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ED Fellowship --> Toxicology > Ingestion/inhalation/exposure > Flashcards

Ingestion/inhalation/exposure Flashcards

1
Q

Discuss risk assessment of button battery ingestion

A

Almost exclusively a peads problem. The majority pass through the GIT easily and without complication. Larger batteries may lodge in the oesophagus causing singificant complications including death particularly if diagnosis si delayed

<20mm are less likle to lodge in the oesophagus and cause complciaitons
>20mm more likley and can cause sever local corrsive injury within 2 hours
Age is an important predictor of severity with the most severe oesophageal injuries and fatalities occurring in childre younger tahn 4 years old
New battery is worse than old
May containt manganese, sliver lithium or zinc but the quantities available for absorption are insufficent to cause systemic heavy metal toxicity

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2
Q

Discuss mechanisms of injury with button battery ingestion

A

The most significant mechanism is the generation of bhydroxide ions at the negative pole of the battery caused by the current created through the adjacent tissue. THe resulting hydroxide acuumulation produces resutls equivalent to localised alkaline corrosive injury with tissue liquefactions and necoriss. Corrisve injury may develop within 2 hours of lodgement.

Potential complciations incude oesophageal perforation, tracheo-oseophageal fistual, aorto-oesophageal fistula and stricture formation.

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3
Q

Discuss IX of button battery

A

History or suspicion of button battery ingestion mandates plan AP and lateral XR of neck, chest and abdo

Typically will ahve a double ring or halo shap on AP view and a step off appearance on lateral

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4
Q

Discuss MX of button battery ingestion

A

Resus
ABCD

D: Endoscopic removal as soon as possible ideally witihin 2 hours of ingestion

  • allows both removal and examination for local complciations
  • a button battery passed through the pylorus in an asymptoamtic child can be left to pass
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5
Q

DIscuss risk assessment of carbon monoxide poisoning

A

Deaths almost always occur prehospital, for those who arrive at hospital risk assessment attempts to identify those at risk of myocardial injury

  • acute deliberate self poisoning by car exhaust fumes usually involves exposure to high concentration of CO for limited duration and lower risk of long term sequalae
  • Accidental occupational exposure often involves exposure to lower concentrations of CO for a prolonged duration and higher risk of long term sequalae

High risk features inlcude

  • signifaicnt loss of conciousness or coma
  • persistnat neurological dysfunction
  • abnormal cerebellar examination
  • metabolic acidosis
  • myocardial ischaemia
  • Age over 55 years

Pregnancy - feotal haemoglobin binds CO more readily and the feotus is at higher risk of complications

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6
Q

Discuss TM and TK of Caborn monoxide poisoning

A

CO has a 210 times the effeinity for HB than o2. binding therefore rends HB o2 transport less effective. Hypoxia resutls. In addition CO binds to intracellular cytochromes. CO also initiates endothelial oxidative injury, lipid peroxidation and an inflammatory cascade. The process is probably responsible for the delayed neurological sequelae

TK: the elimination half life of CO is determined by the dissolved o2 tension of the blood and varies as follows

  • 21% 240 minutes
  • 100% o2 - 90 minutes
  • 100% o2 at 3 atmospheres: 23 minutes
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7
Q

Discuss clijnical features of CO toxicity

A

Most patients present with headache, nasuea and varying degrees of altered mentation, which rapidly resolve with o2 therapy. transient LOC is common

CNS

  • headache, nausea, dizziness
  • confusion poor concentration, MMSE errors
  • incooridnation and ataxia
  • seizures and coma

CVS

  • Tachy and hypertension
  • ischaemic ECG changes
  • Hypotension
  • Dysrhythmias
  • acute MI

Respiratory
-Non cardiogenic pulmonary oedema

Metabolic

  • lactic acidosis
  • Rhabdomyolysis
  • hyperglycaemia

Other

  • DIC
  • BUllae, alopecia, sweat gland necoriss

Peresistent neurological sequale are usually evident from the time of poisoning and seen in up to 30% of survivors at 1 month

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8
Q

DIscuss Ix of CO poisonoingn

A

CO levels
-confirms the diagnosis and loosely correlates to symptoms when measured shortly after the terminaiotn of exproure
-<10% -background level of a smoker
-10% usually asymptomatic - slight headache
-20% dizziness nasuea dyspnoea throbbing headache
-30% vertigo ataxia visual disurbance
40% confusion coma seizures syncope
50% CVS and resp failure, dysrhythmias, seizures and death

Serum lacatate
-FBC ,EUC, TNI, bHCG,

CT head or MRI brain may demonsetrate cerebral oemea, atrophy basal ganglia injury or corical demyelination in severe cases

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9
Q

DIscuss management of CO poisoning

A

RESUS
ABCD

D: Remove from exposure and apply supplemental o2
E: Enhanced by
#normobaric o2 : all patient should receive 100% o2 or high flow o2 via a non rebreather until all symptoms ahve resolved and for at least 8 houors
-pregnant patient should receive 100% o2 for 24 hours while feotal wellbeing is being assessed
#Hyperbaric oxygen
-may be indicated in patients with one or more of the risk factors listed above
-all pregnant patients should be considered for HBO
A: nil
D:

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10
Q

Discuss risk assessment of corrosives

A

Causes injury to the upper airway and GI tract. Upper airway injury is a life threatening emergency.

