In Copyright Since September 11,
2000 This web site is in no manner affiliated with any Kaiser entity and the for profit Permanente Link for Translation of the Kaiser Papers PATHFINDER(search)
| ABOUT US |
CONTACT
| WHY
THE KAISERPAPERS
| RESEARCH GUIDES BY SUBJECT | A READER'S GUIDE | Kaiser Diagnostic and Treatment Documents NOVEMBER 1999 KAISER PERMANENTE CLINICAL PRACTICE STATEMENT for ADULT SEPSIS ENDORSED BY:
GUIDING PRINCIPLES Prevention of sepsis is facilitated by: recommending vaccinations, such as pneumovax and influenza; the appropriate early treatment of pneumonia, urinary tract, and other infections; use of sterile precautions; routine hygiene; and judicious use of Foley catheters and other invasive devices. See Table I for conditions leading to high risk for sepsis. The early recognition of sepsis is vital to prevent disease progression and increased risk of mortality. It is important to continually monitor vital signs, urine output and mental status and to pay close attention to deteriorating trends. See Table 2 for definitions of different stages of sepsis. Septic patients require rapid treatment tuith antibiotics and fluids. Do not delay antibiotic treatment if cultures can not be readily obtained. See Tables 3 and 4 for antimicrobial recommendations and treatment algorithm.
|
||||||||||||||||||||||||||||||||
Determine advance directives,
patient preferences
for care, and establish code status with a physician order.
These should be documented and
respected at all times,
and treatment plans modified accordingly. Many recent studies evaluating innovative therapies have failed to show any improvement inpatient outcomes. Therefore, this clinical practice statement emphasizes standard therapies. TREATMENT GOALS Attain the following treatment goals as rapidly as possible. See Table 4 for treatment algorithm. * Systolic blood pressure ³90 mm Hg or MAP ³6 0-70 mm Hg *SaO2 ³90% * Urine output > 0.5cc/kg/hr * Resolving acidosis * Improved mental status The goal of the clinical practice statement - to promote early recognition of sepsis in adults to facilitate early intervention in order to reduce morbidity and mortality. Audience - all physicians treating patients in the hospital and emergency department, hospital and emergency nurses, as well as physicians and nurse practitioners seeing patients in the outpatient and urgent care setting. Development - by a multidisciplinary team of intensivists, hospital based specialists, emergency and primary care physicians, and emergency and intensive care nurses. Widely reviewed throughout the Northern California region. To be reviewed at least every two years and revised as needed. Foundation - due to insufficient evidence from large, randomized, controlled clinical trials, the Statement is based upon standard practice, expert opinion, and, when available, well- designed, randomized, controlled clinical trials. INTRODUCTION Certain segments of the population are particularly prone to developing sepsis.Preventive measures, such as the pneumovax and influenza vaccines and limited use of invasive devices, are vital for these groups. It is especially important to consider sepsis in any high-risk patient who meets the criteria for systemic inflammatory response syndrome (SIRS). | ||||||||||||||||||||||||||||||||
Table
I. Conditions Leading to High Rick for Sepsis *Age > 65 * Chronic liver disease *Chronic lung disease *Chronic renal disease *Diabetes mellitus *Heart disease *Hematologic disorder *Immunodeficiency *Indwelling catheters *Infection in previous year *Malignant neoplasm *Non-cardiac vascular disease *Organic cognitive disorder *Spinal cord injury *Substance abuse *Adapted from Quartin,30 Kreger24 ACCM/SCCM
DEFINITION
Systemic inflammatory response syndrome is the term applied to the diffuse inflammatory reaction as a result of any physiologic insult, such as trauma, bums, pancreatitis, toxins or infection. Regardless of etiology, SIRS is manifested by two or more of the following symptoms: fever or hypothermia, tachycardia, tachypnea, and leukocytosis. SIRS involves all organs and cells, and is triggered by a host of endogenous inflammatory mediators. Once initiated, the inflammatory response may continue even after the inciting insult has been resolved. Although the SIRS definition is broad, it should be used to screen patients who are at risk for developing sepsis. The SIRS criteria21,32 have proved sensitive for early identification of patients with sepsis. A study of the history of 50% - 90% SIRS followed 2527 patients admitted to the hospital who met these criteria. Among them, 26% (649) developed sepsis, 18% (467) severe sepsis, and 4% (110) septic shock. The median interval and likelihood of progression to sepsis was related to the number of SIRS criteria met on presentation. The mortality rate increased from 6% if two out of four criteria were met, to 18% if all four criteria were met. The mortality rate progressed from 7% in SIRS to 46% in septic shock (Table 2). *The goal is to recognize sepsis as early as
