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

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