Pediatric Poisonings

Epidemiology99% of ingestions by children under 6 are unintentional.Approximately 40% of ingestions reported to the poison center by adolescents are intentional.Approximately 56% of adolescent ingestions are by females.

DefinitonThe poison means to injure or kill with a substance that in known or discovered to be harmful .The term poisoning cannotes clinical symptomatology, it also implies that the toxic exposure is unintentional .The term overdose implies intentional toxic exposure , either in the form of a suicide attempt os as inadvertent harm secondary to puposeful drug abuse .The terms poisoning and drug overdose often are used interchargeably , especially when prescription drugs are the agents , even though definiton a drug overdose does not produce poisoning unless it causes clinical symtoms

The general approach to poisoning 1.Stabilization2. Laboratory assessment3.Decontamination of the gastrointestinal tract , skin , eyes4.Administrate of an antidote5.Elimination enhacement of the toxin 6.Observation and disposition

1.Stabilization Resuscitation with establisment of the airway , adequate support of ventilation .Particular attention should be dirrected to abnormalities in the cervical spine and temporomandibular joint

Continous cardiac and pulse oximetry monitoring

Maintenance of blood pressure and tissue perfusion ( may require the peovision of volume , correction of acid base disturbance , administration of pressor agents )

History The following questions may be revealing

What other medicines are in the house?What was the patient doung that day?Have there been recent emotionally or traumatic events ?Is the patient eating a special diet or taking a new health food , alternative medication or performance enhancer ?Could the patient inadvertently have taken too much of prescribed medication ?If it can be identified , is the substance non toxic?

Physical examinationBody temperature hypotermia( exposure to cold , hypoglicemia , barbiturates , ethanol ,overdose ) , hypertemia(LDS , cocaine , slicylates poisoning)Bradycardia overdose of digitalis ,beta blokers , calcium channel blokers but also it may be seen iwith hypotermia and spinal cord injury Hypertension intoxication with cocaine ,amphetamines , sympathomimetics Lungs inhalation of toxic gase s may produce wheezing - tricyclic antidepressant overdose pulmonary edema - pneumothorax in patients who smoke cocaine , methamphetaminaPupils pinpoint pupils overdose clonidine , opiates , organophosphate insecticids Level of consciousness

2.Laboratory assessmentComplet blood count Determination of serum electrolytes , glucose , BUN , creatinine and calcium , urinalysis ,prothrombin time , hepatic enzymes Pulse oxymetry , 12 lead electrocardiography Arterial blood gases The measurement of serum salicylate and acetaminofen levels is generally added in the case of the patient with overdose of un unknown substance , because these agents are often co- ingestants or are contained in combination drugsPerforming a urine pregnancy test in teenager girls is wise Urinary drug screening Chest radiography aspiration pneumonia , pulmonary edema ,Ct scan if underlying trauma is suspected Lumbar punction for ruling out meningitis in a patient with fever and coma

The range of dermal toxins is broad Most of these substances are corrosive agents capable of producing burns that may become full thickness( i.e third degree)Other types of agents are irritants , sensitizers , allergens , vesicants and exfoliantsThe skin of infants is notable for beeing more permeable than that of adults to substances of all classesIf the victim is immersed in atoxic fluid , the first step is his or her extrication , the victim should be disrobe , wash with water Emmergency medical personel should provide themselves every level available of self- protection 3.Decontamination of the gastrointestinal tract , skin , eyes

3.Decontamination of the gastrointestinal tract , skin , eyesInitial management of all chemical ocular injuries requires immediate decontamination by irrigation Early application of a topical anesthetic is recomandated to facilitate irrigation and anhance the patient comfort The most commonly available solution include sterile water , normal saline an lactated RingerThe upper and the lower eyelids should be retracted ,inspected for retained solid material and injury and irrigated Immediate refferal to an ophthalmologist is necessary for all significant burns

3.Decontamination of the gastrointestinal tract , skin , eyesGastric lavage involves blind placement of a large bore gastric tube into the stomach , in a patient who can either protect his or her airway or in whom the airway has been protected by an endotracheal tube , with the goal of removing toxicant remaining in the stomach through a combination of instillation of water or physiological saline , followed by suction or gravity induced drainage The cycle of instillation/drainage is repeated until the effluent in clear or until several liters of water /saline have been passed through the tube. Left recumbent Trendelenburgs position to reduce the risk of aspirationIndications recent ingestion( less than 1 hr , unless the ingestion involves agents that decrease gastric motility such as anticholinergics)Contraindications low viscosity petroleum products , corrosive and inability to protect the aiwayAdverse effects hypoxia , perforation of the gastrointestinal tract or pharynx, aspiration pneumonitis , electrolyte abnormalities

