Volume 24 • Number 1 In This Issue - ACEP SSO Service · Volume 24 • Number 1 September ......

Volume 24 • Number 1

September

2009

In This IssueLesson 1 Diabetic Ketoacidosis and Hyperosmolar Hyperglycemic State . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Page 2 The Drug Box . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 0 The LLSA Literature Review . . . . . . . . . . . . . . . . . . . . . . . . . . . . Page 11Lesson 2 The Vomiting Child . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .Page 12 The Critical Image . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Page 20 CME Questions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Page 21 The Critical ECG . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Page 24

ContributorsTiong Beng Sim, MD, wrote “Diabetic Ketoacidosis and Hyperosmolar Hyperglycemic State.”

Dr. Sim is a research fellow in the emergency department at Cleveland Clinic Foundation, Cleveland, Ohio, an associate consultant in the emergency department at National University Hospital, Singapore, and clinical teacher, Yong Loo Lin School of Medicine, National University of Singapore.

Lee S. Benjamin, MD, FACEP, and Katherine A. Lewis, MD, wrote “The Vomiting Child.” Dr. Benjamin is an assistant professor in the divisions of Emergency Medicine and Pediatric Emergency Medicine at Duke University School of Medicine in Durham, North Carolina. Dr. Lewis is an attending emergency physician at Inova Fairfax Hospital in Falls Church, Virginia.

Sharon E. Mace, MD, FACEP, reviewed “Diabetic Ketoacidosis and Hyperosmolar Hyperglycemic State” and “The Vomiting Child.” Dr. Mace is professor of medicine at the Cleveland Clinic Lerner College of Medicine, Case Western Reserve University, director of the Observation Unit and director of Pediatric Education and Quality Improvement at the Cleveland Clinic Foundation, and faculty for the MetroHealth Medical Center Emergency Medicine Residency Program in Cleveland, Ohio.

Frank LoVecchio, DO, MPH, FACEP, reviewed the questions for these lessons. Dr. LoVecchio is research director at the Maricopa Medical Center Emergency Medicine Program and medical director of the Banner Poison Control Center, Phoenix, Arizona, and a professor at Midwestern University/Arizona College of Osteopathic Medicine in Glendale, Arizona.

Louis G. Graff IV, MD, FACEP, is Editor-in-Chief of Critical Decisions. Dr. Graff is professor of traumatology and emergency medicine at the University of Connecticut School of Medicine in Farmington, Connecticut.

Contributor DisclosuresIn accordance with ACCME Standards and ACEP policy, contributors to Critical Decisions in Emergency Medicine must

disclose the existence of significant financial interests in or relationships with manufacturers of commercial products that might have a direct interest in the subject matter. Authors and editors of these Critical Decisions lessons reported no such interests or relationships.Method of Participation

This educational activity consists of two lessons with a posttest and should take approximately 5 hours to complete. To complete this educational activity as designed, the participant should, in order, review the learning objectives, read the lessons, and complete the online posttest. Release date May 1, 2009. Expiration date April 30, 2012.Accreditation Statement The American College of Emergency Physicians (ACEP) is accredited by the Accreditation Council for Continuing Medical Education (ACCME) to provide continuing medical education for physicians. ACEP designates this educational activity for a maximum of 5 AMA PRA Category 1 Credits™. Physicians should only claim credit commensurate with the extent of their participation in the activity. Approved by ACEP for 5 Category I credits. Approved by the American Osteopathic Association for 5 hours of AOA Category 2-B credit (requires passing grade of 70% or better).Target Audience This educational activity has been developed for emergency physicians.

Critical Decisions in Emergency Medicine

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Lesson 1

Diabetic Ketoacidosis and Hyperosmolar Hyperglycemic State

Tiong Beng Sim, MD

n ObjectivesOn completion of this lesson, you should be able to:

1. Identify potentially life-threatening hyperglycemic diabetic emergencies.

2. Describe the clinical presentations of diabetic ketoacidosis (DKA) and the hyperosmolar hyperglycemic state (HHS) and their diagnostic criteria.

3. Evaluate the precipitating causes of DKA and HHS.

4. Describe the management of DKA and HHS.

5. State the main complications of each diabetic emergency, and discuss the management of each

n From the EM Model5.0 Endocrine, Metabolic, and

Nutritional Disorders

5.4 Glucose Metabolism

Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS) represent the two most serious and life-threatening complications of diabetes mellitus. DKA is the most common cause of diabetes-related death in childhood and also carries significant mortality risk in adults. Annually, DKA accounts for approximately 100,000 hospitalizations in the United States and is responsible for more than $1 billion in health-care and related costs per year.1

Timely diagnosis and therapy are critical to reducing mortality and morbidity.

Case Presentations

n Case OneAn 8-year-old girl presents with

severe shortness of breath. She has had multiple episodes of diarrhea and vomiting over the past 24 hours. The mother adds that her daughter has been losing weight recently and attributes it to fussy eating habits. She also notes that the child has been drinking water excessively and urinating frequently. She does not have any previous medical illnesses.

On arrival, the patient is very tachypneic with Kussmaul breathing. Vital signs are blood pressure 55/24, pulse rate 145, respiratory rate 48, and temperature 38°C (100.4°F). Clinical examination reveals a severely dehydrated restless child with a fruity odor. The abdomen is diffusely tender and distended, with diminished bowel sounds. A

bedside capillary glucose reading is high. Arterial blood gas (ABG) measurement with the patient on oxygen via nonrebreathing mask shows pH 7.02, Po2 320, Pco2 20, HCO3 12 mEq/L, sodium 138 mEq/L, and potassium 5 mEq/L. A urinary catheter is inserted.

n Case TwoA 75-year-old man arrives

by ambulance. He was found unconscious at home. The son says that his father had been taking fluids poorly for the past few days and has had a productive cough associated with a fever. The patient has a history of diabetes mellitus and renal impairment and is poorly compliant with medications. On route to the hospital, the patient had a focal seizure that was aborted with intravenous lorazepam given by the paramedics.

On arrival at the emergency department, the patient is drowsy and vomits. Vital signs are blood pressure 150/80, pulse rate 135, respiratory rate 22, temperature 39.5°C (103.1°F), and pulse oximetry 95% on nonrebreathing mask. He appears sallow and dehydrated. The pupils are equal in size, and the neurologic examination shows diminished power on the left. On auscultation, crackles are heard over the right lung base.

The patient is intubated immediately to protect the airway, in view of his obtundation.

A bedside glucometer reading is high. A chest radiograph shows a

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right lower-lobe consolidation. Initial ABG readings on 100% oxygen show pH 7.38, Po2 110, Pco2 35, HCO3 20, oxygen saturation 98%, sodium 146, and potassium 4. The glucose is 950 mg/dL. A septic workup is performed. An emergent computed tomography (CT) scan of the head is normal.

PathophysiologyUnderstanding the pathogenesis

of DKA and HHS gives insight into the principles of their management. The underlying mechanism of DKA is a net reduction of insulin’s effective action as a result of resistance or decreased secretion and a concomitant elevation of insulin counterregulatory hormones such as glucagon, catecholamines, cortisol, and growth hormones. This leads to increased gluconeogenesis, hepatic and renal glucose production, and impaired peripheral utilization of glucose. The net result is hyperglycemia and increased hyperosmolality in the extracellular space. The hormonal alterations also promote release of free fatty acids from adipose tissue (lipolysis) into the circulation which are subsequently converted to ketone bodies (-hydroxybutyric acid and acetoacetate) in the liver, leading to ketonemia and acidosis.2 The overall effect culminates in the two cardinal features of DKA: hyperglycemia and ketonemia. Hyperosmolarity but not acidosis is prominent in HHS, because the insulin level in HHS is sufficient to counteract lipolysis and ketogenesis but not adequate to facilitate peripheral tissue use of

glucose. In practice, however, it is common to see a mixed picture of both DKA and HHS. Both conditions are associated with glycosuria and osmotic diuresis, with tremendous loss of water and electrolytes in the process.

DKA is also a pro-inflammatory state, resulting in release of reactive oxidative species such as elevation of C-reactive proteins and other cardiovascular risk markers, like lipid peroxidation markers, which return to normal levels on intense treatment of the DKA episode.3 The clinician should therefore be wary of this and cautious in using the markers to diagnose an infective process or cardiovascular event, although one should look actively for triggering factors.

DiagnosisA high degree of suspicion with

timely diagnosis and management are critical for better outcomes in these acute life-threatening metabolic disorders, especially in the extremes of age. DKA could well be the initial presentation of type I diabetes mellitus (formerly known as juvenile-onset or insulin-dependent diabetes mellitus) in children. Up to 40% of elderly patients who present with hyperglycemic crisis do not have a prior history of diabetes, and delayed recognition of hyperglycemic symptoms could lead to severe dehydration.4 The mortality rate for DKA is less than 5%, but the mortality rate for HHS remains alarmingly high at 33% in those over age 80, with death caused

by the precipitating illness rather than metabolic derangements.5 The prognosis for both conditions is worse at the extremes of age and in the presence of coma, which indicates severe hyperosmolality and hemodynamic instability.6

Clinicians must therefore be quick to diagnose these conditions from their varied presentations and identify any underlying precipitating illnesses and render timely and appropriate treatment to reduce morbidity and mortality. Many previously undiagnosed patients are seen in physicians’ office or emergency departments before they become critically ill. Checking the glucose may be life saving.

CRITICAL DECISIONWhat presentations should raise suspicion of DKA or HHS, especially in patients who do not have a prior history of diabetes mellitus?

DKA and HHS can fall anywhere along the disease continuum of metabolic derangements. In many cases, a mixed picture can occur depending on the duration of illness and the nature of the precipitating cause, and this has implications for management.6

Typically, DKA evolves over a short time frame—less than 24 hours, while HHS tends to evolve over a few days leading to a more severe dehydration and hyperosmolality. The symptoms of uncontrolled diabetes usually precede metabolic decompensation. The clinical picture includes polyuria, polydipsia, weight loss, malaise, dehydration, blurred vision, vomiting,

What presentations should raise suspicion of DKA or • HHS, especially in patients who do not have a prior history of diabetes mellitus?When is abdominal pain truly an acute abdomen?• What are the diagnostic criteria for DKA and HHS?• Is a venous or capillary blood gas a good substitute for • an arterial blood gas?

What are the major considerations for managing • hyperglycemic crises?What are the potential complications that the clinician • needs to be aware of while managing hyperglycemic crises?

Critical Decisions


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abdominal pain, weakness, altered mental state, and coma. Dehydration can be worsened by the concomitant use of diuretics.

Physical signs include Kussmaul breathing (which is a compensatory mechanism for severe metabolic acidosis), accompanied by a fruity acetone odor. Signs of dehydration include tachycardia, hypotension, dry mucous membranes, and decreased skin turgor. Up to 25% of patients have emesis, which can have a “coffee ground” appearance secondary to gastric erosions and hypertonicity-induced gastroparesis.7 A rectal examination should be performed to look for occult gastrointestinal hemorrhage and perirectal abscess. Sources of infection should be sought.

Mental status can range from alertness to lethargy, obtundation, and coma. The level of consciousness correlates more with the severity of osmolality rather than acidemia, which explains why altered sensorium and coma are seen more commonly in HHS and signs of acidosis are usually absent in HHS. In some patients with HHS, focal neurologic signs such as

hemiparesis and seizures (partial motor seizures are more common than generalized) are the dominant clinical findings.2

Although infections are common precipitants of both DKA and HHS, patients can be normothermic or even hypothermic because of peripheral vasodilation. Severe hypothermia is an indicator of poor prognosis.8

CRITICAL DECISIONWhen is abdominal pain truly an acute abdomen?

