Respiratory Rate :
Respiratory Rate :
37.8 º C
38.2 º CSEPT. 15, 2009 (11:00am)SEPT. 15, 2009 (12:00nn)
Pulse Rate :
Pulse Rate :
Blood Pressure :
Blood Pressure :
Respiratory Rate :
Respiratory Rate :
1. NaCl TabTID
8:00am; 2pmNot administered
2. N – Acetylcystein 600mgq6h
8:00am; 2pm; 8pm; 2amNot administered
3. Clindamycin 30mg Cap NGTBID
12:00 nnDone at 12:10 nn
NURSING CARE PLANASSESSMENTDIAGNOSISINFERENCEPLANNINGINTERVENTIONRATIONALEEVALUATIONSubjective Data:
“Lagi syang nilalagnat. Kapag hinihipo mo syamararamdamanmong mainit talaga katawannya.”
He alwaysgets sick. Whenyou touch himyou will really feel that histemperature isincreased.
), asverbalized by thepatient’sdaughter.Risk for infection r/tcompromisedimmunesystem.Sepsis is aclinical term todescribesymptomaticbacteremia, withor without organdysfunction.Sustainedbacteremia, incontrast totransientbacteremia, mayresult to asustained febrileresponse thatmay beassociated withorganAfter 8 hours of nursinginterventions,will achievetimely healingand free fromfurther infections.
Provideisolation andmonitor visitors asindicated;
Wash handsbefore andafter eachcare activity;
Body substanceisolation shouldbe used for allinfectiouspatients.Reserveisolation/restriction maybe needed toprotect theimmunosuppressed patient.
Reduces risks of crosscontaminationbecause glovesAfter 8 hours of nursinginterventions, thepatient was able toachieve timelyhealing and freefrom further infections.
S. S., a 65-year-old man who lived alone, was cutting vegetables and accidentally cut his finger. He casually washed the bleeding site, put a Band-Aid on the deep cut and continued cooking. Two days later, he removed the Band-Aid but the cut appeared open and oozing. Later that day, he replaced the Band-Aid with a fresh one. A few days later he noticed that his finger had become very red and swollen and he could see a small amount of pus at the site. He had also developed a low grade fever and malaise. The following day he went to see his physician who cleaned the cut and gave him a broad-spectrum antibiotic. However, S. S did not follow the dosing instructions and stopped taking the antibiotic when he felt better after 3 days. A few days later, he developed a high fever, chills, severe fatigue, tachycardia, and growing mental confusion. A relative visiting S. S called 911 and he was taken to the local emergency room. On admission, his temperature was 40 �C, his blood pressure was 88/60 mm Hg, his respiratory rate was 22, his pulse was 111. Blood chemistry revealed a BUN of 55 mg/dl and creatinine of 1.8 mg/dl. Blood cultures grew out Gram-negative rods that were identified as E. coli. He was diagnosed with severe septic shock as a result of inadequate treatment of a wound infection.Laboratory values on admission:
S. S was transfused, given fluids, appropriate antibiotics, and PEEP assisted ventilation. It was considered that if he continued to deteriorate, with an increased risk of death as indicated by an acute physiology and chronic health evaluation score (in critically ill patients) APACHE II score greater than or equal to 25 or dysfunction of two or more organs, he would be given activated protein C (Drotrecogrin Alfa), recently reported to decrease mortality and to ameliorate organ dysfunction in patients with severe sepsis.
Septic shock results from a complex progression of disease that is described as severe infection and moves from a systemic inflammatory response syndrome (SIRS) to sepsis and severe sepsis to septic shock. Left untreated, septic shock can lead to death, with or without multiple organ dysfunction syndrome (MODS).
It is particularly important to recognize the problem as early as possible and treat accordingly, especially since mortality rates for sepsis (16 to 20 percent) and septic shock (20 to 50 percent) vary based on the type of infectious organism, underlying illness or complication, timing and the kind of antimicrobial therapy, and degree of system failure present. Thus, it is critical to understand the pathophysiology, symptoms, assessment techniques, and available treatment options.
