preventative measures in ICU

wolfgang

pathophysiology of VTE

virchow’s triad

components of virchow’s triad

* stasis
* vascular injury
* hypercoagulable state

$ICU patient have **all 3** of these$

formation of VTE

VTE starts as DVT

usually starts in legs due to decreased movement=decreased blood flow from lack of movement

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DVT can turn into PE

risk factors for VTE (5)

* cancer
* previous VTE
* obesity
* trauma
* surgery

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drug options for VTE prophylaxis

* heparin
* LMWH
* fondaparinux
* DOACs

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heparin for VTE prophylaxis

@@most common agent@@

* 5000 units SQ Q24H or 5000 units SQ Q8H
* no renal dose adjustment required

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examples of LMWH

* enoxaparin
* dalteparin

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enoxaparin and dalteparin dosing for VTE prophylaxis

enoxaparin: requires renal adjustment

* 40 mg Q24H or 30 mg Q12H
* CrCl

fondaparinux for VTE prophylaxis

* the only synthetic agent
* not routinely used in critically ill patients
* CI in CrCl < 30

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DOACs in VTE prophylaxis

no role in ICU patients

mechanical methods for VTE prophylaxis

$sequential compression devices$

**use:**


1. combination with prophylaxis for increased risk
2. monotherapy for patients with increased bleed risk

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when can you not use mechanical methods for VTE prophylaxis

* if pt has injury to leg
* if pt has an ACTIVE DVT (could break off)

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how to treat patients with multiple risk factors for VTE

should get pharmacologic and mechanical interventions

major effects of VTE prophylaxis

* bleeding
* heparin-induced TCP

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who should not receive pharmacologic VTE prophylaxis

patients with platelets

bleeding due to VTE prophylaxis

prophylaxis does not cause major VTE bleeding

heparin-induced TCP due to VTE prophy

$immune mediated disorder$

* presents as low platelets in the presence of heparin or LMWH leads to thrombosis (stroke, MI, VTE)

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dosing of VTE prophylaxis drugs in obesity/edema

obesity raises risk of VTE, but could also cause patients to be under-dosed = more risk

stress ulcer

stress-related mucosal damage

* can develop 24 hours after ICU admission

pathophys of stress ulcers

acid hypersecretion in response to gastrin stimulation of parietal cells

independent risk factors for stress ulcers

need $ONE$ to qualify for prophylaxis:

* coagulopathy: platelets

drugs that can be used for stress ulcer prophylaxis

* antacids
* sucralfate
* H2 receptor antagonists
* PPIs

antacids for stress ulcer prophy

not effective and associated with higher mortality

sucralfate for stress ulcer prophy

don’t work as well and have increased risk of toxicity

what do H2 receptor antagonists for stress ulcer prophy require

renal dosing

what occurs over time with H2 antagonists

tachyphylaxis

\-drug stops working

dosage forms of H2 antagonists for stress ulcer prophy

IV and enteral

ADRs of H2 antagonists

* TCP
* mental status changes
* noxocomial pneumonia

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dosing of H2 antagonists for stress ulcer prophy

famotidine 20 mg IV or PO Q12H

ADRs of PPIs

* GI
* nosocomial pneumonia
* C.diff
* fractures
* electrolyte disturbances

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effects of hyperglycemia

* dysregulation of NO function
* impaired neutrophil fxn
* increase production of pro-inflammatory cytokines

target glucose range

140-180 mg/dL

what is the main risk of acute glucose control

$hypoglycemia$

\-it is easy to overshoot, and hypoglycemia is a much more acute risk of poor outcomes/mortality

level to treat hypoglycemia

treatment for hypoglycemia

* discontinue insulin
* administer dextrose: 25 g IV
* re-evaluate insulin/glucose control

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what to do if a patient’s glucose begins to trend under goal but patient is not hypoglycemic

decrease insulin dose or re-evaluate need for insulin

oral antidiabetic agents for glucose control

not routinely used

slinding/correctional scale for glucose control

most common initial method of ICU glucose control

\-use short/rapid acting insulin

\-short: 0-18 units Q4H

\-rapid: 0-6 units TID

how to treat patients with high insulin requirements

basal alone

\-started as a low dose and increased carefully as needed

\-not used as routine control