Hyperthyroidism is 10 times more common in women. Insufficiency of TH is referred to as hypothyroidism,

 

Hyperthyroidism is 10 times more common in women.

Insufficiency of TH is referred to as hypothyroidism,

and 95% of the time it is caused by dysfunction of the

thyroid gland. One of the more common causes of hypothyroidism is Hashimoto thyroiditis, an autoimmune

condition in which the body produces antibodies to the

TSH receptor, which block signaling, and does not allow

production of TH. Other causes include iodine deficiency,

infiltrative diseases affecting the thyroid gland, or administration of drugs ( eg, arniodarone). At its extreme, hypothyroidism can manifest as myxedema coma, a severe and

288

THYROID EMERGENCIES

life-threatening state that occurs more frequently in the

elderly.

CLINICAL PRESENTATION

� History

Depending on the degree of abnormality, patients will

present with varied severity of symptoms. Patients with

earlier stages of thyrotoxicosis will report excessive sweating, weight loss, palpitations, anxiety, and heat intolerance.

Patients in thyroid storm will present with symptoms of

thyrotoxicosis in addition to fever, tachycardia, altered

mental status, and often congestive heart failure. In elderly

patients, there is a rare form of thyrotoxicosis referred to as

apathetic hyperthyroidism, presenting with lethargy,

altered mental status, blepharoptosis (drooping of the

upper eye lid), weight loss, and atrial fibrillation leading to

congestive heart failure.

On the opposite side of the spectrum, patients with hypothyroidism complain of fatigue, depression, weight gain, cold

intolerance, and dry skin. In its severe state, myxedema coma,

patients present with altered mental status, bradycardia,

hypothermia, hypoventilation, and hypotension.

Both thyroid storm and myxedema coma usually occur

in patients with previously diagnosed thyroid disorders

and are usually precipitated by other factors, such as

infection, trauma, diabetic ketoacidosis, stroke, surgery, or

medication noncompliance.

� Physical Examination

Clinical findings in both hyper- and hypothyroidism are

summarized in Table 68-1. Not all the signs and symptoms

will be present in every patient. Frequent findings in

patients with hyperthyroidism owing to Graves disease

include goiter, exopthalmos, palmar erythema, and tachycardia (Figure 68-1). In thyroid storm, in addition to those

findings, patients will have altered mental status, fever,

hypertension, and frequently atrial fibrillation.

Hypothyroid patients will present with fatigue, periorbital

edema, hair loss, and dry skin. Myxedema coma patients

will have altered mental status, hypothermia, hypotension,

and myxedema (non-pitting peripherial edema owing to

the accumulation of mucopolysaccharides in the skin).

DIAGNOSTIC STUDIES

� Laboratory

It is important to note that both thyroid storm and myxedema coma are clinical diagnoses and are not defined by

absolute levels of hormones. The main test used for

assessment of thyroid function is ISH level, and its use as

a single test is appropriate for an initial evaluation of thyroid function. In patients with an intact hypothalamicpituitary-thyroid axis, small changes in the level of TH

will lead to significant changes in ISH levels. In a majority

of cases, normal ISH effectively excludes dysfunction of

Table 68-1. Comparison of clinical presentation

of patients with hyper- and hypothyroidism.

System Hyperthyroid Hypothyroid

Vital signs Tachycardia Bradycardia

Hypertension Hypotension

Fever Hypothermia

General Weight loss Weight gain

Hyperkinesis Fatigue/lethargy

Anxiety Depressed

HEENT Goiter Periorbital edema

Exophthalmos Loss of outer third of

Lid lag* the eyebrows

Hoarse voice

Hair loss

Cardiovascular Arrhythmias (atrial Bradycardia

fibril lation)

Widened pulse pressure

Lungs Dyspnea ± pleural effusion

Abdomen Diarrhea Constipation

Skin Warm Cool

Moist Dry

Palmar erythema Rough skin

Nonpitting edema

Neuro Altered mental status Altered mental status

Hyperreflexia Memory impairment

Delayed deep tendon

reflexes**

Note: The degree of symptoms depends on severity of disease.

