Exam 3: the end is near Flashcards
if a child presents with an altered level of consciousness, metabolic disturbances, neurologic dysfunction, cardiac/pulmonary distress: ___
it is important to include toxic exposures as part of differential
supportive care in peds tox includes:
-begins with airway stabilization
-early antidote admin (if indicated)
what lab values do we want to initially get in children who present with toxicities?
-alcohol ingestion –> serum osmolality
-BBs or CCBs –> electrocardiogram
-always serum concentrations of acetaminophen
Gastric decontamination in peds tox: AC
-activated charcoal (consider use within 1 hr in pts with a potentially toxic ingestion)
–> dose: 0.5 - 1 g/kg
-multiple dose activated charcoal: use to prevent prolonged absorption or enterohepatic recirculation
–> dose: LD of 1 g/kg followed by 0.5 g/kg every. 4-6 hrs for up to 24 hrs
Gastric decontamination in peds tox: whole bowel irrigation
-performed using polyethylene glycol AND electrolyte solution
–> consider in pts who have ingested: sustained- release, enteric coated, iron or other metals
(can be given orally but admin via NG tube is easier in kids)
–> dose: 0/5 L/hr (small kids) up to 1.2-2 L/hr in older kids and adults for 4-6 hrs
**do NOT use miralax
Acetaminophen in ped tox
toxic ingestion: > 200 mg/kg (oral) or >. 60 mg/kg (IV) in kids
-GI decontam: AC within 1 hr
-Antidote: NAC (use IV & to prevent hyponatremia in children, product should be diluted to a concentration of 40 mg/dL)
Ethylene Glycol in ped tox
-engine coolant - has a sweet taste so kids and pets love it
-give IV pyridoxine 100 mg/day + thiamine 100mg/day until ethylene glycol metabolites are eliminated
Antidote: ethanol or fomepizole
Methanol in peds tox
ex: solvents, antifreeze, fuels, windshield washer fluid
-formaldehyde and formic acid cause lead to metabolic acidosis and blindness
-give folic acid 1 mg/kg (max 50 mg) every 4-6 hours for 24 hrs
Antidote: ethanol or fomepizole
Ethylene Glycol + Methanol Antidotes: ethanol (10%)
- can be oral or IV
LD: 8 mL/kg over 1 hr
Infusion: 0.8 mL/kg/hr
–> want serum concentrations of 100-150
Disadvantages: - requires central venous catheter
-central nervous system depression
-respiratory depression
-therapeutic drug monitoring
Ethylene Glycol + Methanol Antidotes: Fomepizole
1st line therapy!!
-load: 15 mg/kg , then 10 mg/kg q 12 h x 4 doses, 15 mg/kg q 12 h until serum concentrations are < 25
Advantages: no alternation in consciousness, no effect on blood glucose or electrolytes, no need for central venous access, no need for intensive care unit monitoring
what to do with a foreign body ingestion
-manual removal if impaction suspected
-battery may become lodged in the esophagus + result in serious life threatening complications
Signs & symptoms: vomiting, diarrhea, abdominal pain, fever, refusal to eat or drink, dysphagia
cough and cold preparations in peds tox
-avoid them in 6 years and younger, most cases lead to death
-GI decontamination: AC
-symptomatic management: htn (labetalol, nicardipine), arrhythmias (amiodarone) and seizures (benzos)
Strategies for poison prevention
-child proof caps
-child proof containers
-storage location
-environmental precautions
-taking appropriate doses
**disposal of unused, expired drugs
-never mix household products (ammonia and bleach = toxic fumes)
valuable information to collect when faced with a potential poisoning
-age and weight
-health history
-time of exposure
-route of exposure
-present symptoms
-exact name of product
-estimate how much may have been ingested
-strength of product
-formulation of product
General tx approach of poisoned pt
1- assess the pt: level of exposure, amount, symptoms
2- self tx (at home)?
