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Board Review 12/17/2012 What topic should we do for January Board Review? A. Adolescent B. Disorders of the eye C. Sports Medicine and Physical Fitness Multiple VERY helpful resources Data on signs and symptoms of toxicities Can help identify unknown toxins Management of ingestions 1-800-222-1222 Always have a high level of suspicion with an ingestion that there may be multiple agents involved i.e. check an acetaminophen level when another ingestion is suspected Very few initial signs/symptoms but high potential for poor outcome if missed Emetics (ie syrup of ipecac) Gastric Lavage Activated Charcoal Cathartics Whole bowel irrigation A 4 year old is brought in by her parents because 20 minutes ago they found her playing with an empty bottle of grandmas atenolol which they knew previously had approximately 15 pills in it. You have a high suspicion that she ingested the medicine. She is anxious appearing but awake and alert with a heart rate of 70 and BP of 82/39. Which of the following would be the most appropriate action at this time? A. Administer syrup of ipecac B. Observation C. Administer activated charcoal D. Administer N-acetylcysteine E. Draw an atenolol level Emetics (ie syrup of ipecac) or gastric lavage No longer recommended for use in the home or ER Only possible use must meet these criteria: Consultation with qualified medical personnel Substantial risk or serious toxicity of the substance ingested No access to any alternative therapy for at least 1 hour Administration within 30-90 minutes of ingestion Administration will not adversely affect later treatment (ie activated charcoal or N-acetylcysteine Absolute contraindications: Severe HTN or bradycardia Risk of or current AMS Ingestion of caustic, corrosive or hydrocarbon substance Activated Charcoal Organic product with numerous micropores that allow a large surface area of absorption **ONLY method of GI decontamination supported by poison control centers** Discussion about use in homes Best if within 60 minutes of ingestion Not for use when ingested substances are alcohols, corrosives, iron, or lithium; caution with hydrocarbons Dosing:0.5-1g/kg (adult range 25-100g); 10:1 ratio of AC to ingested toxin Can drink or give via OG/NG Contraindicated in patients with unprotected airway Cathartics (laxatives) Limited use; ? Benefit Sometimes given with dose of AC Whole bowl irrigation Enteral administration of osmotically balanced solution Can be used after AC Used for “body packers” A 3yo boy is brought to the ER at 7AM after his parents found him unresponsive in bed. The last time they saw him was at 2AM while they were cleaning up from a cocktail party. On exam he has diaphoresis and moans to painful stimuli. His vitals are T96.4, HR145, RR20, BP 83/34, Sp02 98%. His pupils are mid-sized and sluggish. Of the following, what is the MOST important test to obtain at this time? A. Acetylcholinesterase determination B. Bedside glucose C. Blood alcohol level D. Serum osmolality E. Urine toxicity Beverages, cough medications, mouthwashes, aftershaves Multiple over-the-counter preparations Clinical features Dose-related CNS depressant Ingestion of 0.5g/kg (1.5ml/kg body weight) can produce intoxication in a young child Induces hypoglycemia (especially in children)** Metabolism of ethanol creates a relative lack of pyruvate blocks gluconeogenesis hypoglycemia Hypothermia, inebriation, vomiting, ataxia, respiratory depression, coma, hypotension, death May mask toxicities from other ingestion drugs** Effects of stimulants are blunted Effects of other depressants may be potentiated Lab workup Ethanol level, serum electrolytes, glucose Watch for hypokalemia Screen for other ingestions Management Supportive, IVFs Correct electrolytes/glucose No antidote; good prognosis Your 3yo child loves blueberry soda. You found him in the garage with an empty bottle of Windex. Upon arrival to the ER the child is lethargic and minimally responsive to painful stimuli. An ABG shows 7.11/30/60/12. All of the following are possible treatment modalities for this child, EXCEPT: A. Ethylene glycol B. Sodium bicarbonate C. Leucovorin D. Folate E. Hemodialysis