Grand Rounds Recap 1.11.23
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R1 Clinical diagnostics: caustic skin injuries WITH Dr. wolski
Severity of caustic skin injuries depends on physical state of substance, concentration, strength, amount, skin characteristics, time of exposure
Algorithm to manage most caustic skin injuries
Safety: scene safety, PPE
Strip: remove clothing
Shower: 45-60 minutes of irrigation time
Size: attempt to estimate the burn size and depth
Sedate: adequate pain control
Stabilize
Chemicals can be associated with systemic toxicity so monitor electrolytes and telemetry
Do not neutralize substances due to possible exothermic reaction
Cement
Typically delayed presentation. Several hours after exposure, patients will develop burning pain, erythema, and vesicles. 24-48 hours after exposure, wounds will ulcerate and develop black necrosis
Treatment: extensive irrigation, debridement, and hydrocolloid dressing
Hydrofluoric Acid
Glass etching/cleaning, ceramic manufacturing, rust removal, automobile wheel cleaners, air conditioner cleaners, germicides, insecticides, tile cleaning, laundry powders, semiconductor production, plastic production
Distinct characteristics
Pain out of proportion to burn appearance
Progressive tissue destruction, with maceration, erythema, edema, ulcers, necrosis, eventually whitish/silvery-gray discoloration
Delay in presentation depending on HF concentration
Systemic effects
Acidemia, hypocalcemia, hypomagnesemia, hyponatremia, hyperkalemia, hyperphosphatemia → cardiac arrhythmias
Tenosynovitis and osteolysis can occur due to depth of HF penetration. Patients may also have nausea, abdominal pain, muscle fasciculations
Pulmonary edema, bronchopneumonia, and tracheobronchial hemorrhage also possible
Treatment
Copious irrigation followed by administration of calcium
All cases: topical calcium gluconate gel
Deep wounds: above plus subeschar calcium gluconate injection
Digital burns: topical treatment + arterial infusion after identifying arterial supply to injury
IV calcium for hypocalcemia
Phenol
Found in soaps, sprays, ointments, as well as industrial production of explosives, fertilizers, rubber
Distinct characteristics: sweet odor, numbness over burns due to anesthetic properties of phenol, dark-colored burns
Systemic effects
Direct damage to renal tubules and glomeruli leading to renal failure
CNS stimulation (hyperreflexia, convulsions) or CNS depression (lethargy, respiratory arrest)
PNS demyelination
Cardiovascular toxicity
Erythrocyte lysis
Central lobar hepatic necrosis
Treatment
DO NOT RINSE. Irrigation with inadequate amounts of water increases risk of absorption by exposing more body surface area to the phenol. Instead, you should wipe phenol off with polyethylene glycol. Alternative solvents include soap and vegetable oil
White Phosphorus
Most frequently used in military, fireworks, insecticides, fertilization as well as illicit methamphetamine production
Combined thermal and chemical burn
Distinct characteristics: yellow flame with white smoke, burn appears yellowish, waxy, and necrotic
Systemic effects
Hypocalcemia, hyperphosphatemia → bradycardia, QT prolongation, ST/T wave changes
Erythrocyte hemolysis
Renal damage
Hepatic necrosis
Treatment
Extensive irrigation, particle removal, and dressing with saline-soaked pads.
Beware
Dry dressings can ignite
Removed particles should be placed in cold water to prevent combustion
Examine debrided wounds twice daily for smoking and missed particles
Of note, you can use a Wood’s lamp for particle visualization
R2 CPC WITH Dr. Shaw and Dr. Hughes
Case: Middle aged female with recent history of molar pregnancy with chief complaint of abdominal pain, vaginal bleeding. Found to have a temperature of 101.2 and tachycardia.
Diagnosis: Gestational trophoblastic disease with secondary hyperthyroidism
Test of Choice: Thyroid Studies
Premalignant: hydatidiform mole (partial, complete)
Malignant: Gestational trophoblastic neoplasia
Gestational Trophoblastic disease: abnormal proliferation of trophoblastic cells
Trophoblasts provide nutrients to the embryo and develop into a large part of the placenta
Secrets hCG early in pregnancy
Clinical signs and symptoms
Hyperemesis
Elevated BP
Enlarged uterus
Vaginal bleeding
Diagnostics
Ultrasound
Laboratory testing
Thyrotoxicosis
Can be complication of GTD
Treatment
Beta-blockers
Glucocorticoids- prevent conversion of T4 to T3
Definitive management: Dilation and curettage
Post-operatively: methimazole, birth control
pediatric simulation
Consider congenital cardiac etiology in a newborn with poor feeding, vomiting, cyanosis, or mottling.
Coarctation typically presents with sudden symptoms of heart failure and shock due to closure of the PDA that has been bypassing the coarc for systemic circulation, so they are often pale, mottled, irritable with hepatomegaly and diminished or absent femoral pulses. Four extremity BPs demonstrate hypotension in bilateral LEs +/- LUE depending on the location of the coarc
In addition to other supportive measures, prostaglandins are administered to keep the PDA open to allow for systemic circulation. The starting dose is 0.05 mcg/kg/min but can be titrated up to 0.1 mcg/kg/min
Risks of prostaglandins include apnea and hypotension, which increase with increasing doses. Be prepared to secure the airway and provide resuscitation as needed. This is a patient you would want to talk to peds cardiac ICU very early in the process to coordinate transfer and care