Category Archives: #FOAMtox

TOXCARD: TOXIC ALCOHOL POISONING

Author: Kristin E. Fontes, MD (Emergency Physician, Santa Barbara Cottage Hospital and Goleta Valley Cottage Hospital) // Edited by: Cynthia Santos, MD (Senior Medical Toxicology Fellow, Emory University School of Medicine), Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital), and Brit Long, MD (@long_brit, EM Attending Physician, San Antonio Military Medical Center)

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Case presentation:

A 28-year-old female is brought to the emergency department by ambulance from home after her roommate found her disoriented and poorly responsive. The roommate reports finding a small container of antifreeze in the patient’s bedroom. Vital signs are as follows: T 37.0C, HR 65, BP 126/76, RR 32, and SpO2 98% on room air.  Venous blood gas shows pH 6.97, pCO2 21, pO2 38, HCO3 4.8, and lactate 6.75.

Question:

What are the laboratory abnormalities that can occur with toxic alcohol poisoning and how can it be treated?

Pearl:

Common features of toxic alcohol poisoning are elevated anion gap metabolic acidosis and elevated osmolar gap (the latter being a distinguishing feature from ethanol poisoning); osmolar gap usually elevated early after ingestion.(1,2)

Recall the toxic alcohol metabolites and their effects:

toxic alcohol metabolism

  • EG toxicity can cause significant renal failure due to oxalate crystal deposition in the kidneys and glycolic acid, which is directly nephrotoxic; hypocalcemia and tetany can also result due to oxalate binding to calcium.(1)
  • MeOH toxicity classically causes visual disturbances (“snowfield” vision) due to formic acid-induced optic neuropathy.(1)
  • Isopropanol toxicity causes ketosis without acidosis (no lactic acid formed!).  Usually benign clinical course but can occasionally cause hemorrhagic gastritis. Fomepizole and HD not usually indicated.(1)
  • Propylene glycol toxicity often due to intravenous medication preparations containing this alcohol (e.g., diazepam, lorazepam, esmolol, nitroglycerin, phenobarbital, phenytoin) can result in severe lactic acidosis.(1)
Treatment Approach:
  • Fomepizole competitively inhibits alcohol dehydrogenase, which is involved in the metabolism of all alcohols, including ethanol. It is given to prevent the buildup of toxic metabolites from ethylene glycol (glycolic acid, glyoxylic acid, and oxalic acid) and methanol (formic acid) whose deposition in tissues can cause irreparable damage.(1)
  • Fomepizole is indicated for MeOH or EG ingestion resulting in a metabolic acidosis with an elevated osmolar gap (not accounted for by ethanol) and a serum MeOH or EG level of at least 20 mg/dL.(1)
  • Fomepizole dosing: 1) Load: 15 mg/kg (max 1.5 g) IV, diluted in 100 mL of normal saline or 5% dextrose, infused over 30 minutes; 2) Maintenance: 10 mg/kg IV every 12 hours for 4 doses, then increase to 15 mg/kg until serum toxic alcohol level is less than 20 mg/dL.(1,3)
  • Hemodialysis is indicated for toxic alcohol poisoning with an elevated osmolar gap and/or severe metabolic acidosis refractory to standard therapy, refractory hypotension, or end organ damage (i.e. acute renal failure).(1,3)
  • Vitamin Supplementation: Give folic or folinic acid to patients with MeOH toxicity to divert metabolism away from formic acid to carbon dioxide and water. Give folic acid, pyridoxine, and thiamine to patients with EG toxicity to divert metabolism to nontoxic metabolites.(1,3)
Main points:

Consider toxic alcohol poisoning in a patient with an unexplained elevated anion gap metabolic acidosis and elevated osmolar gap. Consider fomepizole and/or HD in patients with severe toxic alcohol poisoning, especially if refractory to standard therapy.

 

References:
  1. Olson KR & California Poison Control System. (2012). Poisoning & drug overdose. New York: Lange Medical Books/McGraw-Hill.
  2. Emmett M and Palmer BF. Serum osmolal gap. In: UpToDate, Forman JP (Ed), UpToDate, Waltham, MA, 2016.
  3. LeBlanc C, Murphy N. Should I stay or should I go?: toxic alcohol case in the emergency department. Can Fam Physician 2009 Jan;55(1):46-9.

