Poisonings and Overdoses (PCP) PDF

Poisonings and Overdoses PCP  Objectives Understand common terms associated with poisoning/OD Understand/differentiate poisoning/OD routes Identify/discuss common overdose/poisons from home, recreation, prescription, and other sources Understand treatment fo...

Poisonings and Overdoses PCP  Objectives Understand common terms associated with poisoning/OD Understand/differentiate poisoning/OD routes Identify/discuss common overdose/poisons from home, recreation, prescription, and other sources Understand treatment for different poisonings/OD Discuss important history taking points  Contents Pharmacokinetics Marijuana General Hx & Tx Household Poisons Alcohol Acids/Bases Ethanol Petroleum products Isopropanol CO & Cyanide Methanol Food Poisoning Sympathomimetics Blister Agents Cocaine Prescription Drugs Methamphetamine Tricyclic Antidepressants MDMA Salicylates Depressants Acetaminophen Benzodiazepines Cholinergics Opiates Organophosphates Gamma-Hydroxybutyrate Anticholinergics Huffing Polypharm is the rule rather than the exception  Definitions Poison A substance, which upon contact or being introduced into an organism, impairs or prevents normal metabolic processes from taking place, thus altering the normal function of organs and tissues Alchemist’s Rule ‘Everything is a poison, it is a matter of dose.’  Definitions What is an overdose? An excessive dose It is the use of any drug in such quantities that acute adverse physical or mental effects occur. It can be deliberate or accidental; lethal or non-lethal.  Routes of Entry Inhalation Absorption Injection Ingestion  Routes of Entry Inhalation Anything airborne can be breathed in Fairly rapid Most frequent route Gases, vapors, smoke, fog, dusts, mists, fumes  Routes of Entry Absorption (Skin and Mucous Membranes) Includes the eyes Generally slower Intact skins provides barrier to some but not all poisons Causes absorption into systemic circulation Affected by blood flow/temp to area Some parts of body absorb more quickly (ie sole of foot vs skin folds) Lipid soluble chemicals more likely to absorb easily through skin (organophosphates)  Routes of Entry Ingestion Patient had to have been awake to take it Slow absorption Intentional Suicide Poisoned by other Unintentional Improper hand washing, smoking, eating, swallowing concentrated solid or liquid aerosols during inhalation Occurs most in children  Routes of Entry Injection Subcutaneously, Intramuscularly, Intravenously IV drug use Accidental high pressure injection Through a laceration Prescribed medication  Degree of Poisoning Factors that effect degree of poisoning include: Concentration Exposure time The substance's affinity for tissue Sensitivity of the exposed tissue Route of entry Age Liver ability  Alcohol Isopropanol Methanol Ethanol (ETOH) ETOH Withdrawal  Alcohol ADME Usually po A Can be absorbed parenterally through inhalation, PR, or IV Distributes equally through all water D carrying potential spaces Alcohol Anhydrase Aldehyde dehydrogenase M ETOH Acetaldehyde Ketones 95% Metabolization E 5% Sweat, urine, respiration  Alcohol MOA Binds to GABA, a receptor protein which causes CNS depression. Continuous stimulation of GABA increases stimulus threshold More ETOH is needed to reach the same effect as dependency increases Sub clinical S/S are caused by the depression of specific areas of the brain responsible for coordination, memory, logic, consciousness, respiration, airway protection etc. Extremely common co-contaminant  Isopropanol Common Sources Rubbing alcohol (70% isopropanol) Antifreeze Skin lotions Cleaning products Death is uncommon Isopropanol has 2-3 times the potency of ethanol and causes more damage to cells.  Methanol (methyl alcohol) Is an industrial solvent therefore found in cleaning supplies Most commonly windshield washer fluid 30 ml (1mg/kg) potentially fatal Alcohol Dehydrogenase Methanol Formaldehyde Formaldehyde causes irreversible systemic tissue damage including eyes (blindness), CNS, kidneys, GI, and liver destruction.  