- Email: [email protected]
Inflammation II: Sepsis
PATHO CORNER
Inflammation II: Sepsis Kim A. Noble, MSN, RN, CPAN IT IS 15:30 ON A FRIDAY afternoon. Dr. Bill, the anesthesiologist who is covering the weekend, walks into the PACU to ask who is working late. Friday evenings are notorious for cases added to the schedule, so you slowly identify yourself as the late person. Dr. Bill tells you that he just saw a very sick 88-year-old patient in the emergency room (ER) who will be coming to the OR as soon as a room is prepared. He tells you she has free air under the diaphragm on x-ray and is quite unstable with severe hypotension and shock. You flash your coworker a look of anxiety and begin to make mental notes of what you need to do to get ready to care for this patient. It is now 18:50 and you just received a call that the sick patient from the ER is coming into the PACU in 30 minutes. There are currently 2 staff nurses in the PACU caring for 1 stable orthopedic patient waiting for a floor bed and 2 patients waiting to go to Phase II. You manage to get all 3 patients discharged from PACU before Sick Sally arrives. Sally is an 88-year-old patient who arrives in PACU with a flurry of activity. You receive the following report: Sally has a history of 3 days of abdominal pain, which according to her daughter was not severe enough to seek medical treatment until today. In the last 24 hours, her pain was accompanied with fever and severe vomiting. Sally has been remarkably healthy, with a medical history of coronary artery disease and stable COPD treated with longstanding steroids and bronchodilators. Sally is 5=2⬙ tall and is reported to weigh 112 pounds. Shortly after arriving in the ED, Sally was found to have a perforated diverticulum on CT scan and was severely hypotensive and confused. She was taken to the OR and after a rapid Journal of PeriAnesthesia Nursing, Vol 20, No 2 (April), 2005: pp 135-140
sequence induction with oxygen, nitrous oxide, 1 mg of midazolam, and succinylcholine, she had a resection of a perforation of the sigmoid colon. She was found to have a large amount of bowel contents in the abdominal cavity requiring copious irrigation and the insertion of multiple drains. The perforation was resected, and a temporary colostomy and end-to-end anastomosis was performed. The surgeon noted a great deal of tissue friability and oozing from the abdominal wound. Sally was not reversed at the end of the case, and the plan is to mechanically ventilate her until she is more hemodynamically stable. During the procedure, Sally remained severely hypotensive despite the administration of 6,500 mL of 0.9% normal saline solution. She was reported to have an estimated blood loss of 2,200 and was given 3 units of packed cells. She is currently receiving 6 g/kg of intropin by pump and has an arterial line in her right radial artery that correlates well to cuff pressures. She has an external jugular introducer with pulmonary artery catheter, as well as two large bore peripheral intravenous lines. You admit Sally to the PACU and begin her care. Your admission assessment notes the following: no neurological response, clear, coarse breath sounds bilaterally via an oral #6.5 endotracheal tube. Her ventilator settings from anesthesia include a tidal volume of 550, rate of 14 breaths
Kim A. Noble, MSN, RN, CPAN, is an assistant professor at Temple University, Philadelphia, PA. Address correspondences to Kim A. Noble, MSN, RN, CPAN, Temple University, CHP Jones Hall #415, 3307 N Broad St, Philadelphia, PA 19140; e-mail address: [email protected]. © 2005 by American Society of PeriAnesthesia Nurses. 1089-9472/05/2002-0010$30.00/0 doi:10.1016/j.jopan.2005.01.006 135
136
per minute, and 100% FiO2. Sally has a midline abdominal dressing that is dry, a left-sided sump drain attached to low continuous wall suction, and 2 decompressed, right-sided bulb suction drains. She has a bagged left-sided colostomy that is nonfunctional at present. Sally has a nasogastric tube that you connect to continuous, low suction after checking tube placement. There is scant blood drainage obtained. She has a urinary catheter that was noted to have drained 50 mL on insertion in the OR and has 30 mL total drainage for the 90-minute operative case. There is no urine in the tubing at present. You note mottled extremities and no palpable pulses below her femoral arteries bilaterally. All invasive lines are noted to be patent, and the following admission data are obtained: VS: BP 79/30 (a-line); HR 146; T 101.9°F (Tympanic); PAP 16/2 with a pulmonary capillary wedge pressure (PCWP) of 3 mm Hg. Your coworker sends a full set of laboratory work for analysis. You know Sally is gravely ill and suspect systemic inflammatory response syndrome (SIRS) after gram-negative septicemia. The following laboratory results are obtained: arterial blood gas: pH 7.21, PCO2 22, PO2 51, HCO3 12, O2 Sat. 88%, Hgb 7.4, Hct 22; bleeding time ⬎ 7 minutes, platelet count of 27,000; fibrin split products ⬎ 300 g/dL; activated partial thromboplastin time (aPTT) ⬎ 120 seconds, prothrombin time (PT) ⬎ 60 seconds, INR (international normalized ratio) ⬎ 4.8, and a plasma fibrinogen 12 mg/dL. In the February 2005 issue of JOPAN, inflammation was briefly described in a case study of a patient with appendicitis. Sick Sally’s illness represents the same protective mechanism amplified because of a systemic response. SIRS is first to be discussed in terms of its pathophysiology and systemic consequences, and then the implications for Phase I PACU care will be discussed.