ToxCard: TCA Poisoning

Author: Tharwat El Zahran, MD (Medical Toxicology Fellow, Emory University School of Medicine) // Edited by: Cynthia Santos, MD (Senior Medical Toxicology Fellow, Emory University School of Medicine), Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital), and Brit Long, MD (@long_brit, EM Attending Physician, San Antonio Military Medical Center) screen-shot-2017-01-08-at-11-30-27-pm
Case Presentation:

2 yo male child presented to the ED with status epilepticus. His parents found an empty bottle of amitriptyline at home. He was intubated, given benzodiazepines and antiepileptic drugs. VS: BP 70/30, T 106 F, RR 24, HR 98, sat 98% RA, glucose 100 mg/dl. EKG is shown below.

EKG TCA PED

Question

What EKG findings occur in tricyclic antidepressant (TCA) poisoning? And how are they treated?

Pearl

TCAs alter the conformation of the sodium channel and slow the rate of rise of the action potential, which produces both negative dromotropic and inotropic effects. Sodium bicarb is the primary treatment for TCA poisoning.

  • All TCA are competitive antagonists of the muscarinic acetylcholine receptors and antagonize peripheral α1 adrenergic receptors.
  • Most prominent effects of TCA overdose result from binding to cardiac Na channels.
  • Acute ingestion 10-20 mg/kg of most TCAs cause cardiovascular and CNS toxicity. In children,  >5mg/kg results in toxicity.(1)
  • Signs of acute cardiovascular toxicity are refractory hypotension, acidosis, and arrhythmias. EKG indicators include intraventricular conduction delay (R shift of QRS axis and prolonged QRS), R in avR≥ 3mm, R/S>0.7 and arrhythmias. A QRS≥100 msec indicates increased incidence of serious toxicity, including coma, intubation, hypotension, seizures, and dysrhythmias. Sinus tachycardia is the most common EKG abnormality. (2)(3)
  • Acute neurological toxicity include AMS, delirium, agitation , seizures, and/or psychotic behavior with hallucinations, lethargy, coma.
Treatment approach
  • If the decision is made to intubate, avoid apnea, consider awake intubation, pretreat w benzos to raise seizure threshold and hyperventilate to promote alkalosis.(4)
  • If the EKG indicates signs of TCA poisoning as mentioned above,  give 1-2 meq/kg of sodium bicarb IV boluses at 3-5 min intervals.(4)
  • Continue bicarb drip until QRS duration <100, vitals stable, Na ~150, pH ~7.55. Watch for hypokalemia and hypocalcemia with bicarb drip.  Consider hypertonic saline (3%) if refractory or if serum pH>7.55.(4)
  • Hypotension unresponsive to sodium bicarb, or fluid boluses should be treated with vasopressors (norepi recommended).(4)
  • Treat dysrhythmias with lidocaine bolus of 1mg/kg IV followed by infusion of 20-50 mcg/kg/min.
  • Benzodiazepines, barbiturates, or propofol are recommended for seizures. Consider continuous EEG monitoring with neuromuscular blockade in refractory cases. Avoid phenytoin.(4)
  • For refractory cardiovascular poisoning consider intralipid or ECMO if available.(4)
Main point

TCAs are sodium channel blockers and primary treatment of TCA poisoning is sodium bicarb. The EKG abnormalities like QRS≥100,  R wave in avR ≥3mm, and R/S> 0.7 can predict significant toxicity.  Sodium bicarb displaces the TCA from the Na binding site by raising the Na+ gradient and increasing the pH.  Prolonged resuscitation might be necessary.

References
  1. Caksen et al. Acute amitriptyline intoxication: an analysis of 44 children. Human & Experimental Toxicology (2006) 25: 107-110
  2. Olgun et al. Clinical, Electrocardiographic, and Laboratory Findings in Children With Amitriptyline Intoxication. Pediatr Emer Care 2009;25: 170-173
  3. Paksu et al. Amitriptyline overdose in emergency department of university hospital: Evaluation of 250 patients. Human and Experimental Toxicology 2014;33:980–990
  4. Goldfrank’s Toxicologic Emergencies, 10th E, Chapter 71: Cyclic Antidepressants, p 972- 982.

