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UBP Pearls > Misc 2 > Flashcards

Misc 2 Flashcards

1
Q

CV changes w/burn injury?

A
  • First, CO dec 2/2 circulating myocardial depressant factors, inc SVR (cat release), dec plasma vol 2/2 protein rich fluid intravasc –> interstitial space, dec coronary blood flow, dec response to cats
  • If resus adequate, capillary integrity normal in 18-48 hrs
  • At 48-72 hrs, get hyperdynamic state! HR and CO increased, (inc cats, SVR dec)
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2
Q

Anesthetic considerations for burn pt undergoing burn excision 48 hrs after event?

A
  • risk of HD instability (transitioning from hypo to hyperdynamic circ state w/in first 72 hrs)
  • burn excisions are at risk for sig blood loss (ensure T&Cs)
  • fluid and lyte management (IV access!)
  • temp control (keep OR 28-32*C, monitor closely)
  • safe placement of monitors
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3
Q

What % of pt’s TBSA would be the limit for an escharotomy?

A

50%! Early extensive a/w/ dec fluid loss, improved CV fxn, dec transfusion, improved survival.

But! Can lead to inc blood loss and have to take into account pt specific situation to see how much they could reasonably handle (can stage them, use epi, turniquets, compression dressings)

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4
Q

Why are burn pts at inc risk of hypothermia? Issues a/w/ this?

A
  • impaired thermoreg
  • anesthetic-induced vasodil
  • surgical skin prep w/alcohol
  • inc O2 consumption
  • arrhythmias
  • coagulopathy
  • inc blood loss
  • infx
  • graft disruption (shivering)
  • dec CO
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5
Q

What is the time period in which you should avoid sux in burn patients? What is the time period where pt is at risk for MOST pronounced K elevation?

A
  • 24 hrs to 2 years after burn
  • 5-15 days after burn is worst time
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6
Q

Diff between tangential vs fascial excision for burn surgery?

A
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7
Q

Multiple considerations and eval of when to transfuse in burn surgery?

A
  • PMH requiring higher Hct levels d/t c/f cardiac dysfxn (HTN, DM, HLD)
  • CO poisoning
  • planned % excision
  • depth and type of excision (tangential, fascial)
  • tumescent fluid use w/epi?
  • current progress of surgery and level of surgical hemostasis
  • HD instability
  • s/s of end organ ischemia
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8
Q

SEs of hyper-alimentation? What to monitor?

A

Hyperglycemia
Cholestasis
Fatty infiltration of the liver
Lyte disturbances

Serum and urinary glu
Liver fxn
Lytes

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9
Q

Benefits of early enteral nutritional support?

A
  • attenuation of hypermetabolic response and muscle protein loss
  • improved wound healing
  • modulated stress hormone levels
  • improved gut muscle integrity
  • dec risk of stress ulcer formation
  • inc risk of sepsis and multi-organ failure 2/2 gut mucosal atrophy, inc microbial translocation
  • improved outcomes
  • do have to be careful of gastric ileus (inc risk of aspiration w/enteral feeds) and intestinal necrosis if pt in shock and try to start feeds too early
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10
Q

What does acute AR lead to?

A
  • vol overload of LV
  • dec effective SV
  • pulm edema 2/2 LVEDP
  • inc myocardial demand
  • dec myocardial blood supply 2/2 dec diastolic pressures in aorta + inc LVEDP
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11
Q

What to do if traumatic epidural placement?

A
  • basically, if nonurgent should delay case for 24 hrs if utilizing systemic heparinization
  • if have to proceed, ensure nl coags prior to removal of drain afterwards. In meantime, q1h neuro exam for s/s of spinal cord compression 2/2 hematoma formation. Utilize narcotic only through it or with low dose concentration LA to preserve LE motor fxn and allow for neuro monitoring
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12
Q

Pros/cons of epidural placement for thoracic aneurysm repair?

