Prompt diagnosis is crucial to the management of sepsis, as initiation of early-goal-directed therapy is key to reducing mortality from severe sepsis.[1]
Within the first three hours of suspected sepsis, diagnostic studies should include measurement of serum lactate, obtaining appropriate cultures before initiation of antimicrobial treatment, so long as this does not delay antimicrobial treatment by more than 45 minutes.[1] To identify the causative organism(s), at least two sets of blood cultures (aerobic and anaerobic bottles) should be obtained, with at least one drawn percutaneously and one drawn through each vascular access device (such as an IV catheter) in place more than 48 hours. [1] If other sources are suspected, cultures of these sources, such as urine, cerebrospinal fluid, wounds, respiratory secretions, should be obtained as well, so long as this does not delay antimicrobial treatment. [1]
Within six hours, if there is persistent hypotension despite initial fluid resuscitation of 30ml/kg, or if initial lactate is ≥ 4mmol/L (36mg/dL), central venous pressure and central venous oxygen saturation should be measured.[1] Lactate should be re-measured if the initial lactate was elevated.[1]
Within twelve hours, it is essential to diagnose or exclude any source of infection that would require emergent source control, such as necrotizing soft tissue infection, peritonitis, cholangitis, intestinal infarction.[1]
}}
Sepsis (/ˈsɛps[invalid input: 'ɨ']s/; from the Greek σῆψις: the state of putrefaction and decay) is a potentially deadly medical condition characterized by a whole-body inflammatory state (called a systemic inflammatory response syndrome or SIRS) caused by severe infection.[2][3] Septicemia (also septicaemia or septicæmia [ˌsɛp.tə.ˈsi.miə])[4] is a related medical term referring to the presence of pathogenic organisms in the bloodstream, leading to sepsis.[5] The term has not been sharply defined. It has been inconsistently used in the past by medical professionals, for example as a synonym of bacteremia, causing some confusion.[3]
Sepsis is caused by the immune system's response to a serious infection, most commonly bacteria, but also fungi, viruses, and parasites in the blood, urinary tract, lungs, skin, or other tissues. Sepsis can be thought of as falling within a continuum from infection to Multiple Organ Dysfunction Syndrome (MODS). [6]
Common symptoms of sepsis include those related to a specific infection, but usually accompanied by high fevers, hot, flushed skin, elevated heart rate, hyperventilation, altered mental status, swelling, and low blood pressure. In the very young and elderly, or in people with weakened immune systems, the pattern of symptoms may be atypical, with hypothermia and without an easily localizable infection. [7][8]
In the United States, severe sepsis contributes to more than 200,000 deaths per year.[9] The incidence of severe sepsis and septic shock has increased over the past 30 years, and the annual number of cases is now >700,000 (~3 per 1000 population). Approximately two-thirds of the cases occur in patients with significant underlying illness. Sepsis-related incidence and mortality rates increase with age and preexisting comorbidity. The rising incidence of severe sepsis in the United States is attributable to the aging of the population, the increasing longevity of patients with chronic diseases, and the relatively high frequency with which sepsis develops in patients with AIDS. The widespread use of immunosuppressive drugs, indwelling catheters, and mechanical devices also plays a role.
Ddx:
TSS Hypovolemia Cardiopulmonary Endocrine ingestion, toxin Anaphylaxis Liver Failure
Nor-epi 1st pressor, crystalloid preferred
Abx within 1 h Anticipate and manage complications source control Consider adjunctive therapy in appropriately selected patients
Editing--------------
Definitions:
Definitions
editAccording to the American College of Chest Physicians and the Society of Critical Care Medicine, there are different levels of sepsis:[3]
- Systemic inflammatory response syndrome (SIRS) is the presence of two or more of the following: abnormal body temperature, heart rate, respiratory rate or blood gas, and white blood cell count.
