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List the abnormal signs and symptoms displayed in these patients after exposure to the unknown chemical. Which of these findings are consistent with inhalation of cyanide?
Abnormal signs and symptoms - nausea, dizziness, light-headedness, weakness, drunken appearance, confusion, mydriasis, hypotension, cherry red-colored skin, mildly elevated BP (some), hypotension (many), nutty-smelling breath, bradycardia, tachypnea, seizures, anxiety, abdominal pain, nausea, emesis, headache, unconsciousness, coma.
Symptoms consistent with cyanide inhalation - nausea, dizziness, weakness, confusion, mydriasis, cherry red-colored skin, hypotension (many), nutty-smelling breath, bradycardia, tachypnea, seizures, anxiousness, emesis, headache, unconsciousness, coma1,2.
List the laboratory tests that may be abnormal in patients exposed to cyanide. Explain the pathophysiology underlying these abnormalities.
Anion gap test (blood or urine) - This test is mainly used for a differential diagnosis of metabolic acidosis. Cyanide poisoning causes an "arrest of aerobic metabolism which leads to a marked accumulation of lactic acid and a profound anion gap metabolic acidosis1."
Arterial/Venous Blood Gases (ABG) & pH test - these are done to evaluate O2/CO2 gas exchange, to monitor respiratory function including hypoxia and acid-base status. With cyanide toxicity, these tests will be abnormal because "cyanide inhibits aerobic respiration, stops ATP generation, and arrests cellular respiration resulting in tissue anoxia1." This lack of oxygen alters the gas exchange as well as the acid-base status of the individual. Venous oxygen levels are also abnormally high in patients with cyanide poisoning due to their inability to utilize oxygen1.
Whole Blood Cyanide test - this is used to establish the diagnosis of cyanide poisoning. Toxic levels (> 1mg/L) of cyanide in the blood will cause an abnormal result for this test.
Electrolyte panel test - Abnormal electrolyte levels will be observed with cyanide poisoning because cyanide forms complexes with cation-containing enzymes ultimately creating an anion gap in the blood1.
Lactic Acid test - The results of this test will be abnormal because with cyanide poisoning, there is a marked accumulation of lactic acid in the body due to a halt in aerobic metabolism. A serum lactate or 10mmol/L or more is an indication of cyanide poisoning1.
What are the potential short- and long-term sequelae from this exposure?
Short term - CV effects (ex: bradycardia, hypotension, pulmonary edema etc), CNS effects (ex: headache, anxiety, confusion, etc), and GI effects (ex: N&V)1.
Long term - neurological and thyroidal disturbances, injury to tissues with high oxygen demand (especially brain and heart), some damage to the basal ganglia eliciting parkinsonian symptoms, and death have been reported1.
What are the goals of pharmacotherapy for these patients1,2?
Stabilize the patient - provide supportive care (ABCs) to prevent/correct life-threatening complications, administer antidote, correct chemical imbalances in blood and control seizures
Decontaminate the patient - any clothing and/or belongings that have been exposed should be removed from patient vicinity.
Remove patient from source of exposure and into fresh air
Monitor for signs of toxicity
What non-pharmacologic measures are available to treat cyanide poisoning?
Supportive care (ABCs & oxygen, IV fluids)
Remove patient from source of exposure and into fresh air (for inhalation) and wash patient's skin and hair with non-toxic, mild detergent and warm water, then rinse thoroughly with water (for dermal exposure)
If ingested, decontaminate within 1hr of ingestion with gastric aspiration or a single-dose of activated charcoal if patient is conscious.
What feasible pharmacotherapeutic alternatives are available for treating cyanide poisoning
Cyanide antidotes (amyl and sodium nitrites, thiosulfate, or hydroxocobalamin)
Outline your pharmacotherapeutic plan for treating cyanide poisoning in these patients. Include dose(s), route(s), and repeat dosing information (if any) for both adult and pediatric patients. Also, describe use of administration devices or ancillary supplies required.
Immediately administer 100% oxygen.
Children (unlabeled use): 70 mg/kg as single infusion (maximum: 5 g); if required, a dose of 35 mg/kg may be repeated.
