Running head: COMPREHENSIVE CLINICAL CASE STUDY
Comprehensive Clinical Case Study
Neeta Monteiro, RN, BSN
Wright State University-Miami Valley College of Nursing and Health
NUR 7201
Dr. Kristine Scordo
July 10, 2013
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History and Physical
Source of Information
Information was obtained from the patient’s mother, since the patient is unresponsive and
unable to provide information. The mother is alert and oriented, speaks English, and is consistent
with the information.
Chief Complaint
Altered mental status
History of Present Illness
Ms. B.H. is a 29 year old Caucasian female patient with a history of depression, anxiety,
and polysubstance abuse, brought in by emergency medical service (EMS) after being found in
altered mental status by her mother. The patient’s mother reports she was last seen normal
around 1400 at a family function. Later that night at around 2330 the patient was found
extremely agitated, combative, and delirious. EMS was called, and patients vital signs included
temperature of 98.6o F, blood pressure of 130/80 mmHg, heart rate of 98 beats/minute,
respiratory rate of 26/minute, and oxygen saturation of 96% on room air. Per the mother, the
patient has been very depressed lately after she broke up with her boyfriend, and was always
talking about harming herself. No pill bottles or drug supplies were found around her. According
to the EMS report, when the patient was asked what was going on, she apparently screamed “I
tried to end it all!” The patient was not able to provide information as to what she did to harm
herself. Subsequently the patient became unresponsive and had to be intubated for airway
protection. She was brought to the emergency department (ED) for further workup.
Family reports that patient has history of cocaine and benzodiazepine abuse. She has
previously attempted suicide by hanging in March 2012. At that time she required intubation. Per
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family she has not used any drugs since then, and has gone back to school. However she has
been drinking up to a pint of vodka a day for the last couple months. Mother denies any recent
fevers, chills, sick exposures, or trauma. Patient lives with her mother.
Laboratory workup in the ED displayed normal plasma electrolytes, and kidney function.
The plasma carbon dioxide level is 7 mEq/L (normal 19-32 mEq/L), anion gap is 33 (normal 1020), calculated serum osmolality is 328 mOsml/Kg/H2O (normal 285-295 mOsm/kg), measured
serum osmolality is 362 mOsm/kg (normal range should not exceed the calculated by >10
mOsm/kg) and osmolar gap is 34 mOsm/kg (normal <10 mOsm/kg). Arterial blood gas (ABG)
assessment presents a pH of 7.23, PCO2 23, HCO3 8, PO2 73, O2 sat 94, base excess -4. Urine
microscopy displayed calcium oxalate monohydrate and dihydrate crystals along with several
erythrocytes in the urine. Urine drug screen was negative for phencyclidine, benzodiazepine,
cocaine, amphetamine, tetrahydrocannabinol (marijuana), opiates, barbiturates and tricyclic
antidepressants. Urine appeared fluorescent on examination under the Wood’s lamp. Urine
pregnancy test is negative. Cardiac enzymes are negative and serum lactate level is 1.1 mmol/L.
Results of the computed tomography (CT) of the head without contrast, chest x-ray, and
electrocardiogram (EKG) is normal. Results of the blood levels for acetaminophen, salicylate,
ethanol, methanol, ethylene glycol, isopropyl alcohol are pending.
Medical History
Childhood Illnesses: She had chickenpox at age 4 years. No other major childhood
illnesses like polio, measles, or rheumatic fever.
Adult Illnesses: History of polysubstance abuse (cocaine, xanax, tobacco, alcohol),
previous suicide attempt by hanging in March 2012, depression, and anxiety.
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Surgeries/procedures: Underwent tonsillectomy at age 14, suction dilatation and
curettage done on11/24/2008.
Medications

Trazadone 50 mg 1 tablet at HS

Citalopram 10 mg 1 tablet po daily

Multi-vitamin one tablet daily po
Allergies: Betadine, sulfonamides, latex, Motrin and tape.
Immunization: Received the flu shot in November 2012. All childhood vaccinations are
up-to-date.
Personal and Social History: The patient is single and does not have any children. She
lives with her mother. She works as a janitor at a local business for the last two years. She has
been working on completing her high school diploma. She smokes one pack of cigarettes per
day, consumes one pint of vodka per day for the last two months, and uses recreational drugs
occasionally. She does not have a regular exercise schedule nor does she participate in any
precise diet regimen.
Family History: The patient’s mother is 56 years old and has history of hypothyroidism,
and diabetes. Father is 61 years old and has history of atrial fibrillation, stroke, hypertension and
hyperlipidemia. The patient has only one brother who is 24 years old and apparently in good
health. Her paternal grandmother (78 years old) has history of hypertension, diabetes, and stroke.
Her maternal grandmother (80 years old) has history of breast cancer and hyperthyroidism. Both
her paternal and maternal grandfathers are deceased due to natural causes of old age.
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Review of Systems
General: Mother reports that the patient has been drinking excessively for the last two
months. She has not been attending school regularly and has been very depressed. She does not
take very good care of herself, and does not participate in an annual medical examination. She is
otherwise in reportedly good health, and has not had any major illnesses recently. No recent
weight gain or weight loss.
Skin/Hair/Nails: No change in skin color. No history of skin disease, hair loss, or change
in texture. No changes in nail.
HEENT: No unusual incidence of headaches, head injury, or vertigo. No difficulty with
vision; does not use corrective glasses or lenses; has had no issues with hearing; no nasal
bleeding or allergies. Does not normally have any problems with eating, chewing and
swallowing. Does not visit the dentist regularly.
Neck: No past issues with pain, problems with range of motion, lumps or swollen glands.
Chest: Has history of asthma. Smokes one pack of cigarettes per day. In March 2012 she
attempted suicide by hanging and required intubation.
Cardiovascular: No history of chest pain, or peripheral edema. No history of
hypertension, murmurs, or coronary artery disease.
