Tests for Premature Rupture of Membranes

Tests for Premature Rupture of Membranes (PPRM)

The tests for PPRM are the most common tests used to detect early signs of cardiac arrest in patients with suspected acute myocardial infarction or sudden death. They have been widely accepted as the gold standard in clinical medicine since they were first described by Cardoso et al. [1]. These tests are now considered to be the best way to diagnose PPRM in patients with known acute myocardial infarction.

However, there is no consensus among experts on how these tests should be performed. There are several different types of PPRM testing available and each one has its own advantages and disadvantages. For example, some studies have shown that electrocardiography (ECG) may provide better results than echocardiogram (EKG). Other studies suggest that the use of magnetic resonance imaging (MRI) may improve detection rates compared to other methods such as computed tomography (CT), ultrasound, or angiograms.

In this article we will discuss the most commonly used tests for PPRM. We will then review their pros and cons, and finally present our recommendations for which type of test is best for your patient based on all the evidence available.

Tests for PPRM

The following tests should all be considered when deciding on which one to use in your PPRM protocol:

Echocardiogram (EKG)

This is one of the most common tests used for PPRM. Echocardiogram uses ultrasound to detect whether there is any perimembranous ventricular septal defect (VSD), which is a hole in the heart. A large ventricular septal defect (VSD) is considered to be a PPRM if it is greater than or equal to 2.5 cm in diameter.

An echocardiogram can also be used to determine the cause of the PPRM. For example, a PPRM in someone with no symptoms can be the result of acute myocardial infarction (AMI). If this is the case then other tests like an angiogram should also be performed to identify the location and extent of the infarct.

Echocardiograms are quick, painless and readily available in most hospitals.

Disadvantages include false positive results, which can lead to unnecessary interventions.


This is an effective and cheap test for diagnosing PPRM. An electrocardiogram detects electrical activity in the heart using electrodes placed at specific locations on the patient’s body. The QT interval is the most useful ECG parameter to predict a PPRM. An increase in QT interval by more than 60 milliseconds is considered to be a positive result.

A conventional ECG can only detect a PPRM if it is large enough to cause blockage of the electrical conduction system of the heart. It is unable to detect small PPRM’s that do not cause any conduction problems, such as those that are still able to contract normally. This means that a patient may still go into cardiac arrest despite having no ECG abnormalities.

Disadvantages include false negative results if the PPRM is of an unusual type or if it has not yet caused any conduction problems.


MRI uses a strong magnetic field to align the electrons within the nitrogen and oxygen molecules that make up biological tissues. These electrons then realign themselves when the magnetic field is turned off, but they do so at different speeds. When the magnetic field is turned back on, the electrons realign themselves again, but they all do so at the same speed. This process produces a signal that is picked up by sensors placed around the patient in the MRI scanner.

These sensors then send these signals to a computer, which displays a picture of the tissue types based on their density. The use of different pulse sequences allows for the production of highly detailed images of specific tissues within the heart.

A PPRM can be detected using an MRI by identifying the level of oxygen saturation in tissue (myocardium and pulmonary tissue). A 20% or more decrease in myocardial or pulmonary tissue oxygenation is considered to be a positive result.

MRI is very accurate at diagnosing a PPRM even if conduction problems have not yet occurred. It can also differentiate between different types of PPRM and an AMI even when both are present.

MRI is, however, expensive and requires the patient to lie within a narrow tube for up to an hour while radio waves emit strong magnetic fields which can interfere with the normal functioning of some medical devices such as pacemakers. It also requires that the patient does not have any metal objects in their body such as shrapnel, surgical clips or hemostats.

Research on the use of hyperpolarized (highly polarized) oxygen MRI is ongoing. The advantage of hyperpolarized oxygen MRI is that it can detect even the smallest PPRM. It also improves the ability to differentiate between a PPRM and an AMI.