- Sepsis is defined as SIRS in response to an infectious process.[10]
- Severe sepsis is defined as sepsis with sepsis-induced organ dysfunction or tissue hypoperfusion (manifesting as hypotension, elevated lactate, decreased urine output, decreased platelets, increased bilirubin, decreased alveoloar oxygenation. [11][12]
- Septic shock is severe sepsis plus persistently low blood pressure following the administration of intravenous fluids.[13]
Sepsis Diagnostic Table:
| General Variables | Inflammatory Variables | Hemodynamic Variables | Organ Dysfunction Variables | Tissue Perfusion Variables |
|---|---|---|---|---|
| Fever >38.3C | Leukocytosis (WBC count >12,000/uL) | Arterial Hypotension ( SBP <90mm HG, MAP <70mmHg, or an SBP decrease >40mm Hg in adults or less than 2 SD below normal for age) | Arterial hypoxemia (PaO2/FIO2<300) | Hyperlactatemia (> 1 mmol/L) |
| Hypothermia (Core Temperature < 36C) | Leukopenia (WBC count <4,000/uL) | Acute Oliguria (urine output < 0.5 mL/kg/hr for at least 2 hrs despite adequate fluid resuscitation) | Decreased capillary refill or mottling | |
| Heart Rate >90/min or more than 2SD above normal value for age >38.3C | Normal WBC count with greater than 10% immature forms | Creatinine increase > 0.5mg/dL or 44.2 μmol/L | ||
| Tachypnea | Plasma C-reactive protein more than 2SD above normal | Coagulation abnormalities (INR > 1.5 or aPTT > 60 s) | ||
| Altered Mental Status | Plasma procalcitonin more than 2SD above normal | Absent bowel sounds | ||
| Significant edema or positive fluid balance (>20mL/kg over 24hr) (Core Temperature < 36C) | Thrombocytopenia (platelet count < 100,000/μL) | |||
| Hyperglycemia (plasma glucose>140mg/dL in the absence of diabetes) | Hyperbilirubinemia (plasma total bilirubin > 4mg/dL or 70 μmol/L) | |||
| Hypothermia (Core Temperature < 36C) | cell
|
Intravenous fluids
editIn EGDT, fluids are titrated in response to heart rate, blood pressure, and urine output; restoring large fluid deficits can require 6 to 10L of crystalloids.[15] In cases where a central venous catheter is used to measure blood pressures dynamically, fluids should be administered until the central venous pressure (CVP) reaches 8–12 cm of water (or 10–15 cm of water in mechanically ventilated patients). Once these goals are met, the mixed venous oxygen saturation (SvO2), i.e., the oxygen saturation of venous blood as it returns to the heart as measured at the vena cava, is optimized. If the SvO2 is less than 70%, blood is given to reach a hemoglobin of 10 g/dl and then inotropes are added until the SvO2 is optimized.[15]
References
edit- ^ a b c d e f g Dellinger, RP (2013 Feb). "Surviving sepsis campaign: international guidelines for management of severe sepsis and septic shock: 2012". Critical Care Medicine. 41 (2): 580–637. doi:10.1097/CCM.0b013e31827e83af. PMID 23353941.
{{cite journal}}: Check date values in:|date=(help); Unknown parameter|coauthors=ignored (|author=suggested) (help) - ^ Levy, Mitchell M.; Fink, Mitchell P.; Marshall, John C.; Abraham, Edward; Angus, Derek; Cook, Deborah; Cohen, Jonathan; Opal, Steven M.; Vincent, Jean-Louis (2003). "2001 SCCM/ESICM/ACCP/ATS/SIS International Sepsis Definitions Conference". Critical Care Medicine. 31 (4): 1250–6. doi:10.1097/01.CCM.0000050454.01978.3B. PMID 12682500.
- ^ a b c Bone, R.; Balk, R.; Cerra, F.; Dellinger, R.; Fein, A.; Knaus, W.; Schein, R.; Sibbald, W. (1992). "Definitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis. The ACCP/SCCM Consensus Conference Committee. American College of Chest Physicians/Society of Critical Care Medicine". Chest. 101 (6): 1644–55. doi:10.1378/chest.101.6.1644. PMID 1303622.
- ^ http://dictionary.reference.com/search?q=Septicemia
- ^ Septicemia at eMedicine Dictionary
- ^ Annane D, Bellissant E, Cavaillon JM (2005). "Septic shock". Lancet. 365 (9453): 63–78. doi:10.1016/S0140-6736(04)17667-8. PMID 15639681.
{{cite journal}}: CS1 maint: multiple names: authors list (link) - ^ Levy MM, Fink MP, Marshall JC; et al. (April 2003). "2001 SCCM/ESICM/ACCP/ATS/SIS International Sepsis Definitions Conference". Crit. Care Med. 31 (4): 1250–6. doi:10.1097/01.CCM.0000050454.01978.3B. PMID 12682500.
