CC Emergencies, Poisoning PDF

1/1/25 1 Acute Inhalation Injuries ▪Leading cause of fire-related deaths through 3 mechanisms ▪ 2 Hypertensive Encephalopathy ▪Goal: decrease SBP by 15-20% or DBP to 100-110 range ▪First line: Nicardipine or Labetalol; Nitroprusside drip ▪ 3 Ischemic Stroke ▪Treat for...

1/1/25 1 Acute Inhalation Injuries ▪Leading cause of fire-related deaths through 3 mechanisms ▪ 2 Hypertensive Encephalopathy ▪Goal: decrease SBP by 15-20% or DBP to 100-110 range ▪First line: Nicardipine or Labetalol; Nitroprusside drip ▪ 3 Ischemic Stroke ▪Treat for BP > 220/120; if so, decrease by 15% to below this threshold ▪First Line: Nicardipine, Labetalol, Nitroprusside ▪Goal: BP < 185/110 if a candidate for thrombolytic therapy only, otherwise, see above goal ▪ 4 Hemorrhagic Stroke ▪BP Goal: SBP 120-160 ▪Nicardipine or Labetalol ▪May need intracranial pressure monitor as well ▪ 5 Aortic Dissection ▪SBP goal 100-120 range ▪Esmolol or Labetalol ▪HR goal < 65 bmp ▪ 6 Hyperthermic Emergencies ▪Life threatening elevation of core body temperature > 40 C (104 F) and is due to a failure of normal thermoregulation 7 Heat Stroke ▪Signs & Symptoms ▪Hypotension ▪GI distress ▪Weakness ▪Outcomes ▪Shock 1 8  ▪Outcomes ▪Shock ▪Multiorgan failure ▪Rhabdomyolysis ▪MI ▪ 8 Severe Hyperthermia (Heat Stroke) Core body temperature > 40.5 C (105 F) ▪May be exertional, caused by exercise in high heat or humidity ▪Nonexertional occurs in elderly or very young during heat waves ▪Elderly persons taking anticholinergic, antiparkinsonian or diuretic drugs are most susceptible Clinical features ▪Hot dry skin, delirium, dilated pupil, muscle rigidity, tachypnea ▪Rhabdomyolysis, DIC, ARDS, renal failure and hepatic dysfunction can occur Treatment ▪Rapid cooling with sponging, fans, cooling blankets or ice baths ▪IV fluids, internal cooling by gastric or peritoneal lavage with iced saline ▪ 9 Heat Stroke Treatment ▪Primary means for non-exertional heat stroke is spraying the patient with a mist of lukewarm water and blowing fans on the patient with ice packs for neck (NOPE), axillary, and groin to help augment cooling ▪Cooling for goal of 101.3 (38.5 C) RECTAL temperature ▪Ice water immersion is recommended for exertional heat stroke in young patients if intubation or close monitoring is not needed ▪ 10 Malignant Hyperthermia ▪Genetically susceptible individuals prone to have malignant hypertension upon exposure to volatile gases 11 Neuroleptic Malignant Syndrome ▪Associated with use of neuroleptic medications and presents with encephalopathy, muscle rigidity, and autonomic instability and fever ▪ ▪Seen more with older typical antipsychotics, but can happen in the 11 ▪ ▪Seen more with older typical antipsychotics, but can happen in the atypical ones such as Olanzapine, Quetiapine, and Risperidone ▪ ▪Similar to serotonin syndrome – but this one lacks myoclonus and hyperreflexia and GI syndrome (usually) ▪ 12 Serotonin Syndrome Potentially life-threatening syndrome that is precipitated by the use of: ▪ 13 Neuro 14 Accidental Hypothermia ▪Young outdoor types or alcoholics/homeless/psychiatric cases ▪Can be of 3 degrees of severity: ▪Severe: < 28.0 (82.4) ▪Moderate: 28-32 (82.4 – 89.6) ▪Mild: 32.0 – 35.0 (89.6 – 95.0) ▪Osborne/J-waves appear at temperatures at less than 33 (91.4F) and should not be confused with cardiac ischemia ▪Requires passive external warming with insulating materials ▪ 15 Hypothermia ▪Mild 32 to 35C: Passive external rewarming ▪Moderate 28 