 

 

Tox Cards: CO Poisoning

Author: Patrick C. Ng (Chief Resident, San Antonio Military Medical Center) // Edited by: Cynthia Santos, MD (Senior Medical Toxicology Fellow, Emory University School of Medicine), Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital), and Brit Long, MD (@long_brit, EM Attending Physician, San Antonio Military Medical Center)
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Case Presentation:
It is a cold day in the middle of December. A 56 yo female and her 29 yo daughter who is 8 months pregnant present to your ED with a chief complaint of generalized weakness and headache for 2 days. They mention that they think they both caught the flu due to the cold temperatures despite turning their heater on high and using oil lamps for extra heat in their apartment. Their vital signs are normal.
Question:
What are the most common signs/symptoms of carbon monoxide (CO) poisoning, and what are the general management plans?
Pearl:

CO poisoning presents with nonspecific symptoms that can be mistaken for other diagnosis such as the flu. Initial treatment includes high-flow supplemental O2. Hyperbaric oxygen therapy (HBOT) may or may not be the “standard of care” (controversial).

  • CO poisoning can be an elusive diagnosis, as non-specific symptoms such as headache, dizziness, nausea, fatigue, and chest pain are non-specific and can be consistent with many other disease processes.(1,2)
  • Key historical clues include people from the same household presenting with symptoms of headache and flu-like symptoms that improve throughout the course of the day (i.e. when patients leave their dwellings for work, school, etc.) and history of exposure to CO sources such as heaters and enclosed garages.(1,2)
  • A co-oximetry is a spectrophotometer that uses many different wavelengths to measure oxygenated hemoglobin (oxyHb), deoxygenated hemoglobin (deoxyHb), as well as carboxyhemoglobin (COHb) and methemoglobin (MetHb) concentrations.(3)
  • The use of greater number of wavelengths in a co-oximeter as compared to a standard pulse oximeter allows the co-oximeter to distinguish between other types of hemoglobin,  whereas a standard pulse oximetry can only distinguish between oxyHb and deoxyHb.(3)
  • Blood COHg levels commonly reaches a level of 10 % in smokers and may even exceed 15 %, as compared with 1 to 3 % in nonsmokers.(2)
  • Standard treatment includes  high-flow O2  via NRB mask (or intubation in severe cases) until symptoms resolve and CO levels return to baseline; pregnant patients should continue for at least 24 hours with fetal wellbeing assessment. Patients also require follow up at 1-2 months for neuropsychiatric assessment.(1,2)
  • Normal half life of Hb-CO is 4-6 hrs with room air oxygen, 40- min with high-flow O2, and 15-30 min with HBOT.(2)
  • Although the indications for HBO are controversial, some recommend HBO for any CO-poisoned patient with mental status change or history of syncope, signs of cardiac ischemia or arrhythmia, history of ischemic heart disease and CO level > 20%, symptoms that do not resolve with normobaric O2 therapy after 4-6 hours, or any pregnant patient with CO > 15%. Coma is generally an undisputed indication for hyperbaric-oxygen therapy.(2)
  • The use of HBO has been reported to reduce the risk of neurological/cognitive sequelae thought to be associated with carbon monoxide poisoning.(4,5)
Main Point:
Carbon monoxide poisoning can be a deadly diagnosis associated with significant morbidity and long-term permanent neurological damage. It can present with very non-specific symptoms. Specific historical clues as well as co-oximetry can help the emergency physician quickly make the diagnosis. High-flow O2 therapy is the initial standard therapy with some advocating HBOT for select severe or at risk cases.
References:
1. Piantadosi CA. Diagnosis and treatment of carbon monoxide poisoning. Respir Care Clin N Am. 1999;5:183-202.
2. Ernst A, Zibrak JD. Carbon Monoxide Poisoning. N Engl J Med 1998;339:1603-1608.
3. Hampson NB. Noninvasive pulse CO-oximetry expedites evaluation and management of patients with carbon monoxide poisoning. Am J Emerg Med. 2012 Nov;30(9):2021-4.

