Misplaced Pages

Sepsis: Difference between revisions

Article snapshot taken from Wikipedia with creative commons attribution-sharealike license. Give it a read and then ask your questions in the chat. We can research this topic together.
Browse history interactively← Previous editNext edit →Content deleted Content addedVisualWikitext
Revision as of 20:02, 23 January 2009 editGor n bein (talk | contribs)Extended confirmed users503 editsm Neonates← Previous edit Revision as of 19:41, 24 January 2009 edit undo98.180.5.84 (talk)No edit summaryNext edit →
Line 16: Line 16:
'''Sepsis''' is a serious ] condition characterized by a half-body ] state (called a ] or SIRS) caused by ].<ref name="pmid12682500">{{cite journal |author=Levy MM, Fink MP, Marshall JC, ''et al'' |title=2001 SCCM/ESICM/ACCP/ATS/SIS International Sepsis Definitions Conference |journal=Crit. Care Med. |volume=31 |issue=4 |pages=1250–6 |year=2003 |month=April |pmid=12682500 |doi=10.1097/01.CCM.0000050454.01978.3B |url=http://meta.wkhealth.com/pt/pt-core/template-journal/lwwgateway/media/landingpage.htm?issn=0090-3493&volume=31&issue=4&spage=1250}}</ref><ref name="1992consensus">{{cite journal |author=Bone RC, Balk RA, Cerra FB, ''et al'' |title=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 |journal=Chest |volume=101 |issue=6 |pages=1644–55 |year=1992 |month=Jun |pmid=1303622 |doi= 10.1378/chest.101.6.1644 |url=http://www.chestjournal.org/cgi/pmidlookup?view=long&pmid=1303622 |format={{dead link|date=January 2009}} &ndash; <sup></sup>}}</ref> The body may develop this inflammatory response to ] in the blood. The related layman's term is '''blood poisoning'''. '''Sepsis''' is a serious ] condition characterized by a half-body ] state (called a ] or SIRS) caused by ].<ref name="pmid12682500">{{cite journal |author=Levy MM, Fink MP, Marshall JC, ''et al'' |title=2001 SCCM/ESICM/ACCP/ATS/SIS International Sepsis Definitions Conference |journal=Crit. Care Med. |volume=31 |issue=4 |pages=1250–6 |year=2003 |month=April |pmid=12682500 |doi=10.1097/01.CCM.0000050454.01978.3B |url=http://meta.wkhealth.com/pt/pt-core/template-journal/lwwgateway/media/landingpage.htm?issn=0090-3493&volume=31&issue=4&spage=1250}}</ref><ref name="1992consensus">{{cite journal |author=Bone RC, Balk RA, Cerra FB, ''et al'' |title=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 |journal=Chest |volume=101 |issue=6 |pages=1644–55 |year=1992 |month=Jun |pmid=1303622 |doi= 10.1378/chest.101.6.1644 |url=http://www.chestjournal.org/cgi/pmidlookup?view=long&pmid=1303622 |format={{dead link|date=January 2009}} &ndash; <sup></sup>}}</ref> The body may develop this inflammatory response to ] in the blood. The related layman's term is '''blood poisoning'''.


'''Septicemia''' is an ill-defined term referring to the presence of bacteria or their toxins in the blood.<ref>{{EMedicineDictionary|septicemia}}</ref> The term improperly mixes components of bacteremia and sepsis, and has been abandoned as a concept.<ref name="1992consensus"/> '''Septicemia''' is an ill-defined term referring to the presence of bacteria or their toxins in the blood.<ref>{{EMedicineDictionary|septicemia}}</ref> The term improperly mixes components of ] and ], and has been abandoned as a concept.<ref name="1992consensus"/>


Sepsis is usually treated in the ] with ] and ]. If fluid replacement is insufficient to maintain blood pressure, specific ] drugs can be used. ] and ] may be needed to support the function of the lungs and kidneys, respectively. To guide therapy, a ] and an ] may be placed. Sepsis patients require preventive measures for ], ]s and ]s, unless other conditions prevent this. Some patients might benefit from tight control of ] with ] (targeting ]), low-dose ] or ] (] ]).<ref name="campaign">{{cite journal |author=Dellinger RP, Levy MM, Carlet JM, et.al, for the International Surviving Sepsis Campaign Guidelines Committee. |title=Surviving Sepsis Campaign: International Guidelines for Management of Severe Sepsis and Septic Shock: 2008 |journal=Crit Care Med |year=2008 |volume=36 |issue=1 |pages=296–327 |pmid=18158437 |url=http://www.ccmjournal.com/pt/re/ccm/searchresults.htm |doi=10.1097/01.CCM.0000298158.12101.41 |doi_brokendate=2008-06-26}}</ref> Sepsis is usually treated in the ] with ] and ]. If fluid replacement is insufficient to maintain blood pressure, specific ] drugs can be used. ] and ] may be needed to support the function of the lungs and kidneys, respectively. To guide therapy, a ] and an ] may be placed. Sepsis patients require preventive measures for ], ]s and ]s, unless other conditions prevent this. Some patients might benefit from tight control of ] with ] (targeting ]), low-dose ] or ] (] ]).<ref name="campaign">{{cite journal |author=Dellinger RP, Levy MM, Carlet JM, et.al, for the International Surviving Sepsis Campaign Guidelines Committee. |title=Surviving Sepsis Campaign: International Guidelines for Management of Severe Sepsis and Septic Shock: 2008 |journal=Crit Care Med |year=2008 |volume=36 |issue=1 |pages=296–327 |pmid=18158437 |url=http://www.ccmjournal.com/pt/re/ccm/searchresults.htm |doi=10.1097/01.CCM.0000298158.12101.41 |doi_brokendate=2008-06-26}}</ref>