mias or severe hypokalemia are present. The rate of infu ­ sion should be no more than 20 mEq/hr, especially when the infusion is to run through a peripheral IV line. Pain

 

mias or severe hypokalemia are present. The rate of infu ­

sion should be no more than 20 mEq/hr, especially when

the infusion is to run through a peripheral IV line. Pain

and burning with peripheral IV potassium replacement

can be treated by slowing down the infusion rate. Avoid IV

potassium in patients in renal failure. Physicians should

treat concomitant hypomagnesemia, as potassium repletion is dependent of magnesium.

DISPOSITION

� Admission

Because of the potential for life-threatening arrhythmias, all

patients with moderate to severe hyperkalemia (K + level

>6.0 mEq/L) or severe hypokalemia (K+ level <2.5 mEq/L)

should be admitted to a hospital bed with a cardiac monitor.

� Discharge

Patients with mild to moderate hypokalemia (K+ 2.5-

3.4 mEq/L) and no clinical symptoms may be discharged

with appropriate oral repletion therapy. Mildly hyperkalemic (K+ level <6.0 mEq/L) who are asymptomatic, have

no ECG changes consistent with hyperkalemia, and have

an identifiable and correctable cause of their hyperkalemia

can be considered for discharge with early follow-up for a

repeat electrolyte panel.

SUGGESTED READING

Gennari FJ. Hypokalemia. N Engl ! Med. 1998;339:451-458.

Kelen GD, Hsu E. Fluids and electrolytes. ln: Tintinalli JE,

Stapczynski JS, Ma OJ, Cline DM, Cydulka RK, Meckler GD.

Tintinalli's Emergency Medicine: A Comprehensive Study Guide.

7th Ed. New York, NY: McGraw-Hill, 20 1 1, pp. 1 1 7-1 29.

Mahoney BA, Smith WAD, Lo DS, Tsoi K, Tonelli M, Clase CM.

Emergency interventions for hyperkalaemia Cochrane Database

Syst Rev. 2005;CD003235:1-28.

Thyroid Emergencies

Monika Pitzele, MD

Key Points

• In a critica lly ill patient with a goiter or history of

hyperthyroidism, consider and treat thyroid storm early.

• Thyroid storm and myxedema coma are clinical

diagnoses that do not depend on the absol ute levels

of thyroid-stimulating hormone and free thyroxine.

INTRODUCTION

Thyroid hormone (TH) is synthesized within the follicular

cells of the thyroid gland. Production begins with the uptake

of iodine into the follicular lumen. Thyroglobulin, produced within the follicular cell, is bound to iodine and then

coupled to produce the thyroid hormones, thyroxine (T 4

)

and triiodothyrinine (T3

). Release of thyroid hormone is

stimulated by one of the hormones secreted by the pituitary

gland, thyroid-stimulating hormone (TSH). In turn, TSH is

regulated by thyroid-releasing hormone (TRH) secreted by

the hypothalamus. High levels of T4 and T3 act to suppress

production of TSH and TRH via a negative feedback loop.

TH released from the thyroid gland is in its less active form,

T4

, which is converted in peripheral organs (kidney and

liver) into its 10 times more active derivative, T3

" The halflife of T 3 is significantly shorter, approximately a day,

compared with 1 week for T4

• In the serum, the majority of

TH is bound to thyroid-binding globulin (TBG), making it

inactive. The only active forms are free T3 and T4

• After TH

enters cells, it binds to its nuclear receptor and regulates

expression of genes involved in lipid and carbohydrates

metabolism and protein synthesis. As a net result of its

action, there is an increase in basal metabolic rate.

Emergencies related to the thyroid gland can be caused

by both excess and deficiency of TH. Excess of TH can

• Myxedema coma should be considered in elderly hypothyroid

patients who present with hypothermia and confusion.

