Reference no: EM133260200

Do a  DRUG STUDY  base on this Case Scenario

Please provide a Quality Answer

Case Scenario of Septic Shock Syndrome caused by S. pneumoniae in an immuno compromised patient despite of vaccination

• The 25-year old male caucasian patient suffered from an autoimmune lymphoproliferative disorder (ALPS) that was treated by splenectomy 24 months before this event. He had no previous episodes of severe infections. In September 24, 2022, he developed malaise, chills and abdominal pain of sudden onset after heavy exercise, and contacted his nearest outpatient clinic. A routine check-up involving ECG, chest X-ray, blood pressure measurement and determination of O₂-saturation showed no significant abnormalities. Blood results showed slightly elevated leukocyte counts with 11.3 G/L, normal red blood cell counts (4.78 T/L) and normal platelets with 294 G/L. The patient was sent home after transfusion of 1 L isotonic infusion solution and symptomatic therapy with Metamizol and Paracetamol.
• Eight hours later, the general condition of the patient worsened rapidly and he had to be hospitalized because at that time he had already developed leukopenia (2.8 G/L), his platelet levels were low (108 G/L) and the serum creatinine was elevated (2.0 mg/dl). Hemostasis parameters were also altered. A rapid test for S. pneumoniae-antigen was positive and although antimicrobial therapy was started immediately, the patient developed hemodynamic problems (systolic RR: 50 mmHg) and had to be transferred to an intensive care unit (ICU). In spite of catecholaminergic therapy, fluid resuscitation and intubation, the organ dysfunction of the patient deteriorated and he developed severe septic shock with metabolic acidosis (lactate 15 mmol/L), anuric renal failure, overt disseminated intravascular coagulation (DIC) and fast spreading necrotic skin lesions, resembling purpura fulminans.
• Thus, the patient received fibrinogen (Haemocomplettan®, CSL Behring) and prothrombincomplex (Beriplex®, CSL Behring) alongside clindamycin, linezolid and intravenous immunoglobulins (Pentaglobin®, Biotest Pharma GmbH) and was transferred to our intensive care unit at the Medical University of Vienna.
• Upon admission, his hemodynamic and respiratory situation was stable. The metabolic acidosis, however, worsened: lactate levels increased to 18 mmol/L and signs of hepatic impairment were detectable with elevated transaminases and hypoglycemia. Moreover, creatine kinase (CK) levels were massively increased at 6678 U/L and myoglobin values were at 11,500 ng/mL. The skin lesions progressed, and confluent lesions spread over the whole face, both hands and both feet. Hemostasis parameters showed thrombocytopenia (33 G/L), a PT of 31%, an aPTT of >180 s, fibrinogen values of 72 mg/dl and massively elevated D-Dimer levels (72.19 μg/ml), resembling septic coagulopathy with purpura fulminans. According to local and international recommendations, coagulation therapy with a plasma-derived protein C concentrate (Ceprotin®, Baxalta), was initiated. An initial bolus dose of 100 U/kg body weight was given, followed by 10 U/kg/h, aiming for plasma protein C activity values of 100 U/dL. Additional hemostatic therapy consisted of fibrinogen and platelet concentrates, antithrombin replacement (aiming for antithrombin levels of 100 U/dL), and low dose heparin infusion (250 U/kg BW/h). Moreover, extracorporeal renal replacement therapy had to be started because of acute renal failure.
• Under this treatment the patient could be successfully stabilized. Although CK and myoglobin values continued to increase during the next 3 days and the face and the limbs of the patient were impressively hypoperfused, there were no signs for a compartment syndrome, and no surgical intervention was necessary. After peaking at day 3 upon admission, CK values decreased within the next weeks until returning into the normal range after 4 weeks. In parallel, also the hemostaseologic parameters improved and the skin situation ameliorated.
• The renal situation, however, remained unchanged and until week 4 no sufficient renal function could be established. Therefore, the patient was changed from continuous hemofiltration to intermittent hemodialysis, which was well tolerated. Creatinine levels were constantly high, peaking with 7.95 mg/dl.
• After 27 days, the patient could be transferred from the intensive care unit to our infectiological ward, where he stayed for another 26 days. Within this stay and under forced fluid substitution, his creatinine levels returned almost into normal range (1.27 mg/dl); also the urine output increased, so renal replacement therapy could be stopped after 4 weeks upon admission. In following, renal function returned to normal. The local skin situation improved constantly, necrotic areas were surgically removed and healed decently.
• The patient could be finally transferred to a rehabilitation center, from which he was discharged fully recovered.