Abdominal pain mimicking an acute abdomen is a common symptom, seen in 50% of patients presenting with DKA. The pain is often diffuse; localized tenderness should alert physicians to look for a secondary etiology. A strong association was observed between abdominal pain and metabolic acidosis but not severity of hyperglycemia or dehydration. In DKA patients with abdominal pain, the mean serum bicarbonate (9 +/- 1 mmol/L) and blood pH (7.12 +/-0.02) were lower than in patients without pain (15 +/- 1 mmol/L and 7.24 +/-

0.09, respectively, both P <.001).9 Cocaine and alcohol abuse are also commonly associated with abdominal pain in DKA. In general, investigation of the etiology of abdominal pain in DKA should be reserved for patients without severe metabolic acidosis (mild DKA), or with pain that persists after the resolution of ketoacidosis, or with localized tenderness, or with acute peritoneal signs.

Precipitating CausesThe two most common triggers of

DKA and HHS are noncompliance with therapy and infection. Other precipitants include cerebrovascular accidents, myocardial infarction, acute abdomen, and drugs. Common drugs that affect carbohydrate metabolism leading to worse diabetes control include steroids, phenytoin, thiazides, oral contraceptives, -blockers, sympathomimetic agents, and antipsychotics. New-onset type I diabetes mellitus can also present with DKA in children and young adults.

DKA HHS

Mild Moderate Severe

Plasma glucose (mg/dL) >250 >250 >250 >600

Arterial pH 7 .25 to 7 .3 7 to 7 .24 <7 >7 .3

Serum bicarbonate (mEq/L) 15 to 18 10 to <15 <10 >15

Urine ketones Positive Positive Positive Small

Serum ketones Positive Positive Positive Small or absent

Calculated serum osmolality (mOsm/kg) Variable Variable Variable >320

Anion gap >10 >12 >12 Variable

Mental state Alert Alert/drowsy Stupor/coma Stupor/coma

Total body water deficit (L) in a 70-kg adult 6 9 (24%)

Age Young Elderly typically

Onset Acute: over hours to days

Chronic: over days to weeks

Seizures Rare Common

Insulin levels Very low to absent Low to normal

Mortality 0% to 10% 20% to 40%

Table 1.Diagnostic criteria and clinical features in both DKA and HHS. Adapted from Kitabchi AE, Umpierrex GE, Murphy MB, et al. Hyperglycemic crisis in adult patients with diabetes: a consensus statement from the American Diabetes Association. Diabetes Care. 2006;29:2740. Used with permission.


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CRITICAL DECISIONWhat are the diagnostic criteria for DKA and HHS?

A mixed picture of both DKA and HHS can occur. Mild ketonemia might be present in patients with HHS who have an admission pH above 7.3 and bicarbonate of more than 20 mEq/L. The severity of DKA is classified as mild, moderate, or severe according to the severity of metabolic acidosis and the presence of altered sensorium (Table 1).2 Knowing the severity and the overlapping presentation can guide in the management of patients.

The therapeutic regimen is tailored according to the prominent clinical features. Cerebral edema is uncommon in adults but is seen in pediatric patients. Undertreatment of HHS increases the risk of mortality. Therefore in patients with HHS, the aim is to correct hyperosmolality rapidly to less than 320 mOsm/L and lower the blood glucose to 250 to 300 mg/dL early. In pediatric patients with DKA, rapid correction of metabolic abnormalities and, consequently, of hyperosmolarity, by administering hypotonic fluids and insulin should be avoided to decrease the risk for precipitating cerebral edema.10

Differential DiagnosisOther causes of ketosis and

acidosis should be considered in patients presenting with DKA. Both starvation and alcoholic ketoacidosis can be distinguished from DKA by a clinical history of starvation and alcohol abuse, respectively, and a blood glucose level that ranges

from mildly elevated (<250 mg/dL) to hypoglycemic levels. The serum bicarbonate level with starvation and alcoholic ketoacidosis is usually not lower than 18 mEq/L, while that of DKA could exhibit a profound acidosis.

Laboratory InvestigationsThe preliminary investigations

should include plasma glucose, BUN, electrolytes and creatinine, serum and urine ketones, osmolality, urinalysis, arterial blood gases, and CBC. An ECG, chest radiograph, and septic workup should be performed if clinically warranted. Table 2 lists common useful calculation formulas.

Several pitfalls must be avoided in interpreting the laboratory results in patients with DKA or HHS. The stress of the DKA will often cause a leukocytosis proportional to the ketone concentration and hemoconcentration. Infection should be considered if the leucocytosis is more than 25,000 or there is an elevated band count.11 The hyperglycemia can cause nonspecific elevation of a variety of enzymes, including hepatic transaminase, lactate dehydrogenase, creatine kinase, amylase, lipase, and triglycerides; results must, therefore, be interpreted with caution.12 Those DKA patients who are vomiting or are on a diuretic may have a superimposed metabolic alkalosis that could mask the severity of their ketoacidosis. A low serum potassium concentration on admission can reflect severe total body potassium deficiency. Because the insulin

therapy of the DKA can further lower potassium levels and potentially provoke respiratory failure and life-threatening cardiac dysrhythmia, potassium should be replaced until the level is more than 3.3 before insulin is started. Finally, a patient’s acidosis could give a false reading of the potassium level. Corrected potassium levels can be estimated by subtracting 0.6 mEq/L from the laboratory potassium value for every 0.1 decrease in pH value noted in the blood gas (Table 2). For example, a patient with a serum potassium value of 5 mEq/L and pH of 6.9 actually has a corrected potassium of only 2 mEq/L, indicating severe hypokalemia and should have immediate potassium replacement, and consideration should be given to withholding insulin therapy until potassium is restored above 3.3 mEq/L.

Pseudohyponatremia can exist as a result of hyperglycemia and the elevated chylomicrons in DKA. The actual sodium level can be calculated (Table 2). If a DKA patient has an increased serum sodium level, this indicates a profound water loss and severe dehydration, with the corrected sodium being even higher.

It is possible for patients to have DKA even when they are euglycemic or with tests negative for urine ketones. Euglycemia has been reported in up to 18% of cases of DKA,13 and the urine dipstick test uses the nitroprusside method which detects the presence of acetoacetate but not -hydroxybutyric acids. Thus the diagnosis can be missed in those

Table 2.Useful formulas in DKA

Anion gap = [Na+ – (Cl- + HCO3-)]

Serum sodium correction = Measured [Na+] + [1 .6 glucose (mg/dL) – 100]/100

Serum potassium correction during acidemia = [K] – (0 .6 mEq/L per 0 .1 drop in pH)

= [K] – (0 .6 mEq/L [7 .4 – measured pH 10])

Serum osmolality (mOsm/L) = 2 [Na+ + K](mEq/L) + Glucose (mg/dL)/18 + BUN (mg/dL)/2 .8

Total body water deficit (L) = 0 .6 body weight (kg) [1 – 140/serum Na+]


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DKA cases in which the predominant ketones are -hydroxybutyric acids.

CRITICAL DECISIONIs a venous or capillary blood gas a good substitute for an arterial blood gas?

The pH is used as one of the diagnostic criteria to categorize the severity of acidemia in DKA patients and is useful therefore in steering treatment plans and disposition in the emergency department. Venous pH correlates very well with the arterial pH as it is only 0.02 to 0.03 units lower than the arterial pH, provided good phlebotomy principles are observed during the blood drawing such as avoiding a long tourniquet time.14-16 Venous pH can therefore be used as a substitute for arterial pH to assess response to therapy while at the same time avoiding pain and potential complications from repeated arterial punctures. Initial blood gas analysis, however, should still be an arterial sample, as recommended by the American Diabetes Association (ADA).2

CRITICAL DECISIONWhat are the major considerations while managing hyperglycemic crisis?

The therapeutic goal of DKA and HHS hinges on correcting underlying pathophysiologic abnormalities. The cornerstones are fluid resuscitation, acid-base and electrolyte correction, insulin therapy, identification of comorbid precipitating factors, and, above all, frequent, meticulous patient monitoring. Comatose patients,

especially if they are vomiting, require immediate intubation to reduce the risk of aspiration. A summary of DKA and HHS management is depicted in Figure 1.

Fluid ResuscitationFluid therapy, the mainstay of

DKA/HHS treatment, is directed toward correction of intravascular and extravascular volume deficits and improving renal perfusion. Fluid replacement also lowers blood sugars independently of insulin therapy, reduces the counterregulatory hormones thereby improving insulin sensitivity, and improves glomerular filtration rate, which in turn enhances the clearance of glucose and ketones from the blood.

In the absence of cardiac compromise, isotonic saline (0.9% NaCl) is infused in adults at a rate of 15 to 20 mL/kg/hour during the first hour.2 Further choice of fluid therapy should be guided by hemodynamic status, hydration status, corrected sodium level, and urinary output.

If the patient remains hypotensive despite initial therapy, deliver another bolus of saline, and consider administering a plasma expander until shock is resolved. If the patient is hemodynamically stable and if the corrected sodium is normal or elevated, infuse 0.45% saline at 4 to 14 mL/kg/hour (range depends on hydration status) evenly over 24 hours. If the corrected sodium is low and the patient is stable, 0.9% saline infusion at a similar rate is recommended.2

Success in fluid therapy is reflected by an improvement in hemodynamic and hydration status and pH values, a satisfactory urine output of 1 to 2 mL/kg/hour, and clinical progress.

Insulin TherapyInsulin therapy improves the

hyperglycemia and ketoacidosis in DKA by inhibiting gluconeogenesis and ketogenesis and decreasing lipolysis.

The use of intravenous insulin infusion has been supported by many randomized controlled trials. Once hypokalemia (K <0.3 mEq/L) and hypotension are excluded, an intravenous bolus of regular insulin at 0.1 unit/kg followed by an infusion at a rate of 0.1 unit/kg/hour should be started as recommended by the ADA.2 In general, any insulin therapy should be withheld if the serum potassium falls below 3 mEq/L and given only after potassium rises above 3.3 mEq/L to avert disastrous cardiac arrhythmias and respiratory failure.

The blood glucose level should be monitored hourly, and if the target glucose lowering rate of 50 to 75 mg/dL per hour is not achieved despite adequate fluid therapy, then the insulin infusion may be doubled every hour to treat possible insulin resistance, which can occur in sepsis, in occult infection, or with intraabdominal pathology.2

When the blood glucose level falls below 250 mg/dL, do not omit insulin infusion but continue at a lower dose of 0.05 to 0.1 unit/kg/hour and add 5% dextrose to the fluid regimen to

Serum Potassium Concentrations (mEq/L)

Potassium Replacement (mEq/L)

>5 .3 Do not give K, but check potassium levels hourly and start replacement when K <5 .3

4 to 5 .3 20

3 to 4 30 to 40

<3 40 to 60 (consider holding insulin temporarily until K >3 .3 )

Table 3.Potassium replacement regimena in adult patients with DKA or HHS

a Ensure satisfactory urine output of 1 mL/kg/hour before initiating potassium replacement .


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Figure 1.Summary protocol of DKA and HHS management. Adapted from Kitabchi AE, Umpierrex GE, Murphy MB, et al. Hyperglycemic crisis in adult patients with diabetes: a consensus statement from the American Diabetes Association. Diabetes Care. 2006;29:2739-2748. Used with permission.