3.Decontamination of the gastrointestinal tract , skin , eyesActivated charcoal binds to diverse substances , rendering them less available for systemic. absorbtion from the gastrointestinal tract Single Dose 1 g/kg in children max dose 50 g , 25-100 g in adults , administred orally( in water ) or via nasogastric tube .Indication , fenitoin, glutetimid , acetaminofen , benzodiazepine poisoning Contraindications ingestion of caustics , in case of risk for gastrointestinal hemorrhage or perforation , in any patient in whom the airway protection is not assured , in case of ileus or mechanical bowel obstructionAdverse reactions and complications vomiting , duarrhea and constipation , pulmonary aspiration , direct administration into the lungs via misplaced nasogastric tube

3.Decontamination of the gastrointestinal tract , skin , eyesMultiple dose activated charcoal used in the case of drugs that undergo extensive enterohepatic or enteroenteric circulation Indication carbamazepine , dapsone , phenobarbital , quinine , theophyline

Contraindications same as for single dose - the presence of decreased peristalsis should provoke cautionCathartics magnesium salts and nondigestible sorbitol . May induce significant harm in children with renal disease .Manitol 20% - dose 4-5 ml/kg , Sorbitol 70% 1-2 ml /kg .Complications nausea , vomiting , hypermagnesiemia and cardiac dysrhythmias , dehydratation .

3.Decontamination of the gastrointestinal tract , skin , eyesWhole bowel irrigation involves administration , by mouth or nasogastric tube , of large amounts of an iso- osmotic polyethylene glycol electrolite solution with the goal of removing unabsorbrd toxicant from the gastrointestinal tract as rapidly as possible by rectal expulsion .Dose 25 ml /kg/hr for 4 -6 hr .Total dose 500 ml /hr under the age of 6 yrs , 1000ml /hr under the age of 10 yrs , 1500-2000 ml /hr in adolescentsIndications iron ,lithium , drug packets Contraindications mechanical or functional obstruction , gastrointestinal haemorrhage

4.Administrate of an antidote Only a small proportion of poisoned patients are amenable to antidotal therapy

Only a few poisoning is antidotal therapy urgent (e.g., CO, cyanide, organophosphate and opioid intoxication)

Specific Intoxications and Their Antidotes

5.Elimination enhacement of the toxin Forced diuresis by administering 2-3 times the maintenance fluid to achieve U.O = 2-5 cc/kg/hr (contraindicated in pulmonary or cerebral edema and renal failure)Urinary alkalinization to eleiminate weak acids(salicylates, barbiturates and methotrexate), can be achieved by adding NaHCO3 to the IV fluids, the goal is urine pH of 7-8 Serum alkalinization in triciclic antidepresant toxicityHemodialysis in low molecular weight substances with low volume of distribution and low binding to plasma proteins (barbiturate , methanol, ettilenglicol , heavy metals , lithium)Hemoperfusion, protein binding is not a limitation

Special Pediatric IssuesALL THINGS TEND TO END UP IN THE MOUTHS OF YOUNG CHILDREN!!

Which is Candy?

Sweet Tarts vs. Ecstacy

Physiologic DifferencesBlood brain barrier still more permeable to toxicologic substances until around 4 months.No studies demonstrating increased permeability, rather this is an estimate based on toxicity noted with smaller doses than expected.

Higher metabolic demands.

Decreased ability to glucuronidate in the infant period. Second trimester pregnancies that were terminated showed only 10% activity of the P-450 system.No better studies to date, but most believe between ages 2-4 years that glucuronidation is equivalent to adults.

Decreased glycogen stores.

Physiologic DifferencesIncreased body surface area can lead to thermoregulatory issues.

Children reside lower to the ground. This puts them at higher risk for ingesting compounds heavier than air. Often adults will NOT have the same exposure.

Inability to avoid hazards they do not read warning labels or Do Not Enter signs.

Acquired methemoglobinemia

- is caused by an external source, usually a drug or medication.

