Exam 4 Flashcards
Most commonly involved drugs in adult poisoning
- analgesics
– sedatives/hypnotics/antipsychotics
– antidepressants
Approach to patient with unknown overdose
- contact Poison Control Center
- obtain H&P and PMH, although may not be possible
- assess underlying conditions, chronic illnesses, suicidal or not?
- MATTERS acronym
MATTERS acronym
- Medication/substance ingested
- Amount ingested
- Time of ingestion
- Toxicology of the drug
- Emesis/presence of pill fragments
- Reasons for ingestion
- Signs and symptoms
Rapid first look: toxidrome oriented physical exam
- vital signs – hypo or hypertensive, brady or tachycardic
- alert, responsive to voice, responsive to pain, or unresponsive
– pupil size, position, nystagmus - mucous Membranes
- skin temperature and moisture
– presence/absence of bowel sounds
– motor tone
General toxicology Diagnostics
- 12 lead EKG
– plain film radiographs; not much benefit unless packing or drug is radiopaque, or looking for aspiration - toxicology screens: acetaminophen, salicylates, “drugs of abuse” immunoassay, comprehensive urine drug screen
- CMP, K, calcium, glucose, liver enzymes, kidney function, CBC, lactate, ABG
ICU admission criteria for toxicology
- hemodynamic instability: hypotension, non-sinus rhythm, hypothermia, hypoxia
- signs of end organ damage: GCS < 13, unable to protect airway, confusion requiring monitoring for respiratory depression, renal failure, hypertensive emergency, heart block (other than first-degree), life-threatening electrolyte imbalances, rhabdomyolysis, DIC, seizures
- if none of the above are present, they can go to a general medical floor
Be aware of post admission delayed toxic effects
- Late toxic effects: sustained release drugs or problems with absorption
– acetaminophen peaks 24 hours post ingestion
– oral hypoglycemics, insulin, TCAs - methanol, Ethylene glycol, isopropyl alcohol peaks over six hours post ingestion
- ingested drug packets
Geriatric considerations for poisoning/toxicology
- Polypharmacy can lead to unintentional overdose; but do NOT rule out intentional overdose
- May have atypical presenting symptoms
– decline in GFR and creatinine clearance
Pathophysiology of acetaminophen toxicity
Small amount is metabolized to a highly toxic reactive intermediate called NAPQI. NAPQI is normally detoxified by glutathione, but when you take too much acetaminophen, the liver runs out of glutathione leaving a build up of the toxic byproduct NAPQI
acetaminophen toxicity presentation
- often asymptomatic or have mild G.I. symptoms at initial presentation
- can cause varying degree of liver injury over the next four days
- Time sensitive: people treated within eight hours of ingestion rarely have hepatotoxicity; hepatotoxicity can occur with ingestion of over 10 g in 24 hours
Four phases of acetaminophen poisoning
- phase 1: <24 hours; anorexia, malaise, pallor, n/v, diaphoresis
- phase 2: 24-48 hours; RUQ pain, abnormal LFTs
- phase 3: 48 to 96 hours; encephalopathy, coagulopathy, hypoglycemia, LFT peaks, rare – pancreatitis, ARF, MI
- phase 4: >96 hours; decreased LFTs, liver transplant, death, or recovery
Diagnostics for acetaminophen toxicity
- plasma acetaminophen level: must be 4+ hours after ingestion to be accurate/have utility
- baseline AST, AL T, PT/INR, creatinine, serum lactate
- toxicology screen
- Rumack-Matthew monogram: used to decide whether to treat with n-acetylcysteine (Mucomyst) or not
G.I.decontamination for acetaminophen overdose
- emesis and gastric lavage are not recommended
– activated charcoal can be considered if presenting within two hours of ingestion - give anti-emetics (especially if giving acetylcysteine orally)
Antidote for acetaminophen overdose
- Acetylcysteine
- if given within 8 HOURS of ingestion, serious hepatotoxicity and death are uncommon (do not delay giving waiting for the 4 hour level and Rumack Matthew nomogram)
Indications for acetylcysteine administration
- suspected single ingestion of > 150 mg/kg and patient with unavailable concentration
