Septic shock is a serious condition with a high mortality rate, especially in infants and those with comorbidities. It occurs when infection leads to systemic inflammatory response syndrome (SIRS) and dysfunction of the cardiovascular system and multiple organs. Pathophysiologically, septic shock involves a cascade of metabolic, hematological and clinical changes mediated by microbial toxins and the host's inflammatory response. Treatment involves rapid identification, source control through drainage or debridement, appropriate antimicrobial therapy, and supportive care including fluid resuscitation and vasopressors to maintain adequate blood pressure and reverse cardiovascular dysfunction.
Septic shock is a serious condition with a high mortality rate, especially in infants and those with comorbidities. It occurs when infection leads to systemic inflammatory response syndrome (SIRS) and dysfunction of the cardiovascular system and multiple organs. Pathophysiologically, septic shock involves a cascade of metabolic, hematological and clinical changes mediated by microbial toxins and the host's inflammatory response. Treatment involves rapid identification, source control through drainage or debridement, appropriate antimicrobial therapy, and supportive care including fluid resuscitation and vasopressors to maintain adequate blood pressure and reverse cardiovascular dysfunction.
Septic shock is a serious condition with a high mortality rate, especially in infants and those with comorbidities. It occurs when infection leads to systemic inflammatory response syndrome (SIRS) and dysfunction of the cardiovascular system and multiple organs. Pathophysiologically, septic shock involves a cascade of metabolic, hematological and clinical changes mediated by microbial toxins and the host's inflammatory response. Treatment involves rapid identification, source control through drainage or debridement, appropriate antimicrobial therapy, and supportive care including fluid resuscitation and vasopressors to maintain adequate blood pressure and reverse cardiovascular dysfunction.
Incidence 0.5: 1000 population. Result in CV dysfunction and MOF
Highest in infants. Depends on Organism Orgs Staph all types Time to tx Strept pneumo Host response to infection and tx Pseudomonas Mediators IL1, 6, kinins, eicasanoids, platelet NN HSV activating factor, NO GBS Survival depends on speed &adequacy of resuscitation. RF Injured children Hypovol - Incr microvasc perm Neonates Arteriolar and venule dilatation, pooling blood Chronic medical probs – CHD, UT abnormalities, Volume loss (poor input, v+d, 3rd spacing) devices Abn Haemodynamic response Fatality Highest for infants and comorbidities 80% kids present wLoc CI +/- abnormal vascular Aetiology Combination of multiple types of shock – tone Infection, 20% hyperdynamic state relative and absolute hypovolaemia, Hypotension not required for diagnosis shock maldistribution Progression – loss cardiac comp for ↓SVR myocardial depression Cap leak, vd, toxin related cardiac multiple metabolic, endocrine and depression haematological problems. Impaired substrate us Cascade of metabolic, haematological and clinical changes – decr tissue perfusion -> anaerobic metabolism -> from invasive infection and microbial toxins. lactic acidosis. Deterioration in O2 consumption SIRS is host dependant response. &extraction Pathophysiological septic shock incompletely understood. Dysregulation glucose, fat, amino acids. Direct effects microbiological agents Changes in glycolysis and gluconeogen early Microbiological toxins Pts inflam response to infection Assessment Activation of endogenous mediators Hx, examination Septic shock 1 JFICM 2010 Jan Kelly Maintain adequate BP (no O2 debt) Restauration preload – incrementally, Skin temperature gradient (>3ºC) attention to signs volume overload. Peripheral perfusion index (variation in pulse Crystalloid vs colloid (SAFE, NEJM 2004- pressure on pulse oximetry) ?alb better than NaCl in septic shock) NIRS – MvSats and Cyt-aa3 saturation RBC if Hct <30% (Hb 8-10) (incr O2 TcO2 and CO3 - ↓TcO2 and ↑CO2 a/w ↓tissue carrying capacity) perfusion Pressors Incr perfusion pressure and CO Not validated Inodilators (dobu, milrinone incr flow) Tissue capnography – sublingual/gastric –art CO2 gradient Inoconstrictors (adrenaline, NA, dopa ↑P) Tx Vaspressin (incr survival adults, kids) Goals Identification of shock state Infection source control Rapid reversal of CV dysfunction and vital fns Culture Blood, urine, other pot infected sites Antimicrobial tx Give adequate abs – narrow at 48-72h Source control (debride, drainage) Ab choice Determined by Age, hx, comorbidity, clinical Monitoring – ECG, pulse ox, BP/IABP, IDC syndrome, gm stain, local resistance patterns. CVL (CVP), pulse pressure variation (preload Hypoglycaemia 0.5-1g/kg glucose =5-10ml/kg D10 dependant till PPV <10%) HCO3 Tx of shock induced met acidosis showed no Lab ABG improvement in CO / decr inotropes. Lactate (adequacy of global O2ation) APC Incr CNS bleeding in kids, no benefit. MvO2Sats Echo Glucocorticoids Up to date 2010: Adults: Beneficial in pts w severe septic Supportive measures shock (systolic BP <90 despite fluids and inotropes for 1h) O2 and ventilator support in adults (grade2B recommended). CV support No good evidence for steroids in mod septic shock. Incr O2 delivery, decr O2 requirements Response to ACTH testing should not be used to select Vol Impr CO by maximizing Starling curve patients as unreliable. Administer for 5-7 days (grade 2C), taper optional.
Septic shock 2 JFICM 2010 Jan Kelly
Fludrocortisone not beneficial (COITTS – grade 2C) Amp + gent cefotaxime Cefotaxime HPA axis may be disturbed in sepsis. CNS susp Cef +vanc Absolute adrenal insufficiency (random cortisol<500nmol/L Pneumonia Fluclox & Fluclox & and incr post ACTH stimulation test <240), relative adrenal gentamicin gentamicin & insufficiency (incr post ACTH stimulation test <240) may roxithromycin GU –No abn Amp & gent Amp and gentamicin benefit from steroids (inconclusive evidence). Low dose Timentin gent Timentin and gentamicin GUT ACTH test probably more sensitive than high dose. Abn GUT Skin/soft Clindamycin, penicillin and gentamicin Kids Appears to benefit some. tissue Limited date in children. Improved outcomes in Orbital Cefotaxime & fluclox dengue shock. Incr mort in heterogeneous cellulitis retrospective cohort. IC / febrile neutropenic Timentin and gentamicin Dose 1-2mg/kg/dose Expert consensus – catecholamine resistant shock / suspected adrenal insufficiency (random cortisol <500nmol/L) defines absolute adrenal insufficiency, indicates need for continued glucocorticoid tx. Calculated free and total cortisol may be more accurate. Dex may be better if ACTH stimulation test planned (hydrocortisone is pharmacological cortisol, binds cortisol binding protein well – other steroids don’t ->?less interference w ACTH stimulation test)
Susp source Neonate Infant 1-3m Ped <3m
<1m Source unk, no Amp & gent Fluclox and gent (vanc if CVL meningitis (vanc if CVL) or EVD) & cefotaxime & cefotaxime Source unk Cefotax and Amp and Fluclox and Septic shock 3 JFICM 2010 Jan Kelly