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52 Cards in this Set

  • Front
  • Back
Nonocclusive bowel necrosis
-A/W early enteral nutrition in critically ill, trauma, burn, postop pts (0.3-8%)
-typically occurs in 2nd week of TF
-tachy, fever, leukocytosis
-patchy distribution like NEC
-increase energy demand?, intraluminal toxin?, (in ileus-->bacterial overgrowth)
Risk factors for decubitus ulcers
Emergency Admission (36x)
elderly age
days in bed
days without nutrition
Catheter-related bloodstream infection
+ catheter tip culture with negative peripheral Bcx --> colonization (removing tip suffices)
+ tip cx + Bcx --> coag neg staph (5-10days) coag + staph (10-14days)
I:E ratio
Physiologic respirations I:E - 1:2
Inverse ratio mech vent --> increase inpiration time, decrease venous return, auto-peep, permissive hypercapnia reduces barotrauma
Stress ulcers
Gastric pH 4 or above
2.5-3% incidence
usually in fundus, body of stomach
impaired mucosal protection
RF: mechanical ventilation & coagulopathy (not steroids)
When do you give prophylaxis for GI ulcers?
-Coagulopathy (plt<50,000, INR>1.5, PTT>2x control -Mechanical ventilation > 48 hours
-History of GI ulceration or bleeding with the past year
-Two or more of the following risk factors — sepsis, ICU admission lasting >1 week, occult GI bleeding lasting ≥6 days, and glucocorticoid therapy (more than 250 mg hydrocortisone or the equivalent).
IUH vs LDMW
Fixed-dose low-molecular-weight heparin treatment appears to be as effective and safe as dose-adjusted intravenous unfractionated heparin for the initial treatment of nonmassive pulmonary embolism.
Stress ulcer prophylaxis
H2 blockers better than sucralfate (1.7 vs 3.8%)
HIT
4-14 days onset
2-5%
plts< 150,000 or <50%
Type 1 HIT
Mild thrombocytopenia, not immune mediated, caused by direct agglutinating effect, not a/w thrombosis, resolves despite continuation of heparin therapy
Type 2 HIT
Severe thrombocytopenia
Immune mediated
A/w venous & arterial thrombosis
stimulates PF4 --> IgG
Treatment of HIT
stop heparin and start argatroban, bivalirudin, lepriudin
Recombinant activated factor VII
approved for hemophilia A or B bleeding
combines with TF to activate factor X and IX
Off label use - emergent reversal of coumadin
pH 7.0 --> ineffective
AE --> 10% HTN
SIRS
Temp >38.5 or < 35
pulse >90
RR >20
PaCO2 <32
WBC >12 or < 4 or >10% bands
Activated protein C
endogenous protein that promotes -fibrinolysis and inhibits thrombosis and inflammation
-reduced levels in septic pts
-reduces mortality by 6% in pts with -severe sepsis
predisposes to severe bleeding (not recommended w/n 96 hours of surgery)
-give within 12-24 hrs for 96 hours
Effective measures in reducing sepsis related mortality
-Correcting central venous PO2 w/n 6 hours
-Steroids for non responders
-Tight glucose (80-120)
Crystalloid vs colloid
SAFE Trial - no diff in mortality or organ failure when given albumin or NS
TRICC report
Restrictive strategy of red cell transfusion was as effective as liberal strategy
Acute adrenal insufficiency
hypotension, hypoNa, hyperK
Corticotropin test
measure serum cortisol before and after 30-60 mins of IV 250mcg 1-24 ACTH
nonresponders should get 50q6
Toxic megacolon
total or segmental nonobstructive colonic dilation of at least 6cm a/w systemic toxicity
Diagnosing Cdif
enzyme immunoassay that rapidly detects toxin A nd B (less sensitive than cytotoxin assay which detects toxin B only)
PEEP
increases FRC, compliance
decreases PIP
can cause hypotension
Tertiary peritonitis bugs
Candida
Enterococcus
staph epidermis
Low dose vasopressin
increases SBP, MAP
Periop B-Blockers
2 or more of Mangano criteria (>65 y.o, HTN, current smoker, chol>240, NIDDM
1 of the following (high risk surgical procedure, IHD, IDDM, CR>2.0, TIA/CVA)
How does hyperglycemia cause infection?
leads to G6PD inhibition --> lower levels of PMN superoxide production --> diminished bactericidal activity
VAP
8 days of antibx
Contrast Induced Nephropathy
-no RCTs proving efficacy of mucomyst or dopamine
-Prehydration with NaHco3 better than saline?
Risk Factors for VAP
>60
>48 hours
COPD
ARDS
Reintubation
Upper extremity DVT factors
Biggest RF --> Central venous cathether
young, lean patients
U/S less sensitive than for lower
treatment --> a/c for 3 months
can lead to PE, SVC syndrome, postthrombotic venous insufficiency
What causes release of renin?
decreased vascular volume
dehydration
negative sodium balance
Where is aldosterone released?
Adrenal zona glomerulosa
What governs aldosterone secretion?
Serum K concentration
Hypernatremia treatment
Half of the sodium deficit should be replaced in the first 24 hours
Fluid of choice for hypochloremic hyponatremic alkalosis
NS (not LR since lactate is converted to bicarb)
Hyperkalemia
peaked t waves
wide qrs
n/v/abd pain
HyperMg
flaccid paralysis
hyporeflexia
HypoMg
hyperreflexia
seizures
torsades de pointes (Vtach with long QT)
HypoCa
paresthesias
perioral tingling
carpal pedal spasm
prolonged QT
Weak antiplatelet agent
ASA via permanent COX1 and COX2 inhibition (stop 5 days before surgery)
Mechanism of clopidogrel and ticlopidine
inhibit ADP receptor mediated platelet aggregation (strong antiplatelet)
Mechanism of abciximab (reropro)
Inhibit GpIIb/IIIa receptor (most potent)
increased bleeding complications
severe thrombocytopenia
Mechanism of cilostazol (pletal)
reversible phosphodiesterase III inhibitor --> increase cAMP--> vasodilation and platelet inhibition
NSAIDs mechanism
reversible inhibit COX-1
LMWH and fondaparinux
bind to heparin beinding site of AT III (inactivates Xa but not IIa the way heparin does)
Abdominal compartment syndrome features
increased intrathoracic pressure
decreased cardiac output
decreased urine output
Mechanism and uses of caspofungin and amphoB
Caspofungin inhibits cell wall syntehsis
Ampho B binds to ergosterol leading to increased cell wall permeability
both can be used for empiric fungal infection
Preop parenteral and enteral nutrition
decreased morbidity for parenteral in severely malnourished
decreased morbidity and mortality in severely malnourished
Why does enteral nutrition cause less infectious complications in critically ill?
decreased hyperglycemia?
preservation of GALT?
What 3 parameters affect PaO2
FiO2
PEEP
I/E
SIADH features
hyponatremia
concentrae urine
high urinary sodium
absence of peripheral edema or dehydration
normal volume status
dcreasd BUN
normal potasim