possible
and to initiate therapy immediately. The progression from sepsis or severe sepsis to septic shocky with its increased mortality, may be prevented by the early initiation of appropriate antibiotic therapy. *A patient can progress rapidly from sepsis to septic shock even when treated appropriately. | ||||||||||||||||||||||||||||||||
| ||||||||||||||||||||||||||||||||
Adapted from
BoneRC6, Rangel-Frallstd2,
Knaus21, Brun-Buisso9
Table 3. Empirical Choice of Antimicrobial Regimes for Sepsis | ||||||||||||||||||||||||||||||||
| ||||||||||||||||||||||||||||||||
* Adjust
Gentamicin or Tobramycin dosage for renal
function per pharmacy protocol. Quantities over 200mg should
be given
over at least two hours. NF - Not in formulary I Not all scenarios can be covered in this table. Call the Infectious Disease consultant prn, especially if resistant organisms are suspected. Revise medication immediately upon receipt of identification and sensitivity results. 2 Choices are not listed in order of preference. Discuss with local Infectious Disease consultant prn. 3 May need adjustment in cases of renal and/or hepatic dysfunction. 4 For management of oncology patients with chemotherapy-induced neutropenia, refer to your local protocol or the on-line clinical library. TABLE 4. TREATMENT ALGORITHM FOR SEPSIS (Systemic Inflammatory Response Syndrome with Clinical Evidence of Potentially Serious Infection) | ||||||||||||||||||||||||||||||||
| ||||||||||||||||||||||||||||||||
Advance directives,
patient preferences for care and code
status should be determined and documented. The patient or agent's preferences should be respected at all times, and treatment modified accordingly The Next 12 Hours | ||||||||||||||||||||||||||||||||
| ||||||||||||||||||||||||||||||||
Subsequent Care | ||||||||||||||||||||||||||||||||
| ||||||||||||||||||||||||||||||||
Advance directives'
patient preferences for care and code
status should be determined and documented, The patient or agent's preferences should be respected at all times, and treatment modified accordingly. Hebert 16 Knaus21, Herbert17, Bakker3, Hayes15 DIAGNOSIS & TREATMENT Sepsis has myriad clinical manifestations. The goal is to recognize sepsis as early as possible and to initiate therapy immediately. See Table I for groups at high risk for sepsis. The progression from sepsis or severe sepsis to septic shock, with its increased mortality, may be prevented by the early initiation of appropriate antibiotic therapy. Frequently, sepsis does not have a source that can be quickly identified. In that case, broad spectrum antibiotic coverage for both Gram negative and Gram positive organisms is recommended in the initial hospital course. Antibiotic therapy may need to be adjusted according to additional information obtained in the course of hospitalization. Cultures of blood, and other appropriate sources, such as urine and sputum, or of spinal, peritoneal, pleural, or joint fluids, should be obtained rapidly, preferably before the institution of antibiotic therapy. However, therapy must not be delayed if cultures cannot be rapidly obtained. It is also important to obtain baseline tests of organ function for future comparison in the event of organ dysfunction (Table 6). If initial evaluation does not reveal the source of sepsis, continue to search for an occult source, such as sub-acute endocarditis or intra-abdominal process. Septic patients may not be febrile, and may be hypothermic. The absence of a fever does not rule out sepsis and may, infact, portend a poorer prognosis. Patients may be afebrile because of unappreciated antipyretic use prior to presentation. In the patient with severe sepsis, initiate fluids and antibiotics as rapidly as possible. A patient can progress quickly from sepsis to septic shock even when treated appropriately. Antibiotics Early institution of empiric antibiotic therapy is of great importance in the management of sepsis (Table 3). When choosing initial antibiotics, consider factors such as the presumed site of infection and the likelihood of nosocomial infection with resistant species. Pulmonary infections are the most common source, followed by genitourinary and gastro-intestinal, depending upon the population. Empiric antibiotic therapy for septic shock usually includes multiple drugs. Advantages include a greater likelihood of antibiotic coverage against the infecting agent, prevention of the emergence of resistant strains, and possible synergistic antibacterial activity of some combinations. The disadvantages include increased risk of toxicity, super-infection with opportunistic organisms (e.g. fungi), and possible antagonism of antibacterial activity. In addition to antimicrobial therapy, measures to eliminate the source of infection should be pursued. Abscess cavities must be drained and intravascular devices or surgical prosthetic materials that are potential sources of infection may need to be removed.
