been studied primarily in patients who present to EDs after a suicide attempt in middle-income countries [34]. BIC includes a 1-hour information session that is administered shortly prior to discharge, and subsequently provides 9 follow-up contact interventions at specified intervals over an 18-month period. Unlike in a typical BCI, the contacts in BIC are conducted by a clinician either face-to-face or over the phone and include standardized assessments of the patient’s condition, although they still do not include psychotherapy. BIC has been shown to reduce suicide attempts, suicide deaths, or both in India [34–36], Iran [34,36,37], China [34,36], Brazil [34,36], and Sri Lanka [34,36] but was not found to directly improve clinical outcomes in a study conducted in French Polynesia [38]. A meta-analysis conducted by Riblet et al concluded that BIC is effective in reducing suicide risk overall [39].

ED-SAFE

The Emergency Department Safety Assessment and Follow-up Evaluation (ED-SAFE) protocol was validated in 8 EDs in 7 states in the US that did not already provide psychiatric services internally [40]. Under this model, all patients in the ED receive a screening for suicide risk, and those with an initial positive screen receive a secondary screen administered by the ED physician, a self-administered safety plan, and a series of up to 11 phone contacts over the following year that are administered by trained mental health clinicians in a central location. The ED-SAFE phone contacts follow the Coping Long Term with Active Suicide Program (CLASP) protocol [41] and provide support around safety planning and treatment engagement. They have the capacity to engage the patients’ significant others directly if a significant other is available and the patient chooses to involve that person.

In a single multicenter study, ED-SAFE reduced the absolute risk of suicide attempt by 5%, and the relative risk by 20% compared to usual treatment [40]. An intermediate phase of the study compared the universal suicide screening alone (ie, without the safety plan or follow-up contacts) with usual care and did not find this to improve outcomes [40].

Case Management

Kawanishi et al conducted a randomized controlled trial of assertive case management, the ACTION-J study, for patients with psychiatric diagnoses who presented with self-harm to 17 participating EDs in Japan [42]. In the ACTION-J study, case managers were mental health clinicians who provided clinical evaluations, treatment planning, encouragement, and care coordination over the course of 7 scheduled face-to-face or phone contacts in the first 18 months, and additional contacts at 6-month intervals until the completion of the trial (up to a total of 5 years) [43]. The comparison intervention, enhanced usual care, consisted of psychoeducation provided at the time of the encounter in the ED without case management services. The assertive case management intervention was associated with a decrease in suicidal behavior in the first 6 months but not for the duration of the study, except in women, for whom the benefit lasted the full 18 months [42]. A subsequent analysis also found a decrease in the total number of self-harm episodes per person-year compared to enhanced usual care, although there was not a difference in the number of participants who experienced a repeat self-harm episode [43]. The benefit was most strongly pronounced among patients who had presented with an index suicide attempt [43].

Morthorst et al applied an alternative case management model for the assertive intervention for deliberate self harm (AID) trial, which took place in Denmark [44]. Participants were aged 12 and older and could have been recruited from medical or pediatric inpatient units as well as the ED after a self-harm event. AID employed psychiatric nurses to provide crisis intervention, crisis planning, problem solving, motivational support, family mediation, and assistance with keeping appointments over a period of 6 months following discharge. Outreach took place over the phone, by text message, in participants’ homes, in cafes, and at health and social services appointments. The intervention required at least 4 contacts, although additional contacts could be made if appropriate. In comparison with a control group, in which participants received only usual care (which included ready access to short-term psychotherapy), the AID intervention was not associated with statistically significant differences in recurrent suicidal behaviors [44]. Subgroup analyses examining adult participants aged 20–39 and 40 and older also did not find differences in recurrent suicidal behavior between groups [44].

The Baerum Model and OPAC

A municipal suicide prevention team that provides comprehensive social services to suicide attempters has operated in Baerum, Norway, since 1983 [45]. Under the Baerum model, patients who attempt suicide, can be discharged from the general hospital without psychiatric admission, and are determined to have a high level of need for support are connected by a hospital-based suicide prevention team to a community-based team consisting of nurses and a consulting psychologist, who subsequently engage patients in own their homes and through follow-up phone calls. The services they provide include care coordination, encouragement, activation of social networks, psychological first-aid, and counseling focused on problem-solving. The ostensible goal of the suicide prevention team is to provide a bridge between inpatient medical care and outpatient mental health treatment; however, the intervention lasts approximately 1 year regardless of whether the patient connects with a treatment program [45].

A retrospective comparison of outcomes between recipients of the original Baerum program and non-recipients failed to find a difference in suicide attempts or suicide deaths between groups [45]. However, this was not a controlled study, and suicide attempters were preferentially referred to the program based on whether they had a higher level of need at baseline. Hvid and Wang adapted this model to patients who presented to EDs and general hospitals in Amager, Denmark [46] and have since conducted a series of randomized controlled trials comparing their adaptation to usual care. The Danish version of the Baerum model, renamed OPAC (for “outreach, problem solving, adherence, continuity”), provides similar case management and counseling services but for a maximum of 6 months. In their studies, OPAC significantly reduced the number of patients with a repeat suicide attempt and the total number of repeat suicide attempts at a 1-year interval, and this effect on total number of suicide attempts was sustained at 5 years [47,48]. Although the OPAC protocol begins with a patient’s presentation to the ED, the intervention is initiated after admission to the general hospital. Therefore, while this may inspire a model that provides similar services directly from the ED to patients who do not require general hospital admission, the existing model is not entirely based in the ED.

Discussion

The needs of suicidal patients are often multidimensional, and in some cases their risks are driven by psychosocial problems in addition to, or instead of, medically modifiable psychiatric conditions [49]. However, developing an ED-based program to support patients who are at risk of suicide after they are discharged from the ED is possible. Many such programs that provide or facilitate caring contacts, family support, case management, and/or treatment engagement with discharged patients have demonstrated that similar strategies may have the potential to impact future suicidal behavior. Nonetheless, it would be a stretch to say that all hospital systems should immediately begin doing so.

A new post-discharge support program is an investment of financial resources, personnel, and sometimes technology. Successful delivery of support or messages in any format requires that the intended recipient be able to receive it via reliable access to a working address, telephone number, or electronic device. Nonetheless, programs that rely on BCIs alone (excluding those conducted via telephone) cost relatively little to implement and thus would require a smaller investment than programs that require synchronous telephone or face-to-face contacts with staff in addition to or instead of BCIs. Costs for synchronous programs will also vary depending on the frequency and duration of contacts and the licensure and training required of the staff who provide them.

A trend toward better outcomes associating with more resource-intensive programs is easy to imagine but has not been definitively demonstrated. The wide variation between protocols in all types of programs makes comparisons between those that do and do not include synchronous contacts, and between types of synchronous contacts, difficult. Meanwhile, the low cost of BCIs alone could increase their attractiveness as an investment regardless of the magnitude of outcome improvement.

Denchev et al constructed a cost/benefit comparison model that included the postcard BCI study conducted by Carter et al [20], the telephone outreach study conducted by Vaiva et al [23], and a study of cognitive behavioral therapy (CBT) [11], all of which showed a clinical benefit. This model relied upon some numeric estimations and did not account for variation in outcomes between individual studies of each intervention strategy. However, it concluded that both telephone outreach and CBT were likely to be cost-prohibitive compared to asynchronous BCIs, which were associated with a reduction in costs overall [28].

Conclusion

There remains much to learn regarding how best to reduce suicide risk among adult patients in the period after discharge from the ED, during which patients with an identified suicide risk are known to be vulnerable. However, providing psychosocial and emotional support to patients with an identified suicide risk after they are discharged from the ED is feasible and may reduce subsequent suicidal behaviors. Templates for providing supportive outreach using different modalities now exist, and these may help guide the ongoing development and widespread adoption of more effective and cost-effective solutions.

Corresponding author: David S. Kroll, MD, dskroll@bwh.harvard.edu.

Financial disclosure: Dr. Kroll has received research funding from Brigham and Women’s Hospital to study and develop technological solutions for supporting suicidal patients after discharge from the emergency department. He has additionally received research funding and a speaking honorarium from Avasure.

From the Department of Psychiatry, Brigham and Women’s Hospital, and Harvard Medical School, Boston, MA.

Abstract

• Objective: To provide a review of emergency department (ED)-based psychosocial interventions that support adult patients with an identified suicide risk towards a goal of reducing subsequent suicidal behavior through the period after discharge, which is known to be a time of high risk for suicidal behavior.
• Methods: Non-systematic review of the literature.
• Results: Multiple methods of engaging patients after discharge from the ED have been shown to reduce subsequent suicidal behaviors. These methods include sending caring letters in the mail, facilitating supportive phone conversations, case management, and protocols that combine different services. Overall, the existing literature is insufficient to recommend widespread adoption of any individual strategy or protocol. However, providing psychosocial and emotional support to patients with an identified suicide risk after they are discharged from the ED is feasible and may reduce subsequent suicidal behaviors. Templates for providing supportive outreach using different modalities now exist, and these may help guide the ongoing development and widespread adoption of more effective and cost-effective solutions.
• Conclusion: Many ED–based interventions that provide enhanced support to patients with suicide risk after they are discharged have demonstrated a potential to reduce the risk of future suicidal behavior.

Key words: suicide; emergency department.

Despite the fact that emergency department (ED) providers often feel unprepared to manage suicide risk, patients with significant suicide risk frequently receive care in EDs, whether or not they have sustained physical injuries resulting from suicidal behavior [1,2]. Patients make greater than 400,000 visits to EDs in the United States each year for suicidal and self-injurious behaviors (suicide attempts and self-injurious behaviors are typically coded in ways that make them indistinguishable from each other in retrospective analyses) [3], and it is estimated that 6% to 10% of all patients in EDs endorse suicidal ideation when asked, regardless of their original chief complaints [4]. Meanwhile, suicide has become the 10th leading cause of death in the United States [5], and the Joint Commission has charged all accredited health care organizations with providing comprehensive treatment to suicidal patients, which may range from immediately containing an acute risk to ensuring continuity of care in follow-up [5].