This is a protein found in heart cells, and its release into the blood indicates diseased heart cells. It has a very short half-life of just a few hours, so it is useful for detecting problems in the short term. For this reason, this test can be useful as a ‘check up’ after any heart attack or episode of chest pains.

A PPRM causes immediate damage to the heart muscle, so the level of troponin will rise immediately. A rise in the level of troponin is considered to be a definitive indicator that a PPRM is present.

Disadvantages of this test include its limited ability to detect a PPRM, as well as the fact that it can only be used in the first few hours after the onset of chest pain. It cannot be used to predict the long-term risk of a PPRM occurring, and it cannot be used to detect a PPRM after the first week. It is also less sensitive at detecting a PPRM than other tests, so if one is present, it will show up as negative.


General treatment of a PPRM is the same as for an AMI: Aspirin, heparin and then Coumadin (warfarin) to inhibit further clot formation. The dose of Coumadin needs to be monitored using an INR (International Normalized Ratio) test. The dose of Aspirin and Heparin is tapered slowly over time.

Post-AMI treatment

It has been found that patients who have previously had an AMI have a 2-4% risk of suffering a PPRM each year. Aspirin and heparin are used widely to prevent further clots forming, but there is no evidence that they prevent a PPRM from occurring.

Coumadin is an anticoagulant which can help prevent clotting, but it also has many well-known and widely-publicised side effects (such as excessive bleeding). These side effects are not usually a problem in the short-term, but as treatment is prolonged they become more of a concern. As a result, the decision to use Coumadin needs to be made on a case-by-case basis by the patient’s cardiologist and their general practitioner.

Risk reduction

The only reliable way to reduce the risk of a PPRM is to take Aspirin daily. The recommended dose is 75-100mg per day. This can be increased to 325mg or even up to 1000mg a day if the patient is at a high risk of suffering a PPRM, such as smokers over the age of 40.

Cigarette smoking increases the risk of blood clots by up to tenfold. The benefits of quitting smoking far outweigh any risks posed by taking a daily dose of Aspirin.

Other factors that increase the risk of a PPRM include obesity, high cholesterol, hypertension and diabetes. A healthy lifestyle and a low fat diet can be effective in combating these risk factors.

Other drugs have been researched for their ability to prevent blood clots, such as the new drug Apixaban. This has been shown to be more effective than Aspirin at preventing clotting, and may become a viable alternative in the future.

Hope this answers your question. I have more details on this subject in my book ‘Heart Disease – Your questions answered’, available on Amazon. If you found this answer helpful, please click on the ‘accept’ button above, to help me know that I’m helping people. Thank you and good luck with everything.

Sources & references used in this article:

The preterm prediction study: prediction of preterm premature rupture of membranes through clinical findings and ancillary testing by BM Mercer, RL Goldenberg, PJ Meis… – American journal of …, 2000 – Elsevier

Reduction of group B streptococcal maternal and neonatal infections in preterm pregnancies with premature rupture of membranes through a rapid identification test by WJ Morales, D Lim – American journal of obstetrics and gynecology, 1987 – Elsevier

A rapid matrix metalloproteinase-8 bedside test for the detection of intraamniotic inflammation in women with preterm premature rupture of membranes by KW Kim, R Romero, HS Park, CW Park, SS Shim… – American journal of …, 2007 – Elsevier

… of insulin-like growth factor binding protein-1 (IGFBP-1), placental alpha-microglobulin-1 (PAMG-1) and nitrazine test to diagnose premature rupture of membranes in … by S Tagore, K Kwek – Journal of perinatal medicine, 2010 – degruyter.com

Qualitative human chorionicgonadotropin testing of cervicovaginal washings for the detection of preterm premature rupture of membranes by AL Cooper, ST Vermillion, DE Soper – American journal of obstetrics and …, 2004 – Elsevier

Vaginal fluid urea and creatinine in diagnosis of premature rupture of membranes by H Kafali, C Öksüzler – Archives of gynecology and obstetrics, 2007 – Springer