labs, Acid base
Toxidromes and withdrawals
Clinical effects and Ekgs
Antidotes
Miscellanous
100
I am suspected in the following presentation:
A 26 y o female who presents with vomiting, diarrhea, GI bleeding, and AMS with following labs:
ABG:7.33, 34, 86
BMP: Na 136/ K 3.3/ Chloride 90/ HCO3 19/ BUN 22/ Cr 0.7/ Gluc 102, Ca 8.2
measured osmolality 292, Calculated osmolality 289
urine and serum drug screen normal
A 26 y o female who presents with vomiting, diarrhea, GI bleeding, and AMS with following labs:
ABG:7.33, 34, 86
BMP: Na 136/ K 3.3/ Chloride 90/ HCO3 19/ BUN 22/ Cr 0.7/ Gluc 102, Ca 8.2
measured osmolality 292, Calculated osmolality 289
urine and serum drug screen normal
What is Iron toxicity?
High anion gap, normal osmolar gap accounted for by the "I" in both MUDPILES and ADICT.
High anion gap, normal osmolar gap accounted for by the "I" in both MUDPILES and ADICT.
100
Occuring 2-4 days after lack of ingestion of a particular substance, I am characterized by confusion, insomnia, vivid hallucinations, delusion, tremor, mydriasis, tachycardia, fever and diaphoresis.
What is Delirium tremens?
Alcohol withdrawal: Generalized coarse tremors starting 6-8 hours after last drink, intensifying up to 24-36 hours. First days: anxiety, insomnia, anorexia, sweating, facial flushing, mydriasis, tachycardia, and hypertension. Altered Mental status, nightmares, auditory hallucinations in 25% patients, peaking 24-36 hours. Generalized tonic-clonic seizures in 1/3 patients, usually within 12-24 hours, status epilepticus in 3%; recurrent szs more likely in those with previous withdrawals.
* Delirium tremens in 5%, 2-4 days after last drink; confusion, insomnia, vivid hallucinations, delusion, tremor, mydriasis, tachycardia, fever, diaphoresis; may last 1-3 days and replapse over weeks.
for DT, aggressive IV fluids, may require high dose bezodiazepines 5-10 mg IV Q1-4 hours
Alcohol withdrawal: Generalized coarse tremors starting 6-8 hours after last drink, intensifying up to 24-36 hours. First days: anxiety, insomnia, anorexia, sweating, facial flushing, mydriasis, tachycardia, and hypertension. Altered Mental status, nightmares, auditory hallucinations in 25% patients, peaking 24-36 hours. Generalized tonic-clonic seizures in 1/3 patients, usually within 12-24 hours, status epilepticus in 3%; recurrent szs more likely in those with previous withdrawals.
* Delirium tremens in 5%, 2-4 days after last drink; confusion, insomnia, vivid hallucinations, delusion, tremor, mydriasis, tachycardia, fever, diaphoresis; may last 1-3 days and replapse over weeks.
for DT, aggressive IV fluids, may require high dose bezodiazepines 5-10 mg IV Q1-4 hours
100
After a characteristic latent period of about 12 hours, severe manifestation of toxicity include anion gap acidosis, visual disturbance, blindness, respiratory failure, seizures and possibly coma.
What is methanol intoxication?
100
100% O2 and sometimes hyperbaric O2 is my antidote
What is carbon monoxide toxicity?
symptoms include headache, AMS, vision changes, and coma. Nausea/vomiting are common. Arryhtmias and myocardial ischemia or infaction. pulmonary edema (primary cardiac disturbance or from smoke inhalation). Delayed neurologic manifestations are common.
symptoms include headache, AMS, vision changes, and coma. Nausea/vomiting are common. Arryhtmias and myocardial ischemia or infaction. pulmonary edema (primary cardiac disturbance or from smoke inhalation). Delayed neurologic manifestations are common.
100
Oxygen saturation gap is useful when you suspect my ingestion
What is Carbon monoxide?
Oxygen saturation gap: differences between oxyhemoglobin percentage as measured by Pulse Oximetry (SPO2), or as estimated from arterial oxygen tension (PaO2), when compared with the oxyhemoglobin percentage (SaO2), as measured by co-oximetry.
