1) According to Barrish where does oozing come from?  Can it be fixed with really high tourniquet pressures?

2) Ideally where do we start in terms of tourniquet pressures for lower extremities?

1) Oozing occurs from intramedullary blood flow and small arterial vessels.  Therefore blowing up the tourniquet to a redonkulus level of 350 is "ridiculous and useless" 

2) Ideally we start at 100mmHG above systolic BP

1) How can tourniquet pain manifest during general anesthesia?

2) When does Tourniquet pain usually manifest?

1) -hypertension

-tachycardia

-diaphoresis

2) within a 45-60 minute time frame under general anesthesia.

Differentiating between true surgical pain and tourniquet pain can be tricky.  

Answer true or false to the aforementioned conundrum: 

1) True surgical pain usually responds to small or moderate doses of narcotic

2) Tourniquet pain usually responds well to narcotics and opiods

3) If the patient becomes hypertensive d/t the tourniquet pain  you should give an antihypertensive.

4) When dealing with the tourniquet pain you should consider if the symptoms are tolerable vs. dangerous and what the pt's comorbidities are. 

5) Don't bother the surgeon regarding tourniquet pain. 

1) True

2) False: Tourniquet pain will often not respond to narcotics and opiods (as anticipated)

3) False:  Okay not entirely false, however, duration of action should be considered because Gayle says, "Once the tourniquet is released you are stuck with it!"

4) Well Um  True.

5) False:  Determine where you are in the case- if closing, the tourniquet may be deflated.  Gayle states, "Work with the surgeon"

Fill in the blanks regarding the theory behind tourniquet pain:

The umyelinated C-fibers (although they block quickly) also become _____1_____ sensitive as the local anesthetic concentration decreases.  This isn't entirely true of ______2______ fibers which seem to remain sensitive to the local.

1) More

2) Alpha-Delta

Of the following, which environments stimulate the C-Fibers?

A) Hypoglycemia

B) Hyperglycemia

C) Acidosis

D) Alkalosis

E) Hypoxemic

F) Chicken Nuggets

A and E are the answer.

What are the anaerobic metabolic components that are responsible for:

- The dramatic decrease in SVR

-Heart rate increase

-increase in core body temperature

when the cuff is deflated??????????

Fill in the blanks you silly little freaks:

After the tourniquet is deflated:  If your pt is  spontaneously breathing you will likely see an _____1______ in minute ventilation.  If the patient is NOT spontaneously breathing, the ETCO2 will ______2______.   The minute ventilation may need to be adjusted to manage the _____3_____ in ETCO2.

1) increase

2) Rise

3) Rise

True or false regarding tourniquet release:

1) Although possible, arrhythmias are uncommon following tourniquet deflation.

2) Blood/ tissue reoxygenation is not as dangerous as the ischemic injury (reperfusion injury)

3) The mechanism of tissue injury via reoxyenation is the development of superoxide radicals that destroy the tissue cells. 

4) Propofol does not help with superoxides.

5) Tourniquets can produce stasis and the formation of emboli. Releasing the tourniquet can release the emboli.

1) true

2) False:  Tissue reoxygenation is equally as dangerous as the ischemic injury

3) True

4) False:  Interestingly, propofol has been found to limit superoxide formation!

5) True

1) What are the contraindications for using a tournequet? 

2) Is sickle cell anemia an absolute contraindication to tourniquet use?

1) significant peripheral vascular insufficiency or calcification

2) No.  Tourniquets have been used safely in patients with Sickle Cell Disease although all of the implications to prevent sickling must be employed.

Fat embolism syndrome is a rare but potentially fatal syndrome. 

How soon does it present after a long bone fracture?

Dyspnea

petechia (upper chest, upper extremities, conjunctiva)

Confusion

• Petechia (20-50% of patients) can be missed because it may resolve quickly
• decline in ETCO2
• Decline in Saturation
• Rise in Pulmonary Artery Pressures
• ischemic like changes on ECG
• Right sided heart strain

• Fat globules are released from fat cells in the bone and enter the circulation

• Fat globules are toxic to capillary-alveolar membranes producing vasoactive substances that result in ARDS.

• The confusion and neurological changes are thought to be due to the same/similar mechanism resulting in damage to capillary structures in the brain.

When do ARDS symptoms occur in regards to fat embolism syndrome?

What does the Chest X-ray look like?

1) 1-3 days after precipitating event

2) CXR takes on a "snow storm" appearance

1) Prophylactic- the bone fractures should be splinted, reduced/stabilized as soon as possible.

2) Supportive: Oxygen therapy, intubation, positive pressure ventilation, high dose corticosteroids.

anything:

-Clot

-Cement

-Fat

-Air

In regards to Pulmonary Embolism answer these True or False questions:

1) Embolism can be caused by positioning, fractures of long bones, injection of cement under high pressure and predisposing medical conditions.

2) Venous thromboembolism is a rare cause of death after surgery or trauma of lower extremities

3) Without prophylaxis, the incidence of  clot/emboli is 1-76%.  Of these 10 to 50% show clinical or laboratory signs. 

4) Surgeons have become much better at employing anticoagulation therapy post surgery.

1) True

2) False: Major cause of death

3) False:  without prophylaxis- incidence of clot/emboli: 40-80%  Of these 1-28% show clinical or laboratory signs. 

4) False: Surgeons fail to employ anticoagulation therapy for fear of bleeding post trauma or surgery.

• right heart strain (RBBB, Right axis deviation, tachycardia
• Decreased Cardiac Output
• Increased pulmonary pressures
• Hypoxemia
• Tachypnea
• Resp. Alkalosis
• Mental Status Changes

1) Hip Arthroplasty

2) Total knee arthroplasty

3) Repair of Hip Fracture

50% of venous thrombi start here.  The other 50% start there. 

Where????

bear

hair

scare

50% start intraoperatively

50% during the post op period 24-48 hours after.

1) Compression stockings are a must

2) Fondaparinux (Arixta) is a pentastarch that binds to Antithrombin III. 

By selectively binding to ATIII, fondaparinux sodium potentiates (about 300 times) the innate neutralization of Factor Xa by ATIII. Neutralization of Factor Xa interrupts the blood coagulation cascade and thus inhibits thrombin formation and thrombus development.

Review some Anticoagulant safety issues regarding Subarachnoid blocks and epidurals:

1) For Low molecular weight heparin: for twice daily dosing- when should the first dose be given?  What do I do if I have an epidural?

2) How about once a day dosing?

1) first dose no earlier than 24 hours postoperatively regardless of anesthetic technique and only in the presence of adequate hemostasis.

-remove indwelling catheters before initiation

-When continuous epidural technique is used- catheters may be left indwelling overnight and removed the following day.  The first dose of LMWH should be administered 2 hours after catheter removal

2) Administer 1st dose 6-8 hours postop.  Administer 2nd dose no sooner than 24 hours after 1st dose. 

-Indwelling catheters my be safely maintained but should  be removed at a minimum of 10-12 hours after last does of LMWH.  Subsequent dosing should be initiated a minimum of 2 hours after catheter removal. 

1) How long should a patient be anticoagulated after surgery to aid in prevention of PE?

(What are the current guidlines?)

2) Risk for clot formation exists for how long after the post-operative period?

1) 7-10 days

2) Up to 2 months!!!!