Adults: Initial dose: 5 g as single infusion; may repeat a second 5 g dose depending on severity of poisoning and clinical response; maximum cumulative dose: 10 g.
Treat with benzodiazepenes
What supportive care measures may be necessary for optimal management2?
Immediately remove the patient/victim from the source of exposure.
Evaluate respiratory function and pulse.
Ensure that the patient/victim has an unobstructed airway.
Assist ventilation as required.
If breathing has ceased (apnea), provide artificial respiration.
Establish secure large-bore intravenous (IV) access.
Monitor for respiratory distress.
Describe the clinical and laboratory parameters required to determine whether treatment for these patients has been successful.
Reversal of metabolic acidosis
Normal values for arterial and venous blood gases
Absence of clinically significant cyanide blood levels
Normal electrolyte values
Reversal of lactate accumulation
How often should the nursing and medical staff attempt to assess and reassess the patients?
Based on the half-life of cyanide (0.7 - 2.1 hrs1), the medical staff should reassess the patients every 1-2 hours.
For patients who are alert and oriented, what information would you share with them about the possible immediate side effects of each of the antidotes?
Cardiovascular: Blood pressure increased (18% to 28%; systolic â‰¥180 mm Hg or diastolic â‰¥110 mm Hg), bradycardia (reflex; mean decrease of 16% in pulse rate)
Central nervous system: Headache (6% to 33%)
Dermatologic: Erythema (94% to 100%), rash (predominantly acneiform; 20% to 44%; can appear 7-28 days after administration and usually resolves within a few weeks)
Gastrointestinal: Nausea (6% to 11%)
Genitourinary: Chromaturia (100%; may last up to 5 weeks after administration but usually clear within several days)
Hematologic: Lymphocytes decreased (8% to 17%)
Local: Infusion site reaction (6% to 39%)
Cardiovascular: Postural hypotension; cutaneous flushing of head, neck, and clavicular area; tachycardia; palpitation; vasodilation; syncope
Central nervous system: Headache, dizziness, restlessness
Dermatologic: Skin rash (contact dermatitis)
Gastrointestinal: Nausea, vomiting
Hematologic: Hemolytic anemia
Ocular: Increased intraocular pressure
Cardiovascular: Tachycardia, syncope, cyanosis, hypotension (associated with rapid infusion), flushing
Central nervous system: Dizziness, headache
Gastrointestinal: Nausea, vomiting
Miscellaneous: Methemoglobin formation
Cardiovascular: Hypotension (rapid infusion)
Dermatologic: Contact dermatitis
Gastrointestinal: Nausea, vomiting
Local: Local irritation
How long might it take for the patients to recover from potential long-term effects of acute cyanide exposure?
Weeks to months
Create a list of potential chemical agents that the patients may have been exposed to based on presenting signs and symptoms
Type II pyrethroids
How serious is this exposure, and what could be some potential sequelae?
Exposure is relatively serious as it could lead to hypertension (cholinergics) acute lung injury, altered mental status, & coma (type II pyrethroids), as well as seizures (both agents).
Other potential sequelae include paresthesias, tinnitus, vegetative nervous disorders, cerebro-organic disorders, visual disturbances (pain, lacrimation, photophobia, conjuctivitis), dysacousia, sensomotor-polyneuropathy most frequently in the lower legs, and fasciculations.
What are the goals of pharmacotherapy in this case?
Provide supportive care to manage
hypersensitivity reactions (using antihistamines),
neurological symptoms (using benzodiazepines)
contact dermatitis (using topical corticosteroids)
Antagonize muscarinic symptoms (with atropine)
Stop aging of enzyme blockade (with 2-PAM)
Prevent and terminate seizures (with diazepam)
How do your goals change if there were 15 patients presenting with these symptoms and differing degrees of severity and exposure?
First identify the patients according to their degrees of severity and exposure
Treat (like above) starting with patients that have the most severe exposures and tailor doses based on these varying severities.
What non-pharmacologic measures are available to treat these patients?
Remove patient from the source of the exposure and into the fresh air.
Monitor for respiratory distress.
Supplemental oxygen should be provided if needed
What feasible pharmacotherapeutic alternatives are available for treating these patients?