Deliberate or unintentional ingesiton of concentrated sulfuric acid, sodium hydroxide solution and solid preparations are associated with severe corrosive injury to the pharynx, upper airway oesophagus and stomach. NOt associated with systemic toxicity

Stridor dyspnoea dysphonia or thorat pain indicates airway injury and an immediate threat to life

Significant gastro oesophageal injury is indicated by any two of

  • stridor
  • drooling
  • vomiting

THe absence of lip or oral burns does not exclude singifaicnt Gastro-oesophageal injury

The following corrosives agents are also associated with severe ssytemic toxicity

  • glyphosate
  • mercuric chloride
  • paraquat
  • potassium permanganate
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11
Q

Discuss clinical features of corrosive ingestion

A
  • Laryngeal oedema may cause rapidly progressive stridor hoarseness and respiratory distress
  • oeophageal perforation and mediastinitis are associated with chest pain dyspneoa fever, subcut emphysema and a pleural rub
  • 30% of patient with grade 2b or 3 injury will develop oesophageal strictures
  • grade 2 and 3 injuries are associated with oesophageal carcinoma
  • perf stomach or intestine leads to clinical features of peritonitis

Patients who ingest a large amount of concentrated acids usually present in shock with profound metabolic acidosis and progress to multi organ failure and death despite laparotomy and surical debridement

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12
Q

Discuss IX fo corrosive ingestion

A

CT/XR

Endoscopy gold standard 
Grading 
-grade 0:noraml 
grade 1: mucosal oedema and hyperaemia 
grade 2 a: supericial ulcers bleeding and exudates
grade 2b: deep or circumferential ulcers 
grade 3a: focal necrosis 
grade 3b: extensive necrosis
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13
Q

Discuss management of corrsive ingestion

A

fResus
ABCD;
-Early ETT or surgical airway
-Do not insert a NGT until after endoscopy
-ABs not indicated unless signs of perforation

D: Mouth is rinsed with water as an immediate first aid

  • do not induce vomiting
  • do not adminisater oral fluids
  • do not administer activated charcoal
  • do not attempt to ph neutralisation

E: nil
A: nil

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14
Q

Discuss risk assessment of cyanide

A

Acute cyanide exposure whether by ingestion of cyanide salts or inhalation of hydrogen cyanide gas is potentially rapdily lethal

Cyanide is the product of combustion of natural substances and synthetic material and therefore commonly produced in fires

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15
Q

Discuss TM and TK of cyanide

A

TM: Binds to the ferric ion of cytochrome oxidase and inhibits oxidative metabolism, leading to lactic acidosis
It stimulates release of biogenic amines resulting pulmonary and coronary vasoconstriction. In the CNS cyanide triggers neurotransmitter release particualry NMDA which leads to seizures.

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16
Q

Discuss clinical features of cyanide toxicity

A

Acute inhalation of cyanide gas leads to LOC within seconds to minutes
Early symptoms include nasuea vomting, headache, dyspnoea, tachypnoea, hyptersion, tachycardai agitation collapse and seizures
Progressive features include hypotension, bradycardia, confusion teatny, drowsiness resp depression and coma

17
Q

Discuss IX of cyanide

A

ABG - serum lactate strongly correlates with severity of intoxication

Cyanide levels - do not aid in acute management but confirm diagnosis
>20mic/L - symptomatic
>40mic/l potentially toxic
>100mic/l lethal

18
Q

Discuss management of cyanide toxicity

A

Resus
ABCD
-cyanide poisoning poses multiple immediate threates to life
-Coma –> need for early Intubation and ventialtion
-Siezures –>
Shock
-Profound lactic acidosis

D: Removal from source
Remove cother and wash skin with soap and water - clothing should be bagged
-cyanide is rapidly absorbed and the onset of symptoms within minutes- resus takes prioty over ddecontaminaion.
-Charcoal is contrainidicated until airway securen

E: nil

A: Hydroxocobalamin, thiosulfate and dicobalt

19
Q

Discuss risk assessment of glyphophate

A

Widely used herbicide - severe toxicity occurs as a result of deliberate ingestion of a concentrated formulation.
It anifest with GI corrosive symptoms and in large ingestions severe HAGMA, hyperkalaemia and CVS collapse

Does is frequently difficult to quantify but correlates to severity
-Acute corrosive injury to the upper airways poses an immediate life threat

  • <50ml 100% - asymptomatic or minor GIT symptoms
  • 50-150ml 100% - GIT only
  • > 150ml - Severe GIT, risk of upper airway swelling, may develop multisystem toxicity, especially metabolic acidosis, hyperkalamia and hypotension
  • > 300 ml - potential fatal, death usually from refractory shock.