Revision as of 19:41, 24 January 2009

For the genus of flies of this name, see Sepsidae. Medical condition
Sepsis
SpecialtyInfectious diseases Edit this on Wikidata

Sepsis is a serious medical condition characterized by a half-body inflammatory state (called a systemic inflammatory response syndrome or SIRS) caused by infection. The body may develop this inflammatory response to microbes in the blood. The related layman's term is blood poisoning.

Septicemia is an ill-defined term referring to the presence of bacteria or their toxins in the blood. The term improperly mixes components of bacteremia and sepsis, and has been abandoned as a concept.

Sepsis is usually treated in the intensive care unit with intravenous fluids and antibiotics. If fluid replacement is insufficient to maintain blood pressure, specific vasopressor drugs can be used. Artificial ventilation and dialysis may be needed to support the function of the lungs and kidneys, respectively. To guide therapy, a central venous catheter and an arterial catheter may be placed. Sepsis patients require preventive measures for deep vein thrombosis, stress ulcers and pressure ulcers, unless other conditions prevent this. Some patients might benefit from tight control of blood sugar levels with insulin (targeting stress hyperglycemia), low-dose corticosteroids or activated drotrecogin alfa (recombinant protein C).

Terminology

Severe sepsis occurs when sepsis leads to organ dysfunction, low blood pressure (hypotension) or insufficient blood flow (hypoperfusion) to one or more organs (causing, for example, lactic acidosis, decreased urine production or altered mental status). Sepsis can lead to septic shock, multiple organ dysfunction syndrome (formerly known as multiple organ failure) and death. Organ dysfunction results from sepsis-induced hypotension (< 90 mmHg or a reduction of ≥ 40 mmHg from baseline) and diffuse intravascular coagulation, among other things.

Bacteremia is the presence of viable bacteria in the bloodstream. Likewise, the terms viremia and fungemia simply refer to viruses and fungi in the bloodstream. These terms say nothing about the consequences this has on the body. For example, bacteria can be introduced into the bloodstream during toothbrushing. This form of bacteremia almost never causes problems in normal individuals. However, bacteremia associated with certain dental procedures can cause bacterial infection of the heart valves (known as endocarditis) in high risk patients. Conversely, a systemic inflammatory response syndrome can occur in patients without the presence of infection, for example in those with burns, polytrauma, or the initial state in pancreatitis and chemical pneumonitis.

Signs and symptoms

In addition to symptoms related to the provoking infection, sepsis is characterized by evidence of acute inflammation present throughout the entire body, and is therefore frequently associated with fever and elevated white blood cell count (leukocytosis) or low white blood cell count and lower than average temperature. The modern concept of sepsis is that the host's immune response to the infection causes most of the symptoms of sepsis, resulting in hemodynamic consequences and damage to organs. This host response has been termed systemic inflammatory response syndrome (SIRS) and is characterized by hemodynamic compromise and resultant metabolic derangement. Outward physical symptoms of this response frequently include a high heart rate (above 90 beats per minute), high respiratory rate (above 20 breaths per minute) and elevated body temperature.

This immunological response causes widespread activation of acute phase proteins, affecting the complement system and the coagulation pathways, which then cause damage to the vasculature as well as to the organs. Various neuroendocrine counter-regulatory systems are then activated as well, often compounding the problem. Even with immediate and aggressive treatment, this may progress to multiple organ dysfunction syndrome and eventually death.

Epidemiology

In the United States, sepsis is the second leading cause of death in non-coronary ICU patients, and the tenth most common cause of death overall according to data from the Centers for Disease Control and Prevention (the first being multiple organ failure). Sepsis is common and also more dangerous in elderly, immunocompromised, and critically ill patients. It occurs in 1%-2% of all hospitalizations and accounts for as much as 25% of intensive care unit (ICU) bed utilization. It is a major cause of death in intensive care units worldwide, with mortality rates that range from 20% for sepsis to 40% for severe sepsis to >60% for septic shock.

Definition of sepsis

Sepsis is considered present if infection is highly suspected or proven and two or more of the following systemic inflammatory response syndrome (SIRS) criteria are met:

Fever and leukocytosis are features of the acute phase reaction, while tachycardia is often the initial sign of hemodynamic compromise. Tachypnea may be related to the increased metabolic stress due to infection and inflammation, but may also be an ominous sign of inadequate perfusion resulting in the onset of anaerobic cellular metabolism.

