JOMA Polymicrobial Septic Shock10.5005/jp-journals-100 with Multiorgan Dysfunction70-0012 CASE REPORT Polymicrobial Septic Shock with Multiorgan Dysfunction in an Otherwise Healthy Immunocompetent Patient 1Anuradha Makkar, 2Inam D Khan, 3KS Rajmohan, 4Syed A Hashmi, 5Lakshmi Nair, 6Alpana Gupta, 7Harleen Chopra, 8Priyanka Banerjee, 9Pragyan S Panda, 10Rajiv M Gupta ABSTRACT Source of support: Nil Background: Sepsis is a significant cause of morbidity and Conflict of interest: None mortality worldwide despite advanced critical life-support. Septic shock and multiorgan dysfunction is the terminal stage INTRODUCTION in critically ill patients leading to perfusion abnormalities, lactic acidosis, oliguria and altered mental status creating a rapid Sepsis is a major cause of morbidity and mortality world- downhill course and mortality. Sepsis ensues through stages wide despite advanced critical life-support. It is the 11th - of exaggerated immune response including systemic inflamma leading cause of death overall with attributable mortality tory response syndrome, in the backdrop of infectious stimuli. to sepsis and severe sepsis being 30 to 50% and 50 to 60%. Case report: Polymicrobial septic shock with multiorgan Following a non-infectious or infectious insult, there is dysfunction leads to demise in an otherwise healthy immuno- competent patient. Microbiological profile revealedEscherichia a preliminary systemic response which becomes over- coli urinary tract infection (UTI), Staphylococcus sciuri bactere- whelming leading to systemic inflammatory response mia, Acinetobacter baumanii ventilator-associated pneumonia, syndrome. When the compensatory anti-inflammatory and central line catheter tip Pseudomonas aeruginosa, thereby reaction fails, it leads to immunomodulatory failure, pointing towards polymicrobial sepsis. Neutropenia of 290/ dL along with serum procalcitonin 5 ng/mL was detected. An severe sepsis, septic shock, and multiorgan dysfunction. autopsy revealed anasarca, bilateral lung abscesses, Hepato- Sepsis ensues prolonged hospital stay and aggressive splenomegaly, intracerebral hemorrhage, consolidated lungs, exposure to a cocktail of antimicrobials thereby increas- myocardial hypertrophy, and acute tubular necrosis were ing healthcare costs and furthering antimicrobial resis- observed. Bacterial colonies from lungs, liver and cerebrospinal tance.1-3 fluid grew Pseudomonas aeruginosa. Septic shock and multiorgan dysfunction is the ter- Conclusion: Polymicrobial sepsis can rapidly deteriorate a minal stage in critically ill patients leading to perfusion patient and mandate aggressive fluid, inotrope, ventilation, dan antimicrobial therapy, notwithstanding challenges in diagnosis, abnormalities, lactic acidosis, oliguria and altered mental prognosis and optimal management. status creating a rapid downhill course and mortality. Sepsis ensues through stages of exaggerated immune Keywords: Atypical pneumonia, Multiorgan dysfunction, Poly- microbial, Sepsis, Septic shock. response including systemic inflammatory response syndrome, in the backdrop of infectious stimuli. Poly- How to cite this article: Makkar A, Khan ID, Rajmohan KS, Hashmi SA, Nair L, Gupta A, Chopra H, Banerjee P, Panda PS, microbial septic shock with multiorgan dysfunction in Gupta RM. Polymicrobial Septic Shock with Multiorgan Dys- an otherwise healthy immunocompetent patient is being function in an Otherwise Healthy Immunocompetent Patient. presented.4 Journal of Medical Academics 2018;1(1):61-64. CASE REPORT 1Professor and Head, 2Associate Professor, 3Senior Advisor A 46-year-old woman with no known history of chronic and Head, 4Asst Professor, 5,6,8,9Assistant Professor, 7Senior disease, presented with mild to moderate grade intermit- 10 Resident, Consultant and Professor tent fever with chills, dry cough without hemoptysis, 1,2,7-9Department of Microbiology, Army College of Medical sore throat, malaise and generalized body aches of two Sciences and Base Hospital, New Delhi, India weeks duration. Initial outpatient workup for tropical 3-6Department of Pathology, Army College of Medical Sciences fever comprising malaria, typhoid, dengue, chikungunya and Base Hospital, New Delhi, India was negative. Subsequently, the patient presented with a 10Department of Microbiology, Army Hospital Research and febrile toxic look, breathlessness at rest, tachycardia 134/ Referral, New Delhi, India min, normal blood pressure with no postural variation Corresponding Author: Inam D Khan, Associate Professor and hypoxemia at room temperature requiring oxygen Department of Microbiology, Army College of Medical Sciences inhalation and was promptly admitted to acute care. and Base Hospital, New Delhi, India Mobile: +918076324060, Examination revealed posterior