Journal of Emergency Nursing
Volume 30, Issue 2 , Pages 113-116, April 2004

A 52-year-old Acyanotic Man With Severe Hypoxia and Profound Metabolic Acidosis Following an Industry Chemical Exposure☆

New Brunswick and Piscataway, NJUSA

Kathleen Evanovich Zavotsky, MS, RN, CCRN, CNS, C, CS, CEN, is Clinical Nurse Specialist, Emergency Department, Robert Wood Johnson University Hospital, New Brunswick, NJ. Philippe Mentler, PharmD, is Emergency Department Pharmacy Resident, Robert Wood Johnson University Hospital, Rutgers the State University of New Jersey, Ernest Mario School of Pharmacy, Piscataway, NJ. Craig Gronczewski, MD, is Emergency Department Attending Physician, Robert Wood Johnson University Hospital, New Brunswick, NJ. Peter Torres, MSN, RN, NP-C, is Staff Nurse, Emergency Department, Robert Wood Johnson University Hospital, New Brunswick, NJ.

Article Outline

 

A 52-year-old man presented to the emergency department complaining of nausea, vomiting, and weakness for several hours beginning when he was at work. Approximately 10 hours earlier, he had physical contact with a liquid chemical believed to be 2,4,5 trichloro-6-carbopentoxyphenyl oxylate. The patient admitted that he had removed his respirator several times while working with the chemical because he was not feeling well. He changed his uniform before leaving work for the day.

Approximately 2 to 4 hours after the exposure, he felt nauseous and began vomiting. He attributed this to the “flu” with which members of his family were ill. When his symptoms became so severe that he was unable to stand without assistance, his family called 911.

Upon arriving at the emergency department, the staff opted to decontaminate the patient because of his poor history and their risk of secondary contamination. During primary decontamination, the staff removed the patient's clothing and escorted him into the decontamination room. Secondary decontamination involved a 15-minute shower with copious amounts of water and a mild soap. The staff performing the decontamination wore personal protective equipment consisting of a Tyvex suit and a positive pressure ventilation hood using supplied air because of the uncertainty of the exposure.

The patient's vital signs after decontamination were as follows: temperature, 37°C (98.6°F); heart rate, 109 beats per minute; respiratory rate, 20 breaths per minute; blood pressure (BP), 110/38 mm Hg; and SaO2, 98% on room air. The patient was awake, alert, and oriented to person, place, and time. He was still vomiting and complained of mild upper abdominal pain. To assist us in caring for this patient, we notified the hospital pharmacist, County HAZMAT Team, nursing supervisor, the Poison Control Center, and the patient's employer, who immediately provided us with the material safety data sheet (MSDS) for 2,4,5 trichloro-6-carbopentoxyphenyl oxylate. This chemical is a colorless solid or liquid form of oxalic acid that is used in the production of glow sticks used for nighttime events. There is no antidote for the exposed patient; the clinical presentation guides treatment.

We hydrated the patient intravenously with 0.9% normal saline solution at 125 mL/hr for 10 hours and administered metoclopramide (Reglan), 10 mg intravenously every 4 hours as needed. His abnormal laboratory results were as follows: white blood cells, 15 thousand/mm3 (normal, 4 to 10 thousand/mm3); lipase, 93 U/L (normal, 15 to 60 U/L); total bilirubin, 1.4 mg/dL (normal, 0.1 to 1.2 mg/dL); aspartate aminotransferase, 50 IU/L (normal, 12 to 45 IU/L); creatinine, 1.8 mg/dL (normal, 0.5 to 1.2 mg/dL); and anion gap, 19.1 mEq/L (normal, 4 to 12 mEq/L). His blood urea nitrogen (BUN) level was 21 mg/dL (normal, 6 to 23 mg/dL). Based on these laboratory findings and the patient's presentation, we evaluated and treated him for acute biliary disease and possible pancreatitis. Results from his chest and abdominal radiographs were negative.

…the patient's employer…immediately provided us with the material safety data sheet for 2,4,5 trichloro-6-carbopentoxyphenyl oxylate. This chemical is a colorless solid or liquid form of oxalic acid that is used in the production of glow sticks used for nighttime events. There is no antidote for the exposed patient; the clinical presentation guides treatment.

After remaining in the emergency department for 10 hours, the patient became acutely confused with a BP of 80/30 mmHg. (This was 18 to 20 hours after exposure.) His heart and respiratory rates increased to 120 beats per minute and 40 breaths per minute. Results of an abdominal ultrasound were negative. The surgical team determined that he did not have an acute abdominal emergency.

