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Journal of Clinical Medicine Research

Case Report

Volume 1, Number 2, June 2009, pages 109-114

Rapid Hemodynamic Deterioration and Death due to Acute Severe Refractory Septic Shock

Sepsis is a clinical syndrome which is characterized by severe infection leading to systemic inflammation and widespread cellular injury [1]. Similar systemic response also occurs in the absence of an infection. This entity is different from culture negative sepsis syndrome, in which case there is an evidence or suspicion of infection, but blood or body fluid cultures are negative [2, 3]. In fact, blood cultures are negative in 30 to 80 percent of patients with sepsis depending on the severity of syndrome [3].

Bloodstream infection is associated with high mortality rates. When bacteremia is associated with severe septic shock, gram negative and gram positive bacteria have comparable outcomes [4]. Dysregulation of anti and pro-inflammatory modulators is currently believed to be the center of pathogenesis of sepsis syndrome. Excessive spill of pro-inflammatory cytokines results in vasodilatation, increased endothelial permeability, leukocyte accumulation and neutrophils degranulation; leading to chain of events ensuing extensive tissue injury [5]. Cellular injury also plays an important role in the pathogenesis of sepsis through local hypoxia, apoptosis of injured cells, and direct cytotoxic effects [6]. Combination of excessive inflammation and cellular injury gives rise to full blown picture of sepsis syndrome (Fig. 1).

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Figure 1. Pathogenesis of sepsis

EGDT has shown to increase survival by 20 % [10], and should be initiated as soon as the diagnosis is suspected. This include invasive hemodynamic monitoring with the aim of maintaining: central venous pressure (CVP) between 8 and 12 mm Hg, mean arterial pressure 65 mm Hg, urine output 0.5 mL/kg/hr, and central venous or mixed venous oxygen (SvO₂) saturation 70%. If the SvO₂ is less than 70% after maintain CVP of 8-12 mm Hg, infusion of packed red blood cells is indicated to maintain hematocrit of at least 30%. Dobutamine infusion is also indicated if cardiac output is compromised [10, 20]. Appropriate cultures should be obtained before starting antibiotics.

Intravenous antibiotics should be started as early as possible and always within the first hour of recognizing severe sepsis and septic shock [20]. The site of infection and responsible microorganisms are usually not known initially in a patient with sepsis. Antibiotic treatment must be guided by the patients susceptibility group and local knowledge of bacterial resistance [21]. Intravenous broad spectrum antibiotics directed against both gram positive and gram negative bacteria should be administered immediately after appropriate cultures have been obtained. Few guidelines exist for the initial selection of empiric antibiotics. If pseudomonas is an unlikely pathogen, combination of vancomycin with either the third or fourth generation cephalosporin, or beta-lactam/beta-lactamase inhibitor, or carbapenem is an excellent initial choice. If pseudomonas is a possible pathogen, combination of vancomycin and two antipseudomonal agents should be considered. Antifungal agent may be considered initially if risk factors for fungal infection are present, or within 48 hours if no improvement occurs [21]. Antimicrobial regimen should be reassessed in 48-72 hours on the basis of microbiological and clinical data [22]. Antibiotics should be stopped if the cause is found to be non-infectious.

Intravenous hydrocortisone is indicated for adult septic shock when hypotension responds poorly to adequate fluid resuscitation and vasopressors. Hydrocortisone dose should be ≤ 300 mg/day. Steroids are not recommended to treat sepsis in the absence of shock unless the patients endocrine or corticosteroid history warrants it [23]. Recombinant human activated protein C should be considered in adult patients with sepsis-induced organ dysfunction with clinical assessment of high risk of death and if there are no contraindications [24].

Our case emphasizes the importance of early recognition and management of septic shock. Gram negative septicemia is notorious for rapid deterioration due to endotoxin release. Multi-organ damage due to septic shock carries poor prognosis, and such patients should be managed aggressively with multidisciplinary approach. This case also highlights the fact that despite optimized treatment, this entity has very high mortality rates as shown in the previous studies. Nonetheless, early recognition, EGDT, and initiation of intravenous antibiotics are key components in treating patients with sepsis and septic shock.

Acknowledgments

The authors do not have any competing interests.

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