- patient with unknown ingestion time and serum level > 10 µg/milliliter
- patient with history of APAP ingestion and evidence of any liver injury
- patient with delayed presentation (>24 hours) with lab evidence of liver injury
Acetylcysteine dosing
20 hour IV protocol
- initial loading dose of 150 mg/kg IV over 15-60 minutes
- then administer a 4 hour infusion at 50 mg/kg at 12.5 mg/kg/hr IV
- finally administer 16 hour infusion at 100 mg/kg at 6.25 mg/kg/hr IV
72 hour PO protocol
- loading dose of 140 mg/kg PO then 70 mg/kg PO q4h for a total of 17 doses for 72 hours
Kings college criteria
- developed to determine which patients with fulminant hepatic failure should be referred for liver transplant
- PH < 7.3, PT < 100, Cr 3.4 mg/dL with grade 3 or 4 encephalopathy
Diagnostics for alcohol and glycol poisoning
- blood ethanol, methanol, ethylene glycol
- serum osmolality
- CMP
- ABG
Ethanol toxidrome
- CNS depression
- ataxia
- dyarthria
- odor of ethanol
Ethanol metabolism
- Gets broken down by liver enzymes to acetaldehyde and then to acetate
- acetaldehyde is toxic to the liver
- this process also creates free radicals which cause more damage
Ethanol management
- IV fluids
- thiamine (B1) deficiency is common in etoh dependence
— Wernicke’s encephalopathy is under-diagnosed and under-treated - if CNS depression: intubate, gastric lavage if < 1 hour
- charcoal NOT helpful
- observe and hold until sober or etoh is < 100 mg/dL
- watch for delirium tremens
- always assess for intent
Isopropyl management
- examples: rubbing alcohol, solvents for cosmetics
- can cause CNS depression: 2x more potent than ethanol and duration of action is 2-4x times longer than ethanol
- lavage and charcoal if within one hour of ingestion
- IV fluids
- if hypotensive despite treatment, HD to remove acetone
Isopropyl metabolism
Broken down by the liver to acetone
Examples of methanol
Found in wood alcohol, paint thinners, fuel additives
Methanol metabolism
Methanol gets broken down by the liver into formaldehyde and then into formic acid which causes metabolic acidosis and tissue injury
- formic acid is the toxic metabolite
Unique methanol symptoms
- takes 12 to 24 hours for methanol to become toxic due to metabolism timeframe
- Visual changes: non-reactive mydriasis, photophobia, papilledema
Methanol management
- lavage if within one hour of ingestion
- folinic acid: facilitates the breakdown of formic acid into CO2 and H2O
- IV NaHCO3 for severe acidosis
- HD for MeOH > 50 ml/dL, severe acidosis, renal failure, or visual symptoms
- antidote: Fomepizole
Fomepizole indications
- anion gap metabolic acidosis, visual disturbances, oxalate crystals in the urine, methanol concentration > 20 mg/dL
- stop the infusion when MeOH < 20 mg/dL or undetectable, normal pH, and is asymptomatic
Ethylene glycol metabolism
Gets broken down into glycoaldehyde and further into glycolic acid (glycolate) which is the toxic metabolite
Presentation of ethylene glycol poisoning
- timing can vary, stages can overlap, multiple organ systems are affected
- neurologic stage: 30 minutes - 12 hours
— glycol acid and calcium oxalate crystals – cerebral edema, seizures, infarction, meningolencephalitis - cardiopulmonary stage: 12-24 hours
— most deaths occur at this stage
— tachycardia, tachypnea, HTN, HF, acute lung injury
— Hypocalcemia: EKG changes are QT prolongation, myocardial depression, arrhythmias - renal stage: 24-72 hours
— due to calcium oxalate crystals deposition in proximal tubules, the most common major complication
— May need short term HD, can take kidneys weeks to months recover
Management of ethylene glycol poisoning
- charcoal and lavage if < 1 hour since ingestion
- correct acidosis with NaHCO3 of pH < 7.2 (used more in methanol poisoning)
- Fomepizole (same dose as MeOH)
- pyridoxine and thiamine IV
- HD for severe cases: glycol level > 50 mg/dL, pH < 7.3, hemodynamically unstable
Assessment findings of opioid overdose
- toxidrome: miosis (constricted pupils), respiratory depression, CNS depression, hypothermia, bradycardia, euphoria to coma