Identify precipitating illness and start IV fluid bolus 15 to 20 mL/kg first hour

Ketoacidosis + hyperglacemia(pH <7.3) (glucose >250 mg/dL)

Hyperglycemia + hyperosmolality + pH >7.3(glucose >600 mg/dL) (serum osmolality >320)

DKA HHS

Insulin PotassiumFluids

Blood pressure 3 to 4 4 to 5<3IV bolus0.1 units/kga

Stable IV infusion0.1 unit/kg/hr

Hourly glucosemonitoring

Unstable

Repeatfluid bolusConsider

colloids/inotropes

Target glucosedrop 50 to 75mg/dL/hour

Hold insulintill K >3.3

Add K 40-60mEq/L

Add K30 to 40 mEq/L

Add K20 to 30 mEq/L

Correctedserum sodium

Low High or normal Yes No

0.9% NaCl(4 to 14

mL/kg/hour)

0.45% NaCl(4 to 14

mL/kg/hour)

Continuesamedose

Doubleinfusion

dose

Venous glucose reaches 250 mg/dL

Add IV 5% dextrose to above fluid regimenDecrease IV insulin to 0.05 units/kg/hour

Maintain glucose between 150 to 250 mg/dL and continue insulin infusionand fluid hydration until ketosis or hyperosmolality resolves

aOmit bolus insulin in pediatric patients


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complete rehydration and to maintain the glucose between 150 to 250 mg/dL until ketosis or hyperosmolality resolves. Dextrose combinations may be increased to 10% if glucose levels remain below 100 mg/dL. If hypoglycemia occurs, insulin may be stopped temporarily and restarted when patients are euglycemic again.

PotassiumDespite total body potassium

depletion, mild to moderate hyperkalemia secondary to cellular efflux is frequently encountered in DKA patients. This resolves readily with insulin therapy, acidosis correction, and fluid resuscitation.

Hypokalemia is a likely complication from DKA therapy as a result of cellular influx. To prevent hypokalemia, the ADA recommends initiating potassium replacement once serum potassium levels drop below 5.3 mEq/L, provided there is a satisfactory urine output of 1 mg/kg/hour. In general, 20 to 30 mEq/L in each liter of infusion fluid is sufficient to maintain the serum potassium between 4 to 5 mEq/L. An alternative regimen is summarized in Table 3.10

BicarbonateThe use of bicarbonate therapy

in DKA remains controversial. The administration of bicarbonate could potentially lead to harmful effects such as rebound alkalosis, worsened hypokalemia, decreased tissue oxygen uptake, paradoxical central nervous system acidosis, and cerebral edema. The consensus is that bicarbonate therapy should not be used for patients in DKA when the pH is above 7, because administration of insulin inhibits lipolysis and leads to resolution of ketoacidosis without any bicarbonate.

The ADA guidelines recommend bicarbonate therapy when the pH is below 7. For a pH between 6.9 and 7, give 50 mmol of bicarbonate in 200 mL sterile water over 1 hour; for a pH below 6.9, give 100 mmol of

bicarbonate in 400 mL sterile water over 2 hours. The venous pH should be assessed every 2 hours until the pH rises above 7, and treatment may be repeated if necessary to achieve the target pH value above 7. The rationale for using bicarbonate when the pH falls below 7 is that severe acidosis can lead to a myriad of adverse effects including negative inotropism, central nervous system depression, peripheral vasodilation, and insulin resistance. However, there are no prospective, randomized studies concerning the use of bicarbonate in patients with pH below 6.9. Another study involving 21 patients also showed no benefit to bicarbonate therapy in patients with pH from 6.9 to 7.1.17

PhosphatePhosphate replacement has

shown no added benefit for most patients with DKA and could cause hypocalcemia.18 However, careful phosphate replacement may be indicated in patients with cardiac dysfunction, anemia, respiratory depression, and severe hypophosphatemia (<1 mg/dL).19 In such cases, 20 to 30 mEq/L of potassium phosphate may be added to the fluid regimen.

Elderly PatientsElderly patients’ response to

these conditions deserves special consideration. Elderly patients are more likely to present with a mixed picture of both DKA and HHS. They have a higher mortality rate, because they generally have more comorbidities and more severe precipitating illness. Those with mental status changes out of proportion to the abnormality of their serum osmolarity could have an additional process such as an intracranial event or occult sepsis.

Seizures in HHS, especially focal seizures, are usually associated with focal neurologic findings that resolve with treatment, but stroke is also common in older patients. Phenytoin is ineffective for control of seizures

caused by HHS and may actually exacerbate HHS by worsening hyperglycemia.20 Benzodiazepines should be tried first, and if they fail, then barbiturates should be considered for seizure control.

In elderly patients and patients with renal or cardiac compromise the fluid resuscitation should be done with caution. Therapy may be guided by invasive monitoring such as central venous line pressures. Frequent assessment of cardiac, renal, and mental status must be performed during fluid resuscitation to avoid iatrogenic fluid overload.

The serum glucose can decline more precipitously in the elderly during therapy, so frequent glucose monitoring is essential in this age group. In older patients with HHS, a glucose level of 250 to 300 mg/dL should be maintained until hyperosmolarity and mental status improve.

Pediatric PatientsPediatric patients also have unique

aspects to their experience with DKA and HHS. Cerebral edema is a rare but potentially fatal complication of DKA that primarily occurs in pediatric patients, especially those with newly diagnosed diabetes. The incidence is between 0.7% and 1%, and mortality rates as high as 70% have been reported.21 It is speculated that excessive rehydration, cerebral hypoxia and ischemia, and increased blood-brain barrier permeability contribute to cerebral edema in this age group, but the actual cause is not well understood.

The clinical features of cerebral edema are a deterioration of consciousness and evidence of increased intracranial pressure (ICP) such as vomiting and headache. Neurologic deterioration can be rapid and heralded by seizures, incontinence, pupillary changes, sustained heart rate deceleration, and an abnormal respiratory pattern (Cheyne-Stokes respirations, grunting) culminating in brainstem


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herniation and cardiopulmonary collapse. The progression is so rapid that papilledema could be absent. The timing of cerebral edema is variable, with most cases occurring between 4 and 12 hours after the start of treatment.21

Treatment of cerebral edema is aimed at lowering ICP by administering mannitol at 1 to 2 g/kg over 15 minutes for maximum effect coupled with ICP monitoring and hypoventilation. The role of dexamethasone and diuretics has not been established.

Preventive measures that might decrease the risk of cerebral edema in high-risk patients include avoidance of insulin bolus, gradual fluid replacement over 48 hours if the patient is stable, cautious sodium replacement, blood glucose reduction of 50 to 100 mg/dL/hour, avoidance of unnecessary bicarbonate therapy in pediatric patients, and the addition of dextrose to the intravenous fluid regimen once blood glucose reaches 250 mg/dL.21

An insulin bolus should be avoided in pediatric patients. The rest of the insulin regimen is similar to that for adults.

CRITICAL DECISIONSWhat are the potential complications that the clinician needs to be aware of while managing hyperglycemic crises?

Major complications to be guarded against are hypoglycemia, hypokalemia, hyperchloremia, fluid overload, acute respiratory distress syndrome, thromboembolism, and rhabdomyolysis.

Case Resolutions

n Case OneFluid resuscitation was begun,

and 500 mL of 0.9% normal saline was administered in the first hour (body weight 25 kg). The corrected potassium was calculated as 2 mEq/L, and potassium replacement was initiated.

Repeat vital signs were blood pressure 75/40 and heart rate 115. A 0.45% saline solution was started at a rate of 10 mL/kg/hour. The patient was closely monitored, and the abdominal tenderness resolved.

A subsequent venous blood gas measurement 1 hour later showed a pH of 7.15 and a bicarbonate of 15. The laboratory venous glucose was reported as 380 mg/dL. The repeat corrected potassium was 3.4 mEq/L, and an insulin infusion was started at 2.5 units/hour (0.1 units/kg/hour). Another 30 mEq/L of potassium was added to the fluid regimen.

She was subsequently admitted to the ICU.

n Case TwoThe patient was fluid resuscitated

with 1 L normal saline in the first hour. An insulin bolus of 8

units was given followed by an infusion of 8 units/hour (weight 80 kg). Intravenous antibiotics were administered in the emergency department.

With the history of renal impairment, a central venous pressure line was inserted in the emergency department to guide fluid therapy. Then, 500 mL of 0.45% sodium was infused hourly, with 20 mEq/L of potassium added after satisfactory urine output of 100 mL in the first hour was obtained.

The serum creatinine and BUN were 2.2 mg/dL and 84 mg/dL respectively. The calculated osmolality was 382 mOsm/L.

Repeat electrolyte studies 1 hour later showed a potassium of 4.4, sodium 145, and bedside capillary glucose 560 mg/dL. Insulin infusion was maintained at 8 units/hour,

Pearls and Pitfalls• DKAandHHSmaywellbethefirstpresentationofdiabetesmellitus.

• Lookforoccultabdominalpathologyifapatient’sabdominalpainfailstoresolveafterresolutionofketosisorifthereislocalizedtenderness.

• Theurinedipsticktestusesthenitroprussidemethod,whichdetectsthepresenceofacetoacetatebutnot-hydroxybutyric,sorelianceonthistestresultalonecanleadtoamisseddiagnosisinpatientsforwhomthepredominantketonesare-hydroxybutyricacids.

• ExercisecautionwhilemanagingDKAandHHSintheextremesofage,becausecerebraledemaandfluidoverloadarepotentialtreatment-relatedcomplicationsinchildrenandtheelderly,respectively.

• Hypokalemiaandhypoglycemiacanoccurasaresultoftreatmentandcouldeasilybeoverlookedinabusyemergencydepartment;carefulandfrequentmonitoringandrepeatbiochemistrypanelsarecriticaltoavoidsuchcomplications.

• Acorrectedpotassiumlevelshouldbeusedinsteadofthelaboratorypotassiumlevel,becausethevaluecanbegrosslylowinthepresenceofacidosis.

• Omittingintravenousinsulincompletelywhentheserumglucosereaches250mg/dLisacommonmistakeasketosisandhyperosmolalitytake1to2daystoresolve.Instead,theinsulininfusiondoseshouldbelowered,and5%dextroseIVintroducedtothefluidregimentomaintainglucosebetween150to250mg/dL.

• BicarbonatetherapyisassociatedwithmanyadverseeventsandshouldnotbeusedinDKApatientswithapHabove7.ItsuseinpatientswithapHbelow7remainscontroversial.


10

because the target glucose drop of 75 mg/dL was achieved. Another 20 mEq/L of potassium was given.

The patient was transferred to the ICU.

SummaryDKA and HHS are serious diabetic

emergencies and can be potentially fatal. Timely diagnosis and effective management involving adequate fluid resuscitation, insulin therapy, correction of acid-base and electrolyte abnormalities, and identification of precipitating pathology are critical for a better outcome. The emergency physician should also be aware of the caveats related to treatment, especially cerebral edema, which can be lethal in the pediatric age group.

References1. Kitabchi AE, Umpierrez GE, Murphy MB, et al.

Management of hyperglycemic crises in patients with diabetes. Diabetes Care. 2001;24(1):131-153.

2. Kitabchi AE, Umpierrez GE, Murphy MB, et al. Hyperglycemic crises in adult patients with diabetes: a consensus statement from the American Diabetes Association. Diabetes Care. 2006;29(12):2739-2748.

3. Stentz FB, Umpierrez GE, Cuervo R, et al. Proinflammatory cytokines, markers of cardiovascular risks, oxidative stress, and lipid peroxidation in patients with hyperglycemic crises. Diabetes. 2004;53(8):2079-2086.

4. Gale EA, Dornan TL, Tattersall RB. Severely uncontrolled diabetes in the over-fifties. Diabetologia. 1981;21(1):25-28.

5. Malone ML, Gennis V, Goodwin JS. Characteristics of diabetic ketoacidosis in older versus younger adults. J Am Geriatr Soc. 1992;40(11):1100-1104.

6. Wachtel TJ, Tetu-Mouradjian LM, Goldman DL, et al. Hyperosmolarity and acidosis in diabetes mellitus: a three-year experience in Rhode Island. J Gen Intern Med. 1991;6(6):495-502.