When an acute suicide risk is identified in the ED, the provider’s immediate next steps should be to place the patient in a safe area under constant observation and to provide an emergency assessment [5,6]. Although psychiatric consultation and/or psychiatric admission may follow this assessment, suicide risk does not require admission in all cases; and some patients with suicide risk may be discharged to an outpatient setting even without receiving a psychiatric consultation [1]. Regardless of whether an outpatient disposition from the ED is appropriate, however, the period that immediately follows discharge is a time of high risk for repeated suicidal behavior and suicide death [7–9], and only 30% to 50% of patients who are discharged from EDs after a self-harm incident actually keep a follow-up mental health appointment [9,10]. Therefore, any support given to patients through this transition out of the emergency care setting could be especially high-yield.

The Joint Commission recommends that all patients with suicidal ideation receive, at minimum, a referral to treatment, telephone numbers for local and national crisis support resources (including the National Suicide Prevention Lifeline 1-800-273-TALK), collaborative safety planning, and counseling to restrict access to lethal means upon discharge [5]. However, some programs have demonstrated the capacity to provide enhanced support to patients beyond discharge from the ED, with some success in reducing the rates of subsequent suicidal behaviors. This non-systematic review describes interventions that can be initiated in the context of an ED encounter with the purpose of reducing future suicidal behavior among adult patients. They are primarily psychosocial rather than clinical. Clinical interventions that apply psychotherapy [11–13] psychopharmacology [14], and specialized inpatient treatments [15] have been studied as well but are beyond the scope of this review.

[polldaddy:10107269]

Interventions to Support Patients At Risk of Suicide After Discharge from the ED

Brief Contact Interventions

The idea that maintaining written correspondence with patients who have a known suicide risk after discharge can reduce subsequent suicide rates originated with a study of psychiatric inpatients conducted by Motto and Bostrom, in which patients who had been admitted for depression but had declined outpatient treatment were randomly assigned to periodically receive letters containing supportive messages from staff members over a period of 5 years [16]. This study remarkably found that these so-called brief contact interventions (BCIs), which were personalized to each recipient but did not contain psychotherapy per se, were associated with a reduced rate of suicide throughout the duration of the program compared with no written contacts [16].

BCIs have since been adapted to other communication formats and have been studied in patients who were discharged directly from the ED after an evaluation of suicide risk or suicidal behavior. Typically, BCIs consist of short, supportive messages that are delivered at regular intervals (often once every 1–2 months) over a period of 1 to 5 years [17,18]. They notably do not contain psychotherapy content, although they may reinforce coping strategies or remind recipients of how to access help if needed [17,19]. They may arrive as postcards [20,21], letters [22], telephone outreach [23–25], or a combination of modalities [26].

Protocols that rely on BCIs alone vary in their structure and have yielded mixed results [18]. A meta-analysis of 12 BCI protocols conducted by Milner et al found that, overall, BCIs administered after a presentation to the ED for self-harm have been associated with a significant reduction in repeat suicide attempts per recipient but not in total suicide deaths [27]. Milner’s group did not recommend large-scale promotion of BCIs based on the inadequacy of data so far, but suggested that this strategy may yet show promise upon further study [27]. A key advantage of BCIs is that they are inexpensive to implement, particularly if they do not include a telephone outreach component [28]. Thus, even if the potential benefit to patients is small, administering BCIs can be cost-effective [28].

It should not come as a surprise, therefore, that the potential for incorporation of BCIs into mobile smartphone technology is currently under investigation. Individuals who own mobile phones typically keep them on their persons and turned on continuously, and thus this is a reliable platform for maintaining contact with a wide range of patients in real-time [17,29]. Developers of at least 2 BCI smartphone programs that rely on mobile text messaging have published their protocols [17,30]. However, whether these programs will succeed in meaningfully reducing suicide rates remains to be determined by future research.

Green Cards

Morgan et al conducted a study in the United Kingdom in which individuals who presented to EDs after a self-harm event received a “green card,” which contained encouraging messages about seeking help and provided contact information for emergency services with 24-hour availability [31]. The green card also facilitated access to a crisis admission if necessary. The green card was distributed first in the ED and a second time by mail 3 weeks later. No suicides occurred in either the intervention or control group, which received usual care, and no statistically significant differences in suicide reattempt rate were found between groups after 1 year [31].

Evans et al studied an updated version of the green card intervention in which the green card facilitated access to an on-call psychiatrist with 24-hour availability by telephone [32]. The updated card included encouraging messages about seeking help similar to the original green card described by Morgan; however, the psychiatry consultation via telephone replaced the offer of hospital admission [32]. This second trial of green cards also failed to show a reduction in the rate of suicide reattempts among green card recipients at 6 months and 1 year [32,33].

Brief Intervention and Contact

The World Health Organization’s Brief Intervention and Contact (BIC) protocol is a standardized, multi-step suicide prevention program that has been studied primarily in patients who present to EDs after a suicide attempt in middle-income countries [34]. BIC includes a 1-hour information session that is administered shortly prior to discharge, and subsequently provides 9 follow-up contact interventions at specified intervals over an 18-month period. Unlike in a typical BCI, the contacts in BIC are conducted by a clinician either face-to-face or over the phone and include standardized assessments of the patient’s condition, although they still do not include psychotherapy. BIC has been shown to reduce suicide attempts, suicide deaths, or both in India [34–36], Iran [34,36,37], China [34,36], Brazil [34,36], and Sri Lanka [34,36] but was not found to directly improve clinical outcomes in a study conducted in French Polynesia [38]. A meta-analysis conducted by Riblet et al concluded that BIC is effective in reducing suicide risk overall [39].

ED-SAFE

The Emergency Department Safety Assessment and Follow-up Evaluation (ED-SAFE) protocol was validated in 8 EDs in 7 states in the US that did not already provide psychiatric services internally [40]. Under this model, all patients in the ED receive a screening for suicide risk, and those with an initial positive screen receive a secondary screen administered by the ED physician, a self-administered safety plan, and a series of up to 11 phone contacts over the following year that are administered by trained mental health clinicians in a central location. The ED-SAFE phone contacts follow the Coping Long Term with Active Suicide Program (CLASP) protocol [41] and provide support around safety planning and treatment engagement. They have the capacity to engage the patients’ significant others directly if a significant other is available and the patient chooses to involve that person.

In a single multicenter study, ED-SAFE reduced the absolute risk of suicide attempt by 5%, and the relative risk by 20% compared to usual treatment [40]. An intermediate phase of the study compared the universal suicide screening alone (ie, without the safety plan or follow-up contacts) with usual care and did not find this to improve outcomes [40].

Case Management

Kawanishi et al conducted a randomized controlled trial of assertive case management, the ACTION-J study, for patients with psychiatric diagnoses who presented with self-harm to 17 participating EDs in Japan [42]. In the ACTION-J study, case managers were mental health clinicians who provided clinical evaluations, treatment planning, encouragement, and care coordination over the course of 7 scheduled face-to-face or phone contacts in the first 18 months, and additional contacts at 6-month intervals until the completion of the trial (up to a total of 5 years) [43]. The comparison intervention, enhanced usual care, consisted of psychoeducation provided at the time of the encounter in the ED without case management services. The assertive case management intervention was associated with a decrease in suicidal behavior in the first 6 months but not for the duration of the study, except in women, for whom the benefit lasted the full 18 months [42]. A subsequent analysis also found a decrease in the total number of self-harm episodes per person-year compared to enhanced usual care, although there was not a difference in the number of participants who experienced a repeat self-harm episode [43]. The benefit was most strongly pronounced among patients who had presented with an index suicide attempt [43].

Morthorst et al applied an alternative case management model for the assertive intervention for deliberate self harm (AID) trial, which took place in Denmark [44]. Participants were aged 12 and older and could have been recruited from medical or pediatric inpatient units as well as the ED after a self-harm event. AID employed psychiatric nurses to provide crisis intervention, crisis planning, problem solving, motivational support, family mediation, and assistance with keeping appointments over a period of 6 months following discharge. Outreach took place over the phone, by text message, in participants’ homes, in cafes, and at health and social services appointments. The intervention required at least 4 contacts, although additional contacts could be made if appropriate. In comparison with a control group, in which participants received only usual care (which included ready access to short-term psychotherapy), the AID intervention was not associated with statistically significant differences in recurrent suicidal behaviors [44]. Subgroup analyses examining adult participants aged 20–39 and 40 and older also did not find differences in recurrent suicidal behavior between groups [44].

The Baerum Model and OPAC

A municipal suicide prevention team that provides comprehensive social services to suicide attempters has operated in Baerum, Norway, since 1983 [45]. Under the Baerum model, patients who attempt suicide, can be discharged from the general hospital without psychiatric admission, and are determined to have a high level of need for support are connected by a hospital-based suicide prevention team to a community-based team consisting of nurses and a consulting psychologist, who subsequently engage patients in own their homes and through follow-up phone calls. The services they provide include care coordination, encouragement, activation of social networks, psychological first-aid, and counseling focused on problem-solving. The ostensible goal of the suicide prevention team is to provide a bridge between inpatient medical care and outpatient mental health treatment; however, the intervention lasts approximately 1 year regardless of whether the patient connects with a treatment program [45].