In children, the SIRS criteria are modified in the following fashion:

Note that SIRS criteria are very non-specific, and must be interpreted carefully within the clinical context. These criteria exist primarily for the purpose of more objectively classifying critically-ill patients so that future clinical studies may be more rigorous and more easily reproducible.

Consensus definitions however continue to evolve with the latest expanding the list of signs and symptoms of sepsis to reflect clinical bedside experience.

To qualify as sepsis, there must be an infection suspected or proven (by culture, stain, or polymerase chain reaction (PCR)), or a clinical syndrome pathognomonic for infection. Specific evidence for infection includes WBCs in normally sterile fluid (such as urine or cerebrospinal fluid (CSF), evidence of a perforated viscus (free air on abdominal x-ray or CT scan, signs of acute peritonitis), abnormal chest x-ray (CXR) consistent with pneumonia (with focal opacification), or petechiae, purpura, or purpura fulminans

The more critical subsets of sepsis are severe sepsis (sepsis with acute organ dysfunction) and septic shock (sepsis with refractory arterial hypotension). Alternatively, when two or more of the systemic inflammatory response syndrome criteria are met without evidence of infection, patients may be diagnosed simply with "SIRS." Patients with SIRS and acute organ dysfunction may be termed "severe SIRS."

Patients are defined as having "severe sepsis" if they have sepsis plus signs of systemic hypoperfusion: either end organ dysfunction or a serum lactate greater than 4 mmol/dL. Other signs include oliguria and altered mental status. Patients are defined as having septic shock if they have sepsis plus hypotension after aggressive fluid resuscitation (typically upwards of 6 liters or 40 ml/kg of crystalloid).

Examples of end-organ dysfunction include the following:

More specific definitions of end-organ dysfunction exist for SIRS in pediatrics.

  • Cardiovascular dysfunction (after fluid resuscitation with at least 40 ml/kg of crystalloid)
    • hypotension with blood pressure < 5th percentile for age or systolic blood pressure < 2 standard deviations below normal for age, OR
    • vasopressor requirement, OR
    • two of the following criteria:
  • Respiratory dysfunction (in the absence of cyanotic heart disease or known chronic lung disease)
    • the ratio of the arterial partial-pressure of oxygen to the fraction of oxygen in the gases inspired (PaO2/FiO2) < 300 (the definition of acute lung injury), OR
    • arterial partial-pressure of carbon dioxide (PaCO2) > 65 torr (20 mmHg) over baseline PaCO2 (evidence of hypercapnic respiratory failure), OR
    • supplemental oxygen requirement of greater than FiO2 0.5 to maintain oxygen saturation ≥ 92%
  • Neurologic dysfunction
  • Hematologic dysfunction
  • Renal dysfunction
  • Hepatic dysfunction (only applicable to infants > 1 month)

Neonatal sepsis

In common clinical usage, sepsis specifically refers to the presence of a serious bacterial infection(SBI) (such as meningitis, pneumonia, pyelonephritis, or gastroenteritis) in the setting of fever. Criteria with regards to hemodynamic compromise or respiratory failure are not useful clinically because these symptoms often do not arise in neonates until death is imminent and unpreventable.

It is difficult to clinically exclude sepsis in newborns less than 90 days old who have fever (defined as a temperature > 38°C (100.4°F). Except in the case of obvious acute viral bronchiolitis, the current practice in newborns less than 30 days old is to perform a complete workup including complete blood count with differential, blood culture, urinalysis, urine culture, and cerebrospinal fluid(CSF) studies and CSF culture, admit the newborn to the hospital, and treat empirically for serious bacterial infection for at least 48 hours until cultures are demonstrated to show no growth. Attempts have been made to see if it is possible to risk stratify newborns in order to decide if a newborn can be safely monitored at home without treatment despite having a fever. One such attempt is the Rochester criteria.

A study performed at Strong Memorial Hospital in Rochester, New York, showed that infants ≤ 60 days old meeting the following criteria were at low-risk for having a serious bacterial illness:

  • generally well appearing
  • previously healthy
    • full term (at ≥37 weeks gestation)
    • no antibiotics perinatally
    • no unexplained hyperbilirubinemia that required treatment
    • no antibiotics since discharge
    • no hospitalizations
    • no chronic illness
    • discharged at the same time or before the mother
  • no evidence of skin, soft tissue, bone, joint, or ear infection
  • WBC count 5,000-15,000/mm
  • absolute band count ≤ 1,500/mm
  • urine WBC count ≤ 10 per high power field (hpf)
  • stool WBC count ≤ 5 per high power field (hpf) only in infants with diarrhea

Those meeting these criteria likely do not require a lumbar puncture, and are felt to be safe for discharge home without antibiotic treatment, or with a single dose of intramuscular antibiotics, but will still require close outpatient follow-up.

Diagnosis

The medical history and clinical examination can provide important elements regarding the cause and severity of sepsis.