• For successful treatment, it is important to try to identify a trigger that pushed the patient into the extreme

state of thyroid storm or myxedema coma.

cause a syndrome referred to as thyrotoxicosis and can be

caused either by excessive production of TH or its

exogenous administration. In its extreme state,

thyrotoxicosis can lead to a life-threatening condition

called thyroid storm, a state manifesting with fever,

tachycardia, and altered mental status.

Hyperthyroidism is the term used when excessive

production of TH by the thyroid is the cause of thyrotoxicosis. One of the most common causes of hyperthyroidism

is Graves disease (approximately 80% of cases), in which

autoimmune antibodies that bind to TSH receptors on the

surface of thyroid cells stimulate production and release of

TH. Other significant causes of hyperthyroidism include

toxic multinodular goiter, thyroiditis, pituitary adenoma,

and reaction to drugs ( eg, lithium, amiodarone and iodine).

POTASSIUM DISORDERS of illnesses that cause potassiwn disorders, such as paralysis, tachycardia, rashes, or striations. Patients with a

 

POTASSIUM DISORDERS

of illnesses that cause potassiwn disorders, such as paralysis, tachycardia, rashes, or striations. Patients with a

hyperkalemia-induced QRS widening may appear bradycardic before degeneration into a sinusoidal rhythm (see

Diagnostic Studies).

DIAGNOSTIC STUDIES

� Laboratory

An electrolyte panel will detect abnormalities of potassiwn

(turnaround time is approximately 30-40 minutes). A

potassiwn level can be obtained using many blood gas analyzers. Advantages include a more rapid turnaround time (2

minutes). However, blood gas analyzers are unable to detect

a hemolyzed sample and therefore may overdiagnose hyperkalemia. A magnesiwn level should be obtained in patients

with hypokalemia, because of the difficulty in correcting low

potassiwn in the setting of low magnesiwn levels.

� Electrocardiogram

Symmetrical T-wave peaking, P-wave flattening, QRS widening, or a sinusoidal pattern are characteristic of hyperkalemia (Figure 67-1). Unfortunately, the electrocardiogram

(ECG) lacks sensitivity to detect elevated potassiwn levels.

Only 50-60% of patients with potassium levels >6.5

mEq/L have any of the preceding ECG findings.

Hypokalemia is manifested by U-waves, T-wave flattening,

and ST -segment depression. Dysrhythmias, including ventricular fibrillation, may occur in patients with severe

hypokalemia or in patients with moderate hypokalemia

and a history of cardiac disease.

MEDICAL DECISION MAKING

Patients with a history consistent with a potassiwn disorder ( eg, missed dialysis, profuse diarrhea) should have

immediate ECG testing performed and should be placed

on a cardiac monitor. An electrolyte panel or arterial

blood gas with electrolytes should be drawn. If an ECG is

consistent with hyperkalemia, therapy should be initiated

immediately, before confirmatory tests. Before treating

isolated hyperkalemia detected on an electrolyte panel,

pseudohyperkalemia (hemolysis) should be ruled out by

communication with the lab. Patients who are dialysis

dependent or who remain hyperkalemic despite treatment should have emergent dialysis arranged. Patients

with hypokalemia should have potassium and magnesium repleted (Figure 67-2).

TREATMENT

� Hyperkalemia

All patients with hyperkalemia should be put on a cardiac monitor, and an ECG should be performed. If QRS

widening or arrhythmias are noted on a rhythm strip or

ECG, calcium, given as calcium gluconate 10% (less irrif>1;e I of t

Figure 67-1 . ECG changes of hyperkalemia. Note the pea ked T waves and widened QRS complex.