Patients with hypotension and hypoperfusion may require as much as 10 liters of isotonic crystalloid fluids and I liter of colloids in the first 24 hours of resuscitation. Fluid Resuscitation Fluid resuscitation is the first step in the management of hypotension/hypoperfusion due to sepsis. Hypovolemia is a common problem as result of vasodilation, capillary leak, poor intake and increased insensible fluid losses. The goals of therapy are to achieve a systolic blood pressure ³ 90 mm Hg, a heart rate of < 110 beats/min, and improvement in mental status and urine output. Patients with severe sepsis/shock may need large volumes of fluid to correct deficits. In the first 24 hours of resuscitation, as much as 10 liters of isotonic crystalloid fluids (normal saline or Ringer's lactate) and 1 liter of colloids may be required.31,35 Fluids should be delivered through two large-bore peripheral IVs or a venous access central line as quickly as possible. Continue to monitor vital signs, urine output and mental status to assure that treatment goals are attained. 18 CRYSTALLOIDS & COLLOIDS Multiple studies have shown that patients in septic shock may be resuscitated with crystalloids, with or without colloid solutions. These studies show no significant difference in mortality rates using colloids compared with crystalloids as long as appropriate resuscitation goals are reached. 10,34 Crystalloid fluids are preferred for resuscitation. If resuscitation goals are not achieved after 4-6 liters of crystalloids, some clinicians add colloids. Studies have shown that adding colloids will increase blood pressure and cardiac index more rapidly and with less volume than crystalloids alone. This is crucial, since leaving the patient with persistent hypotension and hypoperfusion will result in multiple organ dysfunction and higher mortality. Larger, well-designed, randomized trials will be required to detect potentially small differences in treatment effects, mortality, and pulmonary function, if they truly exist. Hetastarch (Hespanâ) and albumin are the most commonly used colloids. Colloid resuscitation can be initiated with a bolus of 250 cc of hetastarch, and repeated as needed.31 This is as effective as albumin and may have fewer adverse effects.l4 Fresh frozen plasma is useful if the patient has coagulopathy (e.g. INR > 2). While aggressive fluid resuscitation may lead to pulmonary edema, this concern should not dissuade physicians from using large amounts of IV fluids when organ hypoperfusion is present. Patients with rales, decreasing oxygen or increased respiratory rate should have a chest x-ray. Fluid resuscitation should not be discontinued unless the x-ray reveals pulmonary edema in the presence of worsening respiratory failure. RED BLOOD CELL COUNT The minimum maintenance range for hemoglobin in critical care patients is thought to be 7-9 gm/dL after considering blood flow, oxygen delivery and coronary ischemia. For patients with signs of hypoperfusion, coronary disease or bleeding, hemoglobin may need to be maintained at a higher level. 17 Code Status & Advance Directives Sepsis treatment may require the use of mechanical ventilation and pressor agents. These aggressive measures are used in refractory septic shock, which has a predicted mortality of 40%-60%, and in multiple organ dysfunction, with a predicted mortality of 50%-90%. The patient's wishes regarding code status, mechanical ventilation, the use of pressors and other treatments should be discussed in the context of the diagnosis of sepsis and existing comorbidities. They should be reviewed with the patient or agent (in cases of altered mental status), written in the orders and respected throughout treatment. Vasopressors