to 32C- decreased shivering: Active external warming ▪Severe less than 28C- COMA: Active internal rewarming 16 Osborne Waves 17 Hypothermia ▪ECMO is recommended for those in cardiac arrest and hypothermia because maximizes the rewarming rate and can allow for hemodynamic support ▪ ▪Normal treatment of ventricular arrhythmias and asystole during hypothermia is ineffective until temperature is > 86.0F (30 C) ▪ ▪Aggressive rewarming is appropriate in all patients in suggestive clinical situation in absence of obvious irreversible signs of death 18  ▪Aggressive rewarming is appropriate in all patients in suggestive clinical situation in absence of obvious irreversible signs of death ▪ 18 Encephalopathy ▪Always give thiamine to prevent Wernicke encephalopathy and dextrose for hypoglycemia unless these diagnoses can be rapidly excluded 19 Alcohol Poisoning ▪Determine if alcohol is the only substance taken as multiple toxins can coexist with alcohol consumption: ▪ 20 Alcohol Poisoning ▪Anion Gap = MUDPILES (MAYBE NOT) ▪Plasma Osmolar Gap: > 10 is abnormal and is characteristic of all alcohols but lacks specificity ▪Gap > 25 highly suggestive of methanol or ethylene glycol poisoning, but gap may be normal later in presentation ▪Early administration of Fomepizole to inhibit alcohol dehydrogenase prevents the formation of toxic metabolites of ethylene glycol and methanol ▪ 21 Rubbing Alcohol ▪Measure serum osmolarity 22 Ethylene Glycol (Anti Freeze) ▪Urinalysis for crystals ▪ 23 Methanol Breakdown ▪Methanol, also known as wood alcohol, is a commonly used organic solvent that, because of its toxicity, can cause metabolic acidosis, neurologic sequelae, and even death, when ingested. ▪. 24 Methanol Breakdown ▪Pathophysiology 25 24 Methanol Breakdown ▪Pathophysiology 25 Methanol Breakdown ▪This may explain the reason for the latency of symptoms between ingestion and effect. 26 Methanol Breakdown ▪The eye damage caused by methanol has been well described. 27 Methanol Breakdown ▪Methanol also affects the basal ganglia. 28 Methanol Breakdown ▪Clinical Presentation:. 29 Methanol Breakdown ▪Neurologic manifestations: 30 Methanol Breakdown ▪Seizures may occur, generally as a complication of the metabolic derangement or as a result of damage to the brain parenchyma. ▪ 31 Methanol Breakdown ▪Vision loss: 32 Methanol Breakdown ▪Physical examination helps to rule out other causes of altered mental status and visual dysfunction, the 2 most common presenting signs of methanol intoxication. 33 Methanol Breakdown ▪With large ingestions of methanol, depressed cardiac contractility heralds circulatory collapse and leads to signs of heart failure, cardiac arrhythmias, or both. ▪Neurologic examination - in addition to the progression of symptoms from drowsiness to stupor to coma, ocular findings in patients with methanol poisoning are prominent during a careful neurologic examination. ▪ 34 35  ▪ 34 Methanol Breakdown ▪Workup: ▪ ▪ 35 Methanol Breakdown ▪Treatment and Management: ▪Prompt medical care is key to avoiding complications secondary to methanol intoxication. ▪Metabolic acidosis in methanol poisoning may necessitate the administration of bicarbonate and assisted ventilation. ▪Antidote therapy, often using ethanol or fomepizole, is directed towards delaying methanol metabolism until the methanol is eliminated from the patient’s system either naturally or via dialysis. ▪Hemodialysis can easily remove methanol and formic acid. 36 Methanol and Metabolism 37 