topic 25 Flashcards
What are 4 steps to the general approach to a toxic patient?
• Vital Signs
– The A,B,C’s – “Treat the patient, not the poison”
- Consider decontamination
- Is there an antidote?
• Can the toxin be removed?
– HD, CAVH, CVVH, CAVHD
What are 4 things that should be considered in the differential diagnosis of a person in a toxic coma?
• Differential diagnosis of a patient in coma:
– Vital signs
– Patient odor
– Physical exam and history
– Consider along with toxic causes other possibilities:
- Metabolic
- Infectious (e.g. meningitis, encephalitis)
- Structural (e.g., tumor, hemorrhage, and edema)
- Vascular (e.g., arteritis)
- Psychiatric causes of brain dysfunction
What are 7 components of the physical exam that will help diagnose a toxic patient?
• Physical Exam
– patient odor
– skin, hair, nails
– pupil changes
– clues in respiratory exam
– clues in cardiovascular exam
– clues in gastrointestinal exam
– Specific “toxidromes”
What are some skin, hair and nail findings that are possible results of poisoning? What could cause them?
- Skin color (cyanosis) – Consider methemoglobinemia
- Nitrates
- Aniline dyes
- Phenazopyridine (Pyridium®)
- Benzocaine – Nail changes
Nail Changes
• white transverse growth arrest bands (Mee’s
lines) seen with heavy metals such as arsenic or
thallium.
Hair changes
Toxic Allopecia
• Differential Diagnosis: – Alopecia totalis – Thallium (~2 wks) – Radiation
What are possible pupil changes and what could cause them?
• Miosis (small pupils) – Opiates – Clonidine – Nicotine – Cholinergic excess (e.g. organophosphate insecticides - must know for boards)
• Mydriasis (dilated pupils) – Sympathomimetics – Cocaine – Amphetamines – Anticholinergics – Antihistamines
What are some clues that can be found in the respiratory exam? What could they be caused by?
• Tachypnea (fast respiratory rate) – Toxins that produce acid metabolites • ethylene glycol, methanol – Toxins that uncouple oxidative phosphorylation • cyanide, carbon monoxide, hydrogen sulfide, salicylates – Toxins that result in hypoxemia • CO, methemoglobin formers – Toxins that stimulate the patient • Sympathomimetics, cocaine, PCP
• Bradypnea (slow breathing)
– Opiates (may have apnea = absent breathing)
– Many other toxins that suppress respirations
• Pulmonary edema
– Many toxins (e.g. heroin, salicylates)
• Hypoxia (consider differential)
What are 4 common antidotes for a toxic patient? What are some possible downsides to using an antidote?
• While determining etiology of coma consider the Basic Four Antidotes: – Oxygen – Naloxone – Thiamine – Dextrose
• Can be downsides to using antidotes
– e.g., arrhythmias & pulmonary edema after
naloxone administration in opiate addicts
– e.g., excessive Methgb after sodium nitrite
What is the antidote for methemoglobinemia? How does it work? When is improvement normally seen? When is it less effective?
- Methylene Blue for methemoglobinemia, which forms when the iron within hemoglobin is oxidized from the 2+ to the 3+ state. It does not carry oxygen.
- Methylene blue is itself an oxidizing agent, which is first converted in vivo to leukomethylene blue, and this reduced form is then able to reduce the hemoglobin back to the oxygen-carrying 2+ state.
• Symptomatic improvement usually occurs within
30 minutes. – A 2nd dose of methylene blue may be required in very severe cases or if there is evidence of ongoing methemoglobin formation.
• Less effective or ineffective in the presence of
glucose-6-phosphate dehydrogenase deficiency since its antidotal action is dependent on nicotinamide-adenine dinucleotide phosphate(NADP+). Exchange transfusion may be necessary in this case.
What are five important questions for the toxic patient history?
– Specific chemical or generic/brand drug name
– If unknown, what meds are available in home?
– Estimate of ingested dose & dosage strength
– Pharmaceutical formulation
• tablet, enteric coated, sustained release
• liquid vs. granules vs. solid
– What drugs are available
• “Medicine Cabinet Manifest”
• Grandparent’s medications
What is a general principle for the clues found in CVS exam? Which drug can cause a wide variety of arrythmias in overdose?
• Effects of toxins and drugs on the cardiovascular
system are complex
• Digoxin is an example of a drug that can cause a
wide variety of arrhythmias in overdose (atrial and ventricular).
Which drugs can cause arrythmias? How do they do it? What might they lead to?
– Prolonged QRS and/or prolonged QT
• e.g., Tricyclic antidepressants
– Poison the sodium channel (widens the QRS)
– Poison the potassium channel (prolongs QTc)
– May lead to tachyarrhythmias such as ventricular tachycardia (VT) or ventricular fibrillation (VF)
Which drugs can cause tachycardia?
• Tachycardia (fast heart rate) – Amphetamines and other stimulants – Antihistamines – Anticholinergic drugs (antimuscarinic) – Caffeine
– Cocaine
– Cyclic antidepressants
– Synthroid® (levothyroxine)
– Withdrawal from sedative/hypnotics/alcohol
Which drugs can cause bradycardia?
• Bradycardia (slow heart rate)
– beta-adrenergic antagonists (β-blocker) (propranolol)
– calcium channel antagonists (diltiazem)
– clonidine
– cardiac glycosides (digoxin)
– opioids
– organophosphate insecticides (muscarinic
stimulation)
What are the effects of an overdose of calcium channel blockers? What is the antidote? What else is it used to treat?
- Calcium channel blockers in overdose may also lead to bradycardia and heart block along with significant hypotension.
- Ca chloride or Ca gluconate
- Used to treat the severe, life threatening hypocalcemia caused by poisoning by hydrofluoric acid, ammonium bifluoride and other fluoride salts.
- Part of the multi-agent therapy for overdoses of calcium channel blockers.
What is the classic symptom of beta blocker intoxication? What else is it used to treat? What are the side effects?
- Bradycardia is classically seen with beta-blocker intoxication.
- Antidote for beta-blocker poisoning. May be of limited benefit in calcium channel blocker overdose
• Bypasses the blocked ß receptor to switch on adenylyl cyclase which increases production of cyclic AMP and activates more cAMP-dependent
phosphokinase.This in turn enhances calcium flux through calcium channels and increases the rate and strength of myocardial contraction.
• Treats hypoglycemia because it stimulates hepatic gluconeogenesis and glycogenolysis.
• Side effects include nausea and vomiting
and rash.