The patient's agitation became unmanageable, so we sedated and intubated him. His temperature increased to 38.9°C (102°F). Results of his laboratory tests revealed that his BUN and creatinine were now 26 mg/dL and 2.3 mg/dL, respectively, with associated oliguria, and a lactate level of 10.16 mmol/L (normal, 0.5 to 2.2 mmol/L), indicating profound metabolic acidosis. We actively resuscitated him with 0.9% normal saline solution administered intravenously at 250 mL/hr and started a phenylephrine (Neosynephrine) drip at 0.1 mcg/kg/min that was titrated to keep his systolic BP >100 mmHg. Results of a urine toxicology screen revealed cocaine and a thiocyanate level >64 mcg/mL (normal for a nonsmoker, 1 to 4 mcg/mL, and for a smoker, 7 to 17 mcg/mL). His drug use may have interfered with our ability to obtain an accurate history.

Because our patient had an acute, unexpected change in his vital signs and symptoms and because he now could not provide us with any information, we called his employer again to ask if the patient could have been exposed to any other chemical. He provided us with an MSDS for acetonitrile.

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Discussion 

Acetonitrile is a very flammable solvent found in industrial and laboratory applications. It is relatively nontoxic, but the liver can convert it to the toxic metabolite cyanide. Toxicity may be delayed for several hours (range, 3 to 24 hours).

Cyanide is one of the most rapidly acting lethal poisons.1 It is commonly found in the end-products of combustion, in cigarette smoke, cosmetic nail glue remover, metal, wood, plants, and the pits of peaches and apricots. Cyanide may result from the breakdown of sodium nitroprusside if the drug is administered at high doses or for prolonged periods. Often a history of cyanide exposure is unavailable, and depending on the hospital setting, it may take several hours or days to receive serum cyanide analysis results.2., 3.

Once absorbed by the body, cyanide causes a shift towards anaerobic metabolism, as demonstrated by our patient's large anion gap, metabolic acidosis, and elevated lactate level. Clinical manifestations begin in highly metabolic and oxygen-dependent tissues, such as the brain and heart. Three to 4 hours after exposure, our patient experienced tachycardia and hyperpnea, typical symptoms of mild cyanide poisoning. Additional symptoms of cyanide toxicity can include headache, dizziness, drowsiness, giddiness, confusion, cardiovascular collapse, arrhythmias, hypotension, seizures, and death. When our patient came to the emergency department, he was unable to ambulate. His condition progressed to a profound alteration in mental status with severe lactic acidosis and hypotension that required intubation 18 to 20 hours after exposure. Small amounts of cyanide are excreted in the lungs and sweat and may produce a bitter almond odor that about 50% of the population can detect.4 None of our staff was able to detect the odor.

Cyanide is one of the most rapidly acting lethal poisons. It is commonly found in the end-products of combustion, in cigarette smoke, cosmetic nail glue remover, metal, wood, plants, and the pits of peaches and apricots.

Suspect cyanide toxicity in all acyanotic patients who have signs of severe hypoxia.5 Dermal decontamination is rarely necessary for cyanide exposures, but EMS or ED staff should remove wet clothing and decontaminate the patient with copious amounts of water and a mild soap. Once we determined that our patient had cyanide toxicity, we administered 300 mg of 3% sodium nitrite intravenously over 10 minutes followed by 12.5 g of 25% sodium thiosulfate intravenously over 10 minutes, according to the directions on the Cyanide Antidote Package (Taylor Pharmaceuticals, Decatur, Ill).6

Nitrites promote the generation of methemoglobin. Cyanide has a greater affinity for methemoglobin than for hemoglobin, so normal cellular gas exchange is preserved. Nitrites also cause vasodilation, which, theoretically, would increase oxygen delivery to tissue.7., 8. Amyl nitrite ampules also are available in the kit, but we did not use them on our patient. The injectable sodium nitrite is preferred over the inhaled amyl nitrite because of its longer half-life and more reliable methemoglobin production.7 Consider using the amyl nitrite ampules for patients who do not have intravenous access or when there may be a delay in administering the intravenous sodium nitrite. Patients should have a methemoglobin level drawn 30 minutes after the dose and, if necessary, have sodium nitrite administered at half the dose at least 1 hour after the first dose.