The Inflammatory Response Gone Astray The inflammatory response couples cellular activity with that of a chemical messenger system
KIM A. NOBLE
to announce the presence and location of damaged tissue or foreign matter, organize the response needed to destroy and remove the invading organisms and damaged tissue, and provide a support structure for healing and the restoration of normal functioning.1 It is an immediate and nonspecific response, meaning as soon as a cell is identified as foreign or injured, an inflammatory response begins and remains in place through the process of clean-up. In Sick Sally’s case, a systemic inflammatory response has been initiated in response to a gram negative septicemia, leading to the amplification of a normally protective and controlled response to a critical level. SIRS is frequently encountered in surgical patients, with approximately 80% of surgical patients in critical care units suffering from this derangement in an inflammatory response.2 According to McCance and Huether,1 “septicemia is the 13th most common cause of death in the US, and the leading cause of death in intensive care units. . .with a mortality rate of 20% to 95%.” SIRS is usually called sepsis when the presence of microorganisms are detected in the bloodstream. The inflammatory response is highly effective on a local level, but when it becomes active on a systemwide basis, fatal consequences may occur. Gram-negative bacteria are normally found in the large intestine and are harmless as long as contained within the lumen of the gastrointestinal tract. When the integrity of the intestinal wall is lost, the gram-negative organisms spill into the abdominal cavity and may make their way into the bloodstream of a patient, causing bacteremia and beginning the inflammatory cascade of SIRS. In addition to releasing exotoxins, irritating proteins released from both gram-positive and gram-negative bacteria during cell growth,1 gram-negative bacteria also contain endotoxins, a fat-based component of their cell wall. Endotoxins are released upon cellular lysis, further amplifying the tissue injury and inflammatory cascade.1 Endotoxins and exotox-
INFLAMMATION II
137
ins directly damage the endothelial cells that form the lining of blood vessels systemwide, causing the release of inflammatory and prothrombotic mediators, the activation of white blood cells (WBC), and the stimulation of the compliment, kinin, and clotting systems.1
free nerve endings and causes pain. Although all 3 systems work through different mediators and mechanisms, all effectively amplify the inflammatory response. In septicemia, each response is an additional layer that may have catastrophic consequences.
The compliment system is a group of plasma proteins that, when activated, each links the next, creating a cascade that ends with several of the final activated proteins able to directly destroy foreign matter. In this way, the compliment system serves as a bridge between the inflammation and immune responses and once fully activated, teams up with the immune system. The plasma proteins involved in this response are labeled C1 through C5-9 and each is linked due to enzymatic action.1 The end result of compliment activation is the stimulation of WBC activity, secretion of inflammatory mediators, and mast cell degranulation, which increases vascular permeability.
In gram-negative septicemia, septic shock develops when vascular permeability and large fluid losses lead to the development of hypoperfusion from profound hypotension. The reduction in vascular resistance and hypotension decreases tissue perfusion and robs the supply of oxygen and nutrients to the tissues, triggering a switch from aerobic metabolism to anaerobic metabolism and the production of lactic acid. Systemwide, this leads to a state of metabolic acidosis. When coupled with the serum presence of multiple inflammatory mediators, there is a direct myocardial depressive effect, decreasing the heart’s ability to respond to the sympathetic nervous system’s call for a compensatory increase in heart rate and contractility. Finally, the alveolocapillary membranes of the lungs are exposed to large numbers of inflammatory mediators, having the entire cardiac output pass through this capillary system with each cardiac cycle. The increased permeability directly decreases the exchange of gasses across the alveolocapillary membrane, effectively filling the alveoli with plasma and cells and deactivating surfactant. Frequently, the lungs are the first organ system to fail, necessitating mechanical ventilation with high concentrations of oxygen and the use of positive end expiratory pressure (PEEP) to improve gas exchange.
