Patient discharged with elevated troponin levels?

MunoRN, RN · May 24, 2019

There are number of causes of troponin increases other than an acute coronary process, particularly relatively mild increases and peaks. An increase in serum troponin levels can take days or weeks to resolve after the cause of the increase has resolved, so mainly what you're looking for is a peak. Primary cardiac causes for the troponin elevation should be evaluated, but there's no reason not to discharge a patient just because their troponin is 0.06.

CPLibra, ADN, BSN, RN · May 25, 2019

Initially the troponin was 0.3 asymptomatic of chest pain, SOB, respiratory distress, NSR. Then the troponin went down to 0.06 asymptomatic, up to 0.08, and then maintained at 0.06 for 1 day. Just after 2 days and a few hours of being admitted, the patient was discharged with the 0.06 troponin. The cardiologist wrote in the notes that the elevated troponin level could be due to either sepsis or due to the UTI.

I am just worried that the nurse discharged the patient prematurely with an elevated troponin.

2Ask · May 25, 2019

Even though 0.06 is technically "high" it is not that high. I work on a floor with lots of kidney failure patients and they have chronically elevated troponins. The cardiologist was aware and not concerned so I wouldn't worry about it. For CYA, I put in a note that the doctor was notified of_____ and no new orders were received.

http://web.labmed.washington.edu/tests/chemistry/TROPIG

sweetlv · May 25, 2019

There are many non-cardiac causes for elevated troponin, such as: Renal failure, PE, Severe pulmonary hypertension, Sepsis, Severe critical illness, Burns, Extreme exertion, etc. If patient's troponin levels came down without cardiac interventions (heparin drip), then it is safe to d/c patient with trending down troponin levels. In fact, they will continue to trend down over few days yet. In addition, you've mentions that patient did not have any cardiac symptoms, which is also very important.

A dx of NSTEMI was most likely given initially because of elevated troponin. Cardiologist was consulted, EGK was done but the troponin was noted trending down. If the troponin would go up, i am pretty sure the nest step would be cardiac cauterization. In addition, pt is in sinus rhythm on monitor. Was the EKG done? Did it show NSR? No SOB with Activity? No pain? No radiating pain? Looks like all those pieces of assessment point that elevated troponin levels were not caused by cardiac issues.

CPLibra, ADN, BSN, RN · May 25, 2019

Patient was brought in due to ALOC and low blood sugar, but in the ER patient was diagnosed with NSTEMI.

In the ER, the patient refused lovenox because the patient verbalized that they do not like lovenox due to fear of bleeding out and do not like injection shots. Patient is also allergic to aspirin. The patient was never on heparin drip. So no cardiac medication interventions were really done, but patient was on some BP meds just to maintain BP due to history of HTN and atorvastatin as ordered by cardiologist. EKG was done and rhythm shows NSR and she was NSR throughout her stay. Patient was on SCD's.

Patient was able to tolerate activity without SOB, respiratory distress, and chest pain. Throughout the time I had the patient for less than 2 days, the patient was asymptomatic and denied SOB, respiratory distress, chest pain, or in general pain anywhere.

And, it is a good point that the patient was possibly given that initial diagnosis NSTEMI just due to the elevated initial troponin. With further work up of labs and what not, troponin did indeed trend down without any cardiac interventions and it was found that patient had positive nitrites for UTI.

However, I'd like to know how long should the patient remain in the hospital to monitor the troponin to trend down or how many trends does it take haha (if there is such a thing)? I suppose my concern is that the patient went from 0.3 down to 0.06, and then up to 0.08, then back down to 0.06 for three consecutive results and got discharged so quick!

Thank you for your replies everyone.

allnurses Guide · May 25, 2019

I have seen something very similar - I came on duty to my psych unit to find out in report that a patient had a CK level of 2300. Normal is 22-198. The whole hospital was worked up about it. I asked if a cardiac work-up had been done at the sending facility and if there was more than 1 CK level. Turns out the ekg was normal, the cardiologist not concerned and the level had actually dropped to 1300 prior to patient being transferred. Still a very high number but not abnormal with certain types of overdose. We drew new labs and level was down to 489. It can take days for these enzymes to go down so as long as the patient is asymptomatic there is little cause for worry.

Hppy

beekee · May 26, 2019

Where I work, this patient wouldn’t have even seen a cardiologist. Discharge based on what you wrote would not be unusual or suspect at all.