Windshield wiper fluid, cooking fuel, perfumes Methanol itself causes n/v, inebriation Metabolites (formaldehyde and formic acid) are more toxic CNS depression, anion gap acidosis (can cause multiorgan dysfunction), optic changes Testing: methanol level, ABGs Treatment: Sodium bicarb for acidosis Folate or leucovorin (can help eliminate formic acid) Ethanol: can help decrease formation of metabolites Hemodialysis for severe cases Most commonly: Antifreeze Causes severe metabolic acidosis and formation of calcium oxalate crystals in vital organs Hypocalcemia Nephrotoxicity Treatment Gastric emptying (if within 1hr) Correction of acidosis and hypocalcemia Thiamine and pyridoxine Cofactors in the non-toxic pathway of ethylene glycol metabolism Hemodialysis Gasoline is most common exposure Irritating to GI and respiratory tract Primary concern: chemical pneumonitis Aspirated low-viscosity hydrocarbons spread to large areas of lung; destroy surfactant; alveolar collapse; VQ mismatch; hypoxemia Direct capillary damage also leads to pneumonitis A2yo boy is brought to the emergency department by his father after they had spent several hours in the garage while the father worked on the car. The father reports that approximately 30 minutes ago he heard the child coughing and found him with an open bottle of lighter fluid in his hands. On exam, the child is awake and alert; temperature is 37.0°C, HR is 120 beats/min, RR is 24 breaths/min, BP is 90/60 mm Hg, and 02 sat 98%. Of the following, the MOST appropriate next step is to: A. Obtain urine tox screen B. Perform gastric lavage C. Reassure the father and discharge the patient home D. Obtain a STAT chest CT E. Place the child under observation Clinical manifestations Initial: oropharyngeal and gastric irritation Coughing and choking: could indicate inhalation of fumes; does not necessarily imply aspiration Vomiting from gastric irritation Aspiration: significant coughing and respiratory distress “petroleum” smell on breath, tachypnea, retractions, bronchospasm, wheezing, rales, Fulminant chemical pneumonitis: marked SOB and hypoxemia Fever within 6 hrs indicates tissue damage (not infection) Pulmonary damage reaches peak at 3 days after aspiration Diagnosis Based on history, signs/symptoms of respiratory involvement If symptomatic: ABG, CXR CXR findings can lag 4-6hrs after aspiration Management Asymptomatic patients: observe for 4-6 hrs If abnormal CXR: consider admitting Symptomatic: admit Supportive care; no use for abx or steroids Prognosis: good Chemical pneumonitis often resolves completely Rarely will have long term problems (pneumatoceles) Amitriptyline, clomipramine, desipramine, etc Used in children to treat enuresis Block acetylcholine, prevent reuptake of norepinephrine, and block sodium channels in the myocardium Clinical toxicity begins with 6-8hrs of ingestion and peaks within 24hrs** Clinical effects: Anticholinergic! Dry mouth, ileus, dilated pupils, urinary retention, tachycardia, HTN, flushed CNS: delirium, agitation, restlessness, hallucinations, convulsions Life threatening toxicity due to cardiac dysrhythmias You are called by the mother of a 3-year-old girl because the child appears confused and is pale and sweating. The mother thinks the child may have taken some of her grandmothers imipramine. You advise her to call 911 to have her taken to the ER. Of the following, what is the most appropriate action to take in the ER? A. CXR to evaluate for pulmonary edema B. EKG to monitor for dysrhythmia C. ECHO to assess cardiac function D. EEG to identify a seizure focus E. Serum measurement of imipramine Work-up Can check serum levels, but results do not contribute to treatment decisions EKG** Can help identify significant conduction defects Prolonged PR Widened QRS Single most useful prognostic indicator for convulsions or dysrhythmias OTc prolongation Rightward shift of axis AV block Ventricular dysrhythmias Management Activated charcoal for GI decontamination CNS toxicity (convulsions) respond to benzos Serial EKGs/monitor for the first 6 hrs after ingestion For cardiac dysrhythmias: Cardiac monitoring Continued until all toxic effects have resolved for 24hrs Sodium bicarb (1-2Meq/kg) Prognosis is good Resolution of toxicity generally in 24-48hrs Can have late (2-5days after overdose) fatal dysrhythmia but this is found in seriously ill patients A 16yo girl is brought to the ER by her parents after she admitted to taking two handfulls of acetaminophen (500mg) because her boyfriend broke up with her. Which of the following is the MOST important piece of information you must obtain in order to determine your next course of action? A. The name and address of the boyfriend B. History of previous suicide attempts C. How long ago the ingestion took place D. A blood gas measurement E. Glucose measurement One of most common medications used to treat fever and pain in children Most common analgesic overdose in children less than 6yo Toxicity arises from metabolism of the drug During hepatic metabolism of large doses, a toxic metabolite accumulates in the hepatocyte and causes damage to liver cells Minimum toxic dose: 140mg/kg Severe toxicity for ingestions >250mg/kg Initial signs/symptoms: nonspecific; nausea/vomiting Within 18-24hrs hepatic damage may become evident with increased LFTs If not treated, hepatic damage may worsen Either gradually resolves OR if severe, will progress to severe hepatic damage hepatic failure Hepatic failure: Coagulation abnormalities Encephalopathy In young children: altered ‘sleep/wake’ cycles, irritability Only accurate predictor of hepatic toxicity from acetaminophen is measurement of a level 4-10hrs after overdose Levels that fall above nomogram line may be associated with hepatic damage Treatment N-acetylcysteine Should be started within 10 hours of ingestion A 7 yo boy is brought to the ER due to altered mental status. He was well when he came home from school, but when he came inside for dinner after playing outside with friends he complained of abdominal pain and had an episode of NBNB emesis. Over the next 30 min he became increasingly lethargic. In the ER, he is unresponsive and drooling. Temp is 98.8, HR is 50, RR is 36, BP is 100/60. Sp02 is 82% on room air. Pupils are small and sluggish. Breath sounds are coarse bilaterally with increased WOB. You suspect a toxin exposure. What is the most appropriate treatment? A. Atropine B. N-actylcysteine C. Naloxone D. Physostigmine E. Ethanol Found in a wide array of products Herbicides, pesticides, lawn care 70% of exposures occur due to ingestion of improperly stored products Mechanism of action: (Cholinergic poisoning) Irreversibly inhibits acetylcholinesterase leads to accumulation of acetylcholine excess acetylcholine overstimulates muscarinic, nicotinic, central receptors Muscarinic: “SLUDGE” (salivation, lacrimation, urination, diarrhea, gastric emesis), miosis, bronchorrhea/resp distress, sweating, bradycardia, hypotension Nicotinic: muscle twitching, weakness, paralysis Central: confusion/AMS, HA, tremor, seizure, coma Treatment Decontamination Skin washing, activated charcoal Blocking effects of excess acetylcholine Atropine: give every 10-30min until muscarinic effects gone Reactivating acetylcholinesterase Pralidoxime: best if given within 24-48hrs Supportive measures Ventilation, IVFs, vasopressors A 2-year-old boy is brought to the emergency department after his father found him with the leaf from a foxglove plant in his mouth. He has had one episode of emesis and is complaining of abdominal pain. On physical examination, his heart rate is 140 beats/min, respiratory rate is 24 breaths/min, blood pressure is 100/60 mm Hg, and oxygen saturation is 100%. His pupils are 4 mm and briskly reactive to 2 mm. The remainder of his examination findings are normal. After administering activated charcoal, what is the most appropriate next step? A. B. C. D. E. Abdominal xray EKG Serum creatine phosphokinase Serum sodium Head CT Ingestions most common in children < 6yo Fewer than 10% result in need for medical treatment Most ingestions are small in quantity and symptoms are generally short-lived GI effects are most common Treatment based on suspected ingestion/symptoms ABCs Decontamination: activated charcoal Reversal: Physostigmine for anticholinergic ingestion Cardiac monitoring for cardiac glycoside ingestion Call poison