Methemoglobin is an aberrant form of hemoglobin arising from oxidation of iron in the normal heme molecule from the ferrous form (Fe2+) to the ferric (Fe3+) form. The presence of ferric heme molecules causes a structural change in the hemoglobin molecule, resulting in reduced oxygen-carrying capacity and impaired unloading of oxygen at the tissue.This left shift in the oxygen saturation curve results in functional anemia.Typically, red blood cells maintain a steady-state methemoglobin level of less than 1% via 2 main enzymatic pathways. Elevation in methemoglobin levels can be caused by congenital enzyme deficiencies or exposure to exogenous oxidizing agents that disrupt the equilibrium established by these pathways.

Causes Nitrates fountain water in the first year of life , Sulfamides , EMLA cream(lidocaine and prolocain),Nitric oxid ,Metoclopramid , Anilin diapers

With a methemoglobin level of 3-15% skin can turn to a pale gray or blue (cyanosis). With levels above 25% the following symptoms may be present:Cyanosis unaffected by oxygen administrationBlood that is dark or chocolate in color that will not change to red in the presence of oxygenHeadacheWeaknessConfusionChest painWhen methemoglobin levels are above 70% death may result if not treated immediately.Blood from the heel sticks is chocolate-brown and does not become pink when exposed to room air. Management

1. Laboratory data methemoglobin > 2% in new borne ,>1,5% in premature new borneChemistry serum electrolytes , liver enzyme , BUN , complete blood count ( CBC)

Management

2. Vital signs cardiac and respiratory stabilisation, seizures treatment , O2 3.Decontamination wash skin , gastric lavage( in case of ingestion)4.For acquired methemoglobinemia the typical treatment is with methylene blue. This is administered with an IV over a five-minute period and results are typically seen within 20 minutes. Methylene blue reduces methemoglobin back to hemoglobin. Dose 1 mg/kg , (concentration 1%) , max dose 7 mg/kgIf symptoms persist after 1 hour, repeat doses are given with caution, as accumulation of the drug can result in increased production of methemoglobin .5 .Ascorbic acid 30 mg/kg iv6.If symptoms persist despite the above-outlined therapy, hemodialysis might be required( metHb> 60% , hemolysis , sulfmethehemoglobinemia

Benzodiazepine Toxicity

Depending on the drug preparation and the presence of co -ingestants , the time from ingestion to appearance of the drug in the systemic circulation is 10-20 min .After absorbtion , benzodiazepines are higly protein bound , ranging from 70%-99%.

Protein binding is greatest with highly soluble drugs(diazepam 99% bound) and least with more water soluble agents( alprazolam 70% bound) .Only unbound drug is available to cross the blood- brain barrier and interact with CNS receptors .

Benzodiazepines are metabolized predominantly in the liver by oxidation and/or conjugation. Elimination of benzodiazepine metabolites usually occurs via renal clearance

Respiratory failure frequent -Triazolam ,Flunitrazepam ,

Paradoxical agitationSlurred speechAltered mental status, impairment of cognitionConfusionDrowsinessComa (Classic-isolated benzodiazepine overdose presents as coma with normal vital signs).Respiratory depressionHypotonia

Diagnosis Qualitative urine screening for the presence of benzodiazepnes or their metabolites provide rapid useful information in evaluation of patients with un unknouwn cause of CNS depression.A negative screening result does not rule out the presence of a benzodiazepine. Qualitative screening of urine or blood may be performed but rarely influences treatment.

Quantitative plasma measurements are not available in most hospitals and provide no significant therapeutic direction to the trating pshysician. Plasma concentration of benzodiazepines correlate very poorly with the severityof toxic effects( CNS depression) or mortality.

Physical Examination

Treatment

Single-dose activated charcoal is not routinely recommended as the risks far outweigh the benefit( fast absorbtion).

Activated charcoal - single dose 1 g/kg

Hypotension - use Dopamine

Coma and respiratory depression - Flumazenil 0,1 mg /kg in 30 sec , if the patient is still in coma after 30 sec a second dose will be use.In long-term benzodiazepine users, Flumazenil may precipitate withdrawal and seizures; in patients taking benzodiazepines for a medical condition, flumanazenil may result in exacerbation of the condition.

