ITE KEY WORDS Flashcards
What is a Bland-Altman Plot?
- A method of data plotting used in analyzing the agreement between two different assays.
- Bland–Altman plots are extensively used to evaluate the agreement among two different instruments or two measurements techniques. Bland–Altman plots allow identification of any systematic difference between the measurements (i.e., fixed bias) or possible outliers.
Femoral Nerve Block Anatomy
Muscles innervated
Cutaneous Innervation
What Distribution is missed?
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Relevant Anatomy
- Femoral nerve (posterior divisions of L2-4) is formed in the psoas major muscle, runs between psoas and iliacus muscles and enters the thigh under the inguinal ligament lateral to the femoral artery, at which point it divides into multiple terminal branches (usually classified as anterior [mostly cutaneous] and posterior [mostly motor]).
- Landmarks and Surrounding Structures: Important landmarks include the femoral crease, ASIS, pubic tubercle, femoral artery (palpable) and veins (not palpable), both located medially.
- Cutaneous Innervation: The femoral nerve blocks the anterior thigh, as well as the medial lower leg (from the saphenous nerve). Note that it misses a portion of the medial thigh innervated by the obturator nerve (which also innervates the medially-located obturator externus, adductors [brevis, longus, and magnus], and gracilis muscles).
- Muscular Innervation: Major muscles supplied by the femoral nerve include the anterior compartment muscles (quadriceps femoris, sartorius, and pectineus muscles), as well as the more proximal iliacus and psoas major muscles.
- Distributions Missed: Medial thigh (obturator nerve)
Neuromuscular blockade and primary hyperparathyroidims
- Hyperparathyroidism is a common cause of hypercalcemia and the effects of calcium at the neuromuscular junction may cause pre-existing muscle weakness. However, this response is unpredictable and though it might seem that the pre-existing muscle weakness associated with hyperparathyroidism would reduce neuromuscular blocker requirements, it has been suggested that hypercalcemia associated with primary HPT may antagonize the effects of non-depolarizing muscle relaxants, making patients more resitant to blockade.
Treatment of Prolonged QT
- May occur with (Jervell and Lange-Nielsen syndrome) or without (Romano-Ward syndrome) deafness. Presents as lightheadedness, syncope, torsades, and cardiac arrest.
- Immediate Treatment with Magnesium Sulfate
- Acute management is based on intravenous magnesium, replacement of potassium and calcium if indicated. Avoid amiodarone in these patients as it may worsen the disease.
- Long term therapy is usually based on beta blockade,
Aspiration Management of LMA
- Initial steps for management of suspected or confirmed pulmonary aspiration of gastric contents in patients with a LMA include
- increasing FiO2 to 100%
- deepening anesthesia
- placing the patient in a head-down position.
- Suctioning should usually be performed and the severity of aspiration assessed using fiberoptic bronchoscopy. Additional measures such as intubating should be based on clinical judgment.
Caudal: Systemic Toxicity
- The incidence of local anesthetic-induced seizures following caudal epidural block is higher than following lumbar or thoracic approaches.
- The relative risk of local anesthetic toxicity follows this order: caudal > brachial plexus block > lumbar or thoracic epidural block.
- Elevation of heart rate by more than 10 beats per minute or an increase in systolic blood pressure of more than 15 mm Hg after injection of epinephrine-containing local anesthetic is suggestive of intravascular injection.
Identify the following block and structures
- Relaxation of the anal sphincter following local anesthetic injection may predict the success for a caudal block.
- This is particularly useful in children because most caudal blocks are performed while the child is anesthetized, and it is not possible to assess the effectiveness of the block by testing for sensory analgesia levels.
- One study demonstrated that the presence of a lax anal sphincter at the termination of surgery correlated with the reduced need to administer opioids perioperatively.