CHAPTER 67

Suspected electrolyte disorder

Electrolyte

panel, mon itor,

ECG

and K· decreases,

admit to mon itored

setting with

nephrology consu lt

· Obta in Mg

level

· Replace K·

· Sea rch for

u nderlying cause

K· < 2.5 mEq/L,

admit to

monitored

setting

K· > 2.5 m Eq/L,

consider

discharge when

correcti ble cause

is identified

.A Figure 67-1. Potassium disorders diag nostic a lgorithm. ECG, Electroca rdiogram.

tation to peripheral veins) or calcium chloride 10% (3x

more calcium) should be administered to stabilize myocardial membranes. Calcium can be repeated every 5 minutes

until the ECG normalizes. The duration of action is 30-60

minutes. Calcium is not indicated in the stable patient

when the ECG shows only peaked T waves. Avoid giving

calcium when treating hyperkalemia with coexisting digoxin

toxicity, because intracellular calcium is already elevated in

digoxin toxicity. Further administration of calcium may

cause asystole and death.

Therapy should also be instituted to induce an intracellular shift of potassium. Insulin 0.1 Unit/kg intravenously

(IV) is administered to shift potassium into the cell via an

intracellular messenger. Within 30 minutes, insulin will

reduce the potassium level by 0.5-1.0 mEq/L. In patients

with normal glucose levels, administer 25-50 g ( 1/2-1 amp)

of dextrose rv. An alternate method in stable patients is to

add 10 Units of regular insulin in 500 mL of D10W and

administer this over a 1-hour period. Patients with chronic

renal failure given insulin should have fingerstick glucose

monitoring initiated, as hypoglycemia is not uncommon.

Nebulized albuterol also shifts potassium back into cells

and may work synergistically with insulin. Albuterol 10-20

mg in 4 mL of NS is given via nebulizer over 10 minutes.

Sodium bicarbonate (NaHC03

) also shifts potassium back

into cells and leads to increased potassium excretion by the

kidneys. One amp (SO mEq) infused over a 5-minute period

has an onset in 5-10 minutes and lasts 2 hours.

POTASSIUM DISORDERS

Finally, potassium elimination therapy should be initiated. Furosemide 20-40 mg IV in patients not already

taking the drug will reduce potassium levels. The onset is

several hours, and the amount of decrease in the potassium level is variable. Cation exchange resins like sodium

polystyrene sulfonate (Kayexalate) remove up to 1 mEq

potassium per gram. A standard dose is 30 g mixed with

50 mL of 20% sorbitol to induce diarrhea. It can be

administered rectally (50 g with 200 mL 20% sorbitol), if

necessary. Onset is delayed and may take more than 4

hours. Dialysis should be activated early for patients in

renal failure. Dialysis is also indicated in refractory cases.

Treatment for the underlying disorder (eg, steroids for

Addisonian crisis, Fab fragments for digoxin toxicity)

should be initiated as soon as possible.

� Hypokalemia

Patients with hypokalemia should be put on a cardiac

monitor. Oral K+ replacement (40 mEq/day) is safe and

generally recommended in patients with mild to moderate

hypokalemia. IV K + should be used if cardiac dysrhyth ­

In HHS, the differential diagnosis includes DKA and alcoholic ketoacidosis. Precipitating causes are varied and are

 

In HHS, the differential diagnosis includes DKA and

alcoholic ketoacidosis. Precipitating causes are varied and are

included or excluded based on history and physical exam.

These include multiple types of medications such as diuretics, lithium, beta-blockers, and antipsychotics; gastrointestinal hemorrhage; ischemia of bowel, myocardium, or brain;

renal insufficiency; trauma; burns; and cocaine toxicity.

For differentiating hyperglycemic conditions, see

Figure 66- l.

TREATMENT

Diabetic patients who are noncompliant or inadequately

treated are frequently seen in the emergency department,

and there is some controversy regarding the best treatment

for these patients once it is determined that they do not

have DKA or HHS. Treatment will depend on the degree of

elevation of the glucose level and the presence of dehydration. Options include initiating or restarting an oral antihyperglycemic medication (ie, glipizide or metformin),

administering N or oral fluids and rechecking the glucose

level, or administering insulin (usually regular insulin SQ)

and rechecking the glucose level. Correction of dehydration

prevents further osmotic diuresis.

The 3 pillars of treatment of D KA are fluids, insulin, and

potassium, which are generally administered in that order.