pharyngeal wall conges- e-mail: [email protected], tion with mucus plugs; bilateral harsh vesicular breath Journal of Medical Academics, January-June 2018;1(1):61-64 61 Anuradha Makkar et al. sounds with fine crackles without associated wheeze or biventricular dysfunction on echocardiography, left chest pain. She was initiated on parenteral co-amoxiclav, and right ventricular ejection fraction 40% each. On 4th amikacin, and clarithromycin while on oxygen support, day, she developed sudden bradycardia with refractory bronchodilators through nebulization and supportive hypotension followed by an asystolic cardiac arrest for therapy. During her illness, her hemoglobin was 8.5 which she was resuscitated and continued on a ventilator mg/dL, leucocytes 12800/cu mm with neutrophils 86% and triple inotropic support while Glasgow Coma Scale and lymphocytes 07%, platelets 77,000/cu mm, normal (GCS) remained E1VTM.1 Further course was complicated peripheral blood smear without atypical lymphocytes or by persistent high fever, stress hyperglycemia requiring toxic granules or malarial parasite. D-dimer was 9 mcg/ insulin, refractory seizure requiring phenytoin, valpro- mL (normal < 0.5 mcg/mL) with normal fibrinogen and ate, phenobarbitone and propofol, upper gastrointestinal co-agulogram. Renal function tests, serum electrolytes, bleed, hypernatremia, a deranged liver function which and liver function tests were within normal limits except was managed conservatively. Iatrogenic pneumothorax lactate dehydrogenase which was 555 IU/mL. Urine was and azotemia were managed by intercostal tube and acidic with increased sugar, protein and leucocytes. Arte- peritoneal dialysis. Microbiological profile revealed rial blood gas, pH and oxygen saturation was maintained. Escherichia coli UTI, Staphylococcus sciuri bacteremia, Aci- Two-dimensional echocardiography revealed normal netobacter baumanii ventilator-associated pneumonia, and cardiac function with an ejection fraction of 65%, normal central line catheter tip Pseudomonas aeruginosa, thereby valves, and pericardium. Ultrasonography abdomen revealed mild splenomegaly with minimal left-sided pointing towards polymicrobial sepsis. Neutropenia of pleural effusion. 290/dl along with serum procalcitonin 5 ng/mL was She deteriorated 12-hours post admission rapidly detected. She sustained cardiac arrest on 14th day from with worsening of breathlessness, hypoxemia on mask which she couldn't be revived. ventilation, impending type-1 respiratory failure, and An autopsy revealed anasarca, ascites, bilateral lung hypotension. She was shifted to intensive care and abscesses, multiple petechiae over the heart and left initiated on mechanical ventilation and inotropes. kidney, congested greasy hepatosplenomegaly, and intra- Antimicrobials were changed to ticarcillin-clavulanate, cerebral hemorrhage in right basal ganglia (Fig. 1). Micro- teicoplanin, levofloxacin, artesunate, and oseltamivir scopically, pus from lung abscess showed Gram-negative along with methylprednisolone, central venous pres- bacilli. Congested and consolidated lungs, myocardial sure guided fluids, stress ulcer prophylaxis, and lung hypertrophy with a mononuclear interstitial infiltrate, protective ventilation. Influenza a seasonal, pandemic macrovesicular liver steatosis and early chronic passive H1N1 and influenza B reverse transcriptase polymerase congestion, congested and dilated splenic red pulp with chain reaction, serology for epstein-barr virus (EBV), attenuated white pulp and acute tubular necrosis were enterovirus and Hantavirus was negative. On 3rd day, observed microscopically. Bacterial colonies in the tissue she was detected to have myocardial dysfunction with spaces of lungs and liver as well as cerebrospinal fluid secondary myocarditis with persistent sinus tachycardia grew Pseudomonas aeruginosa which showed similar for 48 hours, elevated natriuretic peptide, creatine-kinase antibiogram typing profile as ante-mortem Pseudomonas muscle/brain and troponin-I, non-specific ST-T changes, (Figs 2 to 4). Fig 1: Lung abscess Fig 2: Congested and consolidated lung 62 JOMA Polymicrobial Septic Shock with Multiorgan Dysfunction Fig 3: Macrovesicular steatosis of liver Fig 4: Acute tubular necrosis DISCUSSION CD4 lymphocytes initially assume a TH1 pheno- type producing pro-inflammatory mediators including Polymicrobial sepsis in this patient was evident from interferon gamma, TNF-a, and IL-2, and later convert fever, tachypnoea, tachycardia, hypotension, PaO /FiO 2 2 to Th2 phenotype producing anti-inflammatory cyto- < 250, metabolic acidosis, azotemia, anemia, leucocytosis, kines including IL-10, IL-4 and IL-13 under the influ- thrombocytopenia, biventricular dysfunction requiring ence of stress hormones such as catecholamines and