All symptomatic patients from elapid envenomation require ICU admission for anticipated respiratory failure. Asymptomatic patients receiving elapid antivenin will need



DISPOSITION

..... Admission

All symptomatic patients from elapid envenomation

require ICU admission for anticipated respiratory failure.

Asymptomatic patients receiving elapid antivenin will need

to be observed for neurologic symptoms. Asymptomatic

patients not receiving antivenin should also be observed

for 24 hours, because risk stratification in these patients

has been found to be so difficult.

..... Discharge

For crotaline snakebites, patients with an apparent "dry

bite" or those without bite marks can be observed in the

ED for 8 hours and discharged without focused therapy.

Patients with minor envenomations, characterized by only

mild local findings on skin examination with the absence

of hematologic or systemic abnormalities, should be

observed for 12-24 hours with repeat blood testing and

may be discharged home without antivenom administra ­

tion if their symptoms remain mild. Patients requiring

antivenom administration should be observed for 18-24 hours

after control of symptoms was obtained. These patients

will also need close outpatient follow-up for repeat

laboratory work to evaluate for any worsening hematologic

abnormalities and must be given very strict discharge

instructions.

SUGGESTED READING

Dart RC, Daly FFS. Reptile bites. In: Tintinalli JE, Stapczynski JS,

Cline DM, Ma OJ, Cydulka RK, Meckler GD. Tintinalli's

Emergency Medicine: A Comprehensive Study Guide.

7th Ed. New York, NY: McGraw-Hill, 20 1 1, pp. 1354-1358.

Hahn IH. Arthropods. In: Nelson LS, Lewin NA, Howland MA,

Hoffman RS, Goldfrank LR, Flomenbaum NE. Goldfrank's

Toxicology Emergencies. 9th ed. New York, NY: McGrawHill Medical, 20 11, pp. 1561-158 1.

Isbister GK, Fan HW. Spider bite. Lancet. 20 11;378: 2039.

Lavonas EJ, Ruha AM, Banner W, at al. Unified treatment algorithm for the management of crotaline snakebite in the

United States: results of an evidence-informed consensus

workshop. BMC Emerg Med. 201 1;11:2.

Riley BD, Pizon AF, Ruha AM. Snakes and other reptiles. In:

Nelson LS, Lewin NA, Howland MA, Hoffman RS, Goldfrank

LR, Flomenbaum NE. Goldfrank's Toxicology Emergencies.

9th ed. New York, NY: McGraw-Hill Medical, 20 1 1,

pp. 1 60 1-1610.

Diabetic Emergencies

Sarah E. Ronan- Bentle, MD

Key Points

• Hyperg lycemia causes an osmotic diuresis that may

result in dehydration.

• Patients with diabetic ketoacidosis (DKA) and

hyperglycemic hyperosmolar state (HHS) are treated

with intravenous fluids and insulin. Potassium

supplementation should begin as soon as the potassium

level is in the normal range.

INTRODUCTION

Diabetes mellitus is a common disorder and is present in

6% of the population in the United States. Diabetes

mellitus is defined as fasting blood glucose > 126 mg/dL on

2 separate occasions or a random glucose >200 mg/dL plus

the classic symptoms of hyperglycemia (ie, polyuria,

polydipsia). Derangement of glucose homeostasis is a

continuum that ranges from hypoglycemia on one extreme

to diabetic ketoacidosis (DKA) on the other end of the

spectrum.

Hyperglycemia, even in the absence of DKA or

hyperglycemic hyperosmolar state (HHS), has many

deleterious effects. An osmotic diuresis occurs when an

elevated glucose level overwhelms the kidneys and begins

to pull electrolytes and water into the urine. In the healthy

individual, serum glucose of 240 mg!dL is required before

glucose is found in the urine. Additionally, hyperglycemia

impairs leukocyte function and wound healing, making

patients prone to infection. Chronic hyperglycemia causes

renal failure, blindness, neuropathy, and atherosclerosis.

Diabetic ketosis is an intermediate metabolic state

between hyperglycemia and ketoacidosis. Patients have an

inadequate amount of insulin to provide the necessary

energy substrates to the cell. As a result, lipolysis is

• Both DKA and HHS are often preci pitated by another

ill ness, frequently infection. An attempt should be

made to search for and treat any precipitating illness.

• When treating patients with HHS, it is important to

follow sodium and serum osmolal ity measurements to

document return to normal values.

stimulated to provide ketone bodies that can be used as

substrates by the brain and other tissues. The ketone

bodiesincludeacetoacetate,acetone,andP-hydroxybutyrate.

DKA is defined as blood glucose >250 mg!dL, serum

bicarbonate < 15 mEq/L, ketonemia, and an arterial pH <7.3.

DKA is present in 5-10% of hospitalized patients. It is the

presenting illness of diabetes mellitus in 1 5-25% of patients.

When making the diagnosis of DKA, the physician should

attempt to determine what has precipitated the illness. The

most common causes of DKA are the "3 I's": insulin lack,

ischemia (cardiac), and infection. The mortality rate of

patients with DKA is approximately 5% and most often is

attributable to concomitant illness.

In DKA, reduced circulatory insulin levels do not allow

glucose to reach the intracellular space. In response, the

cell stimulates lipolysis, which provides the body with

glycerol (substrate for gluconeogenesis) and free fatty

acids. Free fatty acids are a precursor to the ketoacids,

acetoacetate, acetone, and P-hydroxybutyrate. The ketone

bodies can be used as an energy source, but when they are

present in excess, metabolic acidosis results.

HHS occurs when a hyperglycemic osmotic diuresis

causes extreme dehydration. Defining features include

a serum glucose >600 mg/dL, plasma osmolality

>320 mOsm/L, and the absence of ketoacidosis. HHS is

280

DIABETIC EMERGENCIES

most common in elderly individuals. It results in <1 o/o of

diabetes-related hospital admissions, but has a reported

mortality rate of 20-60%. HHS occurs when a prolonged

osmotic diuresis from hyperglycemia results in severe dehydration and an elevated serum osmolality. Concurrent

medical illness is very common and is often a precipitating

cause of HHS.

CLINICAL PRESENTATION

� History

Patients with hyperglycemia report polydipsia and

polyuria. They may also present with blurry vision owing

to changes in the shape of the lens induced by osmotic

movements of water. Recovery is spontaneous, but may

take up to 1 month.

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