7. Kitabchi AE, Umpierrez GE, Murphy MB, et al. Hyperglycemic crises in diabetes. Diabetes Care. 2004;27 Suppl 1:S94-S102.

8. Matz R. Hypothermia in diabetic acidosis. Hormones. 1972;3(1):36-41.

9. Umpierrez G, Freire AX. Abdominal pain in patients with hyperglycemic crises. J Crit Care. 2002;17(1):63-67.

10. Magee MF, Bhatt BA. Management of decompensated diabetes. Diabetic ketoacidosis and hyperglycemic hyperosmolar syndrome. Crit Care Clin. 2001;17(1):75-106.

11. Slovis CM, Mork VG, Slovis RJ, et al. Diabetic ketoacidosis and infection: leukocyte count and differential as early predictors of serious infection. Am J Emerg Med. 1987;5(1):1-5.

12. Vantyghem MC, Haye S, Balduyck M, et al. Changes in serum amylase, lipase and leukocyte elastase during diabetic ketoacidosis and poorly controlled diabetes. Acta Diabetol. 1999;36(1-2):39-44.

13. Cydulka RK, Pennington J. Diabetes mellitus and disorders of glucose homeostasis. In: Marx JA, ed. Rosen’s Emergency Medicine: Concepts and Clinical Practice. 6th ed. Philadelphia, PA: Mosby Inc; 2006:1751.

14. Kreshak A, Chen EH. Arterial blood gas analysis: are its values needed for the management of diabetic ketoacidosis? Ann Emerg Med. 2005;45(5):550-551.

15. Hale PJ, Nattrass M. A comparison of arterial and non-arterialized capillary blood gases in diabetic ketoacidosis. Diabet Med. 1988;5(1):76-78.

16. Kelly AM. The case for venous rather than arterial blood gases in diabetic ketoacidosis. Emerg Med Australas. 2006;18(1):64-67.

17. Morris LR, Murphy MB, Kitabchi AE. Bicarbonate therapy in severe diabetic ketoacidosis. Ann Intern Med. 1986;105(6):836-840.

18. Fisher JN, Kitabchi AE. A randomized study of phosphate therapy in the treatment of diabetic ketoacidosis. J Clin Endocrinol Metab. 1983;57(1):177-180.

The Drug Box

19. Keller U, Berger W. Prevention of hypophosphatemia by phosphate infusion during treatment of diabetic ketoacidosis and hyperosmolar coma. Diabetes. 1980;29(2):87-95.

20. Trence DL, Hirsch IB. Hyperglycemic crises in diabetes mellitus type 2. Endocrinol Metab Clin North Am. 2001;30(4):817-831.

21. Shastry RM, Bhatia V. Cerebral edema in diabetic ketoacidosis. Indian Pediatr. 2006;43(8):701-708.

Regular Insulin

Mechanism of Action Promotes tissue uptake of potassium, glucose, and phospateInhibits gluconeogenesis, lipolysis, and ketoacid production

Indications Diabetic ketoacidosisDiabetic hyperglycemic hyperosmolar syndromeAlcoholic ketoacidosis

Dosing Loading (optional): 0 .1 units/kgInfusion rate: 0 .1 units/kg/hour

Side Effects HypoglycemiaHypokalemia

Contraindication/Precautions Monitor potassium levels closely; add potassium chloride to intravenous fluid as neededMonitor blood glucose at least hourly while the patient is on an insulin drip

Regular Insulin

By Amy Niertit MD, Summa Health System Emergency Medicine Residency

There are many forms of insulin available today, each with varying indications and kinetics . This article focuses on the administration of regular insulin to severely hyperglycemic patients and patients suffering from diabetic ketoacidosis (DKA) . In the setting of DKA, insulin should be administered intravenously only and not subcutaneously or intramuscularly, because absorption via these routes can be unpredictable . Intravenous loading doses are not recommended in children and are controversial in adults . Insulin should be administered in a patient very early in the treatment of DKA and continued for at least 12 hours or until the anion gap resolves .

Feature Editor: Michael S . Beeson, MD, FACEP


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The LLSA Literature Review“The LLSA Literature Review” summarizes articles from ABEM’s “2010 Lifelong Learning and Self-Assessment Reading List.”

Many of these articles are available online in the ACEP LLSA Resource Center (www.acep.org/llsa) and on the ABEM web site.

Do Opiates Affect the Clinical Evaluation of Patients With Acute Abdominal Pain?Reviewed by Ronak B. Patel, MD, MPH, and J. Stephen Bohan, MD, MS, FACEP; Harvard Affiliated Emergency Medicine Residency; Brigham and Women’s Hospital

Ranji SR, Goldman LE, Simel DL, et al. Do opiates affect the clinical evaluation of patients with acute abdominal pain? JAMA. 2006;296(14):1764-1774.

The most common chief complaint in emergency depart-ments is abdominal pain, and 15% to 30% of these visits are true emergencies requiring surgical intervention. The practice of surgery has argued for withholding analgesics in patients under evaluation for acute abdomen, because of concerns that the analgesia could obscure the examination findings and lead to misdiagnosis and management error. Be-cause of this, patients with abdominal pain can wait several hours before receiving adequate pain relief. This study pro-vides a systematic review of the literature and metaanalysis to determine if opiates affect the clinical evaluation of patients with abdominal pain.

The investigators systematically searched the literature for placebo-controlled trials with some form of randomization that studied the effect of opiates on patients with abdominal pain. There were three primary outcomes: whether opiates affect the history, whether they affect the physical examina-tion, and whether they result in management errors. A total of 12 studies with 15 comparisons overall were reviewed (9 adult trials and 3 pediatric). Only 11 of the 15 comparisons obtained significant analgesia with opiates compared with placebo. None of the studies directly evaluated the effect of opiates on history. Among the studies reporting on changes in the physical examination, there was a nonsignificant trend towards alterations in the examination findings, which be-came significant among the comparisons with adequate analgesia. Despite this alteration, there was no significant difference in management errors in any of the individual comparisons or the metaanalysis in terms of both delayed and unnecessary surgery. In fact, there was a nonsignificant trend towards fewer unnecessary surgeries among patients receiving opiates.

Although this study had some methodological limitations such as the heterogeneity of the included comparisons and

minimal blinding, it adds to the literature supporting opi-ate administration to patients with abdominal pain with the authority that systematic reviews and metaanalysis can of-fer. Most clinicians emphasize that the history provides the greatest information towards diagnoses, but no studies ex-amined opiate effect on history. And, although there may be some alteration in physical examinations findings, there was no significant difference in management error. Additionally, the increased use of imaging and various other diagnostic tools in the evaluation of abdominal pain further supports the use of analgesics, because these objective modalities should remain unchanged by opiates even with changes in the physical examination. This study puts to rest the ques-tion of whether opiates should be given to patients under evaluation for abdominal pain: The answer is yes.

HighlightsAbdominal pain is the most common chief complaint in • emergency departments.

The tradition of withholding opiate analgesia from patients • with abdominal pain is changing, but wide differences in practice still remain.

This systematic review with metaanalysis finds no difference • in management error between patients receiving adequate analgesia and those who did not.

Withholding adequate analgesia in patients presenting with • abdominal pain to today’s emergency departments is not justified by the current evidence.


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Lesson 2

Lee S. Benjamin, MD, FACEP, FAAP, and Katherine A. Lewis, MD

The Vomiting Child

n ObjectivesOn completion of this lesson, you should be able to:

1. Describe the common etiologies of vomiting in pediatric patients based on the patient’s age.

2. Identify and provide initial management for a vomiting child at risk for surgical emergencies.

3. Predict when vomiting is a symptom of systemic disease.

4. Decide when vomiting is a symptom of central nervous system disease.

5. Describe the utility of imaging studies in evaluating a vomiting child.

6. Discuss the utility of oral rehydration therapy, the role of antiemetics, and the indications for intravenous fluid in the treatment of a vomiting child

n From the EM Model1.0 General Signs, Symptoms, and

Presentations

1.2 Abdominal

Vomiting is responsible for more than 2% of all emergency department visits and is among the 10 most common chief complaints for all patients presenting to emergency departments. It is associated with several common conditions, making it a symptom that every emergency physician should be familiar with.1 Most children will have nonforceful regurgitation during their first year of life rather than a forceful expulsion of gastric contents from the oropharynx and nasopharynx. Emergency physicians must be able to identify the etiologies that could place a vomiting child at risk for significant morbidity or mortality.

Because of the wide variety of etiologies and organ systems involved with vomiting, no one management strategy is always successful. Myriad potentially dangerous diagnoses must be considered and not only the vomiting but also the underlying etiology must be treated. Commonly, a complete history and physical examination will identify essentially well children with self-limited disease. These children will not need laboratory or radiographic evaluation; however if significant underlying disease is suspected, diagnostic modalities become essential.

Case Presentations

n Case OneA 5-day-old infant is brought to

the emergency department by her parents, who are concerned because the baby has been vomiting. The

mother describes the vomiting as green and nonbloody. She denies fever and says there has been no diarrhea and no sick contacts. The child was born at full term, with no complications. She has been breastfeeding without difficulty until today.

Physical examination reveals a normal female newborn sleeping comfortably. Vital signs are heart rate 140, respiratory rate 40, and tympanic temperature 36.7°C (98.1°F). Her breath sounds are clear, and heart sounds are normal. Abdominal examination reveals a soft, nontender, nondistended abdomen, without organomegaly or mass. The umbilical stump is clean and dry, with no surrounding erythema. The child has no problems with feeding, yet afterwards vomits bright green material.

n Case TwoA 2-year-old boy is brought to the

emergency department after falling off a table. The fall was witnessed by the mother. He fell off of the side of the table, landing on the back of his head. He cried immediately and proceeded to vomit several times. He is developmentally appropriate and has no significant past medical or surgical history. On evaluation, the child is awake and alert, with vital signs within a normal range for his age. He is sitting quietly with his mother in no distress or obvious discomfort. He has no signs of obvious head injury. His neck is nontender, with normal


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range of motion without discomfort. On neurologic examination he is awake, sitting quietly in his mother’s arms, appropriately consolable. He has no focal neurologic deficit, he has normal reflexes, and he ambulates without difficulty.

The Problem of Pediatric Vomiting

Vomiting can be caused by numerous etiologies related to several organ systems. Common conditions that lead to vomiting in children can involve the gastrointestinal (GI) tract, central nervous system, renal system, endocrine system, respiratory system, and genitourinary system. Further complicating the evaluation, vomiting may also be a manifestation of psychiatric and toxic disease states (Table 1). Regardless, as the clinician seeks the underlying etiology, initial stabilization depends on resuscitating the ill patient while evaluating and treating for the suspected underlying condition.

The goals of the evaluation should be, first, to rule out acute surgical processes, and second, to evaluate for life-threatening medical diseases. A thorough history and physical examination likely will identify the underlying process. However, judicious use of laboratory and radiographic evaluation can be necessary to identify those children at risk for significant disease. This discussion will focus on recognizing atraumatic abdominal processes mandating further management, indicators of intracranial injury, and potentially life-threatening diseases.

History and Physical Examination

CRITICAL DECISIONWhat clinical symptoms and signs indicate a potential surgical etiology of vomiting?

When considering surgical processes, understanding the common etiologies that occur in each age group provides a meaningful context in which to approach the evaluation. In newborns, anatomic anomalies are common; however, as children get older, they develop surgical processes more consistent with adult disease.