Similar to the compliment system is the clotting cascade; it also is a system of plasma proteins and cofactors found in the serum. Once activated, it leads to the cascading activation of each link in series, ending in the formation of the fibrin meshwork associated with clotting. This cascade also leads to the release of proinflammatory factors, which further amplifies the response. As with the compliment system, there are protective antifactors found within the cascade, which function in the control and reduction of the cascade effect. In sepsis, the systemic response magnifies at such a rapid rate, both the compliment and clotting system antifactors are ineffective.1 The final backup system to become involved is the kinin system, working primarily through the mediator bradykinin, causing the continuation of vascular permeability, leading to the loss of plasma and cells from the vascular space into the surrounding tissues. In addition, bradykinin activates additional WBCs and causes the secretion of prostaglandins that directly irritate
The activation of the clotting cascade leads to the development of systemic microclotting, called disseminated intravascular coagulation (DIC), which depletes the clotting factors and platelets, leading to oozing and hemorrhage that is particularly problematic in surgical patients. This is clearly seen in several of Sally’s postoperative laboratory work results. The prothrombin time, INR, and activated partial thromboplastin time are used as indicators of the time
KIM A. NOBLE
138
required for a clot and fibrin to form. These 2 tests measure the activity of the clotting cascade in 2 different areas. To have both severely prolonged, as indicated by these results, indicates a widespread activation and depletion of clotting factors, as seen in DIC. Sally’s decreased platelet count would support the diagnosis of DIC, because it would indicate widespread platelet aggregation. The normal platelet count is 150,000 to 400,000, so Sally’s platelet count of 27,000 indicates a severe depletion, which will contribute to bleeding. Sally’s decreased hemoglobin (7.4) and 2,200-mL blood loss would seem excessive for the procedure and would confirm a coagulation disorder. Finally, an elevation in fibrin split products (also called fibrin degradation products or fibrin breakdown products) indicates the activity of the antifactors or the “brakes” of the clotting cascade, in a normal response, leading to the degradation of fibrin. An elevation in fibrin split products indicates excessive clotting and breakdown of clots and is diagnostic for the development of DIC.3 The presence of bacteria and inflammatory mediators in the serum are detected by the hypothalamus, causing an elevation of temperature, and a hypermetabolic state. This further taxes a system that has reached the maximum of functioning in an attempt to compensate for the hypovolemia and decreased vascular resistance. This is further complicated by the presence of an aged or suppressed immune system or preexisting medical disease.
Implications for the PACU Patient By applying the pathophysiological basis for SIRS to the patient you are recovering in the Phase I PACU, there are several direct implications for patient care as follows.
alveolocapillary membrane, requiring the use of mechanical ventilation. Condition permitting, Sally must be adequately paralyzed and sedated to allow for ease of ventilation. An ongoing assessment of the patient’s response to these agents, as well as lung sounds and ETT placement must be conducted. As ventilator settings are implemented, additional ABGs may be ordered. These results must be obtained and reported in a timely fashion and any new orders implemented. Frequently, the hypoxia associated with this disorder is refractory to increases in inspired oxygen, but the addition of PEEP keeps the alveoli open and improves the diffusion of gasses while not requiring the use of toxic oxygen concentrations. PEEP may have the negative effect of decreasing the cardiac output by reducing the venous return to the heart; therefore, the effectiveness of PEEP must be evaluated by using continuous hemodynamic monitoring. In addition, the correction of Sally’s reduced hemoglobin and hematocrit must be included to ensure adequate oxygen delivery to her tissues. Alteration in Fluid Balance
Sick Sally is in the early stages of septic shock and, therefore, has severe increases in vascular permeability leading to losses of large amounts of fluid from the vascular space into the interstitial spaces. This leads to the development of refractory hypotension despite aggressive hydration. Frequent monitoring of heart rate and blood pressure, pulmonary artery waveform tracing, as well as cardiac output and pulmonary capillary wedge pressures (PCWP) are needed. Sally’s admission PAP reading of 16/2 and PCWP of 3 mm Hg indicate a significant need of fluid administration. Urinary output must be monitored and reported and may be used as additional indices of fluid status.
