WILKINSON & SHEERIN
Good Housekeeping: STRESS ULCER and VTE prophylaxis
Andy Wilkinson and Eamonn Sheerin are registrars currently working in ICU in Sydney. They are relatively new to ICU and have been looking into why we do some of what we do on our daily ward rounds.
This podcasts focuses on ways of remembering the important things that can be forgotten, and in particular stress ulcer prophylaxis and venous thromboembolism (VTE) prophylaxis.
Click READ MORE for the podcast, and links...
Listen to the talk here:
For more on FAST HUG IN BED Please look here
The alternative (more hardcore) version is DANISH BUG FEST
D e-escalte - especially anti-biotics, review other meds that may no longer be needed
A nalgesia - Is that why they're hypertensive & tachycardic?
N asogastric Tube - need one? Need to remove one?
I ndwelling Catheter - Pull it out ASAP
S edation - What's the RASS? Can you cut back?
H ead of bed 30 degrees - Not amazing evidence but we do it.
B owel care - Many patients need aperiants. Look for, prevent and investigate diarrhoea.
U lcer prophylaxis - listen to the podcast!
G lycaemic control - here's a podcast & review
F eeding and Fluids - are you feeding? what are you giving? should you be giving less fluid?
E nvironment - think delirium avoidance. Prevention is better than cure! What would you want in ICU?
S kin - pressure areas can get infected; rashes may be significant.
T hromboembolism prophylaxis - listen to the podcast!
Notes to go with the Eamonn's Stress Ulcer Prophylaxis section:
Q1. What are we trying to prevent?
Stress ulcers are gastric mucosal erosions that can develop in patients with a serious illness or severe injury. Unlike peptic ulcers, which tend to develop in the antrum or duodenum, stress-related mucosal injuries typically occur in the acid-producing areas of the stomach (i.e., corpus and fundus). Stress ulcers, unlike peptic ulcers, tend to cause gastrointestinal (GI) bleeding and are not associated with abdominal pain. The mucosal changes of stress-related mucosal injury mainly involve small erosions that do not lead to bleeding but may develop into deeper ulcers, which cause bleeding.
Endoscopy performed within 72 hours of a major burn or cranial trauma reveals acute mucosal abnormalities in greater than 75 percent of patients[i]. Incidence of clinically significant bleeding range from 1.5 to 8.5 percent among all ICU patients[ii], but may be as high as 15 percent among patients who do not receive stress ulcer prophylaxis[iii].
Q2. Which pharmalogical agents should we use?
Q3. Who should we be giving prophylaxis to?
A multicenter prospective cohort study of 2252 ICU patients identified two major risk factors for clinically important GI bleeding (defined as overt GI bleeding leading to hemodynamic deterioration or requiring blood transfusion)[v] due to stress ulceration:
The incidence of clinically important GI bleeding among patients with one or both of these risk factors was 3.7 percent. In patients with neither RF the incidence was 0.1 percent, and the study concluded that prophylaxis was not indicated in these patients.
The American Society of Health-System Pharmacists has developed one of the most comprehensive evidence-based guidelines for SUP.[vi]
These are summarised here.
Enteral nutrition alone may reduce the risk of overt GI bleeding due to stress ulceration and that stress ulcer prophylaxis may be ineffective or harmful among patients who are receiving enteral nutrition:
It is uncertain this is sufficient to justify withholding stress ulcer prophylaxis from patients who are at high risk for gastrointestinal bleeding even if they are receiving enteral nutrition.
Q4. Are there any potential harms of prophylaxis?
Community acquired pneumonia
Therefore remembering to discontinue prophylaxis when the patient is no longer at high risk for stress ulceration can reduce the cost of stress ulcer prophylaxis. Such prophylaxis is unnecessary because the reduction in the rate of nosocomial gastrointestinal bleeding among non-critically ill patients is minuscule due to the low baseline risk. Despite this, several studies have demonstrated a high rate of ongoing stress ulcer prophylaxis among patients who are discharged from the ICU.
Notes to go with Andy's VTE prophylaxis section:
Q1. Why do we employ VTE prophylaxis?
Pulmonary embolism remains the most common preventable cause of hospital death.
In the absence of appropriate prophylaxis, the incidence of DVT in hospital patients where objective diagnostic screening tests have been used to detect asymptomatic events has ranged from 10 to 80 percent in various medical and surgical groups.