Methemoglobinemia is intrinsically toxic at concentrations >30%, causing hypoxia, cardiovascular collapse, and death. However, reports cite therapeutic efficacy with methemoglobin concentrations as low as 2%. The maximum desired levels for methemoglobin are 20% to 30%, to prevent toxicity from the sodium nitrite.8., 9. Methylene blue may be used in instances of significant methemoglobinemia toxicity. Our patient's methemoglobin level at 30 minutes was 6.1%.

Suspect cyanide toxicity in all acyanotic patients who have signs of severe hypoxia.

Sodium thiosulfate enhances the body's own mechanism of cyanide detoxification by allowing enzymatic pathways to convert the cyanide bound methemoglobin into thiocyanate, a nontoxic substance that is readily excreted by the kidneys. Adverse effects are relatively nontoxic but may include abdominal pain, nausea, and vomiting and seem to be related to the rate of infusion. Our patient did not experience any adverse effects during the treatment. Immediately following the administration of the sodium nitrite, sodium thiosulfate, and 2000 mL of intravenous fluid, our patient's condition began to improve. His BP was 119/57 mmHg; heart rate, 106 beats per minute; and his temperature was 38.3°C (101°F). We titrated the phenylephrine down slowly to keep his systolic BP >100 mmHg and transported him to the Coronary Care Unit, where he continued to stabilize. His metabolic acidosis and BUN and creatinine levels returned to normal within 12 hours.

Staff in the ICU monitored our patient for approximately 72 hours. He had an acute episode of confusion shortly after being transferred to a medical-surgical floor, and the staff treated him with sodium nitrate and sodium thiosulfate as a precaution; acetonitrile has an unpredictable rate of absorption and a long half life (32 to 36 hours) with delayed effects. He was discharged home after 6 days in the hospital, without any detected permanent effects of the cyanide toxicity.

Patients who come in with hazardous material exposures usually have been involved in industrial or agricultural accidents.

Chemical hazards are relatively uncommon and statistically represent less than 1% of all ED admissions.10 Patients who come in with hazardous material exposures usually have been involved in industrial or agricultural accidents.10 The ED staff has to weigh the protection of staff, patients, and families over the care of the victim. Patients who do not divulge information about their potential contamination place emergency care providers as well as other patients at risk.

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References 

  1. Kampe S, Iffland R, Korenkov M, Diefenbach C. Survival from a lethal blood concentration of cyanide associated intoxication. Anaesthesia. 2000;55:1189–1191
  2. Brueske P. ED management of cyanide poisoning. J Emerg Nurs. 1997;23:569–573
  3. Baud FJ, Borron SW, Megarbane B, Trout H, Lapostolle F, Vicaut E, et al.  Value of lactic acidosis in the assessment of the severity of acute cyanide poisoning. Crit Care Med. 2002;30:2044–2050
  4. Mushoff F, Schmidt P, Dalrup T, Burkhard M. Cyanide fatalities: case studies of four suicides and one homicide. Am J Forensic Med Pathol. 2002;23:315–320
  5. Greenfield RA, Brown BR, Hutchins JB, Iandolo JJ, Jackson R, Slater LN, et al.  Microbiological, biological, and chemical weapons of warfare and terrorism. Am J Med Sci. 2002;323:326–340
  6. Cyanide antidote kit for the treatment of cyanide poisoning. Decatur (IL): Taylor Pharmaceuticals; 1998;
  7. Baskin S, Horowitz A, Nealley E. The antidotal action of sodium nitrite and sodium thiosulfate against cyanide poisoning. J Clin Pharmacol. 1992;32:368–375
  8. Kerns W, Isom G, Kirk M. Cyanide and hydrogen ions. In: Goldfrank's Toxicologic Emergencies. 7th ed. New York: McGraw-Hill; 2002;p. 1498–1510
  9. Hall AH, Doutre WH, Ludden T, Kulig KW, Rumack BH. Nitrite/thiosulfate treated acute cyanide poisoning: estimated kinetics after antidote. J Toxicol Clin Toxicol. 1987;25:121–133
  10. Scientific Applications International Corporation . Chemical incident module-hospital emergency management: concepts and implications of WMD incidents. Washington: Office of Domestic Preparedness, Office of Justice Programs, United States Department of Justice; 2002;

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Further reading 

    ☆ Anne Marie Lewis RN, BSN, BA, MA, CEN

    PII: S0099-1767(04)00064-9

    doi:10.1016/j.jen.2004.01.013

    Journal of Emergency Nursing
    Volume 30, Issue 2 , Pages 113-116, April 2004

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