Methanol (methyl alcohol) Tx Prehospital Standard care Rapid transport  Methanol (methyl alcohol) Tx Clinical Aldehyde Acetate Methanol Formaldehyde NAC Tissue damage Ethanol  Ethanol (ethyl alcohol) Common Sources Alcohol Aftershaves Perfumes Mouthwashes Tx Standard care Recovery position Search for trauma (head injury)  Alcohol Withdrawal Excitatory Inhibitory Due to constant surplus of ETOH, cells lose GABA receptors. After Balance of excitatory ETOH is taken away, and inhibitory (GABA) the net result is excess neurotransmitter excitatory stimulation. receptors No chronic alcohol use Chronic alcohol use  Alcohol Withdrawal 24-72 Hrs > 7 days Moderate symptoms Symptoms develop. Seizures. generally taper Worsening mild off. May last symptoms. several weeks 8 Hrs Up to 7 days Mild symptoms Symptoms peak ++ autonomic DT may occur tone spontaneously. Seizures highly possible  Alcohol Withdrawal Mild symptoms ++ Autonomic activity Pallor Diaphoresis Essentially a prolonged Tremors anxiety attack Insomnia Abdominal pain Mood swings Palpitations Moderate symptoms Worsening mild symptoms Seizures HTN Essentially like a Hyperthermia sympathomimetic OD Mild confusion Delirium Tremens Hallucinations Agitation Delirium  Alcohol Withdrawal Delirium tremens showing Delirium tremens showing hallucinations and seizures and agitation. complete detachment This is post liberal from reality lorazepam use.  Alcohol Withdrawal “I've been through this severe kind of withdrawal many times. What you don't know is we're 100% conscious, fighting off unspeakably horrible hallucinations, and mental/physical anguish. Be assured he'd rather be dead than on that bed. Give him a gun and he'd pull the trigger instantly. 7 days later? He's a regular guy again. Alcohol... it gets thats bad. yes.” “I know exactly how this guy feels, DTs from alcohol withdrawal is agonizing, I wanted to die so it would be over.Very Scary.For those of you who think alcohol is not a drug and it's withdrawal is not as bad as heroin, your wrong!!” “I just went through this about 2 weeks ago they gave me everything that they could without overdosing me: tranxene orally and ativan IV. I wish I could explain what it feels like but there really is no words its just the most painful and horrifying thing that you could ever imagine.” “Guys i'm scared I'm going to be going into detox soon. PLEASE pray for me. Yes, it is going to be medically supervised.”  Sympathomimetics-Cocaine Can be snorted, injected, inhaled, or taken orally. Causes an increase in serotonin, NE, and dopamine in the CNS which leads to feelings of euphoria, excitement, and energy. Primary concern is cardiotoxicity and agitation  Sympathomimetics-Cocaine S/S ++ Sympathetic tone Tachycardia Tachypnea Mydriasis Hyperthermia Diaphoresis Chest pain Bruxism HTN These Stimulus hypersensitivity S/S are all subclinical findings of “normal” cocaine use. Unexplained sympathetic tone should prompt questions about drug use. The plateau of cocaine toxicity occurs at ~ 4 hours  Sympathomimetics-Cocaine Clinically significant S/S CVS Arrhythmias Significant chest pain CNS Encephalopathy (Seizures & coma) Excited Delirium Bruxism is repeated clenching of the Blood/MSK jaw. Rhabdomyolysis Drug associated delirium with Renal failure hyperthermia is associated with a Significant Hyperthermia significantly increased mortality rate, often due to poor airway management.  Sympathomimetics Crack Cocaine Crack is produced when the hydrochloride molecule removed, which frees the basic cocaine molecule, the so-called freebase. Heating does not destroy freebase, rather it melts at 98°C and vaporizes at higher temperatures; these are physical properties that allow it to be smoked. Same effects as IV cocaine  Sympathomimetics Amphetamines Examples Meth MDMA Ecstasy Mechanism of action and presentation nearly identical to Cocaine. Increases CNS and PNS Epi, NE, and Dopamine levels  Sympathomimetics Meth Relevant differences from cocaine: Duration of action up to 20 hours Dopamine Units Released MDMA (4 hours) 200 Cocaine (1 hour) 100-200 Sex (results may vary) 100-200 Meth (20 hours) 1250-highly addictive!  