A retrospective comparison of outcomes between recipients of the original Baerum program and non-recipients failed to find a difference in suicide attempts or suicide deaths between groups [45]. However, this was not a controlled study, and suicide attempters were preferentially referred to the program based on whether they had a higher level of need at baseline. Hvid and Wang adapted this model to patients who presented to EDs and general hospitals in Amager, Denmark [46] and have since conducted a series of randomized controlled trials comparing their adaptation to usual care. The Danish version of the Baerum model, renamed OPAC (for “outreach, problem solving, adherence, continuity”), provides similar case management and counseling services but for a maximum of 6 months. In their studies, OPAC significantly reduced the number of patients with a repeat suicide attempt and the total number of repeat suicide attempts at a 1-year interval, and this effect on total number of suicide attempts was sustained at 5 years [47,48]. Although the OPAC protocol begins with a patient’s presentation to the ED, the intervention is initiated after admission to the general hospital. Therefore, while this may inspire a model that provides similar services directly from the ED to patients who do not require general hospital admission, the existing model is not entirely based in the ED.

Discussion

The needs of suicidal patients are often multidimensional, and in some cases their risks are driven by psychosocial problems in addition to, or instead of, medically modifiable psychiatric conditions [49]. However, developing an ED-based program to support patients who are at risk of suicide after they are discharged from the ED is possible. Many such programs that provide or facilitate caring contacts, family support, case management, and/or treatment engagement with discharged patients have demonstrated that similar strategies may have the potential to impact future suicidal behavior. Nonetheless, it would be a stretch to say that all hospital systems should immediately begin doing so.

A new post-discharge support program is an investment of financial resources, personnel, and sometimes technology. Successful delivery of support or messages in any format requires that the intended recipient be able to receive it via reliable access to a working address, telephone number, or electronic device. Nonetheless, programs that rely on BCIs alone (excluding those conducted via telephone) cost relatively little to implement and thus would require a smaller investment than programs that require synchronous telephone or face-to-face contacts with staff in addition to or instead of BCIs. Costs for synchronous programs will also vary depending on the frequency and duration of contacts and the licensure and training required of the staff who provide them.

A trend toward better outcomes associating with more resource-intensive programs is easy to imagine but has not been definitively demonstrated. The wide variation between protocols in all types of programs makes comparisons between those that do and do not include synchronous contacts, and between types of synchronous contacts, difficult. Meanwhile, the low cost of BCIs alone could increase their attractiveness as an investment regardless of the magnitude of outcome improvement.

Denchev et al constructed a cost/benefit comparison model that included the postcard BCI study conducted by Carter et al [20], the telephone outreach study conducted by Vaiva et al [23], and a study of cognitive behavioral therapy (CBT) [11], all of which showed a clinical benefit. This model relied upon some numeric estimations and did not account for variation in outcomes between individual studies of each intervention strategy. However, it concluded that both telephone outreach and CBT were likely to be cost-prohibitive compared to asynchronous BCIs, which were associated with a reduction in costs overall [28].

Conclusion

There remains much to learn regarding how best to reduce suicide risk among adult patients in the period after discharge from the ED, during which patients with an identified suicide risk are known to be vulnerable. However, providing psychosocial and emotional support to patients with an identified suicide risk after they are discharged from the ED is feasible and may reduce subsequent suicidal behaviors. Templates for providing supportive outreach using different modalities now exist, and these may help guide the ongoing development and widespread adoption of more effective and cost-effective solutions.

Corresponding author: David S. Kroll, MD, dskroll@bwh.harvard.edu.

Financial disclosure: Dr. Kroll has received research funding from Brigham and Women’s Hospital to study and develop technological solutions for supporting suicidal patients after discharge from the emergency department. He has additionally received research funding and a speaking honorarium from Avasure.

ANSWER

The radiograph shows an avulsion fracture of the right iliac crest. While the patient does have a growth plate in this location, there is asymmetry between the right and left sides.

Pelvic avulsion fractures can be easy to overlook and are often misdiagnosed as strains. Providers must remember that the pelvis serves as an insertion site for multiple muscles; in both adolescent and adult patients, certain activities (eg, sprinting, jumping, kicking) can increase tension and result in a bone avulsion. Affected patients typically report a popping sensation, pain with range of motion, and point tenderness over the fracture.

Avulsion fractures can usually be identified on x-ray; CT and MRI are used only when definitive diagnosis is unclear. Treatment consists of conservative management—rest, protected weight bearing, and physical therapy. Surgery is typically reserved for those with > 2 cm displacement of the fracture fragment.

In athletes, a gradual return to sports is advised, with full participation at four to 12 weeks postinjury. Possible complications include recurrent symptoms, prolonged healing time, nonunion, malunion, or hip weakness.

This patient was placed on crutches with non-weight-bearing status for one week. She used OTC pain medication as needed. The patient completed a four-week course of physical therapy and returned to full weight-bearing status. After six weeks, the patient had returned to full activity with pain-free range of motion and full strength.

ANSWER

The radiograph shows an avulsion fracture of the right iliac crest. While the patient does have a growth plate in this location, there is asymmetry between the right and left sides.

Pelvic avulsion fractures can be easy to overlook and are often misdiagnosed as strains. Providers must remember that the pelvis serves as an insertion site for multiple muscles; in both adolescent and adult patients, certain activities (eg, sprinting, jumping, kicking) can increase tension and result in a bone avulsion. Affected patients typically report a popping sensation, pain with range of motion, and point tenderness over the fracture.

Avulsion fractures can usually be identified on x-ray; CT and MRI are used only when definitive diagnosis is unclear. Treatment consists of conservative management—rest, protected weight bearing, and physical therapy. Surgery is typically reserved for those with > 2 cm displacement of the fracture fragment.

In athletes, a gradual return to sports is advised, with full participation at four to 12 weeks postinjury. Possible complications include recurrent symptoms, prolonged healing time, nonunion, malunion, or hip weakness.

This patient was placed on crutches with non-weight-bearing status for one week. She used OTC pain medication as needed. The patient completed a four-week course of physical therapy and returned to full weight-bearing status. After six weeks, the patient had returned to full activity with pain-free range of motion and full strength.

ANSWER

The radiograph shows an avulsion fracture of the right iliac crest. While the patient does have a growth plate in this location, there is asymmetry between the right and left sides.

Pelvic avulsion fractures can be easy to overlook and are often misdiagnosed as strains. Providers must remember that the pelvis serves as an insertion site for multiple muscles; in both adolescent and adult patients, certain activities (eg, sprinting, jumping, kicking) can increase tension and result in a bone avulsion. Affected patients typically report a popping sensation, pain with range of motion, and point tenderness over the fracture.

Avulsion fractures can usually be identified on x-ray; CT and MRI are used only when definitive diagnosis is unclear. Treatment consists of conservative management—rest, protected weight bearing, and physical therapy. Surgery is typically reserved for those with > 2 cm displacement of the fracture fragment.

In athletes, a gradual return to sports is advised, with full participation at four to 12 weeks postinjury. Possible complications include recurrent symptoms, prolonged healing time, nonunion, malunion, or hip weakness.

This patient was placed on crutches with non-weight-bearing status for one week. She used OTC pain medication as needed. The patient completed a four-week course of physical therapy and returned to full weight-bearing status. After six weeks, the patient had returned to full activity with pain-free range of motion and full strength.

ANSWER

The radiograph shows rib fractures on the left side (arrows); on the same side, there is a moderate-sized pleural effusion—presumably a hemothorax from the trauma.

A closer look at the mid-thoracic spine reveals some irregularity and possible deformity—note the slight offset. This finding is strongly suspicious for a fracture.

A subsequent CT revealed a thoracic burst fracture with retropulsion into the spinal canal.

ANSWER

The radiograph shows rib fractures on the left side (arrows); on the same side, there is a moderate-sized pleural effusion—presumably a hemothorax from the trauma.

A closer look at the mid-thoracic spine reveals some irregularity and possible deformity—note the slight offset. This finding is strongly suspicious for a fracture.

A subsequent CT revealed a thoracic burst fracture with retropulsion into the spinal canal.

ANSWER

The radiograph shows rib fractures on the left side (arrows); on the same side, there is a moderate-sized pleural effusion—presumably a hemothorax from the trauma.

A closer look at the mid-thoracic spine reveals some irregularity and possible deformity—note the slight offset. This finding is strongly suspicious for a fracture.

A subsequent CT revealed a thoracic burst fracture with retropulsion into the spinal canal.

In June 2017, a 4-year-old boy died 1 week after being knocked over and briefly submerged while playing in knee-deep water. This story was widely reported as a case of a rare occurrence called “dry” or “secondary” drowning, depending on the source.¹ The media accounts went viral, spreading fear in parents and others learning about these alleged conditions from the news and social media.

Many alleged cases of dry drowning are reported every year, but each has been found to have a recognized medical source that has a legitimate medically recognized diagnosis (which dry and secondary drowning are not).

Drowning is one of the most common causes of death in children, and so we ought to make sure that the information we share about it is accurate, as it is vital to effective prevention, rescue, and treatment.

Unfortunately, medical providers, medical journals, and the mass media continue to disseminate misinformation on drowning.² These reports often prevail over updated information and hinder accurate understanding of the drowning problem and its solutions.

Every death is tragic, especially the death of a child, and our heartfelt sympathies go out to the family in this alleged drowning case, as well as to all families suffering the loss of a loved one to drowning. However, in the 2017 case, the cause of death was found on autopsy to be myocarditis not related in any way to drowning. As often happens in such situations, this clarification did not receive any media attention, despite the wide reporting and penetration of the original, erroneous story.

We hope our review will reduce misunderstanding among the public and healthcare providers, contribute to improved data collection, and help to promote interventions aimed at prevention, rescue, and mitigation of drowning incidents.

WHAT IS DROWNING?

