Management of septic shock with a norepinephrine-based haemodynamic algorithm

Hernández, Glenn; Bruhn, Alejandro; Romero, Carlos; Larrondo, Francisco Javier Ocharan; Fuente, René de la; Castillo, Luis; Bugedo, Guillermo

doi:10.1016/j.resuscitation.2005.01.009

Cited by 23 publications

(26 citation statements)

References 38 publications

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“…This was already described elsewhere, but only for PAO 2 /FIO 2 ratio. 24 The maintenance or further reduction of NE dose found at t [12][13][14][15][16][17][18][19][20][21][22][23][24] suggests that beneficial effects resulting from 6-hour HVHF are permanent and without a rebound response to shock, at least for 24 hours.…”

Section: Discussionmentioning

confidence: 99%

“…Sepsis and septic shock criteria were defined according to Bone et al 14 Thirty-one consecutive adult patients with full commitment for resuscitation and undergoing severe septic shock defined as norepinephrine (NE) requirement Ն0.3 g ⅐ kg Ϫ1 ⅐ min Ϫ1 to maintain mean arterial pressure (MAP) between 70 mm Hg and 80 mm Hg 15 and progressive lactic acidosis were included. All patients were refractory to previous management for at least 6 hours according to Surviving Sepsis Campaign (SSC) guidelines.…”

Section: Patients Data Collection and Hemodynamic Managementmentioning

confidence: 99%

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Effectiveness of short-term 6-hour high-volume hemofiltration during refractory severe septic shock

Tapía

Chinchón

Morales

et al. 2012

Journal of Trauma and Acute Care Surgery

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Section: Discussionmentioning

confidence: 99%

Section: Patients Data Collection and Hemodynamic Managementmentioning

confidence: 99%

Effectiveness of short-term 6-hour high-volume hemofiltration during refractory severe septic shock

Tapía

Chinchón

Morales

et al. 2012

Journal of Trauma and Acute Care Surgery

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“…Our local management algorithm for septic shock has been published elsewhere [9, 11–14]. Septic patients presenting a circulatory dysfunction at the emergency department (ED) or the pre-ICU service were subjected to vigorous fluid resuscitation and basal measurements of lactate (Radiometer ABL 735, Copenhagen Denmark).…”

Section: Methodsmentioning

confidence: 99%

Persistent Sepsis-Induced Hypotension without Hyperlactatemia: A Distinct Clinical and Physiological Profile within the Spectrum of Septic Shock

Hernández

Bruhn

Castro

et al. 2012

Critical Care Research and Practice

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Introduction. A subgroup of septic shock patients will never develop hyperlactatemia despite being subjected to a massive circulatory stress. Maintenance of normal lactate levels during septic shock is of great clinical and physiological interest. Our aim was to describe the clinical, hemodynamic, perfusion, and microcirculatory profiles associated to the absence of hyperlactatemia during septic shock resuscitation. Methods. We conducted an observational study in septic shock patients undergoing resuscitation. Serial clinical, hemodynamic, and perfusion parameters were registered. A single sublingual microcirculatory assessment was performed in a subgroup. Patients evolving with versus without hyperlactatemia were compared. Results. 124 septic shock patients were included. Patients without hyperlactatemia exhibited lower severity scores and mortality. They also presented higher platelet counts and required less intensive treatment. Microcirculation was assessed in 45 patients. Patients without hyperlactatemia presented higher PPV and MFI values. Lactate was correlated to several microcirculatory parameters. No difference in systemic flow parameters was observed. Conclusion. Persistent sepsis-induced hypotension without hyperlactatemia is associated with less organ dysfunctions and a very low mortality risk. Patients without hyperlactatemia exhibit less coagulation and microcirculatory derangements despite comparable macrohemodynamics. Our study supports the notion that persistent sepsis-induced hypotension without hyperlactatemia exhibits a distinctive clinical and physiological profile.

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“…Exclusion criteria were (1) patients extremely ill, in whom survival interval was expected to be less than 48 hours, (2) use of any external vitamin supplement within one week before enrollment, (3) onco-hematological, and (4) chronic renal failure patients. All patients were managed according to a standard hemodynamic and respiratory algorithm [17]. …”

Section: Methodsmentioning

confidence: 99%

Lipoperoxidation and Protein Oxidative Damage Exhibit Different Kinetics During Septic Shock

Andresen

Regueira

Bruhn

et al. 2008

Mediators of Inflammation

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Septic shock (SS)-related multiorgan dysfunction has been associated with oxidative damage, but little is known about the temporal damage profile and its relationship to severity. The present work investigated prospectively 21 SS patients. Blood samples were obtained at diagnosis, 24, 72 hours, day 7, and at 3 months. At admission, thiobarbituric acid reactive substances (TBARSs), plasma protein carbonyls, plasma protein methionine sulfoxide (MS), ferric/reducing antioxidant power (FRAP), total red blood cell glutathione (RBCG), uric acid (UA), and bilirrubin levels were increased (P < .05). Total radical—trapping antioxidant potential (TRAP) and vitamin-E were similar to controls, and vitamin-C was decreased (P < .05). During evolution, TBARS and RBCG increased (P < .001), vitamin-E levels remained stable, whereas plasma protein carbonyls and MS, TRAP, vitamin-C, reduced glutathione, and UA levels decreased (P < .006). After 3 months, plasma protein carbonyls and MS persisted elevated. More severe patients exhibited higher TBARS, TRAP, FRAP, vitamin-C, UA, and bilirrubin levels. Our results suggest early and persistent oxidative stress during septic shock and a correlation between increasing levels of lipoperoxidation and sepsis severity.

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Management of septic shock with a norepinephrine-based haemodynamic algorithm

Cited by 23 publications

References 38 publications

Effectiveness of short-term 6-hour high-volume hemofiltration during refractory severe septic shock

Effectiveness of short-term 6-hour high-volume hemofiltration during refractory severe septic shock

Persistent Sepsis-Induced Hypotension without Hyperlactatemia: A Distinct Clinical and Physiological Profile within the Spectrum of Septic Shock

Lipoperoxidation and Protein Oxidative Damage Exhibit Different Kinetics During Septic Shock

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