- IF MIOSIS AND RESPIRATORY DEPRESSION, ALWAYS CONSIDER OPIOID OVERDOSE
- non-cardiogenic pulmonary edema especially with heroin
- GI: Decreased bowel sounds and motility, ileus, nausea and vomiting
Opioid overdose management
- G.I. decontamination: no charcoal, no emesis, whole bowel irrigation for body packers (contraindicated if packages are leaking or bowel perforation)
- HD
- Surgery for a bowel obstruction or necrotic bowel syndrome
- antidote: naloxone
— goal is not a normal LOC, but adequate ventilation and spontaneous respirations
— 0.2-1 mg for apneic, minimum 2mg for cardiopulmonary arrest
Examples of cholinergics
- Direct cholinergic receptor stimulus: bethanechol (urecholine), pilocarpine
- acetylcholinesterase inhibitors: insecticides, organophosphates, neostigmine
Cholinergic toxidrome
Salvation, lacrimation, diaphoresis, vomiting, urination, defecation, bronchorrhea, muscle fasciculations, weakness, bradycardia, seizures
Management of cholinergic overdose
- aggressive dermal and G.I. decontamination: charcoal and lavage if < 1 hour of exposure
- treat seizures with benzos: lorazepam and diazepam
- antidotes
— atropine 2mg followed by double doses every 5 minutes until secretions are controlled
— 2-PAM can be given in severe cases
Anticholinergic overdose toxidrome
- Altered mental status, dry flushed skin, urinary retention, decreased bowel sounds, dry mucous membranes
- dry as a bone, red as a beat, hot as a hare, blind as a bat, mad as a Hatter, stuffed as a pipe
- can’t see, can’t pee, can’t sit, can’t shit
Anticholinergic overdose management
- observation, monitoring, supportive care
- Control agitation: benzos, phyostigmine
Beta blocker overdose assessment and findings
- cardiac: bradycardia, brady-dysrhythmias, conduction abnormalities, hypotension
- pulmonary: bronchospasm/constriction
- CNS: depressed LOC, seizures, coma
Beta blocker overdose diagnostics
12-lead EKG: progressively worsening sinus bradycardia, increased PR intervals, loss of atrial activity, AV junctional rhythm, widening QRS complex, AV block, idioventricular rhythm, asystole
Beta blocker overdose management
- hypotension: 20 ml/kg IVF, Trendelenburg positioning
- Inotropes: dopamine, milrinone (effect contractility)
- chronotropes: atropine, epinephrine (effect heart rate)
- HD, temporary pacemaker, CPR
Calcium channel blocker overdose assessment and findings
- CNS: Drowsiness, seizures, altered LOC
- cardiac: bradycardia, tachycardia, hypotension
- GI: Enteric dysmotility, bowel perforation
Calcium channel blocker overdose diagnostics
EKG: Bradycardia, tachycardia (reflects secondary to vasodilation), AV blocks, BBB, ST-T-wave changes
Calcium channel blocker overdose management
- G.I. decontamination: charcoal if < 1 hour since ingestion, gastric lavage, whole bowel irrigation
- hypotension: 1L boluses NS or LR
Digitalis overdose assessment and findings
- CNS: drowsiness, lethargy, headache, hallucinations
- cardiac: palpitations, dyspnea, bradycardia
- Visual: photophobia, yellow halo around lights, snowy vision
- GI: Anorexia, nausea, vomiting, abdominal pain
Digitalis overdose diagnostics
- SERUM DIGOXIN LEVEL: toxic = > 0.2 mg/dL
Digitalis overdose management
- G.I. decontamination: charcoal if within 6-8 hours of ingestion
- correct electrolyte imbalances
- antidote: digoxin immune fab (Digiband)
Salicylate overdose assessment and findings
- TINNITUS, TACHYPNEA, FEVER
- Altered mental status, tachycardia, diaphoresis
Salicylate overdose diagnostics
- serum salicylate level is symptomatic at 40 mg/dL, severe intoxication at > 70 mg/dL
Salicylate overdose management
- G.I.decontamination with activated charcoal
- urine excretion or alkalization
— LR or NS 10-20 ml/kg/hr until urine output of 1-1.5 ml/kg/hr is established
— IF > 40 mg/dL: 100 mEq NaHCO3 in 1L D5W - HD if serum level > 120 mg/dL, pulmonary edema, or volume overload
Benzodiazepine overdose toxidrome
CNS depression, ataxia, dysarthria, bradycardia, respiratory depression, dizziness, hypotension
Benzodiazepine overdose antidote
- Naloxone: 0.05 mg initially, increase PRN