3- referral to hospital: if its moderate to severe exposure or intentional ingestions
ABCDEs of management of a poisoned pt
-airway
-breathing
-circulation
-dextrose/decontamination
-EKG/elimination
Activated charcoal in a poisoned pt
-absorbant: 1 g/kg
-time window: 1 hr
-substances that will NOT bind: ionized metals, alcohols, gasoline
ADrs: vomiting, black tarry stools; want pts to have a protected airway
whole bowel Irrigation in poisoned pts
-polythylene glycol + electrolytes (1-2 L/hr PO/NG until rectal effluent is clear
-goal is to minimize time in GI tract for absorption
-beneficial for XR products and body packets
Orogastric lavage in poisoned pts
“stomach pumping”
-potential to produce serious toxicity
-use when no antidote exists
-time window gives reason to believe agent may still be in stomach
Hemodialysis in poisoned pts
-use when other elimination strategies are not effective/contraindicated
-potential to produce serious toxicity
-agent able to be removed through filtration
Anticholinergic toxidrome
-delirious
- high HR, pupils, BP, RR, temp
-signs: blindness, confused, hot, dry membranes, urinary retention, redness/flushing, tachycardia, no bowel sounds + hypertensive
Antidote: physostigmine (unpopular tho)
sedative- hypnotic toxidrome
-diazepam/ ethanol
-can see dec HR, BP, RR, hyperflexia
S&S: unresponsive but has response to painful stimuli
Adrenergic/Sympathomimetic toxidrome
-methamphetamine/ cocaine
-all vital signs inc, tremors
-S&S: agitation, SWEATY and bowel sounds present
Opioid toxidrome
-heroin/morphine
-decrease in all vitals, hyperflexia
S&S: unresponsive, unresponsive to painful stimuli, low HR + RR, see pinpoint pupils, bowel sounds are absent
Cholinergic toxidrome
(pesticides)
-dec pupil size, BP, HR, inc bowel sounds
SLUDGE: salivation, lacrimation, urination, defecation, gastric cramps, emesis
KILLER B’S**: bradycardia, bronchorrhea, bronchospasm (these will kill you, focus tx on these)
cholinergic toxidrome antidote
1: Atropine: 1 mg IB- titrate to effect,
-Pralidoxime (2-PAM): not used too often, but mainly for nerve gas agents/chemical warfare
Opioid receptors
-MU receptor: central pain analgesia, respiratory depression
-Kappa receptor: spinal analgesia, miosis (small constricted pupils)
-Delta receptor: central and spinal analgesia, cough suppression
exs of opioid agonists
-codeine
-fentanyl
-heroin
-morphine
-hydrocodone
-oxycodone
ex of opioid partial agonist
-busprenorphine (still hits on the opioid receptors)
ex of opioid agonist-antagonist
-nalbuphine
-butorphanol
-pentazocine
ex of opioid antagonist
-naloxone (used to reverse the opioids)
-methylnaltrexone, naltrexone, alvimopan (all used for substance use disorders, opioid induced constipation etc)
Opioid clinical presentation & management
Prezzy: decreased mental status, pinpoint pupils, decreased bowel sounds, depressed respiration
-management: administer antidote (naloxone), #1: PROTECT AIRWAY!