Serotonin Syndrome 38 Carbon Monoxide ▪Smoke inhalation as leading cause of accidental exposure ▪Higher affinity for hemoglobin binding and will form carboxyhemoglobin which is ineffective at transport of oxygen à tissue hypoxia ▪Headaches, confusion, nausea/vomiting, and loss of consciousness can occur ▪DOES NOT LOWER OXYGEN SATURATION on pulse oximetry ▪Co-oximetry – measures carboxyhemoglobin levels used to make diagnosis ▪< 3% is normal, but can be 10-15% in heavy smokers ▪ 39 Carbon Monoxide ▪Cardiac ischemia is common in these patients, and they can have delayed cognitive dysfunction usually and may not arise until months later if they survive that amount of time ▪ ▪ 40 41  ▪ 40 Increased Carboxyhemoglobin Level ▪Functional anemia- one third of this patient’s blood is not carrying oxygen. Heart get’s pissed. I NEED O2. HAVE SOME TROPONIN JERK 41 42 Cyanide Poisoning ▪Usually through fires and occupational exposure but rarely from medications like sodium nitroprusside ▪Cyanide disrupts oxidative phosphorylation forcing cells into anaerobic metabolism ▪Severe multiorgan dysfunction with coma, seizures, and cardiovascular symptoms such as hypotension, bradycardia, heart block and ventricular arrhythmias ▪Presentation is non-specific ▪Lactic acidosis ▪Bright red venous blood ▪Cherry red skin color (classic, but infrequent) ▪Prompt empiric treatment is critical as labs will not return in time to save the patient ▪ 43 Cyanide Poisoning ▪Treatment: ▪Hydroxocobalamin binds intracellular cyanide to form cyanocobalamin which is harmless. ▪Nitrites induce production of methemoglobin – binds cyanide to form much less toxic cyanomethemoglobin. ▪Sodium thiosulfate is sulfur donor promoting conversion of cyanide to thiocyanate which is well tolerated in absence of AKI ▪IF CO poisoning is suspected as well à do not give nitrites as methemoglobinemia can impair oxygen delivery and worsen CO toxicity ▪ 44 Toxicity & Treatments of Drugs of Abuse Initial stabilization includes intubation for airway protection in those with decreased mental status, but a trial of naloxone is warranted any time opioid overdose is suspected, with increasing serial doses and 44 with decreased mental status, but a trial of naloxone is warranted any time opioid overdose is suspected, with increasing serial doses and even a drip might be required in some patients Might THINK about high doses ▪ 45 Flumazenil ▪GABA antagonist for overdose is controversial as this may cause rapid reversal and send patients of long time abuse into seizure activity ▪Benzo overdose is usually low risk, and should just be given supportive therapy ▪ 46 Acetaminophen ▪Acetaminophen: ▪Increased LFTs, INR, and cerebral edema & vomiting ▪N-acetylcysteine is the treatment ▪Transfer to liver transplant center if severe symptoms 47 Salicylates ▪Respiratory alkalosis/anion gap acidosis, tinnitus, agitation, confusion ▪Bicarbonate drip : Urine pH: 7.5 – 8.0 is goal, HD if AKI or severe toxicity ▪Alkalizes the urine and allows you to piss out the aspirin products ▪ ▪ ▪ 48 Metformin Toxicity ▪Poisons the mitochondria. Lactic Acidosis ▪Labs: FSBG, ABG/VBG, Chem 8, Mag / Ca/ Phos, Coags, Lactate, Beta-hydroxybutyrate, LFT. RULE OUT INFECTION ▪TX: Support care, Glucose management, fluids, HCO3, HD, Methylene blue 49  Methylene blue 49 Sulfonylureas ▪Hypoglycemia, confusion, seizures, anxiety, tremors, diaphoresis ▪ ▪Dextrose + Octreotide + Glucagon = temporizing measure ▪ ▪Monitor for hypoglycemia for 48 hours