If you suspect CO, cyanide, hydrogen sulfide, presence of an acquired hemoglobinopathy (methemoglobinemia), arterial blood must be analyzed by a co-oximeter, to measure concentrations of oxyhemoglobin, deoxyhemoglobin, methemoglobin, and carboxyhemoglobin.
Oxygen saturation gap: differences between oxyhemoglobin percentage as measured by Pulse Oximetry (SPO2), or as estimated from arterial oxygen tension (PaO2), when compared with the oxyhemoglobin percentage (SaO2), as measured by co-oximetry.
If you suspect CO, cyanide, hydrogen sulfide, presence of an acquired hemoglobinopathy (methemoglobinemia), arterial blood must be analyzed by a co-oximeter, to measure concentrations of oxyhemoglobin, deoxyhemoglobin, methemoglobin, and carboxyhemoglobin.
200
I am suspected in the following presentation:
A 52 year old homeless man is brought by EMS after losing consciousness; his friend mentioned prior to the episode that he was flushing, complaining of headache, dizziness, was having nausea and vomiting, and then lost consciousness. Labs are:
ABG: 7.32, 32, 56
bmp: Na 135, K 3.3, Cl 109, HCO3 16, BUN17, Cr1.1, Gluc82. Ca8.2
Calculated osmolality 281, measured osmolality 303
, you notice a particular odor (not particularly unpleasant).
Diagnosis confirmed by measuring the serum level.
A 52 year old homeless man is brought by EMS after losing consciousness; his friend mentioned prior to the episode that he was flushing, complaining of headache, dizziness, was having nausea and vomiting, and then lost consciousness. Labs are:
ABG: 7.32, 32, 56
bmp: Na 135, K 3.3, Cl 109, HCO3 16, BUN17, Cr1.1, Gluc82. Ca8.2
Calculated osmolality 281, measured osmolality 303
, you notice a particular odor (not particularly unpleasant).
Diagnosis confirmed by measuring the serum level.
What is isopropanol toxicity?
Normal anion gap, high osmolar gap: acetone, mannitol, diethyl ether.
Isopropanolol is a component of rubbing alcohol and some other household components that may be intentionally abused by alcoholics as an alternative to ethanol. Clinical manifestation include GI irritation, upper GI bleeding, CNS depression, respiratory depression and ketosis. Diagnosis should be considered in patients with CNS depression, particularly when presenting with fruity breath (due to acetone production), unexplained ketosis, or an elevated serum osmolal gap.
Normal anion gap, high osmolar gap: acetone, mannitol, diethyl ether.
Isopropanolol is a component of rubbing alcohol and some other household components that may be intentionally abused by alcoholics as an alternative to ethanol. Clinical manifestation include GI irritation, upper GI bleeding, CNS depression, respiratory depression and ketosis. Diagnosis should be considered in patients with CNS depression, particularly when presenting with fruity breath (due to acetone production), unexplained ketosis, or an elevated serum osmolal gap.
200
My intoxication syndrome is described as a triad of depressed level of consciousness, mitotic pupils and decreased respirations.
What are opioids?
200
Do not use beta blockers to treat hypertension caused by my ingestion.
What is Cocaine?
Hypertension best treated with sedation and if necessary Ca channel blockers, sodium nitroprusside, or phentolamine. Pure beta blockers are contraindicated; unopposed alpha adrenergic activity may cause HTN or coronary vasospasm.
Other medications contraindicated: Phenothiazines and butyrophenone antipsychotics, succinylcholine, Class Ia antiarrhythmics (procainamide).
Hypertension best treated with sedation and if necessary Ca channel blockers, sodium nitroprusside, or phentolamine. Pure beta blockers are contraindicated; unopposed alpha adrenergic activity may cause HTN or coronary vasospasm.
Other medications contraindicated: Phenothiazines and butyrophenone antipsychotics, succinylcholine, Class Ia antiarrhythmics (procainamide).
200
Nausea and vomiting from my oral form may delay treatment; thus anti emetic therapy may be required.
