Comprehensive Clinical Case Study



Comprehensive Clinical Case StudyNeeta Monteiro, RN, BSNWright State University-Miami Valley College of Nursing and HealthNUR 7201Dr. Kristine ScordoJuly 10, 2013History and PhysicalSource of InformationInformation 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 ComplaintAltered mental status History of Present IllnessMs. 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 HistoryChildhood 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.MedicationsTrazadone 50 mg 1 tablet at HSCitalopram 10 mg 1 tablet po dailyMulti-vitamin one tablet daily poAllergies: 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 SystemsGeneral: 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 ExaminationVitals: 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 DiagnosisAfter 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 DiagnosisEthylene glycol toxicityMethanol toxicitySalicylate poisonLactic acidosisAlcoholic ketoacidosisEthylene 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 DiagnosisThe 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 TestRationaleElectrolytesTo assess sodium, potassium, calcium, magnesium, phosphorus, and chloride levelsTo assess anion gapHypokalemia is seen in salicylate poisoningSerum glucoseTo rule out diabetic ketoacidosis and alcohol ketoacidosisSalicylate overdose can increase blood glucose initiallyBlood Urea Nitrogen CreatinineBUN/Creatinine ratio To assess kidney functionTo assess if uremia is the cause of anion gap metabolic acidosisEthylene glycol toxicity can cause renal tubular necrosisBlood Calcium levelThe association of oxalate (metabolite of ethylene glycol) with calcium causes the ionized calcium levels to decrease.Hepatic aminotransferases (ALT, AST)To assess liver functionElevated 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 levelTo 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 injuryComplete blood cell count To assess for anemia, infection, and level of platelets.Nitroprusside reaction testTo rule out DKA and AKA for assessing the presence of acetoacetate, beta hydroxybutyrateThe test is used to assess ketone bodies in the urine. Salicylate poisoningNitroprusside 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 gapsPatients with AKA may not have markedly positive tests for ketones, but the beta-hydroxybutyrate levels will usually be elevatedPregnancy testTo check if patient is pregnant. Done in women of reproductive stage. Calculated serum osmolalitySerum 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 acidosisCalculated serum osmolatity (SO) is measured as followsSO= 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 gapThe test assesses the possible cause of high anion gap metabolic acidosisTo obtain the osmolal gap subtract the calculated osmolality from the measured osmolalityA 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 poisoningIsopropanol 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 metabolitesIngesting small amounts of the toxic components may not always increase the osmolal gap affecting the treatment planCalculation of anion gapHigh levels indicate the presence of high anion gap metabolic acidosisBlood ketonesTo assess or rule out DKA and AKATo assess the cause of high anion gap metabolic acidosisSerum methanol levelWhen osmolar gap is high the cause is usually due to the ingestion of toxic alcohol such as methanolTo detect the presence of methanol level in the blood when intoxication is suspectedIf 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 byproductSerum ethylene glycol levelWhen osmolar gap is high the cause is usually due to the ingestion of the compoundTo 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 acidToxic metabolite of ethylene Glycol, is definitive diagnosisBlood ethanol levelWhen osmolar gap is high the cause may be due to the ingestion of the ethanolConcurrent 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 reducedBlood acetaminophen levelTo rule out concurrent ingestion of acetaminophenECGTo rule out cardiac involvementSinus tachycardia is seen in salicylic acid poisoningTo rule out electrical conduction dysfunction caused by elements that influence the QRS or QTc intervalsQTc interval may be prolonged in patients with ethylene glycol toxicity due to the association of