Gastrointestinal: Normally does have a good appetite, with no recent changes in weight.
Has not had nausea, vomiting, or diarrhea. No history of gastro-esophageal reflex disease, ulcers,
hepatic dysfunction, appendicitis, or colitis. Has regular bowel movements.
Genitourinary: Usually has no problem with frequency, urgency or pain. Has not had
any recent urinary tract infection.
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Reproductive: Had suction dilatation and curettage, done on11/24/2008, due to uterine
fibroids. She does not have any children. Patient broke up with her boyfriend couple months ago.
Mother is unsure if the patient is presently sexually active or has any other significant person in
her life. She does not visit the gynecologist regularly.
Musculoskeletal: No past history of joint disease, arthritis, or fractures. No joint pain,
rigidity, inflammation, malformation, or limitation in range of motion.
Neurological: No issues with seizures or stroke. Has had blackouts due to excessive
alcohol use in the past. No issues with weakness, tremors, paralysis, numbness or tingling in the
past.
Psychological: Has history of depression, cocaine and benzodiazepine abuse, and was
hospitalized in March 2012 for suicidal attempt with hanging. At that time she required
intubation and mechanical ventilation. She broke up with her boyfriend couple months ago and
has been very depressed since then. She started drinking up to a pint of vodka a day for the last
couple months. Patient refused to visit her psychiatrist and does not take her prescribed
citalopram and trazadone regularly.
Physical Examination
Vitals: Temperature 96.4o F, BP 97/61 mmHg, pulse 127/minute, RR 20/minute, SpO2
on ventilator assist control mode, TV 550, PEEP 5, RR 12/minute, FiO2 60%. Height is 5’5”,
and weighs 135 pounds.
General: She is intubated and sedated. She does not appear to be in any distress, resting
comfortably. Physically well developed and nourished.
Skin/Hair/Nails: Skin is clean, dry, and intact. Skin is cool, dry and intact. No skin
hyperpigmentation, pruritus, or rash. No needle tracks seen. Moderate amount of hair on scalp,
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equally distributed. Hair is soft with no hair parasites. Nails are smooth, curved and clean. Has
pink nail beds with no clubbing noted.
HEENT: Normocephalic and atraumatic head, with no lesions or lumps. Face is
symmetric, no weakness, or involuntary movements. Eyes unable to assess visual acuity due to
patient being sedated. Has normal corneal reflex. Pupils are equal, round, reactive to light, 2 +.
No scleral icterus. No discharge. Ears no mass, lesions or drainage, with pale gray tympanic
membrane. Hearing not tested. Nose, nares clear, mucosa is pink, no lesions. No septal deviation
noted. Mucous membrane is moist. Poor dentition with several missing teeth and many dental
carries.
Neck: Neck supple with full range of motion. Symmetric, no masses, tenderness, or
lymphadenopathy. Trachea is midline. No jugular vein distention noted. Carotid arteries pulses
are 2+ bilaterally, with no bruits appreciated.
Chest: Patient is intubated. Symmetric chest rise. Lungs are clear to auscultation
bilaterally. No rales, rhonchi or wheezes noted. Lung fields are resonant.
Cardiovascular: Precordium, no abnormal pulsation, no heaves. Apical pulse at 5th
intercostal space in left mid-clavicular line, no thrills. S1, S2 normal. No S3, or S4. Tachycardia
with regular rhythm. No murmurs, rubs, or gallops. Pulses 2 + in bilateral radial, posterior tibial
and dorsalis pedis. No edema.
Breast: Breasts are symmetric. No retractions, dimpling, discharge or lacerations.
Contour and consistency of breast is smooth and consistent. No lumps or tenderness, no
lymphadenopathy.
Gastrointestinal: Abdomen is flat and symmetric. Bowel sounds are positive with no
bruits. Tympany prevails in all four quadrants. Liver span is 7.5 centimeters, in right mid
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clavicular line. Abdomen is soft, no organomegaly, masses, rebound tenderness, or inguinal
lymphadenopathy.
Genitourinary/Rectal: External genitalia have no lesions, or discharge. Patient has an
indwelling urinary catheter in place. Urine appearance is clear yellow, with adequate urinary
output. Anus, no hemorrhoids, bleeding, fissures, or obvious lesions.
Musculoskeletal: No swollen or inflamed joints. No clubbing or cyanosis noted.
Neurological: Patient is sedated. Unable to verbalize due to endotracheal tube placement.
Pupils are equal 2+ bilaterally. She has a positive gag and cough reflex; moves all her extremities
spontaneously and equally. Follows few simple commands such as hand squeeze. Deep tendon
reflexes are 2 +.
Psychiatric: Patient has a history of depression, anxiety, and previous suicidal attempt by
hanging in March, 2012. Was appropriately treated and discharged, with patient regaining
baseline health status. Has history of smoking, alcohol and substance drug abuse. She recently
broke up with her boyfriend. She has not been taking her medications regularly.
Differential Diagnosis
After acknowledging the findings from the complete history and physical examination,
laboratory and radiological diagnostic tests, the patient appears to be having signs and symptoms
caused by an increased anion gap metabolic acidosis. The patients ABG results include pH 7.23,
PCO2 23, HCO3 8, PO2 73, O2 sats 94%, base excess -4, which is indicative of severe metabolic
acidosis. The patient’s anion gap is 33 (normal is 10-20), calculated serum osmolality is 328
mOsmo/kg, measured serum osmolality is 362 mOsmo/kg, and osmolar gap is 34 (normal is
<10). The high osmolar gap in the presence of high anion gap metabolic acidosis indicates that
there is another osmotically active solvent in the blood serum (Mount & DuBose, 2012).