The identification of the causative microbe in sepsis can provide useful information. Imaging (such as chest X-rays or CT scans) and laboratory techniques (such as urine microscopy or lumbar puncture) are often necessary to find the source of the infection. The exact causative organism is confirmed by microbiological culturing in the laboratory (blood cultures and cultures from suspected sites of infections such as urine cultures, sputum cultures, and so on). However, this is a slow process as it takes a few days to grow up the cultures and correctly identify the pathogens. New molecular diagnostic tests are now available that uses genetic material from the pathogen to quickly (within hours) provide results. However, current practice is to directly prescribe broad spectrum antibiotics to the patient.

The effects of the condition on the function of the organs should be documented to guide therapy. This can involve measurement of blood levels of lactate, blood gas sampling, and other blood tests. Because patients on the intensive care unit are predisposed to hospital-acquired infections (especially related to the presence of catheters), they may require surveillance cultures.

Treatment

Adults and Children

The therapy of sepsis rests on antibiotics, surgical drainage of infected fluid collections, fluid replacement and appropriate support for organ dysfunction. This may include hemodialysis in kidney failure, mechanical ventilation in pulmonary dysfunction, transfusion of blood products, and drug and fluid therapy for circulatory failure. Ensuring adequate nutrition—preferably by enteral feeding, but if necessary by parenteral nutrition—is important during prolonged illness.

A problem in the adequate management of septic patients has been the delay in administering therapy after sepsis has been recognized. Published studies have demonstrated that for every hour delay in the administration of appropriate antibiotic therapy there is an associated 7% rise in mortality. A large international collaboration was established to educate people about sepsis and to improve patient outcomes with sepsis, entitled the "Surviving Sepsis Campaign." The Campaign has published an evidence-based review of management strategies for severe sepsis, with the aim to publish a complete set of guidelines in subsequent years.

Early Goal Directed Therapy (EGDT), developed at Henry Ford Hospital by E. Rivers, MD, is a systematic approach to resuscitation that has been validated in the treatment of severe sepsis and septic shock. It is meant to be started in the Emergency Department. The theory is that one should use a step-wise approach, having the patient meet physiologic goals, to optimize cardiac preload, afterload, and contractility, thus optimizing oxygen delivery to the tissues. A recent meta-analysis showed that EGDT provides a benefit on mortality in patients with sepsis. As of December 2008 some controversy around its uses remains and a number of trials are ongoing in an attempt to resolve this.

In EGDT, fluids are administered until the central venous pressure (CVP), as measured by a central venous catheter, reaches 8-12 cm of water (or 10-15 cm of water in mechanically ventilated patients). This may require around 6 liters of isotonic crystalloid solution, rapidly administered. If the mean arterial pressure is less than 65 mmHg or greater than 90 mmHg, vasopressors or vasodilators are given as needed to reach the goal. 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. Elective intubation may be performed to reduce oxygen demand if the SvO2 remains low despite optimization of hemodynamics. Urine output is also monitored, with a minimum goal of 0.5 ml/kg/h. In the original trial, mortality was cut from 46.5% in the control group to 30.5% in the intervention group. The Surviving Sepsis Campaign guidelines recommends EGDT for the initial resuscitation of the septic patient with a level B strength of evidence (single randomized control trial).

Most therapies aimed at the inflammation process itself have failed to improve outcome, however drotrecogin alfa (activated protein C, one of the coagulation factors) has been shown to decrease mortality from about 31% to about 25% in severe sepsis. To qualify for drotrecogin alfa, a patient must have severe sepsis or septic shock with an APACHE II score of 25 or greater and a low risk of bleeding.

During critical illness, a state of adrenal insufficiency and tissue resistance (the word 'relative' resistance should be avoided) to corticosteroids may occur. This has been termed critical illness–related corticosteroid insufficiency. Treatment with corticosteroids might be most beneficial in those with septic shock and early severe acute respiratory distress syndrome (ARDS), whereas its role in other patients such as those with pancreatitis or severe pneumonia is unclear. These recommendations stem from studies showing benefits from low dose hydrocortisone treatment for septic shock patients and methylprednisolone in ARDS patients. However, the exact way of determining corticosteroid insufficiency remains problematic. It should be suspected in those poorly responding to resuscitation with fluids and vasopressors. ACTH stimulation testing is not recommended to confirm the diagnosis. Glucocorticoid drugs should be weaned and not stopped abruptly.

Neonates

Note that in neonates, sepsis is difficult to diagnose clinically. They may be relatively asymptomatic until hemodynamic and respiratory collapse is imminent, so if there is even a remote suspicion of sepsis, they are frequently treated with antibiotics empirically until cultures are sufficiently proven to be negative. In addition to fluid resuscitation and supportive care, a common antibiotic regimen in infants with suspected sepsis is a beta-lactam antibiotic (usually ampicillin) in combination with an aminoglycoside (usually gentamicin) or a third-generation cephalosporin (usually cefotaximeceftriaxone is generally avoided in neonates due to the theoretical risk of kernicterus.) The organisms which are targeted are species that predominate in the female genitourinary tract and to which neonates are especially vulnerable to, specifically Group B Streptococcus, Escherichia coli, and Listeria monocytogenes (This is the main rationale for using ampicillin versus other beta-lactams.) Of course, neonates are also vulnerable to other common pathogens that can cause meningitis and bacteremia such as Streptococcus pneumoniae and Neisseria meningitidis. Although uncommon, if anaerobic species are suspected (such as in cases where necrotizing enterocolitis or intestinal perforation is a concern, clindamycin is often added.