oxalic acid with calcium thereby causing hypocalcemia.ABGTo assess the pH, PCO2, Bicarbonate, PO2, oxygen saturation and base excess. To assess acid base abnormalities and oxygenation statusProthrombin Time (PT)PT will be prolonged in salicylate poisoningUrine microscopy for oxalate crystalsIn 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 specificityUrinalysis To check for hemoglobinuria, myoglobinuria, and infectionUrine ketones to rule out DKAAssess urine osmolalityTo assess the presence of glucose in urine, indicative of DKAUrine testing under the Wood’s lampIn 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 ketonesTo rule out DKATo assess the cause of high anion gap metabolic acidosisUrine 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 involvementGlomerular Filtration Rate (GFR)The most important diagnostic indicator of renal injury is a glomerular filtration rate (GFR) of less than 30 ml per hourMonitoring 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 suspectedRenal ultrasoundExcellent test for diagnosing AKIChest x-ray To assess for underlying infectionTo assess for pulmonary edema- salicylate poisoning can damage the lung endothelium causing leakage of fluid in the surrounding tissueHead CT without contrastTo rule out intracranial involvement such as edema, bleeding, and tumor. (Foster, Mistry, Peddi, & Sharma, 2010; Galla, Kurtz, Kraut, Lipschik, & Macrae, 2009)Prioritized PlanThe 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. EthanolIf 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 CareTemperature, 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 UpEffectiveness 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).ReferencesBeatty, L., Green, R., Magee, K., & Zed, P. (2013). A systematic review of ethanol and fomepizole use in toxic alcohol ingestion. Emergency Medicine International, 2013, 1-14 Retrieved from , J. (2009). Fomepizole for ethylene glycol and methanol poisoning. New England Journal of Medicine, 360(21), 2216-2223. Doi: 10.1056/NEJMct0806112Bronstein, A. C., Spyker, D. A., Cantilena, L. R., Green, J. L. Rumack, B. H., & Giffin, S. L. (2010). 2009 Annual Report of the American Association of Poison Control Centers’ National Poison Data System (NPDS): 27th Annual Report. Clinical Toxicology (Philadelphia, P.A.), 48(10):979-1178. Retrieved from Foster, C., Mistry, N. F., Peddi, P. F., & Sharma, S. (2010). The Washington manual of medical therapeutics. Philadelphia, PA: Lippincott Williams & Wilkins. Galla, J. H., Kurtz, I., Kraut, J. A., Lipschik, G. Y., & Macrae, J. P. (2009). Chapter 5. Acid-base disorders. In E. V. Lerma, J. S. Berns, A. R. Nissenson (Eds), Current Diagnosis and Treatment: Nephrology & Hypertension. Retrieved July 12, 2013 from , T., & Anderson, I. B. (2012). Chapter 68. Ethylene glycol and other glycols. In: K. R. Olson (Ed), Poisoning & Drug Overdose. 6e. Retrieved July 12,2013 from , M. (2012). Toxic alcohols. Clinical Laboratory News, 38(2), 1-6. Retrieved from publication/cln/2012/February/pages/ToxicAlcohol.aspxKraut, J. A. & Kurtz, I. (2008). Toxic alcohol ingestion: Clinical features, diagnosis, and management. Clinical Journal of the American Society of Nephrology, 3(1), 208-225. Retrieved from , J. (2012). Methanol and ethylene glycol intoxication. Critical Care Clinics, 28, 661-711. Retrieved from , M., Curry, S. C., Ruha, A. M., Pizon, A. F., Boyer, E., Burns , J.,… Gerkin, R. (2012). Ethylene glycol elimination kinetics and outcomes in patients managed without hemodialysis. Annals of Emergency Medicine, 59(6), 527-531. Retrieved from Lexi Comp, Inc. (2013). Lexi-DrugsTM: Fomepizole [Smart-phone application]. Accessed July 15, 2013. Mount, D. B., & DuBose, T. D. (2012). Chapter e15. Fluid and electrolyte imbalances and acid-base disturbances: Case examples. In D. L. Longo, A. S. Fauci, D. L. Kasper, S. L. Hauser, J. L. James, & J. Loscalzo (Eds), Harrison’s Principle of Internal Medicine, 18e. Retrieved July 11, 2013 from Board of Nursing, (OBN). (2013). The formulary developed by the Committee on Prescriptive Governance. Retrieved from , R., Ferguson, D., Smart, M., & Archie, T. (2002). Treatment of ethylene glycol poisoning. American Family Physicians, 1(66), 807-813. Retrieved from http;//afp ................
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