Sympathomimetics MDMA Relevant differences from cocaine: Duration 4-6 hrs Seizures are often caused by hyponatremia due to excessive water intake. Water intake is caused through a combination of hyperthermia, physical activity, and vasopressin release that is specific to MDMA  Depressants Opiates Examples: – Codeine – Fentanyl – Morphine – Demerol – Heroin  Depressants Opiates Endogenous opioids in the body (enkephalins) stimulate Mu, Kappa, and Delta receptors Effects Analgesia Decreased LOC Respiratory depression Miosis Opiates mimic the effects of Hypotension enkephalins in the CNS Decreased gastric motility  Depressants Opiate Withdrawal Chronic use of opiates requires a larger dose to achieve the same affect Euphoria is habituated faster than respiratory depression Sudden discontinuation of opiates, or narcan, will precipitate a withdrawal syndrome  Depressants Opiate Withdrawal 6 hrs Flu like symptoms Anxiety 72 Hrs-1 week NVD Severe abdominal cramps Severe anxiety Opiates-Tools for safe injection  Opiates Pharmacological Tx Naloxone (Narcan) Competitive opioid antagonist Shorter duration of action than opioid narcotics Methadone Long acting (24-36hr) opioid agonist. Methadone is usually given on a daily basis and decreases withdrawal symptoms which allows patients to continue with, and show up to, tapering detox programs. Suboxone (Buprenorphine + Naloxone) A long acting PARTIAL opioid agonist that does not produce a euphoria or respiratory depression. Naloxone is added to prevent euhporia or apnea that may be achieved with high doses of IV use.  Depressants Benzodiazepine Benzodiazepines are sedative-hypnotic agents Commonly are used for a variety of situations that include seizure control, anxiety, alcohol withdrawal, insomnia, control of drug-associated agitation Examples: Valium, Ativan, Versed, Rohypnol  Depressants Benzodiazepine Benzos mimic GABA Gamma-aminobutyric acid (GABA) is the major inhibitory neurotransmitter in the CNS Enhanced GABA neurotransmission results in Sedation Striated muscle relaxation Anticonvulsant effects Vasodilation  Depressants Benzodiazepine S/S: Nystagmus Hallucinations Slurred speech Ataxia Coma Weakness Altered mental status, impairment of cognition Amnesia Respiratory depression Hypotension  Depressants GHB Gama-Hydroxybutyrate GABA B receptor antagonist (different GABA than Ethenol and Benzos) Very narrow margin of safety (5:1) 1.5g (1g/ml)=euphoria vs 5-10g = respiratory arrest Onset 30 minutes Duration 4-6 hours  Depressants GHB S/S Sub clinical Euphoria Disinhibition Amnesia Clinically relevant Coma GHB OD showing confusion and Seizures decreased coordination. As Apnea intoxication progresses to apnea Hypotension patients will move between unconsciousness and violence on Bradycardia a minute to minute basis.  Depressants-Huffing Inhalants include any chemical that is intentionally taken via the pulmonary route to produce a mind-altering "buzz" or high. Example: solvents, aerosols, adhesives, fuels, dry-cleaning agents, tape-head cleaners, correction fluid, and propellants used in whipped cream (whip-its) and cooking sprays The typical abusers of inhalants are those aged 10-15 years, although use in children as young as 7 and 8 years has been reported.  Depressants-Huffing Most inhalants are central nervous system depressants. Inhalants do cause adverse medical effects on almost every system in the body. Both short- and long-term toxic effects occur. Acute neurologic symptoms include euphoria, auditory and visual hallucinations, slurring of speech, ataxia, diplopia, painful burns, tremulousness, and ataxia Most due to hypoxic event Short-term effects include diplopia, impaired memory, slurred speech, seizure, or even death from cardiac arrhythmias. Long-term chronic effects can cause permanent ataxias or sensorimotor peripheral neuropathies. Marijuana  Marijuana Most commonly inhaled (Onset within minutes) or absorbed po (onset within 1-2 hours) Overdoses are S/S generally well Euphoria tolerated by adults, but may cause Relaxation hypoventilation, Amnesia coma, and aspiration risk in Altered perception of time children. Accidental Enhanced tactile experiences ingestion is 600% more common in Tachycardia some states after Anxiety possible legalization.  