control for ANY question** They can help identify unknown plant Plant Toxic part Toxin/Class Clinical Features Datura (jimson weed) Atropa belladonna (nightshade All parts Atropine, scopolamine, hyoscyamine (anticholinergics) CNS: hallucinations, agitation Cardiac: HTN, tachycardia Other: blurred vision, dry mouth, flushing, hyperthermia Solanum (tomatoes, potatoes, eggplant) Blossoms or unripe buds Anticholinergics As above parasympathetic Miosis, bronchorrhea, GI distress, neuromuscular derangement Cardiac glycosides CNS: sedation Cardiac: conduction abnormalities (PR prolongation, QT shortening, bradycardia, ventricular arrhythmia) Hyperkalemia Tobacco plant Digitalis (foxglove), Convallaria (lily of the valley) Nerium (oleander) All, especially seeds Mistletoe berries Berries Prunus (cherries, apricots, peaches, apples, plums) Seeds, pits Mushrooms (ie Amanita) GI distress Cyanide Potentially lethal amatoxins Nausea, vomiting, diarrhea Late onset: fulminant hepatitis A 2 year old boy is brought to the ER because he has been difficult to arouse for an hour. The child is somnolent and responsive only to pain. His temperature is 101.5, HR 130, RR 56, and BP 90/60. ABG reveals pH 7.28/CO2 20/HCO3 15. The patient and his mom have been staying with grandma for the holidays. Mom is healthy, but the grandma takes a few different medications. The most likely explanation for this child’s findings is A. Intracranial hemorrhage B. Acetaminophen ingestion C. Metoprolol ingestion D. Sepsis E. Aspirin ingestion Remains one of the most serious ingestions in the pediatric population Toxic dose for a child = >150mg/kg Salicylates are found in various household products (not just in Aspirin tablets) Mouthwash Face cleanser Powders Bismuth compounds ETC… Symptoms Nausea and vomiting from DIRECT gastric irritation. Altered hearing…usually tinnitus Fever Altered mental status Agitation Seizures Stupor and coma Signs Tachypnea Tachycardia Non-cardiac pulmonary edema (due to increased vascular permeability) Anion gap metabolic acidosis!! Methanol toxicity Uremia Diabetic Ketoacidosis Paraldehyde ingestion Iron/INH toxicity Lactic acidosis Ethylene glycol ingestion SALICYLATES So be sure to rule these things out! Respiratory alkalosis **in young children the metabolic acidosis tends to predominate Global hypokalemia due to K+ excretion in the urine Initial alkaline urine HCO3 excreted in response to the respiratory alkalosis Later…acidic urine as the kidney tries to preserve K+ in exchange for H+ (which is excreted) Paradoxic aciduria in the face of respiratory alkalosis is a hallmark of aspirin toxicity Salicylate levels Peak 4-6 hours after ingestion Correlate poorly with clinical symptoms Should be followed q2-4 hours until decreasing or <30mg/dL You are admitting a patient to the PICU with findings suspicious for Aspirin toxicity. The patient was initially awake upon presentation and was already given activated charcoal. The initial salicylate level was 80mg/dL. You know that aside from supportive care, the next BEST step to enhance salicylate elimination is… A. Gastric lavage B. Alkalinization of the urine C. N-acetylcysteine D. 100% Oxygen E. Acidification of the urine Upon presentation Activated charcoal if the patient is alert Gastric lavage is NOT usually recommended UNLESS Ingestion was a large, life-threatening dose Brought to medical attention within 1 hour Correction of metabolic derangements and dehydration Fluid boluses Alkalinization to enhance salicylate elimination Goal serum pH 7.5 , goal urine pH >7.5 Rec: 1-2 mEq/kg bolus of NaHCO3 followed by a NaHCO3 drip **Add K+ to fluids of patients without renal failure Dialysis if level >100mg/dL or other worrisome signs Intubation can suppress hyperventilation and may be dangerous! Has no color, odor, or taste Has come to be known as the “silent killer” Accounts for most of the poisoning deaths in the US 300-500 people die annually from unintentional poisoning We, as pediatricians, need to be able to recognize the signs and symptoms CO is inhaled and absorbed into the bloodstream Forms carboxyhemoglobin by binding to hemoglobin with an affinity 250x that of oxygen Unable to transport oxygen