Diluted solutions pose little risk when ingested with toxicity confined to minor GI irrittation

20
Q

Discuss TM and TK of glyphosphate

A

TM: Poorly understood but does not inhibit cholinesterase enzymes. Toxicity though to be due predominantly to the surfactant and other co-formulants

TK: GLyphosate is poorly but rapidly absorbed following ingestion with peak concentrations occuring within 4 -6 hours. It is not metabolised but eliminaterd unchanged by the kidneys with an elimination half life of 4-6 hours. prolonged in renal impairment

21
Q

Discuss clinical features of glyphoshate intoxication

A

GIT:

  • corrosive injury to the oropharynx, oesophagus, stomach and duodenum manifests with nausea, vomtiing, diarrhoea and abdominal pain
  • corrosive injury is rarely severe and grade 3 injuries are not reported after glyphosate ingestion

CVS:

  • myocardial depression
  • hypotension
  • CVS collapse

Resp

  • upper resp irritation and drooling
  • aspiration pneumonitis
  • non cardiogenic pulmonary odema

Metabolic
-hyper k
HAGMA

22
Q

Discuss IX

A

ECG, BGL, paracetamol

EUC- LFT - K and hepatic/renal dysfunction
ABG
CXR
Endoscopy and CT chest not usually required as severe corrisve injury of the GIT is not usual

23
Q

DIscuss managment of glyphosate ingestion

A

ABCD
A: intuabte early if sings of airway burns
B: may develop ARDS so lung protective
C: fluid resus and tropes as needed

D: Nil
E: HD enhances the elimination of glyphosate but is not generally indication
A: nil
D: Patients who are clinically well after 4 hours of observation may be discharged
-Patient with known ingestion of >150ml og 100% should be admitted to high dependency unit or ICU in anticipation of muti-organ effects

24
Q

Discuss risk assessment of hydrofluoric acid

A

Found in car wheel cleaners, rust removing solutions and in preparations for glass etching and toher industrial processes.
Exposure may be dermal inhalationla, ocular, or oral.

  • Any dermal exposure may lead to delayed severe pain and tissue injury
  • inhalational exposure can lead to pulmonary injury
  • systemic life threatening flurosis is associated with ingestion or extensive dermal expsoure
  • –dermal exposure with 100% HF to 2.5%
  • –dermal exposure with 70% to 8% BSA
  • –dermal exposure with 23% to 11% BSA
  • –ingestion of >100ml of low concentration 6% by an adult
  • –ingestion of any volume of higher concentration

Children any ingestion

25
Q

Discuss PK and PD of hydrofluric acid

A

TM: -fluride ions bind directly with calcium and magneisums as well as interfering with cellular potassium channels to cuase cell dysfunction and death. Ssytemic toxicity and ventricular dysrhythmias are secondary to hypocalcaemia, hyperkalaemai, hypomag, and acidosis

TK: readily absorbed after ingestion or dermal contact - penetrates deeply into tissues to release fluoride ions

26
Q

Discuss clinical features of hydrofluric acid exposure

A

Dermal

  • skin contact with HF in concentration <50% is not immediatly painful and may go unnoticed for several hours
  • gradual onset of severe deep unremitting pain develops at contact site wihtout obvious erythema or blistering
  • pallor and blanching appear after several hours
  • blistering or tissue loss is delayed many hour or days
  • pain usually last less than 24-36 hours
  • very large exposure reuslts in systemic flurosis

Inhalation

  • immediate onset of mucosal irrtation followed by delayed onset of dyspnoea cough and wheeze
  • non cardiac pulmonary odema may occur in sever cases

Ingestion

  • low concentrations are minimally corrosive to the GIT
  • patient may experience vomiting, mil throat pain, dysphagia and abdominal pain
  • cardiac arret from systemic flurosis may occur wihtout warning 30 minutes to 6 hours post ingestion

Systemic effect (flurosis)

  • hypocalcaemia and hypomagnesaemia manifest as tetany and QT prolongation
  • Ventricualr dysrhytmias and cardiac arrest
27
Q

Discuss IX of hydrofluric acid

A

ECG, BGL and paracetamol

Serial ECG for patient with potential systemic HF poisoning every 2 hours until cardiac monitorign is not required
-degree of QT prolongation is a useful marker of hypocalcamiea

Serum or ionised calcium and mag
– measure at presentation and 4 hours in all patient with systemic symptosm