A consensus committee of the World Health Organization defined drowning as “the process of experiencing respiratory impairment from submersion/immersion in liquid.”³ The process begins when the victim’s airway goes below the surface of the liquid (submersion) or when water splashes over the face (immersion). If the victim is rescued at any time, the process is interrupted, and this is termed a nonfatal drowning. If the victim dies at any time, this is a fatal drowning. Any water-distress incident without evidence of respiratory impairment (ie, without aspiration) should be considered a water rescue and not a drowning.

Rarely do minimally symptomatic cases progress to death, just as most cases of chest pain do not progress to cardiac arrest.⁴ Nonetheless, rescued drowning victims can deteriorate, which is why we encourage people to seek medical care immediately upon warning signs, as we do with chest pain. For drowning, such warning signs are any water distress followed by difficulty breathing, excessive coughing, foam in the mouth, or abnormal behavior.

A SERIOUS PUBLIC HEALTH ISSUE

Drowning is a serious and neglected public health issue, claiming the lives of 372,000 people a year worldwide.⁵ It is a leading cause of death in children ages 1 to 14. The toll continues largely unabated, and in low- and middle-income nations it does not attract the levels of funding that go to other forms of injury prevention, such as road safety.

Nonfatal drowning—with symptoms ranging from mild cough to severe pulmonary edema, and complications ranging from none to severe neurologic impairment—is far more common than fatal drowning.⁶ For every fatal drowning, there are at least 5 nonfatal drowning incidents in which medical care is needed, and 200 rescues are performed.^7–10

In the United States, drowning accounts for almost 13,000 emergency department visits per year and about 3,500 deaths.^7,8

In Brazil, with two-thirds the population of the United States, drowning accounts for far fewer hospital visits but about twice as many deaths. In Rio de Janeiro, where a highly effective and specialized prehospital service is provided at 3 drowning resuscitation centers staffed by medical doctors, an analysis of the 46,060 cases of rescue in 10 years from 1991 to 2000 showed that medical assistance was needed in only 930 cases (2%).¹⁰ The preventive and rescue actions of parents, bystanders, lifeguards, and prehospital rescue services significantly reduce the number of drowning deaths, but these groups do not consistently gather data on nonfatal drowning that can be included in a comprehensive database.

DROWNING IS A PROCESS

When a person in the water can no longer keep the airway clear, water that enters the mouth is voluntarily spit out or swallowed. Within a few seconds to minutes, the person can no longer clear the airways and water is aspirated, stimulating the cough reflex. Laryngo­spasm, another myth concerning drowning, is presumed to protect the airways but does not, as it is rare, occurring in less than 2% of cases.^11,12

If the person is not rescued, aspiration of water continues, and hypoxemia leads to loss of consciousness and apnea within seconds to a few minutes, followed by cardiac arrest. As a consequence, hypoxemic cardiac arrest generally occurs after a period of tachycardia followed by bradycardia and pulseless electrical activity, usually leading to asystole.^13,14

The entire drowning process, from water distress to cardiac arrest, usually takes a few minutes, but in rare situations, such as rapid hypothermia, it can go on for up to an hour.¹⁵ Most drowning patients have an otherwise healthy heart, and the apnea and hypoxemia precede the cardiac arrest by only a few seconds to minutes; thus, cardiac arrest is caused by the hypoxemic insult and not by ventricular dysrhythmias.^6,16

Drowning can be interrupted at any point between distress and death. If the person is rescued early, the clinical picture is determined by the reactivity of the airway and the amount of water that has been aspirated, but not by the type of water (salt or fresh).

Another myth is that drowning in salt water is different from drowning in fresh water. Both salt water and fresh water cause similar surfactant destruction and washout and disrupt the alveolar-capillary membrane. Disruption of the alveolar-capillary membrane increases its permeability and exacerbates shifting of fluid, plasma, and electrolytes into the alveoli.¹³ The clinical picture of the damage is one of regional or generalized pulmonary edema, which interferes with gas exchange in the lungs.^6,13,17

Animal studies by Modell et al showed that aspiration of just 2.2 mL of water per kilogram of body weight is sufficient to cause severe disturbances in oxygen exchange,¹⁷ reflected in a rise in arterial pH and a drop in partial pressure of oxygen. The situation must be similar in humans. In a 70-kg person, this is only about 154 mL of water—about two-thirds of a cup.

The combined effects of fluid in the lungs, the loss of surfactant, and the increase in capillary-alveolar permeability can result in decreased lung compliance, increased right-to-left shunting in the lungs, atelectasis, alveolitis, hypoxemia, and cerebral hypoxia.¹³

If the victim needs cardiopulmonary resuscitation, the possibility of neurologic damage is similar to that in other cardiac arrest situations, but exceptions exist. For example, in rare cases, hypothermia provides a protective mechanism that allows victims to survive prolonged submersion.^4,15

The duration of submersion is the best predictor of death.¹⁸ Underwater, people are not taking in oxygen, and cerebral hypoxia causes both morbidity and death. For this reason, reversing cerebral hypoxia with effective ventilation, oxygen, and chest compression is the priority of treatment.

“Near drowning,” “dry drowning,” “wet drowning,” “delayed drowning,” and “secondary drowning” are not medically accepted diagnoses,^3,4,19 and many organizations and lifesaving institutions around the world discourage the use of these terms.^19,20 Unfortunately, these terms still slip past the editors of medical journals and are thus perpetuated. The terms are most pervasive in the nonmedical media, where drowning seems to be synonymous with death.^3,19,21 We urge all authors and stakeholders to abandon these terms in favor of understanding and communicating drowning as a process that can vary in severity and have a fatal or nonfatal outcome.

Near-drowning

Historically, drowning meant death, while near-drowning meant the victim survived, at least initially (usually for at least 24 hours).

Before 2002, there were 13 different published definitions of near-drowning.^21,22 This variability has caused a great deal of confusion when trying to describe and monitor drowning.

A person can drown and survive, just as a person can have cardiac arrest and survive.^4,21 Just as there is no recognized condition of “near-cardiac arrest,” there is also no condition of near-drowning. Using near-drowning as a medical diagnosis hides the true burden of drowning and consequently amplifies difficulties in developing effective prevention, rescue, and treatment programs.

Dry drowning

Dry drowning has never been an accepted medical term, although it has been used to describe different parts of the drowning process. While many authors use it as a synonym for secondary drowning (described below), in the past it was usually used in cases in which no water was found in the lungs at autopsy in persons who were found dead in the water.^2–4,21 This occurred in about 10% to 15% of cases and was also called drowning “without water aspiration.”

Perhaps some victims suffer sudden cardiac death. It happens on land—why not in the water? Modell et al stated, “In the absence of the common finding of significant pulmonary edema in the victim’s respiratory system, to conclude his or her death was caused by ‘drowning without aspiration’ is unwise.”²³

Laryngospasm is another proposed explanation. It could play a role in the fewer than 2% of cases in which no other cause of death is found on clinical examination or autopsy,^11,12,19,23 but it does not occur in most cases of drowning, or it is brief and is terminated by the respiratory movements that allow the air in the lung to escape and water to be inhaled.

The problem with the term dry drowning is the harm caused by misdiagnosing cases of sudden death as drowning, when an alternative cause is present. Most importantly, the management is the same if small amounts of water are present or not; therefore, no clinical distinction is made between wet and dry drowning.

Secondary drowning

Secondary drowning, sometimes called delayed drowning, is another term that is not medically accepted. The historical use of this term reflects the reality that some patients may worsen due to pulmonary edema after aspirating small amounts of water.

Drowning starts with aspiration, and few or only mild symptoms may be present as soon as the person is removed from the water. Either the small amount of water in the lungs is absorbed and causes no complications or, rarely, the patient’s condition becomes progressively worse over the next few hours as the alveoli become inflamed and the alveolar-capillary membrane is disrupted. But people do not unexpectedly die of drowning days or weeks later with no preceding symptoms. The lungs and heart do not “fill up with water,” and water does not need to be pumped out of the lungs.

There has never been a case published in the medical literature of a patient who underwent clinical evaluation, was initially without symptoms, and later deteriorated and died more than 8 hours after the incident.^6,10,21 People who have drowned and have minimal symptoms get better (usually) or worse (rarely) within 4 to 8 hours. In a study of more than 41,000 lifeguard rescues, only 0.5% of symptomatic patients died.⁶

Drowning secondary to injury or sudden illness

Any injury, trauma, or sudden illness that can cause loss of consciousness or mental or physical weakness can lead to drowning. Physicians need to recognize these situations to treat them appropriately. Drowning that is secondary to other primary insults can be classified as²⁴:

• Drowning caused by injury or trauma (eg, a surfing, boating, or a hang-gliding accident)
• Drowning caused by a sudden illness such as cardiac disease (eg, myocardial ischemia, arrhythmias, prolonged QT syndrome, hypertrophic cardiomyopathy) or neurologic disease (eg, epilepsy, stroke)
• Diving disease (eg, decompression sickness, pulmonary overpressurization syndrome, compression barotrauma, narcosis [“rapture of the deep”], shallow water blackout, immersion pulmonary edema).

PREVENTION IS BEST

Drowning is a leading and preventable cause of death worldwide and for people of all ages. The danger is real, not esoteric or rare, and healthcare providers should use any opportunity to discuss with patients, parents, and the media the most important tool for treating drowning: primary prevention.

For example, small children should be continuously and uninterruptedly supervised within arm’s reach while in the water, even if a lifeguard is present. Other preventive measures are lifejackets, fences completely enclosing pools or ponds, and swimming and water safety lessons. Drowning often occurs in a deceptively pleasant environment that may not seem dangerous.

When preventive measures fail, responders (usually a health professional is involved) need to be able to perform the necessary steps to interrupt the drowning process.