ERAS Protocol
Fluid therapy for traumatic brain injury
The choice of fluid should fulfill this utmost goal by augmenting oxygen delivery to the brain. Non-blood fluid, such as crystalloid and colloid, may help to treat hypotension and increase cerebral perfusion pressure (CPP), thus increase cerebral blood flow (CBF); however, it does not increase blood hemoglobin concentration and may actually decrease blood oxygen content due to hemodilution. Hypotonic, low sodium and dextrose-containing fluids should be avoided. 0.9% normal saline (NS) or even 3% NS should be considered if a crystalloid is chosen. The use of albumin in trauma victims is controversial. Most trauma centers choose not to use it. Mannitol is often adopted to decrease brain water and augment intravascular volume in patients with increased intracranial pressure. Red blood cell transfusion not only increases intravascular volume and facilitate CPP management but also augment blood oxygen content via the increase in hemoglobin.
Post op nausea Treatment
1) 5-HT3 receptor antagonist (e.g., ondansetron): commonly used in the perioperative management of PONV. Better at preventing vomiting than nausea. The recommended dose for ondansetron is 4mg at the end of the surgery. Do not re-dose unless more than 6 hours have elapsed since the last dose was administered, including in the immediate post-operative period. An adverse effect is QTc prolongation.
2) NK-1 receptor antagonist (e.g., aprepitant): more effective than ondansetron. Recommended to give prior to the start of surgery.
3) Corticosteroids (e.g., dexamethasone): recommended dosing is 4 mg at the beginning of the surgery due to long onset time.
4) Dopamine-2 receptor antagonist (e.g., droperidol, metoclopramide, Prochlorperazine): droperidol is effective as an anti-emetic. Recommended dosing is 0.625 to 1.25 mg at the end of surgery. Metoclopramide is considered a weak anti-emetic. The effective dose for metoclopramide is 25 to 50 mg. Metoclopramide 10mg is not recommended for PONV. Also, metoclopramide is not recommended as an antiemetic for patients who have received prophylactic ondansetron intraoperatively.
5) Anti-cholinergics (e.g. scopolamine patch): need to apply prior to going back to the operating room due to its 2 to 4 hour onset time. Can cause visual changes, dry mouth, and dizziness.
Therapeutic Hypothermia: Electrolyte Abnormalities
Type 1 vs Type 2 Alveoli
Type 1: Small, involved in gas exchange
Type 2: Produce surfactant
Brugada Syndrome Anesthetic Considerations
- Brugada syndrome is a rare autosomal dominant disease & is associated with sudden cardiac death from ventricular fibrillation or tachycardia (VT/VF), especially in Southeast Asian males
Anesthetic Considerations
Potential for hemodynamic collapse due to VT & VF
Avoid exacerbating factors of Brugada (ST Elevation):
Parasympathetic nervous system stimulation (increase in vagal tone)
Medications
Avoid BB, alpha agonists, neostigmine
Avoid class Ia antiarrhythmic (procainamide)
Electrolyte abnormalities: ↑↓K, ↑Ca
Fever
Considerations of AICD if in situ (only known treatment)
Preparations for treating Brugada Exacerbations or cardiac arrest:
All patients without AICD need defibrillator & pads in OR
Atropine, Ephedrine, Isoproterenol
Resuscitation drugs should be available
Typical ECG findings
Characteristic findings are RBBB & ST elevation in V1-V3
Pathophysiology of delayed hemolytic transfusion reaction
- Delayed hemolytic transfusion reactions (DHTRs) occur in patients who have received transfusions in the past. These patients may have very low antibody titers that are undetectable on pretransfusion testing, so that seemingly compatible units of red blood cells (RBCs) are transfused. Exposure to antigen-positive RBCs then provokes an anamnestic response and increased synthesis of the corresponding antibody. After several days, the antibody titer becomes high enough to hemolyze transfused RBCs. The frequency of DHTRs is estimated to be approximately 1 case per 5400 red cell units transfused.
DHTRs are a potentially life-threatening complication of sickle-cell disease (SCD) treatment.
Diffusion Hypoxia Prevention with N2O Use
Diffusion Hypoxia has proven to be avoided by administration of oxygen for 10 minutes from cessation of nitrous oxide anaesthesia.