21/2017
CytoSorb in distributive shock with multi-organ failure in the context of acute, severe exudative pancreatitis

Dr. Bernd Yuen, Frau Dr. Pamela Dreessen, Frau Dr. Barbara Lienhardt Nobbe Interdisciplinary Intensive Care Unit, Spital Bülach, Switzerland

Summary:

This case study reports on a 67-year-old male patient, who was admitted to the Emergency Department with diffuse abdominal pain and recurrent vomiting for 24 hours.

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Case presentation

  • Rapid transfer to the interdisciplinary intensive care unit (ICU) with the diagnosis of acute severe pancreatitis with pronounced lactic acidosis and encephalopathy
  • Medical history revealed laparoscopic appendectomy in 2007 for an acute appendicitis, a laparotomy in 2007 because of a gangrenous cholecystitis as well as an idiopathic edematous pancreatitis in 2008. In addition, he had arterial hypertension managed with perindopril.
  • On admission to the ICU, the patient was disoriented and encephalopathic, with a blood pressure of 130/80/65 mmHg, a sinus tachycardia of 125/min, an SpO2 of 91% with 3 liters of O2 nasal and a temperature of 37.5 ° C
  • The initial blood gas analysis showed a lactic acidosis with a pH of 7.28 (BE -6.1 mmol/L, lactate 10.7 mmol/L)
  • He had signs of marked volume deficiency with hemoconcentration (hemoglobin of 21.0 g/dl, hematocrit 64%) and a completely collapsed inferior vena cava on sonography
  • Furthermore, he had an activated coagulation with an INR of 2.4, as well as a thrombocytopenia of 122,000/μl
  • CRP was 212 mg/l and procalcitonin was 9.1 ng/ml
  • Despite aggressive volume resuscitation, the patient deteriorated continuously over the next 12 hours
  • Hemodynamically, the patient became catecholamine-dependent, because of progressive respiratory failure he was intubated and mechanicaly ventilated, due to decreased urinary output to less than 0.5 ml/kgKG/h as well as persistent severe lactic acidosis CRRT was initiated
  • He also had a paralytic ileus with increasing intra-abdominal hypertension up to a maximum bladder pressure of
    22 mmHg, and a septic cardiomyopathy with positive cardiac biomarkers and a diffuse severely impaired systolic pump function (EF 25%) as well as low cardiac index of 2.0 l/min/m2
  • Due to the catecholamine- and volume-refractory shock, continuing vasoactive and volume therapy was guided by using advanced hemodynamic monitoring with the PiCCO system
  • To maintain a MAP of at least 60 mmHg, norepinephrine doses of up to 55 μg/min were required
  • Due to the low cardiac index, dobutamine up to 200 μg/min and also levosimendan were given
  • In addition, hydrocortisone was used as an adjunctive therapy at a dose of 4×50 mg/d
  • At this time, the physicians decided to add an additional treatment using CytoSorb due to the severe distributive and cardiogenic shock with severe capillary leak

Treatment

  • Two consecutive treatments with CytoSorb for a total treatment time of 36 hours (1st  treatment for 12 hours, 2nd  treatment for 24 hours)
  • CytoSorb was used in conjunction with CRRT (Multifiltrate, Fresenius Medical Care) performed in CVVHD mode
  • Blood flow rate: 110 ml/min
  • Anticoagulation: citrate
  • CytoSorb adsorber position: pre-hemofilter

Measurements

  • Hemodynamic parameters and demand for catecholamines
  • Inflammatory parameters (leucocytes, CRP, PCT)
  • Lactate

Results

  • Hemodynamically, impressive stabilization was noted, so that norepinephrine therapy could be reduced from 55 μg/min to 10 μg/min within 24 hours and consecutively stopped after 48 h. At the same time, lactate levels normalized accompanied by a reduction in volume requirements
  • After the patient had a total balance of +13 liters in the first 36 hours, the balance could be reduced to +1.5 liters over the next 24 hours. Negative balance could already be achieved from the third day onwards.
  • The course of the inflammatory parameters was as follows: CRP showed a peak at 432 mg/l after 48 hours and continued to decrease thereafter. PCT showed its highest value of 9.1 ng/ml at the first day and declined thereafter
  • Minimal diuresis was always maintained during CRRT and improved continuously so that CRRT could be stopped after 50 hours and diuresis could be stimulated by furosemide.

Patient Follow-Up

  • Percutaneous tracheostomy had to be performed on day 8 because of a protracted wake-up response due to multifactorial, metabolic-inflammatory encephalopathy and prolonged weaning
  • Due to the abdominal hypertension, the patient was on parenteral nutrition in the first days. After stabilization he was successfully converted to enteral nutrition.
  • Finally, the patient could be de-cannulated on day 21 and was transferred hemodynamically stable and neurologically aware to the peripheral ward
  • While still in the hospital, his condition improved so impressively that he was able to walk on his own and was able to feed himself independently.

CONCLUSIONS

  • CytoSorb treatment resulted in rapid hemodynamic stabilization with shock-reversal within less than 48 hours
  • The capillary leak also improved while volume requirements decreased significantly and the patient could be in negative balance from the third day onwards. This also had a positive impact on the course of the grade III abdominal hypertension.
  • Application of CytoSorb therapy was simple and without complications