Granulocyte-macrophage colony stimulating factor (GM-CSF) is often used in neonatal sepsis, however a recent study found that while GM-CSF corrects neutropenia if present, it has no effect on reducing sepsis or improving survival.

Prognosis

This section needs expansion. You can help by adding to it. (July 2008)

Prognosis can be estimated with the MEDS score. Approximately 20–35% of patients with severe sepsis and 40–60% of patients with septic shock die within 30 days. Others die within the ensuing 6 months. Late deaths often result from poorly controlled infection, immunosuppression, complications of intensive care, failure of multiple organs, or the patient's underlying disease.

Prognostic stratification systems such as APACHE II indicate that factoring in the patient's age, underlying condition, and various physiologic variables can yield estimates of the risk of dying of severe sepsis. Of the individual covariates, the severity of underlying disease most strongly influences the risk of dying. Septic shock is also a strong predictor of short- and long-term mortality. Case-fatality rates are similar for culture-positive and culture-negative severe sepsis.

ICD-9-CM coding guidelines (USA)

Septicemia, Systemic inflammatory response syndrome (SIRS), Sepsis, Severe sepsis, and Septic Shock

1) SIRS, Septicemia, and Sepsis

  • (a) The terms septicemia and sepsis are often used interchangeably by providers, however they are not considered synonymous terms. The following descriptions are provided for reference but do not preclude querying the provider for clarification about terms used in the documentation:
    • (i) Septicemia generally refers to a systemic disease associated with the presence of pathological microorganisms or toxins in the blood, which can include bacteria, viruses, fungi or other organisms.
    • (ii) Systemic inflammatory response syndrome (SIRS) generally refers to the systemic response to infection, trauma/burns, or other insult (such as cancer) with symptoms including fever, tachycardia, tachypnea, and leukocytosis.
    • (iii)Sepsis generally refers to SIRS due to infection.
    • (iv) Severe sepsis generally refers to sepsis with associated acute organ dysfunction.
  • (b) The Coding of SIRS, sepsis and severe sepsis: The coding of SIRS, sepsis and severe sepsis requires a minimum of 2 codes: a code for the underlying cause (such as infection or trauma) and a code from subcategory 995.9 Systemic inflammatory response syndrome (SIRS).
    • (i) The code for the underlying cause (such as infection or trauma) must be sequenced before the code from subcategory 995.9 Systemic inflammatory response syndrome (SIRS).
    • (ii) Sepsis and severe sepsis require a code for the systemic infection (038.xx, 112.5, etc.) and either code 995.91, Sepsis, or 995.92, Severe sepsis. If the causal organism is not documented, assign code 038.9, Unspecified septicemia.
    • (iii)Severe sepsis requires additional code(s) for the associated acute organ dysfunction(s).
    • (iv) If a patient has sepsis with multiple organ dysfunctions, follow the instructions for coding severe sepsis.
    • (v) Either the term sepsis or SIRS must be documented to assign a code from subcategory 995.9.
    • (vi) See Section I.C.17.g), Injury and poisoning, for information regarding systemic inflammatory response syndrome (SIRS) due to trauma/burns and other non-infectious processes.
  • (c) Due to the complex nature of sepsis and severe sepsis, some cases may require querying the provider prior to assignment of the codes.

2) Sequencing sepsis and severe sepsis

  • (a) Sepsis and severe sepsis as principal diagnosis: If sepsis or severe sepsis is present on admission, and meets the definition of principal diagnosis, the systemic infection code (e.g., 038.xx, 112.5, etc) should be assigned as the principal diagnosis, followed by code 995.91, Sepsis, or 995.92, Severe sepsis, as required by the sequencing rules in the Tabular List. Codes from subcategory 995.9 can never be assigned as a principal diagnosis. A code should also be assigned for any localized infection, if present. If the sepsis or severe sepsis is due to a postprocedural infection, see Section I.C.1.b.10 for guidelines related to sepsis due to postprocedural infection.
  • (b) Sepsis and severe sepsis as secondary diagnoses: When sepsis or severe sepsis develops during the encounter (it was not present on admission), the systemic infection code and code 995.91 or 995.92 should be assigned as secondary diagnoses.
  • (c) Documentation unclear as to whether sepsis or severe sepsis is present on admission: Sepsis or severe sepsis may be present on admission but the diagnosis may not be confirmed until sometime after admission. If the documentation is not clear whether the sepsis or severe sepsis was present on admission, the provider should be queried.

3) Sepsis/SIRS with Localized Infection: If the reason for admission is both sepsis, severe sepsis, or SIRS and a localized infection, such as pneumonia or cellulitis, a code for the systemic infection (038.xx, 112.5, etc) should be assigned first, then code 995.91 or 995.92, followed by the code for the localized infection. If the patient is admitted with a localized infection, such as pneumonia, and sepsis/SIRS doesn’t develop until after admission, see guideline I.C.1.b.2.b). If the localized infection is postprocedural, see Section I.C.1.b.10 for guidelines related to sepsis due to postprocedural infection.

