This Rockall score calculator stratifies mortality risk caused by hemorrhage after bleeding in the upper GI according to clinical patient data. Below the form you can read more about the scoring system, its criteria and result interpretation.
How does this Rockall score calculator work?
This health tool is a scoring system that stratifies mortality risk of hemorrhage in the upper GI and allows for quick intervention, either endoscopy or surgical. It covers both clinical criteria and endoscopic findings and can provide outcome results and specific risk percentages. The Rockall score calculator uses the following criteria:
■ Age – as a risk factor, elderly people are more susceptible to GI bleedings;
■ Presence of shock symptoms – monitors heart rate and blood pressure and the lower these are, the lower the hemorrhage risk;
■ Presence of comorbidities – increases risk, especially digestive or cardiac related conditions such as CHF, CAD, renal or liver failure and most cancer types;
■ Endoscopic diagnosis findings that increase risk of poor outcome in patients with GI bleeding acute or in history:
- Stigmata of recent hemorrhage;
- Mallory-Weiss tear;
- Other upper GI bleeding causes;
- Upper gastrointestinal tract cancer;
- Dark spots;
- Blood in upper GI tract;
- Adherent clot, visible vessel;
- Vessel that is actively bleeding or spurting.
One of the criticisms of the Rockall bleeding mortality risk model is that despite the specific predictability it has in mortality percentages, its criteria assessment can be at times much more subjective than that in the Glasgow Blatchford bleeding risk score, allowing the clinician maybe too much space in evaluating the severity of systemic disease. Plus compared to the other score, Rockall focuses on the general status while Blatchford is concerned more on the clinical presentation and symptoms.
Rockall risk scoring interpretation
Once the assessment is completed, the resulting score based on the addition of the points awarded to each question ranges between 0 and 12.
Scores below 3 are considered low risk while everything above 3 is high risk both for rebleeding and mortality, with risk percentages growing exponentially to the score.
|0 - 2||3.50 - 5.30%||0 - 0.20%|
|8 - 12||41.80%||41.10%|
The low risk scenario presentation would have following clinical and laboratory variables:
■ No shock symptoms with a normal heart rate.
■ No comorbidities.
■ No lesion or stigmata of recent hemorrhage or very little indication.
■ No blood, clots or visible vessels in the upper GI tract
Acute upper gastrointestinal bleeding (UGIB)
This is a condition of the upper GI, often resulting in medical emergencencies and use of endoscopy therapy such asclips, thermocoagulation, epinephrine injections in case the bleeding is extended.
Risk assessment is vital in order to quickly instill the right therapy and to diminish need for blood transfusion, complications risks, the risk of further surgical intervention and even diminish mortality risk.
The most common risk factors for UGIB are:
■ Helicobacter Pylori infection (present in 64% of cases);
■ Adheres to gastric epithelium, predisposing underlying mucosa to injury by toxins;
■ Aspirin or NSAID use;
■ Elderly (especially over age 70 years);
■ Male gender (twice as common as female).
Acute, massive gastrointestinal bleeding is often due to:
■ Peptic Ulcer Disease;
■ Gastric Ulcer;
■ Duodenal Ulcer;
■ Arteriovenous malformation;
■ Esophageal Varices;
■ Gastritis or Duodenitis;
■ Mallory-Weiss tear;
■ Gastrointestinal malignancy;
■ Aortic Stenosis;
■ Chronic Renal Failure.
In the above discussed conditions, mortality rates are quite high due to the seriousness, emergency and risk of complications these types of bleedings carry. There is a high risk of erosions into larger vessels and the risk of massive hemorrhage or of diffuse bleeding that won’t stop even after intervention.
1) Rockall TA, Logan RF, Devlin HB, Northfield TC. (1996) . Gut; 38(3):316-21.
2) E Vreeburg, C Terwee, P Snel, E Rauws, J Bartelsman, J Meulen, G Tytgat. (1999) . Gut; 44(3): 331–335.
3) Sanders DS, Perry MJ, Jones SG, McFarlane E, Johnson AG, Gleeson DC, Lobo AJ. (2004) . Eur J Gastroenterol Hepatol; 16(5):487-94.05 Sep, 2015 | 0 comments