STEMI Conference
If a patient has the clinical picture of ACS with anterior ST depression you can activate the the Cath lab for suspected posterior MI. The cardiologists present did not feel it was a requirement to have ST elevation on the the posterior EKG to activate the cath lab for suspected posterior MI. Anterior horizontal ST depression can be enough with the right clinical picture. There is not a lot of data regarding the sensitivity and specificity of the posterior EKG. The cardiologists felt the posterior EKG is very specific but the sensitivity is not known and may be too low.
New Left Bundle Branch Block in the setting of chest pain is very controversial. A new LBBB when compared to an EKG from a year ago may not be an MI. A new LBBB when compared to an EKG from a week ago is a different story and more concerning.
New LBBB from MI will arise from an LAD occlusion. With LAD occlusion, you should have echo findings of anterior wall motion abnormality to go along with the EKG findings. Wall motion abnormalities will help identify AMI in the setting of LBBB. The cardiologists felt that an AMI causing a new LBBB will cause the patient to be ill appearing. It is a relatively large infarct.
There was consensus that a new LBBB is not very specific for AMI. Sgarbossa criteria are specific but insensitive. Cardiologists want to be called on cases with concern for AMI in the setting of new LBBB.
Patients who have had a valve replacement and are sub-therapeutic on their INR can embolize to the coronary arteries causing AMI. We think of embolic phenomena going to the brain most commonly. The cardiologists have noted that emboli can also cause AMI.
Steroids are arthrogenic and can increase the risk of AMI.
Ryan/Hawkins Oral Boards
Case 1. Patient presents unresponsive. EMS gave him narcan with no response. In the ED the patient was intubated. His blood sugar was normal. Further history by EMS revealed the patient ingested GHB. GHB overdoses frequently result in intubation and the patient later wakes up and self-extubates or can be extubated relatively quickly.
γ-Hydroxybutyrate (GHB) is an endogenous molecule as well as a drug. GHB was originally used as an IV anesthetic, primarily in several European countries. In recent years, it has been marketed as a drug for body builders to improve body mass and reduce fat, as well as for use as a hypnotic, antidepressant, anxiolytic, and cholesterol-lowering drug.16 GHB has been found in drug-facilitated sexual assaults.17 Sodium oxybate (the sodium salt of GHB) is currently approved only for use within a highly regulated setting for the treatment of narcolepsy.18 In some European countries, GHB or sodium oxybate is used as a treatment for alcohol dependence and withdrawal.19 GHB can be formulated as a clear liquid or in solid form as a capsule, tablet, or white powder. GHB has many vernacular names, including "liquid ecstasy," "Georgia Home Boy," "G," and "Grievous Bodily Harm."
GHB has a steep dose–response curve with a narrow therapeutic ratio; doses of 10 milligrams/kg result in short-term amnesia, doses of 20 to 30 milligrams/kg result in sedation and drowsiness, and doses exceeding 50 milligrams/kg result in seizure, coma, respiratory depression, and cardiac depression.22 Bradycardia, hypothermia, and either miosis or mydriasis can occur.20 During recovery, the patients often wake up surprisingly quickly as opposed to the more prolonged awakening phase seen after an overdose with other sedatives. Despite co-ingestants being commonly encountered, most patients fully regain consciousness within 6 hours. The co-ingestion of ethanol can worsen hypoxia and possibly result in a longer elimination half-life of GHB.23
Treatment is largely supportive.20 Intubation is generally unnecessary, even in patients with severely depressed consciousness (Glasgow Coma Scale score ≤8) because patients are usually able to protect their airway and maintain ventilation.24 Once the patient is awake and alert, assuming no co-ingestants or secondary complications such as aspiration, the patient can be medically discharged or transferred. (Tintinalli 8th ed.)
Dr. Carlson comment: You can never be faulted for intubating these patients to protect their airway.
Case2. Patient was at a party and injured his shoulder.
Case 3. Pregnant woman presents seizing. Patient was treated with IV magnesium and IV lorazepam. Seizure was terminated. A magnesium drip was started. OB was consulted for urgent delivery of the baby.
Bartgen Study Guide Heme-Onc
Leukemia buzz words: Problem of bone and blood, so back pain, fever, hematologic abnormalities, hepatosplenomegaly are the buzz words.
Platelet transfusion thresholds for thrombocytopenia: ICH and surgery is 100K, GI or other serious bleeding is 50K, LP is 50K, asymptomatic is 20K, Central Line is 20K.