Respiratory support may be necessary

Barbiturate toxicity

Long action > 48 hr ( fenobarbital , mefobarbital) Medium action (amobarbital)Short action 3-4 hr(ciclobarbital,secobarbital)VeryShort < 30 min (thiopental)

Barbiturates mainly act in the CNS, though they may indirectly affect other organ systems. Direct effects include sedation and hypnosis at lower dosages

1. The CNS depressant effect mimics that of ethanol(ataxia ,slurred speech lethargy ,coma) 2. Coma - decreased pupillary light reflex ,decreased deep tendon reflexes , myosis in severe cases. 3. Respiratory exam -acute respiratory distress syndrome ,apnea,hypoxia

4. Cardiovascular exam hypotension,tachycardia,bradycardia,diaphoresis,shock 5. Renal dysfunction due to acute tubular necrosis( muscle necrosis and calcification may be associated with acute renal failure)

Physical Examination

6. Coma blisters are lesions that occur in the setting of a variety of neurological diseases. Although most commonly associated with barbiturate overdose, they can be seen in the setting of coma due to other etiologies. Blisters develop 4872 h after the onset of unconsciousness.They typically appear as blanchable erythematous pathches at pressure points of the skin .A biopsy of the lesion shows epidermal or subepidermal blisters with characteristic necrosis of the sweat glands .Over the next 2-3 days these patches become blisters or erosions , but they usually heal spontaneously over 1-2 weeksPhysical Examination

ManagementAttention to the airway and hypoxiaVital signs( risk of cardiovascular compromise and hypotermia)Ruling out hypoglicemia ( missing diagnosis can have grave consequences)Activated charcoal 1 g/kg , for patients who have a compromised airway , endotracheal intubation is advised prior to giving charcoalLaboratory evaluation basic electolites and glucose . Serum barbiturate levels can be useful in gauging the clinical course of therapy , screenin assays employing semiquantitative immunoassays of serum and urine are readly avilable . BUN , hepatic enzymes may have increased values .ECG ,EEG

ManagementUrine alkalinization is of theoretical value in the treatment of phenobarbital overdose but not overdose of other barbiturates According of the theory of ion trapping , phenobarbital , as a weak acid , will be poorly reabsorbed by the renal tubules if it can be ionized in the milieu of an alkaline urine (NaHCO3 1-2 mEq/kg until urinay Ph 7,5- 8 ) Such alkalinization is rarely achieved in clinical practce without the unwanted effects of metabolic alkalosis or hypernatremia .Multiple dose activated charcoal has been shown to be more effective in decreasing phenobarbital half life in adults and neonates .Extracorporeal removal by hemodialysis or hemoperfusion is also effective in removing the barbiturates , although they are reserved for the most severe cases

PesticidesSpecifically organophosphates and carbamates.

They work by inhibiting acetylcholinesterase.

Present with cholinergic symptoms

Cholinergic Symptoms

Cholinesterase - 2 forms1 . RBC form - true cholinesterase2. plasma form - pseudocholinesterase.

Cholinesterases hydrolyze the neurotransmitter acetylcholine into inactive fragments.Organophosphates form an initially reversible bond with the enzyme cholinesterase. The organophosphate-cholinesterase bond can spontaneously degrade, reactivating the enzyme, or can undergo a process called aging( the first 72 hours ,Oxime treatment can be used)The process of aging results in irreversible enzyme inactivation

Inactivation of the enzyme acetylcholine will accumulate at the synapse, leading to overstimulation and disruption of nerve impulses. Nicotinic stimulation at the motor endplate(Skeletal-muscle depolarization and fasciculations)Muscarinic effects occur at the postganglionic parasympathetic synapses, causing smooth-muscle contractions in various organs

Muscarinic SymptomsSweatingMiosisLacrimation and salivationBronchorrheaBradycardiaEmesis, diarrhea, Abdominal cramping and intestinal hypermotilityUrinary incontinence

Nicotinic SymptomsRemember the days of the week !MydriasisTachypneaWeaknessTachycardiaFasiculationsPediatric patients tend to present with a predominance of nicotinic symptoms!!!

Central nervous systemAnxietySeizuresCentral respiratory paralysisAltered level of consciousness and/or hypotonia

Weakness from Pesticides

Intermediate Syndrome- IMS -proximal muscle weakness , weak neck flexors ,respiratory failure -onset 24- 72 h after acute cholinergic crisis , can last several days or weeksDelayed polyneuropathy -symmetric demyelinisation processpatient notice the onset of weakness and paresthesias about 3-6 month after initial ilnessno known treatment , resolution over 6 month to 1 year

Laboratory test CBC count to rule out infectious causes.Chemistry tests may be useful in ruling out electrolyte disturbances, renal and liver testRBC cholinesterase tests may reveal decreased activity, which confirms the diagnosis.Chest x ray , ECG

TreatmentDecontamination involves removing all of the patient's clothing and washing him or her with water and soap.Ensure airway support and ventilationCirculatory support with intravenous (IV) access, fluids, and cardiac and pulse oximetry monitoringGastric decontamination with activated charcoal should be performed in cases of ingestion.