NewbornsBilious Emesis. There are

numerous surgical conditions that could present with vomiting as a chief complaint. Bilious vomiting indicates intestinal obstruction until it is proved otherwise. Although patients with obstruction can appear ill—or even in shock—bilious emesis might be the only sign. Clinicians should assume that a neonate with bilious vomiting has an obstruction and should image the abdomen with plain radiography. A nondiagnostic abdominal film should not reassure the physician; plain films are negative in up to 56% of neonatal obstructions.2 If an etiology is not obvious on plain radiographs, the clinician should obtain an upper GI contrast study to rule out malrotation and volvulus, true surgical emergencies that lead to tissue ischemia and necrosis and mandate immediate intervention. Other obstructive conditions that might

present with bilious emesis include intestinal atresias, Hirschsprung disease, meconium ileus, meconium plug, and left microcolon. If an obstructive process is identified, the physician should initiate intravenous fluid resuscitation and emergently consult pediatric surgery.

Fortunately, more than 60% of all newborns presenting with bilious vomiting have nonsurgical, nonemergent processes. If obstruction can be ruled out, if no other etiology is identified, and if the patient is otherwise well appearing and tolerating oral intake, the patient is likely to have a benign course.3

Projectile Vomiting. The symptom of projectile vomiting, nonbilious in nature, should alert the clinician to gastric outlet obstruction. Pyloric stenosis is a newborn disease occurring most commonly at 4 to 6 weeks of life, presenting with progressive failure to tolerate feeds associated with forceful, projectile vomiting. Patients can appear dehydrated or emaciated, yet hungry. Caucasian first-born male babies appear to be at highest risk, yet there are both genetic and environmental factors contributing to the disease. The result is an abnormally thickened pylorus commonly palpated on examination, and referred to as the “olive”.

When pyloric stenosis is clinically suspected, finding the “olive” is diagnostic. The classic electrolyte abnormality of hypokalemic, hypochloremic metabolic alkalosis can be present. Radiographic strategies include ultrasonography and upper GI contrast study. The

Which clinical symptoms and signs indicate a potential • surgical etiology of vomiting? How should clinicians evaluate bloody emesis in pediatric • patients? What symptoms and signs suggest a central nervous • system process as the etiology of vomiting?

When should the clinician consider vomiting as a • symptom of a systemic process? What is the utility of imaging in the evaluation of a • vomiting child? At what point should a dehydrated child receive • intravenous fluid supplementation?

Critical Decisions


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Table 1.Etiology of pediatric vomiting based on agea,b

System Newborn <6 weeks Infant <1 year Child <12 years Adolescent 12 years to adult

Gastro-intestinal

Physiologic regurgitationGastroesophageal refluxGastroenteritisDietary intolerancePyloric stenosisIncarcerated herniaNecrotizing enterocolitisMalrotation/volvulusHirschsprung diseaseDiaphragmatic herniaCongenital atresiasHepatobiliary disease

Gastroesophageal refluxGastroenteritisDietary intoleranceAppendicitisIntussusceptionMalrotation/volvulusHirschsprung diseasePyloric stenosisIncarcerated herniaHepatobiliary diseasePancreatitis

GastroenteritisAppendicitisPeptic ulcer diseaseMalrotation/volvulusIntussusceptionIncarcerated herniaGastroparesisHepatobiliary diseasePancreatitis

GastroenteritisAppendicitisIncarcerated herniaGastroparesisHepatobiliary disease Pancreatitis

Infectious Urinary tract infectionSepsisMeningitis and encephalitis

Urinary tract infectionOtitis media and sinusitisSepsisMeningitis and encephalitis

Urinary tract infectionOtitis media and sinusitisPharyngitisPneumoniaMeningitis and encephalitisSepsis

PyelonephritisPharyngitisSepsisMeningitis and encephalitis

Neurologic HydrocephalusIntracranial hemorrhageFeeding intolerance associated with neuromotor disorders

Minor head trauma HydrocephalusIntracranial hemorrhageIntracranial tumor

Minor head traumaMigraine headacheIntracranial hemorrhageIntracranial tumorIntracranial arteriovenous malformation

Migraine headachePseudotumor cerebriIntracranial tumorIntracranial arteriovenous malformationIntracranial hemorrhage

Metabolic/ Endocrine

Adrenal crisisInborn errors of metabolism

Adrenal crisisInborn errors of metabolismPorphyria

Diabetic ketoacidosisAdrenal crisisPorphyria

Diabetic ketoacidosisHyperthyroidismPorphyria

Other Feeding intolerance due to cardiac/pulmonary disordersObstructive uropathy

Posttussive emesisToxic ingestionForeign body ingestion or bezoarMunchausen syndrome by proxyObstructive uropathyReye syndrome

Posttussive emesisToxic ingestion and withdrawalEpididymitisTesticular torsionOvarian torsionForeign body ingestion or bezoarHeat exhaustionHenoch-Schönlein purpuraGlomerulonephritis Renal tubular acidosis Munchausen syndrome by proxyReye’s syndromeCyclic vomiting

Toxic ingestion and withdrawalDrug abuseAnorexia and bulimiaPregnancyPelvic inflammatory diseaseEpididymitisTesticular torsionTuboovarian abscessOvarian torsionNephrolithiasisHeat exhaustionHenoch-Schönlein purpuraGlomerulonephritisRenal tubular acidosis

aListed from common to rare etiologies in descending order; italics represents potential surgical managementbAlways consider traumatic etiologies, unintentional or intentional


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ultrasonography finding of an elongated pylorus with wall thickness greater than 3 mm indicates a positive study.4 With equivocal cases, real time observation is likely to resolve the question.5 Treatment is surgical, and emergent consultation should be obtained.

Other etiologies of nonbilious emesis in this age group include preampullary duodenal stenosis, gastroesophageal reflux, pylorospasm, and hiatal hernia.4

Abdominal Distension. A newborn with vomiting and abdominal distension should be considered at risk for surgical disease. Necrotizing enterocolitis presents with vomiting, abdominal distension, and ill appearance. Fever and bloody stools may accompany these signs. This is a disease primarily of preterm children, with bacterial translocation into the bowel lumen with potential bowel perforation. Plain radiographs might identify pneumatosis intestinalis (air within the bowel wall), however necrotizing enterocolitis is ultimately a clinical diagnosis. Rapid fluid resuscitation, antibiotics for GI pathogens, and immediate surgical referral are necessary. Incarcerated hernias can present similarly, with a palpable, tender mass commonly found in the inguinal area. The skin overlying the hernia is frequently erythematous, and the testicle can appear dark blue because of venous congestion, which could lead to testicular infarction. Appendicitis, rare in this age group, could also present with vomiting, abdominal distension, and possibly shock, and carries a high mortality rate in neonates.6

InfantsIntermittent Abdominal Pain.

Intussusception is the telescoping of one segment of intestine with its vascular supply into another, potentially leading to intestinal ischemia and necrosis. Children with this disease present with vomiting, commonly in conjunction with severe

intermittent abdominal pain that spontaneously resolves. The child may become sleepy or lethargic after pain resolution, but on awakening, can appear playful and fully recovered. This is most often a disease of infants, but it can occur in the early school age years.

Pathologic lead points usually serve to drag one segment of intestine into the other. The most common lesions include Meckel diverticulum, intestinal polyps, duplication cysts, and lymphomas. Henoch-Schönlein purpura, cystic fibrosis, and celiac disease can also contribute.7

Symptoms predictive of intussusception include vomiting and rectal bleeding; signs include abdominal mass, commonly described as “sausage shaped,” abdominal tenderness, and guaiac-positive stool.8 When tissue ischemia occurs, patients can present with abdominal pain, vomiting, and grossly bloody or “currant jelly” stools (from the appearance of stool mixed with mucus). Ill-appearing patients and those in shock require rapid resuscitation and immediate surgical consultation. For the well-appearing child, both ultrasonography and contrast enemas are useful for diagnosis, the prior being noninvasive, the latter having the advantage of being therapeutic as well as diagnostic. Fluoroscopy-guided hydrostatic reduction of intussusception is the most commonly used initial treatment modality in the well-appearing child; however ultrasonography-guided reduction is becoming more common and spares the patient the radiation exposure of fluoroscopy.9 If hydrostatic reduction fails, or if the rare complication of intestinal perforation occurs, surgical intervention is indicated. Because of the potential need for urgent/emergent surgery, hydrostatic reduction is most safely performed at institutions having surgical backup available.

Tenderness. Appendicitis can present much more vaguely in infants and young children than in older

children and adolescents and, rarely, might present without tenderness. However, the clinician must consider the child with persistent tenderness on abdominal examination, lacking definitive diagnosis, as being at risk for appendicitis. The symptoms of vomiting and diarrhea, as well as signs of fever, tenderness, and abdominal distension can be present. However diagnosis is rarely made before appendiceal rupture and peritonitis. Delay in diagnosis is common, with up to a 94% perforation rate with a 9.3% mortality rate in children under 2 years of age.10 Patients in all age groups, including infants, are also at risk for incarcerated hernias.

Older Children and Adolescents Tenderness. Older children

and adolescents share risks for appendicitis and incarcerated hernias. Appendicitis is most common in the second decade of life, and several symptoms and signs on examination suggest its presence. Pain migrating to the right lower quadrant, fever, vomiting, diarrhea, rebound tenderness, guarding, rectal tenderness when present, and psoas sign when present significantly add to the probability of appendicitis, as does a WBC count of more than 10,000.11

Genitourinary Symptoms and Signs. A girl with pelvic pain and abdominal tenderness could have pelvic inflammatory disease with tuboovarian abscess or ovarian torsion. Pelvic examination is indicated, possibly with imaging studies and gynecologic consultation. Pelvic ultrasonography is useful in identifying female ovarian pathology, however it can be misleading in ruling out ovarian torsion, as up to 54% of torsions have arterial flow on ultrasonography. The most common ultrasound finding for torsion is an enlarged ovary.12 If this diagnosis is suspected, the clinician should obtain emergent gynecologic consultation. In boys, testicular pain, swelling,


16

and tenderness suggest possible torsion. In either sex, flank pain, dysuria, and hematuria can represent nephrolithiasis, in which renal obstruction should be considered. A septic appearing patient with flank tenderness and suspected urinary tract infection could have a perinephric abscess.

CRITICAL DECISIONHow should clinicians evaluate bloody emesis in pediatric patients?

Although most commonly benign, bloody emesis in children can signify life-threatening disease and can occur in all age groups (Table 2). If the bleeding is self-limited in a well-appearing patient with a suspected benign etiology such as swallowed blood from breast feeding or epistaxis, no workup is indicated. Additionally, what caregivers describe as blood may simply be a mimicker, such as ingested products that are red in color. If a patient has symptoms or signs of severe blood loss as evidenced by recurrent hematemesis

or hematochezia/melena, light-headedness, syncope, and signs of shock, the clinician should initiate intravenous fluid resuscitation, nasogastric tube insertion to quantify ongoing loss, and treatment of the underlying condition. Iced saline lavage is no longer recommended as treatment. Cross and type-matched blood should be available if needed. Coagulopathy should also be considered and treated when present. With ongoing blood loss or suspected perforation, the clinician should ensure surgical backup. Imaging modalities to assist the diagnosis include angiography and nuclear imaging for brisk bleeds; endoscopy is the most useful study to identify and treat upper GI bleeding.

The most common cause of severe upper GI bleeding in children is variceal bleeding secondary to portal hypertension. Many patients with acute variceal hemorrhage are previously healthy, and this will be their first presentation of liver disease. However, those with chronic liver

disease will likely have stigmata on examination. During resuscitation, treatment should focus on stabilizing vital signs and decreasing blood loss, using intravenous octreotide to lower variceal pressure. Endoscopy is indicated emergently for failure of medical treatment, allowing banding or sclerotherapy of the bleeding vessel.13

CRITICAL DECISIONWhat symptoms and signs suggest a central nervous system process as the etiology of vomiting?

