Barounis/Dodd/Ketterhagen Central Line Simulation Lab
Our awesome EM Intensivists taught us how to optimally place a central line. I can’t do justice to all the teaching they did but here are just a few fine points I picked up.
When putting your sterile gown on by yourself, Velcro the neck first before you put your arms through the sleeves.
The plastic adhesive strips in the sterile probe cover package can be used to tape the probe cord to the drape so the probe doesn’t fall off the patient.
Line up bevel of needle with the numbers on the barrel of the syringe so you know where the bevel is.
When you are locating the IJ in the neck, keeping the probe pointed at the floor instead of aiming it toward the neck will help keep the orientation of the IJ and IC more true.
Once you have punctured the skin, move the ultrasound probe with your needle so that you always have the tip in view and can visualize exactly where you enter the vessel.
When making the cut with a scapel put the blunt side of the scapel towards the wire.
Hawkins Case Presentation and Ortho Xrays
45 yo male presents with altered mental status. Patient was reported to be intoxicated and vomiting. In ED patient was found to have head laceration and rash. He was hypotensive and tachycardic.
Patient was in detox recently and was on multiple medications including antabuse.
DDX=disulfiram reaction, ETOH intoxication, serotonin syndrome, ICH, toxic ingestion, dehydration, sepsis, anaphylaxis.
Patient had improving blood pressure and rash with IV fluids. Mental status worsened with a GCS of 7-8. Patient is next intubated.
Disulfiram reactions can result in tachycardia, hypotension and cardiovascular collapse.
Other tha ETOH, disulfiram reactions can also be caused by chlorpropamide, flagyl and griseofulvin.
The duration of the disulfiram-alcohol reaction varies from 30 to 60 minutes in mild cases to several hours and is largely dependent on the amount of alcohol that needs to be metabolized. Due to vomiting and volume depletion, serum glucose, electrolytes, and kidney function should be evaluated. Since only small amounts of ethanol can precipitate a disulfiram–ethanol reaction, it may be useful to confirm the presence of ethanol with a blood concentration. Patients with cardiovascular instability should have an ECG. Symptomatic and supportive care is the mainstay of treatment. Most patients with hypotension respond to intravenous 0.9% sodium chloride. Refractory hypotension is rare, but if necessary, a vasopressor can be administered. A direct-acting adrenergic agonist such as norepinephrine should be used since disulfiram inhibits dopamine β-hydroxylase (DBH), an enzyme necessary for norepinephrine synthesis. As such, indirect vasopressors, such as dopamine, that require functioning norepinephrine synthesis may be less effective.
For further symptomatic care, antiemetics can be administered, and for cutaneous flushing, a histamine (H1) receptor antagonist, such as diphenhydramine, can be given.101 Most patients with a disulfiram–ethanol reaction have mild symptoms, are hemodynamically stable, and can be safely discharged following resolution of symptoms.
Fomepizole may halt the accumulation of acetaldehyde and thus cease severe disulfiram–ethanol reactions. Fomepizole, an inhibitor of alcohol dehydrogenase, may terminate the progression of the disulfiram reaction by blocking ethanol metabolism to acetaldehyde (Antidotes in Depth: A30). In a study of alcoholics, fomepizole decreased acetaldehyde concentrations and improved clinical symptoms in those experiencing a disulfiram–ethanol reaction.59 A recent case series reported two patients who developed severe disulfiram–ethanol reactions with hypotension and tachycardia unresponsive to fluids who were treated successfully with a single dose of fomepizole.97 One patient improved clinically 90 minutes after administration of fomepizole and the other within 30 minutes. (Goldfrank’s Toxicologic Emergencies)
Segond Fracture is associated with an ACL tear
Montaggia vs Galeazzi
Katiyar Toxicologic Emergencies Hallucinogens
Hallucinogenic botanicals include morning glory and Hawaiian baby woodrose.
Magic Mushrooms are a source of psilocybin.
Ayahuasca and the Yakee plant are plants in the amazon that contain the compound N,NDMT a potent short-acting hallucinogen.