Note: The term urosepsis is a nonspecific term. If that is the only term documented then only code 599.0 should be assigned based on the default for the term in the ICD-9-CM index, in addition to the code for the causal organism if known.

4) Bacterial Sepsis and Septicemia: In most cases, it will be a code from category 038, Septicemia, that will be used in conjunction with a code from subcategory 995.9 such as the following:

  • (a) Streptococcal sepsis: If the documentation in the record states streptococcal sepsis, codes 038.0, Streptococcal septicemia, and code 995.91 should be used, in that sequence.
  • (b) Streptococcal septicemia: If the documentation states streptococcal septicemia, only code 038.0 should be assigned, however, the provider should be queried whether the patient has sepsis, an infection with SIRS.

5) Acute organ dysfunction that is not clearly associated with the sepsis: If a patient has sepsis and an acute organ dysfunction, but the medical record documentation indicates that the acute organ dysfunction is related to a medical condition other than the sepsis, do not assign code 995.92, Severe sepsis. An acute organ dysfunction must be associated with the sepsis in order to assign the severe sepsis code. If the documentation is not clear as to whether an acute organ dysfunction is related to the sepsis or another medical condition, query the provider.

6) Septic shock

  • (a) Sequencing of septic shock: Septic shock generally refers to circulatory failure associated with severe sepsis, and, therefore, it represents a type of acute organ dysfunction. For all cases of septic shock, the code for the systemic infection should be sequenced first, followed by codes 995.92 and 785.52. Any additional codes for other acute organ dysfunctions should also be assigned. As noted in the sequencing instructions in the Tabular List, the code for septic shock cannot be assigned as a principal diagnosis.
  • (b) Septic Shock without documentation of severe sepsis: Septic shock indicates the presence of severe sepsis. Code 995.92, Severe sepsis, must be assigned with code 785.52, Septic shock, even if the term severe sepsis is not documented in the record. The “use additional code” note and the “code first” note in the tabular support this guideline.

7) Sepsis and septic shock complicating abortion and pregnancy: Sepsis and septic shock complicating abortion, ectopic pregnancy, and molar pregnancy are classified to category codes in Chapter 11 (630-639). See section I.C.11 (of the official coding guidelines).

8) Negative or inconclusive blood cultures: Negative or inconclusive blood cultures do not preclude a diagnosis of septicemia or sepsis in patients with clinical evidence of the condition, however, the provider should be queried.

9) Newborn sepsis: Code 771.81, Septicemia of newborn, should be assigned with a secondary code from category 041, Bacterial infections in conditions classified elsewhere and of unspecified site, to identify the organism. A code from category 038, Septicemia, should not be used on a newborn record. Do not assign code 995.91, Sepsis, as code 771.81 describes the sepsis. If applicable, use additional codes to identify severe sepsis (995.92) and any associated acute organ dysfunction.

10) Sepsis due to a Postprocedural Infection

  • (a) Documentation of causal relationship: As with all postprocedural complications, code assignment is based on the provider’s documentation of the relationship between the infection and the procedure.
  • (b) Sepsis due to postprocedural infection: In cases of postprocedural sepsis, the complication code, such as code 998.59, Other postoperative infection, or 674.3x, Other complications of obstetrical surgical wounds should be coded first followed by the appropriate sepsis codes (systemic infection code and either code 995.91or 995.92). An additional code(s) for any acute organ dysfunction should also be assigned for cases of severe sepsis.

11) External cause of injury codes with SIRS: Refer to Section I.C.19.a.7 (of the official coding guidelines) for instruction on the use of external cause of injury codes with codes for SIRS resulting from trauma.

12) Sepsis and Severe Sepsis Associated with Non-infectious Process: In some cases, a non-infectious process, such as trauma, may lead to an infection which can result in sepsis or severe sepsis. If sepsis or severe sepsis is documented as associated with a non-infectious condition, such as a burn or serious injury, and this condition meets the definition for principal diagnosis, the code for the non-infectious condition should be sequenced first, followed by the code for the systemic infection and either code 995.91, Sepsis, or 995.92, Severe sepsis. Additional codes for any associated acute organ dysfunction(s) should also be assigned for cases of severe sepsis. If the sepsis or severe sepsis meets the definition of principal diagnosis, the systemic infection and sepsis codes should be sequenced before the non-infectious condition. When both the associated non-infectious condition and the sepsis or severe sepsis meet the definition of principal diagnosis, either may be assigned as principal diagnosis. See Section I.C.1.b.2)(a) for guidelines pertaining to sepsis or severe sepsis as the principal diagnosis. Only one code from subcategory 995.9 should be assigned. Therefore, when a non-infectious condition leads to an infection resulting in sepsis or severe sepsis, assign either code 995.91 or 995.92. Do not additionally assign code 995.93, Systemic inflammatory response syndrome due to non-infectious process without acute organ dysfunction, or 995.94, Systemic inflammatory response syndrome with acute organ dysfunction.