Alteration in Gas Exchange
As with any other PACU patient, the maintenance of adequate gas exchange is the first nursing priority. Sick Sally’s low PO2 and saturation on her admission ABG indicate a significant barrier to normal gas exchange across the
Alteration in Cardiovascular Functioning
Sally’s history of CAD usually indicates a decrease in the lumen of the coronary vessels and the delivery of oxygen to myocardial tissue, adding additional risk for the development of
INFLAMMATION II
cardiac consequences in her hypermetabolic state. Her heart rate of 147 must be lowered because increases in heart rate lead to increased myocardial oxygen requirements, as well as a decrease in the time of ventricular filling and nutrient delivery to the myocardium. Improving Sally’s fluid status with the administration of blood products and crystalloids will ease the workload of the heart, as will the treatment with pharmacologic agents used to control the heart rate. These agents will require very careful monitoring because of their vasodilatory effects, applying further strain on the heart muscle. Serial electrocardiograms and cardiac enzyme measurements are needed to monitor Sally’s cardiac status. Pharmacologic agents may be used to protect and maintain an adequate cardiac blood supply. In addition to intropin, a chemical precursor of norepinephrine used to increase cardiac contractility and dose-related vasoconstriction of peripheral and renal arterioles, other pharmacologic agents may be used to augment preload, contractility, and afterload. These agents must be carefully titrated to hemodynamic effect. An additional risk for the delivery of oxygen to Sally’s myocardium is her low hemoglobin, which requires rapid and adequate correction with the administration of whole blood. With the administration of large quantities of banked blood products, there is the need to monitor Sally’s serum calcium, because the preservatives used in some blood preparations may deplete serum calcium, adding strain on the contractility of the heart.
139
will need the careful monitoring of all drainage tubes for bleeding, and the amount must be measured and reported. Alteration in Stress Response
Sally has a history of steroid-dependent COPD, and she will exhibit adrenal insufficiency when faced with the stressful situation of emergent surgery and critical illness. She will require the administration of stress doses of steroids and monitoring of their effect(s). The functioning of her immune system may be affected by the chronic use of exogenous steroids, as well as the condition of her connective tissue and her ability to heal a surgical wound. Sally’s blood sugar may also be elevated and require frequent monitoring and sliding scale insulin administration. Alteration in Temperature Regulation
Sally’s immediate postoperative fever is very troublesome because she had several factors that should contribute to a decrease in core body temperature, such as the cooling effect of the OR environment and the administration of cool blood products and intravenous and irrigation solutions. Sally has also been receiving long-standing steroid administration, leading to a decreased febrile response. Her elevation in temperature contributes to her hypermetabolic state, requiring an increase in oxygen consumption. Normothermia should be maintained through the administration of antipyretics and the use of a cooling blanket as needed. Potential for Septicemia
Potential for Bleeding
Sally’s admission laboratory data indicate the development of disseminated intravascular coagulation (DIC), a disorder resulting from massive stimulation of the clotting cascade, resulting in systemic microclotting and the depletion of platelets and clotting factors. Sally had a 2,200-mL blood loss in the OR and only received approximately 1,000 mL banked blood. This coupled with her postoperative Hgb of 7.4 will require the administration of packed cells, as well as fresh frozen plasma and platelets. She
A final need of Sally is for the treatment of her underlying disorder, sepsis, leading to the development of SIRS. Culturing of blood, urine, sputum, wounds, and invasive lines are needed to isolate the causative organism and to identify specific antibiotic sensitivities. Broad spectrum antibiotics will be ordered and should be given on a routine basis.4 A deterioration of Sally’s condition should be expected with antibiotic administration because as the gram-negative bacteria lyse and die, there will be an increased release of endotoxin, further triggering inflam-
KIM A. NOBLE
140
matory mediator release. Once the microorganism sensitivities are identified, appropriate antibiotic selections may be made. Sick Sally represents a critically ill patient exhibiting an extreme response to an inflammatory trigger. Her care would require intensive Phase I management, and through the application of the pathophysiology to the disease process, a PACU nurse is better equipped to anticipate the
needs of this very challenging postanesthesia patient.
Acknowledgments The author thanks her coworkers in Phases I and II and the Anesthesia Department at Jeanes Hospital in Philadelphia, PA—a very special group of people who have served as consultants, editors, and friends.