Cannabinoid Hyperemesis Syndrome Long term chronic users are at risk of developing use related cyclical vomiting and intense abdominal cramping Home remedies include hot showers Generally resolves within 10 hrs of stopping marijuana use Haldol has been found to be effective for Tx  Common Poisonings Household products Plants Petroleum products Industrial products Agricultural products Organophosphates Acids & Alkalis  Household Poisons Acids and Bases Commonly a cleaning agent (ie bleach) Damage is dose dependant Acids cause burning of the esophagus, ulceration, and GI irritation. Chemically buffered in the duodenum with the body's natural HCl acid. Bases cause liquefaction of tissue for hours and is more difficult to buffer in the GI tract.  Household Poisons Acids and Bases Tx: Supportive care Transport Do NOT encourage vomiting  Household Poisons Petroleum Products MOA and Tx is similar for Acids and Bases Brake fluid, Gasoline, Oil Damage is caused by direct trauma to cells in contact with the product Widespread trauma can eventually lead to MODS  Household Poisons CO and Cyanide CO binds to Hgb 210x more than Cyanide inhibits the mitochondria’s O2. Therefore no O2 is ability to create ATP from Oxygen transported to the mitochondria. Created from combustion of Created from incomplete specific products such as plastics combustion of products  Household Poisons CO and Cyanide The end result is a failure for cells to carry out aerobic respiration which leads to lactic acidosis, cell death, MODS, and patient death. Tx Oxygen-100% oxygen reduces the duration of CO’s effects from 6 hours to 2 hours by competitively binding on Hgb sites Hyperbaric chamber-Reduces duration of CO’s effects to 30 minutes by increasing the PO2 in the blood. Cyanocobalamin (Vit B12)-binds to an inactivates the cyanide molecule  Household Poisons CO and Cyanide Hyperbaric chamber. No other treatments can be done during treatment therefore there is no benefit of a hyperbaric chamber for patients with any significant trauma or resuscitation needs.  Household Poisons Food Poisoning Food acts as a source or bacterial infection Causes gastroenteritis Generally self limiting. Risk of hypovolemia from excessive vomiting may require IV fluids.  Household Poisons Blister Agents Ammonia Cleaner Chlorine Bleach  Household Poisons Blister Agents Chlorine gas is an acid that causes direct trauma to the respiratory system Inhalation→ Inflammation→ Pulmonary Edema→ Hypoxia→ Death Tx is high flow oxygen and rapid transport before the tissue damage overwhelms BLS airway management. Do not enter a potentially unsafe scene until fire has cleared it or the patient is brought outside  Rx Drugs-Salicylates Used primarily to treat inflammation ASA--------------------325mg/tab Bengay topical------15mg/ml For an average 14 kg Oil of wintergreen--1400mg/ml toddler death can occur Pepto bismol--------15mg/ml with ingestion of only: 150mg/kg--------Mild toxicity 21 adult ASA tablets >500mg/kg------Lethal toxicity 1 teaspoon of oil of wintergreen 1 bottle of pepto bismol  Rx Drugs-Salicylates Salicylates cause damage through 2 primary mechanisms Directly poisonous to neural tissue Dramatically increases metabolism and breakdown of fuel sources in the body while inhibiting aerobic respiration. Early Transitionary Late 4-12 hours ~24 hrs Tinnitus Worsening ~4 hrs for ped N/V/D symptoms Metabolic acidosis Diaphoresis Agitation Rhabdo Respiratory Delirium Seizures/Coma alkalosis Hyperthermia Hyperthermia Dehydration  ASA Tx: Supportive care Manage airway during seizures Manage hyperthermia Rapid transport for gastric lavage if acute ingestion  Rx Drugs-Acetaminophen Anti Inflammatory & Antipyretic Death occurs due to direct damage to the liver which occurs ~ 12 hours post ingestion With early treatment (< 8hrs), it is easily treated with minimal Tylenol extra damage. strength-20 tablets toxic dose for acute ingestion Lethal dose 150mg/kg or 10g for adults  Rx Drugs-Acetaminophen Acetaminophen Toxic metabolite Large amounts of acetaminophen Normal overwhelm normal metabolism and takes a pathway side pathway which creates a toxic metabolite, eventually causing liver damage Harmless metabolite Liver damage  Rx Drugs-Acetaminophen Acetaminophen Toxic Tx metabolite NAC (given at the Normal hospital within 8 hours) pathway joins with the toxic