TreatmentAtropine 0.02 mg / Kg IV. Repeat as needed and titrate to respiratory secretions. It will likely take massive doses!!(every 3-5 min)Toxogonin (for Romania) 4-8 mg/kg iv in 30 min , will adm again after 4-6 h Pralidoxime (2-Pam) 20-40 mg / Kg bolus followed by 10-20 mg / Kg /hour infusion.Fresh frozen plasma 10 ml/kg Remember to send RBC and Plasma Cholinesterase levels upon arrival and daily.

Corrosive injury

Clinical Presentation

1.Hyperacute phase - ( first minutes 1 h ) - retrosternal pain , dysphagia , hematemesis , salivation , dysphagia ,agitation, septic shock.Oropharyngeal examination ( specialist physician) hiperemia , edema , burns , false membranes2.Acute phase next 3 weeks , clinical signs of postcaustic esophagitis and complications (hematemesis , melenic stool , caustic laringitis secondary to glotic edema, respiratory distress , coughing , bronhospasm , asphyxia, esophageal or gastric perforation , abdominal pain ).The test of choice for proper stageing of esophageal burn severity is upper gastrointestinal endoscopy .3. Subacute phase 3- 6 weeks .General state will improve , patient without fever , without dysphagia .Systemic infections and aclorhidria can develop .Esophageal strictures ( corrosive alkalis) and piloric stenosis( corrosive acids) shall constitute in this phase .4.Chronic phase after 6 weeks , dysphagia for solid food and hipersalivation , dehydration , malnutrition. Treatment for esophageal strictures -repetead bougienage can be started in this phase +/- gastrostomy .

Hospital management -Intensive Care Unit -Otolaringologic exam

-General status , shock signs( arterial hypotension)

-Chemistry Complete blood count (CBC), electrolyte levels, BUN levels, creatinine level, and ABG levels may all be helpful as baseline values and as indications of systemic toxicity.

- Chest radiograph - pneumomediastinum , mediastinitis, pleural effusions, pneumoperitoneum, aspiration pneumonitis, or a button battery (metallic foreign body). The absence of findings does not preclude perforation or other significant injury.

- Endoscopy in the first 24 h but not in the first 4 h after ingestion

Treatment

- protection of the airway

-intravenous acces and fluid resuscitation , broad spectrum antibiotics

- Ranitidin 5 mg /kg , Omeprazol 1 mg /kg /iv

-Analgesic +/-narcotics Algocalmin ,Piafen , Morphine

-Steroids - Dexamethasone 1 mg /kg iv , the next 21 days orally may reduce the scars severity

- Liqiud food will be administred after 3- 4 days( milk , water )

Carbon Monoxide (CO)An odorless, colorless, tasteless gasResults from incomplete combustion of carbon-containing fuelsGasoline, wood, coal, natural gas, propane, oil, and methaneAffects 40 50,000 Americans annually who need to seek careKills an additional 6,000 persons annually in the USACO is the #1 cause of poisoning in industrialized countries

What Effect Does Carbon Monoxide Have on Hemoglobin? Hemoglobin molecules each contain four oxygen binding sitesCarbon monoxide binds to hemoglobinThis binding reduces the ability of blood to carry oxygen to organsHemoglobin occupied by CO is called carboxyhemoglobinBody systems most affected are the cardiovascular and central nervous systems

Effects of Carbon MonoxideOxygen cannot be transported because the CO binds more readily to hemoglobin (Hgb) displacing oxygen and forming carboxyhemoglobinPremature release of O2 prior to reaching distal tissue leads to hypoxia at the cellular levelInflammatory response is initiated due to poor and inadequate tissue perfusionMyocardial depression from CO exposure Dysrhythmias, myocardial ischemia, MIVasodilation from increased release of nitric oxide; worsening tissue perfusion and leading to syncope

Half-life of Carbon Monoxide Half-life time required for half the quantity of a drug or other substance to be metabolized or eliminated

CO half-life on 21% room air O2 4 - 6 hoursCO half-life on 100% O2 80 minutesCO half-life with hyperbaric O2 22 minutes