Endoscopy
-may be indicated for evaluation of extent of corrosive injury

28
Q

Discuss management of HF

A 
REUSUS 
ABCD
-IV calcium at bedside and available for all patient 
In the event of Ventricular dysrythmia 
1) intubate and hyperventilate
2) administer 10% calcium gluconate 60mls or calcium chloride 10% 20mls every 5 minutes until ROSC 
3) administer bicarb 100mEq IV
4) admin mag sulfate 10mmol IV

D:

  • dermal exposure - remove clothing irrigate thoroughly wiht water
  • ingfestion - nil
  • ocular exposure – irrigate thourghly

E: nil
A: calcium
-calcium chloride and gluconate as above
-calcium gluconate gel is indicated for all symptomatic patients following dermal expsoures
-if pain refractory clacium gluconate is adminsited by either subcut, regional intravenous or intra arterial infusion

Do not use regional anaetheisa for pain relief as relief from pain is an indication of adeqaute calcium use. If calcium gel not available can be made by mixing lubricant jelly with 10% calcium gluconate

29
Q

Discuss risk assessment of Paraquat

A

Widely used herbicide that is potentially lethal following ingestion of as little as a mouthful. If the dose is insufficient to cause fulminating MOF and death severe GIT corrosive injury and rapid onset of pulmonary fibrosis are common.

GIT corrosive injury is virtually universal after exposure
Survival after acute paraquat poisoning is related to dose and this in turn is strongly influenced by the circumsatnce of poisoning and the formulation.
-Deliberate self poisoning with concentrated formulations is almost invariably fatal
-accidental ingestions have a better survival rate.

DOSE
<30mg/kg – mild to moderate GIT effects with full recovery expected
30-150mg/kg - severe GIT corrosive injury followed by MOF over 2-6 days then pulmonary fibrosis several days post ingestion - mortality very high
>150mg/kg - fulminant MOF and alveolitits resulting in progressive refractory hypoxia metabolic acidosis renal and hepatic injury and CVS collapse. Mortality universal with death occuring wihtin 12 hours.

30
Q

Discuss TM and TK of paraquote poisoning

A

TM: Caustig agent specifically transported into pneumocytes where it cuases superoxide production and depletes superoxide dismutase and NADPH. Oxygen free radicals cause lipid peroxidation further free radical production and damage to cell membrane integrity.

TK: Rapid but incomplete absorption. Bioavailability increases with dose and kinectics become linear. Peak levels occur wihtin 2-4 hours. Oral absorption is further reduced by the presence of food in the stomach. Inhalational and dermal absorption are minimal through intact skin. Distributionis rapid to highly vascular tissue suchas the kidney liver heart and lung. Nil metabolism and excreted via the kidney.s

31
Q

Describe clinical features of paraquat

A

Initially may appear well but complain of oral burns
Central toungue ulceration and GIT symptoms are universal. Corrosive injury may be severe. Oesophageal perf and mediastinitis are reported

Following large ingestions multiple organ effects become apparent within hours. Tachycardia and tachypnoea accompany metabolic acidosis with elevated lactate. CVS collapse and MOG may lead to death wihtin 24 hours.

Time progression

1) immediate - vomiting and VIT injury
2) hours - corrosive injury to lips and oral cavity. HAGMA
3) <48 hours - progressive acidosis, CVS instability, renal failure, hepatic injury and progressive hypoxaemia in large ingestions
4) >48 hours - progressive pulmonary injury with rapid development of pulmonary fibrosis

32
Q

Discuss IX of paraquat

A

CXR - fibrosis and aspiration

Urinary paraquat

ABG
-lactate >4.4 is associated with fatal outcome

Serum paraquat levels - not avialable to add in clincial management but invaluable for prognosis

33
Q

Discuss management of paraquat poisoning

A

RESUS

  • Only tox in which decontamination take priority over resus or transport to hospital and ideally it occurs at the scene
  • Patients who arrive acutely unwell after deliberate self poisoning with large ingestion should be managed palliatively as soon as the diagnosis is established
  • the aim in moderate overdose is to improve prognosis to reduce the dose that reaches the lung via decontamination and HD
  • Immediate airway is not usually required howevere stridor, dysphagia and dysphonia indicate airway injury and potential imminent airway compromise.
  • no o2 unless spo2 <90%

D:

  • at scene administer food or soil to adsorb paraquat and reduce GIT absorption
  • Administer 50g of charcoal immediatly on arrival
  • fullers earth is clay soil which has been traditionally used but is now often not aviailable and offfers no advantage of charcoal

E: HD - useful for moderate OD - not indicated in splashes and will not prevent fatal outcome in deliberate large od
-most beneficial if able to be performed within 2 hours.

A: nil specific
-reasonable to trial NAC

ED Fellowship --> Toxicology (23 decks)

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