The first challenge is to recognize when someone in the water is at risk of drowning and needs to be rescued.²⁵ Early self-rescue or rescue by others may stop the drowning process and prevent most cases of initial and subsequent water aspiration, respiratory distress, and medical complications.

DON’T BECOME A VICTIM

Rescuers must take care not to become victims themselves. Panicked swimmers can thrash about and injure the rescuer or clutch at anything they encounter, dragging the rescuer under. And the rescuer can succumb to the same hazards that got the victim into trouble, such as strong currents, deep water, or underwater hazards.

Certified lifeguards are trained to get victims out of the water safely. The American Red Cross slogan “Reach or throw, don’t go” means “Reach out with a pole or other object or throw something that floats; don’t get in the water yourself.”

WHAT TO TELL THE PUBLIC

While some journalists acknowledge that the terms dry drowning and secondary drowning are medically discredited, they still use them in their reports. The novelty of this story—and its appeal to media outlets—is precisely the unfamiliarity of these terms to the general public and the perceived mysterious, looming threat.

We often hear that these terms are more familiar to the public, which is likely true. More concerning, some physicians continue to use them (and older definitions of drowning that equate it with death) in media interviews, clinical care, and publications. The paradox is that we, the medical community, invented these terms, not patients or the media.

As clinicians and researchers, we should drive popular culture definitions, not the other way around. Rather than dismiss these terms as “semantics” or “technicalities,” we should take the opportunity to highlight the dangers of drowning and the importance of prevention, and to promote simpler language that is easier for us and our patients to understand.^19,21

Healthcare providers should understand and share modern drowning science and best practices, which will reduce fear, improve resource utilization, and prevent potentially deadly consequences due to misunderstanding or misinterpretation of incorrect terminology.

WHEN PATIENTS SHOULD SEEK CARE

Anyone who experiences cough, breathless­ness, or other worrisome symptoms such as abnormal mentation within 8 hours of a drowning incident (using the modern definition above) should seek medical advice immediately.

We tell people to seek care if symptoms seem any worse than the experience of a drink “going down the wrong pipe” at the dinner table.²¹ But symptoms can be minimal. Careful attention should be given to mild symptoms that get progressively worse during that time. These cases can rarely progress to acute respiratory distress syndrome.

Table 1 explores who needs further medical help after being rescued from the water.²⁶

In most of these cases, it is most appropriate to call an ambulance, but care may involve seeing a doctor depending on the severity of the symptoms.^6,21 Usually, drowning patients are observed for 4 to 8 hours in an emergency department and are discharged if normal. Symptoms that are more significant include persistent cough, foam at the mouth or nose, confusion, or abnormal behavior, and these require further medical evaluation.

Patients should also seek medical care even if they are 100% normal upon exiting the water but develop worrisome symptoms more than 8 hours later, and providers should consider diagnoses other than primary drowning. Spontaneous pneumothorax, chemical pneumonitis, bacterial or viral pneumonia, head injury, asthma, chest trauma, and acute respiratory distress syndrome have been mislabeled as delayed, dry, or secondary drowning.^3,4,19,21

In June 2017, a 4-year-old boy died 1 week after being knocked over and briefly submerged while playing in knee-deep water. This story was widely reported as a case of a rare occurrence called “dry” or “secondary” drowning, depending on the source.¹ The media accounts went viral, spreading fear in parents and others learning about these alleged conditions from the news and social media.

Many alleged cases of dry drowning are reported every year, but each has been found to have a recognized medical source that has a legitimate medically recognized diagnosis (which dry and secondary drowning are not).

Drowning is one of the most common causes of death in children, and so we ought to make sure that the information we share about it is accurate, as it is vital to effective prevention, rescue, and treatment.

Unfortunately, medical providers, medical journals, and the mass media continue to disseminate misinformation on drowning.² These reports often prevail over updated information and hinder accurate understanding of the drowning problem and its solutions.

Every death is tragic, especially the death of a child, and our heartfelt sympathies go out to the family in this alleged drowning case, as well as to all families suffering the loss of a loved one to drowning. However, in the 2017 case, the cause of death was found on autopsy to be myocarditis not related in any way to drowning. As often happens in such situations, this clarification did not receive any media attention, despite the wide reporting and penetration of the original, erroneous story.

We hope our review will reduce misunderstanding among the public and healthcare providers, contribute to improved data collection, and help to promote interventions aimed at prevention, rescue, and mitigation of drowning incidents.

WHAT IS DROWNING?

A consensus committee of the World Health Organization defined drowning as “the process of experiencing respiratory impairment from submersion/immersion in liquid.”³ The process begins when the victim’s airway goes below the surface of the liquid (submersion) or when water splashes over the face (immersion). If the victim is rescued at any time, the process is interrupted, and this is termed a nonfatal drowning. If the victim dies at any time, this is a fatal drowning. Any water-distress incident without evidence of respiratory impairment (ie, without aspiration) should be considered a water rescue and not a drowning.

Rarely do minimally symptomatic cases progress to death, just as most cases of chest pain do not progress to cardiac arrest.⁴ Nonetheless, rescued drowning victims can deteriorate, which is why we encourage people to seek medical care immediately upon warning signs, as we do with chest pain. For drowning, such warning signs are any water distress followed by difficulty breathing, excessive coughing, foam in the mouth, or abnormal behavior.

A SERIOUS PUBLIC HEALTH ISSUE

Drowning is a serious and neglected public health issue, claiming the lives of 372,000 people a year worldwide.⁵ It is a leading cause of death in children ages 1 to 14. The toll continues largely unabated, and in low- and middle-income nations it does not attract the levels of funding that go to other forms of injury prevention, such as road safety.

Nonfatal drowning—with symptoms ranging from mild cough to severe pulmonary edema, and complications ranging from none to severe neurologic impairment—is far more common than fatal drowning.⁶ For every fatal drowning, there are at least 5 nonfatal drowning incidents in which medical care is needed, and 200 rescues are performed.^7–10

In the United States, drowning accounts for almost 13,000 emergency department visits per year and about 3,500 deaths.^7,8

In Brazil, with two-thirds the population of the United States, drowning accounts for far fewer hospital visits but about twice as many deaths. In Rio de Janeiro, where a highly effective and specialized prehospital service is provided at 3 drowning resuscitation centers staffed by medical doctors, an analysis of the 46,060 cases of rescue in 10 years from 1991 to 2000 showed that medical assistance was needed in only 930 cases (2%).¹⁰ The preventive and rescue actions of parents, bystanders, lifeguards, and prehospital rescue services significantly reduce the number of drowning deaths, but these groups do not consistently gather data on nonfatal drowning that can be included in a comprehensive database.

DROWNING IS A PROCESS

When a person in the water can no longer keep the airway clear, water that enters the mouth is voluntarily spit out or swallowed. Within a few seconds to minutes, the person can no longer clear the airways and water is aspirated, stimulating the cough reflex. Laryngo­spasm, another myth concerning drowning, is presumed to protect the airways but does not, as it is rare, occurring in less than 2% of cases.^11,12

If the person is not rescued, aspiration of water continues, and hypoxemia leads to loss of consciousness and apnea within seconds to a few minutes, followed by cardiac arrest. As a consequence, hypoxemic cardiac arrest generally occurs after a period of tachycardia followed by bradycardia and pulseless electrical activity, usually leading to asystole.^13,14

The entire drowning process, from water distress to cardiac arrest, usually takes a few minutes, but in rare situations, such as rapid hypothermia, it can go on for up to an hour.¹⁵ Most drowning patients have an otherwise healthy heart, and the apnea and hypoxemia precede the cardiac arrest by only a few seconds to minutes; thus, cardiac arrest is caused by the hypoxemic insult and not by ventricular dysrhythmias.^6,16

Drowning can be interrupted at any point between distress and death. If the person is rescued early, the clinical picture is determined by the reactivity of the airway and the amount of water that has been aspirated, but not by the type of water (salt or fresh).

Another myth is that drowning in salt water is different from drowning in fresh water. Both salt water and fresh water cause similar surfactant destruction and washout and disrupt the alveolar-capillary membrane. Disruption of the alveolar-capillary membrane increases its permeability and exacerbates shifting of fluid, plasma, and electrolytes into the alveoli.¹³ The clinical picture of the damage is one of regional or generalized pulmonary edema, which interferes with gas exchange in the lungs.^6,13,17

Animal studies by Modell et al showed that aspiration of just 2.2 mL of water per kilogram of body weight is sufficient to cause severe disturbances in oxygen exchange,¹⁷ reflected in a rise in arterial pH and a drop in partial pressure of oxygen. The situation must be similar in humans. In a 70-kg person, this is only about 154 mL of water—about two-thirds of a cup.

The combined effects of fluid in the lungs, the loss of surfactant, and the increase in capillary-alveolar permeability can result in decreased lung compliance, increased right-to-left shunting in the lungs, atelectasis, alveolitis, hypoxemia, and cerebral hypoxia.¹³

If the victim needs cardiopulmonary resuscitation, the possibility of neurologic damage is similar to that in other cardiac arrest situations, but exceptions exist. For example, in rare cases, hypothermia provides a protective mechanism that allows victims to survive prolonged submersion.^4,15

The duration of submersion is the best predictor of death.¹⁸ Underwater, people are not taking in oxygen, and cerebral hypoxia causes both morbidity and death. For this reason, reversing cerebral hypoxia with effective ventilation, oxygen, and chest compression is the priority of treatment.

“Near drowning,” “dry drowning,” “wet drowning,” “delayed drowning,” and “secondary drowning” are not medically accepted diagnoses,^3,4,19 and many organizations and lifesaving institutions around the world discourage the use of these terms.^19,20 Unfortunately, these terms still slip past the editors of medical journals and are thus perpetuated. The terms are most pervasive in the nonmedical media, where drowning seems to be synonymous with death.^3,19,21 We urge all authors and stakeholders to abandon these terms in favor of understanding and communicating drowning as a process that can vary in severity and have a fatal or nonfatal outcome.