4. Tibbles PM, Perrotta PL. Treatment of carbon monoxide poisoning: a critical review of human outcome studies comparing normobaric oxygen with hyperbaric oxygen. Ann Emerg Med. 1994;24:269-276.
5. Weaver LK, Hopkins RO, Chan KJ, et al. Hyperbaric oxygen for acute carbon monoxide poisoning. N Engl J Med 2002;347:1057–1067

Treatment for Salicylate Poisoning

Author: Sean Kolowich (Emory University School of Medicine) // Edited by: Cynthia Santos, MD (Senior Medical Toxicology Fellow, Emory University School of Medicine), Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital) and Brit Long, MD (@long_brit)

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Case presentation:

A 53 year-old previously healthy female is brought into the ED by family members 4 hours after ingesting 100 tablets of aspirin (325mg, unknown formulation). She has no complaints and denies any co-ingestions. VS: Temp 98.1 (oral), HR 93, BP 136/87, RR 20, pulse ox 98% on room air. CMP and ECG are unremarkable, ASA 47.1 mg/dL, ABG pH 7.48, pCO2 20, pO2 122.

Question:

What treatments should a salicylate poisoned patient receive?

Pearl/Pitfall: 

Patients with salicylate poisoning should receive IV bicarb to alkalinize the urine. Indications for hemodialysis include cerebral edema, pulmonary edema, renal failure, intractable acidosis, clinical deterioration, or ASA level > 100 mg/dL or > 70 mg/dL if chronic.

  • Support ABCs, prevent further organ toxicity by encouraging salicylate elimination
    • Alkalinize the serum/urine
      • 1-2 mEq/kg sodium bicarb. IV bolus followed by sodium bicarb. infusion (3 amps into 1L D5W) @ 1.5-2 X maintenance rate
        • goal serum pH ~7.5
        • goal urine pH >7.5
  • Salicylate overdose + IV sodium bicarbonate therapy = potential hypokalemia
    • Avoid hypokalemia because it prevents alkalization of the urine ® prolonged elimination of salicylate
      • goal K+ 4.0 to 4.5 mEq/L
    • Monitor calcium levels (ionized/total); IV NaHCO3 can cause hypocalcemia
  • Consider glucose supplementation if altered mental status
    • Serum glucose may be normal but CNS levels may be low 2/2 effects of salicylates
  • Indications for extracorporeal treatment (intermittent hemodialysis is ECTR of choice):
    • Salicylate level > 100 mg/dL (> 90 mg/dL if impaired kidney function) or > 70 md/dL if chronic.
    • Cerebral edema (altered mental status, seizures)
    • Renal failure
    • Pulmonary edema or new hypoxemia requiring supplemental O2
    • IF standard therapy fails AND:
      • Salicylate level > 90 mg/dL (> 80 mg/dL if impaired kidney function)
      • Systemic pH < 7.20
  • Continue IV sodium bicarb therapy b/w ECTR sessions
Main Point:

Patients presenting with acute salicylate toxicity should receive supportive care and alkalinization with IV sodium bicarbonate. Hemodialysis should be considered early in treatment and is indicated if there is evidence of end organ damage (AMS, ARDS), failure of standard therapy, or severely elevated salicylate levels.

 

References:

  1. Lugassy DM. Salicylates. In: Hoffman RS, Howland M, Lewin NA, Nelson LS, Goldfrank LR. Eds. Goldfrank’s Toxicologic Emergencies, 10e. New York, NY: McGraw-Hill; 2015.
  2. Levitan R, Lovecchio F. Salicylates. In: Tintinalli JE, Stapczynski J, Ma O, Yealy DM, Meckler GD, Cline DM. eds. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 8e. New York, NY: McGraw-Hill; 2016.
  3. Juurlink DN, Gosselin S, Kielstein JT, et al. Extracorporeal Treatment for Salicylate Poisoning: Systematic Review and Recommendations From the EXTRIP Workgroup. Ann Emerg Med 2015; 66:165

Limitations of CIWA score

Author: Cynthia Santos, MD (Senior Medical Toxicology Fellow, Emory University School of Medicine) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital) and Brit Long, MD (@long_brit)

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Case Presentation:

You are working a busy ED shift and are also managing a handful of boarded patients admitted to your ICU. Nursing resources are especially strained today. One of your intubated patients that you admitted for alcohol withdrawal starts having a seizure. His vitals are T 101F, HR 135, BP 175/100, RR 16, O2 sat 89% on 40% O2.