if large ingestions ▪ 50 51 Treatment of Status Epilepticus ▪0-5 min ▪First line à IV Lorazepam 0.1mg/kg (max 4mg/dose) q 5 min with max of 8-10mg or respiratory depression ▪IV Lorazepam 4mg ▪IM Midazolam 10mg ▪Also give 100mg IV Thiamine & IV Dextrose 50% 50mL (if hypoglycemic or alcoholic) ▪5-10 min ▪IV Fosphenytoin 20 PE/kg @ 150PE/min ▪IV Phenytoin 20mg/kg @ 50mg/min ▪IV Valproate 30mg/kg @ 3mg/kg/min ▪ 52 Treatment of Status Epilepticus ▪If convulsions continue (10-20 min) ▪Intubate the patient ▪IV anesthetic with antiepileptic properties and titrate to EEG and watch BP. May require IV Vasopressors to maintain a MAP greater than 65 ▪Midazolam 0.2 mg/kg bolus; then 0.05-2.0 mg/kg/h ▪Propofol 2-4 mg/kg bolus; then 20-65 mcg/kg/min ▪Pentobarbital 5-15 mg/kg bolus; then 0.5 – 5 mg/kg/hr. ▪If convulsions discontinued prior to intubation (10-20 min) ▪Obtain head CT ▪If persistent AMS à continuous EEG monitoring ▪ 53  ▪ 53 Non-convulsive Seizure ▪8-48% of comatose patients may have non-convulsive seizures. Delay in diagnosis and treatment is associated with a higher mortality ▪No single clinical symptom. ▪Subtle signs: ▪ 54 Calcium Channel Blocker Overdose ▪Gastrointestinal Detoxification- ▪Calcium- ▪Give Glucagon – ▪Vasopressors- ▪Insulin- ▪Methylene Blue- ▪Lipid Emulsion Therapy- ▪ 55 B-Blockers/CCB: ▪Bradycardia, hypotension, AMS in b-blockers ▪Atropine 1mg IV x 3 doses ▪Glucagon & calcium chloride ▪Vasopressors & transcutaneous pacemaker ▪High dose insulin & glucose ▪IV lipid emulsions ▪Add these treatments in sequence or all at once if severe in presentation ▪ 56 Digoxin Toxicity ▪Bradycardia, arrythmias, nausea/emesis, abdominal pain, confusion, weakness, and colored vision changes. (Yellow Halos around Objects) ▪Van Gogh- Starry nights. (Fox Glove Tea) ▪Most urgent step ▪ECG ▪Potassium level will be elevated 57 Digoxin Toxicity ▪MC manifestation of digoxin toxicity 57 Digoxin Toxicity ▪MC manifestation of digoxin toxicity ▪GI disturbance, Nausea and Vomiting ▪Can have any cardiac rhythm disturbance ▪MC cardiac dysrhythmia with digoxin ▪Paroxysmal atrial tachycardia with block ▪Severe acute toxicity- severe bradycardia, heart block, hyperkalemia 58 Strongest indication for Digoxin Immune Fab ▪Arrythmia ▪CNS disturbance ▪Hyperkalemia. Greater than 5 mEq/L ▪NO HD. It is too small, can not take it out ▪If no Fab. Atropine or cardiac pacing 59 TCA Overdose ▪Pharmacology ▪Anticholinergic ▪Alpha-Blocker ▪Serotonin, Norepinephrine and Dopamine reuptake inhibition ▪Signs of toxicity ▪QRS prolongation ▪Hypotension, Tachycardia, Respiratory depression 60 TCA Overdose ▪Laboratory Monitoring ▪Serial ECG, Chem 8, Mag, Phos, CPK, Hepatic Enzymes ▪Treatment ▪Charcoal less than 2 hours of exposure ▪Supportive care ▪Serum Alkalinization ▪Fat Emulsion 61 TCA’s ▪Hypotension, sedation, seizures, anticholinergic signs (agitation) ▪Bicarbonate infusions titrate to QRS (greater than 100 ms) ▪Benzodiazepines for seizures ▪PHYSOSTIGMINE CONTRAINDICATED 62 61 ▪Benzodiazepines for seizures ▪PHYSOSTIGMINE CONTRAINDICATED ▪ 62 Antihistamines ▪Anticholinergic signs + agitations/seizures ▪Benzodiazepines for seizures ▪Physostigmine if isolated anticholinergic overdose. Requires constant cardiac monitor & bedside atropine ▪ 63 SSRI/SNRI ▪Agitation, clonus, hyperreflexia, rigidity, fever, tachycardia ▪Benzodiazepines, cyproheptadine if severe ▪Venlafaxine has increased cardiac toxicity ▪ 64 Stuporous, disoriented and obtunded. Pills taken 45 mins prior ▪Naloxone, Thiamine and Dextrose ▪If no improvement ▪Intubate and lavage ▪When is answer flumazenil ▪??? Of seizures ▪ 65 Gastric Lavage ▪Contraindicated ▪After 2 hours- after 2 hours only 15% of the pills are left ▪Caustics ▪Lets TALK BEZOARS 66 Amitriptyline Overdose 67 Valproic Acid Overdose ▪Labs: Ca, Mg, Phos, LFT, CPK, Ammonia and Valproic ▪Toxic level: Greater than 200 mg/ kg ▪Levels ▪Greater than 450 mg/mL. IV L carnitine ▪Greater than 900 mg/mL. Consider HD (Also cerebral edema, coma, shock, pH less than 7.1 ▪Hyperammonemia (WATCH FOR CEREBRAL EDEMA). IV 68 69  coma, shock, pH less than 7.1 ▪Hyperammonemia (WATCH FOR CEREBRAL EDEMA). IV dextrose (suppresses gluconeogenesis), L-arginine 68 69 Signs and Symptoms Consistent with Elevated ICP Impending Herniation ▪Concern for IMPENDING HERNIATION ▪Dilated and non-reactive pupils ▪Asymmetric pupils ▪No motor response ▪Progressive decline in neurologic condition ▪Cushing’s response ▪Hypertension ▪Bradycardia ▪Irregular respirations ▪ 70 Medical Treatment of Elevated ICP ▪Mannitol ▪Administer 1.5 to 2 mg/ kg IV over 30 mins. If imminent decline is suspected ▪0.25 g /kg every 6 to 8 hours. Hold if serum mOsm/L is greater than 320 ▪Repeat dose associated with rebound cerebral edema ▪May cause kidney injury ▪Hypertonic saline: First line treatment ▪Volume expander and can be used if patient hypotensive with elevated ICP ▪23.4% 20 to 30 mL. If imminent decline is suspected ▪3% Saline with target serum sodium of 145-155 mEq/L ▪Hyperventilation on the ventilator: Not used much anymore ▪PaCO2 28 to 35 mmHg ▪Short term stabilization but associated with rebound elevated ICP ▪ 71 Organophosphates or Nerve Gas ▪SOB, excessive salivation, diarrhea, weak muscles, polyuria, and abdominal cramping. constricted pupils and wheezing 71 ▪SOB, excessive salivation, diarrhea, weak muscles, polyuria, and abdominal cramping. constricted pupils and wheezing ▪Blocking of acetyl cholinesterase ▪What first in management. Anticholinergic ▪Atropine ▪Most specific treatment ▪Pralidoxime ▪ 72 Lithium Intoxication ▪GI distress, confusion, agitation, ataxia, irregular coarse tremors, myoclonus, and DI ▪Photophobia, hyperthermia, seizures, coma, rigidity, myoclonus, hyporeflexia, cogwheel rigidity ▪Supportive therapy, IV Hydration ▪HD- serum lithium greater than 4 mEq/L OR IF levels greater than 2.5 mEq/L Plus signs of lithium toxicity 73 Bupropion Intoxication ▪Inhibition of dopamine and norepinephrine re-uptake ▪Cardiotoxicity- inhibition of gap junctions (Prolonged QRS and systolic heart failure). Blockage of cardiac potassium channels. Increased QTc ▪UDS- amphetamines ▪Dosing- 3 grams (Seizures) 10 grams (Toxicity) 74 Bupropion Intoxication ▪Latent phase (Sustained 24 hrs.), Neurotoxicity (Dilated pupils, delirium) Seizures, Cardiotoxic (Prolonged QRS/ QTc) (VA ECMO- refractory shock) ▪TX: Whole bowel irrigation (sustained release) ▪Supportive Care: Intubation, Vasopressors, Lipids, VA ECMO 75 Black Widow Spider Bite ▪Nausea and Vomiting, Waves of muscular pain, ABD Pain/ Cramping, Weakness, Tremors ▪Most common electrolyte abnormality ▪Hypocalcemia ▪Best initial therapy ▪Calcium 76  ▪Best initial therapy ▪Calcium ▪Most effective therapy ▪Anti venin ▪ ▪ 76 Critical Illness Myopathy ▪Steroids, Neuromuscular blocking agents, sepsis ▪Flaccid quadriparesis ▪Proximal greater than distal muscles ▪Respiratory weakness ▪Normal sensation ▪DX: EMG ▪Biopsy: Myopathy with loss of myosin ▪TX: Reduce Sedation, Physical Therapy