References 1. McCance KL, Huether SE: Pathophysiology: The Biologic Basis for Disease in Adults & Children (ed 4). St. Louis, MO, Mosby, 2002 2. Urden LD, Stacy KM, Lough ME: Thelan’s Critical Care Nursing: Diagnosis and Management (ed 4). St. Louis, MO, Mosby, 2002
3. McMorrow ME, Malarkey L: Laboratory and Diagnostic Tests: A Pocket Guide. Philadelphia, PA, Saunders, 1998 4. Drain CB: PeriAnesthesia Nursing: A Critical Care Approach (ed 4). St. Louis, MO, Saunders, 2003
Inflammation II: Sepsis Kim A. Noble, MSN, RN, CPAN IT IS 15:30 ON A FRIDAY afternoon. Dr. Bill, the anesthesiologist who is covering the weekend, walks into the PACU to ask who is working late. Friday evenings are notorious for cases added to the schedule, so you slowly identify yourself as the late person. Dr. Bill tells you that he just saw a very sick 88-year-old patient in the emergency room (ER) who will be coming to the OR as soon as a room is prepared. He tells you she has free air under the diaphragm on x-ray and is quite unstable with severe hypotension and shock. You flash your coworker a look of anxiety and begin to make mental notes of what you need to do to get ready to care for this patient. It is now 18:50 and you just received a call that the sick patient from the ER is coming into the PACU in 30 minutes. There are currently 2 staff nurses in the PACU caring for 1 stable orthopedic patient waiting for a floor bed and 2 patients waiting to go to Phase II. You manage to get all 3 patients discharged from PACU before Sick Sally arrives. Sally is an 88-year-old patient who arrives in PACU with a flurry of activity. You receive the following report: Sally has a history of 3 days of abdominal pain, which according to her daughter was not severe enough to seek medical treatment until today. In the last 24 hours, her pain was accompanied with fever and severe vomiting. Sally has been remarkably healthy, with a medical history of coronary artery disease and stable COPD treated with longstanding steroids and bronchodilators. Sally is 5=2⬙ tall and is reported to weigh 112 pounds. Shortly after arriving in the ED, Sally was found to have a perforated diverticulum on CT scan and was severely hypotensive and confused. She was taken to the OR and after a rapid Journal of PeriAnesthesia Nursing, Vol 20, No 2 (April), 2005: pp 135-140
sequence induction with oxygen, nitrous oxide, 1 mg of midazolam, and succinylcholine, she had a resection of a perforation of the sigmoid colon. She was found to have a large amount of bowel contents in the abdominal cavity requiring copious irrigation and the insertion of multiple drains. The perforation was resected, and a temporary colostomy and end-to-end anastomosis was performed. The surgeon noted a great deal of tissue friability and oozing from the abdominal wound. Sally was not reversed at the end of the case, and the plan is to mechanically ventilate her until she is more hemodynamically stable. During the procedure, Sally remained severely hypotensive despite the administration of 6,500 mL of 0.9% normal saline solution. She was reported to have an estimated blood loss of 2,200 and was given 3 units of packed cells. She is currently receiving 6 g/kg of intropin by pump and has an arterial line in her right radial artery that correlates well to cuff pressures. She has an external jugular introducer with pulmonary artery catheter, as well as two large bore peripheral intravenous lines. You admit Sally to the PACU and begin her care. Your admission assessment notes the following: no neurological response, clear, coarse breath sounds bilaterally via an oral #6.5 endotracheal tube. Her ventilator settings from anesthesia include a tidal volume of 550, rate of 14 breaths
Kim A. Noble, MSN, RN, CPAN, is an assistant professor at Temple University, Philadelphia, PA. Address correspondences to Kim A. Noble, MSN, RN, CPAN, Temple University, CHP Jones Hall #415, 3307 N Broad St, Philadelphia, PA 19140; e-mail address: [email protected]. © 2005 by American Society of PeriAnesthesia Nurses. 1089-9472/05/2002-0010$30.00/0 doi:10.1016/j.jopan.2005.01.006 135
136
per minute, and 100% FiO2. Sally has a midline abdominal dressing that is dry, a left-sided sump drain attached to low continuous wall suction, and 2 decompressed, right-sided bulb suction drains. She has a bagged left-sided colostomy that is nonfunctional at present. Sally has a nasogastric tube that you connect to continuous, low suction after checking tube placement. There is scant blood drainage obtained. She has a urinary catheter that was noted to have drained 50 mL on insertion in the OR and has 30 mL total drainage for the 90-minute operative case. There is no urine in the tubing at present. You note mottled extremities and no palpable pulses below her femoral arteries bilaterally. All invasive lines are noted to be patent, and the following admission data are obtained: VS: BP 79/30 (a-line); HR 146; T 101.9°F (Tympanic); PAP 16/2 with a pulmonary capillary wedge pressure (PCWP) of 3 mm Hg. Your coworker sends a full set of laboratory work for analysis. You know Sally is gravely ill and suspect systemic inflammatory response syndrome (SIRS) after gram-negative septicemia. The following laboratory results are obtained: arterial blood gas: pH 7.21, PCO2 22, PO2 51, HCO3 12, O2 Sat. 88%, Hgb 7.4, Hct 22; bleeding time ⬎ 7 minutes, platelet count of 27,000; fibrin split products ⬎ 300 g/dL; activated partial thromboplastin time (aPTT) ⬎ 120 seconds, prothrombin time (PT) ⬎ 60 seconds, INR (international normalized ratio) ⬎ 4.8, and a plasma fibrinogen 12 mg/dL. In the February 2005 issue of JOPAN, inflammation was briefly described in a case study of a patient with appendicitis. Sick Sally’s illness represents the same protective mechanism amplified because of a systemic response. SIRS is first to be discussed in terms of its pathophysiology and systemic consequences, and then the implications for Phase I PACU care will be discussed.