CO PoisoningSymptoms are often vague, subtle, and non-specific; can easily be confused with other medical conditions; Flu nausea, headachesFood poisoning - nauseaCardiac and respiratory conditions shortness of breath, nausea, dizziness, lightheadednessCO enters the body via the respiratory systemPoisoning by small amounts over longer periods of time or larger amounts over shorter time periods

Assessment for CO ExposureEMS may be summoned to monitor the air quality for the presence of carbon monoxideAirborne CO meters are used and documentation made whether there is a patient transport or notA more immediate concern is the level of CO in the patients bloodRAD 57 monitors are a non-invasive tool that allows results in less than 30 secondsRapid diagnosis leads to rapid and appropriate treatment

RAD 57 DeviceUsed like a pulse oxNon-invasive toolReadings within secondsHelps to quickly hone in a diagnosisUsed in ED and in the field

GuidelinesSpCO level readingsSpCO levels 5%5-10% normal in smokersIn non-smokers, treat with 100% O2EMS should be transported for further evaluation

SpCO levels >10%100% O2 and ED transportAssess the signs and symptomsSpCO levels >25%100% O2 and ED transportConsider a facility with hyperbaric chamber(infants , myocardial hypoxia , HbCO> 20-40%)

Signs and Symptoms CO PoisoningCarboxyhemoglobin levels of

Signs and Symptoms CO PoisoningCarboxyhemoglobin levels of 21 40%Moderate severityWorsening headacheConfusionSyncopeChest painDyspneaTachycardiaTachypneaWeakness

Signs and Symptoms CO PoisoningCarboxyhemoglobin levels of 41 - 59%Severe Dysrhythmias, palpitationsHypotensionCardiac ischemiaConfusionRespiratory arrestPulmonary edemaSeizuresComaCardiac arrest

Signs and Symptoms CO PoisoningCarboxyhemoglobin levels of >60%FatalDeath

Cherry red skin is not listed as a signAn unreliable findingRemember that SpO2 may be falsely normal

Pulse OximetryDevice to analyze infrared signalsMeasures the percentage of oxygenated hemoglobin (saturated Hgb)Can mistake carboxyhemoglobin for oxyhemoglobin and give a false normal level of oxyhemoglobinNever rely just on the pulse oximetry reading; always correlate with clinical assessment

Pulse CO-oximeter Device Hand-held deviceAttaches to a finger tip similar to pulse ox deviceMost commonly measured gases in commercial devices include Carbon monoxide (SpCO)Oxygen (SpO2)Methemoglobin (SpMet)Other combustible gases Without the device, need to draw a venous sample of blood to test for CO levels

Treatment CO PoisoningIncreasing the concentration of inhaled oxygen can help minimize the binding of CO to hemoglobinSome CO may be displaced from hemoglobin when the patient increases their inhaled oxygen concentrationsTreatment begins with high index of suspicion and removal to a safer environmentImmediately begin 100% O2 delivery , hyperbaric chamber

Treatment CO PoisoningGuidelines from different sources may vary when to initiate treatment based on SpCO levelsTreatment levels vary significantlyIf you do not have a CO-oximeter to use, maintain a heightened level of suspicion and base treatment on symptomsMonitor for complicationsSeizures(diazepam)Cardiac dysrhythmiasCardiac ischemia

Long Term Effects CO ExposureHypoxemia follows CO exposureEffects of hypoxemia from CO exposure is dependent on presence of underlying diseasesHypoxemia can cause the formation of free radicals dangerous chemicals

Long Term Cardiovascular EffectsMyocardial injury from hypoxia and cellular damagePump failureCardiac ischemiaLater development cardiovascular complicationsPremature death especially if myocardial damage at the time of initial exposure Factors increasing myocardial injury riskMale genderHistory hypertensionGCS

Long Term Neurological EffectsEffects are primarily affective (mood) and cognitive (thought)Increased depression and anxiety regardless if exposure accidental or suicidal attemptPhenomenon called delayed neurological syndrome (1 - 47% of cases)More likely if there was a loss of consciousnessBehavioral and neurological deteriorationMemory loss, confusion, ataxia, seizures, urinary & fecal incontinence, emotional lability, disorientation, hallucinations, mutism, cortical blindness, psychosis, gait disturbances, Parkinsonism

Mushroom poisoning Poisonous mushrooms contain compounds that are toxic to humans and animalsMode of action well known yet generally there are few antidotes available7 major toxin groups are recognized as poisonous and an 8th toxin group of mainly gastrointestinal irritantsToxins organized into 4 major categories based on physiological action

Mushroom poisoning - 2 major categories on the basis of the time from ingestion to the development of symptoms