My IV form is associated with higher rates of anaphylactoid responses; may be treated with decreased infusion rates and antihistamines
My IV form is associated with higher rates of anaphylactoid responses; may be treated with decreased infusion rates and antihistamines
What is N-acetylcysteine NAC?
200
Activated charcoal absorbs most toxins except 3 ingestions.
Hints: one makes you tipsy, the other stabilizes your mood, and the last makes you stronger.
Hints: one makes you tipsy, the other stabilizes your mood, and the last makes you stronger.
What are alcohols, lithium and iron?
300
We (one category) should be listed under UH's urine drug screen.
AMPHETAMINES 1000 NG/ML
BARBITURATES 200 NG/ML
CANNABINOIDS 50 NG/ML
COCAINE 300 NG/ML
METHADONE 300 NG/ML
OPIATES 300 NG/ML
PCP 25 NG/ML
PROPOXYPHENE 300 NG/ML
AMPHETAMINES 1000 NG/ML
BARBITURATES 200 NG/ML
CANNABINOIDS 50 NG/ML
COCAINE 300 NG/ML
METHADONE 300 NG/ML
OPIATES 300 NG/ML
PCP 25 NG/ML
PROPOXYPHENE 300 NG/ML
What are Benzodiazepines?
BENZODIAZEPINES 200 NG/ML
BENZODIAZEPINES 200 NG/ML
300
My early withdrawal presents with lacrimation, rhinorrhea, perspiration and yawning
What are opiates?
Patients with pure opioid withdrawal maintain normal mental status, therefore AMS should prompt a search for other factors contributing to the patient's condition.
Patients with pure opioid withdrawal maintain normal mental status, therefore AMS should prompt a search for other factors contributing to the patient's condition.
300
My overdose can cause an anticholinergic clinical picture but is predominantly characterized by severe cardiovascular and neurological toxicity.
What are tricyclic antidepressants TCA?
300
Precaution should be taken in the presence of a mixed overdose of an opioid and this substance when administering naloxone.
What is Cocaine?
Administration of naloxone may provoke serious sympathomimetic toxicity by removing the protective opioid-mediated CNS depressant effects.
Initial dose of 0.4 to 2.0 mg IV PRN, Question diagnosis, if no response is observed after 10 mg of naloxone have been administered.
neonates; initial doses of 10 to 30 mcg/kg IV are recommended.
Administration of naloxone may provoke serious sympathomimetic toxicity by removing the protective opioid-mediated CNS depressant effects.
Initial dose of 0.4 to 2.0 mg IV PRN, Question diagnosis, if no response is observed after 10 mg of naloxone have been administered.
neonates; initial doses of 10 to 30 mcg/kg IV are recommended.
300
Urine alkalinization enhances my elimination.
As a matter of fact, my moderately severe toxicity not meeting criteria for hemodialysis is the strongest indication for urine alkalnization.
Other hint: My toxicity can present with High anion gap acidosis.
As a matter of fact, my moderately severe toxicity not meeting criteria for hemodialysis is the strongest indication for urine alkalnization.
Other hint: My toxicity can present with High anion gap acidosis.
What are salicylates?
Urine alkalinization is a method of enhancing renal elimination of certain poisons by increasing urine pH to levels>7.5 through the administration of IV sodium bicarbonate (1-2mEd/kg IV during 3-4 hours). supplement with K if needed, and monitor urine pH every 1 hour, and serum electrolytes Q2-4 hours.
Urine alkalinization is a method of enhancing renal elimination of certain poisons by increasing urine pH to levels>7.5 through the administration of IV sodium bicarbonate (1-2mEd/kg IV during 3-4 hours). supplement with K if needed, and monitor urine pH every 1 hour, and serum electrolytes Q2-4 hours.
400
A 4 year old was playing in the garage with her cousin when she developed an unsteady gait, ataxia, myoclonic jerks, and started vomiting. Her mother noted a green puddle of automotive fluid on the floor. She took her to the ED to be evaluated.
I am the metabolite of the ingested agent that cause tissue injury.
I am the metabolite of the ingested agent that cause tissue injury.
What is oxalate?