If
the patient
remains hypotensive after aggressive resuscitation
with fluids and Adrenal insufficiency should be considered in patients with septic shock who do not respond to fluids and pressors.36 It is thought to occur in 30%-40% of critically ill patients, but can be easily overlooked. Adrenal failure/insufficiency or hemorrhage is found on autopsy in 30%-50% of patients in refractory septic shock. It is vital that physicians be aware that this is a treatable component of shock. The classic laboratory features of hyponatremia, hyperkalemia and acidosis are often absent, and should not be relied upon. Since the use of short-duration stress-dose steroids is safe, it is advisable to over-suspect and treat, rather than miss this diagnosis.28 If the patient has
hypotension that is refractory to fluids
and pressors, a random cortisol level surgery, sepsis or hypotension, will have random cortisol levels > 20 mcg/dL. If the random level is < 20, steroids should be continued, as adrenal failure is likely.
| ||||||||||||||||||||||||||||||||
| ||||||||||||||||||||||||||||||||
Titrated to achieve
MAP³
60-70 mm Hg Even in the absence
of adrenal failure, a significant
improvement in hemodynamics This
practice is in strong contrast to previous use
of high-dosage corticosteroid. (two grams Hemodynamic Monitoring
CLINICAL
MANIFESTATIONS Hypothermia Pulmonary
Manifestations The metabolic
acidosis and increased minute ventilation
of sepsis place a very high demand It
is crucial to
review the patient or agent's preferences
for aggressive treatment and Mechanical
Ventilation If the pCO2
on arterial blood gas measurements
is higher than the calculated
| ||||||||||||||||||||||||||||||||
Expected pCO2:
a. [(Measured HCO3
x 1.5)+8] ± 2 OR b. ³ the last 2 digits of the pH Example of ABG showing respiratory muscle fatigue pH = 7.20, measured pCO2= 28, measured serum HCO3 = 8 [8 x 1.5]+8 ± 2 = 20 ± 2 Thus, the expected pCO 2should be from 18-22. Since the measured pCO2 = 28, this patient has both respiratory acidosis and metabolic acidosis. *These formulae do not apply to patients with chronic CO, retention. | ||||||||||||||||||||||||||||||||
Multiple Organ
Dysfunction (MOD) CONTACT INFORMATION Permanente computer
network. dysfunction (see Table 6 for criteria). The etiology of MOD is very complex and not yet clearly understood. A patient's prognosis is related to age and the number of organ systems involved. The average risk of death increases by 20 percent with the failure of each additional organ system.22,16 Several studies have shown4,9,21,32 that mortality was 30-40% with single organ dysfunction, greater than 60% with two dysfunctional systems and more than 90% in patients with three or more dysfunctional systems. DISCHARGE EVALUATION The
following should
be evident before patient discharge
is considered: | ||||||||||||||||||||||||||||||||
| ||||||||||||||||||||||||||||||||
Modified
from Rangel-Frausto32,
Hebert, 16
andKollef23 REFERENCES
2.