A

PROS:
- postop pain control
- improved resp fxn (dec atelectasis, pulm infx, resp failure, prolonged mech vent)
- improved GI motility
- improved graft patency 2/2 reduced coag response
- dec postop MI (attenuation of stress response + coronary art dilation)

CONS:
- potentially interferes w/MEP/SSEP monitoring (should dose only w/narcotics during case, then LA afterward)
- epidural/spinal hematoma (delay systemic heparin for 60min after placement, minimize dose, remove after complete restoration of motor fxn to avoid dx confusion and nl coag)

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13
Q

What is it called when you “blood let” the patient, save all of that separately, give that same amount in crystalloid to restore blood volume (so you’re making them “anemic” so that when you inevitably lose blood, it’s diluted and still have concentrated full blood saved up?

A few relative C/Is to doing this?

A

Acute normovolemic hemodilution (good b/c dec risk of infx, transfusion rxn, RBC alloimmunization). Shown to save ~1-2u pRBCs at most.

The reduction of [RBC] is ass w/dec blood viscosity –> dec PVR and inc CO, which helps to maintain adequate O2 delivery to tissues despite dec Hct

C/Is:
- Hct < 33, smoker w/pulm disease, renal impairment (2/2 DM, HTN, etc) since difficult to excrete fluid load
- conditions that would make an inc in CO undesirable (like AS) that you’d have w/fluid load
- pre-existing coagulopathy
- Ischemic cardiac disease (should limit initial reduction in Hct to avoid end-organ ischemia)

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14
Q

What’s a good “end point” irt allowable blood loss for someone who has CAD?

A

Hct ~27, so a Hb of 9. I think this is a good limit for SCD as well from what I remember

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15
Q

How does mild and more deep hypothermia result in coagulopathy? Testing for this?

A
  • mild (33-37): cold-induced defects in pltlt aggregation and adhesion. Coags not affected. So should use TEG instead of PTT
  • deeper (<33): pltlt and coag enzyme activity are abnl, could use either test
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16
Q

Describe how a TEG works

A

It measures the viscoelastic properties of blood during induced clot formation

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17
Q

Cross reactivity % for 1st and 2nd/3rd generation cephalosporins w/PCNs?

A

0.5%
Near zero

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18
Q

Mechanism behind “red man syndrome”? S/s? Tx?

A

Rapid admin of vanco (should be 10mg/kg over 60 mins) –> histamine release

  • hypoTN (most common)
  • pruritis, flushing, upper body erythema, cardiac arrest
  • Can give antihistamine (diphenhydramine, cimetidine) 1 hr before vanco can attenuate hypoTN 2/2 dec in SVR
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19
Q

What is arachnoiditis? Causes? S/s? Dx? Tx?

A
  • infl of meninges, subarachnoid space
  • direct injury to spine (trauma, surgery, many LPs), infx, chemicals (dye, preservatives in epidural LAs and steroids), chronic compression of spinal nerves (DDD, spinal stenosis)
  • back pain worse w/activity, sensory/motor abnlties, bowel/bladder/sexual dysfxn
  • CT, MRI
  • similar to other chronic pain issues irt tx: PT, pain meds (NSAIDs, narcs, corticosteroids, anti-spasm/convulsants), IT pump, TENS, spinal cord stimulator
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20
Q

Ddx for prolonged NM blockade?

A
  • myasthenia gravis
  • pseudocholinesterase deficiency
  • drug error, defective n stimulator
  • underlying NM disease (Eaton-Lambert syndrome, botulism toxin, ALS, MS, muscular dystrophy)
  • lyte abnlties, hypothermia, acidosis, hypercarbia
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21
Q

Optic and Bulbar findings of pt w/MG? Tx?

A
  • ptosis, diplopia
  • inability to clear secretions, difficulty breathing, pulm aspiration (presence of these bulbar sxs suggest more severe dz)
  • AChE (pyridostigmine)
  • immunosuppressants (steroids, azathioprine, cyclophosphamide, cyclosporine)
  • thymectomy (production of ABs mostly produced here)
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22
Q

Signs of cholinergic crisis? Tx?