See Section I.C.17.g (of the official coding guidelines) for information on the coding of SIRS due to trauma/burns or other non-infectious disease processes.

See also

References

  1. Levy MM, Fink MP, Marshall JC; et al. (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); Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  2. ^ Bone RC, Balk RA, Cerra FB; et al. (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. {{cite journal}}: Explicit use of et al. in: |author= (help); External link in |format= (help); Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  3. Template:EMedicineDictionary
  4. ^ Dellinger RP, Levy MM, Carlet JM, et.al, for the International Surviving Sepsis Campaign Guidelines Committee. (2008). "Surviving Sepsis Campaign: International Guidelines for Management of Severe Sepsis and Septic Shock: 2008". Crit Care Med. 36 (1): 296–327. doi:10.1097/01.CCM.0000298158.12101.41. PMID 18158437. {{cite journal}}: Unknown parameter |doi_brokendate= ignored (|doi-broken-date= suggested) (help)CS1 maint: multiple names: authors list (link)
  5. Lockhart PB, Brennan MT, Sasser HC, Fox PC, Paster BJ, Bahrani-Mougeot FK (2008). "Bacteremia associated with toothbrushing and dental extraction". Circulation. 117 (24): 3118–25. doi:10.1161/CIRCULATIONAHA.107.758524. PMID 18541739. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  6. Wilson W, Taubert KA, Gewitz M; et al. (2007). "Prevention of infective endocarditis: guidelines from the American Heart Association: a guideline from the American Heart Association Rheumatic Fever, Endocarditis, and Kawasaki Disease Committee, Council on Cardiovascular Disease in the Young, and the Council on Clinical Cardiology, Council on Cardiovascular Surgery and Anesthesia, and the Quality of Care and Outcomes Research Interdisciplinary Working Group". Circulation. 116 (15): 1736–54. doi:10.1161/CIRCULATIONAHA.106.183095. PMID 17446442. {{cite journal}}: Explicit use of et al. in: |author= (help); Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  7. Martin GS, Mannino DM, Eaton S, Moss M (2003-04-17). "The epidemiology of sepsis in the United States from 1979 through 2000". N Engl J Med. 348 (16): 1546–54. doi:10.1056/NEJMoa022139. PMID 12700374.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  8. ^ Goldstein B, Giroir B, Randolph A (2005). "International pediatric sepsis consensus conference: definitions for sepsis and organ dysfunction in pediatrics". Pediatr Crit Care Med. 6 (1): 2–8. doi:10.1097/01.PCC.0000149131.72248.E6. PMID 15636651.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  9. ^ Levy MM, Fink MP, Marshall JC, Abraham E, Angus D, Cook D, Cohen J, Opal SM, Vincent JL, Ramsay G (2003). "2001 SCCM/ESICM/ACCP/ATS/SIS International Sepsis Definitions Conference". Crit Care Med. 31 (4): 1250–1256. doi:10.1097/01.CCM.0000050454.01978.3B. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  10. Abraham E, Singer M (2007). "Mechanisms of sepsis-induced organ dysfunction". Crit. Care Med. 35 (10): 2408–16. doi:10.1097/01.CCM.0000282072.56245.91. PMID 17948334. {{cite journal}}: Unknown parameter |doi_brokendate= ignored (|doi-broken-date= suggested) (help)
  11. Dagan R, Powell KR, Hall CB, Menegus MA (1985). "Identification of infants unlikely to have serious bacterial infection although hospitalized for suspected sepsis". J. Pediatr. 107 (6): 855–60. doi:10.1016/S0022-3476(85)80175-X. PMID 4067741. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  12. ^ Rivers E, Nguyen B, Havstad S; et al. (2001). "Early goal-directed therapy in the treatment of severe sepsis and septic shock". N. Engl. J. Med. 345 (19): 1368–77. doi:10.1056/NEJMoa010307. PMID 11794169. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link)
  13. Jones AE, Brown MD, Trzeciak S; et al. (2008). "The effect of a quantitative resuscitation strategy on mortality in patients with sepsis: a meta-analysis". Critical care medicine. 36 (10): 2734–9. doi:10.1097/CCM.0b013e318186f839. PMID 18766093. {{cite journal}}: Explicit use of et al. in: |author= (help); Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  14. McKenna M (2008). "Controversy swirls around early goal-directed therapy in sepsis: pioneer defends ground- breaking approach to deadly disease". Ann Emerg Med. 52 (6): 651–4. doi:10.1016/j.annemergmed.2008.10.013. PMID 19048659. {{cite journal}}: Unknown parameter |month= ignored (help)
  15. Bernard GR, Vincent JL, Laterre PF, LaRosa SP, Dhainaut JF, Lopez-Rodriguez A, Steingrub JS, Garber GE, Helterbrand JD, Ely EW, Fisher CJ Jr (2001-03-08). "Recombinant human protein C Worldwide Evaluation in Severe Sepsis (PROWESS) study group. Efficacy and safety of recombinant human activated protein C for severe sepsis". N Engl J Med. 344 (10): 699–709. doi:10.1056/NEJM200103083441001. PMID 11236773.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  16. ^ Marik PE, Pastores SM, Annane D; et al. (2008). "Recommendations for the diagnosis and management of corticosteroid insufficiency in critically ill adult patients: consensus statements from an international task force by the American College of Critical Care Medicine". Crit. Care Med. 36 (6): 1937–49. doi:10.1097/CCM.0b013e31817603ba. PMID 18496365. {{cite journal}}: Explicit use of et al. in: |author= (help); Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  17. Annane D, Sebille V, Charpentier C, Bollaert PE, Francois B, Korach JM, Capellier G, Cohen Y, Azoulay E, Troche G, Chaumet-Riffaut P, Bellissant E (2002-08-21). "Effect of treatment with low doses of hydrocortisone and fludrocortisone on mortality in patients with septic shock". JAMA. 288 (7): 862–71. doi:10.1001/jama.288.7.862. PMID 12186604.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  18. Meduri GU, Headley AS, Golden E; et al. (1998). "Effect of prolonged methylprednisolone therapy in unresolving acute respiratory distress syndrome: a randomized controlled trial". JAMA. 280 (2): 159–65. doi:10.1001/jama.280.2.159. PMID 9669790. {{cite journal}}: Explicit use of et al. in: |author= (help); Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  19. Meduri GU, Golden E, Freire AX; et al. (2007). "Methylprednisolone infusion in early severe ARDS: results of a randomized controlled trial". Chest. 131 (4): 954–63. doi:10.1378/chest.06-2100. PMID 17426195. {{cite journal}}: Explicit use of et al. in: |author= (help); Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  20. Sprung CL, Annane D, Keh D; et al. (2008). "Hydrocortisone therapy for patients with septic shock". N. Engl. J. Med. 358 (2): 111–24. doi:10.1056/NEJMoa071366. PMID 18184957. {{cite journal}}: Explicit use of et al. in: |author= (help); Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  21. Steinberg KP, Hudson LD, Goodman RB; et al. (2006). "Efficacy and safety of corticosteroids for persistent acute respiratory distress syndrome". N. Engl. J. Med. 354 (16): 1671–84. doi:10.1056/NEJMoa051693. PMID 16625008. {{cite journal}}: Explicit use of et al. in: |author= (help); Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  22. Annane D, Sébille V, Bellissant E (2006). "Effect of low doses of corticosteroids in septic shock patients with or without early acute respiratory distress syndrome". Crit. Care Med. 34 (1): 22–30. doi:10.1097/01.CCM.0000194723.78632.62. PMID 16374152. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  23. |journal=The Lancet |title=Granulocyte-macrophage colony stimulating factor administered as prophylaxis for reduction of sepsis in extremely preterm, small for gestational age neonates (the PROGRAMS trial): a single-blind, multicentre, randomized control trial |author=Carr et al |Year=2009 |Pages=226-33 |Volume=373
  24. Shapiro NI, Wolfe RE, Moore RB, Smith E, Burdick E, Bates DW (2003). "Mortality in Emergency Department Sepsis (MEDS) score: a prospectively derived and validated clinical prediction rule". Crit. Care Med. 31 (3): 670–5. doi:10.1097/01.CCM.0000054867.01688.D1. PMID 12626967.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  25. United States. National Center for Health Statistics. "ICD-9-CM Official Guidelines for Coding and Reporting". Washington: GPO, 2008.