The Inflammatory Response Gone Astray The inflammatory response couples cellular activity with that of a chemical messenger system
KIM A. NOBLE
to announce the presence and location of damaged tissue or foreign matter, organize the response needed to destroy and remove the invading organisms and damaged tissue, and provide a support structure for healing and the restoration of normal functioning.1 It is an immediate and nonspecific response, meaning as soon as a cell is identified as foreign or injured, an inflammatory response begins and remains in place through the process of clean-up. In Sick Sally’s case, a systemic inflammatory response has been initiated in response to a gram negative septicemia, leading to the amplification of a normally protective and controlled response to a critical level. SIRS is frequently encountered in surgical patients, with approximately 80% of surgical patients in critical care units suffering from this derangement in an inflammatory response.2 According to McCance and Huether,1 “septicemia is the 13th most common cause of death in the US, and the leading cause of death in intensive care units. . .with a mortality rate of 20% to 95%.” SIRS is usually called sepsis when the presence of microorganisms are detected in the bloodstream. The inflammatory response is highly effective on a local level, but when it becomes active on a systemwide basis, fatal consequences may occur. Gram-negative bacteria are normally found in the large intestine and are harmless as long as contained within the lumen of the gastrointestinal tract. When the integrity of the intestinal wall is lost, the gram-negative organisms spill into the abdominal cavity and may make their way into the bloodstream of a patient, causing bacteremia and beginning the inflammatory cascade of SIRS. In addition to releasing exotoxins, irritating proteins released from both gram-positive and gram-negative bacteria during cell growth,1 gram-negative bacteria also contain endotoxins, a fat-based component of their cell wall. Endotoxins are released upon cellular lysis, further amplifying the tissue injury and inflammatory cascade.1 Endotoxins and exotox-
INFLAMMATION II
137
ins directly damage the endothelial cells that form the lining of blood vessels systemwide, causing the release of inflammatory and prothrombotic mediators, the activation of white blood cells (WBC), and the stimulation of the compliment, kinin, and clotting systems.1
free nerve endings and causes pain. Although all 3 systems work through different mediators and mechanisms, all effectively amplify the inflammatory response. In septicemia, each response is an additional layer that may have catastrophic consequences.
The compliment system is a group of plasma proteins that, when activated, each links the next, creating a cascade that ends with several of the final activated proteins able to directly destroy foreign matter. In this way, the compliment system serves as a bridge between the inflammation and immune responses and once fully activated, teams up with the immune system. The plasma proteins involved in this response are labeled C1 through C5-9 and each is linked due to enzymatic action.1 The end result of compliment activation is the stimulation of WBC activity, secretion of inflammatory mediators, and mast cell degranulation, which increases vascular permeability.
In gram-negative septicemia, septic shock develops when vascular permeability and large fluid losses lead to the development of hypoperfusion from profound hypotension. The reduction in vascular resistance and hypotension decreases tissue perfusion and robs the supply of oxygen and nutrients to the tissues, triggering a switch from aerobic metabolism to anaerobic metabolism and the production of lactic acid. Systemwide, this leads to a state of metabolic acidosis. When coupled with the serum presence of multiple inflammatory mediators, there is a direct myocardial depressive effect, decreasing the heart’s ability to respond to the sympathetic nervous system’s call for a compensatory increase in heart rate and contractility. Finally, the alveolocapillary membranes of the lungs are exposed to large numbers of inflammatory mediators, having the entire cardiac output pass through this capillary system with each cardiac cycle. The increased permeability directly decreases the exchange of gasses across the alveolocapillary membrane, effectively filling the alveoli with plasma and cells and deactivating surfactant. Frequently, the lungs are the first organ system to fail, necessitating mechanical ventilation with high concentrations of oxygen and the use of positive end expiratory pressure (PEEP) to improve gas exchange.