Vomiting is one of the most common complaints in patients with increased intracranial pressure. Tumors, obstructive hydrocephalus, and intracranial hemorrhage all commonly present with vomiting as a chief complaint. In children with sudden death due to obstructive hydrocephalus, vomiting was the single symptom common to all patients, with six of seven patients having no known neurologic disease.14

Common Uncommon

Neonate Swallowed maternal blood Stress gastritis or ulcer

Milk protein sensitivity Esophagitis

Trauma (nasogastric tubes) Vascular malformation

Hemorrhagic disease of newborn

Congenital coagulation factor deficiency

Coagulopathy associated with infection

Infant Mallory-Weiss tear Stress gastritis or ulcer

Esophagitis Acid peptic disease

Vascular malformation

GI duplication

Gastric/esophageal varices

Bowel obstruction

Child/Adolescent Esophagitis Vasculitis

Esophageal varices Bowel obstruction

Mallory-Weiss tear Crohn disease

Acid-peptic disease Hemobilia

Gastritis, especially H. pylori

Caustic ingestion

Table 2.Etiology of upper GI bleeding by patient age.a From: Chawla S, Seth D, Mahajan P, Kamat D. Upper gastrointestinal bleeding in children. Clin Pediatr (Phila). 2007;46(1):16-21. Reproduced with permission.

aAlways consider traumatic etiologies, unintentional or intentional


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Vomiting in conjunction with a history of hydrocephalus with an indwelling shunt should raise the suspicion of shunt malfunction and recurring hydrocephalus.15 Recurrent vomiting with history of head trauma indicates potential intracranial hemorrhage. Family history of subarachnoid hemorrhage or coagulopathy suggests intracranial hemorrhage as well. Symptoms of somnolence and headache worse in the morning could indicate increased intracranial pressure secondary to a mass.

On examination, signs of a central nervous system process include altered or depressed mental status, seizure, bradycardia and hypertension consistent with pending cerebral herniation, increasing head circumference in an infant, papilledema, sunsetting eyes (loss of upward gaze), stiff neck worrisome for intracranial bleeding or meningitis, and focal neurologic deficits indicating possible mass.

Vomiting in conjunction with headache, fever, stiff neck, or altered mental status suggests meningitis. Yet these symptoms are rarely all present, even in adults who tend to present more classically.16 In a child with fever, vomiting, and headache, lacking definitive diagnosis, the clinician should consider initiating management and evaluation for meningitis. If bacterial meningitis is highly suspected, intravenous antibiotics should be initiated, and the practitioner should perform lumbar puncture and cerebrospinal fluid analysis. If the clinician suspects increased intracranial pressure or if the patient has a focal neurologic deficit, performing a computed tomography (CT) scan of the brain prior to lumbar puncture is prudent.

If head trauma is associated with signs of significant head injury, the clinician should consider CT imaging as well. The otherwise well-appearing child with recurrent emesis after minor head trauma is at increased risk for intracranial injury and should

undergo CT imaging to rule out intracranial hemorrhage.17

CRITICAL DECISIONWhen should the clinician consider vomiting as a symptom of a systemic process?

Extra-gastrointestinal symptoms or signs could indicate systemic disease. A history of medication or drug ingestion or underlying endocrinopathy or nephropathy necessitates evaluation for expected complications. In the previously well child, symptoms of cough, dysuria, headache, rash, and fever could indicate an infectious etiology such as pneumonia, urinary tract infection, meningitis, meningococcemia, or other forms of sepsis. Recurring emesis associated with dehydration, weight loss, and diffuse abdominal pain could represent diabetic ketoacidosis. Neurologic symptoms of lethargy or seizures in neonates or infants should raise concern for inborn errors of metabolism. Hypoglycemia and hyperammonemia are common laboratory associations.18 Amenorrhea points toward pregnancy-related issues.

Physical examination signs such as ill appearance, unexplained abnormalities of vital signs, neck stiffness, pharyngeal exudate, cardiac murmur, pulmonary crackles, persistent abdominal tenderness, rash, and focal neurologic deficit should heighten the clinician’s suspicion of underlying extraintestinal disease. Persistent tachycardia out of proportion to fever, pain, or dehydration could indicate myocarditis, sepsis, or drug ingestion. A gravid uterus raises suspicion of obstetric complications. Rashes consistent with scalded skin syndrome, rickettsia, or meningococcemia should be sought. Fingernail and tooth damage may point toward bulimia nervosa. Poor muscle tone may be indicative of an inborn error of metabolism.

If extra-gastrointestinal findings are present, these symptoms or signs

should guide the evaluation. The clinician should immediately treat suspected dangerous conditions, while ordering appropriate laboratory and radiographic evaluation and obtaining indicated consultations in the emergency department.

DiagnosisMost vomiting children will not

require much more than a careful history and physical examination to clarify the diagnosis. Occasionally simple laboratory tests such as blood glucose, group A streptococcus, urinalysis, and pregnancy testing could be necessary. Chemistry panels containing sodium, potassium, chloride, BUN, and creatinine are often not needed unless the child has an underlying health problem or the vomiting has been prolonged.19

If there is a concern for infection, sepsis, or underlying malignancy, a CBC might be indicated. Concern for neonatal jaundice or liver, gallbladder, or pancreatic disease will lead to more specialized blood testing, but such is rarely indicated.

CRITICAL DECISIONWhat is the utility of imaging in the evaluation of a vomiting child?

The standard imaging test for a suspected diagnosis can vary depending on a particular hospital’s resources, the time of day, surgeon or radiologist preference, and local tertiary care center resources and practices.

Ultimately, the suspected diagnosis should guide radiographic evaluation with a goal of limiting unnecessary radiation exposure to the patient. Suspected surgical processes will commonly require emergent radiographic evaluation. Plain films can identify obvious obstruction, intestinal atresias, and pneumatosis intestinalis, but more advanced studies are often necessary. Ultrasonography is becoming favored for the evaluation of a number of disease states and has the added advantages of being noninvasive and avoiding radiation


18

exposure. Ultrasonography is used to diagnose and evaluate reduction of intussusception, to diagnose pyloric stenosis and appendicitis, and even to screen for malrotation.

Upper GI contrast radiographs are commonly employed to evaluate for malrotation and volvulus and are useful for pyloric stenosis as well, but they expose the patient to radiation. CT of the abdomen carries a high radiation load; however it is useful in diagnosing appendicitis, obstruction not evident on plain radiographs, and other surgical processes.

Indications for ordering a head CT when there is a suspicion of a neurologic cause of vomiting must take into account the entire clinical picture. Clearly, a head CT is indicated in children if there is a concern for increased intracranial pressure due to a ventriculoperitoneal shunt failure or the presence of tumor or other intracranial lesions. Persistent vomiting as a symptom in minor head trauma is a criteria used in several decision rules to determine the need for CT to rule out intracranial injury.17,20

ManagementManagement of the ill-appearing or

unstable vomiting child begins prior to establishing a definitive diagnosis. The teen suicide attempt by overdose or the infant with metabolic disease may require airway management or intubation. Asthma patients with posttussive emesis require attention to their primary respiratory disease, with support of oxygenation and ventilation. Children in adrenal crisis, those with increased intracranial pressure due to trauma, neonates with pyloric stenosis, and the teen with diabetic ketoacidosis will require careful cardiac monitoring, fluids, or pressor support in addition to subspecialty consultation.

CRITICAL DECISIONAt what point should a dehydrated child receive intravenous fluid supplementation?

Many vomiting children are brought to the emergency department due to concern for dehydration. The question the clinician must answer is does this child require rehydration and, if so, how should the child

be rehydrated? In cases of severe dehydration, the clinician must rapidly resuscitate ill or unstable children with isotonic intravenous fluid boluses. Once the patient is resuscitated, the clinician must supply both maintenance fluids as well as additional fluid to compensate for ongoing losses. With mild to moderate dehydration, the American Academy of Pediatrics and the World Health Organization recommend a trial of oral rehydration therapy (ORT). Despite perceptions of parental preferences, many parents can be taught ORT and might use it at home if one of their children becomes dehydrated in the future.21

As a practical matter, ORT can be difficult because of parental compliance, nursing staff availability, or intractable vomiting. In these situations, insertion of a nasogastric tube for rehydration might still be an option.19 Antiemetics could be useful as well. Antiemetics used in the adult population such as promethazine and prochlorperazine are dangerous in young children and should not be used. Recent research has focused on ondansetron. Studies have shown that both oral and intravenous ondansetron are beneficial in reducing vomiting during rehydration; however they may not affect admission rates and rates of return to the emergency department after discharge.22

DispositionWhen the etiology is clear in a

well-appearing child who is tolerating oral fluids, clinicians may consider discharge home with close outpatient followup. For children who require ORT, the decision to send the child home will depend in part on the ability of the parents to continue oral rehydration and their comfort with how their child responds to treatment. Children with a benign etiology for vomiting who require intravenous hydration may be sent home when they can hydrate orally. When possible, contact the child’s pediatrician prior to discharge and

Pearls and Pitfalls• Biliousemesisinanewborn

indicatesintestinalobstruction,requiringsurgicalintervention,untilitisprovedotherwise.

• Unexplainedabnormalitiesinvitalsignsandthepresenceofextra-gastrointestinalfindingsmayindicateunderlyingsystemicdisease.

• Intracranialprocessescanpresentwithvomitingastheonlysymptom;howeverdepressedmentalstatusandotherneurologicfindingscommonlyaccompanycentralnervoussystemdisease.

• Useofultrasonographylimitsradiationexposuretochildrenwhorequireimagingtoevaluateforcommonsurgicaldiseases.

• MostchildrenwithvomitinganddehydrationfromgastroenteritiscanberehydratedwithORT.OndansetroniseffectiveindecreasingvomitingduringORT;howeveritmightnotaffectratesofadmissionorreturntotheemergencydepartment.

• Promethazineiscontraindicatedinchildrenyoungerthan2yearsoldbecauseofthepossibilityoffatalrespiratorydepression;itshouldbeusedwithcautioninolderchildren.Prochlorperazineisalsonotrecommendedinchildrenyoungerthan2years.

• Whenasurgicalemergencyissuspected,theemergencyphysicianshouldensuretimelypediatricsurgeryevaluationorarrangetransfertoafacilitywithpediatricsurgerycapabilitywithoutdelay.


19

arrange close followup. This should reduce the likelihood of return to the emergency department and will ensure that chronic problems receive appropriate long-term care. If the clinician suspects pregnancy, drug use, psychiatric problems, or child abuse, then social work, psychiatry, or protective services can be useful in providing additional resources to ensure the health of the patient. When a surgical etiology or significant medical disease is suspected, immediate subspecialty consultation or transfer to a tertiary care facility is indicated.

Case Resolutions

n Case OneAssuming intestinal obstruction,

the clinician obtained an upper GI contrast study that revealed malrotation. The physician maintained the child NPO, provided intravenous fluid resuscitation, and consulted pediatric surgery. The child was taken immediately to the operating room, where surgeons found ischemic yet viable intestine. They performed a Ladd procedure to correct the malrotation. The infant did well and was discharged home after an 8-day hospital stay.

n Case TwoA CT scan of the brain was

performed, revealing no intracranial injury and no skull fracture. The patient was treated symptomatically and observed in the emergency department observation unit because of his continued vomiting. His neurologic examination results did not change overnight. The following morning the child was doing well, eating without difficulty, and was discharged home with a diagnosis of concussion. He was asymptomatic with normal examination results at the time of discharge.

Summary Vomiting is a common chief

complaint in children, and it is usually due to benign processes. The

goal of the clinician is to identify those children who have significant underlying disease. The clinician must rapidly identify surgical processes and initiate stabilization and emergent surgical referral. Unexplained abnormalities in vital signs and extra-gastrointestinal symptoms could point toward underlying systemic disease or central nervous system disease. Blood in vomitus is commonly benign, however continued bleeding or unstable vital signs mandate thorough investigation. Once determining that the vomiting is of benign etiology, the clinician should focus on oral rehydration therapy in the mildly to moderately dehydrated patient, and ensure close outpatient followup when discharging the patient.

