This case clearly demonstrates that one should always take the Troponin T level seriously even in the presence of renal failure.
The case is from an international hospital outside of Japan and it has been anonymised for patient confidentiality.
A female patient was admitted into another hospital with appetite loss.
She was a known heavy drinker and smoker with a history of poorly treated diabetes mellitus and hypertension.
She had become abruptly unwell one week before with appetite loss and apparently little other symptoms. She had refused to take food or water and four days prior to admission had stopped taking her medications.
She denied nausea, vomiting, jaundice, abdominal pain, constipation, diarrhoea, weight loss, cardiac and respiratory symptoms.
She was taking Acarbose and Perindopril and she had no drug allergies of note.
Family and social history were unknown.
Physical examination by the resident was apparently unremarkable including the vital signs.
However, chest Xray revealed evidence of an enlarged heart and signs of heart failure as evidenced by upper lobe diversion of blood.
Laboratory data revealed evidence of renal failure with a BUN 100 and creatinine of 3.2. Na & K were normal.
Liver function was abnormal consistent with an alcoholic hepaitis picture.
Blood sugar was 350.
Serum and urine ketones were negative.
CK was 1000, CK-MB was normal. Troponin T was 2.1
ABG revealed a compensated metabolic acidosis. Bicarbonate was 18 and BE -4. Lactate level had not been measured.
ECG revealed ST elevation on a background of a wide QRS complex
Senior doctors reviewed the patient and it was considered that the patient might have developed an acute coronary syndrome plus or minus diabetic ketoacidosis aside from the alcoholic hepatitis.
However, a junior resident had discussed the case with a cardiologist from another hospital by telephone, and had therefore not been able to see the patient, who considered the raised Troponin-T to be as a result of the renal impairment in the absence of an echocardiographic report.
The patient was re-examined and a pan-systolic murmur was heard near the apex of the heart with loss of splitting during respiration.
Nevertheless, it was still considered highly likely that an Acute Coronary Syndrome had occurred, as it had not been ruled out, and an echocardiogram was performed.
The echo clearly showed diffuse hypertrophy of the myocardium but with an infero-apical area of hypokinesis and rupture of the interventricular septum to a size of 5-6mm.
The renal ultrasound scan ruled out obstruction and showed the kidneys to be of normal size suggesting that the insult on the kidneys was acute rather than chronic.
1) Silent AMI due to severe, chronic diabetes mellitus
2) Rupture of myocardium due to 1 above
3) Pre-renal +/- intrinsic renal dysfunction
4) Metabolic acidosis due to AMI (lactic acidosis), renal failure, hepatic damage
Moral Of The Story
MI can present in atypical ways. In this case, the patient lost her appetite ! The diabetes contributed to the 'Silent' nature of the cardiac event. Despite renal failure being present and there being a raised Troponin-T, it does not rule out the presence of a new AMI. Certainly there have been many studies showing that renal failure increases the Troponin level correlated to the degree of renal impairment, but such patients are in fact, high risk for myocardial events in any case. Hence, a Troponin-T in renal failure has to be taken seriously and not overlooked as merely trivial.
Moreover, the idea of DKA is good because AMI can precipitate DKA in a diabetic although that is typically in Type 1 patients rather than type 2 patients, which the patient was not in this case.
The criteria for DKA are as follows:
pH < 7.3
BE > -10
Blood sugar > 200mg/dl (>11.1mmol/L)
Ketones +/++/+++ on the urine dipstick
This patient had none of the above except for the raised glucose and hence, DKA seems actually less likely in this patient.
However, renal failure with a myocardial infarction and hepatic damage seem more likely the causes of the metabolic acidosis and the fact that there was respiratory compensation goes somewhat against DKA. Most DKA patients are severely ill with Kussmaul respiration at presentation and they rarely attain a respiratory compensation. Moreover, the time scale is not compatible with DKA. This patient had a one week history of illness whereas most DKA patients (particularly type 1 patients) present within hours !
So, in summary, do not overlook the Troponin T in patients with renal failure especially when there are additional ECG changes consistent with Acute Coronary Syndrome. The raised CK and abnormal ECG were new problems, and every problem must have an assessment and a plan. You must exclude cardiac causes first. Do not let the opinions of other deter you from doing a thorough investigation of causes when the index of suspicion still remains high.
Have a great weekend !!!