The initial N fluid given is 1 L of 0.9 normal saline (NS)

over 30-60 minutes. Depending on the size of the patient,

often a second liter of 0.9 NS is also administered. Then

switch to 0.45 NS. Be careful to avoid fluid overload in

patients with congestive heart failure. General total body

water depletion in patients with DKA is 6-8 L.

Insulin can be initiated after the first liter of fluids. An

N bolus (0.15 U/kg) is optional. Start an N infusion of

0. 1 U/kg/hr of regular insulin. Continue N insulin until

the pH is >7.3 and the anion gap has closed. Switch to D5

0.45 NS when the glucose level is <250 mg/dL.

Treatment with supplemental potassium depends on

the initial potassium level. For K >5.5 mEq/L: hold

treatment. If K 3.5-5.5 mEq/L: add 1 0-20 mEq to each liter

of IV fluids if renal function is normal. If K <3.5 mEq/L:

add 40 mEq to each liter of N fluids if renal function is

normal. If K <3.5 mEq/L: do not administer insulin until

the serum K is >4.0 mEq/L.

It is important to monitor serum glucose and serum

electrolytes, including magnesium and phosphate regularly,

as electrolyte shifts occur quickly in DKA. Obtain serum

glucose once every hour after starting an insulin drip.

Check electrolytes every 2-4 hours. Magnesium and

phosphate replacement may be required.

In HHS, the average fluid deficit is 8-12 L. Use 0.9 NS for

the initial resuscitation (1 L). Switch to 0.45 NS at a rate of

200-500 rnL/hr. Goal is 3-4 L over the initial 4-hour period.

The corrected serum sodium and the serum osmolarity

should be gradually returned to normal over a 24- to

36-hour period. Insulin N infusion can be started after

initiating infusion of N fluids. A total of 0.1 U/kg/hr of

regular insulin is given if the K >3.3 mEq/L. Potassium

replacement is similar to that in patients with DKA. Frequent

monitoring of glucose and electrolytes is necessary to avoid

iatragenic electrolyte abnormalities, such as hypokalemia.

DIABETIC EMERGENCIES

DISPOSITION

.... Admission

Admission is indicated for patients with DKA and HHS.

An intensive care unit (ICU) setting is appropriate for all

patients with HHS. In DKA, AMS or pH <7.0 generally

necessitate ICU admission.

..... Discharge

Discharge is appropriate for patients with hyperglycemia

once DKA and HHS have been excluded. Patients should

be given instructions to obtain close follow-up.

SUGGESTED READING

Chansky ME, Lubkin CL. Diabetic ketoacidosis. I n: Tintinalli JE,

Stapczynski JS, Ma OJ, Cline DM, Cydulka RK, Meckler GD.

Tintinalli's Emergency Medicine: A Comprehensive Study Guide.

7th ed. New York, NY: McGraw-Hill, 201 1, pp. 1432-1438.

Graffeo CS. Hyperosmolar hyperglycemic state. I n: Tintinalli JE,

Stapczynski JS, Ma OJ, Cline DM, Cydulka RK, Meckler GD.

Tintinalli's Emergency Medicine: A Comprehensive Study Guide.

7th ed. New York, NY: McGraw-Hill, 201 1, pp. 1 440-1444 .

Kitabchi AE, Umpierrez GE, Miles JM, et al. Hyperglycemic crises in adult patients with diabetes. Diabetes Care. 2009;32: 1335.

Nugent BW. Hyperosmolar hyperglycemic state. Emerg Med Clin

North Am. 2005;23:629.

Potassium Disorders

Brooks L. Moore, MD

Key Points

• Obtain an electrocardiogram (ECG) early in patients with

suspected hyperkalemia and never ignore a K+ >6.0 mEq/L.

• Patients with ECG changes consistent with hyperkalemia

require prompt treatment to avoid a life-threatening

dysrhythmia.