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Some of the factors that contribute to the occurrence of increased anion gap metabolic
acidosis include diabetes ketoacidosis, alcohol ketoacidosis, lactic acidosis due to tissue hypoxia,
renal failure, and ingestion of toxic substances such as methanol, ethylene glycol, salicylates, and
acetaminophen. The patient’s osmolal gap is 34. An osmolal gap of greater than 10 is mostly
suggestive of methanol or ethylene glycol toxicity. Ruling out the following differential
diagnosis will assist the practitioner in confirming the absolute diagnosis of the patient
(Jiranantakan, & Anderson, 2012).
Pertinent Differential Diagnosis

Ethylene glycol toxicity

Methanol toxicity

Salicylate poison

Lactic acidosis

Alcoholic ketoacidosis
Ethylene Glycol Toxicity. Ethylene Glycol (EG) is the main element found in antifreeze.
EG has a sugary taste and therefore may lead to intentional as well as unintentional ingestion.
Unintentional ingestion is usually seen in animals and children. Accidental or purposeful
ingestion of antifreeze causes toxicity as seen in the patient. The progression of EG inebriation
occurs in three phases. The first stage usually instigates within half an hour with symptoms such
as drunkenness, deliriousness, headache, and abdominal distress. This stage continues for
approximately twelve hours with more serious central nervous system (CNS) involvement such
as convulsions and unresponsiveness caused by cerebral swelling. The second stage involves the
12 to 24 hour period post ingestion of EG. During this stage the symptoms manifestation
involves cardiorespiratory abnormalities such as dysrhythmias, fluctuation in blood pressure,
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respiratory failure requiring intubation, and signs and symptoms of heart failure caused by the
deposition of calcium oxalate crystals. The third stage comprises of the 24 to 72 hour period with
the indications of acute renal failure sometimes requiring hemodialysis in severe intoxication
(Kruse, 2012).
Toxicity seen in EG poisoning begins to occur due to the accumulation of the toxic
metabolites glycolic, glyoxylic, and oxalic acids which are the byproducts of EG metabolism.
Oxalic acid freely associates with calcium and produces calcium oxalate crystals, which gets
deposited in the brain and kidney causing destruction of the organs. Therefore appearance of
calcium oxalate crystals in the urine microscopy is classically seen in EG toxicity. End organ
damage also occurs by the lethal reaction of glycolic and glyoxylic acids. The accumulation of
these acids is the cradle for anion gap metabolic acidosis, rapid breathing, seizures and
unresponsiveness, heart related dysrhythmias and acute kidney injury (AKI). Renal failure also
leads to delayed excretion of the metabolites causing further damage (Jiranantakan, & Anderson,
2012).
Diagnosis of EG toxicity may not always be direct; therefore focusing on the pertinent
history, presenting signs and symptoms, high anion gap and osmolar gap is imperative. High
levels of EG, elevate the measured serum osmolality, thereby increasing the osmolar gap; the
buildup of the metabolites glycolic, glyoxylic, and oxalic acids causes the upsurge in the anion
gap and a lowering of the plasma bicarbonate level. The simultaneous presence of elevation in
the serum osmolality along with elevated anion gap is a vital clue to toxic ethylene alcohol
ingestion. Assessing concurrent intoxication with ethanol is vital information since ethanol
hinders the breakdown of the primary alcohol ethylene glycol. In situations such as the patient’s,
when the ingestion is not witnessed or the cause of severe metabolic acidosis is unknown,
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assessment of urine under a Wood’s lamp may be helpful. If the urine appears fluorescent, this
may be suggestive of ethylene glycol ingestion. However, this test is not highly specific or
sensitive, limiting its supportive function. Furthermore, the appearance of calcium oxalate
crystals (needle shaped monohydrate crystals and envelope shaped dihydrate crystals) in the
urine supports the diagnosis. The association of oxalate with calcium causes the ionized calcium
levels to decrease. Assessment of ethylene glycol level in the blood will confirm the diagnosis,
although results of the test may not be readily available. Ethylene glycol levels in the blood
greater than 50 mg/dL is commonly associated with severe poisonousness. Treatment should not
be postponed till the availability of results due to the fatality of the toxicity if treatment is
delayed. When treated promptly, kidney injury is usually not permanent. The estimated toxic
amount of ethylene glycol is 1.0 to 1.5 ml/kg. Therefore in patients presenting with increased
anion gap metabolic acidosis, EG intoxication should be ruled out primarily (Mount & DuBose,
2012).
In the present situation, the patient presents with agitation, combativeness and
deliriousness. The patient’s neurological status has deteriorated requiring intubation. The patient
has severe anion gap metabolic acidosis, with a pH of 7.23. The patient has a high osmolal gap
of 34 mOsm/kg, there are calcium oxalate crystals seen in the urine, and the urine appeared
fluorescent under the Woods lamp. Putting all the pieces of information together, ethylene glycol
toxicity is the most likely diagnosis in the patient, although the final confirmation can be made
after obtaining the results of the serum ethylene glycol level by gas chromatography (GC). GC is
the gold standard for the measurement of toxic alcohol levels in the blood. Treatment should not
be delayed due to the non-availability of the toxic alcohol levels due to the deleterious effects of
the toxic metabolites. Ruling out the other possible causes of increased anion gap metabolic
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acidosis will assist the practitioner in further tapering the differential diagnosis list (Jiranantakan,
& Anderson, 2012).