Near-drowning

Historically, drowning meant death, while near-drowning meant the victim survived, at least initially (usually for at least 24 hours).

Before 2002, there were 13 different published definitions of near-drowning.^21,22 This variability has caused a great deal of confusion when trying to describe and monitor drowning.

A person can drown and survive, just as a person can have cardiac arrest and survive.^4,21 Just as there is no recognized condition of “near-cardiac arrest,” there is also no condition of near-drowning. Using near-drowning as a medical diagnosis hides the true burden of drowning and consequently amplifies difficulties in developing effective prevention, rescue, and treatment programs.

Dry drowning

Dry drowning has never been an accepted medical term, although it has been used to describe different parts of the drowning process. While many authors use it as a synonym for secondary drowning (described below), in the past it was usually used in cases in which no water was found in the lungs at autopsy in persons who were found dead in the water.^2–4,21 This occurred in about 10% to 15% of cases and was also called drowning “without water aspiration.”

Perhaps some victims suffer sudden cardiac death. It happens on land—why not in the water? Modell et al stated, “In the absence of the common finding of significant pulmonary edema in the victim’s respiratory system, to conclude his or her death was caused by ‘drowning without aspiration’ is unwise.”²³

Laryngospasm is another proposed explanation. It could play a role in the fewer than 2% of cases in which no other cause of death is found on clinical examination or autopsy,^11,12,19,23 but it does not occur in most cases of drowning, or it is brief and is terminated by the respiratory movements that allow the air in the lung to escape and water to be inhaled.

The problem with the term dry drowning is the harm caused by misdiagnosing cases of sudden death as drowning, when an alternative cause is present. Most importantly, the management is the same if small amounts of water are present or not; therefore, no clinical distinction is made between wet and dry drowning.

Secondary drowning

Secondary drowning, sometimes called delayed drowning, is another term that is not medically accepted. The historical use of this term reflects the reality that some patients may worsen due to pulmonary edema after aspirating small amounts of water.

Drowning starts with aspiration, and few or only mild symptoms may be present as soon as the person is removed from the water. Either the small amount of water in the lungs is absorbed and causes no complications or, rarely, the patient’s condition becomes progressively worse over the next few hours as the alveoli become inflamed and the alveolar-capillary membrane is disrupted. But people do not unexpectedly die of drowning days or weeks later with no preceding symptoms. The lungs and heart do not “fill up with water,” and water does not need to be pumped out of the lungs.

There has never been a case published in the medical literature of a patient who underwent clinical evaluation, was initially without symptoms, and later deteriorated and died more than 8 hours after the incident.^6,10,21 People who have drowned and have minimal symptoms get better (usually) or worse (rarely) within 4 to 8 hours. In a study of more than 41,000 lifeguard rescues, only 0.5% of symptomatic patients died.⁶

Drowning secondary to injury or sudden illness

Any injury, trauma, or sudden illness that can cause loss of consciousness or mental or physical weakness can lead to drowning. Physicians need to recognize these situations to treat them appropriately. Drowning that is secondary to other primary insults can be classified as²⁴:

• Drowning caused by injury or trauma (eg, a surfing, boating, or a hang-gliding accident)
• Drowning caused by a sudden illness such as cardiac disease (eg, myocardial ischemia, arrhythmias, prolonged QT syndrome, hypertrophic cardiomyopathy) or neurologic disease (eg, epilepsy, stroke)
• Diving disease (eg, decompression sickness, pulmonary overpressurization syndrome, compression barotrauma, narcosis [“rapture of the deep”], shallow water blackout, immersion pulmonary edema).

PREVENTION IS BEST

Drowning is a leading and preventable cause of death worldwide and for people of all ages. The danger is real, not esoteric or rare, and healthcare providers should use any opportunity to discuss with patients, parents, and the media the most important tool for treating drowning: primary prevention.

For example, small children should be continuously and uninterruptedly supervised within arm’s reach while in the water, even if a lifeguard is present. Other preventive measures are lifejackets, fences completely enclosing pools or ponds, and swimming and water safety lessons. Drowning often occurs in a deceptively pleasant environment that may not seem dangerous.

When preventive measures fail, responders (usually a health professional is involved) need to be able to perform the necessary steps to interrupt the drowning process.

The first challenge is to recognize when someone in the water is at risk of drowning and needs to be rescued.²⁵ Early self-rescue or rescue by others may stop the drowning process and prevent most cases of initial and subsequent water aspiration, respiratory distress, and medical complications.

DON’T BECOME A VICTIM

Rescuers must take care not to become victims themselves. Panicked swimmers can thrash about and injure the rescuer or clutch at anything they encounter, dragging the rescuer under. And the rescuer can succumb to the same hazards that got the victim into trouble, such as strong currents, deep water, or underwater hazards.

Certified lifeguards are trained to get victims out of the water safely. The American Red Cross slogan “Reach or throw, don’t go” means “Reach out with a pole or other object or throw something that floats; don’t get in the water yourself.”

WHAT TO TELL THE PUBLIC

While some journalists acknowledge that the terms dry drowning and secondary drowning are medically discredited, they still use them in their reports. The novelty of this story—and its appeal to media outlets—is precisely the unfamiliarity of these terms to the general public and the perceived mysterious, looming threat.

We often hear that these terms are more familiar to the public, which is likely true. More concerning, some physicians continue to use them (and older definitions of drowning that equate it with death) in media interviews, clinical care, and publications. The paradox is that we, the medical community, invented these terms, not patients or the media.

As clinicians and researchers, we should drive popular culture definitions, not the other way around. Rather than dismiss these terms as “semantics” or “technicalities,” we should take the opportunity to highlight the dangers of drowning and the importance of prevention, and to promote simpler language that is easier for us and our patients to understand.^19,21

Healthcare providers should understand and share modern drowning science and best practices, which will reduce fear, improve resource utilization, and prevent potentially deadly consequences due to misunderstanding or misinterpretation of incorrect terminology.

WHEN PATIENTS SHOULD SEEK CARE

Anyone who experiences cough, breathless­ness, or other worrisome symptoms such as abnormal mentation within 8 hours of a drowning incident (using the modern definition above) should seek medical advice immediately.

We tell people to seek care if symptoms seem any worse than the experience of a drink “going down the wrong pipe” at the dinner table.²¹ But symptoms can be minimal. Careful attention should be given to mild symptoms that get progressively worse during that time. These cases can rarely progress to acute respiratory distress syndrome.

Table 1 explores who needs further medical help after being rescued from the water.²⁶

In most of these cases, it is most appropriate to call an ambulance, but care may involve seeing a doctor depending on the severity of the symptoms.^6,21 Usually, drowning patients are observed for 4 to 8 hours in an emergency department and are discharged if normal. Symptoms that are more significant include persistent cough, foam at the mouth or nose, confusion, or abnormal behavior, and these require further medical evaluation.

Patients should also seek medical care even if they are 100% normal upon exiting the water but develop worrisome symptoms more than 8 hours later, and providers should consider diagnoses other than primary drowning. Spontaneous pneumothorax, chemical pneumonitis, bacterial or viral pneumonia, head injury, asthma, chest trauma, and acute respiratory distress syndrome have been mislabeled as delayed, dry, or secondary drowning.^3,4,19,21

In June 2017, a 4-year-old boy died 1 week after being knocked over and briefly submerged while playing in knee-deep water. This story was widely reported as a case of a rare occurrence called “dry” or “secondary” drowning, depending on the source.¹ The media accounts went viral, spreading fear in parents and others learning about these alleged conditions from the news and social media.

Many alleged cases of dry drowning are reported every year, but each has been found to have a recognized medical source that has a legitimate medically recognized diagnosis (which dry and secondary drowning are not).

Drowning is one of the most common causes of death in children, and so we ought to make sure that the information we share about it is accurate, as it is vital to effective prevention, rescue, and treatment.

Unfortunately, medical providers, medical journals, and the mass media continue to disseminate misinformation on drowning.² These reports often prevail over updated information and hinder accurate understanding of the drowning problem and its solutions.

Every death is tragic, especially the death of a child, and our heartfelt sympathies go out to the family in this alleged drowning case, as well as to all families suffering the loss of a loved one to drowning. However, in the 2017 case, the cause of death was found on autopsy to be myocarditis not related in any way to drowning. As often happens in such situations, this clarification did not receive any media attention, despite the wide reporting and penetration of the original, erroneous story.

We hope our review will reduce misunderstanding among the public and healthcare providers, contribute to improved data collection, and help to promote interventions aimed at prevention, rescue, and mitigation of drowning incidents.

WHAT IS DROWNING?

A consensus committee of the World Health Organization defined drowning as “the process of experiencing respiratory impairment from submersion/immersion in liquid.”³ The process begins when the victim’s airway goes below the surface of the liquid (submersion) or when water splashes over the face (immersion). If the victim is rescued at any time, the process is interrupted, and this is termed a nonfatal drowning. If the victim dies at any time, this is a fatal drowning. Any water-distress incident without evidence of respiratory impairment (ie, without aspiration) should be considered a water rescue and not a drowning.

Rarely do minimally symptomatic cases progress to death, just as most cases of chest pain do not progress to cardiac arrest.⁴ Nonetheless, rescued drowning victims can deteriorate, which is why we encourage people to seek medical care immediately upon warning signs, as we do with chest pain. For drowning, such warning signs are any water distress followed by difficulty breathing, excessive coughing, foam in the mouth, or abnormal behavior.