Similar to the compliment system is the clotting cascade; it also is a system of plasma proteins and cofactors found in the serum. Once activated, it leads to the cascading activation of each link in series, ending in the formation of the fibrin meshwork associated with clotting. This cascade also leads to the release of proinflammatory factors, which further amplifies the response. As with the compliment system, there are protective antifactors found within the cascade, which function in the control and reduction of the cascade effect. In sepsis, the systemic response magnifies at such a rapid rate, both the compliment and clotting system antifactors are ineffective.1 The final backup system to become involved is the kinin system, working primarily through the mediator bradykinin, causing the continuation of vascular permeability, leading to the loss of plasma and cells from the vascular space into the surrounding tissues. In addition, bradykinin activates additional WBCs and causes the secretion of prostaglandins that directly irritate
The activation of the clotting cascade leads to the development of systemic microclotting, called disseminated intravascular coagulation (DIC), which depletes the clotting factors and platelets, leading to oozing and hemorrhage that is particularly problematic in surgical patients. This is clearly seen in several of Sally’s postoperative laboratory work results. The prothrombin time, INR, and activated partial thromboplastin time are used as indicators of the time
KIM A. NOBLE
138
required for a clot and fibrin to form. These 2 tests measure the activity of the clotting cascade in 2 different areas. To have both severely prolonged, as indicated by these results, indicates a widespread activation and depletion of clotting factors, as seen in DIC. Sally’s decreased platelet count would support the diagnosis of DIC, because it would indicate widespread platelet aggregation. The normal platelet count is 150,000 to 400,000, so Sally’s platelet count of 27,000 indicates a severe depletion, which will contribute to bleeding. Sally’s decreased hemoglobin (7.4) and 2,200-mL blood loss would seem excessive for the procedure and would confirm a coagulation disorder. Finally, an elevation in fibrin split products (also called fibrin degradation products or fibrin breakdown products) indicates the activity of the antifactors or the “brakes” of the clotting cascade, in a normal response, leading to the degradation of fibrin. An elevation in fibrin split products indicates excessive clotting and breakdown of clots and is diagnostic for the development of DIC.3 The presence of bacteria and inflammatory mediators in the serum are detected by the hypothalamus, causing an elevation of temperature, and a hypermetabolic state. This further taxes a system that has reached the maximum of functioning in an attempt to compensate for the hypovolemia and decreased vascular resistance. This is further complicated by the presence of an aged or suppressed immune system or preexisting medical disease.
Implications for the PACU Patient By applying the pathophysiological basis for SIRS to the patient you are recovering in the Phase I PACU, there are several direct implications for patient care as follows.
alveolocapillary membrane, requiring the use of mechanical ventilation. Condition permitting, Sally must be adequately paralyzed and sedated to allow for ease of ventilation. An ongoing assessment of the patient’s response to these agents, as well as lung sounds and ETT placement must be conducted. As ventilator settings are implemented, additional ABGs may be ordered. These results must be obtained and reported in a timely fashion and any new orders implemented. Frequently, the hypoxia associated with this disorder is refractory to increases in inspired oxygen, but the addition of PEEP keeps the alveoli open and improves the diffusion of gasses while not requiring the use of toxic oxygen concentrations. PEEP may have the negative effect of decreasing the cardiac output by reducing the venous return to the heart; therefore, the effectiveness of PEEP must be evaluated by using continuous hemodynamic monitoring. In addition, the correction of Sally’s reduced hemoglobin and hematocrit must be included to ensure adequate oxygen delivery to her tissues. Alteration in Fluid Balance
Sick Sally is in the early stages of septic shock and, therefore, has severe increases in vascular permeability leading to losses of large amounts of fluid from the vascular space into the interstitial spaces. This leads to the development of refractory hypotension despite aggressive hydration. Frequent monitoring of heart rate and blood pressure, pulmonary artery waveform tracing, as well as cardiac output and pulmonary capillary wedge pressures (PCWP) are needed. Sally’s admission PAP reading of 16/2 and PCWP of 3 mm Hg indicate a significant need of fluid administration. Urinary output must be monitored and reported and may be used as additional indices of fluid status.