INTRODUCTION

Potassiwn (K +) is involved in maintaining the resting cell

membrane potential. Small shifts in potassiwn c oncentration

result in problems with muscle and nerve conduction, leading

to potentially life-threatening disorders of the cardiac and

neuromuscular systems. The normal plasma concentration of

potassiwn is 3.5-5.5 mEq/L. Hyperkalemia is defined as

potassiwn level >5.5 mEq/L. It can be classified as mild

(5.6--6.0 mEq/L), moderate (6.1-7.0 mEq/L), and severe

(>7.0 mEq/L). Hyperkalemia is present in approximately So/o

of hospitalized patients. If not treated promptly, two thirds of

patients with severe hyperkalemia (>7.0 mEq/L) will die.

Etiologies include pseudohyperkalemia (red blood c ell hemolysis, white blood cell count > 200,000, or platelet count

> 1 million), transcellular shifts (acidosis or insulin defi ­

ciency), medications (digoxin, succinylcholine, angiotensinconverting enzyme inhibitors, nonsteroidal anti-inflammatory

drugs, or spironolactone), cell breakdown (crush injury,

burns, twnor lysis), increased intake (conswnption of fruits

or salt substitutes), or impaired excretion (renal failure,

Addisonian crisis, or type 4 renal tubular acidosis).

Hypokalemia is defined as potassiwn level <3.5 mEq/L.

Mild hypokalemia is present when the serwn potassiwn

concentration is between 3.1 and 3.4 mEq/L. Moderate

(2.5-3.0 mEq/L) and severe ( <2.5 mEq/L) hypokalemia are

less common. Approximately 15o/o of emergency department

• The most common cause of hypokalemia in a patient in

the emergency department is diuretic (loop or thiazide)

use.

• Replacing K+ via the oral route is safe and is the preferred

method for cases of mild to moderate hypokalemia.

patients are mildly hypokalemic. The percentage increases to

80o/o in patients taking diuretics, especially loop or thiazide

diuretics. Etiologies for hypokalemia include decreased

intake, transcellular shifts (respiratory or metabolic alkalo ­

sis), medication effects (diuretics, insulin, or �-2 adrenergic

stimulation), thyrotoxicosis, hypokalemic periodic paralysis,

or excessive losses from the renal (hyperaldosteronism,

Cushing syndrome, type 1 renal tubular acidosis) or gastrointestinal (vomiting, diarrhea) systems.

CLINICAL PRESENTATION

� History

Symptoms of hyperkalemia and hypokalemia are vague and

frequently include fatigue and generalized weakness. Other

features include paresthesias, nausea, vomiting, constipation,

abdominal pain, psychosis, or depression. A history of vomiting, diarrhea, renal failure, thyroid disease, adrenal disease, or

use of offending medications should raise suspicions.

� Physical Examination

Patients with potassium disorders may not have any physical manifestations. In an unresponsive patient, evidence of

dialysis access (arteriovenous [AV] fistulae, AV grafts, or

tunneled catheters) may provide an indication of the possibility of these conditions. Patients may also display signs

284

Patients with DKA present with often vague complaints such as nausea, fatigue, or generalized weakness. Vomiting and abdominal pain may be present. Altered mental status

 

Patients with DKA present with often vague complaints

such as nausea, fatigue, or generalized weakness. Vomiting

and abdominal pain may be present. Altered mental status

(AMS) also occurs in severe disease and is closely correlated

with a high serum osmolality.

In patients with HHS, AMS is the most common presentation. Additional neurologic complaints include seizures,

hemiparesis, and coma. Coma is present in only 10% of cases.

� Physical Examination

Patients with hyperglycemia or diabetic ketosis may exhibit

evidence of mild dehydration.

In DKA, vital signs are often abnormal, with tachycardia and tachypnea, with characteristic Kussmaul respira ­

tions. If there is severe dehydration or sepsis, hypotension or

hyperthermia may be present. Hypothermia is a poor prognostic sign. Fruity odor on the breath owing to ketonemia

may be present. Evidence of dehydration includes dry

mucous membranes, decreased skin turgor, and tachycardia.