A SERIOUS PUBLIC HEALTH ISSUE

Drowning is a serious and neglected public health issue, claiming the lives of 372,000 people a year worldwide.⁵ It is a leading cause of death in children ages 1 to 14. The toll continues largely unabated, and in low- and middle-income nations it does not attract the levels of funding that go to other forms of injury prevention, such as road safety.

Nonfatal drowning—with symptoms ranging from mild cough to severe pulmonary edema, and complications ranging from none to severe neurologic impairment—is far more common than fatal drowning.⁶ For every fatal drowning, there are at least 5 nonfatal drowning incidents in which medical care is needed, and 200 rescues are performed.^7–10

In the United States, drowning accounts for almost 13,000 emergency department visits per year and about 3,500 deaths.^7,8

In Brazil, with two-thirds the population of the United States, drowning accounts for far fewer hospital visits but about twice as many deaths. In Rio de Janeiro, where a highly effective and specialized prehospital service is provided at 3 drowning resuscitation centers staffed by medical doctors, an analysis of the 46,060 cases of rescue in 10 years from 1991 to 2000 showed that medical assistance was needed in only 930 cases (2%).¹⁰ The preventive and rescue actions of parents, bystanders, lifeguards, and prehospital rescue services significantly reduce the number of drowning deaths, but these groups do not consistently gather data on nonfatal drowning that can be included in a comprehensive database.

DROWNING IS A PROCESS

When a person in the water can no longer keep the airway clear, water that enters the mouth is voluntarily spit out or swallowed. Within a few seconds to minutes, the person can no longer clear the airways and water is aspirated, stimulating the cough reflex. Laryngo­spasm, another myth concerning drowning, is presumed to protect the airways but does not, as it is rare, occurring in less than 2% of cases.^11,12

If the person is not rescued, aspiration of water continues, and hypoxemia leads to loss of consciousness and apnea within seconds to a few minutes, followed by cardiac arrest. As a consequence, hypoxemic cardiac arrest generally occurs after a period of tachycardia followed by bradycardia and pulseless electrical activity, usually leading to asystole.^13,14

The entire drowning process, from water distress to cardiac arrest, usually takes a few minutes, but in rare situations, such as rapid hypothermia, it can go on for up to an hour.¹⁵ Most drowning patients have an otherwise healthy heart, and the apnea and hypoxemia precede the cardiac arrest by only a few seconds to minutes; thus, cardiac arrest is caused by the hypoxemic insult and not by ventricular dysrhythmias.^6,16

Drowning can be interrupted at any point between distress and death. If the person is rescued early, the clinical picture is determined by the reactivity of the airway and the amount of water that has been aspirated, but not by the type of water (salt or fresh).

Another myth is that drowning in salt water is different from drowning in fresh water. Both salt water and fresh water cause similar surfactant destruction and washout and disrupt the alveolar-capillary membrane. Disruption of the alveolar-capillary membrane increases its permeability and exacerbates shifting of fluid, plasma, and electrolytes into the alveoli.¹³ The clinical picture of the damage is one of regional or generalized pulmonary edema, which interferes with gas exchange in the lungs.^6,13,17

Animal studies by Modell et al showed that aspiration of just 2.2 mL of water per kilogram of body weight is sufficient to cause severe disturbances in oxygen exchange,¹⁷ reflected in a rise in arterial pH and a drop in partial pressure of oxygen. The situation must be similar in humans. In a 70-kg person, this is only about 154 mL of water—about two-thirds of a cup.

The combined effects of fluid in the lungs, the loss of surfactant, and the increase in capillary-alveolar permeability can result in decreased lung compliance, increased right-to-left shunting in the lungs, atelectasis, alveolitis, hypoxemia, and cerebral hypoxia.¹³

If the victim needs cardiopulmonary resuscitation, the possibility of neurologic damage is similar to that in other cardiac arrest situations, but exceptions exist. For example, in rare cases, hypothermia provides a protective mechanism that allows victims to survive prolonged submersion.^4,15

The duration of submersion is the best predictor of death.¹⁸ Underwater, people are not taking in oxygen, and cerebral hypoxia causes both morbidity and death. For this reason, reversing cerebral hypoxia with effective ventilation, oxygen, and chest compression is the priority of treatment.

“Near drowning,” “dry drowning,” “wet drowning,” “delayed drowning,” and “secondary drowning” are not medically accepted diagnoses,^3,4,19 and many organizations and lifesaving institutions around the world discourage the use of these terms.^19,20 Unfortunately, these terms still slip past the editors of medical journals and are thus perpetuated. The terms are most pervasive in the nonmedical media, where drowning seems to be synonymous with death.^3,19,21 We urge all authors and stakeholders to abandon these terms in favor of understanding and communicating drowning as a process that can vary in severity and have a fatal or nonfatal outcome.

Near-drowning

Historically, drowning meant death, while near-drowning meant the victim survived, at least initially (usually for at least 24 hours).

Before 2002, there were 13 different published definitions of near-drowning.^21,22 This variability has caused a great deal of confusion when trying to describe and monitor drowning.

A person can drown and survive, just as a person can have cardiac arrest and survive.^4,21 Just as there is no recognized condition of “near-cardiac arrest,” there is also no condition of near-drowning. Using near-drowning as a medical diagnosis hides the true burden of drowning and consequently amplifies difficulties in developing effective prevention, rescue, and treatment programs.

Dry drowning

Dry drowning has never been an accepted medical term, although it has been used to describe different parts of the drowning process. While many authors use it as a synonym for secondary drowning (described below), in the past it was usually used in cases in which no water was found in the lungs at autopsy in persons who were found dead in the water.^2–4,21 This occurred in about 10% to 15% of cases and was also called drowning “without water aspiration.”

Perhaps some victims suffer sudden cardiac death. It happens on land—why not in the water? Modell et al stated, “In the absence of the common finding of significant pulmonary edema in the victim’s respiratory system, to conclude his or her death was caused by ‘drowning without aspiration’ is unwise.”²³

Laryngospasm is another proposed explanation. It could play a role in the fewer than 2% of cases in which no other cause of death is found on clinical examination or autopsy,^11,12,19,23 but it does not occur in most cases of drowning, or it is brief and is terminated by the respiratory movements that allow the air in the lung to escape and water to be inhaled.

The problem with the term dry drowning is the harm caused by misdiagnosing cases of sudden death as drowning, when an alternative cause is present. Most importantly, the management is the same if small amounts of water are present or not; therefore, no clinical distinction is made between wet and dry drowning.

Secondary drowning

Secondary drowning, sometimes called delayed drowning, is another term that is not medically accepted. The historical use of this term reflects the reality that some patients may worsen due to pulmonary edema after aspirating small amounts of water.

Drowning starts with aspiration, and few or only mild symptoms may be present as soon as the person is removed from the water. Either the small amount of water in the lungs is absorbed and causes no complications or, rarely, the patient’s condition becomes progressively worse over the next few hours as the alveoli become inflamed and the alveolar-capillary membrane is disrupted. But people do not unexpectedly die of drowning days or weeks later with no preceding symptoms. The lungs and heart do not “fill up with water,” and water does not need to be pumped out of the lungs.

There has never been a case published in the medical literature of a patient who underwent clinical evaluation, was initially without symptoms, and later deteriorated and died more than 8 hours after the incident.^6,10,21 People who have drowned and have minimal symptoms get better (usually) or worse (rarely) within 4 to 8 hours. In a study of more than 41,000 lifeguard rescues, only 0.5% of symptomatic patients died.⁶

Drowning secondary to injury or sudden illness

Any injury, trauma, or sudden illness that can cause loss of consciousness or mental or physical weakness can lead to drowning. Physicians need to recognize these situations to treat them appropriately. Drowning that is secondary to other primary insults can be classified as²⁴:

• Drowning caused by injury or trauma (eg, a surfing, boating, or a hang-gliding accident)
• Drowning caused by a sudden illness such as cardiac disease (eg, myocardial ischemia, arrhythmias, prolonged QT syndrome, hypertrophic cardiomyopathy) or neurologic disease (eg, epilepsy, stroke)
• Diving disease (eg, decompression sickness, pulmonary overpressurization syndrome, compression barotrauma, narcosis [“rapture of the deep”], shallow water blackout, immersion pulmonary edema).

PREVENTION IS BEST

Drowning is a leading and preventable cause of death worldwide and for people of all ages. The danger is real, not esoteric or rare, and healthcare providers should use any opportunity to discuss with patients, parents, and the media the most important tool for treating drowning: primary prevention.

For example, small children should be continuously and uninterruptedly supervised within arm’s reach while in the water, even if a lifeguard is present. Other preventive measures are lifejackets, fences completely enclosing pools or ponds, and swimming and water safety lessons. Drowning often occurs in a deceptively pleasant environment that may not seem dangerous.

When preventive measures fail, responders (usually a health professional is involved) need to be able to perform the necessary steps to interrupt the drowning process.

The first challenge is to recognize when someone in the water is at risk of drowning and needs to be rescued.²⁵ Early self-rescue or rescue by others may stop the drowning process and prevent most cases of initial and subsequent water aspiration, respiratory distress, and medical complications.

DON’T BECOME A VICTIM

Rescuers must take care not to become victims themselves. Panicked swimmers can thrash about and injure the rescuer or clutch at anything they encounter, dragging the rescuer under. And the rescuer can succumb to the same hazards that got the victim into trouble, such as strong currents, deep water, or underwater hazards.

Certified lifeguards are trained to get victims out of the water safely. The American Red Cross slogan “Reach or throw, don’t go” means “Reach out with a pole or other object or throw something that floats; don’t get in the water yourself.”