Naloxone use in opioid overdose
-non- opioid dependent: IV 0.4 mg
-opioid dependent pt: IV 0.04 mg and titrate to effect (increase by 0.04 mg; want to avoid acute withdrawal)
-bystanders: IN 4 mg (narcan)
-continuous infusion: 1/2 initial bolus dose and 2/3 of new bolus dose per hour
SEs: runny nose, flash pulmonary edema –> associated with high doses of naloxone upfront (acute precipitated withdrawal)
Naloxone induced pulmonary edema
-adrenergic response: tachycardia, tachypnea, hypertension
-shift in blood volume into the pulmonary vasculature: pulmonary vasoconstriction, pulmonary HTN, fluid leakage into lungs
TX: diuretics
Prevention: smaller initial doses of naloxone
Loperamide (used for opioid overdose)
-OTC anti-diarrheal
-inhibits intestinal peristalsis through u-opioid receptor agonism
Clinical presentation: opioid overdose, severe cardiac arrhythmias (when ppl abuse this med for its opioid effects)
-BBB: P-glycoprotein: usually shunts it from the BBB but in high doses the opioid can inhibit this and get into the BBB
-co administration of PGP inhibitors can enhance effects
Loperamide overdose management
Respiratory depression: Naloxone
Cardiac disturbances:
–> IV magnesium (for long QT intervals)
–>sodium bicarbonate
–> IV isoproterenol
–> transcutaneous pacing
- and then CPR and ACLS
Benzo overdose: drugs
-benzos work on Cl channels, binding helps facilitate GABA binding, opens up Cl- channels + CL- will flow causing inhibition of the CNS
Drugs: alprazolam, chlordiazepoxide, diazepam, lorazepam, midazolam, oxazepam
Flumazenil (used in benzo overdose)
-dose: 0.2 mg IV over 15 secs (peds- 0.01 mg/kg IV)
-competitiive antagonist at benzo receptor site (kicks off the benzos)
-onset: 1-2 mins
duration: variable, may need re dosing
Benzo withdrawal symptoms
-severe sleep disturbances
-irritability
-increased tension and anxiety
-panic attacks
-sweating
-dry retching and nausea
-palpitations
-headache
-psychotic reaction
-seizures (can be lethal)
To use or not to use flumazenil?
-benzos protectant effect, relatively non-lethal component of toxicity (death is usually due to losing the airway)
-benzo reversal can potentially cause lethal seizures
What to do in a polysubstance overdose
-elimination: activated charcoal
-administer antidotes: NAC
-supportive care: benzos (SO if you give flumazenil, you could reverse any protective effects that the benzos might be giving - so the drug really is controversial)
when is it safe to use flumazenil?
1- procedural sedation: being put to sleep for a short period of time, use on pts if its safe + wont precipitate a benzo withdrawal. may not completely remove the respiratory depression but will perk them up
2- unintentional, pediatric exposure: use where you dont want to do a lot of work up in peds. peds are usually not benzo dependent
effects of THC
-THC is the main component of marijuana that is responsible for the major psychoactive effects
–> mood elevation, euphoria, relaxation, creative thinking, and increased sensory awareness
Cannabinoid receptors
CB1: high levels int he brain regions, lack of CB1 receptors in the brainstem also explains lack of coma and respiratory depression seen with cannabis use
CB2: high levels expressed in periphery, expressed on a number of immune cells, isolated agonism of CB2 receptors has been the target for novel pharmaceutical candidates as anti-inflammatory agents
Medical conditions that MJ can treat
-anorexia
-anxiety
-asthma
-depression
-epilepsy
-glaucoma
-head injury
-insomnia
-mograine headaches
-multiple sclerosis
-muscle spasticity and spasms
-N/V
-pain
-parkinsons
-tourette syndrome
Clinical effects of phytocannabinoids: wanted effects
-mood elevation
-euphoria
-relaxation
-creative thinking
-increased sensory awareness
-appetite stimulation
-nausea suppression
Clinical effects of phytocannabinoids: paradoxical effects
-short-term memory difficulties
-agitation
-feeling tense
-anxiety
-dizziness
-lightheadedness
-confusion
-loss of coordination
Synthetic Cannabinoids
-sold as different types of smokables, incents etc that ppl smoke to get high
-synthetic cannabinoids are full agonists: higher receptor affinity & longer half-lives
Clinical effects of synthetic cannabinoids: desired effects
-mood elevation
-euphoria
-relaxation
-creative thinking
-increased sensory awareness
Clinical effects of synthetic cannabinoids: unwanted effects
-tachy/bracdycardia
-agitation
-irritability
-nausea
-vomiting
-drowsiness
-lethargy
-confusion
-seizures
-chest pain
-AKI
-CNS depression
-tremors
SO MUCH MORE!