A

MUDPILES - everything parasymp
- constricted pupils
- salivation, diaphoresis
- diarrhea, N/V, abd cramps
- urinary urgency/freq
- weakness and muscle fasciculation
- bradycardia

  • consider intubation (if weak, etc), d/c any anticholinesterases, give anticholinergic (like atropine), supportive care, plasmophoresis/IVIG if severe
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23
Q

What is it called when you don’t have a normal response to heparin administration? ACT still remains low. Ddx?

A
  • ATIII deficiency (in which case, you’d admin FFP)
  • causes are defects in production, loss (nephrotic syndrome), consumption (sepsis, trauma)

-ATIII is protease that binds to thrombin, X, XI, XII, XIII. Heparin works by binding/complexing w/ATIII and enhancing its activity by 1000x

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24
Q

2 main ddx for hypoTN and inc in PAP after giving protamine?

A
  • protamine induced histamine release –> inc PVR and dec SVR
  • type III protamine rxn (protamine-heparin complex induces release of thromboxane A2 in pulm circuit –> inc in PAP –> R HF). No great way to prevent this, but diluting and administering slowly (5-10 mins) “seems a reasonable approach”
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25
Q

What is acromegaly a/w/?

A
  • big hands, feet, nose, mandible, tongue, soft palate, tonsils, epiglottis, glottic stenosis
  • HTN, insulin resistance
  • accelerated atherosclerosis
  • osteoarthritis, skeletal m weakness, arthritis
  • CM
  • OSA
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26
Q

Common causes of PVCs?

A
  • systemic uptake of cocaine (nasally inserted cocaine pledgets)
  • epi within LA mixture
  • hypoxia, cardiac ischemia, air embolism, lyte abnlties, anesthetic induced cardiac depression
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27
Q

What is lupus? Possible manifestations?

A
  • AI disease –> systemic chronic infl (vasculitis) and tissue damage. Must have 3 or more of:
  • ANAs, rash (malar or discoid), nephritis, polyarthritis, thrombocytopenia/anemia/etc (ensure pt doesn’t have s/s of coagulopathy, ensure pltl count and no downtrend if placing a neuraxial), serositis (pericarditis/pleuritis), neuro disorder, photosensitivity
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28
Q

Anesthetic considerations for SLE?

A
  • diff airway: edema, cricoarytenoid arthritis, c-spine arthritis
  • periop coagulation: thrombocytopenia (inc bleeding), antiPlipid ABs (DVT, stroke, PE)
  • pulm: infx, effusion, ILD, pneumonitis
  • cardiac: pulm HTN, HTN, CAD, pericarditis/effusion, valve issues
  • renal: CKD (lupus nephritis)
  • SEs of immunosuppressants
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29
Q

Pathogenesis of acute porphyrias? Preop eval?

A
  • deficiency of enzyme in heme biosynthetic pathway –> accumulation of porphyrins –> abd pain, N/V, psychiatric, ANS instability, seizures, resp failure, lyte abnlties
  • should look for all of these clinical manifestations, when last attack happened, precipitation of that, tx, etc. If current s/s, elective case should be postponed. Otherwise try to optimize ANS, vol status, lytes
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30
Q

How to dec risk of triggering a porphyric crisis?

A
  • avoid/dec fasting, dehydration, stress, infx
  • ensure hydration, give versed, can give 10% glu for carb source, avoid certain drugs
31
Q

Tx of an acute porphyria attack?

A
  • d/c any porphyrinogenic drugs
  • ensure adequate ventilation, oxygenation, hydration, analgesia, anxiolysis, lytes
  • give carbs (D10NS)
  • give antiemetic, BB (if tachy/HTN), BDZ/propofol for seizure (others unsafe)
32
Q

C/Is to ECT?

A
  • intracranial mass lesion
  • vascular AVMs
  • recent MI (<3mo), stroke (<1mo)
  • inc ICP from any cause
  • pheo
33
Q

Physiologic changes during ECT?