WHAT TO TELL THE PUBLIC

While some journalists acknowledge that the terms dry drowning and secondary drowning are medically discredited, they still use them in their reports. The novelty of this story—and its appeal to media outlets—is precisely the unfamiliarity of these terms to the general public and the perceived mysterious, looming threat.

We often hear that these terms are more familiar to the public, which is likely true. More concerning, some physicians continue to use them (and older definitions of drowning that equate it with death) in media interviews, clinical care, and publications. The paradox is that we, the medical community, invented these terms, not patients or the media.

As clinicians and researchers, we should drive popular culture definitions, not the other way around. Rather than dismiss these terms as “semantics” or “technicalities,” we should take the opportunity to highlight the dangers of drowning and the importance of prevention, and to promote simpler language that is easier for us and our patients to understand.^19,21

Healthcare providers should understand and share modern drowning science and best practices, which will reduce fear, improve resource utilization, and prevent potentially deadly consequences due to misunderstanding or misinterpretation of incorrect terminology.

WHEN PATIENTS SHOULD SEEK CARE

Anyone who experiences cough, breathless­ness, or other worrisome symptoms such as abnormal mentation within 8 hours of a drowning incident (using the modern definition above) should seek medical advice immediately.

We tell people to seek care if symptoms seem any worse than the experience of a drink “going down the wrong pipe” at the dinner table.²¹ But symptoms can be minimal. Careful attention should be given to mild symptoms that get progressively worse during that time. These cases can rarely progress to acute respiratory distress syndrome.

Table 1 explores who needs further medical help after being rescued from the water.²⁶

In most of these cases, it is most appropriate to call an ambulance, but care may involve seeing a doctor depending on the severity of the symptoms.^6,21 Usually, drowning patients are observed for 4 to 8 hours in an emergency department and are discharged if normal. Symptoms that are more significant include persistent cough, foam at the mouth or nose, confusion, or abnormal behavior, and these require further medical evaluation.

Patients should also seek medical care even if they are 100% normal upon exiting the water but develop worrisome symptoms more than 8 hours later, and providers should consider diagnoses other than primary drowning. Spontaneous pneumothorax, chemical pneumonitis, bacterial or viral pneumonia, head injury, asthma, chest trauma, and acute respiratory distress syndrome have been mislabeled as delayed, dry, or secondary drowning.^3,4,19,21

A 55-year-old man with no significant medical history presented to the emergency department with left-sided flank pain that had begun 3 days earlier. He described the pain as continuous, sharp, and aggravated by movement. He worked in construction, and before the pain started he had moved 8 sheets of drywall and lifted 5-gallon buckets of spackling compound. He denied any associated chest pain, palpitations, dyspnea, cough, or lightheadedness. His family history included sudden cardiac death in 2 second-degree relatives.

On arrival in the emergency department, his vital signs were normal, as were the rest of the findings on physical examination except for reproducible point tenderness below the left scapula.

Laboratory workup revealed normal blood cell counts, liver enzymes, and kidney function. His initial troponin test was negative.

The patient was referred to an electrophysiologist for further evaluation, but he returned to his home country (Haiti) after discharge and was lost to follow-up.

WOLFF-PARKINSON-WHITE PATTERN VS SYNDROME

WPW syndrome is a disorder of the conduction system leading to preexcitation of the ventricles by an accessory pathway between the atria and ventricles. It is characterized by preexcitation manifested on electrocardiography and by symptomatic arrhythmias.

In contrast, the WPW pattern is defined only by preexcitation findings on electrocardiography without symptomatic arrhythmias. Patients with WPW syndrome can present with palpitation, dizziness, and syncope resulting from underlying arrhythmia.¹ This is not seen in patients with the WPW pattern.

A short PR interval with or without delta waves can also be seen in the absence of an accessory pathway, eg, in hypoplastic left heart syndrome, atrioventricular canal defect, and Ebstein anomaly. These conditions are termed pseudopreexcitation syndrome.²

Our patient presented with severe musculoskeletal pain that precipitated the electrocardiographic changes of the WPW pattern and resolved with adequate pain control. The WPW pattern can be unmasked under different scenarios, including anesthesia, sympathomimetic drugs, and postoperatively.^3–5

Catecholamine challenge has been used to unmask high-risk features in WPW syndrome.³ Our patient may have had a transient spike in catecholamine levels because of severe musculoskeletal pain, leading to unmasking of accessory pathways and resulting in the WPW pattern on electrocardiography.

Most patients with the WPW pattern experience no symptoms, but a small percentage develop arrhythmias.

In rare cases, sudden cardiac death can be the presenting feature of WPW syndrome. The estimated risk of sudden cardiac death in patients with the WPW pattern is 1.25 per 1,000 person-years; ventricular fibrillation is the underlying mechanism.⁶ As our patient had a family history of sudden cardiac death, he was considered at high risk and was therefore referred to an electrophysiologist.

A 55-year-old man with no significant medical history presented to the emergency department with left-sided flank pain that had begun 3 days earlier. He described the pain as continuous, sharp, and aggravated by movement. He worked in construction, and before the pain started he had moved 8 sheets of drywall and lifted 5-gallon buckets of spackling compound. He denied any associated chest pain, palpitations, dyspnea, cough, or lightheadedness. His family history included sudden cardiac death in 2 second-degree relatives.

On arrival in the emergency department, his vital signs were normal, as were the rest of the findings on physical examination except for reproducible point tenderness below the left scapula.

Laboratory workup revealed normal blood cell counts, liver enzymes, and kidney function. His initial troponin test was negative.

The patient was referred to an electrophysiologist for further evaluation, but he returned to his home country (Haiti) after discharge and was lost to follow-up.

WOLFF-PARKINSON-WHITE PATTERN VS SYNDROME

WPW syndrome is a disorder of the conduction system leading to preexcitation of the ventricles by an accessory pathway between the atria and ventricles. It is characterized by preexcitation manifested on electrocardiography and by symptomatic arrhythmias.

In contrast, the WPW pattern is defined only by preexcitation findings on electrocardiography without symptomatic arrhythmias. Patients with WPW syndrome can present with palpitation, dizziness, and syncope resulting from underlying arrhythmia.¹ This is not seen in patients with the WPW pattern.

A short PR interval with or without delta waves can also be seen in the absence of an accessory pathway, eg, in hypoplastic left heart syndrome, atrioventricular canal defect, and Ebstein anomaly. These conditions are termed pseudopreexcitation syndrome.²

Our patient presented with severe musculoskeletal pain that precipitated the electrocardiographic changes of the WPW pattern and resolved with adequate pain control. The WPW pattern can be unmasked under different scenarios, including anesthesia, sympathomimetic drugs, and postoperatively.^3–5

Catecholamine challenge has been used to unmask high-risk features in WPW syndrome.³ Our patient may have had a transient spike in catecholamine levels because of severe musculoskeletal pain, leading to unmasking of accessory pathways and resulting in the WPW pattern on electrocardiography.

Most patients with the WPW pattern experience no symptoms, but a small percentage develop arrhythmias.

In rare cases, sudden cardiac death can be the presenting feature of WPW syndrome. The estimated risk of sudden cardiac death in patients with the WPW pattern is 1.25 per 1,000 person-years; ventricular fibrillation is the underlying mechanism.⁶ As our patient had a family history of sudden cardiac death, he was considered at high risk and was therefore referred to an electrophysiologist.

A 55-year-old man with no significant medical history presented to the emergency department with left-sided flank pain that had begun 3 days earlier. He described the pain as continuous, sharp, and aggravated by movement. He worked in construction, and before the pain started he had moved 8 sheets of drywall and lifted 5-gallon buckets of spackling compound. He denied any associated chest pain, palpitations, dyspnea, cough, or lightheadedness. His family history included sudden cardiac death in 2 second-degree relatives.

On arrival in the emergency department, his vital signs were normal, as were the rest of the findings on physical examination except for reproducible point tenderness below the left scapula.

Laboratory workup revealed normal blood cell counts, liver enzymes, and kidney function. His initial troponin test was negative.

The patient was referred to an electrophysiologist for further evaluation, but he returned to his home country (Haiti) after discharge and was lost to follow-up.

WOLFF-PARKINSON-WHITE PATTERN VS SYNDROME

WPW syndrome is a disorder of the conduction system leading to preexcitation of the ventricles by an accessory pathway between the atria and ventricles. It is characterized by preexcitation manifested on electrocardiography and by symptomatic arrhythmias.

In contrast, the WPW pattern is defined only by preexcitation findings on electrocardiography without symptomatic arrhythmias. Patients with WPW syndrome can present with palpitation, dizziness, and syncope resulting from underlying arrhythmia.¹ This is not seen in patients with the WPW pattern.

A short PR interval with or without delta waves can also be seen in the absence of an accessory pathway, eg, in hypoplastic left heart syndrome, atrioventricular canal defect, and Ebstein anomaly. These conditions are termed pseudopreexcitation syndrome.²

Our patient presented with severe musculoskeletal pain that precipitated the electrocardiographic changes of the WPW pattern and resolved with adequate pain control. The WPW pattern can be unmasked under different scenarios, including anesthesia, sympathomimetic drugs, and postoperatively.^3–5

Catecholamine challenge has been used to unmask high-risk features in WPW syndrome.³ Our patient may have had a transient spike in catecholamine levels because of severe musculoskeletal pain, leading to unmasking of accessory pathways and resulting in the WPW pattern on electrocardiography.

Most patients with the WPW pattern experience no symptoms, but a small percentage develop arrhythmias.

In rare cases, sudden cardiac death can be the presenting feature of WPW syndrome. The estimated risk of sudden cardiac death in patients with the WPW pattern is 1.25 per 1,000 person-years; ventricular fibrillation is the underlying mechanism.⁶ As our patient had a family history of sudden cardiac death, he was considered at high risk and was therefore referred to an electrophysiologist.