Oxalate is the metabolite in ethylene glycol that causes tissue injury by combining with calcium to form calcium oxalate. Calcium oxalate can cause widespread tissue damage.
Oxalate is the metabolite in ethylene glycol that causes tissue injury by combining with calcium to form calcium oxalate. Calcium oxalate can cause widespread tissue damage.
400
My clinical toxidrome mnemonic is SLUDGE
What is cholinergic intoxication?
Salivation
Lacrimation
Urination
Diarrhea
Gastrointestinal distress
Emesis
Salivation
Lacrimation
Urination
Diarrhea
Gastrointestinal distress
Emesis
400
EKG#1
What is TCA cardiotoxicity?
Classical EKG changes are: sinus tachycardia, QTc prolongation, QRS complex widening, right axis deviation, and positive R waves in lead aVR. Treatment is based on EKG findings. Usually therapy is started when QRS is greater than 100ms.
consider TCA toxicity in any patient with confusion or coma, especially if tachycardia and QRS prolongation.
Classical EKG changes are: sinus tachycardia, QTc prolongation, QRS complex widening, right axis deviation, and positive R waves in lead aVR. Treatment is based on EKG findings. Usually therapy is started when QRS is greater than 100ms.
consider TCA toxicity in any patient with confusion or coma, especially if tachycardia and QRS prolongation.
400
I should be given as an antidote for ingestion related cardiotoxicity in the setting of ventricular arrythmias or QRS prolongation >100 ms.
What is sodium bicarbonate?
400
We many cause false positive results in opiate urine screens.
"not poppy seeds!"
"not poppy seeds!"
What are quinolones?
500
A 14 year old was prescribed macrobid and pyridium for a UTI. She presents 3 days later to the ED with dizziness and cyanosis. Methylene blue was administered and had no effect on her condition.
In understanding the possible causes of her persistent cyanosis, checking a blood test is useful to point to this disorder.
In understanding the possible causes of her persistent cyanosis, checking a blood test is useful to point to this disorder.
What is G6PD deficiency?
The patient's presentation was consistent with methemoglobinemia, which is treated with methylene blue. Many drugs including local anesthetics, sulfonamide antibiotics, phenazopyridine, dapsone, and chloroquine can cause methemoglobinemia.
Methemoglobinemia usually responds to methylene blue. Since it did not in this case, other causes of the cyanosis must be excluded or treated. Phenazopyridine can cause sulfhemoglobinemia, which is similar to methemoglobinia, but does not respond to methylene blue. Other explanations for a failure of methylene blue to reduce the methemoglobin might include the presence of Glucose 6 Phosphate Dehydrogenase deficiency or a deficiency of NADPH reductase.
The patient's presentation was consistent with methemoglobinemia, which is treated with methylene blue. Many drugs including local anesthetics, sulfonamide antibiotics, phenazopyridine, dapsone, and chloroquine can cause methemoglobinemia.
Methemoglobinemia usually responds to methylene blue. Since it did not in this case, other causes of the cyanosis must be excluded or treated. Phenazopyridine can cause sulfhemoglobinemia, which is similar to methemoglobinia, but does not respond to methylene blue. Other explanations for a failure of methylene blue to reduce the methemoglobin might include the presence of Glucose 6 Phosphate Dehydrogenase deficiency or a deficiency of NADPH reductase.
500
My intoxication causes hypotension, bradycardia, hypopnea, bradypnea, CNS depression and coma.
I killed Marilyn Monroe
What are barbiturates?
500
What is digoxin toxicity?
GI symptoms: anorexia, N/V, diarrhea
CNS symptoms: dizziness, impaired color perceptions
EKG abnormalities: supraventricular dysrrythmias, AV node block, ST depressions in lateral leads.
GI symptoms: anorexia, N/V, diarrhea
CNS symptoms: dizziness, impaired color perceptions
EKG abnormalities: supraventricular dysrrythmias, AV node block, ST depressions in lateral leads.
500
I should be used for ventricular arrythmias caused by cocaine.
What is a benzodiazepine?
500
Rumack-Matthew nomogram is used to guide my antidote administration.
What is Acetaminophen toxicity?