HomeBound · May 26, 2019

Just another little tidbit...if you drew the trop with a tourniquet---especially if you left it on "too long"---this can raise the trop level artificially. Saw this happen a gazillion times. If you draw from a peripheral IV, using a band....it's just not ideal. I know it sounds stupid--but it's true.

magellan · May 27, 2019

Troponin is a regulatory protein complex that is integral to muscle contraction. Troponin is attached to the protein tropomyosin and lies within the groove between actin filaments in muscle tissue. Being the heart which is muscular in nature, the troponin will increase when the heart is injured like in the cases of cardiac stroke, traumatic injuries etc. However, there are at least 640 to 800 muscles elsewhere in the body so any part of that muscular system gets injured, the troponin and other heart/cardiac (it's a muscle) enzymes such as CPK, MB will definitely be increased. It can be the muscle attached to the kidneys, bones, liver, arms, lungs, abdomen, fingers, legs, thighs, back, chest, etc. Likewise, because the heart is a muscle, it has a properties that can be stretched or enlarged as a compensatory mechanism just like in cases of congestive heart failure that will stretch as far as it will allow the body to do so. Just like the bodybuilder where they have the ability to make their muscles more pronounced and toned in their abs, deltoid, gluteal etc., from weight lifting. The heart will have the ability to do that. In cases where the the doctor will diagnose as the patient's troponin is related to cardiac in nature, the patient should present other symptoms that is, having some chest pain which should always occur with the diagnosis of stroke because, it's for sure, the injury is coming from the heart. Other symptoms that should be considered is shortness of breath (there's no more oxygen in the heart), irregularity or abnormal cardiac rhythm on EKG such as afib, vtach, sinus brady, sinus tachy etc. These are just some of the situation wherein we can truly diagnose that troponin is coming from the heart. Otherwise, when these symptoms are not related, the troponin levels that are increased can be attributed to other parts of the body, like going to the gym often and you keep using all your muscle of the body for so long. These muscles can get tired, fatigue and much worse injured so the cardiac enzymes will be released to the blood stream from the muscle because it got injured and traumatized then eventually your CPK, MB, troponin will increase during blood work. In cases, also that the during lung problems or kidney problems where the muscle attached to it greatly overworked, then the enzymes will also increase. The enzymes are being released to the blood stream when there is a break of the integrity of the muscles. When the muscles are over stretched, injured, sprained etc. But they will present symptoms not similar to the heart or cardiac in nature. It's probably they will present, pain while breathing in case of lung problems then pain in the flank for kidney problems. Therefore, it's not really easy to diagnose a person with cardiac issues because of troponin level but with more further workup and history taking, for sure, we will not make any stone unturned.

magellan · May 27, 2019

For follow up, so when troponin, CPK, MB and other isoenzymes are increased it is a pathognomonic for muscles injury but we have to know where because there are about 640 to 800 muscles in the body. So we need further work up and history taking to identify which part of the body is injured so we can provide adequate treatment for that particular organ or body part. Therefore, there are other cases when the troponin, CPK, MB is increased not only because it's cardiac in nature. But it's always muscular in nature because, those enzymes are attached to it no more than anywhere else but MUSCLES.

2Ask · May 27, 2019

4 hours ago, magellan said:
Troponin is a regulatory protein complex that is integral to muscle contraction. Troponin is attached to the protein tropomyosin and lies within the groove between actin filaments in muscle tissue. Being the heart which is muscular in nature, the troponin will increase when the heart is injured like in the cases of cardiac stroke, traumatic injuries etc. However, there are at least 640 to 800 muscles elsewhere in the body so any part of that muscular system gets injured, the troponin and other heart/cardiac (it's a muscle) enzymes such as CPK, MB will definitely be increased. It can be the muscle attached to the kidneys, bones, liver, arms, lungs, abdomen, fingers, legs, thighs, back, chest, etc.

Correction, cardiac troponins are specific to the heart. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1770452/

The mechanism of increased cardiac troponins in CKD (renal) patients is not well understood but the enzymes don't come from a muscle attached to the kidney, they still come from the heart. Apparently running the body with a damaged kidney is tough on the heart, makes the heart work harder, causes transient demand ischemia with the release of cardiac troponins from the overworked heart but does not mean the patient is having an acute MI. Same with sepsis, heart failure, PE, afib, and SVT (troponins can be elevated but not necessarily acute MI.)

Quote
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1770452/
Although cardiac troponin measurements are of diagnostic and prognostic importance in patients with acute coronary syndromes, the broad range of conditions associated with raised cardiac troponin values has the potential for causing diagnostic confusion and generating clinical dilemmas in patient management. For example, should all renal failure patients with raised cardiac troponin concentrations be referred for coronary angiography, or should patients with a raised troponin after an episode of rapid atrial fibrillation or supraventricular tachycardia be diagnosed as myocardial infarction and undergo risk stratification investigations and be enrolled on a cardiac rehabilitation programme? Similarly, should patients on the intensive care unit with septicaemia or multiorgan failure and raised cardiac troponin be initiated on antithrombotic agents? These questions regarding clinical management emphasise the fact that sole reliance on raised cardiac troponin measurements for the diagnosis of myocardial infarction could lead to inappropriate investigations and treatments that are potentially harmful and expensive. These issues are particularly relevant when one considers that up to 30% of patients with raised cardiac troponins do not have conventional acute coronary syndromes. 17