Reduces oxygen delivery to the tissues by interfering with the dissociation of oxygen from the remaining oxyhemoglobin molecules People (and organs) with higher metabolic rates are affected most Infants and children are at a greater risk Neurologic, cardiac, and pulmonary manifestations are seen more often People living in the same home present with similar, nonspecific symptoms Fatigue Dizziness Headache Nausea Irregular breathing or dyspnea on exertion Palpitations Irritability/confusion/irrational behavior Patients may appear pale or cyanotic Symptoms can progress to LOC and death Symptoms may improve when patient leaves the place of exposure A 5 year old boy is brought to the ED for 2 days of HA, nausea, and vomiting. He is afebrile and does not have diarrhea. Everyone at home, including the dog, has the same symptoms. On PE, he is mildly irritable but alert and oriented, and his mucous membranes appear bright red. His lung exam is clear, but he does have some mild increased WOB. Sats are 100% on RA. What is the MOST appropriate next step? A. Admit the patient for continuous pulse ox monitoring B. Place the patient on 2L of O2 at 40% FiO2 C. Obtain a carboxyhemoglobin measurement D. Administer IV Methylene Blue E. Arrange for emergent hyperbaric oxygen therapy Measurement of carboxyhemoglobin levels can confirm exposure. Extent of exposure and/or measure CO-Hb levels may not correspond to severity O2 saturations obtained by routine pulse ox is falsely normal because O2-Hb and CO-Hb cannot be differentiated on standard pulse ox techniques ABG: metabolic acidosis with a normal PaO2 Separate patient from the source of CO exposure Decrease oxygen consumption by maintaining bedrest and diminishing anxiety Oxygen Should be provided until symptoms resolve and CO-Hb levels decrease to 5% or less 100% O2 via non-rebreather mask Decreases elimination half-life of CO to 1 hour Ventilatory support if needed Hyperbaric oxygen Indications for use are debatable EKG monitoring for cardiac dysrhythmia Counsel parents on important sources of exposure for children Traveling in vehicles Living in homes with poorly ventilated gas cooking and heating appliances Vehicles idling in attached garages Carbon monoxide detectors Show promise Effect on saving lives has not been demonstrated Corrosives are concentrated acid, alkaline, or oxidizing agents Many are common household products Laundry detergent Toilet bowl cleaner Stain and mildew removers Various cleaners Batteries Bleaches ETC! These products are often attractive to children and easily accessible in the home. Depend on the amount and pH of the substance and the nature of the contact Drooling, dysphagia Stridor or wheezing Burns on the mucosa, lips, chin, hands, nose, and chest Odynophagia Dysphonia Nausea/vomiting Chest pain Hoarseness Hematemesis A 3 year old boy was admitted for inpatient observation after presenting to the ER with a suspected corrosive ingestion. The patient was initially stable with no mucosal burns in his oropharynx. In fact, his examination on admit was normal except for fussiness. 48 hours later, the patient begins with gross hematemesis. Which agent was MOST likely ingested? A. An acidic corrosive B. Ethanol C. An alkaline corrosive D. Diet coke E. Acetaminophen Alkaline ingestions Cause deep, more extensive burns that may take longer to heal Cause liquefactive necrosis and tissue edema that affects the squamous epithelium Tend to injure the esophagus and pharynx Acidic ingestions Burn the top layer or skin, so children tend to stop drinking these substances more quickly Cause coagulation necrosis Squamous epithelium of OP and esophagus are fairly resistant MORE likely be transported straight to the stomach and manifest a little later Severe hematemesis, gastritis, strictures, gastric outlet obstruction A 2-year-old boy is brought to the emergency department after his mother found him with an open bottle of toilet bowl cleaner. She reports that he had spilled some on his shirt and had some on his face, but she does not know if he drank any of it. The child is awake and alert, and his vital signs are normal. He is drooling slightly, but examination of his oropharynx reveals