Test 2: Orthopedics (pt 2/4) Flashcards
What are benefits to use of a pneumatic tourniquet?
-Relatively bloodless field during extremity surgery
-Minimize intraoperative blood loss
-Aid in identification of vital structures
-Expedite the procedure
When are tourniquets applied?
After initiation of anesthesia. Need multimodal anesthesia before the tourniquet is inflated. Will still see BP rise with use.
The ischemic pain associated with tourniquet application is similar to that of thrombotic vascular occlusion/peripheral vascular dz.
What is the timing precautions associated with duration of tourniquet application?
-Document time of inflation/deflation
-Set alarm for 60 min intervals - communicate with surgery
-Maximum of 2 hours considered safe!!
-If >2 hrs, consider deflation for 15- 20 min, then reinflate
-Pressure in which it is inflated to depends on pt’s BP and shape/size of extremity
What happens with deflation of the tourniquet?
Release of metabolic waste into systemic circulation
-Transient changes in hemodynamics or pulse ox readings (hypotension, hypoxia)
-Most of these changes resolve quickly, except in patients with extreme conditions r/t cardiac or vascular status (metabolic acidosis, hyperkalemia, myoglobinemia, myoglobinuria, and renal failure)
What are symptoms reported with tourniquet pressurization (awake patients)?
-Dull aching, which progresses to burning and excruciating pain that may require GA
-Once pain begins, it is often resistant to analgesics and anesthetic agents, regardless of anesthetic technique
What is the pain associated with C Fibers (Unmyelinated)?
-Dull, aching pain
-Small, slow-conducting, unmyelinated C fibers
What is the pain associated with A-Delta Fibers (Myelinated)?
-Pinprick, tingling, and buzzing sensations, even after deflation
-Burning, tingling pain
-Larger, faster, myelinated A Delta Fibers
What should you be sure to include with pain mgmt for tourniquets?
Regional Anesthesia (multimodal)
Which patients are at highest risk for Venous Thromboembolism (VTE)?
-Total Hip (THA)
-Total Knee Arthroplasty (TKA)
-Pelvic Fx
What is the etiology for developing Venous Thromboembolism (VTE)?
Venous stasis, hypercoagulability, vascular trauma
What are the S/Sx of a Pulmonary Embolism (PE)?
Dyspnea, chest pain, tachycardia, shock
What are the S/Sx of a DVT?
Painful swelling of extremity, fever
What are the pharmacologic recommendations to prevent VTE?
-Low molecular weight heparin (not for hip fx surgery)
-Low dose unfractionated heparin
-Adjusted-dose Vit K antagonist
-ASA
-Intermittent pneumatic compression device (IPCD) for a minimum of 10-14 days
-However, impacts RA and Neuraxial anesthesia
When should low molecular weight heparin be started?
> 12 hrs preop or >12 hrs postop
Increased risk for bleeding
What are the clinical features associated with Bone Cement Implantation Syndrome (BCIS)?
-Hypoxia, hypotension, cardiac arrhythmias, increased pulmonary vascular resistance, unexpected loss of consciousness when regional anesthesia is administered, and cardiac arrest.
-Most commonly associated with hip arthroplasty, but may occur during other procedures including Knee arthroplasty and vertebroplasty
-Estimated to occur in 2-17% of surgeries
What are the theories behind the etiology of BCIS?
-Involve the role of emboli formed during cementing and prosthesis insertion
-Several mechanisms such as histamine release, complement activation, and endogenous cannabinoid-mediated vasodilation have been proposed.
How do you manage BCIS?
-Optimize BP prior to cementing
-100% FiO2, pressure bags available for rapid IV fluid administration, IV fluid bags full or nearly full
-Vasporessors as needed
-Communicate with team!! And document time on anesthesia record
Patients with one long bone fracture have approximately a ____% chance of developing fat emboli syndrome (FES), and patients with bilateral long bone fractures have a ___% chance.
3%; 33%
Pelvic fxs also at risk
What causes the hypoxia associated with fat embolism?
The seeding of fat cells from the disrupted bone marrow into the venous circulation and eventually lodge in the pulmonary arterial circulation. The resultant pulmonary capillary obstruction leads to diffuse interstitial edema, alveolar collapse, and subsequent reactive hypoxic pulmonary vasoconstriction.