Methanol Intoxication. Methanol is an alcohol that is present in products such as
windshield fluid, fuels, and moon shine alcohol. Unlike ethylene glycol, consuming methanol
causes burning, and is distasteful. Therefore methanol is not as commonly ingested as ethylene
glycol. The toxic byproduct of methanol metabolism is formic acid, which is accountable for the
anion gap metabolic acidosis in methanol intoxication. Signs and symptoms of methanol
intoxication may range from abdominal distress, mild neurological symptoms, throbbing
headache, to lethargy, seizures and coma. Formic acid also causes vision loss due to irreversible
damage to the optic nerve classically seen with methanol toxicity. Performing a detailed
funduscopic assessment will reveal accumulation of blood in the fundus, causing bulging of the
disk and/or degeneration of the fundus. The buildup of methanol in the plasma can lead to
elevation in the serum osmolality, and the amassing of the metabolite formic acid causes the
upsurge in the anion gap, and a lowering of the plasma bicarbonate level. The simultaneous
presence of elevation in the serum osmolality along with elevated anion gap is a vital clue to
toxic methanol ingestion, which is similar to EG toxicity. Assessing concurrent intoxication with
ethanol is vital information since ethanol hinders the breakdown of the primary alcohol methanol
(Kraut & Kurtz, 2008). In methanol toxicity Kussmaul seizures can occur, and signs of metabolic
acidosis may be present such as Kussmaul respirations. Serum toxicology screen will be positive
for methanol, although the results may not be easily obtainable; osmolar gap is present along
with an increased anion gap and the serum lactate levels may be elevated (Krasowski, 2012).
Although the patient is presenting with elevation in the serum osmolality and elevated
anion gap, these abnormalities are also seen with other toxic alcohol ingestions such as EG.
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Examination of the patient’s fundus did not reveal any abnormality, and the serum lactate levels
were within normal range. Furthermore calcium oxalate crystals are not usually seen with
methanol toxicity unless there is concurrent intoxication, which is a possibility. The absolute
ruling out of methanol intoxication is possible when the results of the blood toxic alcohol levels
are available. Practitioners should not delay the treatment due to non-availability of the drug
levels, since management of EG intoxication and methanol intoxication are almost analogous
(Kraut & Kurtz, 2008).
Salicylate Poisoning. Salicylate intoxication occurs due to consumption of salicylates,
triggering perplexing acid-base disturbances presenting initially as respiratory alkalosis and later
as anion gap metabolic acidosis with wide anion gap. Patients with salicylate poisoning usually
present with nausea, vomiting, hematemesis, abdominal pain, fever, malaise, confusion,
delirium, coma, and seizures. Electrolyte abnormalities are common, along with renal
insufficiency, pulmonary edema, and electrocardiogram abnormalities such as sinus tachycardia.
Severe toxicity occurs when drug levels > 300 mg/kg. The blood glucose is usually normal or
decreased, ketones are not present in the blood and serum osmolality is normal. It should be
noted that salicylates may cause false-positive or false negative urinary glucose determination
(Foster, Mistry, Peddi, & Sharma, 2010).
The patient is presenting with tachypnea, confusion, delirium, and wide anion gap
metabolic acidosis, therefore including salicylate poisoning in the differential diagnosis seems
appropriate. However the patient also has elevated serum osmolality, her temperature is within
normal range and she does not have signs of pulmonary edema rendering salicylate poisoning
highly unlikely. The differential diagnosis may be ruled out when the results of the blood
toxicology results are available, although salicylate poisoning seems unlikely (Brent, 2009).
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Lactic Acidosis. An important factor causing increased anion gap metabolic acidosis is
lactic acidosis. Lactic acidosis occurs due to the accumulation of lactate in the blood, caused by
decreased oxygen rich blood supply to the tissues, which then switch to anaerobic metabolism
causing buildup of lactate. Therefore, levels greater than 5 mmol/mL of lactate in the serum,
along with low pH (<7.3), blood bicarbonate levels of less than 8 mEq/L, and anion gap of more
than 30 mEq/L are indicative of lactic acidosis. Signs of lactic acidosis are hypotension,
tachypnea, nausea, lethargy, restlessness, tachycardia, irregular heart rate, and abdominal
discomfort. In lactic acidosis there is usually wide anion-gap metabolic acidosis as seen in the
patient along with elevated serum lactate levels confirming the diagnosis. The patient’s lactate
level is 1.1 mmol/L, which is within normal range ruling out lactic acidosis as one of the causes.
Glycolate, a byproduct of ethylene glycol metabolism, can lead to a falsely elevated lactic acid
level, causing misdiagnosis and leading to inappropriate patient management. Considering the
patients history, there is no evidence that the patient has any underlying infection, tissue
hypoperfusion, diabetes, or genetic disorder that could lead to lactic acidosis. Her temperature is
within normal range, there is no elevation in WBC, and chest x-ray did not show any infiltrates.
Therefore lactic acidosis may be ruled out in the patient (Galla, Kurtz, Kraut, Lipschik, &
Macrae, 2009).
Alcohol Ketoacidosis (AKA). AKA is seen in patients who are addicted to alcohol and
in whom alcohol is the main source of energy due to poor oral intake. The ketoacidosis occurs
when the individual does not consume alcohol for some time and caloric consumption is
reduced. In AKA the anion gap is high, the metabolic acidosis is usually moderately high,
accompanied with high plasma ketones, absent blood alcohol, and hypoglycemia. The patient is
presenting with a pH of 7.23, anion gap of 33 and PCO2 of 23. Moreover, as per the patient’s
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history she has been drinking one pint of vodka per day for the last several months; but there is
no information regarding the date and time of her last alcoholic drink. There is a possibility that
the patient may not have consumed alcohol for some time and has been starving herself, making
AKA a possible differential diagnosis. However there are no ketones detected in the plasma, and
the patient’s blood sugar is within normal range generating AKA as an unlikely diagnosis (Galla,
Kurtz, Kraut, Lipschik, & Macrae, 2009).
Final Diagnosis
The confirmation of the absolute diagnosis was made when the toxic drug levels were
available. The patient’s serum ethylene glycol level by gas chromatography (GC) displayed the
level as 310 mg/dL; levels >50mg/dL are considered toxic. GC is the gold standard for the
measurement of toxic alcohol levels in the blood. The patient’s blood levels did not display the
presence of any ethanol, methanol, isopropyl alcohol, salicylates or acetaminophen. Therefore
the patient was treated appropriately for ethylene glycol toxicity (Jiranantakan & Anderson,
2012).
