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Flashcards in Caustics Deck (20):

List 8 factors that influence extent of injury from caustic exposure

1. Type of agent
2. concentration
3. volume
4. viscosity
5. duration of contact
6. pH/pKa
7. titratable alkali (acid) reserve)
8. presence/absence of food in tomach


what are the 4 classic phases of caustic damage

1. necrosis, invasion by bacteria and PMNs
2. vascular thrombosis
3. sloughing of superficial layers over 2-5d
4. granulation formation, collagen deposition and reepithelialisation (1wk to months)


how do strictures form after caustic injury

contraction of scarred mucosa


what are the endoscopy grades of caustic injury

1st degree: edema/hyperemia
2nd degree: superficial ulcers/whitish membranes, exudates, friability, hemorrhage
IIa: not circufrential
iib: almost circumfrential
3rd degree: full thickness, necrotic mucosa, frank perforation


risk of stricture with grades of caustic injury

1st: none
2nd: 15-30% (circumfrential 75%)
3rd : 90%


when should endoscopy be performed? and why

less than 24hr. longer than that and the risk of perforation increases


indications for endoscopy

1. intentional ingestion
2. S/S: vomiting, drooling, dysphonia


How are phenol and formaldehyde caustic

protoplasmic poisons cause protein denaturation, coagulation necrosis


what are the manifestations of phenol and formaldehyde poisoning

dysrhythmias, seizures, coma hypotension


how do you treat topical phenol exposure and why

irrigate with PEG, if you irrigate with water the phenol may penetrate deeper.


define caustic

an agent capable of causing tissue injury on contac
acid pH less than 3, alkali pH greater than 11


household alkali examples

liquid drain cleaner (KOH, NaOH)
crystal drain cleaners (NaOH)
oven cleaners (NaOH)
rust remover (NaOH)


household acid examples

Liquid drain cleaners (H2SO4)
rust remover (HF)
Toilet bowl/swimming pool cleaner (HCl)


Differentiate types of injuries caused by acids/alkalis

acids: coagulation necrosis
aklali: liquefication necrosis


what is the risk and treatment of hydrogen peroxide ingestion

gas emboli, need to image to look for these in chest, abdo and portal system-->Tx: hyperbaric O2


how is dermal HF acid exposure result in marked toxicity

permeable, dissociates, causes hypoCa, hyperk causing dysrhythmias and death. concentrated 2%TBSA can be fatal


List systemic complications of HF exposure

cardiac: prolonged QT, Hypo Mg, HypoCa, VF/VT
hemorrhage: hypoCa disrupts coagulation cascade
opthalmic: corneal ulcers, edema, necrosis
inhalational exposure: mucosa and pulmonary irritant,


List 5 injuries related to disc battery ingestion:

1. pressure necrosis: from obstruction
2. caustic injury: leaking of alkaline medium
3. electrical injury
4. heavy metal toxicity
5. ulceration, perforation, fistulas


What is the evaluation and management of button disc battery ingestion?

- Radiography for position of battery
o Airway or Esophageal: Immediate emoval
o Gastric or intestinal: Stool monitoring and repeat radiography 1 weekif it does not pass


What are your steps for mgmt of Severe Systemic HF toxicity: IF signs of severe toxicity develop (arrhythmias),

need rapid IV infusion
– CaCl or Ca-gluconate à May need several grams
– 4 g IV MgSO4 over 20min
– Treat hyperK and acidosis
– Aggressive monitoring of Mg, K, Ca
+/- HD if renal function compromised