External links

Intensive care medicine
General terms
Conditions
Organ system failure
Shock sequence
SIRS
Sepsis
Severe sepsis
Septic shock
Multiple organ dysfunction syndrome
Other shock
Cardiogenic shock
Distributive shock
Anaphylaxis
Obstructive shock
Neurogenic shock
Spinal shock
Vasodilatory shock
Organ failure
Acute renal failure
Acute respiratory distress syndrome
Acute liver failure
Respiratory failure
Multiple organ dysfunction syndrome
Complications
Iatrogenesis
Diagnosis
Life-supporting treatments
Drugs
ICU scoring systems
Physiology
Organisations
Related specialties
Pseudomonadota-associated Gram-negative bacterial infections
α
Rickettsiales
Rickettsiaceae/
(Rickettsioses)
Typhus
Spotted
fever
Tick-borne
Mite-borne
Flea-borne
Anaplasmataceae
Hyphomicrobiales
Brucellaceae
Bartonellaceae
β
Neisseriales
M+
M−
ungrouped:
Burkholderiales
γ
Enterobacteriales
(OX−)
Lac+
Slow/weak
Lac−
H2S+
H2S−
Pasteurellales
Haemophilus:
Pasteurella multocida
Aggregatibacter actinomycetemcomitans
Legionellales
Thiotrichales
Vibrionaceae
Pseudomonadales
Xanthomonadaceae
Cardiobacteriaceae
Aeromonadales
ε
Campylobacterales
Blood film findings
Red blood cells
Size
Shape
Colour
Inclusion bodies
Other
White blood cells
Lymphocytes
Granulocytes
Other

Template:Link FA

Categories: