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Surgery > nutrition > Flashcards

nutrition Flashcards

1
Q
A

-12-25kcal/kg the first 7-10 days of ICU stay
-less calories is better (used to be 30)
-refeeding syndrome- arrythmia from the electrolytes
-entral and parentral nutrtion simultaneously
-nepro- feeding for renal pts
-pulmo care- respiratory pts -> low carbs?
-high carbs -> higher endogenous production of CO2 -> acidosis
-use 80% of wt for obese pts
-CC of tube feed = CC of water
-1200CC of tube feed -> 1200 CC of water a day
-200ml of water through feeding tube 6x a day

-wt x 1.2-2 = protein

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2
Q

small intestine

A

-duodenum- iron
-jejunum- folate
-ileum- b12

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3
Q

daily protein

A

-1.2-2.0 g/kg/day of protein
-lower for renal disease
-higher for burns, obesity, trauma

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4
Q

EN vs PN

A

-the same

-SPN is not beneficial to start early (before day 7)

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5
Q

mixed oil

A

-either mixed-oil lipid injectable emulsions (olive oil, triglycerides, oils) or 100% soybean oil lipid injectable emulsions who are candidates for PN within first week

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6
Q

fish oil

A

-either fish oil- or non-fish oil-containing lipid injectable emulsions be provided to pts who are candidates for PN within first week

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7
Q

enteral nutrition

A

-first line
-initial rate- 50 mL/hour.
-Increase by 25 mL/hour q 4–8 hours until the target rate

-complications
-aspiration
-perforation
-respiratory failure
-

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8
Q

left shift vs right shift

A

LEFT SHIFT
-increase affinity for O2
-decrease CO2
-decrease H+
-decrease 2,3DPG
-decrease temp
-HbF

RIGHT SHIFT
-decrease affinity for O2
-increase CO2
-increase H+
-increase 2,3 DPG
-increase temp

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9
Q

anion gap

A

-Na - (Cl + HCO3)
-<12 is normal

-anion gap acidosis- MUDPILES- methanol, uremia, DKA, propylene glycol, INH, lactic acidosis, ethylene glycol, salicylates

-GOLD MARK- ethylene/propylene Glycol, Oxoproline, L/D lactate, Methanol, ASA, renal failure, Ketoacidosis

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10
Q

coagulation 10a

A

-10a - what triggers prothrombin -> thrombin
-thrombin trigger fibrinogen -> fibrin
-fibrin polymer -> clot

-heparin, enoxaparin -> inhibit thrombin

-Ca- when you give pts a lot of blood -> hypocalcemia
-supplement Ca

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11
Q

TEG

A

-FFP- coagulation factors
-cryo- fibrinogen -> clots
-platelets, FFP, desmopressin- increase the strength of clot (MA)
-lysis in 30 - slow down thrombosis with tranexamic acid (TXA) or aminocalproic acid -> increase clot stability

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12
Q

the bleeding pt

A

-vascular integrity
-platelets
-coagulation system
-look for liver and renal ds
-dilutional
-hypothermia
-meds
-technical issues!!!!!

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13
Q

surgical bleedings

A

-75-90% due to technical error
-forgot to put a clip on something
-acquired or congenital coagulopathies contribute to the dilemma
-results in:
-hemodilution- too much fluid, not enough blood
-hypothermia
-consumption of clotting factors
-acidosis

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14
Q

congenital and acquired bleeding

A

-congenital:
-hemophilia
-VWD- prolonged bleeding time- HISTORY

-acquired:
-vit K deficiency
-liver ds- not enough bile
-renal failure- platelet dysfunction
-meds- ASA, plavix
-hypothermia
-splenic pooling-
-massive transfusion syndrome- Ca being used up
-DIC

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15
Q

hypercoagulable states

A

ARTERIAL
-antiphospholipid
-prothrombin 20210 mutation
-HIT syndrome

VENOUS
-factor V leiden
-prothrombin 20210 mutation
-protein C deficiency
-protein S deficiency
-AT 3 deficiency

-virchow triad- intimal damage, stasis (bed rest), hypercoagulable (surgery, tumors, trauma)

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16
Q

replacement therapy

A

-1 PRBC
-1 FFP
-1 platelets
-Ca
-blood warmer - quality of platelets

-inadequate or overzealous resuscitation
-dilutional complications
-citrate toxicity
-hyperkalemia
-hypothermia
-hypokalemia
-acidosis
-late complication- transfusion acute lung injury, SIRS, sepsis, thrombosis (too much cryo, FFP, platelets)

17
Q

heparin induced thrombocytopenia (HIT)

A

-immunologic response
-platelets aggregate and form a clot
-10% of pts on heparin -> most are non-immune (good!)
-More common with UFH (5%) than LMWH (1%)
-heparin > enoxaparin
-can be seen with heparin flushes (not really used anymore -> now normal saline flushes), heparin coated catheters, heparin during dialysis
-swan gantz coated in heparin

