comprehensive clinical case study - neeta...

Running head: COMPREHENSIVE CLINICAL CASE STUDY 1

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

COMPREHENSIVE CLINICAL CASE STUDY 2

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


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 10-

20), 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.


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.


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.


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,


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


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).


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,


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,


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


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.


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).


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


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 Rationale

Electrolytes To assess sodium, potassium, calcium, magnesium, phosphorus, and chloride levels

To assess anion gap

Hypokalemia is seen in salicylate poisoning


Serum glucose To rule out diabetic ketoacidosis and alcohol ketoacidosis

Salicylate overdose can increase blood glucose initially

Blood Urea Nitrogen

Creatinine

BUN/Creatinine ratio

To assess kidney function

To assess if uremia is the cause of anion gap metabolic acidosis

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 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 acidosisDiagnosis 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/LElevated lactate levels are seen in tissue hypoperfusion, metformin toxicity, sepsis, renal and hepatic injury

Complete blood cell count To assess for anemia, infection, and level of platelets.

Nitroprusside reaction test 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 beta-hydroxybutyrate 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.


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


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


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


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


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)

The most important diagnostic indicator of renal injury is a glomerular filtration rate (GFR) of less than 30 ml per hour

Monitoring urine output, cysteine C, complete blood count, creatinine phosphokinase, hyperkalemia, hypocalcemia, urine sodium, urine osmolality, calculating fractional excretion of sodium.

To assess kidney function if kidney injury is suspected

Renal ultrasound Excellent test for diagnosing AKIChest x-ray 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)


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


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


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)


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).


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


<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


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


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


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).


References

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