- Flumazenil: begin at 0.2 mg IV
Antidepressant overdose assessment and findings
- CNS: altered LOC, delirium, seizures, psychotic behavior, hallucinations, stupor, coma
- cardiac: hypotension, dysrhythmias, tachycardia, torsades
- pulmonary: acute lung injury, hypo ventilation, aspiration pneumonitis secondary to CNS depression, ARDS
- anticholinergic: hypothermia, dry skin and mucous membranes, decreased gastric motility, urinary retention
Antidepressant overdose diagnostics
- 12-lead EKG: QTc prolongation, QRS prolongation
Antidepressant overdose management
- Dysrhythmias: give sodium bicarb until pH is 7.45-7.55 (do not give procainamide, beta blockers, or calcium channel blockers)
- hypotension: isotonic IVF, NaHCO3
- convulsions: benzodiazepines
- G.I. decontamination: activated charcoal
General information about trauma
- top etiologies: MVC’s, falls, violence, being struck by/against an object
- # 1 under recognized public health problem in the United States
Golden hour
- patient has 60 minutes from time of injury to receive definitive care after which morbidity and mortality increase significantly
- historically has been a tri-modal distribution of death but now is bi-modal
Advanced trauma life support underlying concepts and basic principles
Underlying concepts
- treat the greatest threat to life first
- never allow the lack of definitive diagnosis to impede the application of indicated treatment
- a detailed history is not essential to begin the evaluation of a patient with acute injuries
Basic principles
- injury kills in a certain reproducible timeframe: ABCDE approach
- Rapid initial assessment & primary treatment
ATLS Basics
Primary survey – very rapid initial assessment, seconds to minutes
Adjuncts to primary survey - additional tools/diagnostics/interventions we have at our disposal
Secondary survey - more detailed head to toe approach
Initiate definitive care – usually happening simultaneously
Tertiary survey - more complete head to toe
Hospital phase - preparing for arrival
- resuscitation area/trauma room/bay with functional airway support, monitoring equipment, protocol to summon additional assistance, warm IV crystalloids, transfer agreements when appropriate, standard precautions
- EFFECTIVE COMMUNICATION
The big six deadly problems
- airway obstruction – tension pneumothorax – open pneumothorax – flail chest – cardiac tamponade – massive external or internal hemorrhage
ATLS primary survey - A
Airway with restriction of cervical spine motion
Assess patency of airway plus simultaneous C-spine immobilization
Gag reflex, pooling or copious secretions/bleeding
Suction
Airway management
Airway maintenance
Drug assisted intubation agents a.k.a. rapid sequence intubation
ATLS – primary survey: airway management
- oxygen, anticipate vomiting, plan for a, B, and C
- predict a difficult airway: LEMON (Look externally (facial trauma, large incisors, beard, large tongue), Evaluate the 3-3-2 rule, Mallampati score, Obstruction, Neck mobility)
- +/- drug assisted intubation (DAI)
ATLS – primary survey: airway maintenance and definitive airways
- Chin lift, jaw thrust, nasal pharyngeal airway, oral pharyngeal airway, extraglottic/superaglottic devices
- definitive airways: oral endotracheal intubation, nasotracheal intubation, surgical airways breakaway cricothyroidotomy, tracheostomy
- indications for a definitive airway: inability to maintain patent airway by other means, inability to maintain adequate oxygenation, obtundation or combativeness resulting in hypotension, GCS < 8
ATLS – primary survey: drug assisted intubation agents
- Etomidate: Little hypotension, no analgesic affect
- ketamine: provides analgesia in addition to analgesic and sedative effect
- midazolam: amnesic properties, can result in hypotension, no analgesic effect
- propofol: dose-related hypotension, no analgesic effect
ATLS – primary survey: Breathing & ventilation
- expose neck and chest
– inspect and determine rate/depth/quality of respirations - auscultate, quick and dirty, do they have bilateral breath sounds?
- breathing management