Severe sepsis/septic shock is a syndrome that is initiated by the host�s innate immune response. Under normal conditions, bacteria commonly enter the bloodstream but are rapidly removed by leukocytes of the innate immune system (monocytes/macrophages and neutrophils) and no symptoms develop. Similarly, this pathway usually resolves small infections of the skin, etc.. Sometimes, however, due to a variety of conditions including a moderate to severe local infection, gum disease, pneumonia or trauma, particularly to the intestine, possibly coupled with inadequate antibiotic therapy, there are too many bacteria to be removed easily by the host, and large numbers of bacteria enter the bloodstream. An infection that is widespread throughout the bloodstream is called sepsis (or septicemia) and can lead to severe symptoms and a life-threatening condition called septic shock.
Etiology Of Sepsis
Sepsis occurs when pathogenic microorganisms cross host barriers and overwhelm defenses. Gram-negative bacteria - such as Escherichia coli, Klebsiella pneumoniae, Pseudomonas aeruginosa, and Neisseria meningitides - are key pathogens. Other causes include Gram-positive organisms such as Staphylococcus aureus, coagulase-negativeStaphylococcus, Streptococcus pneumoniae, Streptococcus pyogenes, and Enterococcus. Rickettsiae, viruses, fungi and polymicrobial sepsis have also been noted as causative agents. In neonates, sepsis is most likely caused by group B Streptococci, E. coli bearing a pathogenic K1 capsule, Klebsiella sp. and Enterobacter sp.
According to the American College of Chest Physicians (ACCP) and the Society of Critical Care Medicine, several physiological effects occur as a result of the systemic inflammatory response syndrome (SIRS). Two or more of the following criteria must be present for a SIRS diagnosis: Body temperature can increase above 38C or drop below 36C; individuals might experience tachycardia (over 90 bpm) or tachypnea (more than 20 breaths per minute or PaCO2 less than 32 mm Hg); and white blood cell counts may be greater than 12,000/mm3, less than 4000/mm3, or over 10 percent band cells. It is important to note that sepsis/septic shock can occur without the identification of bacteria in the blood.
As the disease progresses to severe sepsis, patients generally experience both earlier symptoms, along with organ dysfunction, hypoperfusion, or hypotension. Confusion or altered mental states, elevated plasma lactate levels, and oliguria (decreased urine output of less than 30 ml) are just some examples of the perfusion abnormalities observed.
|Table 1: Definitions of Sepsis-Related Terms (adapted from the Society for Critical Care Medicine)|
From: Schrier and Wang, NEJM 2004, 35:159-169.
Russell, J.A. Management of Sepsis. 2006. NEJM. 355:1699-1713.
Bone, R. C., C. L. Sprung, and W. J. Sibbald. 1992. Definitions for sepsis and organ failure. Crit Care Med
Members of the American College of Chest Physicians/Society of Critical Care Medicine Consensus
Conference Committee.1992. Definitions for sepsis and organ failure and guidelines for the use of
innovative therapies in sepsis. Crit Care Med 20: 864�874
Levy, M. M., M. P. Fink, J. C. Marshall, E. Abraham, D. Angus, D. Cook, J. Cohen, S. M. Opal, J. L. Vincent, and G. Ramsay. 2003. 2001 SCCM/ESICM/ACCP/ATS/SIS International Sepsis Definitions Conference. Intensive Care Med 29:530-538.
Hotchkiss, R. S., and I. E. Karl. 2003. The pathophysiology and treatment of sepsis. N Engl J Med
Janeaway JA, Travers P, Walport M and M.J. Shlomchik (eds). Immunobiology, 6th ed. Garland Science, NY 2005.
Internet Links - Microbiology:
QUESTIONS: The innate immune response to bacteria is initially driven by the interaction of bacteria and/or their products with innate immune cells. Severe sepsis/septic shock can result from an early, overactive innate immune response following bacterial infection resulting in overproduction of inflammatory mediators that lead to a cascade of events, potentially ending in death, often within only a few days.
1. What cells are the major components of the innate immune response and what is their primary function?
2. Describe how endotoxin (LPS) from Gram-negative bacteria activates cells of the innate immune system?
2a.) What products are produced by this activation?
2b.) Which of these products contribute to the cascade of events leading to further deterioration of the patient?
3. What is chemotaxis?
3a.) How do neutrophils get from the blood to sites of infection? What molecules are involved in transmigration (diapedesis) across the endothelium?
4. Complement plays an important role in innate immunity. What are three major functions of complement in innate immunity and describe them.
5. What is phagocytosis? Describe in detail the events leading to killing of bacteria by phagocytosis.
6. What did S. S. do wrong?