52-year old woman with a history of chemotherapy for coat cell lymphoma in 2011, splenectomy in 2013 and autologous bone marrow transplantation in 2014 was admitted to the medical intensive care unit (ICU) after having fever up to 38.7 °C and malaise for 24 h. On admission, she was somnolent; the skin was cold, wet and pale; body temperature was 38 °C, blood pressure 50/40 mmHg and puls 120/min. She was eupnoeic with oxygen saturation (SatO2) of 100% by pulse oximetry, inspiring 2 L of oxygen by nasal cannula. Clinical examination revealed rales over both lungs and tachycardia without heart murmurs. Abdomen was soft and painless with audible peristalsis. Standard electrocardiogram (ECG) showed sinus tachycardia of 125/min.
On admission, we started continuous ECG monitoring, pulse oximetry, non-invasive blood pressure measurements and inserted central venous, arterial and urine catheters to measure central venous pressure intermittently, arterial blood pressure continuously and diuresis per hour.
We suspected sepsis with septic shock and immediately started treatment of shock and diagnostic procedures for sepsis. We managed shock initially by rapid infusion of crystalloids until we confirmed fluid unresponsiveness by ultrasound of inferior vena cava, demonstrating its diameter of 2.2 cm, that did not change with inspiration. Therefore, we started noradrenalin infusion within the first 15 min and up titrated it to 66μg/min. In addition, bedside echocardiography showed decreased ejection fraction (EF) of the left ventricle to 20%. We added dobutamine infusion, but also glucocorticoids and later on vasopressin to reach normotension.
From the very start we suspected pneumonia on clinical grounds and confirmed it by bilateral infiltrates on chest rentgenograph. Among admission laboratory data we observed lactacidosis (arterial pH 7.24, bicarb 13.4 mmol/l, pCO2 4.24 kPa, pO2 13 kPa, lactate 7.5 mmol/l), thrombocytopenia (62 × 103/μL), leucocytosis, increase of procalcitonin to 100 ng/ml, C-reactive protein (CRP) to 166 mg/l, N-terminal-pro brain natriuretic peptide (NT-proBNP) to 2114 pmol/l, myoglobin to 482μg/l, and serum creatinine to 288 μg/l. Admission SOFA score was eight. We collected hemocultures, urinoculture and aspirates as soon as possible and after that immediately administered imipenem 500 mg/6 h IV.
After the first 24 h positive pneumococcal urine antigen confirmed streptococcal pneumonia. We continued imipenem therapy and adjusted the dose to renal failure. Other microbiological cultures remained negative. Together with the specialist for infectious disease we decided to continue imipenem therapy due to prior disease, including splenectomy.
After 24 h of ICU-stay the patient needed 40% oxygen by mask to achieve satisfactory blood gases (pH 7.2, bicarb 15 mmol/l, paCO2 5.35 kPa, paO2 8.5 kPa), her body temperature was 38 °C. SatcvO2 was 76.1%. Luckily, the patient did not need neither non-invasive, nor invasive ventilation during the entire ICU stay.
In spite of all treatments, after the first 24 h multiorgan failure syndrome persisted, including severe systolic myocardial dysfunction with left ventricular EF of 20%, measured by echocardiography. SOFA score at that time was 12.
After 36 h of ICU stay resistant septic shock with high-dose catecholamine support, left ventricular dysfunction with EF of 20% persited and renal failure (serum creatinine 379μmol/l, daily urine output < 500 ml) worsened. SatcvO2 was 78%, body temperature 37 °C and SOFA score increased to 13.
In addition to echocardiography, Pulse Contour Cardiac Output (PiCCO) catheter was inserted to improve hemodynamic monitoring and demonstrated cardiac index (CI) of 3.3 l/min/m2) with stroke volume (SV) of 50 ml, increased global end-diastolic index (GEDI) to 1023 ml/m2 and extra vascular lung water index (ELWI) to 13.3 ml/kg and decreased systemic vascular resistance index (SVRI) of 1672 dyn.s.cm− 5.m2.
Persistant hemodynamic instability and worsening renal failure led to the decision to start continuous veno-venous hemofiltration (CVVH) combined with hemoadsoption treatment by CytoSorb® membrane for the next 24 h. The goal was to improve hemodynamic situation and modulate the inflammatory response in our splenectomised septic patient. Before the start of blood purification therapy, we measured serum IL-6 level, which was 114 pg/ml.
After only 24 h of CVVH with concomitant use of a single CytoSorb® membrane EF increased to 45%. PiCCO measurements improved as follows: GEDI changed to 805 ml/m2, ELWI to 11.2 ml/kg, SVR to 1888 dyn.s.cm− 5.m2 and CI to 3.95 min/m2 and SV to 61 ml. The patient’s temperature was 37 °C and SOFA score 11. IL-6 dropped from 114 pg/ml to 14,2 pg/ml after termination of hemoadsoption therapy.
We could stop the use of dobutamine, norepinephrine and vasopressin. The next day SOFA score was seven. Serum lactate and arterial pH turned to normal within few days, as well as CRP, procalcitonin (Fig. 1), leucocyte and platelet count after 14 days (Fig. 2). Table 1 presents the course of the treatment.
For regeneration of the kidney function the patient received CVVH intermittently for another 21 days. She was discharged from ICU after 10 days and from the hospital after 76 days.