Alteration in Gas Exchange
As with any other PACU patient, the maintenance of adequate gas exchange is the first nursing priority. Sick Sally’s low PO2 and saturation on her admission ABG indicate a significant barrier to normal gas exchange across the
Alteration in Cardiovascular Functioning
Sally’s history of CAD usually indicates a decrease in the lumen of the coronary vessels and the delivery of oxygen to myocardial tissue, adding additional risk for the development of
INFLAMMATION II
cardiac consequences in her hypermetabolic state. Her heart rate of 147 must be lowered because increases in heart rate lead to increased myocardial oxygen requirements, as well as a decrease in the time of ventricular filling and nutrient delivery to the myocardium. Improving Sally’s fluid status with the administration of blood products and crystalloids will ease the workload of the heart, as will the treatment with pharmacologic agents used to control the heart rate. These agents will require very careful monitoring because of their vasodilatory effects, applying further strain on the heart muscle. Serial electrocardiograms and cardiac enzyme measurements are needed to monitor Sally’s cardiac status. Pharmacologic agents may be used to protect and maintain an adequate cardiac blood supply. In addition to intropin, a chemical precursor of norepinephrine used to increase cardiac contractility and dose-related vasoconstriction of peripheral and renal arterioles, other pharmacologic agents may be used to augment preload, contractility, and afterload. These agents must be carefully titrated to hemodynamic effect. An additional risk for the delivery of oxygen to Sally’s myocardium is her low hemoglobin, which requires rapid and adequate correction with the administration of whole blood. With the administration of large quantities of banked blood products, there is the need to monitor Sally’s serum calcium, because the preservatives used in some blood preparations may deplete serum calcium, adding strain on the contractility of the heart.
139
will need the careful monitoring of all drainage tubes for bleeding, and the amount must be measured and reported. Alteration in Stress Response
Sally has a history of steroid-dependent COPD, and she will exhibit adrenal insufficiency when faced with the stressful situation of emergent surgery and critical illness. She will require the administration of stress doses of steroids and monitoring of their effect(s). The functioning of her immune system may be affected by the chronic use of exogenous steroids, as well as the condition of her connective tissue and her ability to heal a surgical wound. Sally’s blood sugar may also be elevated and require frequent monitoring and sliding scale insulin administration. Alteration in Temperature Regulation
Sally’s immediate postoperative fever is very troublesome because she had several factors that should contribute to a decrease in core body temperature, such as the cooling effect of the OR environment and the administration of cool blood products and intravenous and irrigation solutions. Sally has also been receiving long-standing steroid administration, leading to a decreased febrile response. Her elevation in temperature contributes to her hypermetabolic state, requiring an increase in oxygen consumption. Normothermia should be maintained through the administration of antipyretics and the use of a cooling blanket as needed. Potential for Septicemia
Potential for Bleeding
Sally’s admission laboratory data indicate the development of disseminated intravascular coagulation (DIC), a disorder resulting from massive stimulation of the clotting cascade, resulting in systemic microclotting and the depletion of platelets and clotting factors. Sally had a 2,200-mL blood loss in the OR and only received approximately 1,000 mL banked blood. This coupled with her postoperative Hgb of 7.4 will require the administration of packed cells, as well as fresh frozen plasma and platelets. She
A final need of Sally is for the treatment of her underlying disorder, sepsis, leading to the development of SIRS. Culturing of blood, urine, sputum, wounds, and invasive lines are needed to isolate the causative organism and to identify specific antibiotic sensitivities. Broad spectrum antibiotics will be ordered and should be given on a routine basis.4 A deterioration of Sally’s condition should be expected with antibiotic administration because as the gram-negative bacteria lyse and die, there will be an increased release of endotoxin, further triggering inflam-
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matory mediator release. Once the microorganism sensitivities are identified, appropriate antibiotic selections may be made. Sick Sally represents a critically ill patient exhibiting an extreme response to an inflammatory trigger. Her care would require intensive Phase I management, and through the application of the pathophysiology to the disease process, a PACU nurse is better equipped to anticipate the
needs of this very challenging postanesthesia patient.
Acknowledgments The author thanks her coworkers in Phases I and II and the Anesthesia Department at Jeanes Hospital in Philadelphia, PA—a very special group of people who have served as consultants, editors, and friends.
References 1. McCance KL, Huether SE: Pathophysiology: The Biologic Basis for Disease in Adults & Children (ed 4). St. Louis, MO, Mosby, 2002 2. Urden LD, Stacy KM, Lough ME: Thelan’s Critical Care Nursing: Diagnosis and Management (ed 4). St. Louis, MO, Mosby, 2002
3. McMorrow ME, Malarkey L: Laboratory and Diagnostic Tests: A Pocket Guide. Philadelphia, PA, Saunders, 1998 4. Drain CB: PeriAnesthesia Nursing: A Critical Care Approach (ed 4). St. Louis, MO, Saunders, 2003