So we need to be picking these patients.
Q2. Who should we be prescribing VTE prophylaxis to?
First we need to identify at risk patients. This is easier in critical care as that tends to include 100% of patients with common risks including - surgery or trauma, cancer, immobility, recent sepsis, presence of a central venous access device, inherited or acquired hypercoagulable states, age, significant medical co-morbidities.
For this reason it is easier to think why we shouldn’t prescribe it. Contraindications include – active bleeding, thrombocytopaenia, active ulcer, severe liver disease, or patients at risk of bleeds - ICH.
This is one of our common subset of patients- post neurosurgery. A systematic review and meta-analysis of randomized clinical trials evaluating VTE prophylaxis in patients undergoing elective cranial neurosurgery has estimated that for every 1000 patients who receive heparin prophylaxis, 91 VTE events will be prevented. Approximately 35 of these will be proximal DVT or PE, and only 9 to 18 will be symptomatic. On the other hand, 7 intracerebral hemorrhages and 28 more minor bleeds were estimated to occur if a heparin preparation is employed, versus none if a mechanical method of thromboprophylaxis is used.
Q3. What do we use to prevent VTE?
We have two methods; drug or mechanical prophylaxis.
The slightly more contentious of the two is drugs. The most commonly used agents are LMWH and unfractionated heparins which are seemingly used interchangeably.
The most recent trial comparing the two in critically ill patients was the PROTECT trial; a randomised, multi centre study in 2011. They compared the LMWH dalteparin and unfractionated heparin with the outcome measure being patients with proximal leg DVTs. With almost 2000 patients in each arm there was no statistically significant difference between the two modalities. However, they did note that there was significantly less PEs with dalteparin, which called into question what we should be using as our main outcome measure for VTE. In terms of complications there was no difference between the two modalities in terms of bleeding and HIT.
So unfortunately neither is statistically preferable, but I think I would take dalteparin.
Why do we not use dalteparin? – might ask you – assuming cost, but not sure.
Q4. What about fondaparinux?
Fondaparinux is a newer agent chemically related to the low molecular weight heparins.
Fondaparinux has been evaluated in the prevention of VTE in patients undergoing orthopaedic surgery, general surgery, and in hospitalized medical patients. Fondaparinux 2.5 mg once/day by subcutaneous injection has been compared with the LMW heparin enoxaparin 40 mg once daily in patients undergoing total hip or total knee replacement, with enoxaparin 30 mg twice daily in patients undergoing total hip replacement, and with enoxaparin 40 mg daily in patients suffering hip fracture. A Meta-analysis of these four available trials concluded that the efficacy of fondaparinux was superior to that of enoxaparin.
Fondaparinux was shown to have efficacy equal to the LMW heparin dalteparin in patients undergoing high risk abdominal surgery, with a similar incidence of major bleeding . In the subgroup of patients with cancer, fondaparinux therapy resulted in a significant decrease in the composite end point of asymptomatic or symptomatic DVT and non-fatal or fatal PE.
Another potential benefit of fondaparinux over LMWH or unfractionated heparin is that the risk for heparin-induced thrombocytopenia (HIT) is substantially lower. Furthermore, there have been case reports of fondaparinux being used to anticoagulate patients with established HIT as it has no affinity to platelet factor-4.
So it could definitely be a drug we start using more.
Q6. Mechanical methods seem fairly self explanatory, is there anything we should be thinking when applying mechanical prophylaxis?
We have two methods which are often applied together - graded compression stockings and intermittent pneumatic compression. These are very useful for the high risk of bleeding patient. Cochrane meta-analysis has concluded that the use of IPC alone was effective in the prevention of DVT in surgical patients (relative risk reduction 54 percent; 95% CI 42 to 63),
Must remember that it is contraindicated in patients with evidence of leg ischemia, peripheral vascular disease and recent skin grafts. There is also a hypothetical concern that patients who have been at bed rest or immobilized for a period of ?72 hours without any form of prophylaxis may be at risk of dislodging recently formed venous clots in the lower extremities following the use of IPC.
Conclude that it is very important in reducing morbidity and mortality. Should be reviewed daily especially in those patients considered contraindicated in case these factors have changed. We know the drugs are good, but no-one is yet unanimous on one.