{{cite journal}}: Explicit use of et al. in:|author=(help)CS1 maint: date and year (link) CS1 maint: multiple names: authors list (link) - ^ Jui J. Chapter 146. Septic Shock. In: Tintinalli JE, Stapczynski JS, Cline DM, Ma OJ, Cydulka RK, Meckler GD, eds. Tintinalli's Emergency Medicine: A Comprehensive Study Guide. 7th ed. New York: McGraw-Hill; 2011. http://www.accessmedicine.com/content.aspx?aID=6364928. Accessed December 11, 2012.
- ^ Munford RS. Chapter 271. Severe Sepsis and Septic Shock. In: Longo DL, Fauci AS, Kasper DL, Hauser SL, Jameson JL, Loscalzo J, eds. Harrison's Principles of Internal Medicine. 18th ed. New York: McGraw-Hill; 2012. http://www.accessmedicine.com/content.aspx?aID=9105972
- ^ Soong, J.; Soni, N. (2012 Jun). "Sepsis: recognition and treatment". Clinical Medicine (London, England). 12 (3): 276–80. doi:10.7861/clinmedicine.12-3-276. PMC 4953494. PMID 22783783.
{{cite journal}}: Check date values in:|date=(help) - ^ Dellinger, R. P.; Levy, M. M.; Rhodes, A.; Annane, D.; Gerlach, H.; Opal, S. M.; Sevransky, J. E.; Sprung, C. L.; Douglas, I. S.; Jaeschke, R.; Osborn, T. M.; Nunnally, M. E.; Townsend, S. R.; Reinhart, K.; Kleinpell, R. M.; Angus, D. C.; Deutschman, C. S.; Machado, F. R.; Rubenfeld, G. D.; Webb, S. A.; Beale, R. J.; Vincent, J. L.; Moreno, R.; Surviving Sepsis Campaign Guidelines Committee including the Pediatric Subgroup (2013 Feb). "Surviving Sepsis Campaign: International Guidelines for Management of Severe Sepsis and Septic Shock: 2012". Critical Care Medicine. 41 (2): 580–637. doi:10.1097/CCM.0b013e31827e83af. PMID 23353941.
{{cite journal}}: Check date values in:|date=(help) - ^ Dellinger, RP (2013 Feb). "Surviving sepsis campaign: international guidelines for management of severe sepsis and septic shock: 2012". Critical Care Medicine. 41 (2): 580–637. doi:10.1097/CCM.0b013e31827e83af. PMID 23353941.
{{cite journal}}: Check date values in:|date=(help); Unknown parameter|coauthors=ignored (|author=suggested) (help) - ^ Cite error: The named reference
Campaign2008was invoked but never defined (see the help page). - ^ Dellinger, RP (2013 Feb). "Surviving sepsis campaign: international guidelines for management of severe sepsis and septic shock: 2012". Critical Care Medicine. 41 (2): 580–637. doi:10.1097/CCM.0b013e31827e83af. PMID 23353941.
{{cite journal}}: Check date values in:|date=(help); Unknown parameter|coauthors=ignored (|author=suggested) (help) - ^ a b Hall, Jesse (2005). Principles of critical care (3rd ed.). New York: McGraw-Hill, Medical Pub. Division. pp. Chapter 46. ISBN 0071416404.
The efficacy of external cardioversion depends on several factors, including the chronicity of the arrhythmia, triggers for the arrhythmia, and the patient's overall health. Electrical cardioversion has an efficacy of nearly 100% in patients with new-onset atrial flutter or atrial fibrillation who do not have structural heart disease. Conversely, those with chronic atrial fibrillation or mitral valve disease have poorer chance of successful cardioversion.