no lesions. Of the following, the MOST appropriate next step is to A. B. C. D. E. Administer activated charcoal Give syrup of ipecac Perform a gastric lavage Observe overnight and the DC without further intervention Consult GI for an urgent endoscopy ABCs…with particular attention to airway! NO syrup of ipecac NO gastric lavage Re-exposes damaged mucosa to same corrosive agent Can lead to more necrosis and further damage Labs/Imaging Electrolytes, BUN/Cr, ABG if respiratory distress CXR to ensure no signs of aspiration pneumonitis, mediastinitis, or pleural effusion Endoscopy Within 12-48 hours!!! Assess extent of injury and look for burns/stricture/bleeding All household products should be moved up and our of the reach of children Corrosives should NOT be placed in unlabeled containers or food containers. They should be kept in the original packaging. Large labels/symbols of poison should be marked on the product, and kids should be taught the meaning of these symbols. 1-800-222-1222 kept close to phone Most health conditions associated with contaminants in food, water, the home, and the community present initially to the primary care physician. Children’s susceptibility to environmental contaminants differs from adults. Fetal development is affected by exposure to drugs, chemicals, and infections. Carcinogenic cells have more time to develop into tumors. Children eat more food, drink more water, and breathe more air than adults on a per kilogram basis…so they receive a “higher dose” of contaminant. Unique developmental stages increase their exposure to certain contaminants. What is the BEST method to screen for ALL types of environmental exposure in your general pediatrics patients? A. B. C. D. E. Obtain lead levels every 2 years on all patients Send a heavy metal screen on everyone Sample the drinking water of your patients Obtain a thorough environmental exposure history Do a personal assessment of all patient homes One of the most important tools in discerning the importance of environmental hazards for health consequences or to prioritize anticipatory guidance is the environmental history! Ask about generally recognized exposures of concern Tobacco smoke, lead, radon, pesticides, parents’ occupations Also focus on more locally relevant factors Toxic waste sites, wood smoke, well water, sports fishing In the context of illness or disease, an environmental history helps discern the link between environmental factors and the nature, onset, worsening, and improvement of symptoms. Community or public drinking water supplies are regularly monitored under the Safe Drinking Water Act. This oversight does not apply to the 15-20% of households in the U.S. that obtain their water from private wells. Asking patients about their sources of drinking water, such as whether it is from a public source or private well is a key component of the environmental history. What are the two MOST COMMON microbiologic WATER contaminants of concern for children? A. B. C. D. E. Salmonella and Listeria E. coli and Campylobacter Toxoplasma and Bacillus cereus E. coli and cryptosporidium H. pylori and Clostridium difficile Arsenic Known human carcinogen and potential neuro-developmental toxin Lead 20% of child’s exposure is attributable to drinking water Leaches into drinking water from lead-containing pipes “run water for 2 minutes before drinking…” Bacteria E. coli and cryptosporidium are the 2 most common Boiling water for at least 1 minute is required for decontamination (due to small size of cryptosporidium) Nitrate Common contaminant in well water from sewage contamination or fertilizer Young infants are at risk for METHEMOGLOBINEMIA due to the conversion of nitrate nitrate in their stomachs Trichloroethylene and perchloroethylene (industrial solvents) Community characteristics, such as proximity to pesticidetreated fields, high-traffic roadways, industrial sites, or waste sites should be assessed because contaminants can affect the health of children. Pesticides Industrial wastes Traffic pollutants The Air Quality Index can provide local information on daily air quality and help guide decisions on outdoor activities. Pets and people can track pesticide