Question:

What are some of the limitations of using the CIWA score?

Pearl:

Although the CIWA score is a widely cited example of symptom-triggered therapy it has several important limitations and can be difficult to properly execute in the emergency department setting.

  • Symptom-triggered treatment for alcohol withdrawal using the CIWA score has many benefits including reduced progression to mechanical ventilation requirement, 4-fold decrease in benzodiazepine requirements, shorter duration of treatment, and shorter hospitalization stays by 2 days when compared to fixed-dosing scheduling.(1)
  • However, an important clinical limitation of CIWA as a tool to assess alcohol withdrawal is that it does not incorporate vital sign assessment, which can be an important and sometimes the only clue available in recognizing inappropriately treated DT patients.(2)
  • The CIWA score also does not address choice of benzodiazepines, frequency of administration, use of adjuvant medications and underlying medical conditions (renal failure, liver failure, respiratory failure, cardiac disease, age, etc.) in treating withdrawal.(2)
  • The CIWA score requires patients to be able to respond to questions and follow commands. This can be difficult in patients with language barriers, altered mental status or who are intubated.(2)
    • For example “Do you feel sick to your stomach, have you vomited?”; “Do you have any itching, pins-and-needles sensations, burnings, or numbness…?” and “Are you seeing anything that is disturbing you?” are some questions asked.
  • Many of the studies that have evaluated CIWA have excluded patients with seizures, which is an important sign of severe withdrawal and should be taken into consideration.(3)
  • Moreover, the CIWA score can be especially difficult to execute properly without adequate nursing staff. Many busy EDs are often understaffed and have limited nursing resources. Thorough staff training is required to appropriate use CIWA.(2) Studies have shown that the CIWA score tends to be administered irregularly by nursing staff, often used for patients who are not appropriate for symptom-guided treatment and can have a higher proportion of protocol errors.(4)
  • Scoring systems are important for symptom-triggered therapy and provide the ability for comparison analysis in clinical trials. However, many other scoring systems exist. An example is the Richmond Agitation Sedation Scale (RASS), which is observer based.(5) Many hospitals have their own scoring systems as well.
Main point:

Symptom triggered therapy has been shown to have better outcomes than fixed benzodiazepine scheduling in managing alcohol withdrawal. The CIWA score is a widely cited method of using symptom triggered therapy. However, physicians should not rely on just the CIWA score and other hospital and research protocols exist. The CIWA score has several important limitations including the exclusion of vital signs as an assessment, reliance of the patient’s ability to answer questions and follow commands, and can be time consuming in a busy ED environment.

References:
  1. Daeppen J, Gache P, Landry U, et al. Symptom-triggered vs fixed-schedule doses of benzodiazepines for alcohol withdrawal. JAMA. 2002;162(10):1117-1121.
  2. Sankoff J, Taub J, Mintzer D. American College of Medical Quality: Accomplishing much in a short time: use of a rapid improvement event to redesign the assessment and treatment of patients with alcohol withdrawal. Am J Med Qual. 2013; 28(2):95-102.
  3. Saitz R, Mayo-Smith MF, Roberts MS, Redmond HA, Bernard DR, Calkins DR. Individualized treatment for alcohol withdrawal: a randomized double-blind controlled trial. JAMA. 1994;272:519-523.
  4. Hecksel KA, Bostwick JM, Jaeger TM, Cha SS. Inappropriate use of symptom-triggered therapy for alcohol withdrawal in the general hospital. Mayo Clin Proc. 2008;83:274-279. 10.
  5. Sessler CN. The Richmond Agitation-Sedation Scale” validity and reliability in adult intensive care unit patients. Am J Respir Crit Care Med. 2002; 166:1338-1344.