Trometamol

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An event is serious (based on the ICH definition) when the patient outcome is:

• * death

• * life-threatening

• * hospitalisation

• * disability

• * congenital anomaly

• * other medically important event

A 68-year-old man exhibited no improvement during treatment with trometamol for lactic acidosis [route and dosage not stated].

The man presented to hospital with two days history of dyspnoea, weakness, shivering, dizziness and diarrhoea. He received oxygen via nasal cannula. He was on unspecified beta blockers for maintaining His BP. He received crystalloid intravascular replacement for BP correction. Physical examination and laboratory results suggested lymphocytopenia and acute kidney injury. His body temperature was 35.9°C. He had complained about pain and paraesthesia in his right foot with a history of peripheral arterial occlusive disease. His anamnesis revealed COPD, gastroesophageal reflux, arterial hypertension and myocardial infarction. He was sent to the specialised COVID-19 intensive care unit for suspected COVID-19 pneumonia and acute peripheral arterial occlusion few hours after the first hospital admission. On ICU admission, he developed acute respiratory failure and septic shock with severe hypotension and metabolic acidosis. Non-invasive ventilation was provided to support breathing and unspecified bronchodilatory therapy was started due to severe bronchial spasm. Chest X-Ray revealed moderate opacities on his both lower lobes. He was started on norepinephrine and empirical therapy with piperacillin/tazobactam and clarithromycin for the possible community acquired pneumonia. He was initiated on camostat mesilate, remdesivir and dexamethasone for suspected SARS-CoV 2 infection. Further analyses of the blood sample revealed lactic acidosis and confirmed progression of acute kidney injury. Buffering therapy with trometamol for lactic acidosis with unspecified crystalloid solutions, did not show improvement of the overall kidney function.

The man received continuous renal replacement therapy with continuous cytokine haemadsorption and citrate anticoagulation. His condition deteriorated rapidly due to severe septic shock. Consequently, increased doses of continuous norepinephrine was complemented by argipressin and dobutamine. Empiric antibacterial therapy was escalated to vancomycin and meropenem. Physical examination revealed acrocyanosis and cold extremities. In the nucleic acid amplification test (NAAT) on the nasopharyngeal swab collected on the day of ICU admission, no SARS-CoV-2- RNA was detected ruling out COVID-19 infection. His respiratory failure and haemodynamic instability proceeded and he required intubation and unspecified catecholamines with further increased doses of norepinephrine, dobutamine and argipressin.

Transoesophageal echocardiography (TEE) revealed hyperdynamic left ventricular ejection fraction Laboratory results and massive mucous bleeding were consistent with onset of disseminated intravascular coagulation (DIC). He had progressive respiratory failure with no significant findings on chest X-ray. Microbiological testing showed gram negative bacteria in three blood samples taken upon ICU admission. At this point, he reported of a light injury by a dog leash, which could form the hypothetical entry point for the gram-negative bacteria. On day two after the hospital admission, the he developed acute liver failure with progressive shock. Transpulmonary thermodilution measurement technology revealed low cardiac output syndrome due to septic cardiomyopathy. Despite the renal replacement therapy, potassium and lactic acid levels were dramatically increased. He died 48h after the first admission to hospital due to severe septic shock with multiorgan failure. Postmortem findings identified the gram negative bacteria as Capnocytophaga canimorsus bacteraemia which was masqueraded as COVID-19 pneumonia.