Diagnostic Tests
Diagnostic tests are very valuable to practitioners because they support the presumptive
diagnosis that is made based on the patient’s clinical presentation and history. Diagnostic test not
only help endorse a particular diagnosis, but also are important to rule out the differential
diagnosis. The diagnostic tests that may be beneficial in managing a patient with ethylene glycol
toxicity are as follows.
Diagnostic Test
Electrolytes
Rationale
To assess sodium, potassium, calcium, magnesium, phosphorus,
and chloride levels
To assess anion gap
Hypokalemia is seen in salicylate poisoning
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Serum glucose
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To rule out diabetic ketoacidosis and alcohol ketoacidosis
Salicylate overdose can increase blood glucose initially
Blood Urea Nitrogen
To assess kidney function
Creatinine
To assess if uremia is the cause of anion gap metabolic acidosis
BUN/Creatinine ratio
Ethylene glycol toxicity can cause renal tubular necrosis
Blood Calcium level
The association of oxalate (metabolite of ethylene glycol) with
calcium causes the ionized calcium levels to decrease.
Hepatic aminotransferases
(ALT, AST)
To assess liver function
Elevated levels indicate liver damage. EG is metabolized by the
liver.
Probable reasons for high AST and ALT are hepatic inflammation,
trauma, damage to the heart, AKI, and drug or alcohol
intoxication.
Serum lactate level
Complete blood cell count
Nitroprusside reaction test
To rule out lactic acidosis, as this is the most usual source of
severe metabolic acidosis.
A serum lactate level of greater than 5 mEq/L is indicative of
lactic acidosis
Diagnosis of lactic acidosis is made when the lactate levels are >5
mEq/L, pH <7.3, blood bicarbonate levels <8mEq/L, and anion
gap is > 30 mEq/L
Elevated lactate levels are seen in tissue hypoperfusion, metformin
toxicity, sepsis, renal and hepatic injury
To assess for anemia, infection, and level of platelets.
To rule out DKA and AKA for assessing the presence of
acetoacetate, beta hydroxybutyrate
The test is used to assess ketone bodies in the urine.
Salicylate poisoning
Nitroprusside reaction test could be slightly positive or negative
with concomitant lactic acidosis.
Serum betahydroxybutyrate levels
Helps distinguish ethylene glycol intoxication from AKA, which
also increases anion and Osmole gaps
Patients with AKA may not have markedly positive tests for
ketones, but the beta-hydroxybutyrate levels will usually be
elevated
Pregnancy test
To check if patient is pregnant. Done in women of reproductive
stage.
Calculated serum
osmolality
Serum osmolality analyzes the aggregate of substances present in
the blood.
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High levels are seen in dehydration, DKA, uremia, substance
intoxication, such as ethylene glycol, methanol, and isopropanol.
To assess the cause of high anion gap metabolic acidosis
Calculated serum osmolatity (SO) is measured as follows
SO= 2 (Na + K) + (glucose/18) + (BUN/2.8)
Measured serum osmolality
Serum osmolality may also be assessed in a direct process by
“freezing point depression”
Osmolal gap
The test assesses the possible cause of high anion gap metabolic
acidosis
To obtain the osmolal gap subtract the calculated osmolality from
the measured osmolality
A high Osmolal gap in the presence of high anion gap metabolic
acidosis indicates that there is another osmotically active solvent in
the blood stream.
An increase in the osmolal gap may be caused by ingestion of
compounds such as ethanol, ethylene glycol, methanol, isopropyl
alcohol.
The osmolal gap test does not have the capacity to distinguish
between as ethanol, ethylene glycol, methanol and isopropyl
alcohol intoxication.
When the osmolal gap is greater than 10 usually indicates that the
elevation is due to either ethylene glycol or methanol poisoning
Isopropanol intoxication can cause osmolar gap, but it does not
cause anion gap metabolic acidosis.
Measuring the osmolar gap can help with the approximation of the
amount of methanol and ethylene glycol ingested.
Osmolal gap is insensitive if test is delayed and when ethylene
glycol and methanol are totally broken down to their metabolites
Ingesting small amounts of the toxic components may not always
increase the osmolal gap affecting the treatment plan
Calculation of anion gap
High levels indicate the presence of high anion gap metabolic
acidosis
Blood ketones
To assess or rule out DKA and AKA
To assess the cause of high anion gap metabolic acidosis
Serum methanol level
When osmolar gap is high the cause is usually due to the ingestion
of toxic alcohol such as methanol
To detect the presence of methanol level in the blood when
intoxication is suspected
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If there is a delay in checking the level of methanol level the test
may be not be accurate due to the compound being already
metabolized into its byproduct
Serum ethylene glycol
level
When osmolar gap is high the cause is usually due to the ingestion
of the compound
To detect the presence of ethylene glycol in the blood if ethylene
glycol intoxication is suspected. Levels greater than 50 mg/dL are
normally linked with severe inebriation.
The test is usually conducted by gas chromatography (GC), and
may not be available readily in all facilities. Therefore treatment
should not be delayed due to the non-availability of the test result.
If there is a delay in checking the level of ethylene glycol the test
may be not be accurate due to the compound being already
metabolized into its byproducts glycolic acid, glyoxylic acid, and
oxalic acid.
Serum glycolic acid
Toxic metabolite of ethylene Glycol, is definitive diagnosis
Blood ethanol level
When osmolar gap is high the cause may be due to the ingestion of
the ethanol
Concurrent ingestion of ethanol with ethylene glycol or methanol
affects the rate at which the toxic alcohols are metabolized.
Absence of alcohol in the blood in patients who are alcoholic
indicates alcohol ketoacidosis.