residues from treated fields to the indoor area and contaminate surfaces where children crawl and play…”take –home pathway.” Children spend most of their time indoors at home. More than 90% of the 2 million poisonings reported each year occur in the home Daily, low-dose exposure to contaminants may increase chronic health risks such as asthma or cognitive/behavioral problems Mold Leaks and water damage increase risk May result in URI symptoms, cough/wheeze/asthma in sensitized individuals Radon Estimated to cause 21,000 lung cancer deaths each year Comes from the radioactive decay of naturally occurring uranium in soil, rock, and water can infiltrate through holes in foundation. All homes below the 3rd floor should be tested!! Carbon Monoxide Improper or inadequate ventilation can allow build-up from household combustion sources (furnace, fireplace, attached garage) Discussion of a functioning CO detector should be a part of anticipatory guidance Household members that work Exposures may be brought home as dust or residues on clothing or shoes, so it is important to ask about parents’ occupations. Examples: farmers with pesticide exposure, painters, renovation workers, chemical plants, etc. Hygeine practices of removing work clothes/shoes and showering before entering the home can reduce the “take-home pathway” Improper remediation and repair may result in concerning indoor exposures. Asbestos Friable ceiling material or degraded insulation around pipes, boilers, and furnaces Use of asbestos-containing building materials has declines since the 1970s Lead Exposure is associated with a reduced IQ and behavioral problems, including ADHD Deteriorating lead-containing paint is the most common cause in young children Lead dust can form when paint is scraped, sanded, or heated Dust accumulates in windowsills, on floors, and in the soil Lead-based paint banned in 1978 Home repairs/renovations should be performed by trained individuals to apply special containment methods Most children will be asymptomatic Nausea/vomiting Management: Supportive care for GI upset Obtain additional history for possibility of co-ingestion (especially in adolescents) Clinical signs Depressed sensorium Bradycardia Hypotension +/- diaphoresis Management Observation on a CR monitor Most common foreign body ingested: COINS 95% will pass within 4-6 days If do not progress past the stomach in 24 hrs they should be removed Esophogeal Proximal esophagus: should be removed ASAP via endoscopy Middle-lower esophagus: observe for 12-24 hrs if asymptomatic Endoscopy if the coin does not pass Management depends on location of battery AP and lat radiographs from mouth to anus Esophageal Batteries lodged in the esophagus should be immediately removed with direct endoscopic visualization Stomach Usually pass in 48hrs Reimage after 48hrs If still present remove Toxic ingestion occurs at doses >40mg/kg of elemental iron Clinical manifestations Phase 1: vague GI complaints (v/d/abd pain) within 6hrs Phase 2: Decreased GI symptoms; deceptive improvement (hours 6-24) Phase 3: multisystem effects Metabolic acidosis Coagulopathy Cardiovascular collapse Phase 4: obstruction due to scarring/stricture Management ANY symptoms within 6 hours bring to medical attention Serum iron level >350, WBC >15, glucose >150 = BAD Symptomatic patient Abdominal films to identify iron tablets Chelation For severe symptoms, anion gap acidosis, iron level >500, pills visible on abdominal film Deferoxamine chelation Causes urine to be pink/red Can be stopped once urine returns back to normal color Anthrax Virtually all cases are cutaneous form Lesions: pruritic papule central bullous lesion becomes necrotic central black painless eschar Surrounding tissue is swollen and red; no tenderness Eschar falls off in 1-2weeks It is important to ask about complimentary/alternative medicines Especially in children with complex medical conditions such as autism Over-the-counter cough and cold preparations have not been adequately studied in children <6yo Not recommended for use to treat common cold Active ingredients for cold medicines Dextromethorphran, antihistamines, pseudoephedrine, guaifenesin Multiple side effects