Urine output may be maintained because of the ongoing

osmotic diuresis. Physical examination may reveal a source

of infection such as pneumonia, pyelonephritis, or cellulitis.

In HHS, physical examination findings are similar to

those of DKA. Patients usually show evidence of severe dehydration. AMS is a hallmark. A focused neurologic examination is indicated in these patients to detect focal neurologic

deficits. Searching for other precipitating causes that can be

seen on physical examination such as infection is imperative.

DIAGNOSTIC STUDIES

� Laboratory

The first most important test to obtain is a fingerstick

blood glucose at the bedside to rapidly establish the

presence of hyperglycemia. The accuracy of these machines

is known to decrease at extreme elevations, and many will

not read values >600 mg/dL.

Obtain serum electrolytes, renal function, serum

osmolality, and urine ketones. In DKA, the bicarbonate level

will be low, and there will be an elevated anion gap. The

serum potassium level is frequently elevated as a result of

acidemia, causing a shift of potassium into the extracellular

space. As treatment is initiated, potassium is drawn back

into the cells, exposing a total body potassium that is low.

Sodium concentration is also frequently low, usually artificially, because water is drawn out of the intracellular space

by the elevated glucose. To account for this, the sodium

concentration is corrected by adding 1.6 mEq/L (correction

factor) for every 100 mg!dL increase in the glucose. A correction factor of 2.4 mEq/L is more accurate for glucose

levels >400 mg!dL. In HHS, the measured (uncorrected)

sodium concentration, glucose level, and blood urea nitrogen (BUN) are used to calculate the serum osmolality:

Serum osmolality (mOsm/L) = 2(Na) + glucose/ IS

+ BUN/2.8

The nitroprusside test used for the detection of ketones

on urinalysis identifies acetoacetate and acetone but does

not detect �-hydroxybutyrate. In DKA, there is a predominance of �-hydroxybutyrate. Despite some earlier concerns

that urine ketones could be falsely normal in DKA because

of the predominance of �-hydroxybutyrate, this has not

turned out to be the case in clinical practice. Urine ketones

can be used as an accurate screen for the presence of serum

ketones. However, it should be remembered that as treatment ensues, a shift to acetoacetate and acetone makes

urine ketones more positive despite adequate t reatment.

The pH of a venous blood gas is an accurate estimation

of the arterial pH in DKA and can be used to guide management. To determine complex acid-base disorders, an

arterial blood gas can be obtained, but this test rarely

impacts treatment decisions.

When there is suspicion of an underlying infection, blood

cultures, urinalysis, and urine culture should also be obtained.

� Electrocardiogram

An electrocardiogram is obtained to evaluate for signs of

hyperkalemia or cardiac ischemia.

� Imaging

A chest x-ray is indicated when clinical symptoms suggest

pneumonia or another concomitant cardiopulmonary illness.

Head computed tomography scan is obtained to rule out

precipitating cranial pathology (ie, stroke, intracranial hem ­

orrhage) if the patient has AMS.

MEDICAL DECISION MAKING

The differential diagnosis of DKA includes all causes of

metabolic acidosis with an anion gap (methanol ingestion,

uremia or renal failure, isoniazid, lactic acidosis, ethylene

glycol ingestion, alcoholic ketoacidosis, salicylate toxicity).

History and laboratory data should provide the clues to

make the appropriate diagnosis. In determining the pre ­

cipitant ofDKA, the differential diagnosis includes sources

of infection, cerebral vascular accident, and acute

CHAPTER 66

Urine for ketones, serum electrolytes

glucose, ± blood gas ± serum Osmolal ity

Figure 66-1. Diabetic emergencies diag nostic algorithm. AG, anion gap; H HS, hyperg lycemic hyperosmolar state; OSM, Osmolal ity.

coronary syndrome. Noncompliance with insulin therapy

is a diagnosis of exclusion.

Often presenting complaints of patients with DKA

include abdominal pain, and thus the differential diagnosis

also includes appendicitis, pancreatitis, and gastroenteritis.

These are ruled in or out primarily based on history and

physical exam.