References Nawar EW, Niska RW, Xu J. National Hospital 1. Ambulatory Medical Care Survey: 2005. Emergency Department Summary. Adv Data. 2007;386:1-32.

Lilien LD, Srinivasan G, Pyati SP, et al. Green vomiting 2. in the first 72 hours in normal infants. Am J Dis Child. 1986;140(7):662-664. (Prospective followup of neonates with bilious vomiting.)

Godbole P, Stringer MD. Bilious vomiting in the 3. newborn: how often is it pathologic? J Pediatr Surg. 2002;37(6):909-911. (Prospective evaluation of consecutive patients presenting with bilious vomiting.)

Hernanz-Schulman M. Infantile hypertrophic pyloric 4. stenosis. Radiology. 2003;227:319–331. (Excellent review article on the imaging of pyloric stenosis.)

Cohen HL, Zinn HL, Haller JO, et al. Ultrasonography 5. of pylorospasm: findings may simulate hypertrophic pyloric stenosis. J Ultrasound Med. 1998;17:705-711. (Discusses limitations of ultrasonography in diagnosing pyloric stenosis and the value of real-time imaging.)

Karaman A, Cavusoglu YH, Karaman I, et al. Seven 6. cases of neonatal appendicitis with a review of the English language literature of the last century. Pediatr Surg Int. 2003;19(11):707-709. (Discusses the difficulty in diagnosing neonatal appendicitis, perforation rates, and decrease in mortality rates over the course of the century.)

Navarro O, Daneman A. Intussusception. Part 7. 3: diagnosis and management of those with an identifiable or predisposing cause and those that reduce spontaneously. Pediatr Radiol. 2004;34(4):305-312. (Review article on intussusception secondary to pathologic lead points.)

Klein EJ, Kapoor D, Shugerman RP. The diagnosis 8. of intussusception. Clin Pediatr. 2004;43:343-347. (Retrospective study identifying history and physical examination findings predictive of intussusception.)

Khanna G, Applegate K. Ultrasound guided 9. intussusception reduction: are we there yet? Abdom Imaging. 2008;33(1):38-40. (Review article.)

Grosfeld JL, Weinberger M, Clatworthy HW Jr. Acute 10. appendicitis in the first two years of life. J Pediatr Surg. 1973;8(2):285-293. (Discusses the difficulty of diagnosing appendicitis in children younger than 2 years and the high perforation rates at diagnosis.)

Bundy DG, Byerley JS, Liles EA, et al. Does this child 11. have appendicitis? JAMA. 2007;298:438-451. (Review article discussing the utility of symptoms, signs, and laboratory results in diagnosing appendicitis.)

Shadinger LL, Andreotti RF, Kurian RL. Preoperative 12. sonographic and clinical characteristics as predictors of ovarian torsion. J Ultrasound Med. 2008;27:7-13. (Retrospective review of 39 patients with proven ovarian torsion. Be wary of ultrasonography.)

Chawla S, Seth D, Mahajan P, Kamat D. Upper 13. gastrointestinal bleeding in children. Clin Pediatr. 2007;46(1):16-21. (Review article.)

Shemie S, Jay V, Rutka J, Armstrong D. Acute 14. obstructive hydrocephalus and sudden death in children. Ann Emerg Med. 1997;29(4):524-528. (Review of seven cases of unexpected sudden death due to obstructive hydrocephalus, highlighting lack of previous diagnosis and seemingly benign initial symptoms.)

Kirkpatrick M, Engleman H, Minns RA. Symptoms 15. and signs of progressive hydrocephalus. Arch Dis Child.1989;64(1):124-128.

van de Beek D, de Gans J, Spanjaard L, et al. Clinical 16. features and prognostic factors in adults with bacterial meningitis. New Engl J Med. 2004;351(18):1849-1859. (Prospective evaluation of meningitis in adults revealing lack of the common triad of fever, neck stiffness, and altered mental status, but almost all had at least two of the four symptoms of headache, fever, neck stiffness, and altered mental status.)

Dunning J, Daly JP, Lomas JP, et al. Derivation of the 17. children’s head injury algorithm for the prediction of important clinical events decision rule for head injury in children. Arch Dis Child. 2006;91(11):885-891. (Prospective study of more than 22,000 children with minor head trauma, developing a highly sensitive decision rule.)

Calvo M, Artuch R, Macià E, et al. Diagnostic approach 18. to inborn errors of metabolism in an emergency unit. Pediatr Emerg Care. 2000;16(6):405-408. (Neurologic and GI findings were the most common noted.)

Nager AL, Wang VJ. Comparison of nasogastric and 19. intravenous methods of rehydration in pediatric patients with acute dehydration. Pediatrics. 2002;109(4):566-572. (Discussion of nasogastric rehydration and the utility of various laboratory tests to assess dehydration and rehydration.)

Oman JA, Cooper RJ, Holmes JF, et al. Performance 20. of a decision rule to predict need for computed tomography among children with blunt head trauma. Pediatrics. 2006;117(2):e238-e246. (Eight-variable decision rule with persistent vomiting.)

Spandorfer PR, Alessandrini EA, Joffe MD, et al. 21. Oral versus intravenous rehydration of moderately dehydrated children: a randomized, controlled trial. Pediatrics. 2005;115(2):295-301. (Description of an oral rehydration protocol, success rates, and parental perceptions.)

Freedman SB, Adler M, Seshadri R, Powell EC. 22. Oral ondansetron for gastroenteritis in a pediatric emergency department. New Engl J Med. 2006;354(16):1698-1705. (Randomized, prospective study of the utility of ondansetron in treating pediatric gastroenteritis.)


20

The Critical Image

This case illustrates several important points:

When intussusception is suspected, rapid diagnostic imaging is essential, as bowel ischemia, perforation, peritonitis, •shock, and even death can result from delay .

Plain films are usually nondiagnostic, although an appearance of bowel obstruction might be seen . More definitive •imaging should be performed as soon as possible .

Ultrasonography has become a mainstay of diagnosis, as it is rapid, noninvasive, does not result in radiation exposure, •and is highly sensitive and specific for the diagnosis of intussusception . The typical appearance is concentric rings with alternating hyperechoic and hypoechoic layers1 (A) .

Air-contrast enema (B) can be both diagnostic and therapeutic . The intussusceptum can be seen as a soft tissue •density within the bowel, silhouetted by air and often preventing proximal reflux of air . The intussusceptum can often be reduced with increased insufflation of air . Failed reduction occurs in 15% to 25% of cases, and a low risk of perforation exists, so surgical consultation simultaneous with enema is routine in many hospitals .2

In this patient, the air-contrast enema pushed the intussusceptum down to the level of the cecum, but air did not reflux into the small bowel, and the intussusceptum remained visible in the cecum . The patient underwent operative reduction of an ileocolic intussusception .1 . Shanbhogue RL, Hussain SM, Meradji M, et al . Ultrasonography is accurate enough for the diagnosis of intussusception. J Pediatr Surg. 1994;29:324-

327; discussion 327-328 .

2 . Meyer JS, Dangman BC, Buonomo C, Berlin JA . Air and liquid contrast agents in the management of intussusception: a controlled, randomized trial . Radiology. 1993;188:507-511 .

Feature Editor: Joshua S . Broder, MD, FACEP

Images courtesy of Emergency Medicine Picture Archiving & Communication System (www .empacs .org) .

A 3-month-old infant presenting with bilious vomiting and intermittent lethargy. Immediate diagnostic imaging was obtained because of concern for a life-threatening process.

Ultrasonography shows ileocolic intussusception

with typical alternating hypo- and hyperechoic

layers

Transverse colon

Intussusception seen as soft tissue silhouette in proximal transverse

colon near hepatic flexure

A B


21

Qualified, paid subscribers to Critical Decisions in Emergency Medicine may receive CME certificates for up to 5 ACEP Category I credits, 5 AMA PRA Category I Credits™, and 5 AOA Category 2-B credits for answering the following questions . To receive your certificate, go to www .acep .org/criticaldecisionstesting and submit your answers online . You will immediately receive your score and printable CME certificate . You may submit the answers to these questions at any time within 3 years of the publication date . You will be given appropriate credit for all tests you complete and submit within this time . Answers to this month’s questions will be published in next month’s issue .

CME Questions

1 . Laboratory findings of glucose of 445 mg/dL, pH 7 .15, and bicarbonate of 14 mEq/L in a 20-year-old man suggest which of the following? A. HHSB. mild DKAC. mixed DKA and HHSD. moderate DKAE. severe DKA

2 . Which of the following medications can mask the symptoms of hypoglycemia in a diabetic patient? A. -blockersB. NSAIDsC. oral contraceptivesD. phenytoinE. thiazides

3 . The most common precipitator of DKA is: A. acute abdomenB. acute myocardial infarctionC. cerebrovascular accidentD. drug-induced reactionE. noncompliance with insulin regimen

4 . Regarding abdominal pain in DKA, which of the following is correct?A. abdominal pain is universally present in DKAB. abdominal pain in DKA correlates with severity of

hyperglycemia or dehydrationC. rapid administration of normal saline is the most common

etiology of abdominal pain in DKAD. investigation of the etiology of abdominal pain in DKA is

indicated in mild DKA or if the pain persists after resolution of acidosis

E. a strong association is observed between severity of metabolic acidosis and abdominal pain

5 . Which of the following is correct regarding laboratory investigations in DKA/HHS? A. elevation of pancreatic enzymes indicates acute pancreatitis in

DKAB. hyperglycemia but not chylomicrons contribute to

pseudohyponatremiaC. leucocytosis is not commonly encountered in DKAD. a patient with a laboratory potassium of 5 mEq/L and a pH of

6.9 has a corrected potassium of approximately 2 mEq/LE. venous pH correlates poorly with arterial pH and therefore

should not be used as a substitute in guiding therapy

6 . A 30-year-old man presents with breathlessness and restlessness associated with vomiting . Vital signs are blood pressure 84/30, pulse rate 140, respiratory rate 42, and oxygen saturation 98% on nonrebreathing mask . The laboratory findings were pH 7 .04, glucose 400 mg/dL, serum sodium 150 mEq/dL, potassium 2 .9 mEq/dL, urea 20 mg/dL . Which of the following management choices is correct?A. 50 mL of 8.4% sodium bicarbonate is indicatedB. colloids 1 L is the initial fluid of choice as the patient is

hypotensiveC. fluid bolus with 0.45% NaCl as the serum sodium is highD. replace potassium urgently as the actual serum potassium is

significantly lowE. start insulin therapy immediately

7 . A 75-year-old bedridden man was brought to emergency department by family members for drowsiness . Left-sided hemiplegia was found on clinical examination . Vital signs are blood pressure 160/100, pulse rate 130, respiratory rate 30, temperature 34 .3°C (93 .74°F), and oxygen saturation 85% on room air . A bedside glucometer reading was high . Urine ketone was negative . The serum sodium was 145 mEq/dL, and the potassium 4 .5 mEq/dL . Venous glucose was 800 mg/dL . ABG on nonrebreathing mask showed pH 7 .25, Po2 88, Pco2 42, HCO3 15 mEq/dL . Which of the following is the best plan of action?A. infection is unlikely as the patient is afebrile, so further testing

is not neededB. intubate immediately to protect the airway, and do chest

radiograph and brain CTC. begin potassium infusion until serum potassium is above 5

mEq/dLD. administer sodium bicarbonate until the serum pH is greater

than 7.35E. infuse up to 100 mL of intravenous normal saline in the first

hour

8 . Laboratory finding of pH 6 .9, bicarbonate 8 mEq/L, and venous glucose of 380 mg/dL in a 2-year-old child with severe gastroenteritis and a body weight of 10 kg prompts:A. aggressive intravenous infusion: 200 mL 0.45% saline in the

initial hourB. fluid bolus of 200 mL normal salineC. insulin bolus of 1 to 2 unitsD. insulin infusion of 5 units/hourE. rapid infusion of 100 mL 8.4% NaHCO3 over 30 minutes for

correction of acidosis


22

9 . With regard to insulin therapy in DKA, which of the following statements is correct? A. add intravenous dextrose 5% when serum glucose reaches 250

mg/dL and drop insulin infusion dose to 0.05 units/kg/hourB. insulin bolus of 0.1 units/kg is indicated in childrenC. intravenous insulin can be stopped when subcutaneous insulin

is introducedD. omit intravenous insulin as serum glucose reaches 250 mg/dL

during treatment to avoid hypoglycemiaE. rarely, hypoglycemia occurs during the treatment of DKA or