1. Early symptom category Symptoms generally appear within the first 30 min 3 hours of mushroom ingestion . Favorable prognosis 2 . Late symptom category Signs and symptoms begin to appear between 6 and 24 hours after ingestion and may include hepatotoxic, nephrotoxic syndromes 1.Early symptom category - clinical exam Muscarinic syndrome - increased salivation, perspiration, lacrimation ,abdominal pain, severe nausea, diarrhea, blurred vision, and labored breathing within 15-30 minutes of mushroom ingestion. Death is rare but may result from cardiac or respiratory failure in severe cases.Coprine poisoning - 0.5-2 hours after ingesting ethanol include headache, nausea, vomiting, flushing, chest pain, and diaphoresis (as is typical of the disulfiram syndrome) and may last for 2-3 hours. Coprine-containing mushrooms generates a metabolite that inhibits acetaldehyde dehydrogenase.Ibotenic acid and muscimol poisoning ( Amanita pantherina) 30 min after ingestion delirium , halucination and coma

Mushroom poisoning - 2 major categories on the basis of the time from ingestion to the development of symptoms

A . Early symptom category Symptoms generally appear within the first 30 min 3 hours of mushroom ingestion . Favorable prognosis B. Late symptom category Signs and symptoms begin to appear between 6 and 24 hours after ingestion and may include hepatotoxic, nephrotoxic syndromes A .Early symptom category - clinical exam Muscarinic syndrome - increased salivation, perspiration, lacrimation ,abdominal pain, severe nausea, diarrhea, blurred vision, and labored breathing within 15-30 minutes of mushroom ingestion. Death is rare but may result from cardiac or respiratory failure in severe cases.Coprine poisoning - 0.5-2 hours after ingesting ethanol include headache, nausea, vomiting, flushing, chest pain, and diaphoresis (as is typical of the disulfiram syndrome) and may last for 2-3 hours. Coprine-containing mushrooms generates a metabolite that inhibits acetaldehyde dehydrogenase.Ibotenic acid and muscimol poisoning ( Amanita pantherina) 30 min after ingestion delirium , halucination and coma

B . Late symptom category

Severe intoxications , requiring Intensive care therapy .

Amanita phalloides poisoning

- Amatoxins are extremely potent hepatotoxins, are actively absorbed from the gastriontestinal tract . Once absorbed through the gut , amatoxins are transported into hepatocytes by non specific transport system .Circulating amatoxin is not metabolized but excreted by the biliary system and the kidney.Enterohepatic recirculation and biliary excretion of amatoxins are significants .They are not denatured by boiling ,and hence cooking deadly Amanita mushroom does not render them nontoxic . Clinical presentation 3 stages Stage 1 - 6- 24 h , after ingestion , - nausea , vomiting , cholera- like diarrhea , metabolic acidosis , anuria , hematuria.Stage 2 12-48 hr after ingestion apparent recovery , levels of hepatic enzyme rise during this stage Stage 3 24-72 hr after ingestion , progresive hepatic and renal failure , coagulopathy, cardiomiopathy , encephalopathy , convulsions , coma , death

Clinical forms

a.Benign forms without hepatic failure , complete cure in 10- 15 days . The patients will have gastroenteric syndrome ( 2- 5 days) , jaundice , hepathomegaly ( 3- 5 days).

b.Severe forms protrombinic activity 80-50% , cure in 3- 5 weeks .The patient will have gastroenteritic syndrome 3- 7days , astenia(2-3 weks) , high levels of hepatic enzymes( 1000-2000ui/l) , jaundice , hepatomegaly +/- digestive haemorrhage

c.Severe forms - hepatic enzymes rise 24-36 hr after ingestion , protrombinic activity< 50% , without encephalopathy ( cure in 4- 8 weeks) or death beetween days 7 -12 . The patient will have severe gastroenteritis , rising hepatic enzymes and toxic hepatitis .

Toxic hepatitis

Definition - citolitic hepatitis with onset in the first 24-36 hr .

Severe evolution in days 4 and 5 , significant augmentation of hepatic enzymes in days 3- 5 . 1.Severe hepatic failure decreased values of factor V < 50 % , without encephalopathy and jaundice 2. Extremely hepatic failure - decreased values of factor V < 50 % , with encephalopathy and jaundice .Renal failure is caused by hypovolemia in the first days , amatoxins will induce tubular necrosis from the day 5 .Biological test - rise of hepatic enzymes after 36 hr .Protrombinic activity will be decreased after 48 hr +/- Disseminated Intravascular Coagulation . Protrombinic activity < 3% and liver enzyme > 9000ui/l involve a severe prognosis .Evolution death in the days7-12 or cure in 2- 4 weeks .Liver cirrhosis is possible .