 | This article needs additional citations for verification. (September 2009) |
| Cardioversion | |
|---|---|
| ICD-9-CM | 99.6 |
| MeSH | D004554 |
Cardioversion is a medical procedure by which an abnormally fast heart rate (tachycardia) or cardiac arrhythmia is converted to a normal rhythm using electricity or drugs. Synchronized electrical cardioversion uses a therapeutic dose of electric current to the heart at a specific moment in the cardiac cycle. Defibrillation uses a therapeutic dose of electric current to the heart at a random moment in the cardiac cycle, and is the most effective resuscitation measure for cardiac arrest associated with ventricular fibrillation and pulseless ventricular tachycardia.[1] Pharmacologic cardioversion, also called chemical cardioversion, uses antiarrhythmia medication instead of an electrical shock.[2]
Synchronized electrical cardioversion
edit
To perform synchronized electrical cardioversion, two electrode pads are used (or, alternatively, the traditional hand-held "paddles"), each comprising a metallic plate which is faced with a saline based conductive gel. The pads are placed on the chest of the patient, or one is placed on the chest and one on the back. These are connected by cables to a machine which has the combined functions of an ECG display screen and the electrical function of a defibrillator. A synchronizing function (either manually operated or automatic) allows the cardioverter to deliver a reversion shock, by way of the pads, of a selected amount of electric current over a predefined number of milliseconds at the optimal moment in the cardiac cycle which corresponds to the R wave of the QRS complex on the ECG. Timing the shock to the R wave prevents the delivery of the shock during the vulnerable period (or relative refractory period) of the cardiac cycle, which could induce ventricular fibrillation. If the patient is conscious, various drugs are often used to help sedate the patient and make the procedure more tolerable. However, if the patient is hemodynamically unstable or unconscious, the shock is given immediately upon confirmation of the arrhythmia. When synchronized electrical cardioversion is performed as an elective procedure, the shocks can be performed in conjunction with drug therapy until sinus rhythm is attained. After the procedure, the patient is monitored to ensure stability of the sinus rhythm.
Synchronized electrical cardioversion is used to treat hemodynamically unstable supraventricular (or narrow complex) tachycardias, including atrial fibrillation and atrial flutter. It is also used in the emergent treatment of wide complex tachycardias, including ventricular tachycardia, when a pulse is present. Pulseless ventricular tachycardia and ventricular fibrillation are treated with unsynchronized shocks referred to as defibrillation. Electrical therapy is inappropriate for sinus tachycardia, which should always be a part of the differential diagnosis.
![[icon]](/wiki/File:Wiki_letter_w_cropped.svg){kind=small} | This section needs expansion. You can help by adding to it. (June 2008) |
Recommended Energy Selection For External Cardioversions[3][4][5]
- For Atrial Fibrillation, 120 to 200 joules for biphasic devices and 200 joules for monophasic devices
- For Atrial Flutter, 50 to 100 joules for biphasic devices and 100 joules for monophasic devices
- For Ventricular Tachycardia with a pulse, 100 Joules for biphasic devices and 200 Joules for monophasic devices
- For Ventricular Fibrillation or Pulseless Ventricular Tachycardia, 120-200 Joules for biphasic devices and 360 joules for monophasic devices
Pharmacological cardioversion
editVarious antiarrhythmic agents can be used to return the heart to normal sinus rhythm. Pharmacological cardioversion is an especially good option in patients with fibrillation of recent onset. Drugs that are effective at maintaining normal rhythm after electric cardioversion, can also be used for pharmacological cardioversion. Drugs like amiodarone, diltiazem, verapamil and metoprolol are frequently given before cardioversion to decrease the heart rate, stabilize the patient and increase the chance that cardioversion is successful. There are various classes of agents that are most effective for pharmacological cardioversion.
Class I agents are sodium (Na) channel blockers (which slow conduction by blocking the Na+ channel) and are divided into 3 subclasses a, b and c. Class Ia slows phase 0 depolarization in the ventricles and increases the absolute refractory period. Procainamide, quinidine and disopyramide are Class Ia agents. Class 1b drugs lengthen phase 3 repolarization. They include lidocaine, mexiletine and phenytoin. Class Ic greatly slow phase 0 depolarization in the ventricles (however unlike 1a have no effect on the refractory period). Flecainide, moricizine and propafenone are Class Ic agents.
Class II agents are beta blockers which inhibit SA and AV node depolarization and slow heart rate. They also decrease cardiac oxygen demand and can prevent cardiac remodeling. Not all beta blockers are the same, some are cardio selective (affecting only beta 1 receptors) while others are non-selective (affecting beta 1 and 2 receptors). Beta blockers that target the beta-1 receptor are called cardio selective because beta-1 is responsible for increasing heart rate; hence a beta blocker will slow the heart rate.
Class III agents (prolong repolarization by blocking outward K+ current): amiodarone and sotalol are effective class III agents. Ibutilide is another Class III agent but has a different mechanism of action (acts to promote influx of sodium through slow-sodium channels). It has been shown to be effective in acute cardioversion of recent-onset atrial fibrillation and atrial flutter.