Toad licking can cause hallucinogenic effect. (Colorado toad). Toad licking also can cause arrythmias.
in one species of toad, Bufo alvarius (Sonoran Desert toad or Colorado River toad).77 Although bufotenine has been classified as a Schedule I substance by the DEA for many years, 5-MeO-DMT was not scheduled until 2009.91 Like DMT, 5-MeO-DMT is rapidly metabolized by intestinal monoamine oxidase enzymes; oral ingestion of toad venom or skins would thus have limited potential as a route of recreational use.21 Methods for extracting and drying B. alvarius secretions for smoking and insufflation are available on the Internet. Death has resulted from wrongful use of Bufo secretions for purposes of aphrodisia.30,55 The toad venom glands also produce cardioactive steroids, called bufadienolides, which cause digoxinlike cardiac toxicity, and in some species, can secrete tetrodotoxin.87,139 (Goldfrank’s Toxicologic Emergencies)
Peyote and mescaline are other hallucinogens. Some cacti available on line contain peyote or mescaline.
Salvia is from the mint family and can be purchased on the internet or at a garden store. The leaves contain hallucinogens.
Nutmeg contains a hallucinogen.
Most hallucinogens affect the serotonin receptors. There may also be sympathomimetic effects.
Hallucinogens are not routinely identified on urine toxicology screens.
Treat hallucinogenic overdoses with benzodiazepines, cooling, and quiet environment.
Katiyar Toxicologic Emergencies Hypoglycemic Agents
Ackee fruit from Jamaica can cause hypoglycemia.
Sulfonylurea medications increase insulin secretion from pancreatic beta cells.
Metformin inhibits gluconeogenesis, enhances glucose transport into muscles. Decreases glucose being released from liver.
Mild changes in renal function or a new drug interaction can be causes of new onset hypoglycemia.
A single large injection of insulin is more dangerous than multiple smaller doses because a large dose creates a “depot effect”. The “depot effect” will result in prolonged release of insulin.
Insulinoma and sulfonylureas will result in elevated c-peptide levels. Synthetic insulin does not have c-peptide.
Treat sulfonylurea toxicity with glucose and food. Also start octreotide. Check the blood sugar Q1 hour. Keep for OBS or admit
Estoos/Kishi/Miner Trauma Lecture: Neck and Above
In the hypotensive trauma patient, consider hemorrhage as #1 cause. After hemorrhage, consider obstructive causes of shock (tamponade or tension pneumothorax).
When exposing the patient make sure you examine the whole body back and front looking for subtle injuries. At the same time consider environmental exposures such as acids, bioterrorism agents, or radioactive contamination. After fully exposing the patient, keep patient warm with blankets and heat to avoid hypothermia.
The GCS is a critical means of communicating the neurologic status of the patient between caregivers as well as a way to monitor the patient’ neurologic status.
Key ED goal for head trauma management is to avoid hypotension and hypoxia. Elevate the head of the bed. Mannitol or hypertonic saline may be used to lower ICP. Avoid mannitol in patients with renal failure. Avoid hypertonic saline in patients with CHF.
Basilar skull fracture=temporal bone fracture.
Traumatic subarachnoid hemorrhages as opposed to aneurysmal subarachnoid hemorrhage are more peripherally located.
Traumatic intraparenchymal hemorrhages are often in frontal or temporal lobes.
DAI has a benign appearing CT head/MRI with a severely affected GCS/mental status exam. Some DAI patients will improve significantly within a year or so. Prognosis is difficult to predict.
Patients with head injury have 50% increased mortality with single episode of hypotension.
Do not use therapeutic hypothermia in traumatic head injury. Recent RCT showed no benefit and trauma surgeons emphasized that hypothermia increases traumatic bleeding.
When intubating patients with significant head injury and you don’t have to do a crash or life-saving emergent intubation, be very careful to avoid any desaturation or hypotension during the intubation.
Unfortunately I missed a significant portion of this outstanding lecture.