Clinical presentation of synthetic cannabinoid used: Signs & Symptoms
-CNS depression
-disorientation
-restlessness/agitation
-hallucinations
-seizures
-combativeness
-anxiety
-mydriasis
-tachycardia
-vomiting
Clinical presentation of synthetic cannabinoid used: lab abnormalities
-dec potassium
-inc blood glucose
-inc creatinine kinase
-inc white blood cells
-inc creatinine/ AKI
synthetic cannabinoid used management
supportive, symptomatic care
-fluid, electrolyte replacement
-anti-emetics
-benzos
-ketamine
-intubation
cannabinoids: hyperemesis syndrome
-dysregulation of endocannabinoid system: desensitization and downregulation of CB1 receptors that generally have antiemetic effects
Diagnosis: hx of regular cannabis use, cyclic nausea and vomiting, generalized, diffuse abdominal pain & compulsive hot showers with symptom improvement
Hyperemesis Syndrome stages
1- pre-emetic or prodromal phase: months - years, diffuse abdominal discomfort, feelings of agitation or stress, morning nausea and fear of vomiting, increased use of MJ to treat
2- hyper-emetic phase: 24-48 hrs, cyclic episodes of nausea and vomiting, diffuse, severe abdominal pain
3- recovery phase: upon total cessation of cannabis, bowel regimens, fluids, electrolyte replacement and full resolution may take ~ 1 month
Hyperemesis Syndrome: clinical management
-hot showers : activate TRPV1
-capsaicin topical cream: activate TRPV1
-haloperidol: anti- nausea
-IV benzos: inhibitory effect on medullary and vestibular nuclei associated with nausea and vomiting
-fluids and electrolytes: supportive care
What is a sympathetic?
-inhibition of norepinephrine and dopamine reuptake, or increased release of neurotransmitters “uppers:
alpha1: vasoconstriction, increased peripheral resistance, increased blood pressure, mydriasis, increased closure of internal sphincter of the bladder
beta1: tachycardia, increased lipolysis, increased myocardial contractility, increased release of renin
Sympathomimetic toxidrome
-increased: BP, HR, RR, temp, pupil size, bowel sounds, diaphoresis
–> agitated, hyperalert, tremors, seizures
General management of sympathomimetic toxicity
supportive care
-elimination strategies (AC)
-#1: benzos
-anti- hypertensives
-fluids
-anti-psychotics
-electrolyte management
-ice baths
-sodium bicarbonate
sympathomimetic toxicity : cocaine
-typical line = 20-30 mg, ingestion of 1 gram is likely to be fatal
-euphoria, seizures, dysrhythmias, hypertension, coronary artery spasm, MI
-can have adulterants like levamisole (causes neutropenia, vasculitis, purpura)
-body backers are at high risk
Management: high dose benzos, supportive care
sympathomimetic toxicity : amphetamines
-MOA: releases catecholamines
-similar effects to cocaine but longer lasting
-causes agitation, seizures, hyperthermia, HTN, delirium
Management: benzos, barbiturates, anti-hypertensives & supportive care
sympathomimetic toxicity: bath salts
synthetic cathinones that cause: agitation, tachycardia, insomnia, paranoia, seizures, violent, unpredictable behavior
management: supportive care
sympathomimetic toxicity: others
-pseudoephedrine
-nootropics: ppl use it to stimulate a creativity boost or improve cognitive function
sympathomimetic toxicity: supportive care
clinical effects: #1- benzos
airway protection: intubation
hyperthermia: ice packs, cool fluids, antipyretics, benzos (high dose)
dysrhythmias: sodium bicarbonate, lidocaine
rhabdomyolysis: fluids