HHS

10 . Which complication of DKA and HHS is associated with the highest mortality rate?A. cerebral edemaB. hypochloremic non-anion-gap acidosisC. hypokalemiaD. rhabdomyolysisE. abdominal pain

11 . A 7-day-old child presents with a complaint of vomiting . The mother provides a cloth with a sample of bright green emesis on it . Which of the following imaging studies is considered the “gold-standard” in the evaluation of this child?A. air-contrast enema of the rectumB. noncontrast CT study of the abdomenC. plain radiograph of the abdomenD. ultrasonography of the gallbladderE. upper GI contrast study of the abdomen

12 . A 13-day-old infant is diagnosed with malrotation . He is in shock and has abdominal rebound tenderness . Which of the following is the most appropriate management of this patient?A. antibiotics and admission to general pediatricsB. intravenous fluid resuscitation and admission to general

pediatricsC. intravenous fluid resuscitation and referral for immediate

operative interventionD. nasogastric tube decompression and admission to general

pediatricsE. rectal tube decompression and admission to general pediatrics

13 . A 14-year-old boy presents for transient confusion and vomiting after a head-to-head collision during football practice . He is now awake and alert but nauseated . He has no findings of significant head injury on examination, and he has a normal neurologic examination . Which of the following statements regarding vomiting in minor head injury is most accurate?A. any vomiting is predictive of intracranial injuryB. family history has no influence on vomiting after minor head

traumaC. persistent vomiting is a symptom of intracranial injuryD. vomiting is common in concussion and does not indicate

intracranial injuryE. vomiting is not an independent predictor of intracranial injury

14 . A 4-year-old child complains of vomiting and fever . He has no diarrhea; he is not in day care and has no known sick contacts . On examination, vital signs are temperature 39 .8°C (103 .6°F), heart rate 184, respiratory rate 34, blood pressure 70/48, and pulse oximetry 98% on room air . His physical examination is notable for ill appearance, yet he is awake and alert . He has clear lungs, a rapid rhythm, a soft, nontender abdomen, and capillary refill of 3 seconds . Which of the following is the most appropriate initial therapy for this patient?A. airway management B. laboratory evaluationC. intravenous antibiotics D. intravenous fluid resuscitationE. supplemental oxygen

15 . An 8-month-old girl presents with a chief complaint of vomiting and abdominal pain . The patient is previously healthy, but over the past 12 hours has developed intermittent abdominal pain, drawing her knees toward her chest, crying in pain, and vomiting, that spontaneously resolves . She has had no diarrhea . On examination she is well appearing, in no distress, afebrile, and with normal vital signs for her age . She has a soft, nontender abdomen, with no hepatosplenomegaly or mass . In the emergency department she has an episode of sudden crying, appearing to be in significant distress, bringing her legs to her chest . Which of the following is most appropriate in the management of this patient?A. chest radiograph B. computed tomography of the chestC. esophagogastroduodenoscopyD. magnetic resonance imaging of the brainE. ultrasonography of the abdomen

16 . A 13-year-old girl presents complaining of abdominal pain and nausea . According to her mother, the patient has not been taking her insulin . On examination the patient is ill appearing; vital signs are blood pressure 80/40, heart rate 140, respiratory rate 32, and temperature 37 .7°C (99 .9°F) . Her abdomen is tender diffusely . Her bedside glucose test measures “high” . Which of the following is the most appropriate initial intervention?A. intravenous antibioticsB. intravenous antiemetics C. intravenous fluidsD. intravenous insulin E. oral antiemetics

17 . A 6-week-old infant is brought to the emergency department for worsening vomiting . The parents state that he has always been a “spitty” baby but that over the past 24 hours he has not been able to tolerate anything by mouth . His emesis is nonbloody, nonbilious, and “violent”—shooting from his mouth and soaking the parents’ clothing and the floor . On examination the child is vigorous, appears hungry, and is afebrile, with normal vital signs for age . Which of the following physical examination findings is most likely present in this patient?A. abdominal distensionB. Murphy signC. olive-shaped mass in the upper abdomenD. psoas signE. sausage-link appearance of abdomen


23

18 . A 15-year-old girl presents complaining of intermittent vomiting for the past week . She has been nauseated but denies diarrhea, fever, dysuria, vaginal bleeding, vaginal discharge, ill contacts, and travel . She cannot recall her last menstrual cycle . She has no history of medical problems . On examination, the patient is well appearing, vital signs are normal, and she has no abdominal findings or back tenderness . Which of the following laboratory studies is most likely to be helpful in the evaluation of this patient at this point?A. absolute blood countB. electrolytes C. pregnancy testD. urine cultureE. vaginal specimens

19 . An 18-month-old child presents with suspected gastroenteritis . When considering use of antiemetics, which of the following is the most appropriate agent for this patient?A. ondansetronB. prochlorperazineC. promethazineD. scopolamineE. trimethobenzamide

20 . A 6-year-old girl presents complaining of 2 days of vomiting and abdominal pain . She is not eating well but is taking liquids without difficulty . On examination she is awake and alert, appears to feel poorly, is febrile to 38 .9°C (102°F), and has an erythematous posterior pharynx with exudate . The abdomen is soft, with minimal tenderness diffusely and no peritoneal signs . She has no signs of dehydration on examination . Which of the following best explains the etiology of emesis in this patient?A. extra-gastrointestinal nonsurgical processB. extra-gastrointestinal surgical process C. GI nonsurgical processD. GI surgical processE. intracranial nonsurgical process

Answer key for August 2009, Volume 23, Number 12

The American College of Emergency Physicians makes every effort to ensure that contributors to College-sponsored publications are knowledgeable authorities in their fields. Readers are nevertheless advised that the statements and opinions expressed in this series are provided as guidelines and should not be construed as College policy unless specifically cited as such. The College disclaims any liability or responsibility for the consequences of any actions taken in reliance on those statements or opinions. The materials contained herein are not intended to establish policy, procedure, or a standard of care.

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The Critical ECG

September 2009 • Volume 24 • Number 1Critical Decisions in Emergency Medicine is the official CME publication of the American College of Emergency Physicians. Additional volumes are available to keep emergency medicine professionals up-to-date on relevant clinical issues.

Editor-in-ChiefLouis G. Graff IV, MD, FACEP

Professor of Traumatology and Emergency Medicine, Professor of Clinical Medicine, University of

Connecticut School of Medicine; Farmington, Connecticut

Section EditorJ. Stephen Bohan, MS, MD, FACEP

Executive Vice Chairman and Clinical Director, Department of Emergency Medicine, Brigham &

Women’s Hospital; Instructor, Harvard Medical School,Boston, Massachusetts

Feature EditorsMichael S. Beeson, MD, MBA, FACEP

Program Director, Department of Emergency Medi-cine, Summa Health System, Akron, Ohio; Professor,

Clinical Emergency Medicine, Northeastern Ohio Universities College of Medicine, Rootstown, Ohio

Joshua S. Broder, MD, FACEP Assistant Clinical Professor of Surgery, Associate

Residency Program Director, Division of Emergency Medicine, Duke University Medical Center, Durham,

North Carolina

Amal Mattu, MD, FACEPProgram Director, Emergency Medicine

Residency Training Program,Co-Director, Emergency Medicine/Internal Medicine Combined Residency Training Program, University of Maryland School of Medicine, Baltimore, Maryland

Associate EditorsDaniel A. Handel, MD, MPH

Director of Clinical Operations, Department of Emergency Medicine, Oregon Health & Science University, Portland,

Oregon

Frank LoVecchio, DO, MPH, FACEPResearch Director, Maricopa Medical Center Emergency

Medicine Program; Medical Director, Banner Poison Control Center, Phoenix, Arizona; Professor, Midwestern

University/Arizona College of Osteopathic Medicine, Glendale, Arizona.

Sharon E. Mace, MD, FACEPAssociate Professor, Department of Emergency

Medicine, Ohio State University School of Medicine; Faculty, MetroHealth Medical Center/Cleveland Clinic Foundation Emergency Medicine Residency Program; Director, Pediatric Education/Quality Improvement and Observation Unit, Cleveland Clinic Foundation,

Cleveland, Ohio

Robert A. Rosen, MD, FACEPMedical Director, Culpeper Regional Hospital,

Culpeper, Virginia

George Sternbach, MD, FACEPClinical Professor of Surgery

(Emergency Medicine), Stanford University Medical Center, Stanford, California

Editorial StaffMary Anne Mitchell, ELS

Managing Editor

Mike GoodwinCreative Services Manager

Jessica HamiltonEditorial Assistant

Lilly E. FriendCME and Subscriptions Coordinator

Marta FosterDirector and Senior Editor

Educational and Professional Publications

Critical Decisions in Emergency Medicine is a trademark owned and published monthly by the American College of Emergency Physicians, PO Box 619911, Dallas TX 75261-9911. Send address changes to Critical Decisions in Emergency Medicine, PO Box 619911, Dallas TX 75261-9911, or to [email protected].

Copyright 2009 © by the American College of Emergency Physicians. All rights reserved. No part of this publication may be reproduced, stored, or transmitted in any form or by any means, electronic or mechanical, including storage and retrieval systems, without permission in writing from the Publisher. Printed in the USA.

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Sinus tachycardia, rate 105, acute anteroseptal MI, left posterior fascicular block (LPFB). ST-segment elevation in leads V1-V4 indicates acute MI; reciprocal ST-segment depression is present in the inferior leads . ST-segment elevation is also noted in lead aVR, a finding that is highly specific for proximal obstruction of the left anterior descending or left main coronary artery . When the amplitude of ST-segment elevation in lead aVR is equal to or greater than 1 .5 mm, the prognosis is poor, with mortality rates as high as 75% .a LPFB, an uncommon finding, is diagnosed based on the presence of a rightward axis, qR complexes in lead III, and rS complexes in leads I and aVL . The differential diagnosis of rightward QRS axis includes LPFB, lateral myocardial infarction, right ventricular hypertrophy, acute (eg, pulmonary embolism) and chronic (eg, emphysema) lung disease, ventricular ectopy, hyperkalemia, overdoses of sodium channel blocking drugs (eg, cyclic antidepressants) . Normal young or slender adults with a horizontally positioned heart can also demonstrate a rightward QRS axis on the ECG .a Yamaji H, Iwasaki K, Kusachi S, et al . Prediction of acute left main coronary artery obstruction by 12-lead electrocardiography . J Am Coll Cardiol. 2001;38:1348-1354 .

Feature Editor: Amal Mattu, MD, FACEP

From: Mattu A, Brady W . ECGs for the Emergency Physician. London: BMJ Publishing; 2003:101,140 . Available at www .acep .org/bookstore . Reprinted with permission .

A 44-year-old man with left chest and arm pain.

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