A
  • initial electrical stimulus: parasymp discharge –> brady, inc secretions, hypoTN
  • 1 min later, seizure –> symp activation –> tachy, HTN, dysrhythmias (causes inc cerebral blood flow, ICP, and cerebral O2 consumption)
34
Q

How to perform ECT anesthetic?

A
  • this was from a pt who was pregnant, but I’m sure much is the same
  • for the muscle relaxation part, can use smaller dose of sux (like 1mg/kg) to attenuate muscle contractions that can –> bone fx, joint dislocations while still allowing for visual confirmation of seizure activity. Alternatively, could use tourniquet technique to extremity
35
Q

After ECT, pt is disoriented, unable to follow commands, blinking rapidly, constantly moving feet —> what’s going on? Tx?

A

Postictal agitation
- Tx: small dose of propofol, BDZ, or precedex

36
Q

How to eval and optimize pt for pheo resection?

A
  • ensure alpha blockade at least 7-10 days prior to elim sxs, normalize BPs
  • admin fluids to restore intravasc vol
  • eval cardiac fxn (high risk for ectopy, CM, MI) w/EKG, CXR, TTE
  • initiate BB to control HR and cat-induced arrhythmias if needed (but only AFTER BP is optimized…< 165/90 x 48hrs. This is bc you don’t want unopposed alpha)
  • pulm fxn
  • consider sedatives for anxiety
37
Q

Drugs that should be avoided in a pheo case? Those that:

A
  • stimulate tumor cells, like sux. And histamine releasing, like morphine, atracurium, sux
  • result in inc symp activity: atropine, ketamine, ephedrine
  • can cause significant HTN: droperidol, reglan, ephedrine
38
Q

AntiHTN meds you could use if doing a pheo?

A
  • nipride (direct vasodilator, quick on/off)
  • phentolamine (longer onset/duration, can cause tachycardia/tachyphylaxis)
  • NTG (can cause tachycardia)
  • esmolol, labetalol
  • Mg (inhibits cat release, direct vasodilator)
39
Q

Are patients s/p pheo resection at risk for hypo vs hyperglycemia? Why?

A
  • hypo!
  • normally, epi/NE stim a2 Rs in pancreatic cells, which INHIBITS release of insulin. So when tumor removed, epi/NE decreases –> lot of insulin released –> hypoglycemia
  • blood glu should be monitored for 24 hrs postop
40
Q

Things to do if pt w/CRF has K of 5.6 needs surgery

A
  • urgency of case
  • check EKG for any hyperK signs
  • avoid sux, K containing solutions
  • prepare to tx w/Ca, glu/insulin, B agonist, hypervent, bicarb
  • ensure defib in room
  • carefully monitor EKG and K levels throughout case
41
Q

Drugs to avoid in CRF patients?

A
  • anything dep on renal elim or have active metabolites that can accumulate
  • pancuronium
  • atropine/glyco
  • ketamine, morphine, diazepam, meperidine
42
Q

How would you intubate a patient w/glottic mass + stridor, sternal retraction, use of accessory muscles?

A
  • would NOT awake fiber an advanced obstructive laryngeal disease d/t risk of complete obstruction as scope passes, difficulty of airway analgesia, technically difficult thru friable tumor
  • instead,
    1) inhalational induction w/spont vent until airway secured
    2) awake elective trach under LA
43
Q

Radiographic findings of foreign body aspiration?

A
  • most things are radiolucent, so not easily directly visualized. But,
  • bronchial obstruction –> hyperinflation, air trapping, atelectasis of affected lung distal to the foreign body
  • significant atelectasis or hyperinflation –> mediastinal shift
44
Q

What is vWD?

A
  • inherited coag disorder d/t qual or quant defects of vWF in plasma
  • vWF mediates pltl adhesion to bv’s, facilitates plt-plt aggregation, carrier protein for F8
  • 3 main subtypes. Type I: most common and mildest. Quant. Primary hemostasis problem (menorrhagia, GI bleeds, gingival, bruising). Type II: qual defects, 4 subtypes. Type III: rarest, most severe. Severe bleeding (hemarthrosis, muscle hematomas, signif bleeding w/surgery)
45
Q

What will different forms of vWD show on coag studies?