Treatment of Amatoxin PoisoningA . Admission in the first 6 hr

Supportive care - pump stomach, restore fluid balanceActivated charcoal to absorb toxins in stomach every 4-6 hrRehydrationOther treatments

Other TreatmentsSeveral drugs are thought to reduce uptake of amatoxins into liver cells based High dose penicillin G (incredibly high levels) - one million units/kg ( max 20 mil ui)Silibinin (water soluble extract of milk thistle) 25mg/kg /day ,every 6 hrCimetidin and N Acetyl cystein

Treatment of Amatoxin Poisoning

B . Admission after 6 hr Bad prognosis hepatic and renal failure , dehydration , encephalopathyTreatment 1. Hydration 2.Activated charcoal to absorb toxins in stomach every 4-6 hr3.Antitoxinic treatment4.Plasmapheresis - separate blood, remove plasma, replace with fresh plasma,5.Liver transplant4.Increased intracranial pressure Manitol 0,25-0,5g/kg

Psychoactive drugs

Legal highs are novel psychoactive substances wich are either synthetic chemicals , plant or fungal material wich are intended to elicit a psyhoactive response , being either stimulant , hallucinogenic , sedative or a combination of the three phenomena .Europe has seen an explosion in the number of new compounds (from 2008 ), that are appearing on the internet wich display high and close structural similarity with existing and controlled drugs of abuse , but wich are marketed as not for human consumption or even as plant food , bath salts , pond clear.

Synthetic compounds are cathinones , cannabinoides , amphetamines , piperazine ( cigarettes , pills , ) -Spice gold , Spice Diamond

Classification

1.Spice products - plants used asn a sunstitute for cannabis( for smokers)

2.Plant food - hallucinogenic or aphrodisiac plants (Scutellaria galericulata skullcap) , cannabinol

3.Bath salts mephedrone , effects cocaine like( nasal bleeding , nasal burns , halucinations, circulation problems , seizures , death)

4.Hallucinogenic plants mushroom (Amanita pantherina , Psilocybe) , piperazine derivates , cactus seeds

5.LSD - Ipomoes violacea and Agryreia nervosa seeds ,

6. Kratom ( Mitragina Speciosa) effects cocaine like ,contain piperazine ,induce addiction

Agryeia nervosa Mitragina Speciosa

Clinical presentation Increased sweating , hyperesthesia , anxiety , paranoia , depression , addictionCardiac involvement in plants alkaloid like Risk of death secondary to cardiac or neurological disturbances

Treatment There is no antidotal therapy Vital sign monitoring

****************************************************************************Pulse oximetry is a noninvasive method to determine oxygen saturation on the Hgb molecule and on some models, the pulse rate. Two wavelengths of light are emitted from the probe. Deoxyhemoglobin and oxyhemoglobin absorb different wavelengths of light at different rates. Pulse oximetry cannot determine the oxygen content of the blood, the amount of oxygen dissolved in the blood, the respiratory rate, the tidal volume or ventilation, cardiac output, or blood pressure. It cannot tell how much hemoglobin is abnormal (in the form of carboxyhemoglobin (COHb) or methemoglobin (MetHb)). In this respect, in the presence of CO poisoning, the pulse ox may give a normal reading when the O2 saturation of the hemoglobin is really low. Important to note is that oximetry readings may lag behind the actual hypoxic event.**Some of the area hospitals have now purchased a CO monitor device. Without the device, blood needs to be drawn and the sample taken to the lab for results.

The Pulse CO-oximeter uses 8 different wavelengths of light to detect different hemoglobin forms. These forms include oxyhemoglobin (O2Hb), deoxyhemoglobin (Hb), carboxyhemoglobin (COHb), and methemoglobin (MetHb). The pulse CO-oximeter provides the following measurements SpO2, SpCO2, SpMet, and pulse rate.**The administration of high flow oxygen will maximize oxygen saturation on available hemoglobin. As oxygen levels increase, some of the CO molecules will be displaced from hemoglobin. The half-life of COHb would be decreased. CPAP can help to fully saturate hemoglobin with oxygen.****************

Pediatric Poisonings

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Transcript of Pediatric Poisonings