-TYPE 1
-non immune response
-mild drop in platelets >100,000
-1-2 days after start of heparin- returns to normal when you stop it
-usually no clinical consequence

-cardiac surgery- blood goes through a pump - platelets destroyed from pump mechanically -> DIFFERENTIATE

18
Q

HIT type 2

A

-immune mediated
-antibody against heparin platelet factor 4 complex
-antibody bind to Fc receptor and activates platelet -> white clots
-life/limb threatening condition
-leads to thrombocytopenia, arterial, and venous thromboses

-thrombotic sequelae:
-venous:arterial thrombosis -> 4:1
-DVT (50%), PE (25%), acute limb ischemia (10-20%), warfarin assoc venous limb gangrene (5-10%), acute thrombotic stroke or MI (3-5%)
-50% risk of thrombosis over 30 days with cessation of heparin alone
-thrombotic tendency exist for at least 40 days after stopping
-overall risk of thrombotic complication 38-76%

-typically occurs 4-14 days after starting heparin (take into consideration of other recent hospitalizations)
-has occurred as soon as 10 hrs after re-exposure to heparin
-has occurred 3-4 days after cessation of heparin

-platelets count decrease to >50% of what it was on admission after 4 days -> particularly if they got unfractionated and LMWH

19
Q

HIT dx and tx

A

-consider in anyone with unexplained drop in platelets <150,000 or 50% decrease while on heparin
-dx is CLINICAL
-do not wait for lab test results to start tx

-tx:
-d/c ALL HEPARIN (LMWH and flushes, catheters)
-treat clinically suspected HIT immediately
-do NOT wait for lab results
-being alternative anticoagulation with direct thrombin inhibitor -> lepirudin (refludan) or argatroban (acova)
-do NOT use warfarin as substitute -> may actually worsen hypercoaguable state
-continue direct thrombin inhibitor until platelets are normal and need for IV anticoagulation has resolved
-overlap DTI with warfarin for at least 3-5 days
-warfarin start when pt is stable and platelets >100,000 and the DTI is therapeutic

-MONITOR- aPTT or factor 10a
-check every 2-4 hrs until its 1.5-2.5x normal
-check at least daily thereafter

20
Q

disseminated intravascular coagulation (DIC)

A

-systemic, thrombo-hemorrhagic disorder characterized by:
-lab evidence of thrombin generation, fibrinolytic activation, and inhibitor consumption
-AND
-clinical evidence of end organ damage

-clot and lyse
-bleed from everywhere

-Condition with direct intravascular activation of the clotting cascade:
-Trauma, especially neurologic
-Intravascular devices
-Burns
-Infection, esp. with gram negatives (Overwhelming sepsis)
-Obstetrical complications- amniotic fluid embolism
-Cancer, esp. leukemias & adenocarcinomas

21
Q

DIC dx

A

-clinical
-peripheral smear- schistocytes and low platelets
-coagulation profile typically reveals:
-elevated PT/aPTT
-low fibrinogen
-elevated D-dimer/FDPs, thrombin time
-often elevated creatinine, LDH, other assoc end organ damage

22
Q

DIC tx

A

-Tx underlying cause- sepsis
-DIC is not a distinct dx/entity
-Factor replacement as needed.
-Coagulation inhibitor replacement with variable success.
-Platelet transfusion as needed when 15 – 20K level is reached, may start at higher level if there is life threatening bleeding, neurosurgical, etc.

23
Q

surgical infections

A

-inflammatory response
-infection- bacterial, fungal, viral
-sepsis -> severe sepsis -> septic shock (organ involvement)
-trauma, aspiration, pancreatitis, burn

-asepsis principles
-source control- imaging
-antimicrobial agents- within 45 mins