Anti-cholinergics (atropine, 2-PAM)
Beta-agonists if bronchospasm is present.
Suppose there are 100 patients in your hospital's Emergency Department needing an antidote, and you only have enough antidote to treat 25 patients. How do you decide who gets life-saving treatment?
I would perform a quick analysis of the patients and try my best to gauge who the antidote can save based on how long their length of exposure and the severity of their symptoms. Patients who have progressed too far into toxicity and cannot be saved will not be given the antidote.
What antidotes are required for this chemical exposure? Provide the adult doses, routes, and repeat dosing information for each antidote3.
No known antidote1
Primarily effective for muscarinic effects; will not reverse nicotinic effects. DIAGNOSTIC DOSE: ADULT: 1 mg IV or IM; CHILD: 0.25 mg (about 0.01 mg/kg) IV or IM. THERAPEUTIC DOSES: ADULT: 2 to 5 mg slowly IV; CHILD: 0.05 mg/kg slowly IV; REPEAT DOSES may be administered every 10 to 15 min as needed to achieve and maintain full atropinization (drying of pulmonary secretions).Â
(Protopam, 2-PAM) and its chloride (US). Severe OP poisoning with nicotinic and/or CNS manifestations should be treated with pralidoxime. ADULT: 1 to 2 g IV at 0.5 g/min, or mixed in 250 ml of NS and infused over 30 min. CHILD: 25 to 50 mg/kg, diluted to a 5% concentration in NS and infused over 20 to 30 min.Â
Â Obidoxime Dichloride
may be a less toxic and more efficacious alternative to pralidoxime. Given as an IM or IV injection of 250 mg. Subsequent injections of 250 mg every 2 hours or continuous infusion of 35 mg/hr may be necessary.Â
Â Â HI-6
an alternative oxime, has excellent acetylcholinesterase regenerating action with VX and very good action with Sarin (GB).
There are special dosing kits and administration devices available for these antidotes. Describe how these kits should be administered4.
If severe signs and symptoms are present, three (3) Atropine auto-injectors and three (3) 2-PAM CL injectors should be administered in rapid succession.
If the patient exhibits SLUDGEM but no central nervous system (CNS) findings are present, then two (2) Atropine auto-injectors and one (1) 2-PAM CL injector should be given.
In either case, remove secretions, maintain patient's airway and, if necessary and the situation permits, use artificial ventilation.
Repeat dosages will be given as specified in the Extended Re-evaluation and Treatment Schedule
If symptoms resolve, then only monitoring is necessary.
Pre-measured doses of auto-injectors should be safe in most adults. It should be noted, however that auto-injectors were designed for a military profile: approximate age 18-35, weight 70 kg. Or 154 lbs., healthy and with no preexisting medical conditions.
Pralidoxime (2-PAM CL) is most effective if administered immediately after poisoning and following but not before Atropine, especially for severe exposures.
If a patient's condition worsens and seizure activity occurs, what class of medications should be used for this chemical-induced seizure?
Outline a monitoring plan to assess if the pharmacotherapy treatment for these patients is successful.
Monitor patients for resolution of respiratory symptoms
Monitor patients for resolution of seizures
Monitor patients for resolution of cholinergic or pyrethroid toxidromes
Do not discontinue treatment until symptoms resolve
What information would you share with the patients about immediate side effects of each of the antidotes?
For the antidote kit:
Atropine may cause chest pain. It may also exacerbate angina or induce a myocardial infarction.
Up to one hour after intramuscular injection of 2-PAM CL some pain may be experienced at the site of injection.
2-PAM CL may cause blurred vision, double vision (diplopia), dizziness, headache, drowsiness, nausea, rapid heart rate (tachycardia), increased blood pressure, and hyperventilation.
Both (Atropine and 2-Pam CL) should be used with caution (but not withheld) in patients with preexisting cardiac disease, high blood pressure, or strokes, particularly in the Extended Re-evaluation and Treatment Phase.
How long might it take for patients to recover from the ocular effects of the chemical exposure?
Could range from days to months to years depending on the symptom in question and the severity of the exposure.