A
  • Mild forms: near normal
  • Severe: prolonged bleeding, thrombocytopenia, prolonged PTT
46
Q

Don’t know pt’s subtybe of vWD…do you admin anything ppx prior to big surgery?

A
  • don’t give DDAVP (works for type I, but not really for type II. Also limited DOA, potential for tachyphylaxis
  • give ppx vWF replacement w/cryo or Humate P
47
Q

How to manage peripheral neuropathy caused intraop?

A
  • review chart, thorough H&P
  • eval type and severity
  • neuro consult w/nerve conduction velocity and EMG studies
  • inform pt and family of concerns and plans for further eval
  • reassure that most cases of peripheral neuropathy resolve w/in 6-12 weeks w/o intervention
48
Q

For how long after an airway fire should you keep a pt intubated?

A
  • 24hrs (inhalational injury can initially seem mild w/minimal e/o mucosal injury, but then progress rapidly to life threatening airway obstruction 2/2 rapidly developing airway edema
  • give steroids, humidified O2, monitor serial XRays x 24 hrs
49
Q

Dose of dantrolene?

A

2.5mg/kg (repeating doses q5-10m PRN to control sxs)

  • also should hyperventilate w/100% O2
  • active cooling measures
  • maintain UOP w/IVFs, mannitol, lasix
  • monitor labs
  • treat hyperK, rhabdo, dysrhythmias PRN
  • continue IV dantrolene for 24-48 hrs
  • monitor in ICU x72 hrs
50
Q

Purpose of pt w/sickle cell disease taking hydroxyurea?

A
  • dec # of sickle crises via ability to inc circ fHb –> dec rate and extent of HbS sickling
  • other mechanisms too, but too detailed
51
Q

What is aplastic crisis?

A
  • BM suppression 2/2 infx (parvo) or folate def –> dec RBC production. This, + sickle cell disease (and dec RBC life span) –> profoud anemia –> cardiac failure + death
  • tx: correcting any folate def + give blood until BM suppression resolves
52
Q

Why is it important to have a hight Hct cutoff for sickle cell patients?

A
  • deoxygenated blood sickles (also has to do with the amount of time that it’s deoxygenated…hence why not all venous blood sickles)
  • should transfuse to Hct >30 but <35 (want to avoid inc viscosity a/w/ over transfusion)
53
Q

What is something postop you can do if your OB patient or any pt who needs neuraxial is at a higher risk of spinal hematoma for whatever reason (low platelets, etc)

A
  • ensure adequate platelet level postop
  • allow for complete resolution of motor/sensory fxn before removing catheter (to allow for better detection of change in motor or sensory fxn a/w/ hematoma formation)
  • can order q1h neuro checks to more quickly ID s/s of epidural hematoma (severe backache, bowel/bladder dysfxn, radiculopathy, tenderness, unexplained fever)
54
Q

What are things intraop that you can do to reduce risk of sickling in SCD pt?

A
  • avoid hypoTN and venostasis w/fluid admin (and L uterine displacement if OB)
  • avoid inc viscosity w/w/ overtransfusion (Hct >35%)
  • preserve adequate Oxygenation w/O2 and O2-carrying capacity w/pRBCs (Hct >30% goal)
  • maintain normothermia (hyper increase oxygen consumption, hypo –> blood stasis)
  • ensure adequate ventilation and tissue perfusion to avoid acidosis, which shifts the curve to the right and causes Hb deoxygenation
55
Q

When should nitrous be avoided in relation to eye surgery? Time periods?

A
  • should be d/c’ed 15min prior to injx of intra-vitreal gas for retinal detachment surgery
  • should be avoided after for variable times depending on what was injx (air: 5d, sulfur hexafluoride: 10d, perfluoropropane: 30d)

**admin of very soluble gas like nitrous –> expansion of intra-vitreal bubble –> inc intra-ocular P, central retinal art occlusion, and retinal/optic n ischemia

56
Q

How to tx acute chest syndrome in SCD pt?