The ketoacidosis occurs when the individual does not consume
alcohol and caloric consumption is reduced
Blood acetaminophen level
To rule out concurrent ingestion of acetaminophen
ECG
To rule out cardiac involvement
Sinus tachycardia is seen in salicylic acid poisoning
To rule out electrical conduction dysfunction caused by elements
that influence the QRS or QTc intervals
QTc interval may be prolonged in patients with ethylene glycol
toxicity due to the association of oxalic acid with calcium thereby
causing hypocalcemia.
ABG
To assess the pH, PCO2, Bicarbonate, PO2, oxygen saturation and
base excess.
To assess acid base abnormalities and oxygenation status
Prothrombin Time (PT)
PT will be prolonged in salicylate poisoning
Urine microscopy for
oxalate crystals
In ethylene glycol poison to assess the presence of oxalate crystals
(needle shaped and envelope shaped) in the urine those are formed
COMPREHENSIVE CLINICAL CASE STUDY
19
by the association of oxalic acid and calcium.
This test is lacks specificity
Urinalysis
To check for hemoglobinuria, myoglobinuria, and infection
Urine ketones to rule out DKA
Assess urine osmolality
To assess the presence of glucose in urine, indicative of DKA
Urine testing under the
Wood’s lamp
In ethylene glycol poison the urine appears fluorescent due to the
presence of fluorescein in antifreeze. Consumption of antifreeze is
the main source of ethylene glycol poisoning.
The test lacks sensitivity and specificity, since all solutions of
ethylene glycol may not contain added fluorescein, nor does all
urine specimens that appear fluorescent are indicative of EG
toxicity.
Urine ketones
To rule out DKA
To assess the cause of high anion gap metabolic acidosis
Urine drug screen
To rule out coexistence of drug overdose with the following
compounds; phencyclidine, benzodiazepine, cocaine,
amphetamine, tetrahydrocannabinol (marijuana), opiates,
barbiturates, and tricyclic antidepressants.
Cardiac enzyme
To assess cardiac involvement
Glomerular Filtration Rate
(GFR)
Monitoring urine output,
cysteine C, complete blood
count, creatinine
phosphokinase,
hyperkalemia,
hypocalcemia, urine
sodium, urine osmolality,
calculating fractional
excretion of sodium.
Renal ultrasound
Chest x-ray
The most important diagnostic indicator of renal injury is a
glomerular filtration rate (GFR) of less than 30 ml per hour
To assess kidney function if kidney injury is suspected
Excellent test for diagnosing AKI
To assess for underlying infection
To assess for pulmonary edema- salicylate poisoning can damage
the lung endothelium causing leakage of fluid in the surrounding
tissue
Head CT without contrast
To rule out intracranial involvement such as edema, bleeding, and
tumor.
(Foster, Mistry, Peddi, & Sharma, 2010; Galla, Kurtz, Kraut, Lipschik, & Macrae, 2009)
COMPREHENSIVE CLINICAL CASE STUDY
20
Prioritized Plan
The management of a patient with ethylene glycol (EG) toxicity should take into
consideration the amount of EG consumed, the time of consumption to commencement of
medical treatment, and information regarding simultaneous use of ethanol. Treatment should not
be delayed due to the high mortality risk associated with EG toxicity. When time of presentation
is delayed, the patient may already be displaying signs and symptoms of multiple organ failure
decreasing the odds of survival. The fundamental approach to EG toxicity management is the
administration of the precise antidote to interrupt the production of the toxic byproducts that are
responsible for multiple organ failure. The two chief antidotes available today for EG
intoxication are ethanol and Fomepizole. Supportive care should be provided similar to taking
care of critically ill patients with multiple organ involvement (Jiranantakan, & Anderson, (2012).
The management of a patient with ethylene glycol poisoning includes the following strategies.
Initial Management
The preliminary step of management involves safeguarding the patient’s airway,
oxygenation and organ perfusion. Severely intoxicated patients will require intubation and
ventilator support. Patient’s admitted with severe ethylene glycol toxicity may benefit from a
medical toxicologist consult, renal/nephrology consult and neurology consult for the evaluation
of anion and osmolar gaps, hemodialysis, and CNS associated complications. Seizures should be
managed by administration of anti-seizure medications such as Lorazepam 1 mg every 4 hours as
needed, and Dilantin 100 mg IV every 8 hours (Jiranantakan, & Anderson, (2012).
Drug of Choice
Ethylene glycol poisoning can cause serious metabolic acidosis, acute kidney injury, and
when not promptly treated may even lead to mortality. The parent compound ethylene glycol by
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21
itself does not cause any major deleterious effects. The toxic effects occur once the liver
metabolizes the compound into its harmful byproducts glycolic acid, glyoxylic acid, and oxalic
acid. The enzyme that is responsible to initiate the metabolism of ethylene glycol in the liver is
alcohol dehydrogenase (ADH). Therefore, inactivating this enzyme will hinder the production of
the toxic metabolites. The drug of choice for the treatment of ethylene glycol poisoning is
Fomepizole which acts by inhibiting the action of ADH. In a retrospective, multicenter cohort
study conducted by Levine and colleagues in 2012, patients with ethylene glycol poisoning were
treated with Fomepizole alone and had good outcomes. Traditionally EG toxicity was treated
with the administration of alcohol intravenously and by hemodialysis. The recent introduction of
the drug Fomepizole in 1997 has replaced the practice of alcohol administration due to its ease of
use and superior outcomes. Ethanol is a competitive ADH substrate, and fomepizole acts as an
ADH inhibitor. However, fomepizole has superseded ethanol as the antidote of choice in most
settings in the United States (Levine et al, 2012).