Annane D, Jars-Guincestre
MC, Paraire F. Incidence
of bilateral hemorrhagic necrotic adrenals
in patients with septic shock: a septic shock. Chest 1991:99:956-62. 4. Beal AL, Cerra FB. Multiple organ failure syndrome in the 1990s: systemic inflammatory response and organ dysfunction. JAMA 1994; 271:226-33. 5. Bollaert PE, Charpentier C, Levy B, et al. Reversal of late septic shock with supra- physiologic doses of hydrocortisone. Crit Care Med 1998:26:645-50. 6. Bone RC. .Let's agree on terminology: definitions of sepsis. Crit Care Med 1991;19:973-6. 7. Bone RC, Fisher CJJr, Clemmer TP, et al. A controlled clinical trial of high-dose methyl- prednisolone in the treatment of severe sepsis and septic shock. NEnglJMed 1987:317: 653-8. 8. Briegel J, Forst H, Haller M, et al. Stress doses of hydrocortisone reverse hyperdynamic septic shock: a prospective, randomized, double- blind, single-center study. Crit Care Med 1999;27:723-32. 9. Brun-Buisson C, Doyon F, CarletJ, et al. Incidence, risk factors, and outcome of severe sepsis and septic shock in adults: a multicenter prospective study in intensive care units. French ICU Group for Severe Sepsis. JAMA 1995:274:968-74. 10. Choi PT-L, Yip G, Quinonez LG, et al. Crystalloids vs. colloids in fluid resuscitation: a systematic review. Crit Care Med 1999;27: 200-10. Clemmer TP, Fisher CJJr, Bone RC, et al. Hypothermia in the sepsis syndrome andclinical outcome. TheMethylprednisolone Severe Sepsis Study Group. Crit Care Med 1992;20:1395-401. Connors AFJr, Speroff T, Dawson NV, et al. The effectiveness of right heart catheterization in the initial care of critically ill patients. SUPPORT Investigators. AMA 1996:279: 889-97. Desjars P, Pinaud M, Potel G, et al. A reappraisal of norepinephrine therapy in human septic shock. Crit Care Med 1987;15:134-7. Ernest D, Belzberg AS, Dodek PM. Distribution of normal saline and 5% albumin infusions in septic patients. Crit Care Med 1999:27:46-50. Hayes MA, Timmins AC, Yau EH, et al. Oxygen transport patterns in patients with sepsis syndrome or septic shock: influence of treatment and relationship to outcome. Crit Care Med 1997:25:926-36. Hebert PC, Drummond AJ, Singer J, et al. A simple multiple system organ failure scoring system predicts mortality of patients who have sepsis syndrome. Chest 1993; 104:230-5. Hebert PC, Wells G, Blajchman MA, et al. A multicenter, randomized, controlled clinical trial of transfusion requirements in critical care. Transfusion Requirements in Critical Care Investigators, Canadian Critical Care Trials Group. NEnglJMed 1999;340:409-17. HopkinsJA, Shoemaker WC, Chang PC, et al. Clinical trial of an emergency resuscitation algorithm. Crit Care Med 1983:11:621-9. Hussain SN, Sirnkus G, Roussos C. Respiratory muscle fatigue: a cause of ventilatory failure in septic shock. JApplPhysiol 1985; 58:2033-40. Kiiski R, TakalaJ. Hypermetabolism and efficiency of CO2, removal in acute respiratory failure. Chest 1994;105:1198-203. Knaus WA, Sun X, Nystrom 0, et al. Evaluation of definitions for sepsis. Chest 1992:101: 1656-62. Knaus WA, Wagner DP. Multiple systems organ failure: epidemiology and prognosis. Crit Care lin 1989:5:221-32.Kollef MH, Eisenberg PR. The relationship of the ACCP/SCCM Consensus Conference classification of sepsis to mortality and multi-organ dysfunction among medical ICU patients.J Intensive CareMed 1996:11: 326-32. Kreger BE, Craven DE, McCabe WR. Gram-negative bacteremia. IV. Re-evaluation of clinical features and treatment in 612 patients. AmJMed 980;68:344-55. Meadows D, Edwards JD, Wilkins RG, et al. Reversal of intractable septic shock with norepinephrine therapy. Crit CareMed 1988:16:663-6. Mimoz 0, Rauss A, Rekik N, et al. Pulmonary artery catheterization in critically ill