nutrition Flashcards
-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
small intestine
-duodenum- iron
-jejunum- folate
-ileum- b12
daily protein
-1.2-2.0 g/kg/day of protein
-lower for renal disease
-higher for burns, obesity, trauma
EN vs PN
-the same
-SPN is not beneficial to start early (before day 7)
mixed oil
-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
fish oil
-either fish oil- or non-fish oil-containing lipid injectable emulsions be provided to pts who are candidates for PN within first week
enteral nutrition
-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
-
left shift vs right shift
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
anion gap
-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
coagulation 10a
-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
TEG
-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
the bleeding pt
-vascular integrity
-platelets
-coagulation system
-look for liver and renal ds
-dilutional
-hypothermia
-meds
-technical issues!!!!!
surgical bleedings
-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
congenital and acquired bleeding
-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
hypercoagulable states
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)
replacement therapy
-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)
heparin induced thrombocytopenia (HIT)
-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
HIT type 2
-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
HIT dx and tx
-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
disseminated intravascular coagulation (DIC)
-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
DIC dx
-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
DIC tx
-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.
surgical infections
-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
wound classification