A
  • provide suppl O2, bronchodilators, incentive spiro, chest physio
  • abx
  • pain control
  • correct anemia w/blood transfusion
  • consider exchange transfusion and/or mech ventilation if severe enough
57
Q

Using a tourniquet in SCD pt?

A
  • prefer not to since regional venostasis, acidosis, deox Hb that occurs distal to it
  • have been used safely in pts if >2hrs
  • if absolutely needed, try to avoid hypoxia, acidosis, dehydration, hypo/hyperthermia as much as possible
58
Q

S/s of thyrotoxicosis?

A
  • cardiac: tachy, arrhythmias, CM, inc SV and CO, dec SVR and PVR
  • neuro: anxiety, agitation, trmors, insomnia, muscle weakness
  • sweating, heat intolerance, weight loss
59
Q

Lambert-Eaton pathophys? What does weakness improve with? Tx?

A
  • ABs to PREjxnl Ca channels –> dec ACh release at motor end plate –> proximal weakness of LEs, sometimes UEs + autonomic dysfxn (dry mouth, impotence, constipation, ortho hypoTN)
  • Improved strength w/activity! (instead of w/rest like in MG)
  • tx the cancer, plasma xchange, IVIG, pred, pyridostigmine (cholinesterase inhibitor which inc ACh at the jxn)
60
Q

Preop HTN - what are some examples of situations where you’d delay the case for improved BP control?

A
  • SBP >180 or DBP >110
  • has SBP >140 and concomitant end-organ damage (LVH, angina, MI, CHF, CAD, stroke, TIA, CKD, retinopathy, PAD)
  • is undergoing cardiac sx, carotid sx, or pheo resection
  • however, decision to delay any case must weigh risk/benefits
61
Q

What steps would you take for a GETA in pt w/SVC syndrome?

A
62
Q

Doing a thoracic AA repair…going to use the clamp and sew technique (no bypass). A few methods for providing renal protection?

A
  • Similar steps to when you do a kidney transplant case (bc you’re interrupting renal blood flow during this procedure too)
  • adequate IVFs
  • avoid contrast dye wherever possible
  • avoid nephrotoxic drugs (NSAIDs, ACEi, ASA, aminoglycosides)
  • use renal protective drugs: mannitol (inc renal blood flow, scavenges free radicals), loop diuretics, low dose dopamine (these inc renal blood flow and UOP)
  • minimize X clamp time
  • systemic/regional hypothermia
63
Q

Are kidneys still at risk if a Xclamp is placed infrarenally?

A
  • Yes! Still a 40% dec in renal blood flow (80-90% when suprarenal X clamp)
  • ATN is what causes postop dysfxn and failure after aortic reconstruction
64
Q

What is the order of artery branches off of the aorta below the diaphragm?

A
65
Q

What are some downsides to induced hypothermia?

A
  • arrhythmias (atrial, ventricular fib)
  • myocardial depression
  • inc metabolic O2 requirements (shivering)
  • coagulopathy
  • on the positive side…hypothermia dec cerebral and spinal cord O2 requirements by 5% for each 1* below 36*C
66
Q

Mechanism behind nipride toxicity? What to give for tx?

A
  • nitroprusside enters RBC –> rxn happens which releases NO and cyanide ions –> ions can do 3 things:
    1) react w/MetHb –> cyanMetHb
    2) react w/thiosulfate –> thiocyanate
    3) bind to cytochrome oxidase (which is what actually causes issues) –> impairs nl tissue O2 utilization –> cyanide toxicity –> met acidosis, inc mixed venous O2, arrhythmias. Chance of this is low if using doses < 0.5mg/kg/h

From ACCRAC epi 265:
- nipride reacts w/oxyHb, transfers electron from oxyHb to nipride –> MetHb. Causes release of NO (therapeutic, causing sm m relaxation) and 5 CN ions (4 of which are converted to thiocyanate in the liver, and excreted in urine , prolonged in renal dysfxn pts. Remaining CN reacts w/MetHb –> cyanMetHb, but when nipride conc exceed capacity of the liver or when sulfur or MetHb stores are depleted –> CN toxicity)

  • tx: d/c infusion, 100% FiO2, and admin: thiosulfate (2nd rxn from above), amylnitrate or Na nitrate (both oxidize Hb to MetHb, inc substrate from 1st rxn), or hydroxocobalamin (combines w/CN –> cyanocobalamin, aka B12). All effectively dec CN from circ to avoid rxn w/cyto oxidase
67
Q

Some postop complications a/w/ aortic aneurysm/dissection repair?