patients: a prospective analysis of outcome changes associated with catheter-prompted changes in therapy. Crit CareMed 1994:22:573-9. Narins RG, Emmett M. Simple and mixed acid-base disorders: a practical approach. Medicine (Baltimore) 1980;59:l6l-87. Oelkers W. Adrenal insufficiency. NEnglJMed 1996:335:1206-12. The Pulmonary Artery Catheter Consensus Conference; consensus statement. Crit Care Med 997;25:910-25. Quartin AA, Schein RM, Kelt DH, et al. Magnitude and duration of the effect of sepsis on survival. Department of Veterans Affairs Systemic Sepsis Cooperative Studies Group. JAMA 1997:277:1058-63. Rackow EC, FalkJL, Fein IA, et al. Fluid resuscitation in circulatory shock: a comparison of the cardiorespiratory effects of albumin, hetastarch, and saline solutions in patients with hypovolemic and septic shock. Crsit are Md 193:11:839-50. Rangel-Frausto MS, Pittet D, Costigan M, et al. The natural history of the systemic inflammatory response syndrome (SIRS): a prospective sMy.JAMA 1995:273:117-23. SchaerGL,FinkMP,ParrilloJE. Norepinephrine alone versus norepinephrine plus low-dose dopamine: enhanced renalblood flow with combination pressor therapy. Grit are Md 195:13:492-6. Schierhout G, Roberts 1. Fluid resuscitation with colloid or crystalloid solutions in critically ill patients: a systematic review of randomised trials. MJ 1998:316:961-4. 35. Shoemaker WC, Appel PL, Kram HB, et al. Hemodynamic and oxygen transport monitoring to titrate therapy in septic shock. NewHoriz 1993:1:145-59. 36. Soni A, Pepper GM,WyrwinskiPM, etal. Adrenal insufficiency occurring during septic shock: incidence, outcome, and relationship to peripheral cytokine levels. ArnJMed 1995:98:266-71. 37. The Veterans Administration Systemic Sepsis Cooperative Study Group. Effect of high-dose glucocorticoid therapy on mortality in patients with clinical signs of systemic sepsis. NEnglJMed 1987:317:659-65. ACKNOWLEDGMENTS Clinical Leader Nazir Habib, MD; Intensivist, Vallejo Work Group Doug Chartier, MD; Chief of Utilization Management, Oakland Jay Colas, RN; Assistant Manager, Emergency Department, Walnut Creek Janice
Manjuck, MD;
Intensivist, San Francisco Bill
Plautz, MD; Emergency
Medicine, South
San Francisco Terry
Segeike, RN; Intensive
Care Unit, Vallejo Kurt
Swartout, MD; Hospital
Based Specialist, Sacramento
Project Management
Laura Finkler, MPH;
TPMG Department of Quality
& Utilization Kathleen
Martin; TPMG
Department of Quality
& Utilization Reviewers
Reviewers who made significant
contributions to the
text: Tricia
Bell, MD; Intensive
Care/Internal Medicine, San
Rafael Eric
Koscove, MD; Chief of
Emergency Medicine, Santa
Clara Chinh Le,
MD; Chair, Chiefs of
Infectious Disease, Santa
Rosa Lou Lehman,
MD, Co-Chair,
Regional Hospital Based
Specialists and Chair,
Regional Chiefs of Critical
Care, San Francisco Lisa
Hammer Reig, PharmD,
Divisional Drug Information/Professional
Services, Southern California
David J. Witt, MD; Chief of
Infectious Disease, South
San Francisco Thanks
to the following
reviewers for their careful
reading and comments: Drew Baker, MD; Chief of Emergency Medicine, Hayward Roger Baxter, MD; Chief of Infectious Disease, OaklandGeorge Bulloch, MD; Chief of Emergency Medicine, Redwood City James Cadden, MD; Chief of Emergency Medicine, Santa Rosa David Campen, MD; Chair, TPMG Formulary Subcommittee, Santa Clara Uli Chettipally, MD; Chief of Emergency Medicine, South San Francisco Michael Coppolino, MD; Critical Care, San Francisco Paul Feigenbaum, MD; Chief of Medicine, San Francisco John Fitzgibbon, MD; Chief of Utilization Management, Sacramento Maurice Franco, MD; Critical Care, Hayward Lauren Freeman, MD; Hospital Based Specialist, South Sacramento Dale Grahn, MD; Chief of Utilization