metabolite to create a safe metabolite to be excreted by the body. Harmless metabolite Liver damage  Rx Drugs-Acetaminophen S/S: Nothing for 12 hours. Then.. RUQ pain NV Liver failure Jaundice Hepatic encephalopathy Hypoglycemia Coagulation dysfunction  Rx Drugs-TCA Tricyclic antidepressants (TCAs) cause the overwhelming majority of antidepressant poisoning resulting in morbidity and mortality A lethal dose of a TCA is only 8 times the prescribed dose Called tricyclic because metabolized three times by liver Each time makes new/different metabolite One of first major anti-depressents Now is last resort because more specific and less dangerous alternatives  Tricyclic Antidepressants (TCA) S/S: Less severe S/S are primarily caused by anticholinergic effects of TCAs Dry as a bone Red as a beet Mad as a hatter Hot as a hare Blind as a bat Peak toxicity occurs within 4 hours and any ingestion > 6 hours ago is unlikely to cause worsening symptoms  Tricyclic Antidepressants (TCA) S/S: (CCCA) Coma Convulsions Cardiac Acidosis Arrhythmias Caused by TCA’s Caused by TCA’s Commonly causes Anaerobic effects on effects on wide complex respiration serotonin and NE serotonin and NE arrhythmias at nerve terminals at nerve terminals, anticholinergic properties, and acidosis All of these are treated with sodium bicarb  Tricyclic Antidepressants (TCA) Examples Elavil Amitriptyline Impril  Cholinergics-Organophosphates Usually found in pesticides and weapons of war (sarin gas) Can be absorbed readily through skin Inhibits acetylcholinesterase, which increases the amount of Ach in the synaptic cleft. Cholinergics-Organophosphates Cholinergics-Organophosphates  Organophosphate Poisoning Muscarinic Effects S - salivation D-Diaphoresis/Diarrhea L - lacrimation U-Urination U - urination M-Miosis B-Bradycardia D - defecation B-Bronchospasm G - gastroenteritis E-Emesis E – emesis L-Lacrimation M - Miosis S-Salivation Organophosphate Poisoning Nicotinic Effects M - mydriasis (pupil dilation) T - tachycardia W - weakness H - hypertension, hyperglycemia F - fasciculations  Organophosphate Poisoning The most immediate danger of organophosphate poisoning is respiratory paralysis and seizures, mediated by constant stimulation by Ach at the NMJ. Fasciculations @ 22 seconds.  Organophosphate Poisoning Tx Standard care Airway management and oxygenation due to respiratory paralysis Aggressive fluid boluses to maintain BP (systolic of 90 or MAP of 65) Atropine (ALS) Versed (ALS)  Anticholinergic Poisoning Decrease the strength of Ach at the muscarinic junction either by increased AchE or competitive inhibition. The muscarinic junction is responsible for the processes involved in SLUDGEM and DUMBBELS Therefor, anticholinergic poisoning does the opposite Dry as a bone Red as a beet Mad as a hatter Hot as a hare Blind as a bat  Treatment for Poisoning Ensure scene safety Decontamination is paramount for treatment of patients. This should begin BEFORE the initial medical management. Remove all clothing and irrigate exposed areas to remove residual material from the skin. Treat pt in well ventilated room or outside Care is required to prevent secondary casualties. Maintain appropriate barrier protection and ventilation.  Treatment for Poisoning Airway management O2 Contact poison control IV therapy ECG ALS back up Notifying receiving treatment center so secondary decontamination area can be set up. Decontaminate yourself AND your truck  Management of Overdose Patient Scene safety LOC (must be continually reassessed) Airway management O2 IV therapy ECG Continual reassessment and management of symptoms as they occur Any other injuries? Excellent history ALS back-up  Special Considerations The following can speed up/slow down poisonings Age Gender Underlying risk factors Previous health considerations Always have a differential diagnosis  History Taking What was taken? Time it was taken? Route it was taken? How much / what concentration? Why it was taken? Any vomiting after ingestion? How many times? Any pill bottles / samples of what was taken?  History Taking For recreational drugs: Was amount / dose / route used usual for you? Was drug supplied by usual supplier or someone new? Questions?