Case Review. In search of an ideal antidote for the management of ethylene glycol
intoxication, Beatty and colleagues conducted a systematic review in 2013. This review included
studies from 1996 to 2010. The review involved 145 studies which included the use of ethanol
and/or fomepizole for the treatment of ethylene glycol toxicity in adults who presented to the ER
within 72 hours of exposure to the toxin. A total of 897 patients were acknowledged; 720 (80%)
were managed with ethanol, 146 (16.3%) were managed with fomepizole, and 33 (3.7%) with
both antidotes. Patients with ethylene glycol toxicity, treated with ethanol had an 18.1%
mortality rate, compared to 4.1% when treated with fomepizole. The disadvantages of using
ethanol as an antidote include the need for a central venous catheter, difficulty in sustaining
acceptable plasma concentration of ethanol, low blood sugar, depression of the central nervous
COMPREHENSIVE CLINICAL CASE STUDY
22
system, bizarre behavior and prolonged necessity to be intubated. Compared to ethanol,
fomepizole had safer side effects, the pharmacokinetics and pharmacodynamics of fomepizole
were well anticipated, the hospital and intensive care unit stay was shorter, and fewer patients
required dialysis. Due to all these major benefits, fomepizole has surpassed ethanol as the key
drug of choice in the treatment of alcohol (Beatty, Green, Magee, & Zed, 2013). According to a
2009 Report by the American Association of Poison Control, fomepizole was utilized in more
than 1740 cases of toxic alcohol consumption, compared to only approximately 95 cases in
which ethanol was executed, therefore displaying its efficacy and success (Bronstein et al.,
2010).
Fomepizole. Fomepizole is the antidote for the treatment of ethylene glycol toxicity. The
brand name of Fomepizole is Antizol. Treatment with Fomepizole should be started promptly
upon suspicion of EG toxicity (Lexi comp., 2013).
Mechanism of Action. Fomepizole antagonizes the action of the enzyme ADH, which
promotes the metabolism of EG, initially to glycoaldehyde. Glycoaldehyde is then transformed
to glycolate, glyoxylate, and oxalate by the oxidation process. Glycolate and oxalate are
accountable for the anion gap metabolic acidosis and acute tubular necrosis of the kidneys
(Comp., 2013).
Pharmacodynamics/Kinetics. The onset of action of Fomepizole is within one to two
hours. It is readily absorbed orally and is rapidly distributed into the body fluid when given
intravenously. It minimally binds to proteins. Fomepizole is metabolized by the liver and
excreted by the kidneys. The half-life of Fomepizole is not known (Lexi Comp., 2013).
Indications. Fomepizole is recommended for the management of EG poisoning. It is also
used as an antidote for methanol intoxication (Lexi Comp., 2013)
COMPREHENSIVE CLINICAL CASE STUDY
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Contraindications. Fomepizole is contraindicated in patients with history of
hypersensitivity to the drug (Lexi Comp., 2013).
Dosage. Initially Fomepizole is given as a loading dose of 15 mg/kg intravenously (IV).
Subsequently the dose consists of 10 mg/kg IV administered every 12 hours for 4 doses. Further
dosages consist of 15 mg/kg every 12 hours while waiting for EG levels to decline to <20
mg/dL, witness improvement of patient’s symptoms, and normalization of pH (Lexi comp.,
2013). If patient develops renal failure and requires hemodialysis, adjustment of dosage is
required (Lexi Comp, 2013).
Precautions. Fomepizole should be administered carefully in patients with liver and
kidney impairment since the drug is metabolized in the liver and excreted by the kidneys. If
severe kidney impairment is noted, and when ingested levels of EG are high, hemodialysis may
be necessary (Lexi Comp., 2013).
Administration. Fomepizole should always be administered diluted in 100 ml of 0.9%
sodium chloride or 5% dextrose solution, and given as a slow IV infusion over a period of half
hour. Fomepizole should never be given as a bolus (Lexi Comp., 2013).
Adverse Effects. Fomepizole can cause the following adverse effects, headache, GI
distress, cardiac dysrhythmia, hypotension, rash, elevated liver enzymes, anemia, phlebitis,
arthralgia, visual changes, anuria, hiccups, pharyngitis, and multi organ failure (Lexi Comp,
2013).
Drug Concentration. Literature supports Fomepizole levels of greater than 0.8 mg/L is
sufficient to deliver continuous inhibition of the enzyme ADH (Lexi Comp., 2013).
Drug Interaction. Fomepizole is not known to interact with other drugs (Lexi Comp,
2013).
COMPREHENSIVE CLINICAL CASE STUDY
24
Ethanol Interaction. The elimination of Fomepizole is decreased by approximately 50%
with the administration of ethanol (Lexi comp., 2013).
Storage. Fomepizole should be stored at room temperature (Lexi Comp., 2013).
Cost. The estimated cost of Fomepizole is approximately $ 370 to 550 per dose (Brent,
2009)
APN Authority to Prescribe: According to the Ohio Board of Nursing, 2013, an
advanced practice nurse (APN) with a valid certificate to prescribe has the authority to prescribe
Fomepizole in the State of Ohio, within the APNs scope of practice.
Ethanol
If the decision is made to give ethanol instead of Fomepizole due to unavailability of the
drug or due to other factors, the regimen of ethanol administration is as follows. The suggested
plasma ethanol concentration is 100 to 150 mg/dL, and may be administered intravenously (IV),
orally, or through a nasogastric tube. IV ethanol should be diluted in a solution of five percent
dextrose, and initially given as a loading dose of 8 to 10 ml/Kg over a half hour period, followed
by a continuous infusion of 1.4 to 2.0 mL/Kg/hour (Scalley, Ferguson, Smart, & Archie, 2002).