A
  • renal failure, AKI (usually ATN)
  • MI
  • pulm insult
  • neuro injury (paraplegia)
  • mesenteric/visceral injury (2/2 ischemia)
  • CVA

More specific to endovasc aneurysm repair:
- endoleaks
- endograft migration
- contrast induced nephropathy
- postimplantation syndrome (endothealial activation 2/2 prosthesis –> fever, infl mediators, leukocytosis. Supportive tx, self resolving

68
Q

Concerns when providing anesthesia in MRI?

A
  • unintentional transfer of ferromagnetic object into scanner room (projectile injury to anyone)
  • dislodgement or malfxn of implanted device (PM, AICD, SCS)
  • magnet induced equip malfxn (pumps etc)
  • thermal injury (so need special cables w/o coiling)
  • hearing loss 2/2 loud scanner
  • patient anxiety
  • kidney injury 2/2 gadnolinium containing contrast agents
  • I would add: unfamiliarity w/OOR environment and use of different equipment etc
69
Q

What are the recommendations irt when you’re supposed to start enteral or TPN in the ICU?

A
  • s/p 8 days in the ICU
  • dec infx, shorter duration of renal replacement therapy, shorter # of days on mech vent, less cholestasis, dec cost
  • however, inadequate nutrition also bad. Delayed wound healing, inc incidence of infx, impaired muscle fxn (delayed mobilization), gut atrophy
  • so, should initiate ENTERAL nutrition w/in first 24-48h of ICU admission
70
Q

Do you d/c enteral nutrition prior to surgery?

A
  • Nope
  • inc risk of hypoglycemia/fluid imbalance
  • low risk of aspiration pneumonitis w/continued infusion
  • current guidelines say to continue pre and intraop
  • However, would still use an OGT to empty stomach, give aspiration ppx, cricoid, RSI, and extubate fully awake
71
Q

Indications for TPN?

A
  • inability/refusal of pt to take PO/enteral
  • short bowel syndrome
  • active GI bleeding
  • abd distention
  • need for bowel rest
  • V/D/malposition of feeding tube, poor gastric emptying, etc
72
Q

Complications a/w/ TPN?

A
  • inc CO2 retention (think about in COPD pt) –> metabolic demand for O2 that can’t be met (so need to lower the resp quotient by dec carb and inc lipid content). This can also –> difficulty w/weaning from vent + muscle weakness from hypoPhos
  • metabolic disturbances (hypo/hyperK, Na, Phos, Mg, glu, acidosis/alkalosis, Ca), refeeding syndrome
  • catheter issues (infx/sepsis, PTX, air embo, tamponade, thrombophlebitis)
  • fatty liver
  • cholecystitis (2/2 inactive GI system)
  • fluid overload
  • HLD, anemia, pancreatitis, fat embo
73
Q

What are the main parts of a proper machine check?

A
  • turn on machine and monitors, calibrate them + alarms
  • verify emergent vent equip available, suction
  • check high P system: the Ecylinders need adequate gas P, central pipeline supply hoses connected and gauges read 50
  • check low P system: check for leaks (+ pressure test), vaporizers are filled, flowmeter check
  • check scavenging system, unidirectional valves, adequate CO2 absorbant
74
Q

Mechanisms that protect against delivery of hypoxic mixture?

A
  • fail safe alarm: sounds if P in O2 pipeline falls <30
  • O2 failure cut off valves: d/c flows of other gasses when O2 P dec < threshold
  • not definitive - need to be vigilant!

UBP Pearls (9 decks)

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