Management of Rhabdomyolysis: Once the patient is in the ED, continue aggressive IV rehydration for the next 24 to 72 hours. One method is rapid correction of the fluid deficit with IV crystalloids followed by infusion of 2.5 mL/kg/h, with the goal of maintaining a minimum urine output of 2 mL/kg/h.11 Another method is a goal of 200 to 300 mL of urine output each hour.12
No prospective controlled studies have demonstrated benefit from alkalinization of the urine with sodium bicarbonate or forced diuresis with mannitol or loop diuretics.12,13,14 Bicarbonate is widely recommended but without an evidence base. If bicarbonate is given, maintain an isotonic solution and avoid metabolic alkalosis or hypokalemia.12 Mannitol may be harmful because it may cause osmotic diuresis in hypovolemic patients.
Hypocalcemia observed early in rhabdomyolysis usually requires no treatment. Calcium should be given only to treat hyperkalemia-induced cardiotoxicity or profound signs and symptoms of hypocalcemia. If hypercalcemia is symptomatic, continue saline diuresis. Treat hyperphosphatemia with oral phosphate binders when serum levels are >7 milligrams/dL. Treat hypophosphatemia when the serum level is <1 milligram/dL. Hyperkalemia, which is usually most severe in the first 12 to 36 hours after muscle injury, can be significant and prolonged. Traditional insulin and glucose therapy, although recommended, may not be as effective in rhabdomyolysis-induced hyperkalemia. The use of ion-exchange resins (e.g., sodium polystyrene sulfonate) is effective. Dialysis may be needed (see chapter 17, Fluids and Electrolytes).
Avoid prostaglandin inhibitors such as nonsteroidal anti–inflammatory drugs because of their vasoconstrictive effects on the kidney. Finally, treat the underlying cause. (Tintinalli 8th edition)
Harwood comment: CPK less than 1000 I don't worry about rhabdo. CPK 2-10,000 most can be treated with oral hydration. >10,000 CPK usually will need IV hydration/OBS.
A late complication of rhabdo is DIC.
Factor 8 replacement for Hemophilia is basically: 50u/kg for head injury and 25u/kg for all other injuries/bleeding. 1 unit/kg of factor 8 will raise factor activity 2%. 50u/kg will get factor activity up to 100%. 25u/kg will get factor activity up to 50%. Give the factor 8 prior to CT for head injury.
Ahmad/Bernard/Destefani/Einstein/Nakitende/Regan Job Search Panel
Plan that it will take several months to get a permanent license in any state.
There are pros and cons to job searching early and late in EM-3 year. Sometimes it's better to lock in the job early. On the other hand, sometimes good jobs open up later in the year.
If you are doing independent contracting as part of your work-mix you need to hire a professional accountant manage your taxes/finances.
Don't be hesitant to ask and negotiate for more $ or time once you are offered the job. Everything is negotiable.
During the interview, no question is off the table.
You can probably create a individualized job for yourself anywhere if you plan it out carefully, have the right skill set, describe it well, list the metrics to measure your performance, and present yourself in excellent fashion to the employer.
There was tons more of great advice that I could not encapsulate in these notes.
Florek Seizures
It is not necessary or recommended to give IV anticonvulsant medications during the course of an uncomplicated seizure, although the practitioner should be ready to administer these medications if seizures do not terminate. Most seizures will self-resolve within 5 minutes. Any unnecessary sedation at this point will complicate the evaluation and result in a prolonged decrease in level of consciousness.7 Seizures that fail to abate after 5 minutes are considered status epilepticus and require more aggressive medical interventions (Tintinalli 8th ed.)
5 Causes of Seizures: 1. Abnormal Vitals(hypoxia, hypotension, hypertension)/Hypoglycemia, 2. Toxic-Metabolic (electrolyte abnormalities, ETOH withdrawal), 3. Infectious, 4. Structural, 5. seizure-like activity.
In nonconvulsive status epilepticus, the patient is comatose or has fluctuating abnormal mental status or confusion, but no overt seizure activity is present. The diagnosis is challenging and is typically made by EEG. Findings suggestive of nonconvulsive status epilepticus include a prolonged postictal period after a generalized seizure; subtle motor signs such as twitching, blinking, and eye deviation; fluctuating alterations in mental status; or unexplained stupor and confusion.25 (Tintinalli 8th ed)
To screen for pseudoseizure you can flush the eye with saline. This can frequently disrupt a pseudoseizure.
Dr. Williamson comment: Consider CT scan of the head for first-time seizures. Instructions for patients with first-time seizure should include no driving or swimming, or dangerous work until cleared by neurologist. Also if you have another seizure, you need to return to the ED.