24
Q

wound classification

A
25
Q

antibiotics

A

-prophylaxis- gram positive (skin)
-Cardiac: Cefazolin, cefuroxime
-Thoracic: Cefazolin, ampicillin-sulbactam
-Gastroduodenal: Cefazolin
-Biliary Tract: Cefazolin, cefoxitin, cefotetan, ceftriaxone, ampicillin-sulbactam
-Laparoscopic Procedures:
-Elective/Low risk: none
-Elective/High risk: Cefazolin, cefoxitin, cefotetan, ceftriaxone, ampicillin-sulbactam
-Appendicitis: Uncomplicated: Cefoxitin, cefotetan, cefazolin + metronidazole
-Small Intestine:
-Nonobstructive: Cefazolin
-Obstructive: Cefazolin + metronidazole, cefoxitin, cefotetan
-Hernia Repair: Cefazolin
-Colorectal: Cefazolin + metronidazole, cefoxitin, cefotetan, ampicillin-sulbactam, ceftriaxone + metronidazole, ertapenem
-Head & Neck:
-Clean: None
-Clean with prosthesis: Cefazolin
-Clean-contaminated cancer surgery: Cefazolin + metronidazole, cefuroxime + metronidazole, ampicillin-sulbactam
-Other clean-contaminated (excludes tonsilectomy and functional endoscpic sinus problems): Cefazolin + metronidazole, cefuroxime + metronidazole, ampicillin-sulbactam
-Neurosurgery: Cefazolin
-C-Section: Cefazolin
-Hysterectomy: Cefazolin, cefotetan, cefoxitin, ampicillin-sulbactam
-Ophthalmic: Topical neomycin-polymyxin B-gramicidin, 4th generation fluoroquinolones
-urologic:
-Lower instrumentation with risk factors for infection: Fluoroquinolone, TMP-SMX, cefazolin
-Clean without entry to urinary tract: Cefazolin (single dose of aminoglycoside with penile prosthesis)
Implanted prosthesis:
Cefazolin + aminoglycoside, cefazolin + aztreonam, ampicillin-sulbactam
-Orthopedic:
-Clean hand, knee or foot without implants: None
-Spinal with and without instrumentation: Cefazolin
-Hip fracture, ORIF device implantation, TJR: Cefazolin

-empiric
-therapeutic- key element is de-escalation

26
Q

hyponatremia

A

-pontine myelinosis if correction of >25 for 24-48 hrs
-limit to 10/day
-cerebral edema
-give hypertonic saline
-DO NOT give sodium bicarb

27
Q

hyperkalemia

A

-hyperkalemia:
-peaked t waves
-stimulate aldosterone -> pee K

-tx:
-CaCl2 10% - 1 ampule
-sodium bicarbonate - 1 ampule
-D50 and insulin 10 u
-beta 2 agonist nebulizer- cellular K increase
-kayexalate
-sodium zirconium cyclosilicate (lokelma)
-dialysis

28
Q

causes of hyperkalemia

A

-Renal dysfunction
-Acidemia
-Hypoaldosteronism
-Drugs
-Excessive intake
-WBC > 100,000
-Platelets > 600,000

-Cell Death
-Rhabdomyolysis
-Tumor lysis- chemo
-Burns
-Hemolysis

-check LDH

29
Q

hypokalemia

A

-repletion is done based on
-say the K you want is 4.5
-(K you want - K you have) / Cr x 100 = K you need to replete

-tx:
-10/hr via IV
-remember to check Mg too

30
Q

hypocalcemia

A

-prolonged QTC interval
-chvostek sign- face
-trousseau sign- carpal spasm

31
Q

hypomagnesemia

A

-energy, muscles, protein
-cant replace K without Mg
-<1.6
-cause- diet, diuretics, gut loss, massive diarrhea, resuscitation, burns, pacreatitis, SIADH, parathyroidectomy, primary hyperaldosteronism
-POST OP AFIB -> GIVE MG !!!!!
-4.2-4.5 POST OP

-weakness, fatigue, MS changes
-hyperreflexia
-seizure
-arrythmia

-tx:
-magnesium sulfate IV
-1g = 8mEg
-infuse at rate of 2g/hr
-emergency- 2g/5 mins

-clinical picture- pt with isolated repaired fracture femur, LOC decreased, seizure -> ekg with torsades

32
Q

hypermagnesemia

A

-iatrogenic, Renal insufficiency, antacid abuse, adrenal insufficiency, hypothyroidism

-S/Sx: N/V, weakness, MS changes, hyporeflexia, paralysis of voluntary muscles
-EKG- AV block and prolonged QT interval
-HYPOTENSION- eclampsia
-prolonged PR interval

Treatment:
-Discontinue source
-normal saline
-IV Calcium Gluconate for acute
-loop diuretics
-then so Dialysis

33
Q

hypophosphatemia

A

-seen in hyperalimentation, after starvation, DKA, malabsorption, phosphate binding antacids, alkalosis, hemodialysis, hyperparathyroidism.
-seen in refeeding syndrome- ate too quick after starvation
-HEAD TRAUMA

-S/Sx:
-myocardial depression due to low ATP
-shift of oxyhemoglobin curve to left due to low 2,3 DPG
-anorexia
-bone pain
-hemolysis
-cardiac arrest

-tx:
-PO replacement! (neutrophos) or
-IV KPhos or NaPhos 0.08-0.20 mM/kg over 6 hrs
-keep phosphorous x calcium ratio < 60
-magnesium is given at the same time!
-need this for ATP -> diaphragm stops working without it -> cant take off vent

34
Q

hyperphosphatemia

A

-renal insufficiency, hypoparathyroidism, may produce metastatic calcification
-tx with restriction and phosphate binding antacid (amphogel)

Surgery (26 decks)

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