Management, Diablo Service Area Chris Gronbeck, MD; Critical Care, San Rafael Jianfei Hu, MD; Hospital Based Specialist, Walnut Creek Daniel Klein, MD; Chief of Infectious Disease, Hayward Aye Koko, MD; Hospital Based Specialist, Fresno David Langkammer, MD; Associate Chief of Medicine, Diablo Service Area Todd Lasman, MD; Pulmonology, Redwood City Eleanor Levin, MD; Chair, Chiefs of Cardiology, Santa Clara Hsiu-Wei Lin, MD; Intensive Care, Walnut Creek Timothy Lockyer, MD; Hospital Based Specialist, Santa Teresa Jeff Lou, MD; Hospital Based Specialist, Santa Teresa Gilbert Mandell, MD; Chief, Pharmacy and Therapeutics and Chief, Hematology/Oncology, South Sacramento Susan Marantz, MD; Chief of Utilization Management and Chief of Critical Care, Santa Rosa Suzanne Mierendorf, MD; Hospital Based Specialist, Santa Clara Robert Mooney, MD; Chief of Emergency Medicine, Walnut Creek Richard K. Morgan, MD; Internal Medicine, Kaiser Stanislaus Bien Nguyen, MD; Chief of Patient Education and Hospital Based Specialist, Santa Teresa Tom Padgett, MD; Chief of Emergency Medicine, San Francisco Alien Parsley, MD; Chief of Outpatient Pharmacy and Therapeutics, Walnut Creek Robert Riesenfeld, MD; Hospital Based Specialist, Walnut Creek Anne Rogers, MD; Critical Care, Walnut Creek Valeric Scheider MD Critical Care Walnut Creek Christina Shih, MD; Assistant Physician-in-Chief, San Francisco and Chair, Regional Chiefs of Emergency Medicine Darshan Sonik, MD; Critical Care, Sacramento Stanley}. Tillinghast, MD; Hospital Based Specialist, South Sacramento Abdul Wali, MD; Chief of Hospital Based Services, Diablo Service Area Joseph Wong, MD; Internal Medicine, Stockton Patricia Z. Wong, RN; Manager, Emergency Department, Fresno J. Susan Yee, RN; Manager, Berkeley Regional Laboratory Editing Kaiser Foundation Research Institute Medical Editing Department Linda Bine; TPMG Communications Department Design & Production GailHolan, CurveyGraphic Design CONTACT INFORMATION Kaiser Permanente Northern California TPMG Department of Quality and Utilization 1800 Harrison Street, 4th floor Oakland, CA 94612 510-987-2950 or tie-line 8-427-2950 To obtain more information about KPNC Clinical Practice Guidelines and Statements, printed copies or permission to reproduce any portion, please contact the TPMG Dept. of Quality & Utilization, or send an e-mail message to clil.EiC.l~l.gzlidelilzes@kp. org KPNC Clinical Practice Guidelines and Statements can be viewed on-line on the Kaiser Permanente Northern California intranet website at htt{)://clinical 'library, ca. kp. org CME Credit: ContinumH Education Credit for physicians and nurses is available for review ol Statement. The CME Pro- and Post-Tests are available on-line at the above website address. This website is accessible only from the Kaiser Permanente computer network. The Permanente Medical Group (TPMG) clinical practice guidelines and statements have been developed to assist clinicians by providing an analytical framework for the evaluation and treatment of selected common problems encountered by patients. These guidelines and statements are not intended to establish a protocol for all patients with a particular condition. While they provide one approach to evaluating a problem, clinical conditions may vary significantly from individual to individual. Therefore, the clinician must exercise independent judgment and make decisions based upon the situation presented. While great care has been taken to assure the accuracy of the information presented, the reader is advised that TPMG cannot be responsible for continued currency of the information for any errors or omissions in this statement, or for any consequences arising from their use. Copyripht 1999 The Permanente Medical Group, Inc. |