Hemodialysis
Although treatment with fomepizole helps inhibit the formation of toxic metabolites to
some extent, it does not totally halt the formation of the metabolites. Even though the body is
well designed to securely breakdown the toxic metabolites, production of enormous quantity of
byproducts renders the body incapable. Therefore, some patient’s will require hemodialysis due
to the long half-life of EG; also EG and its metabolites are minute compounds that can be easily
dialyzed. A nephrologist should be consult when ethylene glycol toxicity is suspected. The
indicators for hemodialysis consist of, deteriorating health status, severe metabolic acidosis (pH
COMPREHENSIVE CLINICAL CASE STUDY
25
<7.3), acute kidney injury (serum creatinine >3.0 mg/dL), electrolyte disorders, and ethylene
glycol levels that are not declining, or insensitivity to the antidote. Even though hemodialysis is
initiated the patient will still require treatment with the antidote while the patient is on dialysis.
The dosage of fomepizole is 15mg/kg IV over half an hour every four hours. The dosage and
time of administration of fomepizole will vary when hemodialysis is stopped depending on the
patient’s clinical status (Kruse, 2012).
Some professionals support the use of recurrent doses of fomepizole without
hemodialysis in patients with mild exposure to ethylene glycol, without pronounced academia,
and/or without kidney injury. There is not adequate evidence available to obviate the use of
hemodialysis in patients with ethylene glycol toxicity. Clinicians are encouraged to make the
decision regarding dialysis on a case to case basis (Kruse, 2012).
According to the American Academy of Clinical Toxicology guidelines, to prevent
Wernicke-Korsakoff syndrome, a daily dose of thiamine 100 mg and vitamin B6 50 mg
intravenously, is recommended in patients who chronically use alcohol, and withdrawal is
anticipated. Administration of sodium bicarbonate may be necessary to correct systemic
academia and prevent end organ damage. A sodium bicarbonate dose of 1-2 mEq/kg may be
given IV as a bolus, and then as a continuous infusion of 132 mEq in one liter of 5% dextrose, to
run at 200 to 250 mL/hour if the patient’s pH is <7.3. Replacement of calcium may be necessary
in patients who develop hypocalcemia, to prevent tetany and seizures (Scalley, Ferguson, Smart,
& Archie, 2002).
Supportive Care
Temperature, blood pressure, heart rate, and respirations should be monitored at least
once every hour and more frequently during the initial course of treatment. The patient should be
COMPREHENSIVE CLINICAL CASE STUDY
26
placed on a continuous cardiac monitor. Blood pressure should be adequately maintained to
prevent hypotension or hypertension. An increase in temperature should be appropriately treated
and if necessary blood cultures and antibiotic therapy should be started if infection is suspected.
Cardiac dysrhythmias are common in toxicity; EKG should be obtained if patient develops
arrhythmia. Monitoring daily weight, intake and output is imperative; inserting a Foley catheter
may be beneficial to monitor strict urine output and assess kidney function. Blood sugar should
be assessed every six hours to prevent hypoglycemia or hyperglycemia. Patients on bed rest
should have bilateral lower extremity sequential compression devices, and Lovenox 40 mg
subcutaneously daily, to prevent deep vein thrombosis. Intravenous fluids may be necessary to
maintain adequate perfusion and hydration. Optimal oral care and suction of secretions is crucial
to prevent the patient from developing secondary infections such as ventilator associated
pneumonia (Krasowski, M. (2012).
Follow Up
Effectiveness of the treatment should be monitored by the assessment of patient’s
condition, anticipating improvement in clinical status. Serial assessment of ethylene glycol levels
in the blood and urine, urine oxalate crystals, osmolality of the blood and urine, hepatic function,
comprehensive metabolic panel to assess renal function and electrolytes, ABGs, and anion and
osmolar gaps, should be carried out throughout the course of treatment to assess the trend in
clinical standing. Since ethylene glycol toxicity causes issues with kidney function, central
nervous depression, and cardiac dysrhythmia, follow up of the patient will depend on the severity
of the underlying effects of the toxicity, and the capacity to treat these conditions. The number of
days the patient may require ventilatory support, the duration of dialysis, and management of
neurological deficits will differ from patient to patient. Nonetheless, all patients will need to be
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27
closely monitored initially in an ICU setting. Every effort should be made to wean the patient off
the ventilator as quickly as possible. As the patient’s condition improves and patient is able to
participate in the care, a behavioral consult and substance abuse counseling should be initiated.
The poison control center should be informed when patients with drug overdose and suicide
attempt are admitted (Mount & DuBose, 2012).
Patients who are completely back to baseline should be discharged to the psychiatric
department for further management of the psychological issues. Some patients may need long
term dialysis, while others may require long term physical therapy and nursing home care.
Depending on each patients needs appropriate referrals should be made. Patients who are being
discharged home should have close supervision during the initial period. Assessment of the
patient’s home situation, support system, and the patient’s ability to cope with lifes stressors is
important if patient is being discharged home. A social service and case management consult
should be initiated to help plan with the discharge process and help introduce the patient back in
the community (Krasowski, 2012).
Health Promotion Activities
Once the patient’s condition improves and she is able to participate in the care, educating
on the hazards of consuming toxic compounds on the brain, heart, liver, kidney and the overall
quality of life is imperative. Teaching should be provided on the ill effects of alcohol ingestion,
with encouragement to stop drinking and using illegal drugs. Offering information regarding
survivor outreach programs will be beneficial to the patient for coping with future life stressors.
All practitioners at every opportunity should enquire, guide, evaluate, support and make
adequate arrangements for the patient to quit smoking. The patient should be reminded to take all
her medications as per the recommendations of the prescriber. The flu and pneumonia vaccine
COMPREHENSIVE CLINICAL CASE STUDY
28
should be offered to all patients that meet the criteria. Instructing the patient on the benefits of
eating healthy and participating in daily physical activity to maintain optimal health is
imperative. The patient should be encouraged to join a social support group, alcohol anonymous,
and develop health habits and participate in healthier hobbies and interests. Involving family in
overall teaching and learning process will provide support and encouragement, and increase the
probability of success and adherence to recommendations (Kraut & Kurtz, 2008).
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