Class IV drugs are calcium (Ca) channel blockers. They work by inhibiting the action potential of the SA and AV nodes.
If the patient is stable, adenosine may be administered first, as the medicine performs a sort of "chemical cardioversion" and may stabilize the heart and let it resume normal function on its own without using electricity.
See also
editReferences
edit- ^ Marino, Paul L. (2014). Marino's the ICU book (Fourth ed.). Wolters Kluwer Health/Lippincott Williams & Wilkins. ISBN 978-1451121186.
- ^ Shea, Julie B.; William H. Maisel (2002). "Cardioversion". Circulation. 106 (22): e176–8. doi:10.1161/01.CIR.0000040586.24302.B9. PMID 12451016.
- ^ Fuster, V; Rydén, LE; Cannom, DS; Crijns, HJ; Curtis, AB; Ellenbogen, KA; Halperin, JL; Le Heuzey, JY; Kay, GN; Lowe, JE; Olsson, SB; Prystowsky, EN; Tamargo, JL; Wann, S; Smith SC, Jr; Jacobs, AK; Adams, CD; Anderson, JL; Antman, EM; Halperin, JL; Hunt, SA; Nishimura, R; Ornato, JP; Page, RL; Riegel, B; Priori, SG; Blanc, JJ; Budaj, A; Camm, AJ; Dean, V; Deckers, JW; Despres, C; Dickstein, K; Lekakis, J; McGregor, K; Metra, M; Morais, J; Osterspey, A; Tamargo, JL; Zamorano, JL; American College of Cardiology/American Heart Association Task Force on Practice, Guidelines; European Society of Cardiology Committee for Practice, Guidelines; European Heart Rhythm, Association; Heart Rhythm, Society (2006 Aug 15). "ACC/AHA/ESC 2006 Guidelines for the Management of Patients with Atrial Fibrillation: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Revise the 2001 Guidelines for the Management of Patients With Atrial Fibrillation): developed in collaboration with the European Heart Rhythm Association and the Heart Rhythm Society". Circulation. 114 (7): e257-354. doi:10.1161/CIRCULATIONAHA.106.177292. PMID 16908781.
{{cite journal}}: Check date values in:|date=(help) - ^ Zipes, DP; Camm, AJ; Borggrefe, M; Buxton, AE; Chaitman, B; Fromer, M; Gregoratos, G; Klein, G; Moss, AJ; Myerburg, RJ; Priori, SG; Quinones, MA; Roden, DM; Silka, MJ; Tracy, C; Smith SC, Jr; Jacobs, AK; Adams, CD; Antman, EM; Anderson, JL; Hunt, SA; Halperin, JL; Nishimura, R; Ornato, JP; Page, RL; Riegel, B; Blanc, JJ; Budaj, A; Dean, V; Deckers, JW; Despres, C; Dickstein, K; Lekakis, J; McGregor, K; Metra, M; Morais, J; Osterspey, A; Tamargo, JL; Zamorano, JL; American College of Cardiology/American Heart Association Task, Force; European Society of Cardiology Committee for Practice, Guidelines; European Heart Rhythm, Association; Heart Rhythm, Society (2006 Sep 5). "ACC/AHA/ESC 2006 Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death: a report of the American College of Cardiology/American Heart Association Task Force and the European Society of Cardiology Committee for Practice Guidelines (writing committee to develop Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death): developed in collaboration with the European Heart Rhythm Association and the Heart Rhythm Society". Circulation. 114 (10): e385-484. doi:10.1161/CIRCULATIONAHA.106.178233. PMID 16935995.
{{cite journal}}: Check date values in:|date=(help) - ^ Link, MS; Atkins, DL; Passman, RS; Halperin, HR; Samson, RA; White, RD; Cudnik, MT; Berg, MD; Kudenchuk, PJ; Kerber, RE (2010 Nov 2). "Part 6: electrical therapies: automated external defibrillators, defibrillation, cardioversion, and pacing: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care". Circulation. 122 (18 Suppl 3): S706-19. doi:10.1161/CIRCULATIONAHA.110.970954. PMID 20956222.
{{cite journal}}: Check date values in:|date=(help)
External links
edit- Cardioversion from the National Institutes of Health
- Pharmacological Cardioversion from the American Academy of Family Physicians
- Synchronized Electrical Cardioversion from eMedicine Online
- Cardioversion from the Heart Rhythm Society
